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

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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.
Original languageEnglish
Pages (from-to)148-155
Publication statusPublished - Jun 2016

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