Causes of anorexia nervosa

The causes of anorexia nervosa are unknown. In addition to gender (female), a number of other risk factors have been identified. In Western society, obesity is considered unattractive and unhealthy, so the desire to be thin is widespread, even among children. More than 50% of prepubertal girls use diets or other methods of weight control. Excessive concern about one's own weight or a history of dieting are predictors of increased risk, especially in people with a genetic predisposition to anorexia nervosa. Studies of monozygotic twins show a concordance rate of over 50%. Familial and social factors are likely to play a role. Many patients belong to the middle and upper socioeconomic classes; they are meticulous, conscientious, and intelligent, with very high standards of achievement and success.

The causes of anorexia are an unsolved problem. Foreign authors often interpret its occurrence from the Freudian standpoint as "unconscious escape from sexual life", "desire to return to childhood", "rejection of pregnancy", "frustration of the oral phase", etc. However, psychoanalytic concepts do not explain the manifestations of the disease, on the contrary, they lead to their incorrect understanding. Both mental changes and humoral factors play a role in the formation of nervous anorexia and its development.

The causes of anorexia should also be sought in premorbid personality traits, physical and mental development, upbringing, and microsocial factors. Nervous anorexia occurs in the pre-, post-, and actual pubertal period, i.e. the background is dysregulatory changes in the endocrine system characteristic of this period. The development of the bulimic form of nervous anorexia is also associated with premorbid features of the hypothalamic-pituitary system function. It has also been established that starvation, leading to exhaustion, causes secondary neuroendocrine and metabolic changes, which in turn affect the function of the cerebral structures of the brain, causing mental changes. A vicious circle of psychobiological disorders is formed. The possible role of the opioid peptide system in regulating eating behavior in patients is being studied.

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Endocrine causes of anorexia

Endocrine disorders in nervous anorexia. The presence of amenorrhea was one of the diagnostic criteria for nervous anorexia. It is the menstrual dysfunction that often makes patients seek medical attention for the first time. The question of whether these changes are primary or secondary is widely discussed. The most common point of view is that the loss of menstruation occurs secondarily, due to weight loss. In this regard, a position was put forward about a critical body weight - a fairly individual weight threshold at which amenorrhea occurs. At the same time, in a large number of patients, menstruation disappears at the very beginning of the disease, when there is no weight deficit, i.e. amenorrhea is one of the first symptoms. It is known that when body weight is restored to the value at which the menstrual function was lost, the latter is not restored for a long time. This makes it possible to think about the primacy of hypothalamic disorders that manifest themselves against the background of special eating behavior in such patients. It is possible that during body weight rehabilitation the fat tissue/body weight ratio may not be restored, and this is necessary for normal menstrual function. The pathogenesis of amenorrhea in female athletes is also associated with a violation of this ratio.

Studies of gonadotropic secretion have revealed a decrease in circulating pituitary and ovarian hormones. When luliberin is administered to patients, a decreased release of LH and FSH is observed compared to healthy people. The question of the possibility of treating amenorrhea associated with disorders at the hypothalamic level is discussed. A correlation has been revealed between hormonal and somatic changes that are responsible for maintaining amenorrhea. Psychogenic factors are important during periods of restoration of menstruation and the onset of disorders.

A study of the secretion and metabolism of sex steroids showed an increase in testosterone levels and a decrease in estradiol, which is explained by changes in the function of the enzyme systems involved in the synthesis of these steroids and metabolism in tissues.

In patients with bulimia, amenorrhea often occurs without a pronounced deficit in body weight. It is possible that the special "vomiting" behavior of patients corresponds to changes in the system of neuropeptides, neurotransmitters of the brain, which affect the hypothalamic mechanisms of regulation of menstrual function.

Laboratory studies show that the levels of free T4 _, total T4 _, and TSH are normal, but serum T3 _in patients with severe weight deficit is reduced, while pituitary thyrotropin (TSH) remains normal, i.e., paradoxical insensitivity of the pituitary gland to a decrease in T3 is observed _. However, with the introduction of thyroliberin, a release of TSH is noted, which indicates normal hypothalamic-pituitary connections. A decrease in T3 _is caused by a change in the peripheral transition of T4 _to T3 _and is regarded as a compensatory reaction that promotes energy conservation in conditions of exhaustion and weight deficit.

