Alcoholic Beverages

[tgkfour1]

How much is too much on a weekly basis. I drink very little.

 

[Fade]

Glass of wine a night is actually good for you.

I drink a beer every other day at most.
So one a day isn't bad but for some people it might start with one drink a day then two then three and so on.

If you go out on the weekends and drink alot then try not to drink during the week.

Gotta remember that stuff is full of carbs and it dehydrates ya.

 

[LAM]

any regular consumption of alcohol can create insulin resistance.

 

[Fade]

What substance in alcohol causes the resistance?

 

[LAM]

 

[Robboe]

Just eating carbs can induce insulin resistance.

It's not so much the carbs themselves, but the metabolites from the hexamine pathway through which cabrohydrates are metabolised.

 

[Fade]

That's what I thought CD. Having anything with sugars in it will cause the samething. It's not alcohol specific.

 

[Robboe]

Just found this man:

Med Hypotheses 2001 Sep;57(3):405-7

Does regular ethanol consumption promote insulin sensitivity and leanness by stimulating AMP-activated protein kinase?

McCarty MF.

Pantox Laboratories, San Diego, California 92109, USA.

There is good reason to believe that regular moderate alcohol consumption promotes insulin sensitivity of skeletal muscle; conceivably, this benefits the protective effects of moderate drinking on vascular health and risk for obesity and diabetes. The mechanism responsible for alcohol's insulin-sensitizing activity remains obscure. As a working hypothesis, it is proposed that metabolism of acetate in peripheral tissues generates sufficient levels of AMP to temporarily stimulate the AMP-activated protein kinase, which in turn induces the synthesis of certain long-lived proteins that act to boost insulin sensitivity and possibly aid the efficiency of fat oxidation as well. Copyright 2001 Harcourt Publishers Ltd.

PMID: 11516237 [PubMed - indexed for MEDLINE]


I'll keep scaning though. Maybe there's a more up to date study, although september 2001 is really recent.

 

[Fade]

So the carbs may not be the cause of the sensitivity.

Possibly aid fat oxidation huh?

 

[Robboe]

Something slightly different:

Metabolism 2000 Nov;49(11):1473-8

Influence of moderate chronic wine consumption on insulin sensitivity and other correlates of syndrome X in moderately obese women.

Cordain L, Melby CL, Hamamoto AE, O'Neill DS, Cornier MA, Barakat HA, Israel RG, Hill JO.

Department of Health and Exercise Science, Colorado State University, Fort Collins 80523, USA.

Epidemiologic studies indicate that alcohol consumption is associated with improved insulin sensitivity; however, scant experimental evidence confirms this observation. To determine the effects of regular moderate wine consumption on insulin sensitivity, 20 overweight women (body mass index [BMI], 29.8 +/- 2.2 kg/m2) participated in a 20-week free-living randomized crossover trial. The subjects, serving as their own controls, consumed wine (190 mL red wine, 13% vol/vol ethanol, 5 days per week) for 10 weeks and abstained for 10 weeks or vice versa. The dependent variables (body weight, BMI, percent body fat, blood pressure, fasting blood glucose and insulin, blood lipids, dietary intake, and insulin sensitivity by intravenous glucose tolerance test [IVGTT]) were measured at the pretest, at the 10-week crossover, and at the 20-week completion of the study. Data were analyzed at the pretest and at completion of the wine drinking and abstention periods of the study using ANOVA by order of treatment. Fasting glucose remained unchanged (mean +/- SD; P > .05) throughout the experiment (pretest, drinking, and abstention, 91.1 +/- 9.2, 91.6 +/- 9.1, and 88.5 +/- 11.2 mg/dL), as did the measures of insulin sensitivity, fasting insulin (pretest, drinking, and abstention, 8.6 +/- 3.3, 8.6 +/- 4.1, and 9.1 +/- 4.7 microU/mg) and the insulin sensitivity index (3.60 +/- 2.96, 3.25 +/- 2.17, and 3.30 +/- 1.84). Body composition and blood lipids also remained unchanged (P > .05) during treatment. Moderate wine consumption at this dose in overweight women did not improve or impair insulin sensitivity, nor did it change any of the known correlates of insulin sensitivity, including body weight and composition, blood lipids, and blood pressure.

Publication Types:
Clinical Trial
Controlled Clinical Trial

PMID: 11092514 [PubMed - indexed for MEDLINE]

 

[Robboe]

Ooooo isn't this all very exciting...

Diabetes Care 2000 Nov;23(11):1630-6

Associations between alcohol consumption and insulin sensitivity and cardiovascular disease risk factors: the Insulin Resistance and Atherosclerosis Study.

