Abdominal type of obesity: causes, degrees, how to get rid of it

Endocrinologists diagnose abdominal obesity when accumulations of excess fat tissue are concentrated in the abdomen and abdominal cavity.

This type of obesity can also be called android obesity (due to the distribution of fat deposits on the body according to the male type), central or visceral. That is, for doctors, these definitions are synonyms, although there are differences between visceral and abdominal obesity: in Latin, abdomen means "stomach", and viscera means "insides". It turns out that in the first case, the anatomical localization of fat is characterized, and in the second, it is emphasized that this fat is not subcutaneous, but internal and is located in the area of the omentum, fat depots of the mesentery and around the visceral organs themselves.

In physiologically normal quantities, this fatty tissue serves as protection for them, but its excess volumes – abdominal obesity – have an extremely negative effect on health.

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Epidemiology

By some estimates, there are nearly 2.3 billion overweight adults in the world, and their number has increased more than 2.5 times in three decades. For example, in the United States, at least 50% of men aged 50 to 79 and about 70% of women in this age group are obese. And obesity combined with diabetes has been diagnosed in 38.8 million Americans, with a 0.8% “male” advantage. About 32% of the adult population of the United States (47 million) have metabolic syndrome.

The number of Canadians over 18 who are obese has risen sharply, although most have a BMI of 35 or less – or class I obesity.

Brazilian pediatric endocrinologists claim that 26.7% of Brazilian boys aged 7-10 years and 34.6% of girls of the same age are either overweight or have some degree of obesity, most often abdominal.

The number of patients with obesity has increased in Australia, Mexico, France, Spain, Switzerland; 27% of cases of obesity diagnosis concern men, 38% – women.

Obesity rates among Britons have increased roughly fourfold over the past 30 years, reaching 22-24% of the UK population.

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Causes abdominal obesity

The key exogenous causes of abdominal obesity are associated with a violation of the physiological proportionality of calorie consumption and expenditure of received energy - with a significant excess of consumption. With a sedentary lifestyle, unused energy in the form of triglycerides accumulates in adipocytes (cells of white adipose tissue). By the way, it is not so much excessive fat consumption that leads to obesity, but food rich in carbohydrates, since excess glucose is easily transformed into triglycerides under the influence of insulin. So, such risk factors for obesity as poor nutrition and lack of physical activity do not cause any doubts.

One of the obvious causes of abdominal obesity in men is alcohol. The so-called "beer belly" appears because alcohol (including beer) provides a lot of calories without any real nutritional value, and when these calories are not burned, fat reserves in the abdominal cavity increase.

Eating disorders are also among the causes of excess weight: many people have the habit of “rewarding themselves with food,” that is, “eating away” stress and any surge of emotion (the pathogenesis of this phenomenon will be discussed below).

Endogenous causes of abdominal obesity are associated with the production of a number of protein-peptide and steroid hormones, neuropeptides and neurotransmitters (catecholamines), as well as with their interaction, the level of sensitivity of associated receptors and the regulatory response of the sympathetic nervous system. Quite often, endocrine problems are genetically determined.

As endocrinologists note, abdominal obesity in men (who initially have more visceral fat than women) is caused by a decrease in testosterone (dihydrotestosterone) levels. A reduction in the production of sex steroids, as it turns out, contributes to an increase in the number of their receptors in tissues, but receptor sensitivity is significantly reduced, so the transmission of signals to the neuroreceptors of the hypothalamus, which regulates most endocrine processes in the body, is distorted.

Abdominal obesity in women usually develops after menopause and is explained by a rapid decline in estradiol synthesis in the ovaries. As a result, not only the catabolism of brown adipose tissue changes, but also its distribution in the body. In this case, abdominal obesity with a normal BMI (i.e., with a body mass index of no more than 25) is often observed. Obesity is promoted by polycystic ovary disease, which reduces the level of female sex hormones. In addition, risk factors for visceral obesity in women include hypothyroidism - a deficiency of the thyroid hormone thyroxine and thyroid-stimulating hormone (synthesized by the pituitary gland), which play an important role in overall metabolism.

Abdominal obesity in women after childbirth threatens those who gain more kilograms during pregnancy than they should (and this is typical for approximately 43% of pregnant women). Increased body weight before pregnancy also contributes to obesity, especially against the background of high levels of the hormone prolactin in the blood (which is produced during lactation and stimulates the conversion of glucose into fat). The development of abdominal obesity after childbirth can be one of the consequences of Sheehan's syndrome, associated with severe blood loss during childbirth, which leads to damage to pituitary cells.

