Now a study by Jennifer Fenn and colleagues from the University of Vermont report significant weight gain with methadone treatment for opioid addiction in a paper published in the Journal of Substance Abuse Treatment.
The retrospective chart review included 96 patients enrolled in an outpatient methadone clinic for ≥ 6 months.
Overall mean BMIs increased by about 3 units (from 27.2 to 30.1), which corresponds roughly to an 18 lb or 10% increase in body weight.
Interestingly, the weight gain was predominantly seen in women, who gained about 28 lbs or 17.5% body weight compared to men, who only increased their weight by about 12 lbs or 6.4%.
As the study did not have access to food records, one can only speculate as to the causes. While better nutrition may well play a role, one could also speculate that there may be some addiction transfer from opioids to calorie-dense foods.
Whatever the cause, clinicians should probably be aware of this potential impact of methadone treatment on body weight, as prevention of excess weight gain may be easier than treating obesity once it is established.
Now a study by Pardis Pedram and colleagues from Memorial University, Newfoundland, examine this issue in a paper just published in PLoS One.
The study looks at 652 adult volunteers (415 women, 237 men) recruited from the general population.
‘Food addiction’ was assessed using the Yale Food Addiction Scale (YFAS), a questionnaire consists of 27 items that assess eating patterns over the past 12 months. The YFAS translates the Diagnostic and Statistical Manual IV TR(DSM-IV TR) substance dependence criteria in relation to eating behaviour (including tolerance and withdrawal symptoms, vulnerability in social activities, difficulties cutting down or controlling use, etc.). The criteria for ‘food addiction’ are met when three or more symptoms are present within the past 12 months together with clinically significant impairment or distress.
Based on these criteria, ‘food addiction’ was present in 5.4% of participants (6.7% in females and 3.0% in males) and increased with obesity status.
Interestingly enough, the clinical symptom counts of ‘food addiction’ were positively correlated with all body composition measurements across the entire sample (p<0.001) – not just in those with higher BMI.
Nevertheless, “food addicts” substantially heavier (11.7 kg), had 4.6 units higher BMI, and had 8.2% more body fat than “non-addicts”. Furthermore, food addicts consumed more calories from fat and protein than controls.
Thus, this study shows that as many as 1 in 20 (or 5%) of the general population may have a diagnosis of “food addiction”. Those who do are substantially heavier than individuals who do not meet these criteria.
Furthermore, individual symptoms of “food addiction” are associated with higher body weight across the entire range of BMI suggesting that even mild to moderate signs of “addiction” (below the threshold of a formal diagnosis) may contribute to weight gain in the general population.
As with all addictions, simply warning about the “evils” or making consumption more difficult (taxing, banning, punishing) is of limited help in addressing the problem. In addition, given that total “food-abstinence” is not an option, the best you can hope for is “harm-reduction” – a rather conservative goal for any addiction.
Clearly, not recognising the potential role of food addiction as a contributor to the obesity epidemic means missing the boat on providing appropriate care to individuals with this condition.
As with other addictions, “Simply say no” approaches are naive at best in addressing the problem.
p.s. Three co-authors of this paper (Danny Wadden, Peyvand Amini and Farrell Cahill) are graduates of the Canadian Obesity Network’s annual Summer Bootcamp.
Earlier this week I blogged about the possible deleterious impact that sleep deprivation, alcohol intake and TV watching can have on food intake.
Now a paper by Jean-Phillipe Chaput and colleagues from the University of Ottawa, published in the APPETITE, suggests that sleep deprivation in turn may contribute to increased alcohol consumption.
This cross-sectional study looked at the association between sleep duration and alcohol consumption in adults (301 men and 402 women aged 18 to 64 years) from the greater Quebec City area.
Participants categorized as short- (⩽6 h), compared to average- (7-8 h) or long- (⩾9 h) duration sleepers, consumed significantly more alcohol and had greater odds of odds of exceeding the recommendations for sensible weekly alcohol intake of 14 drinks for men and 7 drinks for women, even after adjusting for relevant confounders.
While this relationship was evident in both sexes, binge drinking (i.e. ⩾5 drinks on one occasion) was more common in men than women. Thus, men sleeping less than 6 hours per night with a disinhibited eating behavior were more likely to report binge drinking (41%).
Based on these findings the authors suggest that the combination of short sleep duration with disinhibited eating behavior is associated with greater alcohol intake in adults, findings that can certainly further explain the strong relationship between not getting enough sleep and weight gain.
