Obesity and hypertension -
To recover from obesity and related conditions, doctors recommend that adults and children maintain a healthy BMI for their age and gender. Treatment for obesity and hypertension begins with making key lifestyle changes. Other effective options may include medications and, as a last resort, surgery.
For children, doctors and researchers suggest focusing on weight management and education. Maintaining a moderate weight and managing your blood pressure can contribute to you living a longer, healthier life. Our experts continually monitor the health and wellness space, and we update our articles when new information becomes available.
Obesity is a health condition that can raise your risk of diseases like diabetes. Learn about childhood obesity, risk factors, classes, and treatment. This article….
Visceral fat is located near vital organs like the liver and stomach. Find out about diagnosis, the complications it may cause, and more. Saying that obesity is only a matter of willpower is nonsense.
There are many factors involved, both internal and external, that affect our eating…. Obesity can affect nearly every system in the body.
Here are the long-term effects of obesity, so you can get started with a healthier lifestyle. In a study of older adults living in long-term care, researchers randomly assigned facilities to use either a potassium-rich salt substitute or….
A recent study has found that tai chi was more effective compared to aerobic exercise in lowering blood pressure among prehypertension patients. Portopulmonary hypertension is a progressive complication of high blood pressure in the veins that lead to your liver.
Renal parenchymal disease is a group of conditions that can develop in the parts of your kidney that filter your urine and produce the hormone…. According to new research, adding salt at mealtime, using a salt shaker for example, is associated with an increased risk of developing kidney disease,.
A Quiz for Teens Are You a Workaholic? How Well Do You Sleep? Health Conditions Discover Plan Connect. How Obesity Can Increase Your Risk for Hypertension and What You Can Do About It. Medically reviewed by Angelica Balingit, MD — By Jennifer M. Edwards on April 28, Can obesity cause hypertension?
Ethnicity, race, and BMI Scientists are beginning to understand the limits of BMI as a health tool. Was this helpful?
Obesity-induced hypertension. How is hypertension treated in people with obesity? Hypertension in children with obesity. How we reviewed this article: Sources.
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Apr 28, Written By Jennifer M. Share this article. Read this next. Obesity: What You Need to Know Obesity is a health condition that can raise your risk of diseases like diabetes. READ MORE. Is BMI an Accurate Predictor of Health? By Katey Davidson, MScFN, RD, CPT. Visceral Fat.
Medically reviewed by Danielle Hildreth, RN, CPT. By Kris Gunnars, BSc. How Does Obesity Affect the Body? Medically reviewed by Angela M. Bell, MD, FACP. Want to Lower Your Blood Pressure? Tai Chi May Work Better Than Aerobics A recent study has found that tai chi was more effective compared to aerobic exercise in lowering blood pressure among prehypertension patients.
Overview of Portopulmonary Hypertension. To date, leptin has been the most thoroughly studied. Leptin is a amino acid peptide that promotes weight loss by reducing appetite and by increasing energy expenditure through sympathetic stimulation to thermogenic tissue.
The absence of leptin or a mutation in the leptin receptor induces hyperphagia and obesity in both rodents and humans. Circulating levels of leptin parallel fat cell mass. Blood pressure and leptin are modestly correlated in normotensive and hypertensive individuals after adjustment for fat mass.
Increased sympathetic outflow is a putative mechanism by which leptin may increase arterial pressure. Leptin activates the sympathetic nervous system both by centrally mediated effects on the hypothalamus and by local peripheral actions. High circulating levels of leptin reportedly account for much of the increase in renal sympathetic tone observed in obese human subjects.
Although acute infusion of leptin produces natriuresis in normotensive rats, the natriuretic effect is attenuated in hypertensive and obese Zucker rats, possibly as a consequence of leptin resistance. Preliminary evidence suggest that other adipocyte-derived peptides may also affect arterial pressure.
Circulating adiponectin levels are decreased in obesity-induced insulin resistance, 70 and some studies suggest that adiponectin is protective against hypertension through an endothelial-dependent mechanism.
