PHOTOS: Image downloaded from https://imgur.com/gallery/rzCOM
Text: Alejandra Misiolek Marín
The addiction to food.
This post is the third and last part explaining the relationship between obesity and the brain.
At the end of the last post, I raised the following questions:
Why are the dopamine circuits increased in obese people? Does obesity cause them to be activated or does a person get fat because they are activated? Which came first, the chicken or the egg?
To answer these questions, we will look at what has been learned from scientific experiments. In one experiment, mice were subjected to a diet rich in hypercaloric foods for 15 weeks to observe changes in dopamine levels. It was found that, on the one hand, the diet led to obesity and, on the other hand, it was shown that in these mice less dopamine was released in the nucleus accumbens and striatum in response to the consumption of the food compared to mice that ate feed. To test whether the response was solely to food or whether it was generalized to substances that increase dopamine levels, the same mice were given amphetamine. It was interesting to note that the dopaminergic response to amphetamine was also attenuated.
How do we interpret these results? On the one hand, we know that obesity causes changes in the brain and not the other way around. However, we seem to be programmed to overeat and choose hypercaloric foods. The changes in the brain are a decreased dopamine response, not only in response to food but also to other stimuli. This means that food no longer gives us as much pleasure when we are obese as it does when we are thin.
But how do we know if the same thing happens in humans?
There are studies that show the same results in humans. For example, in another study conducted with women who gained weight over a period of 6 months, it was found that, compared to those who did not gain weight, they suffered a decreased response of striatal body activity in response to tasty foods.
In addition, it has been shown that obese people have a decreased response to food consumption compared to lean people (Volkow, 2011), and what actually decreases is the signaling of dopamine D2R receptors in response to the consumption of hypercaloric foods. In other words, obese people have less availability of D2R receptors compared to individuals with normal BMI. (Kenny, 2011)
We know that these receptors are to blame for what is happening because of studies that have been done with D2R receptor knockdown mice (mice that have been bred in the laboratory directly without these receptors). When these mice gain weight, they show an acceleration in compulsive consumption behaviours compared to mice with D2R receptors.
On the other hand, studies show that weight loss in obese individuals is related to increased density of D2R receptors in the striatum. (Wang et al., 2008). And this confirms that obesity is the egg and change is the chicken.
So, these studies seem to contradict the results of the previous studies described in the previous post. However, this contradiction is apparent because it actually leads us to a new hypothesis, which synthesizes the previous ones: while hyperactivation of the dopaminergic system has created a very high expectancy prior to consumption, the response to actual consumption is diminished, so overconsumption of hypercaloric meals may represent an attempt to compensate for deficient D2R signaling related to the reward deficit in obese individuals. (Geiger et al., 2009; Johnson, 2010; Kenny, 2011).
Since obesity is characterized by overconsumption despite the desire to limit it and one’s knowledge of the negative health consequences, we can conclude that drug addiction follows a similar pattern – loss of control and inhibition despite the devastating effects on the individual. So, obesity and addiction share the traits of compulsive disorders. In other studies, it has been shown that obese mice continued compulsive consumption despite punishment. On the other hand, the same aversive stimuli interrupted the consumption of thin mice. We can conclude that obesity is the determinant of food addiction.
- Geiger, B. M., Haburcak, M., Avena, N. M., Moyer, M. C., Hoebel, B. G., & Pothos, E. N. (2009). Deficits of mesolimbic dopamine neurotransmission in rat dietary obesity. Neuroscience, 159(4), 1193-1199.
- Johnson, P. M., & Kenny, P. J. (2010). Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats. Nature neuroscience, 13(5), 635.
- Kenny, P. J. (2011). Reward mechanisms in obesity: new insights and future directions. Neuron, 69(4), 664-679.
- Stice, E., Yokum, S., Blum, K., & Bohon, C. (2010). Weight gain is associated with reduced striatal response to palatable food. Journal of Neuroscience, 30(39), 13105-13109.
- Volkow, N. D., Wang, G. J., & Baler, R. D. (2011). Reward, dopamine and the control of food intake: implications for obesity. Trends in cognitive sciences, 15(1), 37-46.
- Wang, Y., Beydoun, M. A., Liang, L., Caballero, B., & Kumanyika, S. K. (2008). Will all Americans become overweight or obese? Estimating the progression and cost of the US obesity epidemic. Obesity, 16(10), 2323-2330.