D

Daily Diary daily activities and transactions of everyday life.

Daily stress is relatively minor, but has the
▶ Diaries potential to disrupt the flow of everyday life and
add to overall levels of stress.
Daily stress can be both anticipated and
unanticipated. Anticipated daily stressors include,
Daily Hassles for example, driving in rush hour traffic on the way
home from work, paying bills, working long
▶ Daily Stress hours, job performance evaluations, or taking
children to after-school activities. Unanticipated
stressors may include arguments with spouse,
car trouble, getting stuck in long lines at the
Daily Mood Variation grocery store, getting sick, losing one’s keys, or
inconveniences due to weather.
▶ Diurnal Mood Variation

Description

Daily Stress Daily stressors are not inherently stressful events,

C. Renn Upchurch Sweeney
VA Salt Lake City Healthcare System,
Salt Lake City, UT, USA
Synonyms
Daily hassles; Everyday problems
Definition
Daily stress is defined as mundane hassles,
strains, or annoyances associated with routine
but they are events that people might appraise as
stressful. The experience of feeling stressed
depends on what events one notices and how
one appraises or interprets these events, which
is referred to as the “primary appraisal.” Events
that are stressful for one person may be routine
for another. For example, one may see an
upcoming job interview as an exciting
opportunity. Others may view it as terrifying.
Theoretically, the person then engages in
a “secondary appraisal” to determine the ade-
quacy of personal and social resources for dealing
with the stressor.
Daily stress is different from major life stressors
such as getting married, death of a loved one, or

M.D. Gellman & J.R. Turner (eds.), Encyclopedia of Behavioral Medicine,

DOI 10.1007/978-1-4419-1005-9, # Springer Science+Business Media New York 2013
D 538
divorce. Unlike life events that call for people to
make adjustments to their lives, daily hassles are
part of everyday life. Daily stress is more frequent
and continuous form of stress than less frequent
events that constitute major life stressors. Because
of its frequency it may be a more important deter-
minant of stress than major life stressors.
Daily stress and minor hassles have been found
to be important forms of stress. Research indicates
that routine hassles may have significant harmful
effects on mental and physical health (i.e., declines
in physical health such as headaches or backaches
or worsening of symptoms in those already suffer-
ing from illness). Minor hassles can produce stress
and aggravate physical and psychological health in
several ways. First, the effect of minor stressors
can be cumulative. Each hassle may be relatively
unimportant in itself, but after a day filled with
minor hassles, the effects add up. The cumulative
impact of small stressors may wear down an indi-
vidual until the person eventually feels
overwhelmed, drained, grumpy, or stressed out.
The aggregate effects of everyday hassles have
the potential to compromise well-being or predis-
pose an individual to become ill. Second, daily
stress can contribute to the stress produced by
major life stressors and influence the relationship
between major life events and illness. That is, daily
stress can contribute to the stress produced by
major life events. If a major life event is experi-
enced at a time when minor life events are also
high in number, the stress may be greater than it
would otherwise be. Alternatively, major life
events, either positive or negative, can also affect
distress by increasing the number of daily hassles
they create.
References and Readings
Cooper, C. L., & Derre, P. (2007). Stress: A brief history
from the 1950s to Richard Lazarus. In A. Monat, R. S.
Lazarus, & G. Reevy (Eds.), The Praeger handbook on
stress and coping (2007th ed., Vol. 1, pp. 7–31).
Westport, CT: Greenwood Publishing.
Kohn, P. M. (1996). On coping adaptively with daily
hassles. In M. Zeidner & N. S. Endler (Eds.),
Handbook of coping: Theory research, & applications
(pp. 181–201). Oxford, England: Wiley.
Dangerous Drinking
Taylor, S. (2006). Health psychology (6th ed.). New York:
McGraw-Hill.
Weiten, W. (1995). Themes and variations (3rd ed.).
Pacific Groove, CA: Brooks/Cole.
Dangerous Drinking
▶ Binge Drinking
Data
J. Rick Turner
Cardiovascular Safety, Quintiles, Durham,
NC, USA
Synonyms
Numerical information; Numerical representa-
tion of (biological, psychological, behavioral)
information
Definition
Data is a plural construct indicating more than
one piece of numerical information. The singular
form of the term is datum. Statistical analysis
(certainly of the type useful in the discipline of
behavioral medicine) almost always uses more
than one piece of numerical information, and
the term datum does not occur again in any
other methodology entry in this encyclopedia.
Description
Accordingly, plural words are used in conjunc-
tion with the word data: “the data are, the data
were, these data, the data show, etc.” If you are
uncertain as to how to construct a phrase includ-
ing the word data, replace the word data in your
mind with the word results. While the terms data
and results are not truly synonymous, the word
results is also a plural construct. This strategy will
Database Development and Management 539 D
therefore likely help you express a phrase includ- data (their age in years and months) they contrib-
ing the word data correctly. ute equally to the total number of subjects in that
Data can generally be classified into one of the category.
following scales of measurement: nominal, ordi-
nal, and ratio. Nominal scales involve names of
Cross-References
characteristics. Common examples from behav-
ioral medicine include sex (male and female sub-
▶ Efficacy
jects in a research study) and race or ethnicity. An
▶ Sample Size Estimation D
ordinal scale is defined as one in which an order-
ing of values can be assigned. Age of study sub-
jects categorized as less than 25 years of age,
25–30 years of age, and 31 years of age and
Database Development and
older is one example. Data measured on a ratio
Management
scale can be manipulated in certain ways not
possible with the previous scales. For example,
J. Rick Turner
someone weighing 220 pounds (lbs) can be said
Cardiovascular Safety, Quintiles, Durham,
to weigh twice as much as another subject
NC, USA
weighing 110 lbs. The same applies for height
and age. The feature of the ratio scale that makes
such comparisons possible is that the value of
Definition
zero on the scale represents a true zero – a weight
of zero and a height of zero (no matter what the
The goal of experimental methodology and oper-
unit of measurement) means that there is no
ational execution in behavioral medicine
weight or height, respectively.
research, like all research, is to provide optimum
You may have noticed what appears to be an
quality data for subsequent statistical analysis
initial contradiction in the previous paragraph:
and interpretation. These data need to be stored
Age is discussed in both the ordinal scale and
and managed. Databases facilitate such storage
the ratio scale discussions. The reason for this
and management. Data management is therefore
apparent paradox is that data can be measured
an important intermediary between data acquisi-
(recorded) on one scale but reported on another.
tion and data analysis.
Imagine that 100 subjects participate in a
research study, and each of their ages is recorded
in years and months. Then, for various reasons, Description
the subjects are each placed into one of three
ordinal categories: those aged less than 25 years Analysis of data collected in behavioral medicine
of age, 25–30 years of age, and 31 years of age clinical trials is typically conducted using files of
and older. This is perfectly acceptable, but any data contained in a database. It is of critical
statistical analysis performed would have to take importance that the data collected from all
into account the scale on which the data are sources are accurately captured in the database.
reported: Different analyses are appropriate for A brief list of such data includes: subject identi-
different kinds of data. fiers (rather than their names); age, sex, height,
It is also of interest to note that, while it and weight; questionnaire data concerning
may be convenient to report the subjects’ ages a multitude of topics; and physiological measure-
in this ordinal fashion, a certain degree of preci- ments made before, during, and possibly after the
sion in the information is lost. For example, two treatment period(s).
subjects aged 26 and 29 years, respectively, A data management plan for a clinical trial is
would both be placed in the middle category. written along with the study protocol and possi-
Therefore, although they provide different raw bly a statistical analysis plan before the study
D 540
commences (statistical details can also be
included in the study protocol). The data man-
agement plan identifies the documentation that
will be produced as a result of all of the data
collected during the conduct of the trial. This
plan covers items such as:
• The form(s) on which raw (source) data will
be recorded.
• Entering data.
• Cleaning the data.
• Creating data reports.
• Transferring data.
• Quality assurance processes.
The quality assurance (QA) component is
vital. While differing definitions of quality activ-
ities can be found, Prokscha (2007) defined qual-
ity assurance (QA) as a process involving the
prevention, detection, and correction of errors or
problems, and quality control (QC) as a check of
the process. The data stored in the database need
to be complete and accurate. Processes that check
data and correct them where necessary (i.e., make
a change to the database) need to be formalized,
and all corrections documented in an audit trail
such that a later audit can reveal exactly how the
final database was created. That is, following
initial data entry, the audit trail will record
“who, what, when, why” information for all
changes subsequently made.
Having collected optimal quality data, first-rate
data management is also critical. Many data that
are collected can now be fed directly from the
measuring instrument to computer databases,
thereby avoiding the potential of human data
entry error. However, this is not universally true.
Therefore, careful strategies have been developed
to scrutinize data as they are entered. The double-
entry method requires that each data set is entered
twice (usually by different operators) and that
these entries are compared by a computer for any
discrepancies. This method operates on the pre-
mise that two identical errors are probabilistically
very unlikely, and that every time the two entries
match the data are correct. In contrast, dissimilar
entries are identified, the source data located, and
the correct data point entry confirmed.
To facilitate the eventual statistical analysis of
the enormous amount of data acquired during a
Database Development and Management
clinical trial, recording and maintaining them
is extremely important. Database development,
implementation, and maintenance therefore
require attention. The goals of a database are to
store data in a manner that facilitates prompt
retrieval while not diminishing their security or
integrity.
There are several types of database models.
Clinical research typically utilizes one of two
types, the flat file database or the relational data-
base. Each has its advantages and disadvantages,
and these will be considered by data managers
before they decide which type to employ. The
flat file database model is simple but restrictive,
and it becomes less easy to use as the amount of
data stored increases. This model can also lead
to data redundancy (the same information, e.g.,
a subject’s birth date, being entered multiple
times) and consequently to potential errors.
This model works well for relatively small
databases.
Relational databases are more flexible, but
they can be complex, and careful initial work is
needed. This work involves initial logical model-
ing of the database. The defining feature of
a relational database is that data are stored in
tables, and these tables can be related to each
other. This reduces data redundancy. Subject
identifiers in one table, for example, can be
related to their heights in another table, their
baseline blood pressure in another table, and so
on, thereby eliminating the need to store identi-
fiers with each individual set of measurements.
Since these databases can contain huge amounts
of tables, use of one of several commercially
available relational database management sys-
tems is typical.
Cross-References
▶ Study Protocol
References and Readings
Prokscha, S. (2007). Practical guide to clinical data man-
agement (2nd ed.). Boca Raton, FL: Taylor & Francis.
Death Anxiety
Dean Ornish
▶ Ornish Program and Dean Ornish
▶ Preventive Medicine Research Institute
(Ornish)
Death
▶ Mortality
Death Anxiety
Chad Barrett
Department of Psychology, University of
Colorado Denver, Denver, CO, USA
Synonyms
Fear of Death; Thanatophobia
Definition
Death anxiety refers the fear of and anxiety
related to the anticipation, and awareness, of
dying, death, and nonexistence. It typically
includes emotional, cognitive, and motivational
components that vary according to a person’s
stage of development and sociocultural life expe-
riences (Lehto & Stein, 2009). Death anxiety is
associated with fundamental brain structures that
regulate fight-or-flight responses and record emo-
tionally charged explicit and implicit memories
(Panksepp, 2004). Cognitive dimensions of death
anxiety can include an awareness of the salience
of death and a variety of beliefs, attitudes,
images, and thoughts concerning death, dying,
and what happens after death (Lehto & Stein,
2009). Death anxiety can be experienced con-
sciously or unconsciously; it can motivate indi-
viduals to ameliorate their death anxiety through
distraction (Greenberg, Pyszczynski, Solomon,
Simon, & Breus, 1994), attempts to enhance
541 D
self-esteem (Bassett, 2007), or by pursuing posi-
tive life changes (Tedeschi & Calhoun, 2004).
Individuals experiences of death anxiety can be
influenced by their developmental stage. Young
adults are mostly concerned about dying too
soon, and adult parents are mostly concerned
about the effect of their possible death on other
family members. Elderly adults are often more
concerned with becoming a burden on others, D
dying alone, or dying among strangers
(Kastenbaum, 2000). Sociocultural influences
can also shape the cognitive, experiential, and
emotional components of death anxiety (K€ubler-
Ross, 2002; Lehto & Stein, 2009).
Description
Most people report some fear of death, but only
a few people report high levels of death anxiety
(Kastenbaum, 2000). According to Noyes et al.
(2000), only 3.8% of respondents indicated that
they were much more nervous than most people
about death or dying, and 9.8% indicated they
were somewhat more nervous than most people.
Stressful experiences can often increase a person’s
level of death anxiety, (e.g., life-threatening
encounters, tragedies, disasters, health problems,
illness, or death of a friend or family member, etc.)
(Kastenbaum). A meta-analysis of research on
death attitudes among older adults indicated that
health problems were associated with elevated
levels of death anxiety (Fortner & Neimeyer,
1999). In a later review of the literature on death
attitudes, Neimeyer, Wittkowski, and Moser
(2004) noted that the relationship between death
anxiety and health problems is sometimes equiv-
ocal. While many studies found positive associa-
tions between health problems and death anxiety,
others found no significant relationship. Neimeyer
et al. discussed more sophisticated studies and
that such conflicting findings may be the result of
moderator variables such as social support, coping
styles, and religious beliefs. Increased social sup-
port, approach- and acceptance-based coping
strategies, intrinsic religiosity, and beliefs in
a positive afterlife are typically associated with
less death anxiety.
D 542
Cross-References
▶ End-of-Life Care
▶ Palliative Care
References and Readings
Bassett, J. A. (2007). Psychological defenses against death
anxiety: Integrating terror management theory and
Firestone’s separation theory. Death Studies, 31,
727–750.
Fortner, B. V., & Neimeyer, R. A. (1999). Death anxiety in
older adults: A quantitative review. Death Studies, 23,
387–411.
Greenberg, J., Pyszczynski, T., Solomon, S., Simon, L., &
Breus, M. (1994). Role of consciousness and accessi-
bility of death-related thoughts in mortality salience
effects. Journal of Personality and Social Psychology,
67, 627–637.
Kastenbaum, R. (2000). The psychology of death (3rd ed.).
New York: Springer.
K€ubler-Ross, E. (2002). On death and dying: Questions
and answers on death and dying; on life after death.
New York: Quality Paper Book Club.
Lehto, R. H., & Stein, K. F. (2009). Death anxiety:
An analysis of evolving concept. Research and Theory
for Nursing Practice: An International Journal, 23,
23–41.
Neimeyer, R. A., Wittkowski, J., & Moser, R. P. (2004).
Psychological research on death attitudes: An over-
view and evaluation. Death Studies, 28, 309–340.
Noyes, R., Jr., Hartz, A. J., Doebbeling, C. C., Malis,
R. W., Happel, R. L., Werner, L. A., et al. (2000).
Illness fears in the general population. Psychosomatic
Medicine, 62, 318–325.
Panksepp, J. (2004). The foundations of human and animal
emotions. New York: Oxford University Press.
Tedeschi, R. G., & Calhoun, L. G. (2004). Posttraumatic
growth: Conceptual foundations and empirical
evidence. Psychological Inquiry, 15, 1–18.
Death Rate
▶ Mortality Rates
Death, Assisted
▶ Euthanasia
Death Rate
Death, Sudden
Ana Victoria Soto1 and William Whang2
1
Medicine – Residency Program, Columbia
University Medical Center, New York, NY, USA
2
Division of Cardiology, Columbia University
Medical Center, New York, NY, USA
Synonyms
Sudden cardiac death
Definition
Death within 1 h of the onset of acute symptoms.
Description
Sudden cardiac death (SCD) is an important
public health problem, with an annual incidence
estimated between 180,000 and 250,000 cases in
the United States. The working definition of SCD
is death within 1 h of the onset of symptoms, in
the absence of preceding evidence of severe
pump failure. In prior decades, the majority of
SCD cases have been estimated to occur due to
rapid cardiac arrhythmia, specifically ventricular
tachycardia (VT) and ventricular fibrillation
(VF). More recent data indicate that VT/VF is
the presenting rhythm in SCD about 30–40% of
the time. SCD may also occur due to life-
threatening slow heart rhythms (bradycardia) or
due to other causes such as massive pulmonary
embolism or intracranial hemorrhage (Hinkle &
Thaler, 1982; Lloyd-Jones et al., 2010).
In prospective cohort studies, women have
a lower incidence of sudden death than men.
Coronary artery disease (CAD) is the most com-
mon finding in SCD and is discovered in as many
as 80% of SCD cases. However, among the large
population of patients with coronary artery dis-
ease, the absolute risk of SCD is still low. In
addition, a substantial proportion of SCDs occur
in the absence of known prior heart disease.
Death, Sudden
Clinical risk factors for SCD have been devel-
oped, and the most reliable of which is reduced
left ventricular ejection fraction by cardiac imag-
ing such as echocardiogram. However, the
prevailing clinical indicators of risk are still lim-
ited in their specificity, and identification of indi-
viduals at high risk remains a major challenge
(Chugh et al., 2008).
Two major mechanisms have been implicated
in SCD in the setting of CAD. First, acute plaque
rupture may lead to coronary artery occlusion,
inadequate blood flow to cardiac muscle (ische-
mia), and subsequent VT and VF. Another poten-
tial mechanism related to CAD results from the
presence of myocardial scar from a prior myocar-
dial infarction. With this myocardial substrate,
heterogeneity in depolarization and conduction
can allow for the development of reentry, in
which a tachycardia circuit develops and which
manifests as VT that can eventually degenerate to
VF. Other underlying cardiac abnormalities can
also predispose to SCD. For instance, cardiomy-
opathies due to causes other than CAD (e.g.,
alcohol, long-standing hypertension, sarcoidosis)
are also associated with SCD. In addition, pri-
mary electrical abnormalities, such as inherited
ion channel disorders, are relatively rare but
potent causes of sustained ventricular arrhythmia
in the absence of structural heart disease
(Virmani, Burke, & Farb, 2001).
The major treatment against SCD is a preven-
tive therapy, the implantable cardioverter-
defibrillator. Randomized controlled trials of
primary prevention ICD therapy have demon-
strated survival benefit in patients with left
ventricular ejection fraction <0.36 and with
symptoms of congestive heart failure (Bardy
et al., 2005; Moss et al., 2002).
A number of studies have noted an association
between psychosocial factors, in particular
depression, and SCD. For instance, Empana
et al. examined data from enrollees of a health
maintenance organization in Washington state, in
a case control study involving 2,228 out-of-
hospital cardiac arrests. Cases of out-of-hospital
cardiac arrest (n ¼ 2,228) among patients aged
40–79 years were identified from emergency
medical service incident reports, and their
543 D
ambulatory medical records were examined for
the existence of depression. Compared with
nondepressed subjects, the adjusted odds ratio
of cardiac arrest was increased in less severely
depressed subjects (OR 1.30, 95% CI 1.04–1.63)
and further increased in severely depressed (OR
1.77, 95% CI 1.28–2.45) (Empana et al., 2006).
In a cohort analysis involving 915 individuals
aged 70 years or older in northern Finland, D
Luukinen et al. found that depression was asso-
ciated with increased risk of sudden death (HR
2.74, 95% CI 1.37–5.50), whereas the risk of non-
sudden death was not significantly increased.
(Luukinen, Laippala, & Huikuri, 2003) In the
Nurses’ Health Study of 63,000 female nurses
without known cardiovascular disease at study
outset, cohort analyses indicated a significant
association between depression and SCD in mul-
tivariable models that included hypertension, dia-
betes, and hypercholesterolemia (HR 2.33, 95%
CI 1.47–3.70). The relationship of depression at
study outset to subsequent SCD appeared to be
related to a specific association with antidepres-
sant use (Whang et al., 2009). A separate cohort
analysis of the Nurses’ Health Study included
72,359 women with no history of cardiovascular
disease or cancer in 1988 and used the Crown-
Crisp Index to assess phobic anxiety. During
12 years of follow-up, women who scored 4 or
greater on the CCI were at higher risk of SCD (HR
1.59, 95% CI 0.97–2.60). After adjustment for
possible intermediaries (hypertension, diabetes,
and elevated cholesterol), a trend toward increased
risk persisted for SCD (P ¼ 0.06) (Albert, Chae,
Rexrode, Manson, & Kawachi, 2005).
Cross-References
▶ Sudden Cardiac Death
References and Readings
Albert, C. M., Chae, C. U., Rexrode, K. M., Manson, J. E.,
& Kawachi, I. (2005). Phobic anxiety and risk of
coronary heart disease and sudden cardiac death
among women. Circulation, 111(4), 480–487.
D 544 Decision Analysis

Bardy, G. H., Lee, K. L., Mark, D. B., Poole, J. E.,

Packer, D. L., Boineau, R., et al. (2005). Amiodarone Decision Making
or an implantable cardioverter-defibrillator for conges-
tive heart failure. The New England Journal of
Medicine, 352(3), 225–237. ▶ Clinical Decision-Making
Chugh, S. S., Reinier, K., Teodorescu, C., Evanado, A.,
Kehr, E., Al Samara, M., et al. (2008). Epidemiology
of sudden cardiac death: Clinical and research impli-
cations. Progress in Cardiovascular Diseases, 51(3),
213–228.
Empana, J. P., Jouven, X., Lemaitre, R. N., Sotoodehnia, N., Deep Sleep
Rea, T., Raghunathan, T. E., et al. (2006). Clinical
depression and risk of out-of-hospital cardiac arrest. ▶ Slow-Wave Sleep
Archives of Internal Medicine, 166(2), 195–200.
Hinkle, L. E., Jr., & Thaler, J. T. (1982). Clinical classifi-
cation of cardiac deaths. Circulation, 65, 457–464.
Lloyd-Jones, D., Adams, R. J., Brown, T. M., Carnethon, M.,
Dai, S., De Simone, G., et al. (2010). Executive
summary: Heart disease and stroke statistics–2010 Defense Mechanism
update: A report from the American Heart Association.
Circulation, 121(7), 948–954.
Luukinen, H., Laippala, P., & Huikuri, H. V. (2003). ▶ Denial
Depressive symptoms and the risk of sudden cardiac
death among the elderly. European Heart Journal,
24(22), 2021–2026.
Moss, A. J., Zareba, W., Hall, W. J., Klein, H.,
Wilber, D. J., Cannom, D. S., et al. (2002). Prophylac-
tic implantation of a defibrillator in patients with
Defensive Coping
myocardial infarction and reduced ejection fraction.
The New England Journal of Medicine, 346(12), ▶ Defensiveness
877–883.
Virmani, R., Burke, A. P., & Farb, A. (2001). Sudden
cardiac death. Cardiovascular Pathology, 10, 211–218.
Whang, W., Kubzansky, L. D., Kawachi, I.,
Rexrode, K. M., Kroenke, C. H., Glynn, R. J., et al.
(2009). Depression and risk of sudden cardiac death Defensive Denial
and coronary heart disease in women: Results from the
Nurses’ Health Study. Journal of the American
▶ Defensiveness
College of Cardiology, 53(11), 950–958.

Decision Analysis
Defensiveness
▶ Clinical Decision-Making
Carolyn Korbel1 and Sonia Matwin2
1
The Neurobehavioral Clinic and Counseling
Center, Lake Forest, CA, USA
Decision Authority 2
Department of Psychiatry, Harvard Medical
School, Boston, MA, USA
▶ Job Demand/Control/Strain

