The polygenic nature of hypertriglyceridaemia: implications for definition, diagnosis, and management
Open accessAbstract
Plasma triglyceride concentration is a biomarker for circulating triglyceride-rich lipoproteins and their metabolic remnants. Common mild-to-moderate hypertriglyceridaemia is typically multigenic, and results from the cumulative burden of common and rare variants in more than 30 genes, as quantified by genetic risk scores. Rare autosomal recessive monogenic hypertriglyceridaemia can result from large-effect mutations in six different genes. Hypertriglyceridaemia is exacerbated by non-genetic factors. On the basis of recent genetic data, we redefine the disorder into two states: severe (triglyceride concentration >10 mmol/L), which is more likely to have a monogenic cause; and mild-to-moderate (triglyceride concentration 2–10 mmol/L). Because of clustering of susceptibility alleles and secondary factors in families, biochemical screening and counselling for family members is essential, but routine genetic testing is not warranted. Treatment includes management of lifestyle and secondary factors, and pharmacotherapy. In severe hypertriglyceridaemia, intervention is indicated because of pancreatitis risk; in mild-to-moderate hypertriglyceridaemia, intervention can be indicated to prevent cardiovascular disease, dependent on triglyceride concentration, concomitant lipoprotein disturbances, and overall cardiovascular risk.
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No randomized controlled trial has yet been reported to investigate whether reducing severe (>500 mg/dL) or moderate (>200 mg/dL) hypertriglyceridemia prevents cardiovascular disease.
“No RCT has yet been reported to investigate the benefit of reducing severe (>500 mg/dL) or moderate (>200 mg/dL) hypertriglyceridemia to prevent CVD.”
From American Association of Clinical Endocrinology Clinical Practice Guideline: Developing a Diabetes Mellitus Comprehensive Care Plan-2022 Update. (2022) · cites this paper as [371]
The “Triglycerides and risk of cardiovascular disease” section says cardiovascular-outcome trials mainly enrolled people without clinically relevant hypertriglyceridaemia, supporting the concern about a lack of targeted evidence. It does not state categorically that no RCT investigated either specified threshold. The “Desirable concentrations” section also reports post-hoc clinical benefit in fibrate-trial participants with triglycerides >200 mg/dL and low HDL cholesterol, though that is not the same as a trial designed for that group. Page numbers were not provided in our copy. (LLM, conf=0.83)
Experimental — accuracy not yet measuredApart from icosapent ethyl, fish oil therapy has not been shown to prevent cardiovascular adverse events.
“To date, aside from icosapent ethyl, fish oil therapy has not been shown to prevent CV adverse events.”
From American Association of Clinical Endocrinology Clinical Practice Guideline: Developing a Diabetes Mellitus Comprehensive Care Plan-2022 Update. (2022) · cites this paper as [371]
The “Omega-3 fatty acids” section (page not provided) reports that omega-3 supplementation was not significantly associated with reductions in all-cause mortality, myocardial infarction, or stroke. This supports the claim’s general point about cardiovascular outcomes, but the paper does not address the stated exception for icosapent ethyl. (LLM, conf=0.88)
Experimental — accuracy not yet measuredRegulatory approvals of fibrates, omega-3 fatty acids, and niacin for patients with triglyceride levels above 500 mg per deciliter were based on their triglyceride-lowering properties in the context of historical data supporting a correlation between incidence of pancreatitis and severity of hypertriglyceridemia.
“The approvals by various regulatory authorities of fibrates, omega-3 fatty acids, and niacin for patients with triglyceride levels above 500 mg per deciliter were based on their triglyceride-lowering properties in the context of historical data that support a correlation between the incidence of pancreatitis and severity of hypertriglyceridemia. 32”
From Olezarsen, Acute Pancreatitis, and Familial Chylomicronemia Syndrome (2024) · cites this paper as [32]
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredPatients with severe hypertriglyceridemia ≥10 mmol/L and chylomicronemia syndrome usually do not develop premature atherosclerosis.
“For example, patients with severe hypertriglyceridemia ≥10 mmol/L and chylomicronemia syndrome have high risk of acute pancreatitis but usually do not develop premature atherosclerosis, probably because chylomicrons and large VLDLs do not traverse the vascular endothelial barrier [33].”
