Fats

TL;DR. Fat is a family, not a substance, and the members behave very differently. Two fatty acids are essential and you will die without them. Trans fats from industrial hydrogenation are the one dietary component with an unambiguous case for elimination, and they have largely been eliminated. Saturated fat is the long-running argument: replacing it with polyunsaturated fat lowers heart disease risk in the trials, replacing it with refined carbohydrate does not, and that nuance is where most of the public confusion lives. Dietary cholesterol turned out to matter much less than assumed for most people, which is why egg guidance changed.

Key takeaways

• Two essential fatty acids: linoleic acid (omega-6) and alpha-linolenic acid (omega-3). Everything else your body can make.
• Trans fats are uniquely harmful and have been banned or effectively removed from the food supply in most of the world since around 2018 to 2023.
• What you replace saturated fat with determines the outcome. Polyunsaturated fat lowers cardiovascular risk; refined carbohydrate does not.
• Dietary cholesterol raises blood cholesterol far less than saturated fat does in most people, which is why per-day egg limits were dropped.
• Omega-3 from oily fish has good evidence for triglycerides and moderate evidence for cardiovascular outcomes; supplements have performed worse than the fish in trials.

The chemistry, in the minimum necessary detail

In short: A fat is three fatty acids on a glycerol backbone, and the double bonds in those fatty acids determine everything about how the fat behaves.

Dietary fat is mostly triglyceride: a glycerol molecule with three fatty acids attached. A fatty acid is a chain of carbon atoms with a carboxyl group at one end.

Two features of that chain determine everything:

Chain length:

Saturation, meaning how many double bonds the chain contains:

The geometry is the whole story. A double bond in the natural cis configuration puts a kink in the chain, so the molecules cannot stack neatly, so the fat is liquid and its membranes are fluid. Saturated chains are straight, stack tightly, and are solid. Trans double bonds have the hydrogen atoms on opposite sides, which removes the kink, so a trans fat is chemically unsaturated and physically behaves like a saturated one. That is precisely why industry made them.

Omega-3 and omega-6

The "omega" number counts carbons from the far end of the chain to the first double bond. This matters because humans lack the enzymes to put double bonds at the omega-3 or omega-6 positions, which is exactly why those two families are essential.

The conversion of plant ALA into EPA and especially DHA is poor in humans: commonly cited figures are 5 to 10 percent conversion to EPA and under 1 to 5 percent to DHA, with conversion somewhat better in women (an oestrogen effect, presumably related to pregnancy). This is the single most important practical fact for vegan and vegetarian diets, and the answer is algal oil, which is where fish get their DHA in the first place.

What your body does with fat

In short: Fat is the energy store, the membrane material, the hormone precursor, and the carrier for four vitamins.

• Energy storage. 9 kcal per gram, stored nearly water-free, against 4 kcal per gram for glycogen stored with three times its weight in water. A person carrying 15 kg of body fat has around 135,000 kcal of stored energy against roughly 2,000 kcal of glycogen. This density is why we store energy as fat and not as starch.
• Cell membranes. Every cell is bounded by a phospholipid bilayer, and the fatty acid composition of your diet measurably changes membrane fluidity and function.
• Hormone and signal precursors. Cholesterol is the starting material for testosterone, oestrogen, cortisol, aldosterone, and vitamin D. Arachidonic acid and EPA are the precursors of eicosanoids: prostaglandins, thromboxanes, leukotrienes, which govern inflammation, clotting, and pain. This is the pathway that aspirin and ibuprofen block (Chapter 66).
• Absorbing vitamins A, D, E, and K, which require fat in the same meal. A fat-free salad genuinely delivers less of the vitamins in it, and studies adding avocado or oil to salad show several-fold increases in carotenoid absorption.
• Insulation and organ protection.

Trans fats: the settled case

In short: Industrially produced trans fat raises LDL and lowers HDL simultaneously, has no known safe level, and has been removed from most of the world's food supply.

