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Portrait of Konrad Bloch
Photo: Peter Geymayer, Self-photographed · Public domain via Wikimedia Commons

Nobel Prize in Physiology or Medicine · 1964

Konrad Bloch

Forced out of Nazi Germany, he helped map how the body builds cholesterol, the chemistry that statin drugs later learned to block.

The Nobel citation: “for their discoveries concerning the mechanism and regulation of the cholesterol and fatty acid metabolism”
Born
January 21, 1912, Neisse, Germany (now Nysa, Poland)
Died
October 15, 2000, Burlington, MA, USA
Shared with
Feodor Lynen
Affiliation at the time
Harvard University, USA

Medicine prize

1964

Shared with 1 other laureate.

Age that year

52years

Born in 1912.

Headline credited impact

34,000–96,000lives saved

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

Sources cited

22

Fact-checked September 24, 2026.

  • Working in Davos in the mid-1930s, he tested fat extracts from tuberculosis bacteria by injecting them into his own arms. He still had the scars in a 1993 interview.
  • In 1936 a Yale professor he had never met, and knew only through letters, gave him a job with no salary. That appointment letter alone won him a US visa.
  • He arrived in America with $100, taught night labs for dental students, and saved enough to bring his brother and then his parents out of Nazi Germany.
  • He spent a summer at a Bermuda research station trying to show that shark livers make squalene, a cholesterol precursor. It failed; his lab later proved it in rats.
  • In 1968 the Munich technical university that had barred him from graduate study in 1934 because he was Jewish gave him an honorary doctorate.

The breakthrough

How living cells build cholesterol, step by step (1942-1964)

Cholesterol is a waxy molecule with 27 carbon atoms arranged in four linked rings and a tail. Every cell in our bodies needs it. By the 1930s chemists knew its shape, but nobody knew how living things build such a complicated molecule. Starting in 1942 at Columbia with David Rittenberg, Bloch fed animals acetic acid, the small two-carbon acid in vinegar, tagged with rare forms of carbon and hydrogen that work like tracking tags. The tags showed up in cholesterol. Using a mutant bread mold that could only grow on acetate, his team then showed that the mold's own sterol was built from acetate alone. Next his lab found that the liver strings acetate-derived pieces into squalene, a 30-carbon chain, and that squalene becomes cholesterol. In 1953 he and the chemist Robert Woodward proposed how squalene folds and closes into rings to make lanosterol, and his lab then showed that lanosterol is trimmed down into cholesterol. Along with Feodor Lynen's group in Munich, John Cornforth and George Popják in Britain, and Karl Folkers's team in the US, his lab filled in the steps in between: acetate becomes mevalonic acid, which becomes a five-carbon building block, and six of these are joined into squalene. Think of an assembly line that snaps identical five-carbon bricks into a chain, then folds the chain into a sculpture. The whole route takes about 30 steps. Bloch also showed that cholesterol is the starting material for bile acids and a female sex hormone.[2],[3],[4],[11]

“I was told by the dean of the school in Munich that I had to leave, because Jews were not allowed to do graduate work.”
Konrad Bloch, Oral history interview with James J. Bohning at Harvard, 22 March 1993, recalling how his studies in Munich ended in 1934.[6]

What it meant for humanity

Bloch's work gave medicine a map of how the body makes its own cholesterol, just as high blood cholesterol was being linked to heart disease. When the prize was presented in 1964, the Nobel committee's speaker said researchers now knew which reactions to study, and predicted specific treatments for the diseases that were the most common cause of death in developed countries. That prediction came true through statins. In his Nobel lecture, Bloch pointed to one step, the conversion of a molecule called HMG-CoA into mevalonic acid, as the likely control point of the whole pathway, citing work by Bucher. Statins block exactly that step. Akira Endo, who discovered the first statin, wrote that most of the pathway was worked out by four biochemists: Bloch, Lynen, Cornforth and Popják. In 1965 Endo had written to Bloch asking to train in his lab, but the class was already full. The first statin reached US patients in 1987. By 2018 an estimated 173 million people in 83 countries used cholesterol-lowering drugs, with statins the most used, and one US study estimated that statins prevented about 40,000 deaths in 2008 alone. Bloch's work reached further. He showed that cholesterol is the raw material for bile acids and a female sex hormone, and the five-carbon building block in his pathway is also the starting point for rubber and many other natural products. Late in his career, a contaminated chemical sample led his lab to a new way to switch off enzymes: a decoy that the enzyme itself turns into a weapon against itself. Bloch later cited Ornidyl (eflornithine), a sleeping sickness drug, as one medicine that works this way. For three decades he also taught Harvard's basic biochemistry course to thousands of students, and he mentored more than 125 young researchers.

