CORRESPONDENCE
liter, a value not significantly dif-
ferent from the expected decrease
of serum sodium (4.4 mEq/liter)
calculated from the dilution of
body water after a water load of 20
ml/kg body weight. We have dem-
onstrated that ANF is secreted in
response to water expansion and
we suggestthat the observed natri-
uresis, with its associated water,
could help to limit volume expan-
sion (Am J Med 1988;84: 409-418).
The contribution of the observed
natriuresis to the fall in the serum
sodium level is probably of minor
importance. In addition, ANF has
been demonstrated to inhibit the
hydro-osmotic action of vasopres-
sin in uitro [2] and thus is thought
to increase the excretion of water
rather than to decrease it. When
antidiuretic hormone is sup-
pressed,asis usual in psychotic pa-
tients with polydipsia and hypona-
tremia, ANF would act asa diuretic
that
_. promotes more . water than so-
dium excretion relative to the re- -
spective concentrations of sodium
in urine and in serum.
The correlation between serum
sodium and body weight in the
polydipsic psychotic patients of
Vieweg et al [3] suggeststhat, in
this condition, as in inappropriate
antidiuresis, the fall in the serum
sodium level is directly related to
the amount of water retained. We
have not recorded accurately the
body weight of our patients in the
chronic state; however, others have
clearly reported that an increase in
body weight is a good index of wa-
ter retention in inappropriate anti-
diuresis [4].
In acute water loading tests, we
measure the body weight before
the administration of water, but we
need not monitor it because
changesin body weight can be de-
duced from the accurately known
external balance of water. An in-
verse correlation between serum
sodium and the calculated body
weight is found in this condition,
suggestingthat the decreasein the
serum sodium level is clearly relat-
ed to the retention of free water.
We have calculated that more than
94 percent of the decreasein serum
sodium is due to water retention.
Finally, we wish to emphasize
that in psychotic patients with
polydipsia and hyponatremia, the
causes of altered water excretion
are multiple and that vasopressin-
induced antidiuresis is only mar-
ginally involved [5,6]. On the con- coronary heart disease(CHD) and
trary, a vasopressin-independent the physical activity of preindus-
defect in water excretion has been trial societies are inadequately
clearly demonstrated [5]. We have supported.
suggestedthat a decreasein solute They point out that hunter-
delivery to the diluting segment of gatherers were stronger and more
the nephron may account for the muscular than succeeding agricul-
defect and have hypothesized that turalists, based upon evidence in
protracted natriuresis secondary to skeletal remains, and suggest
ANF secretion induced by the large therefore that the intensity of in-
intake of water may be responsible termittent peak demands on the
for it [7]. The idea is based on our musculoskeletal system is more im-
demonstration that, even in portant than the mere number of
healthy subjects, the administra- hours worked in the development
tion of an acute water load in- of muscularity. They alsopoint out
creasesANF secretion and the uri- the importance of endurance activ-
nary sodium excretion [8]. ities in our evolutionary past, as
ELIE COGAN, M.D., Ph.D. suggestedby the superior aerobic
MARIE-FRANCE DEBOWE, B.S. fitness measured in several prelit-
THIERRY PEPERSACK, M.D. erate populations. Finally, they
PHILIPPE DEMAEYER, M.D. generalize from clinical and post-
MAURICE ABRAMOW, M.D., Ph.D. mortem investigations of preliter-
Free University of Brussels ate societies today, which indicate
(U.L.B.)
1020 Brussels, Belgium that these societies experience lit-
tle or no CHD. This lack of CHD is
1. Cooke CR, Turin MD, Walker WG: The syndrome of presumably becauserisk factors for
inappropriate secretion of antidiuretic hormone
(SIADH): pathophysiologic mechanisms in solute and
the development of atherosclerosis
volume regulation. Medicine 1979; 58: 240-251. were souncommon in such cultures
2. Dillingham MA, Anderson RJ: Inhibition of vaso- and becausethey “led lives charac-
pressin action by atrial natriuretic factor. Science terized by considerable physical
1986: 231: 1572-1573.
3. Vieweg V. Godleski L. Yank G: Diurnal variation of
exertion.” We believe it is prema-
serum sodium and ADH among patients with psycho- ture to suggestthat physical fitness
sis, intermittent hyponatremia and polydipsia (PIP (basedon fitness testing of contem-
syndrome) (letter). Neuroendocrinol Lett 1987; 9: porary traditional societies) and
219.
