home Auditorium 7 Metabolic syndrome, what to do, how to treat? Metabolic syndrome

Metabolic syndrome, what to do, how to treat? Metabolic syndrome

The availability of high-calorie food, personal transport, and sedentary work have led to the fact that in developed countries almost a third of the population has metabolic problems. Metabolic syndrome is a complex of such disorders. It is characterized by obesity, excess cholesterol and insulin, and a deterioration in the flow of glucose from the blood into the muscles. Patients have high pressure, constant fatigue, increased hunger.

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Ultimately, metabolic disorders lead to atherosclerosis, thrombosis, diabetes, heart disease, and strokes. It is predicted that in the next decade there will be 1.5 times more people with metabolic syndrome, and in the elderly group the prevalence of the disease will reach 50%.

Metabolic syndrome - what is it?

Back in the sixties of the last century, a connection was identified between excess weight, type 2 diabetes, angina pectoris and hypertension. It was found that these disorders are more common in people with android type obesity, when more fat is deposited in the upper part of the body, mainly in the abdomen. In the late 80s, the final definition of metabolic syndrome was formed: it is a combination of metabolic, hormonal and accompanying disorders, the root cause of which was increased production insulin.

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Due to hormonal characteristics, metabolic syndrome Diagnosed more often in men. This is why they are more likely to die from heart disease. vascular diseases. In women, the risk increases significantly after menopause, when estrogen production stops.

The main provocateur of metabolic syndrome is considered to be increased tissue resistance to the hormone insulin. Due to excess carbohydrates in food, there is more sugar in the blood than the body needs. The main consumer of glucose is muscles; during active nutrition, they need tens of times more. In the absence of physical activity and excess sugar, body cells begin to restrict the passage of glucose into themselves. Their receptors stop recognizing insulin, which is the main conductor of sugar in the tissue. It is gradually developing.

The pancreas, having received information that glucose began to enter the cells more slowly, decides to speed up the metabolism of carbohydrates and synthesizes an increased amount of insulin. An increase in the level of this hormone stimulates the deposition of adipose tissue, ultimately leading to obesity. Simultaneously with these changes in the blood, dyslipidemia occurs - low-density cholesterol and triglycerides accumulate. Changes normal composition blood has a pathological effect on blood vessels.

In addition to insulin resistance and hyperinsulinemia, the causes of metabolic syndrome are:

A significant increase in visceral fat due to excess calories in food.
Hormonal disorders - excess cortisol, norepinephrine, lack of progesterone and growth hormone. In men - a decrease in testosterone, in women - its increase.
Excessive intake of saturated fat.

Who is more susceptible to MS?

Regular screening to identify metabolic syndrome is recommended for all individuals at risk.

Signs of belonging to this group:

periodic increase in blood pressure (> 140/90);
body weight above normal or abdominal obesity (in the abdomen);
low level of physical activity;
adherence to unhealthy diet;
increased hair growth on the face and limbs in women;
diagnosed diabetes mellitus or;
cardiac ischemia;
problems with blood vessels in the legs;
atherosclerosis and disorders cerebral circulation;
gout;
polycystic ovary syndrome, irregular menstruation, infertility in women;
erectile dysfunction or decreased potency in men.

Symptoms of metabolic syndrome

Metabolic syndrome begins with minimal metabolic disorders, develops slowly, gradually accumulating concomitant diseases. It does not have any obvious signs - pain, loss of consciousness or high temperature, so changes in the body are usually not paid attention to, only to be realized when metabolic syndrome manages to cause significant harm to the body.

Typical symptoms:

food without fast carbohydrates does not bring satisfaction. A meat dish with salad is not enough, the body requires dessert or pastries with sweet tea;
delaying food intake leads to a feeling of irritation, worsens mood, and causes anger;
in the evening you feel increased fatigue, even if you have been absent all day physical activity;
weight increases, fat is deposited on the back, shoulders, and abdomen. In addition to subcutaneous fat, the thickness of which is easy to feel, the volume of the abdomen is increased due to fat deposits around the internal organs;
it’s difficult to force yourself to get up earlier, walk an extra kilometer, take the stairs on foot instead of the elevator;
starts periodically palpitations caused by increased insulin levels in metabolic syndrome;
sometimes felt in the chest Blunt pain or feeling of squeezing;
the frequency of headaches increases;
dizziness and nausea appear;
areas of redness are visible on the neck and chest due to vasospasm;
increased fluid intake due to a constant feeling of thirst and dry mouth;
The regularity of bowel movements is disrupted, and constipation is common. Hyperinsulinemia in metabolic syndrome contributes to a slowdown in digestion. Due to excess carbohydrates, gas formation increases;
sweat production increases, especially at night.

It has been established that a predisposition to metabolic disorders is inherited, so the risk group also includes persons whose parents or siblings have abdominal obesity, high blood pressure, diabetes mellitus or insulin resistance, heart problems, and varicose veins.

Signs of a metabolic symptom revealed by the results of a blood test:

Laboratory analysis	Results indicating metabolic syndrome, mmol/l	Reason for deviation from the norm
Fasting glucose	in the elderly > 6.4	Poor supply of glucose from the blood to the tissues; sugar does not have time to normalize even after 8 hours of sleep.
	> 7.8 at the end of the test	Slowing of glucose uptake into cells due to insulin resistance and low energy requirements.
Lipoprotein cholesterol high density	< 1 у мужчин, < 1,2 у женщин	The level decreases due to physical inactivity and lack of unsaturated fats in the diet.
Low-density lipoprotein cholesterol	> 3	The increase is due to an excess of fatty acids entering the blood from visceral fat.
Triglycerides	> 1,7	They come from food and adipose tissue and are synthesized by the liver in response to excess insulin.
Uric acid	> 0.42 in men, > 0.35 in women	The level increases when metabolic syndrome affects the metabolism of purines, an important component of cell nuclei.

Diagnosis of MS

A patient's history of metabolic syndrome increases the likelihood of death from a heart attack by 23 times; in half of the cases, these disorders lead to diabetes mellitus. That is why it is important to make a diagnosis at an early stage, while deviations from the norm are minor.

If you suspect metabolic syndrome, you should contact an endocrinologist. Other specialists may be involved in the treatment of concomitant diseases - a cardiologist, vascular surgeon, therapist, rheumatologist, nutritionist.

The procedure for diagnosing the syndrome:

Questioning the patient to identify signs of metabolic disorders, poor heredity, level of activity and dietary habits.
Collecting an anamnesis of the disease: when abnormalities became noticeable, did obesity appear, did blood pressure rise, did high sugar occur.
In women, the state of the reproductive system is determined - past illnesses, pregnancies, regularity of menstruation.
Physical examination:

the type of obesity and the main areas of growth of adipose tissue are determined;
waist circumference is measured. When WC > 80 cm in women and 94 cm in men, metabolic syndrome is observed in most cases;
The waist to hip ratio is calculated. A coefficient above one for men and 0.8 for women indicates high probability metabolic disorders;
body mass index is calculated (the ratio of weight to the square of height, weight is expressed in kg, height in m). A BMI above 25 increases the risk of metabolic syndrome; with a BMI > 40, the likelihood of the disorder is considered extremely high.

Direction to biochemical tests to identify abnormalities in the composition of the blood. In addition to the above studies, tests for insulin and leptin may be prescribed:

Increased insulin most often means insulin resistance in the patient. Based on the level of fasting glucose and insulin, one can judge the severity of resistance in a patient and even predict the imminent development of diabetes mellitus;
Leptin increases with obesity, excess nutrition, leading to an increase in blood sugar.

