Charles Rotimi, Ph.D.

Dr. Charles Rotimi is a biochemist and a genetic epidemiologist in the National Human Genome Center, Department of Microbiology, College of Medicine, Howard University. He received his undergraduate education from the University of Benin in Nigeria before immigrating to the United States for further studies. Dr. Rotimi started his education in the US at the University of Mississippi where he obtained a masters degree in Health Care Administration. He obtained a second masters degree and a doctorate in epidemiology from the University of Alabama at Birmingham School of Public Health. He is currently Associate Professor in the Department of Microbiology and Director of Genetic Epidemiology, National Human Genome Center at Howard University in the College of Medicine. His long-term scientific interest is directed at understanding the patterns and determinants of common complex diseases including diabetes, hypertension and obesity in populations of the African Diaspora. Collectively, diabetes, hypertension, obesity and their complications explain over 80% of the well-documented health disparity that exists between African Americans and their White counterparts in the US. Contemporary populations of African descent now live in very different social settings, from traditional to fully westernized lifestyles, with varying degrees of genetic admixture. Dr. Rotimi believes that studying these diverse populations may help explain phenomenon like the monotonic increase in hypertension rates as one moves from rural west Africa (about 7%) through the black nations of the Caribbean (about 26%) and the US (about 34%). Taking advantage of the huge contrast in the distribution of risk factors in these contemporary African populations, Dr. Rotimi uses genetic epidemiology models to test whether high rate of diseases like diabetes, hypertension and obesity among African Americans is the result of exposure to higher levels of environmental risk factors, an increased genetic susceptibility, or an interaction between adverse environments and deleterious genes.

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