Adrenal Cortex

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Two main hormone groups of adrenal cortex are glucocorticoids and mineralocorticoids, but also androgens, estrogens and progesterons are produced there.

Adrenal cortex is a very important relay point of the whole endocrine system.

All adrenocortical hormones are made from cholesterol. There are eight key enzymes necessary for the production of various adrenocortical hormones, and every one of them may be deficient due to faulty genes. The result is the classical excess of hormones produced in the steps just preceding the disruption of biochemical chain reaction, and lack of hormones beyond the point of disruption as described in the chapter on ‘Genetic diseases’.

The lack of glucocorticoids leads to an increased release of corticotrophin-releasing hormone (CRH) of hypothalamus, and thereby of adrenocorticotropic hormone (ACTH) of anterior lobe of pituitary, and that in turn leads to a further increase of concentration of the hormonal precursors just before the disruption of biochemical chain reaction, causing various glucocorticoid, mineralocorticoid androgenic, gestagenic or estrogenic effects in the patient.

The most common of these genetic enzymatic defects is lack of 21Alpha-hydroxylase that leads to the lack of cortisol, increased production of androstendione and testosterone, a cause of virilisation in females, and adrenogenital syndrome in males, i.e. precocious pseudopuberty.

Glucocorticoids, mainly cortisol,

- stimulate gluconeogenesis in liver,

- inhibit glucose intake by cells,

- stimulate lipolysis,

- stimulate protein breakdown in tissues,

- stimulate protein production in liver,

- support production of erythrocytes, platelets, and neutrophil granulocytes,

- decrease lymphocyte, monocyte, eosinophil and basophil counts,

- act as immunosuppressants, also by limiting production of antibodies,

- suppress inflammation, and healing by inhibition of connective tissue proliferation,

- lower plasma level of calcium and phosphorus by inhibition of calcitriol.

Mineralocorticoids increase renal retention of Na+ and water, and stimulate elimination of K+, Mg++, H+ , by kidneys, as well as potassium intake.

Adrenocortical hormonal insufficiency can be the result of decreased function of adrenal gland, i.e. Addison’s disease, genetic defects, autoimmune inflammation of adrenals, TB, enzymopathies, or of lower level of ACTH, i.e. defect of anterior lobe of pituitary.

The massive therapeutic use of corticosteroids has been one of the big successes of modern medicine but there are many drawbacks to that story as well. The secondary lesions of adrenal glands are more frequent today than primary diseases. The widespread therapeutic use of corticoids in inflammatory conditions, allergies, immune system deficiencies, autoimmune diseases, cancer, skin diseases, etc., brought on an atrophy of adrenal cortex due to competitive inhibition. In other words the adrenal cortical function is suppressed by exogenous intake of hormones for long periods of time, e.g. for years, often in high doses, and at non-physiological intervals. The functional non-use causes the morphological atrophy of endocrine structures so that eventually adrenal glands can no longer produce sufficient quantities of their hormones. Fetal precursor cell transplantation of diencephalon, entire pituitary, adrenal cortex, liver, spleen, bone marrow, generally solves this problem.

Growth takes place in three phases: * the 1st phase, during the first two - three years of life, is ‘genetic’, characterized by a high speed of growth,

- the 2nd phase, from 4th - 5th to 8th – 12th years of life, is ‘pituitary’, regulated by diencephalon/hypothalamus/ pituitary, stimulated by growth hormone system, characterized by a slow and steady growth, with a yearly increase of 4 to 6 cm. - hormones of adrenal cortex are responsible for the stimulation of gonads into initiation of the 3rd, i.e. pubertal, phase of growth, controlled by adrenocortical and sex hormones.

There is an involution of adrenal glands after birth. After 6th – 8th year of age the adrenal glands and gonads begin to grow rapidly, reaching the culmination between 14 and 18 years of age. Whereas the corticosteroids show a nearly linear rise from birth, the production of gonadotropins, 17-ketosteroids, and sex hormones begins between 6 and 8 years of age only, but then the rise of their levels is parallel with those of corticosteroids.

The growth of the entire body, and bony growth, are controlled by adrenocortical and sex hormones working in synchrony. These two groups of hormones initiate the 3rd phase of growth at the beginning of puberty, and terminate the growth by closure of epiphyses at the end of puberty. The earlier these two groups of hormones act, the earlier the pubertal growth outburst sets in, but is also finished earlier. As a result, the final stature is lower in girls, than in boys, particularly those that start later, as in northern countries. The same applies to some racial groups. To stimulate the 3rd stage of growth and development fetal precursor cell transplants of adrenal cortex, gonads, hypothalamus, is used.

If there is a delay of development in the 2nd phase, then fetal precursor cell transplantation of diencephalon, hypothalamus and anterior lobe of pituitary, is indicated, and if there is a delay in the 3rd phase, then fetal precursor cell transplantation of adrenal cortex, gonad, is mandatory.

Since the beginning and end of puberty has moved into earlier years, there is much less time now for the therapy of growth disorders.

Retarded puberty is the result of constitutional factors, malnutrition and other unfavorable environmental conditions, hypogonadism, such as in Turner’s syndrome, congenital hypothyreoidism, lack of pituitary gonadotropins in panhypopituitarism, pituitary nanism. Retarded appearance of secondary sex characteristics is due to an insufficiency of adrenal cortex. Fetal precursor cell transplantation of gonads, placenta, adrenal cortex, diencephalon, hypothalamus, pituitary, thyroid, thymus, is recommended.


Missing puberty is rare and occurs in dystrophia adiposo-genitalis, Prader-Willi syndrome, various inter-sex conditions.