New markers of coronary heart disease

New markers of coronary heart disease

A detailed discussion of new biochemical and genetic markers of cardiovascular diseases (CVD) is presented in a separate article on the site. In general, several hemostatic and inflammatory markers, new lipid parameters, cell adhesion molecules, markers of infection and oxidative stress are associated with the stages of atherogenesis, thrombosis or cardiovascular events (SSSob).

Of these new risk factors (RF), only the level of CRP added prognostic information to general risk prediction models, such as the Framingham Risk Scale. High levels of CRP serve as a prognostic factor for cerebral stroke (MI), recurrent coronary events and cardiovascular death. The Centers for Disease Control and Prevention and American Heart Association guidelines endorse the definition of CRP as an adjunct to risk assessment, especially for those in the intermediate risk zone.

In the United States, recently obtained results for women show that 20–30% of people at risk of 5–20%, according to APT III, can be reclassified into a higher or lower group after measuring the level of CRV. Approval of the definition of SRV partially reflects the low cost of assessment, especially in comparison with other approaches to screening based on complex visualization technologies, such as CT, or the definition of calcification of spacecraft. In general, when the level of SRV is used in the general risk prediction algorithm, its values ​​<1.1–3 and> 3 mg / l correspond to the low, intermediate, and high risk of future vascular diseases. Adding a high level of CRP to the formal definition of MS also improves predictive accuracy with respect to vascular events or diabetes. To date, other inflammatory markers, such as lipoprotein-associated phospholipase A2, fibrinogen, and ligand CD40, are of limited value if CRP levels are known.

Other new risk factors (RF) – lipoprotein (a) and homocysteine ​​- are of limited value in general screening, but may be useful in the presence of a premature disease in families prone to atherosclerosis, when there are no clusters of traditional RF. In relation to lipoprotein (a), the availability of an assessment, regardless of apo re-screening, is a significant achievement that helps resolve the inconsistencies of previous reports.

A general restriction on the use of these new markers is the lack of data showing that reducing their level will lead to a decrease in vascular risk, therefore their use is limited to a risk assessment and a motivation for lifestyle changes. For example, although statin therapy reduces CRP, a post-hoc analysis suggests improved outcomes in individuals with elevated CRP, prospective studies testing the use of CRP to control statin treatment are only starting. Similarly, although folate decreases homocysteine, there is no evidence that this approach reduces vascular risk. The potential clinical benefits of these markers and today’s results regarding their modification are presented in a separate article on the site.

A number of common genetic polymorphisms are associated with coronary risk factors (RF). For example, carriers of a common mutation in the MTNFR gene have elevated levels of homocysteine ​​and multiple inherited lipid metabolism abnormalities associated with HLP and an increased vascular risk. Similarly, almost 50% of variations in the level of CRP are inherited. However, there is no evidence that screening for this polymorphism adds essential information to more easily detectable levels of homocysteine, lipids or CRP. Data concerning arterial thrombosis contrasts with data from venous thrombosis, when an assessment of factor V Leiden and prothrombin mutation is clinically useful. Thus, although genetic screening is a promising way to identify individuals at risk for future events, its role in primary and secondary prevention of atherothrombotic diseases remains unproved today. However, the time will come when genetic screening will play a role in identifying individuals at increased risk for appropriate therapy to reduce the risk of subsequent events.

The effectiveness of the treatment of stress and depression in coronary heart disease

The effectiveness of the treatment of stress and depression in coronary heart disease

The study of psychosocial factors as possible risk factors for coronary heart disease (RF KBS) is difficult due to the inaccuracy of definitions and units of measurement. Psychosocial factors such as depression, chronic hostility, social exclusion, and a feeling of lack of social support have always been associated with the risk of coronary heart disease.

However, it is necessary in further work to confirm this relationship and establish the effectiveness of interventions. With regard to the existence of a link between vascular risk and such psychosocial factors as work-related stress, type A behavior and anxiety, the data are heterogeneous.

Studies of therapeutic interventions, although not blind, noted the importance of improving psychosocial factors as part of preventive programs, especially with secondary prophylaxis.

The strongest evidence was obtained for patients after myocardial infarction (MI). Although many data show that stress and depression after MI are common and predictors of subsequent events, the results of interventions are limited. A meta-analysis of 37 small studies on the training of patients with coronary heart disease (CHD) in stress management showed that these efforts can reduce heart mortality by 34% and repeated myocardial infarction by 29%, possibly due to the favorable effect on blood pressure, cholesterol and MT. smoking, FA and eating habits.

