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Overweight, obesity, and weight reduction in hypertension

Overweight, obesity, and weight reduction in hypertension
Literature review current through: Jan 2024.
This topic last updated: Oct 19, 2021.

INTRODUCTION — Excess weight typically raises blood pressure, and weight loss usually lowers blood pressure [1]. In addition to increasing the risk of hypertension, overweight and obesity increase cardiovascular risk through adverse effects on lipids, insulin resistance, and other cardiometabolic processes. Other adverse effects of overweight and obesity include higher risks of cancer, chronic kidney disease, osteoarthritis, other comorbidities and increased all-cause mortality [2]. The relationship between adiposity and these outcomes is direct and progressive (ie, risk increases as adiposity increases) [3]. (See "Overweight and obesity in adults: Health consequences".)

EFFECTS OF ADIPOSITY ON BLOOD PRESSURE

Epidemiology — Increased adiposity, whether assessed as higher body mass index (BMI), higher weight, or larger waist circumference, is strongly associated with higher blood pressure and development of hypertension [4-7]. In the Nurses' Health Study [4], for example, BMI at age 18 years and at midlife was positively associated with the occurrence of hypertension (figure 1). Weight gain was also associated with increased risk; the relative risks of hypertension in women who gained 5.0 to 9.9 kg and ≥25.0 kg were 1.7 and 5.2, respectively (figure 2).

It is difficult to determine the fraction of hypertension that can be attributed to overweight and obesity. In the Framingham Heart Study, in which participants who were prospectively followed for up to 44 years [8], it was estimated that excess body weight (including overweight and obesity) accounted for approximately 26 percent of cases of hypertension in men and 28 percent in women. In the Nurses' Health Study, in which women were followed for up to 16 years, the fraction of new hypertension cases attributable to overweight and obesity was 40 percent [6]. Hence, while overweight and obesity increase the risk of hypertension, it is well-recognized that hypertension is commonplace in nonoverweight individuals and that factors other than excess weight raise blood pressure.

Pathogenesis — The rise in blood pressure seen with obesity is initially associated with an elevation in cardiac output and a relatively normal systemic vascular resistance (SVR) [9]. However, normotensive individuals with obesity have the same cardiac output but an SVR that is below that of lean normotensives. Thus, the hemodynamic difference between hypertensive and normotensive people with obesity is an elevation in SVR in hypertensives, a difference similar to hypertensive and normotensive lean subjects [9]. In addition, individuals with obesity may have increased activation of the renin-angiotensin-aldosterone system [10].

These hemodynamic alterations, plus abnormalities in lipid and glucose metabolism, appear to be related to fat distribution, not just total body weight [3,11]. Specifically, the risk of obesity-related abnormalities is greatest in those patients with abdominal (also called "upper body" or "central") obesity.

Numerous mechanisms by which overweight and obesity raise blood pressure have been proposed [3,12,13]. It is likely that several mechanisms are operant simultaneously.

Renal injury — Increased renal tubular sodium reabsorption impairs pressure natriuresis and plays an important role in initiating obesity-related hypertension [13]. Potential mediators of abnormal kidney function include (1) physical compression of the kidneys by fat in and around the kidneys, (2) activation of the renin-angiotensin-aldosterone system, and (3) increased sympathetic nervous system activity. Increases in systemic blood pressure and glomerular hyperfiltration subsequently lead to renal injury and chronic kidney disease.

Hyperinsulinemia and insulin resistance — There may be a central role for peripheral insulin resistance, leading to impaired glucose tolerance and hyperinsulinemia, in the development of obesity-related hypertension [14]. Hyperinsulinemia might increase blood pressure through increased sympathetic activity [15], volume expansion from increased renal sodium reabsorption [16], endothelial dysfunction [17], upregulation of angiotensin II receptors [17], and decreased cardiac natriuretic peptide [12].

Sleep apnea syndrome — Patients with obesity often have sleep-disordered breathing and sleep apnea, both of which raise blood pressure [18]. (See "Obstructive sleep apnea and cardiovascular disease in adults", section on 'Hypertension'.)

