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Twenty-three healthy males, aged 23 to 62 years, were examined by M-mode echocardiography and systolic time intervals for 3 h after (1) ethanol 1 g/kg by mouth taken over 60 minutes; (2) atenolol 100 mg by mouth; (3) ethanol (1 g/kg) + atenolol (100 mg). The peak mean blood ethanol (± s.e.) was 112 ±4 mg/100 ml in test 1 and 104 ± 7 mg/100 ml in test 3. During increasing blood ethanol, heart rate (HR), systolic blood pressure (BP), cardiac output (CO) and echocardiographic indices of left ventricular (LV) function were significantly augmented, while total peripheral resistance (TPR) decreased. During declining blood ethanol, systolic BP, L V end-diastolic and end-systolic diameters, stroke volume (SV) and circumferential wall stress were significantly reduced; echocardiographic indices of LV function were unaltered, but the pre-ejection period/LV ejection time ratio was increased, Atenolol decreased llR, systolic BP, SV, CO, and all estimates of LV function, but increased TPR. Ethanol + atenolol tended to cause smaller depressions in the indices of LV function than did atenolol alone, in spite of similar plasma atenolol concentrations (n = 6). It is concluded that ingestion of modest doses of ethanol evokes vasodilation and enhances LV function during increasing blood ethanol, and reduces LV preload and afterload during decreasing blood ethanol without impairing contractility. Social drinking and beta blockade seem not to have any harmful acute combined effects on the heart and circulation, at least in normal subjects. [ABSTRACT FROM PUBLISHER]

Acute effects of alcohol on the peripheral nerves of seven patients with diabetic polyneuropathy and 13 healthy subjects were examined neurophysiologically. Ethanol (1 g/kg) caused a slight increase in skin temperature and motor conduction velocity in both groups. Motor distal latencies decreased in the healthy subjects, but increased among polyneuropathic patients after the consumption of alcohol. Diabetic nerves appear most susceptible to the acute effects of alcohol. [ABSTRACT FROM AUTHOR]

The effect of alcohol on exercise-induced changes in serum glucose, serum free fatty acids, and serum insulin was studied in healthy male volunteers by performing an exhaustive ergometer exercise: (1) followed by alcohol intoxication (induced by 1.5 g of alcohol/kg of body weight); (2) during alcohol intoxication (induced by 0.8 g of alcohol/kg of body weight); and (3) during hangover (13 hr after a dose of 1.5 g of alcohol/kg of body weight). Acute alcohol intake immediately before exercise inhibited the exercise-induced increase in mean serum glucose concentration and caused a mild decrease in serum glucose levels during recovery from exercise. Exercise during hangover also resulted in decreased glucose levels during recovery from exercise. Alcohol administration immediately before or after exercise inhibited the postexercise increase in mean serum free fatty acids concentration. This was not seen during hangover, when blood alcohol concentration had already reached 0. In conclusion, alcohol interferes with the metabolism of carbohydrates during and after anaerobic exercise by decreasing the availability of circulating glucose. Furthermore, during recovery from exercise, alcohol decreases the supply of free fatty acids for the body.

The combined effect of alcohol and physical exercise on the serum levels of testosterone, luteinizing hormone, and cortisol was studied in healthy male volunteers by performing an exhaustive ergometer exercise (1) followed by alcohol intoxication (induced by 1.5 g of alcohol/kg body weight), (2) during alcohol intoxication (induced by 0.8 g of alcohol/kg body weight), and (3) during hangover (13 hr after a dose of 1.5 g of alcohol/kg body weight). Physical stress immediately before alcohol administration prolonged the depressant effect of alcohol on testosterone secretion. This seemed to be mainly a consequence of direct inhibition at the testicular level, even though the role of luteinizing hormone as a contributory regulatory factor cannot be totally ruled out. Cortisol response to exercise was not modified by alcohol under any of the experimental conditions.

