While classical bipolar disorder with episodes of euphoric mania interspersed with episodes of depression is one of the clearest clinical syndromes in psychiatry, the boundaries of bipolar disorder remain contested. As case definition is central to epidemiology, all the contested boundaries of bipolar disorder could influence prevalence rates and our understanding of risk factors. Some of the major boundary issues for bipolar disorder include the overlap of bipolar disorder with psychotic features, with schizoaffective disorder and schizophrenia, and the overlap of bipolar disorder with unipolar major depression when patients who present primarily with depression have brief or mild episodes of hypomania. There is also an overlap of bipolar disorder with apparent personality disorder, especially Cluster B personality disorders such as borderline and narcissism, and the issue of when hyperthymic personality merges into bipolar disorder.^(2,3) When bipolar disorder is comorbid with substance abuse there are also important diagnostic issues.

Another important issue in determining caseness of bipolar disorder for epidemiological surveys is symptom pattern and duration. A number of the diagnostic instruments for assessing bipolarity in population surveys limit the questions on mania to a type of symptom profile characterized by euphoria, grandiosity, increased energy, and decreased sleep. Whether the commonly used epidemiology interviews adequately detect those individuals who have manic episodes characterized by irritability, anger, and activation is very debatable. The other key diagnostic issue is what criteria are used to categorize the minimum duration for hypomania; is four days too long, is even two days too long? Furthermore, as insight is sometimes impaired in hypomania and mania, and as these are low prevalence disorders, the accuracy of case detection of bipolar disorders in populations remains an issue for further research.⁽⁴⁾

Population studies such as the ECA, and its related cross-national studies, and the NCS reported that the lifetime prevalence of bipolar disorder varies from 0.3 to 1.5 per cent. The NCS data include only bipolar I data, while the ECA includes bipolar I and bipolar II disorder.^(4,5) In all studies, the six-month prevalence is not much lower than the lifetime prevalence of bipolar disorder. These findings reflect the high degree of chronicity and/or recurrence associated with bipolar disorder. Broader definitions of mania/hypomania have resulted in lifetime prevalence rates increasing to about 4 per cent.⁽⁶⁾

In these population studies, the mean age of onset of bipolar disorder has varied from 17 to 27 years. However, as age of onset is not normally distributed, the mean is a slightly misleading variable; in clinical samples, while the mean age of onset may be in the twenties, the most common age of onset are the teenage years.

In bipolar disorder, the prevalence in males and females is similar. This is in contrast to the reasonably consistent female excess found in major depression.

In the NCS, all identified bipolar I individuals suffered from at least one, and often up to three or more, comorbid disorders. The most common comorbid disorders included the full range of anxiety disorders, alcohol and drug dependence, and conduct disorder or other antisocial behaviours.

Alcohol and drug abuse and/or dependence are commonly comorbid with bipolar disorder. Old studies found that binge drinking was especially common in bipolar individuals and that this binge pattern of drinking was more associated with manic episodes than with depressive episodes. Clinical studies find that bipolar patients with comorbid substance dependence are less compliant with prescribed mood stabilizers and have more frequent hospital readmissions. Stimulant abuse/dependence rates are especially increased in bipolar disorder.

Individuals with bipolar disorder have the full range of anxiety disorders, including phobias, panic disorder, and obsessive–compulsive disorder. Perhaps surprisingly, comorbid rates of these anxiety disorders tend to be higher in bipolar disorder than in major depression.

Another area of high comorbidity with bipolar disorder is that of childhood conduct disorder and attention deficit disorder. One of the issues in understanding this high rate of comorbidity is whether childhood conduct disorder and/or childhood attention-deficit disorder are sometimes the first manifestations or precursors of bipolar disorder. Certainly, if the pattern of conduct-disorder symptoms or attention-deficit symptoms is episodic rather than consistent over time, the issue becomes whether these are not early manifestations of bipolar disorder rather than truly independent comorbid conditions. The other key diagnostic controversy in this area is the status of juvenile or childhood bipolar disorder.

