Hereditary obesity: Prader-Willi syndrome. How to overcome hereditary obesity

Mesenchymal dystrophies (stromal vascular dystrophies) - metabolic disorders that develop in the stroma of organs.

Classification

Depending on the type of substances whose metabolism is disrupted, three groups of mesenchymal dystrophies are distinguished:

1. Mesenchymal dysproteinoses(protein metabolism disorders)
2. Mesenchymal lipodystrophies(lipid metabolism disorders)
3. .

TO mesenchymal dysproteinosis include (1) mucoid swelling, (2) fibrinoid changes, (3) extracellular hyalinosis, and (4) amyloidosis.

Mesenchymal lipodystrophies

Mesenchymal lipodystrophies (mesenchymal lipidoses) include (1) metabolic disorders of acylglycerols (neutral fats), as well as (2) cholesterol and its esters (cholesterides). Acylglycerols include three classes of compounds - mono-, di- And triglycerides. Metabolism disorders of neutral fats ( acylglyceroses) are local (local) and generalized (widespread) in nature, accompanied by accumulation (cumulative dystrophies) or depletion (resorptive dystrophies) of tissue lipids. Disorders of cholesterol and cholesterol metabolism ( cholesterosis) manifest themselves as a deficiency of these substances in the body ( Bessen-Kornzweig disease), and their excessive concentration in some tissues ( atherosclerosis, xanthomatosis, lipoid arc of the cornea). The term is sometimes used as a synonym for cholesterosis cholesterol diathesis.

I. Acylglyceroses

1. Generalized cumulative acylglyceroses ( obesity, hereditary hyperacylglycerolemia)
2. Generalized resorptive acylglyceroses ( cachexia, )
3. Local cumulative acylglyceroses ( lipomatosis, Vacat obesity)
4. Local resorptive acylglyceroses ( focal necrosis of adipose tissue, regional lipoatrophy).

II. Cholesterosis (cholesterol diathesis).

1. Resorptive cholesterosis ( Bessen-Kornzweig disease)
2. Cumulative cholesterosis [ atherosclerosis, xanthomatosis, lipoid arc of the cornea].

Among generalized cumulative acylglyceroses, obesity is of primary importance, but this group of mesenchymal lipodystrophies also includes hereditary diseases accompanied by the development of hyperacylglycerolemia. Classic example hereditary hyperacylglycerolemia is Buerger-Grütz disease (hyperlipidemia type Ia), in which the enzyme is missing lipoprotein lipase, as a result of which the neutral fat of chylomicrons is not broken down and these particles remain in the bloodstream for a long time ( hyperchylomicronemia). In addition to chylomicrons in hereditary hyperacylglycerolemia, the content of very low density lipoproteins- particles also rich in neutral fats.

Obesity

Obesity (general obesity, obesity, adipositas) is a pathological process accompanied by a significant increase in the body’s mass of white adipose tissue. The total amount of acylglycerols also increases significantly. Minimum indicator excess of “standard” body weight in obesity is 20% in men and 25% in women (it is with such excess body weight that a statistically significant increase in secondary morbidity and mortality is observed). Obesity is one of the most common diseases in developed countries peace. The process often develops after 40 years, mainly in women. Obesity is often accompanied by the development parenchymal lipodystrophy of the liver(fatty hepatosis).

If available infant excess body weight due to excessive development of adipose tissue, the term “obesity” is not used: traditionally, this condition is designated by the concept paratrophy.

Classification

Forms of obesity are classified as follows:

I. Etiological principle

1. Primary (nutritional-constitutional) obesity
2. Secondary ( symptomatic ) obesity[hereditary and acquired variants].

Forms of secondary acquired obesity:

• Endocrine obesity
• Cerebral (hypothalamic) obesity
• Duodenal (duodenoprival) obesity[when deleting duodenum]
• Hypoxic obesity (primary Pickwickian syndrome)
• Iatrogenic obesity[for example, long-term use of β-blockers inhibits lipolysis].

II. Expressiveness of the process

1. I degree(excess of body weight over “standard” by no more than 29%)
2. II degree (30-49%)
3. III degree (50-99%)
4. IV degree(100% or more).

III. Preferential localization of fat deposits

1. Symmetric (universal) type
2. Asymmetrical types(top, middle, bottom).

IV. Micromorphological features of white adipose tissue

1. Hypertrophic obesity
2. Hyperplastic obesity
3. Mixed obesity.

V. Morphogenesis of obesity

1. Dynamic phase(body weight increases)
2. Static phase(body weight is relatively constant).

Symmetric and asymmetric types of obesity

According to external manifestations they distinguish symmetric And asymmetrical types of obesity. At symmetrical type white adipose tissue relatively evenly distributed over different parts of the body. At top type fatty tissue is expressed in the area of ​​the face, back of the head, neck, shoulder girdle and mammary glands. At average type development of subcutaneous tissue of the anterior abdominal wall (“fat apron”) is noted, with bottom type- in the area of ​​the buttocks, thighs and legs. The top type corresponds android, or " apple"(typical for men), lower - gynoid, or " pyriform"(typical for women), obesity. This distribution is caused by the different sensitivity of lipocytes to sex hormones: lipocytes of the upper half of the body are more sensitive to androgens, therefore the predominance of androgens over estrogens is accompanied by the development top type obesity. The android type of obesity is often combined with impaired glucose tolerance or diabetes, hyperlipidemia, arterial hypertension, hyperandrogenism and hirsutism in women.

Hyperplastic and hypertrophic obesity

Based on the micromorphological characteristics of adipose tissue, there are hypertrophic And hyperplastic obesity. The number of white adipose tissue cells reaches a maximum during puberty (in women there are about 40 billion of them, in men it is half as much, which is associated with the suppressive effect of testosterone on the development of adipose tissue). Diagnosis of hypertrophic and hyperplastic obesity is carried out using a biopsy of fatty tissue.

Hypertrophic obesity characteristic of a disease that appears in adulthood, it develops against the background of persistent hyperglycemia and secondary hyperinsulinemia, it is characterized by an increase in the volume of lipocytes due to the accumulation of acylglycerols in their cytoplasm. Thus, with an increase in cell diameter by 2 times, the amount of neutral fat in it increases 8 times. The total number of fat cells does not change significantly in this type of obesity. Despite the decrease in the sensitivity of hypertrophied adipocytes to insulin, the sensitivity of these cells to lipolytic hormones (sex and thyroid hormones) increases, so a significant decrease in adipose tissue mass is possible conservative methods treatment. Correction of body weight in hypertrophic obesity is necessary because... it is accompanied by pronounced metabolic disorders and leads to severe changes, primarily in the cardiovascular system.

Against, hyperplastic obesity characterized by an increase in the number of lipocytes, the content of acylglycerols in the cell does not change. This type of obesity is not associated with increased concentrations of glucose and insulin in the blood. Metabolic disorders in hyperplastic obesity are not pronounced, so its course is usually benign, but it is difficult to reduce the mass of hyperplastic adipose tissue using conservative methods. In some cases, obesity combines signs of hypertrophy and hyperplasia of adipocytes. Hyperplastic or mixed obesity is observed in individuals who have been overweight since childhood.

