From Cod Liver Oil to EPA and DHA: Who Found Omega-3s and When

Omega-3 supplements did not start as omega-3 supplements. Cod liver oil was a remedy for rickets long before EPA entered the record in 1970s Greenland studies. This history follows the trials and the Eastern texts.

**Jump to:** [Eastern medicine](#eastern-medicine-what-the-texts-record) | [Greenland studies](#where-the-fats-were-named) | [Trials](#the-first-large-trial-gissi-prevenzione) | [Global positions](#global-positions-side-by-side) | [FAQ](#frequently-asked-questions) ## The short version Omega-3 supplements did not start as omega-3 supplements. The fish-derived remedy with the fullest Western record is cod liver oil. For generations it was prescribed for a range of complaints before anyone could name the fats in it. A 2019 historical review in PubMed says cod liver oil had been used since 1700 as a nonspecific treatment for a range of diseases, and that occasional papers before 1900 pointed to its efficacy for rickets ([According to PubMed, Hernigou and colleagues, 2019](https://doi.org/10.1007/s00264-019-04288-z)). EPA and DHA, the two fats the modern label is named for, entered the research record in the 1970s. EPA appears by name in a 1978 Lancet paper by Danish researchers who had studied the blood fats of Greenland Inuit. This article runs two threads. The Western thread goes from cod liver oil to the Greenland studies, the Japanese trials and the present-day regulatory positions. The Eastern thread covers traditional medical texts. Historical uses are reported as history, not as evidence for use today. ## Where the omega-3s come from Fish do not make the omega-3s they carry. The US National Institutes of Health Office of Dietary Supplements says that DHA and EPA are originally synthesized by microalgae at the base of the marine food chain, and that fish acquire them as they move up the food chain ([NIH ODS, Omega-3 Fatty Acids](https://ods.od.nih.gov/factsheets/Omega3FattyAcids-HealthProfessional/)). The same fact sheet says the omega-3 content of fish varies widely. Cold-water fatty fish such as salmon, mackerel, tuna, herring and sardines contain high amounts. Bass, tilapia, cod and shellfish contain less. Cod liver oil is a different product from the oil in a fillet. The rickets story belongs to the liver oil and its vitamin D, which is a separate thread from the omega-3 fats. A 2022 review by Miller and Imel identifies vitamin D3 as the antirachitic agent in cod liver oil ([According to PubMed, Miller and Imel, 2022](https://doi.org/10.1159/000527011)). ## Eastern medicine: what the texts record Donguibogam, a Korean medical text by Dr. Heo Jun, was published in 1613. A 2016 review in PubMed says the distinctive system of traditional Korean medicine was established shortly after the book appeared, and that UNESCO registered the book on its cultural heritage list in 2009 ([According to PubMed, Song, Won and Kim, 2016](https://doi.org/10.3831/KPI.2016.19.002)). We have found no documented medical use of fish oil or fish liver in the Eastern texts reviewed here. ## Cod liver oil and rickets Rickets is the disease that gave cod liver oil its clinical record. Hernigou and colleagues write that cod liver oil was first proposed as a medicine for rickets in Northern Europe at the end of the eighteenth century. They say the link between rickets and nutritional deficiency was suspected and then demonstrated between 1880 and 1915 ([According to PubMed, Hernigou and colleagues, 2019](https://doi.org/10.1007/s00264-019-04288-z)). Their review describes a 1930s public health campaign that used irradiated ergosterol from yeast to enrich milk and other foods with vitamin D, and says that campaign succeeded in eradicating rickets. They also note that rickets was first recognized as a disease of urban living people. Miller and Imel give the parallel track. Sniadecki first advocated treatment by exposure to sunshine in 1822. Contemporaneously, several British physicians advocated cod liver oil, and the review says both approaches were successful ([According to PubMed, Miller and Imel, 2022](https://doi.org/10.1159/000527011)). Work in 1924 showed that exposure to ultraviolet light gave fats and other foods antirachitic properties. The review also states that vitamin D3, the antirachitic agent in cod liver oil, was produced by ultraviolet radiation of 7-dehydrocholesterol. ## Where the fats were named The research that named EPA started in Greenland, with a plasma study and a diet study by Danish researchers. Four papers from that work are indexed