Monday, January 30, 2006

Alcohol

Alcohol stimulates a feeling of well being and euphoria, and can eliminate social inhibitions. Learn how it effects your performance and what alcohol does to your system!

Introduction
Alcohol is a general term denoting a family of organic chemicals with common properties. Members of this family include ethanol, methanol, isopropanol, and others. This introduction discusses the physical, chemical, and physiological aspects of the most commonly ingested of these - ethanol.
Ethanol is perhaps the most widely consumed drug on Earth. With the exception of its effects on heart disease, few people would claim it is good for you. But, because of its legality, omnipresence, and just the fact that it is so much fun, most think very little of having a few beers or even a few six packs. This includes many athletes.

However, it is far from being a harmless vice, even in non-alcoholics. It affects numerous neurotransmitters, metabolic processes, and hormones -- and many of these effects go beyond the time period of intoxication. These have ramifications, not only for general health, but as you will see, body composition as well.
We will first look at the basic science of ethanol, and then we will turn to its effects on body composition in the second installment. We will not be looking at the effects of chronic ethanol consumption, addiction, and withdrawal, as they are not relevant to what I consider as my target audience. Suffice it to say such a lifestyle is utterly incompatible with getting the most out of one's exercise and nutritional efforts.

Biochemistry
Ethanol, in addition to being a drug, is also a nutrient. However, unlike the other nutrients such as carbs, fat and protein, the body lacks the ability to store ethanol. It is also the only toxic macronutrient. These two characteristics lead to some important consequences -- namely, it must be metabolized, and this metabolism take precedence over all other nutrients.

It is metabolized by one of two pathways, depending on blood levels. The primary is to aldehyde, via alcohol dehydrogenase (ADH). However, at high levels, what is known as the microsomal ethanol oxidizing system (MEOS) becomes a significant pathway. Both result in conversion to acetate, then acetyl-CoA -- where it can either a) enter the tricarboxylic acid cycle and be oxidized into CO2 and water, or b) be stored a fat.

Pharmocokinetics
Ethanol is readily bioavailable with oral administration, however, oral clearance rate and % absorption decrease in the post-prandial state (i.e. with food), due to the presence of ADH activity in the stomach. The more food in the stomach, the longer the ethanol stays there to be metabolized before it reaches the bloodstream. The type of food will effect this, with protein and fat having the greater effect. Fat, due to slowing transport into the small intestine, protein, probably through direct binding with the ethanol molecule.
The type of drink can also effect blood alcohol levels obtained - particularly in the fed state. For instance, after a meal, a less concentrated drink (such as a beer) will be absorbed more quickly than a more concentrated one (such as a shot) -- and, in rats, this led to an 80% higher peak blood alcohol level and 95% higher overall absorption. However, on an empty stomach, the opposite was found, though the magnitude of the difference was not as strong.

It is also interesting to note that when large amounts are taken in, absorption can exceed systemic distribution, thus exceptionally high concentrations can occur in arterial blood, and, therefore, the brain. This is why bonging 6 beers right in a row hits you harder than drinking 8 drinks over 2 hours. Despite popular opinion to the contrary, women do not metabolize ethanol more slowly than men - the opposite is in fact true. Failure to take into account differences in total body water (i.e. LBM) between men and women has accounted for much of this confusion. However, when normalized for total body water, women metabolize ethanol 33% faster than men, due to a proportionally larger liver.
Due to limitations of ADH, metabolism of ethanol follows zero-order, straight line kinetics - meaning it is broken down at a constant rate (about a drink per hour, 5oz) rather than having a half-life as most drugs do.
DHT has been shown to decrease breakdown of ethanol by increasing the breakdown of ADH, thus a good testosterone cycle will increase susceptibility to intoxication.


Aggression
There exists a real and significant relationship between ethanol and aggression, which might be of particular importance to athletes who are supplementing with exogenous androgens or an EC stack, or any other things which could already be facilitating aggressive behavior.