Pressure measurement, cardiogram recording.
If you are obese, creating a nutrition plan may require:

bioimpedansometry to assess the content of water and fat in the body;
indirect calorimetry to calculate how many calories the patient’s body needs per day.

The diagnosis of “metabolic syndrome” is excluded in the latest international classification of diseases. Based on the results of the study, the conclusion describes all components of the syndrome: hypertension (ICD-10 code I10), obesity (code E66.9), dyslipidemia, impaired glucose tolerance.

Treatment of metabolic syndrome

The basis of treatment for metabolic syndrome is getting rid of excess weight. To do this, the composition of the diet is adjusted, its caloric content is reduced, and daily physical education classes are introduced. The first results of such non-drug treatment become visible when a patient with abdominal obesity loses about 10% of weight.

Additionally, the doctor may prescribe vitamins, nutritional supplements, and medications that improve carbohydrate metabolism and correct blood composition.

According to clinical guidelines For the treatment of metabolic syndrome, patients are not prescribed medications for the first 3 months. Their diet is adjusted and physical activity is introduced. As a result, along with weight loss, blood pressure and cholesterol often normalize, and insulin sensitivity improves.

The exception is patients with a BMI > 30 or a BMI > 27 in combination with hypertension, impaired lipid metabolism or type 2 diabetes. In this case, it is preferable to treat metabolic syndrome and concomitant obesity with drug support.

For morbid obesity, it is possible to use bariatric surgery methods: gastric bypass and band gastroplasty. They reduce the volume of the stomach and enable a patient with an eating disorder to feel full from a smaller portion of food.

If blood counts have not returned to normal within 3 months, medications are prescribed to treat remaining problems: fat and carbohydrate metabolism correctors, blood pressure lowering agents.

Use of drugs

Group of drugs	Active substance	Operating principle	Trade names
Help with weight loss
Lipid-lowering drugs	Orlistat	Inhibits the absorption of fat from the intestines, 30% of triglycerides are excreted in feces, which reduces the calorie content of food.	Orsoten, Xenical, Orlixen, Listata
Correction of carbohydrate metabolism
Biguanides	Metformin	They reduce insulin resistance and glucose synthesis in the liver, and reduce its entry into the blood from the small intestine. Taking it for metabolic syndrome reduces the risk of diabetes by 31%.	Glucophage, Bagomet, Siofor, Glycon
Alpha-glucosidase inhibitors	Acarbose	Disturbs the work of enzymes that break down polysaccharides. As a result, less sugar enters the blood.	Glucobay
Correction of lipid metabolism
Statins	Rosuvastatin	Effectively reduce bad cholesterol (up to 63% of the original figures). Used to treat atherosclerosis in diabetes mellitus and metabolic disorders.	Rozulip, Roxera
Statins	Atorvastatin		Atoris, Liprimar, Tulip
Fibrates	Fenofibrate	Reduce blood triglycerides, increase good cholesterol.	Traykor, Lipantil
A nicotinic acid, its derivatives	Nicotinic acid + laropiprant	Suppresses the release of fatty acids from visceral fat. Laropiprant eliminates the side effects of taking nicotine.	Threadaptive
Cholesterol absorption inhibitors	Ezetimibe	Blocks the transfer of cholesterol from food through the epithelium small intestine into the blood.	Ezetrol, Ezetimibe, Lipobon
Normalization of pressure
ACE inhibitors	Fosinopril	Dilate blood vessels. Does not reduce activity if there is excess fat. They do not have a negative effect on metabolism.	Monopril, Fosicard
ACE inhibitors	Ramipril		Hartil, Amprilan
Calcium channel blockers	Verapamil	Blocks the flow of calcium into blood vessels, which leads to their expansion. Used to treat myocardial ischemia and nephropathy in diabetes mellitus.	Isoptin, Finoptin
Calcium channel blockers	Felodipin		Felodip

The choice of the direction of treatment and specific means is the prerogative of the attending physician. All of the above drugs are quite serious and, if taken incorrectly, can not only not cure metabolic syndrome, but also aggravate its course.

Diet

The only one real way treatment of excess weight in metabolic syndrome – creating a long-term energy deficit. Only in this case the body uses fat reserves to produce energy. Abdominal obesity is a chronic disease. Even after losing weight to normal, there is always a threat of relapse. Therefore, there is nothing left to do but treat metabolic disorders continuously, for the rest of your life, mainly through non-drug methods - physical education and proper nutrition. After achieving the desired result, the efforts of doctors and the patient should be aimed at maintaining it for a long time.

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Calorie intake is calculated in such a way that the patient loses no more than 2-4 kg per month. An energy deficit is created due to a strong reduction in animal fats and partial reduction in carbohydrates. The minimum daily caloric intake for women is 1200 kcal, for men - 1500 kcal, and fats should account for about 30%, carbohydrates - 30-50 (30% - if sugar is elevated or significant insulin resistance is detected), proteins - 20-30 (if not nephropathy).

Principles therapeutic nutrition for metabolic syndrome:

At least 3 meals, preferably 4-5. Long “hungry” intervals are unacceptable.
Unsaturated fats(fish, vegetable oil) should make up more than half of their total number. Eating animal fats should be accompanied by a portion of greens or raw vegetables.
Best sources protein – fish and dairy products. Meat: poultry and beef.
Slow carbohydrates are preferred (). Sweets, baked goods, white rice, fried potatoes are replaced with buckwheat and oatmeal, bran bread.
Food should provide at least 30 g of fiber per day. To do this, the menu should have a lot of fresh vegetables.
With high blood pressure, salt is limited to 1 teaspoon per day. If you gradually add less salt to your food, you can get used to the new taste of the food in a couple of weeks.
To increase potassium intake, you need to include green vegetables, legumes, and raw carrots in your diet.
There should be at least 30 ml of liquid per 1 kg of body. Tea, juices and other drinks are replaced clean water. The only exception is rosehip decoction.

Treatment of obesity should be periodic: we actively lose fat for six months, then for the same period we slightly increase the calorie intake so that the weight stabilizes. If you need to lose more weight, repeat the cycle.

If you stick to it for a long time low calorie diet, the body’s metabolism slows down, according to various sources, by 15 to 25%. As a result, the effectiveness of weight loss decreases. To increase energy expenditure in the treatment of metabolic syndrome, physical activity is required. Also, with active muscle work, insulin resistance decreases, triglyceride levels drop, good cholesterol increases, the heart trains, lung capacity and oxygen supply to organs increases.

It has been established that patients with metabolic syndrome who have introduced regular exercise into their lives are much less likely to experience relapses of the disease. Aerobic exercise is the best way to prevent metabolic slowdown. Power training with high weights are undesirable, especially if the pressure periodically rises.

Aerobic training is any sport in which most of the muscles work for a long time and the heart rate increases. For example, running, tennis, cycling, aerobics. Classes begin gradually so as not to overload patients with metabolic syndrome, most of whom last played sports in their distant youth. If there are doubts that the patient is able to cope with them, they test the functioning of the heart and blood vessels on a treadmill or exercise bike - a treadmill test or bicycle ergometry.

Start training with 15 minutes of walking, gradually increasing the speed and duration to an hour a day. To get the desired effect, training should be done at least three times a week, and preferably daily. The minimum weekly duration of exercise is 150 minutes. A sign of effective training is an increase in heart rate to 70% of its maximum frequency (calculated as 220 minus age).

In addition to a healthy diet and physical activity, treatment for metabolic syndrome should include stopping smoking and severely limiting alcohol. Living without tobacco leads to an increase in good cholesterol by 10%, without alcohol - it reduces triglyceride levels by 50%.