in PubMed. A 1971 Lancet report by Bang, Dyerberg and Nielsen is titled "Plasma lipid and lipoprotein pattern in Greenlandic West-coast Eskimos" ([According to PubMed, Bang and colleagues, 1971](https://doi.org/10.1016/s0140-6736(71)91658-8)). In 1975, Dyerberg, Bang and Hjorne reported the fatty-acid composition of plasma lipids in 130 Greenland Eskimos. They compared them with 32 Greenland Eskimos living in Denmark and 31 Caucasian Danes. The Greenland group had a much higher proportion of palmitic, palmitoleic and timnodonic acids, and markedly lower linoleic acid. Their total polyunsaturated fatty acid concentration was lower than in the other groups ([According to PubMed, Dyerberg, Bang and Hjorne, 1975](https://doi.org/10.1093/ajcn/28.9.958)). The authors noted that an earlier study had found markedly lower plasma lipid levels in Greenland Eskimos than in Western populations, and that coronary atherosclerosis seemed far less common among them. They found these observations hard to combine with their fatty-acid results, and suggested the difference might be qualitative rather than quantitative. In 1978, Dyerberg, Bang, Stoffersen, Moncada and Vane published "Eicosapentaenoic acid and prevention of thrombosis and atherosclerosis?" in The Lancet. They reported that EPA did not induce platelet aggregation in human platelet-rich plasma. They noted that Eskimos had high EPA levels, low arachidonic acid levels, a low incidence of myocardial infarction and a tendency to bleed. They wrote that dietary enrichment with EPA might protect against thrombosis ([According to PubMed, Dyerberg and colleagues, 1978](https://doi.org/10.1016/s0140-6736(78)91505-2)). ## What the Greenland studies did and did not show The Greenland work found something real. The fatty-acid pattern in plasma and diet differed sharply from Danish patterns, and the traditional diet was built on seal and fish. In 1980, Bang, Dyerberg and Sinclair analyzed diets collected from 50 adults in the winter of 1976. Seal and fish were the predominant foods. The ratio of polyunsaturated to saturated fatty acids was 0.84 in the Eskimo diets, against 0.24 in Danish diets. The authors wrote that the rarity of ischemic heart disease in Greenland Eskimos "may partly be explained" by the antithrombotic effect of long-chain polyunsaturated fatty acids, especially eicosapentaenoic acid ([According to PubMed, Bang and colleagues, 1980](https://doi.org/10.1093/ajcn/33.12.2657)). What the studies did not show matters just as much. The four papers above are observational or laboratory studies. Their abstracts describe population blood and diet measurements and platelet tests in the laboratory, and they frame a protective effect as a possibility. The step from "this population has a distinctive fat profile" to "this fat protects the heart" needed trials. The first large trial discussed here, GISSI-Prevenzione, was published in 1999. ## Burr and Burr, 1929 George and Mildred Burr published "A new deficiency disease produced by the rigid exclusion of fat from the diet" in the Journal of Biological Chemistry in 1929, volume 82, pages 345 to 367. The DOI is . PubMed indexes a 1973 reprint of the paper in Nutrition Reviews under the same title ([According to PubMed, Burr and Burr, 1973](https://doi.org/10.1111/j.1753-4887.1973.tb06008.x)). A 2012 commentary in the same journal, "Essential fatty acids: the work of George and Mildred Burr," lists both the 1929 paper and the Burrs' 1930 paper, "On the nature and role of the fatty acids essential in nutrition," volume 86, pages 587 to 621 ([According to PubMed, 2012](https://doi.org/10.1074/jbc.O112.000005)). The 1929 title names the condition: a deficiency disease produced by excluding fat from the diet. The 1930 title turns to the fatty acids themselves. The modern omega-3 answer is narrower, and it appears in the US section below. ## Japan: EPA ethyl ester from Mochida The Japanese EPA story also has a drug-development thread. Mochida Pharmaceutical's Fuji Central Research Laboratory in Shizuoka reported in 1995 that ethyl EPA (EPA-E), given to cholesterol-fed rabbits, decreased total cholesterol in the very-low-density and intermediate-plus-low-density lipoprotein fractions ([According to PubMed, Yano and colleagues, 1995](https://doi.org/10.1248/yakushi1947.115.10_843)). In 2022, Mochida researchers reported a 12-week phase 3 trial of MND-2119, a self-emulsifying formulation of highly purified EPA-E that can be taken once daily. In people with high triglycerides, its triglyceride reduction at 2 g a day was non-inferior to