When I began my Ph.D. research comparing diet responses across varying genetic backgrounds, I ambitiously expected to identify the “best” dietary pattern for health. But, it was quickly apparent that the data did not match the story in my head. As highlighted in the journal Genetics, my study showed there is no “one-size-fits-all” diet for optimal health and personalized, or precision diets, should allow for better health outcomes.
There is a never-ending debate about what makes a healthy diet. In academia, scholars argue about the health effects of various fatty acids and micronutrients.
The debate is just as fierce in the public sector, where gurus proselytize on the benefits of fruit-only diets, or meat-only diets, and everything in between.
I went to graduate school with the intention of settling this debate. I thought, given proper study design, science would tell us what to eat.
But, science gives complicated answers.
It turns out, there is no single dietary pattern that will improve everyone’s health because diets affect us differently based on many factors, most importantly our genetics.
Here’s how we figured out the importance of genetics in nutrition…
In Dr. David Threadgill’s Laboratories at NC State and Texas A&M, my colleagues and I investigated whether three popular diets could promote better health than an American diet across individuals with different genetics.
Our mouse models allowed us to control environment and genetics, impossible in human studies.
We studied diets of human populations with historically positive health outcomes, a Mediterranean diet, a Japanese diet, and a ketogenic diet.
We formulated mouse versions of the human diets, matching the macronutrient ratios, lipid profiles, and types of ingredients. We went as far as including red wine and green tea extracts in the Mediterranean and Japanese diets, respectively. It was the next best thing to making mouse-sized linguini and sushi.
We fed the four diets to four mouse strains, each with unique genetics. Within each strain, mice are genetically identical, just like identical twins. Feeding the diets to a given strain allowed us to compare the health effects of the diets in a consistent genetic background.
The genetic variation between any two strains is similar to the variation between two unrelated people. Comparing the diet responses between strains allowed us to identify how genetics influence the health effects of a given diet.
The American diet was not great for the health of any of the mice. However, the strains varied in the severity of negative health effects. Some of the mice became super fat and had uncontrolled blood sugar. Others got a little chunky but showed few signs of poor health. It depended on genetics.
Our mouse data matched previous observations in people. On average, the American diet is not great for human health. Yet, some people eat terribly without obvious signs of health problems, whereas others quickly gain weight and eventually develop diabetes and heart disease from an American diet.
Next, we sought to identify an alternative diet that would yield better health. Mediterranean and Japanese diets were good candidates, as they were traditionally associated with longevity and low rates of chronic disease. Or, maybe the Maasai in Africa, who ate a high-fat ketogenic diet and had great health, actually had it right. We put all three to the test.
The Mediterranean diet generally improved cholesterol profiles of the mice, again matching the observations of human studies. But, many of the mice still became obese. The Mediterranean diet prevented fatty liver disease in some, but not all of the mice. It depended on genetics.
The Japanese diet looked promising. Most of the mice maintained a healthy weight, normal cholesterol, and good blood sugar control. Yet, one type of mouse developed liver dysfunction from the diet. Most, but not all, of the mice had beneficial outcomes from the Japanese diet. It depended on genetics.
The ketogenic diet had the most diverse health effects. Some mice became obese, and some had poorly controlled blood sugar. Meanwhile, other mice maintained a low body fat percentage and appeared very healthy. Again, it depended on genetics.
The bad news from our study was that we did not find a single diet that could improve the health of all individuals.
The good news was that at least one diet improved health in each genetic background.
We found that a diet really cannot be called “healthy” without considering the individual eating the diet, and particularly the individual’s genetic makeup.
Of course, these were mouse studies. So, do we humans respond in the same way?
The data suggests that we do. Similar interpersonal variations in diet responses are often observed, though not often discussed, in human studies. The evidence suggests that people vary in how a diet affects their health.
Emerging from this study and related research is a growing field known as “precision dietetics,” which aims to expand our knowledge of nutrition and genetics and meld this knowledge into individualized nutrition recommendations.
Soon, we hope to better predict how nutrition influences health on an individualized basis in order to provide meaningful, personalized dietary guidance that result in real health benefits.
Until then, we can use what science has demonstrated, certain dietary patterns generally yield positive health outcomes, but individual results results may vary. Starting with these generally healthy approaches, we can adjust our diet to find what works for us.