Abstract
It has become widely accepted that the immune system, and specifically increased levels of inflammation, play a role in the development of depression. However, not everyone with increased inflammation develops depression, and as with all other diseases, there are risk factors that may contribute to an increased vulnerability in certain individuals. One such risk factor could be the timing of an inflammatory exposure. Here, using a combination of PubMed, EMBASE, Ovid Medline and PsycINFO, we systematically reviewed whether exposure to medically related inflammation in utero, in childhood, and in adolescence, increases the risk for depression in adulthood. Moreover, we tried to determine whether there was sufficient evidence to identify a particular time point during the developmental trajectory in which an immune insult could be more damaging. While animal research shows that early life exposure to inflammation increases susceptibility to anxiety- and depressive-like behaviour, human studies surprisingly find little evidence to support the notion that medically related inflammation in utero and in adolescence contributes to an increased risk of developing depression in later life. However, we did find an association between childhood inflammation and later life depression, with most studies reporting a significantly increased risk of depression in adults who were exposed to inflammation as children. More robust clinical research, measuring direct markers of inflammation throughout the life course, is greatly needed to expand on, and definitively address, the important research questions raised in this review.
Highlights
One of the most important developments in translational mental health is the observation that the inflammatory system is involved in the pathogenesis of major depressive disorder (MDD) (Bufalino et al 2013; Valkanova et al 2013; Zunszain et al 2013; KiecoltGlaser et al 2015; Miller & Raison, 2015)
Given that neural development extends from the embryonic period through to adolescence (Rice & Barone, 2000; Johnson, 2001), and that this coincides with the development of the immune system (Hannet et al 1992; Osugi et al 1995; Holt & Jones, 2000) we focus on studies reporting exposure to increased inflammation in three developmental life stages: antenatal, childhood, and adolescence
It seems plausible that women in the Japanese cohort may have had diets rich in omega-3 fatty acids, which may have bestowed some protection against depression (Lin & Su, 2007; Sublette et al 2011; Martins et al 2012)
Summary
One of the most important developments in translational mental health is the observation that the inflammatory system is involved in the pathogenesis of major depressive disorder (MDD) (Bufalino et al 2013; Valkanova et al 2013; Zunszain et al 2013; KiecoltGlaser et al 2015; Miller & Raison, 2015). Exposure to increased inflammation may play a causal role in the pathogenesis of depression, as shown from research detailing how a high proportion of patients undergoing treatment with interferon (IFN)-α, a cytokine used for cancer or viral hepatitis C, go on to develop depression (Capuron et al 2001; Bonaccorso et al 2002; Horikawa et al 2003; Loftis & Hauser, 2004; Raison et al 2005). As with all other diseases, there are risk factors that contribute to an increased vulnerability in certain individuals Such risk factors could include the type, severity, frequency and/or the timing of an inflammatory challenge. Research has already shown that the timing and/or age at exposure may be an important predictor of future psychopathology, with exposure to adverse experiences in early life being consistently associated with increased susceptibility to a variety of neuropsychiatric disorders (Turecki et al 2014; Visser et al 2014; Kalmakis & Chandler, 2015; Trotta et al 2015)
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