Origins of Depression in Later Life

8/12/2019 Origins of Depression in Later Life

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INVITED REVIEW

Origins of depression in later life

D A N G . B L A Z E R I I * A N D C E L I A F. H Y B E L S

Duke University Medical Center,Department of Psychiatry and Behavioral Sciences,Durham,NC,USA

ABSTRACT

Background. Despite the burden of depression in late life, its origins present a paradox toinvestigators and clinicians alike.

Method. We review biological (genetics and heredity factors, neurotransmitter dysfunction,endocrine changes, vascular disorders, and medical co-morbidities), psychological (personalityattributes, neuroticism, cognitive distortions, and the lack of emotional control and self-efficacy)and social (stressful life events, bereavement, chronic stress or strain, socio-economic disadvantageand impaired social support) origins of late-life depression based upon an extensive though notexhaustive review of the extant literature. In addition, modifying psychological and social factorsare discussed.

Results. Older adults appear to be at greater risk for major depression biologically, such asdepression resulting from vascular changes, yet the frequency of depression is lower comparedto younger adults. Older adults may be protected psychologically due to factors such as socio-emotional selectivity and wisdom, compared to younger adults, and perhaps relatively protected

from social risks.

Conclusions. A biopsychosocial approach to evaluating the origins of late-life depression isheuristically valuable, a continual reminder of the many factors that contribute to the onset andpersistence of clinically significant symptoms in late life.

INTRODUCTION

Depressive symptoms and disorders are fre-quent causes of emotional and physical suffer-ing, decrease the quality of life and increase the

risk for death among older adults (Berkmanet al. 1986; Blazer et al. 2001 ; Blazer, 2003).Even so, the origins of late-life depressionpresent a paradox to investigators and cliniciansalike. Older adults appear to be at greaterbiological vulnerability to depression, yet com-munity surveys in Western societies haverepeatedly documented a lower frequency oflate-life depressive symptoms and cases of

depressive disorders in controlled analysescompared to midlife (Blazer et al . 1991;Weissman et al. 1991) Therefore, a biopsycho-social model of etiology (Engel, 1977, 1980;Blazer, 2002 ; Lindau et al. 2003) is especiallyapplicable to the elderly primarily because itreminds us that the origins of late-life depressionare multiple and range across all three domains.Even so, this model can be misleading given thetight connection between the domains. Forexample, psychological dimensions have bio-logical mechanisms and biological models implyinput from the environment.

Psychological and social factors may be moreprotective against depressive symptoms anddisorders in later life compared to earlier stages

of the life-cycle. This paradox, however, mustnot blind us to the adverse consequences of

* Address for correspondence: Dan G. Blazer II, M.D., Ph.D.,

Box 3003, Duke University Medical Center, Department ofPsychiatry and Behavioral Sciences, Durham, NC, 27710, USA.

(Email: [email protected])

Psychological Medicine, 2005,35, 112. f 2005 Cambridge University PressDOI: 10.1017/S0033291705004411 Printed in the United Kingdom

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severe late-life depression, including an in-creased risk for non-suicide mortality (Schulzet al . 2002), suicide (Conwell et al . 2002),physical disability (Berkman et al. 1986) andrisk of adverse outcomes for specific illnesses,such as cardiovascular disease (Sullivan et al.1997) and diabetes (Blazer et al. 2002a).

The multiple biological, psychological, andsocial causes of depressive symptoms and dis-orders in late life, however, are not competingbut complementary and almost always trans-actional. For example, vulnerability to socialstressors often derives from underlying biologi-cal mechanisms that interact with social riskfactors. In this article we provide a representa-tive but not comprehensive review, focusingupon more recent studies of the origins of late-life depressive symptoms and disorders, that is,depression experienced by older adults whether

that depression had its onset in later life orearlier in the life-cycle. Where possible we

distinguish those studies that explore the originsof depressive symptoms from those that focuson diagnosed disorders such as major de-pression. We also distinguish those origins thatare specific to older adults from those that affect

adults across the life-cycle including olderadults, as summarized in Table 1.

We divide the review into biological, psycho-logical, and social origins more for convenienceof organization than to suggest that thesedomains cannot be connected theoretically ordemonstrably. We stop short, however, of pro-viding a grand model of the web of causation(MacMahon & Pugh, 1970), for if the plethoraof studies emerging in recent years has taught usanything, it taught us the danger of potentially

limiting our inquiries to fit the Procrustean bedof such models.