Bell RA, Mayer-Davis EJ, Martin MA, D'Agostino RB Jr, Haffner SM.

Department of Public Health Sciences, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157-1063, USA. rbell@wfubmc.edu

OBJECTIVE: Light-to-moderate alcohol consumption has been associated with reduced cardiovascular disease (CVD) mortality, which may be explained by increased insulin sensitivity (SI) and an improved lipoprotein and blood pressure profile. Prior research has shown improved SI with light-to-moderate alcohol intake even though somewhat imprecise measures of SI were used. RESEARCH DESIGN AND METHODS: Relationships between alcohol use and SI and CVD risk factors were assessed in a cross-sectional analysis of 1,196 white, African-American, and Hispanic men and women from the Insulin Resistance and Atherosclerosis Study (IRAS). Five categories of previous-year alcohol use (never, <0.5 drinks/day, 0.5-0.99 drinks/day, 1-2.99 drinks/day, and > or =3 drinks/day) and log SI + 1 (frequently sampled intravenous glucose tolerance test with Bergman minimal model analysis), log fasting insulin, log triglycerides, HDL cholesterol, and systolic/diastolic blood pressure were examined using analysis of variance. RESULTS: Univariate analysis showed an inverse U-shaped relationship between SI and alcohol intake, with a peak at the 0.5-0.99 drinks/day category. A U-shaped relationship was observed between fasting insulin and the lipid and blood pressure measures. After adjustment for demographic (clinic, sex, ethnicity, age), lifestyle (smoking, dietary energy/fat intake, physical activity), and physical (BMI, waist circumference) variables, the alcohol/insulin association was attenuated, but the association with lipids and blood pressure remained for high-intake categories. CONCLUSIONS: These data suggest that the enhanced SI associated with light-to-moderate alcohol consumption may be a function solely of a BMI and central adiposity profile more favorable to higher SI.

Publication Types:
Multicenter Study

PMID: 11092284 [PubMed - indexed for MEDLINE]

 

[Robboe]

Originally posted by Fade99
Possibly aid fat oxidation huh?

Dude, don't try using that an excuse



hee hee.

 

[Fade]

Hell with it.

For the sake of science I'll drink alot of beer over the next month. I'll keep my diet the same.

We'll see what happens.

 

[Robboe]

Originally posted by LAM
any regular consumption of alcohol can create insulin resistance.

I suspect the study (studies) showing this were done with large quantities of alcohol over a period of time, right?

 

[Robboe]

A-ha!

Eur J Clin Invest 2000 Apr;30(4):297-301

Alcohol consumption and insulin resistance in young adults.

Flanagan DE, Moore VM, Godsland IF, Cockington RA, Robinson JS, Phillips DI.

University of Southampton, Southampton; Imperial College School of Medicine, London, UK. daniel@flanagan.freeserve.co.uk

BACKGROUND: Alcohol may have a cardioprotective effect. One possible mechanism is by reducing insulin resistance, a known cardiovascular risk factor. The aim of this study was to assess the relationship between alcohol consumption, insulin resistance and other parameters determining glucose tolerance in 154 young men and women. SUBJECTS AND METHODS: Subjects completed a questionnaire documenting weekly alcohol consumption. Insulin sensitivity and glucose tolerance were measured using the intravenous glucose tolerance test with minimal model analysis. Height, weight, usual level of exercise, smoking habits and socio-economic status were also recorded. RESULTS: Insulin sensitivity correlated inversely with body mass index (r = - 0.529, P < 0.001) but not with level of physical fitness. Women were significantly less insulin sensitive than men (4.19 and 5.63 104 min-1 pmol-1 L-1, respectively; P < 0.001). Insulin sensitivity correlated positively with alcohol consumption and this trend remained significant allowing for body mass index and gender (beta = 0.17, P < 0.014). First-phase insulin secretion showed a weak but non-significant trend in the opposite direction. Fasting glucose, fasting insulin and glucose tolerance showed no relationships with alcohol consumption. CONCLUSION: These data suggest a close relationship between alcohol consumption and insulin resistance in young adults. Regular alcohol consumption is associated with decreased insulin resistance and this may partly explain the cardioprotective effect of alcohol.

PMID: 10759877 [PubMed - indexed for MEDLINE]

 

[Robboe]

Another:

Alcohol Clin Exp Res 1999 Mar;23(3):471-5

Glucose metabolism, insulin-like growth factor-I, and insulin-like growth factor-binding protein-1 after alcohol withdrawal.

Passilta M, Kervinen K, Kesaniemi YA.

