weight reduction and obesity
TRANSCRIPT
CLIN. AND EXPER. HYPERTENSION, 21(5&6), 763-768 (1999)
WEIGHT REDUCTION AND OBESITY
Lewis Landsberg, M.D. Department of Medicine
Northwestern University Medical School Chicago, Illinois 606 1 1
Key Words: Blood pressure, diet, insulin, sympathetic nervous system
ABSTRACT
Obesity and hypertension are intimately linked. Weight loss lowers blood pressure and improves the blood pressure response to sodium restriction and antihypertensive medications. In addition to the effects of energy restriction, diets rich in fruits and vegetables (and hence potassium) and rich in low fat dairy products (and hence rich in calcium and magnesium), high in fiber, and low in saturated fat also lower blood pressure independent of sodium and energy content. These dietary modifications, along with weight loss are beneficial in patients only mildly overweight and, because of beneficial effects on other cardiac risk factors should be part of the therapeutic regimen in all obese hypertensive patients.
OBESITY AND HYPERTENSION
The association of hypertension and obesity is well-recognized (1, 2). In
the Framingham Study, the incidence of obesity in the most obese subgroup of the
cohort approached 50% (3). Likewise, a substantial portion of individuals with
essential hypertension are obese. Body fat distribution plays an important
independent role in this association as well (1, 4). The abdominal, upper body fat
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pattern is more closely associated with hypertension than BMI or percent body fat
(1). Recent weight gain is also a very highly significant factor in predicting the
development of hypertension (1, 3). Obesity, moreover, increases resistance to
antihypertensive therapy and interferes with achieving target BP levels (5).
The underlying mechanisms that relate body weight and blood pressure
remain incompletely understood, but insulin mediated sympathetic stimulation
appears to play a role (6). Recent evidence suggests that leptin may also be
involved (7).
EFFECT OF LOW ENERGY DIETS AND WEIGHT LOSS
Both caloric restriction and weight loss have independent, separable
effects on blood pressure (1, 8, 9). Low energy diets reduce blood pressure
without concomitant sodium restriction (lo), although the effects of salt
restriction are additive or synergistic with those of weight loss (11). The
mechanisms involved are not known with certainty, but early in the course of low
energy intake negative sodium balance (natriuresis of fasting) may contribute
along with lowered levels of insulin; with reduction in body fat mass
improvement in insulin sensitivity and diminished sympathetic nervous system
activity (6, 12) are probably involved. Small amounts of weight loss in only
mildly obese patients, can, when combined with sodium restriction, have
clinically important results (1 1, 13, 14).
DIET COMPOSITION
In the last few years impressive evidence from prospective studies has
indicated that, in addition to energy content, mineral and macronutrient
composition influence blood pressure. The well-publicized clinical trial, “Dietary
Approaches to Stop Hypertension” (DASH study) examined the impact of diet
composition independent of energy content in 459 individuals randomized to 1 of
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WEIGHT REDUCTION AND OBESITY 765
3 diets for an 8 week period (1 5) . Energy and sodium content was equivalent in
all 3 groups. As compared with the control (“typical” U.S. diet) a diet rich in
h i t s and vegetables (second group) lowered blood pressure significantly. The
third group, a combination diet, low in total and saturated fat, rich in fruit and
vegetables, and rich in low-fat dairy products produced an even greater fall in
blood pressure (5.5 mm/hg systolic and 3.0 mm/hg diastolic as compared with the
control diet. The blood pressure changes were achieved 2 weeks into the
intervention diet and were sustained for the remainder of the 8 week trial. In the
133 subjects with hypertension (BP greater than or equal to 140 mmhg systolic or
equal to or greater than 90 mm/hg diastolic) the decreases in blood pressure were
substantially greater with a reduction in a systolic of 11.4 and diastolic 5.5 mm/hg
respectively as compared with control diet. Examination of the composition of
the various diets suggests that decreased saturated fat, increased potassium,
magnesium and calcium, and perhaps increased dietary fiber and protein were
associated with the hypotensive effect. This short-term study demonstrates
convincingly that these dietary components, independent of changes of energy
content and sodium, influence blood pressure. Consistent findings were reported
in another 10 week study of subjects with hypertension, dyslipidemia, or diabetes
although in this latter study energy and sodium restriction apparently contributed
to the hypotensive response (1 6).
