There's something poignant about the possibility that one of the reasons obese people eat too much is because they are unable to take pleasure in the taste of their food. But according to a new study published in Science, that's exactly what happens:
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.
The experiment was elegantly designed. Subjects were given sips of a chocolate milkshake inside an fMRI machine. The activation of the striatum - an area rich in dopamine neurons and involved in the processing of hedonic rewards - was then monitored. Sure enough, obese people tended to have reduced activation in the striatum: they kept on sipping the milkshake in a manic search for satisfaction. A second study found that, over time, people with a polymorphism that leads to reduced dopamine receptors in the striatum also tended to put on weight, suggesting that obesity is, at least in part, triggered by a shortage of neural pleasure. Of course, this contradicts the popular (and deeply unfair) cultural stereotype of obesity, which assumes that people who are overweight are gluttons, unable to resist temptation. In fact, they are the opposite of gluttons: the reason they eat too much is because they don't enjoy their food enough. They keep on sipping the milkshake precisely because it isn't pleasurable. The finding reminds of that old Jewish joke in the beginning of Annie Hall:
There's an old joke - um... two elderly women are at a Catskill mountain resort, and one of 'em says, "Boy, the food at this place is really terrible." The other one says, "Yeah, I know; and such small portions."
For another really cool finding on obesity and dopamine, check out this blog post.
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I immediately wonder whether this effect also applies to sex, drugs, gambling, and anything else people get addicted to, and/or make self-destructive decisions concerning...
I'd be curious to know which set of responses formerly obese people--people who had been obese but who have changed their diet and exercise regimens such that they no longer are obese--have. If their brains tend to react in the way that the'lean' people's brains react, then it may be that this is something changeable. If not, then they are certainly making herculean efforts to be more healthy.
Interesting. It has also been shown that anorexics have unusually high dopamine receptor activity (in the basal ganglia), suggesting that dopamine receptor sensitivity would be (roughly) inversely correlated to food consumption. I wouldn't have expected a uniform trend from one extreme to the other -- wonder what happens in the middle with average-weight people or bulimics.
A quick pubmed search reveals that most studies seem to be looking at genetic factors. I like that the study you cited looks at a direct biological output (dopamine sensitivity). The paper below demonstrates why genetic studies often fail to demonstrate causality:
Prog Neuropsychopharmacol Biol Psychiatry. 2008 Apr 1;32(3):620-8. Epub 2007 Oct 10
OBJECTIVE: The sensitivity of dopamine reward pathways has been implicated in the risk for various psychiatric disorders including compulsive overeating. The evidence is divided, however, about the direction of causal association. One argument is that a Reward Deficiency Syndrome is the risk factor, while others contend that hyper-sensitivity to reward enhances the motivation for pleasurable activities like eating. Unfortunately, little human research has bridged the gap between psychological and neurobiological approaches to brain reward functioning and disorder. The present study addressed this issue by implementing psychological and biological markers of reward sensitivity in the assessment protocol. METHODS: Adults with binge eating disorder (BED) were compared to samples of normal-weight and obese controls on two personality measures of reward sensitivity and were genotyped for six markers of the DRD2 dopamine receptor gene. RESULTS: Genotype x Group ANOVAs revealed significant main effects and an interaction on the personality measures for Taq1A. BED and obese subjects reported greater reward sensitivity than normal-weight controls, but only among those carrying the A1 allele. We also found that normal-weight controls with at least one copy of the T allele of the C957T marker had significantly lower reward sensitivity scores than any of the other groups who did not differ from each other. CONCLUSIONS: Given evidence linking the A1 allele with reduced receptor density, an inverse relationship was expected between psychological measures of reward sensitivity and presence of the A1 allele. One explanation for our findings could be that the BED and obese participants possess another genetic variant that interacts with the A1 allele to produce higher dopamine activity. These findings have implications for future studies of the molecular genetics of BED and obesity, and for behavioural and pharmacologic therapies targeting these conditions.
