When depression also reveals a violation of the secretion of growth hormone secreted by the pituitary gland during human sleep, hence we can assume some of the mechanisms of sleep disorders in depression. Violation of the secretion of another hormone of the pineal gland (pineal gland) – melatonin may to some extent explain the seasonality of exacerbations of depression in some of its variants. The altered circadian rhythm of melatonin release was noted in the majority of patients.
When depression does not change the blood content of adrenocorticotropic hormone of the pituitary gland in response to the introduction of the hormone hypothesis Lamus corticoliberin (Holsboer F. et al., 1984), but the content of the latter in the cerebrospinal fluid increases (Nemeroff C. et al., 1984). Various researchers have demonstrated an increase in the number of corticoliberin and vasopressin neurons in the paraventricular nuclei of the hypothalamus (Raandshe-er F. et al., 1994).
Thyroid
The fact that its cause is hypothyroidism, characterized by thyroid insufficiency, is evidence of the role of the endocrine factor in the genesis of depression. At the same time, it is known that the human brain is extremely sensitive to the deficiency of thyroid hormones. It should be noted that latent hypothyroidism can be detected on the basis of an increase in blood levels of thyroid-stimulating hormone of the pituitary gland, which stimulates the activity of thyroid hormones. Depression in hypothyroidism is associated with a decrease in the number of biologically active substances in the human central nervous system. As a result of therapy with thyroxin and antidepressants, there is an increase in the activity of thyroid hormones and a decrease in the severity of stable or refractory depression to drug therapy.
A reduced response to protimile stimulation (synthetic thyreiberin) indicates impaired hypothalamus function during depression. Excessive response to stimulation of protilerine, on the contrary – to the thyroid gland insufficiency.
Adrenal glands
Numerous studies indicate an increase in the blood of a patient with depression in the content of the adrenal hormone cortisol, which actively reacts to the state of stress (Hailbreich U. et al., 1985). In addition, an increase in the total mass of the adrenal glands was found (Nemeroff C. et al., 1984). Domestic scientists recorded a distinct increase in blood cortisol, especially in those who experienced anxiety. And, on the contrary, as they get out of depression, in most cases the content of this hormone in the blood decreases. With depression, the daily rhythm of cortisol release is distorted (normally, its level rises in the morning and falls at midnight). An increase in cortisol has been observed to decrease the number of neurotransmitters that are actively involved in the pathogenesis of depression. It should be noted that the decrease in the concentration of cortisol depends on the severity and duration of depression, this is explained by the depletion of the capabilities of the hypothalamus, pituitary and adrenal glands with a prolonged increase in the functional activity of these structures of the body during the illness.
One of the methods for diagnosing depression is the hormone test for suppressing cortisol with dexamethasone. With the introduction of a small dose of the synthetic analogue of the hormones glucocorticoids – dexamethasone, in a depressed state, the secretion of the adrenal hormone cortisol and adrenocorticotropic hormone of the pituitary is not suppressed (Carroll B. et al., 1981).
The dexamethasone suppression test is not positive for every person suffering from depression, but as they get out of the disease, if there has been a change in the cortisol content, it is normalized. Hence the need for a re-dexamethasone test in individuals with depressive spectrum disorders.
Disorders of the depressive spectrum occur in such diseases of the adrenal glands as Itsenko Cushing’s syndrome and Addison’s disease.
In the period of depression, there is a decrease in the functional capabilities of glucocorticoid endings of the nerve cells of glucocorticoid receptors (Modell S. et al., 1997) and an altered state of corticosteroid receptors (Von Bardeleben U., Holsboer E, 1989). There is a point of view according to which the body of a patient with depression cannot independently complete the stress response due to an imbalance of sensitive nerve cell endings.
A high level of cortisol and a low level of steroid hormone dehydroepiandrosterone adrenal glands (DHEA) are assumed to be unfavorable prognostic indicators for the prognosis of depression. The ratio of DHEA to cortisol was changed during the recurrent depression and remained unchanged during its first episode. This circumstance may indicate the depletion of the anabolic possibilities of the organism as the duration of the disease.
In addition to the genetic factors responsible for cortisol receptor imbalance, as moments promoting the development of depression, long-lasting stressful influences carried out at an early age are singled out, during the period that is especially sensitive for the body when central mechanisms of endocrine organs regulation are formed (hypothalamic-pituitary-adrenal system).
Exposure to high concentrations of the stress hormone – cortisol can lead to a persistent decrease in the number of glucocorticoid receptors, which, in turn, is a risk factor for the development of depression. As a stressful effect, contributing to the release of cortisol, highlight the early deprivation of maternal care, sexual and physical violence. Thus, the receptor hypothesis brings together biological and psychological models for the development of depression (Dinan T., 1994).
Restoration of the normal functioning of the endocrine system can be an indicator of sustained remission in depression, while the absence of a change in hormonal parameters indicates a lack of improvement.