Tests can now be conducted in which DNA is analysed to estimate the chance of developing diseases such as heart disease or lung cancer in smokers. It was thought that risk estimates derived from these genetic tests may motivate people to change their behaviour in order to reduce the identified risks. In the current review, we assessed the effect of communicating disease risk estimates from genetic tests on risk-reducing behaviours and motivation to undertake such behaviours.
A systematic search located 14 papers reporting the results of 13 eligible studies: seven clinical studies and six analogue studies (studies in which participants are given hypothetical scenarios asking them to imagine receiving genetic test based disease risk estimates).
Five clinical studies assessed smoking cessation, with statistical combination of the results revealing no statistically significant effects on smoking cessation in either the short-term (< six months) or long term (> six months). Two clinical studies assessed dietary behaviour and showed that communicating genetic test-based risk estimates did change people's behaviour.The two studies assessing physical activity and the one study assessing medication or vitamin use aimed at reducing disease risks did not show that communicating DNA-based disease risk estimates had an effect on behaviour.
For the six analogue studies, statistical combination of the results revealed a statistically significant effect of genetic test based disease risk estimates on intention to change behaviour only. There was no evidence of any unintended detrimental effects on motivation or mood.
In summary, the limited amount and quality of evidence currently available suggests that communicating genetic test based disease risk estimates may have little or no effect on behaviour, but may have a small effect on intentions to change behaviour. Larger and better quality trials are needed.
Mindful of the weak evidence based on a small number of studies of limited quality, the results of this review suggest that communicating DNA-based disease risk estimates has little or no effect on smoking and physical activity. It may have a small effect on self-reported diet and on intentions to change behaviour. Claims that receiving DNA-based test results motivates people to change their behaviour are not supported by evidence. Larger and better-quality RCTs are needed.
There are high expectations regarding the potential for the communication of DNA-based disease risk estimates to motivate behaviour change.
To assess the effects of communicating DNA-based disease risk estimates on risk-reducing behaviours and motivation to undertake such behaviours.
We searched the following databases using keywords and medical subject headings: Cochrane Central Register of Controlled Trials (CENTRAL, The Cochrane Library, Issue 4 2010), MEDLINE (1950 to April 2010), EMBASE (1980 to April 2010), PsycINFO (1985 to April 2010) using OVID SP, and CINAHL (EBSCO) (1982 to April 2010). We also searched reference lists, conducted forward citation searches of potentially eligible articles and contacted authors of relevant studies for suggestions. There were no language restrictions. Unpublished or in press articles were eligible for inclusion.
Randomised or quasi-randomised controlled trials involving adults (aged 18 years and over) in which one group received actual (clinical studies) or imagined (analogue studies) personalised DNA-based disease risk estimates for diseases for which the risk could plausibly be reduced by behavioural change. Eligible studies had to include a primary outcome measure of risk-reducing behaviour or motivation (e.g. intention) to alter such behaviour.
Two review authors searched for studies and independently extracted data. We assessed risk of bias according to the Cochrane Handbook for Systematic Reviews of Interventions. For continuous outcome measures, we report effect sizes as standardised mean differences (SMDs). For dichotomous outcome measures, we report effect sizes as odds ratios (ORs). We obtained pooled effect sizes with 95% confidence intervals (CIs) using the random effects model applied on the scale of standardised differences and log odds ratios.
We examined 5384 abstracts and identified 21 studies as potentially eligible. Following a full text analysis, we included 14 papers reporting results of 7 clinical studies (2 papers report on the same trial) and 6 analogue studies.
Of the seven clinical studies, five assessed smoking cessation. Meta-analyses revealed no statistically significant effects on either short-term (less than 6 months) smoking cessation (OR 1.35, 95% CI 0.76 to 2.39, P = 0.31, n = 3 studies) or cessation after six months (OR 1.07, 95% CI 0.64 to 1.78, P = 0.80, n = 4 studies). Two clinical studies assessed diet and found effects that significantly favoured DNA-based risk estimates (OR 2.24, 95% CI 1.17 to 4.27, P = 0.01). No statistically significant effects were found in the two studies assessing physical activity (OR 1.03, 95% CI 0.59 to 1.80, P = 0.92) or the one study assessing medication or vitamin use aimed at reducing disease risks (OR 1.26, 95% CI 0.58 to 2.72, P = 0.56).
For the six non-clinical analogue studies, meta-analysis revealed a statistically significant effect of DNA-based risk on intention to change behaviour (SMD 0.16, 95% CI 0.04 to 0.29, P = 0.01).
There was no evidence that communicating DNA-based disease risk estimates had any unintended adverse effects. Two studies that assessed fear arousal immediately after the presentation of risk information did, however, report greater fear arousal in the DNA-based disease risk estimate groups compared to comparison groups.
The quality of included studies was generally poor. None of the clinical or analogue studies were considered to have a low risk of bias, due to either a lack of clarity in reporting, or where details were reported, evidence of a failure to sufficiently safeguard against the risk of bias.