EPA-E at 1.8 g a day. The abstract states that in Japan EPA-E is taken twice or three times a day for dyslipidemia ([According to PubMed, Mori and colleagues, 2022](https://doi.org/10.1016/j.jacl.2022.06.007)). In 2025, a 12-week phase 3 trial in China tested MND-21, a highly purified ethyl icosapentate soft capsule, in people with severe hypertriglyceridemia. Triglycerides fell by a mean of 18.38% at the 3,600 mg dose, against 8.11% on placebo (P = .049). One of the trial's authors is a clinical research author at Mochida Pharmaceutical, and the abstract says MND-21 has not yet been approved for severe hypertriglyceridemia ([According to PubMed, Wang and colleagues, 2025](https://doi.org/10.1016/j.jacl.2025.12.007)). A 2020 PubMed-indexed survey of Japanese pharmacists names Epadel among the EPA/DHA products that patients used when they had adverse events ([According to PubMed, Chiba and colleagues, 2020](https://doi.org/10.1248/yakushi.19-00256)). ## The first large trial: GISSI-Prevenzione The first large trial discussed here is GISSI-Prevenzione. It was published in The Lancet in 1999 under the title "Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after myocardial infarction" ([PubMed record](https://pubmed.ncbi.nlm.nih.gov/10465168/)). The trial enrolled 11,324 patients who had survived a recent heart attack, within three months of the event. They were randomly assigned to n-3 polyunsaturated fatty acids at 1 g a day, vitamin E at 300 mg a day, both, or neither, for 3.5 years. According to PubMed, the n-3 group had a 10% relative reduction in the primary endpoint of death, non-fatal heart attack and stroke in the two-way analysis (95% CI 1 to 18). The four-way analysis gave 15% (95% CI 2 to 26). The benefit was attributed to fewer deaths, including cardiovascular deaths. Vitamin E showed no benefit. The authors called the n-3 result "clinically important and statistically significant." The people in this trial had already had a heart attack, so the trial does not test prevention in healthy adults. ## Japan: EPA added to statins The Japanese EPA Lipid Intervention Study, known as JELIS, asked a different question. Yokoyama and colleagues randomized 18,645 Japanese patients with total cholesterol of 6.5 mmol/L or higher. One group received 1,800 mg of EPA a day with a statin. The other received a statin alone. Patients were recruited between 1996 and 1999 and followed for five years. The trial's aim was framed around patients in Japan who eat a large amount of fish ([According to PubMed, Yokoyama and colleagues, 2007](https://doi.org/10.1016/S0140-6736(07)60527-3)). At a mean follow-up of 4.6 years, the primary endpoint of major coronary events occurred in 2.8% of the EPA group and 3.5% of the controls, a 19% relative reduction (p=0.011). Sudden cardiac death and coronary death did not differ between the groups. In patients with a history of coronary artery disease, major coronary events were reduced by 19% (8.7% against 10.7%, p=0.048). In the subgroup without that history, the 18% reduction was not statistically significant (p=0.132). The authors call EPA "a promising treatment" for prevention of major coronary events, especially non-fatal coronary events, in Japanese patients with high cholesterol. The trial was randomized and open-label, with a blinded endpoint analysis, as its title says. ## Cognition: a 24-month trial in England and Wales Dangour and colleagues tested cognition in older people. They randomized 867 cognitively healthy adults aged 70 to 79, recruited through 20 general practices in England and Wales. The active group took daily capsules providing 200 mg of EPA and 500 mg of DHA. The control group took olive oil, and the intervention lasted 24 months ([According to PubMed, Dangour and colleagues, 2010](https://doi.org/10.3945/ajcn.2009.29121)). Serum EPA and DHA rose in the active group. The primary outcome was the California Verbal Learning Test. Cognitive scores did not change over 24 months, and the analysis showed no significant difference between the arms on the primary or any secondary cognitive outcome. The authors wrote that the lack of decline in the control arm and the relatively short intervention period may have limited their ability to detect an effect. That is the authors' caveat, not a finding that the supplement works. ## 2018 and 2019: two large trials, two results REDUCE-IT tested icosapent ethyl, a highly purified EPA ethyl ester, in 8,179 patients who were taking statins and had fasting triglycerides of 135 to 499 mg/dL. Participants received 2 g twice a day, or