From Quantifying atherogenic lipoproteins for lipid-lowering strategies: Consensus-based recommendations from EAS and EFLM (2020) · cites this paper as [33]
The Monogenic hypertriglyceridaemia section (page not provided) says patients with monogenic disorders and triglycerides >10 mmol/L usually do not develop premature atherosclerosis, probably because chylomicrons cannot traverse the vascular endothelial barrier. The Introduction also identifies severe hypertriglyceridaemia as a risk factor for acute pancreatitis. The claim extends the atherosclerosis finding to patients with severe hypertriglyceridaemia and chylomicronemia syndrome generally; the source makes it specifically about monogenic disorders. (LLM, conf=0.86)
Experimental — accuracy not yet measuredSevere hypertriglyceridemia (≥500 mg/dL) is associated with serious non-cardiovascular complications, including non-alcoholic fatty liver disease, steatohepatitis, and acute pancreatitis.
“Furthermore, severe hypertriglyceridemia (≥ 500 mg/dL) is associated with serious non-cardiovascular complications, including non-alcoholic fatty liver disease, steatohepatitis, and acute pancreatitis [11, 12].”
From The Efficacy and Safety of Plozasiran on Lipid Profile in Dyslipidemic Disorders: A Systematic Review and Meta-Analysis (2026) · cites this paper as [12]
The Introduction and the Management section identify severe hypertriglyceridaemia as a risk factor for acute pancreatitis, but define severe as >10 mmol/L (>885 mg/dL), not ≥500 mg/dL. The Secondary causes section describes non-alcoholic fatty liver disease as a factor associated with increased risk of hypertriglyceridaemia, not as its complication; no passage found supports steatohepatitis as a complication. Page numbers were unavailable in our copy. (LLM, conf=0.89)
Experimental — accuracy not yet measured
In patients with mild-to-moderate hypertriglyceridemia, defined as 2-10 mmol/L, elevated baseline and on-treatment apoB helps identify the atherogenic dyslipidemia related to remnant lipoproteins combined with small dense LDL particles that is not reflected by LDLC and non-HDLC.
“In patients with mild-to-moderate hypertriglyceridemia, defined as 2-10 mmol/L [33], elevated baseline and on-treatment apoB helps identify the atherogenic dyslipidemia related to remnant lipoproteins combined with small dense LDL particles that is not reflected by LDLC and non-HDLC.”
From Quantifying atherogenic lipoproteins for lipid-lowering strategies: Consensus-based recommendations from EAS and EFLM (2020) · cites this paper as [33]
In patients with mixed hyperlipidemias, routine genetic testing is not warranted.
“In patients with mixed hyperlipidemias, routine genetic testing is not warranted [33].”
From Quantifying atherogenic lipoproteins for lipid-lowering strategies: Consensus-based recommendations from EAS and EFLM (2020) · cites this paper as [33]
Chylomicrons and large VLDLs probably do not traverse the vascular endothelial barrier.
“probably because chylomicrons and large VLDLs do not traverse the vascular endothelial barrier [33].”
From Quantifying atherogenic lipoproteins for lipid-lowering strategies: Consensus-based recommendations from EAS and EFLM (2020) · cites this paper as [33]
Patients with severe hypertriglyceridemia ≥10 mmol/L and chylomicronemia syndrome have high risk of acute pancreatitis.
“For example, patients with severe hypertriglyceridemia ≥10 mmol/L and chylomicronemia syndrome have high risk of acute pancreatitis but usually do not develop premature atherosclerosis, probably because chylomicrons and large VLDLs do not traverse the vascular endothelial barrier [33].”
From Quantifying atherogenic lipoproteins for lipid-lowering strategies: Consensus-based recommendations from EAS and EFLM (2020) · cites this paper as [33]
Extreme elevations of plasma triglyceride levels above 10 mmol/L increase the risk for acute pancreatitis.
“Extreme elevations of plasma TG levels (>10 mmol/L or >880 mg/dL) increase the risk for acute pancreatitis10–13”
Triglyceride levels above 10 mmol/L confer a high risk of pancreatitis, with risk increasing significantly when triglyceride levels are above 20 mmol/L.
“TG levels >10 mmol/L (>880 mg/dL) confer a high risk of pancreatitis with the risk increasing significantly when TG levels are >20 mmol/L.”
