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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Contents
- 1 Can alcohol temporarily raise triglycerides?
- 2 Why are my triglycerides suddenly so high?
- 3 Do triglycerides change from day to day?
- 4 Is high triglycerides permanent?
- 5 What alcohol is best for high triglycerides?
- 6 How long do you have to not drink alcohol before a cholesterol test?
- 7 Why did my triglycerides go up so much in one year?
- 8 Why are my triglycerides high even though I eat healthy?
- 9 Can a hangover cause high triglycerides?
Can alcohol temporarily raise triglycerides?
High Triglycerides and Alcohol Use – Alcohol contains a lot of sugar and calories, and thus can elevate triglycerides in the body. Consuming large amounts of alcohol can increase the release of VLDL, increase the flow of free fatty acids to the liver from fat tissue, and impede the body’s ability to break down fat.
- In addition to raising triglyceride levels in the blood, overindulging in alcohol is linked to alcoholic fatty liver disease, pancreatitis, and cardiovascular disease.
- There have been conflicting findings regarding whether light use of alcohol may be beneficial to the cardiovascular system.
- For instance, one meta-analysis (a study that analyzes results from multiple studies) found that individuals with low consumption of alcohol and no episodes of drinking heavily had a lower risk of ischemic heart disease than those who never drank, those who occasionally drank heavily, and those who chronically drank heavily.
Yet, another more recent meta-analysis found that, although the overall analysis showed there was a lower risk of death from coronary heart disease for individuals with low consumption of alcohol, this correlation was not present in better quality studies, studies that controlled for heart health, or studies on individuals younger than 56.
- Thus, the connection some studies have found between light alcohol use and cardiovascular health may actually be due to factors other than light consumption of alcohol.
- The American Heart Association (AHA) recommends that if you already drink alcohol, you should drink in moderation.
- However, they advise that if you don’t already, you should not start, as drinking alcohol increases the risk of several health problems.
The AHA asserts that, although there may be some cardiovascular benefits from alcohol consumption which should be further researched, they do not currently recommend drinking alcohol to obtain these possible benefits. Rather, they recommend consulting with a doctor about improving your cholesterol and blood pressure, exercising, eating healthy, and controlling your weight.
Regular physical activity Losing weight Staying away from refined carbohydrates and sugar Decreasing or stopping alcohol use Eating healthier fats, such as fats from plants and fish
The only way for an individual to determine if their triglycerides and/or cholesterol levels are too high is to have their levels checked through a blood test. Any adult who has never had their cholesterol and triglyceride levels checked, or who has not had them checked in several years, should discuss with a health care professional whether a screening for lipid disorders is appropriate for them.
Additionally, anyone who finds that their use of alcohol is causing them problems or otherwise interfering with their ability to function normally should see a health care professional that can evaluate them for an alcohol use disorder, Addiction is a chronic disease that, if left unaddressed, can result in disability or death.
Research-based treatment for addiction can help individuals learn to manage their alcohol use disorder and avoid relapse.
Can a weekend of drinking increase triglycerides?
Is Alcohol to Blame for High Cholesterol and Triglyceride Levels? and are two forms of blood-borne fat that appear in the human circulatory system. People with too much LDL (“bad”) cholesterol or triglycerides in their bloodstreams can develop substantially increased risks for serious forms of heart disease.
- In a study published in December 2013 in the journal Alcohol, a team of Japanese researchers looked at the connection between LDL and triglyceride levels and occasional or habitual heavy consumption of,
- Does heavy drinking of alcohol affect triglycerides and cholesterol levels? This was the question the researchers wanted to answer.
They found that even occasional heavy drinking can increase both triglycerides and bad cholesterol.
How long does it take to normalize triglycerides?
Exercising Routinely – Exercise helps reduce “bad” LDL cholesterol by increasing “good” HDL cholesterol. Studies have shown that moderate-intensity aerobic exercise performed five days a week for 30 minutes or more can raise HDL to levels where it can counter the harmful effects of LDL.
- Even so, it can take six months to a year to achieve beneficial results, which is why it is important to make exercise a habit you can sustain.
- You can do so by choosing aerobic activities you enjoy and that are appropriate for your age, like brisk walking, jogging, cycling, swimming, or dancing.