Synonyms
Decision Latitude
Avoidant coping; Defensive coping; Defensive
▶ Job Demand/Control/Strain denial; Repression; Repressive coping
Defensiveness
Definition
Defensiveness is defined as a coping strategy that
is characterized by a general orientation away
from threatening self-relevant information and
a denial or minimization of negative affects
such as distress, anxiety, or anger.
Description
Defensiveness is characterized by a general
orientation away from threatening self-relevant
information and a denial or minimization of
negative affects such as distress, anxiety, or
anger (Weinberger, Schwartz, & Davidson,
1979). Self-relevant information that is perceived
as being inconsistent with personal goals and
beliefs is likely to trigger defensive coping reac-
tions (Croyle, Sun, & Hart, 1997). Defensiveness
appears to occur normatively in response to self-
relevant health risk information, but also to vary
across individuals as a more enduring orientation
to coping with distress. There is much conceptual
overlap between defensiveness, repressive cop-
ing, avoidant coping, and denial in the literature,
in that each share a core coping process of min-
imizing, denying, or repressing distress, negative
affect, or distressing information to serve emo-
tion regulation goals (Myers, 2010).
Defensiveness has been most frequently
assessed through the use of measures of
self-reported defensiveness (Weinberger et al.,
1979), such as the Marlowe-Crowne Social
Desirability Scale (MCSD; Crowne & Marlowe,
1960). Those who score high on social desirabil-
ity are thought to minimize, deny, or repress
negative emotions such as anxiety and anger,
reflecting a defensive or self-deceptive
orientation to the self that involves avoidance
of distress-arousing thoughts. Measures of
self-reported trait anxiety are also frequently
used in conjunction with the MCSD to identify
those who minimize or deny negative affects and
who score high on defensiveness to capture a true
defensive or, interchangeably, repressive coping
group (Myers, 2010; Weinberger et al., 1979).
Those who have a defensive or repressive coping
545 D
style are less likely to report negative affect,
distress, somatic symptoms, and chronic
stress across a variety of tasks, experimental
conditions, and self-report measures. Although
defensive/repressive copers deny distress in
response to stressful experimental conditions,
physiological indicators of distress are often
observed.
Defensiveness occurs rather frequently in the D
population. It has been estimated that 10–20% of
the general population, 30–50% of those with
particular chronic illnesses, and up to 50% of
the elderly use defensive or repressive coping
strategies (see Myers, 2010 for a review). In the
context of behavioral medicine, defensiveness
appears to prompt cognitive, behavioral,
and physiological variations, which may have
important implications for health. Specifically,
the current literature suggests that:
1. Defensiveness is associated with information
processing variations that occur normatively
in response to self-relevant health threat
information.
2. Defensiveness may have direct effects on
physiological functioning.
3. Defensiveness is associated with greater
morbidity and mortality in a number of
chronic illnesses and disease states.
Defensive Cognitive Processing
Defensiveness influences the way that informa-
tion is processed when threatening self-relevant
information is perceived. Defensive cognitive
processing variations appear to occur norma-
tively in response to perceiving personally threat-
ening health risk information. Defensive denial
processes tend to appear early in the health-threat
appraisal process and tend to diminish over time.
They are less extreme when individuals are aware
of direct actions to eliminate the threat, and
are less common when positive states and
experiences (e.g., positive mood, optimism,
self-affirmation) are bolstered prior to threat
perception, or when active coping alternatives
are available and reasonable to execute.
Defensive cognitive processing variations such
as (a) minimization of the seriousness of health
threats, (b) self-serving prevalence estimates,
D 546
(c) tendencies to denigrate the accuracy or valid-
ity of an undesirable test result, and (d) biased
processing of health risk information occur
frequently in response to perceived health-threat
information. These normative defensive pro-
cesses may play an important role in regulating
emotional distress in the short term so that
rational health-protective actions can be
identified, enacted, and maintained (Croyle
et al., 1997; Wiebe & Korbel, 2003).
Physiological Effects of Defensiveness
An emerging literature has identified links
between a generalized defensive or repressive
coping style and physiological variations in
responding which may have direct impacts on
health (see Myers, 2010 for a review). It has
been hypothesized that the effort required to
repress, minimize, or deny negative thoughts
and emotions characteristic of defensive coping
may result in heightened autonomic reactivity
and may impact cardiovascular arousal. Defen-
siveness has been associated with increased
cardiovascular reactivity to stress via increased
sympathetic demand when defensive processes
are initiated and maintained. Homeostatic
changes in baseline cardiovascular functioning
are thought to occur over time in response to
increased sympathetic reactivity. Cardiovascular
disease risk may be increased in defensives
through a physiological mechanism of increased
stress reactivity, possibly triggering changes in
vascular functions or structure that may alter
resting blood pressure levels.
Increased Prevalence of Morbidity and
Mortality among Defensive Copers
There is an extensive body of literature that links
trait-like defensive and repressive coping with
poor physical health (see Myers et al., 2007 for
a comprehensive review). Repressive/defensive
coping appears to both contribute to poor health
and disease progression, and to also be used more
frequently among those with chronic illnesses.
There is a fairly extensive literature linking
repressive coping with increased risk for mortal-
ity in coronary heart disease (CHD) and myocar-
dial infarction (MI). Repressive coping is
Defensiveness
associated with a twofold increased risk of
death, MI, and other cardiac events. In addition,
heightened levels of defensiveness are associated
with hypertension, high blood pressure, as well as
high lipid and glucose levels. For example, high
scores on the MCSD have been associated with
elevated blood pressure and heart rate reactivity.
Additional support for the association between
defensiveness and elevated blood pressure in the
general population was found in Jorgensen,
Johnson, Kolodziej, and Schreer (1996)
meta-analysis. Further, a meta-analysis by
Mund and Mitte (2011) suggested that repressive
copers are at greater risk of developing cancer
and coronary heart disease.
Cross-References
▶ Cancer Risk Perceptions
▶ Cognitive Distortions
▶ Coping
▶ Defensive Coping
▶ Denial
▶ Health Behaviors
▶ Repressive Coping
References and Readings
Crowne, D. P., & Marlowe, D. (1960). A new scale of
social desirability independent of psychopathology.
Journal of Consulting Psychology, 24(4), 349–354.
Croyle, R. T., Sun, Y., & Hart, M. (1997). Processing risk
factor information: Defensive biases in health-related
judgments and memory. In K. Petrie & J. Weinman
(Eds.), Perceptions of health and illness: Current
research and applications (pp. 267–290). London:
Harwood Academic.
Jorgensen, R. S., Johnson, B. T., Kolodziej, M. E., &
Schreer, G. E. (1996). Elevated blood pressure and
personality: A meta-analytic review. Psychological
Bulletin, 120(2), 293–320.
Mund, M., & Mitte, K. (2011). The costs of repression:
A meta-analysis on the relation between repressive
coping and somatic diseases. Health Psychology.
doi:10.1037/a0026257. Nov 14, 2011 (No pagination
specified).
Myers, L. (2010). The importance of the repressive coping
style: Findings from 30 years of research. Anxiety,
Stress, and Coping, 23(1), 3–17.
Degenerative Diseases: Disc or Spine
Myers, L., Burns, J. W., Derakshan, N., Elfant, E.,
Eysenck, M. W., & Phipps, S. (2007). Current issues
in repressive coping and health. In J. Denollet, I.
Nyklicek, & A. Vingerhoets (Eds.), Emotion regula-
tion: Conceptual and clinical issues (pp. 69–86). New
York: Springer.
Weinberger, D. A., Schwartz, G. E., & Davidson, R. J.
(1979). Low-anxious, high-anxious and repressive
coping styles: Psychometric patterns and behavioral
responses to stress. Journal of Abnormal Psychology,
88, 369–380.
Wiebe, D. J., & Korbel, C. (2003). Defensive denial,
affect, and the self-regulation of health threats. In L.
Cameron & H. Leventhal (Eds.), The self-regulation of
health and illness behavior (pp. 184–203). New York:
Harwood Academic.
Degenerative Diseases: Disc or Spine
Daniel Gorrin
Department of Physical Therapy, University of
Delaware, Newark, DE, USA
Definition
The intervertebral disc is a structure located
between adjacent vertebral bodies that functions
primarily as a shock absorber. The disc is com-
prised of a fibrocartilaginous outer layer called
the annulus fibrosus and a gelatinous inner
layer called the nucleus pulposus (made up of
collagen fibrils embedded within a water/
mucopolysaccharide mix). The disc is connected
to the cartilaginous end plates located on the
cranial and caudal aspects of the vertebral bodies.
The end plates assist in providing the disc with
nutrients.
Degenerative disc disease is a potential cause
of back pain marked by an atraumatic, gradual
onset of symptoms. Due to its primary function as
a shock absorber, the disc is subject to significant
“wear and tear” during the course of a lifetime.
As the patient increases in age, the disc may
undergo a degenerative process in which water
is lost from the nucleus pulposus and replaced
with fibrocartilage. Systemic, cellular, and
biochemical changes related to aging may also
contribute to degeneration of the disc. Pain
547 D
resulting from degenerative disc disease is
thought to be caused by a combination of irrita-
tion of the disc’s nociceptive fibers and inflam-
matory products found within the damaged disc.
The degenerative process can also affect the
outer layer of the disc, the annulus fibrosis, which
could increase the risk of a herniation of the
nucleus pulposus. Tears in the annulus or degen-
eration of the annulus can limit the structure’s D
ability to contain the gel-like nucleus. Release
of the nucleus can cause impingement and irrita-
tion of the surrounding spinal nerve roots or even
the spinal cord itself. This condition (commonly
referred to as a “bulging” or “herniated” disc) can
result in localized pain at the site of the herniation
or pain in the areas supplied by the nerve
(radiculopathy).
Patients who experience degenerative disc
disease or a disc herniation are likely to regain
full function with non-operative treatment. Phys-
ical therapy interventions including mobilization,
manipulation, traction, core stabilization exer-
cises, electrical stimulation, and biofeedback are
used in treatment of these conditions. Appropri-
ate pharmacological intervention, nerve root
injections, and epidural injections can also help
provide pain relief. Operative treatment may be
indicated if the patient presents with severe
neurological deficits or receives no benefit from
conservative treatment.
References and Readings
Boyling, J. D., & Palastanga, N. (1994). Grieve’s modern
manual therapy (2nd ed.). New York: Churchill
Livingstone.
Drake, R. L., Wayne Vogl, A., & Mitchell, A. W. M.
(2010). Gray’s anatomy for students (2nd ed.).
Philadelphia: Churchill Livingstone Elsevier.
Magee, D. J., Zachazewski, J. E., & Quillen, W. S. (2009).
Pathology and intervention in musculoskeletal reha-
bilitation (1st ed.). St. Louis, MO: Saunders Elsevier.
McGill, S. (2002). Low back disorders: Evidence based
prevention and rehabilitation (1st ed.). Champaign,
IL: Human Kinetics.
Yue, J. J., Guyer, R. D., Johnson, J. P., Khoo, L. T., &
Hochschuler, S. H. (2011). The comprehensive treat-
ment of the aging spine: Minimally invasive and
advanced techniques (1st ed.). Philadelphia: Elsevier
Saunders.
D 548
Degenerative Diseases: Joint
Beth Schroeder
University of Delaware, Newark, DE, USA
Synonyms
Chronic inflammatory polyarthritis; RA
Definition
Rheumatoid arthritis (RA) is a chronic inflamma-
tory condition that affects the synovium of joints
in the body. While the exact cause of RA is
unknown, it is considered to be an autoimmune
condition, in which the body attacks its own
healthy cells. In a normal, healthy joint, the syno-
vial membrane provides synovial fluid that
functions to reduce friction and lubricate the
joint surfaces and to provide nutrients to the car-
tilage. With RA, the synovial membrane becomes
inflamed and thickens, forming a pannus.
A pannus is an accumulation of tissue that ulti-
mately causes damage to structures in the joint
capsule, such as the cartilage, subchondral bone,
and even ligaments.
RA presents with periods of both exacerbation
and remission. The typical signs and symptoms
of RA include pain, morning stiffness, swelling,
and decreased mobility of the affected joints.
Normally, multiple joints are affected in
a symmetric pattern, with both sides of the body
being affected. The small joints of the hands and
feet are the most common joints to be affected,
as well as the cervical spine. As the condition
progresses, laxity in the ligaments supporting
the joint may develop, causing joint deformities
or dislocations.
RA’s symptoms are not only musculoskeletal,
but the condition can also affect the cardiovascu-
lar, renal, and pulmonary systems that may also
present in this condition, including fatigue, loss
of appetite, and decreased endurance. In some
patients, firm skin nodules may form in areas
Degenerative Diseases: Joint
such as the elbows or fingers. It usually presents
between the ages of 20–50 years old, and females
are more affected.
Although there is no cure for RA, there are
pharmacotherapy treatment options that target
the pain and inflammation with hopes of slowing
the progressive of the disease. The use of
medications includes analgesics, nonsteroidal
anti-inflammatory drugs (NSAIDs), corticoste-
roids, disease-modifying antirheumatic drugs
(DMARDS), and biologic response modifiers
(BMRs). Physical therapy is also a critical com-
ponent in the management of RA. During periods
of an active flare, joint protection and rest are the
most important. Exercise, though, should still be
a component of treatment, organized into short
bouts with frequent rest periods to limit fatigue.
In order to prevent deformations and maintain
adequate range of motion, it is very important
that patients consistently change positions of the
affected joints. If swelling is not present, it is also
recommended that light stretching be done.
Because the manifestations of RA are irrevers-
ible, management and treatment of RA is
a lifelong process. It is essential for patients to
work closely with their health care providers in
order to establish an individualized treatment
plan in order to maintain as much functional
independence as possible.
References and Readings
A.D.A.M. Medical Encyclopedia [Internet]. Rheumatoid
arthritis. Atlanta, GA: A.D.A.M.; #2010. [Last
reviewed February 07, 2010; cited April 18, 2011];
[about 6 p.]. Retrieved from http://www.ncbi.nlm.
nih.gov/pubmedhealth/PMH0001467/
Goodman, C. C., & Fuller, K. S. (2009). Pathology: Impli-
cations for the physical therapist (3rd ed.). St. Louis,
MO: Saunders Elsevier.
Kisner, C., & Colby, L. A. (2002). Therapeutic exercise.
Philadelphia: F.A. Davis Company.
Degenerative Parkinsonism
▶ Parkinson’s Disease: Psychosocial Aspects
Degrees of Freedom
Degrees of Freedom
J. Rick Turner
Cardiovascular Safety, Quintiles, Durham,
NC, USA
Definition
Degrees of freedom may be defined as the
number of squares of deviations from the mean
minus the number of independent linear restric-
tions placed upon the quantities involves. For n
numbers there are n squares of deviations from
the mean, of which only (n  1) are independent.
That is, when (n  1) are specified, the nth is also
specified.
Description
This is the most esoteric definition in the
Methodology category of entries, and please do
not be concerned if it sounds a little hard to
digest. The following scenario will make it
much clearer.
Suppose you are asked a question: “Choose
any five numbers that add up to 100.” How much
choice do you actually have? A few moments’
thought will reveal that you only have four
choices. You can choose any four numbers you
wish, but having done so, you have no choice
about the fifth. Whatever the sum of the four
numbers you have chosen, only one number will
take you from there to 100, and hence you have
no choice.
Now consider this issue in a slightly different
way, but one that is precisely equivalent:
“Choose any five numbers that have a mean of
20.” This is an equivalent task since any five
numbers that have a mean of 20 will add up to
100. Therefore, once again, there are only four
choices: These four choices precisely determine
the value that must be chosen as the fifth. Hence,
in a group of scores with a fixed mean, there is
one less degree of freedom than the total number
549 D
of scores. This explanation ties in to the informa-
tion provided in the entry titled “▶ Variance,” in
which the calculation of variance from a term
called “the sum of squares” is described: Vari-
ance is obtained by dividing the sum of squares
by the degrees of freedom.
A word of further explanation is in order here.
While the term (n  1) is used by the majority of
statisticians, it is possible that you might on occa- D
sion see the term n used as the denominator
instead of (n  1) when calculating variance.
The mathematical reasoning behind the state-
ment that (n  1) is the better choice is beyond
the scope of this encyclopedia’s discussions.
Nonetheless, a simple explanation makes the
point.
Whenever a single research study is
conducted, a sample of study participants is cho-
sen from the population of all individuals who
could theoretically have participated as subjects.
The data collected from the subjects who did
participate facilitate the precise calculation of
the variance in the characteristic of interest to
the researchers (reduction in blood pressure,
reduction in an assessment of depression, etc.).
However, this precisely calculated value is not of
primary interest. What is of most interest is an
estimate of the variance that would be seen in the
general population of individuals who may be
exposed to the intervention of interest if the
study reveals that the intervention is both safe
and also of therapeutic benefit. That is, the goal
is to use statistical methodology to estimate in an
optimum manner how well the results of a single
experimental study will generalize to the general
population of patients should the intervention
become widely used. The best estimate of the
population variance is generated by the use of
(n  1) as the degrees of freedom, that is, as the
denominator when the sum of squares is divided
by the degrees of freedom.
Cross-References
▶ Standard deviation
▶ Variance
D 550
Dekker, Joost
Joost Dekker
Department of Psychiatry and Department of
Rehabilitation Medicine, VU University Medical
Centre, Amsterdam, The Netherlands
Biographical Information
Joost Dekker was born in Doetinchem, the
Netherlands, on June 23, 1951. He received
a BSc in chemistry (Utrecht, 1973, cum laude)
and MSc in psychology (Utrecht, 1980). He
obtained his PhD in 1988 (Utrecht, cum laude).
He is a licensed health psychologist. He was
senior researcher at the WHO Collaborating Cen-
ter on Quality of Life in Relation to Health Care,
Amsterdam (1987–1988), and senior researcher
and subsequently head of the research department
at the Netherlands Institute of Primary Health
Care, Utrecht (1988–2001). He was also director
of the Institute of Health and Welfare Studies,
Amsterdam (2001–2007).
Dekker is currently Professor of Allied Health
Care at the Department of Psychiatry and the
Department of Rehabilitation Medicine, VU
University Medical Center, Amsterdam, the
Netherlands (1997–present). He is chair of the
research track Soma & Psyche in the Mental
Health research program, EMGO Institute for
Health and Care Research, and leader of the
Quality of Life research program, Cancer Center
Dekker, Joost
Amsterdam. He is “dosent” of Psychological
Aspects of Rehabilitation at the Faculty of Sports
and Health Sciences, University of Jyv€askyl€a,
Finland.
Dekker’s research concerns behavioral factors
in somatic disease, in the clinical epidemiological
tradition. He focuses on musculoskeletal disor-
ders, neurological disorders, and – recently –
cancer. He has obtained grants from numerous
agencies, including the Ministry of Health,
Netherlands Organization for Health Research
and Development, and NGOs. He is (co)author
of more than 225 international peer-reviewed
scientific publications, more than 80 national
peer-reviewed scientific publications, and more
than 90 scientific publications in books, reports,
and other journals. He served as editor in chief
(2007–2011) and associate editor (1993–2006) of
the International Journal of Behavioral Medicine.
He performs editorial services for a wide range of
scientific journals and has supervised 21 success-
fully defended PhD theses.
Dekker is president elect of the International
Society of Behavioral Medicine (2010–2012)
and will serve as president from 2012 to 2014.
Other positions in ISBM include member of the
Board (2007–present), member of the Governing
Council (1994–2006), chair of the Strategic
Planning Committee (2004–2006), chair of the
Nominations Committee (2006), and co-chair
(1996–1998) and chair (1998–2002) of the
Education and Training Committee. He is
involved in other international and national
boards and committees. Examples include the
Society of Behavioral Medicine, the Cochrane
Collaboration, Netherlands Health Council,
Netherlands Health Research Council,
Netherlands Behavioral Medicine Federation,
and Royal Netherlands Society of Physiotherapy.
He has contributed to the organization of
numerous international and national conferences.
Major Accomplishments
Dekker developed the theory on behavioral and
neuromuscular factors in activity limitations in
Dekker, Joost
osteoarthritis. The theory provides an integrated
model of how behavioral factors (negative affect
and avoidance of activities) and neuromuscular
factors (muscle weakness, poor proprioception,
and laxity of joints) interact, resulting in activity
limitations in this clinical condition. Empirical
support for the theory has been obtained
in cross-sectional and longitudinal research
(Dekker, Tola, Aufdemkampe, & Winckers,
1993; van der Esch, Steultjens, Knol, Dinant, &
Dekker, 2006; van der Esch et al., 2007;
Steultjens, Dekker, & Bijlsma, 2002).This theory
was used to develop therapeutic approaches
aimed at improved performance of activities in
osteoarthritis. Examples include “behavioral
graded activity” and “stability training.” These
therapeutic approaches have been and are being
evaluated in randomized clinical trials, which are
providing evidence in support of these
approaches (Pisters, Veenhof, Schellevis, de
Bakker, & Dekker, 2010; Veenhof et al., 2006).
He contributes to the integration of psychol-
ogy and rehabilitation (including rehabilitation
medicine, physiotherapy, and occupational ther-
apy). This integrated approach results in novel
theories and innovative treatments. The previ-
ously mentioned research on activity limitations
in osteoarthritis illustrates the integration of psy-
chology and rehabilitation. Other examples
include the development of therapeutic
approaches for neurological patients, specifically
stroke patients with apraxia (Donkervoort,
Dekker, Stehman-Saris, & Deelman, 2001;
Donkervoort, Dekker, & Deelman, 2006;
van Heugten et al., 1998) and patients with
dementia (Graff et al., 2006).
Dekker also contributes to the scientific foun-
dation of rehabilitation medicine, physiotherapy,
and occupational therapy. This work concerns the
application of the International Classification of
Functioning in these disciplines (Dekker, 1995),
summarizing the evidence in support of exercise
therapy in a wide range of disorders (Baar,
Assendelft, Dekker, Oostendorp, & Bijlsma,
1999; Smidt et al., 2005), assessing prognostic
factors for quality of life (Braamse et al., 2011;
van der Waal, Terwee, van der Windt, Bouter, &
Dekker, 2005), summarizing the evidence in
551 D
support of occupational therapy in numerous dis-
orders (Steultjens, Dekker, Bouter, Leemrijse, &
van den Ende, 2005), assessing the impact of
comorbidity on pain and activity limitations
(van Dijk et al., 2010), and contributing to the
development of measurement instruments and
clinimetrics (Dekker, Dallmeijer, & Lankhorst,
2005).
He strongly supports the implementation of D
his research into clinical practice. This has
resulted in the foundation of an outpatient clinic
for advanced rehabilitation in osteoarthritis, the
development and implementation of a national
consensus on the treatment of osteoarthritis
(van den Ende et al., 2010), and the implementa-
tion of screening and treatment for psychological
distress in patients with multiple sclerosis and
cancer.
In the role of editor in chief, Dekker
contributed to the definition of the profile of the
International Journal of Behavioral Medicine
(Dekker, 2007). IJBM has been defined as an
interdisciplinary journal, publishing research on
factors relevant to health and illness. The scope of
IJBM extends from biobehavioral mechanisms,
clinical studies on diagnosis, treatment, and reha-
bilitation to research on public health, including
health promotion and prevention. IJBM is an
international journal: manuscripts originate
from all over the world, addressing issues related
to both local and global health.
Cross-References
▶ Arthritis
▶ Cancer Survivorship
▶ Chronic Pain
▶ Evidence-Based Behavioral Medicine
(EBBM)
▶ Exercise
▶ International Society of Behavioral Medicine
▶ Neurological
▶ Occupational Therapy
▶ Physical Therapy
▶ Psychometrics
▶ Quality of Life: Measurement
▶ Rehabilitation
D 552
References and Readings
Baar, M. E. V., Assendelft, W. J. J., Dekker, J.,
Oostendorp, R. A. B., & Bijlsma, J. W. J. (1999).
Effectivenss of exercise therapy in patients with oste-
oarthritis of the hip or knee: A systematic review of
randomized clinical trials. Arthritis & Rheumatism, 42,
1361–1369.
Braamse, A. M., Gerrits, M. M., van Meijel, B., Visser, O.,
van Oppen, P., Boenink, A. D. et al (2011). Predictors
of health-related quality of life in patients treated with
auto- and allo-SCT for hematological malignancies.
Bone Marrow Transplant. doi:10.1038/bmt.2011.130.
Dekker, J. (1995). Application of the ICIDH in survey
research on rehabilitation: The emergence of the func-
tional diagnosis. Disability and Rehabilitation, 17
(3–4), 195–201.
Dekker, J. (2007). Defining the profile. International
Journal of Behavioral Medicine, 14, 1–2.
Dekker, J., Dallmeijer, A. J., & Lankhorst, G. J. (2005).
Clinimetrics in rehabilitation medicine: Current issues
in developing and applying measurement instruments 1.
Journal of Rehabilitation Medicine, 37(4), 193–201.
Dekker, J., Tola, P., Aufdemkampe, G., & Winckers, M.
(1993). Negative affect, pain and disability in osteoar-
thritis patients: The mediating role of muscle weak-
ness. Behavior Research and Therapy, 31, 203–206.
Donkervoort, M., Dekker, J., & Deelman, B. (2006). The
course of apraxia and ADL functioning in left hemi-
sphere stroke patients treated in rehabilitation centres
and nursing homes. Clinical Rehabilitation, 20(12),
1085–1093.
Donkervoort, M., Dekker, J., Stehman-Saris, F. C., &
Deelman, B. G. (2001). Efficacy of strategy training
in left hemisphere stroke patients with apraxia:
A randomised clinical trial. Neuropsychological Reha-
bilitation, 11, 549–566.
Graff, M. J., Vernooij-Dassen, M. J., Thijssen, M.,
Dekker, J., Hoefnagels, W. H., & Rikkert, M. G.
(2006). Community based occupational therapy for
patients with dementia and their care givers:
Randomised controlled trial. British Medical Journal,
333(7580), 1196.
Pisters, M. F., Veenhof, C., Schellevis, F. G.,
de Bakker, D. H., & Dekker, J. (2010). Long-term
effectiveness of exercise therapy in patients with oste-
oarthritis of the hip or knee: A randomized controlled
trial comparing two different physical therapy inter-
ventions. Osteoarthritis and Cartilage, 18(8),
1019–1026.
Smidt, N., de Vet, H. C., Bouter, L. M., Dekker, J.,
Arendzen, J. H., de Bie, R. A., et al. (2005). Effective-
ness of exercise therapy: A best-evidence summary of
systematic reviews. The Australian Journal of Physio-
therapy, 51(2), 71–85.
Steultjens, M. P., Dekker, J., & Bijlsma, J. W. (2002).
Avoidance of activity and disability in patients with
osteoarthritis of the knee: The mediating role of muscle
strength. Arthritis and Rheumatism, 46(7), 1784–1788.
Delay Discounting
Steultjens, E. M., Dekker, J., Bouter, L. M.,
Leemrijse, C. J., & van den Ende, C. H. (2005). Evi-
dence of the efficacy of occupational therapy in differ-
ent conditions: An overview of systematic reviews.
Clinical Rehabilitation, 19(3), 247–254.
van den Ende, C. M., Bierma-Zeinstra, S. M.,
Vlieland, T. P., Swierstra, B. A., Voorn, T. B., &
Dekker, J. (2010). Conservative treatment of hip and
knee osteoarthritis: A systematic, step-by-step
treatment strategy. Nederlands Tijdschrift voor
Geneeskunde, 154, A1574.
Van der Esch, M., Steultjens, M., Harlaar, J., Knol, D.,
Lems, W., & Dekker, J. (2007). Joint proprioception,
muscle strength, and functional ability in patients with
osteoarthritis of the knee. Arthritis and Rheumatism,
57(5), 787–793.
van der Esch, M., Steultjens, M., Knol, D. L.,
Dinant, H., & Dekker, J. (2006). Joint laxity and the
relationship between muscle strength and functional
ability in patients with osteoarthritis of the knee.
Arthritis and Rheumatism, 55(6), 953–959.
van der Waal, J. M., Terwee, C. B., van der Windt, D. A.,
Bouter, L. M., & Dekker, J. (2005). The impact of non-
traumatic hip and knee disorders on health-related
quality of life as measured with the SF-36 or SF-12.
A systematic review. Quality of Life Research, 14(4),
1141–1155.
van Dijk, G. M., Veenhof, C., Spreeuwenberg, P., Coene, N.,
Burger, B. J., van Schaardenburg, D., van den Ende,
C. H., Lankhorst, G. J., Dekker, J. (2010). CARPA
Study Group. Prognosis of limitations in activities in
osteoarthritis of the hip or knee: a 3-year cohort study.
Archives of Physical Medicine and Rehabilitation,
91:58–66.
van Heugten, C. M., Dekker, J., Deelman, B. G., van
Dijk, A. J., Stehmann-Saris, J. C., & Kinebanian, A.
(1998). Outcome of strategy training in stroke patients
with apraxia: A phase II study. Clinical Rehabilitation,
12(4), 294–303.
Veenhof, C., Koke, A. J., Dekker, J., Oostendorp, R. A.,
Bijlsma, J. W., van Tulder, M. W., et al. (2006). Effec-
tiveness of behavioral graded activity in patients with
osteoarthritis of the hip and/or knee: A randomized
clinical trial. Arthritis and Rheumatism, 55(6), 925–934.
Delay Discounting
▶ Impulsivity
Deliberate Self-Harm
▶ Suicide
Dementia
Delta Sleep
▶ Slow-Wave Sleep
Dementia
Bonnie Levin
Department of Neurology, University of Miami
Medical Center, Miami, FL, USA
Synonyms
Cognitive impairment; Cortical dementia;
Dementing illness
Definition
Dementia is a disorder characterized by
a progressive decline in intellectual function or
behavior severe enough to cause impairment in
social and occupational functioning.
Description
The term dementia is derived from the Latin
words de (“without”) and mens (“the mind”).
The most widely used criterion for diagnosing
dementia is the DSM-IV, which defines dementia
as a disorder characterized by progressive decline
in intellectual function or behavior severe enough
to cause impairment in social and occupational
functioning. Memory loss is the hallmark feature
as well as impairment in one or more cognitive
abilities, including language, reasoning, execu-
tive function, praxis, and visuospatial skills.
The DSM-V, which is expected to be
published in 2012, has adopted the term
“Neurocognitive Disorders” and further
subdivided it into “Major” and “Minor” to
replace the DSM-IV classification of “Delirium,
Dementia, and Amnestic and Other Cognitive
Disorders.”
553 D
There are four dementia syndromes that account
for approximately 90% of cases. They are
Alzheimer’s disease, vascular dementia, dementia
with Lewy bodies, and frontotemporal dementia.
Alzheimer’s disease: Alzheimer’s disease
(AD) is the most common dementia accounting
for 50% of all cases. The major pathology is an
abnormal extracellular accumulation of beta-
amyloid peptide and intracellular accumulation D
of tau protein. Beta-amyloid is believed to be the
main component of senile plaques (SPs) and tau
is involved in the development of neurofibrillary
tangles (NFT). Neuropathological examination
of AD brains reveals that most cases of AD
have a combination of NFT and SP. The NFTs
initially appear in the hippocampus and entorhi-
nal cortex and then extend to the neocortex. SPs
tend to be seen more in the association cortex.
Memory changes have been correlated with hip-
pocampal and entorhinal pathology whereas
more global cognitive decline is seen with neo-
cortical involvement. AD onset is typically insid-
ious, often taking years before the correct
diagnosis is made. The first clinical criteria
based on consensus were published in l983,
referred to as the NINCDS-ADRDA. The
advancement in MR imaging, PET imaging,
CSF assays, and other biomarkers have shown
that the older criteria are no longer well suited
to diagnose AD and newer guidelines for all-
cause dementia and AD dementia, which is fur-
ther subdivided into amnestic and non-amnestic
presentations, have recently been published
(Dubois et al., 2007).
Cardinal features of the disease are progres-
sive decline in mental status functions, including
memory loss, and one or more cognitive impair-
ments involving language, executive, visuospa-
tial/perceptual dysfunction, apraxia, and agnosia.
The cognitive deficits seen in AD are progressive
and interfere with activities of daily living
(ADL). The average time course for AD is
between 8 and 12 years after diagnosis, but it
can last as long as 20. It is now accepted that
there is a prodromal phase in which individuals
exhibit mild cognitive impairment, also referred
to as MCI, before reaching the threshold for early
dementia (Peterson, 2000).
D 554
There are three stages of AD. In mild AD,
individuals typically present with problems
recalling recent events with relative sparing of
older memories. Other frequent cognitive prob-
lems include difficulty in solving problems and
carrying out complex multi-step tasks, making
sound decisions, planning difficulties, and prob-
lems in holding information in mind. Changes in
personality are also common, with irritability and
apathy among the most frequent complaints
voiced by caregivers. Individuals in the early
stages of AD may also exhibit empty speech,
problems finding words, and have difficulty
expressing their ideas. In the midstage or moder-
ate AD, individuals become more confused and
their memory loss is more pervasive. They may
have difficulty retrieving older memories such as
their address, school they attended, or names of
relatives. Assistance with basic ADLs such as
grooming, toileting, and other self-care activities
may be necessary. Personality changes are more
pervasive and it is not unusual for caregivers to
report aggression and paranoia. In the late or
severe stage of AD, afflicted individuals have
lost the ability to communicate beyond occa-
sional words or phrases and require full time
assistance for all self-care activities. At this
stage, motor symptoms are common as well as
loss of bowel, bladder, and swallowing abilities.
Most AD patients die of complications of chronic
illness (pneumonia).
Vascular dementia: It is estimated that nearly
two thirds of individuals who experience a stroke
will have some degree of cognitive impairment,
with roughly a third exhibiting frank dementia
(Selnes & Vinters, 2006). Cognitive impairment
resulting from vascular factors has been termed,
“vascular cognitive impairment” or VCI. Various
components of the “metabolic syndrome,” a term
that refers to a cluster of cardiovascular risk fac-
tors, including diabetes, hypertension, hyperlip-
idemia, hypertriglycemia, and impaired glucose
tolerance, have been linked to age-related cogni-
tive decline. Postmortem studies have revealed
that VCI can also coexist with AD pathology, and
those with both pathologies show a greater degree
of cognitive impairment (REF). Since many of
the vascular risk factors can be modified
Dementia
following changes in one’s lifestyle (diet, exer-
cise, not smoking, etc.) and medication, it may be
possible to improve or even decrease the inci-
dence of VCI with the appropriate intervention
(Gorelick et al., 2011).
Dementia with Lewy bodies: Dementia with
Lewy bodies (DLB), also known as Lewy body
dementia, Lewy body disease, and cortical Lewy
body disease, is the second most common demen-
tia after Alzheimer’s disease. DLB can present as
a movement disorder resembling Parkinson’s dis-
ease with cognitive changes or with memory and
dysexecutive changes suggestive of Alzheimer’s
disease with visual hallucinations and/or delu-
sions. Other presenting features of DLB include
fluctuating levels of attention, characterized by
drowsiness, starring off, lethargy, a history of
falling, sleep-related disturbances, and auto-
nomic dysregulation involving body temperature,
blood pressure, urinary difficulties, constipation,
and swallowing difficulties. Risk factors are age
(>60 years), gender (male), and family history.
Frontal temporal dementia: Frontal temporal
dementia (FTD) is a category of conditions
involving atrophy and neuronal loss of the frontal
and temporal lobes, resulting in prominent lan-
guage impairment and behavioral decline. It is
the most prevalent dementia among younger indi-
viduals. It is estimated that between 20% and
50% of individuals with dementia under
65 years of age have FTD (REF). Three FTD
syndromes have been proposed: behavioral vari-
ant, semantic dementia, and progressive
nonfluent aphasia. In the behavioral variant, neu-
ropsychiatric features, characterized by emo-
tional dysregulation, are prominent early in the
disease. Social inappropriateness, lack of insight,
apathy, disinhibition, and diminished activity are
frequent as well as more extreme behaviors
including poor hygiene, hyperorality, shoplifting,
and other impulse control problems. This variant
is often misdiagnosed as depression due to the
apathetic behavioral style. Frank psychosis is
unusual but seen most often among individuals
with Alzheimer’s disease (Cardarelli, Kertesz, &
Knebl, 2010; Neary et al., 1998). In semantic
dementia, patients present with fluent speech
that is devoid of meaning and may contain
Dementia
semantic paraphasias. The central feature is lan-
guage output characterized by the use of words
that approximate the intended word, such as
“thing to eat with” for knife or “clothes” for
skirt. In addition, this variant is also associated
with associative agnosia, or the inability to rec-
ognize and assign meaning to objects and facial
recognition deficits, including well-known
figures such as celebrities (Cardarelli et al.,
2010; Neary et al., 1998). The third variant, pro-
gressive nonfluent aphasia, is characterized by
speech that is agrammatical, nonfluent, stuttering
or halting, and effortful. Word retrieval difficul-
ties or frank anomia are common with phonemic
paraphasias such as saying “dat” for cat or
“drother” for mother. Other impairments include
difficulties with comprehension, reading, and
repetition. Median survival for FTD is compara-
ble to AD, approximately 9 years. Since there is
no treatment for FTD, intervention is at the level
of establishing behavioral management strategies
for issues related to behavioral conduct and psy-
chological counseling for caregivers and family
members (Cardarelli et al., 2010; Neary et al.,
1998).
Other Dementias
Treatable Dementia
There are a number of treatable dementias. The
most common are those resulting from metabolic
disorders such as a vitamin B-12 deficiency, nor-
mal pressure hydrocephalus, chronic substance
abuse, subdural hematoma following trauma
and hypothyroidism. For this reason, it is impor-
tant to first rule out the treatable dementias with
the help of a careful medical work-up, blood
tests, and neuroimaging.
Rapidly Progressive Dementia (RPD)
There is a group of dementing conditions that
develop subacutely and involve rapid decline of
cognitive, behavioral, and motor function.
A variety of etiologies can lead to RPD including
neurodegenerative, toxic-metabolic, neoplastic,
infectious, and inflammatory conditions
(Geschwind, Shu, Harman, Sejvar, & Miller,
2008; Rosenbloom & Alireza, 2011).
555 D
The most widely studied RPD subgroup is the
prion disease Creutzfeldt-Jakob disease or CJD.
The sporadic form of CJD (sCJD) typically pre-
sents with mental status alterations characterized
by dementia and/or psychiatric changes accom-
panied by cerebellar and extrapyramidal symp-
toms. sCJD onset is usually between 50 and
70 years and is equally prevalent in males and
females, with a short median survival of 5 D
months. Of note, psychiatric complaints and
behavioral symptoms such as depression, malaise
and marked anxiety can precede the dementia and
movement disorder. The EEG in the later stages
of the disease has a distinctive diagnostic pattern
of periodic sharp waves. The other form, referred
to as variant CJD (vCJD), is rarer and can affect
either young or older adults. Mean age of onset is
29 years and typically presents as a psychiatric
disturbance lasting 6 or more months before
other symptoms begin. Although the classic
EEG pattern described above for sCJD is
not typically present, the diagnostic feature of
vCJD is the pulvinar sign on MRI (Geschwind
et al., 2008).
Assessment of Dementia
The diagnosis of dementia should be ascertained
through a combination of careful history taking,
an interview with the patient and an informant,
and neuropsychological testing performed by
a qualified professional. The type of cognitive
battery used to assess dementia will depend on
several factors, including the time allotted for
assessment, the willingness of the patient to par-
ticipate in the testing process, and clinician
availability.
Assessment of dementia requires an under-
standing of the normative aging process, brain
anatomy and neural circuitry, and neuropathol-
ogy. The mental status evaluation should focus
on three components: cognition, personality/
mood, and behavioral function. The type of
examination can vary from bedside screening to
a comprehensive evaluation.
The most widely known measure is the Mini-
Mental State Examination (MMSE), a short
screening instrument developed in the l970s to
assess cognition in the elderly. It is untimed,
D 556
consists of 11 questions and a total possible
score of 30 points. Originally designed for
psychogeriatric patients (Rosenbloom & Alireza,
2011), this measure has been used to assess men-
tal status in a wide variety of neurologic and
general medical disorders as a dementia screen,
not as a diagnostic tool. Its purpose is threefold:
to screen for cognitive impairment, to assess
severity of impairment, and to monitor change
over time with repeated assessments.
There are many advantages of the MMSE,
some of which include the ease of administration,
the availability of international translations, the
use of cutoff scores that make inter-study com-
parisons easier, and the availability of norms for
age and education. However, there are several
drawbacks to the MMSE (Nieuwenhuis-Mark,
2010). One criticism of this screening instrument
is that it relies heavily on intact verbal skills,
a problem for those with limited language ability
or with a low educational level. Also there is
a lack of consensus as to which cutoff score is
best to use and whether the norms have been
collected on representative samples. Although
the MMSE has wide international use and has
been translated into many different languages,
there are questions as to whether the translations
are really comparable to the original test due to
the fact some of the items may not be relevant in
other cultures (e.g., reciting “no, ifs, ands, and
buts”). The most serious criticism is that the
MMSE was developed as a cognitive screen,
but it is widely used as a diagnostic tool and has
been shown to be insensitive in discriminating
between age-related cognitive change, mild
cognitive impairment, and early dementia
(Mitchell, 2009).
Ideally, bedside examinations and screening
measures should be supplemented with more
comprehensive testing using standardized neuro-
psychological measures with known reliability
and sensitivity for detecting cognitive impair-
ment. A qualified neuropsychologist will select
measures designed to assess specific cognitive
abilities including general intelligence, language
abilities (e.g., verbal fluency, word retrieval,
comprehension), conceptual reasoning and
abstraction, perception, spatial cognition
Dementia
(visuoconstructive graphomotor and assembling
abilities), attention and memory (working mem-
ory, verbal and nonverbal immediate and delayed
recall), motor speed and the executive functions
(e.g., skills involved in planning, organization,
set shifting, goal setting, and problem solving).
Additional questionnaires are frequently
included to assess a patient’s emotional status,
in particular symptoms of anxiety and depres-
sion. A major goal of the neuropsychological
evaluation is to identify a specific pattern of cog-
nitive change associated with a particular demen-
tia. Another goal is to provide a baseline from
which to compare future evaluations. A third goal
is to identify cognitive strengths and weaknesses
that can be used to address treatment and man-
agement issues.
Prevention of Dementia
There is compelling evidence from basic and
clinical research that aerobic exercise may be
neuroprotective. Transgenic mouse models, epi-
demiologic, biomarker, and prospective clinical
studies have linked exercise with improved cog-
nition and provided evidence that physical activ-
ity directly modulates known risk factors
associated with dementia, including obesity, vas-
cular disease, hypertension, diabetes, inflamma-
tion, and cardiovascular disease. The mechanism
by which increased physical activity improves
cognition is not known. It has been proposed
that physical exercise may reduce beta-amyloid
deposits in the brain, increase synaptogenesis
and plasticity, boost endorphins and growth
factors, or increase brain perfusion (Savica &
Peterson, 2011).
Education and intellectual stimulation have
also been credited with having a neuroprotective
role against dementia and cognitive decline
(Stern, 2002). Numerous observational studies
have shown a strong and positive association
between higher intellectual activities and reduced
cognitive decline. A lower educational level is
associated with a 30% increased risk of having
AD. It is possible that higher education is a proxy
for higher SES which confers an advantage in
terms of overall health, lifestyle, and reduced
stress.
Dementia Screening Tests
More recent studies have provided prelimi-
nary evidence showing that cognitive training,
i.e., mental exercises to improve memory, rea-
soning, and processing, may improve cognition
and instrumental activities of daily living. Pre-
liminary evidence has shown in animals that
increased mental activity is linked to increased
brain volume (Willis et al., 2006).
Diet: Although it has long been held that diet is
linked to cognition, the evidence remains contro-
versial. Most attention has centered on the
Mediterranean diet, one which is high in vegeta-
bles and non-saturated fat, and linked to a lower
risk of cognitive decline. It is argued the diet is
high in antioxidants and its relationship to reduc-
ing oxidative stress is the key factor responsible
for improved cognition (Savica & Peterson, 2011).
Social Networks: There are several studies
suggesting that social connectivity, as defined
by participation in social activities and
maintaining interpersonal relationships, may be
protective against cognitive decline. Conversely,
social disengagement, loneliness, and not living
with a partner have been found to be linked to
AD, although this association did not apply to
those who were divorced or widowed (Seeman,
Lusignolo, Albert, & Berkman, 2001). A valid
criticism of these studies is that it is difficult to
know whether reduced social connectivity is
a risk factor or an actual symptom of AD, given
that social withdrawal is a feature of early
dementia.
Cross-References
▶ Aging
▶ Alzheimer’s Disease
▶ Cognitive Function
▶ Cognitive Impairment
▶ Geriatrics
References and Readings
Cardarelli, R., Kertesz, A., & Knebl, J. A. (2010).
Frontotemporal dementia: A review for primary care
physicians. American Family Physician, 82,
1372–1377.
557 D
Dubois, B., Feldman, H. H., Jacova, C., Dekosky, S. T.,
Barberger-Gateau, P., Cummings, J., et al. (2007).
Research criteria for the diagnosis of Alzheimer’s dis-
ease: Revising the NINDS-ADRDA criteria. Lancet
Neurology, 8, 734–746.
Geschwind, M. D., Shu, H., Harman, A., Sejvar, J. J., &
Miller, B. (2008). Rapidly progressive dementia.
Annals of Neurology, 64(1), 97–108.
Gorelick et al. (2011). Inclusion of stroke in cardiovascu-
lar risk prediction instruments: A statement for
healthcare professionals from the American Heart D
Association/American Stroke Association. Stroke, 42,
2672–2713.
Mitchell, A. J. (2009). A meta-analysis of the accuracy of
the mini-mental state examination in the detection
of dementia and mild cognitive impairment. Journal
of Psychiatry Research, 43(4), 411–431.
Neary, D., Snowden, J. S., Gustafson, L., Passant, U.,
Stuss, D., Black, S., et al. (1998). Frontotemporal
lobar degeneration: A consensus on clinical diagnostic
criteria. Neurology, 51(6), 1546–1554.
Nieuwenhuis-Mark, R. E. (2010). The death knoll
for the MMSE: Has it outlived its purpose? Journal
of Geriatric Psychiatry and Neurology, 23(3),
151–157.
Peterson, R. C. (2000). Mild cognitive impairment: Tran-
sition between aging and Alzheimer’s disease.
Neurologia, 15, 93–101.
Rosenbloom, M. H., & Alireza, A. (2011). The evaluation
of rapidly progressive dementia. Neurologist, 7(2),
67–74.
Savica, R., & Peterson, R. C. (2011). Prevention of
dementia. Psychiatric Clinics of North America,
34(1), 127–145.
Seeman, T. E., Lusignolo, T. M., Albert, M., & Berkman, L.
(2001). Social relationships, social support, and patterns
of cognitive aging in healthy, high-functioning older
adults: MacArthur studies of successful aging. Health
Psychology, 20(4), 243–255.
Selnes, O. A., & Vinters, H. V. (2006). Vascular cognitive
impairment. Nature Clinical Practice Neurology, 2,
538–547.
Stern, Y. (2002). What is cognitive reserve? Theory
and research application of the reserve concept.
Journal of International Neuropsychology Society, 8,
448–460.
Willis, S. L., Tennstedt, S. L., Marsiske, M., Ball, K.,
Elias, J., Koepke, K. M., et al. (2006). Long-term
effects of cognitive training on everyday functional
outcomes in older adults. Journal of the American
Medical Association, 296(23), 2805–2814.
Dementia Screening Tests
▶ Screening, Cognitive
D 558
Dementing Illness
▶ Dementia
Demographics
J. Rick Turner
Cardiovascular Safety, Quintiles, Durham,
NC, USA
Synonyms
Subject characteristics
Definition
Demography can be defined as the statistical
science focusing upon the distribution, density,
vital statistics, and various other defining charac-
teristics of human populations. Demographics
therefore include characteristics such as sex,
age, race/ethnicity, height, weight, and socioeco-
nomic class.
When reporting a research study, it is neces-
sary to provide a summary of the relevant demo-
graphic characteristics of the subjects who
participated in the study. Ultimately, the goal of
a clinical study is not to provide precise informa-
tion for that particular subject sample but to
collect information that generalizes to the popu-
lation from whom that particular sample was
chosen. Therefore, a given subject sample needs
to reflect that population adequately for such
generalization to be meaningful.
Not all demographic information is always of
relevance. In some studies, perhaps a clinical trial
of a new drug, it may not be necessary to report
the socioeconomic status of the study participat-
ing in the study. If there is no biologically
plausible reason to think that individuals
from different socioeconomic strata would
respond differently to the drug, it is not necessary
to report this information. In contrast, sex and
Dementing Illness
age may be considered to be of considerable
relevance if there are biologically plausible rea-
sons to think that these factors may influence drug
responses.
Cross-References
▶ Generalizability
Demyelinating Disease
▶ Multiple Sclerosis: Psychosocial Factors
Denial
Alefiyah Z. Pishori
Department of Psychology, University of
Connecticut, Storrs, CT, USA
Synonyms
Coping strategies; Defense mechanism
Definition
The psychological concept of denial refers to
a cognitive and emotional coping strategy involv-
ing the negation of a fact or reality. In the context
of health psychology, denial refers to the nega-
tion of a health problem, effecting either oneself
or someone else. Individuals experiencing denial
refuse to believe facts that are difficult to face,
such as being diagnosed with a terminal or
chronic illness. Denial is a common and normal
process; it can be either protective or harmful in
managing a health problem, depending on the
extent of the denial and how it impacts individ-
uals’ decision making. For instance, denial has
been identified as a useful and necessary first step
in the process of coping with a terminal or life-
threatening illness to allow individuals to adjust
Denial
to the situation. However, denial can become
a problem when it persists and prevents individ-
uals from actively coping with the truth and/or
receiving necessary care and treatment for their
illnesses. Family members or friends of an indi-
vidual diagnosed with an illness may also engage
in denial; they may cope with the experience of
learning their loved one is ill by rejecting the
idea. If their denial persists as well, they may
advise their loved one to not seek treatment or
reject the truth regarding what is happening to
their loved one.
Description
Denial as a psychological process has a long his-
tory, originating with Sigmund Freud’s theory of
defense mechanisms. Freud conceptualized
defense mechanisms as strategizes utilized by
individuals to protect themselves from difficult
memories by distorting them or making them
inaccessible to consciousness; denial was one
such strategy. Over time, theorists have identified
different types of denial that an individual may
experience or engage.
Defensive Denial
Defensive (or pathogenic) denial is a specific
form of denial in which individuals use defensive
processes to manage their emotional responses
and allow for appropriate decisions regarding
health threats. This is a dynamic process that
accommodates new information and can be dis-
tinguished from other forms of denial that ignore
reality. Defensive denial minimizes threats but is
responsive to reality and information regarding
the situation. It may lead to the minimization of
health threats, protective social comparisons that
minimize the individuals’ risks, or questioning
the validity of health threat information. It is
unclear how defensive denial impacts behavior,
although it has been suggested that it may
decrease negative affect and thus allow individ-
uals to engage in protective health behaviors
(Wiebe & Korbel, 2003). However, if a person
experiencing pathogenic denial is not exposed to
information regarding the seriousness of the
559 D
situation, he/she may not recognize the truth of
his/her situation (Janis, 1983).
Malignant Denial
Malignant (or pathological) denial is
a maladaptive form of denial that prevents indi-
viduals from receiving necessary treatment for
their conditions. What makes this form of denial
malignant is the impact it has on health-care D
decisions: individuals will ignore doctors and
refuse treatment. For instance, individuals suffer-
ing from psychological conditions, such as sub-
stance abuse and eating disorders, often deny
they have a problem and refuse help or treatment.
Individuals with infectious diseases who are
experiencing malignant denial may engage in
behaviors that put others at risk of becoming
infected as well (Kalichman, 2009). Thus, this
form of denial is a serious concern as it can
negatively impact both an individual’s own and
others’ health.
Denial versus Avoidance
Denial must be distinguished from avoidance.
Avoidance refers to individuals’ refraining from
reminders of the truth, although they are cogni-
tively aware of the facts, whereas denial suggests
that individuals have refused to accept the facts.
Thus, an avoidant individual may recognize he/
she is ill but refrain from going to the doctor for
treatment, while an individual in denial would
refuse to see the doctor because he/she would
not acknowledge he/she had an illness. Although
these concepts are often confused and the terms
used interchangeably, they are conceptually
distinct.
Cross-References
▶ Avoidance
▶ Defensiveness
References and Readings
Breznitz, S. (1983). The denial of stress. New York: Inter-
national Universities.
D 560
Cohen, S. (2001). States of denial: Knowing about atroc-
ities and suffering. Malden, MA: Blackwell.
Janis, I. L. (1983). Preventing pathogenic denial by means
of stress inoculation. In S. Breznitz (Ed.), The denial of
stress (pp. 35–76). New York: International Universi-
ties Press.
Kalichman, S. (2009). Denying AIDS: Conspiracy theo-
ries, pseudoscience, and human tragedy. New York:
Copernicus Books.
Wiebe, D., & Korbel, C. (2003). Defensive denial, affect,
and the self-regulation of health threats. In L. D.
Cameron & H. Leventhal (Eds.), The self-regulation
of health and illness behavior (pp. 184–203).
New York: Routledge.
Dependence, Drug
John Grabowski
Department of Psychiatry, Medical School,
University of Minnesota, Minneapolis, MN, USA
Synonyms
Drug abuse; Substance abuse; Substance use
disorders
Definition
Problematic use of drugs altering behavior and
psychological function is categorized in terms of
patterns and consequences of use. The common
worldwide codification of these disorders is
found in International Statistical Classification
of Diseases and Related Health Problems 10
(ICD-10), which refers to these disorders as Men-
tal and behavioral disorders due to psychoactive
substance use. The generic ICD-10 definition is:
“a wide variety of disorders that differ in severity
and clinical form but that are all attributable to
the use of one or more psychoactive substances,
which may or may not have been medically pre-
scribed.” The American Psychiatric Association
codification of these disorders is found in the
Diagnostic and Statistical Manual – Fourth Edi-
tion (DSM-IV), which uses the diagnostic label of
Substance-Related Disorders. The generic
DSM-IV definition is: “The Substance-Related
Dependence, Drug
Disorders include disorders related to the taking
of a drug of abuse (including alcohol), to the side
effects of a medication, and to toxin exposure.”
While “dependence” historically has had
a precise scientific definition, common use is
often confused with “abuse,” “addiction,” and
other terms.
Description
Determinants of Dependence
Problematic use of drugs altering behavior and
psychological function (“psychoactive drugs”) is
determined by circumstances of use, route of
administration, dose, and drug or medication.
Direct biological and behavioral effects of
a chemical or drug determine the likelihood of
drug taking. The “abuse liability” or “abuse
potential” is determined with standardized
preclinical/animal laboratory procedures. In
these experiments, the test drug is made available
through an intravenous line, as a liquid for oral
consumption, or on occasion as vapor or smoke.
The animal has the opportunity to press a lever or
engage in some other response producing drug
delivery. The rate of responding and frequency of
drug delivery are compared to the vehicle, or
solution without drug (placebo). If the drug is
“self-administered” at higher rates than vehicle,
it is deemed to have “rewarding” or reinforcing
effects that will sustain drug seeking and
drug taking.
Within a series of similar drugs (e.g., stimu-
lants, anxiolytics) the relative reinforcing
effect can be established as a hierarchy from
least to most reinforcing. In turn, this is charac-
terized as relative abuse liability. Generally,
though not always, the animal self-administration
patterns predict the likelihood of human
self-administration. In these experiments, food
and water may be concurrently or sequentially
available for comparison to drug intake or to
determine the effect of drug on other behaviors.
Numerous comparisons can be made, and other
paradigms implemented, to further characterize
the properties and behavioral consequences of
drug self-administration. In animals, the core
Dependence, Drug
biological effects of the agents are examined and
in humans a variety of self-report descriptive
measures, such as “liking,” “willingness to take
again,” and “unpleasant effects” are also deter-
mined. Arguably, it is the balance of immediate
pleasurable to unpleasant effects that determine
possible persistent use. Untoward effects that fol-
low excessive use, for example, “hangovers” are
not necessarily deterrents to resumption of drink-
ing alcohol. Ultimately, when use persists and
dependence emerges, a variety of untoward out-
comes occur. Continued use in patterns that
produce hazardous and debilitating outcomes
(biological, behavioral, social) are key features
in determination of dependence.
Within drug self-administration studies,
whether with nonhuman animals or humans,
dose-ranging studies are conducted with, for
example, “low,” “medium,” and “high” doses,
again with comparison to placebo. The result is
often, though not always an inverted U-shaped
curve with lower doses consumed less than inter-
mediate doses, while very high unit doses may
generate less drug taking (due to increasing
adverse effects or satiating doses achieved with
less output). In some instances, for example, sed-
atives, the medication itself may impair ability to
continue self-administration. Other experimental
strategies determine whether changes in intake
are due to incapacitating effects of the drug, titra-
tion to seek optimal effect, adverse effects at
a particular dose, or other factors. While
the interactions may be complex, dose is an
important factor in self-administration and
establishing drug dependence.
The route of administration (intravenous,
inhalation, insulfflation, oral) may alter the
likelihood of drug dependence. More rapid
onset is typically observed with intravenous and
inhalation routes and it is generally thought that
this may increase the probability of persistent
use. However, individual preferences or dislikes
may intervene; for example, many people are
unwilling to use injection paraphernalia. Still,
while IV heroin use produces a singular and
pronounced effect, orally ingested opioids for
nontherapeutic purposes can also produce pro-
found dependence. Most agents with moderate
561 D
to high abuse potential can be expected to be
associated with dependence in some people,
regardless of route, when used outside of
therapeutic regimens.
Other factors important to use and ultimately
dependence may include drug availability and
social circumstances. Social factors are com-
monly important in initial use even though later
use may be solitary. The relative ease of D
obtaining a drug makes initial exposure and
frequent use more likely for those individuals
who are responsive to the effects. Still, most
individuals exposed to drugs do not proceed to
a level of use that can be categorized as depen-
dence. Knowing who will, or will not proceed to
dependence, that is, who is vulnerable to effects
of a particular drug and likely to engage in
persistent use is a matter of considerable interest.
Behavioral/Psychological and Physical
Dependence
The various diagnostic and scientific schemata
may differentiate or emphasize two aspects of
dependence that are commonly inseparable:
behavioral or psychological dependence and
physical dependence. As drug action and deter-
minants of persistent use have been more
effectively delineated, these distinctions may be
less useful but are separable in some
circumstances.
Drug dependence typically refers to persistent
use despite problems across the spectrum of
personal and social activities as well as
biological/medical and psychological harm. In
current terminology, dependence refers to
patterns of behavior that precede, are concurrent
with, and follow use. Drug seeking
(soliciting/purchasing drugs from others) can be
elaborate and time consuming. The behavior of
drug taking, legal or illegal, is typically
characterized by ritualized events.
These behaviors may be socially accepted as
well as being behaviorally and psychologically
relatively benign, for example, persistent
coffee/caffeinated beverage consumption at
moderate doses. Caffeine, most commonly
through coffee or carbonated beverage consump-
tion, is thought to be the most widely used drug in
D 562
the world. In this example, two prominent
ritualized patterns exist. One entails the legal
purchase of beans or ground coffee, special
home apparatus for grinding and preparing coffee
along with the spectrum of containers from which
it is consumed. A second pattern that has evolved
in recent decades stems from the long-standing
practice of coffee with meals or in coffee shops.
Now, the elaborate rituals are well represented by
Starbucks, Caribou, and other chains as well as
myriad local purveyors. The user determines size
(volume), dose (singles, doubles, triples), dairy
product additions ranging from skimmed milk to
heavy cream, additional additives be they spices
or liqueur flavorings. The use, dose, drug-taking
style, may differ from person to person and time
to time for the particular person. Persistent
caffeine use has clear biological and psycholog-
ical effects and cessation of use leads to an array
of symptoms.
Heroin use likewise entails procedures and
rituals: mixing, drawing drug into a syringe,
tying off an extremity to gain access to a vein
and injection. Use by smoking or insufflation is
also accompanied by a systematized approach to
self-administration. These events may be solitary
or in groups. The consequences of drug adminis-
tration are then experienced. Heroin or other per-
sistent opioid use for nontherapeutic purposes
often follows a course of increasing dosing as
tolerance emerges to the euphoriant effects,
increase in associated illegal contacts during
drug seeking, increasing cost, and deterioration
of social circumstances. Tolerance is not
consistent across all effects. Thus, diminished
euphoriant effect leading to higher dosing with
opioids is not matched by tolerance to respiratory
depressant effects and death may ensue. In the
case of potent stimulants, cardiovascular
excitation/dysfunction or seizures occur as
doses increase despite reduction in perceived
euphoriant effects. These patterns of use in the
face of untoward consequences are emblematic
of dependence.
The behaviors immediately following drug
use are dependent on the characteristics of the
agent. Sedating drugs produce feelings of
euphoria or pleasure, varying levels of lethargy
Dependence, Drug
and somnolence to virtual unconsciousness, and
at the extreme, death, usually from respiratory
depression. Stimulant-type drugs generate pat-
terns of energized behavior ranging from active
euphoria and self-confidence to highly stereo-
typic behaviors, hallucinations, and psychosis,
and at the extreme, death due to cardiovascular
accident or collapse.
Dependence may also refer to a biological
state, historically referred to in pharmacology as
“addiction” or more recently as “physical
dependence,” in which a distinctive profile and
sequence of symptoms emerges when use is
discontinued. The constellation of symptoms
observed on abrupt discontinuation in the
presence of physical dependence is referred to
as a “withdrawal syndrome” (composed of with-
drawal signs and symptoms). The consistency of
such patterns is most evident for drugs with
sedative-like properties such as opiates
(e.g., heroin), benzodiazepines (e.g., diazepam),
barbiturates (e.g., pentobarbital), and alcohol.
These symptoms are typically the reverse of
those associated with high-dose drug use; for
example, with opioids, behavioral activation,
increases in respiration, and increased gastroin-
testinal activity over baseline emerge. Direct
physical symptoms dissipate over days but
behavioral and biological symptoms that have
been conditioned by repeated pairings of drug
self-administration and previously neutral
environmental stimuli may persist for months.
They may be elicited by environmental circum-
stances in which drug use or withdrawal symp-
toms previously occurred. In the case of
stimulants, behavioral malaise, impairment in
performance, diminution of blood pressure, and
other symptoms are common. For the licit drug
caffeine, the most pronounced withdrawal
symptoms are headache, inattention and associ-
ated performance deficits, and fatigue. The
constellation of symptoms is often
a determinant of reemergent drug seeking and
drug taking, or in treatment jargon, “relapse.”
As noted, in special circumstances, the
components of dependence may be separable.
This is informative with respect to the contribu-
tion of environmental circumstances, behavioral
Dependence, Drug
consequences, and biological underpinnings.
These separable determinants can be examined
in the laboratory, for example, by comparing the
behavior of animals that have learned to
self-administer drugs to those that have passively
received the drugs. Comparable instances exist in
humans. Remarkable resilience and persistence
of behavior emerges for individuals using psy-
choactive drugs to excess, be the drug stimulant
or sedative like. However, patients receiving high
doses of intravenous opioids in hospital settings
for pain, invariably have a pattern of biological
adaptations characteristic of dependence that dic-
tate physiological sequelae to abrupt cessation of
dosing will occur. Thus, for example, the consti-
pation associated with high-dose opioid use is
followed by increased gastrointestinal motility.
Still, it is extraordinarily uncommon on recovery
and discharge from the hospital for these patients
to engage in the patterns of drug seeking and drug
taking that are evident in individuals whose use
was established through illicit acquisition and
seeking euphoriant effects. Similarly, patients
treated with methadone or buprenorphine for
previous heroin dependence, are, on one hand
physically dependent and tolerant to many opioid
effects at a stable dose, but unlikely to seek and
use illicit opioids. In other circumstances, for
example, treatment of attention deficit-
hyperactivity disorder, drugs with some
dependence liability are used effectively for
treatment and diminish the likelihood of illicit
drug use and abuse; thus treating one disorder
diminishes a range of problems, including pro-
pensity to illicit drug use. These examples point
to the importance of a range of environmental and
behavioral factors contributing to substance use
disorders.
Acquisition, Maintenance, and Elimination
of Drug Dependence
In the laboratory, nonhuman subjects
(e.g., rodents, primates) generally self-adminis-
ter, or will work to obtain, the same agents that
are taken by humans in both laboratory and
natural settings. Conversely, discovery of a drug
used for euphoriant purposes in human
populations, can generally be translated into
563 D
animal paradigms with evidence of
self-administration. There are some exceptions
and special cases; for example, nonhuman organ-
isms rarely self-administer hallucinogens, but for
a variety of pharmacological and social reasons,
these are not self-administered by humans in the
same way as, for example, heroin. Persistent
harmful heroin, cocaine, alcohol, or other drug
use is clearly distinctively different from either D
therapeutic drug use or even “controlled” licit or
illicit drug use.
Acquisition of drug taking is essentially
a social and cultural phenomenon. For legal
psychoactive drugs (e.g., alcohol), society sets
relatively clear rules and norms generally with
a view to harm reduction and control. Most
people conform to the accepted social and legal
constraints while some go on to dependence. For
illegal drug use, the social group sets the norms.
Both entail socially driven exposure.
Stable use of legal drugs may differ consider-
ably within and across drugs. Caffeinated
beverages may be consumed consistently
throughout the day with late day cessation to
permit undisrupted sleep. Historically,
nicotine/cigarettes were consumed in virtually
all social and nonsocial environments during the
“maintenance phase.” Here the change in social
norms over many decades has resulted in limited
venues for use, dramatic increases in prices, and
remarkable reductions in use across the popula-
tion in some countries, while unfettered use is
permitted and maintained in other countries,
thus pointing to the importance of social deter-
minants in use and maintenance. Illegality of
a drug sets maximum constraints on some aspects
of use that must be circumvented but also estab-
lishes a separate market beyond regulatory
control. Even with the alternative social
constraints, not all individuals who use, be it
stimulants (e.g., cocaine), opioids (e.g., heroin),
or marijuana, go on to dependence.
Some of the factors that contribute to
increased reinforcing effectiveness when a drug
is self-administered (immediacy of effect,
genetic makeup) have been considered. Yet the
factors leading to transition from casual, stable,
or infrequent use of a drug, legal or illegal, to
D 564 Depression

