Longevity Library · Lab reference

Written by Daniel Tagge, MD
Updated October 7, 2026
Reviewed October 10, 2026
26 sources · Measured in mg/dL

TriglyceridesFasting triglycerides · Non-fasting triglycerides · TG

Name: Triglycerides: normal range, what the evidence supports, and what moves it
Creator: Daniel Tagge, MD
Published: 2026-10-07

Laboratories call triglycerides under 150 mg/dL normal, the Copenhagen cohorts found heart attack risk already higher above about 88 than below it, the American Heart Association has called a fasting value under 100 'optimal', and genetic studies show the risk travels with the number of ApoB particles, so a triglyceride number is best read as a signal about remnant particles and insulin resistance rather than a target of its own.

Triglycerides are the fat carried in ApoB particles, mostly VLDL and its remnants, and they rise with carbohydrate, alcohol, weight and insulin resistance. The printed cutoff of 150 mg/dL comes from a 2001 US panel; cohorts show risk rising from the lowest band upward, and Mendelian randomization shows the effect is carried by particle number. They move a lot from day to day, and with meals.

01 · The scale

Where the laboratory range and the evidence sit.

Risk rose from the lowest band upward in cohorts: Copenhagen adults with non-fasting triglycerides above about 88 mg/dL already carried higher heart attack and pancreatitis risk than those below, guidelines mark under 150 as lower risk, and genetics show the effect is carried by the ApoB particle count rather than the triglyceride itself.

0100150200300400500600

Common laboratory 'normal'
0 to 150 mg/dL · NCEP ATP III 2001
Lowest-risk reference band in Copenhagen (under about 88)
0 to 88 mg/dL · Nordestgaard 2007; Pedersen 2016
'Optimal' fasting value proposed by the AHA (under 100)
0 to 100 mg/dL · AHA 2011
Borderline high; look for other risk factors
150 to 199 mg/dL · NCEP ATP III 2001; ESC/EAS 2019
High; non-fasting 200 or more calls for a fasting repeat
200 to 499 mg/dL · NCEP ATP III 2001; AHA 2011
Very high; pancreatitis risk, severe hypertriglyceridemia
500 and above mg/dL · NCEP ATP III 2001; ACC 2021

Laboratory range
Evidence supports
Guideline goal or unstudied
Higher risk in studies

Scale in mg/dL. Some laboratories report mmol/L; divide mg/dL by about 88.6 for mmol/L. Bands show where studies found something, not a recommendation for any one person.

02 · What it is

What Triglycerides measures.

Triglycerides are carried in triglyceride-rich VLDL particles and their remnants, each of which also carries one apolipoprotein B, so a plasma triglyceride concentration reflects how many of those ApoB particles are in circulation. Fasting values rise with visceral fat, insulin resistance, diabetes and fatty liver, which is why the number is read as a metabolic marker as much as a lipid.^1,2Grade A

A triglyceride value is unusually unstable. The American Heart Association's statement puts the median intra-individual variation at 23.5 percent, against 4.9 percent for total cholesterol, and in 51 volunteers measured on three occasions the day-to-day variability of triglycerides was 20 percent. Over years the number is about as stable as blood pressure: within-person correlation 0.64 over four years and 0.63 over twelve.^2,3,4Grade B

Because triglyceride-rich remnants are what the number tracks, a non-fasting value carries at least as much risk information as a fasting one. In 26,330 healthy women followed 11 years, non-fasting triglycerides predicted cardiovascular events more strongly than fasting ones; in the Emerging Risk Factors Collaboration the hazard ratios were at least as strong in people who had not fasted.^5,6Grade A

03 · The laboratory range

What a laboratory calls normal.

Under 150 mg/dL printed as normal by US laboratories, with 150 to 199 borderline high, 200 to 499 high and 500 and above very high.

