PHOTOS: Image downloaded from slothilda.com
Text: Alejandra Misiolek Marín
In this post I will analyze the topic of vicious circles in obesity and the role of the reward circuit and dopaminergic pathways.
It is a very extensive topic so I will divide it into several parts.
Why are we talking about obesity?
According to the longitudinal study published in NEJM (2017) in which the development of obesity was investigated in 195 countries over 25 years, 107.7 million children and 607.7 million adults were obese in 2015. Given that during the last 40 years in 70 of these countries obesity rates have doubled and 4 million people a year die because of it, it seems that we are facing a global pandemic, in the face of which it is important to understand its causes.
How can we control the intake at the psychobiological level?
Intake control is achieved through the collaboration between two parallel systems:
- On the one hand, the homeostatic pathway, which is responsible for maintaining the balance between hunger and satiety. This pathway acts thanks to hormonal regulators such as, for example, leptin and ghrelin. These hormones act on our brain, and specifically on the circuits of the hypothalamus. The hypothalamus is a very important structure in our brain in terms of food, as it regulates what we eat to maintain the right balance of energy levels. Dysfunctions of the components of this system, such as congenital leptin deficiency, can result in a constant positive energy balance and the development of obesity.
- On the other hand, we have the reward system that regulates eating behavior. This system is responsible for the pleasure we feel when we eat. We will focus more on this pathway because it is where psychology and medicine converge. This pathway includes the dopamine circuits (mesolimbic dopaminergic pathway) and the limbic regions*, to which the hypothalamus belongs. It is here, in the hypothalamus, that these two systems collaborate.
For these reasons, eating is determined by basal metabolism, by the amount of stored fat and the secretion of hormones and peptides. On the other hand, it is influenced by the hedonic sensations that food transmits to us.
To put it another way and with an example: an obese person who has a lot of adipose tissue, secretes a lot of leptin that blocks the desire and decreases the intake because the energy balance is positive. Is this so?
In theory yes, but from experience we know that it is not. Why?
Because eating activates the very powerful reward circuit (dopaminergic) and we perceive dopamine as pleasure: when we binge eat, the dopamine raises and we feel pleasure.
It has been proven that foods with little taste are not usually consumed in excess while tasty and calorie-rich foods are still consumed, even if the necessary levels of energy (satiety) have been achieved. Thus, it is this hedonic/dopaminergic pathway that allows us to voluntarily ignore physiological satiating cues and continue eating in a satiated state. Obtaining the pleasurable effects of tasty foods is a very powerful motivational force that in certain individuals can overcome homeostatic signals and explains the very rapid growth of obesity rates in industrialized societies.
The key question is: Why do both laboratory animals and humans continue to eat to the point of obesity? What is wrong with the control system I have just described?
This and many other related questions I will answer in the next post.
*nucleus accumbens and striatum receive dopaminergic input from the ventral tegmental area and substantia nigra; the lateral hypothalamus regulates the reward response; and the orbitofrontal cortex and amygdala encode information related to the value of eating, at the cognitive and emotional levels, respectively.
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.