Professor
Center for Metabolic and Liver Diseases

I seek to discover and therapeutically control the metabolic origins of common diseases.
From human twin studies and human genome sequence comparisons, it has become evident that genetics plays a limited and minor role in the origins of common disease. In general, the rarer a disease is, the more likely it is to be of genetic origin. The more common a disease is, the more likely it is to be of environmental and metabolic origin.
Non-infectious common diseases include Alzheimer’s disease, obesity-associated Type 2 Diabetes, most cancers, colitis and the intestinal bowel diseases, multiple sclerosis and various autoimmune syndromes. These diseases originate primarily from environmental and metabolic factors.
Disease has been defined as “active or passive disturbances of cells,” and that “the key to every biological problem must finally be sought in the cell.” From these axioms, attention to the varied composition of normal and diseased cells is essential.
Of the four building blocks and macromolecules of all cells, only two are intrinsically encoded: the nucleic acids DNA and RNA and their encoded proteins. The other two components of the cell are lipids (fats) and glycans (sugars), neither of which is directly encoded by DNA and thus cannot be predicted. Instead, they are metabolic products. We and others have found that lipids and glycans represent the origins of various common diseases and syndromes, including autoimmune disease, diabetes, colitis, and sepsis.
Our research will continue to focus on missing pieces of the puzzle of disease origins with the intent to identify novel and effective preventatives, treatments and cures.