The possible mechanisms by which it does this are several. As an anxiolytic, it can reduce fear of retaliation and consequences of behaviors, as a psychomotor stimulant, it can increase sensation-seeking behavior, and as an analgesic, it can reduce the perception of consequences of painful stimuli.
Another interesting possibility, is that ethanol disrupts executive cognitive functioning (ECF). ECF encompasses higher order mental abilities such as abstract reasoning, attention, planning, self-monitoring, and the ability to adapt future behavior based on feedback from the outside world - basically ECF is the ability to use the above to consciously self-regulate goal directed behavior.

ECF is governed by the prefrontal cortex, and patients with lesions in this area have been noted to have decreased regulation of social behavior, including a "disinhibition syndrome" characterized by impulsivity, socially inappropriate behavior, and aggression - sound at all familiar? :) Lower scores on tests of ECF processes, such as the ability to inhibit aggression to obtain a monetary reward, have been reported for both prefrontal cortex lesioned patients and those intoxicated with ethanol. It should also be noted that it is on the ascending limb of the blood ethanol curve - i.e. when blood ethanol levels are increasing - when effects on ECF are particularly apparent.

The neurotransmitter, serotonin, has been implicated in this ethanol induced aggression as well. Decreases in serotonin levels, as well as 5-HT receptors, have been correlated with aggressive behavior. Acute ethanol consumption decreases the availability of the 5-HT precursor l-tryptophan to the brain. Therefore, it might not be a bad idea to take 25-50mg of 5-HTP if you are prone to aggressive behavior when drinking.

Memory
The NMDA receptor complex is implicated in memory loss and blackouts from ethanol. This is due to its suppression of long-term potentiation (LTP) in the hippocampus. LTP is a sustained increase in synaptic efficacy following brief intense stimulation of presynaptic inputs - basically; it is a physiological change by which memories are formed.

NMDA activation is required for the induction, but not sustaining of LTP, and as mentioned, ethanol results in the blockade of NMDA receptor transmission. Indeed, ethanol has been directly shown to inhibit LTP in concentrations as low as 5mM (equivalent to 1-2 drinks).

This effect is very much dose dependent (as well as exhibiting interindividual differences and tending to be related to rapidly rising blood ethanol levels) and exists as a continuum, with lower concentrations producing minor loss and concentrations between 50-100mM (20+ drinks) producing so-called "blackouts".
Contrary to popular notion, the occurrence of more frequent blackouts is not a predictor of subsequent alcoholism. Blackouts and short-term memory deficits have been found to be related, so if you want to test whether your drunken friend will experience a blackout the next day, ask him about a conversation 5 minutes earlier, and if he does not remember it at all, you will know that he will.

GABA, dopamine, and serotonin are also likely to be involved in ethanol induced memory disruption, though the data for both is scarce at present. With serotonin, this is likely due to decreased availability of tryptophan and has been shown to be reversible with an SSRI. Thus, 25-50mg of 5-HTP is again recommended.

Tolerance
Tolerance is the diminution of the effectiveness of a drug after a period of prolonged or heavy use of that drug or a related drug (cross-tolerance). There are two types of tolerance at work with alcohol. The first is metabolic tolerance in which the alcohol is metabolized at a higher rate (up to 72% more quickly) in chronic users. Because of the higher metabolic rate for alcohol lower peak blood alcohol concentrations are achieved by chronic alcohol users than the average drinker when the same amount of alcohol is ingested. The second is functional tolerance in which there is an actual change in the organ or system's sensitivity to the drug. Studies have shown that chronic alcohol users can have twice the tolerance for alcohol as an average person. It is important to note however that even in light of these tolerance factors, it has been shown conclusively that even in heavy alcohol users functional impairment is clearly measurable at the blood alcohol concentration levels that are currently used for traffic law enforcement and safety sensitive job performance.
Long Term Effects
Structural damage to the brain resulting from chronic alcohol abuse can be observed in different ways:
Results of autopsy show that patients with a history of chronic alcohol abuse have smaller, less massive, and more shrunken brains than nonalcoholic adults of the same age and gender.