Plasma triglyceride levels range from 0.33 to 120 mmol/L, reflecting variability in the rates of secretion and clearance of triglyceride and apoB in VLDL and chylomicrons.
“Plasma TG levels range from 0.33 to 120 mmol/L (30 to 10 000 mg/dL)13,17 (Figure 6), reflecting variability in the rates of secretion and clearance of TG and apoB in VLDL and chylomicrons.61,77”
Heterozygous loss-of-function mutations have also been identified in some patients with polygenic severe hypertriglyceridaemia.
“Heterozygous LOF has also been identified in some patients with polygenic severe hypertriglyceridaemia.13,57”
High plasma TG levels meeting mild-to-moderate hypertriglyceridemia strongly enhance the risk of cardiovascular disease.
“High plasma TG levels that meet the definition of mild-to-moderate hypertriglyceridemia (2–10 mmol/L [175–885 mg/dL]) strongly enhance the risk of cardiovascular (CV) disease [1, 2].”
Doses of about 2-4 g of prescription-grade OM3FAs reduce plasma TG levels by about 30%.
“Doses of about 2–4 g of prescription-grade OM3FAs, mainly containing eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), reduce plasma TG levels by about 30% and are indicated for prevention of pancreatitis in patients with severe hypertriglyceridemia [1, 3].”
Mendelian randomization studies indicate a direct causal relationship between TG-rich lipoproteins and coronary heart disease.
“However, Mendelian randomization studies indicate a direct causal relationship between TG-rich lipoproteins and coronary heart disease [1, 2].”
Hypertriglyceridaemia prevalence is approximately 10% in the adult population, with considerable interregional variation.
“Its prevalence is ∼10% in the adult population with considerable interregional variation.1–5”
From Clinical review on triglycerides (2020) · cites this paper as [2]
Elevated TG is frequently associated with pathological HDL particles that may contribute to ASCVD risk.
“In addition, elevated TG is frequently associated with pathological high-density lipoprotein (HDL) particles that may contribute to ASCVD risk.2”
From Clinical review on triglycerides (2020) · cites this paper as [2]
The graded intervention approach in Table 5 is based on evidence from multiple meta-analyses and randomized controlled trials showing consistent and graded reduction in atherosclerotic cardiovascular disease risk with reductions in total cholesterol and LDL-C.
“This graded approach is based on evidence from multiple meta-analyses and individual randomized controlled trials (RCTs), which show a consistent and graded reduction in ASCVD risk in response to reductions in TC and LDL-C levels (see Recommendations for cardiovascular disease risk estimation below) [31-41].”
From 2019 ESC/EAS guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk (2019) · cites this paper as [36]
The greater the absolute LDL-C reduction, the greater the reduction in cardiovascular risk.
“the greater the absolute LDL-C reduction, the greater the CV risk reduction [35,36,50,115].”
From 2019 ESC/EAS guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk (2019) · cites this paper as [36]
The absolute benefit of statin treatment was lower in primary prevention populations, who are typically at lower risk.
“The absolute benefit from statin treatment was lower in people in primary prevention, who are typically at lower risk [36,38,214,215].”
From 2019 ESC/EAS guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk (2019) · cites this paper as [36]
In people without a history of vascular disease, statin therapy reduced all-cause mortality by 9% per mmol/L LDL-C reduction.
“In those without a history of vascular disease, statin therapy reduced the risk of all-cause mortality by 9% per mmol/L reduction in LDL cholesterol.”
From 2019 ESC/EAS guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk (2019) · cites this paper as [36]
In the CTT meta-analysis of low-risk vascular disease, the relative risk reduction of major vascular events per mmol/L LDL-C reduction was at least as large in low-risk individuals, i.e. in primary prevention.
“In the CTT meta-analysis of treatment in people with a low-risk of vascular disease [36], the relative risk reduction of major vascular events per mmol/L reduction in LDL-C was at least as large in low-risk individuals (i.e. in primary prevention).”
From 2019 ESC/EAS guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk (2019) · cites this paper as [36]
The overall benefit of statins on other stroke subtypes greatly outweighs the small and uncertain hazard of haemorrhagic stroke.
“Note, however, that the overall benefit on other stroke subtypes greatly outweighs this small (and uncertain) hazard [34,36].”