Biological origins

The discovery of biological risk factors and theirputative mechanisms has been a fertile area ofbasic and clinical research into the origins oflate-life depression.

Genetics and heredity

Twin studies of older adults in Scandinavia

provide insight into the relative contribution ofheredity and environment to reported depress-ive symptoms. Among elderly twins in Sweden,for example, genetic influences accounted for16% of the variance in total depression scoreson the Center for Epidemiologic StudiesDepression Scale (CES-D) and 19% of somaticsymptoms. Genetic influences, however, con-tributed to a minimal amount of the variancesymptoms of depressed mood and positive affect(Gatz et al. 1992). Therefore, not all depressivesymptoms appear to be equally influenced byheredity.

Major depression is more common amongwomen compared to men and this differencepersists into late life (Krause, 1986). Many fac-tors have been suggested to explain these dif-ferences, such as selective survival. For example,men die earlier and mortality may be affected bygenetic factors (Hazzard, 1999). Since men andwomen are seldom compared in matchedanalyses, examining older unlike-sex twin pairsprovides an opportunity to explore these sex

differences. In one such study, women had ahigher frequency of depressive symptoms and

Table 1. General and age-specific risk andprotective factors for depression in later life

General risk factors (factors that predispose to depressivesymptoms and disorders across the life-cycle including later life)

Biological risksHereditary (e.g. findings from twin studies)Female sexUnderactivity of serotonergic neurotransmissionHypersecretion of cortisol (associated with hippocampal

atrophy)Low levels of testosterone

StrokeMedical illness and functional impairmentAlcohol abuse and dependence

Psychological risksPersonality disorderNeuroticismLearned helplessnessCognitive distortions

External locus of controlSocial risks

Stressful life events and daily hasslesBereavementSocio-economic disadvantageImpaired social support

Specific risk and protective factors (factors that are especiallyrelevant to depressive symptoms and disorders in later life)

Biological risksGenetic polymorphisms or mutations (such as CADASIL)Low levels of DHEACortical and subcortical ischemiaAlzheimers disease

Psychological protective factors

Socio-emotional selectivityWisdom

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depressive diagnoses and the sex differenceincreased over time (Takkininet al. 2004). Evenso, the likelihood of identifying a mood disorderin the relative of an older adult is lower than inmidlife (Hopkinson, 1964; Brodatyet al. 2001).

Most hypothesized genetic markers for late-life depression have not stood the test of well-controlled studies, yet some present intriguingpossibilities. Despite the considerable interest inthe e4 allele of the apolipoprotein E gene, noassociation was found in a community samplebetween the E4 allele and depressive symptoms(Blazer et al. 2002 b) Other investigators haveconcentrated on genes that may be associatedwith cerebral vascular lesions associated withdepression. In one study, patients with late-

onset major depression exhibited a higher fre-quency of C677T mutation of the MTHFR(methylene tetrahydrofolate reductase) enzymecompared to controls. This mutation may placeolder persons at risk for major depression as-sociated with cerebral vascular lesions (vasculardepression) (Hickie et al. 2001). A rare disease,CADASIL (cerebral autosomal dominant ar-teriopathy with subcortical infarcts and leu-koencophalopathy), derives from the notch 3gene. Depression is one of the initial symptoms

in this condition. Investigators who analyzedthree longitudinal twin studies of the elderly inSweden (mean age 73 years), found an associ-ation between the 5-HTR2A gene promoterpolymorphism and depressive symptoms for theA/A genotype (Jansson et al. 2003). These pre-liminary findings suggest that genetic poly-morphisms or mutations may predispose olderadults to vascular depression (Desmond et al.1999; Krishnan, 2002).

Neurotransmitter dysfunction

Underactivity of serotonergic neurotrans-mission has been the focus of much research onthe pathophysiology of depression in youngeradults. Other neurotransmitter systems, such asnorepinephrine and dopamine dysfunction,have also been implicated as well but weconcentrate on serotonin neurotransmission.Although serotonin activity, specifically, 5-HT2A receptor binding, decreases dramaticallyin a variety of brain regions through midlife,there is less decrease from midlife to late life. In

one study, the investigators found that 5-HT2Areceptors in normal subjects decreased markedly

from young adulthood to midlife (70 % from thelevels at age 20 years through the fifth decade),and then leveled off as age advanced (Shelineet al. 2002). The activity of these receptors,however, may vary with age.

