Obesity—Not Just a Cosmetic Problem

Dear blog readers, dear Peak customers, the issues of being overweight and obesity are increasingly casting a shadow over our society. Many of today’s lifestyle-related diseases stem from a lifestyle that causes body fat levels to rise dramatically.

For athletes, stored fat is essentially excess weight that accumulates mainly around the hips, abdomen, buttocks, or thighs. Many of us have declared war on these fat deposits—mostly for aesthetic reasons—and want to get rid of them or prevent them from forming in the first place. When it comes to “excess body fat,” there is both a cosmetic issue and, more importantly, a health problem that should not be underestimated. For me, this was reason enough to take a closer look at this topic. My goal was to shed light for you, dear readers, on some connections between body fat and health that may not be obvious at first glance.

The Development of Obesity and Its Effects

Causes of Obesity

Obesity is the term used to describe excessive body fat and represents the stage beyond being simply overweight. Several factors can contribute to its development. The main causes include genetic factors, lack of physical activity, certain medical conditions such as hypothyroidism, and a high-calorie diet (exceeding one’s energy needs).

Obesity and Its Effects

Unfortunately, it is not enough to simply acknowledge that obesity exists and assume that, aside from its visual appearance, it has no further negative effects.

Quite the contrary:

A whole range of diseases can be attributed to obesity.

The main problem is insulin resistance.

A major problem associated with obesity is the development of insulin resistance in muscle cells (primarily skeletal muscles). The muscle cell’s receptor no longer responds sensitively enough to insulin and consequently has difficulty allowing glucose into the cell. The glucose remains in the blood, causing the pancreas to try—by force, so to speak—to push the nutrients into the cell by producing excess insulin.

WE ARE IN THE PREDIABETIC STAGE

An untreated prediabetic condition leads to the development of type 2 diabetes, hypertension (high blood pressure), and dyslipidemia (abnormal lipid profile in the blood)

Adipose Tissue as an Endocrine Organ

This naturally raises the question of how an increase in body fat can have such an effect on metabolism. This is due to the fact that our adipose tissue, as an endocrine organ, influences metabolism by releasing certain hormones.

Metabolic Syndrome and Obesity

The insulin resistance caused by obesity promotes the development of what is known as metabolic syndrome. This is the “deadly quartet”—a combination of obesity, lipid metabolism disorders, high blood pressure, and insulin resistance.

Abdominal-visceral fat deposits are considered particularly dangerous. They have the greatest impact on energy metabolism. We’ll learn why this is the case later on.

What Is Abdominal-Visceral or Gluteal-Femoral Fat?

Distinction

The term “abdominal-visceral” refers to fat “stored in the free abdominal cavity,” which surrounds our organs and the digestive system. It is not directly visible but is noticeable as an enlargement of the abdominal volume.

“Gluteal-femoral” refers to fat deposits “on the hips, thighs, or buttocks.”

Subcutaneous fat is the third group. Since it is stored under the skin, it is the most visually noticeable. Metabolically speaking, however, it plays a rather passive role.

Waist circumference is routinely measured to assess the risk of obesity. It is now considered a more meaningful measure of obesity than BMI or the waist-to-hip ratio.

What happens when there is an excess of visceral fat?

An increase in visceral fat deposits leads to the increased release of free fatty acids into the bloodstream via the liver. This triggers further metabolic effects.

First, there is increased β-oxidation of free fatty acids in the skeletal muscles, resulting in an increased incidence of glucose intolerance.

Second, the production of VLDL by the liver increases, leading to hyperlipidemia—that is, an increased level of lipids in the blood (blood fats).

Ultimately, the breakdown of insulin in the liver is reduced, resulting in hyperinsulinemia—an increased presence of insulin in the bloodstream.

Why is visceral fat, of all things, so dangerous?

It is a fact that conditions such as type 2 diabetes or cardiovascular diseases occur more frequently in people with abdominal-visceral obesity.

Gender Differences

Men are genetically predisposed to develop this type of fat deposit more readily. The gynoid fat distribution, which is more common in women and involves fat deposits in the buttocks and on the thighs, carries a significantly lower risk.

Metabolic Activity of Adipose Tissue

The reason for these differences lies in the fact that the two fat distribution patterns have different metabolic effects.

Abdominal-visceral adipose tissue is more sensitive to lipolytic hormones—such as catecholamines, growth hormone, testosterone, and estrogen—than gluteal-femoral tissue; that is, these hormones release fatty acids from the cells into the bloodstream more rapidly. We have already explained above the consequences of an excessive supply of free fatty acids without a corresponding metabolic need.

