Author’s Accepted Manuscript

Quality of life is associated with chronic

inflammation in depression: a cross-sectional study

M Faugere, J-A Micoulaud-Franchi, C Faget-

Agius, C Lançon, M Cermolacce, R Richieri

www.elsevier.com/locate/jad

PII: S0165-0327(17)30792-9
DOI: https://doi.org/10.1016/j.jad.2017.11.061
Reference: JAD9375
To appear in: Journal of Affective Disorders
Received date: 19 April 2017
Revised date: 3 October 2017
Accepted date: 12 November 2017
Cite this article as: M Faugere, J-A Micoulaud-Franchi, C Faget-Agius, C
Lançon, M Cermolacce and R Richieri, Quality of life is associated with chronic
inflammation in depression: a cross-sectional study, Journal of Affective
Disorders, https://doi.org/10.1016/j.jad.2017.11.061
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 Quality of life is associated with chronic inflammation in depression: a cross-sectional study

Faugere M1,2*, Micoulaud-Franchi J-A3,4, Faget-Agius C1,2, Lançon C1,2, Cermolacce M5, Richieri R1,2,6

1
Department of Psychiatry, La Conception University Hospital, 13005 Marseille, France.

2
EA 3279 – Self perceived Health Assessment Research Unit, Aix-Marseille University, 13005,
Marseille, France.

3
Department of Clinical Neurophysiology, Sleep Clinique, Pellegrin University Hospital, 33076
Bordeaux, France.

4
Bordeaux University, USR CNRS 3413 SANPSY, Research Unit, 33000 Bordeaux, France. 5 SHU Adult
Psychiatry, Sainte Marguerite University Hospital, 13274 Marseille, France.

6
Department of Psychosis studies, Institute of Psychiatry, Psychology and Neurosciences, King’s
College London, United Kingdom.

*Corresponding author at: Service du Pr C. Lançon, Pôle Psychiatrie Centre, CHU La Conception, 147
bd Baille, 13005 Marseille, France. Tel: +33 (0)6 50 27 07 07; Fax: +33 (0)4 91 43 55 61. Email address:
melanie.faugere@ap-hm.fr (Melanie Faugere)

Abstract

Background

Inflammation may play a crucial role in the pathophysiology of depression. However, the association
between chronic inflammation and health outcomes in depression remains unclear, particularly for
patient-reported outcomes.

Methods

The aim of this study was to investigate the relationship between quality of life (QoL) (physical and
mental health, assessed by the SF-36) and chronic inflammation assessed using C-reactive protein
(CRP) in patients with current major depressive disorder.

Results

One hundred eighty-one patients with depression were enrolled in this study. After adjusting for key
socio-demographic, clinical and biological confounding factors, patients with high levels of CRP (>3.0
mg/L) had worse physical health than those with normal CRP levels (OR= 0.95, 95% CI=0.92-0.99).

1
Significant associations were found between a higher rate of metabolic syndrome (OR=0.10, 95%
CI=0.02-0.41) and high CRP levels.

Limitations

The cut-off point for high cardiovascular risk was used to define the two groups: normal CRP level
and high CRP level. CRP was the sole marker of inflammation in this study and was collected at only
one time point. The design of this study is cross-sectional and there are no conclusions about the
directionality of the association between QoL and inflammation in depression. QoL was assessed only
by SF-36 scores.

Conclusion

This study found an association between SF-36 physical health score and CRP in patients with
depression, thereby showing the need to consider physical well-being in depression. This paves the
way for interventions to act both on inflammation and QoL in patients with depression.

Keywords

Quality of life, inflammation, C-reactive protein, depression

1. Introduction

Depression is the single most prevalent mental disorder in the general population and the leading
cause of disability worldwide. It combines affective symptoms (mood disorder, feeling of
worthlessness, anhedonia, lack of concentration) and somatic symptoms (fatigue, sleep disturbances,
decreased appetite, loss of weight). Depression affects psychosocial functioning and quality of life
(QoL). Patients with depression report a wide range of functional impairments and lower QoL (IsHak
et al. 2011), including mental (e.g., social functioning) and physical health (e.g., bodily pain).

