The impact of genetic testing for Crohn's disease, risk magnitude and graphical format on motivation to stop smoking: an experimental analogue study.

Genetic tests may motivate risk-reducing behaviour more than other types of tests because they generate higher risk magnitudes and because their results have high personal relevance. To date, trial designs have not allowed the disentangling of the effects of these two factors. This analogue study examines the independent impacts of risk magnitude and provenance, and of risk display type, on motivation to quit smoking. A total of 180 smokers were randomly allocated to one of the 18 Crohn's disease risk vignettes in a 3 (risk provenance: family history. genetic test mutation positive. genetic test mutation negative) x 3 (risk magnitude: 3%, 6%, 50%) x 2 (display: grouped or dispersed icons) design. The 50% group had significantly higher intentions to quit than the 3% group. A significant risk provenance x magnitude interaction showed that participants in 50% or 6% groups were equally motivated, regardless of risk provenance, while participants in the 3% group had higher intentions associated with a mutation negative result than with a result based on family history alone. Grouped icon displays were more motivating than the dispersed icons. Using genetic tests to estimate risks of common complex conditions may not motivate behaviour change beyond the impact of the numerical risk estimates derived from such tests.

Estimating risks of common complex diseases across genetic and environmental factors: the example of Crohn disease.

BACKGROUND: Progress has been made in identifying mutations that confer susceptibility to complex diseases, with the prospect that these genetic risks might be used in determining individual disease risk. AIM: To use Crohn disease (CD) as a model of a common complex disorder, and to develop methods to estimate disease risks using both genetic and environmental risk factors. METHODS: The calculations used three independent risk factors: CARD15 genotype (conferring a gene dosage effect on risk), smoking (twofold increased risk for smokers), and residual familial risk (estimating the effect of unidentified genes, after accounting for the contribution of CARD15). Risks were estimated for high-risk people who are siblings, parents and offspring of a patient with CD. RESULTS: The CD risk to the sibling of a patient with CD who smokes and carries two CARD15 mutations is approximately 35%, which represents a substantial increase on the population risk of 0.1%. In contrast, the risk to a non-smoking sibling of a patient with CD who carries no CARD15 mutations is 2%. Risks to parents and offspring were lower. CONCLUSIONS: High absolute risks of CD disease can be obtained by incorporating information on smoking, family history and CARD15 mutations. Behaviour modification through smoking cessation may reduce CD risk in these people.