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New Diseases, Old Ideas

Interest in differential susceptibility persisted throughout the 20th century. Alcohol remained a concern, as in a 1917 account of a doctor’s trip from Massachusetts to Florida. He wrote appalling things about suffrage and segregation but saved his worst for alcohol: “An educated white man under the influence of liquor is a sad and disgusting sight. A negro under the same conditions is a tiger let loose, a volcano to be fled by everyone.” Only prohibition could ensure the safety of “the wives and daughters of every man.”

Cancer, a so-called “disease of civilization,” was thought to be rare in non-White people. In 1881 a New York physician asserted the “remarkable fact that negro women never have cancer of the uterus.”30 Frederick Hoffman, known for his quantitative assessment of racial susceptibility, observed in 1923 that “Among our native Indians cancer is very seldom met with among those who are of pure blood.” By the late 20th century, however, cancer had crossed the color line.

Heart disease was also viewed through a racial lens. Whereas coronary heart disease — another “disease of civilization” — was considered rare among Black Americans, syphilitic heart disease was thought common, a reflection of the racialized discourse that motivated the U.S. Public Health Service study in Tuskegee. Paul Dudley White wrote in 1933 that “with perfect justification we should expect to find syphilis of aorta and heart much more commonly among the more primitive Negroes in the South than in a highly cultured white community in New England.” Meanwhile, there was “exceptionally little cardiovascular syphilis in the Jewish race, in large measure, I believe, because of the traditionally moral upbringing and the lack of promiscuity that are characteristic of the Jews.”

A counter-discourse to racialized medicine emerged in the late 19th and early 20th centuries, though it was rarely reflected in the Journal. Sociologist W.E.B. Du Bois had called attention to the social origins of the ill health of Black people as early as 1899. Black physicians also became prominent critics of medical racism. By the late 20th century, robust evidence challenged assertions of race differences and determinism. When the Department of Health and Human Services launched its “Healthy People 2000” campaign, it proclaimed that “Narrowing the gaps between the life expectancies of different populations, including blacks, Hispanics, American Indians, Asian Americans, and low-income people, is a primary target of our initiatives.” Though such calls have increased, and progress has been made, health inequities persist.

Debating Nature and Nurture

Confronted with evidence of health inequities, medical researchers have generally attributed the disparities to intrinsic differences between groups (e.g., genetics, heredity), to health-affecting behaviors (e.g., diet or smoking), or to environmental conditions (e.g., poverty). There are often ample data to support each explanation. With little consensus or guidance about which ones to emphasize, investigators make choices that shape our understanding of where responsibility for health lies, and of possible interventions. Many emphasize intrinsic causes of health inequities, which absolve researchers and their readers of responsibility for intervening (e.g., to provide care or to reform social and economic conditions).Such tensions continue to infiltrate writings in this Journal about diabetes, tuberculosis, and infant mortality, among other health problems.

Diabetes, for example, was once deemed rare among Indigenous Americans. By the 1960s, however, the Akimel O’odham (formerly the Pima) had “the world’s highest reported incidence.” In 1965, researchers began a long-term study in the Gila River Indian Community in Arizona. They explained that “Pima Indians have two distinct advantages as subjects for the investigation of diabetes: a high degree of genetic homogeneity and a high prevalence of diabetes mellitus.” Assuming that there was a “strong genetic predisposition,” they searched for suspect genes — without success. Doubts emerged. Obesity and diabetes had been rare among the Akimel O’odham earlier in the century: had their environment changed? Even though they lived on both sides of the U.S.–Mexico border, diabetes was prevalent only in their U.S. communities, which pointed to social and environmental causes. Yet faith in racial genetics persists. Medical schools continue to teach about so-called Pima diabetes “without sufficient explanation of historical and social causes.”