Etiology and pathogenesis of obesity

Any form of obesity is essentially nutritional, i.e. associated with excessive eating behavior ( polyphagia, or hyperphagia, the extreme degree of severity of which is called bulimia). However, when they talk about the etiology of obesity, they mean the reasons leading to excessive food activity. In this regard, there are four main etiological factors obesity: (1) insufficient mobilization of fats from the depot (“greedy lipocyte syndrome”), (2) inhibition of lipolysis under the influence of hormones (lipolytic deficiency and antilipolytic excess), (3) damage to the hypothalamic saturation center and (4) chronic hypoxia. As a rule, the listed factors act interconnectedly in different combinations, but one of them usually dominates.

Insufficient mobilization of fats from the depot is primarily due to hyperinsulinemia, which occurs with insulin resistance in peripheral tissues. Typically, hyperinsulinemia in obesity is secondary, especially in primary obesity. It is associated with the dispersion of cytolemmal insulin receptors over the surface of a sharply enlarged fat cell and with the influence of counterinsular factors produced, in particular, by the lipocytes themselves (primarily TNF-α). Hypertrophy of fat cells, causing a decrease in their sensitivity to insulin, closes one of the vicious circles in the pathogenesis of obesity. Insulin is an antilipolytic hormone, blocking the activity triglyceride lipase adipocytes. The resulting hypoglycemia stimulates eating behavior due to the activation of the hunger center. The second vicious circle is formed glucocorticoids, the production of which often increases in obesity.

Factors predisposing to obesity. Contribute to the development of obesity, burdened heredity, physical inactivity, large portions of food, predominance of fats in food and protein deficiency (lack of protein weakens the specific dynamic effect of food), as well as nycphagy(eating mainly late in the evening and at night). It is believed that abundant protein and carbohydrate foods are not factors predisposing to obesity, although opinions differ regarding carbohydrate foods.

The role of thyroid hormones and brown fat. Overeating does not always lead to obesity. Typically, this speeds up metabolism due to greater formation triiodothyronine, which does not allow acylglycerols to actively accumulate in fat depots. In addition, when overnutrition growth noted brown adipose tissue, whose cells intensively oxidize triglycerides, dissipating excess energy with heat.

Erysichthon syndrome

Obesity is based on an increase in the concentration of fats in the blood (hyperlipidemia). Nutritional hyperlipidemia aptly named by a number of authors Erysichthon syndrome. The story of this character from ancient Greek myths, reinterpreted by Ovid, is also interesting from a medical point of view.

Erysichthon(literally translated from ancient Greek as “defender of the lands”) - the son of the Thessalian king Triops (which is why he sometimes goes by the name Triopeus), who himself later became king. He was distinguished by extreme disrespect for the gods (“ ...despising the divinity of the Most High, I never smoked incense on the altars in their honor"). By cutting down an oak tree in a sacred grove, and thereby destroying the beloved dryad nymph Demeter (Ceres), he incurred the wrath of the goddess. Before her death, the dryad cursed Erysichthon, and her sisters informed Demeter about the sacrilege of the Thessalian king. The angry Demeter terribly punished Erysichthon, asking the goddess of hunger to endow him with an eternal, unquenchable passion for food. She fulfilled the will of Demeter, appearing to the sleeping Erysichthon:

Meanwhile, the sweet dream of Erysichthon was caressing his wings

Soft: he reaches out to temptingly dreamed dishes,

Works with his mouth in vain; wears jaw on jaw,

The seduced woman tries to swallow imaginary food with her throat.

But not luxurious food, but only empty air.

Having woken up, Erysichthon begins to greedily absorb food, and can no longer stop (“ He hungers for more, the more he fills his insides. ... any food in it only attracts new food. He is there, but the womb is empty."). Soon the king squandered all his wealth in a vain attempt to quell the pangs of hunger. He only had his daughter Mnestra left, and Erysichthon sold her, wanting to be satisfied. But divine punishment is inevitable - Erysichthon dies, devouring his own body:

After greed has exhausted everything,

Again and again delivering food to the dashing illness,

Tear apart your members, gnaw Erysichthon with your teeth

He began: he nourished the body, decreasing in body - unhappy!

(Publius Ovid Naso. Metamorphoses. Translation S. Shervinsky).

Primary obesity

Primary obesity- obesity developing as a result of absolute or relative deficiency of the hormone in adipose tissue leptin. Since the cause of primary obesity has been established, it should not be named idiopathic, as was previously accepted. Leptin is secreted by “well-fed” lipocytes and, through its own receptors in the cytolemma of neurons in the saturation center, promotes the production of glucagon-like peptide I, which in turn slows down production neuropeptide Y neurons of the hunger center. Neuropeptide Y is currently considered the main mediator of hunger; it stimulates eating behavior.

There are two forms of primary obesity:

1. Absolute leptin deficiency(deficiency of the hormone itself) - 20% of cases of primary obesity
2. Relative leptin deficiency(decreased sensitivity to the hormone leptin receptors of the saturation center) - 80% of cases of obesity. Relative leptin deficiency manifests itself hyperleptinemia.

Despite established cause primary obesity, in practice it is usually diagnosed by excluding other (secondary) forms of the disease.

Endocrine obesity

Endocrine obesity- obesity developing under the influence of hormones. By modern ideas, any form of obesity can be classified as endocrine disorders: with primary obesity, metabolism is primarily disrupted leptin, with cerebral - neuropeptide Y And glucagon-like peptide I.

However, according to established tradition, there are four main forms of secondary endocrine obesity:

1. Obesity with hypercortisolism(primary and secondary)
2. Obesity with hyperinsulinism
3. Obesity with hypogonadism
4. Obesity with hypothyroidism.

Glucocorticoid hormones and insulin are antilipolytic, sex and thyroid hormones - to lipolytic, therefore the high content of glucocorticoids ( hypercortisolism) and insulin ( hyperinsulinism), as well as a decrease in the level of sexual ( hypogonadism) and thyroid ( hypothyroidism) hormones contribute to obesity.

1. Obesity with hypogonadism. Hypogonadism causes obesity in adiposogenital dystrophy. At the core adiposogenital dystrophy (Frohlich syndrome) is an acquired deficiency of pituitary gonadotropins. Their deficiency leads to insufficient synthesis and secretion of sex hormones. The disease manifests itself in prepubertal or pubertal age with two main syndromes caused by hypogonadism: (1) hypogenitalism(underdevelopment of the genital organs and secondary sexual characteristics) and (2) obesity. Characterized by predominant deposition of fat in the face (“doll face”), chest, abdomen and hips. The limbs are complete. Obesity of the gynoid type often develops. Mostly boys are affected. Lawrence-Moon-Biedl disease- congenital variant of adiposogenital dystrophy. Peripheral forms of hypogonadism are also accompanied by the development of obesity. With eunuchoidism, fat is predominantly deposited in the shoulder girdle, chest, abdomen and hips. Similar external manifestations occur with obesity in men in menopause. A decrease in ovarian function is accompanied by the accumulation of fat on the shoulders (“menopausal hump”), chest, abdomen, and thighs.

