Obesity: The Dopamine Connection

In a recent news article, there is a surprising revelation, that obese people have fewer dopamine receptors. The article author links this to a state akin to addiction (with amphetamine etc) as in addicted individuals too the dopamine system is involved and after prolonged usage of the drug, the dopamine receptors become less in the system.

It turns out that food also affects the brain’s dopamine systems. When Volkow, who is also director of the National Institute on Drug Abuse, and her colleagues compared brain images of methamphetamine users with obese people, they found both groups had significantly fewer dopamine receptors than healthy people. Even more interesting: The higher the body mass index, the fewer the dopamine receptors — a finding that may open the door to a better understanding of why it is so difficult for some people to lose weight and keep it off.

What role dopamine may play in obesity — and how eating affects it — is still to be determined. No one knows when the obese people in the study lost their dopamine receptors in the brain or if that loss could be reversed with weight loss. Are some people more susceptible to the effects of eating sugary, high-fat fare because they start out with lower levels of dopamine receptors in the brain? Or could eating those foods decrease dopamine receptors? Might food additives, preservatives and other substances also have an effect on dopamine receptors?

While several alternatives are provided above as to why this link exists, I would like to advance my own thoughts on the matter. First and foremost, I would like to speculate that when we eat something , we get a dopamine rush, and all of us carve food (get hungry) when we haven’t had a food-associated-dopamine-rush for a long time. Now, if the dopamine rush that we feel, when eating, is not strong enough, we would still feel hungry. This cycle may lead to obesity. Now, from the above study it is clear, that obese people have fewer Dopamine receptors than the rest of us. thus, when they eat something, though the dopamine released in synapses may be the same as that in normal people, due to lesser dopamine receptors, they will experience a subdued dopamine rush. To compensate for this they may overeat and thus gain weight.

This theory (which seems so obvious, once stated) also explains the fact that why people on anti-psychotics sometimes gain weight as a side effect. the anti-psychotics (most of them) work as dopamine antagonist; i.e. they bind to the dopamine receptors and thus make fewer dopamine receptors available. Thus, with reduced bind able dopamine receptor sites, the food we eat, would not lead to a dopamine rush of great magnitude; thus causing overeating and weight gain.

Here, I would like to highlight that dopamine and serotonin system interact a lot, and as indicated in a previous post, those people who have low serotonin levels in brain (i.e. are depressed) also have reduced sensitivity to sweet taste. Thus, they too overeat sweet items to compensate for their reduced sweet taste. Having low serotonin and fewer D2 receptors, may be a potentially deadly condition that may lead to more food craving (especially sugary food) and may lead to obesity.

Hat tip: Center for emotional wellbeing.

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2 thoughts on “Obesity: The Dopamine Connection

  1. joe85022

    Being obese and a smoker this blog has given me a lot of insight. Dopamine is not only related to food but also to nicotine. The lack of dopamine receptors might explain why nicotine is so addictive in my family. But, I can tell that I did quit smoking for awhile and started eating healthy and exercising more. I lost about 30 pounds in five months. Unfortunately I started smoking again but have maintained the weight loss. I think the key to countering it is in exercise including some for of weightlifting not just walking or running. It made a huge difference for me.

  2. Gladina

    Another less painful method to possibly increase dopamine receptors as well as reduce chronic elevated insulin levels (which is also a cause for overeating and not ever feeling ‘full’) is to of course use a moderate ketogenic diet which is high in fat, moderate in protein and low carbohydrate. I’m not stating anything new here, just that I realize that such a diet can address the insulin problem as well as the dopamine problem.

    Once you get an individual eating this way, it would be interesting to see if that person develops another non-food habit which is in an attempt to still raise dopamine receptor sensitivity. If this was the case, it would then strongly support the dopamine hypothesis of obesity and would then support proponents like Stephen Guyenet and his ‘low food reward’.

    Regardless, even if he WAS somehow correct in his thinking that obesity stems from the brain, I still don’t believe in his prescription of low reward food such as the use of starches etc. Even if the primary reason really WAS reduced dopamine receptor sensitivity which lead to over-eating, the effects of elevated insulin are now the PRIMARY problem. The only way ‘fix’ this is through moderate ketogenic diet. This diet will do two things: it will reduce insulin levels (as we all know) in the context of feeling satiated as well as restore dopamine sensitivity. The neuro-protective effects of ketone bodies in the brain has been well researched and supported though the use for epilepsy, Alzheimers and even Parkinson’s Disease.

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