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Portrait of Joseph L. Goldstein
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Nobel Prize in Physiology or Medicine · 1985

Joseph L. Goldstein

With Michael Brown he found the LDL receptor, the cell's doorway for cholesterol, explaining inherited heart attacks and how statins work.

The Nobel citation: “for their discoveries concerning the regulation of cholesterol metabolism”
Born
April 18, 1940, Sumter, SC, USA
Shared with
Michael S. Brown
Affiliation at the time
University of Texas Southwestern Medical Center at Dallas, USA

Medicine prize

1985

Shared with 1 other laureate.

Age that year

45years

Born in 1940.

Headline credited impact

85,000–240,000lives saved

Deaths prevented or postponed by statin therapy worldwide (1987-2025). How it was built

Sources cited

29

Fact-checked September 24, 2026.

  • Goldstein and Michael Brown met as medical interns in Boston in 1966 and became bridge partners at the NIH. They have worked together since 1972.
  • By their own count in 2012, their 40-year partnership was the longest scientific collaboration in Nobel history.
  • At the 1985 Nobel banquet he joked that their true 'collaborative age' was 45 times 44, or 1,980 years, surely old enough for the prize.
  • In Seattle he and colleagues found that the common form of familial hypercholesterolemia affects about 1 in 500 people, and 1 in 25 heart attack survivors.
  • A former postdoc in their lab, Thomas Südhof, cloned the LDL receptor gene there and went on to win a Nobel Prize of his own in 2013.

The breakthrough

The LDL receptor: how cells pull cholesterol out of the blood (1973-1974)

Cholesterol is not simply a villain. Every cell needs it to build its outer membrane, and the body makes hormones from it. It travels through the blood packed inside tiny particles called LDL. In 1972 Goldstein and Michael Brown set out to understand familial hypercholesterolemia (FH), an inherited disease in which blood LDL is about twice normal, or six to ten times normal in the rare severe form. In that severe form, children can have heart attacks. Working with skin cells grown in dishes, they found in 1973 that normal cells stop making their own cholesterol when LDL is around, but cells from children with severe FH keep making it. In 1974 they showed why: normal cells have receptors on their surface that grab LDL, and the FH cells lacked them. Think of each receptor as a docking bay. LDL particles dock, that patch of membrane folds inward and carries them inside, and the cell unpacks the cholesterol. The docking bays then return to the surface to be used again. When a cell already has plenty of cholesterol, it builds fewer docking bays, so more LDL stays in the blood, where it can build up in artery walls. This uptake route, called receptor-mediated endocytosis, turned out to be a general way cells take in many substances. It also explained how statins work: by blocking cholesterol production in the liver, they make liver cells build more receptors, which pull LDL out of the blood.[1],[3],[4],[7],[8],[9],[10]

“To them, it was not a question of physiology or medicine. To them, medicine was physiology.”
Joseph L. Goldstein, Speech at the Nobel Banquet, 10 December 1985, describing physician-scientists such as Archibald Garrod, Oswald Avery and Peyton Rous.[5]

What it meant for humanity

Before Goldstein and Brown, doctors knew that high blood cholesterol went with heart attacks, but not how the body controlled it. Their work supplied the missing mechanism. It showed that familial hypercholesterolemia, which affects about 1 in 500 people and accounts for about 5% of heart attacks before age 60, is caused by faulty LDL receptors. By 2009 more than 1,100 different mutations in the receptor gene had been found in patients. The larger effect came through statins. Akira Endo reported the first statin in 1976, and Merck's lovastatin (Mevacor) became the first approved statin in 1987. Brown and Goldstein explained why these drugs lower LDL so well: starving the liver of its own cholesterol makes it build more LDL receptors, which clear LDL from the blood. In 1981 they confirmed this in dogs. In 1994 the 4S trial showed that a statin could prolong life in people with heart disease. Across 26 large trials, each 1 mmol/L cut in LDL cholesterol lowered heart attacks, strokes and procedures to reopen or bypass heart arteries by about a fifth, and deaths from any cause by about a tenth. By 2018 an estimated 173 million people were taking cholesterol-lowering drugs, with statins the most used type. Access is still very uneven: in 41 low- and middle-income countries, only about one in ten people eligible for preventive statins took them. The same receptor biology also pointed to newer drugs. Researchers found that a protein called PCSK9 destroys LDL receptors, and antibodies that block it cut LDL by up to 60% in early trials when added to a statin.