placebo. The trial was published online in 2018 and appears in volume 380 of the New England Journal of Medicine ([According to PubMed, Bhatt and colleagues, 2018](https://doi.org/10.1056/NEJMoa1812792)). The primary composite endpoint occurred in 17.2% of the icosapent ethyl group and 22.0% of the placebo group (hazard ratio 0.75; 95% CI 0.68 to 0.83). The record also reports more hospitalizations for atrial fibrillation or flutter in the icosapent ethyl group, at 3.1% against 2.1%. Serious bleeding occurred in 2.7% against 2.1%, with a reported P value of 0.06. The trial was funded by Amarin Pharma. VITAL tested marine n-3 fatty acids at 1 g a day, in a factorial design that also tested vitamin D. It enrolled 25,871 adults in the United States: men aged 50 and older and women aged 55 and older. The n-3 group had 386 major cardiovascular events against 419 on placebo (hazard ratio 0.92; 95% CI 0.80 to 1.06). Invasive cancer was not reduced (hazard ratio 1.03). The authors reported a lower rate of total myocardial infarction (hazard ratio 0.72) and no reduction in total stroke (hazard ratio 1.04). Their conclusion was that n-3 fatty acid supplementation "did not result in a lower incidence of major cardiovascular events or cancer than placebo" ([According to PubMed, Manson and colleagues, 2018](https://doi.org/10.1056/NEJMoa1811403)). ## Why the trials disagree The trials do not test the same question. GISSI-Prevenzione tested 1 g a day of n-3 polyunsaturated fatty acids after a heart attack. JELIS tested 1,800 mg a day of EPA with statins in Japanese patients with high cholesterol. REDUCE-IT tested 4 g a day of a purified EPA ethyl ester in statin users with high triglycerides. VITAL tested 1 g a day of marine n-3 in adults at usual risk. The populations, doses and products differ, and so do the outcomes. This article reports each result as measured. It does not rank the trials against each other, and it does not treat any one of them as settling the question for the others. ## Global positions, side by side Each position below gives what the body said and when. The positions are listed by region and are not ranked against each other. **United States.** The NIH Office of Dietary Supplements fact sheet for health professionals says the Institute of Medicine set adequate intakes for omega-3s but no specific intake for EPA, DHA or other long-chain omega-3s. For people aged one and older, the adequate intake applies only to alpha-linolenic acid, which the fact sheet describes as the only essential omega-3 ([NIH ODS, Omega-3 Fatty Acids](https://ods.od.nih.gov/factsheets/Omega3FattyAcids-HealthProfessional/)). The American Heart Association's 2018 science advisory, by Rimm and colleagues, concludes that 1 to 2 seafood meals a week should be included to reduce the risk of congestive heart failure, coronary heart disease, ischemic stroke and sudden cardiac death, especially when seafood replaces less healthy foods. The advisory addresses seafood, not supplements ([According to PubMed, Rimm and colleagues, 2018](https://doi.org/10.1161/CIR.0000000000000574)). **European Union.** EFSA's 2010 opinion on dietary reference values for fats set an adequate intake of 250 mg a day of EPA plus DHA for adults. It set a DHA intake of 100 mg a day for infants over six months and young children under 24 months, and proposed 100 to 200 mg of preformed DHA on top of the adult intake during pregnancy and lactation (EFSA Journal 2010;8(3):1461, https://www.efsa.europa.eu/en/efsajournal/pub/1461). EFSA's 2012 opinion on tolerable upper intake levels found data insufficient to set an upper limit for EPA, DHA or DPA. It said that supplemental EPA plus DHA up to about 5 g a day, and EPA alone up to 1.8 g a day, raise no safety concerns for adults. It noted that dietary recommendations for EPA and DHA based on cardiovascular risk for European adults fall between 250 and 500 mg a day (EFSA Journal 2012;10(7):2815, https://www.efsa.europa.eu/en/efsajournal/pub/2815). **United Kingdom.** The 2004 advice on fish consumption, a joint statement from the Scientific Advisory Committee on Nutrition and the Committee on Toxicity, published for the Food Standards Agency and the Department of Health, endorsed the population recommendation to eat at least two portions of fish a week, one of them oily. It said the same recommendation should apply to pregnant women. It estimated that two portions a week, one white and one oily, contain approximately 0.45 g a day of long-chain n-3 fatty acids (Advice on fish consumption: benefits and risks, 2004, paragraph 1.10, https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/338801/SACN_Advice_on_Fish_Consumption.pdf). **Canada.