Does Alcohol Cause High Cholesterol?

Does Alcohol Cause High Cholesterol
How does alcohol raise your cholesterol? –

When you drink alcohol, it’s broken down and rebuilt into triglycerides and cholesterol in the liver. 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. The liver can’t work as well as it should and can’t remove cholesterol from your blood, so your cholesterol levels rise. Alcohol can lead to the combination of a high triglyceride level along with low HDL cholesterol. This can lead to heart disease.

Is it OK to drink alcohol if you have high cholesterol?

– For most people, light to moderate drinking is unlikely to negatively affect cholesterol levels. In fact, it may improve HDL cholesterol levels and even reduce the risk of heart disease. However, heavy drinking impairs heart health and may raise total cholesterol and triglyceride levels.

Total cholesterol: 200 mg/dL (5.2 mmol/L) or less LDL cholesterol: 130 mg/dL (3.4 mmol/L) or less HDL cholesterol: 40 mg/dL (1 mmol/L) or higher in males and 50 mg/dL (1.3 mmol/L) or higher in females

Although maintaining healthy cholesterol levels is essential to reducing heart disease risk, many factors contribute to this condition, including blood pressure, genetics, and sex ( 19 ). Maintaining a healthy diet and lifestyle — which includes limiting alcohol, keeping a moderate body weight, staying active, and following a nutritious diet — promotes healthy cholesterol levels and reduces your risk of heart disease and other conditions.

How much does alcohol raise cholesterol?

Heavy alcohol use In one study, binge drinking (8 or more drinks for women and 10 or more drinks for men per day) led to a 2 to 8 times higher risk of high triglyceride and total cholesterol levels.

What is the best alcohol to drink to lower cholesterol?

08 /10 Alcohol – Moderate alcohol consumption can increase HDL levels in the blood. Red wine can be the alcohol of choice as it possesses antioxidant properties. Studies reveal that moderate consumption of red wines can not only lower cholesterol levels but help prevent certain heart diseases.

Which alcoholic drink is worse for cholesterol?

This is How Drinking Alcohol Affects Your Cholesterol Does Alcohol Cause High Cholesterol The habits you develop in your daily life contribute to your health in both positive and negative ways. If you’re looking to make some positive lifestyle changes to contribute to your health, start with choosing nutritious foods, getting plenty of exercise, and avoiding smoking.

Your alcohol intake matters, too. In moderate amounts, red wine is commonly linked to healthy cholesterol levels. But drinking more hard liquor, beer, mixed drinks, and excess red wine has a negative impact on your cholesterol levels. At Westmed Family Healthcare, we want you to understand the connection between alcohol and cholesterol.

Here’s some information about cholesterol and how drinking affects your heart health.

Does stress cause high cholesterol?

How Does Stress Effect Cholesterol? | High Cholesterol Everyday Health: How does stress contribute to cholesterol? Dr. Stuart Seale: Studies have shown that stress increases cholesterol not only in the short-term but can also affect even years down the road.

  1. The cause for this isn’t exactly known.
  2. Other studies have shown that stress itself isn’t really the only culprit but that how an individual reacts to and manages stress is also important.
  3. Those who manage stress in unhealthy ways (via hostility, social isolation, or self-blame, for example) tend to have lower levels of (good) cholesterol.

Dr. Lisa Matzer: Stress is known to increase cholesterol levels and in particular the bad, The amount of stress in your life isn’t as important as how you deal with it. The more anger and hostility that stress produces in you, the higher (and worse) your LDL and tend to be.

  • Stress encourages the body to produce more energy in the form of metabolic fuels, which cause the liver to produce and secrete more of the bad cholesterol, LDL.
  • Also, stress may interfere with the body’s ability to clear lipids. Dr.
  • Jacob DeLaRosa: One theory is that stress hormones’ function is to provide fuel for a potential fight-or-flight situation.

