View Full Version : alcohol versus testosterone

10-29-2007, 01:16 PM
that's just something that highschool football coaches tell their players.

alcohol can reduce test slightly if enough of it is consumed.
Let's now turn to some studies that looked directly at testosterone levels following acute alcohol administration. In adult males, 1.3g/kg of ethanol (about 10 drinks for a 200 lb person), caused a significant decrease vs. basal levels at the 60 minute mark. Differences for the next two hours were not significant, though the researches did not utilize a control group, so the natural morning rise in testosterone could have masked any effects ( 38 ). 1.5g/kg lowered levels by an average of 23% over a 24 hour period ( 28 ). 1.75g/kg lowered levels by 27% and 16% at 12 and 24 hours, respectively ( 34 ). Adolescent males admitted to the hospital for alcohol intoxication were found to have 21% lower testosterone levels than controls (36).

A couple of studies have looked at alcohol and exercise. 1.5g/kg depressed testosterone by more than 20% by 1 hour and was still depressed by the same margin at hour 10 ( 37 ). Interestingly, when the same ethanol dose was preceded by an exercise session, the suppressive effect continued for 22 hours -- and when exercise was performed during a hangover, significant suppression ( 21-32% ) vs. ethanol alone continued for 26 hours. Compared to control, both ethanol groups had significantly lower testosterone levels for 42 hours - this is almost 2 full days. A much smaller intake (.83g/kg) did not result in a significant decrease ( 35 ).

All of this is at what are fairly moderate doses. Let's take a look at binge drinking doses.

Probably for ethical reasons, doses equating to 20+ drinks have not been studied in humans, so we must settle for rat data, but considering the effects at lower doses seem quite similar, these studies are likely quite relevant -- and could actually underestimate the effect, since, as we mentioned, these doses resulted in much lower blood alcohol levels in rats than humans.

3g/kg caused massive suppression of testosterone ( 67 ). Between hours 1.5 and 96 (yes, 4 days later), testosterone was reduced between 50-75% and, even a full week later, it was still down 40%. By week two, it was finally back to control level. 3g/kg also reduced HCG stimulated testosterone secretion by 75% ( 66 ). In male macaque monkeys, 2.5 and 3.5g/kg reduced testosterone levels by 63 and 70%, respectively ( 68 )

One study in adolescent rats found that testosterone levels doubled for the first 3 of weeks of ethanol ingestion ( 69 ) -- however, this was with an intake equal to 90 drinks per day for a 200 lb person. If anyone tries this, please report back with your results.

On the other hand, levels below 1g/kg seem to have no deleritous effects ( 35, 70 ).

10-29-2007, 01:17 PM
(that was written by "par deus" somewhere, I don't feel like copy/pasting all the references for that but if anyone wants one just tell me the numbers and I'll post the source)

10-29-2007, 07:13 PM
do you know if xanax lowers test? i hear its nearly the same chemical makeup as alcohol.

10-29-2007, 07:22 PM
Xanax acts on benzodiazepine receptors.

Alcohol acts on GABA receptors.

They are both CNS depressants, which I suppose is the mechanism of action that is inhibiting testosterone.

I would say that while you cannot extrapolate with certainty from these studies, you could be pretty sure that xanax will also lower test.

10-29-2007, 08:28 PM
Jimmy Beam and coke does a body good. Stop reading and start eating. Weak, small, and ripped is no way to go thru life.

10-29-2007, 10:38 PM
Whiskey dick. That's my anecdotal evidence that alcohol lowers test.

That and the fact that I always feel weaker when I lift after a night of drinking (although that may have more to do with dehydration)

10-30-2007, 08:41 AM
do you know if xanax lowers test? i hear its nearly the same chemical makeup as alcohol.
doubtful but if someone knows more I'd like to see it. I'm almost positive the effects would be minimal if anything.

Xanax acts on benzodiazepine receptors.

Alcohol acts on GABA receptors.

They are both CNS depressants, which I suppose is the mechanism of action that is inhibiting testosterone.

I would say that while you cannot extrapolate with certainty from these studies, you could be pretty sure that xanax will also lower test.
there are no benzodiazepine receptors, xanax hits gaba subtype a.

I don't think alcohol is as specific in its gaba targeting nor do I think that's the primary test lowering mechanism - will briefly check on that.

