Effect of Mirtazapine Treatment on Body Composition and Metabolism
J Clin Psychiatry 2006;67:421-424
© Copyright 2014 Physicians Postgraduate Press, Inc.
Purchase This PDF for $40.00
If you are not a paid subscriber, you may purchase the PDF.
(You'll need the free Adobe Acrobat Reader.)
Receive immediate full-text access to JCP. You can subscribe to JCP online-only ($86) or print + online ($156 individual).
With your subscription, receive a free PDF collection of the NCDEU Festschrift articles. Hurry! This offer ends December 31, 2011.
If you are a paid subscriber to JCP and do not yet have a username and password, activate your subscription now.
As a paid subscriber who has activated your subscription, you have access to the HTML and PDF versions of this item.
Click here to login.
Did you forget your password?
Still can't log in? Contact the Circulation Department at 1-800-489-1001 x4 or send email
Objective: Weight gain is a common side
effect of psychotropic medications. Mirtazapine, a widely used antidepressant, induces adverse
metabolic effects such as an increase in body
weight. The aim of this study was to investigate the
influence of mirtazapine treatment on body weight, body fat mass, glucose metabolism,
lipoprotein profile, and leptin and its soluble receptor in
a prospective, controlled study design.
Method: Seven women who met the
ICD-10 diagnostic criteria for a depressive episode
(ICD-10: F31-F33) were assigned to monotherapy
with mirtazapine and observed for a 6-week period. Seven mentally and physically healthy
female volunteers matched for age and body weight served as a control group. Data were
collected from November 2002 to December 2003.
Results: The mean ± SD body weight
increased from 63.6 ± 13.1 kg to 66.6 ± 11.9 kg during mirtazapine treatment (p =
.027). Fat mass increased in study subjects from 20.9 ± 9.6 kg to 22.1±9.3 kg
(p=.018). Insulin, glucose, and the homeostasis model assessment (HOMA) index for insulin
resistance and lipid parameters remained stable. Leptin concentrations increased from
23.0 ± 17.1 ng/mL to 40.9 ± 27.2 ng/mL (p = .018), whereas
the soluble leptin receptor concentrations
remained stable during mirtazapine treatment. In the
control subjects, the investigated parameters
remained stable. Between-group analyses of change
scores revealed significant differences for body
weight (p = .010), body mass index (p = .013), fat
mass (p = .035), and leptin (p = .013).
Conclusion: The antidepressant therapy
with mirtazapine was associated with a significant
increase in body weight, body fat mass, and leptin concentration. In contrast to other
psychotropic medications inducing weight gain, such as
some second-generation antipsychotics, mirtazapine treatment did not influence the glucose