The relationship of serotonin depletion can beinvestigated indirectly by observing radioiso-tope-labeled or tritiated imipramine binding(TIB) sites on platelets in the elderly. There is asignificant decrease in binding sites in olderpeople with major depression compared tonormal controls and subjects with Alzheimersdisease, but no decrease in binding capacity(Nemeroffet al. 1988).

Endocrine changes

Hypersecretion of corticoptropin-releasing fac-tor (CRF) has been associated with depression.CRF is thought to mediate sleep and appetitedisturbances, reduced libido, and psychomotorchanges (Arboreliuset al. 1999). CRF, however,is also diminished with normal aging (Gottfries,1990). Aging is associated with an increased re-sponsiveness of dehydroepiandrosterone sulfate(DHEA-S) to CRF (Luisi et al. 1998). Lowlevels of DHEA have been associated withhigher rates of depression and a greater number

of depressive symptoms in community-dwellingolder women (Yaffeet al. 1998).Total serum testosterone levels decline with

aging yet we do not know the level at whichthese levels become abnormal (Liverman &Blazer, 2004). Testosterone levels were lower inelderly men with dysthymic disorder than inmen without depressive symptoms in one study(Seidman et al. 2001), yet the efficacy of testos-terone treatment for major depression in menhas not been established (Liverman & Blazer,2004). Hormone replacement in women hasbeen associated with some improvement inmood (Sherwin & Gelfand, 1985).

Anatomical changes have been associatedwith endocrine dysregulation as well as late- lifedepressive symptoms, suggesting a viciouscycle downward to chronic and moderatelysevere depressive symptoms. For example,depressive symptoms have not only been associ-ated with atrophy of the hippocampus, theyhave been hypothesized to cause the atrophy(Sheline et al. 1996; Sapolsky, 2001; Steffens

et al. 2002). Cumulative stress over the life-cyclemay lead to a sustained increased secretion of

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cortisol which in turn causes loss of pre-existinghippocampal neurons (Sapolsky, 1996), a lossthat may be prevented in part by use of anti-depressant medications (Czehet al. 2001).

Depressive symptoms can lead to increased

cortisol secretion (Davis et al. 1984). Cortisolinhibits neurogenesis leading to hippocampalvolume loss that may mediate the cognitivesymptoms of depression (Sapolsky, 2001). Othermechanisms that have been proposed to explainvolume loss have been described above and in-clude glutamate neurotoxicity (Sheline, 2003)decreased brain-derived growth factor (Sheline,2003), decreased neurogenesis (Gould et al .1999), and loss of plasticity. For example, earlylife stress may produce a permanent hypersen-

sitivity to stress, with the production of ongoingHPA axis dysregulation and with repeated epi-sodes of major depression plasticity may giveway to permanent damage (Heimet al. 2000).

Vascular depression

The association of depressive symptoms andvascular risk factors has long been known (Post,1962). For example, major depression is a fre-quent outcome of stroke (Robinson & Price,1982), occurring in approximately one-third of

all ischemic stroke survivors (Parikhet al. 1990).Hypertension has also been associated withincreased risk of major depression (Rabkin et al.1983), although the literature is not consistent(Lynesset al. 2000).

Boosted by new tools of inquiry, especiallymagnetic resonance imaging (MRI), investi-gators have proposed a vascular-based de-pression among the elderly (Post, 1962;Krishnanet al. 1988; Coffey et al. 1990; Kumaret al. 2002; Olinet al. 2002). In one study of 139depressed older adults, 54% met neuroimagingcriteria for subcortical ischemic vasculardepression. Age was most strongly associatedwith the increased prevalence of these changes.Lassitude, a history of hypertension, and pooreroutcome were also positively associated with thediagnosis, whereas a family history of mentalillness and loss of libido were negativelyassociated with the diagnosis (Taylor et al.2003 ; Krishnanet al. 2004). Vascular depressionis linked with white-matter hyperintensities(WMH), bright regions seen in the brain par-

enchyma on T2-weighted MRI scans (Krishnanet al. 1997; Guttmannet al. 1998). These lesions

are thought to represent injury to white-mattertracks and may contribute to the disruptionof neural circuits associated with depression(Tayloret al. 2003).

