Addictive behaviors present a challenge, because it is problematic for an observer to understand just 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 steadily to overeat inspite of the resulting health problems and compromised function. In recent years, we’ve learned a good deal concerning 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 most 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 appealing and harder to resist. There’s some evidence from neuroimaging that, even with years of abstinence, these pathways may never return with their preaddiction state, raising the possibility of relapse with reexposure. Overeating clearly shares factors with other addictive behaviors. The overeater persists even yet in the facial skin of negative physical consequences and societal disapproval, includes a high frequency of relapse, and clearly finds rewards in the behavior which are not readily apparent to the observer and that override well-known negative consequences. Recent studies in human and animal subjects claim that a number of the same neurotransmitter systems active in addiction may be active in the persistence of harmful eating behaviors. Nora Volkow, one of many nation’s premier researchers on addictive behaviors, has proposed a common model for both obesity and drug abuse and addiction, with dopamine pathways in the brain playing a key role. In most 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 a result of 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, contact with the food 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 challenging combination to overcome despite having the most effective of intentions. In a study considering gender differences in brain response to food stimulation, Volkow and her colleagues6 found male subjects had a larger power to inhibit brain activation in a reaction to food stimulation in multiple regions, including the amygdala, hippocampus, insula, orbitofrontal cortex, and striatum. Volkow et al hypothesized that difference in power 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 enhance the addictive eating pattern, ultimately causing the familiar cycle of successful dieting followed by a rebound to the pre-diet weight or even higher.7 Imaging studies of obese and lean individuals that 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 mental performance and decreased activation in the striatum. This decreased activity may reflect a genetically mediated decrease in dopamine signaling because region, leading these individuals to overeat to pay for the hypofunctional dorsal striatum.8,9 The continued growth of obesity in our society inspite of the proliferation of “lite” and “low-fat” foods emphasizes that there surely is no shortcut to healthy eating, and a recently available commentary in the Journal of the American Medical Association points out that even efforts to curb calorie intake through the usage of artificial sweeteners may not trump neurobiology. The author cites an observational study that found a dose–response relationship between usage of diet drinks and measurement of adiposity with time, as well as studies finding daily consumption of such drinks connected with metabolic syndrome and threat of diabetes, even though 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 regarded as one of the very most addictive substances. The chance 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 widely praised for addressing tobacco addiction during his term in office, has joined the struggle against obesity. In a recent book, he calls for retraining our brains, suggesting that we must make the exact same change in societal attitudes toward the acceptability of eating calorie-rich foods that individuals 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 their own lifelong struggle to resist those very foods. However intellectually appealing his arguments may be, experience, including their own, suggests that these behavioral changes are difficult to maintain long-term, and the information from neuroimaging studies confirm that the formerly obese individual’s neurobiology may be producing a silent but very powerful opposition to such change. For some would-be dieters, an ice cream soda will continue to look more appealing than brussels sprouts, and their very own neurotransmitters will continue to urge them in the direction of the fats and sugars that will bring satiation and neurologic reward. A recent article in the New Yorker reviewed a number of the societal factors that also militate against dietary behavior change, including a decline in the expense 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.