Interaction between corticosterone and insulin in obesity: regulation of lard intake and fat stores

Passive elevations in glucocorticoids result in increased insulin and abdominal obesity with peripheral wasting, as observed in Cushing's syndrome, with little effect on chow intake. In the absence of insulin (streptozotocin-induced diabetes) diabetic rats markedly increase their chow intake in proportion to glucocorticoids. Given a choice of lard or chow, diabetic rats first eat lard, then reduce caloric intake to normal for 48 h before returning to hyperphagia on chow alone. We performed three experiments to determine the relationship of corticosterone and insulin to lard intake, chow intake, body weight, hormones, and fat depots. The results of these studies clarify the actions of both circulating glucocorticoids and insulin on caloric intake in adult male rats. Our experiments show that glucocorticoids provoke dose-related increases in total caloric intake that persist for days and weeks; the results also suggest that increasing insulin concentrations stimulated by glucocorticoids determine the amount of fat intake. Furthermore, we show that lard intake is associated with increasing insulin concentrations. Additionally, the results in adrenalectomized and adrenalectomized, streptozotocin-induced diabetic rats strongly suggest that it is a combination of corticosterone and insulin that increases abdominal fat depot weight. Independently of the hormonally manipulated rats, the results also show that intact rats voluntarily eat a considerable and stable proportion of their daily calories as lard when given a choice between lard and chow. These results suggest that some human obesities may result from elevated glucocorticoids and insulin increasing the proportional intake of high density calories.     

Increase in Alcohol Intake,Reduced Flexibility of Alcohol Drinking,and Evidence of Signs of Alcohol Intoxication in Sardinian Alcohol‐Preferring Rats Exposed to Intermittent Access to 20% Alcohol

Background: This study assessed in Sardinian alcohol‐preferring (sP) rats a procedure known to promote alcohol drinking and based on the intermittent (once every other day) access to 2 bottles containing alcohol (20%, v/v) and water, respectively (Wise, 1973). Methods: To this end, sP rats were exposed – under the 2‐bottle choice regimen – to: (i) 10% (v/v) alcohol with continuous access (CA10%; i.e., the procedure under which sP rats had been selectively bred); (ii) 10% (v/v) alcohol with intermittent access (IA10%); (iii) 20% (v/v) alcohol with continuous access (CA20%); (iv) 20% (v/v) alcohol with intermittent access (IA20%; the “Wise” condition) (Experiment 1). Additional experiments assessed the influence of (i) adulteration with quinine of the alcohol solution (Experiment 2) and (ii) concurrent presentation of a saccharin solution (Experiment 3) on alcohol drinking under the CA10% and IA20% conditions. Finally, it was assessed whether alcohol drinking under the CA10% and IA20% conditions resulted in motor incoordination at the Rota‐Rod task, as a possible sign of alcohol intoxication (Experiment 4). Results: Daily alcohol intake markedly escalated in rats exposed to the IA20% condition, averaging 9.0 g/kg (in comparison with the average intake of 6.5 g/kg in the CA10% rat group). CA20% and IA10% rats displayed intermediate values of daily alcohol intake between those of CA10% and IA20% rats. Alcohol intake was virtually abolished by addition of quinine or by concurrent presentation of the saccharin solution in CA10% rats; conversely, alcohol intake in IA20% rats was only partially affected by gustatory aversion or concurrent presentation of an alternative reinforcer. Finally, alcohol intake in IA20%, but not in CA10%, rats resulted in clear motor‐incoordinating effects. Conclusions: These data suggest that the “Wise” procedure is effective in inducing marked increases in alcohol intake in sP rats. These increases are associated with a reduced flexibility of alcohol drinking (suggesting the development of “behavioral” dependence) and produce signs of alcohol intoxication that are not detected when sP rats are exposed to the more conventional CA10% condition.     