** Health Canada's Dietary Reference Intakes tables for macronutrients, issued in 2005, set an adequate intake for alpha-linolenic acid of 1.6 g a day for men aged 19 to 30 and 1.1 g a day for women aged 19 to 30. The acceptable macronutrient distribution range for n-3 fatty acids is 0.6% to 1.2% of energy, and a footnote says up to 10% of that range can be consumed as EPA and/or DHA. The table gives no separate reference value for EPA or DHA ([Health Canada, Dietary reference intakes tables: reference values for macronutrients](https://www.canada.ca/en/health-canada/services/food-nutrition/healthy-eating/dietary-reference-intakes/tables/reference-values-macronutrients.html)). **Japan.** The Ministry of Health, Labour and Welfare's Dietary Reference Intakes for Japanese, 2025 edition, published in October 2024, sets one adequate intake for n-3 fatty acids as a group, covering alpha-linolenic acid, EPA and DHA. It is based on median intake. The adult values run from 1.6 to 2.3 g a day by age and sex, and pregnant and lactating women have 1.7 g a day. The Ministry of Agriculture, Forestry and Fisheries summary, updated in January 2025, notes that EPA and DHA come mainly from seafood ([MAFF, Health effects of fats, updated 9 January 2025](https://www.maff.go.jp/j/syouan/seisaku/trans_fat/t_eikyou/fat_eikyou.html)). **Agreement and disagreement.** The UK and EU positions agree on the main point: eat fish, and some of it oily. They differ in units. The UK counts portions, the AHA counts seafood meals, the EU sets an EPA plus DHA amount, Japan sets one combined n-3 amount, and Canada sets an alpha-linolenic acid intake with a footnote for EPA and DHA. The US fact sheet sets an intake for alpha-linolenic acid and none for EPA or DHA. EFSA's 250 to 500 mg a day figure is framed as a dietary recommendation for EPA and DHA, not as a supplement dose. ## Mercury: the caveat on fish Fish advice has a second half. In 2020, Chang and colleagues published an exposure study in Chemosphere on methylmercury in saltwater fish and processed foods eaten in Taiwan. It drew on national survey data from 2005 to 2008. The average estimated intake was 7.9% of the tolerable daily intake for women of child-bearing age, and 13.6% for children. The 95th percentile for consumers only reached 90.4% of the tolerable daily intake in one group and 185% in the other. The highest methylmercury level among the samples was in fried Spanish mackerel. The authors wrote that excessive fish intake may cause health hazards because of methylmercury ([According to PubMed, Chang and colleagues, 2020](https://doi.org/10.1016/j.chemosphere.2020.128249)). The same abstract notes that saltwater fish is rich in EPA and DHA, so the fish that carries the omega-3s also carries the mercury question. ## What the evidence shows now, and where it is disputed Here is the plain reading of the trials above. **Trials that reported fewer events.** GISSI-Prevenzione, in people after a heart attack, with 1 g a day of n-3 polyunsaturated fatty acids. JELIS, in Japanese patients on statins with high cholesterol, with 1,800 mg a day of EPA. REDUCE-IT, in statin users with high triglycerides, with 4 g a day of EPA ethyl ester. **Trials that did not.** VITAL, in adults at usual risk, with 1 g a day of marine n-3. Dangour and colleagues' 24-month cognition trial in healthy older adults. **Disputed: the cause of the difference.** The positive results may belong to EPA alone, to the dose, to the population, or to the statin background. The trials differ on all four, and their designs cannot separate these causes. **Disputed: the safety figures.** REDUCE-IT reported more hospitalizations for atrial fibrillation or flutter in the icosapent ethyl group (3.1% against 2.1%). Its serious bleeding difference had a reported P value of 0.06. Both figures are in the record, and both belong in any honest summary of that trial. **Disputed: how much fish.