Groundbreaking genetic research has found, for the first time, that your genes may influence how you respond to a specific diet. The latest findings suggest that the way each person’s body metabolizes particular types of food is highly individualized. The healthiest food option for one person, may not be the optimal dietary choice for someone else.
This research was conducted by William Barrington, Ph.D., a researcher from North Carolina State University in the laboratory of David Threadgill, Ph.D., at Texas A&M University. These findings will be presented in a lecture, "Pathophysiological Responses to Dietary Patterns Differ with Genetic Backgrounds," at The Allied Genetics Conference on July 15, 2016 in Orlando, Florida.
Based on this cutting-edge research, it appears that one reason most diets fail may be due to a previously unrecognized genetic component—which determines how each person's unique body metabolizes different foods.
If, in fact, there isn't a "one size fits all" way to eat healthiest, following strict dietary rules may actually backfire—especially if you aren't genetically suited for the particular type of rigid diet you're consuming. For example, the Mediterranean diet (which has been hailed as being universally healthy) may actually not be as healthy for some people as eating a typical Western diet.
This new study has broad implications. First, individuals who want to eat the healthiest diet for their personal well-being may someday be able to pinpoint what type of diet is actually best for him or her via genetic testing. Second, these findings might evolve into a call-to-action for the U.S. Food and Drug Administration (FDA) to fine-tune dietary recommendations that reflect the need for more personalized 'precision nutrition.' In a statement, Barrington said,
"There is an over-generalization of health benefits or risks tied to certain diets. Our study showed that the impact of the diet is likely dependent on the genetic composition of the individual eating the diet, meaning that different individuals have different optimal diets.
We've largely viewed diet the same way for the last 100 years—assuming that there is one optimal diet. Now that we've identified that this is likely not the case, I think that in the future we will be able to identify the genetic factors involved in the varying responses to diet and use those to predict diet response in humans."
For this study, the researchers used four mouse strains to represent models of genetic diversity. All of the mice in each strain shared the same genetic composition, thus representing the genetics of one person. The genetic differences between any two strains of mice would parallel that of two unrelated people.
Over the course of six months, the mice received food equivalent to today's Western diet, a traditional Japanese diet, a traditional Mediterranean diet, or a high fat, low carb Atkin's-like 'ketogenic' diet. Some of the mice were given standard mouse chow for comparison. All of the mice were allowed to eat as much food as they desired, while the researchers kept close tabs on how much each had consumed.
Throughout this experiment, the researchers were fastidious about matching the test diets closely with what the human equivalent would be for eating the same diet. For example, the Japanese diet used rice as the main carbohydrate and included green tea extract to mimic the effects of this bioactive compound. For the Mediterranean diet, wheat was the main carbohydrate, and red wine extract was included to imitate this key dietary component.
After analyzing the data, the researchers found that the health-related response to each diet was strongly dependent on the strain of a particular mouse. While mice eating the Western diet generally showed negative health effects (including obesity, fatty liver disease, and higher cholesterol) the severity of these health effects varied widely depending on the strain. In fact, one strain of mice was largely resistant to any negative health effects from eating a Western diet.
Interestingly, the Western diet and the ketogenic diet, which are both high in fat, showed opposite responses for two strains of mice. For one strain, the researchers found very negative health effects on the Western diet, but observed zero negative health effects when this strain ate the ketogenic diet. On the flip side, a different strain of mice who ate the ketogenic diet was actually much healthier when they ate the Western diet.
For all of the strains of mice, the ketogenic diet increased calorie burn without any increase in activity level. That said, some strains of mice ate so much on this diet that they still became obese and experienced negative health effects.
To complicate matters further, the researchers also found that the causes for obesity varied between each strain and appeared to go beyond just calories in and calories out. Some mice on a specific diet ate more calories, and this caused them to become obese... However, other mice on a different diet ate fewer calories but still became obese.
When it comes to broad sweeping dietary guidelines, there appears to be little concrete empirical evidence to support certainty when giving nutritional advice.
"Given the metabolic and genetic similarity of humans and mice, it is highly likely that the level of diversity of diet response seen in our study will also be observed in humans," Barrington concluded. "Since there are different optimal diets for different individuals, this underscores the need for precision nutrition, which would identify optimal dietary patterns for each person."
Moving forward, the researchers are going to work on identifying specific genes and biological mechanisms involved in the varying responses to diets. Eventually, this type of research could lead to genetic testing that identifies who is most likely to benefit (or experience negative health effects) by eating a particular diet.