The pathophysiological mechanisms of depression are not fully understood. Recently, the role of the
immune systems has been emphasized in the development of depression (Dowlati et al. 2010). In
particular, a meta-analysis showed that elevated C-reactive protein (CRP), a classical and reliable
marker of chronic inflammation that is easily measured in blood, is consistently associated with
depression (Haapakoski et al. 2015). However, the relationship between type or clinical severity of
the disorder and elevated CRP levels is not consensual (Song et al. 2015; Hamer et al. 2009; de
Menezes et al. 2017).

Some studies have investigated how QoL may be associated with chronic inflammation. In non-
psychiatric populations, elevated CRP levels were reported to be associated with lower QoL in the

2
general population (Hamer and Chida 2011), and in several chronic diseases (e.g., diabetes
(Cummings, King, and Mainous 2003)). In psychiatric populations and in particular in schizophrenics,
QoL has been associated with chronic inflammation as measured by CRP levels (Faugere et al. 2015).
However, no study to date has specifically investigated the relationship between impaired QoL and
elevated CRP levels in patients with depression.

The aim of this study was to investigate the relationship between QoL and chronic inflammation as
assessed by CRP in patients with depression, in addition to considering key socio-demographic,
biological and clinical confounding factors. We hypothesize that in major depressive disorder,
patients with elevated CRP levels have lower QoL than those with normal levels.

2. Methods
2.1 Study participants

The study evaluated all prospective patients attending daytime hospital hours in our university and
psychiatric hospital over a period of 5 years from October 2010 to May 2015. The inclusion criteria
were as follows: (1) age 18-85 years old, (2) diagnosis of major depressive disorder according to the
DSM-IV-TR criteria, (3) antidepressant medication stable for a minimum of 3 months, and (4) French
as native language. The exclusion criteria were as follows: (1) diagnoses other than major depressive
disorder on axis 1 of the DSM-IV-TR, except for nicotine dependence, (2) major non-psychiatric
disease, (3) mental retardation and (4) any identifiable acute, intermittent or chronic infection or
being on routine anti-inflammatory or immunosuppressive therapy. The data collection was
approved by the Commission Nationale de l’Informatique et des Libertés (CNIL number 1223715).
The study was designed in accordance with the Declaration of Helsinki and French good clinical
practice. All of the patients were informed of the study and gave written informed consent.

2.2 Data Collection.

The following data were collected:

1. Socio-demographic information: gender, age, educational level, professional activity.

2. Clinical characteristics: duration of disorder; body mass index (BMI); tobacco consumption;
alcohol consumption assessed by the Alcohol Use Disorders Identification Test
(AUDIT)(Saunders et al. 1993); depressive symptoms based on the Beck Depression Inventory
(BDI)(Beck et al. 1961), the Hamilton Depression Rating Scale (HDRS)(Hamilton 1960) and the
Montgomery and Asberg Depression Rating Scale (MADRS)(Montgomery and Asberg 1979).

3
 3. Drug information: antidepressant medications (presence of Selective Serotonin Reuptake
Inhibitor (SSRI) or Serotonin-Norepinephrine Reuptake Inhibitor (SNRI)), presence of
benzodiazepines and presence of mood stabilizers.
4. Metabolic Syndrome (Grundy 2005).
5. QoL measurement: QoL was assessed using The Short Form (36) Health Survey (Ware,
Kosinski, and Keller 1994) (SF-36) which has two global scores: SF-36 physical health and SF-
36 mental health. Global scores range from 0, indicating the lowest QoL, to 100, the highest
QoL.
6. Chronic inflammation marker: serum CRP levels were determined using sensitive regular
immunoassays (ELISA). The results were expressed as milligram per liter. The detection limit
was 0.08 µg/ml. Patients were classified into two groups: normal CRP level (≤3.0 mg/l) and
high CRP (>3.0 mg/l)(Wysokiński et al. 2014).

2.3 Statistical analysis

The characteristics of the entire group of patients with depression were expressed in proportions or
as mean and standard deviations. Socio-demographic and clinical characteristics, drug information,
biological characteristics and QoL were compared between the two groups (normal CRP level vs. high
CRP) using the Student t-test for continuous variables and the Chi-squared test for categorical
variables.

A multivariate logistic regression was then performed to estimate the adjusted odds ratio (OR) and
its corresponding 95% confidence interval (CI) for an association between SF-36 physical and mental
health global scores (independent variable) and CRP (dependent variable), with adjustment for
confounding factors selected from the univariate based on threshold p-value ≤0.20 (education level,
rate of metabolic syndrome, BDI score and SF-36 physical health global score were selected). A set of
additional variables were included in the model because of their socio-demographic interest (gender,
age, duration of disorder and tobacco consumption)(Wysokiński et al. 2014).