The printed categories come from the 2001 National Cholesterol Education Program Adult Treatment Panel III: normal under 150 mg/dL, borderline high 150 to 199, high 200 to 499, very high 500 and above. The panel's own rationale was that elevated triglycerides are an independent coronary risk factor because partially degraded VLDL, the remnant lipoproteins, are atherogenic. Earlier US panels had set the 'desirable' line at 250 (1984) and 200 (1993) before it was lowered to 150.^7,2Grade A

The 2019 European dyslipidaemia guideline sets no triglyceride goal but states that under 1.7 mmol/L (150 mg/dL) indicates lower risk and that higher levels indicate a need to look for other risk factors. For samples drawn without fasting, the European consensus asks laboratories to flag 175 mg/dL and above instead of 150, because the maximal mean rise after an ordinary meal is about 26 mg/dL.^1,8Grade A

The American Heart Association's 2011 statement went one step lower and proposed an 'optimal' fasting triglyceride under 100 mg/dL as a parameter of metabolic health, noting that such levels are common in low-risk countries while US medians run about 106 in women and 122 in men, and that the lowest risk of incident and recurrent cardiovascular disease has consistently sat with the lowest fasting triglycerides. It is a designation, not a treatment target, and no trial has tested it.²Grade A

04 · The evidence

What the studies support.

In the Copenhagen City Heart Study, 7,587 women and 6,394 men were followed for a mean of 26 years with a non-fasting triglyceride at baseline. Against people below 1 mmol/L (88.5 mg/dL), the adjusted hazard ratio for heart attack was already 1.7 in women and 1.4 in men at 88.5 to 176 mg/dL, rising to 5.4 in women and 2.4 in men at 442.5 mg/dL and above, with the same stepwise pattern for ischemic heart disease and death. This is an association in a cohort, adjusted for the usual risk factors.⁹Grade B

Across 29 Western prospective studies, 262,525 people and 10,158 coronary cases, the top third of long-term triglyceride values carried an adjusted odds ratio of 1.72 against the bottom third. The association weakened considerably once established risk factors were accounted for, and in the Emerging Risk Factors Collaboration's 302,430 people, the adjusted hazard ratio for triglycerides fell to 0.99 while non-HDL cholesterol carried 1.50: the European guideline summarizes this as the association becoming null after adjustment for non-HDL cholesterol, the sum of all ApoB-carrying particles.^4,6,1Grade A

Genetics point the same way. In 73,513 Copenhagen residents, a genetic increase of 1 mmol/L (39 mg/dL) in non-fasting remnant cholesterol carried a causal odds ratio of 2.8 for ischemic heart disease, independent of HDL cholesterol. Across 17 studies with 62,199 participants, genetically higher triglycerides raised coronary risk (odds ratio 1.62 per log unit), though the signal was not robust once variants shared with HDL and LDL cholesterol were accounted for.^10,11Grade B

The decisive study compared triglyceride-lowering LPL variants with LDL-lowering LDLR variants in 654,783 people. Per 10 mg/dL lower ApoB, each lowered coronary risk by the same amount (odds ratios 0.771 and 0.773), even though the LPL score lowered triglycerides by 69.9 mg/dL and the LDLR score lowered LDL cholesterol by 14.2. After adjusting for ApoB, triglycerides no longer predicted coronary disease (odds ratio 1.014). The European guideline concludes that the causal effect of triglyceride-rich lipoproteins is determined by the circulating concentration of ApoB particles, not by their triglyceride content.^12,1Grade A

Triglycerides are also a working proxy for insulin resistance. In 258 overweight non-diabetic adults measured by the insulin suppression test, a fasting triglyceride of 130 mg/dL or a triglyceride-to-HDL ratio of 3.0 identified the insulin-resistant third with sensitivity of 67 and 64 percent and specificity of 71 and 68 percent, about as well as the metabolic syndrome criteria; in 449 apparently healthy adults a ratio of 3.5 or more best predicted insulin resistance and small, dense LDL. Both are cross-sectional and mostly white samples.^13,14Grade C

At the far end, pancreatitis. In 116,550 Copenhagen adults followed a median of 6.7 years, the adjusted hazard ratio for acute pancreatitis against people under 89 mg/dL was 1.6 at 89 to 176, 2.3 at 177 to 265 and 8.7 at 443 mg/dL and above, a steeper gradient than for heart attack (1.6 and 3.4 at the same bands). The American Heart Association puts the conventional threshold for triglyceride-induced pancreatitis at 1,000 mg/dL and notes that only about 20 percent of people at such levels develop it.^15,2Grade B

05 · What moves it

The levers with evidence behind them.

What is listed here has been tested. The size of each effect, and the size of the study, are in the sentence, so a small effect reads as a small effect.