The prevalence of sleep apnea is approximately 40 percent in moderately overweight individuals and between 40 and 90 percent in adults with obesity [19]. This contrasts with the prevalence of obstructive sleep apnea in the general population (13 to 30 percent among adult men and 6 to 19 percent among adult women) [20]. In this context, it is likely that sleep apnea contributes to elevated blood pressure in patients who are overweight or obese. Activation of the sympathetic nervous system, enhanced aldosterone levels, and increased levels of endothelin by repeated episodes of hypoxia are thought to be responsible in part for the elevation in blood pressure in this disorder [21,22]. (See "Evaluation of secondary hypertension".)

Leptin-melanocortin pathway — The correlation between the serum concentration of leptin, a protein that signals the brain about the quantity of stored fat, and body fat content in humans is approximately 0.9. This and other observations have led to speculation that, with increasing adiposity, leptin acts as a negative feedback "adipostatic" signal to brain centers controlling energy intake (figure 3) [23] (see "Obesity: Genetic contribution and pathophysiology"). There is evidence that leptin may have a role in obesity-related hypertension, particularly via increased sympathetic activity [14].

The melanocortin receptor, which is expressed on downstream targets of leptin- and insulin-responsive neurons, is involved in the regulation of energy balance and may also modulate blood pressure [24]. As an example, the increase in sympathetic nerve activity induced by hyperinsulinemia can be diminished by antagonizing the melanocortin receptor [25].

Genetic susceptibility — There is substantial interindividual variability in the association of adiposity and blood pressure; hence, it is likely that an additional factor or factors modify the relationship of weight with blood pressure. One such factor is genetic susceptibility. Another possibility is that the effects of insulin on blood pressure may in part be mediated by other factors, such as the melanocortin pathway, as noted above.

WEIGHT REDUCTION TO LOWER BLOOD PRESSURE

General approach — Weight loss can lower blood pressure and, along with other lifestyle interventions, is recommended in hypertensive patients who are overweight or obese [26-29].

Options for weight loss in hypertensive patients who are overweight or obese are similar to those in nonhypertensive patients. The approach to weight loss in such patients is presented elsewhere. (See "Obesity in adults: Overview of management".)

Effects of weight loss interventions on blood pressure

Behavioral weight loss (lifestyle modification) — Behavioral weight loss programs primarily emphasize a reduction in calorie intake in order to achieve initial weight loss. Calorie reduction is more important than selecting a diet with a specific macronutrient composition (such as a low-fat or a low-carbohydrate diet) [30,31]. (See "Obesity in adults: Dietary therapy", section on 'Our approach'.)

Increased physical activity is also important, particularly to maintain weight loss, once achieved [32]. However, it is difficult to achieve and sustain calorie imbalance through physical activity alone. (See "Obesity in adults: Behavioral therapy".)

Behavioral weight loss lowers blood pressure in nonhypertensive individuals (and thereby can prevent the development of hypertension). Weight loss also lowers blood pressure when used as initial therapy in hypertensive patients (before drugs are initiated), when used as a cointervention with other nondrug therapies that reduce blood pressure (such as sodium reduction), and when used in conjunction with antihypertensive drug therapy [27,32]. Among those taking antihypertensive medications, behavioral weight loss can permit some patients to withdraw medication and still maintain blood pressure control.

The magnitude of the effect of behavioral weight loss on blood pressures was examined in a systematic review of eight trials of hypertensive patients; the mean reduction in systolic/diastolic blood pressure was 4.5/3.2 mmHg [33]. However, the reduction in blood pressure with weight loss is dose dependent (ie, greater weight loss produces a greater reduction in blood pressure) (figure 4) [30,32-34].

There are a variety of approaches to behavioral weight loss, such as clinician-directed behavioral weight loss, commercial weight loss programs, internet-based programs, mobile phone apps, and wearable physical activity monitors. Our approach to behavioral weight loss is presented elsewhere. (See "Obesity in adults: Behavioral therapy", section on 'Our approach'.)

Weight loss drugs — Weight-reducing drugs have diverse effects on blood pressure, largely dependent on their mechanism of action [35]. Many weight loss medications, particularly sympathomimetic amines, raise blood pressure despite a decrease in weight. However, some weight loss medications (eg, orlistat, which blocks fat absorption, and glucagon-like peptide-1 [GLP-1] agonists) can lower blood pressure. (See "Obesity in adults: Drug therapy".)

Weight loss surgery — Patients with marked obesity may require surgical therapy to produce and maintain an adequate degree of weight loss. (See "Obesity in adults: Overview of management".)

