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Estimates of the lifetime risk for manic–depressive I disorder from epidemiological studies have ranged from 0.2 to 0.9%. The Epidemiological Catchment Area (ECA) study found a lifetime prevalence rate of 1.2% for combined type I and type II variants. These rates are approximately tenfold greater than the preva-lence rate for schizophrenia and about one-fifth that for major depressive disorder. Little is known regarding the prevalence of cyclothymic disorder. The National Comorbidity Survey Repli-cation (NCD-R) found a considerably higher lifetime prevalence of bipolar I-II disorders of 3.9% (Kessler et al., 2005). The life-time prevalence for all mood disorders was 20.8%. Unlike major depressive disorder, manic–depressive disorder has an approxi-mately equal gender distribution. Few consistent data are avail-able regarding differences in prevalence across ethnic, cultural, or rural–urban settings. However, one of the more intriguing puzzles is the tendency of manic–depressive disorder to occur in higher socioeconomic strata than schizophrenia, which tends to aggregate in lower socioeconomic strata. Although many theo-ries have been advanced to explain this phenomenon, no certain mechanism has been identified. However, several issues are clear. First, the finding is most likely not exclusively due to diagnos-tic bias (i.e., overdiagnosing persons of lower socioeconomicclass with schizophrenia more frequently than manic–depressive disorder and the converse in persons of higher socioeconomic class). Secondly, the upward socioeconomic “drift” is not due to highly impaired patients “dragged” upward by higher function-ing family members who are normal or who have adaptive sub-syndromal manic–depressive spectrum characteristics; rather, patients themselves, at least those with type II disorder, are in many cases highly successful and occupy higher socioeconomic levels. Thirdly, the findings are not limited to the USA but have been replicated in European samples.
Of particular interest in regard to the epidemiology of manic– depressive disorder is that the incidence of manic–depressive dis-order (and depressive disorders) appears to have increased since the 1940s. Reasons for this are not clear, although environmental factors, either physiological or psychosocial, may be responsible. For instance, exposure to increasingly severe social stressors, or the breakdown of cultural supports that may buffer stresses, may contribute; increases in exposure to putative environmental toxins might also be considered. In addition, in those families afflicted with manic–depressive disorder across generations, those in later generations tend to have earlier onset. This may be due to changes in genetic loading across generations or to environmental factors either within the family or in the wider environment. Regardless of the cause, the increasing incidence and earlier onset of manic–de-pressive disorder indicate that this illness is not likely to decrease in importance as a clinical and public health issue.
Alcohol and drug abuse and dependence represent the most consistently described and most clinically important psychi-atric comorbidities with manic–depressive disorder. Whereas rates of alcohol abuse combined with alcohol dependence are from 3 to 13% in the general population, lifetime rates for al-cohol dependence from ECA data indicate that they are greater than 30% in persons with manic–depressive I disorder (Regier et al., 1990). Further, ECA lifetime rates for drug dependence in individuals with manic–depressive I disorder are greater than 25% and rates for any substance abuse or dependence are above 60%. Comparable rates for alcohol, drug, or any substance abuse or dependence in major depressive disorder in ECA data are, respectively, 12%, 11% and 27%. Thus, manic–depres-sive disorder represents an enriched sample for substance use disorders, with substantially greater rates than for the general population or even those with unipolar depression. The reasons for the co-occurrence of manic–depressive disorder and sub-stance dependence are not clear. In addition to self-medicat-ing for depression, mania and intensifying the manic experi-ence with stimulants, it is possible that some common genetic predisposition for mood instability is associated with both manic–depressive mood phenomenology and increased craving for substances, and the predominant phenotypic expression is then determined by other genetic or environmental factors. Ac-cording to this hypothesis, some persons possessing the gene develop manic–depressive disorder, some develop substance dependence and some develop both. Regardless of the mecha-nism, comorbid substance dependence represents an important clinical challenge for clinicians treating persons with manic– depressive disorder.
Lifetime anxiety disorders have been described in as many as 44% of individuals with manic–depressive disorder. Other psychiatric comorbidities have been described in modest proportions of manic–depressive patients. Interestingly, data in-dicate that comorbidity may be higher in women with manic–de-pressive disorder than in men which may contribute to the ten-dency for the female gender to be associated with more complex forms of manic–depressive disorder such as rapid and dysphoric mania.
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