This is likely due to an increased abundance of β-adrenergic receptors and a reduced abundance of antilipolytic α-adrenergic receptors in visceral fat cells.

Conclusion

Secretory Activity of Adipose Tissue

In addition to the aforementioned varying sensitivity of adipose tissues to certain glandular hormones, our adipose tissue (again, primarily the visceral component) produces its own biologically active compounds and thus exerts a significant influence on metabolism. These effects further promote the development and persistence of metabolic syndrome.

Adipose Tissue and Estrogen

Along with the ovaries and the placenta, adipose tissue is the most important producer of estrogen in women. The stromal cells of adipose tissue responsible for this have relatively high activity of the enzyme aromatase, which is required for estrogen biosynthesis from androgens. In the gonads (testes or ovaries), so-called gonadotropins (sex hormones) act as inducers (triggers) of enzyme activity.

In adipose tissue, growth factors—primarily platelet-derived growth factor (PDGF) and glucocorticoids—are jointly responsible for this process.

For overweight women, this means, on the one hand, that estrogen reduces the risk of osteoporosis; however, it also increases the risk of developing estrogen-dependent tumors, such as endometrial (uterine) or breast cancer.

Adipose tissue, high blood pressure, and angiotensinogens.

High blood pressure

Adipose tissue is, after the liver, the second most important organ for the production of angiotensinogen. Angiotensinogen is a protein involved in blood pressure regulation. It influences the renin-angiotensin-aldosterone system (RAAS). Obesity leads to increased production of this protein and, consequently, to a predisposition to hypertension.

The primary trigger for obesity-mediated hypertension is sodium retention. In addition to the aforementioned activation of the RAAS, this is caused by activation of the sympathetic nervous system (mediated, among other things, by leptin) and changes in the kidneys due to increased intrarenal pressure resulting from visceral fat accumulation.

Further Effects of Angiotensinogen

It is speculated that angiotensin II, formed from angiotensinogen, may lead to the formation of preadipocytes, which in turn promote the formation of new fat cells. Furthermore, angiotensinogen promotes local insulin resistance, inhibits cell division and cell development, and, via angiotensin II, promotes the production of inflammatory mediators.

Obesity promotes high blood pressure, insulin resistance, and possibly the formation of new fat cells.

Adipose tissue and TNF-α.

Studies have shown that obesity leads to increased production of tumor necrosis factor-alpha (TNF-α). This is present as an inflammatory marker in numerous tissues and is secreted, among other places, in adipose tissue. Fat cell volume correlates with the amount of TNF-α and the expression of its receptors. It inhibits the formation of new fat cells, impairs insulin action (insulin resistance), inhibits glucose transport, stimulates lipolysis, and is therefore partly responsible for insulin resistance in skeletal muscle.

Obesity directly promotes insulin resistance

Adipose Tissue and Leptin

Leptin is a hormone produced in adipose tissue that directly influences the regulation of hunger and satiety. It is released in proportion to fat mass and, depending on its binding to the leptin receptor in the hypothalamus, leads to a reduction in the sensation of hunger or an increase in the sensation of satiety. Leptin is secreted according to a specific circadian rhythm. Significantly higher leptin levels are observed at night.

The goal of this regulation is to maintain a balanced body fat content, achieved through an increase or decrease in adipose tissue mass depending on nutritional status.

Interesting.

Relationship Between Leptin and Other Neurotransmitters

A high level of insulin in the blood does not cause any short-term change in leptin secretion. However, prolonged hyperinsulinemia causes leptin concentrations to rise. Glucocorticoids and estrogens also increase leptin synthesis. Androgens and catecholamines, on the other hand, tend to lead to a decrease in leptin levels.

Leptin and Thermogenesis

Changes in leptin levels affect not only eating behavior but also thermogenesis—that is, the dissipation of energy in the form of heat production as part of metabolic activity.

An excess of food normally leads to increased thermogenesis via rising leptin levels. During fasting, thermogenic activity decreases as leptin levels drop.

Obesity and Leptin—So Why Do We Still Gain Weight?

The system described above is sophisticated and should, in theory, prevent a pathological excess of body fat from developing in the first place. Studies of obese individuals also show that their leptin levels are generally high.

The reason obesity persists is that leptin receptors in the brain become desensitized. Leptin secreted by fat cells thus leads—depending on the degree of resistance—to satiety signals being sent less quickly or not at all, and thermogenesis does not increase in activity either.