Insulin resistance may be a link between obesity and hypertension. Obesity is associated with resistance to insulin-stimulated glucose uptake and hyperinsulinemia, and weight loss increases insulin sensitivity. Release of free fatty acids due to excess adipose tissue lipolysis in upper body obesity contributes to the metabolic abnormalities and possibly to the vascular dysfunction associate with upper body obesity.
However, many of these studies have been conducted at supraphysiologic concentrations of free fatty acids, and consequently these observations should be considered tentative. In several rodent models of experimental hypertension, hypertension can be ameliorated or prevented by chemically diverse agents that increase insulin sensitivity or have a primary lipid-lowering effect e.
Lifestyle interventions for treatment of obesity include emphasis on nutrition, physical activity, and behavior modification. The increasing prevalence of obesity, including childhood obesity, has stimulated interest in developing and evaluating strategies for obesity prevention.
Effective strategies for preventing and controlling overweight and obesity over a short term have been implemented in worksite settings. These interventions have combined instruction in healthier eating with a structured approach to increasing physical activity in the workplace.
The majority of studies were of short term. Nearly all studies resulted in some improvement in diet and physical activity. Some studies that focused on either diet or physical activity alone, but not in combination, had a small but positive impact on BMI.
In two small towns in France, a comprehensive and innovative community-based program to prevent obesity in schoolchildren involved the mayor, teachers, health-care providers, food providers, sports associations, the media, scientists, and various branches of town government.
Families were offered cooking workshops and families at risk were offered individual counseling. Between and , the prevalence of overweight in children had fallen to 8.
This total community approach is now being extended to towns in Europe under the name EPODE Ensemble, prevenons l'obesite des enfants Together, let's prevent obesity in children.
Several different diets have been advocated for the treatment of obesity e. As recently reviewed, 83 behavioral packages may include food diaries and activity records, control of stimuli that activate eating, slower rate of eating, goal setting, behavioral contracting and reinforcement, nutrition education, meal planning, social support, cognitive restructuring and problem solving.
Incorporation of increased physical activity e. Nevertheless, the recidivism rate is high. Two medications are currently available in the United States for the treatment of obesity: i orlistat—an inhibitor of pancreatic lipase that reduces intestinal digestion of fat and ii sibutramine—a serotonin—norepinephrine reuptake inhibitor.
In adolescents, metformin has recently been shown to cause a small but statistically significant decrease in BMI when added to a lifestyle intervention program. In addition to weight loss and other lifestyle modifications, many if not most obese, hypertensive patients ultimately require treatment with one or more antihypertensive agents for blood pressure control.
There is little clinical trial data to indicate that any one class of agents is superior to others. Most guidelines do not recognize obese patients as a special population, and do not make specific recommendations for the pharmacologic treatment of hypertension associated with obesity.
The general principles of pharmacotherapy for obese patients are not different from nonobese patients, but there are a few caveats. The capacity of thiazide diuretics to lower blood pressure in obese hypertensive patients is well established, 92 and the adverse metabolic effects of diuretics insulin resistance, dyslipidemia, hypokalemia are dose related.
ACE inhibitors, and possibly angiotensin II receptor blockers, increase insulin sensitivity and reduce diabetes risk. The antihypertensive potencies of lisinopril and hydrochlorothiazide were reportedly similar in a study of predominantly white, obese, hypertensive patients.
β-Blockers may more effectively decrease blood pressure in obese than in lean hypertensives, perhaps because they decrease cardiac output and plasma renin activity, both of which are increased in obese patients.
However, β-blockers may be associated with weight gain and have negative effects on glucose metabolism. In the final analysis, similar to treatment of all hypertensive patients, combinations of agents with complimentary mechanisms may be required to achieve blood pressure goals.
Selection of drugs should be individualized, taking into account the severity of hypertension, other CVD risk factors, comorbid conditions, and practical considerations related to cost, side effects, and frequency of dosing. Obesity-related hypertension is a multifactorial phenotype determined by the interaction of genes and environments.
However, currently identified genomic factors account for only a small percent of the heritable risk of this phenotype.
