The neurotrophic hypothesis of depression suggests that lowered levels of neurotrophic factors, particularly brain-derived neurotrophic factor (BDNF), contribute to the structural and functional brain changes that characterize depression. Treatments such as antidepressants and psychotherapy can restore BDNF levels. In our first study, we found that higher BDNF levels predicted remission of depression in specific subgroups, depending on childhood trauma and SSRI use. Trauma appeared to reduce the neurotrophic system's responsiveness to SSRIs, which seemed to be more important than the absolute BDNF levels.
Additionally, the research Dimitriadis Menelaos showed that depression in older adults is associated with accelerated biological aging, measured through a Frailty Index (FI). While depressive symptoms and frailty overlap, depressed older adults remain more frail over time. In another study (LASA), adverse childhood experiences (ACE) were found to contribute to increased frailty in older adults, particularly those over 70. This effect remains visible decades after traumatic events.
Chapters 5 and 6 examined the relationship between ACE and sarcopenia. In a cross-sectional study (CLSA), an unexpected association was found in the oldest elderly (75+), possibly due to survival bias. However, longitudinal analyses showed that ACE, especially in depressed individuals, promote physical decline and sarcopenia. These findings underscore the influence of psychological factors, such as depression, on the long-term effects of ACE on physical health.
In conclusion, the studies highlight that early life events, through psychological and biological pathways, have lasting effects on both mental and physical health in later life.