  • Familial hypercholesterolemia, which Goldstein and Brown traced to faulty LDL receptors, affects about 1 in 500 people and accounts for about 5% of heart attacks in people under 60.[4],[7]
  • In 1981 they showed in dogs that a statin raises the number of LDL receptors in the liver, sharply lowering LDL in the blood. They later traced this effect to the SREBP control system they discovered in 1993.[2],[10],[11]
  • Across 26 trials with about 170,000 people, each 1 mmol/L cut in LDL cholesterol lowered heart attacks, strokes and artery-opening procedures by about a fifth, and deaths from any cause by 10%.[12]
  • An estimated 173 million people in 83 countries used cholesterol-lowering drugs in 2018, with statins the most used type. Yet in 41 low- and middle-income countries, only about 1 in 10 people eligible for preventive statins took them.[15],[16]
  • Receptor-mediated endocytosis, the uptake route they described for LDL, proved to be a general way cells take in hormones, enzymes and even some viruses.[4],[7]
  • Their lab trained many scientists. One former postdoc, Thomas Südhof, cloned the LDL receptor gene there and later won the 2013 Nobel Prize in Physiology or Medicine.[24]

Impact in numbers

Goldstein and Brown turned cholesterol from a statistical risk factor into a biological mechanism that doctors could target. The main measurable result is statin therapy, the most used type of cholesterol-lowering drug; an estimated 173 million people took such drugs in 2018. We estimate that statins prevented or postponed roughly 1.7 to 4.8 million deaths from 1987 to 2025. We credit Goldstein with only 5% of that, and Brown with the same, because Akira Endo discovered the first statin, Merck brought the first one to market, and large trials proved statins save lives. We also count a harm: statins cause a small rise in new diabetes diagnoses. Much of their contribution cannot be counted: the concept of receptor-mediated endocytosis, the genetic explanation of familial hypercholesterolemia, the SREBP system that governs how cells make fats and cholesterol, and the receptor biology behind newer PCSK9-blocking drugs. Their lab also trained scientists who made major discoveries of their own.

HealthFundamental science

Each number is the laureate’s credited share of a real-world outcome, cumulative to 2025. The whole outcome, the share of credit, and the reasoning are shown so you can check the arithmetic. Outcomes shared with other laureates are counted once on the impact page.

  • Medium confidenceRippleModeledHealth

    Deaths prevented or postponed by statin therapy worldwide (1987-2025)

    85,000–240,000

    lives saved, credited share

    That is 5% of 1.7–4.8 million lives saved since 1987.

    How this number was built

    Users: Blais et al. estimate 173M people on lipid-lowering drugs in 2018 (83 countries); per-capita use rose ~50% from 2008, so ~110M in 2008. Assume statins are 85%: ~95M (2008), ~147M (2018). Person-years: 1987-2008 ramp from zero = 0.7-1.0B; 2008-18 = 1.2B; 2018-25 = 1.0B (flat) to 1.2B (4%/yr growth). Total 2.9-3.4B. Effect: CTT's 21 statin-vs-control trials had ~12,400 deaths in ~620,000 person-years (~2%/yr) and 10% fewer deaths per ~1 mmol/L LDL cut, about 2 deaths averted per 1,000 person-years. Real-world use (lower risk, doses, adherence): 0.6-1.4. Result 1.76M-4.76M, rounded to 1.7M-4.8M. Check: Grabowski et al. put US deaths averted at ~40,000 in 2008 alone. Share 0.05, same for Brown (0.10 together): Endo found the first statin, Merck brought one to market, and trialists proved statins save lives.[10],[11],[12],[14],[15]

    Sources: Cell (via PubMed Central); Proceedings of the Japan Academy, Series B (via PubMed Central); The Lancet (via PubMed Central); Health Affairs (PubMed record); Atherosclerosis (PubMed record)

  • HarmLow confidenceRippleModeledHealth

    Extra diabetes diagnoses caused by statin therapy worldwide (1987-2025)

    105,000–255,000

    people harmed, credited share

    That is 5% of 2.1–5.1 million people harmed since 1987.