2. Obesity with hypercortisolism. Hypercortisolism underlies Cushing's disease and syndrome(Itsenko-Cushing). Fat accumulates mainly in the face (“moon face”), neck, upper torso and abdomen. A fatty “buffalo hump” forms in the area of ​​the cervical vertebrae. The limbs are thin. Rough purplish-red stripes appear on the skin of the abdomen, thighs, shoulders, and mammary glands ( striae- ruptures of subcutaneous fat), sometimes with hemorrhages along the periphery. In approximately 10% of patients, obesity does not develop, but a typical redistribution of fat occurs. Juvenile basophilism (hypothalamic syndrome of puberty, pubertal-juvenile dyspituitarism) is also manifested by hypercortisolism (secondary hypercortisolism). In addition, there is an increase in the production of somatotropic and gonadotropic hormones. Hyperfunction of the adenohypophysis is caused by hyperproduction of the corresponding releasing factors by the neurosecretory cells of the hypothalamus. In the pituitary tissue the number of basophilic cells increases (hence the term basophilism). The disease develops during puberty and is manifested by obesity, in which fat in subcutaneous tissue It is distributed evenly, but sometimes it is deposited mainly in the lower part of the body, which in young men causes a certain feminization of appearance. Unlike obesity of the Cushing type, the limbs in juvenile basophilism remain plump. Striae are thin, pink, without hemorrhages.

3. Obesity with hyperinsulinism. Hyperproduction of insulin is characteristic of diabetes mellitus type II and is especially pronounced in tumors of insulinocytes ( insulinoma). In this case, obesity develops with a uniform distribution of fat or android type.

4. Obesity with hypothyroidism. Obesity with hypothyroidism ( myxedema) is associated with a decrease in basal metabolism. Excess body weight is caused not only by obesity, but also by “mucosal edema” of tissues, which enhances the impression of obesity.

In addition to the listed forms, endocrine obesity includes epiphyseal obesity at Marburg-Milk syndrome(hyperfunction of the pineal gland due to hyperplasia of pinaeocytes or tumors from them - pinealomas).

A peculiar variant of endocrine obesity is duodenal (duodenoprival) obesity, developing in patients who have had their duodenum removed. Many duodenal hormones regulate the feeling of hunger; the main duodenal hunger inhibitor is cholecystokinin Therefore, when this organ is removed, polyphagia and obesity occur after some time.

Cerebral obesity

Cerebral (hypothalamic) obesity associated with neuronal damage saturation center (satiety center). The nature of the pathological process in the brain can be different - inflammation, tumor, injury, etc. At the same time safe hunger center (appetite center) is activated, which determines excessive eating behavior. The satiety center is located in the ventromedial zones of the hypothalamus, the hunger center is located in the lateral zones. Bilateral destruction of the ventromedial zones leads to severe obesity in experimental animals as a result of polyphagia; damage to the lateral zones can cause refusal to eat ( aphagia) and death from exhaustion. And, on the contrary, chronic stimulation of the ventromedial nuclei of the hypothalamus with implanted electrodes causes aphagia, and the lateral ones - polyphagia. Cerebral obesity is characterized by a rapid increase in body weight after a skull injury, encephalitis or a brain tumor. Body weight may increase even with normal appetite, although polyphagia is common. Obesity is usually symmetrical and reaches high degrees.

Cerebral obesity also includes obesity with Barraquer-Simons disease(Barraquer-Simons), developing in children and young women after cerebral form rheumatism (chorea minor) and diffuse diseases connective tissue. Barraquer-Simons type obesity is characterized by predominant fat deposition in the thighs, buttocks and anterior abdominal wall. Blue-purple striae appear on the skin of the shoulder girdle. Interestingly, the fat of the upper half of the body atrophies, starting from the head (“dead man’s head”), so this disease can also be attributed to local resorptive acylglyceroses.

Cerebral obesity has a unique pathogenesis when Stewart-Morgagni-Morel syndrome, in which hyperostosis of the skull bones and obliteration of their sinuses develop. Probably, as a result of this, blood circulation in the diencephalon of patients is disrupted and selective damage to the saturation center occurs. Mostly girls get sick. Fat is deposited in the abdominal area (android type of obesity).

Hypoxic obesity

Hypoxic obesity (primary Pickwickian syndrome) is caused by chronic hypoxia due to neurogenic hypoventilation of the lungs. Lipocytes are derivatives of poorly differentiated cells of fibroblastic differentiation, which are capable of actively proliferating at low partial pressure of oxygen in the environment. Typically, prolonged hypoxia provokes the growth of only fibrous tissue, but in some cases this also occurs with white adipose tissue. Some authors believe that hypoxic obesity is cerebral in nature.

Primary Pickwickian syndrome involves (1) a breathing disorder, primarily during sleep, which causes restless sleep and is accompanied by unusually intense snoring; (2) compensatory daytime sleepiness (patients fall asleep immediately when out of active activity) and (3) obesity. The syndrome is named Pickwickian by book title Charles Dickens "The Pickwick Papers", one of whose characters (Joe) suffered from this symptom complex. Obesity in primary Pickwickian syndrome is usually of the moderate type. Patients develop right ventricular failure (cor pulmonale).

It is necessary to distinguish from the primary secondary Pickwickian syndrome, developing against the background of existing obesity.

Hereditary obesity

TO hereditary forms of obesity include any cases associated with an inherited gene defect. Some diseases manifested by hereditary obesity can be attributed to endocrine or hypothalamic types of obesity. For example, when Lawrence-Moon-Biedl disease obesity is endocrine in nature. Gierke's disease(type I glycogenosis) is accompanied by constant hypoglycemia due to the absence of a violation of glycogenolysis, as a result of which patients often eat a lot, trying to suppress attacks of bulimia. Fat is deposited mainly in the subcutaneous tissue of the face. Gierke's disease is also characterized by hepatic steatosis. The pathogenesis of obesity in other hereditary diseases is not clear (for example, in Prader-Willi and Carpenter syndromes).

Complications

The main complication of obesity is atherosclerosis associated with hyperlipidemia. The risk of developing arterial hypertension, diabetes mellitus, cholelithiasis increases significantly, varicose veins veins lower limbs, gout, acute appendicitis, liver cirrhosis (in men) and a number of malignant tumors. Excess body weight clearly shortens life expectancy. In addition, myocardial lipomatosis, peripheral hyperestrogenia, hypoventilation syndrome (secondary Pickwickian syndrome) and overload of bones and joints (primarily the spine) develop.

Visceral lipomatosis. Obesity is characterized not only by an increase in the volume of fatty tissue, but also by the proliferation of adipose tissue in the stroma of internal organs ( visceral lipomatosis). Most dangerous myocardial lipomatosis: In areas of severe lipomatosis, rupture of the heart wall may occur. Visceral lipomatosis is combined with the android type of obesity. Lipocytes of internal organs are more sensitive to catecholamines and secrete more TNF-α (cachectin), which has counter-insular potential. Due to this, visceral lipocytes make the greatest contribution to the development of insulin resistance in obesity.

Peripheral hyperestrogenism. In obese patients, the peripheral metabolism of sex hormones is disrupted. In adipose tissue, the aromatization of androgens is accelerated, in particular testosterone and androstenedione into estradiol and estrone, respectively, which leads to hyperestrogenism, which contributes to the occurrence of metrorrhagia And benign breast dysplasia, and for men - gynecomastia, reducing hair growth on the face and body. At the same time, sexual function is impaired in both men and women.

Regional cumulative acylglyceroses include (1) lipomatosis and 2) Vacat obesity.

Lipomatosis

Lipomatosis. Term lipomatosis used in two meanings: (1) focal proliferation of adipose tissue without clear boundaries (for example, myocardial lipomatosis in obesity) and (2) multiple lipomas(tumors of white adipose tissue). In some cases, these processes are combined. Solitary lipomas and hibernomes(tumors of brown adipose tissue) can also be classified as regional cumulative acylglycerosis. Lipomas are usually soft, encapsulated, not fused with the surrounding tissues, yellow in the section and on the surface, with a diameter usually from 1 to 10 cm. The number of lipomas with lipomatosis in one patient can vary, sometimes exceeding 100 nodes.