4. Leaf A, Bartter FC. Santos RF, Wrong 0: Evidence
intense physical activity (based on
in man that urinary electrolyte loss induced by pitres- skeletal remains of ancient hunter-
sin is a function of water retention. J Clin Invest 1953; gatherers) are the factors protect-
32: 868-078. ing preliterate societies today
5. Goldman MB, Luchins DJ. Robertson GL: Mecha-
nisms of altered water metabolism in psychotic pa-
against the development of CHD.
tients with polydipsia and hyponatremia. N Engl J Vigorous aerobic physical activi-
Med 1988: 318: 387-403. ty can improve physical fitness, yet
6. Berl T: Psychosis and water balance. N Engl J Med physical fitness has been associ-
1988: 318: 441-442. ated with decreased CHD in only
7. Cogan E. Debieve M-F. Calderon P. Nortier J. De-
maeyer P. Abramow M: Mechanisms of altered water two studies, one of them our own
metabolism in psychotic patients with polydipsia and [1,2]. It is not physical fitness, but
hyponatremia (letter). N Engl J Med (in press). reported physical activity, that has
8. Cogan E. Debieve M-F. Calderon P. Nortier J. Abra-
mow M: Natriuresis and atrial natriuretic hormone
been associated with decreased
secretion induced by water drinking in healthy hu- CHD in most medical research
mans (abstr). Kidney Int 1988; 33: 258. studies. Recently it has been pro-
posed that it may not be physical
fitness, but rather physical activi-
ty, that protects against CHD [3].
CHRONIC DEGENERATIVE The intensity and duration of
DISEASES IN EVOLUTIONARY physical activity that is most pro-
PERSPECTIVE tective against CHD has not yet
To the Editor: been defined.
Eaton et al (Am J Med 1988; 84: Evidence from the Masai sup-
739-749) have done an admirable ports the suggestion that low-in-
job of pulling together a wide vari- tensity physical activity may pro-
ety of research findings that sup- tect against CHD, and that physi-
port their hypothesis that a mis- cal fitness may be an associated,
match, between modern man’s ge- rather than a causal, CHD risk fac-
netic constitution and “civilized” tor. Of the preindustrial cultures
lifestyle is the causeof most chron- mentioned by Eaton et al, the Ma-
ic degenerative disease today. sai, a traditional semi-nomadic
However, their conclusions about pastoral tribe in East Africa, have
October 1988 The American Journal of Medicine Volume 85 595
CORRESPONDENCE
probably been the most compre-
hensively studied with regard to
their absence of CHD. The Masai
have been the subjects of so many
medical studies, not only because
of their lack of CHD, but also be-
cause their dietary staple is milk,
with saturated fat constituting 66
percent of their total caloric intake
[4]. Intimal thickening and consid-
erable atherosclerosis have been
noted in the coronary arteries of el-
derly male Masai, but at the same
time their coronary vessels appear
to enlarge with age and become
wide enough to prevent occlusive
coronary disease [5].
Although it has been suggested
that the Masai’s protection against
CHD is provided by their excep-
tional levels of physical fitness
[4,5 , the day-to-day physical ac-
tivi 1y associated with these levels
of fitness has never been studied,
and vigorous exertion is reported to
be rare among Masai adults [6]. A
pilot study we conducted in Masai-
land suggests that it is indeed rare
for adult Masai to participate in
physical activity that is more vigor-
ous than walking.
If extensive walking is sufficient
to protect us from CHD in the pres-
ence of a high-fat diet, this would
have important public health im-
plications. There is a need to docu-
ment the actual intensity and du-
ration of daily physical activities in
the few remaining traditional cul-
tures that have a recorded paucity
of CHD in order to clarify these re-
lationships.
ALLAN V. ABBOTT, M.D.
RUTH K. PETERS, s~.D.
University of Southern California
School of Medicine
Parkview Medical Building
B-207
1420 San Pablo Street
LOSAngeles, California 90033
1. Peters RK. Cady LD Jr, Bischoff DP. Pemstein L.
Pike MC: Physical litness and subsequent
infarction in healthy workers. JAMA 1983: 249:
3052-3056’.
2. Wllhelmsen L. Tibblin G. Awell M. et al: Physical
activity, physical fitness and risk of myocardial
tion. Adv Cardiol 1976; 18: 217-230.
3. LaPorte RE. Adams LL, Savage CID. ef &The spec-
trum of physical activity, cardiovascular
health: an epidemiologic perspective. Am J Epidemiol
1984: 120: 507-515.
4. Mann GV, Shaffer RD, Anderson RS. Sandstead
HH: Cardiovascular disease in the Masai. J Ather-
oscler Res 1964; 4: 289-312.
5. Mann GV. Spoerry A, Gray M. Jarashow D: Athero-
sclerosis in the Masai. Am J Epidemiol 1972: 95: 26-
37.