    How this number was built

    Same 2.9-3.4B statin person-years (1987-2025) as the benefit claim (Blais). CTT 2024 individual-patient meta-analysis (19 placebo trials, 123,940 people): in people without diabetes, low/moderate-intensity statins added 1.2 new diagnoses per 1,000 person-years (RR 1.10, placebo 1.2%/yr); high-intensity raised diagnoses 36%, or 4.3 per 1,000 at that 1.2%/yr baseline. MEPS 2008-19: 20% of US statin use was high-intensity (less abroad and earlier, so 5-20%) and 18% of users already had diabetes, so 82% of person-years are at risk. Low: rates cut by a third for real-world dose and adherence, 5% high-intensity: (0.95 x 0.8 + 0.05 x 2.9) x 2.9B x 0.82 = 2.1M. High: (0.8 x 1.2 + 0.2 x 4.3) x 3.4B x 0.82 = 5.1M. CTT: about 62% of new diagnoses were in people already in the top quarter of baseline blood sugar. Share 0.05, matching the benefit claim; Brown gets the same.[15],[28],[29]

    Sources: The Lancet Diabetes & Endocrinology (PMC full text); Saudi Pharmaceutical Journal (PMC full text); Atherosclerosis (PubMed record)

The double edge

Goldstein's own discoveries have no known harmful use, but the statin therapy they helped explain has real, if uncommon, side effects. A 2016 Lancet review by leading trial researchers estimated that treating 10,000 people for five years with a standard statin dose causes about 5 cases of muscle damage (myopathy), 50 to 100 new cases of diabetes and probably 5 to 10 bleeding strokes. The same treatment prevents a heart attack, stroke or artery-opening procedure in 500 to 1,000 of those people. One statin, cerivastatin, was withdrawn worldwide in 2001 after 52 deaths were linked to severe muscle breakdown, which was about 10 times more common with it than with other statins. Many patients also blame statins for muscle aches. The Lancet review was written partly to answer such claims: it concluded that most of these complaints are not caused by the drug, and warned that exaggerated fears lead people at risk to stop treatment. Readers should also know that since 1991 Goldstein, like Brown, has been a director of Regeneron, a drug company that sells a PCSK9-blocking cholesterol drug.

  • Moderate

    Side effects of statins

    Per 10,000 people treated for five years with a standard statin dose, a 2016 Lancet review estimated about 5 cases of myopathy, 50 to 100 new cases of diabetes and probably 5 to 10 bleeding strokes. A 2010 meta-analysis of 13 trials found one extra diabetes diagnosis for every 255 people treated for four years.[13],[17]

  • Moderate

    Cerivastatin withdrawal

    Cerivastatin was withdrawn worldwide in 2001 after it was linked to 52 deaths from rhabdomyolysis, a breakdown of muscle that can cause kidney failure. Risk was highest at the full dose or when taken with the drug gemfibrozil, and this muscle breakdown was about 10 times more common than with other statins.[18]

  • Minor

    Dispute over side-effect claims

    Public claims that statins commonly cause side effects remain contested. A 2016 Lancet review concluded that almost all muscle symptoms blamed on statins in routine practice are not caused by them, and warned that exaggerated claims may keep people at risk from taking the drugs.[13]

  • Minor

    Board seat at a cholesterol-drug maker

    Since 1991 Goldstein has sat on the board of directors of Regeneron, as has Michael Brown. Regeneron sells alirocumab (Praluent), a PCSK9-blocking drug that lowers LDL by leaving more LDL receptors on liver cells. The role is publicly disclosed. We list it as a financial tie, not as evidence of wrongdoing.[26],[27]

Against the odds

Goldstein did not face persecution, and we found no record that he personally met antisemitism. He did grow up in a very small Jewish minority in the rural South. Kingstree's Jewish families were too few to form a congregation until 1945, and before that many worshipped at home or traveled to other towns. A woman who grew up there in the 1920s and 1930s recalled lonely Sundays and a teacher who made her stay seated while the class sang Christian songs. More Jewish families arrived in the early 1940s, and in 1948 the new congregation built its own synagogue, Temple Beth-Or. Nationally, most US medical schools had limited Jewish admissions with quotas since the 1920s, and these did not disappear until about 1970, a few years after Goldstein earned his MD. In 1958, when Goldstein was 18, men from antisemitic hate groups were arrested over the bombing of Atlanta's leading synagogue, the fourth Southern synagogue bombed in little more than a year. Goldstein's own path ran through public schools in Kingstree, a Virginia university and a young Texas medical school, whose chairman of medicine offered him a faculty job if he trained in genetics. Like most young people from Kingstree's Jewish community, he did not move back. Kingstree's congregation later dwindled and stopped holding services in 2004.

