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Discontinuing antidepressants, lowering dose alleviates treatment-induced type 2 diabetes
Japanese adults may be at greater risk for type 2 diabetes if they take antidepressants, but high HbA1c can be addressed by taking a lower dose or discontinuing the drugs, according to findings published in Diabetes Care.
“Long-term antidepressant use might increase the risk of type 2 diabetes mellitus in a time- and dose-dependent manner,” Kazuo Mishima, MD, PhD, of the department of neuropsychiatry at Akita University Graduate School of Medicine in Akita, Japan, and colleagues wrote. “Discontinuation of antidepressant therapy and reduction of the antidepressant dose after type 2 diabetes mellitus onset improved glucose tolerance.”
Mishima and colleagues assessed the risk for type 2 diabetes among 45,265 adult residents of Japan with health insurance who used antidepressants (mean age, 41.4 years; 31.1% women) and a propensity-score matched cohort of 45,265 similar adults who did not use antidepressants (mean age, 46.8 years; 31% women). The researchers identified antidepressant prescriptions and type 2 diabetes diagnoses via medical records collected from 2005 to 2016 and assessed dosage of antidepressants via amitriptyline equivalents per month.
Prior to matching, 50,770 participants used antidepressants and 1,950 of them developed type 2 diabetes. In addition, the pre-matching cohort of those not using antidepressants was made up of 708,647 participants, of whom 3,275 developed type 2 diabetes.
Using the matching groups, the researchers found that type 2 diabetes risk was greater for those who took at least 182.9 amitriptyline equivalents per month, or a high dose, for at least 25 months, or long term, compared with those who were not prescribed antidepressants. (HR = 3.95; 95% CI, 3.31-4.72). Similarly, type 2 diabetes risk was greater for those who took between 91.4 and 182.8 amitriptyline equivalents per month, or a moderate dose, for between 12 and 24 months, or for an intermediate term (HR = 2.52; 95% CI, 2.04-3.11), and for those who took fewer than 91.4 amitriptyline equivalents per month, or a low dose, for fewer than 12 months, or for a short term (HR = 1.27; 95% CI, 1.16-1.39). Type 2 diabetes risk was also greater for those who took a moderate dose for a short term (HR = 1.77; 95% CI, 1.45-2.17), a high dose for a short term (HR = 2.54; 95% CI, 1.62-3.99), a low dose for an intermediate term (HR = 1.44; 95% CI, 1.21-1.72), a high dose for an intermediate term (HR = 3.32; 95% CI, 2.2-5.01), a low dose for a long term (HR = 2.14; 95% CI, 1.94-2.36) and a moderate dose for a long term (HR = 2.58; 95% CI, 2.3-2.89).
“Further studies are needed to assess whether there are differences in vulnerability to antidepressant-induced diabetes among ethnicities and to identify which classes of antidepressants are associated with diabetes risk,” the researchers wrote. “To control medical costs, diabetes onset due to antidepressants should be considered when patients with a high risk of diabetes are offered treatment with antidepressants.”
Among participants who used antidepressants and went on to have diabetes, HbA1c returned to normal for 97.5% of those who discontinued the drugs and for 94% of those who lowered their dosage by 50%.
“Our results suggest that reducing the dose of or discontinuing causative antidepressants within 1 year of type 2 diabetes onset alleviates impaired glucose tolerance, which in turn strongly suggests a causal relationship between antidepressant administration and type 2 diabetes onset,” the researchers wrote. “HbA1c level should be regularly monitored in patients taking antidepressants in order to inform the decision to reduce or discontinue antidepressant use, if possible, when impaired glucose tolerance is observed.” – by Phil Neuffer
Disclosure: Mishima reports he has received research support from the Japanese Ministry of Health, Labour and Welfare, speaker honoraria and research grants from Eisai and Takeda Pharmaceutical, speaker honoraria from Astellas Pharma, Janssen Pharmaceuticals and Merck Sharp & Dohme, and research grants from Nobelpharma.
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