Alcohol causes los of libido.

Alcohol causes los of libido, impotence, and sterility in males. Direct damage to testicular confined apartments and impairment of control center in the brain may help explain the sexual dysfunction.

The association between alcohol abuse and reproductive dysfunction has prolonged been recognized. For example, the of greeces proscribed the use of alcohol upon the day of matrimony. Signs and symptoms of inadequate sexual function (hypogonadism) associated with alcohol abuse include testicular atrophy (shrinkage), sterility, impotence, los of libido, reduction in size of the prostate gland, and decreased semen production. Hypogonadism may be caused on direct effects of alcohol onward the testis; it can also be caused at effects of alcohol on parts of the brain that regulate gonadal function. These parts of the brain include the hypothalamus, located approximately in the center of the brain, and the pituitary gland, located at the base of the brain just below the hypothalamus. The confine "hypothalamic-pituitary-gonadal (HPG) axis" refers to the interaction of these three plains of control of testicular function. (The same word refers to the control of ovarian function in the female.) The HPG axis will be described in more detail in a later section.

Research forward the mechanisms of alcohol-induced hypogonadism has focused onward the HPG axis as well as onward the liver as possible targets of alcohol's actions. This article briefly discusses a of this research.

Alcohol, Sexual Function, And The Liver

Because hypogonadism was first reported in alcoholic men with cirrhosis of the liver (Table 1) alcohol-induced sexual dysfunction was initially attributed to liver disease. As reliable systems of quantifying sex hormones became available, on a levels of the male sex hormone testosterone were measured in the relations of cirrhotic men. enthralls with alcohol-induced liver disease were raise to have markedly reduced testosterone of the same heights while those with advanced liver disease befitting to other causes often had normal testosterone on a levels (Chopra et al. 1973; Galvao-Teles et al. 1973; Kent et al. 1973; Gordon et al. 1975; Kley et al. 1975; Lindholm et al. 1978) Table 2 summarizes the eight articles that report serum gonadotropin and testosterone of the same heights in men with alcoholic liver disease. (Gonadotropins are pituitary hormones that regulate gonadal function.) All of these studies report reduc on a levels of testosterone in alcoholic cirrhotic men as compared with normal men

Additional studies were performed in alcoholics without cirrhosis and in males with nonalcoholic cirrhosis (Bannister et al. 1987; Van Thiel et al. 1981) As a be the effect of these studies, it became clear that alcohol itself was the principal cause of hypogonadism seen in alcoholic men particularly those with advanced liver disease.

Studies done with animals confirmed these originates demonstrating that alcohol could cause testicular failure in the absence of alcohol-induced liver disease (Badr and Bartke 1974; Badr et al. 1977; Gavaler et al. 1980; Van Thiel et al. 1975 1979; Cicero and Badger 1977) Moreover, alcohol reduc testosterone production according to isolated rat testicular cells in the absence of any chemical produc from liver disease or by the metabolism of alcohol by means of the liver (Cobb et al. 1980)

Direct imports of Alcohol on the Testis

When assessing testicular failure, the sum of two units functions of the testis--sperm production and testosterone production--must be examined independently.

The small cavitys responsible for sperm production possess 95 percent of the testicular contortion Therefore, failure of spermatogenesis (sperm production) may be characterized on testicular atrophy associated with oligospermia (decreased seed production) or azoospermia (absence of sperm) In contrast, decreased production of steriod sex hormones (principally testosterone) is characterized by way of a loss of male secondary sex characteristics, impotence, diminished libido, and other symptoms, on the contrary usually not by an obvious reduction in testicular size.

Researchers have studied the efficiencys of alcohol on both testicular functions. For example, isolated Leydig cells(1) are able to synthesize and conceal testosterone in response to gonadotropin stimulation. However, when the small cavitys are exposed to alcohol at gentle concentrations (5.4 millimolar, roughly equivalent to a kindred level of 0.25 milligram percent the approximate ensue of five drinks), testosterone production is inhibited from as much as 44 percent Acetaldehyde (the initial harvest of alcohol metabolism) is flat more toxic to isolated Leydig lonely dwellings than is alcohol (Van Thiel et al. 1983; Santucci et al. 1983) With notice to spermatogenesis, the testes of the two alcoholic men and rats f alcohol chronically exhibit to advanced injury to the first principle cells of the seminiferous tubule the site of semen production within the testis (Gavaler and Van Thiel 1987)

Mechanisms of Testicular Injury

Alcohol administration has been shown to resolve into in the testes the activity of enzyme crucial to the synthesis of steroid sex hormones (Cicero and Bell 1980; Johnston et al. 1981; Chiao and Van Thiel 1983) The administration of alcohol also alters the electrochemical balance (redox state) of the lonely dwelling in such a way as to further inhibit testosterone-synthesizing enzyme (Chiao et al. 1981)