The following has been reprinted from NC Research Campus,
Eat a healthy and balanced diet. That is the first advice that people who need to reduce their risk for cardiovascular disease (CVD) receive.
But what if some nutrients in “healthy” foods interact with an individual’s genetic make-up in a way that actually increases their risk for CVD.
That is the question that Brian Bennett, PhD, is trying to answer. Bennett is an assistant professor of genetics, nutrition and heart disease with the UNC Chapel Hill Nutrition Research Institute (NRI) at the NC Research Campus in Kannapolis. He is pushing the boundaries of nutrigenomics, which is the study of how genes and diet interact, to reveal new clues about individual susceptibility for atherosclerosis and other forms of CVD.
In peer-reviewed journal articles published in the past year, Bennett pioneered findings on the connection of CVD and genetic-nutrient pathways, genes and gut microbiota. He has also established new research models for the study of nutrigenomics as it relates to heart disease.
Systems Genetics and Cardiovascular Disease
Bennett specifically studies atherosclerosis. More commonly known as hardening of the arteries. It is caused by plaque, which is made up of cholesterol, fatty substances, cellular waste, calcium and other substances building up in the arteries as people age. The plaque restricts blood flow making the arteries less flexible, which raises the risk of heart attack, stroke and other forms of CVD.
In journal article published in G3: Genes, Genomics and Genetics in October 2014Bennett worked with scientists at Jackson Laboratory, UNC Chapel Hill and the NRI to identify Apobec 1 on Chromosome 6 as a gene related to the development of atherosclerosis.  Apobec1 is an “editing enzyme” that regulates low-density lipoprotein (LDL), the “bad” cholesterol that contributes directly to atherosclerosis.
The buildup of plaque also creates inflammation in the arteries of the heart.  In a paper published in BMC Med Genomics in August 2014, Bennett and his colleagues analyzed a pathway of genes that identified a gene called Cd44 as a “critical mediator of atherosclerosis.” The research showed that alterations in the expression of Cd44 “mediate inflammation” related to atherosclerosis “through a complex transcription network involving a number of previously uncharacterized genes.”
“Our systems genetics approach, which attempts to model the link between genetic differences and disease susceptibility, is a powerful approach to understand disease,” Bennett said. “We are building on our previous studies and now are focused on how these underlying genetic variations interact with dietary components to affect susceptibility to cardiovascular disease.”
Understanding Diet and Genetic Susceptibility
Bennett’s lab is also looking for clues regarding how diet affects individual susceptibility to CVD. He studies specific gut microbiota and a metabolite (TMAO) related to “cardiometabolic health”. He determined that differences in the microbiota were maintained due to diet. This research established a model for further studies of gut- CVD connection. The results were published in the journal Mammalian Genome in August 2014.
“A focus of my laboratory is to understand how differences in the bacteria that line our digestive tact affect susceptibility to cardiovascular disease.  This aspect of biology and its impact on human health has grown tremendously in the last few years,” Bennet explained.
In Bennett’s research he employs a variety of in-bred and out-bred mouse models, computational analysis and cell culture. He also takes advantage of the scientific expertise and instrumentation at the David H. Murdock Research Institute, which is located on the NCRC.
“I like to use newer more advanced mouse genetic approaches to look at how gene and diet interact to affect cardiovascular disease,” Bennett explained. “The goal is to understand the genetics of heart disease and discover better and more effective therapeutic targets for CVD.