Effects of Alcohol Abuse on Reproductive Function in Women

 Alcohol abuse and alcoholism are associated with disorders of reproductive function in both men and women. Amenorrhea, anovulation, and luteal phase dysfunction may occur in alcohol-dependent women and alcohol abusers. Yet there has been relatively little research on the consequences of alcohol abuse for female reproductive function. Recent clinical and survey studies of alcohol effects on pituitary gonadotropins and gonadal steroid hormones in women are reviewed. Experimental studies of the acute and chronic effects of alcohol on the hypothalamic-pituitary-gonadal axis in normal women and in animal models are also described. Recent studies of the acute effects of alcohol on opioid antagonist and synthetic LHRH-stimulated pituitary gonadotropins are summarized. Possible mechanisms underlying alcohol-induced disruptions of menstrual cycle regularity are discussed. The adverse effects of alcohol on reproductive function in men are well documented. Impotence and diminished sexual interest are common clinical complaints among alcohol-dependent men. Testicular atrophy, low testosterone levels, and gynecomastia are often associated with chronic alcohol abuse (). There is now considerable evidence that alcohol inhibits Read more […]

Studies of Acute Alcohol Effects in Women and Animal Models

Alcohol Effects on Basal Hormone Levels Another approach to examination of alcohol’s toxic effects on reproductive function is to administer a single acute dose of alcohol to a normal healthy woman or experimental animal and measure the effects on pituitary and ovarian steroid hormones. Through a systematic manipulation of alcohol dose and changes in hormone levels, it should be possible to establish whether alcohol primarily disrupts hypothalamic, pituitary, or ovarian function. Surprisingly, studies of acute alcohol administration have shown that alcohol has minimal effects on basal hormone levels. Alcohol did not significantly suppress LH or estradiol in normal women or in female macaque monkeys. These data suggest that a single episode of intoxication is probably not sufficient to suppress normal basal hormone levels and that repeated episodes of intoxication are required to produce the hormonal correlates of amenorrhea, anovulation, and luteal phase dysfunction observed in clinical studies. One procedural difficulty affecting all investigations of acute alcohol effects on basal hormone levels is that studies have usually been conducted during the early follicular or luteal phase of the menstrual cycle, when basal Read more […]

Clinical Studies of Reproductive System Dysfunctions in Alcoholic Women

Alcoholic women may have several disorders of menstrual cycle function, including amenorrhea, luteal phase dysfunction, anovulation, and, in some instances, early menopause. Most available information about alcohol effects on reproductive function has been derived from clinical studies of alcoholic women during sobriety. Evidence of menstrual cycle dysfunctions is based on clinical history information and endocrine evaluations at the time of admission for treatment of alcohol-related medical problems. Disorders such as liver disease and pancreatitis, often complicated by malnutrition or other infectious disorders, are observed clinically. Since these medical disorders can also contribute to reproductive system dysfunctions, it is not possible to attribute abnormal menstrual cycles to alcohol alone. However, recent replications of these reproductive disorders in animal models under controlled conditions and in healthy social drinkers increase confidence in the validity of the clinical observations. Amenorrhea Amenorrhea refers to the complete cessation of menses. Amenorrhea has been consistently reported by alcoholic women, and this condition may persist for several months or for many years. Data from two clinical Read more […]

Drug-Drug Interactions of Amphetamines

Adrenergic neuron blocking drugs Amphetamines and other stimulatory anorectic agents, apart from fenfluramine, would be expected to impair the hypotensive effects of adrenergic neuron blocking drugs such as guanethidine. Not only do they release noradrenaline from stores in adrenergic neurons and block the reuptake of released noradrenaline into the neuron, but they also impair re-entry of the antihypertensive drugs. Alcohol Alcohol increases blood concentrations of amphetamines. Barbiturates Barbiturates can enhance amfetamine hyperactivity. Benzodiazepines Benzodiazepines can enhance amfetamine hyperactivity. Estradiol Preclinical studies (as well as anecdotal clinical reports) have shown that estrogens, through effects on the central nervous system, can influence behavioral responses to psychoactive drugs. In an unusual crossover study, the subjective and physiological effects of oral D-amfetamine 10 mg were assessed after pretreatment with estradiol. One group of healthy young women used estradiol patches (Estraderm TTS, total dose 0.8 mg), which raised plasma estradiol concentrations to about 750 pg/ml, and a control group used placebo patches. Most of the subjective and physiological effects of amfetamine Read more […]

Potential Mechanisms of Alcohol-Induced Bone Disease

The normal growth of bone cells depends upon a variety of orchestrated factors, including adequate nutrition and the function and interaction of various hormones and intercellular regulating factors. Research in this area suggests that while the exact mechanism through which alcohol affects the integrity of the skeleton is not known, much has been learned. Even so, likely candidates have not been clearly identified. Chronic consumption of relatively low amounts of alcohol (one to two drinks per day for women; three to four drinks per day for men) can interfere with the normal metabolism of nutrients. As a result of poor diets, impaired nutrient absorption, or increased renal excretion, alcoholics often have deficiencies in minerals such as calcium, phosphate, and magnesium, as well as low levels of vitamin D, which is necessary for the absorption of calcium from the intestinal system. However, there is little histomorphometric evidence that nutritional deficiencies related to alcohol use are a major cause of alcohol-induced bone disease. Another candidate that may contribute to alcohol-induced bone disease is calcitonin, a peptide produced by the thyroid gland. Calcitonin inhibits bone resorption, in effect protecting Read more […]