Impact of communicating genetic and phenotypic risk of coronary heart disease on health-related behaviour: the INFORM randomised controlled trial

Talk Code: 
Barbora Silarova
Barbora Silarova, Stephen J Sharp, Adam S Butterworth, Emanuele Di Angelantonio, Christine Girling, Kathryn Lawrence, Joanne Lucas, Carmel Moore, Rupert A Payne, Guy Shefer, Zoe Tolkien, Juliet Usher-Smith, Matthew Walker, John Danesh, Simon Griffin
Author institutions: 
MRC Epidemiology Unit, University of Cambridge, Institute of Metabolic Science, Cambridge, CB2 0QQ, UK, Department of Public Health and Primary Care, Strangeways Research Laboratory, Wort’s Causeway, Cambridge, CB1 8RN, UK


Identification of individuals at high risk of coronary heart disease (CHD) using risk scores enables efficient targeting of preventive interventions and is a key component of many primary prevention strategies such as NHS Health Checks. Limitations of previous studies have prevented reliable inference about the benefits and harms of providing individuals with information about their genetic and phenotypic risk of CHD. We aimed to quantify the short-term effects of provision of phenotypic and genetic CHD risk information, alongside lifestyle advice, on change in objectively-measured health behaviours and cardiovascular risk factors.


In a parallel-group, open randomised trial, we allocated 953 male and female blood donors (mean (SD) age = 56.7 (8.8)) with no previous history of CHD to either no intervention (control group, n= 237) or to one of three active intervention groups: i) web-based lifestyle advice only (n= 239); ii) lifestyle advice plus information on estimated 10-year CHD risk based on phenotypic characteristics (n= 239); and iii) lifestyle advice plus information on estimated 10-year CHD risk based on phenotypic and genetic characteristics (n= 238). The primary outcome was change in physical activity from baseline to 12 weeks (measured by Axivity Accelerometer®). Secondary outcomes included: cardiovascular risk factors; perceived risk; and psychological outcomes.


926 (97%) participants completed the trial. There were no significant intervention effects on physical activity defined as average acceleration over the observation period (difference in adjusted mean change from baseline): group with lifestyle advice only vs control group 0.08 m/s2 (95% CI -1.14 to 1.30); genetic group vs phenotypic group -0.36 m/s2 (95% CI -1.57 to 0.86); phenotypic group and genetic group vs. control group -0.56 m/s2 (95% CI -1.62 to 0.49) and phenotypic group and genetic group vs. lifestyle group -0.64 m/s2 (95% CI -1.69 to 0.41). Provision of lifestyle advice alone and alongside risk information was associated with increases in self-reported fruit and vegetable intake (difference in adjusted mean change from baseline): lifestyle advice vs control group 0.61 servings/day (95% CI 0.39 to 0.83); phenotypic group and genetic group vs. control group 0.47 servings/day (95% CI 0.28 to 0.67) with no differences between genetic and phenotypic risk information. There were no significant differences in cardiovascular risk factors, perceived risk; and psychological outcomes between trial groups.


Provision of CHD risk information alone (either based on phenotype or genotype) is unlikely to enhance preventive strategies but neither does it cause psychological harm in the short-term. Provision of lifestyle advice alone or alongside CHD risk information might improve fruit and vegetable intake. We will interpret this finding in the light of data for change in plasma carotenoids (an objective measure of fruit and vegetable intake) which we will present at the meeting.

Submitted by: 
Barbora Silarova
Funding acknowledgement: 
INFORM is funded by European Commission Framework 7 EPIC-CVD Grant agreement no: 279233. NHS Blood and Transplant funded the INTERVAL trial. DNA extraction and genotyping in INTERVAL/INFORM was funded by the UK National Institute of Health Research. The coordinating team for INTERVAL/INFORM at the Cardiovascular Epidemiology Unit of the University of Cambridge was supported by core funding from: UK Medical Research Council (G0800270), British Heart Foundation (SP/09/002), British Heart Foundation Cambridge Cardiovascular Centre of Excellence, and UK National Institute for Health Research Cambridge Biomedical Research Centre.