Weight loss
lowers it, roughly in proportion to the weight lost
Across 73 randomized trials with 32,496 overweight adults, each kilogram lost through lifestyle change lowered triglycerides by about 4 mg/dL at 12 months. The AHA and ACC statements put a 5 to 10 percent weight loss at about a 20 percent fall in triglycerides, and note that in some people the fall reaches 70 percent.^16,2,17Grade A
Cutting added sugar and fructose
lowers it, independent of weight
In 39 randomized trials, higher free-sugar intake raised triglycerides by 0.11 mmol/L (about 10 mg/dL), and the effect was clearest in trials that held calories and weight constant. The AHA statement reports the lowest triglycerides in US adults when added sugar was under 10 percent of energy, with values 5 to 10 percent higher above that.^18,2Grade A
Lower-carbohydrate eating
lowers it more than a low-fat diet, with a trade-off
In 11 randomized trials of six months or longer with 1,369 participants, a low-carbohydrate diet lowered triglycerides 0.26 mmol/L (about 23 mg/dL) more than a low-fat diet and raised HDL cholesterol, but it also raised LDL cholesterol by 0.16 mmol/L (about 6 mg/dL). The AHA statement adds that replacing any class of fat with carbohydrate raises fasting triglycerides across 60 controlled feeding studies.^19,2Grade A
Aerobic exercise
lowers it modestly, most when it starts high
Pooling six randomized trials of aerobic exercise with a prudent diet in 559 adults, triglycerides fell 10.6 mg/dL, about 18 percent, against controls. The AHA statement puts the effect at 20 to 30 percent when the starting value is above 150, the activity moderate to intense and calories also reduced.^20,2Grade B
Alcohol
raises it, acutely with a meal and chronically in excess
Moderate drinking in 44 intervention studies did not change fasting triglycerides, but alcohol taken with a fatty meal adds to the post-meal triglyceride peak by acutely inhibiting lipoprotein lipase, and the AHA estimates an ounce of alcohol a day at 5 to 10 percent higher triglycerides than in non-drinkers. The ACC pathway describes excess alcohol as producing marked elevations, often 250 mg/dL or more, that can precipitate pancreatitis.^21,22,2,17Grade B
Marine omega-3 fatty acids at prescription doses
lowers it by dose; outcome benefit is disputed
Triglycerides fall by roughly 5 to 10 percent per gram of EPA and DHA, and at 4 grams a day by 30 percent or more in people with very high values. Whether that lowering prevents events is unsettled: in 8,179 statin-treated patients with triglycerides of 135 to 499, purified EPA cut the primary cardiovascular endpoint from 22.0 to 17.2 percent over 4.9 years (hazard ratio 0.75) with more atrial fibrillation; in 13,078 similar patients, a combined EPA and DHA product against corn oil did nothing (hazard ratio 0.99). Over-the-counter fish oil at one gram was tested in neither.^23,2,24,25Grade B
Lipid-lowering medication
lowers it by class, 10 to 50 percent
The AHA statement tabulates triglyceride reductions of about 10 to 30 percent for statins and 30 to 50 percent for the fibrate class, and the ACC pathway notes that high-intensity statins lower triglycerides more than lower doses. The pathway reserves triglyceride-directed drugs for people at high risk whose values stay at 150 or above after lifestyle change and treatment of secondary causes; whether to treat is a physician's decision about the whole picture.^2,17Grade A

06 · Reading it well

Caveats, and what belongs with a physician.

Fasting or not changes the number, not the meaning. After an ordinary meal the maximal mean rise is about 26 mg/dL, which is why non-fasting flags sit at 175 rather than 150; a high-fat meal of around 50 grams can push the value up by half or more, so the AHA asks for a fasting repeat within two to four weeks when a non-fasting value reaches 200. The European consensus suggests fasting when a non-fasting value exceeds 440 mg/dL. A single value near any cutoff deserves a second draw.^8,2,3Grade A

Alcohol the evening before, especially with a fatty dinner, raises the next morning's triglycerides through an acute inhibition of lipoprotein lipase and extra VLDL secretion; a surprising value after a dinner out is a reason to repeat, not to conclude.²²Grade C

Triglycerides matter through particle number. Once ApoB is known, triglycerides add no independent coronary risk in Mendelian randomization, so a high triglyceride is a reason to measure ApoB rather than a target to chase on its own; the European guideline prefers ApoB over LDL cholesterol whenever triglycerides are high.^12,1Grade A