- Exercising, along with the appropriate diet, can also help you manage your weight and shed excess pounds.
This is especially important if you have obesity (defined as a body mass index over 30). People with obesity may require an hour of physical activity on most days to achieve sustainable weight loss.
Can you drink alcohol night before triglycerides test?
Blood cholesterol tests – Cholesterol is a fatty substance in the blood. High cholesterol can lead to an increased risk of certain health conditions. Blood cholesterol tests, also known as lipid profiles, assess the quantities of fats in the blood. The different fats tested for include:
high-density lipoprotein cholesterol, also known as “good” cholesterollow-density lipoprotein cholesterol, also known as “bad” cholesteroltriglycerides
The amounts of these fats will increase if a person has recently eaten food. That is why people are asked not to eat for 9–12 hours before the test, which helps give an accurate profile of the amounts of these fats in the blood. Research has suggested that fasting may not be necessary before all cholesterol and triglyceride tests.
Why are my triglycerides suddenly so high?
Lifestyle factors that can raise your triglycerides – Lifestyle factors have a powerful effect on your triglyceride level. That’s because your body converts extra calories into triglycerides. So, if you’re consuming sugars, fats or alcohol that your body doesn’t use right away, your triglycerides can go up. Factors that can lead to high triglycerides include:
Drinking too much alcohol, Eating too many refined carbohydrates (like white bread) or sugars. Eating too much saturated fat. Not moving around enough (sedentary lifestyle).
How long after quitting drinking does cholesterol go down?
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.
Do triglycerides change from day to day?
Clinlab Navigator Lipid and lipoprotein concentrations vary during the normal course of daily activity. Studies have demonstrated that within person variability is sufficient to make an individual move in and out of the predefined risk categories defined by the National Cholesterol Education Program (NCEP).
Interval | Total-C | HDL-C | LDL-C | TG |
Day | 2.5% | 4.5% | 7.8% | 36% |
Month | 4.8% | 7.7% | 9.6% | 24% |
Year | 6.1% | 8.4% | 13.6% | 26% |
Triglycerides fluctuate widely, even during a single day, because they exhibit diurnal variation. Triglyceride concentration is lowest at 3 a.m., rises until mid-afternoon and decreases thereafter. Cholesterol and LDL cholesterol are not subject to diurnal variation, but are affected by seasonal variation.
Variable | Effect |
Menstruation | 6-9% TC increase in follicular phase |
Pregnancy | 30% TC & 200% TG increase at term |
Acute illness | 15% TC & 25% HDL decrease |
Weight loss | 10% TC, 10% HDL, 40% TG decrease |
Exercise | 3-7% TC decrease & 3-10% HDL increase |
Smoking | 3% TC & 9% TG increase, 6-11% HDL decrease |
Posture | 10-20% higher standing than lying |
Specimen handling | Stable for 3 days |
Besides biological variation, lipid values are also dependent on the laboratory’s analytical performance. Today’s chemistry analyzers are very precise; analytical variation in reputable laboratories is less than one half of biological variation. The coefficient of variation at Saint Luke’s Hospital Laboratory is 2.2% for cholesterol, 3.8% for HDL cholesterol and 4.2% for triglycerides.
Lipid | Result (mg/dL) | Significant Change |
Cholesterol | 180 | 32 |
200 | 35 | |
220 | 39 | |
240 | 43 | |
260 | 46 | |
280 | 50 | |
300 | 53 | |
HDL | 25 | 7 |
30 | 8 | |
35 | 10 | |
40 | 11 | |
45 | 12 | |
50 | 14 | |
55 | 15 | |
60 | 16 | |
65 | 18 | |
Triglycerides | 100 | 84 |
150 | 126 | |
200 | 168 | |
250 | 210 | |
300 | 252 | |
350 | 293 | |
400 | 336 | |
450 | 378 | |
500 | 420 |
Cholesterol concentration must change at least 18%, HDL cholesterol 27% and triglycerides 84% before one can be assured that the difference is not simply due to intra-individual and analytical changes. : Clinlab Navigator
Do heavy drinkers have high triglycerides?
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.
Can fasting too long affect triglycerides?
