Bipolar disorder - Etiology

Etiology
''According to the U.S. government's National Institute of Mental Health (NIMH), "There is no single cause for bipolar disorder—rather, many factors act together to produce the illness." "Because bipolar disorder tends to run in families, researchers have been searching for specific genes passed down through generations that may increase a person's chance of developing the illness." "In addition, findings from gene research suggest that bipolar disorder, like other mental illnesses, does not occur because of a single gene.".

It is well established that bipolar disorder is a genetically influenced condition which can respond very well to medication (Johnson & Leahy, 2004; Miklowitz & Goldstein, 1997; Frank, 2005). (See treatment of bipolar disorder for a more detailed discussion of treatment.)

Psychological factors also play a strong role in both the psychopathology of the disorder and the psychotherapeutic factors aimed at alleviating core symptoms, recognizing episode triggers, reducing negative expressed emotion in relationships, recognizing prodromal symptoms before full-blown recurrence, and, practising the factors that lead to maintenance of remission (Lam et al, 1999; Johnson & Leahy, 2004; Basco & Rush, 2005; Miklowitz & Goldstein, 1997; Frank, 2005). Modern evidence based psychotherapies designed specifically for bipolar disorder when used in combination with standard medication treatment increase the time the individual stays well significantly longer than medications alone (Frank, 2005). These psychotherapies are interpersonal and social rhythm therapy for bipolar disorder, family focused therapy for bipolar disorder, psychoeducation, cognitive therapy for bipolar disorder, and prodrome detection. All except psychoeducation and prodrome detection are available as books. Abnormalities in brain function have been related to feelings of anxiety and lower stress resilience. When faced with a very stressful, negative major life event, such as a failure in an important area, an individual may have his first major depression. Conversely, when an individual accomplishes a major achievement he may experience his first hypomanic or manic episode. Individuals with bipolar disorder tend to experience episode triggers involving either interpersonal or achievement-related life events. An example of interpersonal-life events include falling in love or, conversely, the death of a close friend. Achievement-related life events include acceptance into an elite graduate school or by contrast, being fired from work (Miklowitz & Goldstein, 1997).

The "kindling" theory asserts that people who are genetically predisposed toward bipolar disorder can experience a series of stressful events, each of which lowers the threshold at which mood changes occur. Eventually, a mood episode can start (and becomes recurrent) by itself. Not all individuals experience subsequent mood episodes in the absence of positive or negative life events, however.

Individuals with late-adolescent/early adult onset of the disorder will very likely have experienced childhood anxiety and depression. Some argue that childhood-onset bipolar disorder should be treated early.

A family history of bipolar spectrum disorders can impart a genetic predisposition towards developing a bipolar spectrum disorder. Since bipolar disorders are polygenic (involving many genes), there are apt to be many unipolar and bipolar disordered individuals in the same family pedigree. This is very often the case (Barondes, 1998). Anxiety disorders, clinical depression, eating disorders, premenstrual dysphoric disorder, postpartum depression, postpartum psychosis and/or schizophrenia may be part of the patient's family history and reflects a term called "genetic loading".

Bipolar disorder is not either environmental or physiological, it is multifactorial; that is, many genes and environmental factors conspire to create the disorder (Johnson & Leahy, 2004).

Since bipolar disorder is so heterogeneous, it is likely that people experience different pathways towards the illness (Miklowitz & Goldstein, 1997).

Recent research done in Japan indicates a hypothesis of dysfunctional mitochondria in the brain (Stork & Renshaw, 2005)''

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