Antipsychotic Medications and Weight Gain in Children and Adolescents

I have previously blogged about the unfortunate effect of atypical antipsychotics on body weight and on the possible strategies that may be effective in dealing with this important complication of psychiatric treatment.

As the number of children and adolescents diagnosed with and treated for psychiatric disorders continues to increase, the use of these medications in this population is of growing concern.

The extent to which atypical antipsychotic medications promote weight gain and increase cardiometabolic risk in children and adolescents was recently addressed by Christoph Correll and colleagues from the Zucker Hillside Hospital, Glen Oaks, NY, in a paper published in JAMA.

The researchers analysed data from a nonrandomized Second-Generation Antipsychotic Treatment Indications, Effectiveness and Tolerability in Youth (SATIETY) cohort study, conducted between December 2001 and September 2007.

Of 505 youth aged 4 to 19 years with 1 week or less of antipsychotic medication exposure, 338 were enrolled (66.9%) of which 272 had at least 1 postbaseline assessment (80.5%), and 205 patients who completed the study (60.7%). Patients were treated for mood spectrum (48%), schizophrenia spectrum (30%), or disruptive or aggressive behavior (22%) disorders.

Treatment with aripiprazole, olanzapine, quetiapine, or risperidone for 12 weeks resulted in weight gain ranging between 8.5 kg with olanzapine (n = 45) and 4.4 kg with aripiprazole (n = 41). A small control group (that refused or were non-adherent with treatment) had no weight gain during the follow up period.

Olanzapine, quetiapine and risperidone adversely effected plasma lipids, while there were no changes in these parameters with aripiprazole or in the untreated controls.

This study not only highlights the clinically important effect of these antipsychotic compounds on body weight but also suggests that there may be important differences in the magnitude of these effects with different medications.

While these adverse effects should certainly not deter from the use of these compounds where absolutely indicated (given the considerable morbidity associated with severe psychiatric disorders), avoidance of weight gain remains an important challenge that needs to be addressed.

AMS
Edmonton, Alberta

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Antipsychotics and Ingestive Behaviour

While I am taking a brief break from clinics and other obligations (including daily blog posts), I will be reposting past articles, which I still believe to be relevant but may have escaped the attention of the 100s of new readers who have signed up in the past months.

The following was first posted on 08/25/08

I have previously blogged on the profound effect of second generation antipsychotics (SGA) on weight gain. A new article by Melissa Blouin and co-workers from Laval University (Quebec City, Canada), published in this month’s issue of OBESITY, now examines the effect of these compounds on appetite, hunger, satiety, restraint and food preferences in SGA-treated patients (n=20) compared to controls (n=18).

Following a standardised breakfast, SGA patients had more hunger, higher cognitive dietary restraint, disinhibition and susceptibility to hunger than controls. In contrast to the controls, disinhibition in SGA-patients was largely triggered by internal cues. Although SGA-patients displayed higher strategic restraint behaviour, they also reported lower satiation after the buffet meal. No differences were found in food preferences.

This study has a number of interesting angles. Not only were the SGA-treated patients more susceptible to hunger, they were also more likely to consciously restrain their food intake, perhaps as a strategy to control their weight. This of course explains in part the fact that they were less likely to feel full or satiated after a meal than the controls.

It is well known that cognitive restraint (i.e. voluntarily trying to limit food intake) produces a tendency to overeat or even binge when restrictions are lifted (e.g. social disinhibition). The ultimate result, paradoxically, is weight gain or re-gain. This counter-regulatory phenomenon has been well described by Janet Polivy (University of Toronto) and essentially shows that food deprivation amongst dieters (achieved with cognitive dietary restriction) produces a tendency to overeat, explaining why long-term dieting does not work for restrained eaters. In other words – trying to simply eat less as a treatment for obesity is doomed to failure!

On a humanitarian note, the SGA-patients appear to be caught in an unfortunate vicious cycle: The antipsychotics alter eating behaviour to increase body weight – patients try to avoid further weight gain by cognitively restraining their food intake – as a result they feel less satiated and end up eating even more.

Complicated!