This sort of stuff fascinates me because I have pretty much always been fat. It's been especially on my mind because 3 years ago through diet and exercise I dropped from 400 pounds down to 160. Then after a month at 160 I developed what I later found out was refeeding edema and started having horrible, horrible food cravings, to the point where I literally could not sleep at night because all I could think about was the time my wife would be gone and I could binge.
I've been on prozac, paxil, and zoloft since then and none of have done one lick of good about eating. The best I can say is that I no longer spend the entire day thinking about when I will be alone and can eat with abandon. On the other hand, I just never stop eating once I start.
This study makes some sense to me because nothing I eat really seems to taste that great and I just keep eating looking for something tastes good or until my stomach hurts.
So now if they could just find a pill for pleasure, I'd be set. :)
When I nervously or mindlessly eat and get into a rote routine of it, I firmly believe that it dulls the receptors just like alcohol diminishes sexual pleasure by dulling the nerve receptors: a little is good, too much is not so good.
I don't have access to the full text of the article, and I'm curious:
1. Did they just assume all the participants liked chocolate milkshakes? (I don't think I'd show much response either, especially if it was a nasty fast-food milkshake, but a really good chocolate truffle, on the other hand...)
2. Did they do anything to control for the guilt and shame women - especially fat women - feel about eating "naughty" foods? Do negative emotions affect those same dopamine circuits?
My personal experience of becoming/being obese is what the researchers initially expected. If these results really show what the researchers claim they do, and "normal" people get even more pleasure from food than I do, then all I have to say is wow.
So I only think I like food?
I recently began experimenting with hormones for menopause symptoms. When I add the progesterone into the mix, I become insatiably hungry. I can not be satisfied. Similar to being pregnant there is some drive to eat.
Not so much like the mind numbing binge type eating. Just a constant ache.
I don t believe binging is in searching for the taste or the will...I think you are looking down the wrong path. I think it is a complete state of euphoria, and out of body experience. Try taking a dog's bowl away when he starts to eat. There is some kind of drive to eat and turns off the
ability to think. Try sharing a popcorn in the theater with a binge eater. They will hold the control of the popcorn and watch every bite you take.
Is this in the adrenals? We get driving pleasure from things that are designed to make us survive...
reproduction, eating, fleeing, fighting?
Maybe if we can understand that...?
In the zoo, when the monkey's are fed.. what happens.
Some eat on the fly, and some hide it? Go back and eat later, alone...?
It is something in the survival mechanics... one gals suspicion.
Begs the question of whether non-obese people eat only until their desire for pleasure is satisfied.
As something of a fitness obsessive I stopped eating for pleasure some years ago. For the most part, I eat the number of calories I've calculated is appropriate given my activity level for the period in question. Yes, I'd rather eat things that taste good than things that taste bad, but I stop eating when I've eaten the appropriate amount, not when I've derived adequate satisfaction from my food. I make exceptions for special occasions but generally this is how I eat.
All this emphasis on whether our food makes us happy enough seems to miss the point. How much food you eat is still a personal decision. It's not dictated to you by the pleasure centers of your brain.
thanks
Who knew obesity could be so complicated
Before you were born, your parents weren't as boring as they are now. They got that way from paying your bills, cleaning your clothes and listening to you talk about how cool you are. So before you save the rain forest from the parasites of your parents' generation, try "delousing" the closet in your own room.
Your school may have done away with winners and losers, but life has not. In some schools they have abolished failing grades; they'll give you as many times as you want to get the right answer. This doesn't bear the slightest resemblance to anything in real life.
Bones begins in the year 2005, and tells the story of a series of case files, solved weekly, by the unlikely alliance of Dr. Temperance "Bones" Brennan's forensic anthropology team at the Jeffersonian Institute (a thinly veiled allusion to the Smithsonian Institution) and FBI Special Agent Seeley Booth. By examining the human remains of the murder victims, Dr. Brennan and her team provide scientific expertise and an outsider's perspective to the world of criminal investigation to the FBI...