Partial hydrogenation was invented to turn cheap liquid vegetable oil into a solid, shelf-stable fat that behaves like butter or lard. Hydrogen is bubbled through oil over a metal catalyst, and stopping the reaction partway converts some double bonds to the trans configuration. The result was cheap, stable, and excellent for baking and frying, and it went into margarine, shortening, biscuits, pastry, and fried food from the 1950s onward.

The health effects, established through the 1990s, are unusually clear-cut:

• Raises LDL cholesterol (the harmful one).
• Lowers HDL cholesterol (the protective one). Almost nothing else in the diet does both.
• Raises lipoprotein(a), an independent risk factor.
• Promotes inflammation and endothelial dysfunction.
• Meta-analyses associate a 2 percent of energy increase in trans fat with roughly a 20 to 25 percent increase in coronary heart disease risk, which is a large effect for a small intake.

The regulatory response was decisive. Denmark limited industrial trans fat in 2003, the US FDA removed the "generally recognised as safe" status for partially hydrogenated oils in 2015 with compliance by 2018 to 2021, the EU set a 2 percent limit from 2021, and the WHO has driven an elimination programme worldwide. It is one of the most successful public health nutrition interventions ever run, and modelling and observational data attribute substantial reductions in cardiovascular events to it.

Two residual notes. Ruminant trans fats occur naturally in small amounts in dairy and beef, produced by bacteria in the rumen, and at typical intakes they do not appear to carry the same risk. And labelling loopholes persist in some jurisdictions where products under a threshold per serving may declare zero; the tell is "partially hydrogenated oil" in the ingredients list.

Saturated fat: the argument, honestly

In short: Saturated fat raises LDL, LDL causes atherosclerosis, and replacing saturated fat with polyunsaturated fat reduces cardiovascular events. Replacing it with refined carbohydrate does not, which is the source of most of the confusion.

This is the longest-running argument in nutrition and it deserves to be laid out carefully rather than settled by assertion.

What is not in serious dispute:

• Saturated fat intake raises LDL cholesterol relative to unsaturated fat. This is reproducible in controlled feeding studies.
• LDL is causal in atherosclerosis. The evidence from genetics (Mendelian randomisation across many variants), from drug trials across multiple mechanisms, and from familial hypercholesterolaemia is about as strong as causal evidence gets in human biology.
• Randomised trials replacing saturated fat with polyunsaturated fat reduce cardiovascular events. The Cochrane review of reducing saturated fat found about a 17 percent reduction in cardiovascular events, driven by the trials where the replacement was polyunsaturated fat.

What is genuinely contested:

• The replacement determines the result. Substitution analyses consistently show: saturated fat replaced with polyunsaturated fat lowers risk; with monounsaturated fat, probably lowers risk; with whole grains, lowers risk; with refined carbohydrate or sugar, no benefit and possibly harm. Advice to "cut fat" in the 1980s and 90s often produced the last of these, and the resulting low-fat high-sugar products are a fair criticism of how the guidance was implemented.
• Not all saturated fats behave alike. Stearic acid (18 carbons, prominent in cocoa butter) is roughly neutral on LDL because much of it is converted to oleic acid. Lauric, myristic, and palmitic acids raise LDL more.
• The food matters, not just the fatty acid. This is the strongest recent finding. Cheese and yoghurt, despite substantial saturated fat, are not associated with increased cardiovascular risk in cohort studies, and fermented dairy is sometimes associated with lower risk. Processed meat, with similar fatty acids, is consistently associated with higher risk. The food matrix (calcium, fermentation products, protein structure, and what else comes with it) appears to matter, and mechanisms are still being worked out.
• The observational meta-analyses (Siri-Tarino 2010, Chowdhury 2014) that found no association between saturated fat intake and cardiovascular disease are real and were widely reported as an exoneration. The standard critique is that observational studies of a single nutrient cannot identify what it was replaced by, and that measurement error in dietary recall is large. Both the findings and the critique are legitimate.