But if this energy is not used, it gradually accumulates as fat tissue. In addition, sugars that are produced with stress are repeatedly left unused and are eventually converted into triglycerides or other fatty acids. Jeanette Bronée, CHHC, AADP: Stress not only increases inflammation in the body but also causes poor eating habits and poor food choices – all of which affect cholesterol levels.

  1. But cholesterol can also be regarded as a stress response from the body.
  2. Pamela Warren, MS, CHN: Staying calm and cool helps manage cholesterol.
  3. Here’s how: When you’re under mental stress, your body is preparing to protect you and assumes a primitive response, called the fight-or-flight response.
  4. During such a situation, the brain produces the hormones cortisol and adrenaline.

The release of these hormones sends signals that increase blood flow to the brain and eventually produces more energy for the body. When cortisol and adrenaline are released, it raises your cholesterol level. Specifically, the release of cortisol raises blood-sugar levels for the body’s use as energy, as it locks away fat so it’s not used during this state as energy.

Therefore, as cortisol is released, it raises the body’s blood-glucose level, which in turn creates more triglyceride production. Higher triglycerides create higher cholesterol levels. Keeping your stress response under control is a great way to manage cholesterol levels for the long term. Inna Topiler, MS, CNS: Stress will increase your,

(Cortisol is a hormone produced by your adrenal glands when you are stressed.) Under stress, cortisol delivers glucose to the body to help the fight-or-flight mechanism function properly. If cortisol is consistently doing this, blood-sugar levels remain constantly high, which can lead to not only hypo/hyperglycemia and diabetes but also elevated cholesterol levels.

  1. Dr. Raja R.
  2. Gopaldas: In modern-day life, stress is inevitable.
  3. Job stress, getting to work, and taking care of the family all contribute to stress.
  4. How we manage stress is important.
  5. There is no doubt that a constant state of emotional stress is directly linked with high cholesterol levels.
  6. Being happy is a fundamental requirement for every human being – so avoid circumstances that make you unhappy! A daily meditation schedule of 15 to 20 minutes will help, and 45 minutes of vigorous exercises (get your heart rate over 120) three times a week will help lower anxiety levels and stress.

Ensuring that you get adequate sleep – about six to eight hours daily (no more or no less – both are detrimental) is important for everyone. : How Does Stress Effect Cholesterol? | High Cholesterol

Is wine good for high cholesterol?

Red Wine and Grape Juice – Alcohol may raise levels of good HDL cholesterol by as much as 5 to 15 percent, research shows — and red wine is particularly beneficial because its polyphenol antioxidants may also lower LDL levels. If you’re not into vino, grape juice can provide some of the same heart-healthy benefits.

How long does it take to lower cholesterol?

– Cholesterol-lowering drugs usually produce a change in LDL within 6 to 8 weeks, It is possible for lifestyle changes to change cholesterol levels within weeks. However, it may take longer, usually about 3 months — sometimes more. Some doctors recommend adding a cholesterol-lowering drug if a person has not lowered their LDL cholesterol after about 12 weeks of lifestyle changes.

Is whisky good for cholesterol?

Whiskey is a dark-grain alcohol made all over the world. It was first developed in medieval Scotland and Ireland. In Gaelic, its name loosely translates to “water of life.” In 16th-century Scotland, apothecaries sold whiskey as a tonic to slow aging, cure congestion, and relieve joint pain,

During American Prohibition, doctors prescribed whiskey to treat pneumonia, high blood pressure, and tuberculosis, Today, whiskey is available by different names based on its production — like single malt, scotch, bourbon, and rye. While these days it’s more likely to be listed on a bar tab than on a prescription pad, modern research has found evidence that may support some traditional claims that whiskey boosts health.

9 Signs & Symptoms of High Cholesterol YOU MUST NOT IGNORE

It’s well documented, however, that high amounts of alcohol can lead to some serious health issues, Whiskey’s potential benefits are associated with its low to moderate consumption. To reduce the risk of alcohol-related harms, the CDC’s 2020-2025 Dietary Guidelines for Americans recommends that adults of legal drinking age can choose not to drink, or to drink in moderation by limiting intake to 2 drinks or less in a day for men or 1 drink or less in a day for women, on days when alcohol is consumed.