The triglyceride-to-HDL ratio as an insulin-resistance marker was derived in one set of volunteers, and it does not transfer to every population. In 98 overweight African American adults the ratio's area under the curve was 0.56, no better than chance, and the lipid criteria found only 17 percent of the insulin-resistant; in people of African descent, insulin resistance often comes with normal triglycerides.²⁶Grade C

A raised triglyceride has causes worth finding before it is treated as a lifestyle problem. The ACC pathway asks for secondary causes to be investigated, singling out diabetes and excessive alcohol, and the AHA statement lists poorly controlled diabetes, hypothyroidism, kidney disease, estrogens, steroids and the third trimester of pregnancy among the conditions that raise it.^17,2Grade A

See a physician

A triglyceride of 500 mg/dL or higher, which the ACC calls severe hypertriglyceridemia and treats first to lower pancreatitis risk; 1,000 or higher needs prompt attention.
Severe upper abdominal pain with nausea or vomiting in anyone known to have high triglycerides.
Triglycerides persistently above 150 together with diabetes, fatty liver, a large waist, high blood pressure or a high ApoB.
A parent or sibling with pancreatitis, very high triglycerides, or a heart attack or stroke before 55 (men) or 65 (women).
A sharp rise after starting a new medication, hormone therapy, or during pregnancy.

This page is education, not individual medical advice, and reading it creates no physician-patient relationship.

07 · Open questions

What the literature does not settle.

No trial has lowered triglycerides toward 100 mg/dL in healthy adults and counted outcomes; the AHA's 'optimal' under 100 is a designation drawn from population patterns, and the lowest-risk Copenhagen band (under about 88) is a reference group, not a tested target.
Whether lowering triglycerides itself helps, beyond lowering ApoB, is unresolved: the two large omega-3 outcome trials disagreed despite similar triglyceride lowering, so the benefit in one may belong to the agent rather than the triglyceride change.
Remnant cholesterol may be the better measure of the particles that do the harm, but it is calculated differently across laboratories and has no agreed cutoff.
The triglyceride-to-HDL ratio has not been validated as an insulin-resistance marker across ancestries, and fasting insulin or a glucose challenge may serve better in people of African descent.
Fasting and non-fasting cutoffs (150 and 175) are consensus conversions, not separately tested thresholds, and most laboratories still print the fasting range on every sample.

08 · In practice

How Dr. Tagge reads it in his own practice.

I like to see fasting triglycerides under 100, and I read them beside ApoB and fasting insulin rather than alone. That number is the AHA's 'optimal' and sits close to the lowest-risk band in the Copenhagen cohorts, but no trial has tested it, so it is my judgment about where a metabolically healthy adult tends to sit, not a target I chase with medication. A high value sends me looking for sugar, alcohol, weight, sleep and insulin resistance first; a value over 500 is a different conversation, about the pancreas, and it happens the same week.

A practice judgment, labeled as one (Grade D): it is how one physician reads the number for the people he cares for, not a recommendation for you.

Questions

A laboratory calls 140 mg/dL normal, and the European guideline reads anything under 150 as lower risk. It sits above the AHA's proposed 'optimal' under 100, and in the Copenhagen cohort people in the 88 to 176 band carried somewhat more heart attack risk than those below 88, so it is a nudge to look at the rest of the picture: ApoB, fasting insulin, waist, alcohol, and whether the draw was fasting. A single value this close to the middle of the range also moves 20 percent from day to day.

No trial defines one. Laboratories print under 150 mg/dL as normal; the American Heart Association proposed under 100 fasting as 'optimal' for metabolic health, because risk in cohorts sat lowest at the lowest values and because low-risk populations commonly run below 100; and in Copenhagen the reference group with the least risk was under about 88. Genetics add that what matters is the number of ApoB particles the triglycerides ride in, so a low triglyceride with a high ApoB is not reassuring, and the reverse is less worrying than it looks.

In the Stanford studies that introduced it, a ratio of 3.0 (in mg/dL) in overweight adults, or 3.5 in a general healthy sample, best separated the insulin-resistant from the rest, with about two-thirds sensitivity and specificity. Lower is better as a rough signal. The ratio was derived in mostly white volunteers and does not work in African Americans, in whom insulin resistance often comes with normal triglycerides, so it is a prompt to measure fasting insulin, not a diagnosis.

10 · Sources

26 sources, read in full.

Numbered in the order they appear. Each line says what this page relies on from the paper; the link opens the record at PubMed or the publisher.