The association of hypertension with obesity is primarily related to visceral obesity, which in turn is associated with insulin resistance and dyslipidemia. Lifestyle and pharmacologic approaches for treating obesity-related hypertension should address overall CVD risk, not simply hypertension.
More work is required to identify culturally sensitive strategies for obesity prevention and their impact not only on body weight, but also on blood pressure, the metabolic phenotypes associated with obesity, and subsequent CVD.
Although several mechanisms have been identified that may account for elevated arterial pressure, currently, there is no compelling evidence to indicate that any one class of antihypertensive agents is particularly advantageous for the treatment of obesity-related hypertension.
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Obesity is most accurately defined as the abnormal or excessive accumulation of adiposity to the extent that health may be impaired 2. However, the methods used to directly quantify body fat are cumbersome, expensive, and not routinely available in daily clinical practice 8.
For this reason, the body mass index BMI; body weight in kg divided by height in m 2 is the most commonly used surrogate marker of adiposity 9. The WHO defines normal weight as BMI However, BMI does not differentiate between lean muscle and fat mass and does not provide any indication of the distribution of body fat.
This is an important consideration as evidence suggests that visceral or retroperitoneal fat i. Therefore, alternative anthropometric measures of adiposity such as waist circumference WC and waist-to-hip ratio WHR have also been utilized This has led to the development of ethnicity-specific cut-offs for BMI, WC and WHR in non-white individuals as predictors of cardiometabolic risk 18 , The deleterious consequences of obesity include an increased risk of death from cardiovascular disease CVD 20 , type 2 diabetes mellitus T2DM 21 , cancer 22 , and chronic kidney disease Hypertension is currently the leading risk factor for morbidity and mortality worldwide, resulting in million disability-adjusted life years and The relationship between obesity and hypertension is well described in children and adults and across both sexes 5 , In concordance with these observations, it has been shown that even modest reductions in weight can decrease BP in hypertensive patients.
For example, in the TOHP II Trials of Hypertension Prevention, phase II study, in which overweight and obese adults were randomized to a weight loss intervention group versus usual care, participants who maintained a weight reduction of 4.
The putative mechanisms underlying obesity-related hypertension are complex and entail interactions between renal, metabolic, and neuroendocrine pathways Figure 1. These mechanisms include: sympathetic nervous system SNS overactivation, stimulation of the renin-angiotensin-aldosterone system RAAS , alterations in adipose-derived cytokines such as leptin, insulin resistance, and structural as well as functional renal changes.
Increased activity of the SNS is believed to play an important role in the development of obesity-related hypertension Physiological manifestations of SNS overactivity include elevations in heart rate, cardiac output, and renal tubular sodium reabsorption; these occur as a direct result of α-adrenergic and β-adrenergic receptor stimulation and indirectly through activation of other systems, such as the RAAS, which is described below.
Muscle SNS activity, as measured by microneurography, increases with even modest weight gain 35 and appears to be highest in patients with both obesity and hypertension Renal SNS activity, as measured by the norepinephrine spillover method, is also elevated in obese individuals Notably, the increased SNS activity associated with obesity is not uniformly distributed across all organs, and predominantly affects the kidneys and skeletal muscle 6.
On the other hand, the chronic elevation in resting heart rate observed in obese individuals is thought to be mediated by reduced parasympathetic tone rather than increased SNS activity 7. Furthermore, SNS overactivity is not ubiquitously observed in all obese patients, and appears to be influenced by factors such as visceral rather than subcutaneous adiposity, ethnicity, and sex For instance, Native American Pima Indians have a high prevalence of obesity, but relatively low rates of hypertension 39 , This suggests that SNS activity is a key determinant of obesity-related hypertension and that sympathetic tone in the presence of excess adiposity is influenced by factors such as ethnicity.
Causative mechanisms of SNS activation in obesity include abnormal adipokine secretion from adipose tissue; stimulation via the RAAS; insulin resistance; and baroreceptor dysfunction 6 , 7 , Furthermore, obesity frequently coexists with obstructive sleep apnea OSA , which results in chronic intermittent hypoxia and leads to the activation of carotid body chemoreceptors that reflexively upregulate SNS activity Some of these mechanisms may also contribute towards the development of hypertension in an SNS-independent manner, which will be discussed below.