Prevention

Every third resident of Russia suffers from metabolic syndrome. To avoid falling into their ranks, you need to lead healthy life and undergo regular examinations.

Eat high-quality, minimally processed foods. A serving of vegetables with each meal and fruit for dessert instead of cake will significantly reduce the risk of violations.
Don't starve, otherwise your body will try to store every extra calorie in reserve.
Bring maximum movement into your life. Organize your day so that it includes a walk before bed and a gym session.
Take advantage of every opportunity to move more - do exercises in the morning, walk part of the way to work, get a dog and walk it.
Find a sport that makes you feel the joy of movement. Choose the most comfortable room, high-quality equipment, bright sportswear. Work out in the company of like-minded people. Only by getting joy from sports can you do it for the rest of your life.
If you are at risk, get your cholesterol tested periodically. If you have diabetes among your relatives or you are over 40 years old, do an additional glucose tolerance test.

As you can see, staying healthy and living a happy life is not that difficult.

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Catad_tema Metabolic syndrome - articles

Metabolic syndrome - the basics of pathogenetic therapy

T. V. Adasheva, Candidate of Medical Sciences, Associate Professor
O. Yu. Demicheva
Moscow State Medical and Dental University
Urban clinical Hospital №11

In 1948, the famous clinician E.M. Tareev wrote: “The idea of hypertension is most often associated with an obese hypersthenic person, with a possible disorder of protein metabolism, with blood clogging with products of incomplete metamorphosis - cholesterol, uric acid...” Thus, more than 50 years ago, the concept of metabolic syndrome (MS) was practically formed. In 1988, G. Reaven described a symptom complex including hyperinsulinemia, impaired glucose tolerance, low HDL cholesterol and arterial hypertension, giving it the name “syndrome X” and for the first time suggesting that insulin resistance (IR) with compensatory hyperinsulinemia. In 1989, J. Kaplan showed that an essential component of the “deadly quartet” is abdominal obesity. In the 90s the term “metabolic syndrome” appeared, proposed by M. Henefeld and W. Leonhardt. The prevalence of this symptom complex is becoming epidemic and in some countries, including Russia, reaches 25-35% among the adult population.

Generally accepted criteria for MS have not yet been developed, presumably due to the lack of common views on its pathogenesis. The ongoing discussion about the validity of using the terms “complete” and “incomplete” MS illustrates the underestimation of a single mechanism that determines the parallel development of all cascades of metabolic disorders in insulin resistance.

IR is a polygenic pathology, in the development of which mutations in the insulin receptor substrate genes (IRS-1 and IRS-2), β 3 -adrenergic receptors, uncoupling protein (UCP-1), as well as molecular defects in proteins of the insulin signaling pathway (glucose transporters) may play a role. ). A special role is played by a decrease in insulin sensitivity in muscle, fat and liver tissues, as well as in the adrenal glands. In myocytes, the supply and utilization of glucose is impaired, and resistance to the antilipolytic action of insulin develops in adipose tissue. Intense lipolysis in visceral adipocytes leads to the release large quantity free fatty acids (FFA) and glycerol into the portal bloodstream. Entering the liver, FFAs, on the one hand, become a substrate for the formation of atherogenic lipoproteins, and on the other hand, they prevent the binding of insulin to the hepatocyte, potentiating IR. Hepatocyte IR leads to a decrease in glycogen synthesis, activation of glycogenolysis and gluconeogenesis. For a long time, IR is compensated by excess insulin production, so the violation of glycemic control does not manifest itself immediately. But, as the function of pancreatic β-cells is depleted, decompensation of carbohydrate metabolism occurs, first in the form of impaired fasting glycemia and glucose tolerance (IGT), and then type 2 diabetes mellitus (T2DM). An additional decrease in insulin secretion in MS is caused by long-term exposure high concentrations FFA on β-cells (so-called lipotoxic effect). With existing genetically determined defects in insulin secretion, the development of T2DM is significantly accelerated.

According to another hypothesis, the leading role in the development and progression of insulin resistance plays adipose tissue abdominal area. A feature of visceral adipocytes is their high sensitivity to the lipolytic action of catecholamines and low sensitivity to the antilipolytic action of insulin.

In addition to substances that directly regulate lipid metabolism, the fat cell produces estrogens, cytokines, angiotensinogen, plasminogen activator inhibitor-1, lipoproten lipase, adipsin, adinopectin, interleukin-6, tumor necrosis factor-α (TNF-α), transforming growth factor B, leptin etc. It has been shown that TNF-α is able to act on the insulin receptor and glucose transporters, potentiating insulin resistance, and stimulating leptin secretion. Leptin (“the voice of adipose tissue”) regulates eating behavior by affecting the hypothalamic satiety center; increases sympathetic tone nervous system; enhances thermogenesis in adipocytes; suppresses insulin synthesis; affects the cell's insulin receptor, reducing glucose transport. In obesity, leptin resistance is observed. It is believed that hyperleptinemia has a stimulating effect on some hypothalamic releasing factors (RF), in particular ACTH-RF. Thus, with MS, mild hypercortisolism is often observed, which plays a certain role in the pathogenesis of MS.

Particular attention should be paid to the mechanisms of development of arterial hypertension (AH) in MS; some of them were unknown until recently, which is why the pathogenetic approach to the treatment of MS was not fully developed.

There are numerous studies devoted to the study of the subtle mechanisms of the influence of insulin resistance and hyperinsulinemia on blood pressure levels.

Normally, insulin has a vascular protective effect due to the activation of phosphatidyl 3-kinase in endothelial cells and microvessels, which leads to expression of the endothelial NO synthase gene, release of NO by endothelial cells and insulin-mediated vasodilation.

Currently, the following mechanisms of the effect of chronic hyperinsulinemia on blood pressure have been established:

stimulation of the sympathoadrenal system (SAS);
stimulation of the renin-angiotensin-aldosterone system (RAAS);
blockade of transmembrane ion exchange mechanisms with an increase in the content of intracellular Na+ and Ca++, a decrease in K+ (increased sensitivity of the vascular wall to pressor influences);
increased reabsorption of Na+ in the proximal and distal tubules of the nephron (fluid retention with the development of hypervolemia), retention of Na+ and Ca++ in the walls of blood vessels with an increase in their sensitivity to pressor influences;
stimulation of proliferation of smooth muscle cells of the vascular wall (narrowing of arterioles and increasing vascular resistance).

Insulin is involved in regulating the activity of the sympathetic nervous system in response to food intake. Experimental studies have found that during fasting, SAS activity decreases, and when food is consumed, it increases (especially fats and carbohydrates).

It is assumed that insulin, passing through the blood-brain barrier, stimulates glucose uptake in regulatory cells associated with the ventromedial nuclei of the hypothalamus. This reduces their inhibitory effect on the centers of the sympathetic nervous system of the brain stem and increases the activity of the central sympathetic nervous system.

Under physiological conditions, this mechanism is regulatory, but with hyperinsulinemia it leads to persistent activation of the SAS and stabilization of hypertension.

Increased activity central departments SAS leads to peripheral hypersympathicotonia. In the kidneys, activation of JGA β-receptors is accompanied by the production of renin, and sodium and fluid retention increases. Persistent hypersympathicotonia in the periphery of skeletal muscles leads to disruption of the microvasculature, first with physiological sparseness of microvessels, and then to morphological changes, such as a decrease in the number of functioning capillaries. A decrease in the number of adequately supplied myocytes, which are the main consumer of glucose in the body, leads to an increase in insulin resistance and hyperinsulinemia. Thus, the vicious circle closes.

