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There are pathways in the brain that reinforce natural behaviors, such as sexual and feeding behaviors, causing individuals to engage in the behaviors repeatedly. Drugs of abuse activate those same pathways, according to Avena. Highly palatable foods, she said, activate brain reward systems beyond what is seen when healthy food is eaten e. Avena's research involves the use of animal models to determine whether DSM-IV and DSM-5 criteria for substance use disorders APA, , apply when the substance in question is a highly palatable food instead of a drug.

That is, instead of giving animals drugs, she and her research team give them delicious foods to eat. Also of note, Avena was drawn to the use of animal models because they allow researchers to examine biological correlates of behavior often impossible to study in humans. Avena started her inquiry into food addiction by looking at sugar Avena et al. She chose sugar for several reasons, including the fact that Americans consume on average 22 teaspoons of added sugar daily NCI, Studies suggest that sugar appears to be one of the ingredients many people find particularly problematic, such that they have difficulty regulating the intake of foods rich in sugar when they try to cut back.


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There also have been several studies finding a correlation between sugar intake and obesity. Thus, for Avena, sugar appeared to be a good ingredient to examine first. In one study conducted by Avena's group Rada et al. By the end of the 3-week period, these rats were bingeing on the sugar solution and showed evidence of tolerance as they were consuming more and more each day, which suggests that an increased amount was needed to achieve the same effect Rada et al.

This bingeing behavior was particularly apparent during the first hour of access to the sugar solution following the hour period of abstinence. Of interest, Avena noted, rats provided with chow and sugar ad libitum one of the control groups did not show this escalation in daily intake. Other control groups included rats that had access to sugar only on days 1, 2, and 21 of the experiment and rats that had hour daily access to chow only no sugar. It was only the rats that were bingeing on the sugar daily that showed increased intake over time.

Avena and her team were curious about whether the overconsuming rats in the test group were releasing dopamine in a way that was consistent with consuming a food or a drug. A hallmark of drugs of abuse is that they can cause a release of dopamine in reward-related regions of the brain, such as the nucleus accumbens, every time they are administered.

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Food also can cause the release of dopamine, according to Avena, but the dopamine release normally wanes when the food is no longer novel and an individual becomes habituated to it. She and her team found that, indeed, rats that were overconsuming the sugar solution were releasing dopamine every time they had access to the sugar. This was as true on day 21 as it was on day 2. Rats in the ad libitum control group and the control group that drank the sugar solution only occasionally, on the other hand, did not show the same release of dopamine over time, nor did the rats that consumed chow and no sugar Rada et al.

According to Avena, these results suggest that there is something about sugar such that when rats overconsume it, they release dopamine in a drug-like way. Other studies have shown that rats that overconsume sugar show physical signs of withdrawal, distress, and anxiety when the sugar is taken away or when they are administered an opioid antagonist, which blocks opioid receptors in the brain Avena et al. Additionally, the reward-related regions of their brains show a decrease in dopamine levels, coupled with an increase in acetylcholine Avena et al.

According to Avena, a similar dopamine-acetylcholine imbalance has been seen during withdrawal from many drugs of abuse, including cocaine, nicotine, and morphine. Craving is a difficult behavior to assess with animal models, in Avena's opinion. She considers it a highly subjective, psychological characteristic. Nonetheless, several researchers have assessed features of craving in rats in an effort to understand its biological basis Avena et al.

The researchers found that the rats prone to binge eating endured greater magnitudes of shock to obtain the treat relative to their binge-resistant counterparts. Other studies have shown that following an abstinence period, rats prone to bingeing on sugar increase their intake of sugar when it is made available Avena et al.

Avena and her team also studied cross-sensitization between overconsumption of sugar and drugs of abuse Avena and Hoebel, ; Avena et al. They found that animals with a history of overeating sugar became hyperactive when administered a very low dose of amphetamine, a potent dopamine agonist, instead Avena and Hoebel, Animals without a history of overeating sugar, on the other hand, did not show the same hyperactivity in response to the same dose of amphetamine.

These results suggest to Avena that there is something about sugar consumption, presumably the effect it is having on the dopamine system, that causes even a very low dose of amphetamine to have this effect. Greater evidence of cross-sensitization was observed when rats with a history of overconsuming sugar were provided with alcohol instead of sugar; they drank more alcohol than did control rats that were exposed to sugar, but did not overconsume it Avena et al.

Avena mentioned that many other food addiction studies have focused on sugar-fat combinations and combinations of other foods. Many researchers have used as a test condition the cafeteria diet, whereby rats have been provided a wide variety of high-fat, high-sugar foods, as well as healthy foods. For example, Geiger and colleagues found that animals on a cafeteria diet became overweight or obese and when provided amphetamine in vivo or in vitro, released much more dopamine than chow-fed control rats.