The findings of brain imaging techniques, such as CT scans consistently show an association between heavy drinking and physical brain damage, even in the absence of chronic liver disease or dementia. Brain shrinking is especially extensive in the cortex of the frontal lobe - the location of higher cognitive faculties. The vulnerability to this frontal lobe shrinkage increases with age. After 40 some of the changes my be irreversible [see below]. Repeated imaging of a group of alcoholics who continued drinking over a 5-year period showed progressive brain shrinkage that significantly exceeded normal age-related shrinkage. Moreover, the rate of shrinkage correlated with the amount of alcohol consumed. The relationship between alcohol consumption and deterioration in brain structure and function is not simple. Measures such as average quantity consumed, or even total quantity consumed over a year, do not predict the ultimate extent of brain damage. The best predictor of alcohol related impairment is: maximum quantity consumed at one time, along with the frequency of drinking that quantity.

In addition to the toxic effects of frequent high levels of alcohol intake, alcohol related diseases and head injuries (due to falls, fights, motor vehicle accidents, etc.) also contribute. Although changes in brain structure may be gradual, performance deficits appear abruptly. The individual often appears more capable than is actually the case, because existing verbal abilities are among the few faculties that are relatively unimpaired by chronic alcohol abuse.

The pathogenic effects of alcohol abuse on Brain are well established, and worthy of your attention. If you or a loved one abuse alcohol fear is the appropriate emotion. Be afraid, be very afraid!

Alcohol and Women: Alert From NIAAA
On the whole, women who drink consume less alcohol and have fewer alcohol-related problems and dependence symptoms than men, yet among the heaviest drinkers, women equal or surpass men in the number of problems that result from their drinking.
Drinking behavior differs with the age, life role, and marital status of women. In general, a woman's drinking resembles that of her husband, siblings, or close friends. Whereas younger women (aged 18-34) report higher rates of drinking-related problems than do older women, the incidence of alcohol dependence is greater among middle-aged women (aged 35-49).

Contrary to popular belief, women who have multiple roles (e.g., married women who work outside the home) may have lower rates of alcohol problems than women who do not have multiple roles. In fact, role deprivation (e.g., loss of role as wife, mother, or worker) may increase a woman's risk for abusing alcohol.
Women who have never married or who are divorced or separated are more likely to drink heavily and experience alcohol-related problems than women who are married or widowed. Unmarried women living with a partner are more likely still to engage in heavy drinking and to develop drinking problems.
Equal proportions of black and white women drink heavily. Black women report fewer alcohol-related personal and social problems than white women, yet a greater proportion of black women experience alcohol-related health problems.

Data from self-report surveys suggest that Hispanic women are infrequent drinkers or abstainers, but this may change as they enter new social and work arenas. Gilbert found that reports of abstention are greater among Hispanic women who have immigrated to the United States; reports of moderate or heavy drinking are greater among younger, American-born Hispanic women.

Women become intoxicated after drinking smaller quantities of alcohol than are needed to produce intoxication in men. Three possible mechanisms may explain this response.
First, women have lower total body water content than men of comparable size. After alcohol is consumed, it diffuses uniformly into all body water, both inside and outside cells. Because of their smaller quantity of body water, women achieve higher concentrations of alcohol in their blood than men after drinking equivalent amounts of alcohol. More simply, blood alcohol concentration in women may be likened to the result of dropping the same quantity of alcohol into a smaller pail of water.

Second, diminished activity of alcohol dehydrogenase (the primary enzyme involved in the metabolism of alcohol) in the stomach also may contribute to the gender-related differences in blood alcohol concentrations and a woman's heightened vulnerability to the physiological consequences of drinking. Julkunen and colleagues demonstrated in rats that a substantial amount of alcohol is metabolized by gastric alcohol dehydrogenase in the stomach before it enters the systemic circulation.

