This research summary is similar to the earlier one where self-control predicted overweight status; Angela and team have co-authored a similar paper, though based on a different data set and controlling for more confounds.
- Self-control is a variable of concern as ” In this obesogenic context, self control, the capacity to regulate behavior, attention, and emotion in the service of personal standards and goals, is required to forego immediate gratification and choose instead options that protect against weight gain.”
- Weight control may be important for teens, not only for its long term health associations, but also because of its impact on physical attractiveness.
- This study was a prospective longitudinal study that looked at over 100 children in a school setting, and measured their self control and BMI while in grade 5 (mean age 10.5) and correlated it with their BMI when in grade 8.
- Self-control was measured using a variety of methods. Students filled 2 self-report measures of self-control: The Impulsivity subscale of the Eysenck I6 Junior Questionnaire and The Brief Self-Control Scale. Parents as well as teachers also filled the informant version of Brief self-control scale. Apart from this Kirby Delay-Discounting Rate Monetary Choice Questionnaire was used to present hypothetical choices between small reward now and large reward later, meant to judge the delay of gratification. Also an actual behavioral delay of gratification task was used to ascertain self-control. A composite measure was created from these measures.
- Potential confounds like demographics (SES), Happiness (measured by SSLS and PANAS-C) and Intelligence (Otis- Lennon School Ability Test—Seventh Edition Level F) were measured and controlled for in the analysis.
- The authors replicated their earlier result that low self-control in childhood, indeed leads to weight gain in transition to adolescence. High self-control, on the other hand, protects children form weight gain.
I had blogged previously regarding the obesity and dopamine connection and how obese people have been shown to have lesser dopamine receptors in the brain. The studies till now were correlational and there was a possibility that eating more food and the resultant obesity may be a cause and may play a part that decreases the dopamine receptors just like in addicted individuals(the addicted people also have less dopamine receptors).
Here is the abstract of the study:
The dorsal striatum plays a role in consummatory food reward, and striatal dopamine receptors are reduced in obese individuals, relative to lean individuals, which suggests that the striatum and dopaminergic signaling in the striatum may contribute to the development of obesity. Thus, we tested whether striatal activation in response to food intake is related to current and future increases in body mass and whether these relations are moderated by the presence of the A1 allele of the TaqIA restriction fragment length polymorphism, which is associated with dopamine D2 receptor (DRD2) gene binding in the striatum and compromised striatal dopamine signaling. Cross-sectional and prospective data from two functional magnetic resonance imaging studies support these hypotheses, which implies that individuals may overeat to compensate for a hypofunctioning dorsal striatum, particularly those with genetic polymorphisms thought to attenuate dopamine signaling in this region.
Now this should not be news to readers of this blog, because this was exactly what I had proposed in my earlier blog pots. Low number of dopamine receptors leading to lower dopamine rush, leading to overeating and obesity. It is heartening to see the same being confirmed; though we will need more evidence to settle the direction of causality.
E. Stice, S. Spoor, C. Bohon, D. M. Small (2008). Relation Between Obesity and Blunted Striatal Response to Food Is Moderated by TaqIA A1 Allele Science, 322 (5900), 449-452 DOI: 10.1126/science.1161550
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.