The simplest measurement allowing to determine the health-threatening type of abdominal obesity is to measure the waist circumference. If the waist circumference is greater than or equal to 88 cm in women and greater than or equal to 102 cm in men, then we recognize abdominal (visceral) obesity, characterized by a high content of visceral dysfunction that is toxic to health.
PER BONDING OBORITY AFFECTS THE ATTACKER AND ITS COMBATS
In people with normal body mass, the fat mass does not exceed 20% of the weight in women and 10% in men. In obese people, it is often over 50% of body weight! A high risk of excess abdominal fat is a particular threat. In contrast to fat accumulated in other parts of the body, including the one in the thighs and buttocks - visceral fat tissue releases to the blood an abnormal profile of biologically active proteins - so-called. adipokines (spec. cytokines) and excessive amount of oxidized lipids and lipoproteins. A particular threat is the abnormal profile of proteins related to the metabolism and transport of lipids - such as: lipoprotein lipase (LPL, lipase lipoprotein), cholesteryl ester transfer protein (CETP, cholesterol transfer protein), apolipoprotein E, etc.
Visceral fat metabolites destroy arteries due to:[4,5,6,14] - excessive synthesis of LDL cholesterol (above the safe standard!)
- promoting the growth of HDL cholesterol deficit (below the safe standard!)
- causing adverse changes in the structure of LDL lipoproteins circulating in the blood - so-called small and dense particles - aggressive and toxic to the walls of the arteries.
- from oxidative LDL lipoproteins circulating in the blood - so-called small and dense lipid particles - aggressive towards the walls of the arteries. [4,3,5,6]
Oxidative stress in the arteries
It can be said that the higher the weight of visceral fat, the more it releases oxidized fatty compounds into the blood and too many pro-inflammatory adipokines (some kind of cytokines); and too little anti-inflammatory (e.g., adiponectin). In total - an excess of oxidant lipids and a distorted profile of these metabolites causes chronic oxidative stress in the blood plasma. A derivative of excess lipid oxidants in the blood plasma is excessive synthesis of LDL cholesterol (the so-called bad and chronic inflammation of the endothelium of the arteries). Particularly active in causing oxidative stress are the secretion of inflammatory mediators secreted by fatty celiac cells, as well as blocking the synthesis of autoregulatory compounds that reduce inflammation. For example, leptin should be kept in mind that some cytokines stimulate, for example, the development of fever or directly affect cytotoxicity of the arteries, and the insulin resistance and its pathogenic effect - hyperglycemia - caused by the disrupted profile of adipokines released by dysfunctional tissue The consequence of chronic hyperglycemia is a decrease in the level of basic physiological antioxidants - such as peroxidase dismutase, peroxidase, or glutathione reductase, which promotes radical oxidation of lipids and lipoproteins in the blood plasma and derivatives of this atherosclerotic and degenerative processes in the endothelium of the arteries.
Pathomechanism of arterial damage[4,3,5,6]
The basic cause of damage to the arteries are generated by the abdominal tissue - oxidative stress and its derivative - excessive synthesis of LDL (so-called bad) cholesterol. This cholesterol is a collection of several highly harmful to the arteries of the fraction: VLDL, IDL, LDL, Lp (a)).As we have already pointed out above - it is harmful to the arteries, among others, because it contains smaller and denser chemical particles that are easier to stick and penetrate into the walls of arterial vessels; as well as deeper penetration of the endothelium. The chemo-physical aggressiveness of LDL cholesterol to the arterial walls also causes a false immune alarm because it imitates the presence of toxic antigens. Some signaling apodicins that have an alarming effect on the immune system may be involved in stimulating this immune response. That's why immune cells appear in the blood - including large macrophages - which absorb significant amounts of lipids and the above-mentioned LDL cholesterol particles. As a result, they become "sticky and heavy" and settle on the endothelium of the arteries, creating lipid atherosclerotic lesions. As a consequence of subsequent complex processes of endothelial degeneration, serious damage to the vessel wall and the formation of atherosclerotic plaque occur in this place. We will remind - Atherosclerosis narrows the arteries "inside", which reduces the lumen of the vessel and hinders blood flow. This forces the heart to more frequent cramps and faster blood circulation, which results in hypertension and an increased risk of heart attack or stroke - caused by blocking the patency of the arteries due to thrombosis caused by the detachment of atherosclerotic plaque from the vessel wall. In addition, an indirect consequence of an abnormal profile of metabolites of dysfunctional visceral tissue is the appearance of excess fibrinogen in the blood. And this additionally increases the risk of arterial and pulmonary clots that arise after the rupture of the atherosclerotic plaque - threatening infarction and stroke.
Indicators of pathogenicity of endocrine metabolites of dysfunctional visceral tissue[4,3,5,6]
- deficiency of adiponectin released into the blood contributes to inflammation of the walls of blood vessels - an excess of C-reactive protein in the blood threatens cardiovascular events - excess fibrinogen disturbs blood clotting - leptin levels in the blood promote atherosclerosis - excess blood angiotensinogen constricts blood vessels and causes hypertension
The deficiency of adiponectin accelerates atherosclerosis[4,5,20].
