Common-sense beliefs about the prevention of Alzheimer's disease

Abstract

Objectives: Common-sense illness beliefs are important because they influence actions that people take to prevent and treat disease. This research (1) asked younger and older adults about their illness representations of Alzheimer's disease (AD) and (2) manipulated beliefs about AD preventability to determine causal relationships in the data.

Method: In Study 1, the beliefs of younger (age 18–38; n = 82) and older (age 58–89; n = 57) adults about the causes of and ways to prevent AD were compared. In Study 2, younger adults were randomly assigned to read information stating either that AD can be prevented or not.

Results: Compared to younger adults, older adults saw themselves as less at risk, t(137) = 3.03, p = 0.003, d = 0.52, were more likely to believe that AD is preventable, t(137) = 5.01, p < 0.001, d = 0.87 and were more likely to report engaging in behaviors to prevent AD, χ ²(1, 139) = 19.01, p < 0.001, r = 0.37. Manipulating beliefs in Study 2 caused those told that AD was preventable to see themselves as less at risk, report more prevention behaviors, and hold those with the disease more responsible for their fate.

Conclusion: These findings highlight the association of illness representations with reports of behavior and show a disconnect between beliefs and what we currently know about AD.

Keywords:

• dementia
• illness perceptions
• risk judgments

Notes

Notes

1. Given the high prevalence of AD in the population (e.g., 24% of adults over age 80 will have AD; Plassman et al., 2007), the level of exposure to AD for our younger adults is not overly surprising. It is probably normative for young adults to have some experience with a family member with impairment (especially given that young adults are likely to have grandparents, great-aunts and uncles, and many may have great-grandparents still living). In our study, asking for family history means that respondents are reporting family prevalence summed over several family members, and so the percentage should be higher than individual population prevalence figures. Thus, we have no reason to believe that our sample of younger adults is different from the general population with regard to AD exposure. In terms of the older sample, it is likely that even in cases of cognitive impairment, many of their older family members did not receive an AD diagnosis (i.e., it was called ‘senility,’ or the individuals died of some other cause before AD could manifest itself), so rates among the older sample may be underestimated. In addition, current generations of older adults are living longer than previous generations, and AD prevalence increases with age, so older adults may have had fewer relatives who lived to ages that put the relatives at the greatest risk for AD.

2. As noted earlier, younger adults reported more family history of AD than did older adults, and family history was correlated with risk judgments (but not with any other measures). Therefore, we also conducted an analysis of covariance on the risk judgments, controlling for family history. Although the effect sizes were reduced, age remained a significant predictor of both absolute (d = 0.51) and comparative (d = 0.48) risk.

3. Due to the wide range of educational attainment in our older sample, we explored the possibility that education could impact beliefs about personal risk. Education did not correlate significantly with absolute (r = −0.099, p = 0.47) or comparative risk perceptions (r = −0.102, p = 0.45); the older sample remained convinced that they are at low risk regardless of education level.