mental health in new zealand from a public health perspective · of about 10 percent (schulberg et...

MENTAL HEALTH INNEW ZEALAND FROM

A PUBLIC HEALTHPERSPECTIVE

MENTAL HEALTH INNEW ZEALAND FROM

A PUBLIC HEALTHPERSPECTIVE

PUBLIC HEALTH REPORT NUMBER 3

Edited by

Pete M EllisWellington School of Medicine

Sunny C D CollingsWellington School of Medicine

Published with the permission of the Director-General of Health

Published in October 1997 by

public health groupministry of health

Wellington, New Zealand

© 1997 Ministry of Health, PO Box 5013, Wellington

ISBN 0-478-20849-9 (Book)

ISBN 0-478-20850-2 (Internet)

Disclaimer

The views expressed in this report are those of the authorsand they do not necessarily represent the views of the Ministry of Health.

SECT ION IV:RISK FACTORS FORSPEC I F I C D ISORDERS

SECT ION IV:RISK FACTORS FORSPEC I F I C D ISORDERS

266 Mental Health in New Zealand from a Public Health Perspective

Mood Disorders 267

CHAPTER 12:MOOD DISORDERS

PATRICK F SULLIVAN AND CYNTHIA M BULIK

This chapter reviews the evidence concerning the prevention of the two cardinal mood disorders,major depression and bipolar disorder. The chapter has three parts. The first two consider the definition,epidemiology, aetiology, and prevention of major depression and bipolar disorder. The final partpresents conclusions and recommendations.

MAJOR DEPRESS ION

DEF IN I T ION OF MAJOR DEPRESS ION

A major problem in attempting to define clinically important depression is the ubiquity of depressivefeelings. In defining clinically notable depression, a key task is to distinguish normal emotions fromabnormal depression. Emotional states like sadness, feeling ‘blue’, or tearfulness are part of normalhuman experience. Normally, these emotions are relatively transient and not associated with significantdistress or functional impairment. On occasion, sadness becomes exaggerated, pervasive, nearlyunshakeable, and is accompanied by real impairment in a person’s life.

Since the times of the ancient Greek physicians, many definitions of depression have been presented.These definitions have in common an attempt to define depressive signs and symptoms that are abnormalin degree and to identify those depressive states whose associated suffering would argue for someform of treatment. One recent definition of significant, ‘major’, depression is that of the DSM-IV

(APA 1994a) that was developed by a task force in the United States and which appears to be an up-to-date, international consensus view that would correspond reasonably closely to what many clinicianswould consider to be a condition worthy of some form of treatment. The core symptoms of significant,‘major’, depression include depressed mood, diminished interest and pleasure in most activities, weightchange, change in appetite, insomnia or hypersomnia, fatigue, poor concentration, feelings ofworthlessness, and suicidal thinking. Five or more of these must be present for at least two weeks, andrepresent a change from previous functioning.

EP IDEMIOLOGY OF MAJOR DEPRESS ION

L i fe t ime P reva lence

The lifetime prevalence of major depression in random community samples is a matter of somecontention (Parker 1987). The available estimates vary greatly depending on factors such as geographiclocation, how a sample was acquired, which diagnostic criteria were used, and how the interviewer


asked about depressive symptoms. Complete coverage of these important technical issues is beyondthe scope of this chapter; however, these factors may cause wide variation in the reported lifetimeprevalence results.

The lifetime prevalence estimates of major depression in international samples of adults thus varywidely: about 2 percent in Hong Kong (Chen et al 1993); 7.8 percent averaged across five cities in theUS (Weissman et al 1991); and 17.1 percent in a national probability sample in the US (Kessler et al1994). Kendler and colleagues compared nine sets of diagnostic criteria in a large epidemiologicalsample: the lifetime prevalence estimates for major depression ranged from 12–33 percent dependingon the criteria used (Kendler et al 1992).

