The endocrine system: alcohol alters critical hormonal balance

Abstract

Alcohol's effects on the hormonal (i.e., endocrine) system have widespread consequences for virtually the entire body. Alcohol-related hormonal disturbances can result in cardiovascular abnormalities and reproductive deficits in both males and females. Other endocrine problems stemming from excess alcohol consumption include immune dysfunction and bone disease. Researchers are exploring ways of using hormonal mechanisms to help treat alcoholics as well as to identify people predisposed to alcoholism.

Figure 1

The hypothalamic-pituitary-adrenal axis. In response to almost any type of stress, either physical or psychological, the hypothalamus secretes corticotropin-releasing factor (CRF), which in turn increases secretion of adrenocortotropic hormone (ACTH) by the anterior pituitary gland. In response, within minutes, the adrenal glands, located atop the two kidneys, increase secretion of cortisol. The released cortisol initiates a series of metabolic effects aimed at alleviating the harmful effects of the stress state and, through direct negative feedback to both the hypothalamus and the anterior pituitary, decreases the concentration of ACTH and cortisol in the blood once the state of stress abates. ⊕ = excites ⊝ = inhibits

Figure 2

The hypothalamic-pituitary-gonadal axis in males and females. The hypothalamus secretes luteinizing hormone-releasing hormone (LHRH), which controls the anterior pituitary gland’s secretion of both follicle-stimulating hormone (FSH) and luteinizing hormone (LH). In the female reproductive axis (A), these two gonadotropic hormones stimulate the ovaries to secrete estrogen and progesterone, which circulate back to the hypothalamic-pituitary unit and either inhibit or excite the production of FSH, LH, and LHRH. In the male reproductive axis (B), the gonadotropic hormones stimulate production of testosterone by the testes; testosterone also feeds back to the hypothalamus and pituitary to inhibit production of LHRH and the pituitary gonadotropins. ⊕ = excites ⊝ = inhibits

Figure 3

Fluctuations in the levels of estradiol, progesterone, luteinizing hormone (LH), and follicle-stimulating hormone (FSH) over the 28-day female reproductive cycle. SOURCE: Adapted from Guyton, A.C. Textbook of Medical Physiology. 7th ed. Philadelphia: W.B. Saunders, 1986. p. 969.

Figure 4

The hypothalamic-pituitary-growth hormone axis. The hypothalamus secretes growth hormone-releasing factor (GRF), prompting the anterior pituitary to secrete growth hormone (GH). The hypothalamus also produces somatostatin, which acts to inhibit GH secretion; the balance of GRF and somatostatin provides the regulatory mechanism for the GH axis. Once GH has been released, a key target for the hormone is the liver, which produces insulinlike growth factor-1 (IGF-1), a chemical that carries out many of the tasks of GH at the cellular level (e.g., normal function of the immune system, carbohydrate and lipid metabolism, and bone growth and development). IGF-1 also feeds back to the hypothalamus and pituitary to reduce GH secretion. GH acts to inhibit its own secretion by inhibiting secretion of GRF and promoting secretion of somatostatin.

Figure 5

The hypothalamic-pituitary-thyroid axis. The hypothalamus produces and secretes thyrotropin-releasing hormone (TRH), stimulating cells of the anterior pituitary to produce thyroid-stimulating hormone (TSH). TSH then stimulates secretion of thyroxine (T₄) and triiodothyronine (T₃) by the thyroid gland, the primary effect of which is to regulate cell metabolism. T₄ and T₃ both feed back to the hypothalamus and the pituitary to reduce TRH and TSH secretion. SOURCE: Guyton, A.C. Human Physiology and Mechanisms of Disease. 5th ed. Philadephia: W.B. Saunders, 1992. pp. 566–568.