Of course, from this study, we don’t really know if the patients’ abnormal behaviour is due to their medications or simply due to their underlying disease. A third group of subjects consisting of psychotic patients treated with older antipsychotic medications may have answered this question.

Nevertheless, the study does demonstrate that we need to be very cautious in simply blaming someone with obesity for their condition. As this study reminds us – trying to not gain weight by simply eating less, is often a prescription for weight gain.

AMS
Edmonton, Alberta

Comments

Antipsychotics and Ingestive Behaviour

I have previously blogged on the profound effect of second generation antipsychotics (SGA) on weight gain. A new article by Melissa Blouin and co-workers from Laval University (Quebec City, Canada), published in this month’s issue of OBESITY, now examines the effect of these compounds on appetite, hunger, satiety, restraint and food preferences in SGA-treated patients (n=20) compared to controls (n=18).

Following a standardised breakfast, SGA patients had more hunger, higher cognitive dietary restraint, disinhibition and susceptibility to hunger than controls. In contrast to the controls, disinhibition in SGA-patients was largely triggered by internal cues. Although SGA-patients displayed higher strategic restraint behaviour, they also reported lower satiation after the buffet meal. No differences were found in food preferences.

This study has a number of interesting angles. Not only were the SGA-treated patients more susceptible to hunger, they were also more likely to consciously restrain their food intake, perhaps as a strategy to control their weight. This of course explains in part the fact that they were less likely to feel full or satiated after a meal than the controls.

It is well known that cognitive restraint (i.e. voluntarily trying to limit food intake) produces a tendency to overeat or even binge when restrictions are lifted (e.g. social disinhibition). The ultimate result, paradoxically, is weight gain or re-gain. This counter-regulatory phenomenon has been well described by Janet Polivy (University of Toronto) and essentially shows that food deprivation amongst dieters (achieved with cognitive dietary restriction) produces a tendency to overeat, explaining why long-term dieting does not work for restrained eaters. In other words – trying to simply eat less as a treatment for obesity is doomed to failure!

On a humanitarian note, the SGA-patients appear to be caught in an unfortunate vicious cycle: The antipsychotics alter eating behaviour to increase body weight – patients try to avoid further weight gain by cognitively restraining their food intake – as a result they feel less satiated and end up eating even more.

Complicated!

Of course, from this study, we don’t really know if the patients’ abnormal behaviour is due to their medications or simply due to their underlying disease. A third group of subjects consisting of psychotic patients treated with older antipsychotic medications may have answered this question.

Nevertheless, the study does demonstrate that we need to be very cautious in simply blaming someone with obesity for their condition. As this study reminds us – trying to not gain weight by simply eating less, is often a prescription for weight gain.

AMS
Edmonton, Alberta

Comments

Antipsychotics and Weight Gain

It is no secret that medications commonly used to treat psychosis can lead to remarkable weight gain. This is particularly true of the second generation antipsychotics clozapine (Leponex, Clozaril) and olanzapine (Zyprexa), but the mechanisms leading to weight gain are poorly understood.

In a recent study Kluge and colleagues from the Max Planck Institute of Psychiatry in Munich, ramdomised 30 patients with schizophrenia, schizophreniform, or schizoaffective disorder in a double-blind, parallel study comparing abnormal eating behavior using a standardized scale to clozapine and olanzapine.

In both treatment groups, there was a significant increase in cravings and in binge eating, whereby the rate of these effects was somewhat higher with olanzepine. Clinical improvements in psychiatric symptoms was comparable.

What the study does not disclose is what one could possibly do to help patients avoid weight gain. The evidence that “lifestyle” interventions are effective in preventing this weight gain is marginal at best. A recent randomized study published in JAMA showed some benefit of prescribing metformin alone or in combination with lifestyle advice.

An earlier double-blind placebo-controlled study in 37 patients on olanzepine showed greater weight loss with sibutramine (Meridia, Reductil) over 12 weeks than on lifestyle alone.

Amantadine, in an even smaller randomised placebo-controlled study in 21 patients, was at least somewhat effective in limiting olanzapine-induced weight gain.

Clearly, addressing weight gain in patients, who need effective antipsychotic medications remains challenging at best.

AMS

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