The literature has emphasised certain aspects of depressive illness that are thought to be more common in old age. They include a preponderance of somatic complaints, excessive hypochondriasis and greater agitation, more frequent delusions compared to young persons (Baldwin, 1997). These findings are not supported fully by empirical evidence, especially when age-related factors are held constant. Blazer et al. (1987) compared young adults with depression and elders with depression, controlling for symptoms which might fortuitously increase with age independent of depression and they found that older community subjects, characterised according to DSM criteria reported more somatic symptoms, had more thoughts about death. Surprisingly, however, it was the younger rather than the older depressives who reported more memory problems. There were no reports of a special “masked” depression occurring in old age.
In an attempt to better capture the nature of late-life depression and other subsymdromal forms of depression, Minor depressive disorder (MnDD) was proposed and included in the DSM-IV for capturing this non-major subsyndromal depressive disorder in the Appendix B of the DSM-IV (American Psychiatric Association). This carries the same criteria as the Major disorder except that instead of 5 other symptoms only 2 -4 others beside anhedonia or aphoria. The term “subsyndromal depressive symptoms” (Judd 1997; Qualls and Knight, 2006) has been used in research but not yet represented in the DSM and it is used to describe a similar profile to the Minor Depression diagnosis. An even broader set of criteria, labelled “”clinical significant nonmajor depression” has recently been proposed (Kumar et al, 2004). Task Force on DSM-IV., 1994; Djernes, 2006).
While the diagnosis of children with depression is increasing there seems to be a tendency to under diagnose the condition among elderly individuals (see Ohayon, 2007; Parashos et al., 2002). There are a number of stereotypes about the elderly, most of which are negative, in our youth-oriented culture (Hummert, Garstka, Shaner, & Strahm, 1994) with therefore, many consider the notion of living beyond 70 to be a bleak concept (Lacey, Smith, & Ubel, 2006). Stereotypes of the elderly could, as suggested by Ruppel et al (2010), contribute to the underdiagnosis of depression in old age. Clinicians are mistaken in the way they are likely to dismiss depression as purely “understandable” because of ill health. Perhaps it is the case that our incorrect stereotypes that depression in the elderly is due to the aging process alone, have overshadowed our ability to recognise real depression in the elderly for what it is. Ruppel et al. (2010) conducted a study testing two different cohorts of adults – a sample from 1989 and a sample taken in 2006 - on whether this stereotype of elderly depression exists. It was found that for both cohorts, despite the identical symptom profiles, the participants attributed age as the cause of the symptoms more often in the elderly than in young persons, to the latter they attributed depressive disorder more often.
This stereotype is inaccurate and helpful. The empirical literature portrays a different picture. Mitchell & Subramaniam (2005) conducted a systematic review focusing on robust studies that have directly compared the prognosis of depression in late life versus midlife. The results indicated that although rates of relapse and recurrence, and outcome was marginally poorer for older adults. However, reaction to treatment is to a large degree positive. It is found that up to 80% of patients will react well to treatment (Dunitz, 1997).
Although it may very well be the case that depression is not a natural part of the ageing process as is misconceived by many, as has been mentioned previously, it may manifest it’s self differently in later life and the reasons for its existence may be different in nature due the different way of life elders generally experience. The risk and protective factors associated with it may also be different to those who experience it in younger years.
Gatz and his colleagues (Gatz, Kasl-Godley & Karel, 1996) proposed a developmental diathesis-stress model that takes both psychological, environmental and biological influences into account. Psychological vulnerability tends to decrease in later –life as does genetic risk. Furthermore according to the theory, other type of biological vulnerability become more frequent, including age-related neurobiological changes that may predispose to depression (Qualls & Knight, 2006). Several lines of research support these propositions. Firstly, when known risk factors for depression are statistically controlled, older adult actually have lower levels of depressive symptoms than do middle-ages adults (Mirowsky & Ross, 1992). Regarding genetics, family history has been found to be less common among older adults with these disorders (Devanand et al., 2004, as cited in Qualls & Knight, 2006). However, there is much empirical evidence that biological factors play a larger role in depression with age.