Impact of Chronic Alcohol Ingestion on Cardiac Muscle Protein Expression

Background: Chronic alcohol abuse contributes not only to an increased risk of health‐related complications, but also to a premature mortality in adults. Myocardial dysfunction, including the development of a syndrome referred to as alcoholic cardiomyopathy, appears to be a major contributing factor. One mechanism to account for the pathogenesis of alcoholic cardiomyopathy involves alterations in protein expression secondary to an inhibition of protein synthesis. However, the full extent to which myocardial proteins are affected by chronic alcohol consumption remains unresolved. Methods: The purpose of this study was to examine the effect of chronic alcohol consumption on the expression of cardiac proteins. Male rats were maintained for 16 weeks on a 40% ethanol‐containing diet in which alcohol was provided both in drinking water and agar blocks. Control animals were pair‐fed to consume the same caloric intake. Heart homogenates from control‐ and ethanol‐fed rats were labeled with the cleavable isotope coded affinity tags (ICAT™). Following the reaction with the ICAT™ reagent, we applied one‐dimensional gel electrophoresis with in‐gel trypsin digestion of proteins and subsequent MALDI‐TOF‐TOF mass spectrometric techniques for identification of peptides. Differences in the expression of cardiac proteins from control‐ and ethanol‐fed rats were determined by mass spectrometry approaches. Results: Initial proteomic analysis identified and quantified hundreds of cardiac proteins. Major decreases in the expression of specific myocardial proteins were observed. Proteins were grouped depending on their contribution to multiple activities of cardiac function and metabolism, including mitochondrial‐, glycolytic‐, myofibrillar‐, membrane‐associated, and plasma proteins. Another group contained identified proteins that could not be properly categorized under the aforementioned classification system. Conclusions: Based on the changes in proteins, we speculate modulation of cardiac muscle protein expression represents a fundamental alteration induced by chronic alcohol consumption, consistent with changes in myocardial wall thickness measured under the same conditions.     

Increase of Rat Alcohol Drinking Behavior Depends on the Age of Drinking Onset

Background Although alcohol drinking onset in younger people is associated with an increased risk of alcohol-related injuries, other factors, such as habituation and susceptibility to alcohol, in the process of aging have not been adequately examined in animal models. In the present study, we determined whether age of drinking onset affected alcohol drinking behavior and led to alcohol tolerance in experimental animals, and extrapolated some of the findings to human alcohol drinking patterns.
Methods In the first experiment, 18 rats that were naive to alcohol were tested at the age of 1, 4, and 10 months with 4 hr of access to 10% (v/v) alcohol. After the time access tests, these animals (1, 4, and 10 months of age) were housed individually and given free access to 10% alcohol solution and tap water. At 3 and 6 months later, all rats that had experienced alcohol drinking were studied for the voluntary consumption of the alcohol solution, alcohol preference, under the two-bottle method in a second experiment.
Results In the 4-hr alcohol-access test, alcohol intake (g/kg/hr) was significantly increased at 0.5 and 1 hr in 1- and 4-month-old naive rats compared with 10-month-old naive rats. The daily alcohol intake (g/kg/day) of rats with drinking onset at 1 month of age was significantly increased at 3 and 6 months after the voluntary alcohol consumption. The daily alcohol intake in the rats with drinking onset at 4 months of age was significantly increased at 6 months only. However, the daily alcohol intake did not change in the rats with drinking onset at 10 months of age through the alcohol preference test.
Conclusions Alcohol drinking behavior in experimental animals depends on the age of alcohol drinking onset.     