We are fortunate to have New Zealand data from several different studies. In Christchurch, the lifetimeprevalence of major depression in adults selected at random from census data was 12.6 percent (WellsJE et al 1989a) and 33.2 percent in another study of adults randomly selected from the national electoralroll (A Beautrais, P Joyce, R Mulder, personal communication, June 1996). The lifetime prevalenceof major depression was 16.7 percent in a cohort of 15-year-olds in Dunedin (Feehan et al 1994) and4.9 percent in a cohort of 15-year-olds in Christchurch (Fergusson et al 1993).

It is reasonable to suspect that the true lifetime prevalence of major depression is in the range of10 –20 percent. This places major depression among the more common human afflictions. Of note,the lifetime prevalence of major depression in Christchurch was among the highest in 12 similarlyconducted studies in nine countries worldwide (Cross-National Collaborative Group 1992).

Current major depression is especially prevalent in primary care medical settings with a point prevalenceof about 10 percent (Schulberg et al 1985; Ormel et al 1994).

Psy ch ia t r i c Comorb id i t y

Major depression often occurs in conjunction with other mental and physical disorders (Maser andCloninger 1990). The causes of overlap between these disorders are complex (Kendler et al 1995) andnot well elucidated (Neale and Kendler 1995). Alcohol dependence, several different anxiety disorders,and eating disorders frequently complicate the clinical portrait of major depression (DepressionGuideline Panel 1993a).

Natu ra l H i s to r y, Morb id i t y and Mor ta l i t y

The natural history of major depression is highly variable. For depressed individuals seen in psychiatricsettings, recovery from the index episode is the norm although persistent depression is found in about10 percent (Piccinelli and Wilkinson 1994). Notably, 75 percent experienced at least one other episodeof depression over a decade of follow-up (Piccinelli and Wilkinson 1994). However, many peoplewho experience a significant depressive syndrome never receive any form of treatment (Regier et al1978, 1993).

Considerable morbidity is associated with major depression. Epidemiological studies of communitysamples (Broadhead et al 1990) and primary care medical attendees (Wells KB et al 1989b) haveshown that the presence of major depression substantially increases the risk of disability and impairedrole functioning. Patients with major depression had similar or worse functioning than those with

Mood Disorders 269

eight major chronic medical conditions (Wells KB et al 1989b). Substantial excess mortality is alsoassociated with major depression due to suicide (Berglund and Nilsson 1987; Zilber et al 1989) andother causes (Tsuang and Woolson 1978; Black et al 1987a; Zilber et al 1989). Up to 15 percent ofpatients hospitalised for psychiatric treatment of depression eventually die by suicide. Despite thesefindings, major depression is substantially underdiagnosed and undertreated (Regier et al 1978; Klerman1989; Klerman and Weissman 1992; Regier et al 1993).

AET IOLOGY OF MAJOR DEPRESS ION

Aet io log i ca l Mode l s

It is probably useful to conceptualise major depression as a ‘complex disorder’ (Lander and Schork1994) that is the result of the interplay of genetic, biological, and environmental factors.

Kendler and colleagues have published an interesting paper that attempted to develop an empiricalmodel that combined and ranked genetic and environmental risk factors for major depression (Kendleret al 1993b). It is important to note that this model attempted to predict new episodes of major depressionover about a two-year period rather than lifetime major depression. These authors studied 680 pairs offemale twins three times over a 30-month period. The model included the interactions among aconsiderable number of variables that included traumatic experiences, genetic factors, personalityvariables, and interpersonal stressors. Strong predictors were recent stressful life events, genetic riskfactors, past history of major depression, and neuroticism. Predictors of intermediate strength wererecent life difficulties, lack of parental warmth, and lifetime traumas. Modest predictors were lack ofsocial support and parental loss.

While this model was clearly preliminary (and only partially successful) it seems to be a clinicallyuseful model that addresses the interaction and relative importance of these variables. It assignedsome meaning to the obfuscating terms ‘multifactorial’ and ‘bio-psycho-social’ and added a sense oforder to the multitude of variables (ie, stressful life events, family history, past history, personality,etc) thought important in the genesis of major depression.

