3 METHODS
5.6 Conclusions, implications of the study and future directions
The studies presented in this thesis provide implications for further research and for promoting public health (please see Table 15).
In particular, the findings in this thesis inform of the premorbid mechanisms of cardio-metabolic diseases and this is an essential finding as T2D and its metabolic consequences pose a threat to individuals and a financial burden to society. As participants with T2D were excluded from the study samples, it seems that psychosocial factors play a role in the development of T2D by inducing IR – a process that may even date back some 10 years (U.K. Prospective Diabetes Study Group, 1995). However, as the causative cascade of events can not be addressed with these studies, future prospective studies are needed to define how these possibly overlapping psychosocial factors contribute to development of IR. Indeed, the causal evidence for an association between psychosocial factors and prediabetes is yet to be established, unlike the well- established link between depression and manifest T2D. Nevertheless, the findings in this thesis suggest that interventions targeted at reducing depressive symptoms already at subclinical level, and the consequences of stress by more efficient coping skills, as well as the causes of sleep complaints, may be beneficial in long-term health promotion. However, if indeed sub-clinical depressive symptoms and stressful life events are found an underlying cause of IR in a longitudinal setting, further studies could also include assessing the effectiveness of interventions in reducing the incidence of T2D. For example, a randomised controlled study could test whether effective prevention or
93
treatment of depression can reduce the incidence of T2D and its health consequences. Currently, there are few promising results implicating that psychological interventions, e.g. psychotherapy, might prove helpful in both alleviating the symptoms of depression and stress and improving glycemic control (Lustman, Griffith, Freedland, Kissel, & Clouse, 1998; Surwit et al., 2002). In addition to being based on a longitudinal setting, future studies addressing the interactions of specific genes and environment with IR are encouraged, as recent findings have implicated that depressive symptoms, poor sleep and stressful life events may share a common genetic background (Caspi & Moffitt, 2006; Grabe et al., 2012; Karg & Sen, 2012; Kendler et al., 1995; Lyssenko et al., 2009; Mulder et al., 2009). Increasingly, it is becoming clear that few genetic and environmental factors act alone, but that instead they regularly act in concert to determine predisposition to psychiatric disorders (Carola & Gross, 2012; Caspi & Moffitt, 2006; Karg & Sen, 2012).
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Table 15. Key findings, implications of the study and future directions. Key findings:
Subclinical depressive symptoms were associated with increasing odds for IR and the MetS
Subjective sleep complaints related to sleep apnea, insomnia and daytime sleepiness were associated with an increase in IR
Antidepressant medication failed to modify the associations of depressive symptoms with IR and the MetS, but it was also found to contribute to IR and the MetS independently
Stressful life events were associated with IR and the MetS
No associations were found between psychosocial factors and insulin secretion The associations above were not driven by latent or established T2D
All findings above were not sex-specific
Implications and future directions:
Controlling for and preventing already the subclinical psychosocial symptoms presented in this thesis may contribute beneficially to somatic health
Prospective studies are needed to confirm the direction of causality between psychosocial measures and IR.
People in a prediabetic condition are a key target group for psychosocial interventions, however, more research is needed to confirm the efficacy of these interventions on both psychological mood and glycemic control
Future studies need to address the gene-by-environment interactions as it is becoming increasingly clear that not only genetics nor solely environmental factors are the cause for psychiatric or somatic illness but they act in concert in contributing to disease onset
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