  • In his 1964 Nobel lecture Bloch pointed to the step from HMG-CoA to mevalonic acid as the likely control point of cholesterol making, citing Bucher's work. Statins block that step.[3],[11]
  • Akira Endo, discoverer of the first statin, credited Bloch, Lynen, Cornforth and Popják with working out most of the roughly 30-step pathway that drug hunters later tried to block.[11],[12]
  • About 173 million people in 83 countries used cholesterol-lowering drugs in 2018, statins most of all; a US study estimated statins averted about 40,000 deaths in 2008 alone.[13],[15]
  • Bloch showed that cholesterol is the raw material for bile acids and a female sex hormone. The 1964 Nobel presenter added that all the body's steroid substances are made from it.[4]
  • A contaminated sample led his lab to 'suicide' enzyme inhibitors. Bloch cited Ornidyl (eflornithine) as a drug built on this idea; WHO calls eflornithine much safer than melarsoprol, an arsenic drug, for one form of sleeping sickness.[6],[18],[19],[20]
  • At the 1964 Nobel banquet, the Karolinska rector told Bloch, Lynen and chemistry laureate Dorothy Hodgkin that their discoveries might give humanity weapons against cardiovascular disease.[5],[11]

Impact in numbers

Bloch's main gift was knowledge: a step-by-step map of how cells build cholesterol and other sterols, worked out alongside Lynen, Cornforth, Popják and others. The most measurable outcome that map fed into is statin therapy. We use the same estimate as our profiles of Joseph Goldstein and Michael Brown: roughly 1.7 to 4.8 million deaths prevented or postponed worldwide from 1987 to 2025, and roughly 1.4 to 4.1 million extra diabetes diagnoses as a side effect. We credit Bloch with only 2% of each, because the chain from his experiments to a pill passes through many hands: Bucher and Lynen's work on the control step, Akira Endo's discovery of the first statin, Merck's development of lovastatin, and large clinical trials. We do not count his other contributions, to steroid hormone biology, to the chemistry of rubber and other isoprene-based natural products, to the role of sterols in cell membranes, or to enzyme-inhibitor drug design, because no honest number exists for them.

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.

  • Low confidenceRippleModeledHealth

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

    34,000–96,000

    lives saved, credited share

    That is 2% of 1.7–4.8 million lives saved since 1987.

    How this number was built

    Range matches Goldstein and Brown. Users: Blais, 173M on lipid drugs in 2018 in 83 countries (used as a near-global total), per-capita use up ~50% since 2008 (~110M then); assume 85% statins: ~95M (2008), ~147M (2018). Person-years: 1987-2008 ramp from zero 0.7-1.0B; 2008-18 1.2B; 2018-25 1.0-1.2B. Total 2.9-3.4B. Effect: CTT 2005 trials had 8,186 deaths in 90,056 people over ~5 yrs (~1.8%/yr) and 12% fewer deaths per mmol/L LDL cut (mean 1.09), ~2.4 averted per 1,000 person-years; real-world 0.6-1.4. 2.9B x 0.6 = 1.74M; 3.4B x 1.4 = 4.76M; rounded 1.7-4.8M. Check: Grabowski, ~40,000 US deaths averted in 2008. Share 0.02: Bloch was one of four who mapped most of the pathway (Endo); Bucher and Lynen pinned down the HMG-CoA step; Endo found the first statin; Merck developed it; trials proved it; Goldstein and Brown get 0.05 each.[11],[12],[13],[14],[15]

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

  • HarmLow confidenceRippleModeledHealth

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

    42,000–102,000

    people harmed, credited share

    That is 2% 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 0.02, matching the benefit claim.[13],[21],[22]

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

The double edge

We found no documented harm from Bloch's own research. The risks lie downstream, in drugs that act on the pathway he helped map. The first such drug, triparanol, blocked a late step in cholesterol making. It entered US use in 1959 and was withdrawn in the early 1960s after serious side effects, including cataracts. Bloch had no part in it. Statins, which block an early step, are far safer but not harmless. An Oxford-led review estimated that treating 10,000 people for five years with a standard statin dose causes about 5 cases of muscle damage, 50 to 100 new cases of diabetes and probably 5 to 10 bleeding strokes, while preventing 500 to 1,000 heart attacks, strokes and artery-opening procedures. The same review found that most muscle aches blamed on statins are not caused by them.