It is possible that the aetiology of major depression often depends upon the interaction of genetic andenvironmental risk factors (what has been termed ‘genetic control of sensitivity to the environment’(Kendler and Eaves 1986)). Under this conceptualisation, the same life events will have markedlydifferent effects depending upon an individual’s genetic complement. For example, stressful life eventsof similar magnitude may or may not trigger major depression in individuals with different genes.

R i sk Fa c to r s

A number of variables have been found to be statistically associated with major depression inepidemiological studies. These factors include: being female (Wells JE et al 1989a; Weissman et al1991; Kessler et al 1993; Weissman et al 1993); birth in more recent age cohorts (Klerman and Weissman1989; Joyce et al 1990; Weissman et al 1991; Cross-National Collaborative Group 1992); beingseparated, divorced or in an unhappy marriage (Weissman 1987); stressful life events (Kendler et al1993b); and subsyndromal depressive symptoms (Horwath et al 1992).


Gene t i c Fa c to r s

A family history of major depression has consistently been found to be a risk factor for major depression(Weissman 1987; Merikangas and Kupfer 1995). These findings suggest the influence of geneticfactors on the liability to develop major depression.

Methodologically rigorous family studies of major depression have demonstrated its familiarity (ie,its tendency ‘to run in families’). First-degree relatives of probands with major depression have increasedrates of major depression in comparison to normal controls and to those with non-affective psychiatricillness (Tsuang et al 1980; Gershon et al 1982; Weissman et al 1984; Andreasen et al 1987; McGuffinet al 1988; Heun and Maier 1993).

Twin studies can estimate the proportion of variance in liability to major depression due to geneticand shared and unshared environmental influences. The proportion of variance for developing majordepression that can be attributed to additive genetic effects is in the 42–54 percent range (Torgersen1986; McGuffin et al 1991; Kendler et al 1992). As determination of lifetime major depression is notparticularly reliable (Bromet et al 1986; Kendler et al 1993a), when measurement error is taken intoaccount, genetic influences may be as high as 71 percent (Kendler et al 1993a).

There have been three adoption studies of major depression. One study showed evidence supportingsignificant genetic influences (Wender et al 1986; Ingraham and Wender 1992), one study reportedequivocal evidence (Cadoret 1978; Cadoret et al 1985), and one study found no significant geneticeffects (von Knorring et al 1983).

Summar y

Overall, our knowledge of the aetiology of major depression is limited. It is a complex disorder andthe available evidence implicates several environmental risk factors and as-yet unspecified geneticrisk factors.

PREVENT ION OF MAJOR DEPRESS ION

Pr imar y P reven t ion

We are aware of no empirical studies of the primary prevention of major depression in the generalpopulation. If we do not know the aetiology of a disorder, preventing its development by interruptionof its causal chain is a challenge. Primary prevention of major depression by interventions in thegeneral population is not likely to be possible until we have a better understanding of its aetiology.

Several other factors diminish the possibility that primary preventive interventions can be developedfor major depression. Firstly, many of the environmental risk factors implicated in the aetiology ofmajor depression may be impossible or prohibitively expensive to correct. For example, it is difficultto imagine how altering the risk factors of sex and age cohort might be accomplished. Secondly, anumber of the environmental risk factors for major depression may well exist in an interconnectedmatrix; altering one factor (even if possible) might have little influence on the other risks in its matrixand hence have little impact on the incidence of major depression.

Despite these difficulties, a few studies have tested the effects of interventions targeting people atrisk. Results have looked promising but methodological problems limit interpretation of the findings.Interventions have included cognitive methods to gain control of mood (Muñoz et al 1995) andmobilisation of protective factors identified in at-risk groups (Vega and Murphy 1990).

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Secondar y P reven t ion

The secondary prevention (decreased prevalence through early detection and treatment) of majordepression is possible and is the type of prevention for which the greatest body of data exists. Thereare a number of screening methods that have been developed and tested by which to detect the presenceof major depression. Examples of these self-report questionnaires are the CES-D (Radloff 1977) andthe Beck Depression Inventory (Beck et al 1961). These questionnaires can be completed in a fewminutes and carry reasonable sensitivity for the detection of significant depression (Weissman et al1977).

