Throughout contemporary medical discourse, health disparities among racial and ethnic groups are often attributed to systemic and structural racism. Furthermore, organizations such as the American Medical Association assert that race itself is a social construct and urge a shift away from viewing race as a “biological risk factor” toward a “deeper understanding of racism as a determinant of health.” Unfortunately, this framing rings hollow and obscures an important fact: Biology can significantly shape health outcomes and disparities. Ignoring this reality only hinders our understanding of why different groups experience distinct patterns of illness and well-being and, in turn, how to treat them most effectively. Put plainly, biology may well be the root cause of these health disparities, and dismissing it comes at the expense of patients.
Take, for instance, acute myeloid leukemia (AML), a blood cancer rooted in genetic alterations and marked by chromosomal abnormalities in more than half of newly diagnosed cases. Even it has been subsumed by the narrative of structural racism. Just a few years ago, the medical journal Blood, published by the American Society of Hematology, printed an entire article titled, “Structural racism is a mediator of disparities in acute myeloid leukemia outcomes.” Biology, in this construct, is effectively dismissed.
Revisiting clinical trial data
Yet, a recent analysis of more than 30 years of clinical trial data opens the door to a different perspective. The study draws on data from 10 phase 2 and phase 3 interventional trials involving newly diagnosed adults with AML. In general, these later-phase trials are considered among the strongest sources of clinical evidence because they use structured designs, defined endpoints, and rigorous methods to evaluate treatment effectiveness and safety.
Moreover, clinical trial participants receive close medical oversight, with regular check-ins, monitoring, and assessments to track their health and safety throughout a given study. In many cases, they are followed more closely than they would be under standard clinical care. Given the highly controlled nature of these interventional trials, any differences in outcomes that emerge are strong indicators of biological effects rather than features of the health care system.
In analyzing the period from 1984 to 2019, the researchers found that Black patients with AML did, in fact, have worse overall survival than their White peers. And while the lead study author, Shella Saint Fleur-Lominy, initially told Medscape Medical News that unaccounted for “social factors” could explain the difference, she also postulated that “there could be other mutations that we don’t know about.”
Indeed, during a media briefing, Saint Fleur-Lominy noted the significant advantage of having participants drawn from clinical trials, which makes the outcomes “less likely related to social factors” and more likely attributable to untested genetic mutations.
Genetic mutations and race
Further, the impact of known mutations is of particular interest as well, particularly with respect to race. A mutation in NPM1, for instance, is associated with significantly worse survival in Black patients with AML compared to Whites. Recent studies by Andrew Stiff, et al., found “evidence of underlying biological differences in patients with NPM1 mutations with respect to genetic ancestry.” And Wang, et al., noted that “growing evidence suggests that NPM1 mutations do not seem to confer as favorable a prognostic impact on Black patients as on White patients treated with intensive chemotherapy.”
What accounts for this difference is yet to be known. Nevertheless, the NPM1 mutation is regarded as “favorable” when it comes to treatment with venetoclax, a medication which received accelerated FDA approval in late 2018. Its impact then wouldn’t be seen in Saint Fleur-Lominy, et al.’s analysis, which ended with 2019 data. Notably, Wang and colleagues reported that before venetoclax became available, non-Hispanic Black patients had a 22 percent higher hazard of death than non-Hispanic Whites. After the drug’s approval, however, this disparity disappeared, as “worse [overall survival] was not observed for [non-Hispanic Blacks].”
Taken together, the above illustrates what should be clear: Biological differences cannot be ignored, despite what progressive ideologues may suggest. The findings presented by Saint Fleur-Lominy, Wang, and other researchers over recent years make clear that biological variability is a critical factor when it comes to AML. Although some may find political favor with describing race as a “social construct,” its relevance to AML risk stratification and therapeutic decision-making cannot be dismissed. For the sake of patient care, biology must remain at the forefront and cannot be cast away to suit a political narrative.
Kurt Miceli is an internal medicine and psychiatry physician.