Insulin, through mitogen-activated protein kinase, enhances the damaging vascular effects due to the stimulation of various growth factors (platelet growth factor, insulin-like growth factor, transforming growth factor P, fibroblast growth factor, etc.), which leads to proliferation and migration of smooth muscle cells, proliferation of vascular fibroblasts walls, accumulation of extracellular matrix. These processes cause remodeling of cardio-vascular system, leading to loss of elasticity of the vascular wall, disruption of microcirculation, progression of atherogenesis and, ultimately, to an increase in vascular resistance and stabilization of hypertension.

Some authors believe that endothelial dysfunction plays a major role in the pathogenesis of hypertension associated with metabolic disorders. In individuals with insulin resistance and hyperinsulinemia, there is a decrease in response to vasodilation and an increase in response to vasoconstriction, which leads to cardiovascular complications.

Metabolic syndrome is characterized by hyperuricemia (according to various sources, it occurs in 22-60% of patients with MS).

It has now been shown that the concentration of uric acid in the blood correlates with triglyceridemia and the severity of abdominal obesity; This phenomenon is based on the fact that increased fatty acid synthesis activates the pentose pathway of glucose oxidation, promoting the formation of ribose-5-phosphate, from which the purine core is synthesized.

Taking into account all the aspects of the problem discussed above, a therapeutic algorithm for a pathogenetic approach to the treatment of metabolic syndrome should be formed.

Treatment of metabolic syndrome

The complex of treatment for metabolic syndrome includes the following equivalent items: lifestyle changes, treatment of obesity, treatment of carbohydrate metabolism disorders, treatment of arterial hypertension, treatment of dyslipidemia.

Lifestyle change

This aspect underlies successful treatment metabolic syndrome.

The doctor’s goal in this case is to form a stable motivation in the patient, aimed at long-term implementation of recommendations on nutrition, physical activity, and taking medications. A “success mindset” allows the patient to more easily endure the hardships that lifestyle changes require.

Changing your diet. The diet of a patient with metabolic syndrome should not only ensure weight loss, but also not cause metabolic disorders and provoke an increase in blood pressure. Fasting in syndrome X is contraindicated, since it is severe stress, and with existing metabolic disorders, it can lead to acute vascular complications, depression, and breakdown in a “food binge.” Meals should be frequent, food should be taken in small portions (usually three main meals and two or three intermediate meals) with a daily calorie content of no more than 1500 kcal. The last meal is an hour and a half before bedtime. The basis of nutrition is complex carbohydrates with low glycemic index, they should be up to 50–60% nutritional value. The glycemic index unit of a food is the change in glycemia after a meal equal to the change in glycemia after consuming 100 g of white bread. Most people have a high glycemic index confectionery, sweet drinks, baked goods, small cereals; their consumption should be eliminated or reduced to a minimum. Low GI in whole grains, vegetables, fruits rich in dietary fiber. The total amount of fat should not exceed 30% of the total calorie content, saturated fat - 10%. Each meal should include an adequate amount of protein to stabilize glycemia and promote satiety. You should eat fish at least twice a week. Vegetables and fruits should be present in the diet at least five times a day. Acceptable quantity sweet fruits depends on the degree of carbohydrate metabolism disorder; in the presence of type 2 diabetes mellitus, they should be sharply limited.

Table salt - no more than 6 g per day (one teaspoon).

Alcohol, as a source of “empty calories”, an appetite stimulant, and a glycemic destabilizer, should be excluded from the diet or reduced to a minimum. If it is impossible to give up alcohol, preference should be given to dry red wine, no more than 200 ml per day.

Quitting smoking is necessary; this significantly reduces the risk of cardiovascular and cancer complications.

Physical activity. According to G. Reaven, 25% of people leading sedentary lifestyle life, insulin resistance can be detected. Regular muscle activity itself leads to metabolic changes that reduce insulin resistance. To achieve a therapeutic effect, it is enough to practice 30 minutes of intense walking every day or 20-30 minutes of jogging three to four times a week.

Obesity treatment

When treating metabolic syndrome, a satisfactory result can be considered a weight reduction of 10-15% in the first year of treatment, by 5-7% in the second year and the absence of relapses in body weight gain in the future.

Following a low-calorie diet and physical activity regimen is not always feasible for patients. In these cases it is indicated drug therapy obesity.

Currently, the drugs orlistat and sibutramine are registered and recommended for long-term treatment of obesity in Russia. The mechanism of their action is fundamentally different, which makes it possible to select the optimal drug in each specific case, and in severe cases of obesity that are resistant to monotherapy, prescribe these drugs in a complex manner.

Treatment of carbohydrate metabolism disorders

The severity of carbohydrate metabolism disorders in metabolic syndrome ranges from minimal (impaired fasting glycemia and glucose tolerance (IGT)) to the development of type 2 diabetes mellitus.

In the case of metabolic syndrome, medications that affect carbohydrate metabolism should be prescribed not only in the presence of T2DM, but also in less severe (reversible!) disorders of carbohydrate metabolism. Hyperinsulinemia requires aggressive therapeutic tactics. There is evidence of the presence of complications characteristic of diabetes mellitus already at the stage of impaired glucose tolerance. This is believed to be due to frequent episodes of postprandial hyperglycemia.

A powerful arsenal of modern hypoglycemic agents allows you to choose the optimal therapy in each specific case.

1. Drugs that reduce insulin resistance

For metabolic syndrome - drugs of choice.

A. Biguanides

Currently, the only biguanide that reduces insulin resistance is metformin. According to the UKPDS results, treatment with metformin in T2DM reduces the risk of death from diabetes by 42%, myocardial infarction by 39%, and stroke by 41%.

Mechanism of action: increasing tissue sensitivity to insulin; suppression of gluconeogenesis in the liver; changing the pharmacodynamics of insulin by reducing the ratio of bound to free insulin and increasing the ratio of insulin to proinsulin; suppression of fat oxidation and formation of free fatty acids, reduction of triglycerides and LDL, increase of HDL; according to some data - a hypotensive effect; stabilization or reduction of body weight. Reduces fasting hyperglycemia and postprandial hyperglycemia. Does not cause hypoglycemia.

It can be prescribed for IGT, which is especially important from the point of view of preventing the development of T2DM.

B. Thiazolidinediones (“glitazones”, insulin sensitizers)

Pioglitazone and rosiglitazone are approved for clinical use.

In Russia, this is a rarely used group of drugs, probably due to the relative novelty, the known risk of acute liver failure and high cost.

Mechanism of action: increase glucose uptake by peripheral tissues (activate GLUT-1 and GLUT-4, suppress the expression of tumor necrosis factor, which increases insulin resistance); reduce glucose production by the liver; reduce the concentration of free fatty acids and triglycerides in plasma by suppressing lipolysis (through increasing the activity of phosphodiesterase and lipoprotein lipase). They act only in the presence of endogenous insulin.

2. α-glucosidase inhibitors

Acarbose drug

Mechanism of action: competitively inhibits intestinal α-glucosidases (sucrase, maltase, glucoamylase) - enzymes that break down complex sugars. Interferes with the absorption of simple carbohydrates into small intestine, which leads to a decrease in postprandial hyperglycemia. Reduces body weight and, as a result, has a hypotensive effect.

3. Insulin secretogens

Drugs of this class are prescribed for metabolic syndrome in cases where it is not possible to achieve satisfactory glycemic control with the help of drugs that reduce insulin resistance and/or acarbose, as well as in the presence of contraindications to them. The risk of hypoglycemia and weight gain with long-term use requires a strictly differentiated approach when choosing a drug. Prescription for NTG is not practiced. The combination of insulin secretogens with biguanides is very effective.