All of the tests were two-sided. Statistical significance was defined as p < 0.05. Statistical analysis was
performed using the SPSS version 18.0 software package (SPSS Inc., Chicago, IL, USA).

3. Results
3.1 Patient characteristics

One hundred eighty-one outpatients with depression participated in the study (Table 1). The mean
age of the patients was 50.73 years (±14.07), and 34.8% were male. They had moderately severe
symptoms with a mean BDI score of 23.28 (±12.38), a mean HDRS score of 16.77 (±8.26), and a mean

4
MADRS score of 20.90 (±12.07). Of the total number of patients, 51.4% were treated by SSRI and
32.6% were treated by SNRI.

3.2 Comparison of patients with normal CRP level and high CRP

Among the 181 patients with depression, 47 (25.97%) had a high CRP level. Compared to patients
with normal CRP levels, those with high CRP levels had a significantly lower education level
(p=0.020), a higher BDI score (p=0.009) and a higher rate of metabolic syndrome (p<0.001).
Concerning QoL, patients with high CRP levels had lower SF-36 physical health scores (p<0.001). SF-
36 mental health scores were not significantly associated with CRP levels.

3.3 Factors associated with high CRP

In the multivariate analyses shown in Table 2, the relationship between SF-36 physical health scores
and CRP levels remained significant after adjusting for socio-demographic, clinical and metabolic
characteristics. Note that, with a multivariate model that did not include BDI, the relationship
between SF-36 and high CRP levels remains significant (data not shown). A higher rate of metabolic
syndrome remained significantly associated with high CRP levels. Depression severity as assessed by
the BDI score did not remain associated with high CRP levels in multivariate analysis. Note that, with
a multivariate model that did not include SF-36, the relationship between BDI and high CRP levels
remain insignificant (data not shown).

4. Discussion

The main finding of this study is the existence of a relationship between physical QoL and chronic
inflammation in patients with depression, after adjusting for key socio-demographic, clinical and
metabolic confounding factors. These findings support previous studies that reported the association
between low QoL levels and high CRP levels in non-psychiatric populations (Hamer and Chida 2011;
Cummings, King, and Mainous 2003) and in patients with schizophrenia (Faugere et al. 2015).
Moreover, these high rates of high CRP levels in our population (26.0% of the patients with MDD had
a high CRP level) are in line with studies that found that more than one third of patients with MDD
have a high CRP level (Wysokiński et al. 2014). However, this prevalence of high levels of CRP in our
study are slightly lower than in previous studies. This trend can be explained by the fact that more
than 60% of the participants are women, who are known to exhibit lower CRP levels than men
(Vetter et al. 2013; Tayefi et al. 2017). No association was found between antidepressant treatment
and CRP levels, which is in line with two previous meta-analyses. The first of Wiedlocha et al., did not
find significant effect of antidepressant medication on CRP (Więdłocha et al. 2017). The authors
reviewed 32 studies measuring the levels of selected inflammation markers (8 studies measured CRP

5
levels) before and at a second time-point during antidepressant treatment. Using the random-effects
model, authors did not find statistically significant effect of antidepressant treatment on CRP levels
(p<0.05). The second, of Hiles and al., reviewed 8 studies measuring CRP, before and after
antidepressant treatment (Hiles et al. 2012). The authors found a marginally significant decrease in
CRP (d=-0.57, p=0.05). The association between antidepressants and inflammation could be better
analyzed with more specific peripheral inflammation markers like IL-6 or IL-10 (Więdłocha et al.
2017; Hiles et al. 2012).