1.
Mach F, Baigent C, Catapano AL, et al.. 2019 ESC/EAS guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk. European Heart Journal. 2020. PMID 31504418. DOI 10.1093/eurheartj/ehz455.
Guideline · No triglyceride goal, but under 1.7 mmol/L (150 mg/dL) indicates lower risk; the causal effect of triglyceride-rich lipoproteins is determined by the ApoB particle concentration, not the triglyceride content.
2.
Miller M, Stone NJ, Ballantyne C, et al.. Triglycerides and cardiovascular disease: a scientific statement from the American Heart Association. Circulation. 2011. PMID 21502576. DOI 10.1161/CIR.0b013e3182160726.
Consensus statement · Proposes an 'optimal' fasting triglyceride under 100 mg/dL; median intra-individual variation 23.5 percent; non-fasting 200 or more prompts a fasting panel; lifestyle and drug effect sizes tabulated.
3.
Bookstein L, Gidding SS, Donovan M, Smith FA. Day-to-day variability of serum cholesterol, triglyceride, and high-density lipoprotein cholesterol levels. Impact on the assessment of risk according to the National Cholesterol Education Program guidelines. Archives of Internal Medicine. 1990. PMID 2383160.
Laboratory method study · In 51 volunteers measured three times, day-to-day variability was 20 percent for triglycerides against 5 percent for total cholesterol.
4.
Sarwar N, Danesh J, Eiriksdottir G, et al.. Triglycerides and the risk of coronary heart disease: 10,158 incident cases among 262,525 participants in 29 Western prospective studies. Circulation. 2007. PMID 17190864. DOI 10.1161/CIRCULATIONAHA.106.637793.
Systematic review and meta-analysis · Adjusted odds ratio 1.72 for the top versus bottom third of usual triglycerides; within-person correlation 0.64 over four years and 0.63 over twelve.
5.
Mora S, Rifai N, Buring JE, Ridker PM. Fasting compared with nonfasting lipids and apolipoproteins for predicting incident cardiovascular events. Circulation. 2008. PMID 18711012. DOI 10.1161/CIRCULATIONAHA.108.777334.
Prospective cohort · In 26,330 healthy women over 11 years, non-fasting triglycerides had a stronger association with cardiovascular events than fasting ones.
6.
Emerging Risk Factors Collaboration; Di Angelantonio E, Sarwar N, et al.. Major lipids, apolipoproteins, and risk of vascular disease. JAMA. 2009. PMID 19903920. DOI 10.1001/jama.2009.1619.
Systematic review and meta-analysis · In 302,430 people, adjusted hazard ratio for coronary disease 0.99 with triglycerides versus 1.50 with non-HDL cholesterol; hazard ratios at least as strong without fasting.
7.
Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Executive summary of the Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). JAMA. 2001. PMID 11368702. DOI 10.1001/jama.285.19.2486.
Guideline · Triglyceride classification: normal under 150 mg/dL, borderline high 150 to 199, high 200 to 499, very high 500 and above; remnant lipoproteins are atherogenic.
8.
Nordestgaard BG, Langsted A, Mora S, et al.. Fasting is not routinely required for determination of a lipid profile: clinical and laboratory implications including flagging at desirable concentration cut-points: a joint consensus statement from the European Atherosclerosis Society and European Federation of Clinical Chemistry and Laboratory Medicine. European Heart Journal. 2016. PMID 27122601. DOI 10.1093/eurheartj/ehw152.
Consensus statement · Maximal mean post-meal rise in triglycerides about 26 mg/dL; flag non-fasting at 175 mg/dL and fasting at 150; consider fasting when non-fasting exceeds 440; pancreatitis referral above 880.
9.
Nordestgaard BG, Benn M, Schnohr P, Tybjaerg-Hansen A. Nonfasting triglycerides and risk of myocardial infarction, ischemic heart disease, and death in men and women. JAMA. 2007. PMID 17635890. DOI 10.1001/jama.298.3.299.
Prospective cohort · In 7,587 women and 6,394 men over 26 years, heart attack risk rose stepwise from the under-88.5 mg/dL band: adjusted hazard ratios 1.7 (women) and 1.4 (men) at 88.5 to 176, up to 5.4 and 2.4 at 442.5 and above.