Abstract – Studies were undertaken to examine triglyceride turnover in obese humans on isocaloric balanced diets and during prolonged (3-5 wk) fasting. The data were related to plasma concentrations of insulin (IRI), glucagon (IRG), and free fatty acids (FFA) and to blood ketone concentrations.
- The triglyceride turnover rates were also related to the plasma triglyceride concentration.
- This relationship was the same in the obese on isocaloric balanced diets as that we have previously observed in lean humans on similar diets.
- The relationship between triglyceride turnover and concentration changed during prolonged fasting in a way that suggested that triglyceride removal was impaired.
This viewpoint is consistent with the known effects of fasting on adipose tissue lipoprotein lipase activity. In another group of fasted obese, refed with a hypocaloric diet, the relationship returned toward normal. In addition to the impaired triglyceride removal, prolonged fasting resulted in a decrease in triglyceride production.
This decrease occurred despite an increase in plasma FFA. After 3-5 wk of fasting the IRI was about 50% of the initial value, while the IRG was the same as the initial value. While triglyceride production fell during fasting, the blood ketone concentration rose. Others have seen similar changes in ketones and triglycerides in livers perfused with medium in which the ratio of insulin to glucagon fell.
The rate of triglyceride production was not related to body weight. However, regardless of nutritional state, it was positively related to the basal plasma insulin levels. These data indicate that, in man as in animal preparations, insulin may regulate hepatic triglyceride production.
Is high triglycerides permanent?
When your triglyceride levels are too high, you may not have symptoms. It’s a “silent” problem with big implications, such as a four-fold increase in the likelihood of having a heart attack or stroke. A simple blood test is all it takes to check your triglyceride levels,
If they’re too high, you can get them back under control, often by changing your daily habits. If you already know that your triglyceride levels are too high, the actions you take now might even save your life. Having high triglycerides could be a sign that you’re becoming insulin -resistant, which means your body isn’t using insulin (a hormone that controls blood sugar ) properly.
When insulin doesn’t do its job, glucose can’t get into your cells. That raises your blood sugar levels, which can lead to pre-diabetes and, eventually, type 2 diabetes, Having diabetes makes you much more likely to have a heart attack and other heart problems, in addition to the risk from your high triglycerides.
Untreated diabetes is a major health threat. To manage it well, you may need to track everything you eat, test your blood sugar, exercise, lose extra weight, take medication as directed, and keep up with your medical appointments. Many people don’t know that they have diabetes. Your doctor should check on whether you do, and if so, help you get both your diabetes and your triglycerides under control.
High triglyceride levels can be a clue that you have fatty liver disease, Poor eating habits lead not only to high levels of fat in the bloodstream (triglycerides) but increased storage of fat throughout the body, including in the liver, Elevations in liver function tests (like ALT and AST) can indicate that fatty liver is present.
Fatty liver usually does not cause symptoms, but unless reversed, fatty liver can lead to permanent liver damage and cirrhosis, If your triglyceride levels are “very high” – above 500 mg/dL – you are more likely to get inflammation in your pancreas, Inflammation of the pancreas (a condition which doctors call pancreatitis ) can cause permanent tissue damage.
Symptoms can include abdominal pain, which may be severe. If you have high triglycerides, your doctor’s treatment should include healthy eating and exercise, Avoiding processed and sugary foods is paramount; these dietary changes alone can have a tremendous impact on your triglyceride levels.
How can I lower my triglycerides in 2 weeks?
– Triglycerides are a type of lipid, or fat, in the blood. Low carbohydrate and high-fiber diets that include oily fish can help lower triglycerides. Other ways to lower triglycerides include limiting added sugar intake, limiting alcohol, keeping carbohydrates to 50–60% or fewer of total daily calories, and limiting intake of saturated and trans fat.
Can triglycerides go away?
What’s the best way to lower triglycerides? – Healthy lifestyle choices are key:
- Exercise regularly. Aim for at least 30 minutes of physical activity on most or all days of the week. Regular exercise can lower triglycerides and boost “good” cholesterol. Try to incorporate more physical activity into your daily tasks — for example, climb the stairs at work or take a walk during breaks.