In the randomized ENRICHD study, 2481 patients were included (26% – with a feeling of low social support, 39% – in clinical depression, and 34% – in both conditions) 4 weeks after MI. 50% of patients were randomized for cognitive behavioral therapy and drug therapy, if necessary, and the other 50% were in the conventional treatment group.

Intervention did not increase survival without events. It did have a positive effect on depression and a sense of social exclusion, however, the relative improvement in the intervention group compared with the conventional treatment group was less than expected, possibly due to the significant improvement in the condition of patients in the control group.

Preliminary evidence suggests that pharmacotherapy for depression after MI, revascularization, or diagnosis of CHD can improve morbidity and mortality. A randomized SADHART study (Sertraline Antidepressant Heart Attack Randomized Trial) showed the safety of sertraline (a selective serotonin reuptake inhibitor) in the treatment of recurrent depression in patients with cardiovascular diseases (CVD).

Sertralin did not affect LV EF, ventricular premature beats, or other cardiac indicators when compared with the placebo group. Depression and mood scales were better in the sertraline group, especially in depressed patients before heart attack, i.e. in a group in which the onset of depression after an attack is particularly likely. The frequency of repeated heart attacks, HF, episodes of chest pain and cardiac death was lower in the sertraline group than in the placebo group.

In the ENRICHD study, the use of antidepressants was also associated with significantly lower levels of nonfatal MI and deaths.

Efficacy of vitamins for coronary heart disease

Efficacy of vitamins for coronary heart disease

Micronutrients and specific foods are studied as substances for reducing the risk of cardiovascular diseases (CVD). Common supplements that many use to reduce the risk of heart disease include multivitamins, vitamins B and folic acid, antioxidants such as vitamins E and C, various carotenoids and ubiquinone (coenzyme Q10).

Foods that can reduce cardiovascular risk (SSR) are whole grains, fiber, fish and fish oil, and soy protein. Observational studies have shown a lower incidence of CHD among those who use antioxidant vitamins and folic acid, but the results of the research are contradictory and their effect is modest.

The significance of randomized clinical trials for heart-healthy foods and nutrients is best illustrated by a description of the advantages and disadvantages of vitamin E. In fundamental research, there is strong evidence that oxidative stress plays an important role in the development of diseases caused by atherosclerosis, and vitamin E can slow down or prevent various stages of atherosclerosis.

By the mid-1990s. observational studies have convincingly shown that high doses of vitamin E reduce the risk of CHD, especially with secondary prophylaxis. However, completed secondary prevention studies have revealed that the addition of vitamin E has little effect on the risk of coronary heart disease (CHD). Similar results were obtained in two long-term primary prevention studies – the Women’s Health Study and the SU.VI.MAX (Supplementation en Vltamines et Mineraux AntioXydants), which evaluated a combination of antioxidants, including vitamin E in a dose of 30 mg.

No significant reduction in the risk of cardiovascular disease (CVD) was found in these studies.

In the study of the cardiovascular effects of antioxidants in women in the framework of secondary prophylaxis, no positive cardiovascular effects were found among those taking any antioxidant: vitamin E, vitamin C or β-carotene for> 9 years. In the GISSI study, 11,324 patients who recently had myocardial infarction were divided into groups:

(1) taking daily supplements containing 1 g of omega-3 PUFA;
(2) taking vitamin E at a dose of 300 mg;
(3) receiving both supplements;
(4) not taking anything.

Observation was conducted 3.5 years. Treatment of omega-3 PUFA, but not vitamin E, reduced the relative risk of the primary endpoint (death, non-fatal MI and MI) by 10% (95% CI 1-18). This beneficial effect was primarily due to the reduced risk of death, and not due to nonfatal MI or cerebral stroke (MI).

Finally, in numerous prospective cohort studies, plasma homocysteine ​​levels have been consistently associated with increased vascular risk. On this basis, it was hypothesized that a decrease in homocysteine ​​with folic acid would lead to a decrease in the frequency of vascular events. However, numerous studies with the addition of folic acid to patients with vascular disease did not reveal a favorable clinical effect.

Recommendations. There are no results of studies supporting the use of food supplements for the prevention of KBS or other cardiovascular events (SSSob). Antioxidants did not show a clear benefit in preventing CHD, but observational studies revealed the possibility of various micronutrients and specific foods to reduce the risk of coronary heart disease (CHD). However, soy protein and isoflavone supplements lost their popularity in 2006, when the ANA, which had previously recommended soy, changed its position after analyzing the results of 22 studies, saying that it could not recommend supplements of isoflavones in pills or in food to prevent heart disease.