Jimmy Beam and coke does a body good.
you're growing on me rh :D - and with too much snow I now understand the need for those foods lol!!

Stop reading and start eating. Weak, small, and ripped is no way to go thru life.
I'm restricting my calories for the starving kids in poor countries :whiner:

nobody on wanna be big wanna be small n weak!! Ripped is cool tho!!

That and the fact that I always feel weaker when I lift after a night of drinking (although that may have more to do with dehydration)

or the gigantic testosterone reduction, the built up toxic metabolites, or the combination of it all!

10-30-2007, 08:50 AM
couldn't find anything quickly about how exactly alcohol lowers test (although I do not think it's solely through inhibiting gaba); that was excerpted from a much larger article, if anyone wants it posted in full lemme know.

Slim Schaedle
10-31-2007, 08:39 PM
Here's a mock study proposal I wrote up for a research methods class.

I figured I would post it here for ****s and giggles.......

Alcohol consumption inhibits the potential gain of lean body mass in weight training individuals

Principle Investigators: Dr. Jeffrey R. Schaedle, Dr. Emilee Anderson, and Dr. Meredith Tyzinski

Our long term objectives are: 1.) to bring forth evidence regarding the effects of alcohol on lean body mass of weight training individuals in both genders and 2.) to increase awareness to weight training individuals on the importance of proper diet in the process of protein synthesis and formation of lean body mass.

Consuming alcohol in conjunction with a prescribed dietary and exercise regimen will negatively impact lean body mass.

Specific Aim 1. Compare individuals that do not consume alcohol to individuals who do consume alcohol and have identical dietary and exercise regimens in relation to lean body mass.

Specific Aim 2. Determine how alcohol inhibits the process of protein synthesis by testing muscle tissue.

Specific Aim 3. To show whether the effect of alcohol on lean body mass gain may differ in males versus females.

The specific aims of this study will be achieved using a randomized single blind utilizing a total of 30 males and 30 females (between the ages of 21-30) who have met the exclusion/inclusion criteria.

Physical activity such as resistance exercise can produce large increases in skeletal muscle mass. The regulation of skeletal muscle mass is a complex phenomenon. In general, muscle hypertrophy is the result of an increase in the size of the existing muscle fibers. Such increase is reflected by the increase in cross-sectional area of the muscle fibers, which in turn is a consequence of the accumulation of contractile proteins within the fiber. Muscle atrophy (also called muscle wasting) is a consequence of the loss of such contractile proteins due to a reduction in muscle fiber cross-sectional area. The maintenance of skeletal muscle mass is the result of the balance between muscle protein synthesis and muscle protein degradation. Hypertrophy occurs as an adaptive response to load-bearing exercise, and as a result of an enhanced rate of protein synthesis. This increase in protein synthesis enables new contractile filaments to be added to the pre-existing muscle fiber, which in turn enables the muscle to generate greater force. Reports have demonstrated that resistance exercise was capable of inducing a sustained increase in protein synthesis rates for at least 24 hours. This increase in protein synthesis was correlated with the activation of the phosphoinositide-3 kinase (PI3K), the mammalian target of rapamycin (mTOR) and the 70 kDa ribosomal S6 protein kinase (S6K1/p70S6k). The increase in skeletal muscle mass is, in part, a consequence of an increase in protein accumulation due to increases in protein synthesis rates. Protein synthesis is regulated at many levels and involves several intracellular signaling mechanisms such as the actions of IGF-1. Increases in muscle load stimulate the expression of a protein growth factor called insulin-like growth factor 1 (IGF-1). IGF-1 stimulation is sufficient to induce hypertrophy of skeletal muscle.

