A Single-Center, Double-Blind, Placebo-Controlled Evaluation of Lamotrigine in the Treatment of Obesity in Adults

Charles H. Merideth, M.D.

Objective: Unlike many pharmacotherapies for mood disorders, lamotrigine has not been shown to be associated with weight gain. This study evaluated the safety and efficacy of lamotrigine, compared with placebo, as a monotherapy for weight loss in obese adult subjects.

Method: Forty subjects were randomly assigned (1:1) to receive lamotrigine 200 mg/day or placebo for up to 26 weeks. Eligibility included a body mass index (BMI) of 30 to < 40. The primary endpoint was the change from baseline to endpoint (week 26) in subject weight. Secondary endpoints included the change from baseline to endpoint in BMI, percent body fat, serum lipid, and glycosylated hemoglobin values, subject satisfaction with treatment, and quality of life.

Results: Mean change in body weight from baseline to endpoint (last observation carried forward) was -6.4 ± 10.26 lb and -1.2 ± 7.09 lb for lamotrigine and placebo, respectively (p = .0623). Baseline body weight was slightly different between treatment groups (lamotrigine mean = 207.9 ± 19.88 lb, placebo mean = 225.0 ± 32.70 lb; p = .0588). There was a statistically significant difference (p = .0421) in mean change in BMI from baseline to endpoint (-1.5 ± 2.78 and -0.1 ± 1.05 for lamotrigine and placebo, respectively). Subjects were more satisfied with lamotrigine treatment compared with placebo (p = .0065). There were no significant differences between treatment groups in other secondary endpoints. The most frequently reported adverse event was mild-to-moderate headache, occurring in both treatment groups.

Conclusion: Lamotrigine demonstrated a statistically significant difference in mean change in BMI and a trend toward a decrease in body weight and was well tolerated.

(J Clin Psychiatry 2006;67:258-262)

Received April 13, 2005; accepted Nov. 22, 2005. From the Affiliated Research Institute, San Diego, Calif.

This paper was supported by an investigator-initiated grant from GlaxoSmithKline, Research Triangle Park, N.C.

This paper was presented in part at the 158th annual meeting of the American Psychiatric Association, May 21-26, 2005, Atlanta, Ga.

Dr. Merideth reports no additional financial or other support.

The author acknowledges Steve Pashko, Ph.D.; Chris K. Southard, M.A.; Thomas Hochadel, Pharm.D.; and Christine K. Thomason, Ph.D., for their contributions.

Corresponding author and reprints: Charles H. Merideth, M.D., Affiliated Research Institute, 8989 Rio San Diego Dr., Suite 350, San Diego, CA 92108 (e-mail: cmeridethmd@ari-inc.com).