There are a number of locations in which screening for major depression could be performed. TheDepression Awareness, Recognition, and Treatment programme of the US National Institute of MentalHealth provided public education about major depression. In New Zealand, the general practice settingwould be an obvious place in which to screen for and treat major depression. The majority of NewZealand adults visit a general practitioner at least once in any two-year period; detection could bereadily accomplished in the surgery.

Once detected, there are a variety of methods by which major depression may be effectively treated.Brief psychological therapies such as cognitive-behavioural therapy (Elkin et al 1985) and interpersonaltherapy (Klerman et al 1984) are of proven benefit in the treatment of major depression. There exist asizeable number of antidepressant medications of proven efficacy and safety. A number of thesetreatments have also been tested in primary care medicine (Schulberg et al 1993).

It is important to note that secondary prevention of major depression is what many general practitioners,psychiatrists, and clinical psychologists do as a matter of course. However, given that only a minorityof individuals with major depression receive any form of treatment (Regier et al 1978; Hornblow et al1990; Regier et al 1993), improvements in detection and treatment are necessary.

Te r t ia r y P reven t ion

Tertiary prevention entails the reduction of complications of an established condition and theminimisation of the risk of recurrence. The extant literature relevant to the tertiary prevention ofmajor depression contains a paradox. The literature tells us that major depression is often a recurrentand even lifelong affliction. However, the majority of treatment research compares the efficacy oreffectiveness of one or several treatments over relatively brief periods (usually less than three months).This important matter has received insufficient attention.

There have been, however, several useful studies. Chief among them have been the MaintenanceTherapies in Recurrent Depression Protocol (Frank et al 1990; Frank et al 1991; Kupfer et al 1992).Key findings from these papers are the utility of maintaining individuals with recurrent depression on‘full’ dosage antidepressant treatment (ie, the amount of medication used to treat the index episode).In addition, there was some evidence to support the use of a specific form of maintenance psychotherapy.These findings have been extended to depression occurring in late life (Reynolds et al 1994).

Despite these studies, there are insufficient data to guide clinicians in the management of a number ofimportant clinical issues. For example, there are limited data concerning the choice of a second treatmentwhen the initial treatment fails; who should and should not be offered maintenance treatment; andwhich personality and environmental variables might be altered to improve outcome.


Secondar y and Te r t i a r y P reven t ion : Rev iews

Several excellent reviews of the treatment of major depression have been published in Australasia(Andrews 1983; Joyce et al 1995) and in the US (Depression Guideline Panel 1993a, 1993b).

B IPOLAR D ISORDER

DEF IN I T ION OF B IPOLAR D ISORDER

Much of what we currently know about bipolar disorder (previously termed manic-depressive disorderor manic-depressive psychosis), systematically and empirically validates astute observations ofclinicians from previous generations. In 1921, Emil Kraepelin in Manic-Depressive Insanity and Paranoia

proposed an understanding of affective illness which has to some extent been upheld in the currentdiagnostic nomenclature of affective illness. Regarding aetiology, however, there is debate as to whethera single process underlies the various forms of affective illness. From Kraepelin’s time forward untilthe late 1950s, disorders as varied as ‘circular insanity’, melancholia, and mania were considered toexist under the general rubric of manic-depressive insanity. Based on genetic and personalityobservations, Leonard (1957; Leonard et al 1962) proposed that a distinction be made between bipolardisorder, in which both depressive and manic episodes are experienced, and monopolar disorder,consisting of either recurrent depressive or recurrent manic episodes.

