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When Diet Meets Gene

The fact that our genes and diet interact is nothing new. Not everyone who eats a lot of junk food becomes overweight. Only some people taste the bitter compounds found in spinach. Then came the unraveling of the human genome, and the field of nutrigenomics soon followed. In nutrigenomics, scientists focus on how our genes influence the requirements and responses to nutrients.

In recent years, spurred by faster and cheaper DNA technologies, nutrigenomics has yielded novel insights into how our genes influence diet’s role in cancer and other chronic diseases. It is helping scientists understand how foods interact with genes and may someday help health practitioners identify who may gain the most cancer-fighting benefit from certain foods.

DNA Double Helix

Finding the Link

“In nutrition, we’ve been treating everyone as if they’re the same, lumping them together, and then we get very noisy data,” says Steven H. Zeisel, MD, PhD, Director of the University of North Carolina’s Nutrition Research Institute and one of the panelists on AICR’s expert report. Imagine dealing with a population in which 40 percent of people have a gene variant that makes them respond to a nutrient. Depending on the mix of study participants, some might respond and others may not, “and so the study concludes it’s nonsense. But if we understood the importance of the gene variant you could predict who would respond. Now [that same study] makes tremendous sense and you can draw a conclusion.”

The majority of research in nutrigenomics involves single nucleotide polymorphisms (SNPs), referred to as “snips.” A SNP is a variant or misspelling in a single “letter” of our DNA (A, C, G, or T), a nucleotide.

Scientists have identified over 10 million SNPs thus far, with some common SNPs occurring in 5 to 50 percent of the population. It is estimated that every person carries approximately 50,000 such genetic misspellings. Many have no effect on gene expression. But a fraction of SNPs appear to play a role in a broad spectrum of cancer-related lifestyle factors, from fat metabolism to how our bodies interact with alcohol, folate, and vegetables.

wheat stocks in field
Choline, found in eggs, meat, and wheat germ, is also needed for healthy fetal development.

SNPs at Work

Studies have found a number of relatively common SNPs influence nutrient requirements. In one of his recent studies, Dr. Zeisel and his colleagues identified a SNP that increases susceptibility to dietary deficiency of choline, an essential nutrient linked to influencing the risk of certain cancers, such as breast and colon. Three of four people in the UNC-area carry this gene variant, noted Dr. Zeisel.

Choline, found in eggs, meat, and wheat germ, is also needed for healthy fetal development. In England, scientists at the Institute of Food Research pinpointed a SNP found in half the population to explain why broccoli may decrease the risk of prostate cancer for some more than others.

Only the Beginning

Given the wealth of unexplored genes, experts say we are only in the early phase of understanding the diet-genotype connection to cancer. And while one SNP might influence how you react to a certain food, other foods may reduce the risk of cancer through different mechanisms.

“At the moment people are picking on the genes they think are important,“ says Richard Mithen, PhD, head of the Plant Natural Products and Health Programme at IFR, and lead author of the broccoli study. Dr. Mithen is beginning a 5-year follow-up study looking at hundreds of polymorphisms. “It’s finding the genes we don’t know about that’s next.”

The dietary advice to eat fruits and vegetables every day, and cut down on red meat and saturated fat is just really sound advice to everyone.” In the coming years, he adds, we hope to offer advice to fine-tune our diets to reduce the risk of progressive diseases like cancer. “But it’s still early.”

—Excerpted from a feature in ScienceNow.

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