Effect of communicating DNA based risk assessments for Crohn's disease on smoking cessation: randomised controlled trial.

OBJECTIVE: To test the hypothesis that communicating risk of developing Crohn's disease based on genotype and that stopping smoking can reduce this risk, motivates behaviour change among smokers at familial risk. DESIGN: Parallel group, cluster randomised controlled trial. SETTING: Families with Crohn's disease in the United Kingdom. PARTICIPANTS: 497 smokers (mean age 42.6 (SD 14.4) years) who were first degree relatives of probands with Crohn's disease, with outcomes assessed on 209/251 (based on DNA analysis) and 217/246 (standard risk assessment). INTERVENTION: Communication of risk assessment for Crohn's disease by postal booklet based on family history of the disease and smoking status alone, or with additional DNA analysis for the NOD2 genotype. Participants were then telephoned by a National Health Service Stop Smoking counsellor to review the booklet and deliver brief standard smoking cessation intervention. Calls were tape recorded and a random subsample selected to assess fidelity to the clinical protocol. MAIN OUTCOME MEASURE: The primary outcome was smoking cessation for 24 hours or longer, assessed at six months. RESULTS: The proportion of participants stopping smoking for 24 hours or longer did not differ between arms: 35% (73/209) in the DNA arm versus 36% (78/217) in the non-DNA arm (difference -1%, 95% confidence interval -10% to 8%, P=0.83). The proportion making a quit attempt within the DNA arm did not differ between those who were told they had mutations putting them at increased risk (36%), those told they had none (35%), and those in the non-DNA arm (36%). CONCLUSION: Among relatives of patients with Crohn's disease, feedback of DNA based risk assessments does not motivate behaviour change to reduce risk any more or less than standard risk assessment. These findings accord with those across a range of populations and behaviours. They do not support the promulgation of commercial DNA based tests nor the search for gene variants that confer increased risk of common complex diseases on the basis that they effectively motivate health related behaviour change. TRIAL REGISTRATION: Current Controlled Trials ISRCTN21633644.

Why does genetic causal information alter perceived treatment effectiveness? An analogue study.

OBJECTIVES: When a health problem is perceived as having a genetic cause, this appears to increase the perceived effectiveness of pharmacological treatments and reduce perceived effectiveness of non-pharmacological treatments. Potential mediators of this effect include causal attributions, perceived severity, and perceived control over the health problem. This study aimed to use experimental methods to establish which beliefs mediate the effect of genetic causal information on perceived effectiveness of treatments. DESIGN: A 4(cause: environmental, family history, genetic test, family history & genetic test)×2(severity: higher or low) between-subjects design using vignettes about heart disease risk, obesity or depression. METHODS: A total of 647 adults, randomly assigned to read one of the experimental vignettes, were interviewed. Key outcomes were perceived effectiveness of medication and of non-pharmacological treatments. Potential mediators of perceived severity, perceived controllability, and causal attributions were also assessed. RESULTS: For heart disease risk, genetic causes reduced perceived effectiveness of non-pharmacological treatments (an effect mediated by causal attributions and perceived control) but did not influence perceived medication effectiveness. For obesity, neither severity nor cause influenced the perceived effectiveness of either treatment. For depression, genetic causes only increased perceived effectiveness of medication for more severe depression, an effect mediated by perceived control. CONCLUSIONS: The impact of genetic causal information on perceived effectiveness of treatments varies with type of health problem. When genetic causal information influences perceived treatment effectiveness, it does so by altering causal attributions and perceived controllability. However, these effects are small and unlikely to translate into clinically meaningful differences in health-enhancing behaviours.

Trial Protocol: Communicating DNA-based risk assessments for Crohn's disease: a randomised controlled trial assessing impact upon stopping smoking.

BACKGROUND: Estimates of the risk of developing Crohn's disease (CD) can be made using DNA testing for mutations in the NOD2 (CARD15) gene, family history, and smoking status. Smoking doubles the risk of CD, a risk that is reduced by stopping. CD therefore serves as a timely and novel paradigm within which to assess the utility of predictive genetic testing to motivate behaviour change to reduce the risk of disease. The aim of the study is to describe the impact upon stopping smoking of communicating a risk of developing CD that incorporates DNA analysis. We will test the following main hypothesis:Smokers who are first degree relatives (FDRs) of CD probands are more likely to make smoking cessation attempts following communication of risk estimates of developing CD that incorporate DNA analysis, compared with an equivalent communication that does not incorporate DNA analysis. METHODS/DESIGN: A parallel groups randomised controlled trial in which smokers who are FDRs of probands with CD are randomly allocated in families to undergo one of two types of assessment of risk for developing CD based on either: i. DNA analysis, family history of CD and smoking status, or ii. Family history of CD and smoking status. The primary outcome is stopping smoking for 24 hours or longer in the six months following provision of risk information. The secondary outcomes are seven-day smoking abstinence at one week and six month follow-ups. Randomisation of 470 smoking FDRs of CD probands, with 400 followed up (85%), provides 80% power to detect a difference in the primary outcome of 14% between randomised arms, at the 5% significance level. DISCUSSION: This trial provides one of the strongest tests to date of the impact of communicating DNA-based risk assessment on risk-reducing behaviour change. Specific issues regarding the choice of trial design are discussed.

The impact of numeracy on reactions to different graphic risk presentation formats: An experimental analogue study.

OBJECTIVES: Numeracy, the ability to process basic mathematical concepts, may affect responses to graphical displays of health risk information. Displays of probabilistic risk information using grouped dots are easier to understand than displays using dispersed dots. However, dispersed dots may better convey the randomness with which health threats occur, so increasing perceived susceptibility. We hypothesized that low numeracy participants would better understand risks presented using grouped dot displays, while high numeracy participants would have good understanding, regardless of display type. Moreover, we predicted that dispersed dot displays, in contrast to grouped dot displays, would increase risk perceptions and worry only for highly numerate individuals. DESIGN AND METHOD: One hundred and forty smokers read vignettes asking them to imagine being at risk of Crohn's disease, in a 2(display type: dispersed/grouped dots) x 3(risk magnitude: 3%/6%/50%) x 2(numeracy: high/low) design. They completed measures of risk comprehension, perceived susceptibility and worry. RESULTS: More numerate participants had better objective risk comprehension, but this effect was not moderated by display type. There was marginally significant support for the predicted numeracy x display type interaction for worry about Crohn's disease, but not for perceived susceptibility to the condition. CONCLUSIONS: Dispersed dot displays somewhat increase worry in highly numerate individuals, but only numeracy influenced objective risk comprehension. The most effective display type for communicating risk information will depend on the numeracy of the population and the goal(s) of the communication.