Lipomas spread throughout the body (including internal organs) are called diffuse lipomatosis. There are children's and adult form diffuse lipomatosis. The childhood form usually appears in the first two years of life.

Symmetrical forms of lipomatosis are especially typical for middle-aged men who have lived for a long time in countries of the Mediterranean region. Many of them have a history of liver disease or chronic alcoholism.

In the practice of a pathologist highest value have diseases of (1) Madelung, (2) Derkum, (3) Rota-Paillard, (4) Launois-Binsau, (5) Verneuil-Poten, (6) Léry, (7) Marañon, (8) Féré-Langmead, (9) Pasteur-Vallery-Rado-Blamoutier, (10) pelvic and (11) steroid lipomatosis, and (12) HIV lipodystrophy, although these lipomatoses are rare in general.

1. Dercum's lipomatosis (lipomatosis dolorosa) [Francis Durcum- American neurologist] is characterized by the appearance of lipoma-like painful nodes in the subcutaneous tissue of the upper extremities, in the skin of the mammary glands, back, anterior abdominal wall, buttocks and thighs. Pain is determined by palpation, pressure and trauma to the node. It is associated with an inflammatory process in the nerve (neuritis). The skin over the nodes is cyanotic, and hemorrhages are common. Micromorphological examination reveals numerous blood capillaries in the tissue of the nodes, and signs of productive inflammation are noted in the nerve trunks. In some lipomas, focal necrosis of adipose tissue occurs and typical lipogranulomas are formed with the presence of giant multinucleated macrophages. The disease is typical for obese women in menopause. With Dercum lipomatosis, atrophic processes develop in endocrine glands ah, first of all thyroid (hypothyroidism).

2. When Madelung syndrome (multiple cervical symmetrical lipomatosis) [Otto von Madelung- German surgeon] in the neck area, adipose tissue grows in the form of multiple painful nodes. The nodes compress the organs of the neck, leading to dysphagia and difficulty breathing. Lipomatosis probably develops against the background of pituitary disorders.

3. When Roth-Paillard syndrome focal growths of white adipose tissue in lumbar region and on the limbs. The nodes are located symmetrically.

4. Launois-Bensau syndrome (symmetrical lipomatosis Launois-Binsault) is characterized by the appearance of symmetrical lipomas in the neck, abdomen and inguinal folds. Particularly characteristic are nodes on the anterior and posterior surfaces of the neck and in the submandibular region. Sometimes this syndrome in the domestic literature is called “Lonois-Vansaud lipomatosis” or “Lenou-Bensau syndrome.”

5. Verneuil-Poten lipomatosis differs in the localization of lipomas in the supraclavicular areas.

6. Lipomatosis Leri (diffuse symmetrical Lehry lipomatosis) - multiple lipomas, located symmetrically on upper limbs, in the buttocks area, less often in other areas of the skin.

7. Marañon lipomatosis (Marañon hypertrophic lipomatosis) - symmetrical widespread lipomatosis with lesions skeletal muscles (intramuscular lipomas). A feature of intramuscular lipomas is their unclear boundaries due to invasive growth. Such a node is fused to the surrounding tissues. Lipomas in this process give the patient the “look of Hercules.”

8. When Fere-Langmead lipomatosis fatty nodes are located on the palms.

9. Pasteur-Vallery-Rado-Blamoutier lipomatosis characterized by the localization of lipomas in the subcutaneous tissue of the lateral surfaces of the chest.

10. Pelvic lipomatosis differs in the location of lipomas in the pararectal and paravesical tissue. Most often the process occurs in people of the Negroid race of different ages.

11. Steroid lipomatosis refers to iatrogenic forms of lipomatosis. It occurs when long-term use glucocorticoid hormone preparations. Lipomas form primarily on the face, anterior chest wall and above cervical vertebrae(“buffalo hump”).

12. When HIV lipodystrophy In addition to various changes in adipose tissue in patients with HIV infection, the growth of adipose tissue in the neck, mammary glands and internal organs may also occur. Lipomatosis is associated with the action of specific antiretroviral drugs ( iatrogenic lipomatosis). On the face and limbs, on the contrary, fatty tissue may disappear. Patients exhibit hyperlipidemia and peripheral tissue resistance to insulin.

Vacat obesity

Vacant obesity(from lat. vacuus- empty) - replacement of atrophied organ parenchyma with white adipose tissue. Vacant obesity is most commonly observed in skeletal muscle. The organ may enlarge (pseudohypertrophy).

Generalized resorptive acylglyceroses

TO generalized resorptive acylglyceroses refer (1) cachexia (exhaustion, marasmus, general pathological atrophy) and 2) . Some authors call cachexia extreme degree depletion (loss of more than half normal weight body), however, in domestic pathological anatomy these concepts are used as synonyms.

Cachexia

Cachexia(from Greek kakos- bad, hexis- condition) develops (1) with complete long-term starvation or malabsorption ( nutritional cachexia , exogenous cachexia), (2) at anorexia nervosa, (3) malignant tumors (“ cancer cachexia"), (4) with atrophy and necrosis of the tissue of the hypothalamus and pituitary gland ( hypothalamic-pituitary cachexia, or Simmonds-Schien disease), (5) for chronic infections (for example, tuberculosis or long-term purulent processes), (6) for burn disease (“burn exhaustion”), (7) for autoimmune diseases, (8) with general chronic congestive hyperemia, and also (9) with metabolic disorders of a number of hormones (severe chronic adrenal insufficiency, hypoinsulinism, hyperglucagonemia, hypersomatostatinemia). “Wound exhaustion” is a variant of cachexia in chronic purulent infection (“purulent-resorptive fever”). The leading role in the development of endogenous forms of cachexia, in addition to the hypothalamic-pituitary one, is given to TNF-α (cachectin), the main producer of which is macrophages. Hypothalamic-pituitary cachexia is caused by damage to the hunger center, as a result of which the main trigger of eating behavior, neuropeptide Y, ceases to be produced. “Cancer cachexia” has a more complex pathogenesis. In addition to the characteristic appearance, secondary lipofuscinosis is typical for cachexia ( brown atrophy myocardium and liver), as well as the concentration of lipochromes in tissues (the remaining adipose tissue acquires a brownish color as a result). There is no fatty tissue, especially subcutaneous tissue. The skin is dry and flabby. Internal organs are reduced. At a certain stage, exhaustion develops arrowroot edema due to a decrease in oncotic pressure in tissues.

Lipotropin overproduction syndrome

Lipotropin overproduction syndrome (hypermuscular lipodystrophy, lipoatrophic diabetes, generalized lipodystrophy syndrome) is a disease in which the synthesis and secretion of lipotropic hormones by the adenohypophysis increases significantly. The syndrome occurs mainly in women and appears in most cases before the age of 40. Peripheral and visceral adipose tissue is practically absent in patients; only fatty tissue is retained on the palms and soles, in the retro-orbital, epidural or para-articular areas, and in acquired forms - on the face. However, some patients experience excess deposition of subcutaneous fat in the face and neck. Lipotropin overproduction syndrome is characterized by severe hyperlipidemia and hyperglycemia against the background of significant hyperinsulinemia, but diabetes mellitus is rarely complicated by ketoacidosis. Hyperlipidemia leads to the development of severe liver steatosis, progressing to cirrhosis, as well as atherosclerosis. There are hereditary (autosomal recessive inheritance) and acquired variants of the disease. It was previously assumed that with this disease there is an increase in the production of somatotropic hormone by the adenohypophysis, as a result of which hypertrophy of skeletal muscles and internal organs develops and, in some cases, growth resumes in adulthood, but this opinion has not been confirmed. Muscle hypertrophy and visceromegaly are caused by severe persistent endogenous hyperinsulinemia. The natural life expectancy of patients is 35-50 years. The prognosis largely depends on the time of manifestation of the disease: the syndrome that develops during puberty has the most unfavorable course. The main causes of death are liver cirrhosis and atherosclerotic vascular lesions (myocardial infarction, ischemic stroke).

