Regular readers of these pages are well aware of the close link between addictions and some forms of overeating. This topic is now nicely addressed in a commentary by Valerie Taylor (McMaster, Hamilton), Claire Curtis and Caroline Davis (both York University, in this week’s edition of CMAJ.

As they discuss,

“The concept of food addiction, which more accurately may reflect addiction to specific components of food, can be described in much the same way as other addictive behaviours. Both food and drugs induce tolerance over time, whereby increasing amounts are needed to reach and maintain intoxication or satiety. In addition, withdrawal symptoms, such as distress and dysphoria, often occur upon discontinuation of the drug or during dieting. There is also a high incidence of relapse with both types of behaviour.“

To further support their arguments, they cite the many imaging studies showing that specific areas of the reward or mesolimbic system, such as the caudate nucleus, the hippocampus and the insula, are activated both by drugs and by food.

Thus, the easy accessibility of highly palatable foods together with our innate preferences for such foods, can increase the likelihood that vulnerable people will “misuse” food, in much the same way that addicts misuse other drugs to blunt negative emotional states, such as depression, anxiety, loneliness, boredom, anger orinterpersonal conflict.

While the concept of addiction should not negate the role of free will and personal choice, it does provide a rationale for the including addiction screens as a routine part of assessment for obesity. It may also help explain the success of lifestyle programs that incorporate pharmacotherapy or behavioural strategies specifically designed to address the addictive component of this illness.

Thus, as pointed out by Taylor and colleagues, there is not only considerable overlap among the medications shown to interfere with food and drug abuse in animal models, but the many behavioural interventions developed for managing addictions (motivational interviewing, cognitive behavioural therapy and 12-step programs), are increasingly recognised as also being helpful in managing obesity.

Health professionals and decision makers charged with tackling the obesity epidemic would do well to familiarise themselves with the science of addictions and utilize learnings from addiction management in their counseling of patients presenting with excess weight.

AMS
Edmonton, Alberta

Yesterday, the draft version of the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) was released for public comment until April 20.

The book, which serves mental health professionals, is also used by insurance companies making decisions on treatment coverage and in courtrooms and schools. It was last revised in 1994.

From what I’ve been able to garner from the news wires, the new Manual now clearly lists and identifies binge eating but not obesity as a mental health disorder.

This is probably a good thing.

While there is no doubt that binge eating disorder is a syndrome that requires specific mental health intervention, the same cannot necessarily be said for all of obesity.

This is not to say that a large proportion of overweight and obese individuals may also have mental health problems ranging from poor body image to major depression, addictions or attention deficit disorder - I have often blogged about this before.

But clearly, not everyone with excess weight also has a mental health diagnosis and certainly not all overweight patients need to be seen by a mental health professional.

Indeed, as previously noted, obesity is really only the clinical manifestation of caloric excess, and is as such more a clinical sign than a discrete entity in itself. It would therefore make no sense to list obesity as a mental illness or to expect that all obese individuals must now seek help from a mental health professional.

Nevertheless, given the importance of mental health problems either as promoters and/or consequences of weight gain or as important barriers to weight management, having mental health expertise in a weight management program is absolutely essential.

I am sure that the DSM-5 will prompt a wide range of debates and discussions and I will certainly take a closer look at the relevant segments of this intimidating document.

The final version of the manual is due to be published in 2013.

Certainly appreciate comments from any of my readers who work in mental health.

AMS

Vienna, Austria

To anyone regularly dealing with overweight and obese patients, the frequent association between excess weight and chronic musculoskeletal pain is no secret.

This association is particularly true for the rather enigmatic syndrome of fibromyalgia, characterised by the presence of generalized pain in muscle and joints, often associated with fatigue, poor sleep, and depression. Patients typically present with exquisite tenderness over discrete anatomical points, commonly referred to as tender points.  While there is still much debate around the exact etiology or even the exact diagnostic criteria (e.g. number of tender points) for fibromyalgia, there is no doubt that the presence of this syndrome can prove a major barrier to weight management.

Indeed, it is not at all clear whether there may in fact be an etiological link between fibromyalgia and obesity. As outlined in a paper by Akiko Okifuji and colleagues from Salt Lake City, UT, published last year in Clinical Rheumatology, 70% of fibromyalgia patients in their study were overweight or obese and presented with elevated levels of IL-6, catecholamines, cortisol, and CRP, all of which are common findings in obese patients. Furthermore, the patients with fibromyalgia, as do obese patients, presented with reduced sleep duration and efficiency. Based on these commonalities, Okifuji and colleagues concluded that excess weight and obesity may well play a role in fibromyalgia and related dysfunction. 

Interestingly, in 2008, Alan Saber and colleagues published an article in Obesity Surgery describing a significant improvement in pain score and points of tenderness in patients with fibromyalgia who underwent laparoscopic Roux-en-Y gastric bypass surgery. Based on these findings, the authors suggested that weight loss may be an important treatment modality for severely obese patients with this syndrome.

