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These findings are share similarities with those involving alcohol dependent or cocaine dependent subjects in which diminished ventral striatal activation has been reported during the anticipation of monetary rewards [ 5051 ].

The ventromedial njde cortex, functionally connected with the womfn striatum, has been implicated in risk-reward decision-making and the processing of monetary rewards [ 435253 ]. Diminished activation of the thuumbnails prefrontal cortex in subjects nure pathological gambling fhumbnails initially reported in studies of gambling urges and mude control [ 4154 ]. A subsequent study found diminished ventromedial prefrontal cortical activation during simulated gambling, rhumbnails degree of activation correlating inversely with gambling severity in the subjects with pathological gambling [ 49 tjumbnails. More recently, subjects Bb substance use disorders with or without pathological gambling showed diminished ventromedial prefrontal cortical activation during performance wkmen the Iowa Gambling Task [ 55 ].

Together, these data suggest dysfunction of ventral fronto-striatal circuitry in pathological gambling and substance dependence that is linked to aspects of reward processing and disadvantageous decision-making. Another recent study examined in healthy subjects the neural correlates of the near-miss phenomenon [ 56 ]. A near-miss situation occurs when the first two reels thumnbails a slot fhumbnails stop on the same symbol and then the third reel locks on a non-matching symbol. While anticipating the stopping of the third reel, activation of reward processing brain regions e.

During the outcome phase, several of these brain regions e. A region that showed deactivation thus appearing to code these events as non-reinforcing was the ventromedial prefrontal cortex. As ventromedial prefrontal cortical activity has also been linked to loss-chasing in healthy subjects [ 57 ], existing data suggest phenomena hypothesized to be associated with the development of pathological gambling are linked to brain regions in which individuals with pathological gambling show functional abnormalities. Treatments Behavioral and pharmacological treatment strategies for pathological gambling and substance dependence also show similarities.

Gamblers Anonymous, based on the step program Alcoholics Anonymous, is the most widely available form of help for individuals with pathological gambling and attendance has been associated with positive treatment outcome [ 5859 ]. Other behavioral therapies, such as cognitive behavioral therapy, have been adopted from the substance dependence field and shown to be efficacious in the treatment of pathological gambling [ 60 ]. Brief interventions, such as those used in medical settings for assistance with smoking cessation, have shown promise in the treatment of pathological gambling [ 61 ], as have motivational interventions that have shown success in the treatment of drug dependence [ 6263 ].

Multiple pharmacotherapies have been investigated in the treatment of pathological gambling [ 19 ]. As with drug dependence, serotonin reuptake inhibitors have shown mixed results in controlled trials [ 196465 ]. Opioid antagonists, such as naltrexone a drug with approval for the indications of opioid and alcohol dependencerepresent the class of drugs that to date has shown the most promise in the treatment of pathological gambling, particularly amongst individuals with strong gambling urges at treatment onset and those with a family history of alcoholism [ 18 ].

More recently and based on work in drug dependence [ 66 ], glutamatergic agents such as N-acetyl cysteine have been investigated and shown preliminary efficacy in the treatment of pathological gambling. Addiction and pathological gambling Pathological gambling and substance dependence show many similarities. Although specific features also likely distinguish pathological gambling from drug dependence much as specific features distinguish specific forms of substance dependence [ 29 ]existing data suggest a particularly close relationship between pathological gambling and substance dependence that warrant their consideration within a category of addictions.

Addiction and obesity A. Neurobiological Links between Obesity and Thkmbnails Addiction Introduction Obesity is increasing significantly Bbw women nude thumbnails represents a public health concern in both the United Thimbnails and now worldwide. The etiology of obesity is extremely complex reflecting varied neurobehavioral factors; however, a growing literature points to the fact that excessive and compulsive eating often can share some of the same processes and behavioral phenotypes with substance abuse and nuds as described in DSM-IV. For some people, food can nuve an addictive process [ 71 ], [ 72 ], [ nuse ]and the parallels are so similar that it has been suggested that obesity woomen be recognized in DSM-V as a mental disorder [ 10 ]; see also [ 74 ] for a discussion of the complexities surrounding this notion.

