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Obesity, Dopamine and Addiction: A Few Speculative Thoughts on “The Biggest Loser”
The New York Times recently published a feature article by Gina Kolata, a well-known journalist on obesity related issues, focusing on the contestants from the popular reality show “The Biggest Loser”.
The popular press doesn’t do enough justice to the interesting results from the original scientific article from Dr. Kevin Hall’s group.
“The Biggest Loser” is not that bad of a weight loss behavioral intervention.
Kolata’s article portrayed “The Biggest Loser” as an ineffective intervention, but this is not the case when the data is examined in context. “The Biggest Loser” is a reality show in which contestants compete to lose as much percent weight in the course of 30 weeks. Winners get paid $250,000. The competition can be thought of as a very extreme version of Contingency Management (i.e. using extreme financial incentives to create behavioral change) as a treatment for obesity. 14 contestants were recruited and studied rigorously at the National Institute of Health started out on average at 328 lbs and lost 128 lbs in those 30 weeks.
Kolata’s article portrayed “The Biggest Loser” as an ineffective intervention, but this is not the case when the data is examined in context.-Sean X. LuoIn the next 6 years, while most gained most of their original weight back, there’s still a mean weight loss of 12% compared to baseline, which is sizable. The Kolata article was quick to obscure this finding. The average weight for the 14 at the end of 6 years is 288 lbs (i.e. on average the contestants lost more than 30 lbs).
Very few, if any, behavioral interventions for obesity can achieve an average rate of 10% weight loss at the end of 6 years. A recent meta-analysis reports that a typical combined behavioral and lifestyle intervention delivered a general medical clinic causes a 3% weight loss . “The Biggest Loser” is actually extraordinarily successful.
This result alone immediately makes me think; what if we do another round of 30 weeks on the same group? Would we then, at the end of another 6 years, get another 10% overall weight loss? If we do this over and over, at the end of 5 rounds (i.e. 30 years), would we get 50% reduction of weight?
Given the average age of these contestants are 35, at the end of 30 years is where they turn 65, and when increased metabolic disorders, such as diabetes, would greatly cause significant medical morbidity and cost the most healthcare dollars.
Relapse to food binges is comparable to relapse to drugs, especially dopamine-releasing drugs of abuse, such as cocaine.
One contestant said, “What people don’t understand is that a treat is like a drug…two treats can turn into a binge over a three-day period. That is what I struggle with.” This type of description is very reminiscent of the classic scenario of using cocaine in binges under impulsive stressors. Contingency Management, as I talked about in an earlier blog post, appears to be dependent on the appropriate functioning of the dopamine system in the brain.
Two other pieces of evidence lead me to the speculation that relapses, in many circumstances, possibly involve the dopamine neurotransmission. First, obesity is over-represented in patients with Attention-Deficit/Hyperactivity Disorder (ADHD), an interesting phenomenon that’s reviewed recently in the American Journal of Psychiatry .
Second, psychostimulants – medications that induce the release of dopamine in the brain – likely can treat Binge Eating Disorder, which is a collection of psychiatric symptoms that primarily manifest as impulsive lack of control over food. Vyvanse is an example of such a drug that was recently FDA approved for this indication. However, not every obese person has Binge Eating Disorder or ADHD, and not every person with Binge Eating Disorder is obese. My conjecture is represented by the following figure:
This suggests treatment possibilities: Future research projects can test adjunct treatment of psychostimulants to see if they prevent relapse, especially for those who are severely obese for: 1) post-bariatric surgery 2) post aggressive weight loss programs, especially for those who are both obese and have ADHD.
“Precision” weight loss treatments require addressing both the metabolic component and the addictive component.
The original research report says “most subjects regained a significant amount of the weight lost during the competition, but there was a wide degree of individual variation and a mean weight loss.” (emphasis mine). “The Biggest Loser” is a better treatment for some than for others, and treatment-patient matching would be highly beneficial.
The biggest finding from the article is that the resting basal metabolic rates dropped for the contestants from 2607 kcal/day to 1996 kcal/day at the end of 30 weeks, and 6 years later was even lower at 1903 kcal/day, even though most of the contestants regained their weight back. However, what exactly is 1900-2000 kcal/day?
The Kolata article made it sound like, as you lose 100 lbs, your metabolic rates slow down to such a degree that you basically will gain weight back even if you starve yourself. This is clearly false.
The Kolata article made it sound like, as you lose 100 lbs, your metabolic rates slow down to such a degree that you basically will gain weight back even if you starve yourself. This is clearly false.-Sean X. LuoTo give you a sense of what 1900 kcal a day feels like, the average daily calorie intake in 1970 in the US is about 2168 kcal/day. What this means is that in order to maintain steady weight, you would have to eat approximately a breakfast muffin less each day compared to an average 1970s resident of the US. This is quite a low caloric intake compared to our current average (2700 kcal/day), but is by no means impossible for most of us to achieve in the long run. Those who gained the weight back likely were genetically “endowed” with the “gift” of a somewhat lower basal metabolic rate, but this effect alone can’t explain everything (i.e. most of us would be able to sustain a 1900-2000 kcal/day diet, even though perhaps we’d feel a bit hungry here and there, as if you were living in the 70s.)
Even though most of us can sustain this 1950 kcal/day diet, most of the contestants for “The Biggest Losers” cannot. Their muscles are a bit more efficient, but their brains are much worse off in being able to appropriately respond and resist food related stimuli. It’s the interaction between the brain and the muscle that creates the severe obesity phenomenon.
Different people are obese for different reasons. Some people are outlandishly obese because they are especially unlucky in hitting multiple of these reasons. Treatment of obesity therefore requires matching treatment to the patient’s particular reason of being obese (a.k.a. “Precision Medicine”). One very interesting finding from the study was that the thyroid system was acting very strangely in the Biggest Losers: while T4 and TSH were normal, T3 dropped significantly at the end of the 30 weeks of the competition.
For the aficionado, TSH is a hormone that should increase in response to dropping T3 in our body in a “feedback” system to maintain a steady metabolic rate. It appears that the natural feedback loop is broken when people starve. Is it possible that supplementing T3 would prevent regaining weight after dramatic weight loss? Is it possible that a combination treatment of psychostimulant with T3 supplement is even more effective? We would have to conduct more research to find out.
Dramatic weight loss programs like “The Biggest Loser” are quite effective as behavioral treatments, though admittedly most of the constants regain most of their weight back, and become obese again in 6 years. Financial incentives can be potent treatments for obesity, just as they are for other substance use disorders.
A more effective treatment program for obesity will require treatment tailoring: one treatment will not fit all.
Image Courtesy of Shutterstock
 Cortese, Samuele, et al. “Association between ADHD and obesity: a systematic review and meta-analysis.” American Journal of Psychiatry 173.1 (2015): 34-43.