More research is needed on fish oil supplements before offering general recommendations. Several recent studies have failed to reveal the benefits of folach supplementation, thus showing that a decrease in homocysteine ​​is not associated with a reduction in vascular risk.

Effect of hormone replacement

Effect of hormone replacement

The physiological effects of exogenous estrogens are consistent with the cardioprotective effect. Estrogens reduce the level of LDL cholesterol and increase the level of HDL cholesterol, reduce the content of lipoprotein (a), plasminogen activator inhibitor 1, insulin levels, inhibit the process of LDL oxidation and improve endothelial function.

The effect of estrogen on inflammation is complex, since fibrinogen level is reduced, and the level of NRW is increased. Many of these effects are expressed when taking estrogen per os and are minimal when transdermally applied, which indicates the effect of the first pass. Estrogens can also improve glucose tolerance.

Despite the results of observational and physiological studies that suggested the favorable effect of hormone replacement therapy (HRT), the results of 7 recently completed randomized studies (5 – for secondary prevention and 2 – for primary prevention) not only failed to confirm the beneficial effect of HRT on the CHD, but showed that combination estrogen and progestin therapy may increase the risk of CHD. This dramatic change in perspective on the effects of HRT illustrates the problems of uncontrolled interference in cohort observational studies and the importance of randomized controlled clinical trials.

Evidence also indicates that age and time from the onset of menopause may alter the effect of estrogen on cardiovascular risk (CCP).

The first HERS study on secondary prophylaxis did not reveal a positive effect of adding estrogen and progestin on the cardiovascular system even with an increase in the observation period. Subsequent studies did not find a favorable effect of HRT or an increase in the risk of KBS events.

One branch of the large-scale WHI study was planned to assess the relative benefit and risk of estrogen plus progestin for 8.5 years in 16,608 women aged 50 to 79 years with an intact uterus at the start of the study. However, after 5.2 years of observation, the study was stopped because the number of cases of invasive breast cancer exceeded the limits of this PE, i.e. risk exceeded the benefit. At that time, the estimated total risk (RR) for coronary heart disease (CHD) was 1.29 (95% CI 1.02-1.63), for MI – 1.41 (95% CI 1.07-1.85 ) and for pulmonary embolism – 2.13 (95% CI 1.39-3.25).

The overall risk (RR) for all cardiovascular diseases (CVD) was 1.22 (95% CI 1.09-1.36). The absolute excess of SSR per 10 thousand person-years associated with taking estrogen and progestin was equal to 7 cases of CHD, 8 cases of MI and 8 cases of pulmonary embolism. The benefit was to reduce the number of fractures and colorectal cancers.

Later, the estrogen branch of the WHI study involving 10,739 healthy women aged 50–79 years without a uterus was also stopped due to a slight increase in the risk of MI, especially in women aged> 60 years. After 6.8 years of follow-up, the use of estrogens was associated with a 39% increase in the risk of MI, an unreliable 9% decrease in the CHD and a 30-39% decrease in the number of fractures. A more thorough study showed that women with recent menopause had a reduced risk of KBS (MI and coronary revascularization) and a more favorable overall index when taking estrogen compared with placebo.

Although menopause clearly increases the risk of coronary heart disease (CHD), a recent study shows that HRT with estrogens and progestins does not protect the cardiovascular system, especially in older women. Will be able to or pet other regimens or drugs HRT to protect the cardiovascular system, will show the results of other studies.

Recommendations. HRT for the prevention of CVDs is no longer recommended by the USPSTF, the North American Menopause Society, AHA or other scientific organizations. Moreover, in 2003, the FDA revised the labels of all drugs for hormone therapy containing only estrogens or their combination with progestins, and obliged to include warning labels about an increased risk of heart disease, MI, MI and breast cancer. Nevertheless, HRT continues to be used in clinical practice for the treatment of moderate and severe symptoms of menopause.

The effectiveness of the treatment of menopause (coronary heart disease)

The effectiveness of the treatment of menopause (coronary heart disease)

Class 3 interventions are associated with a risk factor (RF), which is still being studied today. For some risk factors (RF), causal dependence with coronary heart disease (CHD) cannot be determined due to limited data. For some DFs with obvious causal dependence, interventions are not yet available. Clinicians should be prepared to discuss these risk factors with their patients, since they are an area of ​​active research and are often in the focus of media attention.