In the current diagnostic classification, the DSM-IV (APA 1994a) upholds the unipolar/bipolardistinction, but brings recurrent mania under the heading of bipolar disorder. The important featuresof mania are abnormally and persistently elevated, expansive or irritable mood lasting at least oneweek, with inflated self-esteem, decreased need for sleep, pressure to talk, racing thoughts, distractibility,increased levels of activity, and excessive involvement in pleasurable activities with a high potentialfor painful consequences, such as sexual indiscretion or unwise business investment.

The hallmark of bipolar I disorder is the presence of at least one manic episode. Although the prototypeof mania is often considered to include euphoric mood, expansiveness and grandiosity, this is not theonly clinical picture of the manic state. Alternative presentations include irritability, rather than euphoria,and mixed affective states. Mixed states (or dysphoric mania) characterise between 5 and 70 percentof individuals with bipolar I disorder with the mean being approximately one-third of bipolar patients(for review, see McElroy et al 1992).

In addition, ‘a spectrum of ambulatory states alternating with milder, short-lived periods of hypomania’has been labelled bipolar II (Akiskal 1995). Hypomanic states are defined as persistently elevated,expansive or irritable moods lasting at least four days. Additional symptoms are required, as in mania,and the symptoms must represent an unequivocal change from normal functioning that is observableby others. The exact nature of bipolar II disorder remains controversial. It has been questioned whetherit represents an independent disorder or a milder form of bipolar I disorder, and whether individualswith bipolar II disorder are more closely akin to those with bipolar I or unipolar depressive disorders.Where sufficient data exist to clarify the distinction between bipolar I and II, the disorders are consideredseparately below.

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EP IDEMIOLOGY OF B IPOLAR D ISORDERS

L i fe t ime P reva lence

The lifetime prevalence in community samples is 0.4 –1.6 percent for bipolar I disorder and 0.5 percentfor bipolar II disorder (APA 1994a). Christchurch data suggest that the lifetime prevalence for amanic episode for individuals between the ages of 18–64 years is 0.7 percent with no significantdifference between the prevalence for males (0.5 percent) and females (0.9 percent) (Wells JE et al1989a). This differs markedly from the 2:1 female:male ratio commonly observed in studies of majordepressive disorder. Bipolar II disorder may however be more common in women (APA 1994a). Aseparate study in Christchurch (n = 1028) found the lifetime prevalence of bipolar I and II to be 1.3percent (A Beautrais, P Joyce, R Mulder, personal communication, June 1996).

Natu ra l H i s to r y : B ipo la r I

Bipolar I disorder is an episodic and recurrent disorder that often runs a chronic course and requiresprophylactic treatment (Angst et al 1978; Post et al 1981). The average age of onset for bipolar Idisorder is between the mid-twenties and mid-thirties (Perris 1982; Endicott et al 1985; APA 1994a).There is some suggestion that first presentation differs by sex, with more males presenting with aninitial manic episode and more females with an initial major depressive episode. Of the individualswho present with a manic episode, the majority will experience future affective episodes (APA 1994a).In terms of the relation between manic and depressive episodes, the pattern can vary across individualsand within an individual over time. About 65–75 percent of manic episodes occur immediately priorto or following a major depressive episode (APA 1994a). There is some suggestion that, with age,interepisode length decreases (Angst et al 1978; Roy-Byrne et al 1985; Goodwin and Jamison 1990),severity increases (Post et al 1981), and duration of hospitalisation for an episode increases (Keck etal 1995). Between 10 and 15 percent of individuals with bipolar I disorder display a clinical coursecharacterised by ‘rapid cycling’, defined as four or more affective episodes (major depressive, manic,or hypomanic) in a 12-month period. Individuals with a rapid cycling pattern may respond less well totreatment (Dunner et al 1976; Misra and Burns 1977; Goodnick et al 1987). Rarely, individuals withbipolar I disorder display very rapid cycling, experiencing switches from depression to mania in a48-hour period (Bunney et al 1965; Jenner et al 1968). Season, treatment with tricyclic antidepressants,and sleep deprivation (eg, travel and the post-partum period) may trigger manic episodes in bipolarindividuals.

