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Animal models of addiction do not generalize well to substance dependence in humans as there are different criteria involved. For example, in animals "addiction" has been traditionally defined by a caged laboratory animal's tendency to press a lever for a reinforcing substance, whereas in humans the criteria for dependence (the clinical term for addiction) include a number of behavioral criteria and consequences that could never exist in laboratory animals (American Psychiatric Association [APA], 2000). These criteria include: tolerance, withdrawal, taking more of a substance than originally intended, a history of unsuccessful attempts to quit, inordinate amounts of time spent in using and seeking the substance, a reduction in activities (occupational, social, or education) due to use, continued usage despite adverse consequences (APA, 2000). Interestingly, only three of these criteria need to be met in a year, so one need not demonstrate significant physical signs such as tolerance and withdrawal in order to be diagnosed with an addiction, whereas in animal models of addiction the animals are often forced to become physically addicted while being maintained on some addictive drug like cocaine.
Deroche-Gamonet, Belin, and Piazza (2004) added some clarity to this dilemma by having rats self-administer cocaine until groups of high or low drug seeking following withdrawal of the drug could be identified. Then, high seeking group was observed to conform to three diagnostic criteria: difficulty stopping intake, high motivation to use, continued use despite harmful consequences (a shock) which are somewhat similar to the DSM-IV criteria. Despite the apparent flaws (e.g., rats deprived of food for a significant period would display the same behavior for food pellets) the authors conclude that animals may display addictive behaviors. Unfortunately, addiction is a much more complex matter than animal models are able to express as the consequences in humans and motivations are related more to more complex behaviors not observed in rats such as cognitions, understanding of right and wrong behaviors, and other behaviors far too complex to be observed in rodents. Moreover, rodents do not seek help to quit using, do not try to quit using, are not chastised by their fellow rodents for being addicts, and do not understand the consequences of usage. Simple stimulus response behavior is certainly a portion of addiction, but this behavior does not define dependence.
However, animal models of addiction have helped to elucidate the neurobiology involved in addiction. This research was originally inspired by a classic study in biological psychology that investigated the reward center of the brain in rats (Olds and Milner, 1954), which borrowed from B.F. Skinner's (1938) instrumental learning paradigm. In the Olds and Milner study rats received direct electrical stimulation, via a surgical procedure, to certain areas of the brain following pressing a lever. Olds and Milner observed that rats would continue to press the lever when the septal area of the brain was stimulated. Consequently, this early research by Olds and Milner suggested that the structures in or surrounding the septal area of the brain play a vital role in reinforcement of behavior and the sensation of reward.
With respect to the pharmacological properties of addiction, it has been discovered that with repeated usage of a drug certain neural pathways associated with reinforcement are altered (Volkow & Li, 2004). The neurotransmitter most often implicated in animal models of addiction is dopamine (DA) although a number of neurotransmitters are involved in different drugs of abuse. The abuse of drugs leads to an increase extracellular dopamine concentrations in limbic system, particularly the nucleus accumbens (Volkow & Li, 2004). This process is similar to any reinforcing behavior except that some researchers believe that the reinforcing effects of substances that are abused are due to the ability of the substances to exceed the time and magnitude of the increase in DA from other "normal" activities that are reinforcing (Volkow & Li, 2004). Volkow goes as far as to say that when someone is addicted to a drug like cocaine their ability not to chose to use the drug has been compromised by these physiological changes (Volkow & Li, 2004); however, this is a ridiculous notion because if this were true then no method outside of medication or surgery would be successful in treating dependence. Addicts to chose to quit and even though they need may need help, being and addict is not an indication that they have lost the ability to chose.
The changes in the brain that occur in binge-eaters are similar to the changes that occur in substance dependence. The most clear common factor between food and drug intake is that both activate the DA link in the reward circuits of the brain (Di Chiara & Imperato, 1988). Blocking these DA receptors reduces behaviors related to feeding in animal models, whereas blocking the mechanisms that inhibit this process lead to binging (Wise & Rompre, 1989). For instance, it has been found that endogenous opioids augment the feeding behaviors of animals. Injections of opioids into the mesolimbic DA system and midbrain (the ends of the reward systems) inhibit the action of GABA (which inhibits dopamine release and thereby inhibits feeding behaviors) and results in a propensity for the animal to eat large quantities of high-fat and high sugar foods (Volkow & Wise, 2005). In contrast, the ingestion of sugary of hi-fat foods and fluids lead to an increase opioid receptor binding within this region (Kelley et al., 2003). Hagan and Moss (1991) previously found that rats maintained on a food deprivation/re-feeding schedule were more responsive to the hyperphagic effects of butorphanol, an opioid agonist, suggesting that binge eating led to alterations within the endogenous opioid system. There have been subsequent studies to support this hypothesis (e.g., Boggiano et al., 2005), whereas the opioid antagonist, naloxone, blocks binge eating in rats that were maintained on a feeding and re-feeding schedule followed by a footshock stress (Boggiano et al., 2005). Thus, animal models of binge eating suggest that there is possibly some disruption in the process of the inhibition of DA in humans that binge eat. However, drugs of abuse actually alter the neurobiology associated with this process by their actions, whereas binge eating does not result is such a dramatic neurobiological alteration and may reflect more innate factors.
It also appears that stress can play an important role in animal models of binge eating. For instance rats deprived or restricted of food do not demonstrate significant increases in food intake once sated; however, if they are given a footshock stress and then allowed free access to food they will overeat significantly (Hagan et al., 2002). But the effect of stress on binge eating in the rats was very specific and the stress must occur following a minimum of three cycles of restriction/re-feeding and had to be in close proximity to the last cycle (Boggiano et al., 2005).
Like the animal models of addiction, animal models of binge eating do not generalize fully to binge eating in humans. For example, food intake is also regulated by a number of mechanisms peripheral to the central nervous system such as blood glucose levels and stomach satiety mechanisms, so the neural changes documented in animal models of binge eating do not fully explain binge eating. Moreover, humans do not entirely act based on stimulus response situations, but are able to delay responses, reflect on choices, and decide what and how much they will eat in a given situation. Their brains are more complex and include sophisticated executive control systems not found in animals. This sophisticated brain also has resulted in technological advances that have taken much of the need for heavy physical activity out of the human lifestyle and replaced it with a number of sedentary activities where eating and drinking fatty and sugary foods are the norm. Binge eating in people is also sensitive to the effects of stress and the specific nature of binge eating depends on the type of stressor (physical or psychological) and its duration (whether it is acute or chronic). Individual differences also play a role based on genetic and environmental factors such as upbringing, the importance of food as a social mechanism, and others (Adam & Epel, 2007). What all this means is that there are critical differences between animal and human studies of binge eating, and therefore major difference between the act of binge eating in people and in animals. The most important difference is that of that of the subjective feelings such as boredom, distress, the abstinence-violation effect, or the perception of a loss of control found in many studies of binging episodes in people cannot be inferred in animal studies. Therefore, models attempting to investigate binge eating in animals can only focus on the precursory circumstances leading to binge eating in people to produce binge related behaviors in animals and cannot address many of the more important issues.
The notion that there exists the potential for a "food addiction" is only made possible by the changes in the diagnostic criteria that are now used to diagnose…[continue]
"Binge Eating Animal Models Of Addiction Do" (2012, September 13) Retrieved October 27, 2016, from http://www.paperdue.com/essay/binge-eating-animal-models-of-addiction-82085
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