Antidepressant use, progression to diabetes linked
However, basis for association remains unclear.
Patients who take antidepressant medications may be at increased risk for developing diabetes, according to results of a new study.
If antidepressants prove to be an independent diabetes risk factor, clinicians will need to consider this when prescribing depression treatment, Richard R. Rubin, PhD, professor of medicine and pediatrics at the Johns Hopkins University, told Endocrine Today.
Rubin and colleagues assessed the association between antidepressant use and diabetes in individuals at high risk for the disease. They evaluated 3,187 participants enrolled in one of three treatment arms in the Diabetes Prevention Program: intensive lifestyle, metformin and placebo.
Depression scores, medication use and diabetes
Researchers from various sites in the United States followed the participants for an average of 3.2 years and found that elevated depression scores consistent with mild depression at baseline and during the study were not associated with progression to diabetes in any of the three treatment arms.
However, antidepressant use at baseline was associated with increased diabetes risk in both the placebo arm (HR=2.25) and intensive lifestyle arm (HR=3.48). Participants who took antidepressants on a continuous basis during the study were also at increased risk for diabetes (placebo arm, HR=2.60; intensive lifestyle arm, HR=3.39). Intermittent use was associated with diabetes risk only in the intensive lifestyle arm (HR=2.07).
|Evaluating Antidepressant Use and Progression to Diabetes: Three Treatment Arms in the Diabetes Prevention Program|
Medication use was not significantly associated with progression to disease in participants in the metformin arm.
According to the researchers calculations, treating 5.4 participants in the placebo arm and 5.2 in the intensive lifestyle arm with antidepressants would cause one additional case of diabetes after three years.
The association between antidepressant use and diabetes risk remained significant when likely mediators were controlled, such as fasting glucose, weight and weight gain, Rubin said.
Women were more likely to use antidepressants at baseline 7.4% of women vs. 2% of men. Prior to this evaluation, only second-generation atypical antipsychotic agents have been associated with increased diabetes risk. Most participants in this study used selective serotonin reuptake inhibitors.
Antidepressant use could simply be a marker for the actual cause of increased diabetes risk, he said. The lingering effects of past depression or the current effects of that depression, even with its symptoms controlled by medication, could explain the association.
Future research should focus on minimizing the potentially adverse effects of antidepressants on glycemic control, according to the researchers. by Katie Kalvaitis
For more information:
- Rubin RR, Ma Y, Marrero DG, et al. Elevated depression symptoms, antidepressant medicine use, and risk of developing diabetes during the Diabetes Prevention Program. Diabetes Care. 2008;31:420-426.
These data are provocative. This raises the question of whether antidepressants can play some kind of etiologic role in the induction of diabetes in people who are susceptible. It makes me wonder whether use of these agents could be doing something bad. I think antidepressants are good at treating depression, and people are going to treat with these drugs even if there is an increased risk for conversion to diabetes in susceptible people. I suppose if you are going to use antidepressants, you should get baseline values on your patients and watch them if it looks like they have any risk factors for diabetes. Based on studies like this one, you want to perhaps screen these patients a little more carefully. The whole issue of depression is hard to quantitate. These researchers are saying that people treated with antidepressants had a higher incidence of conversion to diabetes. But the reasons are apparently not clear. There was no association with body weight gain. This study also raises the question, to which we do not have an answer at the moment: can this be replicated in other studies? Maybe we need a large-scale clinical trial to look at this.
Philip Levy, MD
Endocrine Today Editorial Board member