In an Australian community sample of 45 to 64 year olds, who are not currently receiving treatment for depression or anxiety and who are unlikely to have significant cognitive impairment, SMC are common, with a prevalence of 12%. In univariate analysis, the vascular risk factors of diabetes, being a current smoker and treatment for hypercholesterolaemia were associated with SMC. In multivariate analyses, when adjusted for psychological distress and demographics, vascular risk factors showed only weak associations with SMC.. This may be because of the confounding effect of gender and education, with post-hoc analyses showing male gender and less education were strongly associated with the presence of vascular risk factors.
The lack of strong association of vascular risk factors with SMC is consistent with Jorm et al. [3
], who reported that diabetes, 'heart troubles' and a history of strokes were not associated with memory complaints in multivariate analysis, in an Australian sample of community-dwelling 60 to 64 years old with generally good cognition. This is also consistent with Stewart et al. [17
] who found that in an Afro-Caribbean population hypertension, diabetes, electrocardiography-defined ischemia, cholesterol or triglyceride levels were not associated with memory complaints (although having had a stroke was a significant risk).
In contrast to vascular risk factors, there was a strong independent association between psychological distress and SMC. This is consistent with other literature [18
] and may reflect the common depressive symptoms of poor memory and concentration. There may also be a tendency in subjects with significant psychological distress to have a negative attribution bias and therefore over-report memory complaints [36
]. Memory complaints in those with high levels of psychological distress may also represent a common underlying pathophysiology. Depression, for example is now recognised as an independent modifiable risk-factor for cognitive decline [37
] and conversion of MCI to dementia [38
]. Several mechanisms have been postulated for this relationship including the neurotoxic effects of chronic hypercortisolaemia, reduced levels of neurotrophic factors [39
], alterations in glial-neuronal networks, vascular disease and inflammatory processes [40
]. Indeed, older patients with depression have reduced hippocampal size, which in turn, is associated with poorer memory [40
Our data shows a strong association between vascular risk and psychological distress. This is consistent with the literature, where the association between vascular risk factors and depression is well documented [23
]. We hypothesised that psychological distress might mediate any relationship between vascular risk factors and SMC. However, the general lack of associations between vascular risk factors and SMC seen in Model 3 would suggest that any such mediation is minimal. Further exploration of these complex relationships is warranted in longitudinal studies.
There are several strengths of this study. It is the largest study to date that examines the relationship between psychological distress, vascular risk factors and SMC. The questions were all taken from validated questionnaires used extensively in Australian populations. Our finding of a SMC prevalence of 12% is consistent with the community samples from the literature [1
The major limitation of this study is the uncertainty regarding the direction of causality of any observed association: for example, it may be that SMC lead to psychological distress, rather than the other way around. We also cannot correlate the measure of SMC with an objective cognitive assessment. We could not specifically exclude cases of dementia or MCI although by limiting the cohort to those aged less than 65, we are unlikely to have many cases. A recent meta-analysis found a dementia prevalence rate of 0.6% for those aged between 60 and 64 years in Australasia [41
]. Also, the ability to complete, sign and return the questionnaire would exclude those with significant cognitive decline. In any event, as seen with stroke, these cases may be unlikely to dramatically affect the results.
The presence of hypertension and hypercholesterolaemia were determined by the prescription of medication for these conditions. There may therefore be undetected individuals with these vascular risk factors and those receiving treatments for these conditions may paradoxically be at a reduced risk.
Finally, there is the effect of the size of the study. Analyses of such large samples may result in Type I errors. Such studies always result in a trade-off between efficiency and the diminution of measurement errors in a large sample against the ability of such measures to provide valid evaluations at an individual level. Although we do not anticipate any significant bias in the response, the error will serve to reduce the observed estimate of the association. The similar results found in the exploratory and confirmatory datasets strengthen the validity of our conclusions.
All our measures are self-report and as such, our exposure may be subject to information bias, with those people reporting SMC potentially being less likely to recall the presence of vascular risk factors. This would lead us to have underestimated any real association between vascular risk factors and SMC.
The participation rate of the 45 and Up Study was low, at 18% for the first 100, 000 participants. Although this raises questions about the representativeness of the sample, comparison with the NSW Population Health Survey demonstrated good generalisability [42