Alcohol and thermogenesis
There's been an ongoing debate for years whether Invalid Link Removed "count" or not. This debate has been spurred on by the fact that drinkers Invalid Link Removed than non-drinkers and studies showing accelerated weight loss when fat and carbs are exchanged for an equivalent amount of calories from alcohol. The connection between a lower body weight and moderate alcohol consumption is particularly strong among women. In men it's either neutral or weak, but it's there.
How can this be explained, considering that alcohol is a close second to dietary fat in terms of energy density per gram? Not to mention the fact that alcohol is consumed via liquids, which doesn't do much for satiety?
Alcohol is labeled as 7.1 calories per gram, but the real value is more along the lines of 5.7 calories due to theInvalid Link Removed (TEF) which is 20% of the ingested calories. This makes the TEF of alcohol a close second to protein (20-35% depending on amino acid composition). The heightened thermogenesis resulting from alcohol intake is partly mediated by Invalid Link Removed.
Is higher TEF a reasonable explanation for lower body fat percentage in regular drinkers? We need to consider that alcohol does not Invalid Link Removed like other nutrients. The disinhibition of impulse control that follows intoxication may also encourage overeating. Ever come home from a party in the middle of the night and downed a box of cereals? That's what I mean.
It's unlikely that the effect of alcohol on body weight in the general population can be attributed solely to the high TEF of alcohol. An alternative explanation is that Invalid Link Removed in the long term.
Another explanation is that regular alcohol consumption affects nutrient partitioning favorably via improvements in insulin sensitivity.
Alcohol, insulin sensitiviy and health
Moderate alcohol consumption Invalid Link Removed, lowers Invalid Link Removed and improves glycemic control. Not only in healthy folks, but also in Invalid Link Removed. There is no clear consensus on the insulin sensitizing mechanism of alcohol, but one viable explanation may be that alcohol promotes leanness by Invalid Link Removed. It's not a stretch to assume that this might have favorable effects on nutrient partitioning in the longer term.
If the effect of alcohol consumption on insulin sensitivity doesn't impress you, then consider the fact that studies have consistently shown that moderate drinkers Invalid Link Removed than non-drinkers. This can be mainly attributed to a lowered risk of cardiovascular disease. However, alcohol also contributes to a healthier and disease-free life by protecting against Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, the Invalid Link Removed, different types of Invalid Link Removed,Invalid Link Removed and many other Western diseases. The list goes on and on.
It can almost be said beyond doubt that moderate alcohol consumption is healthier than complete abstinence. With this in mind, it's strange that the fitness and health community shun alcohol. This irrational attitude seems to be grounded in the beliefs that alcohol is fattening and will hamper muscle gains. So let's take a look at that.
Alcohol, hormones and training
You've probably heard that alcohol intake lowers testosterone. While this is true, the actual impact has been widely exaggerated. Invalid Link Removed that had men and women consume 30-40 g alcohol per day, showed a 6.8% reduction in testosterone for the men and none for the women at the end of the study-period. That's three beers a dayfor three weeks and a measly 6.8% reduction in testosterone for the men. What kind of an effect would you think a few beers on an evening once or twice a week would have? Hardly any.
For alcohol to significantly lower testosterone, you need to do some serious drinking. ~120 g alcohol, the equivalent of 10 beers, will Invalid Link Removedfor up to 16 hours after the drinking binge. If you Invalid Link Removedthat you are admitted to the hospital, you get a similar effect with a reduction of about -20%.
A few studies have looked at alcohol consumption in the post-workout period. One study examined the hormonal response to Invalid Link Removed using 70-80 g alcohol, equivalent to 6-7 beers. Talk about "optimizing" nutrient timing. Anyway, despite this hefty post-workout drinking binge, no effect on testosterone was found and only a very modest effect on cortisol was noted. The latter is as expected, considering the effect of alcohol on catecholamines. Citing directly from this paper, this quote sums up the scientific findings regarding the effects of alcohol on testosterone:
"Although the majority of studies involving humans show no ethanol effect on serum luteinizing hormone (LH), some data have demonstrated an increase while others have supported a decrease"
- Invalid Link Removed.
