The third post in this series is a continuation of the second, in that we will continue looking at the psychology and neuroscience behind food addiction. Post IV will begin looking at the cultural aspects related to food addiction and compulsive overeating, so stay tuned.
Homeostatic and hedonic hungers, while fundamentally different in motivation, are both evolutionary important. Both motivations would’ve helped drive an individual to eat plenty of calories in order to satisfy the body’s energy needs in times of food scarcity or uncertainty. Thus, humans either learned, or innately possessed, the ability to eat past satiety. Hypothetically, if a hunter-gatherer were to stop eating at the first sign of satiety then experience a prolonged period of time between their next meal, say the hunting was slow or they were traveling through an area with little vegetation, they would put their body at risk for usurping its energy stores. To protect against this, they would use hedonic hunger to override homeostatic hunger. We still possess this ability today. Though because we live in a time of food abundance, developing the habit of continually eating past our homeostatic set-points has proven to be severely detrimental to health and the main cause of obesity. The theory of ‘motivating operations’ (Tapper, 2005) focuses on explaining the motivations for food seeking. However, they completely ignore any aspect of overeating. They claim that food seeking will increase and hedonic enjoyment of food will be enhanced with deprivation. The reverse implies that with satiety, seeking behaviors and enjoyment of food will decrease. This does not account for the phenomenon that is binge eating. However, ‘motivating operations’ remains somewhat in line with the incentive sensitization model in that they both involve a decrease in food liking during overeating. When wanting increases due to sensitization, liking decreases.
The ยต-opioid system plays a key role in hedonics. In a study using highly-palatable foods (high sugar and fat), opioid administration to sated rats resulted in a stronger desire for food than seen in rats who had been deprived of food (Hayward & Low, 2005). Opioids are thought to increase the hedonic properties of food. More evidence comes from a study where administration of opioids in the nucleus accumbens of rats induced episodes of binge eating on fat (Hayward & Low, 2005). Taken alone, a pure fat foodstuff, such as Crisco, has very little rewarding taste properties unless it is mixed with another highly-palatable food such as sugar. Therefore this study serves as a good indicator of the role of opioids in increasing a food’s hedonic qualities, suggesting that individuals with food addiction may be hypersensitive to opioids in the brain or have an overactive reward system. Sugar is thought to act in the brain similarly to an opioid. Referring back to the aforementioned Avena et al. (2008) study, recall that they found that rodents on a high sugar chow diet exhibit addictive-like behaviors as the researchers increased daily sugar intake over a period of 28 days. The rats also exhibit opioid-like withdrawal symptoms when given the opioid antagonist naloxone (3 mg/kg). Their symptoms included anxiety, teeth chattering, tremor, head shakes, and a drop in body temperature (Avena et al, 2008) suggesting that natural rewards such as sugar act on similar neural substrates as illicit drugs. Hopefully now the correlation between compulsive overeating and other addiction disorders is becoming apparent.
Homeostatic and hedonic hungers, while fundamentally different in motivation, are both evolutionary important. Both motivations would’ve helped drive an individual to eat plenty of calories in order to satisfy the body’s energy needs in times of food scarcity or uncertainty. Thus, humans either learned, or innately possessed, the ability to eat past satiety. Hypothetically, if a hunter-gatherer were to stop eating at the first sign of satiety then experience a prolonged period of time between their next meal, say the hunting was slow or they were traveling through an area with little vegetation, they would put their body at risk for usurping its energy stores. To protect against this, they would use hedonic hunger to override homeostatic hunger. We still possess this ability today. Though because we live in a time of food abundance, developing the habit of continually eating past our homeostatic set-points has proven to be severely detrimental to health and the main cause of obesity. The theory of ‘motivating operations’ (Tapper, 2005) focuses on explaining the motivations for food seeking. However, they completely ignore any aspect of overeating. They claim that food seeking will increase and hedonic enjoyment of food will be enhanced with deprivation. The reverse implies that with satiety, seeking behaviors and enjoyment of food will decrease. This does not account for the phenomenon that is binge eating. However, ‘motivating operations’ remains somewhat in line with the incentive sensitization model in that they both involve a decrease in food liking during overeating. When wanting increases due to sensitization, liking decreases. 