The vascular depression impairments re-

semble impairments exhibited in frontal lobesyndromes. MRI of depressed patients has re-vealed structural abnormalities in areas relatedto limbic-cortical-striatal-pallidal-thalamic-cor-tical pathways (George et al. 1994), includingthe frontal lobes (Krishnan et al. 1993), caudate(Krishnan et al. 1992), and putamen (Husainet al. 1991; Sheline, 2003). In three-dimensionalMRI studies of mood disorders, many of thestructures that compose this tract have beenfound to have volume loss or structural abnor-

malities (Sheline, 2003).Recent interest has also focused on a smaller

size of the orbital frontal cortex in late-life de-pression (Lai et al. 2000). The frontal whitematter (not gray matter) lesions of vascular de-pression are associated with increased myoino-sitolcreatinine and cholinecreatinine ratios.These changes may reflect biological changes innon-neural (glial) tissue, which in turn affectssynaptic activity (Kumar et al. 2002). Whetherinvestigators hypothesize endocrine dysregula-

tion or vascular changes, a major advance in thefield is the concept that older adults may be atgreater risk for depressive symptoms and majordepression because key pathways have beendisrupted.

Cognitive function in late-life major de-pression supports these neuroanatomic findings,specifically the disruption of functional path-ways. For example, disruption of the limbic-cortical-striatal-pallidal-thalamic-cortical path-ways leads to impairment in visuospatial ability,memory, speed of information processing, andexecutive functioning, with executive deficitsbeing particularly related to late age at onset offirst lifetime depressive episode (Alexopouloset al. 2000; Lesser et al. 2000; Butters et al.2004). Given that late-life major depression ischaracterized by slowed information processing,which affects all realms of cognition, this sup-ports the concept that frontostriatal dysfunctionplays a key role.

Alzheimers disease

Clinically significant depressive symptoms canbe identified in approximately 20% of



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Alzheimers disease (AD) patients (Reifleret al.1982; Patterson et al. 1990). Major depressionwith cognitive impairment (even if the cognitiveproblems remit) increases the risk for AD over 5years (Alexopoulos et al . 1993). Depressive

symptoms may be common even in older peoplewith mild dementia of the AD type (Rubinet al. 2001). Given the co-morbidity of majordepression and AD, the depression/dementiasyndrome may have in large part a commonpathophysiology (Olin et al. 2002). The mech-anisms, however, have yet to be worked out.

Medical and psychiatric co-morbidity

Depression frequently results from and compli-cates the recovery of older patients who experi-

ence myocardial infarction and other heartconditions (Sullivan et al . 1997), diabetes(Blazer et al. 2002a), hip fracture (Magazineret al. 1990), and stroke (Robinson & Price,1982). In a study of community-dwellingMexican American elderly, depressive symp-toms were associated with diabetes, arthritis,urinary incontinence, bowel incontinence, kid-ney disease, and ulcers (Black et al. 1998 a). Ingeneral, poor functional status secondary tophysical illness and dementing disorders are

perhaps the most important cause of late-lifedepressive symptoms (Hays et al. 1997; Bruce,2001). In one study, depressive symptomsincreased the risk for activities of daily livingdisability and mobility disability over 6 years by67% and 73% respectively (Penninx et al .1999).

Health status consistently is associated withdepressive symptoms in cross-sectional studiesof older adults (Kraaij et al. 2002). Yet it is notclear whether a change in health status leads to achange in depressive symptoms (Fiske et al.2003). In one study, health status was correlatedwith depressive symptoms but new illnesses inthe previous 3 years did not consistently predictincreases in depressive symptoms (Fiske et al.2003). In the same study, there was no interac-tion between age and health, suggesting thathealth is not more important in predictingdepressive symptoms in late life than it is earlierin life.

Depressive symptoms and disorders in latelife co-occur with psychiatric disorders as well.

On balance, the co-morbidity of late-lifedepression with other psychiatric disorders is

less frequent that earlier in the life-cycle (thedementing disorders being an exception). Thereason is that other psychiatric disorders are lessfrequent in late life compared to younger ages.Alcohol use and major depression are asso-

ciated in community studies of older adults(Devenand, 2002), Anxiety is commonly co-morbid with depressive symptoms, whether ornot the symptoms meet criteria for a depressivedisorder (Blazeret al. 1987).