Calories: 123Protein: 0 gramsFat: 0 gramsCarbohydrates: 0 gramsFiber: 0 gramsSugar: 0 grams

Whiskey is a source of:

Phosphorus Thiamine (Vitamin B1) Zinc Iron Niacin (Vitamin B3)

It also contains ellagic acid, an antioxidant found in berries, While more research is needed, studies show ellagic may kill cancer cells and reduce tumor growth. Calories from spirits are essentially the same but whiskey has no carbohydrates or sugar,

Its ellagic acid content may also reduce bodily inflammation and lower the risk of obesity, Research suggests that there are other health benefits to drinking whiskey. However, these benefits are all associated with moderate consumption — heavy drinking can lead to serious health issues. A glass of whiskey a day may offer health benefits like: Heart Health Whiskey has high levels of polyphenols, plant-based antioxidants linked with lowering your risk of heart disease,

The polyphenols in whiskey have been shown to decrease “bad” cholesterol (LDL) and increase “good” cholesterol (HDL) levels, and reduce triglycerides, or fat in your blood. Bad cholesterol and triglycerides can clog your arteries, while good cholesterol helps to keep them clear.

  • Maintaining healthy levels can help prevent heart disease and stroke,
  • Relief of Cold Symptoms Whiskey can temporarily widen your blood vessels,
  • In small amounts, this can help clear mucus congestion in your sinuses and chest, which lets your body better deal with sickness and infection,
  • This effect may also relieve other symptoms of a cold or flu, like coughing or wheezing,

Immune System Support Scientists are unsure why, but several studies link moderate alcohol consumption to improved immunity of diseases and improved responses to vaccines. Studies show lower rates of the common cold, faster removal of bacteria, and better antibody response in people who have a daily drink compared to those who don’t.

However, much more research is needed to understand this effect. Brain Health The plant-based antioxidants in whiskey may help maintain a healthy chemical balance in your brain. Research shows small amounts of whiskey — especially aged varieties — increases our activity in the brain’s GABA neurotransmitter, responsible for things like nervous system function and memory.

See also:  Does Alcohol Have Benefits?

One study found that people who consumed one to six drinks weekly had a lower risk of dementia than non-drinkers. Another showed that moderate alcohol intake might reduce cognitive decline in people with Alzheimer’s Disease, Whiskey’s potential health benefits are associated with low to moderate amounts.

  • Over time, high alcohol consumption can increase your risk of chronic disease and other health issues.
  • Talk to your doctor to make sure alcohol is safe for you, and consider the following health risks: Heart Problems Whiskey’s heart benefits come with small doses.
  • Heavy alcohol use can lead to high blood pressure, high cholesterol, and heart disease.

Mental and Cognitive Health While low amounts may support brain health, in excess, studies show alcohol can disrupt how memories form. Over time, this can lead to cognitive decline. Heavy alcohol use is also linked to depression, anxiety, and alcohol dependence,

  1. Liver Damage Because your liver breaks down alcohol in your body, heavy drinking can lead to liver disease,
  2. High amounts of alcohol cause fatty deposits in your liver and scarring, which can eventually cause liver failure,
  3. Cancer Risk Studies show excessive alcohol consumption can increase your cancer risk, especially for cancer of the mouth, throat, esophagus, liver, colon, pancreas, and breast,

Immune System Function High amounts of alcohol can weaken your immune system, reducing your body’s ability to fight off infection and raising your risk of chronic diseases. Pregnancy Concerns Research shows that any amount of alcohol can cause problems with a baby’s growth during pregnancy.

How long does it take for your cholesterol to go down after quitting alcohol?

3-4 Weeks – At 3 weeks of not drinking, most drinkers have successfully reduced their risk of heart disease, including stroke, high cholesterol, and high blood pressure. Their kidney health and even their vision may improve. For dependent drinkers, blood pressure may reduce to normal levels by the 3rd or 4th week.