To study the effects of prolonged moderate alcohol intake on bone and mineral metabolism, 60 g/day of ethanol was administered to 10 healthy male volunteers during 3 weeks. The drinking period was preceded and followed by an abstinence period of 3 weeks. The serum level of osteocalcin decreased by 30% towards the end of the alcohol period (P less than 0.01), recovering by 25% after the termination of drinking (P less than 0.01). The serum level of intact parathyroid hormone increased to the end of the drinking period (P less than 0.05). After stopping drinking it came back to baseline (P less than 0.05) within a week. The serum levels of 25(OH)D3, 1,25(OH)2D3, 24,25(OH)2D3, the serum and urinary levels of calcium, and the intestinal absorption of calcium measured by stable strontium remained practically unchanged throughout the whole observation period. We conclude that prolonged moderate alcohol intake impairs osteoblastic function, leading to lowered serum levels of osteocalcin, but it does not derange vitamin D metabolism.

Background: Persons with chronic alcoholism frequently have hypocalcemia, hypomagnesemia, and osteoporosis. The short-term effects of alcohol ingestion on calcium and magnesium metabolism are poorly understood, however., Methods: We measured serum calcium, magnesium, and phosphate concentrations in 17 normal men and 7 normal women before and at intervals up to 16 hours after the ingestion of 1.2 to 1.5 g of alcohol per kilogram of body weight over a 3-hour period (doses sufficient to cause acute intoxication). Urinary excretion of calcium, magnesium, and phosphate and serum calciotropic hormone levels were measured in 16 of these subjects. As a control, the same measurements were made after the ingestion of fruit juice instead of alcohol., Results: The mean (+/- SE) peak blood alcohol level in the men was 37.5 +/- 1.6 mmol per liter, and in the women it was 38.0 +/- 3.2 mmol per liter. In the men the mean serum parathyroid hormone concentration decreased from 16.1 +/- 2.1 to 6.8 +/- 0.9 ng per liter at the end of the three-hour drinking period. The value at this time was 30 percent of that at the end of the three-hour session during which the men drank fruit juice (P = 0.004). The serum concentration of ionized calcium reached a nadir eight hours after the beginning of alcohol administration (decreasing from 1.18 +/- 0.01 to 1.15 +/- 0.01 mmol per liter; P less than 0.001 as compared with values during the fruit-juice study), and urinary excretion of calcium increased from 0.34 +/- 0.08 to 0.36 +/- 0.08 mmol per hour (P less than 0.01 as compared with values during the fruit-juice study). Serum parathyroid hormone levels exceeded base-line values during the last 4 hours of the 16-hour study period; this increase was accompanied by a decrease in the urinary excretion of calcium. Both serum levels of magnesium (in the first 6 hours) and urinary levels (in the first 12 hours) increased after the ingestion of alcohol. In the women, serum parathyroid hormone levels decreased from 29.2 +/- 2.8 to 17.3 +/- 2.6 ng per liter two hours after the administration of alcohol was begun (P less than 0.001) and increased above base-line values during the last four hours of the study period. The serum concentration of ionized calcium decreased from 1.20 +/- 0.01 to 1.16 +/- 0.01 mmol per liter, reaching a nadir 8 to 12 hours after alcohol administration was begun (P less than 0.001)., Conclusions: Short-term alcohol administration causes transitory hypoparathyroidism. This decline in the secretion of parathyroid hormone accounts at least in part for the transient hypocalcemia, hypercalciuria, and hypermagnesuria that follow alcohol ingestion.

The combined effects of alcohol intoxication and intense physical exercise on the adrenergic system were studied in eight healthy male volunteers. Ethanol (0.8 g/kg body weight) was administered perorally to bring about a mean serum concentration of 21 mmol/liter (0.1%); each subject also participated in an identical control session without alcohol. Acute alcohol intake alone did not change the concentrations of plasma adrenaline or noradrenaline or the density, affinity, and functioning (ability to mediate catecholamine-stimulated production of cAMP) of lymphocytic beta-adrenergic receptors. In contrast, acute ergometer exercise brought about an approximately 10-fold increase of plasma adrenaline and noradrenaline concentrations, a 2- to 3-fold increase of beta-adrenergic receptor density and an enhancement of isoproterenol-stimulated cAMP production. Alcohol intake immediately before the ergometer exercise did not modify these changes. In conclusion, acute physical exercise activates the human adrenergic system, with an increase of both plasma catecholamines and lymphocytic beta-adrenergic receptors. Moderate alcohol intoxication does not affect exercise-induced alterations of these parameters.

