Abstract

report important new data that confirm links between posttraumatic stress disorder (PTSD) symptoms and eating disordered behaviors. Furthermore, they extend those links with PTSD to the ingestion of sugary sodas and fast foods, a finding that persists despite race or ethnicity, marital status, education, income level, and body mass index (BMI). Although PTSD and its symptoms have previously been associated with bingeing or purging behaviors or both, as well as smoking cigarettes, this is the first study to demonstrate a connection between PTSD (and, hence, traumatic experiences) and the frequency of ingesting particular types of foods, for example, sugary sodas and fast foods. An emerging body of evidence over the last few years has characterized highly palatable foods, such as those found in fast food restaurants, as potentially addictive and acting very much like licit and illicit substances of abuse in the brain. Specifically, high concentrations of refined sugar, fat, salt, and caffeine are common components of fast food menus, and it has been posited that all these foodstuffs have addictive properties. The results of the Hirth et al. article have important and far-reaching implications. For one, their data help to elucidate the underlying mechanisms and behavioral pathways of how trauma and subsequent PTSD eventually lead to an increased chance of developing one or more of the leading causes of death in the United States. In addition to an array of medical disorders, it is well established that PTSD is associated with significantly higher rates of substance use disorders, other comorbid psychiatric disorders, and a variety of selfdestructive and impulsive behaviors, including suicide. These data also suggest that the ingestion, and especially overingestion, of fatty or sugary energy sources may be just another strategy that traumatized individuals use to numb themselves from their unpleasant feeling states and memories. In essence, certain foods can act just like other substances that alter brain chemistry and, hence, consciousness. Much work in the neurosciences has been done to establish the neurochemical mechanisms underlying these phenomena. Using food to self-medicate dysphoric states is by no means a new idea. For some time now, many people who have struggled with compulsive overeating have identified their problem as a food addiction. In 1956, Randolph first described the phenomenon of food addiction and linked it with addictive drinking. Overeaters Anonymous (OA), which was founded in 1960, defined compulsive overeating as a progressive, addictive illness and focused on refined sugar as the addicting agent, a conclusion that is no longer so far-fetched. In addition, those with overt eating disorders have described using food to self-medicate as well as being addicted to bingeing or purging behaviors. Not only do these behaviors often become habitual methods of affect regulation, but eating foods with high hedonic value can quickly, inexpensively, and legally offer a modicum of comfort and relief, however transiently, and only more problems ensue. During the last several years, mainstream science has begun to accept the notion that certain foods can act like other addicting substances in the brain, despite having other peripheral metabolic effects that substances of abuse do not necessarily have. It has been shown in both animal and human experiments that food intake and drug use both cause dopamine release in parts of the brain that mediate pleasure and emotion. Furthermore, the degree of dopamine release correlates with the sense of subjective reward or experience of pleasure from both food and drug use. Similar patterns of brain activation as seen on functional magnetic resonance imaging (MRI) in response to food and drug cues have also been found. Other studies demonstrate that food can stimulate the opiate system and that there are striking similarities in use and withdrawal patterns of sugar and of classic drugs of abuse. In addition, there often appear to be reciprocal relationships among food and other substances, in that people may gain weight when they stop smoking or drinking. Taken together, these observations support the conclusion that food and classic addictive substances compete for the same brain pathways and may serve the same purposes psychologically. This reorientation toward entertaining the concept of food addiction has been a result of the fact that at least one third of people in the United States are obese, and the mortality and morbidity associated with obesity have become a major focus throughout medicine and public health. Even though the results of the study by Hirth et al. did not find that women with PTSD symptoms had higher BMIs than those women without such symptoms, these data are relevant to an increase in the understanding of the current obesity epidemic. Other investigators have reported that obese patients have high rates of trauma and PTSD. That women with PTSD symptomatology were engaged in more strategies to lose weight, for

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