Dataset Information

Human microbiome variation associated with race and ethnicity emerges as early as 3 months of age.

ABSTRACT: Human microbiome variation is linked to the incidence, prevalence, and mortality of many diseases and associates with race and ethnicity in the United States. However, the age at which microbiome variability emerges between these groups remains a central gap in knowledge. Here, we identify that gut microbiome variation associated with race and ethnicity arises after 3 months of age and persists through childhood. One-third of the bacterial taxa that vary across caregiver-identified racial categories in children are taxa reported to also vary between adults. Machine learning modeling of childhood microbiomes from 8 cohort studies (2,756 samples from 729 children) distinguishes racial and ethnic categories with 87% accuracy. Importantly, predictive genera are also among the top 30 most important taxa when childhood microbiomes are used to predict adult self-identified race and ethnicity. Our results highlight a critical developmental window at or shortly after 3 months of age when social and environmental factors drive race and ethnicity-associated microbiome variation and may contribute to adult health and health disparities.

SUBMITTER: Mallott EK

PROVIDER: S-EPMC10434942 | biostudies-literature | 2023 Aug

REPOSITORIES: biostudies-literature

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Human microbiome variation associated with race and ethnicity emerges as early as 3 months of age.

Mallott Elizabeth K EK Sitarik Alexandra R AR Leve Leslie D LD Cioffi Camille C Camargo Carlos A CA Hasegawa Kohei K Bordenstein Seth R SR

PLoS biology 20230817 8

Human microbiome variation is linked to the incidence, prevalence, and mortality of many diseases and associates with race and ethnicity in the United States. However, the age at which microbiome variability emerges between these groups remains a central gap in knowledge. Here, we identify that gut microbiome variation associated with race and ethnicity arises after 3 months of age and persists through childhood. One-third of the bacterial taxa that vary across caregiver-identified racial catego ...[more]

PMID: 37590208

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Project description:Fifty years ago, Richard Lewontin found that the vast majority of human genetic variation falls within (~85%) rather than between (~15%) racial groups. This result has been replicated numerous times since and is widely taken to support the notion that genetic differences between racial groups are trivial and thus irrelevant for clinical decision-making. The aim of this study was to consider how the apportionment of pharmacogenomic variation within and between racial and ethnic groups relates to risk disparities for adverse drug reactions. We confirmed that the majority of pharmacogenomic variation falls within (97.3%) rather than between (2.78%) the three largest racial and ethnic groups in the United States: Black, Hispanic, and White. Nevertheless, pharmacogenomic variants showing far greater within than between-group variation can have high predictive value for adverse drug reactions, particularly for minority racial and ethnic groups. We predicted excess adverse drug reactions for minority Black and Hispanic groups, compared to the majority White group, and considered these results in light of the apportionment of genetic variation within and between groups. For 85% within and 15% between group variation, there are 700 excess adverse drug reactions per 1,000 patients predicted for a recessive effect model and 300 for a dominant model. We found high numbers of predicted Black and Hispanic excess adverse drug reactions for widely prescribed platinum chemotherapy compounds, such as cisplatin and oxaliplatin, as well as controlled narcotics, including fentanyl and tramadol. Our results indicate that race and ethnicity, while imprecise proxies for genetic diversity, correlate with patterns of pharmacogenomic variation in a way that is clearly relevant to medical treatment decisions. The effects of this variation is particularly pronounced for Black and Hispanic minority groups, owing to genetic differences from the majority White group. Treatment decisions that are made based on (assumed) White pharmacogenomic variant frequencies can be harmful for minority groups. Ignoring clinically relevant genetic differences among racial and ethnic groups, however well-intentioned, will exacerbate rather than ameliorate health disparities.

Project description:ImportanceBreast cancer (BC) is the second leading cause of cancer death in women, and there is a substantial disparity in BC mortality by race, especially for early-onset BC in Black women. Many guidelines recommend starting BC screening from age 50 years; however, the current one-size-fits-all policy to start screening all women from a certain age may not be fair, equitable, or optimal.ObjectiveTo provide race and ethnicity-adapted starting ages of BC screening based on data on current racial and ethnic disparities in BC mortality.Design, setting, and participantsThis nationwide population-based cross-sectional study was conducted using data on BC mortality in female patients in the US who died of BC in 2011 to 2020.ExposuresProxy-reported race and ethnicity information was used. The risk-adapted starting age of BC screening by race and ethnicity was measured based on 10-year cumulative risk of BC-specific death. Age-specific 10-year cumulative risk was calculated based on age group-specific mortality data without modeling or adjustment.Main outcomes and measuresDisease-specific mortality due to invasive BC in female patients.ResultsThere were BC-specific deaths among 415 277 female patients (1880 American Indian or Alaska Native [0.5%], 12 086 Asian or Pacific Islander [2.9%], 62 695 Black [15.1%], 28 747 Hispanic [6.9%], and 309 869 White [74.6%]; 115 214 patients died before age 60 years [27.7%]) of any age in the US in 2011 to 2020. BC mortality per 100 000 person-years for ages 40 to 49 years was 27 deaths in Black females, 15 deaths in White females, and 11 deaths in American Indian or Alaska Native, Hispanic, and Asian or Pacific Islander females. When BC screening was recommended to start at age 50 years for all females with a 10-year cumulative risk of BC death of 0.329%, Black females reached this risk threshold level 8 years earlier, at age 42 years, whereas White females reached it at age 51 years, American Indian or Alaska Native and Hispanic females at age 57 years, and Asian or Pacific Islander females 11 years later, at age 61 years. Race and ethnicity-adapted starting ages for Black females were 6 years earlier for mass screening at age 40 years and 7 years earlier for mass screening at age 45 years.Conclusions and relevanceThis study provides evidence-based race-adapted starting ages for BC screening. These findings suggest that health policy makers may consider a risk-adapted approach to BC screening in which individuals who are at high risk are screened earlier to address mortality due to early-onset BC before the recommended age of mass screening.

Dataset Information

Human microbiome variation associated with race and ethnicity emerges as early as 3 months of age.

Publications

Human microbiome variation associated with race and ethnicity emerges as early as 3 months of age.

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