Department of Internal Medicine and Biocenter Oulu, University of Oulu, Finland.

Alcohol abusers often present with deteriorated glucose metabolism and insulin resistance. Changes in other glucoregulators, such as insulin-like growth factor-I (IGF-I) and IGF-binding protein-1 (IGFBP-1) may also be related to alcohol abuse. We studied the effects of alcohol withdrawal on blood glucose, serum insulin and C-peptide, and plasma IGF-I and IGFBP-1 levels in 27 noncirrhotic male alcoholics aged 43 +/- 9.0 (mean +/- SD) years on four consecutive days immediately after withdrawal. A 4-day monitoring period was conducted in four healthy nonalcoholic control men. The groups were similar in age and body mass index. Glucose, insulin, IGF-I, and IGFBP-1 did not differ significantly between the groups at the baseline, but C-peptide was higher in alcoholics (p < 0.01). After alcohol withdrawal, serum insulin and C-peptide levels increased in close correlation with each other (r = 0.82, p < 0.001). During the 4-day observation period in alcoholics, IGFBP-1 levels declined by 59%, whereas IGF-I increased by 41% (p < 0.001 for both comparisons). The change in insulin correlated inversely with the change in IGFBP-1 levels (r = -0.39, p < 0.05). In the control group, glucose, insulin, IGF-I, and IGFBP-1 remained unchanged during the 4-day monitoring period, whereas some reduction was observed in C-peptide. In conclusion, alcohol withdrawal enhances insulin production, as seen in increased C-peptide levels. An inverse correlation between the changes in insulin and that in IGFBP-1 might suggest that inhibition of IGFBP-1 by insulin remains largely unchanged during the acute phase of alcohol withdrawal.

PMID: 10195820 [PubMed - indexed for MEDLINE]

 

[Robboe]

Hmmmm...Fade, this touches on what you mentioned earlier with the fat oxidisation:

Obes Res 2002 Apr;10(4):245-52

Alcohol consumption in the severely obese: relationship with the metabolic syndrome.

Dixon JB, Dixon ME, O'Brien PE.

Monash University Department of Surgery, Alfred Hospital, Melbourne, Victoria, Australia. john.dixon@med.monash.edu.au

OBJECTIVE: The aim of this study was to examine the association between the clinical and biochemical features of the metabolic syndrome and quantity and type of alcohol intake in the severely obese. RESEARCH METHODS AND PROCEDURES: A cross-sectional study was performed in 486 consecutive severely obese subjects. Data on alcohol consumption was collected by serial clinical interviews and a questionnaire. The relationship between alcohol intake and the clinical and serum chemistry features of the metabolic syndrome was analyzed by multiple statistical techniques. Laboratory measures included lipid profile, fasting blood glucose, hemoglobin A1c, and fasting serum insulin. An indirect index of insulin resistance was calculated using the log-transformed fasting insulin and glucose product. RESULTS: There were 486 subjects, 84% women, with a mean age of 40.6 +/- 10 years (range, 16 to 71 years) and a body mass index of 45.3 +/- 7 kg/m(2) (range, 34 to 77 kg/m(2)). Alcohol consumers (N = 276) showed a marked reduction in the adjusted odds ratio of type 2 diabetes (odds ratio = 0.29; 95% confidence interval, 0.16 to 0.55) compared with rare or nonconsumers (N = 210). There was a U-shaped relationship between the amount and frequency of alcohol consumption and fasting triglyceride, fasting glucose, hemoglobin A1c, and index of insulin resistance measurements. Consumers of < 100 g/wk had more favorable measures. The effect was attenuated when diabetics were excluded from the analysis. Timing of alcohol consumption did not influence outcome measures. DISCUSSION: Light-to-moderate alcohol consumption is associated with a lower prevalence of type 2 diabetes, reduced insulin resistance, and more favorable vascular risk profile in the severely obese. We would propose that light to moderate alcohol consumption should not be discouraged in the severely obese.

PMID: 11943832 [PubMed - indexed for MEDLINE]

 

[Fade]

One drink a day is good....one case a day is bad.

 

[Robboe]

true dat.

Anyhoo, this one is just for shits and giggles. A kinda "Everything you ever didn't need to know about alcohol, but you're gonna find out anyway".

Nippon Eiseigaku Zasshi 2001 Jan;55(4):607-17


[Effects of ethanol on the nervous and vascular systems: the mechanisms of alcohol-induced hypertension]

[Article in Japanese]

Wakabayashi I, Hatake K.

Department of Hygiene & Preventive Medicine, School of Medicine, Yamagata University, Yamagata, 2-2-2 Iida-Nishi, Yamagata 990-9585, Japan.

