THE NEUROBIOLOGY OF BINGE EATING

 THE NEUROBIOLOGY OF BINGE EATING

Introduction

Various studies have been carried out to investigate overeating in both clinical and pre-clinical research. This has been as a result, in part, of the scientific interest to understand the etiology as well as treatment methods for the increasing problem of obesity. Rats have been commonly used in the development of the models of binge eating. According to Avena (2007) palatable diets have been used in most of the studies in inducing overeating in the animals. The results of the studies are pertinent to the reported neurobiology of addition. Nevertheless, it has been noted that non-homeostatic feeding behavior or over-eating can happen without necessarily causing an increase in body weight or becoming obese. It is common knowledge that increased body weight or being obese can have detrimental implications on physiology, neural processes, and behavior. It is also important to understand the way these factors are impacted by overeating behavior (Rebecca et al. 2011).

Animal models of binge eating

One of the animals models used in explaining binge eating is the sugar addiction model. A study carried out in 1987 study revealed that sugar operated as a kind of analgesic drug. Morphine blocker was found to work positively in blocking the effects of the drug. Just like drug addition, it was revealed in the study that animals can become addicted to sugar (Hagan, et al. 2002). DesMaisons (1998) highlighted that idea of sugar addiction as a quantifiable physiological state. She suggested that this state was as a result of opioid receptors activation. The hypothesis of her model was that sugar addiction fell in the same DSM IV for other drug abuse.

In 2002, fifteen years after the model was suggested, a study carried out at Princeton started revealing the neurochemical implications of sugar. The study suggested that as a result, sugar could play the role of a gateway drug. In the study, chow was fed to rats, together with a 25 percent solution of sugar the same concentration as available in soft drinks. The results of the study were collected one month later (Deroche-Gamonet, Belin and Piazza, 2004). It was revealed that the rats had become addicted to the solution; they were also revealed to eat less chow and had an increased intake of the sugary drink to 200 percent. It is asserted by the sugar firms that the same kinds of effects are evident in animals consuming drinks which tasted sweet, even if they did not have any calories. Nevertheless, it is suggested by some researchers that the caloric value may not have any impact. It is sugar as well as the taste of sweetness that cause brain stimulation through activation of endorphin receptor regions. These are the same chemicals which use of morphine and heroine activate in the brain (Rebecca et al. 2011).

According to Hagan, et al. (2002) another study carried out in 2008, revealed that sugar has effects on dopamine and opioids in the brain. This means that there is the possibility of having addictive possibility. The study referred to bingeing, craving withdrawal, and cross-sensitization, and provided each of the factors with operational definitions demonstrating that bingeing of sugar acts as a reinforcer. The behaviors are suggested to be associated with neurochemical alterations occurring in the brain when one is addicted to drugs.         

Research has developed methods of diagnosing food addiction with the application of the model. To establish the guidelines for identification of addicted individuals, such methods or scales as the Yale Food Addiction Scale, have been created. This tool is the initial psychometrically validated method for the establishment of the criteria for food addiction, on the basis of DSM-IV criteria for substance abuse modification. Together with the development of definite identifying behavioral method, studies of genetics and the brain have supported the idea that food addiction is as possible as drug addiction and can be easily diagnosed using the same methods used in the diagnosis of drug addiction (Volkow and Li, 2004).  

One of the main strengths of the model is that it is the very first model that has established an inclusive set of criteria related to addiction when rats are fed with palatable food (Deroche-Gamonet, Belin and Piazza, 2004). This means that the model presents an effective mechanism in the study of mechanisms of the brain related to regular binge-like bouts. The model has the potential of helping with the creation of pharmacotherapies with the aim of suppressing bingeing or possible food addiction. These kinds of treatments might be important in those persons with binge eating disorders comorbid substance use. Avena (2007) posits that an additional strength of the model is that, given the fact that the bingeing animals do not necessarily become obese or overweight; it is possible to separate the behavioral factor of binge-type eating. This is particularly important given that the implications of overweight or obesity can cause alterations in the brain which has an impact on reward. This means that by separating the factor of binge-type and the results of overweight, it is possible to determine the impact of bingeing palatable food.

Other studies have revealed opposing results that have suggested indications of addiction when utilizing other alternating sucrose access programs. Irregular access to sucrose cross-sensitizes with a drug such as cocaine. There is thus, facilitated sensitizing of the DA agonist quinpirole. Additionally, in the animals, anxiety-like behaviors have been revealed where there is restricted availability of diet high in sucrose. Some studies have also noted some behavioral and physiological alterations that propose a negative state in animals which consume sugar sporadically. For example, the withdrawal of sugar has been shown to lower the temperature of the body as well as instigating some indications of aggressive behavior (Berridge, 2009).   