Risk factors for alcoholic liver disease in China

AIM: To examine the association of daily alcohol intake,types of alcoholic beverage consumed, drinking patterns and obesity with alcoholic liver disease in China.METHODS: By random cluster sampling and a 3-year follow-up study, 1 270 alcohol drinkers were recruited from different occupations in the urban and suburban areas of Xi‘an City. They were examined by specialists and inquired for information on: Medical history and family medical history, alcohol intake, types of alcoholic beverage consumed, drinking patterns by detailed dietary questionnaires. Routine blood tests and ultrasonography were done.RESULTS: Multivariate analysis showed that: (1) The risk threshold for developing alcoholic liver disease was ingestion of more than 20 g alcohol per day, keeping on drinking for over 5 years in men. The highest OR was at the daily alcohol consumption ≥160 g, the occurrencerate of ALD amounted to 18.7% (P<0.01). No ALD occurred when ingestion of alcohol was less than 20 g per day. (2) 87.9% of all drank only at mealtimes. The cumulative risk of developing ALD was significantly higher in those individuals who regularly drank alcohol without food than in those who drank only at mealtimes, especially for those who regularly drank hard liquors only and multiple drinks (P<0.05). (3) The alcohol consumption in those with BMI ≥25 was lower than in those with BMI<25, but the risk increased to 11.5%, significantly higher than that of general population, 6.5% (P<0.01). (4) Abstinence and weight reduction could benefit the liver function recovery.CONCLUSION: In the Chinese population the ethanol risk threshold for developing ALD is 20 g per day, and this risk increases with increased daily intake. Drinking 20 g of ethanol per day and for less than 5 years are safe from ALD. Drinking alcohol outside mealtimes and drinking hard liquors only and multiple different alcohol beverages both increase the risk of developing ALD. Obesity also increases the risk, Abstinence and weight reduction will directly affect the prognosis of ALD, Doctor‘s strong advice might influence the prognosis indirectly.     

Relation between alcohol intake, myocardial enzyme activity, and myocardial function in dilated cardiomyopathy. Evidence for the concept of alcohol induced heart muscle disease

Detailed drinking histories were taken in 38 patients in whom dilated cardiomyopathy was diagnosed by cardiac catheterisation and left ventricular biopsy. On the basis of the drinking history twenty patients were classified as being in an abstinent or light drinking group and eighteen patients as being in a heavy drinking group (daily alcohol intake in excess of 80 g or cumulative lifetime intake exceeding 250 kg). Activities of myocardial creatine kinase, lactate dehydrogenase, alpha hydroxybutyric dehydrogenase, malic dehydrogenase, and aspartate amino-transferase were all higher in the heavy drinkers and myocardial enzyme activity correlated with cumulative lifetime alcohol intake, maximum daily intake, and recent daily intake. Activities of creatine kinase, alpha hydroxybutyric dehydrogenase, and malic dehydrogenase correlated with ejection fraction, irrespective of the alcohol intake of the patient. These findings were not altered by exclusion of patients with hypertension. The results indicate that among patients with dilated cardiomyopathy there is a group characterised by a high alcohol intake and raised myocardial tissue enzymes which supports the concept of alcoholic heart muscle disease as a distinct entity.     

Alcohol Self-Administration in a Nonrestricted Access Situation with Alcohol-Preferring (P) Rats

Genetic variables have been implicated as contributing factors in the development of alcoholic behavior. Rats bred selectively for alcohol preference have been used in laboratory studies to investigate the role of such variables. In the present study, rats from the alcohol preferring (P) line were placed in operant chambers in which food pellets, water, and 10% ethanol (v/v) were available continuously for 23 hr/day. Food pellets (45 mg) were presented on an FR 1 schedule of reinforcement, while ethanol was presented in a 0.1 ml dipper on an FR 4 schedule of reinforcement. Water was available in a drinking tube with licks monitored by a drinkometer. Data were analyzed in terms of both total daily intakes and computer defined bouts. The P rats showed greater daily ethanol intakes compared with Long-Evans (LE) animals previously studied under similar access conditions. The major difference in intake was a result of the P rats having a greater number of daily ethanol drinking bouts, while having only a slight increase in individual bout size. These data indicate that genetic selection for ethanol preference may result in the regulation of ethanol intake by means of changes in the frequency of ethanol drinking bouts but not by changes in bout size.     

Relation between alcohol intake, myocardial enzyme activity, and myocardial function in dilated cardiomyopathy. Evidence for the concept of alcohol induced heart muscle disease.