Perhaps counselling patients on sleep hygiene may do more for them than asking them to simply eat less and move more.
Chaput JP, McNeil J, Després JP, Bouchard C, & Tremblay A (2012). Short sleep duration is associated with greater alcohol consumption in adults. Appetite PMID: 22841812
Yesterday, I posted on the recent Senate Committee call on the FDA to ease the path to approval of new obesity, which it described as “a significant unmet medical need.”
In my commentary, I suggested that one solution to better balancing risk and benefit would be to subcategorize obesity into meaningful subtypes, ideally based on an objective aetiological framework.
In a paper just published in Appetite, Caroline Davis and colleagues from Toronto’s York University provide evidence suggesting that ‘food addiction’ (FA) may be a valid clinical sub-phenotype of obesity.
The researchers examined the validity of the Yale Food Addiction Scale (YFAS) – the first tool developed to identify individuals with addictive tendencies towards food – in a sample of obese adults (aged 25-45 years) and non-obese controls.
In their analysis, the researchers focused on three domains relevant to the characterization of conventional substance-dependence disorders: clinical co-morbidities, psychological risk factors, and abnormal motivation for the addictive substance.
Not only were their results strongly supportive of the ‘food addiction’ construct demonstrated validity of the YFAS, in addition, those who met the diagnostic criteria for food addiction had a significantly greater co-morbidity with Binge Eating Disorder, depression, and attention-deficit/hyperactivity disorder compared to their age- and weight-equivalent counterparts.
Those with FA were also more impulsive and displayed greater emotional reactivity than non-FA obese controls. They also displayed greater food cravings and the tendency to ‘self-soothe’ with food.
As the authors conclude:
“These findings advance the quest to identify clinically relevant subtypes of obesity that may possess different vulnerabilities to environmental risk factors, and thereby could inform more personalized treatment approaches for those who struggle with overeating and weight gain.”
From a treatment perspective, these would be the patients, who would perhaps be most responsive to behavioural and pharmacological treatments aligned with an addiction paradigm.
In contrast, non-food addicted obese individuals will likely be far less responsive to these approaches.
Thus, while it may make sense to expose individuals with food addiction to drugs like buproprion, naltrexone, or rimonabant, non-addictive obese individuals may neither respond well nor warrant the risk of these drugs for treating their obesity.
As long as we continue on the path to developing obesity treatments using an outdated and simplistic ‘let’s-get-anyone-with-a-BMI-higher-than-X-to-lose-weight’ approach, we will never get a good handle on risk benefit ratios, let alone, get any closer to ‘aetiology based’ treatments.
Davis C, Curtis C, Levitan RD, Carter JC, Kaplan AS, & Kennedy JL (2011). Evidence that ‘food addiction’ is a valid phenotype of obesity. Appetite PMID: 21907742
The latter system is also involved in other hedonic behaviours ranging from alcohol and recreational drug use to other “pleasurable” activities like sex, shopping, or gambling, all of which can manifest themselves as addictions.
It may therefore not be surprising, that Caroline Davis and colleagues from York University, Toronto, in a paper just published in the International Journal of Obesity, report that a common genetic variant of the mu1 opiate receptor is associated with increased preference for sweets and fatty foods.
The researchers studied the relationship between variants of the OPRM1 gene and measures of food preferences and eating behaviours in 300 healthy adult men and women recruited from the community.
Individuals with the G/G genotype of the functional A118G marker of the OPRM1 gene reported higher preferences for sweet and fatty foods compared with the other two groups. These food preferences were clearly related to all measures of overeating, which in turn accounted for a substantial proportion of the variance in BMI.
Thus, the authors conclude that some of the diversity in the preference for highly palatable foods can be explained by genotypic differences in the regulation of mu opioid receptors that play a key role in the appetite and reward system (in addition, these receptors may also have a role in regulating the homeostatic system).
Obviously, individuals carrying this genetic variant may have a much harder time saying “no” to sweets and fatty foods, than individuals without this variant. Even if the number of people with this genetic variant may have not changed in recent years, the current abundance of cheap sweet and fatty foods clearly poses a far greater challenge to carriers of this gene.
I wonder how many of my readers would suspect that they may have this genetic variant of the opiate receptor gene and, if they do, I’d love to hear how they cope with passing up the sweets.
Davis C, Zai C, Levitan RD, Kaplan AS, Carter JC, Reid-Westoby C, Curtis C, Wight K, & Kennedy JL (2011). Opiates, overeating and obesity: a psychogenetic analysis. International journal of obesity (2005) PMID: 21266954