10.
Varbo A, Benn M, Tybjærg-Hansen A, Jørgensen AB, Frikke-Schmidt R, Nordestgaard BG. Remnant cholesterol as a causal risk factor for ischemic heart disease. Journal of the American College of Cardiology. 2013. PMID 23265341. DOI 10.1016/j.jacc.2012.08.1026.
Mendelian randomization · In 73,513 Copenhagen residents, a genetic 1 mmol/L (39 mg/dL) increase in non-fasting remnant cholesterol carried a causal odds ratio of 2.8 for ischemic heart disease, independent of HDL cholesterol.
11.
Holmes MV, Asselbergs FW, Palmer TM, et al.. Mendelian randomization of blood lipids for coronary heart disease. European Heart Journal. 2015. PMID 24474739. DOI 10.1093/eurheartj/eht571.
Mendelian randomization · Across 17 studies with 62,199 participants, genetically higher triglycerides raised coronary risk (odds ratio 1.62 per log unit), but the estimate was not robust after adjusting for HDL and LDL cholesterol.
12.
Ference BA, Kastelein JJP, Ray KK, et al.. Association of triglyceride-lowering LPL variants and LDL-C-lowering LDLR variants with risk of coronary heart disease. JAMA. 2019. PMID 30694319. DOI 10.1001/jama.2018.20045.
Mendelian randomization · In 654,783 people, LPL and LDLR scores lowered coronary risk identically per 10 mg/dL lower ApoB (odds ratios 0.771 and 0.773); after adjusting for ApoB, triglycerides no longer predicted coronary disease (odds ratio 1.014).
13.
McLaughlin T, Abbasi F, Cheal K, Chu J, Lamendola C, Reaven G. Use of metabolic markers to identify overweight individuals who are insulin resistant. Annals of Internal Medicine. 2003. PMID 14623617. DOI 10.7326/0003-4819-139-10-200311180-00007.
Cross-sectional study · In 258 overweight non-diabetic adults, triglycerides of 130 mg/dL and a triglyceride-to-HDL ratio of 3.0 identified insulin resistance with sensitivity 67 and 64 percent and specificity 71 and 68 percent.
14.
McLaughlin T, Reaven G, Abbasi F, et al.. Is there a simple way to identify insulin-resistant individuals at increased risk of cardiovascular disease?. American Journal of Cardiology. 2005. PMID 16054467. DOI 10.1016/j.amjcard.2005.03.085.
Cross-sectional study · In 449 apparently healthy adults, a triglyceride-to-HDL ratio of 3.5 or more best predicted insulin resistance and small, dense LDL.
15.
Pedersen SB, Langsted A, Nordestgaard BG. Nonfasting mild-to-moderate hypertriglyceridemia and risk of acute pancreatitis. JAMA Internal Medicine. 2016. PMID 27820614. DOI 10.1001/jamainternmed.2016.6875.
Prospective cohort · In 116,550 Copenhagen adults, adjusted hazard ratios for acute pancreatitis against under 89 mg/dL were 1.6 at 89 to 176, 2.3 at 177 to 265 and 8.7 at 443 and above; for heart attack 1.6 and 3.4 at the lowest and highest bands.
16.
Hasan B, Nayfeh T, Alzuabi M, et al.. Weight loss and serum lipids in overweight and obese adults: a systematic review and meta-analysis. Journal of Clinical Endocrinology and Metabolism. 2020. PMID 32954416. DOI 10.1210/clinem/dgaa673.
Systematic review and meta-analysis · Across 73 randomized trials with 32,496 patients, each kilogram lost through lifestyle intervention lowered triglycerides by 4.0 mg/dL at 12 months.
17.
Virani SS, Morris PB, Agarwala A, et al.. 2021 ACC expert consensus decision pathway on the management of ASCVD risk reduction in patients with persistent hypertriglyceridemia: a report of the American College of Cardiology Solution Set Oversight Committee. Journal of the American College of Cardiology. 2021. PMID 34332805. DOI 10.1016/j.jacc.2021.06.011.
Consensus statement · Persistent hypertriglyceridemia is fasting 150 mg/dL or more (non-fasting 175) after lifestyle change and secondary causes; severe is 500 and above; lifestyle lowers triglycerides 10 to 70 percent; excess alcohol can precipitate pancreatitis.
18.
Te Morenga LA, Howatson AJ, Jones RM, Mann J. Dietary sugars and cardiometabolic risk: systematic review and meta-analyses of randomized controlled trials of the effects on blood pressure and lipids. American Journal of Clinical Nutrition. 2014. PMID 24808490. DOI 10.3945/ajcn.113.081521.
