If your 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 obesity, which is a common cause of the so-called. metabolic syndrome which consists of specific symptoms of diabetes and hypertension, and in the blood excess of oxidized lipids toxic to the arteries, including bad LDL cholesterol.
Definition of metabolic syndrome
At the beginning, let us remind you that the metabolic syndrome is not a specific disease, but a well-defined set of symptoms and metabolic causes, whose combined occurrence means a high risk of other dangerous diseases. Generally, it can be said that it is a co-occurrence of such conditions as obesity and hypertension with disturbed metabolism of glucose metabolism, excessive triglyceride concentration in blood and simultaneous deficiency of "good" HDL cholesterol.
We recognize the metabolic syndrome when three of the following 5 disorders occur simultaneously: [4,7,10] 1 / Obesity, including especially dangerous visceral obesity 2 / Disturbance of glucose tolerance, which means pre-diabetic status 3 / Increased level of fat in blood - so-called triglycerides - which means atherosclerosis 4 / Too low level of "good cholesterol" HDL - which means atherosclerosis risk 5 / Elevated arterial pressure - which means a threat of cardiovascular events
Detailed criteria for the diagnosis of a person with metabolic syndrome:
(Criteria according to the International Diabetes Association (IDF) from 2005)
Waist circumference in a woman - equal to or greater than 88 cm; in a man equal to or greater than 102 cm;
and in addition if you experience at least two of the following adverse health conditions: - fasting blood glucose level equal to or higher than 100 mg / dl (or treatment of type 2 diabetes) - triglyceride level in blood equal to or higher than 150 mg / dl (or treatment of dyslipidemia) - concentration of the so-called good cholesterol (HDL) in the blood - in women lower than 50 mg / dl, while in men lower than 40 mg / dl - blood pressure equal to or higher than 130/85 mm Hg (or treatment of hypertension).
Excess glucose in the blood leads to diabetes
Hormones produced by adipose tissue may disturb the production of insulin. In response to the variable level of glucose and insulin in the blood - adipocytes secrete actively biological substances with the role of hormones called adipokines - such as: adiponectin, apelin, leptin, visfatin, resistive, etc. These substances are characterized in that, depending on their concentration in blood may stimulate or block the production and secretion of insulin from the pancreas. It is believed that apelin and visfatin are the most dependent on pancreatic secretion and effective insulin action. In total, the hormones secreted by adipose tissue, depending on their concentration in the blood, may contribute to insulin sensitivity or vice versa to insulin resistance of tissues. In the case of abdominal (visceral) obesity, fat cells - adipocytes - strongly secrete adipokines that disturb the production of insulin by the pancreas, which consequently unimoblows cellular glucose burning. Blocking pancreatic insulin production and increasing insulin resistance leads to a serious disease that is diabetes.
Excessive glucose concentration in the blood generates free radicals and accelerates atherosclerosis
Let us remind you that oxidative stress is a condition bad for the health of the arteries, characterized by the presence of a large number of free oxygen radicals in the blood - for example, oxidized lipids of the VLDL, IDL and LDL fractions. Frequent contact of free oxygen radicals with the walls of the arteries promotes damage to their endothelium.The damage pathomechanism consists in the oxidation (oxidation) of delicate endothelial cell structures and consequently on the degeneration of proteins, lipids and nucleic acids from which they are built. The primary cause of pathology is ineffective neutralization of excess oxygen free radicals by physiological antioxidants (antioxidants). And the deficiency in the blood of antioxidants is the excess of glucose - characteristic for the metabolic syndrome (hyperglycemia). Hyperglycemia causes a decrease in the concentration of the most important physiological antioxidants - such as peroxidase dismutase, peroxidase, or glutathione reductase. What's more, chronic oxidative stress stimulates immune cells - monocytes - to release inflammatory cytokines and oxidized lipids into the blood. Then the so-called Foam cells and consequently there is a significant damage to the vessel wall and the formation of atheromatous plaque at this site. Free oxygen radicals also contribute to the increase in vascular contractility and to excessive blood clotting. This set of pathological factors - first, it raises blood pressure and promotes the separation of atherosclerotic plaque from the wall of the artery; in the case of detachment of the plaque - it threatens the formation of massive thrombi threatening the heart attack around it.