Many previous experimental and epidemiological studies have shown that alcohol consumption has a positive correlation with the incidence of hypertension. The effects of ethanol on the nervous and vascular systems in relation to the mechanisms of alcohol-induced hypertension proposed so far are reviewed here. Alcohol ingestion influences many pathophysiological functions which regulate blood pressure, as follows: 1) Sympathetic nervous activity is increased after drinking. 2) Ethanol acts directly on the contractility of vascular smooth muscle. Ethanol acutely contracts some arteries and increases their contractile responses to agonists, while it also displays inhibitory effects on vasocontractility in other arteries. Thus, ethanol has two opposite actions, both of which depend on the kinds of vessels and animal species used for the experiments. Intra- and extracellular Ca2+ mobilization and activation of the contractile apparatus have been suggested as mechanisms for ethanol's vasocontractile actions. 3) Chronic alcohol ingestion has been reported to induce a deficiency of blood and intracellular magnesium, which influences cellular Ca2+ homeostasis through attenuation of plasmalemmal ATPase activity. Direct alcohol effects on cardiovascular systems may not be involved in hypertension that develops after long-term habitual drinking. 4) Ethanol affects vascular endothelial functions, inhibiting endothelial NO- and EDHF-dependent vasorelaxations. 5) The serum levels of vasoactive substances such as cathecolamines, renin-aldosterone, prostacyclin, and endothelin have been reported to be affected by alcohol ingestion or ethanol in vitro. 6) In heavy drinkers, alcohol withdrawal results in an elevation of blood pressure due to sympathetic nervous stimulation. 7) Long-term heavy drinking often results in the development of insulin resistance and glucose intolerance, which in turn triggers hypertension. 8) The difference in the genetic polymorphism of acetaldehyde dehydrogenase among Japanese people may not be directly related to development of alcohol-induced hypertension. As mentioned above, alcohol shows multiple actions on various factors regulating blood pressure. More detailed and integrated mechanisms for alcohol-induced hypertension, which is not a homogeneous disease, remain to be clarified.

Publication Types:
Review
Review Literature

PMID: 11265132 [PubMed - indexed for MEDLINE]

 

[Robboe]

More saying moderate intake is better than over-the-top consumption:

Novartis Found Symp 1998;216:159-67; discussion 167-72

Do known cardiovascular risk factors mediate the effect of alcohol on cardiovascular disease?

Criqui MH.

University of California, San Diego, Department of Family and Preventive Medicine, La Jolla 92093-0607, USA.

The association between alcohol intake and atherosclerotic cardiovascular disease (CVD) in epidemiological studies is consistent and shows some protection from CVD at consumption levels of one to two drinks per day, but a sharp increase in CVD associated with three or more drinks per day. Analyses of potential mediators of effects of alcohol on CVD show that it increases high density lipoprotein (HDL) cholesterol levels and favourably influences thrombotic factors, especially fibrinogen, and also fibrinolytic factors. Some evidence also suggests moderate alcohol consumption may reduce insulin resistance. However, studies also show an adverse effect of alcohol, particularly at higher doses, on blood pressure (leading to hypertension) and directly on the myocardium (leading to arrhythmias and myocardiopathy). Statistical modelling of the alcohol-CVD relationship is consistent in several studies, with a protective pathway via elevated HDL cholesterol and an adverse pathway through elevated blood pressure. Other possible mediators influenced by alcohol have not yet been examined in this type of analysis. The French Paradox has led to speculation that wine is the only protective alcoholic beverage for CVD, or at least that it has a stronger effect. Multiple non-ethanol components of wine have been studied in the laboratory and have been shown to have antioxidant or anticoagulant effects. Although wine does appear more protective in ecological studies, studies within cohorts show similar effects across alcoholic beverages, suggesting confounding in ecological studies by diet, lifestyle, or other variables. The key component of alcoholic beverages thus appears to be ethanol, consistent with the known potent effects of ethanol on HDL cholesterol and thrombotic factors. The upswing in CVD risk with three or more drinks per day is sharp and emphasizes that benefit from alcohol is limited to moderate consumption only. This upswing also cautions against any public health recommendation to drink alcohol, since many persons will not or cannot limit their intake to moderate levels.

Publication Types:
Review
Review, Tutorial

PMID: 9949792 [PubMed - indexed for MEDLINE]

 

[w8lifter]

Damn Chicken Baby! You ain't being so lazy today Awesome! Spank you

 

[LAM]

Originally posted by The_Chicken_Daddy
I suspect the study (studies) showing this were done with large quantities of alcohol over a period of time, right?

yes...