To study the mechanism of the reduced serum selenium concentration in patients with liver damage we administered 200 micrograms (2.53 mumol) selenium daily as selenium-rich yeast to 8 patients with primary biliary cirrhosis and 8 healthy controls over 16 weeks. Initially selenium concentrations in serum were 24% lower (P less than 0.001) in patients than controls. During supplementation serum selenium levels increased in both groups but the difference between them persisted. Throughout the study whole blood selenium levels and glutathione peroxidase activities were also somewhat lower (P = NS) in patients than controls. Selenium supplementation had no effect on whole blood glutathione peroxidase activities in either group. The basal 24 h urinary excretion of selenium was similar in both groups but was increased more by supplementation in patients than controls. Selenium administration did not influence the liver function of the patients. We conclude that impaired hepatic production of selenium-containing serum compounds is the most likely explanation for the reduced serum selenium concentration in patients with primary biliary cirrhosis.

The effects of acute alcohol ingestion were studied on pulsatile secretion of immunoreactive luteinizing hormone (LH), follicle-stimulating hormone (FSH), and growth hormone (GH), and on serum bioactive LH, testosterone, cortisol, and prolactin. A dose of 1.5 g ethanol per kg of body weight was administered by mouth to eight healthy male volunteers (aged 20 to 26 years) during 3 hr from 1800 to 2100 hr. Blood samples were collected every 20 min for 20 hr until 1400 hr of the following day. Each subject served as his own control in an identical experiment without ethanol, carried out at least 1 month later. Ethanol ingestion decreased serum testosterone concentration on average by 23% (p less than 0.05) between 10 and 16 hr after starting the drinking. The mean levels of LH and FSH and the mean number and amplitude of LH and FSH pulses remained unchanged. Ethanol ingestion did not affect the biological activity of LH. In each subject alcohol administration reduced the nightly peak of GH secretion, and in addition, changed the timing of this peak in most subjects. Only marginal changes were found in the prolactin levels but ethanol ingestion increased the cortisol levels on average by 36% (p less than 0.05) between 11 and 14 hr after the start of drinking. We conclude that the decrement in serum testosterone evoked by ethanol is not attributable to impaired pulsatile secretion of gonadotropins nor to reduced biological activity of LH. In contrast, ethanol profoundly suppressed the pulsatile secretion of growth hormone.

To study the effect of prolonged ethanol consumption on calcium metabolism and on the prevalence of osteoporosis we examined 38 Finnish noncirrhotic male alcoholics (30-55 years of age) with dietary interviews and biochemical measurements and by measuring the bone mineral content of the forearm using single photon absorptiometry (SPA) and the bone mineral density of the spine, humerus and proximal femur using nonquantified computer tomography (CT) and dual-energy x-ray absorptiometry (DEXA). In comparison two groups of healthy controls were studied. The mean daily dietary intake of calcium was 1.3 g in the patients and 1.2 g in the controls. The dietary intake of vitamin D was equal in the study groups, too. The serum levels of calcium, phosphate and parathyroid hormone did not show any difference between the patients and controls but in the alcoholics the urinary excretion of calcium was reduced by 42% (p less than 0.0001) as compared to the controls. The serum levels of 25-hydroxyvitamin D3, 1,25-dihydroxyvitamin D3, and 24,25-dihydroxyvitamin D3 were reduced in the alcoholics by 40% (p less than 0.0001), 23% (p less than 0.01), and 48% (p less than 0.0001), respectively, as compared to the controls. The alcoholic men had normal levels of serum testosterone and they did not have hypercortisolism. The bone mineral content of the dominant forearm measured by SPA was similar in the study groups as were the bone mineral densities (BMD) of the lumbar and humeral areas measured by CT. The BMD at the lumbar, femoral neck, Ward's triangle and trochanter sites measured by DEXA did not differ, either.(ABSTRACT TRUNCATED AT 250 WORDS)