A previous study found a small but significant association between elevated inflammatory markers
and the development of depressive symptoms (Valkanova, Ebmeier, and Allan 2013). Specifically, our
results are in line with findings that showed that somatic symptoms (i.e. chronic pain, changes in
appetite, lack of energy, sleep disturbances…) in depression are more strongly associated with CRP
levels than affective symptoms (Elovainio et al. 2009). They are also in line with data that showed
that the progression of chronic inflammatory disease may exert a significant negative impact on QoL.
This hypothesis may be supported by the sickness behavioral model (Dantzer et al. 2008). CRP is a
general marker of inflammation that is functionally involved in the development of symptoms of
sickness (as feeling depressed and irritable, having fragmented sleep or cognitive disorders) through
direct effects on the central nervous system (Dantzer et al. 2008). These symptoms are well known to
impact QoL negatively in non-psychiatric populations (Dantzer et al. 2008). Our results suggest that
they may also be related to poor QoL in patients with depression, as already shown in patients with
schizophrenia (Faugere et al. 2015). The relationship between quality of life and CRP was
independent of metabolic syndrome. However, our results also confirmed an association between
high CRP and high rates of metabolic syndrome, as previously seen in patients with MDD (Chirinos et
al. 2017), but also in schizophrenia (Vuksan-Cusa et al. 2013) and in the general population (Frohlich
et al. 2000). There is evidence that, in the presence of metabolic syndrome, an expansion of adipose
tissues could release pro-inflammatory molecules (Monteiro and Azevedo 2010). Thus, further
studies are needed to investigate the relationship between CRP level, metabolic syndrome and
somatic symptoms related to sickness behavior. These future findings could be very useful for
therapeutic applications in patients with depression (Ellul et al. 2016).

Several limitations should be considered in this study. First, there is the problem of the definition of
the groups (normal and high CRP level). While there are no generally accepted criteria for relapse, we
chose the most consensual definition in the recent scientific literature, which is recognized as the
cut-off point for high cardiovascular risk (Wysokiński et al. 2014). Second, CRP was the sole marker of

6
inflammation. Although CRP is strongly associated with IL-6 activity, we did not directly assess any of
the cytokines. Future studies with extensive assessment of inflammatory markers may be required
(Więdłocha et al. 2017; Hiles et al. 2012). Third, we measured CRP levels at only one time point, yet
repeated testing has been recommended to confirm elevated plasma levels because concentrations
can be affected by acute infection. However, patients with acute infections were excluded and did
not alter any of the results. Fourth, the cross-sectional design of the study precludes any conclusions
about the directionality of the association between QoL and inflammation in depression. Fifth, we
investigated only SF-36 scores. More studies are needed to explore the relationship between more
specific physical symptoms and CRP levels and would likely offer interesting interventional prospects
for acting both on inflammation and QoL in patients with depression. Seventh, BDI was associated
with CRP in univariate analysis but not in multivariate model. It could be interesting to explore which
BDI items are related to high CRP levels, probably because they are BDI items specifically associated
with high CRP, in particular items concerning physical health. Lastly, a certain number of patients
treated by mood stabilizers are probably pharmacoresistant. Nevertheless, we reassessed the
analyses by removing patients with mood stabilizers and found no differences in the results (data not
shown).

Despite these limitations, our study shows that chronic inflammation is moderately associated with
lower QoL levels in patients with depression and indicates the need for further research exploring
the relationship between physical health and inflammation in depression.

Conflicts of interest

None

Funding

This research did not receive any specific grant from funding agencies in the public, commercial or
not-for-profit sectors.

Acknowledgements

Our thanks to all the patients, staff who helped with the study and Ms Eile Gibson.

Authors Contributions

M.F. and J.A.M.F. wrote the manuscript. All authors designed the study and wrote the protocol. M.F.,
J.A.M.F. and C.L. conducted the literature search. R.R., C.F.A. and M.C. recruited the patients. M.F.
and J.A.M.F conducted the statistical analyses. All authors contributed to and approved the final
manuscript.