The risk associated with menopause (menopause). Up to 45 years, a relatively small number of women in the United States and other developed countries suffer from cardiovascular diseases (CVD). However, by age 60, CVDs have become the leading cause of death among women. Although the incidence of CHD in men of any age is higher, as is mortality from CHD, this gap is significantly reduced after natural menopause or bilateral removal of the ovaries in women.

The increased risk of coronary heart disease (CBS) after menopause can be explained by adverse changes in lipid and carbohydrate metabolism, which leads to an increase in LDL cholesterol and reduced HDL cholesterol, an increase in glucose tolerance (IGT) changes in hemostatic factors and vascular function. These changes have long been associated with a decrease in endogenous estrogen, which usually accompanies menopause.

Many observational studies have suggested that the use of hormonal drugs after menopause reduces the risk of KBS. A meta-analysis of 40 cohort and case-control studies showed a 50% reduction in the risk of KBS after using estrogens. In an early analysis of the Nurses’ Health Study, one of the largest cohort studies that studied this issue, the risk of KBS was 50% lower in women who took estrogens (relative risk 0.51; 95% CI 0.37-0.70).

These data, together with the known beneficial effects of estrogen per os on the lipid profile, became the basis for the widespread use of hormone therapy after menopause for the prevention of CVD.

Efficacy of alcohol for coronary heart disease

Efficacy of alcohol for coronary heart disease

Alcohol consumption has a complex effect on cardiovascular diseases (CVD). Observational studies have shown that consuming large amounts of alcohol increases total mortality (OS) and mortality from cardiovascular disease (CVD).

In contrast,> 100 prospective studies showed an inverse relationship between low and moderate alcohol consumption and the risk of heart attacks, ischemic stroke, peripheral arterial disease (PAD), sudden cardiac death (SCD) and death from all cardiovascular causes. The effect is relatively permanent and corresponds to a risk reduction of 20-45%.
Moderate alcohol consumption is associated with a decrease in USA in primary and secondary prevention in both men and women. The mechanisms underlying the effect of moderate alcohol consumption (1-2 servings per day) contribute to the increase in cholesterol level of cholesterol levels, improve fibrinolytic ability, reduce platelet aggregation and CRP levels.

Studies have clearly shown the protective effect of alcohol on cholesterol. Although there is an assumption about the unique cardioprotective properties of red wine, most studies have found the same positive effect of different types of alcohol when it is moderately consumed.

Recommendations for taking alcohol. Although the association of alcohol with a reduced risk of coronary heart disease (CHD) is probably causal, individual and community recommendations must take into account the complexity of the metabolic, nutritional and psychological effects of alcohol. The consumption of small or moderate portions of alcohol or a large amount of alcohol causes a protective or harmful effect, respectively.

All patients should be advised to avoid excessive alcohol consumption. For certain patients, a discussion about alcohol can be part of routine preventive counseling. In general, 1-2 servings of alcohol (drink) are safe for men, but for women it is more reasonable to limit themselves to smaller doses, because they usually have less body mass (MT) and there are differences in hepatic metabolism.

However, counseling must be strictly individual; when discussing the problem of alcohol consumption, other coronary risk factors (RF) (especially hypertension and diabetes), as well as a family history of liver disease, alcoholism, breast cancer or colon should be taken into account.

Endpoints for nutritional studies of patients with coronary heart disease (CHD)

Endpoints for nutritional studies of patients with coronary heart disease (CHD)

There are very few studies that have studied the effect on KBS of only a modified diet. In the Lyon Diet Heart Study, in which 605 patients undergoing myocardial infarction participated, patients were randomized into 2 groups: (1) on a diet of the Mediterranean type; (2) on a typical western diet. After 46 months of follow-up, the risk of cardiovascular death or MI was 65% less in the Mediterranean diet group.