Regional resorptive acylglyceroses include two groups of pathological processes: (1) focal necrosis of adipose tissue ( liponecrosis, steatonecrosis) and (2) local atrophy of white adipose tissue ( regional lipoatrophy).

Focal necrosis of adipose tissue

The main non-infectious processes in which focal necrosis of adipose tissue, are the following forms of regional acylglyceroses:

1. Weber-Christian disease (spontaneous panniculitis)
2. Traumatic lipogranuloma
3. Pancreatic liponecrosis
4. Insulin liponecrosis.

In addition, adipose tissue necrosis develops when cold, post-steroid(when stopping taking glucocorticoid hormones) and reactive(secondary change against the background of other diseases) panniculitis, as well as in newborns ( necrosis of the subcutaneous tissue of newborns) and children early age (acute multinodular disseminated non-recurrent liponecrosis).

Weber-Christian disease- autoimmune damage to adipose tissue. At the site of necrosis of adipose tissue, a node is formed, located in the hypodermis at different depths. The diameter of individual nodes ranges from a few millimeters to 10 cm or more. Nodes can be located on any part of the skin; they are rarely isolated. The favorite localization of nodes is the skin of the extremities. Sometimes nodes merge into conglomerates. Large nodes contain cavities with a yellowish foamy mass ( fatty detritus) and clinically simulate an abscess or phlegmon. The disease begins with symptoms of general intoxication, with the exception of the Rothmann-Makai variant, and proceeds with relapses and remissions. The duration of spontaneous panniculitis varies: from several weeks to several decades, more often from a week to a year.

There are four forms of Weber-Christian disease:

• Spicy(rare fatal course of the disease with severe liver damage)
• I'll sharpen it up(moderate form, reminiscent of sepsis, with moderate liver damage)
• Chronic(proceeds favorably with long-term remissions without liver damage)
• Rothmann-Makai form(proceeds favorably, there is no general intoxication reaction).

At changed adipose tissue reveals a lymphohistiocytic infiltrate, foci of lipocyte necrosis with the presence foam macrophages and the formation of characteristic fatty cysts. During the resorption of detritus, it grows in its place. fibrous tissue, giving density to the lesions.

Traumatic lipogranuloma- focal necrosis of fatty tissue in its place mechanical damage with the subsequent development of productive inflammation. This process is often incorrectly called “traumatic oleogranuloma.” Oleogranuloma (lat. oleum- oil) - a focus of productive inflammation at the site of administration of vegetable fat (oil solution of the drug).

Pancreatic liponecrosis (pancreatic lipodystrophy) - necrosis of adipose tissue, developing under the influence of pancreatic enzymes (with acute pancreatitis, disintegrating malignant tumors of this organ).

Insulin liponecrosis (insulin lipodystrophy) occurs at insulin injection sites. At the same time, dense, flattened nodes with a diameter of 2 to 20 cm with a depression in the center and clear boundaries are formed in the subcutaneous fatty tissue. The skin over the node does not move, because soldered to him. Nodules may appear in areas distant from the injection sites.

Regional lipoatrophy

TO regional lipoatrophy can be attributed to the one mentioned in the section “Cerebral obesity” Barraquer-Simons disease(lipoatrophy of the upper body and obesity of the lower). Other local lipoatrophies are also known: autosomal dominant lipoatrophy of the extremities, circular and semicircular lipoatrophy of the extremities, girdle abdominal lipoatrophy in infants, etc.

Cholesterosis

Disturbances in the metabolism of cholesterol and cholesterol are manifested primarily by their accumulation in tissues ( cumulative cholesterosis), especially in the wall of arteries and in the skin, but a hereditary disease with cholesterol deficiency is known ( resorptive cholesterosis). Cholesterol refers to necessary substances: steroid hormones, vitamin D, bile acids are synthesized from it, it is part of the biomembranes of all cells, so cholesterol deficiency leads to no less devastating consequences for the body than its excess.

Resorptive cholesterosis

Cholesterol deficiency is observed in children with hereditary Bessen-Kornzweig disease, in which a defect in the enzymes for the synthesis of cholesterol in various cells of the body is formed. The most severe changes occur in the brain: its underdevelopment (hypoplasia) is associated precisely with a deficiency of cholesterol and cholesterol. Underdevelopment of brain tissue is accompanied by oligophrenia.

Cumulative cholesteroses

Distinguish hereditary And purchased forms cumulative cholesterosis. The accumulation of cholesterol and cholesterol in tissues is primarily due to their intake from food ( exogenous cholesterol), although a certain role is played by the high synthetic activity of cells ( endogenous cholesterol). Cholesterol and cholesterol are deposited most often in the walls of arteries ( atherosclerosis), dermis ( xanthomatosis) and in outer shell eyes ( lipoid arc of the cornea). The range of altered tissues in hereditary cumulative cholesterosis is significantly wider: for example, with Tangier Island diseases Characterized by the accumulation of cholesterol in the palatine tonsils (“orange tonsil disease”) and in other lymphoid organs.

The main reason for the accumulation of cholesterol in tissues is the insufficiency of the mechanism for its reverse transport. The key factor reverse cholesterol transport systems(from the periphery to the liver, from where its excess is removed from the body with bile) are high density lipoproteins, more precisely the protein included in their composition apoprotein A. Apoprotein A is synthesized by hepatocytes and integumentary enterocytes; it has a unique ability to absorb cholesterol and its esters (“cholesterol magnet”). High-density lipoprotein particles collect cholesterol not only in the interstitial sector, but also inside cells. In humans (as well as higher apes and pigs), there is a species-specific (characteristic of all representatives of the species) deficiency of apoprotein A and, accordingly, high-density lipoproteins. Animals with high content of these lipoproteins do not suffer from cholesterol diathesis, even with constant use cholesterol-rich foods. Some people are also quite different high concentration apoprotein A (“longevity syndrome”).

Mesenchymal carbohydrate dystrophies

Mesenchymal carbohydrate dystrophies include (1) disorders of glycosaminoglycan metabolism which include hereditary diseases mucopolysaccharidoses, and 2) disorders of glycoprotein metabolism (mucus tissue).

Mucopolysaccharidoses

Mucopolysaccharidoses- thesaurismosis, accompanied by the accumulation of glycosaminoglycans in tissues. The term “mucopolysaccharidoses” comes from the outdated designation of proteoglycans (neutral mucopolysaccharides) and their constituent glycosaminoglycans (acidic mucopolysaccharides). Mucopolysaccharidoses are characterized by gargoylic syndrome(from fr. gargouille- a grotesque figurine resembling a person, which was used to decorate roofs, cornices and other details of old houses): a massive skull, short neck, receding wide nose bridge, hypertelorism, thick lips, high palate, fused eyebrows, large tongue.