It seems that the fitness mainstream, which has been most adamant about propagating the "alcohol-zaps-testosterone-myth", have cherry-picked a bunch of studies to base their claims on. Well, no big surprise there. We've been through this many times before with meal frequency and countless other diet myths.
When it comes to recovery after strength training, moderate alcohol consumption (60-90 g alcohol) does not accelerate Invalid Link Removed or affect Invalid Link Removed.
However, the research is a bit mixed on this topic. Invalid Link Removed, which used a very brutal regimen of eccentric training only, followed by alcohol intakes in the 80 g range (1 g/kg) noted impaired recovery in the trained muscles. I should note that eccentric training is hard to recover from and the volume used here was pretty crazy.
Another study looked at Invalid Link Removed followed by post-workout alcohol intakes in the 120 g range (1.5 g/kg) and saw significant suppression of testosterone that carried over to the next day.
The common denominator among these two studies is either extremely tough training or unusually high alcohol intakes in the post-workout period. Unless you're in the habit of going bar-hopping after 50 reps of eccentric leg extensions to failure, this stuff does not apply to you. Yet it's studies like these that gets the attention among the alcohol-alarmist fitness crowd.
What about protein synthesis? Strangely enough, the acute effects of alcohol on muscle protein synthesis in normal human subjects are non-existent in the scientific litterature. It has only been studied in chronic alcoholics, which have reduced rates of muscle protein synthesis. Invalid Link Removed, which causes muscle loss, is one unfortunate side-effect of alcohol abuse. However, Invalid Link Removedshowed that alcoholics without myopathy had lower body fat percentage and the same amount of lean mass as non-drinkers. So much for the argument that alcohol makes all your muscles fall off.
If you put any stock in Invalid Link Removed, it's clear that alcohol affects protein synthesis negatively. Then again, results from rat studies are almost never directly applicable to human physiology. There are profound differences in how humans and rodents cope with macronutrients and toxins.
Alcohol and fat storage
Let's quickly review how nutrients are stored and burned after a mixed meal.
1. Carbs and protein suppress fat oxidation via an elevation in insulin. However, these macronutrients do not contribute to fat synthesis in any meaningful way by themselves.
2. Since fat oxidation is suppressed, dietary fat is stored in fat cells.
3. As the hours go by and insulin drops, fat is released from fat cells. Fat storage is an ongoing process and fatty acids are constantly entering and exiting fat cells throughout the day. Net gain or loss is more or less dictated by calorie input and output.
If we throw alcohol into the mix, it gets Invalid Link Removed in the in the substrate hierarchy: alcohol puts the breaks on fat oxidation, but also suppresses Invalid Link Removed.
This makes sense considering that the metabolic by-product of alcohol, acetate, is toxic. Metabolizing it takes precedence over everything else. This quote sums up the metabolic fate of alcohol nicely:
"Ethanol (alcohol) is converted in the liver to acetate; an unknown portion is then activated to acetyl-CoA, but only a small portion is converted to fatty acids.
Most of the acetate is released into the circulation, where it affects peripheral tissue metabolism; adipocyte release of nonesterified fatty acids is decreased and acetate replaces lipid in the fuel mixture."
- Invalid Link Removed (1999).
Acetate in itself is an extremely poor precursor for fat synthesis. There's simply no metabolic pathway that can make fat out of alcohol with any meaningful efficiency. Studies on fat synthesis after substantial alcohol intakes are non-existent in humans, but Invalid Link Removed(from quotation) estimated de novo lipogenesis after alcohol consumption to ~3%. Out of the 24 g alcohol consumed in this study, a measly 0.8 g fat was synthesized in the liver.
The effect of alcohol on fat storage is very similar to that of carbs: by suppressing fat oxidation, it enables dietary fats to be stored with ease. However, while conversion of carbs to fat may occur once glycogen stores are saturated, DNL via alcohol consumption seems less likely.