persistent, compulsive-like use by any given indi-
vidual is not well understood.
Elimination of drug use and termination of
self-administration and dependence can be
studied in the animal laboratory and some find-
ings are translatable to the human case. In the
human natural environment, elimination or ces-
sation may result from a variety of self-imposed
regimens or externally applied circumstances.
Severe dependence typically requires a course
of specific treatment for the substance use disor-
der(s). For drugs that produce profound with-
drawal syndromes, for example, alcohol, the
first phase may require intensive medical man-
agement. However, this is distinct from the typi-
cally required course of treatment involving
cognitive behavior therapy, substantial social
and behavioral adjustments, and possibly main-
tenance medications.
McKim, W. A. (2007). Drugs and behavior: An introduc-
tion to behavioral pharmacology (6th ed.). Upper
Saddle River, N.J: Pearson Prentice Hall.
Thompson, T., & Unna, K. R. (Eds.). (1977). Predicting
dependence liability of stimulant and depressant
drugs. Baltimore: University Park Press.
World Health Organization. (1992). ICD-10 classifications
of mental and behavioural disorder: Clinical descrip-
tions and diagnostic guidelines. Geneva: Author.
Depression
▶ Beck Depression Inventory (BDI)
▶ Negative Thoughts
▶ Pregnancy Outcomes: Psychosocial Aspect
Depression Assessment

▶ Depression: Measurement
Cross-References

▶ Addictive Behaviors
▶ Cognitive Behavior Therapy Depression Diagnosis
▶ Substance Abuse: Treatment
▶ Depression: Measurement

References and Readings

American Psychiatric Association. (2000). Diagnostic

Depression: Measurement
and statistical manual of mental disorders (4th ed.,
text rev.). Washington, DC: Author. Samantha Yard and Kimberly Nelson
Carroll, M. E., & Overmier, J. B. (Eds.). (2001). Animal Department of Psychology,
research and human health: Advancing human welfare
through behavioral science [electronic resource].
University of Washington, Seattle, WA, USA
Washington, DC: American Psychological Association.
Fischman, M. W., & Mello, N. K. (Eds.). (1989). Testing
for abuse liability of drugs in humans. National Synonyms
Institute on Drug Abuse. Rockville, MD: U.S. Dept.
of Health and Human Services, Public Health Service,
Alcohol, Drug Abuse, and Mental Health Administra- Depression assessment; Depression diagnosis
tion, National Institute on Drug Abuse; [Washington,
DC: Supt. of Docs., U.S. G.P.O., distributor].
Higgins, S. T. (1997). Applying learning and conditioning
theory to the treatmentof alcohol and cocaine abuse.
Definition
In B. Johnson & J. Roache (Eds.), Drug addiction
and its treatment (pp. 367–386). Philadelphia: The measurement of depression is a process
Lippincott-Raven. conducted by clinicians and researchers for the
Johanson, C. E., Schuster, C. R., Hatsukami, D., &
Vocci, F. (2003). Abuse liability assessment of
purpose of (1) identifying people who may
CNS drugs. Drug and Alcohol Dependence, 70(3), require treatment for depression, (2) identifying
S1–S114. people who meet specific diagnostic criteria for
Depression: Measurement
depression, and (3) quantifying the severity of
depressive symptomatology.
Description
Depression is defined by a cluster of behaviors
and symptoms that have both mental and physical
manifestations and affect a wide range of func-
tionality. Specific criteria for depression include
experiencing persistent depressed mood or loss of
interest or pleasure in most things along with at
least four out of the following additional markers:
sleep disturbance, feelings of worthlessness or
guilt, appetite or weight changes, concentration
problems, decreased energy, psychomotor retar-
dation or agitation, and suicidality. Depression is
ideally diagnosed through a face-to-face inter-
view with a trained mental health professional
based on the current versions of the Diagnostic
and Statistical Manual of Mental Disorders
(DSM) or the International Classification of
Disease (ICD) criteria. It is also important to
note that symptoms that do not meet criteria can
be impairing and thus may be important to mea-
sure as well. As such, depression can be measured
both categorically (i.e., meeting diagnostic
criteria or not) and continuously (i.e., symptom
severity). Depression measurement can be bro-
ken down into three distinct functions: screening,
diagnosis, and quantification of symptoms.
Instrument choice should be made according to
these functions, in addition to what population is
being assessed, what specific hypotheses are
being tested, and if there is a desire to compare
the results to other research findings.
Screening instruments are designed to capture
anyone who could potentially meet diagnostic
criteria for depression and should be referred for
further evaluation. They can additionally be used
to estimate the prevalence of possible depression
in a given setting. They typically do not require
a lot of time, have empirically supported cutoff
criteria, and can be self-administered or adminis-
tered by a nonclinician. As screening instruments
are unable to diagnosis depression on their own,
further assessment by a clinician is needed to
establish a diagnosis.
565 D
Diagnosis of depression is typically done
through a face-to-face interview with a trained
clinician. Sometimes, as is typical in medical
settings, this occurs only with those patients
who have been screened as possibly depressed
with the final diagnosis confirmed by a clinician.
In research settings, the gold standard for depres-
sion diagnosis is a standardized diagnostic inter-
view, such as the Structured Clinical Interview D
(SCID) or the Composite International Diagnos-
tic Interview (CIDI). Structured diagnostic inter-
views can take over an hour depending on the
patient and are typically administered by a clini-
cian who has also been shown to reliably distin-
guish cases from among multiple participants. It
is important to note that diagnostic interviews are
meant to categorize individuals as diagnosed or
not but will not capture people who fall just
below the criteria, yet are still impaired.
Symptom rating scales offer a continuous
assessment of depression severity. They are typ-
ically brief, can be self-administered or adminis-
tered by a nonclinician, and may include a cutoff
for screening purposes. They are particularly use-
ful in monitoring changes in depression symp-
toms over time, and thus can be used in both
clinical and research settings to evaluate treat-
ment effects. Although many symptom rating
scales have established clinical significance or
severity cutoff values, they are unable to diag-
nose depression on their own; thus, assessment by
a clinician or a structured diagnostic interview is
needed for diagnosis.
There are multiple things to consider when
making a depression measurement choice. First,
depression and depressive symptoms can
co-occur with or result from a variety of physical
conditions such as hypothyroidism, cancer,
diabetes, HIV/AIDS, heart disease, medication
side effects, substance withdrawal, and other
illnesses. Therefore, evaluating for additional
medical issues can be important in the assessment
of depression. Second, practical considerations
should be taken into account, including the
length, whether it assesses specific aspects of
depression (i.e., measurement of suicidality and
somatic symptoms separately), reading level,
response formats, need for training to administer,
D 566 Depression: Measurement

Depression: Measurement, Table 1 Twenty-two most commonly used and validated measures of depression
Clinical Depression Time frame
Measure No. of items Assessment type Administration cutoff? specific? assessed
BDI; BDI-PC 7, 13, 21 Screening; symptom Self Yes Yes Today
rating
CES-D 10, 20 Screening; symptom Self Yes Yes Past week
rating
CGI 3 Symptom rating Clinician No No Varies
CIDI Variable Diagnostic Interviewer No Yes Past year
CIS-R Variable Diagnostic Interviewer No No Varies
DADS/DUKE- 7 Screening Self Yes No Past week
AD
DEPS 10 Symptom rating Self Yes Yes Past month
GHQ-12 12 Symptom rating Self No No Past few
weeks
HADS 14 Diagnostic Self Yes No Currently
HAM-D/HDRS 17–29 Symptom rating Clinician No Yes Varies
HSCL 13, 25 Screening; symptom Self Yes No Past week
rating
QIDS/IDS 16, 30 Diagnostic; symptom Clinician; self No Yes Past week
rating
K6/K10 6, 10 Symptom rating Self; interviewer Yes No Past month
MADRS 10 Symptom rating Clinician No Yes Varies
MDI 10 Diagnostic; symptom Self Yes Yes Past
rating 2 weeks
MINI Variable Diagnostic Clinician No No Lifetime
PHQ/PRIME- 2, 9 Screening; diagnostic Self; clinician Yes Yes Past
MD month/
2 weeks
SCID Variable Diagnostic Clinician No No Lifetime
SCL-90-R; BSI 53, 90 Symptom rating Self Yes No Past week
SDDS-PC 5 Screening; diagnostic Self; clinician No Past month
SQ 1 Screening Self No Yes Past year
ZSDS 20 Screening; symptom Self Yes Yes Recently
rating
CES-D Center for Epidemiologic Studies Depression Scale, CGI Clinical Global Impression, CIDI Composite Interna-
tional Diagnostic Interview, CIS-R Revised Clinical Interview Schedule, DADS/DUKE-AD Duke Anxiety Depression
Scale, DEPS The Depression Scale, GHQ-12 General Health Questionnaire, HADS Hospital Anxiety and Depression
Scale, HAM-D/HDRS Hamilton Depression Rating Scale, HSCL Hopkins Symptom Checklist, QIDS (IDS) [Quick]
Inventory of Depressive Symptoms, K6/K10 Kessler Psychological Distress Scale, MADRS Montgomery-Asberg
Depression Rating Scale, MDI Major Depression Inventory, MINI Mini-International Neuropsychiatric Interview,
PHQ Patient Health Questionnaire, PRIME-MD Primary Care Evaluation of Mental Disorders, SCID Structured
Clinical Interview for DSM Disorders, research version, SCL-90-R Symptom Check List Revised, BSI Brief Symptom
Inventory, SDDS-PC Symptom Driven Diagnostic System-Primary Care, SQ Single Question, ZSDS Zung Self-Rating
Depression Scale
Note: Some measures come in more than one version with varying lengths and differences in administration

and whether it can be used to assess treatment
response and severity of depression along with
being able to diagnose. Finally, the Depression
Task Force for the DSM-V is considering chang-
ing the criteria for depression to include
a specification of the severity of depression,
using the Patient Health Questionnaire (PHQ-9)
or the Clinical Global Impressions (CGI) scale.
This forthcoming change in criteria may influ-
ence the choice to include the PHQ-9 or CGI in
the measurement of depression before measures
are adapted to the new criteria.
Depression: Symptoms
Below we have provided Table 1 with the
twenty-two most commonly used and validated
measures of depression. For each measure, we
indicate the number of items, type of measure
(i.e., screening, diagnostic, and/or symptom rat-
ing scale), who can administer the measure (i.e.,
clinician, interviewer, self), whether it has any
established cutoffs for severity or clinical signif-
icance, whether the scale or one of the subscales
assesses depression specifically – as opposed to
general psychological distress or mental illness,
and the timeframe the assessment covers.
Cross-References
▶ Depression: Symptoms
References and Readings
Sharp, L., & Lipsky, M. (2002). Screening for depression
across the lifespan: a review of measures for use in
primary care settings. American Family Physician,
66(6), 1001–1008.
Simoni, J. M., Safren, S. A., Manhart, L. E., Lyda, K.,
Grossman, C. I., Rao, D., et al. (2010). Challenges in
addressing depression in HIV research: Assessment,
cultural context, and methods. AIDS and Behavior.
doi:10.1007/s10461-010-9836-3. Advanced online
publication.
Williams, J., Noël, P., Cordes, J., Ramirez, G., &
Pignone, M. (2002). Is this patient clinically
depressed? Journal of the American Medical Associa-
tion, 287(9), 1160–1170.
Depression: Symptoms
Ellen-ge Denton
Department of Medicine Center for Behavioral
Cardiovascular Health, Columbia University
Medical Center, New York, NY, USA
Synonyms
Diagnostic features of depression
567 D
Definition
Major depressive disorder (MDD) criteria
requires five or more diagnostic features, with
either (1) depressed mood or (2) anhedonia
being present during the same 2 week period
and a change in previous daily functioning.
Diagnostic features include (1) depressed
mood (feeling sad or empty); (2) markedly dimin- D
ished interest or pleasure in almost all activities
(anhedonia); (3) weight loss or weight gain (at
least 5% body weight change in a month),
increased or decreased appetite; (4) insomnia or
hypersomnia; (5) feelings of restlessness or feel-
ing slowed down (psychomotor agitation or retar-
dation); (6) fatigue, loss of energy; (7) feelings of
worthlessness, excessive or inappropriate guilt;
(8) diminished ability to think or concentrate,
indecisiveness; and (9) recurring thoughts of
death and/or suicide.
Dysthymic disorder or a chronic depressive
disorder requires depressed mood, for more
days than not, over a period of 2 years, and two
or more of the diagnostic features previously
mentioned. During the 2-year period, symptoms
of depressed mood and the minimum of two
diagnostic features are to have never remitted
for more than 2 months at a time.
Diagnostic features include (1) poor appetite
or overeating, (2) insomnia or hypersomnia,
(3) low energy or fatigue, (4) low self-esteem,
(5) poor concentration or difficulty making deci-
sions, and (6) feelings of hopelessness.
• Depression symptoms must cause clinically
significant distress or interfere with daily func-
tioning (i.e., social, occupational) or daily tasks.
• Depression symptoms are not due to a general
medical condition or due to the direct physio-
logical effects of a substance.
• Depression symptoms are not better accounted
for by bereavement.
Description
Symptoms of depression can be categorized by
a marked change in a person’s (1) physical well-
being, evidenced by changes in sleep and eating
D 568
behaviors; (2) emotional well-being, such as feel-
ings of sadness and/or hopelessness; and
(3) thoughts. For example, negative thought pat-
terns. Hallmark symptoms of depression are loss
of interest in activities (anhedonia) and
a depressed mood (melancholia), as at least one
of these symptoms are necessary for MDD diag-
nostic criteria. Depression symptoms can have
catatonic features, melancholic features, atypical
features, and postpartum onset.
Depression symptoms may present differently
among children and adolescents. Some children
may present with mood irritability or a failure to
make expected weight gains. Diagnostic duration
of symptoms for children and adolescents is typ-
ically at least 1 year.
Depression diagnosis is two times more likely
among women than men. Women’s increased
likelihood for depression is found in the general
population, across cultural groups and across
demographic groups (Bromet et al., 2011).
Although studies have not concluded that depres-
sion symptoms differ by gender (Kessler,
McGonagle, Swartz, Blazer, & Nelson, 1993),
some studies suggest men exhibit more external-
izing symptoms of depression (angry outbursts,
irritability, withdrawal, blunted affect, etc.) while
comparatively, women have more melancholic
symptoms of depression (sadness, guilt, etc.)
(Hatzenbuehler, Hilt, & Nolen-Hoeksema, 2010).
Depressive symptoms are quite common in
several biomedical health conditions and have
been shown to predict worse prognosis in
heart disease (Bush, 2002; Frasure-Smith &
Lesperance, 2006), even if at low levels. Because
depression is a heterogeneous construct with
multidimensional characteristics, the cardiovas-
cular literature has begun to identify depression
symptom clusters that are associated with worse
coronary heart disease outcome. For example,
some authors have found somatic depressive
symptoms to be associated with cardiac disease
severity (de Jonge et al., 2006; Watkins et al.,
2003). A recent study comparing cognitive affec-
tive symptoms to somatic affective depressive
symptoms found that somatic affective symp-
toms predicted worse cardiovascular outcome
while cognitive affective symptoms did not
Depression: Symptoms
(Martens, Hoen, Mittelhaeuser, de Jonge, &
Denollet, 2009). Somatic affective symptoms
include sadness, dissatisfaction, pessimism, sui-
cidal ideas, crying, work difficulty, insomnia,
fatigability, loss of appetite, somatic preoccupa-
tion, and loss of libido.
References and Readings
American Psychiatric Association. (1994). Diagnostic
and statistical manual of mental disorders (4th ed.).
Washington, DC: Author.
Bromet, E., Andrade, L., Hwang, I., Sampson, N.,
Alonso, J., de Girolamo, G., et al. (2011). Cross-
national epidemiology of DSM-IV major depressive
episode. BMC Medicine, 9(1), 90.
Bush, D. E. (2002). Cardiac disease and depression in the
elderly. Cardiology in Review, 19(11), 10–15.
de Jonge, P., Ormel, J., van den Brink, R. H. S., van
Melle, J. P., Spijkerman, T. A., Kuijper, A., et al.
(2006). Symptom dimensions of depression following
myocardial infarction and their relationship with
somatic health status and cardiovascular prognosis.
The American Journal of Psychiatry, 163(1), 138–144.
Frasure-Smith, N., & Lesperance, F. (2006). Depression
and coronary artery disease. Herz, 31(Suppl. 3), 64–68.
Goldberg, D., Kendler, K. S., Sirovatka, P. J., & Regier,
D. A. (2010). Diagnostic issues in depression and
generalized anxiety disorder: Refining the research
agenda for DSM-5. Arlington, VA: American Psychi-
atric Association.
Hales, R. E., Yudofsky, S. C., & Gabbard, G. O. (2008).
The American psychiatric publishing textbook of
psychiatry (5th ed.). Arlington, VA: American
Psychiatric.
Hatzenbuehler, M. L., Hilt, L. M., & Nolen-Hoeksema, S.
(2010). Gender, sexual orientation, and vulnerability
to depression. In J. C. Chrisler & D. R. McCreary
(Eds.), Handbook of gender research in psychology
(pp. 133–151). New York: Springer.
Kessler, R. C., McGonagle, K. A., Swartz, M., Blazer,
D. G., & Nelson, C. B. (1993). Sex and depression in
the National Comorbidity Survey I: Lifetime preva-
lence, chronicity and recurrence. Journal of Affective
Disorders, 29(2–3), 85–96.
Martens, E. J., Hoen, P. W., Mittelhaeuser, M.,
de Jonge, P., & Denollet, J. (2009). Symptom dimen-
sions of post-myocardial infarction depression, disease
severity and cardiac prognosis. Psychological Medi-
cine, 40(05), 807.
Watkins, L. L., Schneiderman, N., Blumenthal, J. A.,
Sheps, D. S., Catellier, D., Taylor, C. B., et al.
(2003). Cognitive and somatic symptoms of depres-
sion are associated with medical comorbidity in
patients after acute myocardial infarction. American
Heart Journal, 146(1), 48–54.
Depression: Treatment
Depression: Treatment
Tatsuo Akechi
Department of Psychiatry and Cognitive-
Behavioral Medicine, Graduate School of
Medical Sciences, Nagoya City University,
Nagoya, Aichi, Japan
Synonyms
Management of depression; Pharmacotherapy for
depression; Psychotherapy for depression
Definition
Effective treatment methods of patients with
depressive disorders
Description
There are several types of treatment for depres-
sion, and these are mainly somatotherapy and psy-
chotherapy. Somatotherapy for depression usually
includes pharmacotherapy and electroconvulsive
therapy (ECT). In addition, other types of
somatotherapy including transcranial magnetic
stimulation (TMS) can be available now in several
countries such as USA (Gelenberg, 2010).
With regard to pharmacotherapy, there are
several different types of drugs, so-called antide-
pressants. Antidepressants include selective
serotonin reuptake inhibitors (SSRI), serotonin
noradrenaline reuptake inhibitors (SNRI), tricy-
clic antidepressants (TCA), tetracyclic antide-
pressants, monoamine oxidase inhibitors
(MAOIs), and other types of antidepressant
drugs (Gelenberg, 2010; Hales & Yudofsky,
2003; Sadock & Sadock, 2003). The effective-
ness of these antidepressants is generally compa-
rable between classes and within classes of
medications. On the other hand, side effect
profiles clearly differ among the different classes
of antidepressants. Pharmacotherapy is most
widely used for treatment of depression.
569 D
Especially pharmacotherapy is recommended as
an initial treatment choice for patients with mild
to moderate major depressive disorder as defined
by DSM-IV-TR. The choice of each antidepres-
sant is usually determined by anticipated side
effects and safety for the individual patient. In
general, the SSRIs and other newer antidepres-
sants are better tolerated and safer than either
TCAs or the MAOIs, although many patients still D
benefit from older drugs including TCAs. During
pharmacotherapy, patients should be carefully and
regularly monitored to evaluate side effects. Over-
all, approximately two-thirds of the patients with
major depression respond to an adequate trial of
antidepressant medication. However, far few
achieve full remission of symptoms.
ECT is recommended as a treatment of choice
for patients with severe major depressive disorder
and those with psychotic features. Other cases
such as a suicidal patient with an urgent need for
response can also be appropriate for ECT treat-
ment. ECT has the highest response and remission
rates among any antidepressant treatment. ECT is
generally provided 2–3 times per week and total of
6–12 treatments. ECT is a safe treatment, and it is
suggested that risks of morbidity and mortality do
not exceed those associated with anesthesia alone.
Side effects of ECT include short-time confusion,
memory impairment, headache, muscle aches,
and so on. ECT is the use of electrically induced
repetitive firings of the neurons in the CNS. The
mechanisms of action of ECT are complex and not
completely understood.
TMS was approved for use in patients with
major depressive disorder in USA. TMS uses
a magnetic field to stimulate or inhibit cortical
neurons. Because the area of cortex stimulated is
related to placement of the coil on the skull, the
coil is most often placed over the left dorsolateral
prefrontal cortex for treatment of depression.
There are few findings regarding long-term fol-
low-up data of TMS treatment effect. So more
longer-term data and further refinement of TMS
are needed.
Regarding psychotherapy, cognitive-behavioral
therapy (CBT) and interpersonal psychotherapy
(IPT) are most well-known and proven psychother-
apeutic approaches for patients with depressive
D 570
disorders (Gelenberg, 2010). CBT combines cog-
nitive psychotherapy with behavioral therapy,
including behavioral activation, and its goal is to
reduce depressive symptoms by challenging and
reversing irrational beliefs and distorted attitudes
and encouraging patients to change their maladap-
tive preconceptions and behaviors in real life. On
the other hand, IPT focus on interpersonal factors
that may interact with the development of depres-
sive disorders. The goal of IPT is to intervene by
identifying the trigger of depression, facilitating
mourning in the case of bereavement, promoting
recognition of related affects, resolving role
disputes and role transitions, and building social
skills to improve relationships and to acquire
needed social supports. Although these psycho-
therapies are recommended as an initial treatment
choice for patients with mild to moderate major
depressive disorder, these should be used in com-
bination with pharmacotherapy for severe major
depressive disorder.
Treatments of depression generally include
several different steps, and these are acute phase
treatment, continuous phase treatment, and main-
tenance phase treatment. Primary aims of the
acute phase treatment are to improve symptoms
of depression and achieve a full return to the
patient’s functioning. Continuous phase treat-
ments are mainly provided to reduce the risk of
relapse for a patient who has been successfully
treated. Regarding patients who have had multi-
ple major depressive episodes or who have
chronic features, maintenance phase treatment
should be considered in order to reduce the risk
of a recurrent depressive episode.
Cross-References
▶ Antidepressant Medications
▶ Cognitive Behavioral Therapy (CBT)
▶ Psychoeducation
▶ Social Support
References and Readings
Gelenberg, A. J. (2010). Practice guideline for the treat-
ment of patients with major depressive disorder
(American journal of psychiatry, 3rd ed., Suppl. 167,
Descriptive Data
pp. 1–118). Washington, DC: American Psychiatric
Association.
Hales, R. E., & Yudofsky, S. C. (2003). Textbook of
clinical psychiatry (4th ed.). Washington, DC: The
American Psychiatric Publishing.
Sadock, B. J., & Sadock, V. A. (2003). Kaplan & Sadock’s
synopsis of psychiatry (9th ed.). Philadelphia:
Lippincott Williams & Wilkins.
Descriptive Data
▶ Aggregate Data
Developmental Disabilities
Monica Dowling
Miller School of Medicine, University of Miami,
Miami, FL, USA
Synonyms
Autism spectrum disorders; Intellectual disability
Definition
Developmental disabilities (DD) is an umbrella
term for a group of interrelated, chronic,
nonprogressive, neurological, or brain-based dis-
orders which are defined as “severe, life-long
disabilities attributable to mental and/or physical
impairments, manifested before age 22, that
result in substantial limitations in three or more
areas of major life activities: capacity for inde-
pendent living, economic self-sufficiency, learn-
ing, mobility, receptive and expressive language,
self-care, self-direction” (Administration on
Developmental Disabilities, 2007). In the case
of young children, DD is likely to result in sig-
nificant limitations. Low IQ scores are typically
associated with DD, and individuals with intel-
lectual disabilities comprise the largest group
considered to have DD (Larson et al., 2000), but
other conditions may impose functional limita-
tions on individuals whose intelligence is at or
Developmental Disabilities
above average. Sensory impairments are
included only as occurring in combination with
impairment in intellectual and adaptive function-
ing. The current conceptualization includes diag-
nostic classifications of intellectual disability
(formerly mental retardation), autism spectrum
disorders (ASD), cerebral palsy (CP), and spe-
cific syndromes whose behavioral phenotype
includes limitations in intellectual and adaptive
functioning (e.g., fragile X, trisomies, Prader-
Willi, Smith-Magenis) but does not specify an
etiology or medical diagnosis.
Description
Epidemiology
Researchers from the CDC estimate the preva-
lence of DD by tracking five conditions: intellec-
tual disability (ID), autism spectrum disorders
(ASD), cerebral palsy (CP), hearing loss, and
vision impairment. The essential features of
ASD are impaired reciprocal social interactions,
delayed or unusual communication styles, and
restricted or repetitive behavior patterns. ID is
defined as a condition marked by an IQ < 70
with concurrent limitations in adaptive function-
ing, previously referred to as mental retarda-
tion. Cerebral palsy is defined as a group of
nonprogressive, but often changing, motor impair-
ment syndromes secondary to brain lesions/anom-
alies arising at any time during brain development
or as a result of neonatal insult.
Developmental disabilities affect approxi-
mately 17% of children younger than 18 years
of age in the USA (Bhasin, Brocksen, Avchen, &
Van Naarden, 2006). In 2006–2008 nearly 10
million children aged 3–17 had a developmental
disability on the basis of parent report (Boyle et
al., 2011). The most recent CDC prevalence esti-
mates of ASD are 1 in 88 children (Baio, 2012).
Population-based estimates of functional limita-
tions and health services utilization among chil-
dren with DD were 4–32 times higher than for
children without DD (Boulet, Boyle, & Schieve,
2009), while the cost to society of ASD alone is
estimated to be $35–$90 billion annually (Ganz,
2007). The CDC estimates that the average
571 D
lifetime cost associated with intellectual disabil-
ity (IQ < 70) is approximately $1,014,000 per
person (in 2003 dollars).
Etiology
The likelihood of identifying an underlying eti-
ology increases with the degree of disability.
Prenatal causes include genetic abnormalities
including chromosomal abnormalities (e.g., D
trisomies, X-linked, microdeletions, and
subtelomeric rearrangements), single gene disor-
ders (e.g., X-linked recessive conditions), and
multifactorial/polygenic conditions (e.g., spina
bifida); congenital infections (e.g., rubella, syph-
ilis); alcohol and other drug or teratogen expo-
sure; and maternal disorders. Perinatal causes
include placental complications, preeclampsia/
eclampsia, birth trauma/anoxia, complications
of prematurity (e.g., IVH), infections (e.g., bac-
terial meningitis), and metabolic abnormalities.
Postnatal causes include infections, trauma, envi-
ronmental pollutants/neurotoxins, malnutrition,
and inborn errors of metabolism (e.g., PKU).
Genetic disorders now account for approxi-
mately 55% of moderate to severe ID (IQ < 50)
and 10–15% of mild ID (IQ 50–70), and these
percentages continue to increase with the use
of new molecular techniques. More than 1,000
genetic disorders leading to developmental
disabilities have been identified, many with
active research programs (Tartaglia, Hansen, &
Hagerman, 2007). Fragile X syndrome (FXS), the
most common form of inherited ID, is caused by
a mutation in a single gene (FMRP1) on the
X chromosome, resulting from expansions of
cytosine-guanine-guanine (CGG) repeats, which
interferes with the normal transcription of
a single protein (FMRP). Other disorders, such
as Smith-Magenis or velocardiofacial syndrome
(also known as 22q11.2 deletion syndrome), are
microdeletion syndromes. Prader-Willi and
Angelman syndromes are both the result of dele-
tions on the same chromosome (15), but the
expression is related to inheritance from either
the father (Prader-Willi) or mother (Angelman).
Still other disorders are characterized by the addi-
tion or absence of an entire chromosome (e.g.,
Down syndrome or trisomy 21; Klinefelter or
D 572
47, XXY; Turner or 45, X), leading to
overexpression or imbalance of many genes and
subsequent abnormalities.
Diagnosis
The American Academy of Pediatrics has
recommended that developmental surveillance
be incorporated into every well-child visit and
that any concerns should be promptly addressed
with standardized developmental screening tests
(AAP, 2006). In addition, screening tests should
be administered regularly at the 9-, 18-, and
24-month visits, including ASD specific mea-
sures. There is no universally accepted screening
tool appropriate for all populations and all ages.
However, accurate, cost-effective, and parent-
friendly questionnaires are available for ages
1 month to 5 1/2 years in multiple languages
(e.g., Ages and Stages Questionnaires, third Ed.,
Brookes Publishing). In addition, tools such as
the M-CHAT and a follow-up interview used to
screen for ASD are available, at no cost (www.
firstsigns.com), covering a range of ages (e.g.,
16–48 months) and in many languages. Once
identified as being at risk, diagnostic develop-
mental and medical evaluations should be pur-
sued, typically involving pediatric subspecialists
and using valid and reliable measures of cogni-
tion, adaptive behavior, communication, social,
and neuropsychological functioning.
Intervention/Current Best Practices
Prevention has focused on educational initiatives
to eliminate or minimize risk factors such as
smoking and alcohol use during pregnancy or
lead and mercury exposure as well as medical
initiatives such prenatal screening and treatment
for infectious disease (e.g., syphilis, CMV),
genetic screening and counseling for carriers of
genetic disorders, and the use of vaccines to pre-
vent maternal or child infections (e.g., rubella,
meningitis) (Brosco, Mattingly, & Sanders,
2006). In addition, early identification and treat-
ment (e.g., newborn screening for genetic and
metabolic disorders and fetal alcohol syndrome)
Developmental Disabilities
have been successful in limiting the impact of
severe developmental disabilities (Powell et al.,
2010; Bertrand, 2009) and pilot programs using
a variety of assays using urine or blood are under
way (e.g., cytomegalovirus). Even late treatment
has been successful in partially reversing the
severe cognitive impact associated with meta-
bolic disorders such as untreated PKU (Grosse,
2010).
Emerging areas of knowledge that influence
practice include targeted pharmacological and
evidence-based treatments for specific disorders
such as fragile X and ASD, as well as a growing
body of clinical guidelines specific to conditions
in the pediatric age range. Evidence-based com-
prehensive treatment programs for young chil-
dren with ASD emphasize behavioral- and/or
development-based models. For example, the
UCLA Young Autism Project, the Princeton
Child Development Institute, and the Douglass
Developmental Disabilities Center utilize tradi-
tional behavioral interventions(e.g., discrete trial
training). The Learning Experiences and Alterna-
tive Program for Preschoolers and their Parents
(LEAP) and the Walden Early Childhood Pro-
gram utilize behavioral interventions in natural-
istic settings and incidental teaching. Division
TEACCH incorporates both behavioral and
developmental approaches, while the Denver
Early Start Model has a developmental orienta-
tion. In addition, care consideration guidelines
are currently being developed for fragile X and
other disorders having unique behavioral pheno-
types (e.g., velocardiofacial, Smith-Magenis),
and as understanding of the underlying mecha-
nisms advances, targeted treatment studies are
under way that may eventually reverse the
neurodevelopmental abnormalities (e.g., medica-
tions that regulate the activity of the mGluR5
pathway in fragile X). At this time, best
practice includes the need for intensive, multidis-
ciplinary treatment programs for individuals
with developmental disabilities and their families
that focus on strengths and include medical,
behavioral, educational, and therapeutic
interventions.
Dexamethasone Suppression Test 573 D
References and Readings Baio, J. (2012, March). Prevalence of autism spectrum
disorders-Autism and Developmental Disabilities
Accardo, P. J. (Ed.). (2008). Capute and Accardo’s Monitoring Network, United States, 2008. MMWR
neurodevelopmental disabilities in infancy and child- Surveillance Summaries, 61(SS03), 1–19.
hood (3rd ed.). Baltimore: Brookes. Tartaglia, N. R., Hansen, R. L., & Hagerman, R. J. (2007).
Administration on Developmental Disabilities. (2007). Advances in Genetics. In S. L. Odom, R. H. Horner,
What are developmental disabilities? Washington, M. E. Snell, & J. Blacher (Eds.), Handbook of devel-
DC: Administration on Developmental Disabilities. opmental disabilities (pp. 98–128). New York:
Retrieved December 28, 2010, from www.acf.hhs. Guilford Press.
gov/opa/fact_sheets/add_factsheet.html D
American Academy of Pediatrics, Council on Children
with Disabilities. (2006). Identifying infants and
young children with developmental disorders in the Developmental Psychology
medical home: An algorithm for developmental sur-
veillance and screening. Pediatrics, 118(1), 405–420.
Bertrand, J. (2009). Interventions for children with fetal ▶ Child Development
alcohol spectrum disorders (FASDs): Overview of
findings for five innovative research projects.
Research in Developmental Disabilities, 30(5), 986–
1006.
Bhasin, T. K., Brocksen, S., Avchen, R. N., & Van Deviance
Naarden, B. K. (2006, January). Prevalence of four
developmental disabilities among children aged ▶ Stigma
8 years: Metropolitan Atlanta Developmental Disabil-
ities Surveillance Program, 1996 and 2000. MMWR
Surveillance Summaries, 55(SS01), 1.
Boulet, S., Boyle, C. A., & Schieve, L. A. (2009). Health
care use and health and functional impact of develop- Dex Suppression Test
mental disabilities among US children, 1997–2005.
Archives of Pediatrics & Adolescent Medicine,
163(1), 19–26. ▶ Dexamethasone Suppression Test
Boyle, C. A., Boulet, S., Schieve, L. A., Cohen, R. H.,
Blumberg, S. J., Yeargin-Allsopp, M., Visser, S., &
Kogan, M. D. (2011). Trends in the prevalence of
deveoplmental disabilities in US children, 1997–
2008. Pediatrics. 127(6), 1034–1042. Dex Test
Brosco, J. P., Mattingly, M., & Sanders, L. M. (2006).
Impact of specific medical interventions on ▶ Dexamethasone Suppression Test
reducing the prevalence of mental retardation.
Archives of Pediatrics & Adolescent Medicine,
160(3), 302–309.
Ganz, M. L. (2007). The lifetime distribution of the incre-
mental societal costs of autism. Archives of Pediatrics Dexamethasone Suppression Test
& Adolescent Medicine, 161(4), 343–349.
Gross, S. D. (2010). Late-treated phenylketonuria and
partial reversibility of intellectual impairment. Child Brigitte M. Kudielka
Development, 81(1), 200–211. Department of Medical Psychology &
Larson, S., Lakin, C., Anderson, L., Kwak, N., Lee, J. H., Psychological Diagnostics, University of
& Anderson, D. (2000). Prevalence of mental retarda-
Regensburg, Regensburg, Germany
tion and/or developmental disabilities: Analysis of the
1994/1995 NHIS-D. MR/DD Data Brief, 2(1), 1–11.
Powell, K., Van Naarden Braun, K., Singh, R., Shapira,
S. K., Olney, R. S., & Yeargin-Allsopp, M. (2010). Synonyms
Prevalence of developmental disabilities and receipt of
special education services among children with an
inborn error of metabolism. Journal of Pediatrics, Dex suppression test; Dex test; DST; HPA axis
156(3), 420–426. negative feedback testing
D 574
Definition
Dexamethasone is a synthetic glucocorticoid
and acts as a ligand of glucocorticoid receptors.
The principle of the dexamethasone suppression
test (DST) is based on this binding capability.
Via receptor binding, dexamethasone exerts
a negative feedback function on the hypothala-
mus-pituitary-adrenal (HPA) axis (de Kloet,
Vreugdenhil, Oitzl, & Joels, 1998). The HPA
axis is a hierarchical hormonal system
encompassing the hypothalamus, the pituitary
gland, and the adrenal cortex with their respec-
tive hormones CRH (corticotropin releasing
hormone), ACTH (adrenocorticotropin hor-
mone), and cortisol. Beside its role in stress
regulation, the HPA axis is vital for supporting
normal physiological functioning. Its function-
ing is controlled by several negative feedback
loops. Generally, the DST is applied as
a standard diagnostic tool to assess feedback
sensitivity of the HPA axis in clinical settings
(e.g., in major depression, posttraumatic stress
disorder, etc.) as well as in psychoneuroendocri-
nological research (e.g., in stress research)
(Bellingrath, Weigl, & Kudielka, 2008; Yehuda
et al., 1993).
The dexamethasone suppression test normally
consists of the oral intake of a single dose of
dexamethasone (see below) which then leads to
the suppression of ACTH at the level of the
pituitary and subsequently to a reduced cortisol
secretion from the adrenal cortex. Of course,
dexamethasone can also be applied intrave-
nously. In contrast to endogenous glucocorticoids
like cortisol, dexamethasone primarily acts at
the level of the pituitary (due to the blood-brain
barrier). Selected doses of dexamethasone vary
depending on the aim of the diagnostic test, the
tested population, or the given research question.
A typical dose to identify individuals with
increased cortisol suppression after dexametha-
sone intake (indicating increased negative feed-
back sensitivity) is the application of 0.5 mg of
dexamethasone. Oral intake normally takes place
at 11 pm and cortisol measurements are repeat-
edly performed during the following morning or
day to account for the normal circadian rhythm of
Dexamethasone Suppression Test
cortisol (and ACTH) with highest levels in the
morning and decreasing levels over the remain-
der of the day (except for stress-related
superimposed hormone surges). After ingestion
of a standard dose of 1 mg of dexamethasone, an
almost complete suppression of the cortisol
secretion in healthy individuals can be expected.
That means, cortisol levels are typically
suppressed to concentrations less than 5 mg/dl
until the following afternoon after the intake of
1 mg dexamethasone the night before. However,
in the normal population up to 10% non-
suppressors can be identified. Fortunately, there
are virtually no side effects reported for a single
dexamethasone intake of 1–2 mg of dexametha-
sone. In different patient groups, either no corti-
sol suppression (e.g., in Cushing’s disease) or
cortisol super-suppression (e.g., in some patients
suffering from posttraumatic stress disorder) can
be observed. For the diagnosis of Cushing’s
disease, dexamethasone doses of up to 8 mg are
applied. However, it is of note here that other
tests need to complement a definite diagnosis of
Cushing’s disease.
In recent years, a much lower dexamethasone
dosage of 0.25 mg was suggested (mainly for
research purposes) to increase the sensitivity of
the DST, called low-dose DST (Cole, Kim,
Kalman, & Spencer, 2000; Yehuda, et al.,
1993). This version of the test is advantageous if
subtle differences are to be detected in HPA axis
negative feedback sensitivity in apparently
healthy individuals (Bellingrath et al., 2008).
After intake of 0.25 mg of dexamethasone,
endogenous cortisol concentrations of about
5 mg/dl can normally be expected.
One should be aware of the fact that an
unequivocal interpretation of DST results should
additionally account for the following two issues:
Since the exact amount of circulating dexameth-
asone is dependent on metabolic functioning,
bioavailability of dexamethasone should be con-
trolled for, especially in certain patient groups
with known metabolic dysfunctions. Further-
more, in order to rule out altered reactivity of
the adrenal cortex to ACTH signals, one should
want to additionally check the extent of ACTH
suppression.
Diabesity in Children
Finally, the DST can also be combined with
other pharmacological provocation tests like the
CRH stimulation tests (Heuser, Yassouridis, &
Holsboer, 1994). Over the last decades, the
combined Dex-CRH test applying a
premedication of 1.5 mg dexamethasone the
night before followed by a CRH application
(e.g., 100 mg or 1 mg/kg body weight) the follow-
ing afternoon proved its usefulness especially for
the assessment of HPA axis feedback regulation
in psychiatric disorders.
Cross-References
▶ ACTH
▶ Adrenal Glands
▶ Adrenocorticotropin
▶ Corticotropin-Releasing Hormone (CRH)
▶ Cortisol
▶ Depression
▶ Endocrinology
▶ Glucocorticoids
▶ Hypothalamic-Pituitary-Adrenal Axis
▶ Pituitary-Adrenal Axis
▶ Stress
References and Readings
Bellingrath, S., Weigl, T., & Kudielka, B. M. (2008).
Cortisol dysregulation in school teachers in relation
to burnout, vital exhaustion, and effort-reward-imbal-
ance. Biological Psychology, 78(1), 104–113.
Cole, M. A., Kim, P. J., Kalman, B. A., & Spencer, R. L.
(2000). Dexamethasone suppression of corticosteroid
secretion: evaluation of the site of action by receptor
measures and functional studies. Psychoneuroendo-
crinology, 25(2), 151–167.
de Kloet, E. R., Vreugdenhil, E., Oitzl, M. S., & Joels, M.
(1998). Brain corticosteroid receptor balance in
health and disease. Endocrine Reviews, 19(3),
269–301.
Heuser, I., Yassouridis, A., & Holsboer, F. (1994). The
combined dexamethasone/CRH test: A refined labora-
tory test for psychiatric disorders. Journal of Psychi-
atric Research, 28(4), 341–356.
Yehuda, R., Southwick, S. M., Krystal, J. H., Bremner, D.,
Charney, D. S., & Mason, J. W. (1993). Enhanced
suppression of cortisol following dexamethasone
administration in posttraumatic stress disorder. The
American Journal of Psychiatry, 150(1), 83–86.
575 D
DHA
▶ Omega-3 Fatty Acids
Diabesity in Children
D
Francine Kaufman
Medtronic, Northridge, CA, USA
Synonyms
Childhood obesity; Obesity
Definition
The association of obesity and diabetes has been
recently referred to as diabesity.
Description
In 2000, then Surgeon General David Satcher
announced that the epidemic of obesity in the
United States was increasingly affecting children
and adolescents (Satcher, 2001). At the time of
the surgeon general’s announcement, approxi-
mately 16% of youth were categorized as being
obese, defined as a body mass index (BMI) greater
than the 95th percentile for age and gender. Over-
all, that same childhood obesity rate persists in the
USA today; however, minority children have sig-
nificantly higher rates. Data from the HEALTHY
study in middle school–aged children showed that
approximately 50% of sixth grade students in
middle schools with a predominate minority pop-
ulation were overweight or obese (BMI  85th
percentile for age and gender) (HEALTHY,
HEALTHY Study Group, 2010).
Concomitant with the rise in childhood obe-
sity is a corresponding increase in the incidence
of the metabolic syndrome and type 2 diabetes in
pediatric subjects. Before the 1990s, it was rare
for most pediatric centers to have patients with
D 576
type 2 diabetes. By 1994, type 2 diabetes patients
represented up to 16% of new cases of diabetes in
children in urban areas, and by 1999, depending
on geographic location, the range of percentage
of new cases of type 2 was between 8% and 45%
(HEALTHY, HEALTHY Study Group, 2010).
The SEARCH study showed that after age
10 years, of all American Indian children who
have diabetes, two thirds have type 2; of all
Hispanic and African American children with
diabetes, approximately a third have type 2; and
only 8% of non-Hispanic White children affected
with the disease have type 2 (SEARCH, 2006).
Therefore, type 2 diabetes occurs mainly in eth-
nic minorities in the United States, as has been
described in children in a number of countries
throughout the world.
A period of prediabetes, defined as either ele-
vated fasting glucose levels, impaired glucose
tolerance, and/or elevated A1C (5.7– < 6.4%),
occurs before the development of frank type 2
diabetes. Type 2 diabetes in children and youth, as
in adults, is caused by the combination of insulin
resistance and relative B cell secretary failure.
Plasma insulin concentrations appear normal or
elevated, but there is a loss of first-phase insulin
secretion that cannot compensate for underlying
insulin resistance. There are a number of genetic
and environmental risk factors for insulin resis-
tance and limited B cell reserve, including
ethnicity, obesity, sedentary behavior, family his-
tory of type 2 diabetes, puberty, high and low
birth weight, and female gender. Family educa-
tion level, SES, maternal diabetes or excessive
weight gain, failure to breast feed, and exposure
to an obesogenic environment are additional risk
factors.
Type 2 diabetes in pediatric subjects has
a variable presentation, although many children
present with symptoms caused by elevated glu-
cose. There is an associated increase in A1C
6.4% which can be used to make the diagnosis.
Few pediatric subjects with type 2 diabetes can be
treated with diet and exercise alone; therefore,
pharmacologic therapy is most often required.
Depending on initial glucose levels and the
degree of symptoms caused by hyperglycemia,
practitioners usually prescribe metformin for
Diabesity in Children
those subjects who are mildly affected, or sub-
jects begin insulin therapy if they have more
significant hyperglycemia. Relatively few pedi-
atric subjects use other or combination therapy.
Unfortunately, while they are undergoing the
present pharmacologic regimens, many patients
appear unable to achieve glycemic targets over
the long term. Specific treatment algorithms for
pediatric patients with type 2 diabetes that are
aimed at achieving glycemic targets have not
been investigated in youth. The ongoing Treat-
ment Options for type 2 Diabetes in Adolescents
and Youth (TODAY) trial, sponsored by the
National Institutes of Health, has investigated
best treatments for type 2 diabetes in pediatric
subjects and will provide evidence for improving
the outcome of pediatric type 2 diabetes.
The term diabesity was coined to raise aware-
ness about the adverse health effects of obesity.
Today, obesity and diabetes has become a health-
care crisis of epidemic proportions. It is a given
that individuals and families must change their
behavior if we are to reverse the present trends.
But they cannot do it on their own. Reversing the
trends will require the coordinated efforts from
local, state, and national governments; public and
private industries; community and religious orga-
nizations; schools; and the health-care system.
Information must be provided, social norms
must change, and, most importantly, an environ-
ment that supports healthy lifestyles must be cre-
ated. Only then will the childhood diabesity
epidemic be reversed.
Cross-References
▶ Obesity in Children
▶ Type 2 Diabetes Mellitus
References and Readings
HEALTHY, HEALTHY Study Group. (2010). A school-
based intervention for diabetes risk reduction. The New
England Journal of Medicine, 363, 443–453.
Kaufman, F. R. (2005). Type 2 diabetes in children and
youth. Endocrinology and Metabolism Clinics of
North America, 34, 659–676.
Diabetes Education
Satcher, D. (2001). The Surgeon General’s call to action
to prevent and decrease overweight and obesity.
Rockville, MD: Public Health Service, Office of
the Surgeon General, United States Department of
Health and Human Services. Available at http://
www.surgeongeneral.gov/topics/obesity/calltoaction/
CalltoAction.pdf
SEARCH Study Group: The Burden of Diabetes Mellitus
Among U.S. Youth. (2006). Prevalence estimates from
the SEARCH for Diabetes in Youth Study. Pediatrics,
118, 1510–1518.
Diabetes
Luigi Meneghini
Diabetes Research Institute, University of
Miami, Miami, FL, USA
Synonyms
Hyperglycemia
Definition
Diabetes (mellitus) is defined as elevated blood
glucose levels (hyperglycemia), which over time
can lead to chronic microvascular complications
such as diabetic retinopathy, nephropathy, and
neuropathy. Diabetes is caused by deficiency in
insulin production (type 1 diabetes), which in
many cases can be accompanied by increased
insulin demand, also known as insulin resistance
(type 2 diabetes). Type 2 is the most common
form of diabetes accounting for 85–90% of all
cases. Diabetes can be diagnosed by way of
a fasting plasma glucose (126 mg/dl), an ele-
vated HbA1c (6.5%) or an oral glucose toler-
ance test (2-h postchallenge plasma
glucose 200 mg/dl). Alternatively, someone
presenting with symptoms of hyperglycemia,
such as excessive thirst or urination, blurring of
vision, or weight loss, combined with a random
plasma glucose of 200 mg/dl, can also be diag-
nosed with diabetes.
Control of hyperglycemia is essential to
reduce the risk of chronic microvascular
577 D
complications associated with diabetes. This can
be done through adopting healthy lifestyle and
dietary habits, the use of oral medications to
lower blood glucose, and/or the use of insulin
replacement therapy. Diabetes is often a familial
disease with genetic and environmental
predisposing factors. First-degree relatives of
individuals with diabetes have an approximate
fivefold to tenfold increase in the risk of devel- D
oping diabetes compared to the general
population.
While diabetes mellitus (“sweet siphon”)
refers to the more common form of diabetes, char-
acterized by hyperglycemia, diabetes insipidus
(“bland or tasteless siphon”) refers to an inability
to retain free water due to deficiencies in the
production or action of antidiuretic hormone
(vasopressin).
References and Readings
Joslin, E. P., & Kahn, C. R. (2005). Joslin’s diabetes
mellitus (14th ed.). Philadelphia: Lippincott Williams
& Willkins.
Diabetes Education
Luigi Meneghini
Diabetes Research Institute, University of
Miami, Miami, FL, USA
Synonyms
Patient education; Self-management education
Definition
Diabetes education is the process of enabling
patients with diabetes to gain knowledge, prob-
lem-solving skills, empowerment, and ability
to manage their condition through the applica-
tion of appropriate treatments and lifestyle
intervention.
D 578 Diabetes Foot Care