Detailed drinking histories were taken in 38 patients in whom dilated cardiomyopathy was diagnosed by cardiac catheterisation and left ventricular biopsy. On the basis of the drinking history twenty patients were classified as being in an abstinent or light drinking group and eighteen patients as being in a heavy drinking group (daily alcohol intake in excess of 80 g or cumulative lifetime intake exceeding 250 kg). Activities of myocardial creatine kinase, lactate dehydrogenase, alpha hydroxybutyric dehydrogenase, malic dehydrogenase, and aspartate amino-transferase were all higher in the heavy drinkers and myocardial enzyme activity correlated with cumulative lifetime alcohol intake, maximum daily intake, and recent daily intake. Activities of creatine kinase, alpha hydroxybutyric dehydrogenase, and malic dehydrogenase correlated with ejection fraction, irrespective of the alcohol intake of the patient. These findings were not altered by exclusion of patients with hypertension. The results indicate that among patients with dilated cardiomyopathy there is a group characterised by a high alcohol intake and raised myocardial tissue enzymes which supports the concept of alcoholic heart muscle disease as a distinct entity.     

Abrupt Termination of an Ethanol Regimen Provokes Ventricular Arrhythmia and Enhances Susceptibility to the Arrhythmogenic Effects of Epinephrine in Rats

Background: Pathologists examining victims of sudden unexpected death encounter alcoholics more often than expected; alcohol may play a role in sudden arrhythmic death. Here we determine whether a pattern of alcohol consumption, chronic ethanol intake, and withdrawal increases the incidence of malignant ventricular arrhythmia and modulates susceptibility to the arrhythmogenic potential of sympathetic stimulation from an epinephrine test in rats. Methods: Male Wistar rats were treated with a continuous ethanol liquid diet for 7 weeks, and then subjected to 1-day withdrawal or 21-day abstinence. Ventricular ectopy was evaluated by 24-hour electrocardiographic telemetry recording; whole-body sympathetic activation, cardiac sympathovagal balance, and susceptibility to ventricular arrhythmia induced by sympathetic stimulation were evaluated based on blood noradrenalin metabolite concentrations, heart rate variability, and a 3-step epinephrine test. Results: Ventricular arrhythmia and related death were observed only in rats at 1 day of withdrawal, but not in nonalcoholic, continuous ethanol intake or 21-day abstinence rats. One-day withdrawal after a 7-week continuous ethanol regimen elevated circulating noradrenalin metabolite levels and induced cardiac sympathovagal imbalance. Deaths related to the epinephrine test and ventricular arrhythmia induced by low doses of epinephrine were observed only in 1-day withdrawal rats. However, all anomalies were normalized by 21-day abstinence. Conclusions: Abrupt termination of a 7-week continuous ethanol regimen is sufficient to enhance the whole-body sympathetic activation and cardiac sympathovagal imbalance that contribute to ventricular arrhythmia and sudden death in alcoholic rats. Those providing medical care for alcoholics, including in cases of legal imprisonment, should be aware of the possibility of enhanced susceptibility to sudden arrhythmic death due to the abrupt termination of a chronic ethanol regimen.     

Intermittent access to 20% ethanol induces high ethanol consumption in Long-Evans and Wistar rats

Background: There has been some difficulty getting standard laboratory rats to voluntarily consume large amounts of ethanol without the use of initiation procedures. It has previously been shown that standard laboratory rats will voluntarily consume high levels of ethanol if given intermittent‐access to 20% ethanol in a 2‐bottle‐choice setting [ Wise, Psychopharmacologia 29 (1973), 203 ]. In this study, we have further characterized this drinking model. Methods: Ethanol‐naïve Long–Evans rats were given intermittent‐access to 20% ethanol (three 24‐hour sessions per week). No sucrose fading was needed and water was always available ad libitum. Ethanol consumption, preference, and long‐term drinking behaviors were investigated. Furthermore, to pharmacologically validate the intermittent‐access 20% ethanol drinking paradigm, the efficacy of acamprosate and naltrexone in decreasing ethanol consumption were compared with those of groups given continuous‐access to 10 or 20% ethanol, respectively. Additionally, ethanol consumption was investigated in Wistar and out‐bred alcohol preferring (P) rats following intermittent‐access to 20% ethanol. Results: The intermittent‐access 20% ethanol 2‐bottle‐choice drinking paradigm led standard laboratory rats to escalate their ethanol intake over the first 5 to 6 drinking sessions, reaching stable baseline consumption of high amounts of ethanol (Long–Evans: 5.1 ± 0.6; Wistar: 5.8 ± 0.8 g/kg/24 h, respectively). Furthermore, the cycles of excessive drinking and abstinence led to an increase in ethanol preference and increased efficacy of both acamprosate and naltrexone in Long–Evans rats. P‐rats initiate drinking at a higher level than both Long–Evans and Wistar rats using the intermittent‐access 20% ethanol paradigm and showed a trend toward a further escalation in ethanol intake over time (mean ethanol intake: 6.3 ± 0.8 g/kg/24 h). Conclusion: Standard laboratory rats will voluntarily consume ethanol using the intermittent‐access 20% ethanol drinking paradigm without the use of any initiation procedures. This model promises to be a valuable tool in the alcohol research field.     

