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 ].
The major mechanism appears to be increased VLDL formation in the liver. Also from studies using alcohol with diet, in which response was intensified 42 or seen only 28 in subjects with HTG due to VLDL elevations as opposed to normolipidemia , it has been suggested that the rise in fasting triglyceride concentration after alcohol ingestion is related to baseline triglyceride concentration.
A previous fasting study in healthy normolipidemic alcoholic men given mL of alcohol orally during a 6-hour period also suggested no relation between the degree of triglyceride response and the basal fasting value. Our patients with HTG were typical of patients with moderate primary VLDL elevation; their HTG was not secondary to the commonly described associations of diabetes mellitus, obesity, heavy alcohol use, or smoking. In these subjects, moderate acute alcohol intake equivalent to about 2 alcoholic drinks, the recommended daily limit for healthy adults 5 in a fasting state did not worsen the HTG.
This finding, however, would not necessarily change standing clinical recommendations 4 , 5 that patients with HTG limit their alcohol intake. Alcohol is frequently consumed with fatty foods and, at least in normolipidemic subjects, the combination of fat and alcohol has a synergistic effect in increasing plasma triglyceride concentrations 25 - 27 as a result of alcohol's inhibition of the lipolysis of intestinally derived lipoproteins. In addition, the low triglyceride-clearing capacity in enhanced postprandial lipemia increases risk for atherosclerosis.
In previous studies of the effects of alcohol intake on fasting plasma triglyceride concentration in patients with HTG, all dietary trials to the best of our knowledge, dietary fat may have been a confounder in the interpretation of data.
Since alcohol suppresses the clearance of intestinally derived lipoproteins, 26 , 27 an overnight fast may not have been long enough in individuals with HTG to achieve such clearance, particularly if fat and alcohol had been consumed together the evening before testing.
In our study, as with the alcohol-induced changes in plasma ethanol concentration, effects on concentrations of NEFAs and acetate the final oxidation product of alcohol were similar in the HTG and non-HTG groups, indicating that there was no significant impairment by alcohol of the pathways leading to these analytes. The correlation between the duration and magnitude of the plasma acetate concentration and the reduced plasma NEFA concentration supports the hypothesis that the alcohol-induced reduction of plasma NEFA concentration is mediated by acetate.
A decrease in plasma NEFA concentration after acute ingestion of alcohol in healthy individuals 14 , 15 , 58 - 61 and subjects with type 2 diabetes mellitus 61 , 62 has been well described. It could occur through several mechanisms, none of which can be cited unequivocally, although some are more likely than others. One possibility is that there is enhanced extraction of NEFAs by hepatic tissues. However, this mechanism seems unlikely.
Hepatic extraction of NEFAs is a direct function of the plasma concentration, 63 and direct measurements have shown a decrease in hepatic extraction following alcohol ingestion. This mechanism is made less likely by the observation that alcohol ingestion does not change the rate of removal of a constant infusion of radiolabeled palmitic acid. No direct experiment has eliminated either of these mechanisms.
Because alcohol inhibits the lipoprotein-mediated hydrolysis of intestinally derived lipoproteins without affecting the release of NEFAs by peripheral tissues, however, it seems likely that it also inhibits hydrolysis of the endogenous plasma triglyceride pool that is composed of VLDL. The subsequent increase in plasma NEFA concentration after the effects of alcohol have subsided, as seen in our study, suggests increased lipolysis, although again it is not known whether the increase is in plasma or in adipose tissue.
However, the simultaneous decline in plasma triglyceride concentration in our non-HTG group suggests that the increased plasma NEFA pool is derived through plasma triglyceride hydrolysis.
The alcohol-induced changes in plasma NEFA concentration may be the key to understanding how alcohol ingestion increases plasma HDL cholesterol concentration.
About half of the well-demonstrated cardioprotective effect of moderate alcohol consumption 10 , 33 , 34 , 64 has been attributed to beneficial effects on HDL cholesterol concentration. Importantly, plasma NEFAs are important regulators of the redistribution of cholesteryl esters that is mediated by cholesteryl ester transfer protein, 69 - 71 and increased NEFA concentrations that are well within the range of those observed physiologically enhance the exchange of plasma VLDL triglycerides for HDL cholesteryl esters.
Conversely, a decrease in plasma NEFA concentration might be associated with increased HDL cholesteryl esters, and since nearly all cholesterol in HDL is in the esterified form, there is an obligatory increase in plasma HDL cholesterol.
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. Gastroenterol Clin North Am. LaRosa JC Triglycerides and coronary risk in women and the elderly review.
Erkelens WBrunzell JD Effect of controlled alcohol feeding on triglycerides in patients with outpatient "alcohol hypertriglyceridemia. Nouv Presse Med. Aust N Z J Med. Md Med J. Ann Intern Med. Wien Med Wochenschr. The focus will be on population, intervention and metabolic studies with respect to alcohol and plasma triglycerides.
Recent findings: Alcohol consumption and fat ingestion are closely associated and stimulated by each other via hypothalamic signals and by an elevated cephalic response. A J-shaped relationship between alcohol intake and plasma triglycerides has been described.
What we eat can have a big effect on our cholesterol and triglyceride levels, so changing your diet is one of the most important things you can do. By continuing to browse the site you are agreeing to our use of cookies. Continue Find out more. How does alcohol raise your cholesterol? So, drinking alcohol raises the triglycerides and cholesterol in your blood.
If your triglyceride levels become too high, they can build up in the liver, causing fatty liver disease. Alcohol can lead to the combination of a high triglyceride level along with low HDL cholesterol.
This can lead to heart disease. Alcohol can affect your health in other ways too: it can lead to weight gain , raising your risk of heart disease it can raise your blood pressure , which also raises your risk of heart disease it can lead to some types of cancer, liver disease, pancreatitis, depression and dependency.
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