The ยต-opioid system plays a key role in hedonics. In a study using highly-palatable foods (high sugar and fat), opioid administration to sated rats resulted in a stronger desire for food than seen in rats who had been deprived of food (Hayward & Low, 2005). Opioids are thought to increase the hedonic properties of food. More evidence comes from a study where administration of opioids in the nucleus accumbens of rats induced episodes of binge eating on fat (Hayward & Low, 2005). Taken alone, a pure fat foodstuff, such as Crisco, has very little rewarding taste properties unless it is mixed with another highly-palatable food such as sugar. Therefore this study serves as a good indicator of the role of opioids in increasing a food’s hedonic qualities, suggesting that individuals with food addiction may be hypersensitive to opioids in the brain or have an overactive reward system. Sugar is thought to act in the brain similarly to an opioid. Referring back to the aforementioned Avena et al. (2008) study, recall that they found that rodents on a high sugar chow diet exhibit addictive-like behaviors as the researchers increased daily sugar intake over a period of 28 days. The rats also exhibit opioid-like withdrawal symptoms when given the opioid antagonist naloxone (3 mg/kg). Their symptoms included anxiety, teeth chattering, tremor, head shakes, and a drop in body temperature (Avena et al, 2008) suggesting that natural rewards such as sugar act on similar neural substrates as illicit drugs. Hopefully now the correlation between compulsive overeating and other addiction disorders is becoming apparent. Individuals with food addiction undoubtedly exhibit certain behaviors and personality traits that are strikingly similar to those of drug addicts. The main difference lies in the fact that food addiction is more accurately referred to as a ‘behavioral addiction:” one involving abuse of natural rewards (Davis et al, 2009). Drugs of addiction also act directly on the brain. Food acts indirectly, through the gut. However, gut peptides have strong connections to the dopaminergic (DA) system (Dagher, 2009), a system closely-linked to liking and wanting of illicit drugs. Eating, unlike drug-taking, is intrinsically required for human survival. And just as higher doses of drugs result in higher potential for addiction, we can see that larger ‘meals,’ or more accurately, binges, can also result in high potential for addiction. Grigson (2002) asserts that foods, like drugs, have the ability to alter brain mechanisms in ways that contribute to their increasingly compulsive use. In their paper on the neurobiology of eating and drug abuse, Corwin & Hajnal (2005) outline four things that must be considered when operationally defining non-homeostatic appetitive behavior: quantity consumed, quality or type consumed, context in which the behavior occurs, and the specific kind of behavior that is directed toward obtaining and consuming the commodity of interest.
These aspects are to be used in for defining all types of non-homeostatic behavior, including compulsive overeating, not just drug addiction behavior. It is normal to overeat on occasion. Such overeating can be effectively regulated by the body’s systems because they are prepared to work harder at certain times than others. This type of overeating is referred to as compensatory. However, when it becomes compulsive, it renders itself dysfunctional because the human body is maladapted to deal with chronic stress to the degree that excessive sugar and fat intake will induce. Long-term health issues follow. Parallels can be made to drug taking in this regard as well. Recreational use, with adequate detoxification periods between use episodes, does not result in chronic negative effects on physical and mental health. However, when use escalates to abuse, extremely negative effects follow.
The neuro-anatomical substrates associated with compulsive overeating are the same as those implicated in all appetitive behaviors, including drug taking. The main regions involved in appetitive behavior are the amygdala, hippocampus, orbitofrontal cortex, insula, and striatum (Dagher, 2009). When considered as a pathway, one entity, these substrates are all implicated in the following: learning about (food) rewards, setting the incentive value of stimuli in the environment, budgeting attention and efforts toward (food) rewards, and integrating homeostatic information about energy stores and gut contents with information about the outside world (availability of food)(Dagher, 2009). These substrates have been found to respond equally to food cues and drugs cues (Dagher, 2009) as well as contain prominent DA projections. When a blockade was applied to this DA pathway, all rodent responding for drugs and food was abolished (Wise et al, 1978). And lesions to these areas impair feeding behavior (Wise et al, 1978). In order to fully understand eating behavior, one must understand the interaction between the gut (enteric nervous system) and the central nervous system. The key players in these interactions are hormones, which project to the hypothalamus.
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