Does your heart improve when you stop drinking?

When a person stops drinking alcohol completely, their heart muscle has the chance to strengthen and will gradually improve over time. However, some heart diseases are chronic, which means a person will never fully recover, even if they quit drinking.

How long does it take for triglycerides to reduce after alcohol?

Background Patients with hypertriglyceridemia (HTG) are generally advised to avoid alcohol, even though moderate alcohol consumption is cardioprotective. Alcohol increases plasma triglyceride concentration transiently in normolipidemic subjects, but whether alcohol consumption per se increases triglyceride concentrations in patients with HTG is unclear. Objective To assess whether baseline fasting triglyceride concentration determines plasma triglyceride concentration after acute oral alcohol intake. Methods Twelve persons with fasting triglyceride concentrations of 2.3 to 8.5 mmol/L (200-750 mg/dL) and 12 persons as a non-HTG group were enrolled. Obesity, current smoking, and history of hypertension, diabetes, or excessive alcohol use were exclusionary. Fasted subjects consumed 38 mL of ethanol in water (equivalent, 2 alcoholic drinks); blood samples were collected at baseline and at intervals thereafter for 10 hours. No less than 1 week later, the subjects consumed water alone in a control test. Results Mean triglyceride values were 4.04±0.41 mmol/L (358±36.9 mg/dL) and 1.00±0.11 mmol/L (89±10.2 mg/dL) for the HTG and non-HTG groups, respectively. Despite similar changes with alcohol feeding in plasma ethanol, nonesterified fatty acid, and acetate concentrations, the groups differed in triglyceride response. At 6 hours (peak) compared with baseline, triglyceride concentration increased only 3% in the HTG group but 53% in the non-HTG group. The former change was not significantly different from the effect with water alone (−9.2% from baseline; P =.43), whereas the latter was (−8.0%; P =.003). Conclusions Acute alcohol intake alone is not an important determinant of plasma triglyceride concentration in individuals with HTG. Other factors, such as the contemporaneous consumption of fat and alcohol, known to increase triglyceride concentrations synergistically in non-HTG individuals, may be more important. HYPERTRIGLYCERIDEMIA (HTG) is a health hazard because it is a risk factor for pancreatitis 1 and, in the view of many authorities, for coronary heart disease and other atherosclerotic disease.2, 3 Primary treatment after control of conditions and discontinuation of drugs that can cause HTG is weight control through exercise and reduction of energy intake and dietary fat. Adjunctive lipid-lowering pharmacotherapy may be considered.4 In addition, consumption of alcohol may be curtailed; clinical recommendations range from complete abstinence for all patients with HTG 5 to restriction of use, after a trial period, in selected patients.4 Indeed, fasting triglyceride concentrations normalize with discontinuation of alcohol intake in some patients, 6 in some instances dramatically and in particular in those with type V hyperlipidemia.7 – 9 Although observational epidemiological studies show little if any association between alcohol intake and concentration of very low-density lipoproteins (VLDLs) or plasma triglyceride, 10 perhaps because of the heterogeneity of triglyceride disorders in etiology and expression, 11 excessive alcohol intake followed only diabetes mellitus as the apparent cause of secondary HTG in a lipid clinic series.12 It is not clear, however, that alcohol per se raises triglyceride concentrations in individuals with HTG. It is the consensus of many studies that alcohol induces transient increases in plasma triglyceride concentrations in normolipidemic subjects, whether it is administered in the fasting state 13 – 16 or preprandially.17 – 22 In a series in which alcohol was given with dinner, the transient increase would have led to the finding of HTG in 25% of the subjects even after an overnight fast.18 Most otherwise healthy alcoholics have normal fasting triglyceride concentrations.23, 24 Also in normolipidemic subjects, contemporaneous ingestion of alcohol and fat induces a lipemia of a magnitude exceeding the sum of the effects of fat and ethanol consumed separately.25 – 27 A lipemic response to alcohol plus fat has been described in studies of subjects with HTG as well, 18, 26, 28 and the response may be exaggerated compared with that in normotriglyceridemic individuals.18, 28 However, to the best of our knowledge, the question of