In the ECA study, 39 per cent of those with bipolar I or bipolar II disorders received outpatient psychiatric treatment within 1 year and about 10 per cent would receive inpatient treatment within a 6-month period. In the NCS study, 45 per cent of those with bipolar disorder had received psychiatric treatment in the previous 12 months; although 93 per cent reported lifetime treatment for their bipolar disorder. However, both of these studies suggest that more than half the individuals with bipolar disorder are not currently in psychiatric treatment and, given the high morbidity and mortality associated with bipolar disorder, this is of major concern.⁽⁴⁾

In considering the risk factors for bipolar disorder, it is useful to separate risk factors into those that are risk factors for lifetime vulnerability (for example genetic factors) and those that are risk factors for the onset of an episode of depression or mania (for example, life events). Thus, in determining risk factors for lifetime vulnerability, genetic factors constitute the largest single risk factor. However, if one is considering who is vulnerable to an episode of mania over the next six months, genetic factors will play a relatively smaller part and predictions may be best based on other factors such as past history, childbirth, being treated for depression with antidepressant medication, and the approach of spring or summer. Genetic risk factors are discussed further in Chapter 4.5.5.

Although organic factors, such as some type of central nervous system damage, are unusual risk factors in young adults, in lateonset bipolar disorder (age of onset more than 50 years) organic disease of the central nervous system is an increasing factor for the development of mania. In younger adults, AIDS and head injury are two important aetiological factors in a limited number of cases of bipolar disorder.

A range of other biological factors are particularly relevant risk factors to the onset of episodes of illness, but they may contribute a relatively small part to lifetime vulnerability. Many women have their first episode of depression or mania in the postpartum period. While a limited number of women may have manic episodes limited to the postpartum period, postpartum episodes of mania are more commonly part of a long-term bipolar disorder and these women will have episodes both precipitated by childbirth and at other times in their life. Indeed, in the postpartum period, having a history of bipolar disorder is one of the strongest risk factors for the development of a postpartum psychosis.

There is substantial evidence that seasonal patterns influence the onset of manic and depressive episodes. There are consistent
findings of an excess of manic episodes in late spring and early summer. To date, however, the nature of the environmental factors that influence this late spring, early summer peak of manic episodes is less clear.

There is also substantial evidence that disruptions of normal biological rhythms may precipitate the onset of manic or depressive episodes. This has been documented in relation to international travel involving east–west or west–east travel with disruption of circadian rhythms. Disruption of circadian rhythms through shiftwork or other factors, which disrupt the normal sleep cycles, may also be important triggers to the onset of episodes of mania. These findings have led to the development of a social rhythm metric, as an adjunct to interpersonal psychotherapy (interpersonal social rhythms therapy) as a treatment for individuals with bipolar disorder.

Adverse life events have been well documented to be precipitants of manic episodes, as well as depression. It appears that life events are more likely prior to the first or second episode of mania and are less likely later in the course of illness. The critical factor in life events triggering mania may be whether there is associated sleep disruption, rather than the ‘psychological’ meaning of the event.

A key issue for the epidemiology of depressive disorders is defining the boundaries of major depression and dysthymia. Depressive symptoms in the community are common, and defining both the symptom count and the duration at which depressive symptoms count as part of a clinical disorder is arbitrary. When Kendler and Gardner⁽⁷⁾ examined the boundaries of major depression as defined by DSM-IV in a population-based twin sample of women, they found that, if a twin had four or fewer depressive symptoms, syndromes composed of symptoms involving no or minimal impairment, and episodes lasting less than 14 days, then the individual’s co-twin was still at an increased risk of major depression. Kendler and Gardner concluded that they could find no empirical support for the DSM-IV requirement of duration for two weeks, five symptoms, or clinically significant impairment. These authors suggested that major depression, as articulated by DSM-IV, may be a diagnostic convention imposed on a continuum of depressive symptoms of varying severity and duration. Wainwright et al.,⁽⁸⁾ using data from the National Psychiatric Morbidity Survey of Great Britain, have also suggested that research should move beyond a binary decision of case versus non-case, and utilize a probablistic measure of psychiatric case status, replacing the arbitrary threshold with a smooth transition. This type of approach allows the benefits of syndrome diagnosis to be retained, while not falling into the dilemma of an arbitrary threshold that lacks validity.