Protein requirements for athletes performing strength training are greater than for sedentary individuals and are above current Canadian and US recommended daily protein intake requirements for young healthy males. Leucine kinetic and nitrogen balance methods have been used to determine the dietary protein requirements of strength athletes compared with sedentary subjects. For strength athletes, low protein diets do not provide adequate protein and result in an accommodated state of decreased whole body protein synthesis. Exercise and physical activity increase energy expenditure up to 10-fold. Evidence has accumulated that amino acids are oxidized as substrates during prolonged submaximal exercise. In addition, studies have determined that both endurance and resistance training exercise increase skeletal muscle protein synthesis and breakdown in the post-exercise recovery period. Studies using nitrogen balance have further confirmed that protein requirements for individuals engaged in regular exercise are increased. The current recommended intakes of protein for strength and endurance athletes are 1.6 to 1.7 g/kg and 1.2 to 1.4 g/kg per day, respectively

Protein synthesis and growth are regulated by signal transduction proteins. The
major mechanism of signal transduction is the phosphorylation or dephosphorylation of proteins. The synthesis of a protein depends on the transcription of DNA into mRNA and on the translation of that mRNA into protein. Nutrition, exercise and hormones affect both transcription and translation in muscle. The second step is translation, which is the actual protein synthesis. It involves, translation initiation, elongation of the peptide chain and termination. Elongation involves the synthesis of peptide bonds between amino acids; it is controlled by eukaryotic elongation factors (eEFs). Translation of the mRNA into peptide is terminated once the stop codon of the mRNA has been reached by the ribosome. A positive regulator of translation and muscle size is IGF-1. IGF-1 was discovered as a growth factor that mediated the effect of growth hormone. Systemic IGF-1 is secreted by liver into the bloodstream and acts as a growth-stimulating second messenger for growth hormone.

The deleterious effects of ethanol on the hypothalamic pituitary growth hormone axis in adult male humans and animals have been well documented. It is also well established that ethanol has toxic effects on testicular function in adult humans and animals. Growth hormone is considered to be an anabolic hormone. The presence of an adequate circulating concentration of GH is necessary for normal accretion of muscle protein in children and the maintenance of lean body mass in adults. Although GH can directly influence various aspects of muscle metabolism, the majority of its effects appear to be mediated indirectly via enhanced synthesis and secretion of insulin-like growth factor (IGF)-I. GH also increases IGF-I in peripheral tissues, such as skeletal muscle. Most studies have shown that chronic alcohol consumption, in rodents or humans, decreases the circulating concentration of IGF-I. Because decreases in IGF-I have been correlated with reductions in muscle protein synthesis, the reduction in IGF-I has been thought to be partly responsible for the alcohol-induced myopathy. The decrease in circulating IGF-I observed following chronic alcohol consumption could be caused by a decrease in plasma GH levels. It has been concluded that acute exposure to ethanol causes a prolonged and severe decrement in serum growth hormone, and attenuation in testosterone secretion.
Insulin-like growth factors-I and -II and insulin are structurally related polypeptides with potent mitogenic and metabolic effects on the central and peripheral nervous systems. These growth factors and their respective receptors are widely distributed throughout the brain, including the hippocampus and cerebellum. Evidence indicates that ethanol can decrease plasma levels of insulin-like growth factors and can also inhibit the growth-promoting and cell survival effects of these growth factors under in vitro conditions.

Studies have been carried out in order to characterize the ability of alcohol to suppress insulin-like growth factor (IGF)-I stimulation of ribosomal S6 kinase 1 (S6K1) and 4E-BP1 phosphorylation, which are central elements in the signal transduction pathway used to coordinate the protein synthetic response and may contribute to the development of alcoholic myopathy. Studies have examined the dose and time dependency of the ability of alcohol to impair signal transduction under basal and IGF-I-stimulated conditions. Additional studies examined the effect of gender, nutritional state, and route of alcohol administration and determined the direct effects of alcohol on muscle metabolism. Phosphorylation of S6K1 and S6 in muscle has been shown to have increased after injection of IGF-I in control rats. In contrast, IGF-I failed to stimulate S6K1 or S6 phosphorylation 2.5 hr after administration of alcohol when blood alcohol concentration was increased between approximately 165 and 300 mg/dl. The effect on S6K1/S6 phosphorylation was observed as early as 1 hr and for up to 8 hr. The ability of alcohol to impair phosphorylation of S6K1 and S6 was independent of gender (male versus female), nutritional status (fed versus fasted), and route of alcohol administration (intraperitoneal versus oral). Furthermore, the suppressive effect of alcohol was still observed in rats pretreated with 4-methylpyrazole, suggesting that the response was independent of the oxidative metabolism of ethanol. Data indicates that acute alcohol intoxication selectively impairs IGF-I signaling via S6K1, and the defect is independent of gender, nutritional state, route of administration, and alcohol metabolism. This IGF-I resistance leads researchers to believe alcohol directly limits the translation of selected messenger RNAs and, ultimately, protein synthesis in skeletal muscle.