- Avoid sugar and refined carbohydrates. Simple carbohydrates, such as sugar and foods made with white flour or fructose, can increase triglycerides.
- Lose weight. If you have mild to moderate hypertriglyceridemia, focus on cutting calories. Extra calories are converted to triglycerides and stored as fat. Reducing your calories will reduce triglycerides.
- Choose healthier fats. Trade saturated fat found in meats for healthier fat found in plants, such as olive and canola oils. Instead of red meat, try fish high in omega-3 fatty acids — such as mackerel or salmon. Avoid trans fats or foods with hydrogenated oils or fats.
- Limit how much alcohol you drink. Alcohol is high in calories and sugar and has a particularly potent effect on triglycerides. If you have severe hypertriglyceridemia, avoid drinking any alcohol.
What alcohol is best for high triglycerides?
Red wine is thought to have heart health benefits exceeding other wines and forms of alcohol because grape skins have a high level of antioxidants, such as resveratrol, which helps increase levels of ‘good’ cholesterol.
What alcohol raises triglycerides?
Beer by itself doesn’t contain any natural cholesterol, but it can raise your triglyceride levels.
How long do you have to not drink alcohol before a cholesterol test?
On Nutrition – In your younger years, how often did you cram for an important test? I know I’m guilty of that one (freshman year History of Western Civilization, I’m looking at you). While shortcuts are great in many areas of life, they’re not so great for actually absorbing information, or when taking a test that may provide important information about your health.
Someone I was talking to recently mentioned that they were having bloodwork done to check their cholesterol and triglyceride levels in a few days. Their previous test results weren’t great, and they were worried that the results on their upcoming test would be worse, since they hadn’t made any diet or lifestyle changes.
“Is there anything I can do in the next few days to make my results better?” they asked. “No, not really,” I said. I should have added, “Why would you want to?” This wasn’t the first time I’ve been asked how to “cram” for a cholesterol test. Many people, consciously or unconsciously, seek their doctor’s approval.
No one likes to get a “failing” grade on their cholesterol test, but even if you could cheat on your test by making last-minute changes you don’t plan to sustain, you would only be cheating yourself. Cholesterol is a waxy, fatty substance in your body that travels through your bloodstream via lipoproteins.
Some is good — which is why our bodies actually make cholesterol — but too much is a risk factor for heart disease. Low-density lipoproteins (LDL), commonly called “bad” cholesterol, transport cholesterol to your body’s tissues and blood vessels, depositing any excess along the walls of your blood vessels.
High-density lipoproteins (HDL), or “good” cholesterol, transport this excess cholesterol away from your blood vessels so it can be removed from your body. Triglycerides are fats that circulate in your bloodstream. High triglycerides and low HDL increase your risk for heart disease and Type 2 diabetes.
Your cholesterol levels are affected by what you eat over time, and any improvements to your diet and lifestyle habits generally take three to six months to have an effect, if they’re going to — some people see better results than others. Improving your diet and increasing physical activity can both lower LDL and triglyceride levels, but exercise does much more than diet for improving HDL numbers.
- What about fasting before your blood test? It used to be standard practice to have everyone fast for up to 12 hours before a cholesterol test, but guidelines have changed recently.
- Whether you need to fast prior to the test depends on your individual risk factors, so follow your doctor’s instructions.
Regardless of whether you need to fast, avoid alcohol for 24 hours before your test and don’t eat a fatty meal the night before — these two things could artificially raise your triglyceride levels. As for long-term changes, start by eating less saturated fat — especially from fatty cuts of meat and processed foods — and increasing fish meals to twice per week.
Go for more fiber-rich carbohydrates — whole grains, beans and lentils, vegetables, fruit — and fewer “simple” carbs such as sugar and white flour. Watch alcohol intake, especially if your triglycerides are high, because alcohol dramatically increases triglyceride levels in some people. If you like having a framework to guide your eating choices, the DASH diet (Dietary Approaches to Stop Hypertension) and the Mediterranean diet both encompass these suggestions.
