Plasma insulin-like growth factor I levels are higher in depressive and anxiety disorders, but lower in antidepressant medication users

It has been postulated that many peripheral and (neuro)biological systems are involved in psychiatric disorders such as depression. Some studies found associations of depression and antidepressant treatment with insulin-like growth factor 1 (IGF-I) - a pleiotropic hormone affecting neuronal growth, survival and plasticity - but evidence is mixed. We therefore studied whether depressive and anxiety disorders were associated with plasma IGF-I, and explored the role of antidepressant medication in this association in a large observational study. The sample consisted of 2714 participants enrolled in The Netherlands Study of Depression and Anxiety, classified as healthy controls (n = 602), antidepressant users (76 remitted and 571 with current depressive and/or anxiety disorder(s), n = 647), persons having remitted depressive and/or anxiety disorder(s) without antidepressant use (n = 502), and persons having current depressive and/or anxiety disorder(s) without antidepressant use (n = 963). Associations with IGF-I concentrations were studied and adjusted for socio-demographic, health, and lifestyle variables. Relative to healthy controls, antidepressant-free individuals with current disorders had significantly higher IGF-I levels (Cohen's d = 0.08, p = 0.006), whereas antidepressant-free individuals with remitted disorders had a trend towards higher IGF-I levels (d = 0.06, p = 0.09). Associations were evident for depressive and for anxiety disorders. In contrast, antidepressant users had significantly lower IGF-I levels compared to healthy controls (d = 0.08, p = 0.028). Our findings suggests that antidepressant medication use modifies the association between depressive/anxiety disorders and plasma IGF-I. These results corroborate with findings of some previous small-scale case-control and intervention studies. The higher IGF-I levels related to depression and anxiety might point to a compensatory mechanism to counterbalance the impaired neurogenesis, although future studies are needed to support this hypothesis. (C) 2016 Elsevier Ltd. All rights reserved.