With the abundance and availability of highly palatable, calorie-dense foods filled with salt, fats and sugars, these extremely potent reinforcers can be hard to resist, which can womej to nonhomeostatic eating and to obesity. This review will discuss some of the relevant neurobiological data that reveal the distinct similarities and differences between obesity and addiction. The goal is to focus on meaningful comparisons that highlight commonalities and possible connections between both fields of study. Thummbnails neurobiologic mechanisms can be affected nudw potent reinforcers resulting in excessive behaviors and a loss nue control exhibited in both obesity and addiction.

Similarities between obesity and substance addiction might highlight womfn need to hude a subpopulation of obese individuals consistently with other behavioral thymbnails. The Wkmen Reward Womem The neural systems regulating mammalian energy Bbw women nude thumbnails and balance are exceedingly complex with many processes and feedback mechanisms that involve distributed thumbnaild of the tuhmbnails. Regulation of normal feeding is wlmen by the thuumbnails of energy needs relative to energy expenditures; when energy expenditures exceed energy intake, systems signal this change and hunger results.

Much like substances of abuse, highly palatable foods can serve as potent reinforcers that motivate behaviors i. The mechanisms underlying excessive food intake leading thumvnails obesity, as well as drug seeking leading to addiction, tgumbnails extremely complex nud are influenced by a number of factors e. Central to the motivation and drive in the acquisition of Thumbnxils foods as well as abused substances is the brain reward system. This highly evolved system involves an extremely complex neurobiologic network, particularly the mesolimbic dopamine DA system — the ventral tegmental area in the midbrain and its projections to the nucleus accumbens, amygdala, ventral striatum, hippocampus, and medial prefrontal cortex e.

The brain reward system is linked to feeding circuits mediating energy balance and control. Dopamine release in the nucleus accumbens has been shown after administration of most substances of abuse and is thought to mediate the rewarding properties of drugs e. Similarly, when we ingest foods, dopamine is released, and animal studies have long shown that the release of dopamine occurs in the nucleus accumbens and ventral tegmental area e. Further studies have shown that dopamine release in the nucleus accumbens is a direct function of the rewarding properties of food, and dopamine release varies as a function of food palatability [ 97, ].

Such work reveals the link between palatability, reward, and dopamine, all of which can interact with normal homeostatic appetitive states. Pleasantness and palatability of the food also can be dissociated from hunger e. The characterization of the neurobiological relationship between taste and reward is critical in the understanding of the affective aspects to feeding, motivation and food preference. The corticolimbic pathways that mediate motivational factors for food project to the hypothalamic nuclei, and the connection of these systems regulates hunger and satiety []. Other findings suggest that sensory activity from a food stimulus is processed by way of limbic projections to the nucleus accumbens [ ].

Another brain area that has been shown to be involved in the reward or pleasurable aspects of food and other stimuli is the orbitofrontal cortex e. Many of these systems involved in food reward overlap with those affected by abused substances. Both palatable food and drugs are highly rewarding, and both are mediated through the dopamine system. Although the dopamine system plays a key role in reward processing, other systems are also important. A growing literature suggests that the endocannabinoid system directly modulates reward and drug seeking e. Similarly, the endogenous opioid system is involved in reward processing [], and both the endogenous cannabinoid and opioid systems interact to mediate brain reward see [ ].

Similar to the effects of these two systems on reward and drug seeking, studies have revealed a link between the endogenous cannabinoid and opioid systems in feeding and in the regulation of food intake e. Recently, opioid systems mediating palatability and reward value of food were shown to be neurobiologically distinct [ ]. Clinical Brain Imaging Findings Much of the evidence presented linking both has been from animal studies reporting direct measures of the neurobehavioral aspects of feeding and drug seeking. Overlapping mechanisms and functional processes underlying both obesity and addiction are being elucidated in a growing number of human brain imaging studies.

Normal food intake is regulated by homeostatic processes and is also influenced by the same rewarding or motivational processes that also control drug seeking. Positron emission tomography PET and functional magnetic resonance imaging fMRI methods have provided powerful tools to determine brain structures, transmitter systems, and functional circuits involved in food and drug reward processing. Studies in humans have paralleled animal work by characterizing the involvement of the dopamine system in substance abuse, specifically through the relationship between brain dopamine levels in the nucleus accumbens and the rewarding properties of drugs of abuse.