6. Mann GV. Shaffer RD, Rick A: Physical fitness and
immunity to heart disease in Masai. Lancet 1965; II:
1308-1310.
Submitted June 15, 1988, and accepted
596 October 1988 The American
The Reply:
Apparently Drs. Abbott and Peters
interpreted our report to the effect
that physical activity was the main
influence acting to protect recent
hunter-gathers, other traditional
peoples, and Paleolithic humans
against coronary heart disease
(CHD). We believe their interpre-
tation is a misconstruction. Be that
as it may, we did not mean to sug-
gest that exercise was the primary
or even necessarily a major factor.
People whose lives include es-
sential elements of our remote an-
cestors’ lifeways are protected
against atherosclerosis because: (1)
They have little or no hyperten-
sion. (Our originally submitted
manuscript, available on request,
included a table listing 26 such cul-
tures with supportive references.)
(2) They have little or no exposure
to tobacco. Our African and Eura-
sian antecedents had none because
tobacco is indigenous to the Ameri-
cas. (3) Their serum cholesterol
levels average below 150 mg/dl (see
Table VI in our report).
There have been many investiga-
tions of the relationship between
physical exercise and CHD. Paf-
fenbarger and Hyde’s [l] work in
this regard is highly informative,
and a recent contribution from the
Centers for Disease Control [2] re-
views 43 such studies. This analysis
concludes that physical inactivity
should be considered a major risk
factor.
Numerous beneficial influences
operated jointly to protect our an-
cestors from CHD. If we can rein-
stibte these elements into our cur-
rent lifestyle, we should be able to
greatly reduce the prevalence of
this disorder in today’s humans.
Our recent monograph f3] explores
this concept in greater detail.
S. BOYD EATON, M.D.
MARJORIE SHOSTAK
myocardial MELVIN KONNER, M.D., Ph.D.
Emory University
Atlanta, Georgia 30322
infarc- 1. Paffenbarger RS. Hyde RT: Exercise as a protec-
tion against heart attack. N Engl J Med 1980: 302:
1026-1027.
disease and
2. Casperson CJ: Protective effect of physical activity
on coronary heart disease. MMWR 1987: 36: 426-
430.
3;Eaton SB. Shostak M, Konner M: The Paleolithic
prescription. New York: Harper & Row, 1988.
PHARMACEUTICAL COMPANY-
SPONSORED SYMPOSIA AND
MEDICAL ETHICS
To the Editor:
I am pleased to announce the re-
August 1, sults of the First Annual Juried
1988
Journal of Medicine Volume 85
Competition for Creative Titling of
a Drug Company-Sponsored Sym-
posium. This competition was es-
tablished in response to pressures
from the academic community [l-
31 for the purpose of recognizing
publishers who have created dis-
tindtive names for symposia that
deal with a specific drug and are
supported by the company that
makes that drug. In evaluating
each entry, the judges consider (1)
creativity and (2) pretension.
The first award has been granted
to Cahners Publishing Company
for their publication entitled,
“Proceedings of a Symposium. Ad-
vanced Technology in Cardiovas-
cular Therapy: Investigators’ Dia-
logue” (Am J Med 1987; 83(suppl
6B): l-33). This publication dealt
with a controlled-release oral dos-
age form of nifedipine and was
sponsored by Pfizer Laboratories.
In giving the award, the jury
cited the imaginative focus on
technology in the title. Through a
clever choice of words that shifted
the emphasisto modern technolo-
gy and altogether away from medi-
cation, the publishers were judged
to have thoroughly (and imagina-
tively) obscured the basic purpose
of the symposium. Essential to re-
ceiving the award for pretension is
that the title promises far more
than it gives. Once again, the ap-
peal to technology and the empha-
sis on the word “advanced” were
what gave this work ascendancy
over the runners-up, which often
simply promised to provide a gen-
eral updating in a field or intensive
teaching about a particular clinical
problem. Although hardly novel,
the concept that a seriesof articles
all sponsored by a single company
and published in a supplementary
issueof a journal might properly be
regarded as a “dialogue” gave fur-
ther support to the selection of this
symposium for the award.
A check for $10 has been mailed
to the President of Cahners Pub-
lishing Company along with a let-
ter of congratulations.
DANIEL M. MUSHER, M.D.
Veterans Administration
Medical Center
2002 Holcombe Boulevard
Houston, Texas 77211
I. Rochmis PG: Seminars for physicians. JAMA 1982;
248: 1580-1581.
2. Soffer A: Hazards in publication of proceedings.
Arch Intern Med 1982: 142: 2074-2076.
3. Musher DM: Antibiotics: the medium is the mes-
sage. Rev Infect Dis 1983: 5: 809-812.
SubmItted February 10. 1986, and accepted August
8, 1988