With that out of the way, we can turn to the ways in which ethanol can affect our fat loss and muscle building efforts.
They are several.
And, they are not good.
Fat Loss
First, unlike most drugs, ethanol is nutritive -- and densely so. It contains 7.1 calories per gram (1) -- almost twice that of carbohydrates and protein. And, unlike the other nutrients, it does not appear to cause a significant amount of satiety (2). In other words, it typically does not replace calories, it adds to them.
Considering oÂ*ne drink (1 beer, 1 shot, 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 oÂ*n 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 oÂ*n if it were light or not). This is pretty much the entire day's calorie allowance for someone trying to lose bodyfat -- and I don't think I have to mention that we often follow this up with a 3 A.M. trip to a fast-food joint or all-you-can-eat buffet where we might get a couple thousand more.
There is some speculation in the literature that ethanol calories do not count, so we need to look at this notion. This idea primarily comes from the fact that epidemiological studies have shown that drinkers have lower Body Mass Indexes (BMI's) than their caloric intake would predict. In men, identical and even lower BMI's, despite calorie intakes several hundred higher than nondrinkers, and in women, it consistently LOWER BMI's despite higher calorie intakes than nondrinkers (3,4,5).
Most of these studies have not looked at actual body composition (3,4,5), thus weight differences could be explained by lower LBM levels -- and this would not be at all surprising considering some of ethanol's effects oÂ*n anabolic hormones which you will find out about later. In addition, both dietary intake and anthropometric measures have merely been self-reported by subjects and obtained by mail by the researchers (6), with the reported daily calorie intake representing oÂ*nly 60-70% of the population's average daily energy needs (7).
However, a more interesting study is oÂ*ne by Addolorato et al. which looked at not oÂ*nly BMI, but body composition (via DEXA) as well, in 34 alcoholics vs. 43 matched controls -- all male (8). The alcoholic group had lower bodyfat levels, but they had identical LBM. oÂ*ne possible explanation is that the alcoholic group had increased levels of extracellular water, as is known to occur in alcoholic cirrhosis (9) and more recently has been found to occur in alcoholics without liver disease (10). It should also be noted that these are chronic alcoholics who could have some metabolic abnormalities that do not pertain to us.
Another study found weight loss with isocaloric substitution of ethanol for carbohydrates as well as less than expected weight gains when ethanol was added to a maintenance diet (11). Though, this could be accounted for to some extent by differences in glycogen storage (unlike carbohydrate, alcohol is not stored as glycogen), as well as muscle (due to hormonal issues -- more oÂ*n this below).
There are also several studies suggesting that alcohol calories do indeed count. Nearly 100 years ago, Atwater and Benedict conducted a series of 13 whole-body calorimetry experiments to test alcohol's nutritive value. They found that the difference in energy given off as heat when alcohol was consumed vs. when it was not was a mere 1% (12). Numerous studies looking at the short-term (less than 4 hours) thermogenic effect of alcohol all found less than 10% dissipation of alcohol energy (13) -- however, it appears that longer studies give a more accurate representation, so we will look at a couple of those.
1.32g/kg (10 drinks for a 200lb person) of alcohol given at meals resulted in a 7% increase in total energy expenditure over 24 hours -- equivalent to 25% of the total alcohol energy (14). Another study using a smaller amount of alcohol (.55g/kg) observed thermogenic dissipation equivalent to oÂ*nly 15% of the total alcohol energy (15).
Two other studies offer strong evidence that alcohol calories count. The first measured body weight and metabolic rate with isocaloric substitution of 75g of alcohol per day for two weeks, finding results identical to that of control (16). A 5 week study using both high (172g/day) and moderate (97g/day) alcohol substitution, along with control, found the fuel value of alcohol to be 95% and 99% of control, respectively, with the high and moderate intakes (17).
Now that we have seen some empirical studies, lets turn to the more basic physiology involved. Ethanol is well digested and absorbed, and losses through breath, sweat, and urine are negligible, so those can be ruled out (1).
At high concentration, the afore mentioned (part 1) Microsomal Ethanol Oxidizing System can come into play -- this results in oxidation of ethanol but with less efficient production of ATP vs. the ADH pathway (18). This hypothesis, however, cannot fully explain the claimed inefficiencies of alcohol metabolism, because the bulk of the energy produced from alcohol is in the final steps of its metabolism -- which is the same in both the MEOS and ADH pathways (3)
Another possibility is a futile cycle involving oxidation of alcohol to aldehyde followed by reduction back to alcohol (19). A few such cycles would completely eliminate net energy gain from alcohol, however, though there is some evidence for the existence of such cycles (20), there is no data oÂ*n its quantitative significance.
Also, as mentioned, ethanol stimulates catecholamine release which could enhance thermogenesis (21). Changes in physical activity is an uninvestigated possibility. There is also data to suggest an interaction between ethanol and leptin, though the consequences of this are yet to be elucidated.
On the other side of the coin, alcohol's metabolic byproduct, acetate, directly suppress fat oxidation (22), as opposed to carbohydrates, whose suppression is mediated by insulin. De novo lipogenesis from ethanol does occur, though it is less than 5% of the total calories -- the rest is oxidized to CO2 and H20 (23). However, as noted in part 1, this oxidation takes priority over fat and carbohydrate oxidation, so with a calorie surplus, it would be expected to result in a shift toward lipogenesis for these substrates.
So, while it should be clear that alcohol calories do indeed count, the notion that ethanol will magically cause fat gain is also mistaken. Basically, as always, it comes down to total caloric intake vs. caloric expenditure -- and ethanol will add about 85 calories per drink to intake, while increasing expenditure by an amount equal to about 15-25% of that value, depending oÂ*n amount ingested.
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.
Growth Hormone
The deleterious effects of ethanol on humans and animals is consistent and well-established in both adults and adolescents, with decreases in GH levels, GH mRNA (24), as well as GH releasing factor mRNA levels (25). In adolescent rats, administration of 3g/kg of ethanol, which, due to the faster metabolism of rats produced blood alcohol levels equivalent to only about 4-6 drinks for humans, caused a massive drop in GH levels to just 4-7% of control by the 1.5 hour mark (26) -- Levels were still down 66-86% after 24 hours. In adult rats, the same 3g/kg caused total suppression of GH release, with 2g/kg causing significant but not total suppression (27).
In young adult male humans, 1.5mg/kg disrupted the nocturnal rhythm of GH secretion in all subjects, as well as decreasing overall release by 30% (28). 1g/kg almost completely inhibited the nocturnal rise in growth hormone levels, while a mere .5mg/kg resulted in levels 1/3 that of control (29). Inhibition of hepatic IGF-1 synthesis (30, 31), and the IGF-1/IGFBP-1 ratio (31, 32), a marker of IGF-1 bioavailability, have also been shown to be negatively effected by ethanol.
) HOW CAN THIS BE?