Plasma catecholamine levels, lymphocytic beta-adrenoceptor densities and lymphocytic cAMP production were studied in 10 male subjects attending a withdrawal clinic after prolonged alcohol abuse. On admission the mean beta-adrenoceptor density was 29 +/- 9 fmol mg-1 protein (about 60% of the mean level of healthy control subjects, P less than 0.002). The following day a significant elevation of the beta-adrenoceptor level up to 46 +/- 19 fmol mg-1 protein (P less than 0.05) took place. This was accompanied by a parallel activation of the beta-adrenoceptor-mediated cAMP production of the lymphocytes. No major changes in beta-adrenoceptor levels or cAMP production took place during the next 7 days. Plasma catecholamine levels were elevated at arrival and decreased steadily during the withdrawal period. In conclusion, chronic alcoholism is associated with a reduction of lymphocytic beta-adrenoceptor density and functioning, which is followed by a rapid reversal during abrupt ethanol withdrawal. Thus an accelerated responsiveness to catecholamines may occur during the first ethanol-free day of chronic alcoholics.

The concentrations of triglyceride, cholesterol, phospholipids, and proteins in the major lipoprotein fractions (very-low-density lipoprotein [VLDL], low-density lipoprotein [LDL], and high-density lipoproteins [HDL] HDL2 and HDL3) were monitored in 20 pregnant women who chronically abused alcohol and in 15 abstinent pregnant women. Five of the alcohol users gave birth to infants with fetal alcohol syndrome (FAS). Lipoproteins were fractionated by sequential flotation from samples taken at 16, 20, 24, 28, 32, 36, and 40 weeks of gestation and 6 to 8 weeks after delivery. In abstinent women, concentrations of VLDL and LDL triglyceride, cholesterol, phospholipids, and proteins increased in late gestation. Concentrations of HDL2-cholesterol, phospholipids, proteins, and total HDL2 were increased during the 16th to 28th weeks, but HDL3 remained unchanged. Alcohol abuse clearly reduced the normal increase in total and LDL-cholesterol, as well as in LDL phospholipids, proteins, and total LDL during the 24th to 40th weeks. LDL changes were most pronounced in alcoholic women who later produced FAS infants. Alcohol abuse also increased HDL3. Furthermore, in alcohol users, the normal increase in VLDL was accentuated, especially so in women with FAS infants, and that of HDL2 was reduced. The significance of the changes found remains obscure, but they may be related to impaired function of the fetoplacental unit.

Serum concentrations of iodothyronines, cortisol, prolactin, testosterone and the respective tropic hormones were measured in 32 noncirrhotic male alcoholics, aged 28-51 years, at the end of a long drinking period and subsequently during ethanol withdrawal over 1-2 weeks. Seven men had testicular atrophy. On admission one patient had high values for serum thyroxine (T4) and free thyroxine index (FT4I). A blunted response of serum thyrotropin (TSH) to thyrotropin-releasing hormone (TRH) was found in 9 men. Apart from a blunted TSH-response in one man the abnormalities disappeared during the first week of alcohol abstinence. Simultaneously the mean levels of serum T4, FT4I, triiodothyronine, free triiodothyronine index and reverse triiodothyronine were reduced by 12, 14, 5, 8 and 21%, respectively, and the mean of the maximum TSH-response to TRH was increased by 55%. At the time of stopping drinking two men had high morning values and six an abnormal diurnal rhythm of serum cortisol. High serum ACTH-levels associated with normal serum cortisol concentrations were found in 12 men. During the first week of alcohol abstinence the mean morning values for serum cortisol and ACTH were reduced by 18 and 42%, respectively. The serum ACTH-levels remained high in 6 men but the abnormalities in cortisol secretion disappeared. On admission four men had low serum concentrations of testosterone which were normalized during ethanol withdrawal over one week. At the same time the mean level of serum testosterone was increased by 19%. Mild hyperprolactinaemia found in 7 patients on admission disappeared in 4 men during the first week of ethanol withdrawal.(ABSTRACT TRUNCATED AT 250 WORDS)

