Can Obesity Cause High Blood Pressure?

As your body weight increases, your blood pressure may increase. In fact, being overweight can increase your chances of developing high blood pressure compared to your goal weight.

Can Obesity Cause High Blood Pressure?

As your body weight increases, your blood pressure may increase. In fact, being overweight can increase your chances of developing high blood pressure compared to your goal weight. About 70 percent of adults in the United States are overweight. You can reduce your risk of high blood pressure by losing weight.

A lesser known system that may play a role in obesity and hypertension is the endocannabinoid system. Obesity is associated with increased levels of endocannabinoids in tissues and circulation, 13-15 In particular, the cannabinoid receptor 1 inverse agonists rimonabant and taranabant produce weight loss and improve obesity-related metabolic disorders, suggesting a role for endocannabinoids in obesity and possibly obesity-related hypertension, 13-15 Considerable evidence suggests that obesity-related hypertension is associated with an increased risk of renal failure. The pathophysiological mechanisms associated with the onset of obesity-related hypertension discussed here demonstrate that hyperfiltration, RAS stimulation and obesity-related structural alterations of the kidney set the stage for progressive renal disease. To these factors must be added the effects of glucose intolerance and diabetes mellitus that are associated with obesity, 3-5 Thus, the combination of obesity, diabetes and hypertension is a potent and dangerous mix in terms of renal function.

Indeed, it is possible that the nexus of these three factors is the cause of the current increase in the prevalence of chronic kidney disease. First, the mainstay of therapy must be weight loss. As difficult as weight loss is to achieve and maintain, it should be a primary goal in the treatment of obesity-related hypertension. Weight loss will reverse many of the pathophysiological mechanisms that underpin hypertension.

Although all structural alterations cannot be reversed, at least some can and the risk of further progression can be mitigated, 2,20-22 Obesity predisposes to hypertension and alters the course of hypertensive cardiovascular disease in ways that are only now beginning to be appreciated. The strong association of obesity with diabetes further complicates the picture in patients with these diseases and complicates the design of effective therapeutic interventions. Although difficult to achieve, weight loss should be the first line of therapy. Pharmacotherapy is effective in controlling blood pressure, but must be used judiciously to avoid worsening glucose tolerance.

Newer agents offer the promise of improved control of blood pressure, weight and metabolic parameters, but the true utility of these agents remains to be determined. Continued research into the mechanisms responsible for obesity-related hypertension should allow more targeted use of pharmacological treatment and help explain many of the unknowns in this field, such as the obesity paradox. Just as it helps reduce the likelihood of heart disease, it will also make stroke less likely. If you have type 2 diabetes, your body's blood sugar level is too high.

You don't handle insulin as well as you should. It's a combination of conditions that put you at risk for other problems, such as heart disease, diabetes or stroke. For example, you may be overweight, especially around the waist, and have high blood pressure, high blood sugar and cholesterol problems. This type of arthritis develops when the tissue that cushions bones, called cartilage, wears down with age.

Osteoarthritis is painful and usually affects the spine, knees, hands and hips. In obesity, however, calcium signalling within blood vessels appears to be impaired. This affects vasodilation and contributes to high blood pressure. Obesity, and in particular central obesity, has been consistently associated with hypertension and increased cardiovascular risk.

Based on population-based studies, risk estimates indicate that at least two-thirds of the prevalence of hypertension can be directly attributed to obesity. In addition to hypertension, abdominal adiposity has also been implicated in the pathogenesis of coronary artery disease, sleep apnoea, stroke and congestive heart failure. Obesity is a major cause of hypertension. This risk has been estimated by the Framingham Heart Study, which suggests that approximately 78% of hypertension cases in men and 65% in women can be directly attributed to obesity.

Discovery; Heart; Prevention Obesity is one of the main causes of high blood pressure, also known as hypertension. We have known for years that there is a connection, but the relationship between the two was not well understood - until now. Both increase the risk of heart disease and stroke. Obesity also increases the risk of diabetes, cancer and other deadly diseases.

If we could offer patients a supplement that, combined with a healthy lifestyle, would reduce their risk of hypertension, it would be like offering them a second chance at a longer, healthier life. Although further research is needed before we can use the results of our study in a clinical setting, we are moving forward with ongoing research. Let's look at the results of this study, our next steps and what patients can do right now to reduce their risks. In our research, we fed lab mice a high-calorie, high-fat diet to make them obese.

As expected, the mice developed hypertension. But what we didn't expect to find was a change in the structure of their immunoglobulin G, or IgG, which is the most common type of antibody found in the circulation. Specifically, we found a change in a series of sugar molecules that bind to IgG. The study showed that the amount of a sugar known as sialic acid in the sugar chain that binds IgG decreases as obesity increases.