Among the endocrine pathological changes, the following risk factors for fat accumulation in the abdominal cavity are distinguished:

• increased synthesis of adrenocorticotropic hormone (ACTH) by the pituitary gland and decreased production of somatotropin, beta- and gamma-lipotropins;
• excessive production of glucocorticoids (steroid hormones) in functional disorders of the adrenal cortex;
• an increase in the synthesis of insulin by the pancreas with a simultaneous reduction in the production of the hormone glucagon (which stimulates lipolysis – the breakdown of triglycerides in fat cells).

In essence, the combination of the listed factors causes abdominal obesity in metabolic syndrome. Abdominal obesity is part of the symptom complex of metabolic syndrome and is directly related to both increased tissue resistance to insulin with the development of hyperinsulinemia and an increase in blood glucose levels, and hyperlipidemia - high levels of triglycerides in the blood and low levels of high-density lipoproteins (HDL). At the same time, according to clinical studies, in 5% of cases, metabolic syndrome is present with normal body weight, in 22% - with excess weight and in 60% of patients with abdominal obesity.

Accumulation of visceral fat in the abdominal cavity can occur with Cushing's syndrome (Itsenko-Cushing's disease); with alcohol-induced pseudo-Cushing's syndrome; with a benign tumor of the pancreas (insulinoma); with inflammatory, traumatic or radiation damage to the hypothalamus, as well as in patients with rare genetic syndromes (Lawrence-Moon, Cohen, Carpenter, etc.).

Abdominal obesity may develop in children and adolescents with Fröhlich's neuroendocrine syndrome (adiposogenital dystrophy), which is a consequence of birth traumatic brain injury, cerebral neoplasms, or infectious brain damage with meningitis or encephalitis.

Certain medications, such as steroids and drugs used for mental illnesses, can lead to obesity.

See also – Causes and pathogenesis of obesity

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Pathogenesis

Disturbances in neuroendocrine regulation of fat metabolism determine the pathogenesis of abdominal obesity. Depending on its characteristics, types of obesity are conventionally divided into endocrine and cerebral.

Thus, despite the fact that obesity is accompanied by an increase in the level of the protein appetite suppressant hormone leptin (synthesized by adipocytes), a person does not feel satisfied with hunger and continues to eat. And here either frequent mutations of the leptin gene (LEP) are to blame, as a result of which the receptors in the hypothalamus nucleus (regulating the feeling of hunger) simply do not perceive it, and the brain does not receive the necessary signal. Or - in parallel with the increase in insulin production by the pancreas - resistance to leptin develops.

In addition, the regulation of food satiety can be disrupted due to functional deficiency of leptin with a decrease in the level of estrogens in the blood. And the pathogenesis of "stress eating" (mentioned above) is due to the release of cortisol into the blood, which suppresses the activity of leptin. In general, a deficiency of this hormone or the indifference of its receptors leads to an uncontrollable feeling of hunger and constant overeating.

With a decrease in estrogen synthesis, a decrease in the production of the neuropeptide hormone melanocortin (α-melanocyte-stimulating hormone) in the pituitary gland is also observed, which inhibits lipolysis in adipocytes. A decrease in the synthesis of the pituitary hormone somatotropin and the adrenal cortex hormone glucagon leads to the same result.

Increased food consumption and abdominal tissue obesity cause more intensive synthesis of the neuropeptide NPY (regulatory hormone of the autonomic nervous system) in the intestine and hypothalamus.

The transformation of carbohydrates into triglycerides and their accumulation in white adipose tissue cells is induced by hyperinsulinemia.

Read also – Pathogenesis of obesity in children

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Symptoms abdominal obesity

The main symptoms of abdominal obesity are: fat deposits in the abdominal area and increased appetite, which provoke a feeling of heaviness in the stomach.

And the first signs of obesity of the initial stage (BMI 30-35) are manifested by an increase in waist size. Read more about what are the degrees of obesity

Experts consider non-specific symptoms of excess visceral fat to include belching, increased intestinal gas formation (flatulence) and blood pressure, shortness of breath even with minor physical exertion, increased heart rate, swelling and sweating.

In addition, blood levels of triglycerides, LDL, and fasting glucose increase.

See also - Symptoms of Obesity

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Complications and consequences

The fat surrounding the abdominal organs exhibits significant metabolic activity: it releases fatty acids, inflammatory cytokines and hormones, which ultimately leads to serious consequences and complications.

Central obesity is associated with a statistically higher risk of cardiovascular disease, hypertension, insulin resistance, and the development of non-insulin-dependent diabetes mellitus (type 2 diabetes).

Abdominal obesity is associated with obstructive sleep apnea and the development of asthma (with obesity, lung volume decreases and airways narrow).

Abdominal obesity in women provokes menstrual cycle disorders and causes infertility. And lack of erection is one of the consequences of abdominal obesity in men.

Recent studies have confirmed that higher amounts of visceral fat, regardless of overall weight, are associated with smaller brain volumes and an increased risk of dementia and Alzheimer's disease.