LONG TERM EFFICACY
Are weight loss and dietary modification feasible long-term strategies in
the treatment of hypertension? Data fiom the Treatment of Mild Hypertension
Study (TOMHS) suggests that over a four year period, weight loss, sodium
restriction, diminished alcohol consumption and increased physical activity can be
sustained, although over time the changes in these variables tend to revert towards
pre-intervention levels (1 3). Blood pressure changes, however, as shown in figure
1 , were sustained in TOMHS over a four year period. Similar results have been
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766 LANDSBERG
TOMHS Lifestyle n=902 Intervention
I Y e a r 4 Y e a r I Y e a r 4 Y e a r
Systolic BP Diastolic BP
Figure 1.
demonstrated in the elderly (1 1). Lifestyle modification, therefore, including
weight loss, exert a modest but clinically significant influence on blood pressure
that is sustained over long periods of time.
SUMMARY
In the treatment of obesity related hypertension caloric restriction and
weight loss play an important role in the overall treatment plan. Obesity is a
significant cause of resistance to antihypertensive therapy and weight loss
increases responsiveness to drugs (5). Increased physical activity facilitates
weight loss, exerts a mild antihypertensive effect, and improves insulin sensitivity
(17). Dietary modification consisting of reduction in saturated fat intake along
with increased intake of potassium, calcium, magnesium, and dietary fiber have
demonstrated efficacy in lowering blood pressure and should exert beneficial
effects on other cardiovascular risk factors. The evidence also suggests that these
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WEIGHT REDUCTION AND OBESITY 767
dietary modiciations may be beneficial in normal weight patients and in those
only modestly obese.
REFERENCES
1. Kreiger DR, Landsberg L. Obesity and Hypertension. In Hypertension: Pathophysiology, Diagnosis, and Management Second Edition, edited by J.H. Laragh and B.M. Brenner, Raven Press, Ltd., New York 1995;140:2367-2388.
2. Shaper AG. Obesity and cardiovascular disease. 1996 The origins and consequences of obesity. Wiley, Chichester (Ciba Foundation Symposium 201) p 90-107.
3. Kannel WB, Brand N, Skinner JJ Jr, et al. The relation of adiposity to blood pressure and development of hypertension. Ann Intern Med 1967;67:48-59.
4. Cassano PA, Segal MR, Vokonas PS, Weiss ST. Body fat distribution, blood pressure, and hypertension: A prospective cohort study of men in the normative aging study. Ann Epidemiol 1990;1:33-48.
5 . Modan M, Almog S, Fuchs A, et al. Obesity, Glucose Intolerance, Hyperinsulinemia, and Response to Antihypertensive Drugs. Hypertension 199 1 ; 17565-573.
6. Reaven GM, Lithe1 H, Landsberg L. Hypertension and Associated Metabolic Abnormalities - The Role of Insulin Resistance and the Sympathoadrenal System. The New England Journal of Medicine 1996; 334:374-381.
7. Haynes W, Sivitz W, Morgan DA et al. Sympathetic and Cardiorenal Actions of Leptin. Hypertension 1997;30[part 2]:619-623.
8. Jung RT, Shetty PS, Barrand M et ai. Role of catecholamines in hypotensive response to dieting. Br Med J 1979; 1 : 12- 1 3.
9. Tuck, ML. Obesity, the sympathetic nervous system, and essential hypertension. Hypertension 1992;19:167-177.
Clin
Exp
Hyp
erte
ns D
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LANDSBERG 768
10.
11 .
12.
13.
14.
15.
16.
17.
Reisin E. Abel R, Modan My et al. Effect of weight loss without salt restriction on the reduction of blood pressure in overweight hypertensive patients. N Engl J Med 1978;298:1-6.
Whelton PK, Appel LJ, Espeland MA, et al. Sodium Reduction and Weight Loss in the Treatment of Hypertension in Older Persons A Randomized Controlled Trial of Nonpharmacologic Interventions in the Elderly (TONE). JAMA 1998;279:839-846.
Beckmann SLY 0 s I, Kjeldsen S, et al. Effect of Dietary Counselling on Blood Pressure and Arterial Plasma Catecholamines in Primary Hypertension. Am J Hypertens 1995;8:704-711.
Elmer PJ, Grimm R, Laing By et al. Lifestyle Intervention: Results of the Treatment of Mild Hypertension Study (TOMHS). Preventive Medicine 1995 ;24:378-388.
Stamler R, Stamler J, Grimm R, et al. Nutritional therapy for high blood pressure: final report of a four-year randomized controlled trial-the Hypertension Control Program. JAMA 1987;257(11): 1484-1491.
Appel LJ, Moore TJ, Obarzanek E, et al. A Clinical Trial of the Effects of Dietary Patterns on Blood Pressure. N Engl J Med 1887;336: 11 17-24).
McCarron DA, Oparil S, Chait A, et al. Nutritional Management of Cardiovascular Risk Factors A Randomized Clinical Trial. Arch Intern Med. 1997; 157: 169-177.
Zachwieja JJ, Exercise as Treatment for Obesity. Obesity 1996; Vol25, Number 4,965-988.
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