This "first-pass metabolism" of alcohol decreases the availability of alcohol to the system. Frezza and colleagues reported that, because of diminished activity of gastric alcohol dehydrogenase, first-pass metabolism was decreased in women compared with men and was virtually nonexistent in alcoholic women.
Third, fluctuations in gonadal hormone levels during the menstrual cycle may affect the rate of alcohol metabolism, making a woman more susceptible to elevated blood alcohol concentrations at different points in the cycle. Research findings to date, however, have been inconsistent.

Drinking also may be associated with an increased risk for breast cancer. After reviewing epidemiological data on alcohol consumption and the incidence of breast cancer, Longnecker and colleagues reported that risk increases when a woman consumes 1 ounce or more of absolute alcohol daily. Increased risk appears to be related directly to the effects of alcohol.

Moreover, risk for breast cancer and lower levels of alcohol consumption are weakly associated. Data from other studies, however, do not concur with these findings, suggesting that more research is needed to explore the relationship between drinking and breast cancer.
Menstrual disorders (e.g., painful menstruation, heavy flow, premenstrual discomfort, and irregular or absent cycles) have been associated with chronic heavy drinking. These disorders can have adverse effects on fertility. Further, continued drinking may lead to early menopause.

Does ALCOHOL affect your strength and performance?
Alcohol is a carbohydrate, but doesn't convert to glucose like most carbs do, but is converted into a fatty acid and is consequently more likely to store as fat. Therefore, if you drink alcohol and exercise, it puts fat metabolism on "hold.”

The caloric content of alcohol is seven calories per gram. A shot of gin contains around 110 cals, while an average 12-oz beer contains 146 cals, 13 gms of carb, and some vitamins and minerals.
It is a Central Nervous System (CNS) depressant and it has the lowest effective dose: lethal dose ratio. This means that there is very little difference in the amount of alcohol that will get you drunk and the amount that will kill you. The reason more don't die from alcohol is because the stomach begins to reject it by vomiting (yum!).

Acute alcohol intoxication results in tremor, anxiety and irritability, nausea, decreased mental function, and vertigo (all of which makes you so attractive to the opposite sex). Chronic alcohol use leads to internal destruction of the liver, heart, brain, muscle (!) and cancer in any or all of them.
Research has shown that small amounts of alcohol may benefit the body. This means 12 oz of beer or a small glass of wine. However, to get the most out of the drink, going with a darker, less processed product is best. Darker beers and wines offer more nutrients.
When it comes to your workouts or athletic competition, alcohol impairs balance and coordination since it affects that CNS. Strength and power are also affected since it dehydrates the body, making muscle and other tissue unable to work optimally.

It Lowers Testosterone
But the biggest kick about alcohol for guys is it lowers testosterone levels! Testosterone is what helps us build muscle. That’s not all, it raises estrogen levels! My god guys, that means it's turning us into a women, no kidding. Changes in body fat storage all throughout the body are possible! Including fat deposition in the chest region. This is insane, and people do this to their bodies for pleasure? Testosterone levels appear below average even up to a week later. So if you are going out and getting drunk every weekend, your testosterone levels may not have been normal for quite some time.

Fat Loss
First, unlike most drugs, ethanol is nutritive -- and densely so. It contains 7.1 calories per gram -- almost twice that of carbohydrates and protein. And, unlike the other nutrients, it does not appear to cause a significant amount of satiety. In other words, it typically does not replace calories, it adds to them.
Considering one drink (1 beer, 1 shot, and 1 glass of wine) has about 12g of ethanol, this can add up in a hurry. I would not consider it unusual for a 200lb person to put down 20 drinks on a good Friday night -- this is about 1600 calories just from the alcohol. That should put to rest the notion that beer makes you fat but hard liquor doesn't (though, the carbohydrates in beer would provide another 500-1000 calories depending on if it were light or not). This is pretty much the entire day's calorie allowance for someone trying to lose bodyfat. I don't think I even have to mention that we often follow this up with a 3 A.M. trip to McDonalds’s, Big Burrito, or Campus Kitchen where we might get a couple thousand more calories.