The current mainstream position, from the WHO, the American Heart Association, and most national bodies: keep saturated fat under about 10 percent of energy, and replace it primarily with unsaturated fat from plants, not with refined carbohydrate. That position is defensible on the trial evidence. Positions substantially more permissive or more restrictive than that require reading past what the trials show.

Coconut oil is worth a paragraph because it is marketed as an exception. It is roughly 80 to 90 percent saturated, mostly lauric acid, and controlled trials show it raises LDL substantially compared with unsaturated oils, more than butter in some studies. The medium-chain triglyceride argument is weak: the MCT research uses purified C8 and C10 fats, while coconut oil's lauric acid (C12) behaves largely like a long-chain fat. It is a fine flavouring ingredient and there is no basis for treating it as a health food.

Dietary cholesterol: the reversal

In short: For most people, dietary cholesterol has a modest effect on blood cholesterol, because the body compensates by making less.

Cholesterol is not a fat; it is a sterol, and it is essential. Your liver makes roughly 1 to 1.5 g a day, several times more than a typical diet supplies. When dietary intake rises, endogenous production falls, which is a homeostatic loop most people's bodies run effectively.

Consequently:

• The US Dietary Guidelines dropped the 300 mg/day limit in 2015, stating that cholesterol is "not a nutrient of concern for overconsumption." Several other national bodies followed.
• Eggs are the food this most affects. Large cohort studies mostly find no association between moderate egg consumption and cardiovascular events in people without diabetes. Findings in people with diabetes are less reassuring and less consistent.
• Roughly a quarter to a third of people are "hyper-responders" whose blood cholesterol does respond noticeably to dietary intake. If your LDL is high and you eat a lot of eggs, it is worth testing the effect of changing that rather than assuming either way.
• Saturated fat still raises LDL more than dietary cholesterol does, which is the reason the two were conflated for so long: the foods often overlap.

The lipid panel, decoded

In short: LDL carries cholesterol out to tissues and deposits it in artery walls; HDL carries it back; triglycerides are circulating fat.

Cholesterol does not dissolve in blood, so it travels in lipoproteins, particles with a fat core and a protein shell.

Two corrections worth making. "Good and bad cholesterol" is a simplification that has aged badly for HDL: raising HDL with drugs (CETP inhibitors, niacin) has repeatedly failed to reduce events in trials, so high HDL appears to be a marker of something healthy rather than a cause of it. Triglycerides respond dramatically to alcohol, sugar, and refined carbohydrate, far more than to dietary fat, which surprises people.

Omega-3 and omega-6, and the ratio argument

In short: Omega-3 from oily fish has solid evidence for triglycerides and reasonable evidence for cardiovascular events; the popular omega-6-is-inflammatory argument is not well supported.

The established benefits of marine omega-3 (EPA and DHA):

• Triglyceride lowering, dose-dependent and substantial at prescription doses (2 to 4 g a day can reduce triglycerides by 25 to 30 percent).
• DHA is structurally essential in retina and brain, and required in pregnancy and infancy for neural development.
• Cardiovascular outcomes: eating oily fish is consistently associated with lower cardiovascular mortality in cohorts. Supplement trials have been mixed: several large ones (VITAL, ASCEND) found no benefit for primary prevention, while REDUCE-IT found a substantial reduction using high-dose purified EPA (icosapent ethyl) in high-risk patients, though its mineral oil placebo has been criticised. The honest summary: eat the fish; supplements are a weaker substitute with an unsettled evidence base.
• Anti-inflammatory effects, modest joint symptom benefit in rheumatoid arthritis.

The omega-6 argument. A widely repeated claim holds that modern diets have an omega-6-to-omega-3 ratio of 15:1 or 20:1 against an ancestral 1:1 to 4:1, that omega-6 is pro-inflammatory because arachidonic acid makes inflammatory eicosanoids, and that seed oils are therefore harmful.