In summary, biological vulnerability to de-pressive symptoms and disorders appears to begreater in later life compared to midlife. Manychanges in the brain coupled with the increasedfrequency of diseases known to be associatedwith depression are typical of the aging process,

especially as the individual advances into the eraof the oldest old (Blazer, 2000). Some biologicalprotective mechanisms may increase with agebut these remain unknown at present.

Psychological origins

Several psychological factors have been pro-posed as causes of depressive symptoms anddisorders in late life, including personalityattributes, neuroticism, cognitive distortions,and emotional control. These factors, however,

are not specific to the origins of depression inolder adults and we, therefore, briefly addressexamples of recent studies.

Personality attributes

A recent study found that older patients with apersonality disorder were four times more likelyto experience maintenance or re-emergence ofdepressive symptoms compared to those with-out. No specific personality disorder traits wereassociated with clinical features of depressionsuch as age of onset and number of previousepisodes, but some of the traits were associatedwith psychological correlates including hope-lessness and ambivalence regarding emotionalexpression (Morse & Lynch, 2004). Whenreviewing personality factors, we must recognizethat a depressed mood may alter behavioralstyles as well as cognition.

Personality also interacts with other factors.In a sample of patients with major depressionand non-depressed controls, the effect of stress-

ful life events was modified by cognitive/personality styles in their association with



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late-onset depression, adjusting for medicalillness and reduced physical functioning. Majordepression was 611 times more likely as afunction of these interactions (Mazure et al.2002). In another study, older adults without

high neuroticism and ongoing life difficultieswere not at increased risk for major depressionsecondary to stressful life events. On theother hand, high neuroticism and long-termdifficulties increased the risk, even without theoccurrence of a stressful life event (Ormel et al.2001).

Neuroticism

Neuroticism, a construct rarely applied bypsychiatrists in North America, is frequentlyassessed in Europe and Australia and has beenconsistently associated with late-life depressivesymptoms in cross-sectional and longitudinalstudies of community samples (Henderson et al.1993, 1997; Lynesset al. 2002). This associationhas been observed in residential homes as well(Eisses et al. 2004). In one follow-up study,older adults with low levels of neuroticism wereless likely to develop a depressive disordercompared to subjects with higher neuroticism(Oldehinkelet al. 2001).

Cognitive distortions

Cognitive distortions (Beck, 1987) have alsobeen proposed as a cause of late-life depressivesymptoms and disorders. This theory proposesthat depressed individuals may overreact to lifeevents or misinterpret these events and exag-gerate their adverse outcome. In a recent studyof the experience and impact of adverse lifeevents comparing older patients with majordepression to patients with dysthymia andhealthy controls, patients with major depressionreported more recent life events with greaternegative impact, particularly interpersonal con-flicts (Devenand et al. 2002). The authors pointout it is not clear if the reported impact reflectsan increased vulnerability or a bias in reportingdue to current depressed mood. In a recentstudy from a community sample, elderly per-sons with more depressive symptoms usedacceptance, rumination and catastrophizing to ahigher extent and positive reappraisal to a lower

extent than those with fewer symptoms (Kraaij& de Wilde, 2001).

Emotional control and self-efficacy

In the Longitudinal Aging Study Amsterdam(Beekman et al. 1995 b), major and minor de-pression and persistence and emergence of de-pressive symptoms over 3 years was predictedby external locus of control (Beekman et al.2001). Higher levels of mastery have been shownto have a direct association with fewer depress-ive symptoms in older adults, and to buffer theadverse impact of disability on depression (Janget al. 2002). Self-efficacy has been shown to havea direct effect and also work indirectly throughits effect on social support to prevent depressivesymptoms in a sample of older adults followedfor 1 year (Holahan & Holahan, 1987).

Social origins

A number of social stressors have also beenproposed as contributing to late-life depressivesymptoms and disorders, including stressfullife events, bereavement, chronic stress or strain,socio-economic status and impaired socialsupport. These factors are not unique to olderadults yet the relative contribution of thesefactors appears to vary across the life-cycle.

Stressful life events

One early study found a strong association be-tween both severe life events (i.e. bereavement,life-threatening illness of someone else, majorpersonal illness, etc.) and social difficulties (dif-ficulties in health of someone close to subject,housing, marital and family relationships, etc.)with the onset of major depression in late life(Murphy, 1982). Those lacking a confidant(e)were particularly vulnerable to the effects of lifestress, supporting the hypothesis that socialsupport may buffer the effect of a stressful event.In contrast, a meta-analysis of 25 studies of therelationship between negative life events anddepression in late life, revealed that the totalnumber of life events and the total number ofdaily hassles were strongly associated withdepressive symptoms, while sudden unexpectedevents were not related to depression score(Kraaijet al. 2002).