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Diagnostics abdominal obesity

Diagnosis of abdominal obesity begins with anthropometry, that is, measuring the patient's waist and hip circumference.

Generally accepted criteria for abdominal obesity: in men, the waist circumference is more than 102 cm (the ratio of waist circumference to hip circumference is 0.95); in women – 88 cm (and 0.85), respectively. Many endocrinologists measure only the waist circumference, since this indicator is more accurate and easier to control. Some specialists additionally measure the amount of fat in the intestinal area (sagittal abdominal diameter).

Weighing is performed and BMI (body mass index) is determined, although it does not reflect the characteristics of the distribution of fatty tissue in the body. Therefore, to measure the amount of visceral fat, instrumental diagnostics are necessary - ultrasound densitometry, computer or magnetic resonance imaging.

Necessary blood tests: for triglyceride, glucose, insulin, cholesterol, adiponectin and leptin levels. Urine tests for cortisol are taken.

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Differential diagnosis

Differential diagnostics and additional examinations are designed to distinguish visceral obesity from ascites, bloating, hypercorticism, and also to identify problems with the thyroid gland, ovaries, pituitary gland, adrenal glands, hypothalamus and pituitary gland.

Treatment abdominal obesity

The main treatment for abdominal obesity is a diet to reduce the calories you eat and exercise to burn off the fat reserves that have already accumulated.

Some medications are used in drug therapy. Orlistat (Orlimax) is used to reduce fat absorption - 1 capsule (120 mg) three times a day (during meals). Contraindicated in urolithiasis, inflammation of the pancreas and enzymopathies (celiac disease, cystic fibrosis); side effects include nausea, diarrhea, flatulence.

Liraglutide (Victoza, Saxenda) lowers blood glucose levels; prescribed in a daily dose of no more than 3 mg. May cause headaches, nausea and vomiting, intestinal problems, inflammation of the gallbladder and pancreas, kidney failure, tachycardia, and depression.

Also read about drugs for the treatment of obesity in the article - Tablets for obesity

It is also recommended to take vitamins, in particular, vitamin PP (nicotinic acid); for directions for use and dosage, see – Nicotinic acid for weight loss

More useful information in the material - Treatment of obesity: an overview of modern methods

Physiotherapy treatment can begin with the simplest thing – regular walking: daily for at least 60 minutes. Swimming, cycling, badminton, tennis, squash, aerobics burn calories well.

You also need to do special exercises to lose belly fat. The main thing is that physical activity should be regular.

Folk remedies

Folk remedies for obesity include appetite suppressants such as bee pollen, fresh plantain leaves, chickweed (Stellaria media) and burdock root. Plantain and chickweed are recommended to be added to salads; a decoction of burdock root (a tablespoon of dry root per 250 ml of water) should be prepared; pollen should be taken 10 g twice a day.

Herbal treatment is also used for abdominal obesity. Fenugreek seeds (Trigonella Foenum-graecum) – a plant of the legume family – are taken orally ground into powder. The saponins, hemicellulose, tannins and pectin contained in it help to reduce the level of low-density cholesterol, removing it with bile acids through the intestines. And isoleucine helps to reduce the rate of absorption of glucose in the intestines, which leads to a decrease in blood sugar levels in patients with type 2 diabetes.

The effect of green tea (Camellia sinensis) for weight loss is provided by epigallocatechin-3-gallate. The following promote weight loss: water infusion of Cissus quadrangularis, black elderberry (Sambucus n igra), dark green garcinia (Garcinia a troviridis), infusion or decoction of leaves and stems of Chinese ephedra (Ephedra sinica) and white mulberry (Morus alba), decoction of Baikal skullcap root (Scutellaria baicalensis) and flowers and leaves of large-flowered bellflower (Platycodon grandiflora).

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Surgical treatment

For any type of obesity, surgical treatment requires special indications and can be performed when all attempts to reduce weight have failed.

Today, bariatric surgery uses operations that modulate the volume of the stomach using: insertion of a balloon into the stomach cavity (with subsequent inflation to the established size), bandaging, bypass, and vertical (sleeve) plastic surgery.

Diet for abdominal obesity

What the diet should be like for abdominal obesity is presented in detail in the previously published material - Diet for Obesity, which provides a list of food products for abdominal obesity (recommended and contraindicated).

For information on foods that promote weight loss, see the article - Fat Burning Foods.

And the basic principles of therapeutic dietetics for obesity of various etiologies and localizations are considered in the material - Dietary correction of obesity and excess body weight

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Prevention

The main prevention of obesity, including abdominal obesity, is healthy eating and maintaining physical activity.

Read more – Modern approaches to obesity prevention

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Forecast

In adults who continue to gain more than 2.5-3 kg per year, the risk of developing metabolic syndrome increases to 45%. In advanced cases, complications accompanying abdominal obesity reduce overall life expectancy by an average of six to seven years.

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