Recommendations for diet. Taking into account the limited research results, it is difficult to answer the patient’s question: “What should I eat to prevent heart disease?” However, based on observational studies, patients should be advised to follow a few general principles that arise from the available data. The basis of an improved diet should be a simple set of rules:

• Total calorie intake must be balanced with energy costs. If body weight (MT) is desirable to reduce, then you need to consume less calories than you spend.
• Avoid simple carbohydrates (sugars and starch) that create a high glycemic load, and replace them with sources of carbohydrates that contain a lot of fiber (whole grains, beans) to slow down the absorption of sugars and reduce the insulin response.
• Maximize the consumption of fruits and vegetables. U.S. The Department of Agriculture recommends 1-2.5 servings of fruit and 1-4 servings of vegetables per day.
• Minimize the consumption of saturated fatty acids and trans fats. Instead, you should choose monounsaturated and polyunsaturated fatty acids, whole grains. It is shown that adequate consumption of omega-3 fatty acids reduces the frequency of CVD, especially the sun. The inclusion in the diet of 2-3 servings of fish per week (especially fat) can help prevent cardiovascular events (SSSob).
• Products containing a lot of unhealthy fats should be replaced by sources of proteins containing low saturated fatty acids (FA) or trans fats. It is necessary to limit salt intake, especially to persons with salt-sensitive blood pressure.

Efficacy of diet for coronary heart disease

Efficacy of diet for coronary heart disease

Diet has a significant effect on the risk of developing coronary heart disease (CHD). Cross-cultural studies have shown that diet plays an important role in relation to both KBS and other chronic diseases. For example, a Ni-Hon-San study found that Japanese immigrants who moved to Hawaii or California, often suffer from coronary heart disease (CHD) and ischemic stroke, like the natives of the United States.

However, understanding the specific components of the Western diet that affect this risk remains in question. Dietary research is difficult because of the complexity of the measurements. Nevertheless, some dietary habits have been well studied. This section will discuss macronutrients (fats, carbohydrates, proteins), as well as alcohol. Supplements, nutraceuticals and specific products are discussed below.

Observational studies of the effectiveness of the diet. In observational studies, nutritional patterns were identified that may affect the risk of CHD. One of the key features of the Western lifestyle is excessive calorie intake compared to their costs. One of the constant findings of observational studies is the fact that people consuming a lot of vegetables and fruits are less likely to develop CHD and stroke.

Other components of the Western diet, which can increase the risk of KBS, are saturated fatty acids and trans fats, simple carbohydrates that create an increased glycemic load, and lack of fiber.

Metabolic studies of the effectiveness of the diet. Metabolic studies have shown that diet is an important component of any prevention program. Diet can have a pronounced effect on weight loss (MT), which, in turn, can positively affect DLP, hypertension and diabetes.

Even without weight loss (MT), a healthy diet can improve the lipid profile and provide the body with nutrients that have a beneficial effect on cardiovascular events (SSSob). The study DASH 459 adults with CAD <160 mmHg. st. and dad <80-95 mm Hg. st. were randomly divided into the following groups:
(1) on a control diet with a small amount of fruits, vegetables, and dairy products with a fat content of 37%;
(2) on a diet rich in vegetables and fruits;
(3) on a combination diet that includes a lot of vegetables and fruits and low-fat dairy products. Both therapeutic diets significantly reduced SBP and DBP in individuals with and without AH.

A review of the results of 147 metabolic studies, prospective cohort and clinical studies showed that at least 3 nutritional strategies are effective in preventing KBS: replacing saturated fatty acids and trans fats with non-hydrogenated unsaturated fatty acids; increased consumption of omega-3 fatty acids in the form of fish or fish oil, or from plant sources; use of a diet rich in fruits, vegetables, nuts, whole grains, and containing a small amount of refined cereal products.

The benefits of physical training.

The benefits of physical training.

Termination of FA leads to an increased risk of CHD. The absence of large-scale randomized primary prevention studies that have studied the beneficial effects of FA makes it difficult to assess the benefits of FA in reducing the risk of CHD. However, FA clearly demonstrated a beneficial effect on cardiovascular RF. Exercise increases the level of HDL cholesterol, lowers cholesterol LDL and TG, increases insulin sensitivity and lowers blood pressure in people with elevated and normal blood pressure. Exercise also improves endothelial function and reduces CRP levels.

In the secondary prevention of the cardio-rehabilitation program with components of physical exercises, they showed a favorable effect in reducing the follow-ups. Combined data from many studies have revealed a decrease in OS and cardiovascular mortality by 25%.

Recommendations on physical inactivity. The ANA recently issued revised dietary and lifestyle guidelines starting at 2 years of age. They recommend FA> 30 minutes on most days of the week, even if the FA is divided into short periods. In addition, the ANA proposes to draw attention to the need to increase the FA, guided by the principle “it is better to move every day than to be moved”.

Previous ACC / ANA recommendations for secondary prevention also motivated patients to be physically active. Exercise may include walking, jogging, cycling, swimming, or other aerobic activities for 30–60 minutes on most days of the week, supplemented by increased activity in everyday life, such as climbing the stairs, whenever possible, instead of using an elevator or an escalator Strength training can give an additional favorable effect. Structured exercise programs can reinforce the patient’s long-term commitment to FT.