There is believed to be a direct connection between physical illness and depression. Central nervous system illness such as Parkinson’s disease and stroke, damage parts of the brain (Wasserman, 2006). Problems with lungs and pancreas, the endocrine system, infections and organic brain tissue can lead to what is known as organic depressions (Baldwin, 1997). Also these illnesses have psychological consequences and the sufferer may become depressed owing to the changed life situation their ill-health brings about. An example is given by Wasserman (2006) that it is estimated that 30% of stroke patients suffer from severe despondency. Yet only a few receive treatment for their despondency. Indirectly, other chronic illnesses which are common in later life can have depressive effects, as they would for any age. Having to live with constant pain, extreme fatigue and pronounced worry may induce a person of any age to succumb to depression. There is also a well-known association between hearing impairment in later life and late-onset persecutory states (Baldwin, 1997).
The mismanagement of drug treatments provided to the elderly can also increase the risk for depression. Polypharmaceutics is extremely common in the elderly yet certain combinations of medicines can trigger depression (Wasserman, 2006). Therefore, it is vital that the prescribing doctor is aware of all previous prescriptions. It can also be the case that elderly people are likely to accidently take the incorrect medicine. Medicines liable to provoke depression include certain cardiac agents, such as digoxin, and drugs that produce blood pressure, such as beta-receptor blockers (Wasserman, 2006).
It is a point of considerable interest and contention as to whether the ageing brain itself is more vulnerable to depression (Dunitz, 1997). According to the amine theory of depression, amine changes may predispose depression or be altered by it. Therefore, the direction of causation is unknown (Baldwin, 1997). However some biological changes associated with ageing are similar to those seen in depression (Baldwin, 2002). Thus both normal ageing and depression are associated with decreased brain concentrations of serotonin, dopamine, noradrenaline, and their metabolites and increased MAO-B activity. However the evidence for this theory is mixed (Baldwin, 2002).
Furthermore links have been established between depression in old age and structural changes in the brain. Changes in the brain structure may be relevant to the well-known finding that disorder which damage the subcortical-frontal circuitry of the brain are associated with a high incidence of depression (Baldwin, 2002). These include Parkinson’s disease, Alzheimer’s disease, stroke and heart disease (Qualls & Knight, 2006). Although elderly people share with younger adults many factors which are aetiologically relevant to depression this is increasing evidence that neurodegenerative change, of a type not yet characteristised but possibly subcortical in location, renders some people in later life vulnerable to depression (Baldwin, 1997)
Epidemiological studies have highlighted an association between hypertension and depression (Alexopoulus et al, 1997). Depression associated with vascular risk factors, referred to as “vascular depression” is characterised by late onset and distinctive symptom profile that includes psychomotor retardation, executive functioning deficits, and impaired insights and is less likely to include agitation and guilt (Alexopoulus et al, 1997).
Another predisposing feature may be that of personality. However, to accurately research this factor can be difficult: differentiating features of the current illness from features of the premorbid personality can be very difficult, and even informants often provide biased accounts. Bergmann (1978) and Dunitz (1997) note that patients with predominantly neurotic symptom profiles of depression were often catagorized as anxiety prone individuals – Bowlby’s attachment theory. DSM III “avoidant” and “dependent” types is associated with late life depression (Abrams et al 1987). Furthermore, according to Murphy (1982) life-long lack of capacity for intimacy seems to be a risk factor for depression. Also, it has been suggested by Baldwin that presence of “senile dysphoria”, which refers to “individuals with long standing coping and relationship difficulties who decompensate psychologically in later life” (Baldwin, 1997, p.538), may have a link with depressive personality disorder. Despite these claims the research, not much evidence has been found to be in accordance with them.
