Addictive behaviors present difficult, as it is problematic for an observer to realize why clearly harmful behaviors are continued. However, we frequently see used alcoholics who drink despite liver damage or social consequences, smokers who smoke despite lung or heart damage, and morbidly obese patients who continue to overeat regardless of the resulting health problems and compromised function. Recently, we have learned a whole lot about the reinforcing effects of addictive substances on the brain. Neurochemical pathways involving such potent neurotransmitters as dopamine, serotonin, gamma-aminobutyric acid, and glutamate are affected by exposure to many substances with the prospect of addiction or abuse. Repeated exposure to these addicting substances results in stimulation and modulation of reward pathways that, subsequently, make such substances more attractive and harder to resist. There is some evidence from neuroimaging that, even with years of abstinence, these pathways may never return to their preaddiction state, raising the likelihood of relapse with reexposure. Overeating clearly shares factors with other addictive behaviors. The overeater persists even yet in the face area of negative physical consequences and societal disapproval, has a high frequency of relapse, and clearly finds rewards in the behavior that are not readily apparent to the observer and that override the most obvious negative consequences. Recent studies in human and animal subjects claim that a few of the same neurotransmitter systems active in addiction may be mixed up in persistence of harmful eating behaviors. Nora Volkow, among the nation’s premier researchers on addictive behaviors, has proposed a common model for both obesity and drug abuse and addiction, with dopamine pathways in mental performance playing a vital role. In every addictive behaviors, she hypothesizes that the addicted individual assigns an enhanced salience or meaning to a certain reinforcer (drugs or food) at the expense of other reinforcers.

This is due to conditioned learning and resetting of the brain’s reward thresholds by repeated stimulation either by substances of abuse or by large quantities of palatable food, usually nutrientdense sugars or fats. In this model, exposure to the meals or drug reinforcer or conditioned cues for consumption triggers the dopamine-modulated neuronal reward and motivation circuits, while inhibiting cognitive control.5 Thus, the drive to eat is stimulated, and the ability to inhibit the drive is diminished, a complicated combination to overcome despite having the very best of intentions. In a study looking at gender differences in brain a reaction to food stimulation, Volkow and her colleagues6 found male subjects had a greater ability to inhibit brain activation in a reaction to food stimulation in multiple regions, like the amygdala, hippocampus, insula, orbitofrontal cortex, and striatum. Volkow et al hypothesized that difference in capability to dampen response to food stimulation can result in a lower capability to suppress hunger in women and the resulting gender difference in obesity. Alternation of access and restriction may improve the addictive eating pattern, resulting in the familiar cycle of successful dieting followed with a rebound to the pre-diet weight as well as higher.7 Imaging studies of obese and lean individuals who are anticipating calorie-rich tasty food versus a tasteless solution demonstrate that obese subjects respond with greater activity in the gustatory and somatosensory regions of the mind and decreased activation in the striatum. This decreased activity may reflect a genetically mediated reduction in dopamine signaling because region, leading these individuals to overeat to pay for the hypofunctional dorsal striatum.8,9 The continued growth of obesity inside our society regardless of the proliferation of “lite” and “low-fat” foods emphasizes that there’s no shortcut to healthy eating, and a recent commentary in the Journal of the American Medical Association highlights that even efforts to curb calorie intake through the utilization of artificial sweeteners might not trump neurobiology. The author cites an observational study that found a dose–response relationship between consumption of diet drinks and measurement of adiposity as time passes, along with studies finding daily usage of such drinks associated with metabolic syndrome and risk of diabetes, although the direction of the causality wasn’t clear. Much more concerning, studies with experimental animals found the drive for sweetness led them to decide on saccharine over intravenous cocaine, previously thought to be one of the very most addictive substances. The risk for the human would-be dieter is that the utilization of these hyper-sweet sugar substitutes may overstimulate sweetness receptors, causing them to revert to an infantile state and building a healthy diet of energy-dilute foods less palatable.10 David Kessler,11 the former chief of the Food and Drug Administration who was simply widely praised for addressing tobacco addiction during his term in office, has joined the struggle against obesity. In a recently available book, he demands retraining our brains, suggesting that individuals must make exactly the same change in societal attitudes toward the acceptability of eating calorie-rich foods that people did toward the acceptability of smoking. He challenges our society to trade the transient neurologic reward of high-sugar/high-fat foods for healthier eating, while acknowledging his own lifelong struggle to resist those very foods. However intellectually appealing his arguments may be, experience, including their own, suggests why these behavioral changes are difficult to maintain long-term, and the info from neuroimaging studies confirm a formerly obese individual’s neurobiology may be producing a silent but very powerful opposition to such change. For many would-be dieters, an ice cream soda will continue to look more inviting than brussels sprouts, and their particular neurotransmitters will continue steadily to urge them in the direction of the fats and sugars that will take satiation and neurologic reward. A recently available article in the New Yorker reviewed a few of the societal factors that also militate against dietary behavior change, including a decline in the cost of fats, oils, and sugars in accordance with other foods, and the successful commercial promotion of larger servings extending even into the house, as newer editions of old standby cookbooks now calculate fewer servings from standard recipes.

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