长期饮酒对大鼠心肌及金属硫蛋白含量的影响

目的研究长期饮酒对大鼠心肌细胞形态、超微结构及心肌中丙二醛（MDA）、金属硫蛋白（MT）含量的影响。方法慢性自由饮质量浓度36％酒精6个月,制备大鼠酒精性心肌病早期模型。观察大鼠心肌细胞形态、超微结构改变及心肌中MDA、MT含量变化。结果实验组大鼠心肌细胞发生炎症反应、超微结构改变和心肌细胞间质充血等损伤,心肌中MDA显著高于对照组（P〈0．01）,MT明显低于对照组（P〈0．01）。结论长期饮酒可致大鼠心肌细胞形态及超微结构损伤,MDA增多,MT减少。     

Effect of moderate semi-starvation on plasma lipids

The effect of a daily intake of 200 kcal for 6 days on blood lipid levels of normal and obese subjects was examined. Subjects exhibited a decrease in body weight of 5.9 percent. Plasma glucose levels decreased with no change in insulin levels. FFA and cholesterol did not change significantly with the low caloric intake. Triglyceride and phospholipid concentrations, elevated in obese subjects before the dietary period, decreased significantly with low caloric intake. In contrast no significant changes were observed in triglycerides or phospholipids in normal subjects. Serum uric acid increased during diet in normal but not in obese subjects. These results show different patterns of changes in plasma lipids in normal and obese subjects on very low caloric intake and raise the possibility of differences in utilization of lipid and protein stores, and may also hint at a role for phospholipids in energy metabolism. Very low calorie and carbohydrate diets may be beneficial for weight reduction in obese subjects without increasing blood lipids.     

Increased Natural Killer Cell Activity in a Model of Immunoglobulin A Nephropathy Secondary to Chronic Alcohol Consumption

We investigated natural killer (NK) cell activity in an animal model of ethanol-induced immunoglobulin A (IgA) nephropathy. Two groups, of 10 rats each, received a continuous intragastric infusion of liquid diet through a permanent cannula for 6 weeks. The alcoholic group was infused additionally with intragastric ethanol, representing from 32% to 40% of the caloric requirement. The group of control rats received an isocaloric diet supplemented with glucose instead of alcohol. IgA nephropathy was observed in all the alcoholic rats but in none of the controls. NK cell activity was investigated in the two groups by measuring the cytotoxicity of spleen cells using the chromium release method. NK cell activity was found to be significantly increased in the alcoholic rats. In view of the known modulation of IgA synthesis by NK cells, we suggest that increased NK cell activity may be a contributing factor to the high levels of circulating IgA seen in IgA nephropathy secondary to chronic alcohol consumption.     

Development of ethanol withdrawal-related sensitization and relapse drinking in mice selected for high- or low-ethanol preference