A. Sulfonylureas

Clinical experience shows that monotherapy with certain insulin secretogens (in particular, glibenclamide) in patients with metabolic syndrome is usually ineffective even in maximum doses due to increasing insulin resistance, the secretory capacity of β-cells is depleted and an insulin-requiring variant of T2DM is formed. Preference should be given to highly selective dosage forms, which does not cause hypoglycemia. It is desirable that the drug can be taken once a day to increase treatment compliance.

These requirements are met by the second generation drug gliclazide. pharmacological form MV (modified release) and the third generation drug glimepiride.

Gliclazide - highly selective drug (specific to the SUR1 subunit of ATP-sensitive potassium channelsβ-cells), restores the physiological profile of insulin secretion; increases the sensitivity of peripheral tissues to insulin, causing post-transcriptional changes in GLUT-4 and activating the action of insulin on muscle glycogen synthetase; reduces the risk of thrombosis by inhibiting platelet aggregation and adhesion and increasing the activity of tissue plasminogen; reduces the level of lipid peroxides in plasma.

Glimepiride complexes with the sulfonylurea receptor SURX. Has a pronounced peripheral effect: increases the synthesis of glycogen and fat by activating the translocation of GLUT-1 and GLUT-4; reduces the rate of gluconeogenesis in the liver, increasing the content of fructose-6-biphosphate. It has lower glucagonotropic activity than other sulfonylurea drugs. Provides a low risk of hypoglycemia - causes a maximum decrease in blood glucose with minimal insulin secretion. Has antiaggregation and antiatherogenic effects, selectively inhibiting cyclooxygenase and reducing the conversion arachidonic acid in thromboxane A 2. It is complexed with caveolin in fat cells, which probably determines the specificity of the effect of glimepiride on the activation of glucose utilization in adipose tissue.

B. Prandial glycemic regulators (short-acting secretogens)

Fast-acting hypoglycemic drugs, amino acid derivatives. In Russia they are represented by repaglinide and nateglinide.

Mechanism of action- rapid, short-term stimulation of insulin secretion by the β-cell due to rapid reversible interaction with specific receptors of ATP-sensitive potassium channels.

It is believed that nateglinide is safer with respect to the development of hypoglycemia: insulin secretion caused by nateglinide depends on the level of glycemia and decreases as the level of glucose in the blood decreases. The possibility of using low doses of nateglinide for IGT in patients at high risk of cardiovascular complications is being studied (NAVIGATOR).

4. Insulin therapy

Early initiation of insulin therapy for metabolic syndrome (except in cases of decompensated diabetes) seems undesirable, as it is likely to aggravate the clinical manifestations of hyperinsulinism. However, it should be noted that, in order to avoid complications of diabetes mellitus, compensation of carbohydrate metabolism must be achieved at any cost. If the effect of the previously listed types of treatment is unsatisfactory, insulin therapy should be prescribed, possibly in acceptable combinations with oral hypoglycemic drugs. In the absence of contraindications, combination with biguanides is preferable.

Treatment of arterial hypertension

Target blood pressure level for the development of type 2 diabetes mellitus -< 130/85 мм рт. ст.; при нарушении функции почек - < 125/75 мм рт. ст.

Ideal antihypertensive drug in this clinical situation, it should have a proven effect on cardiovascular end points, not have negative metabolic effects, influence the pathogenetic links of hypertension in insulin resistance and have a number of protective effects (cardio-, nephro-, vasoprotection) with a beneficial effect on endothelial function, platelet-vascular hemostasis and fibrinolysis.

ACE inhibitors

ACE inhibitors are the drugs of choice in the discussion clinical group. This is due, firstly, to the pathogenetic validity of their use (activation of the RAAS in IR) and, secondly, to a number of advantages of drugs of this class:

reducing insulin resistance and improving glycemic control;
absence negative influence to lipid and purine metabolism(FASET, ABCD, CAPPP, HOPE, UKPDS);
vasoprotective effect - regression of vascular remodeling; anti-atherosclerotic effect (SECURE - HOPE-substudy);
nephroprotective effect in diabetic and non-diabetic forms of nephropathy (FACET, MICRO-HOPE, REIN, EUCLID, AIPRI, BRILLIANT);
correction of endothelial dysfunction, beneficial effect on platelet hemostasis and fibrinolysis: NO, prostacyclin, ↓endothelin, endothelium-dependent hyperpolarization factor, ↓procoagulant potential, tissue plasminogen activator, ↓platelet aggregation (TREND).

Thus, ACE inhibitors meet all the requirements for an antihypertensive drug for patients with metabolic syndrome.

β-blockers

Prescribing β-blockers to patients with metabolic syndrome has an undeniable pathogenetic advantage due to the presence of hypersympathocotonia, the mechanisms of which were discussed above. However, for a long time in this clinical group, these drugs were prescribed taking into account a number of restrictions; it was also believed that patients with diabetes mellitus they are contraindicated due to their negative effect on carbohydrate and lipid metabolism.

However, the results of UKPDS and other studies have proven the effectiveness and safety of the use of selective beta-blockers in patients with metabolic disorders and type 2 diabetes. All adverse side effects were mainly associated with the use of non-selective and low-selective β-blockers.

Thus, in patients with metabolic syndrome, it is possible to use highly selective β-blockers (betaxolol, bisoprolol, nebivolol, etc.) in the composition combination therapy in small doses.

Diuretics

Along with β-blockers, thiazide and thiazide-like diuretics are considered first-line drugs for long-term treatment of patients with uncomplicated hypertension. However, as in the case of β-blockers, the use of drugs in this group has a number of limitations due to the development side effects: decreased sensitivity of peripheral tissues to insulin with compensatory hyperinsulinemia, increased glycemia, adverse effect on lipid profile(increased levels of triglycerides, total cholesterol, low-density lipoprotein cholesterol in the blood), impaired uric acid metabolism (hyperuricemia).

Many multicenter prospective studies have noted a high incidence of diabetes mellitus in patients with hypertension when treated with thiazide and thiazide-like diuretics. The thiazide-like diuretic indapamide, which combines the properties of a diuretic and a vasodilator, has a lesser effect on metabolic risk factors. According to the literature, with long-term therapy, indapamide does not have a negative effect on carbohydrate and lipid metabolism and does not worsen renal hemodynamics, which makes it the drug of choice in this clinical group.

Calcium antagonists

Currently, many years of discussion about the effectiveness and safety of calcium antagonists have been summed up.

Numerous multicenter studies have proven a reduction in the risk of cardiovascular complications (STOP-2, NORDIL, INSIGHT, VHAT, NICS-EH, HOT, ALLHAT) during therapy with these drugs. In addition, calcium antagonists have a number of advantages that justify their use in patients with metabolic syndrome:

decreased insulin resistance, decreased basal and glucose-stimulated insulin levels;
no negative impact on carbohydrate and lipid purine metabolism;
vasoprotective effect - regression of vascular remodeling, anti-atherosclerotic effect (INSIGHT, MIDAS, ELSA);
nephroprotective effect (proven for non-hydropyridine drugs);
correction of endothelial dysfunction - an increase in NO due to antioxidant mechanisms (superoxide dismutase activity, ↓NO destruction), improvement of platelet-vascular and fibrinolytic components of hemostasis (↓platelet aggregation, ↓thrombomodulin).

Preference should be given to non-hydropyridine and dihydropyridine drugs long acting due to the ability of short-acting calcium antagonists prescribed in large doses, increase the risk of cardiovascular complications.

AT 1-angiotensin receptor blockers

On modern stage this group of drugs is one of the most actively studied.

