Whole Health Source: Sleep and Genetic Obesity Risk

Evidence is steadily accumulating that insufficient sleep increases the risk of obesity and undermines fat loss efforts.  Short sleep duration is one of the most significant risk factors for obesity (1), and several potential mechanisms have been identified, including increased hunger, increased interest in calorie-dense highly palatable food, reduced drive to exercise, and alterations in hormones that influence appetite and body fatness.  Dan Pardi presented his research at AHS13 showing that sleep restriction reduces willpower to make healthy choices about food.

We also know that genetics has an outsized influence on obesity risk, accounting for about 70 percent of the variability in body fatness between people in affluent nations (2).  I have argued that “fat genes” don’t directly lead to obesity, but they do determine who is susceptible to a fattening environment and who isn’t (3).  I recently revisited a 2010 paper published in the journal Sleep by University of Washington researchers that supports this idea (4).


Dr. Nathaniel Watson and colleagues used twins to tease apart what proportion of obesity risk is due to genes vs. environment, and if sleep duration influences that relationship.  Consistent with other studies, genetics explained 60 percent of the variability in body fatness between participants.  Also consistent with other studies, people who slept less tended to be fatter.  However, what sets this study apart is that they determined how sleep duration influences the relationship between genetics and body fatness.

What they found is nothing short of remarkable.  In people sleeping less than 7 hours per night, genetics determined 70 percent of body fatness, while the environment (lifestyle/diet and ‘random’ effects) explained only 30 percent.  In people sleeping more than 9 hours per night, genetics only explained 32 percent of body fatness, while environment explained 68 percent.  In other words, in people who sleep more than 9 hours, the environment and not genes was the primary determinant of body fatness.

The result was summarized in the following graph:



According to the authors, short sleep duration appears to favor the expression of genetic risk factors for obesity:

Our work suggests latent genetic variability in susceptibility to obesity requires activation by sleep curtailment.

In other words, in an obesity-promoting (low-sleep) environment, people who are genetically susceptible to obesity gain fat, while in a non-obesity-promoting (high-sleep) environment, genetic risk factors are less relevant and don’t influence body fatness as much.  “Obesity genes” act primarily in an obesity-promoting environment.

As a whole, I find the sleep-obesity research quite compelling.  This is one of the reasons why the Ideal Weight Program focuses on improving sleep quantity and quality, a strategy that sets it apart from nearly every other fat loss program.  We combine a tracking system that provides consistent objective feedback on sleep habits, with sleep guidance that helps overcome barriers to restorative sleep.