Fat Metabolism
Studies show that even small amounts of alcohol have a large impact on fat metabolism.
In this study, eight men were given two drinks of vodka and lemonade separated by 30 minutes. Each drink contained just under 90 calories. Fat metabolism was measured before and after consumption of the drink.
For several hours after drinking the vodka, whole body lipid oxidation (a measure of how much fat your body is burning) dropped by 73%.
The reason why alcohol has this dramatic effect on fat metabolism has to do with the way alcohol is handled in the body. When alcohol is consumed, it readily passes from the stomach and intestines into the blood and goes to the liver. In the liver, an enzyme called alcohol dehydrogenase mediates the conversion of alcohol to acetaldehyde.

Acetaldehyde is rapidly converted to acetate by other enzymes. So rather than getting stored as fat, the main fate of alcohol is conversion into acetate, the amount of acetate formed is dose dependant on the amount of alcohol consumed. For example, blood levels of acetate after drinking the vodka were 2.5 times higher than normal. In addition, it appears this sharp rise in acetate puts the brakes on fat loss.
The type of fuel your body uses is dictated to some extent by availability. Unfortunately when acetate levels rise, your body burns the acetate preferentially, since acetate is basically the same product of beta oxidation of fatty acids and glycolysis (glucose to pyruvate to acetate), but it doesn't' require the metabolic work to produce.

So the body simply burns the acetate first, and with the rapid rise seen with alcohol intake, basically pushes fat oxidation out of the metabolic equation.
Because acetate is readily formed from alcohol it can be worse than taking in carbs as far as affecting fat metabolism. That's because glucose has to be sequentially metabolized through various steps to form acetate while acetate is formed from alcohol in just a few steps.
Also alcohol has more calories than carbs. That's why even the low carb beers contain under 100 calories even though they only have about 2.5 grams of carbs and .5 grams of protein. While the carbs and protein only make up 12 calories, the 12 grams of alcohol make up the remaining 80 or so calories.
9 calories per gram of FAT
4 calories per gram of PROTEIN
4 calories per gram of CARBOHYDRATE
7 calories per gram of ALCOHOL

Muscle Gains
If the caloric content of ethanol has not convinced you that it is not the best thing for body composition, its effects on muscle building hopefully will. Ethanol has been consistently shown to result in sustained, significant decreases in testosterone and GH levels -- as well as to increase cortisol in many studies (Hopefully, and in depth analysis of the importance of these hormones on body composition is not necessary). In addition, it also directly inhibits protein synthesis.

Alcohol & Muscle Growth
Importantly for today's discussion, it appears that alcohol use inhibits muscular protein synthesis. In fact, this inhibitory effect of alcohol is most pronounced in fast muscle fibers, especially after prolonged alcohol use.
The scenario would be detrimental for any athlete trying to gain muscle mass and strength through training for improved overall body composition. After all, isn't the goal of training to increase muscle protein synthesis? The problem is that creatine allows us to work harder, which is generally a good thing.
However, this would also mean that muscle recovery is more critical while supplementing with creatine. Now, as alcohol consumption inhibits protein synthesis, a potentially fruitless situation may arise by mixing the two. That is, creatine and alcohol.

Finally, there is also some indication that creatine also stimulates protein synthesis. This effect may underlie part of creatine's benefit. If so, then alcohol consumption would offset this benefit of creatine as well.
Note: Keep in mind these important points:
Alcohol inhibits protein synthesis in fast muscle fibers. Protein synthesis is essential for muscle growth and development. Protein synthesis is important for muscle recovery.
Creatine increases the work output of fast muscle fibers. Thus, fast muscle recovery is more critical during supplementation. Creatine may increase protein synthesis as part of its benefit.
Alcohol may be particularly damaging during creatine supplementation.