Description (nurse, dietitian, pharmacist, etc.) develop and

implement educational interventions based on
Diabetes is a chronic condition whose manage- a curriculum that relies on current evidence and
ment and control is highly dependent on both practice guidelines. Patients need to receive
appropriate treatment prescriptions and patient a documented individual assessment and educa-
implementation of those recommendations. tion plan, with a personalized follow-up plan for
Proper diabetes management requires a high ongoing education and support. Measurement of
degree of involvement on the part of the patient patient-defined goals forms the basis for patient
if it is to be successful. Education for patients reassessment and ongoing support and education.
with diabetes requires transfer of knowledge, as The DSME also needs to measure and document
well as problem-solving skills, that incorporates the effectiveness of the education process and
the needs, goals, and experiences of patients use this opportunity for continuous quality
with diabetes, with the ultimate objective of improvement.
supporting “informed decision making, self-care
behaviors, problem solving, and active collabo-
ration with the health-care team.” The implemen-
Cross-References
tation of appropriate treatment prescriptions and
self-management behaviors needs to ultimately
▶ Patient Education
lead to improved clinical outcomes, health, and
▶ Self-management Education
quality of life.
Diabetes self-management standards have
been modified over the years to incorporate evi-
dence-based recommendations. Guiding princi- References and Readings
ples for these standards, which need to be
adhered to by any entity seeking accreditation Funnell, M. M., Brown, T. L., Childs, B. P., Haas, L. B.,
Hosey, G. M., Jensen, B., et al. (2011). National stan-
for their educational activities, dictate that diabe- dards for diabetes self-management education. Diabe-
tes education should improve clinical outcomes tes Care, 34(Suppl 1), S89–S96.
and quality of life, incorporate empowerment
models, and individualize the educational
approach to include behavioral and psychological
strategies that are culturally and age appropriate.
Group education, ongoing reassessment and edu- Diabetes Foot Care
cation, and behavioral goal setting are critical
elements to successful patient education pro- Kathleen Michael
grams. The American Diabetes Association has School of Nursing, University of Maryland,
published specific standards for diabetes self- Baltimore, MD, USA
management education (DSME) that address
several areas. DSME programs need a clear orga-
nizational structure, mission statement, and goals Synonyms
that are overseen by an advisory group, which
include representatives from health profes- Diabetic foot care
sionals, patients, community, and other stake-
holders. The DSME programs need to determine
the specific educational needs of their target Definition
populations and identify appropriate resources
to meet those needs; they must designate Routine care of the feet for individuals who have
a professional coordinator to manage the pro- diabetes, including inspection, skin and nail care,
gram. Professional and experienced educators and prevention of injury.
Diabetes Prevention Program
Description
Diabetes may cause nerve damage that affects
feeling in the feet. Diabetes may also reduce
blood flow to the feet, making it harder to heal
injuries or to resist infection.
Most people with diabetes can prevent serious
foot problems by taking some simple actions.
Routine foot care should include an annual foot
exam by a healthcare provider, or more often if
foot problems are present. The exam includes
evaluation for injuries or breaks in the skin, nail
problems, pain, sensitivity, or changes in foot
shape or skin color. In some cases, healthcare
providers may recommend specially fitted shoes.
Individuals with diabetes should inspect their
feet every day, looking for red spots, cuts, swell-
ing, or blisters. They should wash feet daily and
apply moisturizing lotion to tops and bottoms of
feet, but not between toes. Toenails should be
trimmed straight across and filed if they can be
easily seen and reached, otherwise a foot care
specialist should trim nails. Shoes and socks
should be worn at all times to prevent injury to
the feet. Other self-care measures to prevent foot
problems include keeping blood glucose levels
controlled, not smoking, and avoiding sitting and
crossing legs for prolonged periods. Increased
activity may promote foot health along with
other overall benefits to the cardiovascular system.
Cross-References
▶ Preventive Care
Diabetes Prevention Program
David G. Marrero
Diabetes Translational Research Center, Indiana
University School of Medicine, Indianapolis,
IN, USA
Synonyms
Type 2 diabetes prevention
579 D
Definition
There are several factors that increase a person’s
risk for developing type 2 diabetes mellitus.
These include increased age, a family history of
diabetes, race (persons of color having greater
risk), obesity, body fat distribution, physical
inactivity, and evidence of a metabolic defect as
measured by either elevated fasting glucose, D
impaired glucose tolerance, or elevated
glycosylated hemoglobin A1c. Because many of
these risk factors are modifiable, notably obesity
and activity patterns, it should be possible to
reduce risk by interventions designed to help
high risk persons reduce weight and increase
their levels of physical activity. There is increas-
ing evidence that this is indeed the case. In 1997,
the Chinese first reported that lifestyle interven-
tion in persons with impaired glucose tolerance
(IGT) resulted in a significant reduction in the
incidence of diabetes, with a 40% reduction
occurring over a 6-year period (Pan et al., 1997).
In 2001, the Finns reported that lifestyle interven-
tion in persons with IGT resulted in a 58% reduc-
tion in 3-year diabetes incidence (Tuomilehto
et al., 2001), and in 2002, the American Diabetes
Prevention Program (DPP) study reported an
identical 3-year reduction in diabetes incidence
(Knowler et al., 2002). This entry focuses on
the DPP.
Description
The DPP was a three-group randomized clinical
trial that was conducted in 27 centers across the
United States. The 3,234 subjects were all
25 years of age or older, had IGT, and a body
mass index (BMI) of at least 24 kg/m2. All ethnic
groups were represented with 45% of the cohort
being African American, Hispanic American,
American Indian, or Asian/Pacific Islander. In
addition, 68% of the cohort was women, 31%
between the ages of 25–44, 49% between 45
and 59, and 20% 60 and above. Subjects were
randomly assigned to a medication condition
(using metformin), a medication placebo control
condition, or a lifestyle intervention. The lifestyle
D 580
intervention was an intensive program with very
specific goals: a minimum of 7% loss of body
weight and maintenance of this weight loss
through the course of the trial and a minimum
of 150 min per week of physical activity with
brisk walking being the standard.
The lifestyle intervention was a 16-session core
curriculum implemented over 24 weeks to account
for holidays and regionally defined special events.
Each session was taught by a lifestyle coach who
worked with the subject one on one. In addition,
subjects had access to a dietitian, a behaviorist,
and exercise physiologist if they so elected. Fre-
quent contact with the lifestyle coach and support
staff was the norm with most subjects following
a weekly meeting schedule (The Diabetes Preven-
tion Program (DPP) Research Group, 2002).
The intervention provided education and
training in diet and exercise methods and behav-
ior modification skills. Emphasis was placed on
the use of self-monitoring techniques to assess
dietary intake and diet composition, active prob-
lem solving to reduce the impact of personal and
social cues to eat in ways counterproductive to
achieving weight goals, and building self esteem,
empowerment, and social support to reinforce
lifestyle modifications. The intervention was
individualized to address social and cultural fac-
tors that impact eating behavior, and a long-term
maintenance program was introduced following
the core curriculum.
The intervention was successful in reducing
the risk for developing type 2 diabetes by 58%.
Subjects in the lifestyle condition lost an average
of 7 kg following the core curriculum and
maintained a negative weight loss with an aver-
age loss of approximately 4 kg and 36 months
postcore. In addition, 74% of the subjects in the
lifestyle condition achieved the minimum study
goal of 150 min of physical activity per week
with the mean activity level at the end of the
core curriculum being 224 min per week. Impor-
tantly, the intervention was effective for all par-
ticipants, regardless of race, age, or gender.
As noted above, this is the same percentage of
risk reduction obtained by the Finns. It is exceed-
ingly rare in the annals of human clinical trials
that two independent studies conducted on
Diabetes Prevention Program
separate continents would report identical find-
ings. A reasonable assumption is that the Finnish
and American trials used identical lifestyle inter-
ventions (both were delivered to individual partic-
ipants rather than in group sessions). However,
they were quite different with the American trial
being substantially more intensive. In the Finnish
trial, each participant in the lifestyle intervention
group had seven sessions with a nutritionist during
the first year of the study and one session every
3 months thereafter (Tuomilehto et al., 2001).
It is tempting to conclude that the American
approach to lifestyle intervention was less effi-
cient than that used by the Finns, but there are
differences between the Finnish and American
participants worth noting. The mean body mass
index (BMI; kg/m2) in the Finnish sample was
about 31, and in the American sample it was
about 34, suggesting that the Americans were
9–10 kg heavier, on average, than the Finns.
The DPP cohort was heterogeneous in terms of
age and race/ethnicity whereas the Finns studied
a fairly homogenous population. In addition,
because of local environmental and cultural dif-
ferences between Finland and the USA, it is
likely there were fewer opportunities for physical
activity for American participants than for Finns.
The prevention of type 2 diabetes is clearly
a behavioral issue that involves implementing
interventions designed to modify eating and
physical activity behaviors. Future efforts need
to consider how to translate efficacy studies such
as those reviewed here into the broader public
health. Such efforts need to involve behavioral
scientists in the design of these interventions.
Cross-References
▶ Diabetes Education
▶ Type 2 Diabetes
References and Readings
Knowler, W. C., Barrett-Connor, E., Fowler, S. E.,
Hamman, R. F., Lachin, J. M., Walker, E. A., et al.
(2002). Reduction in the incidence of type 2 diabetes
with lifestyle intervention or metformin. The New
England Journal of Medicine, 346, 393–403.
Diabetes: Psychosocial Factors
Pan, X. R., Li, G. W., Hu, Y. H., Wang, J. X., Yang, W. Y.,
An, Z. X., et al. (1997). Effects of diet and exercise in
preventing NIDDM in people with impaired glucose
tolerance. The Da Qing IGT and Diabetes Study. Dia-
betes Care, 20, 537–544.
The Diabetes Prevention Program (DPP) Research Group.
(2002). The Diabetes Prevention Program (DPP):
Description of lifestyle intervention. Diabetes Care,
25, 2165–2171.
Tuomilehto, J., Lindström, J., Eriksson, J. G., Valle, T. T.,
Ämalainen, H., Lanne-Parikka, P., et al. (2001). Pre-
vention of type 2 diabetes mellitus by changes in
lifestyle among subjects with impaired glucose toler-
ance. The New England Journal of Medicine, 344,
1343–1350.
Diabetes: Psychosocial Factors
Maartje de Wit
Medical Psychology, VU University Medical
Center, Amsterdam, North Holland,
The Netherlands
Definition
Diabetes psychosocial factors are those factors
associated with the psychological and social
well-being of people with diabetes, as well as
how those factors are related to diabetes-related
self-management behaviors and glycemic
control.
Description
The daily self-care of patients with diabetes
mellitus type 1 or 2 is crucial for achieving
blood glucose targets. Self-management is the
foundation of diabetes treatment. A good under-
standing of the changes and challenges faced by
people with diabetes is therefore essential in
guiding these patients. We should remember
that despite medication and improvements in
administration systems, over one third of patients
have long-term poorly controlled diabetes and
thus a greatly increased risk of micro- and
macro-vascular complications (Harris, 2000;
Writing Team for the Diabetes Control and
581 D
Complications Trial/Epidemiology of Diabetes
Interventions and Complications Research
Group, 2002). Psychological and social factors
play an important role in the self-management
of diabetes. This involves more than just knowl-
edge of the patient. Research on self-care of dia-
betes patients shows that especially perceptions,
attitudes, emotions, and social support are impor-
tant in the process of behavior change. D
Adaptation and Self-management
Diabetes is a chronic disease that puts specific
demands on the daily life of patients. The most
important task is keeping blood glucose values
within normal limits in different situations. This
requires the patient to be always aware of the
effects of diet, physical activity, and glucose-
lowering medication. Patients using insulin are
advised to monitor their blood glucose levels
frequently, to anticipate changing circumstances,
and if necessary, to correct the glucose concen-
tration in a timely manner. Fluctuations in blood
glucose levels are often unavoidable. Low blood
glucose (hypoglycemia) may seriously disrupt
daily functioning and thus lead to frustration
and anxiety in patients as well as in their family
members.
Many patients with type 2 diabetes have, in
addition to impaired glucose regulation, meta-
bolic problems requiring a change of lifestyle
and drug treatment. An increasing number of
patients with type 2 diabetes need to take several
oral medications each day, and many of them also
need daily insulin injections. For many, this treat-
ment appears a difficult task, which translates
into poor treatment adherence. Diabetes is truly
regarded as one of the most psychologically dam-
aging chronic diseases with a high risk of
“burnout.”
After Diagnosis
The adjustment process starts with the diagnosis.
In type 1 diabetes, the majority of cases are diag-
nosed early in childhood and impact the entire
family. Understandably, the diagnosis causes
strong feelings of fear and uncertainty. Most chil-
dren and their parents appear to adjust quite well
to the new situation after some time (Anderson,
D 582
2003). Successful adaptation depends on the
family situation and the quality of care provided.
Generally, during adolescence, a worsening of
diabetes is seen. Increasing insulin resistance
plays a role, but also the tendency of adolescents
to diminish their attention to their diabetes and to
take more risks. Conflicts may arise in the family,
which in turn contribute to poorer adjustment of
blood glucose of youths. However, young people
with diabetes tend to rate their psychosocial
well-being equal to that of their healthy peers
(de Wit et al., 2007).
Diabetes mellitus type 2 is, in most cases,
diagnosed in adulthood although in recent years
the mean age at diagnosis has decreased.
Research shows that when type 2 diabetes is
diagnosed at an early stage, this causes little or
no emotional reaction (Adriaanse & Snoek,
2006). This is presumably because a medical
treatment is usually not an issue and initially
“only” lifestyle changes of patients are requested.
Longitudinal research has shown that the signif-
icance of diabetes and the psychological impact
of this disease changes over time (Thoolen,
de Ridder, Bensing, Gorter, & Rutten, 2006). It
is therefore important not only to pay attention to
adaptation problems soon after diagnosis, but
also in the subsequent treatment process. In
patients with type 1 or type 2 diabetes, possible
health complications may occur that seriously
complicate daily functioning and adversely affect
quality of life.
Social Support
Social support is a complex construct, but gener-
ally is found to have positive effects on diabetes
management. Research has demonstrated
positive effects on adherence and control for
both structural support (e.g., family, friends,
co-workers, density of support networks) and
functional support (e.g., diabetes-specific help,
communication style, cohesiveness). Especially
in adolescents, the importance of a supportive
family has been shown. Open, empathic commu-
nication within families and continued parental
involvement in diabetes care is important
for achieving good adherence and glycemic
outcomes (Anderson, 2003). Evaluation of
Diabetes: Psychosocial Factors
interventions designed to enhance support, such
as social skills training, and improved under-
standing about diabetes for families, has revealed
positive effects on adherence and control. Several
trials have demonstrated that group instruction to
impart diabetes knowledge and coping skills pro-
duces better results than individualized instruc-
tion. Support provided through self-help groups
or through a mentor (a well-adjusted patient) has
been promoted but not researched in the context
of diabetes.
Quality of Life
Diabetes, with daily requirements for self-
monitoring and management in order to avoid
the short-term consequences of hypoglycemia
and the long-term complications associated with
hyperglycemia, has a substantial impact on daily
life. The demands of daily self-care can easily
interfere with normal routines and friendships,
thereby compromising emotional and social
well-being. Attaining strict glycemic control as
well as good quality of life (QoL) is a challenge
for people with diabetes, their families, and
health-care providers. This has led to consider-
able interest in diabetes-specific quality of life,
assessed through a wide range of concerns
including morale, well-being, depression, and
role functioning. Studies looking into the rela-
tionship between diabetes control and QoL find
low correlations, if any, although there is
evidence to suggest that patients suffering from
diabetes-related complications (neuropathy, reti-
nopathy, nephropathy) on average report lower
levels of QoL compared to patients without sec-
ondary complications (Snoek, 2000). In children,
the relationship between glycemic control and
QoL is complex and inconsistent across studies
as well (Bryden et al., 2001; Hoey et al., 2001; de
Wit et al., 2007).
Psychiatric Comorbidity
Diabetes has long been associated with the
psychological constitution of patients. Their
mental state was considered to be the cause of
the disease or as a factor in diabetes regulation.
Diabetes: Psychosocial Factors
Indeed, a meta-analysis does show that depres-
sion increases the risk of developing type 2
diabetes by 30%, taking known risk factors into
account (Knol et al., 2006). There is evidence that
patients with poorly controlled type 1 diabetes, as
measured by levels of glycosylated hemoglobin
(HbA1c), can be distinguished psychologically
as a group from patients with well-controlled
diabetes on measures of depression and eating
disorders. In patients with type 2 diabetes,
there is also evidence of a relationship between
depression and poorer glycemic control. There is
increasing evidence that psychiatric comorbidity
is more frequent in adults as well as adolescents
with diabetes than in the general population
(Anderson, Freedland, Clouse, & Lustman,
2001; Bryden et al., 2001), with adverse conse-
quences for diabetes control. Below three major
mental disorders that can complicate the treat-
ment of diabetes are discussed.
Eating Disorders
Food and postponement of food are inextricably
linked to a disturbance of blood glucose control
in people with diabetes. Time to think about what
you eat and when, can result in feelings of frus-
tration and “binge eating,” especially if the diet is
restrictive. This may explain the increased prev-
alence of “binge eating disorder” in female
patients with type 2 diabetes (Kenardy et al.,
2001). In girls with type 1 diabetes, the preva-
lence of bulimia nervosa is elevated (Colton,
Olmsted, Daneman, Rydall, & Rodin, 2004).
Eating disorders almost always go along with an
elevated HbA1c, frequent fluctuations in blood
glucoses, and a greatly increased risk of early
development of microvascular complications.
Underdosing of insulin as a way to lose weight
is not uncommon, particularly among adolescent
girls. Among girls with type 1 diabetes, 10%
admit to skipping some insulin injections,
and 7.5% report injecting less insulin than is
required in order to lose weight (Neumark-
Sztainer et al., 2002). The treatment of severe
eating disorders in diabetes is complex and
requires a close collaboration between diabetes
clinicians and professionals of clinics specialized
in eating disorders.
583 D
Anxiety
Extreme anxiety may affect diabetes control,
primarily by the disturbing effect of stress hor-
mones, but also by avoidance behavior. One must
be careful in giving alarming information like
risk of diabetes-related health complications
(“fear appeals”) if one wants to encourage
patients to improve self-management. Most dia-
betes patients are already concerned about the D
potential complications of their illness, and fur-
ther increasing this fear probably does more harm
than good. Two fears specific to patients with
diabetes require special attention, namely, fear
of injections and self-monitoring of blood glu-
cose and fear of hypoglycemia. Although the
prevalence of extreme anxiety for the injection
of insulin and for self-monitoring of blood glu-
cose is low among diabetic patients using insulin
(0.3–1.0%), this fear may be accompanied by
great distress and poor diabetes regulation. More-
over, 40% of patients with a phobic fear of injec-
tions also have a phobia of pricking the finger to
obtain a blood sample. Data on the effects
of psychological treatment for self-testing or
injection fear are scarce. Both phobias are often
associated with other psychiatric disorders,
which makes these patients particularly vulnera-
ble (Mollema, Snoek, Ader, Heine, & van der
Ploeg, 2001).
Hypoglycemia remains the major side effect
of intensive insulin therapy. Exact data are
lacking, but a large proportion of patients using
insulin have frequent worries about hypoglyce-
mia. More uncommon is a phobic fear of hypo-
glycemia which can arise once a patient
experienced a severe hypoglycemia with loss
of consciousness. Patients with a compulsive or
panic disorder can be extremely afraid of hypo-
glycemia without ever having had a real risk.
A complicating factor is that anxious patients
often do not know whether the symptoms of
sweating, dizziness, and heart palpitations they
are experiencing are due to dropping blood glu-
cose levels or a panic attack. It is understandable
that phobic patients may pursue “safe” blood
glucose levels, which translates into a higher
HbA1c. Patients with milder forms of fear benefit
from hypoglycemia prevention training, which
D 584
aims to improve their symptom perception and
better recognition of risk factors for hypoglyce-
mia (Cox et al., 2001). Phobic patients and part-
ners can benefit from cognitive behavioral
therapy where they can learn to examine how
realistic their views on hypoglycemia are and
replace irrational thoughts with more adaptive
cognitions.
Depression
Mood disorders are twice as common in patients
with diabetes compared to the general popula-
tion. The prevalence of moderate to severe
depression among both type 1 and type 2 diabetes
patients is estimated at 10–20% (Anderson et al.,
2001). For adolescents with type 1 diabetes, the
risk of depression is 2–3 times higher compared
to their healthy peers (Hood et al., 2006). The
relationship between diabetes and depression is
not entirely clear. Probably biochemical and psy-
chosocial factors play a role. Patients with
depressive symptoms have poorer glycemic con-
trol and more complications and are more often
hospitalized. Early recognition and treatment of
depression in people with diabetes will probably
result in major health benefits. Both psychologi-
cal and pharmacological treatments of depression
in diabetes patients are proven to be effective
(Katon et al., 2004).
Sexual Problems
It is estimated that approximately 50% of men
with a diabetes duration greater than 5 years have
some degree of erectile dysfunction, with adverse
effects on their perceived quality of life. It seems
that these sexual problems are not often discussed
with health-care professionals (De Berardis et al.,
2002). Neuropathy and metabolic disorders
are considered as the main causes of erectile
dysfunction, but acute fluctuations in blood glu-
cose and psychological factors may play a role as
well. Drug treatment of erectile dysfunction,
sometimes in combination with psychotherapy
or marriage counseling, may be effective.
Less is known about sexual dysfunction in
women with diabetes, but recent research
among women with type 1 diabetes showed that
they have more problems with sexual arousal and
Diabetes: Psychosocial Factors
lubrication compared to healthy women. Sexual
problems in female patients are often associated
with depressive symptoms, making it difficult to
determine cause and effect.
Conclusion
Successful management of diabetes requires con-
siderable motivation and adaptability of the
patient. Because people with diabetes are at
increased risk for psychological problems that
may complicate self-management behaviors,
attention to the psychosocial functioning of
patients is important in all phases of treatment.
The fact that depression and other psychosocial
problems are often not recognized and discussed
calls for systematic monitoring of psychological
well-being of diabetic patients as part of the reg-
ular appointments. Research into the effects in
youth and adults with diabetes has shown that
such an approach is feasible and that the well-
being of patients and their satisfaction with care
increase (Pouwer, Snoek, van der Ploeg, Ader, &
Heine, 2001; de Wit et al., 2008). Nurses can play
an important role in such approach. Additional
psychological assessment and intervention can be
provided as needed. Diabetes is a largely self-
managed disease. Consequently, if the patient is
unwilling or unable to self-manage his or her
diabetes on a day-to-day basis, outcomes will be
poor, regardless of how advanced the treatment
technology is. Cognitive, emotional, behavioral,
and social factors have a vital role in diabetes
management, particularly because research has
shown depression and other psychological
problems are prevalent and negatively impact
on well-being and metabolic outcomes. There
is more to diabetes than glucose control; a
biopsychosocial approach is required for optimal
results. Motivational counseling and behavior
change programs in type 2 diabetes have been
shown to be effective in improving adherence
and warrant further dissemination in primary
and secondary care. In type 1 diabetes, adoles-
cents are at increased risk of coping difficulties
and poor diabetes outcomes, and warrant special
attention. For all age groups, monitoring of
Diabetes: Psychosocial Factors
patients’ emotional well-being as an integral part
of routine diabetes care is recommended. Discus-
sion of quality-of-life issues in the context of
clinical diabetes care in itself promotes increased
adherence and patient satisfaction, and has
proven to increase recognition of signs of emo-
tional problems and “diabetes burnout.” Integrat-
ing psychology in diabetes management can help
to effectively tailor care to the patient’s individ-
ual needs and improve outcomes.
Cross-References
▶ Quality of Life
▶ Self-management
▶ Self-monitoring
▶ Self-regulation Model
References and Readings
Adriaanse, M. C., & Snoek, F. J. (2006). The psycholog-
ical impact of screening for type 2 diabetes. Diabetes/
Metabolism Research and Reviews, 22(1), 20–25.
Anderson, B. J. (2003). Diabetes self-care: Lessons from
research on the family and broader contexts. Current
Diabetes Reports, 3(2), 134–140.
Anderson, R. J., Freedland, K. E., Clouse, R. E., &
Lustman, P. J. (2001). The prevalence of comorbid
depression in adults with diabetes: A meta-analysis.
Diabetes Care, 24(6), 1069–1078.
Bryden, K. S., Peveler, R. C., Stein, A., Neil, A., Mayou,
R. A., & Dunger, D. B. (2001). Clinical and psycho-
logical course of diabetes from adolescence to young
adulthood: A longitudinal cohort study. Diabetes
Care, 24(9), 1536–1540.
Colton, P., Olmsted, M., Daneman, D., Rydall, A., &
Rodin, G. (2004). Disturbed eating behavior and eating
disorders in preteen and early teenage girls with type 1
diabetes: A case-controlled study. Diabetes Care,
27(7), 1654–1659.
Cox, D. J., Gonder-Frederick, L., Polonsky, W.,
Schlundt, D., Kovatchev, B., & Clarke, W. (2001).
Blood glucose awareness training (BGAT-2): Long-
term benefits. Diabetes Care, 24(4), 637–642.
de Wit, M., Delemarre-van de Waal, H. A., Bokma, J. A.,
Haasnoot, K., Houdijk, M. C., Gemke, R. J., et al.
(2007). Self-report and parent-report of physical and
psychosocial well-being in Dutch adolescents with
type 1 diabetes in relation to glycemic control. Health
and Quality of Life Outcomes, 5, 10.
de Wit, M., Delemarre-van de Waal, H. A., Bokma, J. A.,
Haasnoot, K., Houdijk, M. C., Gemke, R. J., et al.
585 D
(2008). Monitoring and discussing health-related qual-
ity of life in adolescents with type 1 diabetes improve
psychosocial well-being: A randomized controlled
trial. Diabetes Care, 31(8), 1521–1526.
De Berardis, G., Franciosi, M., Belfiglio, M., Di Nardo, B.,
Greenfield, S., Kaplan, S. H., et al. (2002). Erectile
dysfunction and quality of life in type 2 diabetic
patients: A serious problem too often overlooked.
Diabetes Care, 25(2), 284–291.
Harris, M. I. (2000). Health care and health status and
outcomes for patients with type 2 diabetes. Diabetes D
Care, 23(6), 754–758.
Hoey, H., Aanstoot, H. J., Chiarelli, F., Daneman, D.,
Danne, T., Dorchy, H., et al. (2001). Good metabolic
control is associated with better quality of life in 2,101
adolescents with type 1 diabetes. Diabetes Care,
24(11), 1923–1928.
Hood, K. K., Huestis, S., Maher, A., Butler, D.,
Volkening, L., & Laffel, L. M. B. (2006). Depressive
symptoms in children and adolescents with Type 1
diabetes: Association with diabetes-specific character-
istics. Diabetes Care, 29(6), 1389.
Katon, W. J., Von Korff, M., Lin, E. H., Simon, G.,
Ludman, E., Russo, J., et al. (2004). The pathways
study: A randomized trial of collaborative care in
patients with diabetes and depression. Archives of
General Psychiatry, 61(10), 1042–1049.
Kenardy, J., Mensch, M., Bowen, K., Green, B.,
Walton, J., & Dalton, M. (2001). Disordered eating
behaviours in women with Type 2 diabetes mellitus.
Eating Behaviors, 2(2), 183–192.
Knol, M. J., Twisk, J. W., Beekman, A. T., Heine, R. J.,
Snoek, F. J., & Pouwer, F. (2006). Depression as a risk
factor for the onset of type 2 diabetes mellitus. A meta-
analysis. Diabetologia, 49(5), 837–845.
Mollema, E. D., Snoek, F. J., Ader, H. J., Heine, R. J., &
van der Ploeg, H. M. (2001). Insulin-treated diabetes
patients with fear of self-injecting or fear of self-
testing: Psychological comorbidity and general
well-being. Journal of Psychosomatic Research,
51(5), 665–672.
Neumark-Sztainer, D., Patterson, J., Mellin, A.,
Ackard, D. M., Utter, J., Story, M., et al. (2002).
Weight control practices and disordered eating behav-
iors among adolescent females and males with type 1
diabetes: Associations with sociodemographics,
weight concerns, familial factors, and metabolic out-
comes. Diabetes Care, 25(8), 1289–1296.
Pouwer, F., Snoek, F. J., van der Ploeg, H. M., Ader, H. J.,
& Heine, R. J. (2001). Monitoring of psychological
well-being in outpatients with diabetes: Effects on
mood, HbA(1c), and the patient’s evaluation of the
quality of diabetes care: A randomized controlled
trial. Diabetes Care, 24(11), 1929–1935.
Snoek, F. J. (2000). Quality of life: A closer look at
measuring patients’ well-being. Diabetes Spectrum,
13, 24.
Thoolen, B. J., de Ridder, D. T., Bensing, J. M., Gorter,
K. J., & Rutten, G. E. (2006). Psychological outcomes
D 586
of patients with screen-detected type 2 diabetes: The
influence of time since diagnosis and treatment inten-
sity. Diabetes Care, 29(10), 2257–2262.
Writing Team for the Diabetes Control and Complications
Trial/Epidemiology of Diabetes Interventions and
Complications Research Group. (2002). Effect of
intensive therapy on the microvascular complications
of type 1 diabetes mellitus. JAMA: The Journal
of the American Medical Association, 287(19),
2563–2569.
Diabetic Foot Care
▶ Diabetes Foot Care
Diabetic Neuropathy
Jenny T. Wang1 and Jason S. Yeh2
1
Department of Medical Psychology, Duke
University, Durham, NC, USA
2
Obstetrics and Gynecology, Division of
Reproductive Endocrinology and Fertility,
Duke University Medical Center, Durham,
NC, USA
Synonyms
Nerve damage
Definition
Diabetic neuropathy is nerve damage resulting
from high blood sugar levels (hyperglycemia)
and poor metabolic health in individuals with
diabetes mellitus. Diabetic neuropathy can affect
any number of organs or organ systems. Although
it can develop after the initial diagnosis is made,
it is commonly used as a symptom to diagnose
diabetes in a patient. A significant percentage of
patients have clinical evidence of nerve damage
at the time of diagnosis, which suggests that even
Diabetic Foot Care
prediabetes can cause early diabetic neuropathy.
In general, the more poorly controlled the diabe-
tes, the more severe the diabetic neuropathy.
Studies have shown that nerve conduction
through the body slows significantly with each
percent rise in glycosylated hemoglobin (HbA1c)
values. The most commonly encountered
forms of diabetic neuropathy include distal sym-
metric polyneuropathy, autonomic neuropathy,
polyradiculopathy, and mononeuropathy.
Distal symmetric polyneuropathy is the most
common type and is often synonymous with
diabetic neuropathy. It is characterized by the
symmetrical damage of sensory nerves that
initially affects the lower extremities. The natural
history of symmetric polyneuropathy illustrates
the principle that the longest axons are affected
first. Consequently, patients initially report
symptoms in their toes and feet, which eventually
progress to the classic bilateral “stocking and
glove” numbness. Individuals with peripheral
neuropathy can experience debilitating pain,
tingling, and numbness in their hands and feet.
Because many patients ultimately lose all sensa-
tion in their feet, they must be fitted with
nonabrasive shoes and are taught to check their
hands and feet daily for abrasions and injuries
that can progress into limb and life-threatening
ulcers.
Autonomic neuropathy includes a wide spec-
trum of symptoms that can affect multiple organ
systems such as the cardiovascular, gastrointesti-
nal, genitourinary, and even the neuroendocrine
system. Its diagnosis can be difficult because of
multiple organ involvement and insidious onset.
Symptoms of cardiac neuropathy include exer-
cise intolerance, resting tachycardia, and silent
myocardial infarction. Neuropathic disease of
the upper gastrointestinal tract can cause dyspha-
gia, retrosternal pain, and “heartburn.” More
concerning is delayed stomach emptying which
can cause nausea, vomiting, early satiety,
prolonged fullness after eating and anorexia.
When autonomic disease affects the lower gas-
trointestinal tract, patients present with severe
constipation, diarrhea, and even bowel
Diabetologist (Diabetes Specialist)
incontinence. Neuropathy affecting the genitouri-
nary system can cause bladder dysfunction, erec-
tile dysfunction, and painful intercourse due to
decreased vaginal lubrication. Less commonly,
neuropathy can even cause hypoglycemia
unawareness where patients become unable to
perceive dangerously low blood sugar levels.
Diabetic polyradiculopathies refer to several
types of asymmetric proximal nerve disease in
the diabetic patient, the most common being dia-
betic amyotrophy and diabetic thoracic polyradi-
culopathy. Diabetic amyotrophy is the more
common of the two and involves an acute onset
of pain followed by weakness involving one
proximal leg, with concurrent autonomic failure
and weight loss. If the disease affects the contra-
lateral leg, symptoms can occur immediately or
much later after the initial episode. No treatments
have been shown to be effective for diabetic
amyotrophy. Thoracic polyradiculopathy,
another type of diabetic polyradiculopathy,
describes an injury of the high lumbar or tho-
racic-level nerve roots. These patients present
with severe abdominal pain and have frequently
undergone multiple studies to identify the cause
of their symptoms.
Lastly, there are two types of diabetic
mononeuropathy: cranial and peripheral. Cranial
lesions commonly affect nerves surrounding
the eye and typically result in unilateral eye
symptoms including pain, drooping eyelid, and
double vision. The most common peripheral
lesions in diabetic patients are median nerve
mononeuropathy at the wrist and common pero-
neal mononeuropathy near the ankle, both of
which can result in pain, drooping, weakness,
and decreased range of motion.
Improving the symptoms of diabetic neuropa-
thy can be difficult; most efforts are made to
prevent the onset and worsening of existing
diabetic neuropathy. Treatment of diabetic neu-
ropathy emphasizes tight blood sugar control,
managing pain symptoms through pharmacother-
apy (i.e., analgesics, certain antidepressants,
steroids) and/or psychosocial interventions
(e.g., meditation, relaxation training), and
587 D
practicing diligent foot care (i.e., washing feet,
inspecting for cuts, bruises, or blisters).
Successful diabetes management is associated
with several behavioral and lifestyle factors,
which have been shown to improve with psycho-
social interventions such as motivational
interviewing, health coaching, and cognitive
behavioral therapy. Well-controlled diabetes is
often the result of adherence to a healthy diet D
and exercise regimen, keeping track of carbohy-
drate intake, frequent and routine checks of blood
sugar levels, taking required amounts of insulin,
and discontinuing negative behaviors such as
smoking or excessive drinking. Modification of
these behaviors in children and adults has
resulted in improvements in diabetes manage-
ment, which can prevent or slow the development
of diabetic neuropathy.
Cross-References
▶ Blood Glucose
▶ Chronic Disease Management
▶ Diabetes
▶ Diabetes Education
▶ Diabetes Foot Care
▶ Hyperglycemia
References and Readings
Kronenberg, H., & Williams, R. H. (2008). Williams text-
book of endocrinology (11th ed.). Philadelphia:
Saunders Elsevier.
Diabetologist (Diabetes Specialist)
Janine Sanchez
Department of Pediatrics, University of Miami,
Miami, FL, USA
Synonyms
Endocrinologist
D 588 Diagnostic Criteria

Definition
Diagnostic Interview Schedule
A diabetologist is a physician with expertise in
diabetes care. The physician is often board certi- J. Rick Turner
fied in pediatric or adult endocrinology with Cardiovascular Safety, Quintiles, Durham,
special interest or extra training in diabetes care NC, USA
or research. However, diabetology is not
a recognized medical specialty and has no formal
training programs. Thus, any physician whose Synonyms
practice and/or research efforts are concentrated
mainly in diabetes care may be considered DIS
a diabetologist/diabetes specialist.

