The finding that a few somatic symptoms in healthy adolescents predicted mental health disorders in adulthood indicates that somatic symptoms either reflect vulnerability for mood disorders or constitute a subclinical mood disorder, rather than being caused by depression.
In addition, monoamine depletion studies demonstrate that, although monoamine systems are probably important in the vulnerability to mood lability, there is no simple direct causal relation between catecholamines and mood, as proposed in the monoamine hypothesis of mood disorders [ 3, 6, 7].
There he is conducting PET scan research, investigating the neurobiological relationships involved in vulnerability to mood disorders.
Participants described distress around their perceived family vulnerability to mood disorders.
Understanding the mechanisms behind these sexual dimorphisms may help unravel the biological bases of the heightened female vulnerability to mood disorders.
Under baseline conditions, the sex-related factor influencing emotionality was sex chromosome complement; however, the effect was in the opposite direction to what we had predicted based on the female vulnerability to mood disorders.
Understanding other symptoms in the context of cognitive dysfunction, such as fatigue, sleep disturbance, affective vulnerability and mood disorders might help determine how these symptoms contribute to the occurrence and persistence of cognitive impairment.
Of course, potential developmental changes induced by GluN2B knockout should not be ruled out especially in light of the importance of circuit maturation changes in vulnerability to mood disorders (Stefani and Moghaddam, 2005; Ansorge et al., 2007).
Research using animal models further demonstrates that lack of early maternal care acts as a risk factor in the regulation of emotional and cognitive responses to stress, 39 which may influence vulnerability for mood disorders.
Baseline changes in neurochemical signaling due to the disease state, as in epilepsy [ 32], altered neurobiology secondary to inflammatory mechanisms associated with disease, as in cancer [ 53, 59], or a combination of these factors seem to interact with sex to alter vulnerability to mood disorders.
Family environment in particular would affect the long-term neurobiological and psychosocial development of the offspring and modulate the vulnerability to mood-, anxiety-, psychosis- or drug use-related disorders [1] [6].