The neural changes that are observed in binge eating

According to Berridge (2009) various neural changes entail needing a reward, enjoying it and creating predictions from cues. These chances are experienced regardless of whether the reward is a drug or a food.  Enjoyment of the reward and wanting the food or drug rewards are behaviors having neural impacts.  The neural chances that occur in bingeing are such changes as in opioid and dopamine receptor binding, acetylcholine and dopamine releasing in the nucleus accumbens, and enkephalin mRNA expression (Szczypka, Rainey and Palmiter, 2000). There is a small part in the nucleus accumbens shell that with the use of endocannabinoid and opioid transmission regulates the craving responses to sweet foods. An important role is played by the ventral pallidum in enjoying the sweet food, as a blocking or abrasion of γ-aminobutyric acid transmission in the part of the brain eliminating liking responses. Alternatively, in the reflexive, wanting is a non-cognitive feeling that depends on the transmission of dopamine from the ventral tegmental part. The chemical is transited to the nucleus accumben, the process also involves the hypothalamus and the amygdale. The main point in this case is that transmission of the chemical tends to be associated with the wanting of the food, and not enjoying or knowledge of the rewards. The release of the chemical can be triggered simply by learning about the cues, such as smell (Volkow and Li, 2004).  

The neural changes that accompany binge-eating are similar to those seen following drug use. The neural changes that accompany binge eating are so similar to those that are evident in the use of drugs. This is because the neural changes work on the idea of reward seeking, whether from the food or drug. The changes start with a behavior that is consciously motivated as a result of expecting a reward.  Various neurotransmitters, such as including γ-aminobutyric acid), dopamine, glutamate, serotonin, acetylcholine and endogenous opioid peptides have been suggested to play a part in the addiction to drugs. Among them, dopamine has been showed to play a major role in the reinforcement of the use of drugs. This has emerged as the case with addition to food. Abuse of drugs or food has been reveled to increase concentrations of the chemical. Particularly, it is evident that the reinforcing impact of drugs or food is caused by the incapacity to exceed the level and period of the rapid increases in dopamine happening when triggered by the reinforcers. The neural effects are the same for drugs and food, only that different foods and drugs triggers the changes differently (Berridge, 2009).  

Experiment

In the experiment, rats are maintained 12-hour food deprivation daily. This is followed by access of 12 hours daily to a 25 percent glucose and chow. There is also a control group that is fed on sugar ad libitum. The results of the experiment are that in a few days, the rats start to increase their consumption of the sweet solution and less consumption of chow. The feeding pattern of the rats completely changes such that they consume larger amounts of sugary solution during the access period. When the solution is withdrawn, there are signs of efforts by the sugar bingeing rats to access the solution. This shows that there is an effect of bingeing on the neurology of the rats that is out of their control. In the study, bingeing has been found to release the neurotransmitter dopamine in the brain (Rebecca et al. 2011).

Similar results are revealed in the form of strong cravings of sweet food on individuals who binge. This is because of the release of dopamine which sends an internal message for them to consume sugary foods even when they are aware of the negative effects. It is only when they consume sugar that they feel satisfied. Just like with the rats, when the sugar is withdrawn the individuals who binge become anxious (Smith and Schneider, 1988).  

The animal model of binge eating

The sugar addiction model, already described earlier in the discussion will be used in explaining sugar addiction on the subjects of the experiment. The model shows that exposure to sugary food or solutions cause addiction on the subjects in the same way drugs do. The model has been used in the interest to understand why addiction to sugar happens in animals exposed to sugary solutions (Smith and Schneider, 1988).  

Testing

Studies of the brain on regions such as the medial orbitofrontal cortex, the anterior cingulate cortex and the amygdale have been used in testing whether they are responsible for individual’s failure to control their consumption of food. This is because these are the parts of the brain that are activated by the use of palatable food. Testing of these parts of the brain with the use of mechanisms such as Scores on the Yale Food Addiction Scale can reveal whether they have a role to play in the craving of some food, similar to craving for drugs. Brain scans can also be used in testing these parts of the brain to come up with conclusive evidence. This is because these changes are more related to binge eating than they are related to increased body weight. This only means that increased body weight cannot be used as a conclusive indicator for food addiction (Smith and Schneider, 1988).

 The treatment of binge eating

The results of the experiment can be used to positively inform the treatment for binge eating. Binge eating has been found to increase the release of dopamine in the brain the same way as addictive drugs. This leads to food addiction or binge eating (Szczypka, Rainey and Palmiter, 2000). This means that with the increase in the release of dopamine, individuals will continue to binge. Withdrawal symptoms are noted in the withdrawal of the food. The results suggest a close association between the levels of dopamine and the urge to eat sugary food. This means that a change in the consumption behavior for people who are already bingeing lies in the changes in the dopamine levels. Regulating the release of the chemical can play a major role in the treatment of bingeing according to the results of the experiment. Research suggests that regulation of the neural chemicals can play a major role in the controlling of bingeing Berner et al. (2011).

Conclusion

Neurological and behavioral research has provided evidence of a similarity between addiction to food and addiction to other drugs.  The similarity has been found stronger in the case of craving for food or drugs. This has led to the lack of control over the craving for eating or using drugs. Research has revealed that the main reason for the inability to control the craving lies in the release of chemicals in the brain such as dopamine. Treatment for bingeing lies in the ability to control the release of these chemicals. A very interesting direction in the research on binge eating is the determination of whether individuals can train to control their craving for the food. If this is possible, it would be an important milestone in the control of obesity and related disorders. The results of such research would also inform health care providers and therapists on advising people to work on their craving.

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