Protein Synthesis
Both ethanol and its metabolic byproduct, aldehyde, have been shown to reduce protein synthesis in skeletal muscle. To make matters worse, it is predominately Type II, fast-twitch fibers that are affected (those responsible for muscle tone and increased metabolism). This is a very bad thing for athletes.
With acute administration of real-world doses (.8 - 2.0g/kg) of ethanol, reductions in protein synthesis of 20-30% have been seen within about one to two hours of administration, this is before the previously reviewed hormonal changes occur, indicating that alcohol is exerting a direct effect. Within 24 hours, decreases of as high as 63% have been shown to occur, which likely reflects the added contribution of negative hormonal changes.

The mechanism behind this is not fully characterized. Reduction in both mRNA and translational efficiency have been observed. The generation of free-radicals, which are known to be increased by ethanol, could be involved. Low levels of selenium and alpha-tocopherol (vitamin E) are found in alcoholics with myopathy (muscle wasting). However, there is also evidence that does not support this theory. Another possibility is direct ischemic damage.

Given alcohol's hormonal effects and its direct effects on protein synthesis, if you are going to indulge in fairly heavy alcohol consumption, it would probably be a very good idea to utilize a topical prohormone formulation (or a short-acting injectable ester of the real thing) the evening of drinking, and the next day in order to minimize the damage to your hard earned muscle.

Alcohol & Anabolic Hormones
Anabolic means to promote growth. Alcohol adversely influences the anabolic properties of two of our principal growth promoting hormones, Insulin and Growth Hormone. Furthermore, most of the anabolic effects initiated by Growth Hormone are mediated by Insulin-like Growth Factor-1 (IGF-1). These hormones are essential for inducing muscle protein synthesis after exercise and are also thought to interact with creatine.
Alcohol causes insulin-resistance as well as hinders the release of Growth Hormone from the brain. Chronic alcohol consumption also reduces our IGF-1 levels. These combined effects will slow muscle development and mitigate our response to creatine.

Finally, Growth Hormone secretion is most important during puberty, when we are growing most rapidly. Anything that interferes with this normal surge in Growth Hormone might have serious developmental consequences. Therefore, adolescent athletes are strongly discouraged from consuming alcohol.

Alcohol and Estrogen
Chronic alcoholics, in addition to being hypogonadal, exhibit sign of overt feminization. There is some evidence to suggest that ethanol might also increase the aromatization of testosterone to estradiol. Consumption of .9 - 2.1g/kg of beer or wine significantly (P <0.05 to P< 0.001) increased estradiol levels in healthy adult humans. A study in rats found levels of estradiol increased by 60% (to go along with 55% lower test levels) - however, this was with the equivalent of about 13 drinks/day for 1-2 months.
In addition, alcohol administration has been shown to increase estrogen receptor density and to decrease levels of an estradiol binding protein -- as well as to lower androgen receptor numbers. However, this has primarily been found in conjunction with alcoholic liver disease, so its relevance to acute consumption in questionable.

Another possibility is the existence of phytoestrogens in alcoholic beverages. Hops, used as a flavoring agent and preservative in beer, contains several powerful phytoestrogens, including 8-prenylnaringenin, genistein, and daidzein. And, congeners, which are found primarily in dark liquors such as bourbon and wines, have been found to contain biochanin A, beta-sitosterol.

Testosterone and Females
Ethanol's effects on the female athlete are also bleak. Because female testosterone production occurs primarily outside the gonadal structures, ethanol's effect on LH is not as relevant -- and its effects on Leydig cells obviously are not at all relevant. In addition, ethanol is known to stimulate adrenal activity -- 25% of female testosterone production is produced as an intermediate in the production of cortisol in the adrenals.
This results in INCREASED testosterone levels in women after ethanol consumption. As little as .4g/kg caused a significant increase in testosterone levels and 1.2g/kg and 2g/kg caused increases of 25% and 54% respectively.

Interestingly, serum epitestosterone is not proportionally increased, nor are urinary levels, thus the testosterone to epitestosterone ratio (T: Ep) used in athletic drug screenings is skewed. The same study mentioned above resulted in a T: Ep ratio of around 4.5 compared to 1.5 before drinking. Individual increases ranged from 1.9 to 8.7 times baseline. Given that the testing cutoff is 6:1, it is easy to see that this could result in a false positive (or perhaps be used as a handy excuse for a true positive).

