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Original Article | ONLINE FIRST

Association Between Common Variants Near the Melanocortin 4 Receptor Gene and Severe Antipsychotic Drug–Induced Weight Gain

Anil K. Malhotra, MD; Christoph U. Correll, MD; Nabilah I. Chowdhury, BSc; Daniel J. Müller, MD; Peter K. Gregersen, MD; Annette T. Lee, PhD; Arun K. Tiwari, PhD; John M. Kane, MD; W. Wolfgang Fleischhacker, MD; Rene S. Kahn, MD; Roel A. Ophoff, PhD; Jeffrey A. Lieberman, MD; Herbert Y. Meltzer, MD; Todd Lencz, PhD; James L. Kennedy, MD
Arch Gen Psychiatry. 2012;69(9):904-912. doi:10.1001/archgenpsychiatry.2012.191.
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Context  Second-generation antipsychotics (SGAs) are increasingly used in the treatment of many psychotic and nonpsychotic disorders. Unfortunately, SGAs are often associated with substantial weight gain, with no means to predict which patients are at greatest risk.

Objective  To identify single-nucleotide polymorphisms associated with antipsychotic drug–induced weight gain.

Design  Pharmacogenetic association study.

Setting  The discovery cohort was from a US general psychiatric hospital. Three additional cohorts were from psychiatric hospitals in the United States and Germany and from a European antipsychotic drug trial.

Participants  The discovery cohort consisted of 139 pediatric patients undergoing first exposure to SGAs. The 3 additional cohorts consisted of 73, 40, and 92 subjects.

Intervention  Patients in the discovery cohort were treated with SGAs for 12 weeks. Additional cohorts were treated for 6 and 12 weeks.

Main Outcome Measures  We conducted a genome-wide association study assessing weight gain associated with 12 weeks of SGA treatment in patients undergoing first exposure to antipsychotic drugs. We next genotyped 3 independent cohorts of subjects assessed for antipsychotic drug–induced weight gain.

Results  Our genome-wide association study yielded 20 single-nucleotide polymorphisms at a single locus exceeding a statistical threshold of P < 10−5. This locus, near the melanocortin 4 receptor (MC4R) gene, overlaps a region previously identified by large-scale genome-wide association studies of obesity in the general population. Effects were recessive, with minor allele homozygotes gaining extreme amounts of weight during the 12-week trial. These results were replicated in 3 additional cohorts, with rs489693 demonstrating consistent recessive effects; meta-analysis revealed a genome-wide significant effect (P = 5.59 × 10−12). Moreover, we observed consistent effects on related metabolic indices, including triglyceride, leptin, and insulin levels.

Conclusions  These data implicate MC4R in extreme SGA-induced weight gain and related metabolic disturbances. A priori identification of high-risk subjects could lead to alternative treatment strategies in this population.

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Figures

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Figure 1. Distribution of antipsychotic drug–induced weight gain in antipsychotic-naive subjects following 12 weeks of treatment with second-generation antipsychotic drugs. The y-axis represents the percentage of subjects in each of the 5 weight gain categories; for example, subjects gaining more than 21% of their baseline weight are indicated in light gray, and subjects gaining more than 14% of their baseline weight are indicated in light blue. ARI indicates aripiprazole; AVG, the average of quetiapine (QTP), risperidone (RIS), and ARI; OLZ, olanzapine.

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Figure 2. Genome-wide association study results. A, Manhattan plot displays statistical significance levels (−log10P values) of correlation and trend tests for change in body mass index (BMI) in the discovery cohort, plotted by chromosomal position for all autosomal single-nucleotide polymorphisms (SNPs). Peak values are observed on chromosome 18, between positions 55.934 and 56.037 megabases (Mb), as detailed in Table 1. B, Quantile-quantile plot displays statistical significance levels (−log10P values) of correlation and trend tests for change in BMI in the discovery cohort, plotted against expected values under the null hypothesis. With the exception of the most strongly associated SNPs on chromosome 18, there is no deviation from the diagonal (λgenomic control = 1.00).

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Figure 3. Single-nucleotide polymorphism rs489693 genotype and antipsychotic drug–induced weight gain in 4 cohorts of subjects. Replic1 indicates the first replication cohort; Replic2, the second replication cohort; Recplic3, the third replication cohort.

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