  • —

    Discrimination

    In Kingstree, where Goldstein grew up, Jewish families long had no synagogue. A woman who grew up there in the 1920s and 1930s remembered a teacher who excluded her from class singing because she was not Christian.[6]

  • —

    Quota

    From the 1920s most US medical schools capped the number of Jewish students. The caps were firmly in place by 1945 and had ended by about 1970. Goldstein entered medical school in Dallas in 1962; we found no record that a quota affected him.[2],[19]

  • 1958

    Antisemitic attack

    In October 1958, when Goldstein was 18, dynamite damaged Atlanta's oldest synagogue, the fourth Southern synagogue bombed in little more than a year. The men arrested belonged to antisemitic hate groups. This is regional context, not an attack on Goldstein.[20]

Jewish background

Both parents JewishRelationship to Jewish identity not documented

Goldstein grew up in a Jewish family in Kingstree, South Carolina, a town of about 5,000. His parents, Isadore E. Goldstein and Fannie Alpert Goldstein, ran a clothing store there: in 1936 the family had taken over Silverman's, a store opened in 1904 by the Jewish merchant David Silverman. Kingstree's Jewish families were too few to form a congregation until 1945, when they joined with nearby towns to form a Conservative one, which built Temple Beth-Or in 1948. The Encyclopaedia Judaica has an entry on him. We found no public statements by Goldstein about his own religious practice or views.[2],[6],[21],[22]

Key dates

  1. 1936

    The Goldstein family takes over Silverman's, a store in Kingstree, South Carolina, founded by a Jewish merchant in 1904.[6]

  2. April 18, 1940

    Born in Sumter, South Carolina, the only son of Isadore E. and Fannie Alpert Goldstein. He grows up in nearby Kingstree, where his parents run a clothing store.[1],[2],[21]

  3. 1962

    Graduates summa cum laude in chemistry from Washington and Lee University in Virginia.[2]

  4. June 1966

    Earns his MD in Dallas and starts his internship at Massachusetts General Hospital in Boston, where he meets Michael Brown.[2],[23]

  5. 1968

    Joins the NIH, working in Marshall Nirenberg's lab and caring for children with severe familial hypercholesterolemia.[2],[10]

  6. 1970

    Trains in medical genetics in Seattle, where his study of heart attack survivors finds that 1 in 25 has the common form of familial hypercholesterolemia.[2]

  7. 1972

    Returns to Dallas to head the medical school's first Division of Medical Genetics. He and Brown begin their joint study of familial hypercholesterolemia.[2],[7]

  8. 1973

    With Brown, shows that cells from children with severe familial hypercholesterolemia fail to switch off cholesterol production in response to LDL.[1],[8]

  9. 1974

    Goldstein and Brown show that normal cells have high-affinity binding sites for LDL, the LDL receptor, and that these patients' cells lack them.[7],[9]

  10. 1981

    Experiments in dogs show that a statin lowers blood LDL by raising the number of LDL receptors in the liver.[10],[11]

  11. December 10, 1985

    Shares the Nobel Prize in Physiology or Medicine equally with Michael Brown for discoveries on the regulation of cholesterol metabolism.[1],[3],[5]

  12. August 31, 1987

    The US FDA approves Merck's lovastatin (Mevacor), the first statin approved for human use.[10],[25]

  13. 1993

    With Brown and their trainees, identifies SREBPs, the proteins that switch on the genes for making cholesterol and fats.[2],[10]

  14. 1996

    Becomes chairman of the Lasker Medical Research Awards jury and later writes essays linking creativity in science and art.[2]