Definition
Cross-References
The National Institute of Mental Health Diagnos-
▶ Diabetes tic Interview Schedule was discussed in the
▶ Endocrinology Archives of General Psychiatry by Robbins,
Helzer, Croughan, and Ratcliff (1981). The inter-
view schedule allowed lay interviewers or
clinicians to make psychiatric diagnoses
References and Readings according to DSM-III criteria, Feighner criteria,
and Research Diagnostic Criteria. It was being
Menon, R. (2003). Pediatric diabetes (1st ed.). Norwell,
MA: Springer. used in a set of epidemiological studies sponsored
Sperling, M. A. (2009). Pediatric endocrinology (3rd ed.). by the National Institute of Mental Health Center
Philadelphia: W.B. Saunders. for Epidemiological Studies. Its accuracy has
been evaluated in a test-retest design comparing
independent administrations by psychiatrists and
lay interviewers to 216 subjects (inpatients, out-
patients, ex-patients, and nonpatients).
Diagnostic Criteria The National Institute of Mental Health
Diagnostic Interview Schedule for Children,
▶ Psychiatric Diagnosis Version 4 (NIMH DISC IV or “DISC”) is a
highly structured diagnostic interview used
to assess psychiatric diagnoses of children and
adolescents. The DISC was designed to
be administered by interviewers with no formal
Diagnostic Features of Depression clinical training following the rules and conven-
tions outlined in the DISC training manual.
▶ Depression: Symptoms The DISC questions elicit the diagnostic
criteria specified in the Diagnostic and Statistical
Manual of Mental Disorders – Fourth Edition
(DSM-IV) and the WHO International Classifica-
tion of Diseases, Version 10 (ICD-10).
Diagnostic Interview The Generic or “12 month” DISC was used
in NHANES. Seven of the 34 diagnostic assess-
▶ Interview ments were included in NHANES over the 6-year
Diaries
period that the DISC was administered: general-
ized anxiety disorder, panic disorder, eating dis-
order, elimination disorders, major depression/
dysthymic disorder, attention deficit disorder/
hyperactivity (ADD/ADHD), and conduct disor-
der. In each module, questions are asked about
specific symptoms during the past year, and then
follow-up questions in cases of positive endorse-
ment. Two of the DISC modules in NHANES,
eating disorder and major depression/dysthymic
disorder, were comprised of two parallel inter-
views. A youth-informant interview (DISC-Y)
administered in-person to children asked questions
about themselves, and a parent-informant inter-
view (DISC-P) administered by telephone to
a parent or caretaker asked questions about their
child. Only the DISC-Y was administered for gen-
eralized anxiety disorder and panic disorder, and
only the DISC-P was administered for elimination
disorder, ADD/ADHD, and conduct disorder.
Depending on the module, responses and diagnos-
tic scores derived from the interviews can be com-
bined or examined separately.
Cross-References
▶ Anxiety Disorder
▶ Depression: Measurement
▶ National Health and Nutrition Examination
Survey (NHANES)
▶ Panic Disorder
References and Readings
Everson-Rose, S. A., & Clark, C. J. (2010). Assessment of
psychosocial factors in population studies. In A.
Steptoe (Ed.), Handbook of behavioral medicine:
Methods and applications (pp. 291–306). New York:
Springer.
Robbins, L. N., Helzer, J. E., Croughan, J., & Ratcliff,
K. S. (1981). National Institute of Mental Health diag-
nostic interview schedule: Its history, characteristics,
and validity. Archives of General Psychiatry, 38,
381–389.
Snowling, M. J., & Hulme, C. (2011). Annual research
review: The nature and classification of reading disor-
ders: a commentary on proposals for DSM-5. Journal
of Child Psychology and Psychiatry, Dec, 5th [Epub
ahead of print].
589 D
Diaries
C. Renn Upchurch Sweeney
VA Salt Lake City Healthcare System,
Salt Lake City, UT, USA
Synonyms D
Daily diary; Event sampling
Definition
Diaries are self-report instruments often used in
behavioral medicine research to examine psycho-
logical processes (i.e., affect, social interaction,
marital and family interactions, stress, physical
symptoms, mental health, well being) within the
natural context of everyday life. Diaries require
study participants to keep track of cognitions,
emotions, or behaviors in a log for a particular
period of time and are designed to “capture life as
it is lived” (Bolger, Davis, & Rafaeli, 2003).
Examples of diaries include paper and pencil
diaries, augmented paper diaries (ancillary
devices are programmed to prompt participants
to respond at a particular time), and electronic
diaries (i.e., palm pilots, PDAs). Diaries can be
collected repeatedly over a number of days, once
daily (daily diary), or even sampled several times
during the day.
Advantages
One advantage of diary methods is that informa-
tion is gathered in the context of the participant’s
everyday life, which may illicit behavior that is
more representative than that observed in the
laboratory setting. Secondly, diary methods
reduce the likelihood of retrospection. That is,
the time between an experience and the
recounting of the experience by the participant
is minimized. By asking the participants to record
information when an event occurs or shortly
thereafter, diaries also reduce biases related to
recall (the greater the time between events and
its recollection, the greater the potential for
D 590
distortion), recency effects (more recent events
are more likely to influence judgments) and
salience (moments of peak intensity or personal
relevance influence judgments more than less
salient experiences). Finally, diary studies elimi-
nate the difficulty of summarizing multiple
events.
Disadvantages
Despite the many advantages of diary methods,
several disadvantages also exist. For example,
diaries require experimenters to conduct training
sessions to ensure that participants understand the
diary protocol, which can be time consuming for
the experimenter. Secondly, diaries can be oner-
ous for participants. The burden of repeated
queries and responses places substantial demands
on the participant and requires a greater level of
participant commitment compared to other types
of research studies. Thirdly, the act of completing
the diary may affect participants’ responses or
alter participants’ understanding of a particular
construct. For example, a more complex under-
standing of the surveyed topic may develop or the
experience of the diary study may change partic-
ipants’ conceptualization of the topic to fit with
those measured in the diary. Finally, participants
may develop a habitual response style when mak-
ing repeated diary entries, which may have neg-
ative consequences. For example, participants
may skim over sections of a diary questionnaire
that rarely apply to them, but inadvertently omit
responses to these questions at relevant times.
Cross-References
▶ Ecological Momentary Assessment
References and Readings
Bolger, N., Davis, A., & Rafaeli, E. (2003). Diary
methods: Capturing life as it is lived. Annual Review
of Psychology, 54, 579–616.
Fiske, S. T., Gilbert, D. T., & Lindzey, G. (Eds.). (2009).
Handbook of social psychology (Vol. 1). Hoboken, NJ:
Wiley.
Diastolic Blood Pressure (DBP)
Green, A. S., Rafaeli, E., Bolger, N., Shrout, P. E., & Reis,
H. T. (2006). Paper or plastic? Data equivalence in
paper and electronic diaries. Psychological Methods,
11, 87–105.
Laurenceau, J., & Bolger, N. (2005). Using diary methods
to study marital and family process. Journal of Family
Psychology, 19, 86–97.
Tennen, H., Affleck, G., & Armeli, S. (2003). Daily pro-
cesses in health and illness. In J. Suls & K. Wallston
(Eds.), The social psychological foundations of
health and illness (pp. 495–529). Oxford, England:
Blackwell.
Diastolic Blood Pressure (DBP)
Annie T. Ginty
School of Sport and Exercise Sciences,
The University of Birmingham, Edgbaston,
Birmingham, UK
Synonyms
Blood pressure
Definition
Diastolic blood pressure is the force exerted by
the artery walls during ventricular relaxation. It is
the lowest pressure measured and normal range
is considered to be <80 mmHg (Tortora &
Grabowski, 1996).
Cross-References
▶ Blood Pressure, Elevated
▶ Blood Pressure, Measurement of
▶ Systolic Blood Pressure (SBP)
References and Readings
Tortora, G. J., & Grabowski, S. R. (1996). Principles of
anatomy and physiology (8th ed.). New York: Harper
Collins College.
Diathesis-Stress Model
Diathesis-Stress Model
Kristen Salomon and Alvin Jin
Department of Psychology, University of
South Florida College of Arts & Sciences,
Tampa, FL, USA
Synonyms
Risk factors
Definition
Diathesis refers to a predisposition or vulnerabil-
ity for the development of a pathological state.
Diathesis-stress models argue that certain patho-
logical states or diseases emerge from the com-
bination of a predisposition with stressful events
(Zuckerman, 1999). Most models specify that
neither the diathesis nor stress alone is sufficient
to produce the disorder. Instead, stress activates
the diathesis, which then leads to the disorder.
More broadly, diathesis-stress models are similar
to the idea of risk-factors for stress-related
diseases.
Description
History
Early diathesis-stress models primarily focused
on psychiatric disorders such as schizophrenia,
depression, and anxiety disorders, born out of the
observation that these disorders tend to be
inherited and yet also show a significant relation-
ship to life stress (Zuckerman, 1999). These early
diathesis-stress models identified fixed biological
and/or hereditary factors as predispositions, and
often argued for singular directionality, i.e., that
the stress acted upon the diathesis. Later, the idea
of diathesis was expanded to include physiologi-
cal, behavioural and psychological diatheses,
some of which may be acquired (Zuckerman).
Broadening the scope of diatheses to include
“non-biological” factors also resulted in
591 D
a change in the presumed directionality, such
that diatheses may influence the experience of
stress.
Diatheses
Zuckerman (1999) has argued that diatheses are
traits, and as such they not only should be present
before the onset of the disorder but also should
not change as the result of the disorder. Diatheses D
may be conceptualized as dichotomous, i.e., pre-
sent or not. However, many diathesis-stress
models suggest that the degree of diathesis pre-
sent sets a threshold of vulnerability to stress. The
greater the level of diathesis present, the less
stress required to activate it and create the path-
ological state (Zuckerman). Some diathesis-
stress theories, such as Fowles (1992) theory of
schizophrenia, argue that stress may not be nec-
essary for the disorder to develop. If the level of
diathesis is high enough, the threshold is met and,
even in the absence of stress, the disorder will
develop (Zuckerman, 1999).
The Role of Stress
One important issue for diathesis-stress models is
the potential confounding of stress with the diath-
esis. For example, if a personality trait, such as
neuroticism, is identified as a diathesis for
a disorder, such as anxiety, then the issue
becomes whether the diathesis is reacting to
stress or is the cause of stress. Therefore, many
diathesis-stress models define stress in terms of
external events rather than defining stress as sub-
jectively reported reactions to events (Monroe &
Simons, 1991). Further, identifying genetic, bio-
logical, and/or physiological diatheses, rather
than psychological ones, also serves to avoid the
problem of confounding (Zuckerman, 1999).
Also, diathesis-stress models often assume that
the stress must occur in close temporal proximity
to the onset of the disorder (Zuckerman, 1999).
Some stress-diathesis models suggest that not
only do diatheses differ by disorder but also by
the type of stress necessary to activate a specific
diathesis. For example, for major depressive dis-
order, stressors that involve loss of one’s social
structure (e.g., job loss, divorce, death of a loved
D 592
one) have been identified as those that combine
with diatheses to produce the disorder (Monroe &
Simons, 1991).
Specifying Diathesis-Stress Models
Conceptualizations of diatheses and stressors that
are binary (present or not) lead to relatively simple
models. If both the diathesis and stress are present,
the disorder will occur, but if one or both are
absent, the disorder should not occur. However,
most research on diathesis-stress models suggests
that neither diatheses nor stress are dichotomous.
Some models have suggested that diatheses are
categorical, such as evidence suggesting that alle-
lic variation in the 5-HTT-linked polymorphic
region (5-HTTLPR) of the serotonin-transporter
gene serves as a diathesis for anxiety-related dis-
orders (Lesch et al., 1996). However, these models
do not consider the polygenic nature of most
disorders and they are likely artificially categoriz-
ing dimensional variability in gene expression
(Zuckerman, 1999). Further, stress is often scaled
in terms of the severity of individual stressors (i.e.,
traumatic stress producing posttraumatic stress
disorder; PTSD) or in the total number of stressors
(i.e., more instances of loss associated with higher
rates of depression). Continuous diatheses and
stressors lead to more complex models. Models
may specify additive effects, such that more stress
is required to bring about the disorder in someone
with less of the diathesis than in someone with
a greater degree of the diathesis. Interactive
models may suggest that if the diathesis is absent,
no amount of stress may bring about the disorder,
but once present, the diathesis can vary in its
loading, thus requiring different amounts of stress
to bring about the disorder. Thus, important ques-
tions to consider when developing diathesis stress
models involve the nature of the diathesis (cate-
gorical, continuous, continuous only if present),
the diathesis threshold necessary for the disorder
to emerge, the type (e.g., loss, fear) and nature
(categorical or continuous) of the stress necessary
to activate the diathesis, the nature of the effects of
each (additive, interactive), and whether the diath-
esis and stress are independent of one another or
correlated.
Diet and Cancer
Current State of Stress-Diathesis Models
Recently, the basic diathesis-stress model has
been expanded to include predispositions that
protect individuals from developing stress-
related disorders, or resilience (Belsky & Pluess,
2009). Instead of focusing on why some people
fall victim to disorders in the face of stress,
resilience research focuses on why some people
seem resistant to a disorder, even in the face
of extreme stress. However, resilience is not
the opposite of diathesis, but instead, individuals
may differ in their overall plasticity to both
negative (i.e., stress) and positive (i.e., support-
ive) environmental influences (Belsky &
Pluess, 2009).
Cross-References
▶ Resilience
▶ Risk Factors
▶ Stress
References and Readings
Belsky, J., & Pluess, M. (2009). Beyond diathesis stress:
Differential susceptibility to environmental influences.
Psychological Bulletin, 135(6), 885–908.
Fowles, D. C. (1992). Schizophrenia – diathesis
stress revisited. Annual Review of Psychology, 43,
303–336.
Lesch, K. P., Bengel, D., Heils, A., Sabol, S. Z.,
Greenberg, B. D., Petri, S., et al. (1996). Association
of anxiety-related traits with a polymorphism in the
serotonin transporter gene regulatory region. Science,
274, 1527–1531.
Monroe, S. M., & Simons, A. D. (1991). Diathesis-stress
theories in the context of life stress research: Implica-
tions for the depressive disorders. Psychological Bul-
letin, 110, 406–425.
Zuckerman, M. (1999). Vulnerability to psychopathology:
A biosocial model. Washington, DC: American Psy-
chological Association.
Diet and Cancer
▶ Cancer and Diet
Dimsdale, Joel E.
Dietary Fatty Acids
▶ Essential Fatty Acids
Dietary Lipids Absorption
▶ Fat Absorption
Dietary Requirements
▶ Nutrition
Dietary Supplement
▶ Nutritional Supplements
Differential Psychology
▶ Individual Differences
Diffuse Optical Imaging (DOI)
▶ Brain, Imaging
▶ Neuroimaging
Diffusion
▶ Dissemination
Dimeric Glycoprotein
▶ Fibrinogen
593 D
Dimsdale, Joel E.
Joel E. Dimsdale
Department of Psychiatry, University of
California San Diego, La Jolla, CA, USA
D
Biographical Information
Joel Dimsdale was born in Sioux City, Iowa, in
1947, and obtained his BA degree in biology
from Carleton College. He then attended
Stanford University, where he obtained an MA
degree in Sociology and an MD degree. He
obtained his psychiatric training at Massachusetts
General Hospital and then completed
a fellowship in psychobiology at the New
England Regional Primate Center. He was on
the faculty of Harvard Medical School from
1976 until 1985, when he moved to University
of California, San Diego (UCSD).
Dimsdale is distinguished professor emeritus
and Research Professor in the department of
psychiatry at UCSD. His clinical subspecialty is
consultation psychiatry. He is an active investi-
gator, a former career awardee of the American
Heart Association, and is past-president of the
Academy of Behavioral Medicine Research, the
American Psychosomatic Society, and the
Society of Behavioral Medicine. He is on numer-
ous editorial boards, is editor-in-chief emeritus of
D 594
Psychosomatic Medicine, and is a previous guest
editor of Circulation. He has been a consultant to
the President’s Commission on Mental Health,
the Institute of Medicine, and is a long-time
reviewer for NIH. He consults to the National
Academy of Sciences regarding behavioral issues
in space. He is a member of the DSM V taskforce
and chairs the workgroup studying somatic
symptom disorders. Dimsdale is the former
chair of the UCSD Academic Senate and
currently chairs the Systemwide University of
California Faculty Welfare Committee.
Dimsdale is an active teacher who supervises
CL psychiatry. He mentors trainees and junior
faculty members from psychiatry, psychology,
pulmonary medicine, nephrology, anesthesiol-
ogy, and surgery. Dimsdale directs UCSD’s
K12 training grant for fostering the careers of
outstanding young clinical faculty.
Dimsdale’s major research interests include
sympathetic nervous system physiology as it
relates to stress, blood pressure, and sleep;
cultural factors in illness; and quality of life. He
is the author of more than 500 publications as
well as the editor of four books.
Major Accomplishments
Dimsdale has been an active investigator who has
mentored generations of medical students, resi-
dents, psychology students, and post docs. He has
been repeatedly tapped for leadership positions in
national organizations, on medical journals, and
in university governance.
References and Readings
Bardwell, W., Moore, P., Ancoli-Israel, S., & Dimsdale, J.
(2003). Fatigue in obstructive sleep apnea is driven by
depressive symptoms and not apnea severity. The
American Journal of Psychiatry, 160, 350–355.
Bardwell, W., Natarajan, L., Dimsdale, J., Rock, C.,
Mortimer, J., Hollenbach, K., & Pierce, J. (2006).
Objective cancer-related variables are not associated
with depressive symptoms in women treated for early-
stage breast cancer. Journal of Clinical Oncology, 24,
2420–2427.
Dimsdale, Joel E.
Dimsdale, J. E. (1974). Coping behavior of Nazi concen-
tration camp survivors. The American Journal of
Psychiatry, 131, 792–797.
Dimsdale, J. (1988). A perspective on type A behavior
and coronary disease. The New England Journal of
Medicine, 318, 110–112.
Dimsdale, J. (2000). Stalked by the past: The impact of
ethnicity on health. Psychosomatic Medicine, 62,
161–170.
Dimsdale, J. (2008). Psychological stress and cardiovas-
cular disease. Journal of the American College of
Cardiology, 51, 1237–1246.
Dimsdale, J., & Creed, F. (2009). The proposed diagnosis
of somatic symptom disorders in DSM-V to replace
somatoform disorders in DSM-IV – A preliminary
report. Journal of Psychosomatic Research, 66(6),
473–476.
Dimsdale, J., Graham, R., Ziegler, M., Zusman, R., &
Berry, C. (1987). Age, race, diagnosis, and sodium
effects on the pressor response to infused norepineph-
rine. Hypertension, 10, 564–569.
Dimsdale, J. E., Hackett, T. P., Hutter, A., Block, P., &
Catanzano, D. (1978). Type A personality and the
extent of coronary atherosclerosis. The American
Journal of Cardiology, 42, 583–586.
Dimsdale, J. E., Hartley, L. H., Guiney, T., Ruskin, J., &
Greenblatt, D. (1984). Post-exercise peril: Plasma cat-
echolamines and exercise. Journal of the American
Medical Association, 251, 630–632.
Dimsdale, J. E., & Moss, J. (1980). Plasma catechol-
amines in stress and exercise. Journal of the American
Medical Association, 243, 340–342.
Dimsdale, J., Newton, R., & Joist, T. (1989). Neuropsy-
chological side effects of beta blockers. Archives of
Internal Medicine, 149, 514–525.
Golomb, B. A., Criqui, M. H., White, H. L., & Dimsdale,
J. E. (2004). Conceptual foundations of the UCSD
statin study: A randomized controlled trial assessing
the impact of statins on cognition, behavior, and
biochemistry. Archives of Internal Medicine, 164,
153–162.
Mills, P., Dimsdale, J., Coy, T., Ancoli-Israel, S., Clausen, J.,
& Nelesen, R. (1995). Beta-two adrenergic receptor
characteristics in sleep apnea patients. Sleep, 18, 39–42.
Ng, B., Dimsdale, J., Rollnik, J., & Shapiro, H. (1996).
The effect of ethnicity on prescriptions for patient
controlled analgesia for post-operative pain. Pain, 66,
9–12.
Profant, J., & Dimsdale, J. (1999). Race and diurnal blood
pressure patterns: A review and meta-analysis. Hyper-
tension, 33, 1099–1104.
Thomas, K., Bardwell, W., Ancoli-Israel, S., & Dimsdale, J.
(2006). The toll of ethnic discrimination on sleep
architecture and fatigue. Health Psychology, 25(5),
635–642.
von Kanel, R., Loredo, J., Ancoli-Israel, S., Mills, P.,
Natarajan, L., & Dimsdale, J. (2007). Association
between polysomnographic measures of disrupted
sleep and prothrombotic factors. Chest, 131, 733–739.
Disability
Ziegler, M., Nelesen, R., Mills, P., Ancoli-Israel, S.,
Clausen, J., Watkins, L., & Dimsdale, J. (1995). The
effect of hypoxia on baroreflexes and pressor sensitiv-
ity in sleep apnea and hypertension. Sleep, 18,
859–865.
DIS
▶ Diagnostic Interview Schedule
Disability
Diane Dixon
Department of Psychology, University of
Strathclyde, Glasgow, Scotland, UK
Synonyms
Activity limitations; Impairment; Participation
restrictions
Definition
The World Health Organization views disability
not as a property of an individual person but as an
interaction between features of a person’s body
and their social and physical environment.
Disability can exist at the level of impairments
(to body structures and functions), activity
limitations, and/or participation restrictions.
Impairments are defined as a significant deviation
or loss in body functions or structures. Activity
limitations are difficulties a person has in
performing activities; an activity is the execution
of a task or action. Participation restrictions are
problems a person experiences in involvement in
life situations; participation is involvement in life
situations.
Governments also define disability within
antidiscrimination legislation and to provide
access to government support and services. For
example, in the United Kingdom, the Equality
Act (2010) considers a person to have
595 D
a disability if they have a physical or mental
impairment that has a substantial and long-term
adverse effect on their ability to perform normal
day-to-day activities.
Description
The World Health Organization estimates that, D
worldwide, 650 million people live with disabil-
ities of various types. It is expected that this figure
will continue to rise as the world’s population
ages and the prevalence of chronic illness
increases. The management of disability is
complex and typically involves multidisciplinary
teams and input from multiple services.
As a consequence, the management of disability
will benefit from the use of theoretical
frameworks that are able to accommodate such
multidisciplinary ways of working.
Conceptualizing Disability
The World Health Organization’s International
Classification of Functioning, Disability and
Health (ICF) provides such an integrative frame-
work (WHO, 2001). A summary schematic of the
ICF is shown in Fig. 1.
The WHO designed the ICF as a classification
system for health and health-related states.
However, the ICF can also operate as a complex
model of health and disability. The ICF identifies
three health components, namely, body structures
and functions, activities and participation, and their
corollaries of impairment, activity limitations, and
participation restrictions (see the “Definition” tab
for a description of each component).
The ICF has several features of particular
relevance to behavioral medicine (Dixon &
Johnston, 2010).
First, the relationships between the compo-
nents are reciprocal. This means that impairments
can cause activity limitations but also that activ-
ity limitations can cause impairments. For exam-
ple, osteoarthritis is a health condition in which
the structure of the hip joint is impaired; this
impairment is experienced as joint stiffness and
pain (impairments). A person with osteoarthritis
of the hip might, as a result of such impairments,
D 596
Disability,
Fig. 1 Summary
schematic of the ICF
Body Structures and
Functions
Impairments
experience difficulties getting up and down stairs
and walking (activity limitations), and these
activity limitations might restrict their ability to
use buses or trains, which might reduce their
ability to visit the cinema in town (participation
restrictions). However, reduced walking might
also cause further impairments in the structure
and function of the hip joint, as muscle strength
weakens with reduced use. Thus, within the ICF,
reductions in impairment can be achieved
through interventions that target activity limita-
tions and vice versa. This makes the ICF suitable
for use by multidisciplinary teams typically
required for the effective management of the
consequences of chronic illness. For example,
medical doctors can intervene surgically or phar-
macologically; allied health professionals can
intervene with a range of therapies, for example,
physiotherapy and speech and language therapy;
social services can intervene with adjustments to
the home environment, for example, provision of
ramp access to the home, an electric wheelchair,
and other assistive devices.
Second, the role of the environment and
personal factors in disability is recognized by the
contextual factors component of the ICF. These
contextual factors enable other disciplines to
contribute to our understanding of disability.
The ICF provides a detailed description of the
environmental factors, which include assistive
products and technologies, the natural and
man-made environment, social services, systems,
and policies. These environmental factors enable
Disability
Health Condition
(disorder or disease)
Participation
Activities
Participation
Activity Limitations
Restrictions
Contextual Factors
• Environmental Factors
• Personal factors
diverse disciplines, such as architecture and town
planning, to contribute to achieving reductions in
disability. The personal factors component is less
well described by the ICF; however, personal
factors have been operationalized in the form of
individual cognitions and emotions. Inclusion of
the personal factors component and the observa-
tion that activity limitations and participation
restrictions are behavior(s) enables psychology
to inform our understanding of disability.
Psychology can be defined as the scientific study
of behavior, and as such, models of behavior and
behavior change can be used to understand the
factors that influence disability. Further, the inclu-
sion of behavioral models of disability delivers the
evidence base on how to intervene to change
behavior (Bandura, 1969; Michie et al., 2009),
which enables reductions in disability to be
achieved, again without the need to reduce chronic
impairments.
A behavioral approach to disability conceptu-
alizes disability as behavior, which is influenced
by the same psychological processes that affect
any other type of behavior. As a consequence, an
individual with a health condition will be
motivated to engage in an activity or participate
in a social situation because it achieves the things
they like, because they believe other people
would like them to do so, and because they
believe they are able to do so. The behavioral
approach can be used to explain, in part, the
so-called disability paradox. The disability para-
dox is the observation that two people, living in
Disability
identical social and environmental situations,
experience different levels of disability, i.e.,
people with severe impairments might report
lower than expected levels of disability, whereas
an individual with mild impairment might
experience higher than expected levels of
disability. This observed discordance between
impairments and activity limitations and
participation restrictions may, in part, be
explained by differences in cognitions, emotions,
or coping strategies. The behavioral approach, in
particular, should not be used to “blame” people
with disabilities for those disabilities. The
behavioral approach does not support the idea
that disability arises because an individual lacks
the motivation to overcome their impairments
and limitations. Rather, the behavioral model
emphasizes that every person is influenced by
biological, personal, social, and environmental
factors, and those influences are unique to each
individual. Indeed, using behavioral models to
conceptualize the personal factors component of
the ICF supports the aim of the WHO to account
for activity and activity limitations in the same
terms for all individuals. Within this integrative
framework, it is only the relative importance of
each factor that differs between people, not the
nature of the factors per se. For example, com-
pared to the significant role of impairment, the
role of motivational factors is likely to be a much
weaker determinant of whether or not a person
who has just had a stroke leaves their home to
walk into town to visit the cinema. However, over
the course of their recovery, the role of impair-
ment factors might reduce and the role of moti-
vational factors might increase, so that 6 months
after their stroke, the individual might not walk
into town to visit the cinema simply because there
are no movies they want (are motivated) to see.
Measuring Disability
Clinical practice and research requires methods
of measurement of disability so that the severity
of a health condition can be assessed and the
effectiveness of interventions evaluated. The
ICF provides detailed descriptions of the body
structures and functions and activities that should
be assessed for any given health condition.
597 D
However, the ICF does not indicate how those
structures, functions, or activities should be
assessed. In general, disability is measured by
assessing the ability of an individual to perform
particular activities relevant to their health con-
ditions. For example, a person who has experi-
enced a stroke might be assessed for their ability
to perform activities of daily living, such as the
ability to dress, to use the stairs, and to transfer D
from bed to chair, whereas a person with
a diagnosis of dementia might be asked to com-
plete measures of cognitive function.
In general, two methods of measurement are
available: self-report and observation. Self-report
requires the individual to describe the limitations
and difficulties they experience. Self-report mea-
sures typically use standard questionnaires, for
example, activities of daily living can be mea-
sured by a wide variety of instruments, including
the Barthel Index, the Sickness Impact Profile
(and its UK equivalent the Functional Limitations
Profile), and the Katz ADL scale. Self-report
measures have the advantage of being suitable
for use in a variety of settings, including the
person’s own home, they are inexpensive, and
can assess a wide range of activities over a long
time course. In addition, proxy reports are some-
times used; proxy reporters are usually the pri-
mary caregiver. However, both self- and proxy
reports have the disadvantage of being open to
reporting errors.
Observational measures require a trained
observer to record whether an individual is able
(or not) to successfully perform relevant and
defined activities. Observational measures are
regarded as being more accurate than self-report
measures but have several disadvantages. They
are restrictive, in that they typically assess only
those activities performed in the limited setting of
the hospital or in the limited period available for
a home visit, and as such, they too might under or
over estimate disability.
Self-report and observational measures can be
supplemented by objective electronic measures,
for example, pedometers provide step counts, and
accelerometers measure activity in general. How-
ever, such devices might have restrictive utility
for particular groups, for example, elderly people
D 598
might walk with a gait that fails to register accu-
rately on pedometers. In addition, with the excep-
tion of a step count, these devices do not
discriminate between particular behaviors, for
example, they are not able to distinguish between
the wide variety of activities of daily living mea-
sured by self-report instruments, and at best they
can discriminate between walking, standing, sit-
ting, and lying.
Information about the WHO-ICF can be found
at: http://www.who.int/classifications/icf/en/ this
site provides a detailed description of the ICF
and contains a great beginner’s guide to
the ICF http://www.who.int/classifications/icf/
training/icfbeginnersguide.pdf
The importance of regarding behavior as
a primary health outcome is made very effec-
tively by Professor Robert Kaplan (Kaplan 1990).
Cross-References
▶ Activities of Daily Living (ADL)
▶ Aging
▶ Chronic Disease Management
▶ Chronic Disease or Illness
▶ Efficacy Cognitions
▶ Functional Capacity, Disability, and Status
▶ Geriatric Medicine
▶ Gerontology
▶ Health Psychology
▶ Illness Cognitions and Perceptions
▶ Independent Living
▶ Measures of Quality of Life
▶ National Institute on Aging
▶ Quality of Life
▶ Self-care
▶ Self-management
References and Readings
Bandura, A. (1969). Principles of behavior modification.
New York: Holt, Reinhart and Winston.
Dixon, D., & Johnston, M. (2010). Disability. In D.
French, K. Vedhara, A. A. Kaptein, & J. Weinman
(Eds.), Health psychology (pp. 317–328). Chichester:
Blackwell.
Disability Assessment
Kaplan, R. M. (1990). Behavior as the central outcome in
health-care. American Psychologist, 45, 1211–1220.
Michie, S., Abraham, C., et al. (2009). Effective tech-
niques in healthy eating and physical activity interven-
tions: A meta-regression. Health Psychology, 28(6),
690–701.
WHO. (2001). International classification of functioning,
disability and health: ICF. Geneva: Author.
Disability Assessment
▶ Health Assessment Questionnaire
Disability-Adjusted Life Years
(DALYs)
Marijke De Couck
Free University of Brussels (VUB),
Jette, Belgium
Definition
The disability-adjusted life year (DALY) has
emerged in the international health policy lexicon
as a measure of overall “disease burden.” It is an
expansion on a previous measure, namely, years
of life lost (YLL), which did not take into account
the impact of disability. DALYs for a disease or
health condition are calculated as the sum of the
years of life lost (YLL) due to premature mortal-
ity in the population and the years lost due to
disability (YLD) for incident cases of the health
condition: DALY ¼ YLL + YLD (World Health
Organization [WHO], 2010). The YLL corre-
spond to the number of deaths multiplied by the
standard life expectancy at the age at which
death occurs. The basic formula for YLL is the
following for a given cause, age, and sex:
YLL ¼ N  L
where:
• N ¼ number of deaths
• L ¼ standard life expectancy at age of death in
years
Disasters and Health: Natural Disasters and Stress/Health
L reflects the difference between the standard
life expectancy at that age and age of death.
Because YLL measure the incident stream of
“lost years of life” due to deaths, an incidence
perspective is also taken for the calculation of
YLD. To estimate YLD for a particular cause in
a particular time period, the number of incident
cases in that period is multiplied by the average
duration of the disease and a weight factor that
reflects the severity of the disease on a scale from
0 (perfect health) to 1 (dead). The basic formula
for YLD is the following:
YLD ¼ I  DW  L
where:
• I ¼ number of incident cases
• DW ¼ disability weight
• L ¼ average duration of the disease until
remission or death (years)
One DALY can be thought of as one lost
year of “healthy” life. The sum of these DALYs
across the population, or the burden of disease,
can be thought of as a measurement of the gap
between current health status and an ideal health
situation where the entire population lives to an
advanced age, free of disease and disability
(WHO, 2010).
Several countries and organizations are using
DALYs to identify health priorities and cost-
effective interventions and to allocate resources
for health (The World Bank, 1993). Several treat-
ments or medications can be compared by this
measure, which has been done in a few studies
(Renaud, Basenya, de Borman, Greindl, &
Meyer-Rath, 2009). DALY also measures psy-
chological factors (e.g., emotional, behavioral,
cognitive, and social functions), which are con-
sidered in the weighted disability. DALY can be
used to compare several kinds of interventions,
like psychological versus pharmacological, as
has been done by several studies (Heuzenroeder
et al., 2004).
However, there are a few disadvantages of the
DALY. It is a metric which is used to provide
a single number to capture all of the health costs
caused by a disease. One DALY could represent
1 year of life lost (due to early death), 1.67 years
599 D
spent with blindness, 5.24 years with significant
malaria episodes, 41.67 years spent with intesti-
nal obstruction due to ascariasis (a parasite), or
many possible combinations of these and other
symptoms (Lopez, Mathers, Ezzati, Jamison, &
Murray, 2006). Thus, the same amount of
DALYs, though numerically identical, could
represent very different disabilities over time,
which may not be comparable. D
Cross-References
▶ Disability
▶ Longevity
▶ Quality of Life
▶ Quality of Life: Measurement
References and Readings
Heuzenroeder, L., Donnelly, M., Haby, M. M.,
Mihalopoulos, M., Rossell, R., Carter, R., et al.
(2004). Cost-effectiveness of psychological and phar-
macological interventions for generalized anxiety dis-
order and panic disorder. The Australian and New
Zealand Journal of Psychiatry, 38, 602–612.
Lopez, A. D., Mathers, C. D., Ezzati, M., Jamison, D. T., &
Murray, C. J. L. (2006). Global burden of disease
and risk factors. Washington, DC: World Bank.
Chapter 1.
Renaud, A., Basenya, O., de Borman, N., Greindl, I., &
Meyer-Rath, G. (2009). The cost effectiveness of
integrated care for people living with HIV including
antiretroviral treatment in a primary health care
centre in Bujumbura, Burundi. AIDS Care, 21,
1388–1394.
The World Bank. (1993). The World development
report 1993. Investing in health. Washington, DC:
Author.
World Health Organization. (2010). Global burden
of disease (GBD). Accessed April 15, 2010, from
http://www.who.int/healthinfo/global_burden_disease/
en/index.html
Disasters and Health: Natural
Disasters and Stress/Health
▶ Psychosocial Factors and Traumatic Events
D 600
Disclosure
Pamela S. King
Pediatric Prevention Research Center,
Department of Pediatrics, Wayne State
University School of Medicine, Detroit, MI, USA
Synonyms
Emotional disclosure
Definition
Disclosure has been defined as sharing of
personal information with others through verbal
communication or written expression of what
individuals verbally reveal about themselves to
others (including thoughts, feelings, and
experiences).
Description
Disclosure can be a complex process. It is often
difficult to know what, how much, when, and to
whom to disclose. Many factors influence the
decision to disclose information, including per-
sonality traits such as anxiety, impulsivity, and
extraversion (see Costa & McCrae, 1992), as well
as social norms, one’s affect, goals, and previous
experiences with disclosure, the behavior of the
confidant, and one’s relationship with the confi-
dant. People often choose not to disclose for fear
of negative consequences (e.g., embarrassing or
hurting one’s confidant, punishment, reduction in
autonomy, rejection, harassment, discrimina-
tion). Although disclosure can result in negative
outcomes, research suggests that disclosure can
be beneficial in a variety of ways. Disclosure
provides people with an opportunity to express
their thoughts and feelings, to elicit social sup-
port, gain new coping strategies, and build inti-
macy in their personal relationships. Disclosure
may also allow people to find meaning in
Disclosure
traumatic experiences, and may promote per-
sonal growth and self-acceptance.
Disclosure has been investigated in a variety
of contexts. Researchers have investigated dis-
closure of a “concealable stigmatized identity,”
such as mental illness, experiences of abuse
or assault, epilepsy, or an HIV-positive diagnosis.
In each of these cases, people have personal
information that is socially devalued but is not
apparent to others. Disclosure has been examined
among people who have a chronic illness that is
not readily apparent, such as cancer or diabetes.
Researchers have also studied disclosure of
health information to family, friends, and health
care providers (e.g., parents disclosing HIV status
to children, adolescents sharing diabetes manage-
ment information with parents). Research within
each of these domains has examined how people
make decisions to disclose, how confidants react
to disclosure, and how people are affected by
their disclosure decisions.
Much of the disclosure literature has focused
on the effects of written disclosure on health out-
comes. These studies use a laboratory writing
technique which typically involves random
assignment to one of two (or more) groups: an
experimental group that discloses emotional
material, and a control group that does not. Both
groups are asked to write about assignments for
3–5 days, for 15–30 min each day. Those
assigned to the control conditions are asked to
write about superficial topics. Those in the exper-
imental group are asked to write about their
thoughts and feelings about an important emo-
tional issue that has affected them and their life.
Writing for both groups is usually done in the
laboratory, with no feedback given. This body
of research suggests that disclosure of emotional
events can have immediate effects on skin con-
ductance, heart rate, and blood pressure. In addi-
tion, written disclosure about emotional issues
can have long-term effects on both immune func-
tioning and health outcomes. Disclosure may
influence health in several ways. First, research
suggests that nondisclosure is a form of inhibition
that requires physiological work, reflected in
autonomic and central nervous system arousal.
Disclosing may reduce inhibition, thus reducing
Discrimination and Health
autonomic and central nervous system arousal
and facilitating better health outcomes. Disclo-
sure may also lead to changes in cognitive pro-
cesses, such as decreases in rumination or
increases in mastery, self-acceptance, and self-
concept, which in turn have benefits for health.
Finally, disclosure may lead to better health by
increasing social support. When individuals dis-
close, they may gain information from others
about effective coping strategies or they may
obtain emotional support, both of which could
contribute to better health outcomes.
Recent research has examined a different form
of disclosure – the link between adolescent dis-
closure to parents and adolescent health out-
comes. Prior research identified parental
monitoring as an important predictor of a variety
of adolescent behaviors including risky sexual
behavior, substance abuse, and poor adherence.
Additional investigation, however, revealed that
measures of parental monitoring were assessing
how much knowledge parents had, rather than
the way in which they obtained that knowledge.
Adolescent disclosure may be the primary source
of parents’ knowledge about adolescents’ activi-
ties. Research indicates that among adolescent
disclosure, parent solicitation, and parent
behavioral control, disclosure is the best predic-
tor of delinquent behavior. Research is now
exploring the role that adolescent disclosure to
parents plays in explaining adolescent health
outcomes, such as adherence to the type 1 diabe-
tes regimen.
Cross-References
▶ Emotional Expression
▶ Expressive Writing and Health
References and Readings
Chaudoir, S. R., & Fisher, J. D. (2010). The disclosure
process model: Understanding disclosure decision
making and postdisclosure outcomes among people
living with a concealable stigmatized identity. Psycho-
logical Bulletin, 136(2), 236–256.
601 D
Frattaroli, J. (2006). Experimental disclosure and its mod-
erators: A meta-analysis. Psychological Bulletin,
132(6), 823–865.
Graybeal, A., Sexton, J. D., & Penneaker, J. W. (2002).
The role of story-making in disclosure writing: The
psychometrics of narrative. Psychology and Health,
17(5), 571–581.
Pachankis, J. E. (2007). The psychological implications of
concealing a stigma: A cognitive-affective-behavioral
model. Psychological Bulletin, 133(2), 328–345.
Pennebaker, J. W. (1995). Emotion, disclosure, & health. D
Washington, DC: American Psychological
Association.
Smetana, J. G., Metzger, A., Gettman, D. C., & Campione-
Barr, N. (2006). Disclosure and secrecy in adolescent-
parent relationships. Child Development, 77(1),
201–217.
Stattin, H., & Kerr, M. (2000). Parental monitoring: A
reinterpretation. Child Development, 71, 1072–1085.
Discrimination
▶ Stigma
Discrimination and Health
Yori Gidron
Faculty of Medicine and Pharmacy, Free
University of Brussels (VUB), Jette, Belgium
Definition
This term refers to deliberate inequalities in
access to and in care for health conditions or to
the unequal exposure to health risks as a function
of people’s ethnic or demographic background
(age, gender, beliefs, skin color, etc.). This prob-
lem exists in both developed and developing
countries. Furthermore, discrimination and
health can even be seen on a more global level –
the inequality in health care between rich and
poor countries and the consequent disease burden
carried by poor countries, where global economic
and political forces sustain this. Numerous
studies show differences between low and high
socioeconomic status (SES) groups on health
D 602
conditions, and there is accumulating evidence
linking actual and perceived discrimination with
poor health conditions (Ahmed, Mohammed, &
Williams, 2007; Williams & Mohammed, 2009).
Importantly, physicians may even provide less
medical advice to people who are less similar to
them, i.e., of lower SES (Tschann, Adamson,
Coates, & Gullion, 1988). This is doubly harmful
since low SES people already have poorer health
risks, and receiving less medical advice may add
to their health risks. Both biological and psycho-
social pathways may link discrimination to poor
health (Ahmed et al., 2007). Biologically, low SES
people may be exposed to poorer environments
(poor sanitation, pollution), whose adverse health
effects are clear – infectious diseases, pulmonary
problems, and possibly cancers.
However, the mere exposure to environmental
stressors (e.g., crowding, social violence) may
add onto these biological agents, in contributing
to either unhealthy behaviors (e.g., heavy alcohol
consumption), or to psychophysiological pro-
cesses such as stress-induced inflammation
(Maes et al., 1998) or stress-induced DNA dam-
age (Gidron, Russ, Tissarchondou, & Warner,
2006), eventually resulting in poorer health.
Clear discrimination leading to health problems
could be seen when urban or even country insti-
tutions marginalize certain parts of society (based
on ethnicity or SES) by pressing them to reside in
poorer and more health-risky areas of cities
(Ahmed et al., 2007). One major challenge to
research and of course to curb this severe problem
is the assessment of discrimination. Its assess-
ment can be done by analysis of legislative
records (institutional discrimination), employ-
ment uptake as a function of ethnicity (control-
ling for education), and at an individual level.
The latter includes various scales such as the
perceived discrimination scale (Williams, Yu,
Jackson, & Anderson, 1997), which assesses
10 daily aspects of discrimination (e.g., being
treated as less intelligent or in a less courteous
manner than others). This domain is a very
important example where behavioral and social
sciences interact with biomedical sciences for
understanding and beginning to ameliorate such
severe health problems at a macro level.
Disease Acuity
Cross-References
▶ Health Disparities
▶ Socioeconomic Status (SES)
References and Readings
Ahmed, A. T., Mohammed, S. A., & Williams, D. R.
(2007). Racial discrimination & health: Pathways &
evidence. Indian Journal of Medical Research, 126,
318–327.
Gidron, Y., Russ, K., Tissarchondou, H., & Warner, J.
(2006). The relation between psychological factors
and DNA-damage: A critical review. Biological
Psychology, 72, 291–304.
Maes, M., Song, C., Lin, A., De Jongh, R., Van Gastel, A.,
Kenis, G., et al. (1998). The effects of psychological
stress on humans: Increased production of pro-
inflammatory cytokines and a Th1-like response in
stress-induced anxiety. Cytokine, 10, 313–318.
Tschann, J. M., Adamson, T. E., Coates, T. J., &
Gullion, D. S. (1988). Behaviors of treated hyperten-
sive patients and patient demographic characteristics.
Journal of Community Health, 13, 19–32.
Williams, D. R., & Mohammed, S. A. (2009). Discrimi-
nation and racial disparities in health: Evidence and
needed research. Journal of Behavioral Medicine, 32,
20–47.
Williams, D., Yu, Y., Jackson, J. S., & Anderson, N. B.
(1997). Racial differences in physical and mental
health: Socioeconomic status, stress and discrimina-
tion. Journal of Health Psychology, 2, 335–351.
Disease Acuity
▶ Disease Severity
Disease Burden
Yori Gidron
Faculty of Medicine and Pharmacy
Free University of Brussels (VUB),
Jette, Belgium
Definition
The term “disease burden” is a term of major
importance in medicine and behavioral medicine.
Disease Management
It refers to the intensity or severity of a disease
and to its possible impact on daily life. Thus, it
could be at times referring to both illness severity
and impact, resulting in confusion between con-
cepts. Concerning disease severity, this reflects
the amount of pathology in a given illness. For
example, disease burden in cancer may be
indexed by level of a tumor marker – e.g.,
CA125 in ovarian cancer, or CEA in colon can-
cer. Additionally, tumor stage could reflect dis-
ease burden as well. In coronary artery disease
(CAD), this can be indexed by the number of
arteries occluded over 50%, or the percentage of
occlusion in a given artery (e.g., 40%, 99%). In
infectious diseases, disease burden could reflect
the amount of viral load in HIV patients.
Concerning a disease’s impact, disease burden
can be measured by its effects on longevity or
on quality of life (QOL). An illness with a high
disease burden would thus impair one’s psycho-
logical, physical, or social functioning aspects of
QOL. For example, a patient with severe CAD
could have debilitating chest pain which reduces
his or her mobility, thus impairs work, elicits
anxiety and depressive reactions, and reduces
his or her social contacts with friends, family,
and work colleagues.
In behavior medicine, researchers often take
into account disease burden as a covariate, when
testing the relation between a psychological fac-
tor and recovery or prognosis, independent of
disease burden. For example, Denollet et al.
(1996) showed that the Type-D personality
(high distress and social inhibition) predicted
mortality in coronary heart disease, independent
of disease burden indexed by number of diseased
vessels and left ventricular functioning. In a study
on patients’ recovery from coronary bypass sur-
gery, Scheier et al. (1989) found that patients’
trait optimism predicted recovery, independent
of disease burden indexed by extent of surgery
and number of occluded vessels. Hundreds of
studies examine disease burden by assessing its
impact on QOL and general well-being. A few
standardized disease burden indices exist includ-
ing the Charlson Index and the index of coexis-
tent disease (Greenfield, Aronow, Elashoff, &
Watanabe, 1988). The former only considers the
603 D
number and severity of comorbid diseases, while
the latter additionally considers patients’ func-
tional status in 12 categories (e.g., feeding, men-
tal status, vision, respiration). Another unique
disease burden index is the Smith index, which
considers in a formula with weights a patient’s
emergency room visits during 6 months, blood
urea nitrogen value, arterial pO2, total white
blood cell count, and presence of anemia. These D
indices can enable researchers in behavior
medicine to assess disease burden in
a standardized manner across patient conditions,
and then examine the role of psychosocial factors
in prognosis, independent of disease burden
estimates. Finally, one may also estimate the
impact of such disease burden indices on psycho-
logical functioning.
References and Readings
Denollet, J., Sys, S. U., Stroobant, N., Rombouts, H.,
Gillebert, T. C., & Brutsaert, D. L. (1996). Personality
as independent predictor of long-term mortality in
patients with coronary heart disease. Lancet, 347,
417–421.
Greenfield, S., Aronow, H., Elashoff, R., & Watanabe, D.
(1988). Flaws in mortality data: The hazards of ignor-
ing comorbid disease. Journal of the American
Medical Association, 260, 2253–2255.
Scheier, M. F., Matthews, K. A., Owens, J. F., Magovern,
G. J., Sr., Lefebvre, R. C., Abbott, R. A., et al. (1989).
Dispositional optimism and recovery from coronary
artery bypass surgery: The beneficial effects on phys-
ical and psychological well-being. Journal of Person-
ality and Social Psychology, 57, 1024–1040.
Disease Management
Harry Prapavessis
University of Western Ontario, London, ON,
Canada
Synonyms
Chronic care; Integrated health care; Managed
care
D 604
Definition
Disease management is a patient centered, inte-
grative health care intervention approach for
managing the signs and symptoms of chronic
diseases in defined populations of individuals.
The main aims of disease management interven-
tions are to optimize care, improve quality of life,
and reduce costs associated with treating chronic
conditions by coordinating patient care using a
multidisciplinary approach.
Description
Disease management came about as a response to
a changing health landscape wherein the preva-
lence and complexity of chronic conditions is on
the rise requiring treatment regimens to adjust.
With traditional approaches, patient information
is spread across practitioners and specialists who
are responsible for disparate aspects of patient care
and respond in reactive ways to acute conditions.
In contrast, disease management approaches plan
for the long-term management of chronic condi-
tions by reducing fragmentation and improving the
continuity and coordination of the patient care
process. This strategy is predicated on the under-
standing that improvements in medical therapy and
self management can reduce the signs and symp-
toms of disease and improve treatment outcomes.
Disease management interventions are based
in both primary care and private sector opera-
tions. While each of these shares the common
goal of improving the health of the patient
(e.g., increase functional ability, improve health
status, reduce hospitalization time, and increase
care compliance with treatment plans) and
decreasing associated costs, different approaches
are taken. Primary care interventions are inte-
grated into the health care delivery system and
focus mainly on communication with patients
and between professionals (e.g., physicians, phar-
macists, nurses, nurse practitioners, physical ther-
apists). Private sector interventions are adjunct to
the health care system (e.g., employers and
insurers) and mainly focus on cost containment.
Three common key agents of change emerge
in disease management literature: the patient, the
Disease Management
health care team, and the environment. The
patient is viewed as an active agent in his or
her own care. It is up to the individual to seek
information and be motivated to carry out the
treatment plan. As such, self-management
(▶ Self-management) interventions are hypothe-
sized to affect outcomes (e.g., health status and
health care use) by producing behavior change.
There are many modifiable lifestyle factors that
can be adopted by the patient to prevent or min-
imize the effects of disease (e.g., adherence to
treatment regimens, physical activity, proper
nutrition, medical screening, limited sun expo-
sure, and substance avoidance). For example,
epidemiological studies reveal that people who
are more physically active have a lower risk of
certain cancers than those who are sedentary.
Evidence of self management interventions
consistently demonstrates self-efficacy, and
knowledge and skills are important mediators to
target behavior change interventions.
The role of the health care team in disease
management is to monitor conditions and to cre-
ate a treatment plan, either alone or with the
patient and health care team. A key challenge
for the health care professional is to keep abreast
of advancing knowledge and expertise necessary
to care for patients. Education, decision-making
support, time, and resources are targets for dis-
ease management intervention that should result
in changed attitudes or behavioral intention,
which is hypothesized to lead to professional
behavior change. Ultimately, professionals who
have increased expertise, knowledge, and support
should provide higher quality treatment thus
improving health outcomes.
Interventions that target the health care envi-
ronment often focus on organizational design and
relational coordination. Effective relational coor-
dination interventions often involve the assembly
of a coordinated (coordination within, across, and
between care teams and community resources)
multidisciplinary patient care team. Effective
organizational design interventions often address
task allocation, information transfer, appoint-
ment scheduling, and case management. These
strategies are based on the belief that seamless
care delivery (e.g., structural, financial, and
Disease Onset
functional) and collaboration among diverse care
providers (e.g., nurses, nurse practitioners, dieti-
cians, social workers, physicians, physician assis-
tants, and public health workers) will improve
health and fiscal outcomes.
Although there is some evidence to support
various disease management strategies, definitive
conclusions about the overall effectiveness on
patient outcomes and cost reduction cannot yet
be made and will require further exploration.
605 D
Definition
A disease is a medical condition that is consid-
ered to be abnormal, impairs bodily functions,
and is associated with specific signs and symp-
toms. The disease onset is the first time that there
has been noted to be a “change” in one’s usual
health status with the identified signs and/or
symptoms being able to be directly attributable D
to a specific disease process.