Serum methanol levels were studied in 16 skid-row alcoholics, 16 alcoholics entering a detoxification unit, 193 drunken drivers, and 50 social drinkers, all of whom had a blood-ethanol concentration exceeding 5 mmol/liter at the time of sampling. Highest mean serum methanol level was found in alcoholics entering detoxification (636 +/- 68 mumol/liter, p less than 0.001 as compared to social drinkers), followed by skid-row alcoholics (567 +/- 105 mumol/liter, p less than 0.001), drunken drivers (231 +/- 11 mumol/liter, p less than 0.001) and social drinkers (127 +/- 10 mumol/liter). During 2 days heavy drinking mean serum methanol concentration in 10 nonalcoholic volunteers increased from 177 +/- 15 mumol/liter 1 h after the beginning of drinking to 322 +/- 29 mumol/liter 42 h after the beginning of drinking (p less than 0.001). In 70 of the drunken drivers urinary methanol concentration was determined as well and a fairly good correlation (r = +0.56, p less than 0.001) between serum and urinary methanol levels were found. Our results suggest that methanol determined either from serum or urine can be used as a biological marker of alcohol abuse.

To explore the role of parental alcohol consumption in miscarriage we interviewed 80 women who miscarried about their own and their partners' drinking habits. A control group of 81 gestational-age-matched women whose pregnancy ended in the delivery of a healthy infant at term were similarly questioned. The use of alcohol by women and men was equally frequent in both groups. Before pregnancy, the mean alcohol consumption per week had been about 1-2 drinks for the women and 4-5 drinks for the men. During the presumed day of conception, 13% of the women who miscarried and 11% of the women in the control group had drunk on average 3-4 drinks; the other women had been abstinent at this time. Of the partners, 13% and 15%, respectively, had taken a mean of 4-5 drinks. In both groups 58% of the subjects continued to consume alcohol during pregnancy. The mean consumption was about one drink a week by the women who miscarried and half a drink a week in the control group. Of women who miscarried, 36 had a blighted ovum and in this subgroup alcohol consumption in both women and men was similar to that in the other women who miscarried and their partners, suggesting that alcohol is not causally related to the development of a blighted ovum. These results suggest that moderate maternal or paternal alcohol consumption does not increase the risk of miscarriage.

Left ventricular function was examined by echocardiography and systolic time intervals in nine healthy male volunteers, who ingested ethanol 0.35 g/kg 4 hr after a 50-mg peroral dose of calcium cyanamide, an aldehyde dehydrogenase inhibitor. Accumulation of acetaldehyde in blood was accompanied by marked increases in heart rate (53%) and cardiac output (78%) as well as by decreases in diastolic arterial blood pressure (19%) and peripheral vascular resistance (46%). Ejection fraction and maximum circumferential fibre shortening velocity increased by 25 and 47%, respectively; the preejection period/ejection time ratio decreased by 31%. 4-Methylpyrazole, an alcohol dehydrogenase inhibitor, efficiently reduced blood acetaldehyde levels when injected intravenously (7 mg/kg) at the height of the reaction. It was as effective as intravenous propranolol (0.1 mg/kg) in attenuating the hyperdynamic circulation and stabilized arterial blood pressure better than propranolol. We conclude that even a very mild alcohol intoxication (30-50 mg/100 ml) causes a marked enhancement of cardiac function, in addition to vasodilation, in subjects with impaired acetaldehyde oxidation. These changes are reversed by preventing acetaldehyde formation through alcohol dehydrogenase inhibition.