U.S. recommendations Primary Prevention Surgeon General’s are a great start — every adult should practice 30-minute moderate or intense FA on most days of the week and higher-intensity FA if it is desirable to reduce MT.

From a practical point of view, advice on physical activity (FA) should begin with her buds at the moment, including FA at work and during leisure. If the estimate indicates that FA is less than optimal, then obstacles to an active lifestyle should be examined. Potential obstacles can usually be the lack of time, energy, desire, and also a safe and convenient place to practice. Other barriers include certain medical conditions, such as osteoarthritis or transferred MI. After evaluating the FA, you should follow the advice to increase the cost of calories in everyday life, for example, advice on walking instead of traveling by car. The physician should recommend a steady increase in FA at rest up to> 30 min per day.

The effectiveness of the treatment of obesity in coronary heart disease

Prevalence of obesity. In the United States, over the past 40 years, the proportion of the population with excess MT (BMI> 25 kg / m2) and obesity (BMI> 30 kg / m2) has steadily increased. According to the 1960-1962 NHANES data, 31.6% of men and women had excess MT (BMI of 25.0-29.9 kg / m2), of which 13.4% were obese.

Today, almost 2 out of 3 Americans are overweight (MT) or obese; according to the NHANES 1999-2000, 64.5% of men and women had excess MT, 30.5% of which were obese.

The prevalence of overweight (MT) and obesity among children and adolescents is increasing in parallel with those in adults. At the age of 6-19 years, 15%, and at the age of 2-5 years, 10.4% were overweight (MT) or obesity. This is an alarming trend, because early obesity is a strong predictor of cardiovascular disease (CVD) in adulthood. It is particularly alarming that excess MT can lead to a dramatic increase in the incidence of DM-2 among children. In some areas of the United States,> 30% of new cases of DM-2 were observed among children, with most cases due to obesity.

Obesity risk. Obesity and overweight (MT) are strongly associated with the risk of coronary heart disease (CHD) and cerebral stroke (MI). Since different criteria were used to determine excess MT and obesity, the information and magnitude of this association with coronary heart disease (CHD) do not fully match. The question of whether overweight (MT) is an independent FD KBS, remains a matter of debate, because impact on the risk of coronary heart disease (CHD) may be mediated by arterial hypertension (AH), dyslipidemia (DLP), impaired glucose tolerance (NTG), inflammatory and hemostatic factors.

However, given the strong association with coronary heart disease (CHD), obesity remains an important and easily measurable risk marker.

Data from a number of cohort and metabolic studies provide similar evidence for a link between excess MT, NFA and impaired health. In a recent, long-term study, women studied obesity and NFA as predictors of CHD risk. Although BMI, the ratio of waist to hip volume, NFA independently contributed to the development of CHD, a study that lasted> 20 years showed that obesity increased the risk more than NFA.

Overweight (MT) increases the risk of metabolic disorders such as AH, DLP, IL and NTG. For example, in the Marks and Spenser Cardiovascular Risk Factor Study 14 077 middle-aged women, there were highly reliable, age-adjusted differences between 7 categories of BMI (from <20 to> 30 kg / m2) for GARDEN and DAD, total cholesterol, serum LDL, cholesterol HDL, TG, apo AI, apo B and fasting glucose levels. Excessive MT is associated in adults and children with increased markers of inflammation, such as CRP and fibrinogen, which are associated with an increased risk of CVD. There is a strong relationship between excess MT and an increased risk of CHD, ischemic MI, DMD-2, and other chronic diseases.

Overweight (MT) is an aggravating individual and economic factor. Estimates for 6 large prospective cohorts indicate that in the US, 280–320 thousand deaths per year are associated with overweight (MT), of which 80% occur in individuals with a BMI> 30 kg / m2. According to a national study of 10 thousand adult Americans, obesity is associated with a large number of chronic disorders and a worse quality of life than smoking or alcohol abuse.

Medical expenses for overweight conditions in 1998 were estimated at $ 78 billion (9% of total medical expenses in the United States). This amount is comparable to the cost of treating diseases associated with smoking. A study that examined the effect of increasing MT among men and women aged 35–65 years with initially excessive MT showed that the 3-year increase in health care costs was $ 561 more in individuals with an increase in MT by> 9 kg over this period compared with individuals whose MT remained stable.