The pathological anatomy of the first six types of mucopolysaccharidoses has been most studied: Pfoundler-Hurler disease (type I), Gunter disease (type II), Sanfilippo disease (type III), Brailsford-Morkio disease (type IV), Scheie disease (type V) and Maroto-Lami (type VI). ).

1. More common Pfaundler-Hurler disease [Reinhard von Pfaundler And Gertrude Gurler- German doctors], which is based on a deficiency α-L-iduronidases. Dermatan and heparan sulfates accumulate in tissues, and their content in urine is significantly increased. Symptoms appear towards the end of the first year of life. The disease progresses rapidly, gargoilism syndrome is combined with deep violations psyche, early corneal opacification, deafness, hepato- and splenomegaly. Death usually occurs at the age of 10-12 years with damage to the brain (usually due to hydrocephalus), heart, or from intercurrent diseases.

At macromorphological study reduced and flattened vertebrae with spiky projections, mushroom-shaped intervertebral discs are found, because they are larger than the diameter of the vertebral body. The tubular bones are curved, the epiphyseal lines are curved, jagged. At micromorphological study violations of periosteal and enchondral ossification are detected due to the deposition of glycosaminoglycans in cartilage tissue and in the periosteum. Chondrocytes are swollen, oval in shape, and do not form cartilaginous columns, so the growth of bones in length is delayed. The ground substance and collagen fibers of tendons, fascia, vessel walls, and heart valves contain a large amount of glycosaminoglycans, which are clearly visible by metachromatic staining. The myocardium is hypertrophied, the valvular and parietal endocardium, the chordae tendineae and the walls of the coronary arteries are thickened. In the mitral and aortic valves, vascularization and calcification, deposition of glycosaminoglycans in the interstitial substance and the presence of cell accumulation gurler. Glycosaminoglycans are found in hepatocytes, macrophages of the spleen and lymph nodes, cells of the adenohypophysis, in the cornea, gonads, soft meninges, peripheral nerves, neurons of the brain and autonomic ganglia. At electron microscopy inclusions corresponding to damaged lysosomes are detected in the cells, having the appearance of light transparent vacuoles, “zebra-shaped” or amorphous bodies.

2. When Gunther's disease dermatan sulfate and heparan sulfate accumulate in tissues due to enzyme deficiency iduronate sulfatase. The type of inheritance is recessive, linked to the X chromosome. The course of the disease is long compared to mucopolysaccharidosis type I. Manifestations are moderate, corneal clouding is absent in most cases, but progressive deafness is characteristic.

3. Sanfilippo disease [Sylvester G. Sanfilippo- American pediatrician]. There are four clinical and laboratory variants of the disease (variant A is caused by a defect heparan sulfate sulfatase, B- α-N-acetylglucosaminidase,C- α-glucosaminide-N-acetyltransferase, D- acetylglucosamine-6-sulfate sulfatase). All variants of the disease are phenotypically identical. The body has an increased content of mainly heparan sulfate, which accumulates in the neurons of the brain, arterial walls, liver and spleen.

4. Brailsford-Morkio disease [James Frederick Brailsford- English doctor, Luis Morquio( -) - Uruguayan pediatrician] is manifested by the accumulation of keratan and dermatan sulfates. Due to the breakdown of metaepiphyseal cartilage, patients are of low or dwarf stature. Intelligence is usually normal.

5. Scheie's disease [Harold G. Scheie- American ophthalmologist] is characterized by the accumulation of mainly dermatan sulfate. The disease manifests itself only in adulthood. Characterized by short or dwarf stature. Intelligence is normal.

6. When Maroteau-Lami disease [Pierre Maroteau- French pediatrician and geneticist, Maurice Lamy(-) - French geneticist] accumulation of dermatan sulfate occurs. Dwarf stature of patients is typical.

Close to mucopolysaccharidoses mucolipidoses And hereditary glycoproteinoses.

Slime tissue

Sliming of tissues- replacement of fibrous and other connective tissues with a mucus-like mass formed during the breakdown of proteoglycans and the release of glycosaminoglycans from them. Tissue mucus occurs when (1) cachexia

Often the cause of a swollen waist and unsightly folds of fat is considered hereditary obesity. But even with “bad” genetics, you can get rid of those extra pounds if your diet is balanced and physical activity is properly selected and regular. Weight normalization is a proven and effective way not only to give the body beautiful and attractive shapes, but also to eradicate various ailments and say goodbye to cellulite.

The connection between obesity and the hormone leptin

Why genetic obesity is the hardest

• Firstly, obesity is “in the blood” of a person from birth. It is difficult for him not only to begin to fight fat deposits, but even to imagine that it is possible to change, to lose the weight that has grown together with him.
• Secondly, overeating from a young age is perceived as normal. Often, nearby relatives also suffer from excess weight and have negative experiences of losing weight.
• Third, usually, only a danger to life, alarming anomalies in the body force a plump person to seek medical help.

All methods of losing weight:

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The main reasons for obesity

• constant overeating;
• unregulated rest and eating patterns, for example, working at night, eating “for future use”, in bursts;
• physical inactivity or pathology that does not allow any physical activity;
• work as a pastry chef, seller of “delicious things”.

Reconsidering childhood habits

How to eat

Stage one

• meat;
• dairy and fermented milk products;
• fish and poultry;
• tongue and liver;
• seafood and eggs.

• broccoli;
• champignons and asparagus;
• celery (leaves) and sauerkraut;
• cucumbers, radishes, turnips;
• fresh almonds and green olives;
• lettuce and zucchini;
• peppers and green beans;
• tomatoes.

Stage two

• eggplants and mushrooms;
• beets and avocados;
• artichokes;
• celery (roots);
• cabbage (Brussels sprouts and cauliflower, kohlrabi and red, white);
• melon and black olives;
• hot peppers and leeks;
• fresh pineapples and apricots;
• gooseberries and strawberries;
• tangerines and kiwis;
• blueberries and blackberries;
• grapefruits and oranges;
• apples and peaches;
• grapes and pears;
• freshly prepared juice from unsweetened fruits.

Stage three

What results to expect

• significant reduction in cravings for sweets;
• disappearance of belching and flatulence;
• improved performance and lack of drowsiness;
• weight loss;
• improving the functioning of the pancreas.

What are the health risks of being overweight?

• Excessive load on the heart muscle. The myocardium enlarges, gets tired, wears out, and its pumping function worsens. Scientists have proven that every 10 kg of excess, excess weight encourages the body to “build” 15 km of new (not shrouded in fat!) vessels.
• Anomalies of the vascular system. Lipoids, mainly bad cholesterol, are deposited on the inner walls of blood vessels. They become overgrown with connective tissue, become denser, their lumen narrows, and, accordingly, patency is impaired.
• Various ailments, including destruction, weakening musculoskeletal system. The spinal column, joints of the feet and hands are mainly affected and deformed. Cases of dislocations and subluxations are common.
• Imbalance in the functions of the sex glands, including impotence in the stronger half, infertility and irregular menstrual cycles in women.
• Frequent infectious (cold) diseases, since the immune system is significantly weakened.

– excess fat deposits in subcutaneous tissue, organs and tissues. It manifests itself as an increase in body weight by 20 percent or more of the average due to adipose tissue. Causes psycho-physical discomfort, causes sexual disorders, diseases of the spine and joints. Increases the risk of developing atherosclerosis, coronary artery disease, hypertension, myocardial infarction, stroke, diabetes mellitus, kidney damage, liver damage, as well as disability and mortality from these diseases. The most effective treatment for obesity is the combined use of 3 components: diet, physical activity and appropriate psychological adjustment of the patient.