Moreover, when their cafeteria diet was replaced with regular lab chow, the rats did not show an increase in release of dopamine. Only when their cafeteria diet was reintroduced did these rats again show an increase in dopamine release. According to Avena, these results suggest that the cafeteria diet had changed the rats' brains in a way that was similar to what is seen in rats that overeat sugar and that caused the animals to react to healthy food differently from the way the rats maintained on a healthy diet reacted.

Since this was a debate, Avena identified several issues raised by critics of this work to consider, or reconsider, in moving forward. Additionally, critics have noted that the construct of food addiction may be fitting for individuals with binge eating disorder but not for understanding obesity. That is a valid criticism, in Avena's opinion, given that much of the laboratory work done to date has aligned food addiction with binge eating. To further understand how the food addiction construct may be helpful for understanding obesity, Avena reminded the audience that care is necessary in defining addiction.

Usually when people think about addiction, they think about an extreme loss of control Altman et al.

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But quoting Rogers , Avena stated that while an extreme loss of control may characterize binge eating, it does not describe well the repeated failure to resist energy-rich foods in large portions that gradually contribute to weight gain. Avena remarked that many people think of the typical addict as someone lying in a gutter with no job and no family. But in reality, the typical addict in American society is a mom driving her kids to soccer practice and smoking cigarettes—someone who is likely a fully functioning individual for whom withdrawal syndrome is not physically life-threatening.

Avena suspects that addiction to palatable foods may be more like addiction to cigarettes than to drugs of abuse, and thereby produce the same type of milder and less pronounced loss of control that is associated with smoking. Peter Rogers's interest in the appropriateness of the addiction model for use with food stems from his interest in understanding human appetite and weight control and his work in caffeine psychopharmacology.

But first, he noted that in his opinion, caffeine illustrates very well the distinction between dependence and addiction. Most people who consume caffeine—who he suggested represent the majority of people on the planet—are dependent on it. If they become tolerant to its psychostimulant effects and it is withdrawn, they become fatigued and tired. But few people who consume caffeine experience the extreme loss of control that is characteristic of addiction. But food is just as addictive as heroin and nicotine, research suggests. Substance abuse and high-glycemic foods—such as white bread and potatoes—trigger the same brain mechanism as that linked to addiction, according to Boston Children's Hospital.

They apparently cause excess hunger and stimulate reward and craving in parts of the brain. There are several ways to define addiction, noted Rogers. Other definitions are milder and imply something that someone simply likes to do frequently or is particularly interested in. The food environment has changed dramatically with the influx of hyperpalatable foods that are engineered in ways that appear to surpass the rewarding properties of traditional foods e.

Foods share multiple features with addictive drugs. Food cues and consumption can activate neurocircuitry e. Animals given intermittent access to sugar exhibit behavioral and neurobiological indicators of withdrawal and tolerance, cross-sensitization to psychostimulants and increased motivation to consume alcohol [3]. Rats consuming diets high in sugar and fat demonstrate reward dysfunction associated with drug addiction , downregulation of striatal dopamine receptors and compulsive eating, including continued consumption despite receipt of shocks [4].

Rogers identified several key points of this summary worth reconsidering i. That argument, he explained, is based on an observed overlap between the brain mechanisms and behavioral processes involved in eating and those involved in psychoactive drug use or abuse. In Rogers's opinion, that overlap by itself is not evidence of addiction; it merely shows that drugs of abuse have engaged some of the same mechanisms engaged by eating.

In Rogers's opinion, that same point could be used to argue that foods therefore pose a relatively low risk of addiction. Another argument put forth for the case of food addiction, one based on animal evidence, is that consumption of certain foods—those high in sugar and fat—causes reward dysfunction and sets in motion a vicious cycle of further overeating. That is, the changes that occur in the reward pathways of the brain lead to overconsumption, which leads to further brain changes, and so on.

Again, the argument goes, there is a parallel with the effects of addictive drugs. The argument is based on evidence such as that reported by Johnson and Kenny , who showed that rats exposed to a cafeteria diet of chocolate, pound cake, sugar frosting, and a variety of other energy-dense foods experienced increased body weight compared with rats fed a standard laboratory diet.

Additionally, by implanting electrodes in the rats' brains that delivered rewarding stimulation when the rats pressed a lever, the researchers found that the rats on the cafeteria diet had a higher current threshold; that is, they experienced less reward for the same amount of stimulation compared with rats fed standard lab chow. The researchers interpreted their results as evidence of brain dysfunction.

He traced his alternative explanation back to a study in which he offered rats either a variety of energy-dense foods or fat, specifically lard, along with their standard diet Rogers, Initially, rats in both groups showed an increase in body weight. Over time, however, the rats' food intake decreased and their rate of weight gain plateaued. Rogers argued that the increased weight gain produced a negative feedback effect on appetite. When the rats were returned to their chow diet, they underate. Light Is the New Black.

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