Research completed on The Biggest Loser contestants showed how much participants' metabolisms changed, even six years after completing the competition. Hall, et al., demonstrated not just a slowed metabolism, but altered circulating levels of the appetite-controlling hormone, leptin.
To learn more about how leptin could have affected the weight regain, I asked Stephan Guyenet, PhD, neurobiologist and writer at Whole Health Source, to explain what all this means about why dieters regain weight.
"We've known for a long time that when a person loses a lot of weight, whether they started off lean or obese, the brain initiates a starvation response designed to regain the lost weight. This includes an increase in hunger and overall food motivation, and a decrease in metabolic rate (calorie burning). We also know that this starvation response happens due to a decline in the circulating level of the fat hormone leptin, because when researchers give small leptin injections to prevent it from dropping during weight loss, the starvation response never kicks in.
Kevin Hall's group has documented a clear example of this in contestants from The Biggest Loser. These people lost an average of 128 lbs (58 kg), and their leptin levels plummeted by 94 percent. After this weight loss, their metabolic rate slowed, and they were burning fewer calories than a person of their current weight should have been, even though they were still technically obese. Again, this is part of the natural starvation response.
The new piece of information that Hall's study added to our knowledge is that this starvation response doesn't go away-- even after 6 years and regaining most of the lost weight. In fact, it got even worse.
This is very different from what happens with weight loss surgeries such as the Roux-en-Y and sleeve gastrectomy procedures. In these cases, the body seems to "defend" a leaner body type, rather than initiating a starvation response to weight loss. So we think that Biggest Loser-type weight loss (portion control plus exercise) and bariatric surgery provoke very different responses from the brain regions that regulate appetite and fat mass. They affect the body weight "set point" in different ways.
This highlights the fact that body weight is biologically regulated, and we can't just expect people to eat less to lose large amounts of weight. We need approaches that target the brain regulation of appetite and body fatness-- like bariatric surgery-- but that ideally don't require modifying the digestive tract! I think there are ways to do this via diet and lifestyle, at least to some extent, but research is ongoing.
If we needed another piece of evidence against the carbohydrate-insulin-obesity hypothesis, this provides it. Despite a 62 percent drop in fasting insulin levels at the end of the weight loss period, which according to the hypothesis should make weight maintenance easier, the unfortunate contestants readily regained weight. Leptin is the primary driver of body fat mass regulation, and insulin does play a role but it may actually be the opposite of what carbohydrate-insulin-obesity advocates suggest."
Though the study did find serum leptin to be significantly lower at the 6 year mark compared to baseline (not adjusted for multiple comparisons), there was no significant correlation between follow-up leptin levels and degree of metabolic adaptation.
"We found no significant correlations between the degree of metabolic adaptation at 6 years and the changes in fasting metabolites and hormones. However, the study was not powered to detect such correlations and it is possible that other unmeasured variables, such as changes in circulating organic pollutants might be more strongly related to metabolic adaptation."