In patients with nervous anorexia, an increase in plasma cortisol has been established, which is associated with a disorder of the hypothalamus-pituitary-adrenal system. To study the pathophysiology of these disorders, patients were administered corticotropin-releasing factor. In this case, a significantly reduced ACTH response to stimulation was noted. Changes in the rhythm of cortisol secretion, the absence of suppression during the dexamethasone test are observed in some mental disorders not accompanied by a deficit in body weight. A number of authors point to a change in the function of adrenal enzymes in patients with nervous anorexia, regulated by propiocortin. A decrease in the excretion of 17-OCS in the urine is associated with a disorder of cortisol metabolism and renal function.

Of particular interest is the state of carbohydrate metabolism in patients with bulimia. They show metabolic signs of starvation (increased beta-hydroxybutyric acid and free fatty acids in the blood) without a pronounced deficit in body weight, as in patients with refusal to eat and weight loss, as well as decreased glucose tolerance, changes in insulin secretion. These factors cannot be explained only as secondary, caused by weight loss and weight loss; they may be associated with specific eating behavior.

Chronic hypoglycemia is observed in patients with food refusal. The literature contains descriptions of hypoglycemic comas in patients with nervous anorexia. The decrease in insulin levels is apparently associated with the state of chronic starvation. The glucagon level remains normal during a long-term illness, increasing only in the first days of food refusal. With glucose loading, its level does not differ from that of healthy people. Nervous anorexia occurs in young girls with diabetes mellitus. Then it is the cause of an unexplained labile course of the disease.

The level of somatotropin is increased in severe conditions of patients and significant body weight deficit. Its paradoxical reaction is noted when glucose is administered. The literature contains reports of osteoporosis in patients with this disease, a disorder in the calcium metabolism system and hormones regulating it; the level of cholesterol and free fatty acids in plasma increases. The state of the liver enzyme systems changes, starting from the early stages of the disease. Kidney function also does not remain intact - minute diuresis, endogenous creatinine clearance, and excretion of electrolytes with urine decrease. These deviations are apparently adaptive in nature.

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Electrolyte Causes of Anorexia

When studying the electrolyte balance in patients with different forms of nervous anorexia, a drop in the potassium level in plasma and cells, intracellular acidosis are noted (although in plasma both alkalosis - in patients with vomiting, and acidosis may occur). Sudden death of patients with nervous anorexia is associated with electrolyte changes at the cellular level. The volume of circulating blood decreases, but when calculated per 1 kg of body weight, hypervolemia is noted (an increase of 46% compared to healthy individuals). It becomes clear that careful intravenous infusions must be administered to such patients. This is associated with the described cases of death due to improper infusion therapy.

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Pathogenesis of nervous anorexia

The basis of the disease is mental changes with the formation of dysmorphophobic experiences, leading to a conscious refusal to eat, pronounced weight loss. Chronic nutritional deficiency largely determines the clinical picture of the disease. Disturbances in the secretion of gonadotropins, a delayed reaction of TSH to TRH, a change in the secretion of STH and cortisol have been identified, which indicates the presence of a hypothalamic defect. With successful treatment of the disease and normalization of body weight, the impaired secretion of hormones is also normalized, which indicates the secondary nature of disorders in the hypothalamus in relation to weight loss. However, the frequent presence of certain neurometabolic-endocrine syndromes in the premorbid period (hypothalamic obesity, primary or secondary amenorrhea or oligomenorrhea), as well as the persistence of amenorrhea in many patients even after complete normalization of body weight and the persistence of impaired plasma LH response to stimulation with clomiphene indicate a possible constitutional inferiority of the hypothalamic-pituitary region, which is involved in the genesis of the disease. Differential diagnosis should be carried out with pathological conditions leading to primary and secondary hypopituitarism with pronounced weight loss. It is also necessary to exclude primary endocrine and somatic pathology accompanied by weight loss.