The secretory activity of visceral adipose tissue is characterized by a deficiency of the adiponectin hormone and the release of excess fatty oxygen free acids (FFA). Adiponectin (adiponectin) produced by fat cells acts as an anti-inflammatory factor in blood plasma. Decreasing the level below the physiological norm results in the maintenance of inflammation in the blood vessels. And what is important, the more adipose fatty tissue grows - the less adiponectin is in the body and the more the vasculitis increases. This creates a vicious circle promoting chronic inflammation in adipose tissue and vessels. And as we know, it causes chronic oxidative stress, which promotes the formation of smaller and denser lipid particles. And these, as we already know, more easily penetrate the arterial walls, intensifying the progression of atherosclerosis. It should also be emphasized that a sufficiently high level of adiponectin in the blood positively affects the metabolism of glucose and promotes the optimization of fatty acid production in the liver and muscles. Therefore, adiponectin is credited with strong antiatherosclerotic effects and increases insulin sensitivity. It is worth emphasizing at the moment that the adipose tissue with non-visceral location has an opposite action, i.e. anti-sclerosis! Adiponectin also inhibits the pathomechanism of cholesterol entry into endothelium of the arteries and smooth muscle proliferation [5].
Abdominal fat cells
- adipocytes - release metabolites toxic to the arteries of the arteries
C-reactive protein threatens blood vessels and heart
Adipocytes of dysfunctional fatty gastric tissue release into the blood significant amounts of so-called C-reactive protein which initiates inflammation in the vessels. Until recently, it was thought that the risk of myocardial infarction was mainly due to the size of coronary artery stenosis with cholesterol deposits. Only molecular tests have shown that the main risk factor of infarction is the inflammatory process in the vessels generated by the excess of this C-reactive protein - usually designated by the abbreviation CRP. Inflammation of the vascular endothelium caused by this protein significantly promotes the detachment of atherosclerotic plaques, and this is the direct cause of thrombus and myocardial infarction. That's why almost every second "infarct" does not show the existence of a popular risk factor for MI.1 - what is the increased level of cholesterol in blood above 200 mg / dl. Currently, it is more and more often believed that a better prognosis of the risk of myocardial infarction is too high levels of CRP in the blood. This protein is produced mainly in the liver and fat cells. Therefore, let us emphasize that the increased concentration of CRP is particularly affected by visceral obesity; next to the influence of some chronic diseases, especially diabetes; and age, smoking, the use of certain drugs. The concentration of CRP in normal human blood usually does not exceed 5 mg / l (usually 0.1-3.0 mg / l), but in people with visceral obesity it may be significantly higher. In this context, it is worth emphasizing once again that a significantly elevated CRP level means a significant increase in vascular risk, in particular the risk of myocardial infarction. [20]
Fibrinogen and other proteins associated with the coagulation system[9,12].
Fibrinogen is a protein usually designated with the abbreviation Fb, which participates in the process of forming a vascular clot that threatens infarction and stroke. Although it is produced in the liver - its particularly high concentration in the blood in people with visceral obesity and low physical activity suggests the existence of addiction to dysfunctional visceral tissue. The high excess of fibrinogen in the blood is largely explained by the disturbed profile of lipids and adipopins produced by this tissue. This promotes the increase in the pro-clotting factor - in addition to fibrinogen - factor VII, tissue inhibitor type 1 plasminogen activator (PAI-1), etc. As a consequence, the above-mentioned increase in the risk of cardiovascular events in the form of myocardial infarction, pulmonary infarction, stroke, etc. - resulting from the correlation of high fibrinogen levels in the blood with high levels of LDL and low HDL cholesterol, high lipid content in the form of triglycerides and frequently coexisting hypertension and diabetes.
Leptin increases the risk of cardiovascular events[6,9].
The leptin hormone synthesized and secreted mainly by fat cells (adipocytes) co-regulates normal blood circulation. (In addition to the already discussed role in the regulation of appetite and energy management of the system). The influence of leptin production disorders on the distortion of the normal profile and level of blood lipids as well as on blood clotting is documented. Under the influence of leptin there is lipolysis, i.e. the release of fat in the form of free fatty acids from adipocytes into the bloodstream. The right level of the hormone limits the release of lipids into the blood. As is known, normalization of the level of these lipids in the blood prevents atherosclerotic processes; on the contrary, their excess favors the progression of atherosclerosis.
Visceral obesity and excess angiotensinogen that shrinks blood vessels[18]
It is thought that visceral obesity may cause the release of adipoky profile into the blood that promotes the occurrence of pathogenic changes in the kidney core, resulting in excessive systemic activation of the renin-angiotensin system. Activation of this system results in the additional local synthesis of angiotensin II in adipose tissue and in a manner independent of the production of physiologically necessary doses for self-regulation of blood pressure. The result is the appearance of a significant excess of angiotensinogen in the blood, which is the endogenous compound that most strongly shrinks the arteries and causes high arterial hypertension.
Hypertension degenerates the walls of the arteries, narrowing their light and facilitating the progression of atherosclerosis, and is not treated with a self-perpetuating disease. Seriously, he is at risk of cardiovascular events, including hypertrophy of the left ventricle, myocardial infarction and stroke.
Representative studies of pathological consequences of abdominal obesity[5, 4,6,14,20]
Post-mortem examinations of young victims of traffic accidents have shown that obesity significantly increases atherosclerotic lesions in coronary vessels. The relationship between visceral obesity and the severity of the atherosclerotic process could only be explained in 15% by the classic risk factors - hypercholesterolemia, hypertension, diabetes and smoking. How much abdominal localization of adipose tissue is dangerous for health has been demonstrated in the HOPE study. During 4.5-year follow-up, the group of 8,800 subjects examined the effect of abdominal obesity on the risk of myocardial infarction and cardiovascular deaths. It was found that the risk of these complications increases linearly with increasing waist circumference.Thus, obesity, like age, elevated blood pressure, smoking, hypercholesterolemia, is an independent risk factor for cardiovascular disease. In this obesity proves to be an independent risk factor for such dangerous cardiovascular complications as left ventricular hypertrophy.
