Why does alcohol increase triglycerides

Our results demonstrate that in subjects with moderate HTG, alcohol alone in modest amounts is not an acute lipemic agent. Given that HTG is a risk factor that is linked to other risk factors, such as a low plasma HDL cholesterol concentration, and that alcohol consumption lowers mortality due to cardiovascular disease, one might question the current recommendation that all patients with HTG should totally refrain from alcohol consumption.

Additional studies of the interaction of different kinds of dietary fat and alcohol, which enhances postprandial lipemia, are needed to develop guidelines that can be tailored to the patient with mild to moderate HTG at risk for cardiovascular disease.

Reprints: Henry J. Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy Continue. Figure 1. View Large Download. Table 1. Toskes PP Hyperlipidemic pancreatitis.

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Effect of ethanol on plasma free fatty acids in man. HDL cholesterol removes extra cholesterol and plaque buildup in your arteries. High cholesterol often has no symptoms, but can lead to serious health issues. Having too many triglycerides in your blood can be harmful and lead to heart disease. Here are some natural ways to lower your triglycerides. Health Conditions Discover Plan Connect.

Medically reviewed by Nancy Choi, M. Healthy cholesterol levels. Beer and cholesterol. Liquor and cholesterol. Wine and cholesterol. How much and how often you drink matters. The takeaway. Read this next. Medically reviewed by Natalie Butler, R. Medically reviewed by Judith Marcin, M.

Does Alcohol Thin Your Blood? Medically reviewed by Alana Biggers, M. The Recommended Cholesterol Levels by Age. Hypertriglyceridemia HT may result from genetically determined disturbances in lipid metabolism but may also be secondary to conditions such as obesity, diabetes mellitus, hypothyroidism, the nephrotic syndrome, and the use of medication. Although its health effects are continuously a subject of debate, alcohol ethanol can be added to this list [ 2 , 3 ].

Since both food and alcohol are known to affect lipid metabolism, a number of studies have been directed to their combined effect. This paper will focus on triglycerides after the consumption of such mixed meals as well as on the observation that alcohol may induce a very severe form of HT, which may be of clinical relevance with an increased risk of pancreatitis [ 4 ].

The metabolic effects of alcohol on the liver and lipid metabolism are known for many years and have been extensively studied by Lieber and many of his coworkers [ 5 ]. By contrast, previous feeding of alcohol for several weeks results in postprandial hyperlipemia after a single dose of the mixed meal and even after such a dose without the alcohol component.

In another rat experiment, Daher et al. In case the animals were put on a moderate alcohol diet for a period of ten weeks, their postprandial HT and hyperchylomicronemia were less pronounced. This is probably related to an adaptive increase of lipoprotein lipase LPL activity in case of chronic moderate alcohol consumption [ 9 ]. In contrast, an acute ingestion of ethanol lowers LPL activity.

Another mechanism which may contribute to postprandial HT is a decrease of lipogenesis and glucose oxidation in adipose tissue, as shown in rats after chronic ethanol feeding [ 10 ]. Kang et al. It has also been shown that the lipemic response to alcohol is related to the stage of liver disease, since in cirrhosis, in contrast to steatosis, fasting lipid response is neglectable, but postmeal chylomicron response is increased [ 12 ].

Apart from serum HT, alcohol may also induce accumulation of triacylglycerols in the liver, leading to steatosis hepatis. This influence of alcohol can be partly explained by impairment of AMP-activated protein kinase AMPK , which enzyme plays a central role in hepatic fatty acid metabolism [ 13 ]. Several dietary regimes have proven to be able to influence this process of alcohol-induced fatty liver including medium-chain triglycerides and fish oil [ 14 , 15 ].

Interestingly, the consumption of alcohol stimulates the intake of fat, while dietary fats stimulate the consumption of alcohol, a vicious cycle probably mediated by hypothalamic peptides [ 16 ].