Natu ra l H i s to r y : B ipo la r I I

Endicott and colleagues (1985) suggested that the average age of onset of bipolar II is similar tobipolar I and younger than unipolar disorder, and that bipolar II and unipolar individuals displaygreater chronic affective symptoms than bipolar I individuals. Angst (1986) suggested that bipolar IIindividuals have earlier age of onset, longer duration of illness, shorter cycles, more episodes, andpoorer recovery than individuals with unipolar disorders. These results were not replicated by Kupfer(Kupfer et al 1988) who only found greater suicide attempts and greater psychomotor retardation inbipolar II individuals in comparison to unipolars. The selection criteria for inclusion in theaforementioned studies may have contributed to the differences observed.


Mor ta l i t y : B ipo la r I

Suicide is a serious risk for individuals with bipolar I disorder. The risk of suicide may be somewhatlower in the short term in bipolar I than unipolar individuals (Perris and D’Elia 1966; Angst et al1979; McGlashan 1984; Weeke and Vaeth 1986) – possibly due to the lower percentage of time spentdepressed. In the long term, suicide rates are approximately equal (Tsuang 1978; Black et al 1987b).

Mor ta l i t y : B ipo la r I I

The risk of suicide in individuals with bipolar II may be higher than in individuals with bipolar I andunipolar disorder (Dunner et al 1976; Endicott et al 1985; Kupfer et al 1988; Bulik et al 1990; Rihmeret al 1990). It is possible that this elevated suicide risk could be secondary to comorbid psychopathologyand diagnostic overlap with alcohol dependence and personality disorders (Rihmer et al 1990), or thatindividuals with frank bipolar I are more likely to receive adequate treatment because of the intensityof their manic episodes. Indeed, hypomanic episodes are often seen by the individual as enjoyable andunworthy of intervention.

Morb id i t y : B ipo la r I

Considerable morbidity is associated with bipolar I disorder. Although many individuals display nointerepisode functional impairment, approximately 20–30 percent of patients display social oroccupational impairment at follow-up (Coryell et al 1987). The excesses of behaviour during themanic episode (eg, excessive spending, indiscrete sexuality, and gambling) can continue to impact onthe individual and the family long after the temporal confines of the manic episode. Considerableburden can also been seen in family members who are confronted with the extreme oscillations intheir loved one’s mood and behaviour.

Psy ch ia t r i c Comorb id i t y : B ipo la r I

Approximately two-thirds of individuals with bipolar I disorder display at least one Axis I comorbidcondition (other psychiatric disorder) (Keck et al 1995). Frequent comorbidity with alcohol or othersubstance use disorders, anxiety disorders, and impulse control disorders has been noted.

Psy ch ia t r i c Comorb id i t y : B ipo la r I I

Individuals with bipolar II disorder have been noted to have higher comorbidity of alcoholism,personality disorders, premenstrual dysphoria (in women) and antisocial personality disorder (in men)than bipolar I or unipolar patients (Endicott et al 1985). In addition, a history of childhood hyperactivityhas been noted to occur frequently in individuals with bipolar II disorder (Endicott et al 1985).

AET IOLOGY OF B IPOLAR I AND I I D ISORDERS

Gene t i c Fa c to r s

Numerous clinical and genetic investigations have examined the degree to which bipolar illness isheritable and distinguishable from unipolar illness on the basis of family, twin, adoption, and linkagestudies. A number of family studies have indicated a higher frequency of affective disorders in the

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families of bipolar individuals than unipolar patients (Dupue and Monroe 1978), with a higherprevalence of bipolar illness in the relatives of bipolar patients (Angst 1966; Perris and D’Elia 1966;Winokur and Tanna 1969). Unipolar disorder is more commonly found among relatives of bipolarsthan relatives of unipolars, yet bipolar disorders are infrequently seen among relatives of clearlydiagnosed unipolar depressives (Perris and D’Elia 1966; Gershon et al 1971; Loranger 1975; Gershonand Hamovit 1979). Although unipolar family histories appear to be relatively pure for unipolar disorder,the family pedigrees of bipolar patients indicate a considerable overlap of unipolar and bipolar pathology(Gershon and Hamovit 1979; Mendlewicz 1979).

