Etiology

If an affective temperament is the underpinning of a mood dysregulation, how does the environment determine whether or not such a genetic predisposition will ever develop into visible symptomatology? Clues to this are found in the field of epigenetics, the study of how the environment affects gene expression. There may be no environmental influence so impactful to the brain and mind as early life attachments. Attachment is regarded to be a homeostatic necessity. Attachment theorists have observed that infants with secure attachments to their caregivers develop the capacity to regulate their physical arousal while those without secure attachments do not. Epigeneticists are beginning to explain the molecular basis for how caregiver behavior affects an individual’s capacity for self-regulation. Studies have shown that the more mother rats lick their pups, the more of the pups’ genes become activated to produce receptors for cortisol, the stress hormone that enables the organism to regulate itself. Humans subjected to chronic stress such as insecure attachments and developmental trauma mount a chronic stress response. In contrast to the acute stress response, in which cortisol production regulates the organism and is time-limited, the chronic stress response is a runaway process. Under chronic stress, cortisol production is ongoing and toxic to the system. Long term cortisol exposure destroys the integrity of crucial structures in the brain associated with mood regulation and stimulates production of the neurotransmitter glutamate, another agent which damages nerve cells throughout the brain. Together, cortisol and glutamate create physiologic and functional disruption of crucial elements in the brain that results in mood dysregulation. The degree to which this process unfolds is a function both of the individual’s biological diathesis and of the environs for its genetic expression.

114If a mood dysregulation emerges from an affective temperament, is it genetic? The determinants of our behavior are dynamic and depend on the ongoing interaction of genetic and environmental factors throughout our lives. Not every gene we are born with is activated or “expressed” in the person we are, and the genes we inherit are altered in our interactions with the world we encounter. The burgeoning science of epigenetics is uncovering the influence of the environment on gene expression (Fagiolini et al., 2009; Tsankova, 2007). In the most material sense, we are truly products of our environments.

We have posited that an affective temperament is a predisposition or “diathesis” to mood dysregulation. According to the epigenetic model, mood dysregulation is partially genetic, the result of this diathesis, and partially the result of the environment. The diathesis-stress model of pathophysiology captures the essence of the interaction between environmental influence and genetic predisposition. According to this model, symptoms of a disorder may emerge if a genetically predisposed organism is subjected to sufficient environmental stress. Thus, individuals vulnerable to mood dysregulation, either by an affective temperament or by genetic relation to others with affective disorders, under sufficient conditions of stress, may become symptomatic. Likewise, that same genetically predisposed individual, if maintained in a protected environment that is sufficiently stress-free, may not display symptoms at all. In one example, constitutionally shy monkeys (i.e., those with a diathesis to withdraw,) when reared by confident mothers, became more confident (Mastropieri & Carroll, 1998; Suomi, 1997). Of course, a genetically vulnerable individual maintained in a stress-free environment may still exhibit symptoms of a disorder if the genetic loading or diathesis is too great.