The endocrine type of obesity develops with pathology of the glands internal secretion: hypothyroidism, hypercortisolism, hyperinsulinism, hypogonadism. With all types of obesity, hypothalamic disorders are observed to one degree or another, which are either primary or occur during the course of the disease.

Obesity symptoms

A specific symptom of obesity is excess body weight. Excess fat deposits are found on the shoulders, abdomen, back, sides of the body, back of the head, hips, and pelvic area, while underdevelopment of the muscular system is noted. The patient’s appearance changes: a double chin appears, pseudogynecomastia develops, fat folds on the abdomen hang down in the form of an apron, and the hips take the shape of riding breeches. Umbilical and inguinal hernias are typical.

Patients with degrees I and II obesity may not present any special complaints; with more severe obesity, drowsiness, weakness, sweating, irritability, nervousness, shortness of breath, nausea, constipation, peripheral edema, pain in the spine and joints are noted.

Patients with grade III-IV obesity develop disorders of the cardiovascular, respiratory, digestive systems. Objectively, hypertension, tachycardia, and muffled heart sounds are detected. Standing tall the dome of the diaphragm leads to the development of respiratory failure and chronic cor pulmonale. Fatty infiltration of the liver parenchyma, chronic cholecystitis and pancreatitis occurs. Pain in the spine, symptoms of arthrosis of the ankles and knee joints. Obesity is often accompanied by menstrual irregularities, including the development of amenorrhea. Increased sweating causes the development of skin diseases (eczema, pyoderma, furunculosis), the appearance of acne, stretch marks on the abdomen, hips, shoulders, hyperpigmentation of the elbows, neck, and places of increased friction.

Obesity various types has similar general symptoms, differences are observed in the pattern of fat distribution and the presence or absence of signs of endocrine or nervous systems. At nutritional obesity body weight increases gradually, fat deposits are uniform, sometimes predominant in the thighs and abdomen. There are no symptoms of damage to the endocrine glands.

With hypothalamic obesity, obesity develops quickly, with a predominant deposition of fat on the abdomen, thighs, and buttocks. There is an increase in appetite, especially in the evening, thirst, night hunger, dizziness, and tremor. Trophic skin disorders are characteristic: pink or white stretch marks (stretch stripes), dry skin. Women may develop hirsutism, infertility, menstrual irregularities, and men may experience deterioration in potency. Neurological dysfunction occurs: headaches, sleep disturbance; autonomic disorders: sweating, arterial hypertension.

The endocrine form of obesity is characterized by a predominance of symptoms of underlying diseases caused by hormonal imbalances. The distribution of fat is usually uneven, with signs of feminization or masculinization, hirsutism, gynecomastia, and cutaneous stretch marks. A unique form of obesity is lipomatosis – benign hyperplasia of adipose tissue. Manifested by numerous symmetrical painless lipomas, it is more often observed in men. There are also painful lipomas (Dercum lipomatosis), which are located on the limbs and trunk, are painful on palpation and are accompanied by general weakness and local itching.

Complications of obesity

Except psychological problems Almost all obese patients suffer from one or a number of syndromes or diseases caused by excess weight: coronary artery disease, type 2 diabetes mellitus, arterial hypertension, stroke, angina pectoris, heart failure, cholelithiasis, liver cirrhosis, sleep apnea syndrome, chronic heartburn, arthritis, arthrosis, osteochondrosis, polycystic ovary syndrome, decreased fertility, libido, disorder menstrual function etc.

Obesity increases the likelihood of breast, ovarian and uterine cancer in women, prostate cancer in men, and colon cancer. There is also an increased risk of sudden death due to existing complications. The mortality rate for men aged 15 to 69 years with an actual body weight that is 20% greater than ideal body weight is one third higher than for men of normal weight.

Diagnosis of obesity

When examining patients with obesity, attention is paid to the medical history, family predisposition, the minimum and maximum weight after 20 years, the duration of the development of obesity, the activities carried out, the patient’s eating habits and lifestyle, and existing diseases are determined. To determine the presence and degree of obesity, the method of determining body mass index (BMI) and ideal body weight (IB) is used.

The nature of the distribution of adipose tissue on the body is determined by calculating a coefficient equal to the ratio of the waist circumference (WC) to the hip circumference (HC). The presence of abdominal obesity is indicated by a coefficient exceeding 0.8 for women and 1 for men. It is believed that the risk of developing concomitant diseases is high in men with WC > 102 cm and in women with WC > 88 cm. To assess the degree of subcutaneous fat deposition, the size of the skin fold is determined.

The most accurate results for determining localization, volume and percentage adipose tissue from total body weight is obtained using auxiliary methods: ultrasound, nuclear magnetic resonance, computed tomography, X-ray densitometry, etc. If patients are obese, they need consultations with a psychologist, nutritionist and physical therapy instructor.

To identify changes caused by obesity, determine:

• indicators blood pressure(to detect arterial hypertension);
• hypoglycemic profile and glucose tolerance test (to detect type II diabetes mellitus);
• level of triglycerides, cholesterol, low- and high-density lipoproteins (to assess lipid metabolism disorders);
• changes in ECG and echocardiography (to identify disturbances in the circulatory system and heart);
• level uric acid V biochemical analysis blood (to detect hyperuremia).

Obesity treatment

Each obese person may have their own motivation for losing weight: a cosmetic effect, reducing health risks, improving performance, the desire to wear smaller clothes, the desire to look good. However, goals for weight loss and its pace should be realistic and aimed, first of all, at reducing the risk of complications associated with obesity. Treatment for obesity begins with diet and exercise.

For patients with BMI

When following a hypocaloric diet, basal metabolism decreases and energy is conserved, which reduces the effectiveness of diet therapy. Therefore, a hypocaloric diet must be combined with physical exercise, increasing the processes of basal metabolism and fat metabolism. Purpose therapeutic fasting indicated for patients undergoing hospital treatment with severe obesity for a short period of time.

Drug treatment of obesity is prescribed when a BMI is >30 or the diet is ineffective for 12 weeks or more. The action of drugs from the amphetamine group (dexafenfluramine, amfepramone, phentermine) is based on inhibition of hunger, acceleration of satiety, and anorectic effect. However, side effects are possible: nausea, dry mouth, insomnia, irritability, allergic reactions, addiction.

In some cases, the administration of the fat-mobilizing drug adiposine, as well as the antidepressant fluoxetine, which changes eating behavior, is effective. The most preferred drugs today in the treatment of obesity are sibutramine and orlistat, which do not cause significant adverse reactions or addiction. The action of sibutramine is based on accelerating the onset of satiety and reducing the amount of food consumed. Orlistat reduces the absorption of fats in the intestines. For obesity, symptomatic treatment of underlying and concomitant diseases is carried out. In the treatment of obesity, the role of psychotherapy (conversation, hypnosis) is high, changing the stereotypes of developed eating behavior and lifestyle.

Forecast and prevention of obesity

Timely, systematic interventions for the treatment of obesity bring good results. Already with a decrease in body weight by 10%, the overall mortality rate decreases by >20%; mortality caused by diabetes > than 30%; caused by accompanying obesity cancer diseases, > than 40%. Patients with I and II degrees of obesity remain able to work; with degree III - they receive disability group III, and in the presence of cardiovascular complications - disability group II.