C.1. Study Overview A total of 60 untrained subjects (between the ages of 21-30) with moderate drinking experience, willing to modify their diet, and incorporate exercise will be enrolled in this proposed study. The subjects who will be recruited for this study should not be on any prescribed medications or agree to initiate the use of new medications. Additionally, subjects must not be overweight or obese according to their BMI index or have any muscular dehabilitation. Subjects must be without any history of sever liver, kidney, or heart diseases. Eligible men and women regardless of ethnicity and race will be recruited from local gyms and health clubs in greater Cincinnati area and randomly assigned by gender to one of the three treatment groups for a period of twelve weeks. All groups will follow the standard diet and exercise regimen of 500 kcal above maintenance (50% kcal intake of carbohydrates), .5g fat/lb LBM (20%), 1 g protein/lb LBM (30%), and one hour of weight training three times a week. Group 1 will serve as the male control group drinking no alcohol. Group 2 will be male and drink six beers per week. Group 3 will be male drinking twelve beers per week. Group 4 will be the control for the female group drinking no alcohol. Group 5 will be female drinking six beers per week. Group 6 will be female drinking twelve beers per week. The alcohol will be Budweiser purchased from the local grocery store. Study participants will be asked to sign a consent form and then randomly assigned to any of the three gender based treatment groups.
Skin fold, height (inches), weight (pounds), BMI, waist circumference, Bod-Pod analysis will be assessed at baseline visits, followed up by Bod-pod, weight (pounds), and skin fold measurements will be measured also during the midpoint visit (45 days after baseline visit) and at the final visit (90 days after baseline visit) under the supervision of Dr. Jeffrey Schaedle. Daily food record will be obtained at the midpoint visit and final visit to ensure that the subjects are following the prescribed diet. The purpose of collecting skin fold measurements, height, weight, BMI, and waist circumference is to provide a baseline for each individual subject for comparison with their individual results at the end of the study. All subjects will be counseled accordingly at the initiation of the study how to follow the prescribed diet. Particularly, study subjects will be asked to refrain from taking or starting a prescribed medication during the study.

C.2. Screening, Baseline, Midpoint, and Final Measurements The screening visit will also involve a short medical history questionnaire to rule out exclusion criteria. This screening questionnaire will identify subjects who meet the inclusion/exclusion criteria. Baseline characteristics and measurements will consist of a single visit to the study site. During the first visit, potential subjects who meet the screening criteria will then be provided with a verbal and written description of the project and with answers to any questions regarding their participation in this study. At this time, the potential subject will be assured that his/her participation is completely voluntary. The subject will then be asked to sign an informed consent form. A copy of the signed consent form will be made available to the subject. Skin fold measurements, height (inches), weight (pounds), BMI, waist circumference, and Bod-pod analysis will be obtained. Also an exact weight training routine and diet plan will be prescribed by a certified strength training coach and registered dietitian. Subjects will then be randomly assigned to any of the three gender based treatment groups for a period of 12 weeks.

All subjects will return for a midpoint visit (45 days) where daily food record will be obtained. Bod-pod analysis, weight, and skin fold measurements will also be assessed. Monthly mailers and random-date phone calls will also be used to monitor compliance and retention of the study participants. At the end of the 12 weeks, subjects will return to the study site for a final visit (90 days after baseline). During this final visit, subjects will be analyzed by weight, skin fold measurements, and Bod-pod. Daily food record will also be completed.

C.3. Sample Size, Power Calculation, and Statistical Analyses An initial sample size of 60 subjects, with attrition rates of 10% for the 12 week treatment duration will produce a final sample size of 9 subjects per treatment group. Distribution across gender will be equal. Descriptive statistics, comprising means, standard deviations, minima and maxima, will be calculated for all variables. Distributions of the response variables will be examined to determine if statistical tests of hypotheses based on the assumption of normality are appropriate, or whether transformed date or non-parametric tests should be used. The baseline tests will be used to compare to the after treatment values among the 3 gender based groups. Lean body mass will assessed comparing the changes in parameters for body weight, skin fold measurements, and Bod-pod values from baseline values.