A reduction in the risk of cardiovascular complications in patients with hypertension during treatment with losartan was shown in the LIFE study. Proven nephroprotective effect for diabetic nephropathy for T2DM (RENALL, IDNT, CALM). In addition, the ability of AT 1-angiotensin receptor blockers to reduce uric acid levels (losartan) has been shown.

The influence of AT 1-angiotensin receptor blockers on the pathogenetic links of hypertension in metabolic syndrome and the absence negative impact on carbohydrate and lipid metabolism make these drugs promising in this clinical group. A multicenter study evaluating the effect of valsartan on cardiovascular events in patients with impaired carbohydrate tolerance (NAVIGATOR) is currently underway. Further study of this group of drugs may place them on a par with ACE inhibitors when we're talking about about the treatment of metabolic syndrome.

α 1-blockers

Until the interim analysis of the ALLHAT trial, which found an increase in cardiovascular events, particularly new cases of heart failure, with doxazosin, drugs in this group were considered among the most promising drugs used to treat patients with metabolic syndrome. This is due to the ability of α-blockers to increase tissue sensitivity to insulin and, as a result, improve glycemic control, correct the lipid profile, and have a beneficial effect on hemostasis and endothelial function.

However, on at this stageα 1 -blockers can only be used as additional drugs in combination therapy for hypertension, including metabolic syndrome.

I 1 -imidazoline receptor agonists

Drugs in this group occupy special place in the treatment of metabolic syndrome due to the correction of one of the main links in the pathogenesis of hypertension - central hypersympathicotonia. These drugs, by reducing central sympathetic impulses, increase the sensitivity of peripheral tissues to insulin, improve glycemic control and reduce the activity of the RAAS.

Unfortunately, there is no data on the effect of I 1 -imidazoline receptor agonists on the prognosis of patients with hypertension, which does not allow recommending drugs of this class as first-line agents in the treatment of hypertension. However, they can be successfully used in combination therapy.

Treatment of dyslipidemia

Lipid-lowering therapy must be carried out in patients with MS and combined with therapeutic effects on IR and glycemia.

Statins are undoubtedly the first-line drugs in the treatment of dyslipidemia in patients with metabolic syndrome due to their good clinical efficacy (25-61% reduction in LDL, reduction in triglycerides) and good tolerability.

For isolated hypertriglyceridemia or severe hypertriglyceridemia, the drugs of choice are fibrates, which are inferior to statins in their effect on LDL, are less tolerated and interact with a large number of medicines. The DAIS and VA HIT studies also demonstrated the beneficial effects of fibrates on cardiovascular risk in T2DM.

Conclusion

Thus, considering MS as a “generalized cardiovascular-metabolic disease” (the term of L. M. Resnick), we propose to focus on pathogenetic approaches to its treatment. It is also important to develop uniform diagnostic criteria and include the diagnosis of “metabolic syndrome” in the list of Medical Economic Standards. From point of view evidence-based medicine It is desirable to conduct targeted multicenter studies of drugs used to treat metabolic syndrome.

Formin(metformin) - Drug dossier

Metabolic syndrome (MS) is a metabolic disorder in which cells lose sensitivity to insulin (a hormone produced by pancreatic cells), which is necessary for glucose to enter the cell and the cell to start working - producing energy. As a result, all insulin remains in the blood. The more insulin, the more fat accumulates, mainly in the abdominal area, around the internal organs (fatty liver, etc.). Modern science has proven that the fat cell produces hormones that contribute to further metabolic disorders, damage to the cardiovascular system, and disruption of the reproductive system.

Metabolic syndrome is "pre-diabetes type 2."

Metabolic syndrome in women and men - symptoms

The first sign of the development of metabolic syndrome is the presence of a woman’s waist circumference of more than 80 cm, and a man’s of more than 94 cm. If the above dimensions are combined with an increase in blood pressure higher than 130/85 mm Hg. Art., a glucose level of more than 5.6 mmol/l, or an increase in cholesterol levels in the blood, then the presence of metabolic syndrome is beyond doubt.

Slide 1. Criteria for metabolic syndrome according to the International Diabetes Federation:

Slide 2. How can we spot metabolic syndrome?

Metabolic syndrome - causes

The main causes of metabolic syndrome:

age-related changes hormonal regulation;
excessive consumption of high-calorie foods;
physical inactivity.

The main “trigger” of all metabolic syndrome processes is INSULIN RESISTANCE - the body’s immunity to insulin.

Insulin ensures that glucose enters the cell. If the cell begins to “starve” from a lack of glucose, then the brain receives a signal that it needs to: 1) urgently eat something sweet (increase the glucose level), 2) urgently increase the production of insulin, which will deliver this glucose to the cell.

In the case of metabolic syndrome, the MECHANISM of glucose delivery into the cell is disrupted, that is, it turns out that there is a LOT of glucose in the blood (“increased sugar levels”), but this glucose does not enter the cell (and the person suffers from weakness and lack of energy).

What is the cause of this “insulin resistance”? The fact is that inside the cell there are regulators that control the level of incoming glucose. If more glucose is supplied than necessary, the cell will die. Therefore, in order for a cell to open the “gate” for the entry of glucose, a whole chain of events involving microRNAs must first occur inside this cell.

The cell needs a lot of nucleotides, which will build microRNAs, which in turn will control the process of glucose uptake. But with age, this building material in the form of nucleotides becomes less and less.

Metabolic syndrome - treatment

First of all, treatment of metabolic syndrome should be aimed at solving the problem of excess weight. Need to increase motor activity, reduce caloric intake.

Very important point: must be added to the diet necessary for the body vitamins and microelements, especially those that help the body build microRNAs that will control the absorption of glucose. The body needs nucleotides.

You can compensate for the deficiency of nucleotides in the body with Dienai drugs. Almost all drugs in the Dienai line are a source of nucleotides.

If we are talking about metabolic syndrome in women, then we can recommend drugs such as Panmelan, Dienay.

At metabolic syndrome in men The drug Tarkus is recommended. Tarkus is a drug that helps male body maintain hormonal levels, maintain testosterone levels (the main male hormone). A decrease in testosterone levels is accompanied by a decrease in muscle mass and strength, an increase in adipose tissue, osteoporosis, a decrease in skin tone and thickness ("flabbiness" of the skin). Meanwhile, an increase in body weight due to adipose tissue leads to a further decrease in testosterone. A “vicious circle” arises when excess body fat over time can turn a man into a creature of the middle sex. The fact is that in the male body, in addition to androgens and testosterone, a small amount of female hormones is always produced, and in the female body - male hormones. If a man's weight is 30% higher than normal, endocrine system suspends the production of testosterone and increases the production of estrogen and progesterone. Under their influence, the male figure takes on effeminate forms. Our drug Tarkus helps the male body produce its own testosterone, thereby helping to overcome this condition.

Metabolic syndrome is not a disease, it is a combination of various symptoms and diseases.

Currently, metabolic syndrome is considered the most important factor risk of cardiovascular diseases.

Heart and blood vessel diseases are the most common cause of death worldwide.

Metabolic syndrome in women is the sum of different factors:

Overweight (obesity).
Disturbed balance of fat and cholesterol.
Hypertension (arterial hypertension).
Pathologically high level blood sugar due to insufficient insulin functioning.

These four factors play important role in the development of vascular diseases. This is thought to double the risk of dying from a heart attack or stroke.

In addition, patients with metabolic syndrome are approximately five times more likely to develop diabetes mellitus (type 2).

Metabolic syndrome in women symptoms:

Symptoms of metabolic syndrome often go undetected for a long time because they themselves do not cause pain or discomfort.

A doctor diagnoses it by chance during a physical examination—or after a heart attack or stroke.