Social supports and intimacy seem to play significant roles in the level of depression in old-age. Murphy’s (1982) data suggests that a confidante may act as a buffer against social losses. Emmerson et al (1989) found a striking effect of the absence of a confidante- bigger effect on men. This area can a difficult area to assess, with one of the reasons being due to the question of using objective or subject measures – each will yield different results. However there seems to be somewhat more support for the hypothesis that there is a direct association between social support and depression as opposed to the alternative that social support acts a buffer, It has been found that social support plays a direct role in decreasing the risk of depression in the presence of a life event (Prince et al, 1997). Murrell et al (1991) found a direct protective relationship between self-esteem and depression, but noted that self-esteem modified the association between life events and later depression scores. In line with this hypothesis and in support of it, Prince et al (1997) reported a number of Social Support Deficits including living alone, having no support neighbours, having one or less supportive friends, being upset or bothered about a relationship with a child, lacking satisfaction with support from friends to all be associated with pervasive depression. It was reported that seeing a relative less often than once a week has a borderline association. The cross sectional design of the study was pertinent to the weakening of the alternative buffer hypothesis because of the blurring of temporal relationships between variables – social support and depression were measured concurrently, but preceding life events were retrospectively identified.
Negative life events as a precipitating factor has been empirically shown to be connected with the onset or level of depression experience in old age. Kraaj, Arensman & Spinhoven (2002) among many other studies found that effect to be a moderate one. According to the research of Murphy (1982) depressed old people are twice as likely to have had experienced at least one life event in the last year. Brown and Harris (1978) found that only the most severely threatening life events were related to depression and Norris & Murrell‘s (1987) research found the effect to usually last less than 6 months. Murphy (1982) found that death of a loved one, life-threatening illness to oneself and to somebody close, major financial problems, peremptory removal from one’s home were all significant factors found to be association with elderly depression. Using a cross-sectional survey interview method, Prince et al. (1997) conducted a study in a series called the Gospel Oak Project, in which they aimed to determine a link between levels of later life depression and a number of factors including life events. With a sample size of 654 adults aged 65 or over and using the List of Threatening Events checklist, it was found that depressed subjects reported more life events than non-depressed subjects. The life events were the same as Murphy’s (1982) study as well as the end of a relationship, theft/loss and problem with close relative or friend as being significant factors. It was found that the onset of a serious illness was had the highest rate of associated prevalence and that both serious illness and bereavement held the highest risk for depression within the first 6 months of the event happening. Interestingly, theft/loss and financial crisis were the most enduring as depression was not dependant on the time of the event. Prince et al (1997) suggest that the enduring life circumstances favouring this event predisposed towards depression.
Late-life depression is a complex, yet its nature is similar to that among other ages in many respects. The current diagnostic systems in place do not seem to be adept at capturing the most commons form experience during age and so changes are needed in order to decrease its current underdiagnosis. Qualls & Knight (2006) suggest that a dimensional approach may be of better use, one that considers the frequency and severity of a range of depressive symptoms. Furthermore, stereotypes associated with old-age depression need to be dissolved, both from the clinical perspective and the layperson’s perspective. The researchers state that they “believe that recognition by non-medical personnel is an important issue because the elderly individuals' families may also play a role in the process of recognizing the symptoms and encouraging their elderly relatives to consult with a physician” (Ruppel et al, 2010, p.). There is, however, a problem with the sample size used throughout this study, so these findings may be debateable.
Moreover, it is important to consider the fact that old-age depression is far more heterogenous and so aetiologies will be multiple and complex. The effects of the risk factors and stressors will manifest themselves differently due to the sets of occurrences that are associated with older adulthood such as physical illness and negative life events. Disregarding depression in old age can have devastating effects, because of the high rate of suicide (Dennis,2009) and because the condition is highly treatable. The number of risk factors and protective an elderly person is different to those of younger years. Therefore, aging can be construed not as an inevitable march towards depression, but rather acts as a catalyst through which depression can occur. There is a need change in the diagnostical systems and attitudes that exist about elderly depression, that reflect the different aetiology behind old depression that causes it to manifest itself differently to other ages.
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