Cross-References
Description
▶ Adherence
Diseases may be identified as having an acute,
▶ Aerobic Exercise
▶ Behavior Change subacute, or chronic onset with symptoms devel-
oping over a wide variety of time from minutes to
▶ Behavior Modification
months. Certain diseases will be easier to identify
▶ Self-management
as to their exact time of origin, or disease onset.
An example would be the onset of nausea and
vomiting from a food-borne toxin that has been
References and Readings
ingested. Other diseases are much harder to char-
http://www.carecontinuum.org/ acterize as to their onset. Alzheimer’s disease, for
Singer, S., Burgers, J., Friedberg, M., Rosenthal, M., example, is rarely identified until it has reached
Leape, L., & Schneider, E. (2010). Defining and mea- clinical significance at which time most individ-
suring integrated patient care: Promoting the next fron-
uals and their close contacts on more careful
tier in health care delivery. Medical Care Research
and Review, 68(1), 112–127. analysis can identify early warning signs that
Wagner, E. H. (2000). The role of patient care teams in appeared years earlier and likely marked the
chronic disease management. British Medical Journal, onset of the disease. While symptoms may present
320(7234), 569–572.
in a classic manner, such as chest pain accompa-
nying the onset of a myocardial infarction, at
times, the presentation is atypical/nonspecific,
Disease Manifestation making the diagnosis as to disease onset challeng-
ing. In the elderly, for example, it is not uncom-
▶ Disease Onset mon for a myocardial infarction to present with no
chest pain but rather shortness of breath being the
initial symptom at disease onset.
There are many examples of diseases that have
Disease Onset variable disease onset. One such example is
coronary artery disease. Individuals who present
Steven Gambert with coronary artery disease prior to age 50 are
Department of Medicine, School of Medicine, more likely to have a genetic predisposition;
University of Maryland, Baltimore, MD, USA individuals affected later in life may have
additional risk factors including dietary
influences and coexisting diseases such as
Synonyms hypertension. Another example of a disease
with a variable disease onset is Alzheimer’s
Disease manifestation disease. Individuals affected prior to age 65 are
D 606 Disease Severity

said to have a presenile dementia of the

Alzheimer’s type and are more likely to have Disease Severity Index
a genetic predisposition for this earlier onset.
Individuals affected after age 65 are said to have ▶ Disease Severity
senile dementia of the Alzheimer’s type (SDAT)
(Bertram & Tanzi, 2008).

Disinhibition
Cross-References
▶ Behavioral Inhibition
▶ Acute Disease ▶ Impulsivity
▶ Alzheimer’s Disease

References and Readings Disparities

Bertram, L., & Tanzi, R. E. (2008). Thirty years of ▶ Health Disparities
Alzheimer’s disease genetics: The implications of
systematic meta-analyses. Nature reviews. Neurosci-
ence, 9(10), 768–778.

Dispersion

Disease Severity J. Rick Turner

Cardiovascular Safety, Quintiles, Durham,
Steven Gambert NC, USA
Department of Medicine, School of Medicine,
University of Maryland, Baltimore, MD, USA
Synonyms

Synonyms Scatter; Variability

Disease acuity; Disease severity index

Definition
Disease severity is a term used to characterize the
impact that a disease process has on the utilization
of resources, comorbidities, and mortality. It is
often used by funding agencies to determine what
is an appropriate payment for hospitalization or
nursing home payments based on Diagnosis-
Related Groups or RUGS (Resource Utilization
Groups). There are several “severity indexes” that
may be used to quantify the severity of illness such
as the Glascow Coma Scale for assessing the sever-
ity of cognitive dysfunction or the Mini-Mental
Examination that quantifies the degree of dementia.
Definition
The spread, or dispersion, of a group of numbers
around a central value is an important character-
istic of a data set. It can be calculated in various
ways. The range, the simplest measure of disper-
sion, is the arithmetic difference between
the largest (maximum) value and the smallest
(minimum) value. However, while it can be
useful in initial “visual inspections” of a data
set, this measure of dispersion is only a rough
guide to the amount of variation present. Because
it only takes into account two values from a data
set, it utilizes a (potentially very) small part of the
information available.
Dispositional Optimism
Imagine a data set containing 100 numbers.
When calculating the range, only two of these
numbers would be used. In other words, 98% of
the available information would not be used in
deriving this measure of dispersion. Consider a
hypothetical data set of 100 numbers where the
minimum value is 20, the maximum value is 80,
and all of the 98 other numbers lie between 55 and
75. Now consider a second hypothetical data set of
100 numbers where the minimum value is again
20, the maximum value is again 80, but the other
98 numbers are spread out between 25 and 55.
While the range would be identical in both cases
(i.e., 60), it is intuitive that the overall natures of
the two sets of numbers are quite different.
Two more sophisticated measures of disper-
sion for a data set are its variance and its standard
deviation. These measures are intimately related
to each other and take account of all values in
the data set.
Cross-References
▶ Standard Deviation
▶ Variance
Disposition
▶ Personality
Dispositional Optimism
Lauren Zagorski
Department of Psychology, The University of
Iowa, Iowa City, IA, USA
Synonyms
Optimism
Definition
Dispositional optimism is a stable personality
trait characterized by general positive
607 D
expectations that influence motivated action.
When confronted with obstacles in achieving
a desired future state, those who are optimistic
anticipate positive outcomes from their actions.
According to this self-regulatory model, opti-
mism plays a role in negative feedback loops
that guide goal-directed behavior. Consequently,
optimistic individuals display a cross-situational
tendency to enhance efforts toward their goals D
instead of disengaging and withdrawing efforts.
It is also theorized that optimism is implicated in
the propensity to attribute the cause of negative
events as external and unstable. This explanatory
style then influences future expectancies and
behavior.
Various investigations of dispositional
optimism have revealed a positive relationship
with problem-focused and engagement coping
strategies. This is the proposed pathway for opti-
mism’s potential benefits for well-being and
adjustment to stressors. Dispositional optimism
has been linked to positive psychological and
physical outcomes among patients with chronic
illnesses including cardiovascular disease, AIDS,
and cancer.
Cross-References
▶ Life Orientation Test (LOT)
▶ Optimism and Pessimism: Measurement
▶ Self-regulation Model
References and Readings
Carver, C. S., & Scheier, M. F. (2002). Optimism. In C. R.
Snyder & S. J. Lopez (Eds.), Handbook of positive psy-
chology (pp. 231–243). New York: Oxford University
Press.
Carver, C. S., Scheier, M. F., & Segerstrom, S. C. (2010).
Optimism. Clinical Psychology Review, 30(7),
879–889. doi:10.1016/j.cpr.2010.01.006.
Scheier, M. F., & Carver, C. S. (1992). Effects of opti-
mism on psychological and physical well-being: The-
oretical overview and empirical update. Cognitive
Therapy and Research, 16(2), 201–228. doi:10.1007/
BF01173489.
D 608
Dispositional Pessimism
▶ Optimism, Pessimism, and Health
▶ Pessimism
Dissemination
Wynne E. Norton
Department of Health Behavior, School of Public
Health, University of Alabama at Birmingham,
Birmingham, AL, USA
Synonyms
Diffusion; Implementation
Definition
Dissemination refers to “the targeted distribution
of information and intervention materials to
a specific public health or clinical practice audi-
ence,” whereas implementation refers to “the use
of strategies to adopt and integrate evidence-
based health interventions and change practice
patterns within specific settings” (National Insti-
tutes of Health [NIH], 2010).
Broadly speaking, dissemination and imple-
mentation science (D&I) is focused on bridging
the research-to-practice gap in health care and
public health. The overall objectives of D&I
research are to understand barriers toward the
effective use of evidence-based health interven-
tions, programs, practices, and treatments in
health care and public health and, importantly,
to create and test strategies to move such health
innovations into everyday settings more quickly,
effectively, and broadly.
D&I science is highly interdisciplinary, draw-
ing on expertise from systems science, psychol-
ogy, sociology, health services research,
organizational behavior, and clinical research,
among other fields. The field has witnessed con-
siderable growth, expansion, and interest among
Dispositional Pessimism
researchers, policymakers, and practitioners in
the United States and international settings in
the past decade. This has included the emergence
of speciality journals (e.g., Implementation
Science), conferences (e.g., National Institutes
of Health Conference on the Science of Dissem-
ination and Implementation), review panels,
funding announcements, and training programs
(e.g., Implementation Research Institute).
References and Readings
Dearing, J. W. (2008). Evolution of diffusion and dissem-
ination theory. Journal of Public Health Management
and Practice, 14(2), 99–108.
Green, L. W., Ottoson, J. M., Garcia, C., & Hiatt, R. A.
(2009). Diffusion theory and knowledge dissemina-
tion, utilization, and integration in public health.
Annual Review of Public Health, 30, 151–174.
Greenhalgh, T., Robert, G., Macfarlane, F., Bate, P., &
Kyriakidou, O. (2004). Diffusion of innovations in
service organizations: Systematic review and recom-
mendations. The Milbank Quarterly, 82(4), 581–629.
Implementation Science. (2011). www.implementa-
tionscience.com
Implementation Research Institute. (2011). http://cmhsr.
wustl.edu/Training/IRI/Pages/ImplementationRe-
searchTraining.aspx
National Institutes of Health. (2010). Program announce-
ment: Dissemination and implementation research in
health (R01). Retrieved from http://grants.nih.gov/
grants/guide/pa-files/PAR-10-038.html
NIH Conference on the Science of Dissemination and
Implementation. (2011). http://conferences.thehill
group.com/obssr/DI2011/about.html
Proctor, E. K., Landsverk, J., Aarons, G., Chambers, D.,
Glisson, C., & Mittman, B. (2009). Implementation
research in mental health services: An emerging sci-
ence with conceptual, methodological, and training
challenges. Administration and Policy in Mental
Health, 36(1), 24–34.
Rabin, B. A., Brownson, R. C., Haire-Joshu, D., Kreuter,
M. W., & Weaver, N. L. (2008). A glossary for dis-
semination and implementation research in health.
Journal of Public Health Management and Practice,
14(2), 117–123.
Dissemination and Implementation
▶ Research to Practice Translation
Distant Intercessory Prayer
Distant Intercessory Prayer
Kevin S. Masters
Department of Psychology, University
of Colorado, Denver, CO, USA
Definition
Distant intercessory prayer is simply defined as
prayer said on behalf of someone else when that
person is not present. This is different from
intercessory prayer in which prayer is also said
on behalf of someone else but the person being
prayed for is present during the prayer.
Description
Intercessory prayer is the age-old practice of
praying for someone else. The first empirical
study on this topic was conducted by Sir Francis
Galton and published in 1872. Galton demon-
strated that individuals who were often prayed
for, in this case, members of the royal family,
did not live longer than others. In the context of
modern behavioral medicine, intercessory prayer
still usually consists of prayer for improvement in
health status or healing. One could serve as one’s
own intercessor (as when praying for oneself) or
could be the recipient of prayers from others,
i.e., intercessors. Prayers said by oneself or by
others in the presence of the recipient of the
prayer could theoretically be effective in
improving health through a number of
mechanisms including not only the actual prayer
itself (i.e., divine intervention or some type of
beneficial energy) but also via social support or
other naturalistic psychological mechanisms.
Distant intercessory prayer, however, occurs
when the intercessor is not physically present
with the recipient of the prayer. In this way,
a more stringent test of the effects of prayer per
se can be tested. Further, some studies in this area
used blinding strategies wherein patients did not
know whether they were in the prayer or
no-prayer group, and other studies went even
609 D
further and included patients who did not even
know they were included in a prayer research
project.
Empirical research on the effects of distant
intercessory prayer has been carried out with
patients experiencing many different disorders
including various forms of cardiac disease,
leukemia, mental health problems, renal failure,
rheumatoid arthritis, infertility, sepsis, and D
alcohol abuse. Reviews and meta-analyses were
conducted by Masters and colleagues (Masters &
Spielmans, 2007; Masters, Spielmans, &
Goodson, 2006) and the more recently published
Cochrane Collaboration Review (Roberts,
Ahmed, Hall, & Davison, 2011). Each of these
analyses found no credible evidence that distant
intercessory prayer was associated with
a beneficial overall effect. The authors of the
Cochrane report carefully pointed out that their
review of the empirical data in no way addresses
metaphysical questions regarding the existence
of God or any deity. Similarly, Masters (2005)
argued that distant intercessory prayer studies
lack a strong theological basis and also produce
noninterpretable findings because, critically, they
are not able to control the amount of prayer deliv-
ered to or for the no-prayer control group. That is,
when a group of researchers assigns individuals
to a no-prayer control group, it only means that
the researchers or their chosen intercessors will
not pray for those individuals. This, however,
does nothing to stop family, close friends,
health-care professionals, or others from praying
for them. There has never been a reason postu-
lated that suggests the prayers of intercessors in
a prayer study would be more effective than those
of others in the patients’ experiential world.
Many other questions remain unaddressed in
these studies including qualifications of interces-
sors, theoretical understanding of both significant
and nonsignificant findings, within group varia-
tions in outcomes, and any firm theory or even
coherent hypothesis to offer an explanation for
the expected effects. One study (Benson
et al., 2006) even suggested that individuals
undergoing coronary artery bypass grafting
who knew they were receiving intercessory
prayer had a higher incidence of complications.
D 610
Finally, in some studies, when significant find-
ings were found, they (a) were not on the vari-
ables that were the object of prayer and (b)
occurred in the absence of controls for multiple
comparisons.
It bears repeating, however, that the argu-
ment here is not against the conduct of inter-
cessory prayer, distant or present, by those who
believe in such practices. Rather, it is an argu-
ment that empirical studies have not demon-
strated an overall superiority for groups in
prayed for versus not prayed for groups and
that, because of the inherent methodological
limitations of such research, these studies are
actually unable to test their central idea/hypoth-
esis and thus will never render a definitive data-
base upon which to ascertain the health effects
of intercessory prayer.
Cross-References
▶ Prayer
References and Readings
Benson, H., Dusek, J. A., Sherwood, J. B., Lam, P.,
Bethea, C. F., Carpenter, W., et al. (2006). Study of
the therapeutic effects of intercessory prayer (STEP) in
cardiac bypass patients: A multicenter randomized
trial of uncertainty and certainty of receiving
intercessory prayer. American Heart Journal, 151,
934–942.
Galton, F. (1872). Statistical inquiries into the efficacy of
prayer. Fortnightly Review, 12, 125–135.
Masters, K. S. (2005). Research on the healing power of
distant intercessory prayer: Disconnect between
science and faith. Journal of Psychology and
Theology, 33, 268–277.
Masters, K. S., & Spielmans, G. I. (2007). Prayer and
health: Review, meta-analysis, and research agenda.
Journal of Behavioral Medicine, 30, 329–338.
Masters, K. S., Spielmans, G. I., & Goodson, J. T. (2006).
Are there demonstrable effects of distant intercessory
prayer? A meta-analytic review. Annals of Behavioral
Medicine, 32, 337–342.
Roberts, L., Ahmed, I., Hall, S., & Davison, A. (2011).
Intercessory prayer for the alleviation of ill health
(Review). The Cochrane Collaboration. New York:
John Wiley and Sons.
Distraction (Coping Strategy)
Distraction (Coping Strategy)
Lara Traeger
Behavioral Medicine Service, Massachusetts
General Hospital/Harvard Medical School,
Boston, MA, USA
Synonyms
Behavioral disengagement; Diversion; Mental
disengagement
Definition
Distraction refers to a classification of coping
strategies that are employed to divert attention
away from a stressor and toward other thoughts
or behaviors that are unrelated to the stressor. In
both adult and pediatric populations, distraction
(for example, focusing on an external object or
imagining a peaceful place) may be used to deal
with pain and discomfort during medical proce-
dures. Other examples of distraction include
daydreaming or engaging in substitute activities
to keep one’s mind from ongoing stressors related
to a chronic illness. There are many ways to
group coping strategies together. For instance,
distraction has been considered a type of emo-
tion-focused coping (Lazarus and Folkman,
1984), which involves minimizing the emotional
distress related to a stressor. Distraction has also
been categorized as passive coping, a type of
coping that has been associated with helpless-
ness, avoidance, and poorer psychological out-
comes in the long term. Examples of distraction
that reflect a sense of helplessness or avoidance
are statements such as “I try to think about any-
thing else but my illness because I’ve quit trying
to deal with it” and “I can’t think about my illness
so I’ve been watching television or movies to
escape.”
Diuretic 611 D
Cross-References Definition

▶ Coping A diuretic is a drug that increases the rate of urine

▶ Passive Coping Strategies flow. As a drug class, the major aim of diuretics is
to decrease extracellular fluid volume, and their
major site of action is the kidneys. Secondarily,
References and Readings diuretics increase extracellular sodium excretion.
Different classes of diuretics work by different
Lazarus, R. S., & Folkman, S. (1984). Stress, appraisal, mechanisms in the kidneys, and they alter cation D
and coping. New York: Springer.
and anion levels in the body as well as renal
hemodynamics.
The main classes of diuretics include carbonic
anhydrase inhibitors, loop diuretics, thiazide
diuretics, potassium-sparing diuretics, and
Distress osmotic diuretics. Carbonic anhydrase inhibitors
(e.g., acetazolamide, dichlorphenamide, and
▶ Mental Stress
methazolamide) work at the proximal convoluted
▶ Psychological Stress
tubule of the nephron, where carbonic anhydrase
▶ Stress
plays a role in sodium bicarbonate reabsorption.
By inhibiting sodium bicarbonate reabsorption,
these drugs cause sodium bicarbonate and water
excretion. Carbonic anhydrase inhibitors are used
Distressed Personality Type clinically to treat severe acute glaucoma because
their effect of decreasing bicarbonate
▶ Type D Personality reabsorption leads to decreased bicarbonate
secretion in the eye and lowers intraocular
pressure.
Loop diuretics (e.g., furosemide, bumetanide,
ethacrynic acid, and torsemide) work at the thick
Disuse Atrophy ascending loop of henle and inhibit the sodium-
potassium-chloride symport, thereby increasing
▶ Sarcopenia
excretion of ions and water. Clinically they are
used to quickly get rid of edema in heart failure,
ascites, and pulmonary edema.
Thiazides (e.g., hydrochlorothiazide, thiazide,
Diuretic chlorthalidone, indapamide, and metolazone)
work at the distal convoluted tubule and inhibit
Nicole Brandt1 and Rachel Flurie2 the sodium-chloride symport. They are used
1
School of Pharmacy, University of Maryland, mainly in hypertension because they lower
Baltimore, MD, USA blood pressure and to a lesser extent to reduce
2
University of Maryland, Baltimore, MD, USA edema.
Potassium-sparing diuretics act by two differ-
ent mechanisms. Spironolactone and eplerenone
Synonyms antagonize aldosterone in the collecting tubules
while amiloride and triamterene block the epithe-
Fluid pill; Water pill lial sodium channels in the collecting tubules.
D 612
They all increase sodium excretion and decrease
potassium and hydrogen excretion. These drugs
may be used in combination with loop or thiazide
diuretics to counterbalance the potassium
wasting of those drug classes. The ones that affect
aldosterone are also used in heart failure.
Osmotic diuretics (glycerine, isosorbide, man-
nitol, and urea) cause excess water excretion
from intracellular compartments thereby increas-
ing urine volume and renal blood flow. They are
used to maintain high urine flow in certain clini-
cal situations (e.g., severe hemolysis or rhabdo-
myolysis) and can be used to reduce intraocular
or intracranial pressure.
There are multiple types of diuretics whose
clinical indications can vary depending on the
patient’s comorbidities. It is imperative with this
class of medications to weigh the impact not just on
efficacy but also how these medications can impact
their quality of life due to issues with urinary
frequency and possibly incontinence.
References and Readings
Brunton, L. L., Chabner, B. A., & Knollmann, B. C.
(2010). Goodman & Gilman’s the pharmacological
basis of therapeutics (12th ed.). New York: McGraw-
Hill Professional.
Trevor, A. J., Katzung, B. G., & Susan, B. (2010).
Masters: Pharmacology: Examination & board review
(9th ed.). New York: McGraw-Hill Medical.
Diurnal Mood Variation
Brant P. Hasler
Psychiatry, Western Psychiatric Institute and
Clinic University of Pittsburgh School of
Medicine, Pittsburgh, PA, USA
Synonyms
Daily mood variation; Diurnal rhythms in mood;
Mood variability
Diurnal Mood Variation
Definition
The term diurnal mood variation is most com-
monly used in the context of the symptomatology
of mood disorders, referring to noticeable diurnal
(daily) changes in overall mood state experienced
by some individuals suffering from depression.
Historically, the specific patterns of these diurnal
mood changes were thought to characterize var-
ious subtypes of depression, although empirical
evidence for this has been mixed. Diurnal mood
variation has been most closely linked to melan-
cholic depression (also known as endogenous or
somatic depression), which was thought to be
characterized by a pattern of feeling worst (most
depressed) upon awakening in the morning, than
feeling progressively better as the day continues
into the afternoon and evening. The opposite
(atypical) pattern – feeling best in the morning,
then worsening over the course of the day – was
considered to be less common, and thought to
characterize atypical (or nonendogenous) depres-
sion. Diurnal patterns in mood have also been
noted in healthy individuals, and a circadian
rhythm component to mood is now well
established, although the specific term “diurnal
mood variation” is less commonly used in this
context.
Description
In the context of depression, diurnal mood varia-
tion is typically assessed by asking the patient to
retrospectively describe the pattern, either during
the course of a clinical interview or as an item on
a questionnaire (e.g., Hamilton Rating Scale for
Depression). Efforts to assess diurnal mood var-
iation prospectively, both within and across days,
suggest that the presence and direction (morning
worse vs. evening worse) of diurnal mood varia-
tion are highly unstable over time, and vary inde-
pendently of overall depressive symptoms
(Gordijn, Beersma, Bouhus, Reinink, &
Van den Hoofdakker, 1994). The instability of
diurnal mood variation, as well as poor agree-
ment between assessment approaches, suggests
that caution is warranted when interpreting
Diurnal Mood Variation
diurnal mood variation as an indicator of depres-
sion subtype (e.g., melancholic vs. atypical). This
caution was underscored by a study of 37 patients
with major depression that found no relationship
between pattern of diurnal mood variation and
either typical (i.e., weight loss and insomnia) or
atypical (i.e., weight gain and hypersomnia)
depressive symptoms (Leibenluft, Noonan, &
Wehr, 1992). Likewise, a much larger dataset of
3,744 outpatients with major depression from the
STAR*D study also suggested a need to revise the
conventional wisdom regarding links between
specific patterns of diurnal mood variation and
depression subtypes (Morris et al., 2007). Specif-
ically, nearly a quarter of patients reported diurnal
mood variation, but the majority of these patients
(48.6%) reported evening worsening in mood,
with only 31.9% or 19.5% reporting morning or
afternoon worsening in mood, respectively. Mor-
ris and colleagues also reported that any diurnal
mood variation, rather than morning worsening,
per se, increased the likelihood of having melan-
cholic symptoms of depression.
Diurnal mood variation is thought to have
clinical relevance as a predictor of treatment
response, although the empirical evidence for
this is mixed. Early studies have suggested that
morning worse morning mood predicted favor-
able treatment responses to total sleep depriva-
tion and tricyclic antidepressants. In contrast,
more recent studies indicated that greater mood
variability, rather than any specific pattern of
diurnal mood variation, is associated with
improved response to total sleep deprivation
treatment (Gordijn et al., 1994), and that diurnal
mood variation does not predict treatment
response to selective serotonin reuptake inhibi-
tors (SSRIs) (Morris et al., 2007).
Although the classic conception of diurnal
mood variation has thus far proven to have argu-
able utility, more sophisticated investigations of
diurnal patterns in mood may still provide impor-
tant insights into the pathophysiology of depres-
sion. These studies are distinguished from past
research by using prospective designs along with
more frequent within-day assessments to provide
greater temporal resolution of mood variability.
A number of studies have been influenced by
613 D
advances in affective science, and thus used sep-
arate scales to assess positive and negative affect
rather than using a unidimensional mood measure
(Watson, 2000). These studies have generally
reported that positive affect shows a 24-h rhyth-
mic pattern, while negative affect lacks system-
atic daily variation. Positive affect is lowest in the
early morning hours, rises throughout the day, to
peak in the late afternoon and early evening, and D
declines during the night. Accumulating evi-
dence indicates that the 24-h patterns in positive
affect are due in part to endogenous circadian
rhythms and not simply a reflection of affective
responses to sociocultural rhythms in the envi-
ronment (Boivin et al., 1997; Murray, Allen, &
Trinder, 2002).
Diurnal rhythms in mood may be altered in
depression, most commonly manifesting as
a blunted peak in positive affect. In a study by
Peeters, Berkhof, Delespaul, Routtenberg, and
Nicolson (2006) depressed individuals reported
lower peaks of positive affect, and these peaks
occured later in the day, compared to healthy
non-depressed individuals. The depressed group
also reported decreased negative affect through-
out the day, with greater moment-to-moment var-
iability. (Negative affect in the healthy group did
not follow a systematic pattern, consistent with
previous reports.) In interpreting these results, the
authors hearkened back to the classic definition of
diurnal mood variation, noting that retrospective
mood evaluation, via a unidimensional mood
construct, likely hinged on an internal calculus
of the varying combinations of positive and neg-
ative affect occurring throughout the day. A more
recent study by Murray and colleagues (Murray,
2007) suggested that changes in the diurnal
rhythms of positive affect are not only apparent
in categorical comparisons of depressed and
healthy individuals, but can also serve to charac-
terize the severity of depression. Compared to
a group with mild depression, the group with
more severe depression had a less discernable
rhythm in positive affect with a notably blunted
peak, along greater overall negative affect
throughout the day. Cumulative evidence indi-
cates that altered circadian function may be pre-
sent in depression.
D 614 Diurnal Rhythms in Mood