Twin and adoption studies have yielded more specific information on the transmission of affectivedisorders. Investigations of monozygotic and dizygotic twins have consistently shown a significantlyhigher concordance rate for manic-depressive illness in monozygotic than dizygotic twins (Harvaldand Hauge 1965; Kringlen 1967; Zerbin-Rudin 1967). More specifically, Allen (1976) has shownsignificantly different rates of concordance between twins diagnosed with unipolar depression (40percent) and with bipolar I disorder (72 percent). These rates were much lower among dizygotic twins(11 percent for unipolar and 14 percent for bipolar; that is, very similar rates). A famous adoptionstudy by Mendlewicz and Rainer (1977) identified the importance of genetic factors in the transmissionof bipolar I disorder. Thus, it appears that bipolar I disorder is a relatively highly heritable conditionand that as yet unknown genetic factors are of aetiological relevance.

L inkage and As so c ia t ion S tud ie s

The genetic mapping of the genes that predispose to bipolar I disorder has attracted considerableresearch interest over the last 30 years, particularly as twin and adoption studies have suggested itshigh heritability. Unfortunately, a fair summary of these studies in the middle of 1996 is that there areno compelling or conclusive leads. In an excellent summary of these studies, Risch and Botstein(1996) note that ‘the recent history of genetic linkage studies for (bipolar disorder) is rivalled only bythe course of the illness itself’ in that there has been intense excitement when a group publishes apositive genetic linkage followed inevitably by dysphoria when non-replications by other groups follow.

The history of these studies strongly suggests that great caution is required when evaluating themolecular genetic studies of complex disorders (Lander and Schork 1994) such as bipolar disorder.However, it is the great hope of many in the field that bipolar disorder will one day yield its secrets.

PREVENT ION OF B IPOLAR I D ISORDER

Pr imar y P reven t ion

Similar to major depressive disorder, we are aware of no studies that address primary prevention ofbipolar disorder in the general population. Much of what we wrote above about the primary preventionof major depression also holds for bipolar disorder.

Secondar y P reven t ion

Any of the secondary preventive approaches for bipolar disorder parallel those outlined for majordepression. There are, however, additional facets to secondary prevention of bipolar disorder whichinclude predicting bipolarity in individuals who present with the first affective episode.


Approximately 10 –19 percent of depressed adolescents will go on to develop bipolar I disorder (APA1994a; Rao et al 1995). Individuals with bipolar I disorder tend to display a greater family history ofbipolar disorder than individuals with major depressive disorder (odds ratio of 3.8) (Winokur et al1993). Similarly, elevated rates of hypomania have been detected in family members of those withbipolar II disorder (Endicott et al 1985). When depressed adolescents present for treatment, carefulscreening for a family history of bipolar disorder or hypomania and ongoing vigilance for the presenceof mixed affective states can serve as early warnings for the possible later development of bipolardisorder. These observations could, obviously, influence the clinician’s choice of pharmacologicaltherapy.

Te r t ia r y P reven t ion

According to the Consensus Development Panel (1985), the definition of relapse is ‘the exacerbationof an ongoing episode after an initial suppression of symptoms’ and the definition of recurrence is ‘anew episode following a complete recovery that has lasted for at least several months’. Preventivetreatment refers to long-term efforts to prevent completely or reduce the intensity and frequency ofrecurrence – which we refer to here as tertiary prevention.

