Eating for pleasure is nothing new. Binge eating disorder is nothing new. Ability to have excess food to binge is.

In nature, there is no free sugar or free fat. Energy is stored in complex whole food packages and one or the other form. Nuts and seeds have their energy stored in the form of fat and grains for example in the form of complex sugars or carbohydrates, and they come with fiber and other substances. Our brain had never been exposed to refined sugar or fat before and especially never been exposed to a combination of the two in high doses all at once. For example, when we eat ice-cream or milk chocolate, we have sugar and fat combination that does not exist in nature. What happens in the brain is the same thing that happens when you inhale crack cocaine.

Crack cocaine itself is a refined product. Cocaine naturally occurs only in the coca plant. You cannot get high at that high level if you chew the leaves as Indian tribes do. It is a traditional stimulant to overcome hunger, fatigue, and thirst.

However, when we extract or in other words refine the cocaine or sugar or fat it is a different story. We can eat poppy seeds as much as we like but when we refine the opium and inject it into the vein or drink the poppy tea, well, here comes the magic dragon. In typical research involved with hunger and weight regulation, the focus was on so-called metabolic or homeostatic hunger. Metabolic hunger is driven by real physiological necessity and is most commonly identified with the rumblings of an empty stomach. By the 1980s researchers had mapped out all of the main hormones and neural connections responsible for metabolic hunger.

By the late 1990s, brain imaging studies and experiments with rodents had begun to reveal a second previously unknown biological pathway. This pathway was underlying the process of eating for pleasure. Like I wrote before in the case of obesity standard regulatory system will tell the brain that we have fat deposits stored for an extended period and that we can endure little hunger. Overeating is a form of drug addiction.

What was found was that extremely sweet or fatty food that we have today but were not present in nature, captivate the brain reward circuit in much the same way that cocaine and gambling can do. Even just seeing the food will trigger the brain response. As quickly as such food meets the tongue, taste buds give signals to different areas of the brain. That will result in a response that will trigger the release of the neurochemical dopamine. Frequently overeating highly palatable foods saturate the cerebellum with a significant amount of dopamine that forces the brain to ultimately adjusts by desensitizing itself, decreasing the number of cellular receptors that identify and respond to the neurochemical.

Having a high and constant dopamine level is a form of stimulus that is over-excessive, something called supernormal stimuli. It is a term that evolutionary biologists apply to represent the stimulus that will evoke a response more significant than the stimulus for which it evolved, even if it is artificial. The food industry uses it all the time almost in every possible way they can think of. They even try to link emotional responses and feelings of social acceptance and wellbeing with supernormal stimuli.

Consequently, as a resistance build-up, people may in truth, proceed to gorge as a process of recollecting or even preserving a sense of well-being. This is possibly the reason why the downregulation of leptin receptors in the brain happens also.

There was a series of research done from 2007 to 2011, at the University of Gothenburg in Sweden. They proved that the release of ghrelin (the hunger hormone) by the abdomen immediately enhances the discharge of dopamine in the brain’s award circuit (1). This is a significant finding. They also discovered that medications that prevent ghrelin from binding to neurons restrain the tendency for overeating in people who are obese.

Under normal conditions, leptin and insulin suppress the release of dopamine. In theory, this should reduce the sense of pleasure as a meal continues. Recent rodent studies suggest that the brain stops responding to these hormones as the amount of fatty tissue in the body increases (2). Thus, continued eating keeps the brain awash in dopamine even as the threshold for pleasure keeps going up. A form of maladaptation to our current environment and way of eating and living. If we switch the stimuli from food to cocaine or nicotine or caffeine, we can suppress the hunger drive. Alternatively, also vice versa. If we stop smoking appetite goes up. Tobacco use was linked to hunger suppressing effects even among Pre-Columbian indigenous Americans. Cigarette smoking for weight loss might not be a good idea, because we will swap one addiction for another. You can try extracted nicotine in products like chewing gum or electronic cigarettes with a caffeine combination. There is, for example, particular drugs that target the brain hunger center for lowering appetite like Belviq, Contrave, Saxenda, Phentermine, and Qsymia. Phentermine is an amphetamine. Regular “speed” can work also. The anti-seizure drug Topamax for epilepsy and migraine headaches lowers the appetite and is registered to treat binge eating disorder. If everything else fails, there are seven weight loss surgeries registered so far, from cutting, stapling to ballooning. All because of supernormal stimuli of refined food.

