For Some, Food ‘Addiction’ Similar to Substance Abuse

By RICK NAUERT PHD


People with eating behaviors that resemble addiction appear to have greater neural activity in certain regions of the brain similar to that of substance abusers, including a heightened response in reward circuitry to food cues — more powerful cravings, in other words.

In a study posted online that will appear in the August print issue of Archives of General Psychiatry, researchers used functional magnetic resonance imaging (fMRI) to study the response of 48 healthy young women in response to cues signaling impending delivery of a highly palatable food (chocolate milkshake) vs. a tasteless control solution; and consumption of a chocolate milkshake vs. a tasteless solution.

The women ranged from lean to obese and had been recruited for a healthy weight maintenance trial. Their eating behavior was assessed using a food addiction scale developed by lead author Ashley Gearhardt, a doctoral student at Yale University.

“Similar patterns of neural activation are implicated in addictive-like eating behavior and substance abuse and dependence,” Gearhardt noted in the study.”Food and drug use both result in dopamine release in mesolimbic regions [of the brain] and the degree of release correlates with subjective reward from both food and drug use.”

Gearhardt and colleagues found that participants with higher food addiction scores showed more activity in brain areas linked with craving. “These findings support the theory that compulsive food consumption may be driven in part by an enhanced anticipation of the rewarding properties of food,” the authors write. “Similarly, addicted individuals are more likely to be physiologically, psychologically, and behaviorally reactive to substance-related cues.”

The researchers said that if certain foods are addictive for some people, that could explain in part why they find it so hard to lose weight and keep it off.

While researchers have speculated that an addictive process may be involved in obesity, the authors said that this is the first study to identify distinctive neural or brain activity in people with addictive eating behavior.

In addition, Gearhardt said, ”If food cues take on enhanced motivational properties in a manner analogous to drug cues, efforts to change the current food environment may be critical to successful weight loss and prevention efforts. Ubiquitous food advertising and the availability of inexpensive palatable foods may make it extremely difficult to adhere to healthier food choices because the omnipresent food cues trigger the reward system.”

Source PsychCentral

Long-Term Antidepressant Treatment Contributes To Significant Increases In Weight Gain And Obesity

On January 18, 2011, in Depression, Medication, by Christopher Fisher, PhD


This study demonstrates that patients using antidepressant medication continuously, mostly serotonin-selective reuptake inhibitors (SSRIs), show significantly more (abdominal) overweight and obesity than those using them intermittently or not at all. Compared with SSRIs, other types of antidepressant medication used (e.g. tricyclic ADs) did not have a significant impact on the anthropometric measures (i.e., measurement of of human physical variations).

In a study published in the last 2010 issue of Psychotherapy and Psychosomatics, a group of researchers of the University of Amsterdam presents new findings on the relationship between weight and recurrent depression.

The literature on the relation between obesity and the recurrent type of major depressive disorder (MDD-R; having had at least 2 major depressive episodes) is limited and equivocal. Most studies on depression and obesity did not distinguish between single and recurrent episodes. However, this distinction may be important because depression is increasingly considered a chronic recurrent disorder with various levels of interepisodic functioning, and evidence is growing that the recurrent type is a distinct one.

Most studies on the relation between depression and obesity did not control for antidepressant (AD) medication use, although a substantial part (20 – 60%) of the recurrently depressed patients use ADs for lengthy periods of time. This study elaborates on their findings by focusing on the relation between obesity and MDD-R and the association between long-term use of ADs and obesity.

To be eligible for this study, patients had to meet the following criteria: (a) at least 2 major depressive episodes in the past 5 years (DSM IV), (b) current remission status, according to DSM-IV criteria, for longer than 10 weeks and no longer than 2 years before, and (c) Hamilton Rating Scale for Depression of <10.

At 2 years, follow-up assessment anthropomorphic parameters were collected of 134 subjects.

To assess relapse/recurrence, the Structured Clinical Interview for DSM-IV (SCID-I) was used. Regarding the use of ADs, two groups were distinguished: those who used Ads throughout the entire 2-year study period (n = 46) and those who did not use ADs continuously, but intermittently (n = 49) or not at all (n = 39). Differences between these groups in BMI, waist circumference, and waist-to-hip ratio were tested stratified by gender.

Overweight and obesity occurred more often in patients with recurrent depression than in the reference group, although statistical significance was reached in women only (74% of this sample). Within the MDD-R patient group, serotonin-selective reuptake inhibitors (SSRIs) were the most commonly used type of AD among the continuous AD users. Compared with SSRIs, other types of ADs used (e.g. tricyclic ADs) did not have a significant impact on the anthropometric measures.

The mean AD equivalent correlated positively with both waist circumference (p = 0.006) and waist-to-hip ratio (p = 0.004), but not with BMI. In addition, mean waist circumference and waist-to-hip ratio scores were consistently higher amongst the continuous AD users compared to intermittent and no AD users. Patients using ADs continuously, mostly SSRIs, show significantly more (abdominal) overweight and obesity than those using them intermittently or not at all. Compared with SSRIs, other types of ADs used (e.g. tricyclic ADs) did not have a significant impact on the anthropometric measures. The authors did find, however, a small association between AD equivalent dosage and waist circumference and waist-to-hip ratio.