** The AHA's 1 to 2 seafood meals a week and the Taiwanese exposure figures are two reference points on the table. Both show that species and portion size matter. The AHA figure counts seafood meals, while the Taiwanese study found the highest mercury levels in particular fish. ## What makes this history interesting The omega-3 story runs in reverse from most supplement histories. The fish-derived remedy with the fullest record was prescribed for rickets, and its antirachitic factor is now identified as vitamin D3. The fats now sold under the omega-3 name came from a separate line of work, the Greenland diet and blood studies of the 1970s, which were observational and laboratory studies. Only after that did trials ask whether these fats change clinical outcomes. The answers depend on which fat, which dose and which people were studied, so the same label can describe very different products. ## Bottom line Eat fish, and count the fish. The AHA's 2018 advisory asks for one to two seafood meals a week. The 2004 UK advice asks for at least two portions a week, one of them oily. A supplement is a separate decision. If you are comparing products, read the Supplement Facts panel for EPA and DHA per serving, check the source (fish, krill or algae), and check the serving size. The per-serving numbers are what the bottle actually delivers. ## Next reads For the cardiovascular context of the trials above, see the [heart and blood pressure guide](/health/heart-blood-pressure-complete-guide). For the cognition trial, see the [brain health guide](/health/brain-health-focus-complete-guide). For the rickets and vitamin D thread, see the [vitamin D guide](/health/vitamin-d-complete-guide). ## Frequently asked questions ### How did cod liver oil become the first omega-3 supplement? It did not, in the sense the label now uses. Cod liver oil was a general remedy, and it was proposed for rickets in Northern Europe at the end of the 1700s. Its antirachitic factor is vitamin D3. EPA entered the research record in the 1970s Greenland work and appears by name in the 1978 Lancet paper. ### Who showed that the body needs certain fats from food? George and Mildred Burr's 1929 paper, "A new deficiency disease produced by the rigid exclusion of fat from the diet," describes a deficiency disease produced by excluding fat from the diet. Their 1930 paper concerns the fatty acids essential in nutrition. The modern US answer is narrower: the NIH fact sheet says alpha-linolenic acid is the only omega-3 essential for people aged one and older. ### When were EPA and DHA identified as separate fats? The Greenland papers name EPA. The 1978 Lancet paper uses the name eicosapentaenoic acid (C20:5 omega-3). Later trials, such as Dangour and colleagues' cognition study, treat EPA and DHA as separate components. ### What did the Greenland Inuit studies find, and what did they not show? They found a plasma and diet pattern unlike the Danish one, with seal and fish as the main foods and a high share of n-3 fats. The 1978 authors reported a low incidence of heart attack among Greenland Eskimos and suggested that dietary EPA might protect against thrombosis. The studies did not show that EPA protects the heart. They were observational and laboratory work, and the antithrombotic idea was written as a possibility. ### Where do fish oil supplements come from today? The NIH fact sheet says the omega-3 fats are originally made by microalgae and move up the food chain into fish. It names salmon, mackerel, tuna, herring and sardines among the fish with high omega-3 content. ### Why do omega-3 products differ so much in EPA and DHA? The amounts are set by each product, not by the word omega-3. The Supplement Facts panel gives EPA and DHA per serving, which is the number to compare. REDUCE-IT tested a highly purified EPA ethyl ester, which is a different product from a mixed EPA and DHA fish oil. ### What did the early trials measure, and what did they miss? GISSI-Prevenzione measured death, non-fatal heart attack and stroke after a heart attack. JELIS measured major coronary events in Japanese patients on statins. Dangour and colleagues measured cognitive tests over 24 months. REDUCE-IT and VITAL measured cardiovascular events. The Dangour authors noted that the relatively short intervention period and the lack of decline in the control arm may have limited detection of an effect. None of these trials tested every population, and their doses and products differ, so none answers the others' question. ### Related reading - [Calcium supplements, from chalk to bone trials](/blog/history/history-of-calcium-supplements-from-chalk-to-bone-trials) - [Turmeric, from Ayurveda to isolation](/blog/history/history-of-turmeric-and-curcumin-from-ayurveda-to-isolation) - [Vitamin C, from scurvy to ascorbic acid](/blog/history/history-of-vitamin-c-from-scurvy-to-ascorbic-acid) - [Folate, from Lucy Wills to fortified bread](/blog/history/history-of-folate-from-lucy-wills-to-fortified-bread) - [how cod liver oil led to the vitamin D origin story](/blog/history/history-of-vitamin-d-from-rickets-to-sunshine-vitamin)