Dr. Bowman was the first African-American tenured professor of medicine at the University of Chicago, and an important figure in the intertwined histories of genetics and bioethics.

Dr. Bowman was born and raised in Washington DC, and attended the Howard University College of Medicine, where he graduated in three years. He completed his internship at Howard, before landing a residency in pathology in Chicago. He then served as pathology chief at Provident Hospital, until the Korean War, when he was drafted into serving as pathology chief for the Army’s Medical Nutrition Laboratory in Denver.

After the war, he moved his family to Shiraz, Iran, where he became interested in favism, a genetic disease that causes red blood cells to break down in response to certain triggers (including fava beans, which is where the name for the condition comes from). He worked to collect samples from various ethnic groups in Iran to try to pin down the genetics of this disease. Through this work, he began collaborating with a researcher at the University of Chicago, where he returned (after some time in London) as the school’s first African-American tenured professor of medicine.

In the early 1970s, when President Nixon passed the National Sickle Cell Anemia Control Act, Dr. Bowman spoke out against the haphazard implementation — both the government and grassroots efforts — to combat this disease that disproportionately impacts African-Americans. He also served as the head of UChicago’s Comprehensive Sickle Cell Center for 11 years.

Both favism and sickle cell anemia are diseases that affect people of African descent more often than other racial groups, and both have been shown to offer protection against malaria as a side effect. Thus, they provide interesting examples to help explain why disease is not always selected against by evolutionary pressures.

Hemoglobin (the molecule in red blood cells that travels through the blood, carrying oxygen) is made up of four proteins: two alpha-globin proteins and two beta-globin proteins. Sickle cell anemia is caused by a mutation in the gene that encodes for beta-globin. The mutation causes a very small change, which has no effect when there’s normal amounts of oxygen around. But when oxygen levels are low, the sickle-cell version of beta-globin likes to clump together instead of getting together with alpha-globin. This causes red blood cells with this mutant hemoglobin to distort into non-round shapes and then burst.

Sickle cell anemia can be quite deadly — why wouldn’t it be selected against by evolution? The answer is something we call “heterozygote advantage”. People with sickle cell disease are protected against malaria, because their red blood cells are fragile and tend to burst, instead of making a nice home for the malaria parasite. So we can think of the sickle cell version of hemoglobin as a “good at preventing malaria” version. However, this version on its own is often deadly…

On the other hand, there’s the healthy version of hemoglobin, which we can think of as a “good at carrying oxygen” version. This version is better at carrying oxygen around the body but leaves you susceptible to getting malaria (if that’s a problem where you live). Thus, there’s an advantage to having one of each version. This works in part because one healthy copy of beta-globin is enough to carry all the oxygen, the vast majority of the time.

In addition to his work on these two diseases, Dr. Bowman was heavily involved in bioethics. He was an early proponent of the idea that you had a right to NOT know genetic information about yourself, and a valued member of the Ethical, Legal, and Social Issues Working Group, which advised the Human Genome Project on potential outcomes of the research beyond the scientific realm.