And as the abundance of sialic acid in the chain decreased, blood pressure increased. These changes were not seen in lean mice fed a typical diet. We determined that changes in the IgG sugar chain have detrimental effects on the cells that form the lining of blood vessels. These cells are part of the body's mechanisms that regulate blood pressure.

We teamed up with Dr Gordan Lauc to see if we could find evidence that this same structural change occurs in humans. We conducted a study in 3,400 volunteers that confirmed that the changes in the IgG sugar chain observed with obesity in mice do, in fact, occur in people. These changes are associated with an increase in a person's systolic blood pressure, the top number seen in a blood pressure reading. We also learned that changes in the structure of the sugar chain also occur as we age, which can make older patients more susceptible to high blood pressure.

From there, we started thinking about how we could use this knowledge to prevent these structural changes from occurring and potentially prevent high blood pressure in our lab mice. We fed another group of mice an obesity-inducing diet, but this time we added a natural chemical known as ManNAc, which is produced during the body's production of sialic acid, to their drinking water. ManNAc is already being studied in patients with hereditary inclusion body myopathy (HIBM), a rare genetic disease that causes reduced sialic acid production. Our research showed that mice taking the supplement did not develop high blood pressure.

Their sugar chain structure remained normal, although they remained obese. What's more, we have data indicating that the supplement may also help prevent the development of diabetes, another important risk factor for heart disease. There is still much work to be done in the field of obesity prevention and treatment. And we are delighted to have the opportunity to potentially help a large volume of patients avoid the hypertension that often complicates obesity.

That said, it is important to emphasise that the dietary supplement used in this study did not cause the mice to lose weight. Rather, it served as a protective agent against damage, but did not address the overall concern. This is similar to how cholesterol medication can prevent plaque build-up, to some extent, even if a patient does not reduce their cholesterol intake. Lifestyle is important, and obesity is a difficult condition to change.

In fact, recent research has shown that obesity is associated with reduced brain tissue volume and function, which can make weight loss difficult. Take a brief survey to find out if bariatric surgery can help you achieve your weight loss goals. In terms of blood pressure, consider making small changes in collaboration with your doctor to achieve a healthy blood pressure. Your doctor may recommend taking blood pressure medication and monitoring your blood pressure at home to get an accurate reflection of your daily numbers.

Researchers and public health officials around the world are joining together to combat the growing obesity epidemic. My colleagues and I at UT Southwestern are focused on preventing some of the serious complications of obesity. Ultimately, we hope our findings will help break the link between obesity and high blood pressure, giving patients one less thing to worry about as they work to improve their health. Next article Improving pre-eclampsia care with new research and prevention strategies Discovery; Your Pregnancy Matters Discovery; Men's Health Cancer; Discovery Brain; Discovery Heart.

Together, PTP1B and SOCS3 could play an important role in modulating the appetitive, metabolic and cardiovascular actions of leptin and contribute to the development of leptin-selective resistance in obesity. The most important thing to remember is that obesity is associated with hypertension, and hypertension is associated with numerous other diseases that can affect overall health and life expectancy. Blockade of the MC4Rs markedly reduced BP in spontaneously hypertensive rats, a non-obese model of hypertension associated with increased SNS activity. The importance of Ang II in stimulating renal NaCl reabsorption and mediating obesity hypertension is supported by experimental animal studies demonstrating that Ang II receptor blockade or ACE inhibition attenuates sodium retention, volume expansion and increased BP in obesity.

For example, glomerular hyperfiltration early in obesity may be replaced by a gradual decrease in glomerular filtration rate because renal injury and nephron loss occur in association with prolonged hypertension, diabetes mellitus and dyslipidaemia. The Framingham Heart Study, a famous 44-year study, estimated that excess body weight (including overweight and obesity), accounted for approximately 26 per cent of hypertension cases in men and 28 per cent in women, and approximately 23 per cent of coronary heart disease cases in men and 15 per cent in women. Activation of LepRs in different regions of the CNS may also contribute to differential control of cardiovascular and metabolic function in obesity. However, further studies are needed to determine how these pathways are regulated in obesity and whether their differential activation contributes to selective leptin resistance.

In contrast to multiple studies in dogs, rabbits and humans suggesting that renal compression contributes to obesity-related hypertension, it does not appear to be an important factor in rodents. Furthermore, the rapid increase in CKD over the past 3 decades has paralleled the increase in obesity and there is evidence that obesity may be an independent risk factor for CKD, beyond its effects in causing hypertension and diabetes mellitus. Obesity has been linked to a number of heart conditions, including coronary heart disease, heart failure and type 2 diabetes mellitus, along with high blood pressure. Obesity is a term used to describe people with a body mass index (BMI) greater than 30, and is a major risk factor for high blood pressure.

There is a clear need to develop a comprehensive strategy to manage the growing number of overweight and obese individuals in the community.

Leave a Comment

Your email address will not be published. Required fields are marked *