In response to yesterday’s post on ADHD and obesity, I was made aware of two recent studies, both relevant to this topic.

In the first, A psycho-genetic study by Caroline Davis and colleagues from York University, Toronto, Ontario, Canada, published in the Journal of Psychiatric Research, the researchers examined whether ADHD symptoms were more pronounced in adults with symptoms of binge eating disorder (BE) than in their non-binging obese counterparts, and whether the links were stronger with inattentive vs impulsive/hyperactive symptoms. They also assessed the role of the dopamine D3 receptor in ADHD symptoms since the DRD3 gene has been associated with impulsivity and drug addiction - both relevant features of ADHD.

In the study that involved 60 cases and 120 controls (60 obese and 60 normal weight), childhood and adults ADHD symptoms were assessed and genotying was performed.

While all of the four ADHD symptom scales were significantly elevated in the BE and obese groups compared to the normal weight group, bearers of three DRD3 genotypes had significantly elevated scores on the hyperactive/impulsive symptom scale.

These results suggest that symptoms of ADHD are more common in obese individuals (irrespective of BED status) and that the D3 receptor may play a role in the manifestation of the hyperactive/impulsive symptoms of ADHD.

In another study, published in this month’s issue of OBESITY by Lance Levy and colleagues from the Nutritional Disorders Clinic, also in Toronto, Ontario, Canada, they describe their success in treating refractory obesity in severely obese adults following the management of newly diagnosed attention deficit hyperactivity disorder.

78 subjects out of 242 consecutively referred severely obese, weight loss refractory individuals were diagnosed as having ADHD, of which 65 received ADHD treatment and 13 remained as controls.

After an average of 466 days of continuous ADHD pharmacotherapy, weight change in treated subjects was -12% of initial weight versus a 3% weight gain in controls.

This study not only confirms that ADHD is a highly prevalent condition in severely obese patients, but that the treatment of ADHD is associated with significant long-term weight loss in individuals with a lengthy history of weight loss failure.

Levy suggests, as I did in earlier postings on this topic, that ADHD should be considered as a primary cause of weight loss failure in obese patients.

As he points out, this finding may also be important for patients seeking obesity surgery, as surgical patients with unmanaged ADHD may display poor compliance with diet and supplement requirements.

AMS
Edmonton, Alberta

p.s. Caroline Davis will be presenting at the upcoming 1st National Obesity Summit, Kananaskis, Alberta, May 7-10, hosted by the Canadian Obesity Network

In my clinical practice I remain impressed by the surprisingly high incidence of attention deficit hyperactivity disorder (ADHD) in my obese patients. Many have had symptoms all their lives, many have kids diagnosed and treated for ADHD, but have never considered that they may have this condition themselves.

Long-time readers of this blog will recall several previous postings on this issue - there is little doubt that ADHD is a major handicap in dealing with a weight problem. Lack of impulse control, difficulty planning and following through on lifestyle changes, compliance problems - all make it difficult for someone with ADHD to tackle their weight problem.

But how close is the relationship between ADHD and obesity in the general population?

Based on previous observations that while ADHD affects ~2.9-4.7% of US adults, this condition is reported to be present in 26-61% of patients seeking weight loss treatment, Sherry Pagoto and colleagues from the University of Massachusetts, MA, USA, revisited this issue in a paper published in this month’s issue of OBESITY.

Using cross-sectional data from the Collaborative Psychiatric Epidemiology Surveys, which includes data from 6,735 US residents (63.9% white; 51.6% female) aged 18-44 years, a retrospective assessment of childhood ADHD and a self-report assessment of adult ADHD were administered.

The prevalence of overweight and obesity was 33.9 and 29.4%, respectively, among adults with ADHD, and 28.8 and 21.6%, respectively, among persons with no history of ADHD. Thus, adult ADHD was associated with a 58% greater likelihood of overweight and 81% greater likelihood of obesity.

Further analyses suggested that binge eating disorder (BED), but not depression, partially mediates the associations between ADHD and excess weight. This is not surprising, given that poor impulse control is likely to affect binge-eating behaviour.