From 2019 ESC/EAS guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk (2019) · cites this paper as [36]
Statin therapy may yield a small increase in the risk of haemorrhagic stroke, but the evidence regarding this risk is uncertain.
“Statin therapy may yield a small increase in the risk of haemorrhagic stroke, but the evidence regarding this risk is uncertain [34,36,251,252].”
From 2019 ESC/EAS guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk (2019) · cites this paper as [36]
This graded approach is based on evidence from multiple meta-analyses and individual RCTs, which show a consistent and graded reduction in CVD risk in response to reductions in TC and LDL-C levels.
“This graded approach is based on evidence from multiple meta-analyses and individual RCTs, which show a consistent and graded reduction in CVD risk in response to reductions in TC and LDL-C levels. 61-71”
From 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias (2016) · cites this paper as [67]
These trials are consistent in showing that the higher the initial LDL-C level, the greater the absolute reduction in risk, while the relative risk reduction remains constant at any given baseline LDL-C level.
“These trials are consistent in showing that the higher the initial LDL-C level, the greater the absolute reduction in risk, while the relative risk reduction remains constant at any given baseline LDL-C level.”
From 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias (2016) · cites this paper as [67]
With increasing knowledge, the importance of a polygenic background to familial hyperlipidaemias is emphasized.
“With increasing knowledge about common polymorphisms and lipoproteins, the importance of a polygenic background to familial hyperlipidaemias is emphasized. 67,122”
From 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias (2016) · cites this paper as [67]
The genetic aetiology of HTG appears very complex, involving both common and rare genetic variants.
“The genetic aetiology for HTG seems to be very complex, with effects of both common and rare genetic variants. 67,304”
From 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias (2016) · cites this paper as [67]
People with FCS cannot metabolize chylomicron-associated TGs.
“People with FCS cannot metabolize chylomicron-associated TGs. 5”
From Familial chylomicronemia syndrome: Bringing to life dietary recommendations throughout the life span (2018) · cites this paper as [5]
When LPL is functioning, it helps metabolize TGs into free fatty acids through the LPL-dependent pathway.
“When LPL is functioning, it helps metabolize TGs into free fatty acids through the LPL-dependent pathway.5”
From Familial chylomicronemia syndrome: Bringing to life dietary recommendations throughout the life span (2018) · cites this paper as [5]
Triglyceride levels in individuals with FCS are often 10-fold to 100-fold or more above normal (<150 mg/dL) and may range from 1500 to 15,000 mg/dL or higher.
“Triglyceride (TG) levels in individuals with FCS are often 10-fold to 100-fold or more above normal (,150 mg/dL) and may range from 1500 to 15,000 mg/ dL or higher.4,5”
From Familial chylomicronemia syndrome: Bringing to life dietary recommendations throughout the life span (2018) · cites this paper as [5]
The importance of a polygenic background to familial hyperlipidaemias is emphasized with increasing knowledge.
“With increasing knowledge about common polymorphisms and lipoproteins, the importance of a polygenic background to familial hyperlipidaemias is emphasized.67,122”
From 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias (2016) · cites this paper as [67]
For reduction of triglycerides, more advice comes from lifestyle changes such as sugar and the Mediterranean diet.
“For the reduction of TG, more advice comes from changes in lifestyle, such as sugar and the Mediterranean diet [12, 13].”
From Effects of aerobic exercise on lipids and lipoproteins (2017) · cites this paper as [12]
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“Furthermore, severe hypertriglyceridemia (≥ 500 mg/dL) is associated with serious non-cardio - vascular complications, including non-alcoholic fatty liver disease, steatohepatitis, and acute pancreatitis [11, 12].”
