Triglycerides
You want them low: lower triglycerides mean a lighter load on the cardiovascular system.
In depth
Circulating fat in transit. More responsive to carbohydrate load and alcohol than to dietary fat — a counterintuitive fact that makes this a sharper dietary readout than cholesterol.
What drives it
Exports liver fat increases it.
Lipoprotein-metabolism review (Endotext NBK326742) — VLDL is the triglyceride-rich lipoprotein that exports hepatic triglyceride into the circulation, raising plasma triglycerides. NBK326742. VLDL is the vehicle: each particle carries one molecule of apoB-100 plus varying triacylglycerol and cholesteryl ester, and its physiological job is transporting energy from the liver to the periphery — so plasma triglyceride is largely a readout of hepatic export. Causal demonstration: adenoviral mtp overexpression raised hepatic VLDL-triglyceride secretion without changing apoB100 synthesis — more triglyceride loaded into the same number of particles, not more particles. And it only worked on an apoB100 background, and only where hepatic triglyceride or apoB100 was already elevated — the export machinery is substrate-limited, not rate-limited, under normal conditions.
Fat uptake enzyme reduces it.
10.1016/S0022-2275(20)38739-3 — Lipoprotein lipase is the enzyme that hydrolyzes triglyceride out of circulating chylomicrons and VLDL, so raising its activity lowers serum triglyceride. In a double-blind randomized controlled trial of mangiferin (97 completers, overweight adults with hyperlipidemia), serum triglycerides fell while lipoprotein lipase activity rose in the same subjects (doi 10.1038/srep10344). Corroborated preclinically in diabetic rats, where hepatic TC and TG fell as LPL and hepatic lipase rose. doi 10.1016/S0022-2275(20
Stops fat storage increases it.
SREBP-1c lipogenic program — ACC and FAS synthesize fatty acids that are esterified into triglycerides. Li 2011, Cell Metab 13:376. Mouse + HepG2. Same dissociation caveat as above. PMC5835560
The Door The Fat Comes In Through increases it.
The uptake arm of the four-pathway balance, stated by two independent reviews. Copenhagen (PMID 29936596): 'hepatic steatosis is a consequence of lipid acquisitION exceeding lipid disposal, i.e., the uptake of fatty acids and DE novo lipogenesis surpassing fatty acid oxidation and export.' Corroborated by PMID 28428362: 'Hepatic lipid accumulation may be induced by 4 separate mechanisms: (1) increased hepatic uptake of circulating fatty acids, (2) increased DE novo fatty acid synthesis, (3) decreased beta-oxidation and (4) decreased hepatic lipid export.' all four arms are now represented here: uptake (cd36, fatp2), de novo lipogenesis (lipogenesis, srebp), oxidation (fatty-acid β-oxidation, ppara), and export (vldl). Lipid export is fully represented here — `vldl` exists with an inhibitory edge into steatosis. No ingredient in the formulas is graded on VLDL export. PMID 29936596
What it drives
It reduces Heart & blood pressure.
TG/ASCVD causality review 2014, JACC — Mendelian-randomization evidence supports triglyceride-rich lipoproteins as a causal contributor to atherosclerotic cardiovascular disease; their remnants penetrate the arterial wall and deposit cholesterol in plaques. doi:10.1016/j.jacc.2014.09.042. Mendelian randomization, which is genetic and therefore not confounded by lifestyle: two-sample MR across large European meta-analyses gives odds ratios for total triglycerides of 1.25 (95% CI 1.13-1.38) for coronary heart disease and 1.24 (1.11-1.38) for myocardial infarction. UK Biobank MR separately finds remnant cholesterol and triglycerides causally associated with progression from a first cardiometabolic disease to multimorbidity. Mechanism: chylomicron and VLDL remnants rapidly penetrate the arterial wall and deposit cholesterol into lesions. Three things that must travel with this number. (1) it is not settled: causality between plasma triglycerides and atherosclerotic disease remains controversial after more than four decades, and the two landmark randomized trials — strength and reduce-it — reported conflicting results. (2) the effect may not survive adjustment: the triglyceride-CHD association diminished to null when adjusted for HDL-C, and the authors draw the practical conclusion themselves — A treatment targeting a triglyceride pathway that does not also raise HDL-C may not be beneficial. Lowering the number is not the same as lowering the risk. (3) APO B is the stronger target: in the same MR, apolipoprotein B raised CHD and MI risk by 44 and 41 percent versus 25 and 24 for triglycerides — particle number beats particle content. And the effect is disease-specific: triglycerides were causal for CHD and MI but not for ischemic stroke. doi 10.1016/j.jacc.2014.09.042.
It increases Clears liver fat.
Named across five reviews of the cardiovascular-renal-hepatic-metabolic syndrome as part of the shared mechanism set: ectopic fat accumulation triggered by metabolic reprogramming, oxidative stress and inflammation induced by energy overload, modified lipids, UREMIC toxins, and senescence, as well as insulin resistance pathways activated by pro-inflammatory factors and lipotoxic products, collectively exacerbate simultaneous hepatic and renal injury. doi 10.1038/s41581-026-01066-0 · PMC11725408
It reduces Lowers cholesterol.
insulin, fasting insulin, type 2 diabetes and blood lipids share one literature: heart, kidney, liver, and metabolic diseases share interlinked pathological mechanisms, including inflammation, oxidative stress, insulin resistance, and endothelial health issues. These four overlap by nature: fasting insulin is the level, insulin is the signaling, type 2 diabetes is the diagnosis and blood lipids are the substrate. The same driver legitimately reaches all four, and a reader should not mistake four arrows for four independent findings. doi 10.1038/s41581-026-01066-0 · PMC11725408
Blends that modulate it
Each blend page names this pathway and carries the study behind its claim.
See it on the map
Open the causal map to follow this pathway upstream and downstream, arrow by arrow, each with its study.