  • 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. Both judged these risks small next to the heart attacks and strokes prevented.[16],[17]

  • Moderate

    Triparanol, an early cholesterol-synthesis blocker

    Triparanol (MER/29), introduced in the US in 1959, was the first cholesterol-lowering drug that worked by blocking cholesterol synthesis, at the pathway's final stage. It was withdrawn in the early 1960s because of serious side effects, including cataracts. Bloch was not involved; we list it because it shows the risks of acting on the pathway.[11]

Against the odds

Bloch grew up in a small Jewish community in Silesia and was studying chemistry in Munich when Hitler took power in 1933. That April, new laws purged Jewish civil servants and capped 'non-Aryan' admissions to German schools and universities at 1.5 percent. Bloch finished his diploma in 1934, but the dean then told him that Jews could not do graduate work. His professor, Hans Fischer, had been willing to take him but doubted he would be allowed to. Two leading German chemists, Fritz Kögl and Alfred Butenandt, also turned him down, and Bloch believed Butenandt knew he was Jewish. He found a temporary job at a research institute in Davos, Switzerland, but his residence permit was running out. The United States required an affidavit of support, and he had no relatives there to provide one. A Yale professor, R. J. Anderson, gave him an unpaid post, and that letter won him a visa in 1936. A Harvard department profile says this spared him a likely fatal return to Germany. He arrived with $100, taught night labs for dental students, and saved to bring his younger brother and then his parents to America. His parents escaped from Berlin in 1941, two weeks before Germany invaded the Soviet Union.

  • 1934

    Discrimination

    Nazi laws of 1933 capped 'non-Aryan' university admissions at 1.5 percent. After Bloch finished his chemistry diploma in Munich, the dean told him Jews were not allowed to do graduate work. Two leading German chemists, Fritz Kögl and Alfred Butenandt, also declined to take him; Bloch believed Butenandt knew he was Jewish.[2],[6],[10]

  • 1934

    Exile

    He left Germany for a temporary research job in Davos, Switzerland. When his Swiss residence permit was about to expire in 1936, an unpaid appointment at Yale got him a US visa.[2],[7]

  • 1936

    Poverty

    He reached the United States with $100 and earned money teaching night labs for dental students. His salary at Columbia in the 1930s rose only from $500 to $1,000 a year.[6]

  • 1941

    Persecution

    His parents remained in Nazi Germany until 1941 and escaped from Berlin two weeks before Germany invaded the Soviet Union, after Bloch saved up to pay their passage. His older sister went to England.[6]

Jewish background

Both parents JewishCulturally Jewish

Bloch was born into a Jewish family; a Harvard faculty memorial calls it highly cultured and prosperous. His father's family had lived in the Silesian town of Neisse for three or four generations. He suggested the family was not very religious, but in a town with a very small Jewish community he took private Hebrew lessons from the rabbi, had a Bar Mitzvah, and was said to be the best Hebrew scholar in town. In 1934 Nazi racial rules ended his studies in Munich because he was Jewish, and all of his immediate family later fled Germany. We found no record of religious practice in his adult life. The Encyclopaedia Judaica has an entry on him.[6],[7],[8],[9],[20]

Key dates

  1. January 21, 1912

    Born in Neisse, Upper Silesia, Germany (now Nysa, Poland), into a Jewish family.[1],[2],[6]

  2. 1930

    Begins studying chemistry at the Technische Hochschule in Munich, where Hans Fischer's teaching draws him to organic chemistry.[2]

  3. 1934

    After earning his diploma, is told Jews cannot do graduate work in Munich; leaves Germany for a research post in Davos, Switzerland.[2],[6]

  4. 1936

    Emigrates to the United States on the strength of an unpaid Yale appointment and enters Columbia University's biochemistry department.[2],[7]

  5. 1938

    Earns his PhD at Columbia and joins Rudolf Schoenheimer's isotope-tracer research group.[2]

  6. 1941

    Marries Lore Teutsch; the same year his parents escape from Berlin shortly before Germany invades the Soviet Union.[2],[6]

  7. 1942

    With David Rittenberg, begins the cholesterol work that shows acetate is a major building block of the molecule.[2],[3]

  8. 1946

    Moves to the University of Chicago, becoming full professor of biochemistry in 1950.[2]

  9. 1952

    His lab shows that rat liver makes squalene from acetate and that squalene is converted into cholesterol.[3]