This effect is clearly related to alcohol and not to the type of drink, since in a similar experiment, no differences were found between wine, beer, and spirits [ 18 ]. In another experiment of these investigators, they showed that TG levels reach their peak three hours after dinner with the same response in men and women [ 19 ]. Even so, the response is not different in men with a low-risk profile for cardiovascular disease compared to men with a high-risk profile [ 20 ].

Since both alcohol and exercise have an effect on postprandial lipemia and TG clearance, their combined effect has been studied. El-Sayed and Al-Bayatti [ 21 ] studied plasma TG concentrations after exercise followed by a diet with and without alcohol.

However, when alcohol was consumed with the lunch, TG concentration increased substantially 5 hours during recovery. The mechanism responsible for this TG rise was not studied, but inhibition of LPL activity by alcohol may play a role. On the other hand, Hartung et al. Even if the diet contains a lot of fat resulting in high postprandial TG levels, the addition of alcohol still has a significant additive effect. Franceschini et al. A similar study was designed by Pownall [ 24 ] in which three different fat loads were given to normal subjects with and without alcohol.

The fat loads consisted of saturated fat, polyunsaturated fat, or polyunsaturated fat with omega-3 fatty acids. Preprandial alcohol increased postprandial lipemia, an effect that was most profound with the saturated fat load. Alcohol had no effect on the plasma concentrations of free fatty acids derived from peripheral tissue but appeared to decrease the plasma concentration of free fatty acids from dietary origin.

These data are highly suggestive for an impairment of chylomicron hydrolysis due to inhibition of LPL. Fielding et al. Because of the increased risk of cardiovascular diseases in diabetes patients and the possible cardioprotective effect of alcohol, Dalgaard et al. Early in the postprandial phase, alcohol suppresses the incretin responses and increases the late postprandial TG levels.

This alcohol-induced suppression of the incretin response resulting in lower insulin levels may contribute to the impaired TG clearance in type 2 diabetes patients but may also be operative in nondiabetics. In contrast to moderate alcohol consumption, excessive intake may cause HT even in the fasting state [ 5 , 17 ].

This effect seems to be more pronounced in African-Americans than in white Americans [ 27 ]. When regular and binge drinkers cut down their alcohol intake, a more or less similar drop 0. Pownall et al. They conclude that alcohol intake alone in not an important determinant of plasma TG concentration in individuals with HT. On the other hand in a recent study analyzing the underlying disorders in patients with severe HT, alcohol proved to be of dominant importance [ 4 ].

In patients with TG levels exceeding Especially, patients with the combination of alcohol abuse, diabetes mellitus, and obesity, for which the authors introduced the term SHIBA syndrome severe hypertriglyceridemia influenced by alcohol , are prone to develop extremely high TG levels. In those cases, there is an increased risk of developing pancreatitis. Both the effects of excessive alcohol intake and the lack of insulin or insulin resistance push TG metabolism in the same direction.

The consumption of alcohol-containing drinks has become an accepted part of lifestyle in most societies. The health effect of alcohol, however, has always been subjected to debate. Moderate alcohol consumption is associated with a lower risk of cardiovascular disorders, and the pattern and amount of alcohol are of more importance than the type of alcoholic beverage [ 2 , 30 ]. One of the underlying mechanisms for this beneficial effect is its influence on lipids especially the increase in plasma HDL-cholesterol [ 31 ].

In case of moderate drinking, 1—3 glasses a day for men and glasses for women, hardly any effect is seen on triglycerides. However, excessive alcohol intake may cause hypertriglyceridemia not only postprandially, but also in the fasting state.

This is mainly due to an increase in the synthesis of large VLDL particles in the liver. When alcohol consumption is accompanied by a meal containing fat, especially saturated fat, it has a significant additive effect on the postprandial triglyceride peak. This peak is for the most part the result of a retardation of chylomicron breakdown and to some extent of that of VLDL remnants.

Most likely, this should be attributed to an inhibition of lipoprotein lipase activity by alcohol. In case of moderate and regular alcohol intake, adaptation restores LPL activity.