At first glance, it would appear that olderadults are at greater risk for depressive symp-toms secondary to stressful life events. Yet three

qualifiers temper the risk among the elderly.First, ongoing difficulties may have a smaller



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effect on the risk for depression in older adultscompared to younger adults (Bruce, 2002).One group found that the onset of depressivesymptoms were not associated with baseline(ongoing) psychosocial stressors but were associ-

ated with factors that changed through time(Kennedy et al. 1990). Second, most stressfulevents that lead to late-life depression are pre-dictable or on time events. For example, deathof a spouse is a severe, at times catastrophic,event that frequently leads to depression. Inearly or midlife it is unexpected and the adjust-ment is especially difficult. In late life, by con-trast, most older people recognize, just byobserving their peers, that death of a spouse isfrequent and have actually rehearsed the event,

such as considering what they might do if aspouse dies.

Third, many events that can lead to de-pression are more frequent early in life com-pared to late life, such as divorce and difficultieswith the law. In one study significant difficultywith the law (something more grave than atraffic violation) was reported during the pre-ceding year by 9% of younger adults comparedto less than 1% among older adults (Hugheset al. 1988).

Bereavement

One life event potentially associated withdepression in late life is bereavement (Clayton,1990). Studies have found bereavement to beassociated with depressive symptoms in olderadults in cross-sectional and longitudinalstudies (Prigerson et al. 1994; De Beurs et al.2001). For example, in a study of 1810 com-munity-dwelling older adults, onset of clinicallysignificant depressive symptoms over a 3-year

follow-up was predicted by death of a partner orother relatives. While other studies have foundbereavement to predict depressive symptoms(Prigerson et al. 1994) others have not (Princeet al. 1998).

Chronic stress or strain

Chronic strain is associated with depression inolder adults. The prevalence of depressivesymptoms in caregivers of people with dementiais 4347% (Livingston et al. 1996; Waite et al.

2004). For this reason, providing support forcaregivers is most important to prevent the

onset and progression of depression in this vul-nerable group of older people. In cross-sectionalanalyses using data from a community study ofolder Mexican Americans, financial strain wasassociated with level of depressive symptoms

(Blacket al. 1998 b).

Socio-economic status

Socio-economic disadvantage was associatedwith prevalence and persistence of depressivesymptoms over 24 years in a sample of com-munity-dwelling adults 50 years or older whooriginally met criteria for major depression(Mojtabai & Olfson, 2004). While level ofeducation did not predict emergence ofdepressive symptoms over 1 year (Beekmanet al. 1995a) in a study from The Netherlands,emergence of depression over a 3-year periodwas predicted by lower level of education(Beekmanet al. 2001).

Impaired social support

Social support is a multifactorial construct,including perception, structure of the socialnetwork, and tangible help and assistance(Turner & Turner, 1999). The most robust

relationship between impaired support and late-life depressive symptoms, however, has beenfound with perceived support (Bruce, 2002). In arecent community study in Hong Kong, im-paired social support and depressive symptomswere associated (including network size, net-work composition, social contact frequency,satisfaction with social support, and instrumen-tal-emotional support) (Chi & Chou, 2001).In longitudinal studies, poor social supportpredicted number of depressive symptoms atfollow-up after 36 years (Henderson et al.1997). Insufficient social network predicted theincidence of major depression in a sample of875 non-depressed elderly people followed for3 years (Forsell & Winblad, 1999).

Support can mediate between risk factors andthe onset of depression. In a recent analysisusing growth-curve modeling, perceived socialsupport was shown to mediate the relationshipbetween disability and depressive symptomsover time (Taylor & Lynch, 2004). In a pro-spective study of 1940 community-dwelling

elderly, the effect of stress on incident depressionwas modified by environmental vulnerability



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including marital status and social support(Geerlingset al. 2000). The importance of socialsupport may vary by sex. In a study of middle-aged and older patients, impaired social supportwas associated with poorer outcome of major

depression in older men but not older women(Georgeet al. 1989; Dewet al. 1997).