Cortisol
Ethanol has been found to both directly, and indirectly -- via increases in ACTH, increase cortisol production. 1.75g/kg increased levels by 152% at 4 hours and was still significantly higher than control at 24 hours in adult males. In addition, consumption of ethanol along with exercise resulted in a 61% increase in cortisol over alcohol alone. A study of adolescents admitted to the hospital with acute alcohol intoxication showed ACTH and cortisol levels 10 and 1.6 times that of controls in females, and 5.9 and 1.4 times as high in males -- however, a general stress response much be considered as a possibility in these circumstances.
Other studies, however, have not found such effects. Thus, some researchers have concluded that any increases in cortisol are due to a stress response from nausea rather than a direct effect of ethanol. And, indeed, in one study, a subject that vomited displayed cortisol levels 5 times as high as his baseline value.

Indirect Effects: Immune System
Even moderate, acute ethanol consumption can significantly influence susceptibility to infections caused by viral and bacterial pathogens -- and alcohol is usually consumed in a social setting, where exposure to pathogens will be increased. Obviously, if one is sick, workouts will suffer. Thus, this is important.
Both in vitro and in vivo administration of ethanol blunts inflammatory cytokine response to bacterial stimulation. Monocyte production of IL-1, IL-6, and TNF-alpha are decreased - leading to defective host defense against microbial infection. In addition, immunomodulatory cytokines such as IL-10 and TGF-beta as well as the prostaglandin PGE2, are increased, leading to a downregulation of production of antigen specific T-cells - increasing susceptibility to viral infections.

Sleep
Though, it is a CNS depressant, and can thus facilitate the onset of sleep, ethanol has negative effects on its quality. Of particular importance is REM sleep, which is the deepest stage of sleep, and is most important for mental and physical recovery. Ethanol reliably disrupts REM sleep, at doses as low as 2-3 drinks. It increases the time to induction of REM as well as total time spent in REM, due to decreases in the number of REM sleep episodes as well as a prolongation of the non-REM phase of the REM-nonREM cycles. These effects are dose dependent, so the more you drink, the more it is affected.

Hangover
The cause of ethanol induced hangover is not fully elucidated, however there are several mechanism likely to contribute. The formation of prostaglandins (PG) is increased by ethanol and the use of aspirin like drugs before and during drinking has been shown to significantly reduce the severity of hangover. The use of linoleic and linolenic acid, which can both act as inhibitors of PG formation, also reduced the severity of hangover. Fish oils, which reduce cytokine formation, might be useful as well.
Congeners -- byproducts of ethanol preparation which occur mainly in dark liquors and wine -- are also a likely culprit -- and indeed in patients consuming 1.5g/kg of ethanol, 33% of those who consumed bourbon reported severe hangover vs. only 3% of those who consumed vodka. In other words, if you can't see through it, don't do it.

Ethanol inhibits anti-diuretic hormone, and hydration attenuates but does not fully relieve hangover symptoms. Aldehyde may be a factor as well -- the use of an herbal preparation called Liv.52 was found to decrease hangover symptoms vs. placebo, and indeed lower aldehyde levels were found. However, this study was done by the makers of the product, so its results could be viewed as questionable. Preventative use of vitamin b6 (400mg before, during, and after) was shown to reduce hangover symptoms by 50%. Other factors contributing to hangovers include lack of sleep, lack of food consumption, increased physical activity while intoxicated, and overall poor physical health.

Conclusion
Health issues aside, it should be clear that the regular consumption of significant quantities of alcohol is absolutely detrimental to one's efforts to improve body composition. . Alcohol decreases muscle protein synthesis, causes insulin-resistance and interferes with the release of Growth Hormone (and, hence, IGF-1) following exercise. However, we all know its consumption is woven into the very fabric of our society, so most of us are not going to do away with it completely. We will have to be content with merely minimizing the negative consequences of its consumption. Other than the numerous specific recommendations that appear in the body of this article, the main general thing you can do is limit total consumption.