  10. 1953

    With Robert Woodward, publishes the scheme for how squalene folds into lanosterol, the first ring-shaped step toward cholesterol.[3]

  11. 1954

    Becomes Higgins Professor of Biochemistry at Harvard, a post he holds until 1982.[2],[7]

  12. 1964

    Shares the Nobel Prize in Physiology or Medicine with Feodor Lynen for discoveries on cholesterol and fatty acid metabolism.[1]

  13. 1988

    Receives the US National Medal of Science.[6],[7]

  14. October 15, 2000

    Dies of complications of congestive heart failure in Burlington, Massachusetts, aged 88.[1],[7]

Sources

  1. 1.Konrad Bloch - Facts · NobelPrize.org (Nobel Prize Outreach)
  2. 2.Konrad Bloch - Biographical (from Nobel Lectures, Physiology or Medicine 1963-1970) · NobelPrize.org (Nobel Foundation), 1964
  3. 3.The Biological Synthesis of Cholesterol (Nobel Lecture, 11 December 1964) · NobelPrize.org (Nobel Foundation), 1964
  4. 4.Award ceremony speech, Nobel Prize in Physiology or Medicine 1964 (Professor S. Bergström) · NobelPrize.org (Nobel Foundation), 1964
  5. 5.Konrad Bloch - Banquet speech (with remarks by Rector S. Friberg) · NobelPrize.org (Nobel Foundation), 1964
  6. 6.Oral history interview with Konrad E. Bloch, conducted by James J. Bohning at Harvard University, 22 March 1993 (transcript) · Science History Institute Digital Collections, 1993
  7. 7.Konrad Bloch, Nobel winner, dies at 88 · Harvard University Gazette, 2000
  8. 8.Pietro de Camilli to Present 2024 Konrad Bloch Lecture on April 11 (includes a profile of Konrad Bloch) · Department of Molecular and Cellular Biology, Harvard University, 2024
  9. 9.Konrad Emil Bloch (Encyclopedia of World Biography; Scribner Encyclopedia of American Lives, entry by David Petechuk; Encyclopaedia Judaica, entry by Samuel Aaron Miller and Ruth Rossing) · Encyclopedia.com (Gale)
  10. 10.Anti-Jewish Legislation in Prewar Germany · United States Holocaust Memorial Museum, Holocaust Encyclopedia
  11. 11.A historical perspective on the discovery of statins (Endo A; Proc Jpn Acad Ser B 86(5):484-493) · Proceedings of the Japan Academy, Series B (via PubMed Central), 2010
  12. 12.A Century of Cholesterol and Coronaries: From Plaques to Genes to Statins (Goldstein JL, Brown MS; Cell 161(1):161-172) · Cell (via PubMed Central), 2015
  13. 13.Trends in lipid-modifying agent use in 83 countries (Blais JE et al.; Atherosclerosis 328:44-51) · Atherosclerosis (PubMed record), 2021
  14. 14.Efficacy and safety of cholesterol-lowering treatment: prospective meta-analysis of data from 90,056 participants in 14 randomised trials of statins (Cholesterol Treatment Trialists' Collaborators; Lancet 366:1267-78) · The Lancet (PubMed record), 2005
  15. 15.The large social value resulting from use of statins warrants steps to improve adherence and broaden treatment (Grabowski DC et al.; Health Aff 31(10):2276-85) · Health Affairs (PubMed record), 2012
  16. 16.Interpretation of the evidence for the efficacy and safety of statin therapy (Collins R et al.; Lancet 388:2532-61) · The Lancet (PubMed record), 2016
  17. 17.Statins and risk of incident diabetes: a collaborative meta-analysis of randomised statin trials (Sattar N et al.; Lancet 375:735-42) · The Lancet (PubMed record), 2010
  18. 18.Trypanosomiasis, human African (sleeping sickness) - Fact sheet · World Health Organization, 2023
  19. 19.Alpha-Difluoromethylornithine, an Irreversible Inhibitor of Polyamine Biosynthesis, as a Therapeutic Strategy against Hyperproliferative and Infectious Diseases (LoGiudice N et al.; Med Sci (Basel) 6(1):12) · Medical Sciences (MDPI) (PubMed record), 2018
  20. 20.Konrad Emil Bloch, 88 (Memorial Minute, Faculty of Arts and Sciences; Daniel Kahne, Charles Lieber, Dudley Herschbach) · Harvard Gazette, 2018
  21. 21.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
  22. 22.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 13 corrections made. How we check

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