the effects of alcohol intake alone in otherwise fasted individuals with HTG has not been addressed. Given that dietary fat could be a confounder in the interpretation of the feeding experiments in subjects with HTG, we undertook a study of the effects of an acute dose of alcohol on plasma triglyceride and nonesterified fatty acid (NEFA) concentrations in a non-HTG group and in subjects with primary moderate HTG. A reduction in plasma NEFA concentration perturbs the activities of several processes involved in normal lipoprotein metabolism, among them lipolysis, 29, 30 cholesteryl ester transfer activity, 31, 32 and esterification of cholesterol.30 Ultimately, clarification of the role of alcohol in the induction of HTG is needed, in particular in light of the conundrum facing clinicians regarding what to recommend to patients about moderate alcohol use to reduce risk for coronary heart disease.33, 34 As in other areas of coronary heart disease risk investigation (eg, the apparent response heterogeneity in the relation of hypertension to sodium consumption 35, 36 or hypercholesterolemia to intake of dietary cholesterol 37 – 39 ), closer examination may be needed to enable a refinement of clinical guidelines. Participants in the study were 12 persons with a fasting triglyceride concentration of 2.3 mmol/L (200 mg/dL) or greater but not exceeding 8.5 mmol/L (750 mg/dL) at screening and 12 normotriglyceridemic persons (non-HTG group). The HTG group was recruited through referrals from collaborating physicians in the Section of Atherosclerosis and Lipoprotein Research at Baylor College of Medicine, Houston, Tex, the non-HTG group through advertisements in the Texas Medical Center, Houston. Men and nonpregnant, nonnursing women aged 21 years or older were eligible. Subjects could not have a history of hypertension or diabetes mellitus, be obese (body mass index ≥30) or current smokers, or take any lipid-lowering medication. They were excluded if they consumed excessive amounts of alcohol (>3 drinks per day) or had never or rarely drunk alcohol. Eligibility was determined from questionnaires except for screening fasting triglyceride concentration (1 determination), body mass index (weight and height measurement), and blood pressure (measurement in addition to self-reported history regarding hypertension; not to exceed 139/89 mm Hg on a single measurement). All blood samples in the study were drawn by trained personnel in the General Clinical Research Center of The Methodist Hospital, Houston. Participants were advised to fast for 12 hours and not to consume alcohol for 24 hours before the alcohol loading test. On the morning of the test, a saline lock with a 3-way stopcock was placed in an upper arm for blood sample collection. The line was kept open with a saline solution drip of 30 mL/h, and after each blood sampling it was flushed with saline solution. Each participant consumed, within 15 minutes of beginning consumption, 38 mL (30 g) of ethanol (Everclear) in 362 mL of water, equivalent to about 2 alcoholic drinks.40 The beverage was served at room temperature. Subjects continued to fast for 10 hours after ingestion; they consumed only drinks with no energy content and were involved in only passive activities during this period. Just before the test drink (baseline), 30 minutes after, and then hourly for up to 10 hours, 5 mL of blood was collected into EDTA and placed on ice. For control testing, the process was repeated no less than 1 week later, with the alcohol replaced by water. The loading tests were conducted in the General Clinical Research Center of The Methodist Hospital. The protocol was reviewed by the Institutional Review Board for Human Subject Research of Baylor College of Medicine and The Methodist Hospital. All subjects gave written informed consent and were compensated for each test. Plasma was isolated from fasting blood samples by using low-speed centrifugation at 4°C. Screening samples were analyzed for total cholesterol, high-density lipoprotein (HDL) cholesterol, triglyceride, and calculated low-density lipoprotein (LDL) cholesterol concentrations. Test samples were analyzed at all time points for triglyceride, NEFA, ethanol, and acetate concentrations after the alcohol challenge, and for triglyceride and NEFA concentrations after subjects were given only water. The LDL cholesterol values were calculated using the formula derived by Friedewald et al 41 ; all other determinations used were by direct measurement with enzymatic methods, using standards supplied by the vendor (Boehringer Mannheim