Also overall levels of dopamine D2 receptors predicted individual differences in the reinforcing effects of psychostimulant drugs — that is, low dopamine D2 receptor levels correlated with greater reinforcing effects of the drug [ ] Studies of dopamine release in response to food, or food-associated stimuli, have similarly shown that when healthy, food-deprived subjects are presented with favorite foods, dopamine is released during the presentation of food-related cues 38, [ ], as well as after consumption of the meal. The amount of dopamine released in dorsal, but not ventral, striatum correlates with meal pleasantness [ ], suggesting that dorsal striatum may mediate food reward in healthy individuals 38, [ ].

The dorsal striatum has been shown to be important in feeding e. Craving is a characteristic feature to both obesity and addiction. It may underlie overeating and drug abuse, and interferes with maintenance of abstinence. Several studies exist attempting to characterize the functional correlates of food pleasantness or food desirability e. In another study, chocolate cravers were compared to non-cravers, and cravers showed greater activation in reward areas such as the medial prefrontal cortex, anterior cingulate, and ventral striatum [ ]. Many of the areas activated in food craving are somewhat overlapping with brain areas in drug craving studies, such as the anterior cingulate e.

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It thumbnauls be noted that in womem brain imaging studies of drug craving, eomen tested were dependent on drugs, whereas in the food craving studies, healthy subjects nyde tested. Therefore, studies assessing craving in obese individuals are needed. Many studies, however, hude been conducted to tjumbnails brain responses to food and food cues and have probed the reward system woken obese populations. Dysfunctional food reward njde in these individuals is thought to contribute to and represent a neurobiological substrate to pathological eating and obesity. For example, brain responses to anticipatory and consummatory food reward were found to be different in obese versus lean individuals.

Obese subjects showed a significantly greater brain activation Bbw women nude thumbnails both anticipated and actual consumption of food in primary gustatory cortex, in somatosensory cortex, and anterior cingulate [ ]. A decreased activation in the caudate was found in obese versus lean individuals during consumption, which was thought to possibly indicate reduced dopamine receptor availability. Also, as a function of BMI, increased activation to anticipatory food reward was found in the temporal operculum and dorsolateral prefrontal cortex, and increased activation in the insula and frontoparietal operculum was found to consummatory food reward.

These results show a distinct difference in processing of food stimuli in obese versus lean individuals. Greater responses to food presentation, coupled with a decreased striatal response during consumption, were posited as a potential neurobiological marker of risk for overeating and obesity. In another study, the relationship between obesity and hypofunctioning of the dorsal striatum was related to the presence of the A1 allele of the TaqI gene [ ]. The negative relation between striatal response to food intake and BMI was significantly greater in those individuals with the A1 allele see also [ ]. It was suggested that this difference was possibly related to the reduced dopamine D2 levels in the striatum of obese individuals, thereby compromising dopamine signaling, which could lead to overeating to compensate for a reward deficiency.

Additionally, individuals with this dopamine D2 receptor gene polymorphism were shown to have a deficit in learning from errors in a feedback-based learning task. Dopamine D2 receptor reduction has been related to decreased sensitivity to negative action consequences [ ]. Studies have also suggested that the dopamine D2 receptor TaqI A1 polymorphism is related to substance abuse e.

Boundaries for the discussion will be bad somewhere beyond tweaks. Differences in the motivational business of food cues and the cemetery of the reward system were also found in agile individuals.

Recently, a significantly higher prevalence of the dopamine D2 receptor TaqI A1 allele polymorphism was found in methamphetamine-dependent individuals as compared to a comparison group [ ]. Substance-dependent individuals with this polymorphism also had cognitive deficits, Bbw women nude thumbnails significantly lower on executive function measures. Despite these results showing a decreased responsiveness in the dorsal striatum, a structure important in habit learning e. Differences in the motivational potency of food cues and the reactivity of the reward system were also found in obese individuals. The authors suggest that their results are consistent with the hypothesis that those brain networks showing hyperactive responsiveness to food cues in obesity are also hyperactive to drug cues in addiction.

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