The study underlines what I have long proposed: assessment for ADHD should be part of routine work up for obesity and weight-related health problems. When present, ADHD can pose a major barrier to obesity management and should be addressed by CBT and/or medications.

AMS
Edmonton, Alberta

Psychological and psychiatric assessment prior to bariatric surgery is an essential part of our current management model and is recommended by all current obesity guidelines. Indeed, there is little doubt that psychiatric diagnoses are relatively common in weight loss-seeking obese individuals. Specifically, the prevalence of binge eating disorder (BED) has been reported to be in the range of 25-40% of all individuals seeking bariatric surgery.

The general notion is that patients with significant BED should undergo cognitive behavioural intervention prior to surgery and that severe BED may be a contraindication to proceeding with any form of weight-loss.

However, contrary to this widely held notion, hard data confirming that the presence of BED is indeed a predictor of poor surgical outcomes is sparse. In fact, most published studies, suggest that weight loss results in BED patients may be as good (or in some cases even better) than in patients without BED!

Nevertheless, there appear to be some important caveats. Thus, in a new study by Sharon Alger-Mayer and colleagues from Albany Medical College, NY, published in this months edition of Obesity Surgery, weight loss outcomes in patients with severe BED (37 out of 157 patients), who managed to lose 10% of body weight prior to surgery and attended all follow-up consultations during the first 12 months following surgery, were similar to the outcomes in patients without BED over 6 years of follow-up.

Note: the two caveats are:

1) losing 10% of their weight prior to surgery and

2) attending all follow-up appointments.

The study of course did not include patients with BED, who did not lose 10% body weight prior to surgery or who failed to attend their follow-up appointments.

Incidentally, depression (Beck’s Depression Inventory) and poor quality of life (SF-36) likewise did not predict weight loss outcomes.

Overall, this study is consistent with previous shorter-term studies that did not find BED to be a negative predictor of surgical outcomes. Nevertheless, the authors still regard psychological and psychiatric assessment an essential part of patient work-up prior to surgery.

Thus, BED should not generally be seen as a contraindication to proceeding with gastric bypass surgery. Does the same apply to other types of surgery such as the gastric sleeve or gastric banding? We’ll have to wait for the appropriate studies.

In the meantime, at our centre, we continue to insist on regular attendance and demonstration of significant lifestyle changes that include diligent food journaling, regular planned exercise, strict attendance of all clinic appointments, and a minimum of 5-10% weight loss in all pateints prior to consideration for surgery (in addition, we insist on smoking cessation, elimination of all pop, juices and carbonated beverages, elimination of all junk foods and high-caloric snacks, and a sound understanding of the risks and benefits of the planned procedure) .

I guess it may be time for a randomized trial to determine if assessment and treatment for BED will help improve surgical outcomes or prove a waste of resources and an unwarranted barrier to sugery.

Till then, I believe it is advisable to err on the side of caution.

AMS
Edmonton, Alberta

On Tuesday, Prime Minister Harper, on behalf of all Canadians, said “We are sorry” to the Aborginal peoples of Canada for putting generations of them through residential schools aimed at removing them from the influence of the wigwam.

These residential schools began in 1920 and attendance for all aboriginal children ages 7-15 years was made compulsory. Children were forcibly taken from their families by priests, Indian agents and police officers. The last federally run residential school was in Saskatchewan and closed its doors in 1996.

In his address, Harper said:

“The Government of Canada built an educational system in which young children were often forcibly removed from their home, often taken far from their communities. Many were inadequately fed, clothed and housed. All were deprived of the care and nurturing of their parents, grandparents and communities.”

This disastrous and cruel policy resulted in much pain and despair in the First Nations’, Inuit and Metis people that lasts to this day (known as the “generational effect”). Sexual, physical and mental abuse was widespread; students were broken in heart and spirit; culture and identities were destroyed.

Much (if not all) of what ails the Aboriginal peoples of Canada can be traced back to this policy – including possibly issues that affect Aboriginal health to this day.