Additional effort should be made to improve tertiary prevention of bipolar I disorder. Although lithiumhas proven to be an invaluable tool in the treatment of this disorder (Angst et al 1970; Baastrup et al1970; Coppen et al 1971; Hullin et al 1972; Prien et al 1984), a 20–30 percent failure rate of long-termtreatment efficacy has been demonstrated (O’Connell et al 1985). Rapid cycling, medication non-compliance, the presence of mood-incongruent psychotic features (Miklowitz 1992), frequent previoushospitalisations, poor social supports, lower social class, current alcohol or drug abuse (O’Connell etal 1985; O’Connell et al 1991), and high familial expressed emotion (Miklowitz et al 1988), have allbeen associated with treatment failure or increased risk of recurrence. These findings have not beenreplicated by all investigators (eg, Carlson and Goodwin 1973; Carlson et al 1977; Roy-Byrne et al1985). Rapid discontinuation of lithium has been associated with an increased risk of recurrence(Faedda et al 1993).

In addition, claims have been made that carbamazapine is of equal efficacy to lithium in the prophylacticmanagement of mania (Post et al 1986, 1991); however, a meta-analysis by Dardennes and colleagues(1995) suggests that this statement is premature and that the data are not yet sufficient to establishtherapeutic equivalence. Reviews of pharmacological interventions for bipolar disorder are available(Prien and Gelenberg 1989).

Bauer and Keller (1994) highlight the ‘efficacy effectiveness gap’ in the treatment of bipolar disorder,wherein the success rates seen in randomised clinical trials (‘efficacy’) are not equivalent to the resultsseen in general clinical practice (‘effectiveness’). Indeed, in a review of the Massachusetts GeneralHospital psychopharmacological database of all patients being treated for bipolar I or II disorder in aone-year open trial, although 90 percent of the sample met criteria for remission during the course ofthe year, only 4 percent of patients experienced an episode-free year (Sachs et al 1994).

Bauer and Keller (1994) highlight the importance of delivering high-intensity pharmacotherapy withas few side-effects as possible, efforts to improve medication adherence, patient education, and illness-management skills to improve outcome in general practice.

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Psychological interventions such as cognitive-behavioural therapy aimed specifically at developingtools for illness management, such as ways of living with a chronic, recurrent illness, recognisingearly warning signs of affective episodes, and assisting with adherence to medication are worthy offurther investigation. It is also worthwhile to determine whether other focal psychotherapies (eg,interpersonal psychotherapy (Klerman et al 1984)) can assist with decreasing the risk of relapse inindividuals with bipolar I disorder (E. Frank, personal communication, June 1992).

Secondar y and Te r t i a r y P reven t ion : Rev iews

Excellent reviews of the treatment of bipolar disorder have been published in Australasia (Andrews1983; Joyce et al 1995) and in the US (APA 1994b).

CONCLUS IONS AND RECOMMENDAT IONS

Many authors have criticised the paucity of attention given to primary prevention in psychiatry and,indeed, to the two cardinal mood disorders. Upon closer inspection, however, this matter is considerablymore complex. As reviewed above, we have but a slight inkling of what is likely to be a complexcausal aetiological chain that results in major depression and bipolar disorder. Until the causes ofthese conditions are better understood, primary preventive efforts are premature. In contrast, secondaryand tertiary preventive efforts for major depression and bipolar disorder are probably feasible. It iscritical for any such programmes to be tested empirically prior to more general implementation.

We close with the following recommendations:

1. Primary prevention of major depression and bipolar disorder is not currently possible. Furtherrigorous investigation of the effectiveness of possible intervention is necessary.

2. The inability to provide primary prevention is in part because the aetiology of major depressionand bipolar disorder is not understood. Studies employing the appropriate scientific methodologyto clarify the aetiology of these disorders would be useful. We suggest that attempting to elucidatethe genetic basis of these conditions would be particularly useful and, should this beaccomplished, the relevant environmental factors could then be delineated.

3. New Zealand data concerning the treatment of major depression and bipolar disorder (secondaryand tertiary prevention) are needed. In particular, we believe that studies of the detection andtreatment of major depression in the general practice setting and of the long-term treatment ofmajor depression and bipolar disorder in the specialist setting are required.

4. Data about mood disorders in Mäori and Pacific people are essentially non-existent. We knowlittle about their prevalence in these population groups nor of the impact of culture upon theirdetection and treatment. Studies employing careful empirical methods to correct thesedeficiencies are essential.


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