Alcohol and Fat Metabolism
Alcohol and Fat Metabolism
The main problem with alcohol is not the number of calories it contains but rather the effect is has on fat metabolism. One study, for example, has shown that even small to moderate amounts of alcohol has a large impact on fat metabolism.[i]
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. And 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. This is one of the reasons for the induction phase of my phase shift diets, including the Metabolic, Anabolic, and Radical Diets. By severely limiting your carb intake your body is forced to rev up it’s fat burning machinery, so that you become fat adapted, and increase the use of protein for some of the functions, such as anaplerosis, that carbs are usually heavily involved in.
In other words, your body tends to use whatever you feed it, and after a time becomes adapted to the macronutrient intake. 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. As well, alcohol decreases not only the breakdown and use of body fat as fuel, it also stimulates new fat formation, known as de novo lipogenesis.
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, as far as caloric content, can be considered part way between carbs and fats, as it has more calories than carbs. That’s why even the low carb beers which contain under 100 calories are off limits in the low carb phase of my diets since even though they only have about 2.5 grams of carbs and .5 grams of protein., the alcohol content is the problem. 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
In summary, while the odd drink or two is acceptable on the Metabolic Diet, it’s important to realize that it can be counter productive in the low carb phase and especially so in the induction stage. As such, it’s best to partake on the higher carb days where the alcohol is more in tune with the metabolism. However, even in this phase it’s important to keep in mind that acute alcohol intoxication impairs protein synthesis and the anabolic hormones.
Alcohol, Carbs and Calories
Alcoholic beverages generally contain alcohol, some or no carbs and calories but not much else. The calories come from the alcohol and sugars, and some protein, usually under 1 gram.
I’ve included the alcohol and calorie content of some alcoholic beverages in the table below. The difference between the alcohol calories and the overall calories are the calories that come from sugars.
Usually the amount of alcohol in a serving is about the same, though the serving size may vary. For example, 12 oz of regular beer contains about the same amount of alcohol as a 5-fluid-ounce glass of table wine.
DRINK SIZE ALCOHOL CALORIES (1)
(fluid ounces) (grams)
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
BRANDY 1-1/2 14 95
CORDIAL OR LIQUEUR 1-1/2 12 160
Dessert sweet vermouth,
port, sherry, etc. 3-1/2 16 160
Dry, table, red or white burgundy,
dry sherry, etc. 5 13 100
Light 5 9 70
Wine spritzer 7 11 85
Wine cooler 12 14 180
Nonalcoholic 5 0 10
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
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
[i] Siler SQ, Neese RA, Hellerstein MK. De novo lipogenesis, lipid kinetics, and whole-body lipid balances in humans after acute alcohol consumption. American Journal of Clinical Nutrition 1999; 70:928-936.
Curr Mol Pharmacol. 2015 Aug 17. [Epub ahead of print]
The hepatic lipidome: a gateway to understanding the pathogenesis of alcohol-induced fatty liver.
Clugston RD1, Gao MA, Blaner WS.
Chronic alcohol consumption can lead to the development of alcoholic fatty liver disease. The underlying pathogenic mechanisms however, have not been fully elucidated. Here, we review the current state of the art regarding the application of lipidomics to study alcohol's effect on hepatic lipids. It is clear that alcohol has a profound effect on the hepatic lipidome, with documented changes in the major lipid categories (i.e. fatty acyls, glycerolipids, glycerophospholipids, sphingolipids, sterol lipids and prenol lipids). Alcohol's most striking effect is the marked change in the hepatic fatty acyl pool. This effect includes increased levels of 18-carbon fatty acyl chains incorporated into multiple lipid species, as well as a general shift toward increased unsaturation of fatty acyl moieties. In addition to our literature review, we also make several recommendations to consider when designing lipidomic studies into alcohol's effects. These recommendations include integration of lipidomic data with other measures of lipid metabolism, inclusion of multiple experimental time points, and presentation of quantitative data. We believe rigorous analysis of the hepatic lipidome can yield new insight into the pathogenesis of alcohol-induced fatty liver. While the existing literature has been largely descriptive, the field is poised to apply lipidomics to yield a new level of understanding on alcohol's effects on hepatic lipid metabolism.
Acta Pharmacol Sin. 2012 May;33(5):652-9. doi: 10.1038/aps.2012.11. Epub 2012 Mar 26.
Chronic ethanol consumption increases the levels of chemerin in the serum and adipose tissue of humans and rats.
Department of Endocrinology, Provincial Hospital Affiliated to Shandong University, Ji'nan, China.
Chemerin is a new adipokine involved in adipogenesis and insulin resistance. Since ethanol affects the insulin sensitivity that is closely associated with adipokines. The aim of this study was to investigate the effects of ethanol on chemerin in humans and rats.
In the human study, 148 men who consumed alcohol for more than 3 years and 55 men who abstained from alcohol were included. Based on ethanol consumption per day, the drinkers were classified into 3 groups: low-dose (<15 g/d), middle-dose (15-47.9 g/d) and high-dose (≥48 g/d). Anthropometric measurements and serum parameters were collected. In the rat study, 27 male Wistar rats were randomly divided into 4 groups administered water or ethanol (0.5, 2.5, or 5 g·kg(-1)·d(-1)) for 22 weeks. The chemerin levels in the sera, visceral adipose tissue (VAT) and liver were measured using ELISA.