7
References

Beck, A. T., C. H. Ward, M. Mendelson, J. Mock, and J. Erbaugh. 1961. “An Inventory for Measuring
Depression.” Archives of General Psychiatry 4 (June): 561–71.
Chirinos, Diana A., Kyle W. Murdock, Angie S. LeRoy, and Christopher Fagundes. 2017. “Depressive
Symptom Profiles, Cardio-Metabolic Risk and Inflammation: Results from the MIDUS Study.”
Psychoneuroendocrinology 82 (August): 17–25. doi:10.1016/j.psyneuen.2017.04.011.
Cummings, Doyle M, Dana E King, and Arch G Mainous. 2003. “C-Reactive Protein, Antiinflammatory
Drugs, and Quality of Life in Diabetes.” The Annals of Pharmacotherapy 37 (11): 1593.
doi:10.1345/aph.1D029.
Dantzer, Robert, Jason C. O’Connor, Gregory G. Freund, Rodney W. Johnson, and Keith W. Kelley.
2008. “From Inflammation to Sickness and Depression: When the Immune System Subjugates
the Brain.” Nature Reviews. Neuroscience 9 (1): 46–56. doi:10.1038/nrn2297.
Dowlati, Yekta, Nathan Herrmann, Walter Swardfager, Helena Liu, Lauren Sham, Elyse K. Reim, and
Krista L. Lanctôt. 2010. “A Meta-Analysis of Cytokines in Major Depression.” Biological
Psychiatry 67 (5): 446–57. doi:10.1016/j.biopsych.2009.09.033.
Ellul, P., L. Boyer, L. Groc, M. Leboyer, and G. Fond. 2016. “Interleukin-1 β-Targeted Treatment
Strategies in Inflammatory Depression: Toward Personalized Care.” Acta Psychiatrica
Scandinavica 134 (6): 469–84. doi:10.1111/acps.12656.
Elovainio, Marko, Anna-Mari Aalto, Mika Kivimäki, Sami Pirkola, Jouko Sundvall, Jouko Lönnqvist, and
Antti Reunanen. 2009. “Depression and C-Reactive Protein: Population-Based Health 2000
Study.” Psychosomatic Medicine 71 (4): 423–30. doi:10.1097/PSY.0b013e31819e333a.
Faugere, Melanie, Jean-Arthur Micoulaud-Fanchi, Marine Alessandrini, Raphaëlle Richieri, Catherine
Faget-Agius, Pascal Auquier, Christophe Lançon, and Laurent Boyer. 2015. “Quality of Life Is
Associated with Chronic Inflammation in Schizophrenia: A Cross-Sectional Study.” Scientific
Reports 5 (June): 10793. doi:10.1038/srep10793.
Frohlich, M., A. Imhof, G. Berg, W. L. Hutchinson, M. B. Pepys, H. Boeing, R. Muche, H. Brenner, and
W. Koenig. 2000. “Association between C-Reactive Protein and Features of the Metabolic
Syndrome: A Population-Based Study.” Diabetes Care 23 (12): 1835–39.
doi:10.2337/diacare.23.12.1835.
Grundy, S. M. 2005. “Diagnosis and Management of the Metabolic Syndrome: An American Heart
Association/National Heart, Lung, and Blood Institute Scientific Statement.” Circulation 112
(17): 2735–52. doi:10.1161/CIRCULATIONAHA.105.169404.
Haapakoski, Rita, Julia Mathieu, Klaus P. Ebmeier, Harri Alenius, and Mika Kivimäki. 2015.
“Cumulative Meta-Analysis of Interleukins 6 and 1β, Tumour Necrosis Factor α and C-
Reactive Protein in Patients with Major Depressive Disorder.” Brain, Behavior, and Immunity
49 (October): 206–15. doi:10.1016/j.bbi.2015.06.001.
Hamer, Mark, and Yoichi Chida. 2011. “Life Satisfaction and Inflammatory Biomarkers: The 2008
Scottish Health Survey1: Life Satisfaction and C-Reactive Protein.” Japanese Psychological
Research 53 (2): 133–39. doi:10.1111/j.1468-5884.2011.00460.x.
Hamer, Mark, Gerard J. Molloy, Cesar de Oliveira, and Panayotes Demakakos. 2009. “Persistent
Depressive Symptomatology and Inflammation: To What Extent Do Health Behaviours and
Weight Control Mediate This Relationship?” Brain, Behavior, and Immunity 23 (4): 413–18.
doi:10.1016/j.bbi.2009.01.005.
Hamilton, M. 1960. “A Rating Scale for Depression.” Journal of Neurology, Neurosurgery, and
Psychiatry 23 (February): 56–62.
Hiles, S. A., A. L. Baker, T. de Malmanche, and J. Attia. 2012. “Interleukin-6, C-Reactive Protein and
Interleukin-10 after Antidepressant Treatment in People with Depression: A Meta-Analysis.”
Psychological Medicine 42 (10): 2015–26. doi:10.1017/S0033291712000128.
IsHak, Waguih William, Jared Matt Greenberg, Konstantin Balayan, Nina Kapitanski, Jessica Jeffrey,
Hassan Fathy, Hala Fakhry, and Mark Hyman Rapaport. 2011. “Quality of Life: The Ultimate