Sources

  1. 1.Joseph L. Goldstein - Facts · NobelPrize.org (Nobel Prize Outreach)
  2. 2.Joseph L. Goldstein - Biographical (from Les Prix Nobel 1985, with 2012 addendum) · NobelPrize.org, 1986
  3. 3.The Nobel Prize in Physiology or Medicine 1985 - Press release · NobelPrize.org (Nobel Assembly at the Karolinska Institute), 1985
  4. 4.A Receptor-Mediated Pathway for Cholesterol Homeostasis (Nobel Lecture, Brown MS and Goldstein JL) · NobelPrize.org, 1985
  5. 5.Joseph L. Goldstein - Banquet speech, 10 December 1985 · NobelPrize.org, 1985
  6. 6.Encyclopedia of Southern Jewish Communities - Kingstree, South Carolina · Goldring/Woldenberg Institute of Southern Jewish Life
  7. 7.History of Discovery: The LDL Receptor (Goldstein JL, Brown MS; Arterioscler Thromb Vasc Biol 29:431-438) · Arteriosclerosis, Thrombosis, and Vascular Biology (via PubMed Central), 2009
  8. 8.Familial hypercholesterolemia: identification of a defect in the regulation of 3-hydroxy-3-methylglutaryl coenzyme A reductase activity associated with overproduction of cholesterol (Goldstein JL, Brown MS) · Proceedings of the National Academy of Sciences (via PubMed Central), 1973
  9. 9.Familial hypercholesterolemia: defective binding of lipoproteins to cultured fibroblasts associated with impaired regulation of 3-hydroxy-3-methylglutaryl coenzyme A reductase activity (Brown MS, Goldstein JL) · Proceedings of the National Academy of Sciences (via PubMed Central), 1974
  10. 10.A Century of Cholesterol and Coronaries: From Plaques to Genes to Statins (Goldstein JL, Brown MS; Cell 161:161-172) · Cell (via PubMed Central), 2015
  11. 11.A historical perspective on the discovery of statins (Endo A) · Proceedings of the Japan Academy, Series B (via PubMed Central), 2010
  12. 12.Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170,000 participants in 26 randomised trials (Cholesterol Treatment Trialists' Collaboration) · The Lancet (via PubMed Central), 2010
  13. 13.Interpretation of the evidence for the efficacy and safety of statin therapy (Collins R et al.) · The Lancet (PubMed record), 2016
  14. 14.The large social value resulting from use of statins warrants steps to improve adherence and broaden treatment (Grabowski DC et al.) · Health Affairs (PubMed record), 2012
  15. 15.Trends in lipid-modifying agent use in 83 countries (Blais JE et al.) · Atherosclerosis (PubMed record), 2021
  16. 16.Use of statins for the prevention of cardiovascular disease in 41 low-income and middle-income countries: a cross-sectional study of nationally representative, individual-level data (Marcus ME et al.) · The Lancet Global Health (via PubMed Central), 2022
  17. 17.Statins and risk of incident diabetes: a collaborative meta-analysis of randomised statin trials (Sattar N et al.) · The Lancet (PubMed record), 2010
  18. 18.Withdrawal of cerivastatin from the world market (Furberg CD, Pitt B) · Current Controlled Trials in Cardiovascular Medicine (via PubMed Central), 2001
  19. 19.Why Did the United States Medical School Admissions Quota for Jews End? (Halperin EC) · The American Journal of the Medical Sciences (PubMed record), 2019
  20. 20.Temple Bombing (Hatfield E) · New Georgia Encyclopedia, 2007
  21. 21.Goldstein, Joseph Leonard (Poliakoff M) · South Carolina Encyclopedia (University of South Carolina)
  22. 22.Goldstein, Joseph Leonard (Encyclopaedia Judaica entry) · Encyclopaedia Judaica, via Encyclopedia.com, 2007
  23. 23.Scientific Side Trips: Six Excursions from the Beaten Path (Brown MS, Goldstein JL; J Biol Chem 287:22418) · The Journal of Biological Chemistry (via PubMed Central), 2012
  24. 24.Thomas C. Südhof - Biographical · NobelPrize.org, 2013
  25. 25.Drugs@FDA: MEVACOR (lovastatin), NDA 019643, approval history · U.S. Food and Drug Administration
  26. 26.Leadership: Board of Directors · Regeneron Pharmaceuticals
  27. 27.PRALUENT (alirocumab) injection: U.S. prescribing information · Regeneron Pharmaceuticals
  28. 28.Effects of statin therapy on diagnoses of new-onset diabetes and worsening glycaemia in large-scale randomised blinded statin trials: an individual participant data meta-analysis (Cholesterol Treatment Trialists' Collaboration) · The Lancet Diabetes & Endocrinology (PMC full text), 2024
  29. 29.Statins utilization trends and expenditures in the U.S. before and after the implementation of the 2013 ACC/AHA guidelines (MEPS 2008-2019) · Saudi Pharmaceutical Journal (PMC full text), 2023

Fact-checked on September 24, 2026 by a separate AI fact-checking pass that re-opened the sources, with 12 corrections made. How we check

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