Cross-References
Diversion
▶ Circadian Rhythm
▶ Depression: Measurement ▶ Distraction (Coping Strategy)
▶ Depression: Symptoms
▶ Depression: Treatment
▶ Hamilton Rating Scale for Depression
(HAM-D) Diversity
▶ Mood
C. Andres Bedoya
Behavioral Medicine Service Department of
References and Readings Psychiatry, Massachusetts General Hospital,
Harvard Medical School, Boston, MA, USA
Boivin, D. B., Czeisler, C. A., Dijk, D. J., Duffy, J. F.,
Folkard, S., Minors, D. S., et al. (1997). Complex
interaction of the sleep-wake cycle and circadian
phase modulates mood in healthy subjects. Archives Synonyms
of General Psychiatry, 54(2), 145–152.
Gordijn, M. C., Beersma, D. G., Bouhus, A. L., Cultural competence; Heterogeneity;
Reinink, E., & Van den Hoofdakker, R. H. (1994).
Multiculturalism
A longitudinal study of diurnal mood variation in
depression; characteristics and significance. Journal
of Affective Disorders, 31(4), 261–273.
Leibenluft, E., Noonan, B. M., & Wehr, T. A. (1992). Definition
Diurnal variation: Reliability of measurement and rela-
tionship to typical and atypical symptoms of depression.
Journal of Affective Disorders, 26(3), 199–204. Diversity involves a difference between an indi-
Morris, D. W., Rush, A. J., Jain, S., Fava, M., Wisniewski, vidual or group in comparison to an established
S. R., Balasubramani, G. K., et al. (2007). Diurnal “norm” (Kato & Mann, 1996). This may be
mood variation in outpatients with major depressive
influenced by context and based on a number of
disorder: Implications for DSM-V from an analysis of
the sequenced treatment alternatives to relieve depres- factors including, but not limited to, ethnicity,
sion study data. The Journal of Clinical Psychiatry, race, culture, gender, age, sexual orientation, reli-
68(9), 1339–1347. gion/spirituality, health status, disability, veteran
Murray, G. (2007). Diurnal mood variation in depression:
A signal of disturbed circadian function? Journal of
status, or socioeconomic status (Jackson, 2006).
Affective Disorders, 102, 47–53. Such factors are not mutually exclusive and may
Murray, G., Allen, N. B., & Trinder, J. (2002). Mood and occur in any myriad of combinations.
the circadian system: Investigation of a circadian com-
ponent in positive affect. Chronobiology Interna-
tional, 19(6), 1151–1169.
Peeters, F., Berkhof, J., Delespaul, P., Routtenberg, J., & Description
Nicolson, N. A. (2006). Diurnal mood variation in
major depressive disorder. Emotion, 6(3), 383–391. The field of behavioral medicine has made
Watson, D. (2000). Mood and temperament. New York:
significant advances over the past three decades,
Guilford Press.
Wirz-Justice, A. (2008). Diurnal variation of depressive providing a strong body of interdisciplinary evi-
symptoms. Dialogues in Clinical Neuroscience, 10(3), dence and theory to support the efficacy of apply-
337–343. ing research and practice for the promotion of
health and prevention of illness (Belar &
Deardorff, 2009; Smith & Suls, 2004). Similar
to the medical field as a whole, however, these
Diurnal Rhythms in Mood advances have historically focused on the expe-
rience of middle-class Euro-American white
▶ Diurnal Mood Variation males and been based on a traditional Western
Diversity
view of health (Kazarian & Evans, 2001; Smith,
Kendall & Keefe, 2002).
Yet demographic diversity within the United
States continues to increase in a number of areas
(Jackson, 2006). For example, the Census Bureau
noted that in 2008, ethnic and racial minorities
consisted of approximately one-third of the pop-
ulation. Census projections indicate that by mid-
century, these minority groups will continue to
increase in number and represent slightly more
than a majority of the population as a whole.
Latinos, in particular, are projected to account
for one in three of all Americans. Over this
period, the average age is also expected to
increase, resulting in a greater proportion of
Americans who are older. Similarly, other
diverse groups are projected to continue to
grow, including the number of people who iden-
tify as members of sexual minority groups.
Diversity is a salient issue as it has a number of
implications regarding the prevalence of illness
and health-related disparities (Agency for
Healthcare Research and Quality, 2009; Smith
& Shuls, 2004). For example, compared to
whites, African Americans experience significant
health disparities in areas such as number of new
cases of AIDS, diabetes-related lower extremity
amputations, and lack of prenatal care within the
first trimester of pregnancy. African Americans,
Asian Americans, and Hispanics over the age 50
are significantly less likely to receive preventa-
tive screenings such as a colonoscopy or
proctoscopy. Similarly, Hispanic and African
Americans with depression are less likely than
whites to receive mental health care.
An increasingly diverse demographic land-
scape will require that behavioral medicine
adapt in order to appropriately address the needs
of diverse groups (Belar & Deardorff, 2009).
Through development of cultural competence
skills, the field can better understand patients’
sociocultural contexts, as well as recognize and
appropriately respond to key cultural features. To
this end, cultural competence involves develop-
ment within three domains: self-awareness of
one’s own attitudes and beliefs; knowledge of
the population of interest; and tools that can be
applied with diverse groups (Jackson, 2006).
615 D
Similarly, cultural competence can be
extended to involve a context competence
(Smith & Suls, 2004). From this point of view,
diversity must be addressed within all aspects of
behavioral medicine – clinical practice, research,
education, and policy.
This provides the opportunity to explore the
ways that sociodemographic characteristics are
linked to health, illness, and related behaviors D
(Smith, Kendall & Keefe, 2002). The call to
address diversity within behavioral medicine pro-
vides the opportunity to establish generalization
of prior findings, as well as explore within-group
differences that are related to health-related
behavior and health outcomes. Such competence
will require added interdisciplinary collabora-
tion, for example, with multicultural psychology,
and involve other levels of systems such as mem-
bers of a community or organization.
Cross-References
▶ Cultural and Ethnic Differences
▶ Cultural Competence
▶ Disability
▶ Discrimination and Health
▶ Ethnic Differences
▶ Gender Differences
▶ Health Disparities
▶ Income Inequality and Health
▶ Minority Health
▶ Religion/Spirituality
▶ Sexual Orientation
▶ Sociocultural Differences
▶ Socioeconomic Status (SES)
References and Readings
Agency for Healthcare Research and Quality. (2009,
March). National healthcare disparities report, 2008.
Retrieved March 1, 2011, from www.ahrq.gov/qual/
qrdr08.htm
Belar, C. D., & Deardorff, W. W. (2009). Clinical health
psychology in medical settings: A practitioner’s
guidebook (2nd ed.). Washington, DC: American
Psychological Association.
Jackson, Y. (2006). Encyclopedia of multicultural
psychology. Thousand Oaks, CA: Sage.
D 616
Kato, P. M., & Mann, T. (1996). Handbook of diversity
issues in health psychology. New York: Plenum Press.
Kazarian, S. S., & Evans, D. R. (2001). Handbook of
cultural health psychology. New York: Academic
Press.
Office of Behavioral and Social Sciences Research,
National Institutes of Health. http://obssr.od.nih.gov/
scientific_areas/social_culture_factors_ in_health/index.
aspx
Office of Minority Health, U.S. Department of Health and
Human Services. http://minorityhealth.hhs.gov/
Smith, T. W., Kendall, P. C., & Keefe, F. J. (2002).
Behavioral medicine and clinical health psychology:
Introduction to the special issue, a view from the
decade of behavior [Special issue]. Journal of Consult-
ing and Clinical Psychology, 70(3), 459–462.
Smith, T. W., & Shuls, J. (2004). Introduction to the
special section on the future of health psychology
[Special issue]. Health Psychology, 23(2), 115–118.
Divorce and Health
Tamara Goldman Sher1 and Kathryn Noth2
1
The Family Institute at Northwestern
University, Evanston, IL, USA
2
Illinois Institute of Technology, College of
Psychology, Chicago, IL, USA
Synonyms
Marital dissolution; Separation
Definition
Divorce is the legal dissolution of a marriage. It is
simultaneously a legal and psychological process
(Margulies & Luchow, 1992). Not all people are
equally distressed by divorce, and a variety factors
contribute to level of distress endured. The degree
of distress that stems from the divorce process and
from divorced marital status predicts mental and
physical health in both the short and long term.
Remarriage can reduce the health risks of divorce.
Possible mechanisms underlying the relationship
between divorce and health (e.g., psychophysio-
logical mechanisms, immune functioning) have
been explored.
Divorce and Health
Description
It has long been understood that marriage, or a
stable, long-term intimate relationship, increases
life expectancy, decreases morbidity, and
enhances quality of life (Burman & Margolin,
1992). In fact, it has been noted that the evidence
linking social relationships to health and
mortality is as strong as that linking cigarette
smoking, blood pressure, and obesity to health
(Umberson, Williams, Powers, Liu, & Needham,
2006). However, it is also understood that
not all marriages protect equally, and a poor
relationship may be more health damaging than
no relationship at all.
A number of studies have also found that
being divorced is more health-damaging than
being married (e.g. Hughes & Waite, 2009;
Kiecolt-Glaser, Kennedy, Malkoff, & Fisher,
1988). In an early study on the effects of marriage
versus divorce on immunity status among
a sample of 32 married versus 32 divorced men,
it was found that separated/divorced men were
more distressed and lonelier and reported
significantly more recent illness than did married
men; the former also had significantly poorer
values on two functional indices of immunity
(antibody titers to two herpes viruses) while not
differing significantly on quantitative indices
(percentages of helper and suppressor cells and
their ratio).
In understanding the complexity of the marital
status/marital quality and health relationship, it is
important to understand the differences between
those who are divorced, those who remain mar-
ried and those who remarry in terms of morbidity
and mortality. In the same study of immunolog-
ical functioning, it was found that among married
men, poorer marital quality was associated with
greater distress and poorer immunological
functioning. Among separated/divorced subjects,
those who had separated within the past year and
who had initiated the separation were less
distressed, reported better health, and had better
immunological functioning than did noninitiators
(Kiecolt-Glaser et al., 1988). Taken together,
the results suggest that while being married can
be advantageous in staying healthy (having
Divorce and Health
increased immunity against disease), the effects
of marriage on health depend on the quality of
that marriage. And, given a poor marriage, it is
better to be the one initiating divorce than the one
who is not the initiator when it comes to immune
functioning. Other researchers have attempted
clarify the psychophysiological mechanisms
underlying the relationship between divorce and
health. One study looked at divorce-related psy-
chological adjustment and blood pressure in
a sample of recently separated or divorced adults
(n ¼ 70). Individuals who reported higher
degrees of divorce-related emotional distress
demonstrated elevated resting blood pressure at
study entry. The same study found that men who
reported greater emotional difficulty associated
with the divorce experience showed greater car-
diovascular reactivity when thinking about the
divorce (Sbarra et al. 2009).
A lot of the early research on health and
marriage compared those who were married
with those who were unmarried on health
outcomes. Fewer studies have examined the
effect of changes in marital status on either
emotional or physical well-being. Two large
sample studies, one of 8,809 people in the United
States (Hughes & Waite, 2009) and one of over
5,000 people in Great Britain (Bennett, 2006),
looked at transitions into and out of marriage.
Results from both studies found a clear positive
effect of marriage. It was also found that a change
in marital status predicted health worsening
(Bennett, 2006; Hughes & Waite, 2009) with a
difference between those who were divorced and
those who were widowed. Interestingly, for the
newly divorced, health problems increased at the
point of the divorce, while for the newly
widowed, problems increased later in time,
perhaps because of a cumulative stress effect
(Bennett, 2006). Finally, results revealed strong
and consistent effects of marriage on later health
in that among those who have ever been divorced
or widowed, the remarried generally show better
health than those who have not remarried
(Hughes & Waite, 2009).
Others have assessed whether findings that
divorce is deleterious to health would hold-up to
longer-term analyses. In a study focused on the
617 D
immediate and the more long-term (10 years
later) effects of divorce on women’s health
(n ¼ 244), it was found that in the years imme-
diately following their divorce, women reported
significantly higher levels of psychological
distress than married women; no differences in
physical illness were found between groups
(Lorenz, Wickrama, Conger, & Elder, 2006).
A decade later, the divorced women reported D
significantly higher levels of illness, even after
controlling for age, remarriage, education,
income, and prior health. The authors concluded
that as a stressor, divorce has a more acute effect
on psychological health, while physical illness
risk accumulates incrementally in response to
the relatively stable dimensions of chronic stress
over time. That is, the divorce process has
more of an acute effect on the psychological
health of women while being divorced is
a chronic stressor, and illness can be understood
as a cumulative response to the concomitant
chronically stressful conditions (e.g., financial
hardship, lack of social support).
In looking at the effects of marriage, marriage
transition, and divorce, there are a number of
confounding issues including gender effects, age
effects, and time married effects that are beyond
the scope of this entry. It is clear that divorce
affects men and women differently and the
young versus the old differently. However, the
issue of the relative impact of marriage, divorce,
and marriage transitions on the health of men
versus women is not a clear one. While some
studies have found differences between men and
women (e.g., Dupre & Meadows, 2007), others
have found no such differences (e.g., Williams,
2003) in health impact. In trying to reconcile
these discrepant findings, some have looked at
the possibility of different mechanisms underly-
ing the effects for men versus women. A number
of studies have associated the mortality disadvan-
tage of divorce on women to the financial losses
resulting from divorce, as opposed to the divorce
itself (Lillard & Waite, 1995; Prigerson,
Maciejewski, & Rosenheck, 1999; Wickrama,
Conger, & Lorenz, 1995). In contrast, men seem
to benefit from the sense of a “settled life” that
marriage provides; they are less likely to engage
D 618
in risky health behaviors and experience gain
from the household tasks taken over by women
in marriage (Lillard & Waite, 1995).
In further trying to elucidate the underlying
mechanisms in the relationship between divorce
and health, some researchers have looked at
divorce and illness prevention behaviors.
However, rather than finding that it is a lack of
illness prevention among the unmarried that leads
to worse health outcomes, the opposite appears to
be the case. A number of studies have in fact
found that marriage decreases healthy behaviors
such as weight control (Lee et al., 2005) and
fitness levels (Ortega et al., 2011). These findings
are consistent among the married versus the
nonmarried and across the divorced versus
remarried, with remarriage showing the same
negative health trends as the continuously
married men and women.
Thus, it remains to be determined why
marriage is protective and divorce is harmful in
terms of health outcomes overall. Other than
general health effects, a number of studies have
investigated more discrete health outcomes
that result from marriage, divorce, and transi-
tions. For example, there have been consistent
findings that distressed marriages lead to more
specific poor health outcomes such as coronary
disease (Eaker, Sullivan, Kelly-Hayes,
D’Agostino, & Benjamin, 2007; Zhang &
Hayward, 2006), slow wound healing (Kiecolt-
Glaser et al., 2005), and cardiac events
(Orth-Gomer et al., 2000) compared to happier
marriages. It has also been found that marital
status determines specific health outcomes. For
example, remarriage after divorce significantly
reduces risk of COPD incidence, even after
adjusting for smoking habit (Noda et al., 2009),
and coronary heart disease mortality among
divorced, widowed, and never married men and
women is greater than among the married
(Lindgarde, Furu, & Ljung, 1987; Weiss, 1973;
Zhang & Hayward, 2006).
It remains a truism that being married or in
another long-term intimate relationship is better
for one’s health than being single, widowed, or
divorced for both general health and a number of
specific health conditions. However, the reasons
Divorce and Health
for these findings are not well understood. It is
clearly not that married people take better care of
themselves physically; in fact, the opposite seems
to be the case. It is possible that the stress of
divorce accounts for these differences but then
again so does the stress of remaining in an
unhappy relationship. For women, this stress
seems to be primarily financial, while for men,
this stress appears more task-oriented. It is also
better to be remarried than to remain divorced or
widowed, although the transitions into and out of
marriage themselves seem to be harmful. Clearly,
more information is needed to understand the
complicated relationships between marital status
and health, marital history and health, and marital
quality and health.
Cross-References
▶ Immune Responses to Stress
▶ Marital Satisfaction
▶ Marriage and Health
▶ Psychophysiological
References and Readings
Bennett, K. M. (2006). Does marital status and marital
status change predict physical health in older adults?
Psychological Medicine: A Journal of Research in
Psychiatry and the Allied Sciences, 36(9), 1313–1320.
Burman, B., & Margolin, G. (1992). Analysis of the
association between marital relationships and health
problems: An interactional perspective. Psychological
Bulletin, 112(1), 39–63.
Dupre, M. E., & Meadows, S. O. (2007). Disaggregating
the effects of marital trajectories on health. Journal of
Family Issues, 28(5), 623–652.
Eaker, E. D., Sullivan, L. M., Kelly-Hayes, M.,
D’Agostino, R. B., & Benjamin, E. J. (2007). Marital
status, marital strain, and risk of coronary heart disease
or total mortality: The Framingham offspring study.
Psychosomatic Medicine, 69(6), 509–513.
Hughes, M. E., & Waite, L. J. (2009). Marital biography
and health at mid-life. Journal of Health and Social
Behavior, 50(3), 344–358.
Kiecolt-Glaser, J. K., Kennedy, S., Malkoff, S., & Fisher, L.
(1988). Marital discord and immunity in males.
Psychosomatic Medicine, 50(3), 213–229.
Kiecolt-Glaser, J. K., Loving, T. J., Stowell, J. R.,
Malarkey, W. B., Lemeshow, S., Dickinson, S. L., et al.
(2005). Hostile marital interactions, proinflammatory
Dizygotic Twins 619 D
cytokine production, and wound healing. Archives of Williams, K. (2003). Has the future of marriage arrived?
General Psychiatry, 62(12), 1377–1384. A contemporary examination of gender, marriage, and
Lee, S., Cho, E., Grodstein, F., Kawachi, I., Hu, F. B., & psychological well-being. Journal of Health & Social
Colditz, G. A. (2005). Effects of marital transitions on Behavior, 44(4), 470–487.
change in dietary and other health behaviors in US Zhang, Z. M., & Hayward, M. D. (2006). Gender, the
women. International Journal of Epidemiology, marital life course, and cardiovascular disease in late
34(1), 69–78. midlife. Journal of Marriage and the Family, 68(3),
Lillard, L. A., & Waite, L. J. (1995). Til death do us part: 639–657.
Marital disruption and mortality. American Journal of
Sociology, 100(5), 1131–1156.
Lindgarde, F., Furu, M., & Ljung, B.-O. (1987). D
A longitudinal study on the significance of environ-
mental and individual factors associated with the
development of essential hypertension. Journal of Dizygotic Twins
Epidemiology and Community Health, 41(3), 220–226.
Lorenz, F. O., Wickrama, K. A. S., Conger, R. D., &
Elder, G. H., Jr. (2006). The short-term and decade- Jennifer Wessel
long effects of divorce on women’s midlife health. Public Health, School of Medicine, Indiana
Journal of Health and Social Behavior, 47(2), University, Indianapolis, IN, USA
111–125.
Margulies, S., & Luchow, A. (1992). Litigation, mediation,
and the psychology of divorce. Psychiatry & Law,
20(4), 483–504. Synonyms
Noda, T., Ojima, T., Hayasaka, S., Hagihara, A.,
Takayanagi, R., & Nobutomo, K. (2009). The health
Fraternal twins; Nonidentical twins
impact of remarriage behavior on chronic obstructive
pulmonary disease: Findings from the US longitudinal
survey. BMC Public Health, 9, 412.
Ortega, F. B., Brown, W. J., Lee, D. C., Baruth, M., Definition
Sui, X., & Blair, S. N. (2011). In fitness and in health?
A prospective study of changes in marital status
and fitness in men and women. American Journal of Dizygotic (DZ) twins are pairs of siblings
Epidemiology, 73(3), 337–344. resulting from the same pregnancy. They develop
Orth-Gomer, K., Wamala, S. P., Horsten, M., Schenck- from two separate eggs that have each been
Gustafsson, K., Schneiderman, N., & Mittleman,
fertilized by a different sperm. These siblings
M. A. (2000). Marital stress worsens prognosis in
women with coronary heart disease: The Stockholm share, on average, 50% of their genes, as do
Female Coronary Risk Study. Journal of the American ordinary full siblings. In contrast to monozygotic
Medical Association, 284(23), 3008–3014. (MZ) twins, who are always same-sex pairs,
Prigerson, H. G., Maciejewski, P. K., & Rosenheck, R. A.
DZ twins can be same-sex pairs or opposite-sex
(1999). The effects of marital dissolution and marital
quality on health and health service use among pairs.
women. Medical Care, 37(9), 858–873. The employment of opposite-sex pairs in twin
Sbarra, D. A., Law, R. W., et al. (2009). Marital dissolu- studies allows assessments of whether genetic
tion and blood pressure reactivity: Evidence for the
and shared environmental familial influences
specificity of emotional intrusion-hyperarousal and
task-related emotional difficulty. Psychosomatic Med- on behavior are different for males and females.
icine, 71(5), 532–540. If there are sex differences, the correlation for
Umberson, D., Williams, K., Powers, D. A., Liu, H., & opposite-sex pairs will typically be lower than
Needham, B. (2006). You make me sick: Marital
that for same-sex pairs.
quality and health over the life course. Journal of
Health and Social Behavior, 47(1), 1–16.
Weiss, N. S. (1973). Marital status and risk factors for
coronary heart disease: The United States health
examination survey of adults. British Journal of Cross-References
Preventive & Social Medicine, 27, 41–43.
Wickrama, K., Conger, R. D., & Lorenz, F. O. (1995).
Work, marriage, lifestyle, and changes in men’s phys- ▶ Monozygotic Twins
ical health. J Behavioral Medicine, 18(2), 97–111. ▶ Twin Studies
D 620
References and Readings
Elston, R. C., Olson, J. M., & Palmer, L. (2002).
Biostatistical genetics and genetic epidemiology
(1st ed.). Chichester: John Wiley and Sons.
Nussbaum, R. L., Mc Innes, R. R., & Willard, H. F.
(2001). Genetics in medicine (6th ed.). Philadelphia,
PA: W.B. Saunders.
Spector, T. D., Snieder, H., & MacGregor, A. J. (2000).
Advances in Twin and Sib-pair analysis (1st ed.).
London: Greenwich Medical Media.
DNA
Edward L. Perkins
Biomedical Sciences, Mercer University School
of Medicine, Savannah, GA, USA
Synonyms
Genetic material
Definition
The acronym DNA is now so well known in
popular as well as scientific literature that it
often appears with no accompanying definition:
The words deoxyribonucleic acid are rarely
heard, but they are what the acronym represents.
DNA is a very large molecule or macromolecule,
with each word of its full name being descriptive
of its nature. Ribose is one form of sugar (along
with glucose, fructose, sucrose, and others). The
prefix “deoxy-” specifies a ribose that has lost one
of its oxygen atoms at a specific site in the mol-
ecule. Nucleic acids are a group of complex com-
pounds derived from carbohydrates, purines and
pyrimidines, and phosphoric acid.
Nucleic acids are found in all living cells, and
also in viruses, which themselves are not actually
“alive” until they hijack another cell’s genetic
material and make it work to their advantage.
Nobel Laureate Sir Peter Medawar has captured
this occurrence very well by calling a virus
DNA
“a piece of nucleic acid surrounded by bad
news” (cited by Bryson, 2004).
DNA molecules contain many copies of four
bases: adenine (A), guanine (G), thymine (T), and
cytosine (C). Each of these bases can be regarded
as a molecule in its own right, being comprised of
carbon, hydrogen, oxygen, and nitrogen atoms.
Adenine and guanine are purines, chemical struc-
tures composed of two carbon rings, and thymine
and cytosine are pyrimidines, which are com-
posed of one ring of carbon atoms.
Purines and pyrimidines join together (or
bond) with a deoxyribose molecule that also con-
tains a phosphate group. The combination of A,
G, T, and C with a deoxyribose molecule leads to
the formation of four different nucleotides, two
purine nucleotides (A and G) and two pyrimidine
nucleotides (T and C). Hundreds of thousands of
individual nucleotides can link together to form
a polynucleotide strand. Each DNA molecule is
comprised of two strands of nucleotides that are
attached together. This molecular structure and
the ensuing three-dimensional molecular geome-
try of DNA lead to its characteristic double helix
nature. Once formed, single strands of DNA are
matched with and then attached to another strand
in a nonrandom manner governed by these rules:
An adenine base can only be matched with and
attached to a thymine base, and a guanine base
can only be matched with and attached to
a cytosine base, leading to A-T and G-C pairings.
The term “complementary bases” reflects that
each of the four nucleotide bases has a comple-
mentary base to which it becomes attached.
A critical consequence of this arrangement is
that once the sequence of nucleotides in one
strand is known, the sequence of nucleotides in
the other strand is known.
Replication, the process by which DNA pro-
duces an exact copy of itself, is facilitated
by this phenomenon. The two polynucleotide
chains that comprise a DNA molecule split
apart from each other, and each then becomes
attached to a newly formed chain, that is, an
exact replicate of its original partner. This cre-
ates two identical DNA molecules, which can
then continue to create replicates in an expo-
nential manner.
DNR Order 621 D
The Relevance of Genetics for Behavioral both genetic predisposition to complex disease
Medicine states and environmental influences that inter-
While this encyclopedia is not focused on molec- act with them.
ular genetics, genetic inheritance is of consider-
able importance in behavioral medicine, and
therefore the information conveyed by this entry Cross-References
and other related genetic entries is deserving
of inclusion. In some cases, inheriting certain ▶ Genetics
alleles can be the sole and readily identifiable ▶ Genomics D
cause of a disease. A case in point is phenylke- ▶ Proteomics
tonuria (PKU), which is inherited in an autosomal
recessive manner. Those who inherit the
disease do not have the ability to create an References and Readings
enzyme called phenylalanine hydroxylase,
which metabolizes the amino acid phenylalanine, Bryson, B. (2004). A short history of nearly everything.
New York: Black Swan.
a component of many foods. Accumulating Watson, J. D. (2006). DNA: The secret of life. New York:
levels of phenylalanine are harmful to the central Alfred A Knopf.
nervous system. Fortunately, a very strict diet McGue, M. (2005). Mediators and moderators of
low in phenylalanine provides successful alcoholism inheritance. In J. R. Turner, L. R. Cardon,
& J. K. Hewitt (Eds.), Behaviour genetic approaches
treatment.
in behavioral medicine. New York: Plenum.
In contrast, for complex diseases of interest in
behavioral medicine, a multi-gene etiology is
typical, and it has proved very difficult to isolate
and identify individual genes/alleles that are
responsible for sizeable amounts of variation in
the dispersion of a disease. What has become
DNA-Methylation
apparent, however, is that environmental (behav-
▶ Methylation
ioral) influences are of great importance in many
such complex disorders. Consider the case of
alcoholism, since it well exemplifies the interest-
ing phenomenon of disposition rather than prede-
termination. Clinical data suggest that, when
inherited, the genes that underlie alcoholism lia- DNR Order
bility confer a vulnerability to alcoholism expres-
sion rather than the certainty of it. Genetic Howard Sollins
inheritance of alcoholism liability can thus be Attorneys at Law, Ober, Kaler, Grimes &
highly sensitive to environmental modulation Shriver, Baltimore, MD, USA
(McGue, 2005).
The role of behavioral influences is impor-
tant both in disease etiology and disease treat-
Synonyms
ment. Given a certain genetic inheritance,
some environments can tend to increase the End-of-life care preferences
likelihood of a disease’s expression, while
others tend to decrease it. This also means
that behavioral interventions can be very suc-
cessful at preventing or ameliorating behavior- Definition
ally influenced conditions of clinical concern.
Thus, behavioral medicine is concerned with Do Not Resuscitate Order: DNR
D 622
Description
Do Not Resuscitate Order: DNR
A do not resuscitate (DNR) order is a directive
that cardiopulmonary resuscitation (CPR) should
not be initiated if an individual’s heart stops or
if the individual stops breathing. State law
determines who may issue a DNR order such as
whether a health-care practitioner other than
a physician is authorized to do so. Health-care
facilities will have established protocols for
resuscitating patients when there is no DNR
order, in accordance with state law. Competent
patients or their authorized decision maker or
proxy should be consulted about any proposed
DNR order. The authority of a decision maker
or proxy to consent to a DNR order can be
affected depending on (a) whether that person is
an agent under an advance directive, representa-
tive under a durable health care power of
attorney, surrogate under state law, or guardian
appointed by a court and (b) the scope of any such
authorizing document. State law also determines
if or how a physician may or may not have
the authority to enter a DNR order without
a direction by a competent patient or authorized
decision maker or proxy, based on a
determination that CPR would be medically
futile in a particular case. Hospitals may have
special procedures, consistent with established
policy and state law, on the circumstances
under which a DNR order may be suspended
during surgery.
Cross-References
▶ End-of-life Care Preferences
References and Readings
Kawana-Singer, M. (2011). Overcoming cultural differences
between patients, caregivers, and providers in providing
quality palliative and end-of-life care: A multicultural
experience. Educational Book.
Doctor-Patient Communication
Doctor-Patient Communication:
Why and How Communication
Contributes to the Quality of
Medical Care
Debra Roter1 and Judith A. Hall2
1
Johns Hopkins Bloomberg School of Public
Health, Baltimore, MD, USA
2
Department of Psychology, Northeastern
University, Boston, MA, USA
Synonyms
Medical dialogue; Medical interaction
Description
The patient–physician relationship and its
expression through the medical dialogue have
been described or alluded to in the history of
medicine since the time of the Greeks. Neverthe-
less, historians of modern medicine have tracked
an undeniable decline in the centrality of com-
munication to the care process. In his study of the
history of doctors and patients, Shorter (1985)
attributes the denigration of communication
through the twentieth century to the ascendancy
of the molecular and chemistry-oriented sciences
as the predominant medical paradigm. This
change was fundamental in directing medical
inquiry away from the person of the patient to
the biochemical makeup and pathophysiology of
the patient. It was not coincidental that it was
during this period of scientific advance that the
practice of interviewing patients from a written
outline designed around a series of yes–no
hypothesis-testing questions largely replaced
unstructured medical histories. Conversation
was largely curtailed by these changes; patients
were restricted to answering the questions asked
and the medical dialogue was recast as a medical
interview with the exchange directed by the
scientist-physician.
Professional dominance of physicians over
patients, and scientific objectivity over the patient
Doctor-Patient Communication
perspective, was noted (and lamented) by influ-
ential authors in the medical and social sciences
(Freidson, 1970; Szasz & Hollender, 1956), but
the issue did not attract the attention of medical
educators and policymakers until communication
was convincingly linked to patient outcomes. It is
in this light that the critical role of technical
advances in the 1960s that made audio recording
of the medical visit logistically possible may be
seen and that the methods that allowed investiga-
tion of the relationships between the medical
dialogue and outcomes may be appreciated.
The objectives of this essay are threefold:
(1) to present evidence establishing the impor-
tance of medical visit communication to a variety
of valued outcomes, (2) to provide insight into
how medical communication is assessed by using
a popular coding method, and (3) to briefly con-
sider future directions for improving medical
communication in light of current national
initiatives in health-care policy and reform.
Why Medical Communication Is Important
Within 20 years of the groundbreaking study
by Barbara Korsch and colleagues (1968)
documenting pediatric visit communication was
described and related to patient satisfaction and
adherence with medical recommendations,
a convincing body of literature had emerged
linking medical communication to patient out-
comes. As reflected in a meta-analysis of medical
communication and its correlates, covering the
period from 1964 to 1988, relationships between
specific elements of medical visit communication
and patient outcomes were apparent in regard to
patient recall of medical information, patient sat-
isfaction, adherence, and patient assessment of
technical care quality (Hall, Roter, & Katz,
1988). These relationships, however, varied
depending on which aspect of communication
was measured. For instance, when the doctor
offered more information, asked fewer questions
overall, but more questions about compliance in
particular, and was more positive and less nega-
tive (both verbally and nonverbally), the patient
was significantly more adherent. Satisfaction was
also found to be higher when the doctor offered
more information, actively enlisted patient
623 D
involvement in care, was more positive (verbally
and nonverbally), engaged in more social conver-
sation, and when there was more visit talk over-
all. Communication predictors of patient recall of
information included more information, positive
talk and partnership building, but less question
asking. Thus, some elements of physician com-
munication like information giving and positive
talk were significantly correlated with all out- D
comes, while elements such as question asking,
partnership building, and overall talk were only
related to particular outcomes.
Although not as commonly studied as satisfac-
tion and adherence, there is a small but extremely
important body of work that has linked doctor-
patient communication to other measures of
outcome, including indicators of patient health
status. Included among these measures are phys-
iologic indicators such as levels of glycosylated
hemoglobin (HbA1c) in the blood of diabetic
patients and blood pressure in hypertensive
patients. In addition, such measures as functional
status (the patient’s sense of his or her ability to
perform usual daily routines) and a patient’s
overall sense of well-being and emotional coping
have been linked to elements of the medical
dialogue (Griffin et al., 2004).
Finally, there are a few studies that have
explored how physicians are affected by factors
associated with the way in which they relate to
patients and perform their work. Among these
outcomes are physician satisfaction and the
likelihood of becoming involved in medical mal-
practice litigation. An appreciation for these
outcomes is underscored by the relatively high
levels of physician stress and burnout, particu-
larly in specialties associated with rising mal-
practice rates, and the medical workforce
shortages made worse by increasing numbers of
physicians taking early retirement. It should not
come as a surprise that many of the predictors of
patient satisfaction also affect physician satisfac-
tion as the communication of emotion is highly
reciprocal. The positive regard associated with
patient satisfaction with care and judgments of
good performance, interpersonal rapport, and
personal warmth and affection are all likely to
inspire physician satisfaction and similar feelings
D 624
of liking. The opposite is true as well; critical
judgments and perceptions of rejection or disre-
gard also inspire similarly negative emotions.
Not only are patient and physician satisfaction
and liking related to one another, but when
these measures of a positive interpersonal and
professional relationship are absent, patient
compliance is lowered, therapeutic effect is
diminished, and physician risk for malpractice
litigation is heightened (see Roter & Hall, 2006
for a review of this literature).
How Communication Is Assessed
A review of the methods used to analyze the
medical communication in the 61 studies
included in the meta-analysis described earlier
found that 28 different coding systems were
used (Roter, Hall, & Katz, 1988). Only three
systems, Bales’ Interaction Process Analysis,
the Verbal Response Mode (VRM), and the
Roter Interaction Analysis System (RIAS), were
used in multiple studies, and these were applied
in only a handful of studies (ranging from five to
seven studies each). The Bales’ system and the
VRM taxonomy were originally devised as
a general-purpose system for coding speech acts
but applied within the medical context, while the
RIAS was developed specifically to reflect com-
munication dynamics of the medical dialogue.
Many of the systems coded information exchange
in some form, while others focused on particular
kinds of expression like empathy or concern.
A subsequent review of communication assess-
ment instruments, covering the period
1986–1996, identified 44 unique instruments,
but only four of these were used in multiple
studies (Boon & Stewart, 1998).
While investigators continue to develop and
apply new coding approaches, the RIAS has
clearly gained prominence in the research litera-
ture with more than 250 published studies using
the system as of 2011. Studies have been
conducted in 23 countries in a variety of medical
care contexts and provider types and specialties
with translations to Spanish, French, German,
Italian, Swedish, Norwegian, Danish, Dutch,
Swiss-German, Portuguese, Japanese, Korean,
Chinese, Arabic, Hebrew, and Swahili. (See
Doctor-Patient Communication
https://riasworks.com for a bibliography of
RIAS studies.) Because of its widespread use,
a brief description of the RIAS and examples of
coding categories will be presented.
Derived loosely from social exchange theories
related to interpersonal influence and problem
solving, the system takes a perspective of the
medical encounter as a “meeting between
experts,” grounded in an egalitarian model of
patient-provider partnership that accounts for
the contributions of each speaker (Roter & Hall,
2006). The basic system is comprised of 40 mutu-
ally exclusive and exhaustive codes applied to all
dialogue statements expressed by each speaker in
the encounter. This is usually the patient and
physician, but may also include one or more
family members or friends accompanying the
patient to the visit or multiple providers including
consultant or attending physicians, nurses, or
technicians. The codes are applied to the smallest
unit of expression to which a meaningful code
can be assigned, generally a complete thought,
simple sentence, phrase, or clause in a compound
statement but sometimes a single word. In addi-
tion to verbal exchange, RIAS coders globally
assess the emotional tone of the visit at the close
of a session for each speaker in terms of overall
levels of irritation, anxiety, dominance, interest,
and friendliness. The global ratings have been
found to capture vocal qualities independent of
literal verbal content and can thereby be consid-
ered as an indicator of nonverbal communication
(Hall, Roter, & Rand, 1981).
A useful framework for organizing and
grounding RIAS-coded communication in the
clinical encounter is the four-function model of
medical interviewing that includes data gather-
ing, patient education and counseling, responding
to emotions, and partnership and activation.
Specific codes and dialogue examples in each of
these areas are presented in Table 1.
Future Directions for Improving Medical
Communication
The appearance of patient-centered medical care
on the national health-care agenda reflects a sea
change in the value attributed to communication
by policymakers, medical educators, and the
Doctor-Patient Communication 625 D
Doctor-Patient Communication: Why and How Communication Contributes to the Quality of Medical Care,
Table 1 Communication functions of the medical visit as reflected in RIAS codes and dialogue examples
Functional
grouping Communication behavior Example of provider dialogue Example of patient dialogue
Data Open-ended question (categories: What can you tell me about the How dangerous is my blood
gathering medical condition, therapeutic pain? How are the meds working pressure? How do the meds
skills regimen, lifestyle and self-care, for you? What are you doing to work? What can I do to keep
psychosocial topics, other) keep yourself healthy? What’s myself healthy? Do you have any
happening with your son? suggestions for getting my son to
go along with the family D
program?
Closed-ended question Does it hurt now? Do you take Is my blood pressure too high
(categories: medical condition, your meds every day? Are you now? Is that white pill the
therapeutic regimen, lifestyle and still smoking? Is your wife back? diuretic? Do you think the patch
self-care, psychosocial topics) that can help me stop smoking?
Patient Information about medical A normal blood pressure for Last time I took it my blood
education condition and symptoms someone with diabetes would be pressure was 130/80
and less than 130/80
counseling Information about therapeutic The medication may make you The medication made me drowsy
skills regimen, procedures and tests drowsy. You need to take it for I took the test and am waiting for
10 days the result
Lifestyle/self-care information Getting plenty of exercise is I get plenty of exercise. I have
always a good idea. I can give been trying to quit
you some tips on quitting
Psychosocial exchange about It’s important to get out and do It’s tough to quit when your wife
problems of daily living, issues something daily. The community smokes
about social relations, feelings, center is good for company
emotions
Counseling statements regarding The medication will not be Not applicable
medical condition/therapeutic effective if you don’t take it as
regimen prescribed; I want you to set up
a routine to take your pills the
same time every day
Counseling statements regarding It is very important for you to get Not applicable
psychosocial and lifestyle issues out of the house everyday! Being
social is good medicine
Relationship Positive talk (categories: You look fantastic, you are doing The new medicine works great
skills agreements, jokes/laughter, great More blood! You’re a vampire!
approvals)
Negative talk (categories: No, it doesn’t look to me like you That new drug you gave me was
disagreements, criticisms) were careful about your salt. The useless
local stores are just not very good How can you eat healthy when
about making fresh vegetables even the hospital cafeteria serves
available junk food?
Social talk (nonmedical chit- How about them O’s last night? I follow the Ravens – I’ve given
chat) up on the Orioles.
Emotional talk (categories: I’m worried about that. I’m sure it I am really worried. I’m going to
concern, reassurance/optimism, will get better. We’ll get through make it work!
empathy, legitimation, this I can see how upset you get when
partnership) you see me in this state
I want to work with you until we
get it right
(continued)
D 626 Doctor-Patient Communication