In obesity, the regulation of hunger, satiety, and thermogenesis functions only to a limited extent or not at all. Despite an existing oversupply of food, no signal of satiety is sent.

Adipose Tissue and Adiponectin

The hormone adiponectin is also produced exclusively in fat cells. It possesses vasodilatory, anti-inflammatory, and anti-atherosclerotic properties. Elevated adiponectin levels are directly correlated with HDL cholesterol levels and inversely correlated with BMI, triglyceride levels, and the levels of certain inflammatory markers.

A large proportion of obese individuals have reduced adiponectin levels.

This reduction is one of the most important factors leading to type 2 diabetes in people with obesity.

Adipose Tissue and Resistin (Resistance to Insulin)

Resistin is a protein produced by adipocytes during adipogenesis (fat tissue formation) and released into the bloodstream. Resistin levels in the blood are elevated in obesity and diabetes, suggesting that it plays a role in the development of insulin resistance. In addition, resistin impairs the development (differentiation) of muscle cells.

Adipose tissue, cytokines, and inflammatory factors.

Obesity leads to increased production of inflammatory markers such as CRP or interleukin 6 (IL-6). These have proatherosclerotic effects, as they, among other things, promote platelet aggregation. IL-6, in particular, is a recognized risk factor for heart attack.

PAI-1 (plasminogen activator inhibitor-1)

PAL-1 is elevated in obesity and leads to an increased tendency toward blood clotting (coagulation disorder). This indicates a link between obesity and blood clotting disorders. PAL-1 is the primary trigger for the body’s natural breakdown of blood clots (fibrinolysis) and can therefore be considered an independent risk factor for thromboembolism (vascular occlusion caused by a dislodged thrombus).

Obesity leads to blood clotting disorders

Pharmacological Treatment of Obesity

Obesity and, consequently, metabolic syndrome can be treated with medication.

The ACE inhibitor ramipril, for example, improves insulin sensitivity and glucose uptake by adipocytes.

Glitazones, an oral antidiabetic medication, are used in the treatment of type 2 diabetes. It increases glucose uptake by cells and promotes the formation and differentiation of fat cells. This improves the physiological function of insulin, lowers blood sugar, and reduces insulin resistance, which in turn decreases the amount of insulin required and relieves the pancreas. Glitazones also block the release of substances that promote insulin resistance, such as TNF-α or free fatty acids, thereby holistically improving the metabolic state in the target cells. Interestingly, glitazones induce a kind of “remodeling” of adipose tissue. Old, insulin-resistant fat cells are induced to undergo apoptosis (programmed cell death), while at the same time new, slender, insulin-sensitive adipocytes are formed. Although antihypertensive and lipid-lowering properties are also present, they are not pronounced enough to allow for the discontinuation of concomitant therapy with antihypertensive and lipid-lowering agents in patients with diabetes.

Liposuction

Liposuction is of very limited use in treating diseases caused by obesity. Only subcutaneous adipose tissue is removed, which is far less metabolically and secretorily active than its visceral counterpart. Triglyceride levels, blood sugar, and cholesterol levels usually remain unchanged.

Summary

Due to its pronounced metabolic and secretory activity, visceral adipose tissue in particular must be regarded as a significant risk factor for obesity-associated diseases with an inflammatory component. As we have seen, adipocytes influence lipid and carbohydrate metabolism and, in turn, produce a variety of their own signaling molecules that affect health.

Diseases such as type 2 diabetes, atherosclerosis, hypertension, heart attacks, and even certain types of cancer can thus be attributed to obesity.

Keeping an eye on one’s body weight and body fat percentage is important not only for aesthetic reasons. Far more “important” is the health aspect underlying a healthy body composition.

I would therefore like to conclude my remarks with the recommendation to use a healthy, balanced diet and sufficient exercise to overcome existing obesity—or to prevent excess fat accumulation from occurring in the first place. Medication should only be used as a supplementary measure, and the “easy route” of liposuction is useless, at least when it comes to diseases related to body fat.

The most important thing is a healthy lifestyle, and this is precisely what I urge all readers to adopt. If you don’t feel up to this challenge on your own, there are doctors, nutritionists, or personal trainers you can turn to.

Follow the example of athletes and declare war on excess fat deposits. Thanks to my explanations, you now know your opponent very well.

Best regards,

Yours,

Holger Gugg

www.body-coaches.de