Factors to confirm metabolic syndrome:

Obesity is clearly visible in metabolic syndrome. The most dangerous thing is obesity of the “apple” type with a beer belly. Less dangerous is the accumulation of fat on the hips - the “pear type”.
Visceral fat (inside the abdomen) is very dangerous. It causes dangerous inflammation, affecting the elasticity of blood vessels and blood clotting.
The liver then loses sensitivity to insulin. Fatty liver, inflammation, cirrhosis, and cancer occur.
There is a danger of getting hypertension and heart attack.
Obesity is the most important risk factor for metabolic syndrome.

Circumference or BMI (body mass index):

Less than 18.5 – you need to get better.
The norm is 18.5 to 24.9.
25.0 to 29.9 – period of pre-obesity.

BMI calculation: your weight on the scale in kilograms / height in meters squared. Example: your weight in the morning is 90 kg: your height in meters (1.60x1.60) = 35.15. We look at the table below - you have stage 2 obesity. Start taking better care of your health.

Average waist circumference figures range from 94 centimeters for men to 80 centimeters for women. Anything higher is dangerous.

Belly measurement:

For women - no more than 88 centimeters.
For men - no more than 102 centimeters.

Obesity degree:

Obesity 1st degree	30,0 34,9
Obesity 2 degrees	35.0 to 39.9
Obesity 3 degrees	40.0 to 44.9
Obesity 4 degrees	Everything above

Impaired fat metabolism, as measured by elevated blood lipid levels:

or low density.
Good (HDL) cholesterol is beneficial.

Cholesterol test standards:

You need to start monitoring yourself more closely when these numbers increase, except for good cholesterol. There are numbers, the higher the better.
It is very difficult to achieve this - he reacts to sports.

High blood pressure:

Even when treatment for high blood pressure has already been started, the risk factor for metabolic syndrome remains.
High blood pressure can lead to headaches, dizziness, nosebleeds, and a feeling of heat in the head. It may occur without any discomfort.
Figures above 130/80 should be alarming.

Insulin resistance:

Increased fasting blood sugar levels or already a manifestation of type 2 diabetes. Let me remind you that the norm for fasting sugar is from 3.0 to 5.6 mmol/liter. Now the norm has been increased to 6.1 mmol/liter.
All these signs are the consequences of a modern lifestyle: lack of exercise, poor diet (too many high-calorie foods, sugar).

Causes of metabolic syndrome in women:

Being overweight with excess belly fat increases your risk of developing metabolic syndrome. Thus, it is considered the most powerful provocateur of the disease.
With metabolic syndrome, the excretion of salts - especially salt (sodium chloride) - through the kidneys is impaired. High sodium levels in the body cause hypertension.
It not only damages organs, but also causes minor damage to the inner wall of the vessel.
It is believed that this keeps fat, cholesterol in them. Over the years, the cardiovascular system becomes increasingly damaged.
Another very serious reason is - hereditary factor. Cells remember everything, and this memory is passed on to generations.
We must not forget about smoking and alcohol - practically this hobby leaves no stone unturned in us, destroying our health to the ground.

Examination and diagnosis of women for metabolic syndrome:

It is better to identify the disease early, and not when you have a heart attack, stroke or the development of arteriosclerosis.

Installed hereditary diseases- diabetes, hypertension or lipid metabolism disorders.
Have there been heart attacks, was there loss of vision?
Blood pressure is measured, waist circumference and weight are measured.
A blood test is prescribed for sugar and cholesterol.
Find out the level of uric acid in the blood.
Urine analysis, including the presence of protein.
Liver enzymes ALT and AST will give a picture of fatty liver.

If diabetes is suspected, a glucose tolerance test is performed:

First, they measure on an empty stomach - if the numbers are elevated, the patient is given a sugar solution of a certain concentration or glucose to drink.
After two hours, glucose levels are measured again.
The diagnosis of diabetes is made when the figure is 11.1 mmol/liter or 200 mg/dc.

By ordering an electrocardiogram (ECG) and an ultrasound (ultrasound), the doctor can determine whether damage to the heart and other organs is already present.

In case of severely clogged blood vessels supplying the heart muscle, or after a heart attack, the ECG will show typical changes.

In turn, ultrasound technology makes it possible to easily detect irregularities in the contractions of the heart muscle.

The most important goal is to reduce visceral fat (abdominal obesity) by about 10 to 15 percent within the first year.

Limit total calories in food by adding vegetables, fruits, fiber, and greens for bulk. We exclude all unhealthy foods: salty, fatty, sweets, flour, semi-finished products, smoked meats.

Quickly digestible carbohydrates containing fat and sweets (ice cream, cakes, buns, semi-finished flour products, candies, cookies) are reduced.

Fat no more than 25-30% of the norm (we count in all products). The most dangerous animal fat.

Saturated – 8-10% of total fat.
Polyunsaturated – less than 10% (unrefined oil is best).
Monounsaturated – 15%.

Reducing salt in the diet - cook without salt, add a little salt at the table sea salt(less sodium). Swelling subsides, the load on the heart decreases, blood pressure and weight drop. 4-5 grams per day is enough.

A lot of dietary fiber(steamed bran, vegetables, salads, cabbage, you can use edible cellulose).

Regular endurance training (at 60% of maximum performance) burns a lot of fat, making muscles more sensitive to insulin.
At first, just walking or riding a bike is enough.
Absolute abstinence from cigarettes and alcohol.
Reduce stress in life as much as possible

If the diagnosis is confirmed, the main goal of treatment is to reduce the risk of secondary damage to all organs.

The main thing in treatment is not to let the disease run rampant in order to avoid any complications: vascular and circulatory diseases.

Treatment involves lifestyle changes:

Lots of sports and exercise.
low fat.
Reduced weight and blood pressure.
Normalization of blood sugar.

In people with metabolic disorders or at very high cardiovascular risk, concomitant drug therapy is required.

To lose weight if necessary:

In critical cases, the doctor may prescribe for emergency weight loss:

Orlistat (binding of lipase in the stomach and intestines and absorption of fats). These drugs are Xenical, Orsoten.
At the same time, fat is removed from the depot.
Cholesterol is more difficult to dissolve, and its entry into the blood decreases.
Visceral obesity decreases.

Reducing blood cholesterol:

Fibrates are among the most important means for the treatment of high blood cholesterol. They help lower “bad” LDL and increase “good” HDL.

Fibrates:

Fenofibrate.
Gemfibrozil.
Bezafibrate.
Clofibrate.

Reduces triglycerides in the blood - taken on an empty stomach.

Statins:

Atorvastatins.
Simvastatins.
Pravastatins.
Rosuvastatins.
Lovastatins.

They perfectly reduce bad cholesterol and total cholesterol, increase good cholesterol - they are prescribed only by a doctor due to side effects.

High blood pressure:

For treatment, so-called ACE inhibitors and ATP blockers are taken, which reduce the tension of the arterial wall, forcing the heart to overcome resistance.
Sometimes two or three small doses of drugs with the same effect are prescribed. There are a lot of them, starting with lisinopril, enalapril, captopril and ending with new generation drugs that are updated very often.
Supplemented with diuretics to reduce fluid in the blood and tissues.
Calcium channel blockers.
A-blockers.
Selective b-blockers.

Read more about the treatment of high blood pressure.

All treatments and medications are prescribed by the doctor, taking into account all concomitant diseases and after a thorough examination.

Insulin resistance and high blood sugar:

Drugs - metformin or acarbose, increase the secretion of insulin from, improve the effect of insulin on cells. Both factors contribute to the fact that sugar from the blood is absorbed by cells.

