George Minot

George Richards Minot (1885–1950) was an American physician who shared the 1934 Nobel Prize in Physiology or Medicine for demonstrating that liver therapy could treat pernicious anemia.

Pernicious anemia: An autoimmune disorder that impairs vitamin B12 absorption and causes megaloblastic anemia and neurological damage. The disease Minot helped make treatable with a liver-rich diet.
Intrinsic factor: A protein produced by stomach parietal cells that enables vitamin B12 absorption in the small intestine. Its deficiency explains why ordinary dietary B12 cannot prevent pernicious anemia.
George Whipple: An American physician whose experiments on anemia in dogs showed that liver could promote blood regeneration. Whipple’s findings prompted Minot to test liver as a treatment for pernicious anemia.
Iron-deficiency anemia: Anemia caused by insufficient iron for hemoglobin production, commonly due to blood loss or inadequate intake. Unlike pernicious anemia, it arises from iron shortage rather than impaired vitamin B12 absorption.
Vitamin B12: A water-soluble vitamin essential for DNA synthesis and normal nervous-system function. The active nutritional factor behind the benefit of liver therapy.
Vitamin B12 absorption: The process by which dietary cobalamin binds intrinsic factor and enters the body through the terminal ileum. Defective absorption is the underlying problem liver feeding temporarily overcame.
William P. Murphy: An American physician who shared the 1934 Nobel Prize for research on liver treatment of pernicious anemia. Murphy worked with Minot to conduct and report the dietary treatment study.
Folic acid deficiency: A deficiency of folate that can cause megaloblastic anemia and other health problems. It can resemble B12 deficiency in blood tests, but does not explain Minot’s treatment response.
Liver therapy: A treatment for pernicious anemia based on eating liver or receiving liver extracts. The intervention Minot and William Murphy established as effective.
Megaloblastic anemia: A blood disorder marked by abnormally large developing red cells, usually caused by impaired DNA synthesis. Pernicious anemia produces this pattern when B12 deficiency disrupts blood-cell development.

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Frederick BantingCompared with: Minot’s work, like Banting’s, shows how clinical treatments could emerge from targeted physiological research.