Section of Old Age Psychiatry, Institute of Psychiatry, London
Department of Epidemiology and Public Health, University College London
Department of Public Health and Primary Care, Institute of Public Health, University of Cambridge
Correspondence: Dr R. Stewart, Section of Old Age Psychiatry, Institute of Psychiatry, De Crespigny Park, Denmark Hill, London SE5 8AF, UK. Tel: 020 7848 0240; fax: 020 7701 0167
Declaration of interest This study was funded by a grant from the Wellcome Trust. R.S. is supported by a Research Training Fellowship from the Wellcome Trust.
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ABSTRACT |
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Aims We examined the association between stroke, vascular risk factors and depression in a community-based Caribbean-born population aged 55-75 years.
Method Vascular risk factors were identified by interview, examination and blood tests. Depression was categorised using the Geriatric Depression Scale. Disablement was assessed as a potential mediating factor.
Results Physical illness and disablement were strongly associated with depression, independent of disablement. Previous stroke was associated with depression, independent of disablement. No vascular risk factors were associated with depression.
Conclusions The risk of depression associated with stroke was not explained by disablement. However, the hypothesis that vascular risk factors are important in the genesis of depression was not supported.
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INTRODUCTION |
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METHOD |
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Entry criteria for the main sample were confirmed at interview: all participants in the study were aged 55-75 years, were born on a Caribbean island (or in Guyana), had at least one parent who was born in a Caribbean nation and were living in community accommodation at the time of assessment. There were no specific exclusion criteria.
Measurements
Participants were assessed at home by research staff. The following
measures are considered in this analysis:
In a separate study the 15-item version of the GDS had been validated in AfricanCaribbean primary care attenders of a similar age range against the Geriatric Mental State GMS-AGECAT standardised psychiatric diagnosis (Abas et al, 1998). Using data made available, GDS-10 scores were derived for participants in that study and sensitivity/specificity calculated against the other scales. A 3/4 cut-off on the GDS-10 scale represented an optimal balance between sensitivity and specificity (0.84 and 0.76, respectively) for pure depression (of mild to moderate severity) according to GMS-AGECAT criteria and this cut-off was therefore used to categorise depression in the study considered here.
Statistical analysis
Primary hypotheses were that vascular risk factors would be associated with
depression independent of measures of disability and handicap and that the
association between measures of physical impairment, disability and handicap
would be explained at least partly by increased vascular disease/risk in more
dependent groups.
STATA 6.0 for Windows software was used. Depression (according to the
GDS-10 cut-off described above) was treated as the principal dependent
variable. Univariate analyses were initially used to examine associations
between depression and all measurements of vascular disease/risk
(2 and two-tailed t-tests, as appropriate). For the
measures of disablement, scores were continuously distributed but the degree
of positive skew precluded transformation. These were subdivided a priori in
order to create approximately equal group sizes, and odds ratios for
depression were calculated across the distribution. Secondary, stratified
analyses were carried out to investigate differences in associations within
subgroups of age, gender, disablement and past psychiatric history. Logistic
regression analysis was used to investigate the role of vascular disease in
the association between depression and disablement, and to investigate
confounding/mediating effects of disablement in associations between
depression and categorical vascular measures (with P values derived
from likelihood ratio tests).
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RESULTS |
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Characteristics of the study population
The sample was evenly distributed in terms of age and gender, 54 (19%) were
categorised as depressed according to a 3/4 cut-off on the GDS-10; 160 (58%)
were receiving treatment for hypertension and 82 (29%) for diabetes; 51 (18%)
had hypertension with proteinuria and/or ECG hypertrophy; and 44 (16%) had
diabetes with glycosuria and/or haemoglobin A1c levels of 8.2% or above. Mean
levels of cholesterol (5.6 mmol/l) and triglycerides (1.5 mmol/l), however,
were lower than would be expected in a UK Caucasian population. Current
smoking was relatively uncommon (25%) and in current smokers, the levels of
smoking were relatively low. Seventeen (6%) gave a history of stroke and the
median reported time since last stroke was 10 years (interquartile range 3-20
years); 13 (5%) had ECG evidence of infarction and 112 (40%) had evidence of
ischaemia. A previous general practitioner (GP) consultation for a psychiatric
problem was reported by 46.3% of subjects with depression and 13.6% of those
without depression. The MMSE scores were 20 or below for 47 (16%)
participants.
Demographic factors and disablement
Univariate associations between depression, demographic factors and
disablement are presented in Table
1. No substantial associations were seen with age, gender,
educational level or occupational social class. Strongly significant
associations were seen, however, between depression and all measures of
disablement.
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Vascular disorders/vascular risk
Characteristics of depression/non-depression groups with respect to
measures of vascular disease/risk are presented in
Table 2. Depression was
positively associated with a previous history of stroke. However, there were
no associations evident for any other factors. Secondary analyses carried out
stratifying for age, gender, disability, presence/absence of a previous
consultation for psychiatric problems and age at first consultation did not
reveal any evidence for obscured associations within subgroups. In addition,
there were no increased rates of depression in groups with more severe
hypertension or diabetes (as defined above).
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Multivariate analyses
The association between depression and previous stroke was examined with
age, gender, number of diagnoses and the three measures of disablement in a
logistic regression model. The strength of the association was reduced after
adjustment but remained significant (OR=3.44, 95% CI 1.09-10.9,
P=0.034). Further adjustment for cognitive impairment made no
substantial difference (OR=3.45). Adjustment for age, gender, previous stroke
and principal vascular risk factors (hypertension, diabetes, ECG ischaemia,
cholesterol and triglyceride levels) made little difference to the
associations between measures of disablement and depression. For example, the
odds ratio for depression across the groups of disability scores displayed in
Table 1 was 2.48 (95% CI
1.72-3.59) unadjusted and 3.04 (95% CI 1.92-4.81) after adjustments.