In general, social support is perceived to beadequate in the elderly, even among clinicalsamples (Blazer, 1982). Although old socialnetworks thin out, new ones emerge for manypeople. Most older people believe that theyhave enough contact with both family andfriends as well as endorse the positive relation-ship that they have with their networks(Cornoni-Huntley et al. 1990). Yet when the

social network is depleted suddenly, eitherthrough loss of a network member (such as aspouse or child) or through a change in thequality of the relationship (such as a disputewithin the family), impaired social supportmay be a most important contributor to late-lifedepression.

Modifying factors

Some psychological factors may modify thebiological and social risks for depression. For

example, most older adults who experience asignificant physical illness do not becomedepressed. The psychological risk factorsdescribed above may not be present and, there-fore, the threshold for the onset of depressivesymptoms may be heightened. In addition, olderpeople may possess unique factors thatactually protect them from the onset of clinicallysignificant depressive symptoms. Two of thesepotential factors are described below.

First, the socio-emotional selectivity theoryhas been proposed to explain differences in theexperience of events across the life-cycle(Carstensen et al. 2000). The theory focused onthe perception by older persons of time left inlife rather than past experiences. Youngeradults, who have much to learn and relativelylong futures, are motivated by pursuit ofknowledge, even when this requires emotionalwell-being to be suppressed. Older adults, incontrast, perceive that they have lived longerthan they will live and therefore de-emphasizenegative experience and prioritize emotionally

meaningful goals. For example, these in-vestigators, in one study, found that negative

emotional experiences (the perception ofstressors) declined from young adulthood untilaround the age of 60 years (Carstensen et al.2000). In addition, periods of highly positiveemotional experience were more likely to endure

as meaningful among older periods comparedto younger adults. In a supporting study,investigators found that age was associated witha self-reported increase in positive affect and adecrease in negative affect (Mroczek & Kolarz,1998). In other words, compared to youngeradults, older adults were more likely to selec-tively optimize the positive in their socialexperiences. This in turn could blunt the harshreality of some of the more negative experiencesamong the elderly and, therefore, protect

against the onset of depressive symptoms.Second, adults are thought to acquire in-

creased wisdom as they age. Although wisdomis a nebulous concept for most epidemiologists,psychiatrists and psychologists, investigatorswith the Berlin Aging group have oper-ationalized the concept and studied it in com-munity samples (Baltes & Staudinger, 2000).They defined wisdom as an expert knowledgesystem concerning the fundamental pragmaticsof life, including knowledge and judgment

about the meaning and conduct of life and theorchestrating of human development towardexcellence while attending conjointly to personaland collective well-being. Five criteria wereassessed: rich factual knowledge; rich pro-cedural knowledge (knowing how to assess, forexample, the ability to develop strategies foraddressing problems); lifespan contextuali-zation (e.g. integrating life experiences); rela-tivism of values and life priorities (e.g. tolerancefor differences in society); and recognition andmanagement of uncertainty (accepting that thefuture cannot be known with certainty and thatour ability to assess our sociocultural environ-ment is inherently constrained). The acquisitionof wisdom over time would appear to protectthe elderly from a spiral down into depressionwhen confronted with a complex of negativeexperiences.

Of course, there is major variability acrossolder adults in terms of their psychologicalmake-up and their acquisition of characteristicssuch as wisdom. Yet studies of normal psy-

chological development, as described above,across the lifespan are critical for a better



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understanding of the risk and protective factorsfor late-life depressive symptoms and disorders.

Summary

The biopsychosocial approach to evaluating the

origins of late-life depression is heuristicallyvaluable, a continual reminder of the manyfactors that contribute to the onset and persist-ence of clinically significant symptoms in latelife. Older adults appear to be at greater risk formajor depression from some biological causes(see Table 1) yet the frequency of majordepression is lower, especially in communitysamples in Western countries. Although psy-chological and social risks for depression inthe elderly are well documented, there is reason

to believe that older adults who are cognitivelyintact and who do not suffer from significantfunctional impairment may be protectedpsychologically due to factors such as socio-emotional selectivity and wisdom and perhapsprotected from some social risk factors com-pared to younger adults.

ACKNOWLEDGMENTS

Supported by grant 5R01-AG20614 from the

National Institute on Aging, and 1 K01MH066380 from the National Institute ofMental Health.

DECLARATION OF INTEREST

None.

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Origins of Depression in Later Life