Abdominal fat cells- adipocytes
- release oxidized lipids and bad cholesterol to the arteries and regulatory proteins that disrupt insulin action and cellular glucose burning into the blood
Obesity and metabolic syndrome raise the level of triglycerides and poor non-HDL cholesterol
The excessive accumulation of fat within the abdominal cavity, which accompanies obesity and the metabolic syndrome, generates or reveals insulin resistance. But this is not the end - at the same time appear further dangerous to health disorders, such as: excessive triglyceride, a deficit of "good" HDL cholesterol, an increase above 130 mg / dl "bad" non-HDL cholesterol. And the already mentioned unfavorable changes in the structure of circulating LDL lipoproteins are born - small and dense particles are formed. Smaller and thicker particles contain more bad cholesterol and more easily penetrate arterial walls - initiating and enhancing atherosclerosis.
Obesity promotes the development of hypertension
Obesity increasing body mass - increases the need for blood rich in nutrients and oxygen. The only way to accelerate blood supply is ... increase the pressure! No wonder that already at 20% overweight - the risk of developing hypertension increases by two! And the bigger it is, the younger the endangered person is! It was estimated that after taking into account other risk factors, each increase in body weight by one kilogram increases the risk of developing hypertension by 4.4%. It is also worth noting that hypertension is also driven as a pathomechanism "in itself". Its essence is acceleration of blood circulation, and this means increased pressure on the walls of the arteries! Increased pressure causes arteries to thicken in order to withstand it. However, they do so without growing "outside" - but to ... "inside"! In other words - the muscularity of the vessels to withstand the increased pressure of the blood flowing faster and faster to the "inside", which reduces the light of the arteries. It forces the heart to increase the effort again, and thus another vicious circle arises. Increased flow rate is a greater pressure on the blood - the effect is increased arterial hypertension and narrows the lumen of blood vessels!
Obesity and metabolic syndrome threaten cardiac performance
For many years, the risk of coronary heart disease has been attributed to the direct influence of the pathologies dependent on obesity presented above. However, in the last 20 years, it has also been recognized that obesity itself influences independently the risk of coronary heart disease. The increase in fat mass causes a significant increase in the body's demand for oxygen and nutrients supplied by the blood. The heart is forced to intensify its pressing effort. Performs much more work; its minute capacity is increased. As a consequence, it leads to overload of the left ventricle and then to its overgrowth and development of heart failure.
Obesity and the risk of thromboembolism
Visceral obesity generates an excess of free oxygen radicals that cause chronic oxidative stress in the blood vessels.Free oxygen radicals increase the risk of venous valve damage and varicose vein disease as well as thromboembolism. It has been documented that the excess body weight of obese people correlates positively with both the risk of developing varicose vein disease and with increased blood clotting. In such situations, a higher blood level is observed: fibrinogen, factor VII, and plasminogen activator inhibitor, which are indicators of increased risk of development and subsequent complications of thromboembolism, including, for example, life-threatening pulmonary embolism.
Obesity combined with metabolic syndrome threatens health and life
The criteria for diagnosis of the metabolic syndrome mentioned at the beginning - such as elevated triglycerides in the blood, too low HDL cholesterol level, elevated blood pressure are at the same time the basic morbid complications of obesity. According to the American Heart Association - obesity, besides cigarette smoking, is a basic risk factor favoring the development of coronary heart disease and hypertension. Numerous WHO reports have shown a significant increase in the risk of developing diabetes, hypertension, the abovementioned disturbances in lipid metabolism, heart failure, as well as gallbladder diseases. What's more, the visceral obesity observed in the metabolic syndrome, with its disturbed hormonal profile and lipid - accelerates and intensifies other derivatives of metabolic syndrome complications - such as: blood hyperhydrosis, osteoarticular degenerative changes, hyperandrogenism, gout, some psychosocial disorders (depression , anxiety, interpersonal interpersonal disorders); sometimes hypnotic apnea. [18] Some epidemiological studies also point to some relative risk of initiation of malignant tumors (breast, endometrium, colon), as well as sexual hormone disorders, impaired fertility, and fetal abnormalities as a result of maternal obesity. Obesity also increases the risk of death in proportion to the increase in BMI [19]. It is also an important factor hindering surgical treatment, worsening the prognosis after injuries or acute infections [16].
Author: mgr farm. Nina Krawczyk
MA in chemistry. foo. Edward Ozga Michalski
LITERATURE
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