The evidence does not support the strong version:

• Increasing dietary linoleic acid does not measurably raise arachidonic acid in human tissue, because the conversion is tightly regulated.
• Controlled trials of increased linoleic acid do not show increases in inflammatory markers.
• Cohort studies find higher linoleic acid intake, and higher linoleic acid measured in blood or tissue (which avoids dietary recall error), associated with lower cardiovascular risk and lower type 2 diabetes risk.
• Major bodies, including the American Heart Association after a formal advisory review, conclude that omega-6 polyunsaturated fat lowers cardiovascular risk when it replaces saturated fat.

What is fair to say: increasing omega-3 is more clearly beneficial than reducing omega-6, and the two are not equivalent levers. The seed oil panic that circulates online substantially exceeds the evidence. What is genuinely true is that seed oils are the fat in most fried and ultra-processed food, so intake correlates with a dietary pattern that is bad for other reasons, and heavily reused frying oil does accumulate harmful oxidation products (Chapter 91).

Cooking fats and smoke points

In short: Match the fat to the temperature, prefer stable fats for high heat, and never reuse oil that has darkened or smells acrid.

Smoke point matters less than oxidative stability, which is set by how many double bonds the fat has. Polyunsaturated oils oxidise fastest, producing aldehydes and other compounds associated with harm. This is why flaxseed oil must never be cooked, why oils should be stored dark and cool, and why deep-fry oil should be discarded once it darkens, foams, smokes early, or smells acrid.

Extra virgin olive oil deserves the correction: it is frequently described as unsuitable for cooking, and testing shows it is one of the more stable oils under heat, because its high monounsaturated content and high polyphenol and vitamin E content resist oxidation. It is fine for normal cooking, and using it for deep-frying is mainly a question of cost and flavour.

The bottom line

• Fat is a family. Chain length and double-bond geometry decide how each member behaves.
• Trans fats are the one clearly settled case: harmful at any realistic intake, and successfully removed from most of the world's food supply.
• Saturated fat raises LDL and LDL causes atherosclerosis. What you replace saturated fat with decides whether you benefit: unsaturated fat and whole grains yes, refined carbohydrate no.
• Dietary cholesterol matters much less than once believed, because the body compensates. Eggs are fine for most people.
• Eat oily fish for omega-3, or algal oil if you do not eat fish. The seed oil panic is not supported by the trial or biomarker evidence; the omega-3 case is much stronger than the anti-omega-6 case.

Sources and notes

Fatty acid chemistry and metabolism follow standard biochemistry texts. Trans fat effects on lipids and cardiovascular risk follow Mozaffarian et al., New England Journal of Medicine, 2006, and the WHO REPLACE programme documentation. The saturated fat replacement evidence follows the Cochrane review by Hooper et al., 2020, and the substitution analyses of Li, Hu and colleagues. The observational meta-analyses that found no association are Siri-Tarino et al., 2010, and Chowdhury et al., Annals of Internal Medicine, 2014, with their standard critiques. The food matrix argument for dairy follows Astrup and Thorning's work and the 2020 Advances in Nutrition consensus. Coconut oil trials are meta-analysed in Neelakantan et al., Circulation, 2020. Dietary cholesterol guidance follows the 2015 US Dietary Guidelines Advisory Committee report. LDL causality follows the European Atherosclerosis Society consensus statement, Ference et al., European Heart Journal, 2017. Omega-3 trials cited are VITAL, ASCEND, and REDUCE-IT. The omega-6 position follows the American Heart Association advisory, Harris et al., Circulation, 2009, and biomarker analyses by Marklund et al. Oil oxidative stability follows de Alzaa et al., Acta Scientific Nutritional Health, 2018.

Open questions. How much of the apparent neutrality of dairy fat is food matrix and how much is residual confounding is unresolved. The REDUCE-IT result remains contested because of its mineral oil placebo, and whether purified EPA differs meaningfully from mixed omega-3 preparations is not settled.

👉 Next: fibre and the microbiome, the part of your food you cannot digest and cannot do without.