It is no secret that obesity and its consequences (e.g. diabetes) are rampant amongst the Aboriginal peoples of Canada. While poverty, breakdown of traditional lifestyle and culture and even genetic factors (thrifty genotype) have all been implicated in this, I wonder how much the misery caused by the residential school program had to contribute.

Early traumatic life experiences including sexual, mental and physical abuse as well as neglect and grief have all been implicated in binge eating disorder (BED) – in its purest form – the uncontrollable urge to devour large quantities of highly palatable high-caloric foods in response to emotional hunger. This behaviour has been interpreted as an emotional coping strategy, “filling the inner void”, building a physical protective barrier, etc., the ultimate result being excessive weight gain with all its consequences (the typical binger does not compensate by purging or excessive exercise).

In “treatment-seeking” patients with obesity, the prevalence of BED is estimated at 20-40%. Although I was unable to find a study that has applied the DSM-IV criteria for BED to an Aboriginal population – my guess is: the rates are probably high!

Given its distinct psychopathology, BED is highly responsive to psychotherapeutic approaches. In contrast, educational initiatives based on simply providing information on healthy lifestyles are useless.

Obesity is never an issue of “choice”. I have yet to meet anyone who “chooses” to be obese. This is most certainly also true for Canada’s Aboriginal population.

I look forward to perhaps one day reading a thesis on “The Role of Residential Schools in the Aboriginal Obesity Epidemic”.

I’d be surprised if the author failed to find a clear link.

AMS
Edmonton, Alberta

Classical Binge Eating Disorder (as defined by DSM-IV) is found in around 20-40% of severely obese patients presenting at bariatric centres (including ours). Numerous studies have shown that patients with BED can achieve significant weight loss, resolution of comorbidities and improvement in quality of life with obesity surgery and therefore should not generally be denied surgery.

Nevertheless, many centres (including ours) are reluctant to operate on patients with active BED fearing poorer outcomes and greater distress. It turns out that we really don’t know much about how bariatric surgery affects eating patterns in patients with BED.

This question was now addressed by Susan Colles and colleagues from Monash University in Melbourne in a study published in the March issue of OBESITY. Colles and colleagues planned to study eating behaviours in 180 patients before and 12 months following laparoscopic adjustable gastric banding (LABG). Of these, 6 did not receive surgery, 1 died of a myocardial infarct and 44 (25% of eligible subjects) did not return for the 12-month survey (more on this later).

While only 14% of patients had BED at baseline, 31% were described as “uncontrolled eaters”, 40% had night eating syndrome (NES) and 26% were “grazers”.

Although all groups, including the “bingers” lost similar amounts of weight and BED reduced to 3% in this group, patients with preoperative BED were most likely to develop uncontrolled eating or grazing. Patients who reported uncontrolled eating or grazing after surgery tended to lose less weight and reported greater psychological distress.

Interestingly, the authors report that the 12-month non-responders were more likely to have had presurgical BED, have lost less weight and attended less clinic appointments. This may be due to patients with these behaviours feeling more ashamed about their “loss of control” and therefore avoiding follow-up visits.

This study highlights the risk of preoperative “bingers” to become “uncontrolled eaters” or “grazers” resulting in psychological distress and poorer weight outcomes. As these patients are more likely to drop out of follow-up they may also be at increased long-term risk of nutritional deficiencies and other long-term complications of bariatric surgery.

In an accompanying paper in the same issue of OBESITY, Colles and colleagues describe how “loss of control” may be at the root of the significant psychological distress of patients with BED resulting in their greater likelihood of seeking out bariatric surgery as a means to control their eating behaviour. This may well in part explain the high prevalence of BED in patients presenting in bariatric clinics.

Clearly, we need to learn more about how to pre-screen patients for potentially poor outcomes and how best to monitor post-surgical patients for the development of aberrant eating behaviours.

Given that BED, once diagnosed, is actually quite responsive to psychological treatments resulting in a remarkably high rate of resolution, I wonder about the rational for operating on patients with active BED - after all weight loss should not be the only parameter by which results of obesity surgery are measured.

AMS
Edmonton, Alberta