Hypertriglyceridemia and pancreatitis in a patient with apolipoprotein E7 (p.[E244K; E245K])/E4
Arai, M., Nishimura, A., Mori, Y., Ebara, T., & Okubo, M. (2014) · Clinica Chimica Acta · doi:10.1016/j.cca.2014.06.001 · Cited by 2 · see citing works
Dietary Interventions for Hypertriglyceridemia
Kirkpatrick, C. F., Petersen, K. S., Kris-Etherton, P. M., & Maki, K. C. (2026) · Current Atherosclerosis Reports · doi:10.1007/s11883-026-01444-w
- Authors
- Hegele, R. A., Ginsberg, H. N., Chapman, M. J., Nordestgaard, B. G., Kuivenhoven, J. A., Averna, M., Borén, J., Bruckert, E., Catapano, A. L., Descamps, O. S., Hovingh, G. K., Humphries, S. E., Kovanen, P. T., Masana, L., Pajukanta, P., Parhofer, K. G., Raal, F. J., Ray, K. K., Santos, R. D., Stalenhoef, A. F. H., Stroes, E., Taskinen, M.-R., Tybjærg-Hansen, A., Watts, G. F., & Wiklund, O.
- Affiliations
- Western University (CA)
- Columbia University (US)
- Inserm (FR)
- University of Copenhagen (DK)
- University Medical Center Groningen (NL)
- University of Palermo (IT)
- University of Gothenburg (SE)
- University of Milan (IT)
- Hôpital de Jolimont (BE)
- Amsterdam UMC Location University of Amsterdam (NL)
- University College London (GB)
- Wihuri Research Institute (FI)
- Institut de Recerca Biomèdica Catalunya Sud (ES)
- University of California, Los Angeles (US)
- Ludwig-Maximilians-Universität München (DE)
- University of the Witwatersrand (ZA)
- St George's Hospital (GB)
- Universidade de São Paulo (BR)
- Radboud University Medical Center (NL)
- University of Helsinki (FI)
- The University of Western Australia (AU)
- Sahlgrenska University Hospital (SE)
- ORCID
- Hegele, Robert A
- Ginsberg, Henry N
- Chapman, M John
- Nordestgaard, Børge G
- Kuivenhoven, Jan Albert
- Averna, Maurizio
- Borén, Jan
- Catapano, Alberico L
- Descamps, Olivier S
- Hovingh, G Kees
- Humphries, Steve E
- Kovanen, Petri T
- Masana, Luis
- Pajukanta, Päivi
- Parhofer, Klaus G
- Raal, Frederick J
- Ray, Kausik K
- Santos, Raul D
- Stroes, Erik
- Taskinen, Marja-Riitta
- Watts, Gerald F
- Wiklund, Olov
- Venue
- The Lancet Diabetes & Endocrinology
- Publisher
- Elsevier BV
- Published
- 2014-08
- Volume
- 2
- Issue
- 8
- Pages
- 655-666
- ISSN
- 2213-8587 (ISSN-L)
- PMC
- PMC4201123
- OpenAlex
- W2125012558
- Semantic Scholar
- c1ba145b0d21fd14d5d928afc61bbde5b3da6e55
- Cited by
- 635
- References
- 69
- Citations by year
- 2026: 39 · 2025: 38 · 2024: 46 · 2023: 48 · 2022: 63 · 2021: 60 · 2020: 61 · 2019: 60 · 2018: 43 · 2017: 55 · 2016: 54 · 2015: 47 · 2014: 18 · 2013: 2 · 2012: 1
- FWCI
- 6.89
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Lancet Diabetes & Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (publishedVersion)
- PubMed Central (acceptedVersion)
- Nova Science Publishers (Nova Science Publishers, Inc.) (submittedVersion, other-oa)
- UWA Profiles and Research Repository (UWA) (submittedVersion, other-oa)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Pure Amsterdam UMC (submittedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (submittedVersion)
- Radboud Repository (Radboud University) (submittedVersion)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (submittedVersion)
- Funders
- Canadian Institutes of Health Research (CTP-79853, MOP-13430, MOP-79523)
- Heart and Stroke Foundation of Canada (NA-6059, PRG-4854, T-6018)
- Western University
- Novartis
- European Atherosclerosis Society
- F. Hoffmann-La Roche
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
- Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Keywords
- hypertriglyceridemia, polygenic inheritance, polygenic risk score, autosomal recessive mutation, triglyceride-rich lipoproteins, familial aggregation, genetic counseling, pancreatitis risk, cardiovascular risk, pharmacotherapy, lifestyle management
- MeSH terms
- Animals, Combined Modality Therapy, Health Promotion, Humans, Life Style, Triglycerides, Hypertriglyceridemia, Biomarkers, Practice Guidelines as Topic, Genetic Predisposition to Disease, Multifactorial Inheritance
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