Biochemicals, Indianapolis, Ind). The HTG and non-HTG groups were compared using χ 2 and 2-sample t tests. Magnitudes of alcohol- and water-induced changes in lipid concentrations were estimated for each subject by using the integrated area under the curve defined by plotting triglyceride or NEFA values vs time during the 10-hour interval. Analyses of covariance adjusted for baseline differences in age and body mass index were used to compare the groups with respect to plasma lipid concentrations at baseline and with respect to alcohol-induced lipemia adjusted for water-induced lipemia. Appropriate transformations to meet the assumptions of the tests were used when needed. Wilcoxon signed-rank tests were used to assess the magnitude of alcohol-induced changes from baseline. Continuous data are reported as mean±SEM. All statistical tests were 2-tailed. Actual P values were reported for all tests; the interpretation of statistical significance, however, was based on keeping the familywise error rate of,05 or greater for each group of related hypotheses. The statistical analyses were performed using commercially available software (STATA Release 5.0, STATA Corporation, College Station, Tex). Mean anthropomorphic data and plasma lipid and lipoprotein values determined at the screening visit are shown for the HTG and non-HTG groups in Table 1, The mean plasma triglyceride concentrations were 4.04±0.41 mmol/L (358±36.9 mg/dL) and 1.00±0.11 mmol/L (89±10.2 mg/dL), respectively. The groups were sex balanced, but the HTG group was significantly older and had a significantly higher body mass index. Therefore, other between-group tests were adjusted for these variables. With those adjustments, other significant differences distinguishing the HTG group were higher total cholesterol and lower HDL cholesterol concentrations. Plasma NEFA concentrations were also higher in the HTG group, but not significantly so ( Table 2 ). Consumption of alcohol led to a rapid rise in mean plasma ethanol concentration in both groups ( Figure 1 ). The peak value, achieved in both groups at the 30-minute measurement, was slightly higher in the non-HTG group, ie, 13.7±1.5 mmol/L vs 10.6±1.3 mmol/L. The difference was not significant ( P =.35) in an analysis adjusted for baseline concentration, age, and body mass index. The rates of alcohol clearance were also similar. Ethanol clearance was estimated from the initial slope of plasma ethanol vs time. On the basis of a first-order regression analysis, the halftimes for the clearance of ethanol were 2.2 and 2.5 hours for non-HTG and HTG groups, respectively. Plasma triglyceride response to alcohol in both groups peaked between 4 and 6 hours, with mean triglyceride concentrations returning to baseline or near-baseline values at 10 hours, as seen in Figure 2, In the HTG group, alcohol had little effect on triglyceride concentration, which at 6 hours was increased only 3% above that at baseline ( P =.94). As seen in Table 2, this was similar to the −9.2% change from baseline after water consumption ( P =.43). The magnitude of the lipemia, expressed in terms of integrated area under the curve (baseline to 10 hours), did not vary significantly according to alcohol or water feeding in the HTG group ( P =.16). In contrast, alcohol had a striking lipemic effect in the non-HTG group. Triglyceride concentration at 6-hour follow-up was increased 53% from baseline, whereas the water-induced change was −8.0% ( P =.003) ( Figure 2 ). The magnitude of the lipemia was also significantly higher ( P =.002) ( Table 2 ). In the HTG group, alcohol induced a 37% decrease in mean plasma NEFA concentration at 30 minutes, which was significantly greater than the 10% water-induced decrease ( P =.003). Similarly in the non-HTG group, NEFA concentration was reduced by 35% and 8.5% at 30 minutes after alcohol and water intake, respectively ( P =.004) ( Table 2 ). Reduction from baseline extended to 4 and 5 hours, respectively ( Figure 3, top). Conversely, plasma acetate concentrations, after initial plateaus, began to decrease 4 and 5 hours after alcohol loading ( Figure 3, bottom), ie, the time interval during which acetate concentrations were elevated corresponded to the interval during which NEFA concentrations were depressed. Finally, the magnitude of the decrease in plasma NEFA concentrations appeared to correlate with the plasma acetate concentration. Maximum acetate concentration was greater in the HTG group (0.98 vs 0.61 mmol/L), and the decrease in plasma NEFA concentration was greater for the HTG group. Our finding