And if your physical activity levels aren’t what they could be — perhaps due to the pandemic — make a plan for gradually, steadily and consistently getting up and moving more. Carrie Dennett: [email protected] ; on Twitter: @CarrieDennett, Carrie Dennett, MPH, RDN, CD is a registered dietitian nutritionist at Nutrition By Carrie, and author of “Healthy For Your Life: A holistic approach to optimal wellness.” Visit her at nutritionbycarrie.com.
Why did my triglycerides go up so much in one year?
What Are the Causes and Symptoms of High Triglycerides? – Causes include obesity, eating too much unhealthy food, genetics, certain illnesses including poorly controlled diabetes, kidney disease, and underactive thyroid (hypothyroidism). Some drugs, such as steroids and birth control pills, and drinking a lot of alcohol can also cause it.
Can you reverse the effects of high triglycerides?
High Triglycerides You can take medicine to lower your triglyceride levels, but the best way is to lose weight, exercise, and cut back on calories.
Why are my triglycerides high even though I eat healthy?
My Cholesterol is Normal, but My Triglycerides are High: Why Is That? – So both your HDL and LDL levels are where they should be, but your triglycerides are still high — why is that? Triglycerides become elevated due to excess calories that do not get burned off, and in turned get stored in fat cells.
Losing 5 to 10 pounds if overweight Avoiding alcohol (even small or moderate amount of alcohol can significantly raise triglycerides) Avoiding foods high in saturated fats (fried foods) Limiting simple carbs that have high processed sugars (white bread, cakes, pastries). Participating in 30 minutes of exercise per day
“All these suggestions and routine follow up with a medical professional will lower you triglyceride level, even despite a low total cholesterol,” Dr. Hanumanthu says.
Learn more about triglyceride levels in our Health Library.
Can a hangover cause high triglycerides?
Can alcohol affect a cholesterol test? – Absolutely. Here’s why. Much of the alcohol that flows into your system after tipping back a glass finds its way to your liver for a digestive after-party. Alcohol is broken down in your liver and reconstructed as cholesterol and triglycerides,
The more you drink, the more your levels of cholesterol and triglycerides rise. As you might imagine, high levels of either type of this waxy fat are not exactly desirable for managing cholesterol or optimal health. “People who drink a lot of alcohol tend to have very high triglycerides,” says Dr. Cho.
“That can be a concern because elevated triglyceride levels can increase your risk for diabetes, pancreatitis and stroke.”
What causes high triglycerides but normal cholesterol?
My Cholesterol is Normal, but My Triglycerides are High: Why Is That? – So both your HDL and LDL levels are where they should be, but your triglycerides are still high — why is that? Triglycerides become elevated due to excess calories that do not get burned off, and in turned get stored in fat cells.
Losing 5 to 10 pounds if overweight Avoiding alcohol (even small or moderate amount of alcohol can significantly raise triglycerides) Avoiding foods high in saturated fats (fried foods) Limiting simple carbs that have high processed sugars (white bread, cakes, pastries). Participating in 30 minutes of exercise per day
“All these suggestions and routine follow up with a medical professional will lower you triglyceride level, even despite a low total cholesterol,” Dr. Hanumanthu says.
Learn more about triglyceride levels in our Health Library.
What makes triglycerides go up and down?
What’s the best way to lower triglycerides? – Healthy lifestyle choices are key:
- Exercise regularly. Aim for at least 30 minutes of physical activity on most or all days of the week. Regular exercise can lower triglycerides and boost “good” cholesterol. Try to incorporate more physical activity into your daily tasks — for example, climb the stairs at work or take a walk during breaks.
- Avoid sugar and refined carbohydrates. Simple carbohydrates, such as sugar and foods made with white flour or fructose, can increase triglycerides.
- Lose weight. If you have mild to moderate hypertriglyceridemia, focus on cutting calories. Extra calories are converted to triglycerides and stored as fat. Reducing your calories will reduce triglycerides.
- Choose healthier fats. Trade saturated fat found in meats for healthier fat found in plants, such as olive and canola oils. Instead of red meat, try fish high in omega-3 fatty acids — such as mackerel or salmon. Avoid trans fats or foods with hydrogenated oils or fats.
- Limit how much alcohol you drink. Alcohol is high in calories and sugar and has a particularly potent effect on triglycerides. If you have severe hypertriglyceridemia, avoid drinking any alcohol.