Tuberculosis investigations show similar tensions. In 1990, Arkansas researchers studied tuberculosis in racially integrated nursing homes. Among people who were tuberculin-negative on arrival, more Black residents (13.8%) than White residents (7.2%) subsequently tested positive. Researchers jumped to race and genetics: “under the same social conditions, blacks are apparently infected more readily by Mycobacterium tuberculosis than whites”; these data “strongly suggest heritable differences.” Skeptics suggested other causes, from differences in baseline health (e.g., nutritional status) to differences in exposure (racial integration did not guarantee equivalent conditions). Some observers argued that this rush to genetic judgment was “a great disservice, since it deters the hunt for remediable causes.”

Other researchers cast doubt on racial explanations for conditions such as low birth weight. Past researchers had argued that racial genetics significantly affected birth weight. But when a study in Illinois compared infants of U.S.-born White women, African-born women, and U.S.-born Black women, birth weights were similar in the first two groups but lower in the third, providing “some evidence against the theory that there is a genetic basis for the disparity. Questions about the role of heredity versus social determinants in disease causation have persisted in the Journal for two centuries with little consistent editorial commentary.

Race and Medicine in the 21st Century

In 2003, the Journal published a debate about the role of race in medicine. On one side, researchers warned that race was a poor proxy for human genetic variation and that racist thinking had corrupted American medicine. On the other, researchers maintained that racial and ethnic categories were useful and that ignoring race would “retard progress in biomedical research and limit the effectiveness of clinical decision making.” One of the Journal’s editors weighed in. Acknowledging that race was “fraught with sensitivities and fueled by past abuses and the potential for future abuses,” she ultimately saw value in its use: “it seems unwise to abandon the practice of recording race when we have barely begun to understand the architecture of the human genome.” This did not resolve the debate.

As costs of genome sequencing fell, researchers plumbed the genetic substructure of human populations and identified genetic variations relevant for pathophysiology and therapeutics. Journals have been quick to publish reports of disease–gene associations, no matter how small their effect, as well as reports of racial differences in allele frequency. This practice persists despite serious skepticism about the idea that race meaningfully reflects ancestry, and therefore genetics. Sophisticated analyses have revealed the social, biologic, and genetic complexity of ancestry and its imperfect mapping onto racial categories. Scholars now interrogate the taxonomies we use to study human difference. In parallel, they have shown how social and economic factors generate health inequities, and how economic and political elites use race theories to defend privilege and power. Current medical writings continue to deploy fundamentally different ideas about race (biologic, social, or both) and about social determinants of health (foregrounded or ignored). Growing evidence suggests that racism is a powerful driver of inequities that were once ascribed to putatively intrinsic racial differences.

Tensions flared amid revelations of inequities during the Covid-19 pandemic, fueling calls for racial reckoning. As a result, debates about the use of race in areas such as diagnostic testing gained visibility. Race adjustments are now being removed from several diagnostic tools (e.g., estimated glomerular filtration rate, pulmonary function tests). But researchers still defend race-based medicine, arguing that race is a “master status”: it can “capture important epidemiologic information, including social determinants of health such as racism and discrimination, socioeconomic position, and environmental exposures,” and it is “directly associated with genetic ancestry and therefore indirectly related to genetic variants that may affect disease and health outcomes.” They warn against “naive ‘color blindness’ that is more likely to perpetuate and potentially exacerbate disparities.” By continuing to present both sides of these debates, the Journal misses an opportunity to pass judgment and exercise much-needed guidance on a matter of great medical, public health, and social importance. More careful and robust research attentive to the legacies of history is essential.

Important questions remain. Even the most basic decisions (e.g., which population descriptors are appropriate when considering human diversity in medical research and practice) are contested. American medicine has long accepted racializing narratives that propagate social perceptions about White superiority. Deliberate thinking and action are required to resist those narratives. We must decide carefully which policies and practices are justified — scientifically and ethically — as we contend with the nature and meaning of human differences. The Journal can act on its commitment to health equity not only by publishing the best, most rigorous research on this important topic, but also by interrogating the racial assumptions and sociopolitical consequences of everything it publishes.