Background: Previous studies have shown that high alcohol consumption is associated with low withdrawal susceptibility, while at the same time, other studies have shown that exposure to ethanol vapor increases alcohol drinking in rats and mice. In the present studies, we sought to shed light on this seeming contradiction using mice selectively bred for High‐ (HAP) and Low‐ (LAP) Alcohol Preference, first, assessing these lines for differences in signs of ethanol withdrawal and second, for differences in the efficacy of intermittent alcohol vapor exposure on elevating subsequent ethanol intake. Methods: Experiment 1 examined whether these lines of mice differed in ethanol withdrawal‐induced CNS hyperexcitability and the development of sensitization to this effect following intermittent ethanol vapor exposure. Adult HAP and LAP lines (replicates 1 and 2), and the C3H/HeNcr inbred strain (included as a control genotype for comparison purposes) received intermittent exposure to ethanol vapor and were evaluated for ethanol withdrawal‐induced seizures assessed by scoring handling‐induced convulsions (HIC). Experiment 2 examined the influence of chronic intermittent ethanol exposure on voluntary ethanol drinking. Adult male and female HAP‐2 and LAP‐2 mice, along with male C57BL/6J (included as comparative controls) were trained to drink 10% ethanol using a limited access (2 h/d) 2‐bottle choice paradigm. After stable baseline daily intake was established, mice received chronic intermittent ethanol vapor exposure in inhalation chambers. Ethanol intake sessions resumed 72 hours after final ethanol (or air) exposure for 5 consecutive days. Results: Following chronic ethanol treatment, LAP mice exhibited overall greater withdrawal seizure activity compared with HAP mice. In Experiment 2, chronic ethanol exposure/withdrawal resulted in a significant increase in ethanol intake in male C57BL/6J, and modestly elevated intake in HAP‐2 male mice. Ethanol intake for male control mice did not change from baseline levels of intake. In contrast, HAP‐2 female and LAP‐2 mice of both sexes did not show changes in ethanol intake as a consequence of intermittent ethanol exposure. Conclusions: Overall, these results indicate that the magnitude of ethanol withdrawal‐related seizures is inversely related to inherited ethanol intake preference. Additionally, intermittent ethanol vapor exposure appears more likely to affect high‐drinking mice (C57BL/6J and HAP‐2) than low drinkers, although these animals are less affected by ethanol withdrawal.     

酒精性肝病并酒精性戒断综合征32例临床分析

探讨酒精性肝病患者中酒精戒断综合征的临床特点,并分析酒精性肝病的严重程度是否影响戒断症状的轻重。回顾性分析了32例酒精性肝病合并酒精戒断综合征的患者,用SPSS统计软件进行统计分析表明酒精性肝病的严重程度并不影响戒断症状的轻重,酒精性肝病的严重程度与饮酒时间密切相关而与平均每天酒量关系不大,而戒断则反之。因此长期酗酒引起酒精性肝病者每天饮酒（精）量越大越容易出现戒断综合征,须提高警惕避免误诊。     

Intermittent versus daily calorie restriction: which diet regimen is more effective for weight loss?

Dietary restriction is an effective strategy for weight loss in obese individuals. The most common form of dietary restriction implemented is daily calorie restriction (CR), which involves reducing energy by 15–60% of usual caloric intake every day. Another form of dietary restriction employed is intermittent CR, which involves 24 h of ad libitum food consumption alternated with 24 h of complete or partial food restriction. Although both diets are effective for weight loss, it remains unknown whether one of these interventions produces superior changes in body weight and body composition when compared to the other. Accordingly, this review examines the effects of daily CR versus intermittent CR on weight loss, fat mass loss and lean mass retention in overweight and obese adults. Results reveal similar weight loss and fat mass loss with 3 to 12 weeks' intermittent CR (4–8%, 11–16%, respectively) and daily CR (5–8%, 10–20%, respectively). In contrast, less fat free mass was lost in response to intermittent CR versus daily CR. These findings suggest that these diets are equally as effective in decreasing body weight and fat mass, although intermittent CR may be more effective for the retention of lean mass.     

Effects of CRF1-receptor and opioid-receptor antagonists on dependence-induced increases in alcohol drinking by alcohol-preferring (P) rats