8
 Outcome Measure of Interventions in Major Depressive Disorder.” Harvard Review of
Psychiatry 19 (5): 229–39. doi:10.3109/10673229.2011.614099.
Menezes, Sara Teles de, Roberta Carvalho de Figueiredo, Alessandra Carvalho Goulart, Maria
Angélica Nunes, Isabela M. Benseñor, Maria Carmen Viana, and Sandhi Maria Barreto. 2017.
“Lack of Association between Depression and C-Reactive Protein Level in the Baseline of
Longitudinal Study of Adult Health (ELSA-Brasil).” Journal of Affective Disorders 208 (January):
448–54. doi:10.1016/j.jad.2016.10.046.
Monteiro, Ros?rio, and Isabel Azevedo. 2010. “Chronic Inflammation in Obesity and the Metabolic
Syndrome.” Mediators of Inflammation 2010: 1–10. doi:10.1155/2010/289645.
Montgomery, S. A., and M. Asberg. 1979. “A New Depression Scale Designed to Be Sensitive to
Change.” The British Journal of Psychiatry: The Journal of Mental Science 134 (April): 382–89.
Saunders, J. B., O. G. Aasland, T. F. Babor, J. R. de la Fuente, and M. Grant. 1993. “Development of
the Alcohol Use Disorders Identification Test (AUDIT): WHO Collaborative Project on Early
Detection of Persons with Harmful Alcohol Consumption--II.” Addiction (Abingdon, England)
88 (6): 791–804.
Song, Bo Mi, Ju-Mi Lee, Wungrak Choi, Yoosik Youm, Sang Hui Chu, Yeong-Ran Park, and Hyeon
Chang Kim. 2015. “Association between C Reactive Protein Level and Depressive Symptoms
in an Elderly Korean Population: Korean Social Life, Health and Aging Project.” BMJ Open 5
(2): e006429. doi:10.1136/bmjopen-2014-006429.
Tayefi, Maryam, Mojtaba Shafiee, Seyyed Mohammad Reza Kazemi-Bajestani, Habibolah Esmaeili,
Susan Darroudi, Samaneh Khakpouri, Maryam Mohammadi, et al. 2017. “Depression and
Anxiety Both Associate with Serum Level of Hs-CRP: A Gender-Stratified Analysis in a
Population-Based Study.” Psychoneuroendocrinology 81 (July): 63–69.
doi:10.1016/j.psyneuen.2017.02.035.
Valkanova, Vyara, Klaus P. Ebmeier, and Charlotte L. Allan. 2013. “CRP, IL-6 and Depression: A
Systematic Review and Meta-Analysis of Longitudinal Studies.” Journal of Affective Disorders
150 (3): 736–44. doi:10.1016/j.jad.2013.06.004.
Vetter, M. L., T. A. Wadden, C. Vinnard, R. H. Moore, Z. Khan, S. Volger, D. B. Sarwer, L. F.
Faulconbridge, and POWER-UP Research Group. 2013. “Gender Differences in the
Relationship between Symptoms of Depression and High-Sensitivity CRP.” International
Journal of Obesity (2005) 37 Suppl 1 (August): S38–43. doi:10.1038/ijo.2013.95.
Vuksan-Cusa, Bjanka, Marina Sagud, Miro Jakovljevic, Alma Mihaljevic Peles, Nenad Jaksic, Sanea
Mihaljevic, Maja Zivkovic, Suzan Kudlek Mikulic, and Sasa Jevtovic. 2013. “Association
between C-Reactive Protein and Homocysteine with the Subcomponents of Metabolic
Syndrome in Stable Patients with Bipolar Disorder and Schizophrenia.” Nordic Journal of
Psychiatry 67 (5): 320–25. doi:10.3109/08039488.2012.745601.
Ware, John E, M Kosinski, and SD Keller. 1994. “SF-36 Physical and Mental Health Summary Scales.”
Boston, MA: The Health Institute, New England Medical Center.
Więdłocha, Magdalena, Piotr Marcinowicz, Renata Krupa, Marlena Janoska-Jaździk, Marta Janus,
Weronika Dębowska, Anna Mosiołek, Napoleon Waszkiewicz, and Agata Szulc. 2017. “Effect
of Antidepressant Treatment on Peripheral Inflammation Markers - A Meta-Analysis.”
Progress in Neuro-Psychopharmacology & Biological Psychiatry, April.
doi:10.1016/j.pnpbp.2017.04.026.
Wysokiński, Adam, Aleksandra Margulska, Dominik Strzelecki, and Iwona Kłoszewska. 2014. “Levels
of C-Reactive Protein (CRP) in Patients with Schizophrenia, Unipolar Depression and Bipolar
Disorder.” Nordic Journal of Psychiatry, December, 1–8. doi:10.3109/08039488.2014.984755.