Systematic review and meta-analysis · Across 39 randomized trials, higher free-sugar intake raised triglycerides by 0.11 mmol/L, independent of weight change.
19.
Mansoor N, Vinknes KJ, Veierød MB, Retterstøl K. Effects of low-carbohydrate diets v. low-fat diets on body weight and cardiovascular risk factors: a meta-analysis of randomised controlled trials. British Journal of Nutrition. 2016. PMID 26768850. DOI 10.1017/S0007114515004699.
Systematic review and meta-analysis · In 11 randomized trials with 1,369 participants, low-carbohydrate diets lowered triglycerides 0.26 mmol/L more than low-fat diets and raised LDL cholesterol 0.16 mmol/L.
20.
Kelley GA, Kelley KS, Roberts S, Haskell W. Efficacy of aerobic exercise and a prudent diet for improving selected lipids and lipoproteins in adults: a meta-analysis of randomized controlled trials. BMC Medicine. 2011. PMID 21676220. DOI 10.1186/1741-7015-9-74.
Systematic review and meta-analysis · Aerobic exercise plus a prudent diet lowered triglycerides 10.6 mg/dL (18.2 percent) across six randomized trials in up to 559 adults.
21.
Brien SE, Ronksley PE, Turner BJ, Mukamal KJ, Ghali WA. Effect of alcohol consumption on biological markers associated with risk of coronary heart disease: systematic review and meta-analysis of interventional studies. BMJ. 2011. PMID 21343206. DOI 10.1136/bmj.d636.
Systematic review and meta-analysis · In 44 intervention studies, moderate alcohol raised HDL cholesterol but did not affect fasting triglyceride levels.
22.
Van de Wiel A. The effect of alcohol on postprandial and fasting triglycerides. International Journal of Vascular Medicine. 2012. PMID 21961068. DOI 10.1155/2012/862504.
Review · Alcohol with a fat-containing meal adds to the postprandial triglyceride peak through acute inhibition of lipoprotein lipase and increased VLDL synthesis.
23.
Skulas-Ray AC, Wilson PWF, Harris WS, et al.. Omega-3 fatty acids for the management of hypertriglyceridemia: a science advisory from the American Heart Association. Circulation. 2019. PMID 31422671. DOI 10.1161/CIR.0000000000000709.
Consensus statement · Prescription omega-3 at 4 g/day lowers triglycerides by 30 percent or more in very high triglycerides; hypertriglyceridemia defined as 200 to 499 mg/dL and very high as 500 and above.
24.
Bhatt DL, Steg PG, Miller M, et al.. Cardiovascular risk reduction with icosapent ethyl for hypertriglyceridemia. New England Journal of Medicine. 2019. PMID 30415628. DOI 10.1056/NEJMoa1812792.
Randomized trial · In 8,179 statin-treated patients with triglycerides 135 to 499 mg/dL, purified EPA 4 g/day reduced the primary endpoint from 22.0 to 17.2 percent over a median 4.9 years (hazard ratio 0.75), with more atrial fibrillation.
25.
Nicholls SJ, Lincoff AM, Garcia M, et al.. Effect of high-dose omega-3 fatty acids vs corn oil on major adverse cardiovascular events in patients at high cardiovascular risk: the STRENGTH randomized clinical trial. JAMA. 2020. PMID 33190147. DOI 10.1001/jama.2020.22258.
Randomized trial · In 13,078 statin-treated high-risk patients with median triglycerides 240 mg/dL, 4 g/day of EPA plus DHA versus corn oil did not reduce major adverse cardiovascular events (hazard ratio 0.99).
26.
Sumner AE, Finley KB, Genovese DJ, Criqui MH, Boston RC. Fasting triglyceride and the triglyceride-HDL cholesterol ratio are not markers of insulin resistance in African Americans. Archives of Internal Medicine. 2005. PMID 15983289. DOI 10.1001/archinte.165.12.1395.
Cross-sectional study · In 98 overweight African Americans, the triglyceride-to-HDL ratio had an area under the curve of 0.56 for insulin resistance and the lipid criteria had 17 percent sensitivity.

Keep reading.

Reading a number well is the start of the work, not the end of it. If you would like a physician to read yours over time, Explore working with Dr. Tagge.