To prevent obesity, a person with normal weight only needs to spend as many calories and energy as he receives during the day. With a hereditary predisposition to obesity, after the age of 40, with physical inactivity, it is necessary to limit the consumption of carbohydrates, fats, and increase protein and plant foods in the diet. Reasonable physical activity is required: walking, swimming, running, visiting gyms. If you are dissatisfied with your own weight, in order to reduce it you need to contact an endocrinologist and nutritionist to assess the degree of violations and draw up an individual weight loss program.

Obesity and heredity

Considering the issue of “obesity and heredity,” it is worth noting that there is still no substantiated evidence that some people have obesity in their genes. There is a possibility of transmitting a hereditary predisposition to obesity, and sometimes only heredity can explain the cause of excess weight.

But still, in most cases, the problem of obesity is associated either with serious disturbances in the functioning of the body, or with an incorrect lifestyle. Some might object by saying that there are many cases of obese parents having obese children. overweight. But even in such cases, the entire responsibility for the occurrence of the problem cannot be placed on hereditary predisposition.

As I already said, such people have a predisposition, but obesity itself develops due to the fact that such families initially already have “destructive” habits, for example, eating large amounts of fatty and high-calorie foods, snacking on chips and crackers, drinking large amounts of sweet soda, sedentary lifestyle, etc. That is why children growing up in such families are already developing from childhood, which subsequently leads to the development of obesity.

So what should you do if a person has a predisposition to developing obesity, and can it be avoided if you take good care of your body? I will try to cover the answers to these questions in detail in this article.

Where does obesity come from?

Let's look at the reasons or a set of reasons that can lead to the development of obesity.

• In first place among the causes of obesity is. You know that if you constantly eat high-calorie foods and regularly overeat, then very soon the body loses its ability to be full, which provokes the consumption of even more food. And when the digestion process is disrupted, obesity is right there, and before you have time to realize that you have a problem, your weight will already begin to go off scale.
• In addition to eating disorders, obesity can develop in people who consider it an unnecessary activity. Such people are accustomed to spending their days sitting in front of the computer and their evenings on the couch in front of the TV.
• When discussing obesity and heredity, we can say that obesity itself is not inherited, but a predisposition to obesity is transmitted. And if you are in the “risk zone”, you need to organize your life more carefully so that there is a place for active types of recreation. There is no need to neglect the rules of rational nutrition.
• Obesity can also develop with serious illnesses. For example, obesity develops with certain tumors or with a malfunction thyroid gland etc. Only a doctor can determine such disturbances in the functioning of the body, therefore, before taking any steps to treat obesity, consultation with a specialist is necessary. Only a doctor can tell you the reason and prescribe the necessary treatment.

The general recommendations of doctors for the treatment of obesity relate to the same lifestyle, and if you want to get rid of excess weight and transform beyond recognition, you will have to be patient and willpower, and then you will succeed.

What to do?

People suffering from obesity should not blame heredity and wait for geneticists to discover the gene responsible for this and create “” in order to rid all of humanity of the problem of obesity in one fell swoop. You need to get down to business yourself, and the desire to ensure that this does not become a result and a properly developed strategy will definitely do their job and save you from this problem for a long time, and maybe even forever.

The first thing people who are obese need to think about is how they eat. To do this, “soberly” assess the nutrition situation. It is very important to admit that you eat “tasty” and “a lot”. And when you recognize this, you will understand where to move. But still, you shouldn’t radically change your eating habits - start with small changes, by giving up some of the most harmful products, or from replacing fatty ones with low-fat analogues. When you get used to this diet, start introducing the following changes and so on until your diet becomes balanced.

Sport is something “scary” for many people, and they don’t even know how to approach it. This is understandable; it is very difficult for a person with excessive body weight not only to run, but even just to walk. It’s difficult, but it’s still necessary. Start with small walks, gradually move to a slow one, do several bends, and gradually your body will be drawn into the process. When excess weight will slowly begin to “melt”, you will be able to afford more complex exercises and activities - aerobics, running.

Another way to overcome obesity is to take natural weight loss medications. Moreover, preference should be given to natural ones, since they also have a healing effect and also do not have side effects, unlike various ones. And in a healthy body, all processes proceed more intensely, and you can lose weight more effectively. By using these drugs, you will “suffer” less from switching to a new diet, because the drug reduces appetite and cravings for sweets. And by combining taking medications with some dietary restrictions and physical activity, you will increase their effectiveness several times, and after some time you will be able to forget about how much suffering your excess weight has brought you.

VES.ru - website - 2006

Genetic predisposition to obesity

Of great importance in a particular disease is gene variability, leading to disruption of the function or amount of protein encoded by a given gene. In particular, this concerns the variability of genes that cause obesity.

There are several gene mutations (changes) that can cause obesity. These mutations most often also contribute to the development of type 2 diabetes mellitus and other endocrine diseases. This is most often associated with mutations in genes encoding proteins of the signaling system responsible for regulating the amount of energy stored as fat in the body.

This signaling pathway begins with the protein Leptin, which is produced by adipose tissue. Moreover, its amount is proportional to the volume of adipose tissue. Leptin activates through a specific receptor (nerve ending) in the hypothalamus (part of the most ancient structure of the brain) and turns on the production of melanocortin, which reduces human food intake. The presence of mutations in almost any of the genes in this chain leads to the development of obesity syndrome.

Congenital leptin deficiency

This is a rare syndrome associated with a gene mutation that shifts the reading frame of gene information located at position ΔG133 (the map of the human genome is almost completely known). In this case, an altered form of leptin appears, which is not secreted by fat cells. Today there are several hundred families in the world where there are people with obesity caused by this mutation. Correction is achieved by introducing the missing leptin into the body.

Congenital leptin receptor deficiency

This is a rare syndrome associated with a mutation in the leptin receptor gene in the hypothalamus. In this case, a form of altered receptor appears that does not bind leptin. Today there are several dozen families in the world that carry this mutation. Correction unknown.

Mutation in the proopiometalocortin (POMC) gene

In this case, a form of altered protein appears in which the amino acid arginine is replaced by glycine at position 236 (Arg236Gly). Occurs in approximately 1% of all cases of hereditary obesity. In addition to obesity syndrome, carriers of this gene have a deficiency of ACTH (adenocorticotropic hormone) and red hair coloring.

Mutation in the PC-1 gene

The function of the protein encoded by this gene is that it forms the hormones ACTH and melanocortin by specifically cutting POMC. In this case, symptoms similar to mutations in the POMC gene develop, with the only difference that hyperproinsulinemia (an increase in the level of insulin precursor in the blood) is also added, since PC-1 also converts proinsulin into active insulin in pancreatic cells.

Mutation in the melanocortin type 4 receptor gene (MC4R)

The most commonly observed genetically determined form of obesity. Occurs in 6% of all cases of obesity. About 15 different mutations in this gene have been described. One of them occurs in 95-99% of cases and affects about 1.3% of the entire human population.

Obesity in carriers of all the above mutations is associated with overeating. People simply do not receive the signal that there is sufficient energy storage in the form of fat in fat cells. But if a mutation in the hormone leptin itself is corrected using injections of the missing protein, then in the presence of mutations in all other genes, correction of food intake is required by all known methods, including using surgical methods.

Unfortunately, not all factors have been identified to date. genetic predisposition influencing the development of obesity. The mechanisms were not found either. effective correction genetic mutations. However, existing knowledge helps predict the possibilities of each type of conservative or surgical treatment. Analysis for the presence of a mutation in one of the listed genes in a patient will allow us to identify a group of people for whom treatment should be immediate and radical.