Whether or not less drastic approaches to weight management can provide benefits remains to be seen. Nevertheless, there have been reports of limited response to education, exercise, and psychological interventions. Thus, currently accepted non-pharmacological treatments for fibromyalgia remain rather limited.

Recently, a Cochrane review concluded that duloxetine is efficacious for treating pain in fibromyalgia and another systematic review found evidence that gabapentin and pregabalin can also reduce pain in these patients. 

Nevertheless, fibromyalgia continues to be a common but largely undertreated problem in overweight and obese patients and can often pose a significant barrier to increasing physical activity or modifying ingestive behaviour. 

As blogged before, assessment for muskuloskeletal pain should be a regular and essential feature of any assessment for overweight and obesity. 

I very much look forward to comments from any readers struggling with fibromyalgia or from colleagues on how they manage this debilitating syndrome.

AMS
Edmonton, Alberta

As blogged before, binge eating disorder (BED) can be diagnosed in as many as in one in four patients presenting in bariatric centres for weight loss.

Typical BED is characterized by frequent and persistent episodes of binge eating accompanied by feelings of loss of control and marked distress in the absence of regular compensatory behaviors. The disorder is associated with specific psychopathology (eg. dysfunctional body shape and weight concerns), psychiatric comorbidity (depression and anxiety disorders), and significant health and psychosocial impairments.

In my experience, the vast majority of patients with BED present with impressive histories of weight cycling, sometimes losing substantial amount of weight, only to soon gain it back. As do many obese patients, including those without BED, they fully believe that losing weight is the only solution to their often complex problems.

Just how futile weight loss attempts can be for patients with BED without primarily addressing the underlying psychopathology is nicely illustrated by Terence Wilson and colleagues from Rutgers University, New Jersey, just published in the Archives of General Psychiatry.

In this study, 205 women and men with a body mass index between 27 and 45 who met DSM-IV criteria for BED were randomised to twenty sessions of behavioural weight loss with moderate caloric restriction and exercise (BWL) or interpersonal psychotherapy (IPT) or 10 sessions of guided self-help cognitive behavioural therapy (CBTgsh) during 6 months.

At the end of the 6 month intervention, a substantially greater number of BWL patients achieved a 5% reduction in body weight (41%) than with IPT (15%) or CBTgsh (15%). At this time, all patients reported a similar reduction in binge-eating episodes.

However, two years later the picture looked quite different: while there were no longer significant weight differences between the groups (which means that the BWL patients regained virtually all the weight they lost), both IPT and CBTgsh were more likely to remain in remission from binge eating than BWL patients. The odds ratios for low and high global Eating Disorder Examination scores were 2.8 for BWL, 2.9 for CBTgsh, and 0.73 for IPT.

Although there was no significant association between sustained remission from binge eating and percent change in weight, a significantly greater proportion (31%) of patients with sustained remission from binge eating during follow-up lost a minimum of 5% of their baseline weight compared with patients who were never in remission (10%).

Not only does this study clearly show that behavioural weight loss is substantially less effective in long-term control of BED than psychological treatments, it also shows that simply losing weight is not a solution. Indeed, because conventional behavioural lifestyle treatments generally focus on dietary restraint, they are far more likely to ultimately promote binge eating than reduce it.

Not surprisingly, the authors conclude that guided self-help based on cognitive behavior therapy should be a first-line treatment option for most patients with BED, with IPT (or full cognitive behavior therapy) used for patients with low self-esteem and high eating disorder psychopathology.

Clearly, simply joining the next weight-loss challenge is not the solution.

AMS
Edmonton, Alberta

Earlier this year, I blogged about a study that linked obesity to brain atrophy. Specifically, that study reported that in individuals with a BMI > 30, atrophy was found in the frontal lobes, anterior cingulate gyrus, hippocampus, and thalamus compared with individuals with a normal BMI (18.5-25). 

Now, a study by Wolfgang Lieb and colleagues from the Framingham Heart Study, just published in JAMA, suggests the opposite.

Admittedly, this study primarily looked at the relationship between plasma leptin levels and the incidence of dementia, based on findings from animal studies suggesting that leptin facilitates long-term potentiation and synaptic plasticity in the hippocampus, promotes β-amyloid clearance, and improves memory function in animal models of aging and Alzheimer disease (AD).

The researchers studied 785 persons from the Framingham original cohort including 198 dementia-free survivors, who also underwent volumetric brain MRI between 1999 and 2005, approximately 7.7 years after leptin was assayed. 

During a median follow-up of 8.3 years higher leptin levels were associated with a markedly lower risk of incident dementia and AD as well as higher total cerebral brain volume and lower temporal horn volume.

Obviously, as one of the major determinants of leptin levels is body mass index, it is therefore not surprising that there was a significant difference in BMI between the lowest (BMI=24) and highest (BMI=32) leptin quartiles.

As with all studies of this nature, associations do not prove causality, so although the authors appear delighted that their findings support their hypothesis, I believe we are far off from recommending that people gain weight to increase their leptin levels to, in turn, lower their risk for dementia.

As so often, further studies appear warranted…

AMS
Chicago, IL