In the high-dose group of humans and middle- and high-dose groups of rats, chronic ethanol consumption significantly increased the serum chemerin level. Both the middle- and high-dose ethanol significantly increased the chemerin level in the VAT of rats. In humans, triglyceride, fasting glucose, insulin and HOMA-IR were independently associated with chemerin. In rats, the serum chemerin level was positively correlated with chemerin in the VAT after adjustments for the liver chemerin (r=+0.768). High-dose ethanol significantly increased the body fat in humans and the VAT in rats.
Chronic ethanol consumption dose-dependently increases the chemerin levels in the serum and VAT. The serum chemerin level is associated with metabolic parameters in humans. The increased serum chemerin level is mainly attributed to an elevation of chemerin in the VAT after the ethanol treatment.
Alcohol Clin Exp Res. 2011 Feb;35(2):229-34. doi: 10.1111/j.1530-0277.2010.01338.x. Epub 2010 Nov 8.
Ethanol-induced alterations in fatty acid-related lipids in serum and tissues in mice.
Department of Obstetrics and Gynecology, Indiana University School of Medicine, Indianapolis, USA.
Chronic alcohol consumption is a major factor for several human diseases, and alcoholism is associated with a host of societal problems. One of the major alcohol-induced metabolic changes is the increased NADH levels, which reduces glucose synthesis and increases fatty acid (FA) synthesis. Probably more important is the induction of FA synthesizing enzymes under the control of sterol regulatory element binding proteins (SREBP), plus increased malonyl-CoA, which blocks FA entry to the mitochondria for oxidation. The changes in FA-related lipids, particularly lysophospholipids and ceramides (Cers), in different tissues in ethanol-fed mice have not been reported.
We systematically determined the levels of FA-related lipids, including FAs, phosphatidylcholines, phosphatidylethanolamines, lysophosphatidic acid, lysophosphatidylcholine, lysophosphatidylethanolamine, lysophosphatidylinositol, sphingomyelins, and ceramides (Cers), in the serum and different tissues by high-performance liquid chromatography-electrospray ionization-tandem mass spectrometry (HPLC-ESI-MS/MS). The study was performed in C57BL/6J mice fed with Lieber-DeCarli diet, in which ethanol was added to account for 27.5% of total calories. The serum and tissues were collected from these mice at the time of killing, and the results were compared to pair-fed controls.
The important observation was that ethanol-induced tissue-specific changes, which were related to different FA chains. Several 22:6 FA, 18:0 FA, 18:0 to 18:3 FA-containing lipids were significantly increased in the serum, liver, and skeletal muscle, respectively. In the kidney, all 22:6 FA-containing lipids detected were increased. In addition, alterations in other lipids in tissues, except adipose tissue, were also observed.
We found tissue-specific alterations in the levels of FA-related lipids after ethanol administration. The implications of these findings pertinent to human physiology/pathology warrant further investigation. More studies are needed to explore the mechanisms on the different effects of ethanol on certain lipids in different tissues.
Am J Clin Nutr. 1999 Nov;70(5):928-36.
De novo lipogenesis, lipid kinetics, and whole-body lipid balances in humans after acute alcohol consumption.
Department of Nutritional Sciences, University of California at Berkeley, CA 94720-3104, USA.
Acute alcohol intake is associated with changes in plasma lipid concentrations and whole-body lipid balances in humans. The quantitative roles of hepatic de novo lipogenesis (DNL) and plasma acetate production in these changes have not been established, however.
We used stable-isotope mass spectrometric methods with indirect calorimetry to establish the metabolic basis of changes in whole-body lipid balances in healthy men after consumption of 24 g alcohol.
Eight healthy subjects were studied and DNL (by mass-isotopomer distribution analysis), lipolysis (by dilution of [1,2,3,4-(13)C(4)]palmitate and [(2)H(5)]glycerol), conversion of alcohol to plasma acetate (by incorporation from [1-(13)C(1)]ethanol), and plasma acetate flux (by dilution of [1-(13)C(1)]acetate) were measured.
The fractional contribution from DNL to VLDL-triacylglycerol palmitate rose after alcohol consumption from 2 +/- 1% to 30 +/- 8%; nevertheless, the absolute rate of DNL (0.8 g/6 h) represented <5% of the ingested alcohol dose; 77 +/- 13% of the alcohol cleared from plasma was converted directly to acetate entering plasma. Acetate flux increased 2.5-fold after alcohol consumption. Adipose release of nonesterified fatty acids into plasma decreased by 53% and whole-body lipid oxidation decreased by 73%.
We conclude that the consumption of 24 g alcohol activates the hepatic DNL pathway modestly, but acetate produced in the liver and released into plasma inhibits lipolysis, alters tissue fuel selection, and represents the major quantitative fate of ingested ethanol.