title: Effect of Alzheimer disease genetic risk disclosure on dietary supplement use.
abstract: BACKGROUND
  Genetic susceptibility testing for Alzheimer disease (AD) with APOE genotype disclosure is not recommended for clinical use but is available through direct-to-consumer (DTC) genetic testing companies. Little is known about whether APOE genotype disclosure would actually prompt changes in nutrition behaviors among at-risk individuals.
  
  
  OBJECTIVE
  We studied the effect of APOE genotype disclosure for AD risk assessment on dietary supplement use in adults with a family history of AD.
  
  
  METHODS
  As part of a secondary analysis of data from the second Risk Evaluation and Education for Alzheimer's Disease Study, we examined the effect of genotype disclosure on health-behavior changes among 272 unaffected first-degree relatives of persons with AD.
  
  
  RESULTS
  Overall, 16% of all participants reported a change in dietary supplement use after AD risk assessment. Participants who learned that they had at least one copy of the risk-increasing epsilon4 allele (epsilon4+) had 4.75 times the odds of reporting a change in dietary supplement use than did their counterparts who had an absence of the risk-increasing epsilon4 allele (epsilon4-) (95% CI: 2.23, 10.10; P < 0.0001) after adjustment for age, sex, race, baseline supplement use, randomization arm, and educational level. There were no significant differences between APOE epsilon4+ and epsilon4- participants in changes in overall diet, exercise, or medications.
  
  
  CONCLUSIONS
  In this sample of first-degree relatives receiving genetic susceptibility testing for AD, an APOE epsilon4+ genotype status was positively associated with dietary supplement use after risk disclosure. Such changes occurred despite the absence of evidence that supplement use reduces the risk of AD. Given the expansion of DTC genetic tests, this study highlights the need for future studies in disease risk communication.
authors.affiliation: Department of Neurology, Boston University School of Public Health, Boston, MA, USA. jvern@psu.edu
authors.forename: Jacqueline A
authors.initials: JA
authors.lastname: Vernarelli
authors.forename: J Scott
authors.initials: JS
authors.lastname: Roberts
authors.forename: Susan
authors.initials: S
authors.lastname: Hiraki
authors.forename: Clara A
authors.initials: CA
authors.lastname: Chen
authors.forename: L Adrienne
authors.initials: LA
authors.lastname: Cupples
authors.forename: Robert C
authors.initials: RC
authors.lastname: Green
mesh_terms: D000368:Aged; D000544:Alzheimer Disease / Q000453:epidemiology / Q000235:genetics*; D053327:Apolipoprotein E4 / Q000235:genetics*; D044383:Black People / Q000235:genetics; D019587:Dietary Supplements / Q000032:analysis* / Q000706:statistics & numerical data; D004522:Educational Status; D005190:Family; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D008297:Male; D008875:Middle Aged; D011897:Random Allocation; D018570:Risk Assessment; D012307:Risk Factors; D044465:White People / Q000235:genetics
chemical_list: D053327:Apolipoprotein E4