Closing Comments
If you're spending your hard earned money on supplements, don't just piss them all out by drinking all night. When you're spending hours lifting, conditioning and practicing for athletics-don't throw it all out the window because you want to party with some friends. Identify your goal and do all things that will help you achieve that goal. If your goal is to get trashed, go for it!
I recommend Killian’s Irish Red (www.killian’s.com).
Don't misconstrue my message. This is not a crusade against alcohol consumption. In fact, an occasional glass of red wine has been shown to possess healthful qualities. In my opinion nothing beats a good Bordeaux.

However, if you're serious about making gains in strength, mass, and/or body composition, then maybe you should abstain from alcohol, especially immediately before bed and after exercise. This precaution is especially important if you are below 20 years of age, when Growth Hormone release is most necessary for normal growth and development. In any case, moderation is always the best policy. Oh yeah, DON'T DRINK AND DRIVE!






























The American Medical Association has defined the blood alcohol concentration level of impairment for all people to be 0.04 grams/100 milliliters of blood (equivalent to .04 grams/210 liters of breath). The following is a generally accepted guide to the affects of alcohol.
Stages of alcohol intoxication
BAC
(g/100 ml of blood
or g/210 l of breath) Stage Clinical symptoms
0.01 - 0.05 Subclinical Behavior nearly normal by ordinary observation
0.03 - 0.12 Euphoria Mild euphoria, sociability, talkitiveness
Increased self-confidence; decreased inhibitions
Diminution of attention, judgment and control
Beginning of sensory-motor impairment
Loss of efficiency in finer performance tests
0.09 - 0.25 Excitement Emotional instability; loss of critical judgment
Impairment of perception, memory and comprehension
Decreased sensitory response; increased reaction time
Reduced visual acuity; peripheral vision and glare recovery
Sensory-motor incoordination; impaired balance
Drowsiness
0.18 - 0.30 Confusion Disorientation, mental confusion; dizziness
Exaggerated emotional states
Disturbances of vision and of perception of color, form, motion and dimensions
Increased pain threshold
Increased muscular incoordination; staggering gait; slurred speech
Apathy, lethargy
0.25 - 0.40 Stupor General inertia; approaching loss of motor functions
Markedly decreased response to stimuli
Marked muscular incoordination; inability to stand or walk
Vomiting; incontinence
Impaired consciousness; sleep or stupor
0.35 - 0.50 Coma Complete unconsciousness
Depressed or abolished reflexes
Subnormal body temperature
Incontinence
Impairment of circulation and respiration
Possible death
0.45 + Death Death from respiratory arrest
















Serving size and contents of commonly used alcoholic beverages.

Drink Size (fluid ounces) Alcohol (grams) Calories
Beer
Beer or ale, regular 12 13 150
Beer, light 12 12 105
Beer, low carb 12 12 95
Beer cooler 12 12 100
Near beer 12 1 30
Wine
Dessert, sweet vermouth, port, sherry, etc. 3-1/2 16 160
Dry, table, red or white burgundy, chablis, champagne, dry sherry, etc. 5 13 100
Light 5 9 70
Wine spritzer 7 11 85
Wine cooler 12 14 180
Non-alcoholic 5 0 10
Liquor
Gin, 90-proof 1-1/2 16 110
Rum, vodka, 80-proof 1-1/2 14 95
Whiskey bourbon, rye, scotch, 86-proof 1-1/2 15 105
Brandy 1-1/2 14 95
Cordial or Liqueur 1-1/2 12 160
Mixed Drinks (2)
Margarita 2-1/2 18 170
Gin and tonic 7-1/2 16 170
Whiskey sour 3 15 125
Daiquiri 2 14 110
Drink Size (fluid ounces) Alcohol (grams) Calories

0 Comments:

Post a Comment

<< Home