Hunger and appetite may sound similar, both resulting from an assortment of biochemicals communicating between the body and the brain. However, biologically, hunger and appetite are miles apart. Hunger is the physical needof the body to sustain itself. Appetite is a desirethat is affected as much by emotions as by physiological factors.
Highlights
- The culprit behind bingeing and emotional eating is a disbalance between the brain’s reward system and dopamine, the “feel-good” hormone,
- Studies have linked obesity and higher BMI to weaker dopamine release in the brain, especially in the dorsal striatum area,
- Reward deficiency syndrome occurs when dopamine fails to actively provide the gratification it should. While one factor for this syndrome is genetic, research shows that eating less can actually alter our brain’s reward system and increase dopamine receptors.
Eating is rarely a simple cycle of ‘get hungry–eat–get full–stop’. The happiness one associates with food makes getting the right nourishment a complex idea, as anyone who has succumbed to indulging in food that makes one “feel” good rather than eating healthy can understand. Certain comfort foods provide instant delight and work well for a while. Indulge the craving too often, and you find yourself wanting that food more and more to feel the same pleasure as before. The culprit behind bingeing and emotional eating is known as reward deficiency syndrome (RDS)—a disbalance between the brain’s reward system and dopamine, the “feel-good” hormone.
Dopamine and food addiction
The human brain is wired to repeat life-sustaining actions by associating them with sensations of pleasure or reward. This is exactly what happens when we eat appetizing food—our brain rewards us with a hit of dopamine.
Complications occur when modern junk food is thrown into the mix. Research reveals that processed or junk food can trigger a far stronger and longer-lasting feeling of reward than healthier, more wholesome foods. Almost all of us have experienced how snacking on a rich dessert can feel far more satisfying than eating a piece of fruit.
When a person frequently does something that produces too much dopamine, its receptors in the brain begin to downregulate—lower their levels—in order to keep things in equilibrium. Fewer receptors demand more dopamine to reach the same amount of gratification and lead to ‘withdrawal’, causing a fall in dopamine activity and setting off craving, unhappiness and the need for another fix. Essentially, one begins to eat more in order to feel as rewarded as before, or develops ‘tolerance’.
Withdrawal and tolerance are classic signs of addiction; in this case, addiction to highly processed, refined food rich in unnatural concentrations of rapidly absorbed sugar, oil and salt.
How obesity rewires the brain
Dopamine alone does not tell us why overeating and the risk of developing obesity are more of a problem for some than others. Some can stop at one cookie or one slice of pizza, but for others, that can be near impossible. This can come down to how our bodies respond to the ‘binge eatability’ of certain foods, and obesity can make one more susceptible to the pull of overeating.
Obese people tend to have a greater desire for food while enjoying it less. Research demonstrates that obese people, who have higher BMIs than normal, react differently to food stimuli than people with normal BMIs. Studies have linked obesity and a higher BMI to weaker dopamine release in the brain, especially in the dorsal striatum area. The dorsal striatum, the area associated with reward and motivation, shows a greater response to food cues than to the actual act of eating itself in obese people; research also correlates a higher BMI with fewer receptors in the dorsal striatum to bind dopamine, thus leading to overeating.
In essence, the reward systems of obese people are wired towards creating a dopamine deficiency, urging them to eat pathologically as compensation. This failure of the dopamine reward system is called reward deficiency syndrome.
Reward Deficiency Syndrome
Reward deficiency syndrome, or RDS, occurs when dopamine fails to actively provide the gratification it should, leading to emotional eating and overeating. Conversely, RDS can often be the consequence of overconsumption as much as a cause of it, meaning that the dopamine release only changes in the wake of changes in eating habits to avoid overstimulation. It is convenient to think of it as building a tolerance to the dopamine released by eating; after a point, it takes more and more for the receptors in the dorsal striatum to be sated.
This point of view is supported by research that shows that people who had lost weight had decreased levels of dopamine receptors, likely in response to increased levels of dopamine. Further research undertaken on subjects two years after their weight loss to assess whether the loss normalized dopamine binding found an increased number of dopamine receptors, thus establishing that reduced receptor availability caused by obesity can be reversed.
Another major reason for fewer dopamine receptors is genealogy. There are five dopamine receptors (DR) genes, named DRD1 through DRD5. Of these, DRD2 occurs in two forms: DRD2 A2, a variant of the gene that is found in two-thirds of the population and carries a reduced risk of RDS; and DRD2 A1 that results in 30-40% fewer receptors and occurs in the remaining population. Research has also established a relationship between obesity and DRD2 A1 and an additional risk of addictive behaviour.
RDS and its role in addictions has been an area of much research. Traditionally, anti-substance abuse programmes and medications for blocking dopamine have been espoused to counter addiction, but a review of the research done on the subject proposes that while this works in the short-term, activating dopamine receptors rather than blocking them might yield better long-term benefits. Research indicates that dopamine agonist therapy, which involves increasing receptors or enhancing dopamine release, can be effective as an adjunct therapy to counter addictions, ADD, depression and obesity.
Conclusion
Popular opinion posits that our consumption of food, in quantity and type, is dependent on the choices we make and the willpower we have, holding us responsible for curbing emotional eating. However, this can be a limited perspective on what is a nuanced science. Overeating and obesity cannot simply be tied down to personal control, food choices or metabolism. They are also dependent on the wiring of our brains and how it responds to the food we do eat, and often the food we wish we were eating, making some people more susceptible to overeating.
Dopamine is the hormone responsible for the gratification we receive from eating foods we enjoy, and failure in providing this gratification is called the reward deficiency syndrome. While one factor for this syndrome is genetic, research shows that eating less can actually alter our brain’s reward system and increase dopamine receptors. A better understanding of the connection between emotions and overeating expands the horizons of our insights into eating right.
Disclaimer: The contents of this article are for general information and educational purposes only. It neither provides any medical advice nor intends to substitute professional medical opinion on the treatment, diagnosis, prevention or alleviation of any disease, disorder or disability. Always consult with your doctor or qualified healthcare professional about your health condition and/or concerns before undertaking a new healthcare regimen including making any dietary or lifestyle changes.
References
- https://www.ncbi.nlm.nih.gov/pubmed/27383008
- https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0117959
- https://www.frontiersin.org/articles/10.3389/fpsyg.2014.00919/full
- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3124340/
- https://www.sciencedirect.com/science/article/
abs/pii/S0140673600036436