There is a group of sensitive individuals that will respond excessively to delicious foods. They would have to excessive response in the brain reward circuit that will dramatically alter their brain chemistry. Overstimulated brain reward circuit will override any self-control mechanism so that willpower will rarely if ever be sufficient to force them to resist eating those foods once they are around creating a binge eating disorder. Researchers at The Scripps Research Institute in Jupiter, Florida found that in rats that have been given unrestricted access to high-calorie foods, their brains showed neurological changes in their reward circuit (3).

High-calorie foods, in this case, were sausage, bacon, cheesecake, and chocolate. It was the first study that showed that the neurological mechanism that drives people into drug addiction is also driving the compulsion for overeating, pushing people into obesity. Some of the rats were given only one hour a day to feast on high-fat foods, while others had unlimited access 24 hours a day. Both groups were given access to a typical, healthy lab rat chow food. The one group that possessed infinite access to high-calorie food ate little to none of the standard bland low-calorie chow alternatives. They quickly had grown obese because they eat as much as they could, about twice the amount of calories as the control. The big surprise was that even the rats that had limited access to junk food did their best to keep up. During that one hour, they ate as much as they can with no stopping. They managed to consume, on average, 66% of their daily calories in the course of that one single hour per day and quickly developed a pattern of compulsive binge eating disorder. It was also observed that a group of obese rats with unlimited access to junk food had shown a severely increased threshold for reward levels. The same thing happens with drug addiction. After showing that obese rats had clear addiction-like food-seeking behaviors and that an increased threshold for reward levels is forcing them to seek more and more to reach the same level of reward the researchers investigated underlying neurological mechanisms that are responsible for these changes.

There is a specific receptor in the brain known to play a significant role in vulnerability to drug addiction, the dopamine D2 receptor. In the brain, there are neurotransmitters like dopamine. Dopamine is a feel-good chemical that will get released when we have some pleasurable experience like sex or food. The D2 receptor responds to dopamine. Cocaine, for example, is a drug that increases dopamine levels in the brain by blocking its retrieval. Overstimulation of the dopamine receptors with any supernormal stimuli will eventually lead to neural adaptation in the form of downregulation of the receptors. Also, this was shown in the study too. Levels of the D2 dopamine receptors were significantly reduced in the brains of obese animals. The same thing happens in drug addicts. To determent the level of influence of dopamine in the rats eating behavior, a virus was inserted into the brains of a test group of animals to knock out their dopamine D2 receptors. Addiction-like behavior happened almost instantly. The next day their brains changed into a state that was consistent with an animal that had been overeating for several weeks. Also, the animals had become compulsive in their eating behaviors and developed binge eating disorder. The research that took three years to finish confirms the addictive properties of junk food.

Animals binge-eating lipids and animals binge-eating sugars experience different physiological effects, but the most substantial impact can be brought by the combination of neural effects from both of these ingredients. Actually, the most desired food for the lab rats appeared to be a food item with the highest combination of fat and sugar: cheesecake.

Related Posts

1. 
   Cause of Obesity- Maladaptation or addiction
2. 
   Hunger- Just a normal “emotion”
3. 
   Minnesota starvation experiment- Why dieting makes us fat. The psychology of hunger.
4. 
   Obesity Risk Factors
5. 
   Refined sugar health risk correlations- Understanding the basics
6. 
   Supernormal stimuli- Binge eating disorder and appetite regulation
7. 
   What Is a Processed Food? -Understanding the Basics

Sources:

Passages selected from a book: “Go Vegan? Review of Science: Part 1” [Milos Pokimica](p36)

1.  The Stomach-Derived Hormone Ghrelin Increases Impulsive Behavior. doi: 10.1038/npp.2015.297
2. Ghrelin and food reward. doi: 10.1016/j.neuropharm.2019.01.001
3. Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats https://doi.org/10.1038/nn.2519
4. Is dopamine a physiologically relevant mediator of feeding behavior? DOI: https://doi.org/10.1016/j.tins.2007.06.004