Background:  Selective breeding of rats over generations and induction of alcohol dependence via chronic vapor inhalation both enhance alcohol consumption in animal models. The purpose of this study was to determine whether dependence-induced increases in alcohol consumption by P rats is sensitive to naltrexone, a general opioid receptor antagonist (but with highest affinity at the μ-opioid receptor at low doses), and the recently characterized small molecule CRF₁-receptor antagonist MPZP ( N,N -bis(2-methoxyethyl)-3-(4-methoxy-2-methylphenyl)-2,5-dimethyl-pyrazolo[1,5- a ]pyrimidin-7-amine).
Methods:  P rats ( n  =   20) were trained to respond for alcohol and water in a 2-lever operant situation during daily 30-minute sessions. P rats were then matched for alcohol intake and exposed to chronic intermittent alcohol vapor ( n  =   10) or ambient air ( n  =   10) for approximately 10 weeks. All rats were then administered MPZP and naltrexone in 2 separate and consecutive Latin-square designs.
Results:  MPZP attenuated dependence-induced increases in alcohol intake by P rats while having no effect on alcohol consumption by nondependent controls. Conversely, operant alcohol responding was reduced similarly in dependent and nondependent P rats by naltrexone.
Conclusions:  These results confirm a role for brain CRF₁-receptor systems in dependence-induced changes in the reinforcing properties of alcohol, and CRF₁-receptor blockade appears to suppress dependence-induced drinking at lower doses in P rats relative to other rat lines. Therefore, brain CRF₁-receptor systems are important in the regulation of dependence-induced alcohol consumption, whereas brain opioid systems are important in the regulation of basal alcohol consumption by rats.     

Dietary Ethanol Does Not Accelerate Bone Loss in Ovariectomized Rats

The abuse of alcohol is a behavior that can significantly compromise skeletal health. Because postmenopausal women are already at risk for low bone mass and osteoporotic fracture, this investigation sought to determine whether high concentrations of dietary ethanol exacerbate the bone loss associated with ovariectomy in rats, an animal model of human postmenopause. Six-month-old Sprague-Dawley rats were ovariectomized or sham-operated and randomly divided into groups fed a modified Lieber-DeCarli liquid diet isoca-lorically supplemented with 0%, 13%, or 35% ethanol (by daily caloric intake), for a period of 2 months. All animals were injected with fluorochromes at the start, 2 weeks, and 2 days before sacrifice to label mineralizing bone surfaces. At sacrifice, blood, uterus, and tibiae were harvested. No differences in serum calcium or cholesterol were found. Serum creatinine was also found to be unvaried, indicating this level of alcohol consumption did not compromise liver function. Dietary alcohol consumption at 35% of daily caloric intake was determined to increase tibial cortical medullary area and en-docortical perimeter, while not affecting cortical area and periosteal perimeter. Ovariectomy significantly increased indices of bone turnover and resulted in cancellous bone loss, whereas alcohol consumption had no additional detrimental effects. This was a consistent pattern for other indices of proximal tibial architecture. In summary, this investigation has found that chronic ingestion of high concentrations of alcohol does not accentuate bone loss in ovarian hormone-deficient adult female rats.     

Alcohol and sauna bathing: effects on cardiac rhythm, blood pressure, and serum electrolyte and cortisol concentrations.

The effect of heavy drinking and sauna bathing on cardiac rhythm, blood pressure, and serum electrolyte and cortisol concentrations was studied in 10 healthy male volunteers. Sauna bathing induced a comparable, significant increase in heart rate with and without alcohol consumption. During sauna bathing without alcohol, systolic blood pressure remained at the baseline level, whereas sauna and alcohol together decreased systolic blood pressure markedly from 136 +/- 4 to 113 +/- 3 mmHg (P less than 0.01). Neither sauna alone, nor sauna combined with alcohol intake, increased the frequency of premature ventricular complexes. Serum potassium, calcium and cortisol concentrations changed slightly during sauna, but alcohol consumption did not contribute further to this. In conclusion, sauna bathing, even in combination with heavy drinking, does not appear to provoke cardiac arrhythmias in healthy young men. However, the risk of hypotension is increased when sauna bathing is combined with alcohol consumption.     

Alcohol Consumption and Hypertension

Many observational studies have shown a relationship between three or more alcoholic drinks daily and hypertension. Reduction in alcohol intake is associated with lowering of blood pressure in randomized clinical trials: each drink per day reduction in intake lowers systolic and diastolic blood pressure by approximately 1 mm Hg. Although regular alcohol consumption seems to reduce the incidence of atherothrombotic cardiovascular events, excessive alcohol intake increases the risk of many medical and psychosocial problems. For persons with hypertension who drink excessively, average maximum alcohol intake of one drink per day in women and two drinks per day in men is a reasonable goal, if drinking is not otherwise contraindicated.