that alcohol intake significantly increased the mean fasting plasma triglyceride concentration (which at 6 hours was 53% above baseline vs an 8% decrease with water alone) in the non-HTG group is consistent with many studies in which alcohol was given orally 14, 15 or intravenously 13, 16 in the fasting state or administered preprandially 17 – 22 to normolipidemic individuals. Trials in which alcohol was administered as part of a diet for days or weeks included isocaloric control, 19, 20 indicating that the increases in fasting triglyceride concentration were not due simply to higher energy intake. The major mechanism appears to be increased VLDL formation in the liver.10, 20, 42, 43 The degree of short-term plasma triglyceride concentration change has been variable, depending on dosage of alcohol, duration of administration, and a variety of genetic and environmental factors.42 – 44 Although a threshold for response, at a daily dose of 75 to 100 mL of alcohol, has been suggested by some studies using basal diet, 45 moderate dosages have increased triglyceride concentration in fasting normolipidemic subjects.46, 47 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.10, 42 In our study, however, designed to assess the question of triglyceride response by baseline concentration, alcohol ingestion did not affect fasting triglyceride concentration in subjects with elevated VLDL concentrations; the 3% increase in plasma triglyceride concentration with alcohol consumption was not significantly different from the 9% decrease with water consumption alone ( P =.43). A previous fasting study in healthy normolipidemic alcoholic men given 225 mL of alcohol orally during a 6-hour period also suggested no relation between the degree of triglyceride response and the basal fasting value.48 The striking difference in effect on plasma triglyceride concentration in our HTG and non-HTG groups occurred despite similar peak plasma ethanol values and rates of alcohol clearance; the peak plasma ethanol concentration in each group was about half of the legal definition of intoxication in Texas (≥0.1 g/100 mL of blood) 49 or closer to the legal limit in some states (≥0.08 g/100 mL of blood).50 Although body mass index was significantly higher in our HTG than in our non-HTG group, weight, given adjustment of the analyses, did not account for the difference in triglyceride response; in a 4-week series, a transient increase in fasting triglyceride concentrations occurred in obese but not in lean subjects with normal lipid concentrations or HTG.42 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.51 – 54 The HTG in our subjects was not linked, as seen in insulin resistance syndrome, 55 to hypertension. 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.26, 27 The effect is more profound with saturated fat than with polyunsaturated fat, apparently related to a greater resistance of saturated fat to hydrolysis.26 The magnitude of the lipemia following an oral fat load is a direct function of fasting triglyceride concentration.56 Thus, the conjunction of saturated fat, ethanol, and HTG could lead to high concentrations of plasma triglyceride, increasing risk for pancreatitis. In addition, the low triglyceride-clearing capacity in enhanced postprandial lipemia increases risk for atherosclerosis.57 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.42 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.59 Alcohol could increase the rate of uptake of NEFAs by peripheral tissues. 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.58 Alternatively, NEFA production by hormone-sensitive lipase in peripheral tissue or by lipoprotein lipase in the plasma compartment could be impaired. 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.64, 65 Alcohol consumption reduces the concentration and activity of cholesteryl ester transfer protein (CETP), 66 – 68 which mediates the exchange of VLDL triglycerides for HDL cholesteryl esters. 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. Thus, elevated plasma NEFA concentrations stimulate a decrease in 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.72 This recommendation does not distinguish between the risk for alcohol-induced pancreatitis in patients with severe HTG and a history of pancreatitis and the benefits of low-dose alcohol consumption in patients with mild to moderate HTG and other risk factors for cardiovascular disease. 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. Accepted for publication August 15, 1998. 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