Doctor-Patient Communication: Why and How Communication Contributes to the Quality of Medical Care,
Table 1 (continued)
Functional
grouping Communication behavior
Partnering Facilitation (categories: asking
skills for patient opinion, asking for
understanding, paraphrase and
interpretation, back-channel)
Orientation (categories:
transitions, directions)
Example of provider dialogue
What do you think it is? What
would help? Do you follow me?
Let me make sure I’ve got it right.
I heard you say you the meds
didn’t work for you
Uh-huh, right, go on, hmm
Ok, well, let’s see
I’d like to do a physical now. Get
up on the table. Now we’ll check
your back
Example of patient dialogue
Do you follow what I’m saying?
Let me make sure I’ve got it right.
I heard you say you that the meds
take time to work and I have to
just keep taking it and be patient
Uh-huh, right, go on, hmm
Alright, now
I’ll get started on filling this form
out while you’re gone

public. The influential Institute of Medicine
report on Health Care Quality identified patient-
centered care as key to any significant future
improvements in health-care quality, alongside
core medical care quality requisites of safety,
timeliness, effectiveness, efficiency, and equity
(Institute of Medicine [IOM], 2001). In a similar
vein, patient-centered communication was recog-
nized as a significant vehicle for the prevention of
medical errors and malpractice litigation (Kohn,
Corrigan & Donaldson, 1999). The scientific evi-
dence reflected in these important reports not
only has implication for the routine practice of
medicine, but it has also influenced national
health policy. The Surgeon General has targeted
an increase in the proportion of persons who report
that their health-care providers have satisfactory
communication skills among the key objectives
for the nation (Surgeon General Report, Healthy
People 2010, Health Objective 11.6). This goal is
integrated into objectives in screening, diagnosis,
treatment, prevention, and hospice care applicable
to chronic diseases and cancer. Most recently,
patient-centered care has been included among
the quality benchmarks for Accountable Care
Organizations as part of the Patient Protection
and Affordable Care Act, Public Law 111–148
(Levinson, Lesser, & Epstein, 2010).
Responding to these same pressures, the
American Association of Medical Colleges
(AAMC) and the Accreditation Council for
Graduate Medical Education (ACGME) have
required documentation of communication skills
training as part of the accreditation criteria for
undergraduate and graduate level medical train-
ing programs. Consequently, virtually all US
medical schools now require that some portion
of their curriculum be dedicated to this area.
Despite this progress, medical education chal-
lenges remain as the intensity and format vary
widely and training is often concentrated in the
first 2 years of training before medical students
begin to see patients (Levinson et al., 2010).
Requirements for medical certification have also
been expanded to include demonstration of profi-
ciency in communication skills as part of the United
States Medical Licensing Exam (USMLE). The
clinical skills portion of the exam assesses candi-
dates’ performance using standardized patients
(actors trained to portray patients) presenting
cases that a physician is likely to encounter in
clinics, doctors’ offices, emergency departments,
and hospital settings (http://www.usmle.org/
index.html). Furthermore, recent changes by
the American Board of Medical Specialties
(ABMS) now require communication skills for
recertification every 5 years (Levinson et al.).
This essay began by suggesting that medicine
had lost its focus on the person of the patient in
embracing the scientific advances of the twenti-
eth century, but there is reason for optimism in
anticipating that the scientific, educational, and
policy advances of the twenty-first century will
return the patient to the center of care. Recogni-
tion of communication’s centrality to the heart
and art of medicine as well as its science is well
Dominant Inheritance
reflected in the words of an early advocate of
biopsychosocial medicine, George Engel, “It is
not just that science is a human activity, it is also
that the interpersonal engagement required in the
clinical realm rests on complementary and basic
human needs, especially the need to know
and understand and the need to feel known and
understood” (Engel, 1988, p. 136).
Cross-References
▶ Health Care
▶ Health Communication
▶ Patient Care
▶ Patient-Centered Care
References and Readings
Boon, H., & Stewart, M. (1998). Patient-physician com-
munication assessment instruments: 1986 to 1996 in
review. Patient Education and Counseling, 35,
161–176.
Engel, G. L. (1988). How much longer must medicine’s
science be bound by a seventeenth century world
view? In K. White (Ed.), The task of medicine:
Dialogue at Wickenburg (pp. 113–136). Menlo Park,
CA: Henry J. Kaiser Family Foundation.
Freidson, E. (1970). Professional dominance. Chicago:
Aldine.
Griffin, S. J., Kinmonth, A. L., Veltman, M. W. M.,
Gillard, S., Grant, J., & Stewart, M. (2004). Effect on
health related outcomes of interventions to alter the
interaction between patients and practitioners.
A systematic review of 35 trials. Annals of Family
Medicine, 2, 595–608.
Hall, J., Roter, D., & Katz, N. (1988). Meta-analysis of
correlates of provider behavior in medical encounters.
Medical Care, 26, 657–675.
Hall, J. A., Roter, D. L., & Rand, C. S. (1981). Commu-
nication of affect between patient and physician.
Journal of Health and Social Behavior, 11, 18–30.
Institute of Medicine. (2001). Crossing the quality chasm:
A new health system. Washington, DC: National
Academy Press.
Kohn, L. T., Corrigan, J. M., Donaldson, MS. (1999). To
err is human: building a safer health care system.
Washington (DC): National Academies Press.
Korsch, B. M., Gozzi, E. K., & Francis, V. (1968). Gaps in
doctor-patient communication: I. Doctor-patient
interaction and patient satisfaction. Pediatrics, 42,
855–871.
Levinson, W., Lesser, C. S., & Epstein, R. M. (2010).
Developing physician communication skills for
patient-centered care. Health Affairs, 29, 1310–1318.
627 D
Roter, D. L. (2000). The enduring and evolving nature of
the patient-physician relationship. Patient Education
and Counseling, 39, 5–15.
Roter, D. L., & Hall, J. A. (2006). Doctors talking with
patients/patients talking with doctors: Improving com-
munication in medical visits (2nd ed.). Westport, CT:
Praeger Publishers.
Roter, D. L., Hall, J. A., & Katz, N. R. (1988). Patient-
physician communication: A descriptive summary of
the literature. Patient Education and Counseling, 12,
99–119. D
Roter, D., & Larson, S. (2002). The Roter Interaction
Analysis System (RIAS): Utility and flexibility for
analysis of medical interactions. Patient Education
and Counseling, 46, 243–251.
Shorter, E. (1985). Bedside manners. New York: Simon
and Schuster.
Szasz, P. S., & Hollender, M. H. (1956). A contribution to
the philosophy of medicine: The basic model of the
doctor? Patient relationship. Archives of Internal
Medicine, 97, 585–592.
Domestic Violence
▶ Family Violence
Dominance
▶ Interpersonal Circumplex
Dominant Inheritance
Laura Rodriguez-Murillo1 and Rany M. Salem2
1
Department of Psychiatry, Columbia University
Medical Center, New York, NY, USA
2
Broad Institute, Cambridge, MA, USA
Definition
A trait with dominant inheritance is expressed
in the presence of the dominant allele, both in
individuals who are homozygous for the locus of
interest (DD, the same alleles) and in those who
are heterozygous (Dd, differing alleles).
Humans have two versions of all autosomal
genes, called alleles, one from each parent.
D 628
Dd dd
Dd dd Dd dd
Dominant Inheritance, Fig. 1 Dominant inheritance
diagram. Highlighted individuals are affected by the
disease given by the dominant D allele
Dominant inheritance refers to the situation when
an allele of a gene is expressed (dominant allele)
over the alternate gene allele, which is masked
(recessive allele). An example of a disease with
dominant inheritance is Huntington’s disease,
where affected individuals carry at least one
defective allele, leading to production of the
defective protein and resulting in disease
(Walker, 2007). To illustrate, the children of an
affected heterozygous parent have a 50% chance
of inheriting the disease allele and of being
affected (see pedigree, Fig. 1). Children of
a homozygous affected parent have a 100%
chance of inheriting the allele and developing
disease.
Cross-References
▶ Allele
▶ Gene
▶ Genotype
Dopamine
▶ Heterozygous
▶ Homozygous
▶ Recessive Inheritance
References and Readings
Lewis, R. (2005). Human genetics. Concepts and
applications (7th ed.). Boston: McGraw-Hill Science/
Engineering/Math.
Strachan, T., & Read, A. P. (2003). Human molecular
genetics (3rd ed.). London/New York: Garland
Science/Taylor & Francis Group.
Walker, F. O. (2007). Huntington’s disease. Seminars in
Neurology, 27(2), 143–150.
Dopamine
Michela (Micky) Marinelli
Department of Cellular and Molecular
Pharmacology, Rosalind Franklin University of
Medicine and Science, North Chicago, IL, USA
Definition
Dopamine is a catecholamine neurotransmitter
produced in dopamine neurons of the brain.
Description
Dopamine is a catecholamine produced in dopa-
mine neurons of the brain.
Anatomy
Approximately, 75% of all of the dopamine cells
of the brain originate in the midbrain. From the
midbrain, three main pathways project to
mesocorticolimbic structures, where dopamine
acts as a neurotransmitter (for review, see
Zahm, 2006).
The mesocorticolimbic or A10 pathway:
Dopamine neurons originate from the ventral
tegmental area and project primarily to the ven-
tral striatum, amygdala, hippocampus, and fron-
tal cortex.
Dopamine
The nigrostriatal, mesostriatal, or A9 path-
way: Dopamine neurons originate from the
substantia nigra pars compacta and project pri-
marily to the dorsal striatum.
The retrorubral or A8 pathway: Dopamine
neurons originate from the retrorubral field pro-
ject primarily to the dorsal and ventral striatum,
hippocampus, and parts of the extended amygdala.
Another dopaminergic pathway originates
from the hypothalamus and projects to the ante-
rior lobe of the pituitary (tuberoinfundibular
pathway or A12 and A14 pathways), where dopa-
mine acts as a neurohormone.
Transmission
Dopamine is stored in synaptic vesicles and
is released upon neuronal depolarization. Once
released, it acts on dopamine receptors.
Dopamine receptors are metabotropic (G-pro-
tein-coupled) receptors. They are divided in two
classes: D1-like (D1, D5 receptors) and D2-like
(D2, D3, and D4), which respectively stimulate
or inhibit adenylyl cyclase and consequent for-
mation of cAMP. Most released dopamine is
cleared from the synapse by reuptake into the
dopamine neurons, via dopamine transporters.
Function
While dopamine released from the tuberoin-
fundibular pathway inhibits prolactin release,
dopamine released in mesocorticolimbic and
motor structures serves to modulate movement,
emotions, and reward.
In particular, the mesostriatal pathway is
mostly involved in movement control: This is
most notable in the neurodegeneration of dopa-
mine neurons of this pathway, which is associ-
ated with ▶ Parkinson’s disease.
Dopamine from the mesocorticolimbic and
mesostriatal pathways plays an important role in
reward. In particular, the activity of dopamine
cells increases in response to unexpected reward-
ing events, or the cues that predict them (Schultz,
2002).
Dopamine is also one of the major players
mediating the rewarding effects in ▶ drug abuse
and drug dependence (Marinelli, Rudick, Hu, &
White, 2006; Volkow, Fowler, Wang, &
629 D
Goldstein, 2002). Addictive drugs have the com-
mon action of increasing dopamine levels in the
striatal complex (Di Chiara & Imperato, 1988;
Imperato et al., 1992). This effect is mediated by
different mechanisms, such as blocking the reup-
take of dopamine at the level of the dopamine
transporter, reversing the transporter from reup-
take to release, or increasing the activity of dopa-
mine neurons. In addition, animal studies show D
that subjects with heightened dopaminergic
transmission are more prone to self-administer
drugs of abuse compared with subjects
expressing reduced dopaminergic transmission.
Furthermore, treatments that decrease dopami-
nergic transmission generally produce
a decrease in drug responding and relapse,
whereas treatments that increase it have opposite
effects (Marinelli et al., 2006). Similarly, human
studies show a positive correlation between dopa-
mine levels and behavioral responses to
psychostimulant drugs (Leyton et al., 2002;
Oswald et al., 2005). While this suggests that
increased dopaminergic tone is a facilitator of
drug abuse, there is also evidence for decreased
dopaminergic tone to play a role (Melis et al.,
2005). Thus, withdrawal from long-term use of
addictive drugs can lead to a hypo-dopaminergic
state that could promote the search for drug, to
counteract the decrease in dopaminergic tone.
These views are not incompatible; thus, it has
been proposed that drug craving and relapse in
the could result from two separate phenomena:
“chronic craving,” which is an attempt to allevi-
ate a state of hypo-dopaminergia and “instant
craving,” which is instead caused by
a temporary increase in dopaminergic tone that
triggers relapse (Childress & O’Brien, 2000;
Franken et al., 2005; Pilla et al., 1999).
Antipsychotic drugs that block dopaminergic
transmission are effective in treating some
aspects of schizophrenia (mostly delusions and
hallucinations), suggesting that hyperdopa-
minergia may underlie these conditions; how-
ever, the matter is controversial because it is
still unclear if patients with schizophrenia have
impaired dopaminergic transmission (Howes &
Kapur, 2009; Moncrieff, 2009; van Os & Kapur,
2009).
D 630 Dorsal Hypothalamic Area

Cross-References van Os, J., & Kapur, S. (2009). Schizophrenia. Lancet,

374, 635–645.
Volkow, N. D., Fowler, J. S., Wang, G. J., & Goldstein,
▶ Drug Abuse R. Z. (2002). Role of dopamine, the frontal cortex and
▶ Neurotransmitter memory circuits in drug addiction: Insight from imag-
▶ Parkinson’s Disease ing studies. Neurobiology of Learning and Memory,
78, 610–624.
Zahm, D. S. (2006). The evolving theory of basal fore-
brain functional-anatomical ‘macrosystems’. Neuro-
science and Biobehavioral Reviews, 30, 148–172.
References and Readings

Childress, A. R., & O’Brien, C. P. (2000). Dopamine

receptor partial agonists could address the duality of
cocaine craving. Trends in Pharmacological Sciences,
21, 6–9. Dorsal Hypothalamic Area
Di Chiara, G., & Imperato, A. (1988). Drugs abused by
humans preferentially increase synaptic dopamine
concentrations in the mesolimbic system of freely ▶ Hypothalamus
moving rats. Proceedings of the National Academy of
Sciences of the United States of America, 85,
5274–5278.
Franken, I. H., Booij, J., & van Den, B. W. (2005). The
role of dopamine in human addiction: From reward to Dorsalgia
motivated attention. European Journal of
Pharmacology, 526, 199–206. ▶ Back Pain
Howes, O. D., & Kapur, S. (2009). The dopamine hypoth-
esis of schizophrenia: Version III–the final common
pathway. Schizophrenia Bulletin, 35, 549–562.
Imperato, A., Mele, A., Scrocco, M. G., & Puglisi-Allegra, S.
(1992). Chronic cocaine alters limbic extracellular dopa- Dorsomedial Nucleus
mine. Neurochemical basis for addiction. European
Journal of Pharmacology, 212, 299–300.
Leyton, M., Boileau, I., Benkelfat, C., Diksic, M., Baker, G., ▶ Hypothalamus
& Dagher, A. (2002). Amphetamine-induced increases
in extracellular dopamine, drug wanting, and novelty
seeking: A PET/[11C]raclopride study in healthy men.
Neuropsychopharmacology, 27, 1027–1035.
Marinelli, M., Rudick, C. N., Hu, X. T., & White, F. J. Dose: Intensity, Response
(2006). Excitability of dopamine neurons: Modulation
and physiological consequences. CNS & Neurological Nicole Brandt
Disorders Drug Targets, 5, 79–97.
Melis, M., Spiga, S., & Diana, M. (2005). The dopamine
School of Pharmacy, University of Maryland,
hypothesis of drug addiction: Hypodopaminergic Baltimore, MD, USA
state. International Review of Neurobiology, 63,
101–154.
Moncrieff, J. (2009). A critique of the dopamine hypoth-
esis of schizophrenia and psychosis. Harvard Review
Definition
of Psychiatry, 17, 214–225.
Oswald, L. M., Wong, D. F., McCaul, M., Zhou, Y., The underlying mechanism of dose intensity and
Kuwabara, H., Choi, L., et al. (2005). Relationships response deals with drug-receptor interactions.
among ventral striatal dopamine release, cortisol
secretion, and subjective responses to amphetamine.
Drugs can bind to a receptor and enhance the
Neuropsychopharmacology, 30, 821–832. effect of that receptor (agonist), inhibit the effect
Pilla, M., Perachon, S., Sautel, F., Garrido, F., Mann, A., of that receptor (antagonist), or enhance the effect
Wermuth, C. G., et al. (1999). Selective inhibition of of that receptor at less than the maximum
cocaine-seeking behaviour by a partial dopamine D3
receptor agonist. Nature, 400, 371–375.
response (partial agonist). Clinically, the goal of
Schultz, W. (2002). Getting formal with dopamine and a drug dose, or dose regimen, is to provide
reward. Neuron, 36, 241–263. a patient with maximal benefit and minimal
Double-Blind Study
toxicity. To accomplish this, one must know
about a drug dose’s pharmacological potency
and maximal efficacy. Potency is defined as the
dose of drug required to produce 50% of the
drug’s maximal effect. The more potent a drug
is, the lower the dose needed to produce a desired
clinical response. Drug potency depends on the
affinity of receptors to bind the drug and how
effectively the drug-receptor interaction leads to
a clinical response. Drug potency is the main
factor considered when deciding a dose to
administer.
A dose’s response relates to how effective
a drug is at a particular dose in relation to clinical
response. How effective a dose is and what type
of response it can have in a patient varies based
on the route of administration, the absorption, the
distribution in the body, and the clearance from
the blood or site of action. When deciding on
a drug and dose, not only does the dose’s efficacy
response have to be taken into account, but the
dose’s toxic response also has to be considered.
Each drug has a therapeutic window and the goal
is to give a dose of drug that is above the bottom
line of that window (clinical efficacy) but not
over the top line of that window (clinical toxic-
ity). In short, the overall aim is to give the
smallest dose possible that has the greatest effi-
cacy and least toxicity.
In addition to the characteristics of the drug
(pharmacokinetics), the intensity and response
are also based on the characteristics of the patient.
The intensity of effect of a drug dose can be
increased or decreased if the patient is
hyperreactive or hyporeactive (compared to the
majority of patients) to the drug. How reactive
a patient is to a drug depends on multiple factors
such as genetics, age, gender, body size,
comorbidities, and concomitant medications
(i.e., drug-drug interactions). There is also the
issue of tolerance that may develop with some
medication classes (e.g., narcotics). Basically,
continued administration leads to decreased
dose intensity, and when this happens, the patient
is said to have built up a tolerance to the drug at
that specific dose. All of these variables need to
be taken into consideration when deciding on
a drug dosing regimen.
631 D
Cross-References
▶ Agonist
References and Readings
Katzung, B. G., Masters, S. B., & Trevor, A. J. (2009). D
Basic & clinical pharmacology (11th ed.). New York:
McGraw-Hill.
Shargel, L., Wu-Pong, S., & Yu, A. B. (2005). Applied
biopharmaceutics and pharmacokinetics (5th ed.).
New York: McGraw-Hill.
Double-Blind Study
J. Rick Turner
Cardiovascular Safety, Quintiles, Durham,
NC, USA
Definition
A double-blind research study is one in which
neither the subject nor the researcher knows
which treatment a subject is receiving.
Employing the double-blind methodology is
a hallmark of pharmaceutical clinical trials. In
some trials, an investigational drug is compared
with a placebo. Both drug products must there-
fore look, smell, and taste the same so that sub-
jects cannot deduce from one of these
characteristics which treatment they are receiv-
ing. These drug products must also be
manufactured, and similarly shipped to the sites
running the trials, in a manner that does not allow
the physician investigators to know which treat-
ment subjects are being administered. The same
applies for a trial in which two active drugs are
being compared. While the double-blind process
takes considerable work, it is certainly possible to
implement it successfully.
This methodology can be much more difficult
to implement in studies of behavioral medicine
interventions.
D 632
Cross-References
▶ Randomization
Drinking
▶ Alcohol Consumption
Drug Abuse
▶ Dependence, Drug
Drug Abuse: Treatment
▶ Substance Abuse: Treatment
Drug and Alcohol Treatment
▶ Substance Abuse: Treatment
Drug Dependence Treatment
▶ Substance Abuse: Treatment
Drug Development
▶ Pharmaceutical Industry:
Development
Drug Rehabilitation
▶ Substance Abuse: Treatment
Drinking
Drug, Adverse Effects/Complications
Nicole Brandt
School of Pharmacy, University of Maryland,
Baltimore, MD, USA
Synonyms
Adverse drug events; Adverse drug reactions
Definition
Adverse drug events (ADE) are noxious events
that occur during the use of a medication, but
there is not always a causal link (ICH, 1994).
An ADE can be a direct injury from the medica-
tion, like an adverse drug effect such as a fall.
It can also be some form of harm due to the way in
which the medication is used, such as
discontinuing the medication abruptly, causing
an adverse drug withdrawal event such as confu-
sion or increased blood pressure (VA, 2006).
Adverse drug reactions (ADR) are
“unintended, harmful responses to a usual dose
of a medication during normal administration,
with a direct causal relationship” (Nebeker,
et al., 2004). Adverse effects or reactions differ
from side effects in that medication side effects
can be beneficial or harmful, while adverse drug
effects are always adverse or negative. Allergic
reactions are a type of adverse effect that is
elicited by the immune system, for example,
hives or shortness of breath. It is important to
monitor for and document drug adverse effects
in order to provide the best possible care and to
prevent subsequent harm (VA, 2006).
References and Readings
Research and
International Conference on Harmonization (ICH).
(1994). Clinical safety data management: Definitions
and standards for expedited reporting The Interna-
tional Conference on Harmonization. Report No.:
E2A. Accessed at http://www.ich.org/fileadmin/
Public_Web_Site/ICH_Products/Guidelines/Efficacy/
E2A/Step4/E2A_Guideline.pdf
Nebeker, J. R., Barach, P., & Samore, M. H. (2004).
Clarifying adverse drug events: A clinician’s guide to
Dunbar-Jacob, Jacqueline
terminology, documentation, and reporting. Annals of
Internal Medicine, 140, 795–801.
VA Center for Medication Safety, VHA Pharmacy
Benefits Management Strategic Healthcare Group
and the Medical Advisory Panel. (2006). Adverse
drug events, adverse drug reactions and medication
errors, frequently asked questions. The Department of
Veterans Affairs. Accessed at http://www.pbm.va.
gov/vamedsafe/Adverse%20Drug%20Reaction.pdf
DST
▶ Dexamethasone Suppression Test
Dual Process Models of Health
Behavior
▶ Temporal Self-Regulation Theory
Dual Systems Models
▶ Temporal Self-Regulation Theory
Dunbar-Jacob, Jacqueline
Faith S. Luyster
School of Nursing, University of Pittsburgh,
Pittsburgh, PA, USA
Biographical Information
633 D
Jacqueline Dunbar-Jacob was born in Detroit,
Michigan. She received her BSN degree from
Florida State University, earned her MS degree
in Psychiatric Nursing from University of
California, San Francisco, and earned her
Ph.D. degree in Counseling Psychology from
Stanford University. In 1984, Dunbar-Jacob
joined the faculty at the University of Pitts-
burgh, Pittsburgh, PA, as assistant professor D
and director of Nursing at Western Psychiatric
Institute and Clinic and later rose through the
ranks in the School of Nursing to become pro-
fessor in 1993. She subsequently received sec-
ondary appointments as professor of
Psychology, Epidemiology, and Occupational
Therapy. Since 2001, she has served as the
dean at the University of Pittsburgh School of
Nursing. She has been internationally recog-
nized for her study of patient adherence to treat-
ments across a variety of patient populations
including rheumatologic conditions, cardiovas-
cular disease, and diabetes.
Major Accomplishments
Dunbar-Jacob’s research has been supported by
the National Science Foundation and several
institutes within the National Institutes of Health
(NIH) including the National Institute of Nursing
Research; National Heart, Lung, and Blood Insti-
tute; and National Institute of Diabetes and
Digestive and Kidney Diseases.
Dunbar-Jacob is director of a P01 program
project grant from the NIH on translating inter-
ventions related to patient adherence and quality
of life. She has served as the director of the
NIH-funded Center for Research in Chronic
Disorders at the University of Pittsburgh. She
has served on three NIH safety and data monitor-
ing boards, as a behavioral scientist for three
NIH-funded multicenter clinical trials, and on
20 NIH working groups addressing research
agendas. She served on the NIH Prevention of
Alzheimer’s Disease Consensus Panel and is cur-
rently a member of the technical expert panel for
the AHRQ comparative effectiveness project on
D 634
adherence interventions. Her work has been rec-
ognized with the PA Nightingale Award for
research, the Pathfinders Award for research by
the Friends of the NINR, and her induction into
the Sigma Theta Tau International Inaugural
Nurse Researcher Hall of Fame.
Her current leadership roles include president
of Friends of the National Institute of Nursing
Research, chair of the Advisory Board for the
Institute for Health Care Communication, and
cochair of the Pennsylvania Center for Health
Careers Supply-Demand Committee. Dunbar-
Jacob has also served as the chair of the AACN
Task Force on the Future of the Research Focused
Doctorate and chair of the Scientific Advisory
Board for NIH Roadmap Initiatives for the
Patient Reported Outcomes Measurement Infor-
mation System (PROMIS). Recently, she was
a fellow in the Robert Woods Johnson Executive
Nurse Fellows Program and a member of the
National Institute of Nursing Research Advisory
Council. She is also past president of the Acad-
emy of Behavioral Medicine Research and past
president of the Society for Behavioral Medicine.
Cross-References
▶ Adherence
▶ Compliance
▶ Nonadherence
▶ Noncompliance
▶ Patient Adherence
References and Readings
Chia, L., Schlenk, E., & Dunbar-Jacob, J. (2006). Effect of
personal and cultural beliefs on medication adherence
in the elderly. Drugs & Aging, 23(3), 191–202.
Dunbar-Jacob, J. (2007). Models for changing patient
behavior. The American Journal of Nursing, 107(6
Suppl), 20–25.
Dunbar-Jacob, J., Bohachick, P., Mortimer-Stephens, M. K.,
Sereika, S., & Foley, S. (2003). Medication adherence
in patients with cardiovascular disease. Journal of
Cardiovascular Nursing, 18(3), 209–218.
Dunbar-Jacob, J., Burke, L. E., Rohay, J. M., Sereika, S.,
Schlenk, E. A., Lippello, A., et al. (1996). Compara-
bility of self-report, pill count, and electronically mon-
itored adherence data. Controlled Clinical Trials,
17(2S), 80S.
Dyadic Stress
Dunbar-Jacob, J., Erlen, J. A., Schlenk, E., Ryan, C.,
Sereika, S., & Doswell, W. (2000). Adherence in
chronic disease. In J. Fitzpatrick & J. Goeppinger
(Eds.), Annual review of nursing research (Vol. 18,
pp. 48–90). New York: Springer.
Dunbar-Jacob, J., Gemmel, L. A., & Schlenk, E. A.
(2008). Predictors of patient adherence: Patient char-
acteristics. In S. A. Shumaker, E. Schron, J. Ockene, &
W. L. McBee (Eds.), Handbook of health behavior
change (3rd ed., pp. 397–410). New York: Springer.
Dunbar-Jacob, J., Houze, M., Kramer, C., Luyster, F., &
McCall, M. (2010). Adherence to medical advice:
Processes and measurement. In A. Steptoe (Ed.),
Handbook of behavioral medicine: Methods and
applications (pp. 83–95). New York: Springer.
Dunbar-Jacob, J., & Mortimer-Stephens, M. (2001).
Treatment adherence in chronic disease. Journal of
Clinical Epidemiology, 54(1), S57–S60.
Dunbar-Jacob, J., & Schlenk, E. A. (1996). Treatment
adherence and clinical outcome. Can we make
a difference? In R. J. Resnick & R. H. Rozensky
(Eds.), Health psychology through the lifespan:
Practice and research opportunities (pp. 323–343).
Washington, DC: American Psychological Association.
Dunbar-Jacob, J., & Schlenk, E. A. (2000). Patient
adherence to treatment regimen. In A. Baum,
T. A. Revenson, & J. E. Singer (Eds.), Handbook
of health psychology (pp. 571–580). Hillsdale, NJ:
Lawrence Erlbaum.
Dunbar-Jacob, J., Schlenk, E. A., Burke, L. E., &
Matthews, J. T. (1998). Predictors of patient adher-
ence: Patient characteristics. In S. A. Shumaker, E.
Schron, J. Ockene, & W. L. McBee (Eds.), Handbook
of health behavior change (2nd ed., pp. 491–511).
New York: Springer.
Dunbar-Jacob, J., Sereika, S., Rohay, J., & Burke, L.
(1998). Electronic methods in assessing adherence to
medical regimens. In D. Krantz & A. Baum (Eds.),
Technology and methods in behavioral medicine
(pp. 95–113). Mahwah, NJ: Lawrence Erlbaum.
Martin, K. A., Bowen, D. J., Dunbar-Jacob, J., &
Perri, M. G. (2000). Who will adhere? Key issues in
the study and prediction of adherence in randomized
controlled trials. Controlled Clinical Trials, 21(5),
195S–199S.
McCall, M. K., Dunbar-Jacob, J., & Puskar, K. (2009).
Promoting medication adherence. Nursing Made
Incredibly Easy, 7(5), 20–25.
Stilley, C., Bender, C., Dunbar-Jacob, J., & Ryan, C.
(2010). The impact of cognitive function on medica-
tion management: Three studies. Health Psychology,
1, 50–55.
Dyadic Stress
▶ Family Stress
Dyslipidemia
Dynorphins
▶ Endogenous Opioids/Endorphins/Enkephalin
Dysfunction Syndrome
▶ Chronic Fatigue Syndrome
Dysfunctional/Dysfunction
▶ Maladaptive/Maladjustment
Dyslipidemia
Ronald Goldberg
Diabetes Research Institute, University of Miami
Miller School of Medicine, Miami, FL, USA
Synonyms
High cholesterol; Hypercholesterolemia;
Hypertriglyceridemia
Definition
The term dyslipidemia refers to an abnormality of
circulating lipoproteins, which are the protein-
lipid complexes that transport the major blood
lipids, cholesterol, and triglyceride through the
circulation. The standard test for circulating
lipids and lipoproteins consists of the measure-
ment of the total serum cholesterol, its low-
density (LDL-C) and high-density lipoprotein
cholesterol (HDL-C) subfractions, and the fasting
triglyceride level. Dyslipidemia is then defined as
a higher than acceptable total cholesterol, LDL-C
or triglyceride level, or a low HDL-C value, or
various combinations of these. The clinical
importance of these abnormalities relates to the
635 D
association of elevated cholesterol, LDL-C, and
in many instances of hypertriglyceridemia with
an increased risk of cardiovascular disease
(CVD). Conversely, HDL-C is inversely associ-
ated with the risk of CVD. Although not readily
measured with standard testing, there are other
circulating atherogenic lipoproteins, such as
intermediate density lipoprotein and lipoprotein
(a), that are believed to increase risk for CVD. D
Very high triglyceride values (>1,000 mg/dl) are
also associated with an increased risk of
pancreatitis.
Etiology
The etiology of dyslipidemia is complex. Primary
forms of dyslipidemia may be due to monogenic
or as yet mostly poorly defined polygenic abnor-
malities of lipoprotein metabolism. Clinically,
these manifest as predominant (and sometimes
severe) hypertriglyceridemia, moderate to severe
elevations in LDL-C, or combinations of these
two abnormalities. Hypertriglyceridemia is com-
monly associated with low HDL-C levels as well
as smaller than normal LDL particles which may
have increased atherogenicity. In addition, iso-
lated HDL deficiencies may primarily be due to
genetic disturbances of HDL metabolism. More
commonly, dyslipidemia is due to effects of sec-
ondary factors acting on the particular genetic
substrate of the individual to produce a range of
lipid abnormalities. Common secondary causes
of hypertriglyceridemia, small LDL particles,
and low HDL-C include abdominal obesity, insu-
lin resistance, and type 2 diabetes, while the most
common reason for an elevated LDL-C is the
high fat diet that is typical of Western societies.
Clinical Evaluation and Intervention
The clinical evaluation of dyslipidemia has been
guided by the recommendations of the National
Cholesterol Education Program (NCEP) which
published its initial Adult Treatment Panel
(ATP I) recommendations in 1987 for diagnosis
and treatment of lipid disorders, and these were
revised in 1994 (ATP II) and 2001 (ATP III) with
an update in 2004. ATP IV will be published in
due course. The current guidelines recommend
that attention to LDL-C should be the first
D 636
priority because of its close association with
CVD event rates, except in patients with severe
hypertriglyceridemia (>500 mg/dl), where
urgent triglyceride lowering to prevent pancrea-
titis should be the initial treatment.
The question of what constitutes an LDL-C
level requiring treatment has undergone consid-
erable evolution as clinical trial data showing
benefit from statin drugs in different population
subgroups have been reported. In essence, the
population is divided into low-risk, moderate-
risk, and high-risk subgroups. Cut points for die-
tary intervention or pharmacologic intervention
have been defined for each group according to
severity of CVD risk and in 30 mg/dl increments
of LDL-C; however, because these cut points and
the targets of treatment are somewhat arbitrarily
defined and are also a subject of debate, these
values are given as a range. Thus, for low-risk
subjects (with no more than one major CVD risk
factor), the cut point for therapeutic lifestyle
changes, focusing largely on lowering choles-
terol, and saturated fat intake is recommended at
130–160 mg/dl, while drug therapy is
recommended at 160–190 mg/dl, aiming for an
LDL-C of 130–160 mg/dl – the average for the
general population.
For those with at least two major risk factors,
but without diabetes or evident CVD, the cut
points for pharmacologic and lifestyle change
are 130–160 and 100–130 mg/dl respectively,
and the goal is <100–130 mg/dl (an LDL-C of
100 mg/dl is considered optimal for the general
population). For highest-risk subjects, a single cut
point for combined lifestyle and drug therapy is set
at 70–100 mg/dl, with a target of 70 mg/dl.
Statin drugs are the first choice, with add-on
agents such as ezetimibe and bile sequestrants
available in the event that statin therapy is inade-
quate or not tolerable. Because LDL-C reflects
only the cholesterol content of LDL and may not
adequately reflect the full range and impact of
atherogenic lipoproteins before and on treatment,
the use of alternative or secondary measures such
as non-HDL-C (calculated by total cholesterol
minus HDL-C) or apolipoprotein B (the protein
component of all atherogenic lipoproteins) has
been proposed.
Dyslipidemia
Elevation in triglyceride levels is less directly
related to CVD risk, and it is likely that there is
considerable heterogeneity in this relationship
across the population. Subjects with triglyceride
values >150 mg/dl are said to have borderline
hypertriglyceridemia, and those with values
>200 mg/dl have hypertriglyceridemia which
should be considered for treatment. In this popu-
lation, non-HDL-C or apolipoprotein B measure-
ments may have special advantages because
hypertriglyceridemia alters the LDL-C value.
The initial approach is therapeutic lifestyle
change in which overweight is an important tar-
get. Medications such as fibrate drugs, high doses
of omega 3 fatty acids, or niacin may be added if
lifestyle therapy is considered inadequate,
although evidence for CVD benefit with these
medications is weaker than that for statin drugs.
Lastly, low HDL-C, defined as <40 mg/dl in
men and <50 mg/dl in women, is considered to
be an independent CVD risk factor. Weight
reduction and increased physical activity may
modestly raise HDL-C and are prudent
approaches to management of low HDL-C. How-
ever, drug therapy with HDL-raising drugs such
as fibrates or niacin remains a challenge because
of the lack of a full understanding of the relation-
ship between HDL and CVD, side effects of
medications, and the paucity of data that this
approach clearly adds to the benefit of statin
therapy. Considerable efforts are being made to
improve our understanding and the management
of dyslipidemia.
Cross-References
▶ Cardiovascular Disease
▶ Cholesterol
▶ Diabetes
▶ Insulin Resistance (IR) Syndrome
▶ Lipid Abnormalities
References and Readings
Lorenzo, C., Williams, K., Hunt, K., & Haffner, S. M.
(2007). The national cholesterol education program-
adult treatment panel III, international diabetes
Dyspnea
federation, and world health organization definitions
of the metabolic syndrome as predictors of incident
cardiovascular disease and diabetes. Diabetes Care,
30, 8–13.
Scott, M., Grundy, S., Cleeman, J., Bairey Merz, C. N.,
Brewer, H. B., Clark, L. T., Hunninghake, D.,
Pasternak, R., Smith, S., Stone, N., & Coordinating
Committee of the National Cholesterol Education Pro-
gram. (2004). Implications of recent clinical trials for
the national cholesterol education program adult treat-
ment panel III guidelines. Journal of the American
College of Cardiology, 44, 720–732.
Dyspnea
Valerie Sabol
School of Nursing, Duke University, Durham,
NC, USA
Definition
Dyspnea, or shortness of breath, is a frequently
reported symptom of unpleasant and/or uncom-
fortable respiratory sensations with many poten-
tial underlying etiologies (e.g., pulmonary
disease, primary manifestation of cardiac disease,
neuromuscular disease, obesity, anxiety). The
American Thoracic Society (1999) defines dys-
pnea as a “subjective experience of breathing
discomfort that is comprised of qualitatively dis-
tinct sensations that vary in intensity; the experi-
ence derives from interactions among multiple
physiological, psychological, social, and envi-
ronmental factors, and may induce secondary
physiological and behavioral responses.”
Although older adults with chronic pulmonary
and/or cardiac disease may have a blunted
response to dyspnea, perhaps as a result of adap-
tation over time, it is still an important clinical
history finding (e.g., acute exacerbation of
a chronic disease process).
There are variations in the clinical reporting of
dyspnea; words used by individuals to describe
their breathing discomfort may provide insight
into the underlying pathophysiology of their dis-
ease. For example, words used to describe diffi-
culty inspiring is associated with upper airway
637 D
obstruction (e.g., aspiration), and words used to
describe difficulty with expiratory flow is associ-
ated with obstruction of the smaller bronchioles
(e.g., asthma). The inability to breathe while in
a recombinant position is known as orthopnea,
and complaints of sudden onset of coughing or
difficult breathing after sleeping in a recombinant
position (typically after 1–2 h) is known as par-
oxysmal nocturnal dyspnea (PND), and is typi- D
cally associated with heart failure. Dyspnea on
exertion (DOE) is common in obstructive and
restrictive pulmonary diseases. Dyspnea that is
described as painful may have an underlying
inflammatory or trauma-related etiology. Signs
of air hunger include mouth breathing, use of
accessory muscles, and/or inability to finish
a sentence without pausing to breathe. Some
individuals, however, are able to adjust their
physical activities to limit or prevent dyspnea
and more objective testing may be warranted.
Depending on the most likely underlying etiol-
ogy, there are several diagnostic studies that could
be used to evaluate dyspnea. For example, exer-
cise testing (e.g., 6-min walk test), spirometry, and
other pulmonary function tests (PFTs), pulse
oximetry, arterial blood gas sampling, blood
chemistries (e.g., b-type natriuretic peptide, ane-
mia, renal function), and chest radiography may
provide information to aid in a differential diag-
nosis and help target treatment strategies. Treat-
ment strategies include self-help strategies (e.g.,
accurate self-assessment and regulation of breath-
ing), smoking cessation, avoidance of infection,
and environmental stressors (e.g., weather
extremes, poor air quality, pollutants), pulmonary
rehabilitation, and chronic disease management.
Cross-References
▶ Anxiety and Heart Disease
References and Readings
American Thoracic Society. (1999). Dyspnea. Mecha-
nisms, assessment, and management: a consensus
statement. American Journal of Respiratory Critical
Care Medicine, 159(1), 321–340.
D 638
Marx, J., Hockberger, R., & Walls, R. (2009). Rosen’s
emergency medicine: Concepts and clinical practice
(7th ed.). Philadelphia: Mosby-Elsevier.
Dysrhythmia
▶ Arrhythmia
Dysthymia
Nina Rieckmann
Berlin School of Public Health, Charité
Universit€atsmedizin, Berlin, Germany
Synonyms
Chronic depression; Chronic depressive disorder;
Dysthymic disorder
Definition
Dysthymia is a form of chronic depression, char-
acterized by persistent (“most of the days, for
more days than not”) depressed mood lasting for
at least 2 years. It is a diagnostic category within
the mood disorders in the current versions of the
Diagnostic and Statistical Manual of Mental Dis-
orders (DSM-IV) and the International Classifi-
cation of Diseases (ICD-10). In addition to
a depressed mood, two or more of the following
symptoms must have been present most of the
time (i.e., the person must not have been symp-
tom-free for more than 2 months at a time):
1. Poor appetite or overeating
2. Insomnia or hypersomnia
3. Low energy or fatigue
4. Low self-esteem
5. Poor concentration or difficulty making
decisions
6. Feelings of hopelessness
In children and adolescents, a dysthymia
diagnosis requires at least 1 year of depressed
Dysrhythmia
or irritable mood, and two of the above symp-
toms. Exclusion criteria are manic, hypomanic
or mixed episodes, presence of a major depres-
sive episode during the first 2 years, and
psychosis.
Description
Dysthymia is a mood disorder of low symptom
intensity. Nevertheless, it is associated with
markedly decreased quality of life, and functional
impairments are significant. While generally able
to cope with everyday life, affected persons
struggle with workplace or school demands,
social and intimate relationships. Lack of energy,
feelings of worthlessness, general negativity and
pessimism are common and foster the stigma of
“character weakness” and interfere with help-
seeking.
The comorbidity with other mental as well as
physical disorders is high. Because of under-
recognition and under-treatment, persons with
dysthymia are high-users of the health-care sys-
tem, which results in substantial direct (health-
care consumption) and indirect (absenteeism,
loss of productivity) costs.
Persons with dysthymia have an increased
lifetime risk of developing a major depressive
episode. When dysthymia worsens into a major
depressive episode, this is termed “double
depression.” Clinically, this form of depression
is distinct from others as it is marked by extreme
hopelessness and a poor prognosis.
Epidemiology and Risk Factors
Reports of the lifetime prevalence of dysthymia
range from 0.1% to 6%, with higher rates in
higher income countries and among females.
Persons with comorbid chronic medical disor-
ders, anxiety disorders, a history of substance
abuse, and personality disorders are at increased
risk for dysthymia and other forms of chronic
depression. A special risk group comprises per-
sons who experience depressive symptoms early
in life (before the age of 21).
Dysthymic Disorder 639 D
Treatment professional depression symptom monitoring,
and patient education about medication side
The most effective treatment for dysthymia con- effects, the importance of medication adherence,
sists of a combination of antidepressant medica- and the connection between psychosocial
tion and psychotherapy. Randomized controlled stressors and symptom recurrence.
trials have shown that both the treatment duration
and the intensity need to be higher for dysthymia
than for major depressive episodes in order to Cross-References
achieve similar response rates. This is possibly D
due to the high rates of comorbidities as well as ▶ Depression: Measurement
the chronic nature of dysthymia, which often ▶ Depression: Symptoms
results in yearlong struggles with everyday social ▶ Depression: Treatment
and occupational life, which are not easily ▶ Mood
overturned (Dunner, 2001). Many factors influ-
ence the choice of treatment: comorbid illnesses,
previous experience with similar medication or References and Readings
psychotherapies, interactions with other medica-
tions, side-effect profile, short- and long-term American Psychiatric Association. (1994). Diagnostic
and statistical manual of mental disorders (4th ed.).
effects, and, most importantly, patient tolerability Washington, DC: Author.
and individual preferences for type of treatment. Dunner, D. L. (2001). Acute and maintenance treatment of
Several guidelines and treatment algorithms are chronic depression. The Journal of Clinical Psychia-
available to guide the initial treatment choices as try, 62(Suppl. 6), 10–16.
Gureje, O. (2011). Dysthymia in a cross-cultural perspec-
well as the dosage augmentation or switches in
tive. Current Opinion in Psychiatry, 24(1), 67–71.
therapy when symptom improvement is Pettit, J. W., & Joiner, T. E. (2005). Chronic depression:
insufficient. Interpersonal sources, therapeutic solutions.
Since residual or subthreshold depressive Washington, DC: American Psychological
Association.
symptoms carry a strong risk of depressive symp-
Trivedi, M. H., & Kleiber, B. A. (2001). Algorithm for the
tom relapse, the treatment goal is complete remis- treatment of chronic depression. The Journal of
sion from all symptoms. Clinical Psychiatry, 62(Suppl. 6), 22–29.
Importantly, any treatment should be followed
by a maintenance phase, which can last as long as
a patient’s lifetime, in order to prevent the recur-
rence of depressive symptoms. Maintenance ther- Dysthymic Disorder
apy can involve the long-term treatment with
efficacious antidepressant medication, regular ▶ Dysthymia