Weight loss surgery (eg, Roux-en-Y gastric bypass) reduces blood pressure at one year, although the effect may not be significantly greater than lifestyle interventions alone [36]. The fall in blood pressure with weight loss is accompanied by a decrease in arterial stiffness [37].

The long-term effects of weight loss surgery on blood pressure were examined in the Swedish Obese Subjects study [28]. Bariatric surgery reduced blood pressure and controlled hypertension at two years compared with no surgery, but there were no differences in blood pressure at six to eight years.

Long-term effects of weight reduction — Contemporary behavioral weight loss programs, on average, achieve approximately 5 percent weight loss by six months. However, most people who lose weight regain some weight over time, possibly because of a persistence of hormonal adaptions to weight loss that reduce total and resting energy expenditure and promote weight (figure 5). These observations suggest that strong mechanisms operate to maintain excess body weight and that weight regain is not merely a loss of motivation to reduce calorie intake and/or increase physical activity. (See "Obesity in adults: Dietary therapy", section on 'Maintaining weight loss' and "Obesity in adults: Overview of management", section on 'Maintenance of weight loss'.)

Long-term effects of weight loss on blood pressure likely depend upon the extent to which weight loss is sustained. In the Framingham Heart Study, the long-term effect of weight loss was evaluated among 623 overweight 30- to 49-year-olds and 604 overweight 50- to 65-year-olds over an eight-year period [38]. Sustained weight loss of 6.8 kg or more was associated with a 22 and 26 percent reduction in relative risk of developing hypertension (defined as 140/90 mmHg) for the two groups, respectively. However, other studies in patients who had sustained weight loss found that, despite initial short-term declines in blood pressure, long-term blood pressure was not reduced [28,39].

The best available evidence suggests that an increase in physical activity should always be added to a reduced calorie intake in order to sustain weight loss [40].

EFFECTS OF ANTIHYPERTENSIVE DRUGS ON WEIGHT AND WEIGHT LOSS — Antihypertensive agents are often necessary if patients cannot maintain a satisfactory blood pressure with lifestyle modification, including weight loss if appropriate. Recommendations for antihypertensive drug therapy in patients with hypertension are discussed in detail elsewhere. (See "Choice of drug therapy in primary (essential) hypertension".)

In general, beta blockers may make weight reduction more difficult. In the Trial of Antihypertensive Interventions and Management (TAIM), for example, the effect of caloric restriction on blood pressure was examined in 878 patients with hypertension treated with atenolol (50 mg/day), chlorthalidone (25 mg/day), or placebo [41]. The mean weight reduction at six months was 3.0 kg among those treated with atenolol compared with 6.9 kg in those treated with chlorthalidone and 4.4 kg among those given placebo. These differences were attenuated but still present at 24 months. How beta blockers impair weight loss is unclear, although reduced sympathetic tone could diminish the basal metabolic rate and/or remove the normal inhibitory effect of catecholamines on appetite.

However, if weight loss is attained, the blood pressure-lowering effect does not depend upon the class of antihypertensive medication taken [42].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Hypertension in adults" and "Society guideline links: Obesity in adults".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topic (see "Patient education: Controlling your blood pressure through lifestyle (The Basics)")

Beyond the Basics topic (see "Patient education: High blood pressure, diet, and weight (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Increased adiposity, whether assessed as higher body mass index (BMI), higher weight, larger waist circumference, or longitudinal weight gain, is strongly associated with higher blood pressure and development of hypertension (figure 1 and figure 2). Excess body weight (including overweight and obesity) accounts for a larger attributable fraction of hypertension. (See 'Epidemiology' above.)

Overweight and obesity may raise blood pressure through a variety of mechanisms, including renal injury, insulin resistance, sleep-disordered breathing, and increased sympathetic activity induced by the leptin-melanocortin pathway. (See 'Pathogenesis' above.)

Weight loss can lower blood pressure and, along with other lifestyle interventions, is recommended in hypertensive patients who are overweight or obese (figure 4). Options for weight loss in hypertensive patients who are overweight or obese (behavioral weight loss, weight loss medications, weight loss surgery) are similar to those in nonhypertensive patients. (See 'Behavioral weight loss (lifestyle modification)' above and 'Weight loss drugs' above and 'Weight loss surgery' above and "Obesity in adults: Overview of management".)

Beta blockers may make weight reduction more difficult to achieve. (See 'Effects of antihypertensive drugs on weight and weight loss' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Norman M Kaplan, MD, who contributed to an earlier version of this topic review.

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