Metformin:

The main drug, which does not stimulate insulin production, is good at reducing insulin resistance. Your own tissues perceive their own insulin better.
Reduces unclaimed insulin in the blood. The feeling of hunger will decrease, you will eat less, and your sugar will decrease.
Slightly reduces the pressure in the blood vessels, decreases.

Surgery:

A fairly common method: bariatric surgery.

They do it for one purpose - to reduce food consumption.

General operations:

Gastric banding.
Gastrectomy (gastric tube, bypass).

They are made to save the life of a sick person.

Prognosis of metabolic syndrome in women:

Good, stable treatment results can be achieved through exercise and diet changes.
Many studies have shown that this behavior produces better results than taking medications.

Do what you can now to prevent metabolic syndrome in women. Don't start the disease.

Good luck!

Which significantly increases the risk of developing cardiovascular pathology, type 2 diabetes mellitus and a number of other diseases. In essence, it is not a disease per se, but rather represents a group of risk factors that often occur together, increasing the likelihood of severe illness.

The term "metabolic syndrome" was introduced relatively recently - in the 80s of the 20th century. This is one of the major health problems in many countries around the world. The number of adults suffering from metabolic syndrome reaches 25-30% in some countries. It is most common in East Asia, Latin America, the USA, and some European countries.

If previously metabolic syndrome was considered a disease of older people, now the percentage of young people suffering from it has increased. It is equally common among both men and women, but recently there has been an increase in incidence among women of reproductive age - this may be due to pregnancy, use oral contraceptives, polycystic ovary syndrome.

In addition to cardiovascular diseases and diabetes, metabolic syndrome leads to non-alcoholic steatohepatitis, a number of oncological diseases, including breast, colon, and prostate cancer. A connection between metabolic syndrome and the occurrence of psoriasis and some neuropsychiatric disorders has also been revealed.

The mechanism of development of metabolic syndrome is not fully understood. Treating patients is quite a challenging task. In some cases healthy image life - proper nutrition, physical activity - reduce the risk of developing serious diseases.

Synonyms Russian

Metabolic Syndrome X, Riven's Syndrome, Insulin Resistance Syndrome, New World Syndrome.

English synonyms

Metabolic syndrome X, cardiovascular metabolic syndrome, dysmetabolic syndrome, syndrome X, Reaven syndrome.

Symptoms

The diagnosis of metabolic syndrome is established when three or more of the following symptoms are present:

abdominal obesity - waist circumference more than 94 cm in men and 80 cm in women;
arterial pressure above 130/80;
increased levels of cholesterol in the blood;
increased levels of triglycerides in the blood;
increase in blood glucose concentration.

General information about the disease

The development of metabolic syndrome is based on both genetic predisposition and a number of external factors: low physical activity, eating disorders. It is believed that the leading role is played by disruption of the functioning of adipose tissue and the development of insulin resistance.

A sign of metabolic syndrome is the so-called abdominal obesity. With it, adipose tissue is deposited on the abdomen and the amount of “internal” fat increases (this may not be visible from the outside). Abdominal fat has increased resistance to insulin, unlike subcutaneous fat.

Insulin is a hormone that is produced by beta cells of the pancreas and is involved in all types of metabolism. Under the influence of insulin, glucose penetrates into the cells of various tissues of the body, where it is used as an energy source. Excess glucose in the liver is stored as glycogen or used for the synthesis of fatty acids. Insulin also reduces the breakdown of fats and proteins. If cell resistance to insulin occurs, the body requires more of this hormone. As a result, the level of insulin and glucose in the blood increases, and the utilization of glucose by cells is disrupted. Excessive concentrations of glucose damage the walls of blood vessels and disrupt the functioning of organs, including the kidneys. Excess insulin leads to sodium retention by the kidneys and, as a result, increases blood pressure.

Adipose tissue dysfunction plays an important role in the development of insulin resistance. For abdominal obesity fat cells enlarged, infiltrated by macrophages, which leads to the release large quantities cytokines - tumor necrosis factor, leptin, resistin, adiponectin and others. As a result, the interaction of insulin with receptors on the surface of cells is disrupted. An additional factor The development of resistance is obesity, since insulin can accumulate in fat cells.

Insulin resistance affects fat metabolism: the level of very low-density lipoproteins (VLDL), low-density lipoproteins (LDL), triglycerides increases, and the concentration of high-density lipoproteins (HDL) decreases. Low-density lipoproteins are a fraction of total cholesterol that is involved in the formation of the cell wall and in the synthesis of sex hormones. However, excess LDL (" bad cholesterol") can lead to the formation of atherosclerotic plaques in the wall of blood vessels and to pathology of the cardiovascular system. High-density lipoproteins, on the contrary, are “good” cholesterol. They are involved in the transfer of excess cholesterol back to the liver, and also prevent the formation of atherosclerotic plaques. Due to the excess of low-density lipoproteins and triglycerides that occurs in metabolic syndrome, the level of “good” cholesterol (HDL) usually decreases.

In addition, with metabolic syndrome vascular wall it becomes tougher, the thrombotic activity of the blood increases, and the amount of pro-inflammatory cytokines increases. All this further increases the risk of cardiovascular disease.

Thus, metabolic syndrome is a complex of pathological conditions that are closely related to each other. The process of development of metabolic syndrome is not fully understood.

In the absence of appropriate treatment, metabolic syndrome can lead to a number of serious diseases over several years: pathology of the cardiovascular system, in particular coronary disease heart, type 2 diabetes. The likelihood of liver damage with the subsequent development of cirrhosis, kidney disease, and cancer also increases.

Who is at risk?

Obese people.
Leading a sedentary lifestyle.
People over 60 years of age.
Patients with type 2 diabetes mellitus or those whose relatives suffer from it.
People with cardiovascular diseases, high blood pressure.
Women with polycystic ovary syndrome.

Diagnostics

Diagnosis of metabolic syndrome is based on examination data, medical history, results of laboratory and instrumental studies. The main diagnostic criterion is abdominal obesity, however, it does not indicate the presence of metabolic syndrome on its own, but in combination with a number of additional symptoms confirmed by tests.

It is important to try to find out the cause of obesity, which may be associated, for example, with diseases of the endocrine system.

Laboratory research

Other research methods

Blood pressure measurement. Metabolic syndrome is characterized by blood pressure above 130/85.
Glucose tolerance test - measuring blood glucose levels before a glucose load (that is, before taking a glucose solution), as well as 60 and 120 minutes after it. Used to diagnose impaired glucose tolerance, which may occur in metabolic syndrome.
Electrocardiography (ECG) is a recording of the potential difference that occurs during heart contractions. Allows you to evaluate the work of the heart, identify signs of acute or chronic heart disease.
Angiography and computed tomography are imaging methods that allow one to assess the state of the cardiovascular system.

Treatment

The mainstay of treatment for patients with metabolic syndrome is achieving and maintaining a normal weight. Diet and exercise are used for this. Normalizing weight and a healthy lifestyle significantly reduces the risk of developing severe complications of metabolic syndrome.

Medicines are used depending on the predominance of certain pathological changes: arterial hypertension, disorders of carbohydrate or lipid metabolism.

Prevention

Balanced diet.
Sufficient physical activity.
Regular preventive examinations for people at risk of developing metabolic syndrome.

Laboratory examination for metabolic syndrome
Plasma glucose
Cholesterol – high density lipoprotein (HDL)
Cholesterol – low density lipoproteins (LDL)
Total cholesterol
Cholesterol – very low density lipoproteins (VLDL)
Triglycerides
Atherogenic coefficient
Serum C-peptide
Microalbumin in urine
C-reactive protein, quantitative
Insulin
Homocysteine