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Table 1. Socio-demographic, clinical and biological characteristics of study sample (n=181). a X2 test
for qualitative variables b Alcohol Use Disorders Identification Test c Beck Depression Inventory d
Hamilton Depression Rating Scale e Montgomery and Asberg Depression Rating Scale f Global
Assessment of Functioning scale g Clinical Global Impression scale h State Trait Anxiety Inventory i
Suicide Behaviors Questionnaire – Revised j Medication Adherence Report Scale k 36-Item Short Form
survey: Scores range from 0 to 100; higher scores represent higher QoL

Whole Group Normal CRP level High CRP Normal

(N=181) ≤3.0mg (N=134) >3.0mg/L (N=47) CRP
level vs.
Mean Mean Mean High
SD SD SD
(%) (%) (%) CRP
p-value
63 49 14
Gender (Male) 0.256a
(34.8%) (36.6%) (29.8%)
Age (years) 50.73 14.07 49.94 14.45 52.98 12.65 0.202
109 87 22
Education level (>12 years) 0.020 a
(60.2%) (64.9%) (46.8%)
37 31 6
Professional activity (yes) 0.093 a
(20.4%) (23.1%) (12.8%)
Duration of disorder
15.35 13.57 15.06 13.50 16.98 13.63 0.405
(years)

93 65 28
Presence of SSRI 0.128 a
(51.4%) (48.5%) (59.6%)
59 46 13
Presence of SNRI 0.257 a
(32.6%) (34.3%) (27.7%)
Presence of 77 52 25
0.062 a
benzodiazepines (42.5%) (38.8%) (53.2%)
Presence of mood 10
14 (7.7%) 4 (8.5%) 0.516 a
stabilizers (7.5%)

64 46 18
Tobacco consumption (yes) 0.375 a
(35.4%) (34.3%) (38.3%)

AUDIT b 6.81 7.90 6.53 6.97 7.61 10.30 0.683

BDIc 23.28 12.38 21.64 11.64 27.71 13.37 0.009
HDRSd 16.77 8.26 16.82 8.38 16.66 8.03 0.920
MADRS e 20.90 12.07 19.73 11.77 24.60 12.48 0.079
GAF f 56.63 16.11 57.73 15.89 53.51 16.49 0.123
CGI g 4.08 1.30 3.98 1.31 4.36 1.24 0.088
STAI-Y h A 50.23 13.50 49.48 13.12 52.42 14.50 0.207
STAI-Y B 56.03 12.16 55.24 11.39 58.16 13.98 0.207
SBQ-R i 10.12 5.48 10.20 5.35 9.88 5.90 0.749
MARS j 6.24 2.04 6.23 2.06 6.28 2.00 0.882

SF-36 k Physical Health 46.41 16.51 48.99 17.29 38.65 10.84 <0.001
SF-36 Mental Health 29.77 16.14 30.56 17.13 27.43 12.64 0.200

Metabolic Syndrome (yes) 19 6 (4.5%) 13 <0.001a

10
 (10.5%) (27.7%)

Table 2. Factors associated with high CRP: multivariate analysis a Confidence Interval b 36-Item Short-
Form survey: Scores range from 0 to 100; higher scores represent higher QoL.

Adjusted odds
Factors 95%CIa p-value
ratio
Gender (Male) 1.08 0.39-3.01 0.881
Age (years) 1.01 0.97-1.05 0.718
Education level (>12 years) 1.90 0.77-4.69 0.162
Duration of disorder (years) 0.99 0.95-1.02 0.416
Tobacco consumption (yes) 1.24 0.45-3.38 0.681
Metabolic syndrome (yes) 0.10 0.02-0.41 0.002
Beck Depression Inventory 1.03 0.99-1.07 0.177
SF-36b Physical Health 0.95 0.92-0.99 0.023
SF-36 Mental Health 1.02 0.98-1.06 0.323

Highlights

 Inflammation may play a crucial role in the pathophysiology of depression.

 Chronic inflammation is associated with quality of life in patients with depression.
 Patients with high CRP levels had worse physical health.
 Physical well-being in depression may act both on inflammation and quality of life.

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