In general, a better understanding of the relationship between obesity and depression that includes understanding the beneficial and adverse effect of psychotropics on appetite, eating behaviour, body weight, and metabolism should improve our ability to prevent and treat both obesity and depression. Thereby, ideally persontailored interventions can be developed, including effective nonpharmaceutical preventive strategies for recurrent depression and extra physical activities with – as added benefit – protection against AD-induced weight gain.

Material adapted from Journal of Psychotherapy and Psychosomatics.

Reference
Lok, A.; Visscher, T.L.S.; Koeter, M.W.J.; Assies, J.; Bockting, C.L.H. ; Verschuren, W.M.M. ; Gill, A. ; Schene, A.H. The ‘Weight’ of Recurrent Depression: A Comparison between Individuals with Recurrent Depression and the General Population and the Influence of Antidepressants. Psychother Psychosom 2010;79:386-388.

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Risk for Alcoholism Linked to Risk for Obesity

ScienceDaily


The researchers noted that the association between a family history of alcoholism and obesity risk has become more pronounced in recent years. Both men and women with such a family history were more likely to be obese in 2002 than members of that same high-risk group had been in 1992.

“In addiction research, we often look at what we call cross-heritability, which addresses the question of whether the predisposition to one condition also might contribute to other conditions,” says first author Richard A. Grucza, PhD. “For example, alcoholism and drug abuse are cross-heritable. This new study demonstrates a cross-heritability between alcoholism and obesity, but it also says — and this is very important — that some of the risks must be a function of the environment. The environment is what changed between the 1990s and the 2000s. It wasn’t people’s genes.”

Obesity in the United States has doubled in recent decades from 15 percent of the population in the late 1970s to 33 percent in 2004. Obese people — those with a body mass index (BMI) of 30 or more — have an elevated risk for high blood pressure, diabetes, heart disease, stroke and certain cancers.

Reporting in the Archives of General Psychiatry, Grucza and his team say individuals with a family history of alcoholism, particularly women, have an elevated obesity risk. In addition, that risk seems to be growing. He speculates that may result from changes in the food we eat and the availability of more foods that interact with the same brain areas as addictive drugs.

“Much of what we eat nowadays contains more calories than the food we ate in the 1970s and 1980s, but it also contains the sorts of calories — particularly a combination of sugar, salt and fat — that appeal to what are commonly called the reward centers in the brain,” says Grucza, an assistant professor of psychiatry. “Alcohol and drugs affect those same parts of the brain, and our thinking was that because the same brain structures are being stimulated, overconsumption of those foods might be greater in people with a predisposition to addiction.”

Grucza hypothesized that as Americans consumed more high-calorie, hyper-palatable foods, those with a genetic risk for addiction would face an elevated risk from because of the effects of those foods on the reward centers in the brain. His team analyzed data from two large alcoholism surveys from the last two decades.

The National Longitudinal Alcohol Epidemiologic Survey was conducted in 1991 and 1992. The National Epidemiologic Survey on Alcohol and Related Conditions was conducted in 2001 and 2002. Almost 80,000 people took part in the two surveys.

“We looked particularly at family history of alcoholism as a marker of risk,” Grucza explains. “And we found that in 2001 and 2002, women with that history were 49 percent more likely to be obese than those without a family history of alcoholism. We also noticed a relationship in men, but it was not as striking in men as in women.”

Grucza says a possible explanation for obesity in those with a family history of alcoholism is that some individuals may substitute one addiction for another. After seeing a close relative deal with alcohol problems, a person may shy away from drinking, but high-calorie, hyper-palatable foods also can stimulate the reward centers in their brains and give them effects similar to what they might experience from alcohol.

“Ironically, people with alcoholism tend not to be obese,” Grucza says. “They tend to be malnourished, or at least under-nourished because many replace their food intake with alcohol. One might think that the excess calories associated with alcohol consumption could, in theory, contribute to obesity, but that’s not what we saw in these individuals.”

Grucza says other variables, from smoking, to alcohol intake, to demographic factors like age and education levels don’t seem to explain the association between alcoholism risk and obesity.

“It really does appear to be a change in the environment,” he says. “I would speculate, although I can’t really prove this, that a change in the food environment brought this association about. There is a whole slew of literature out there suggesting these hyper-palatable foods appeal to people with addictive tendencies, and I would guess that’s what we’re seeing in our study.”

The results, he says, suggest there should be more cross-talk between alcohol and addiction researchers and those who study obesity. He says there may be some people for whom treating one of those disorders also might aid the other.

This work was supported by grants from the National Institute on Alcohol Abuse and Alcoholism and the National Institute on Drug Abuse of the National Institutes of Health.

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Washington University School of Medicine.