Despite the state of volume expansion and sodium retention associated with obesity, which would normally suppress the RAAS, several reports indicate that obese individuals have higher levels of plasma renin activity, angiotensinogen, angiotensin-converting enzyme ACE , and aldosterone compared to lean individuals 44 , Activation of the RAAS leads to increased formation of angiotensin II, which induces systemic vasoconstriction and simulates the production of aldosterone from the adrenal cortex.
Both angiotensin II and aldosterone increase renal tubular sodium reabsorption and water retention, resulting in intravascular volume expansion and hypertension. Several mechanisms are responsible for RAAS activation in obesity. It has been recognized that a bidirectional interaction exists between the SNS and the RAAS, such that the RAAS increases sympathetic tone and, reciprocally, the SNS activates the RAAS This drives the release of renin from the juxtaglomerular cells of the kidney.
Renin secretion is also upregulated secondary to physical compression of the kidney by excess visceral and retroperitoneal fat 7. This leads to decreased renal tubular blood flow and sodium delivery, which is sensed by the macula densa, which in turn stimulates renin secretion through tubuloglomerular feedback Adipocytes also possess their own intrinsic RAAS and appear to be major producers of angiotensinogen and angiotensin II Interestingly, mice with adipocyte-specific deficiency of angiotensin are protected from the development of hypertension, despite being fed an obesogenic diet Additionally, adipocytes have been shown to secrete mineralocorticoid-secreting factors that stimulate aldosterone production from the adrenal gland independently of angiotensin II 50 , The role of RAAS activity in the pathogenesis of obesity-related hypertension in humans is supported by the finding that pharmacologic blockade with ACE inhibitors ACEIs , angiotensin II receptor blockers ARBs , and mineralocorticoid receptor antagonists MRAs significantly lowers BP in obese patients 52 - Increased renal sodium reabsorption and volume expansion play an important role in initiating hypertension associated with obesity.
As mentioned above, excess visceral and retroperitoneal adiposity can lead to mechanical compression of the kidneys.
In addition, the accumulation of peri-renal fat may induce inflammation and expansion of the renal medullary extracellular matrix, which leads to compression of the renal medulla This results in diminished renal tubular blood flow, which prolongs the duration of time in which fractional sodium reabsorption can occur.
Consequently, decreased sodium delivery distally to the macula densa stimulates a feedback-mediated reduction in renal afferent arteriolar resistance, an increase in renal blood flow, and stimulation of renin secretion from juxtaglomerular cells 7.
Website performance optimization services of obesity are rising in htpertension Obesity and hypertension and the rest Anti-cellulite body wraps the world, causing hypergension diseases like stroke, type Obeesity diabetes, osteoarthritis, Anti-cellulite body wraps disease, and hypertension high blood pressure. BOesity blood pressure itself can lead to Anti-cellulite body wraps attacks and Obewitymaking obesity one of the leading risk Natural prebiotics supplements for illness and death. Understanding obesity and hypertension and how they are linked is the first step to lowering your risk and protecting your health. We make it easy for you to participate in a clinical trial for High blood pressure, and get access to the latest treatments not yet widely available - and be a part of finding a cure. Hypertension is the medical term for high blood pressure. Blood pressure is the amount of force the blood exerts against the walls of the arteries. It is normal for blood pressure to rise and fall slightly throughout the daybut blood pressure is considered high when it stays elevated for too long. Obesity Obssity overweight are common Obesity and hypertension in anv Anti-cellulite body wraps States. According to the National Hypertensiln, Lung, and Blood Institute, Farro grain uses 75 Lean mass tracking of all U. adults over 20 years old fall into one of the two categories. Obesity generally describes an increase of fat cells in the body or an increase in their size. It can be caused by:. Obesity is a cause for concern as it increases your risk of many health conditions, including heart disease, diabetes, and hypertension.
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