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DISCUSSION |
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Study limitations
The most important considerations in interpreting these findings relate to
the representativeness of participants compared to the source population.
Various selection processes may have operated in the sampling procedure, which
involved recalled ethnicity by practice staff, and, from results within one
practice, it can be estimated that the sampling frame represented
approximately 75% of the source population. Unfortunately, due to time and
staffing restraints, it was not feasible to contact all persons of unknown
ethnicity for all practices because only 10% of these were potentially
eligible for the study. Refusal rates, in addition, were relatively high but
comparable with another community-based study of a similar population
(Chaturvedi et al,
1993). It is important to consider how selection processes might
have affected results and, in particular, whether they would have obscured an
association between depression and vascular risk factors. It is likely that
higher levels of physical morbidity would be represented in individuals who
were approached to take part compared with the source population (because they
were known to practice staff), but the extent and direction of bias are
unknown with respect to depression. However, prevalence rates of mild to
moderate depression in community samples of older people have been estimated
as being between 10 and 20% (Beekman et
al, 1999), and the prevalence of an equivalent level of
disease severity in this study is within this range. This suggests that over-
or underrepresentation of depression in this study is at least not
substantially different from other community surveys. The fact that it is
towards the upper end of this range suggests that selection bias would, if
anything, exaggerate an association between depression and vascular risk
factors. An additional consideration is that observed associations of
depression with measures of disablement were comparable in strength to
findings from other community studies
(Prince et al, 1997). Any bias obscuring an association between depression and physical health would
therefore have to be specific to vascular disorders, which is an unlikely
situation.
If depression was associated with increased rates of mortality or institutionalisation of people with vascular disease, then associations might be underestimated or missed in this cross-sectional, community-based study. However, the only vascular condition associated with depression was stroke, which would be expected to be one of the most vulnerable to prevalence bias. A shorter duration of depressive episodes in people with vascular disease would be unlikely because vascular disease has, if anything, been reported to be associated with a more prolonged duration of depression (Hickie & Scott, 1998).
A further issue to consider in the light of negative findings is that of statistical power. This study was designed primarily to investigate the association between vascular risk disorders (such as hypertension and diabetes) and cognitive impairment. Negative findings for less-prevalent cardiovascular disorders such as myocardial infarction should be treated with caution because this study would lack the power to detect associations. Possible sources of measurement error (which would reduce the strength of associations) particularly include the less-than-perfect sensitivity/specificity of the depression screen, the use of self-reported diagnoses, the measurement of blood pressure at a single time point and the non-fasting nature of lipid levels. However, upper confidence intervals of odds ratios calculated for the associations between depression and more common disorders such as hypertension or diabetes were small compared with the effects of general physical morbidity and do not suggest the substantial effects that were missed.
Implications for the vascular depression
hypothesis
A significant association was found between stroke and depression in this
study. Although this was a single finding in the context of multiple analyses
and may therefore represent type 1 error, it is consistent with other research
reporting raised rates of depression after stroke
(Pohjasvaara et al,
1998). There is disagreement as to whether increased rates of
major depression within the first few months following stroke are mediated
through pathways of cerebral damage or psychological impact
(Gainotti et al,
1999). Our results suggest that risk of mild to moderate levels of
depression remains raised over a considerably longer period following stroke
in this population and that this is not fully explained by effects on
function. Other possible pathways would include the effect of cerebral damage
but may also involve psychological factors specific to the diagnosis of
stroke. In view of the long period that had elapsed since the last stroke in
most cases, mediating processes can be assumed to be chronic and may
predominantly affect duration rather than incidence of depression.
Despite well-recognised associations between stroke and depression and the increased frequency of magnetic resonance imaging white matter hyperintensities (of suspected ischaemic origin) in older persons with depression (O'Brien et al, 1996), there has been little evidence that vascular risk factors are an important cause of depression at a population level. Two large studies reported no association between blood pressure and depressive symptoms (Friedman & Bennet, 1977; Jones-Webb et al, 1996) and depression is associated with, if anything, low rather than raised lipid levels (Horsten et al, 1997). Increased levels of depression have been described in association with diabetes but it has been suggested that these may largely be accounted for by worse overall physical health and function (Rajala et al, 1997). Many of the risk factors for vascular disease were associated with relative cognitive impairment in this study (results submitted; details available from R.S. upon request), suggesting at least some degree of cerebral effect in at-risk groups. However, there was no evidence to suggest that this degree of effect was associated with depression at a population level in the absence of clinical stroke. The generalisability of results from this study requires consideration:
Public health implications
Poor physical health is well established as a risk factor for depression in
later life. From a public health perspective, the nature of potential
interventions to reduce depression associated with poor health will depend on
how this association is mediated. Effects through cerebrovascular disease and
white matter damage would suggest that interventions should focus on more
rigorous identification and control of vascular risk disorders. However,
effects through the impact of disablement and impaired function would suggest
that more appropriate interventions would be to minimise disablement
associated with physical ill health or to improve psychological adjustment to
disablement. Our findings with respect to stroke suggest a relatively small
but independent impact on depression at a population level compared with
disablement, which requires further investigation. However, with respect to
more commonly occurring conditions, the evidence from both this and other
studies is that, for mild to moderate levels of depression, it is the personal
impact of impaired function that is most important rather than
condition-specific effects.
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Clinical Implications and Limitations |
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LIMITATIONS
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ACKNOWLEDGMENTS |
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Received for publication February 25, 2000. Revision received June 23, 2000. Accepted for publication June 28, 2000.