title: Effect of communicating genetic and phenotypic risk for type 2 diabetes in combination with lifestyle advice on objectively measured physical activity: protocol of a randomised controlled trial Impact of direct-to-consumer genomic testing at long term follow-up Utility of genetic and non-genetic risk factors in prediction of type 2 diabetes: Whitehall II prospective cohort study A randomized trial of the clinical utility of genetic testing for obesity: Design and implementation considerations Personalized Genetic Risk Counseling to Motivate Diabetes Prevention The Cochrane Collaboration’s tool for assessing risk of bias in randomised trials Impact of Delivery Models on Understanding Genomic Risk for Type 2 Diabetes Behavioral Consequences of Testing for Obesity Risk Disclosure of Genetic Information and Change in Dietary Intake: A Randomized Controlled Trial Genetic Susceptibility Testing and Readiness to Control Weight: Results from a Randomized Controlled Trial Personalized Nutrition by Prediction of Glycemic Responses Design and baseline characteristics of the Food4Me study: a web-based randomised controlled trial of personalised nutrition in seven European countries Information and Risk Modification Trial (INFORM): design of a randomised controlled trial of communicating different types of information about coronary heart disease risk, alongside lifestyle advice, to achieve change in health-related behaviour Psychological impact of genetic testing for familial hypercholesterolemia within a previously aware population: A randomized controlled trial Does Type 2 Diabetes Genetic Testing and Counseling Reduce Modifiable Risk Factors? A Randomized Controlled Trial of Veterans The clinical application of genetic testing in type 2 diabetes: a patient and physician survey Psychological responses to genetic testing for weight gain: a vignette study. Why prospective registration of systematic reviews makes sense
abstract: Type 2 diabetes ( T2D ) is associated with increased risk of morbidity and premature mortality . Among those at high risk , incidence can be halved through healthy changes in behaviour . Information about genetic and phenotypic risk of T2D is now widely available . Whether such information motivates behaviour change is unknown . We aim to assess the effects of communicating genetic and phenotypic risk of T2D on risk-reducing health behaviours , anxiety , and other cognitive and emotional theory-based antecedents of behaviour change . In a parallel group , open r and omised controlled trial , approximately 580 adults born between 1950 and 1975 will be recruited from the on-going population -based , observational Fenl and Study ( Cambridgeshire , UK ) . Eligible participants will have undergone clinical , anthropometric , and psychosocial measurements , been genotyped for 23 single-nucleotide polymorphisms associated with T2D , and worn a combined heart rate monitor and accelerometer ( Actiheart ® ) continuously for six days and nights to assess physical activity .  Participants are r and omised to receive either st and ard lifestyle advice alone ( control group ) , or in combination with a genetic or a phenotypic risk estimate for T2D ( intervention groups ) . The primary outcome is objective ly measured physical activity . Secondary outcomes include self-reported diet , self-reported weight , intention to be physically active and to engage in a healthy diet , anxiety , diabetes-related worry , self-rated health , and other cognitive and emotional outcomes . Follow-up occurs eight weeks post-intervention . Values at follow-up , adjusted for baseline , will be compared between r and omised groups . This study will provide much needed evidence on the effects of providing information about the genetic and phenotypic risk of T2D . Importantly , it will be among the first to examine the impact of genetic risk information using a r and omised controlled trial design , a population -based sample , and an objective ly measured behavioural outcome . Results of this trial , along with recent evidence syntheses of similar studies , should inform policy concerning the availability and use of genetic risk information . Current Controlled Trials IS RCT Background There are few empirical data to inform the debate surrounding the use and regulation of direct-to-consumer ( DTC ) genome-wide disease risk tests . This study aim ed to determine the long term psychological , behavioural , and clinical impacts of genomic risk testing for common disease . Methods The Scripps Genomic Health Initiative is a prospect i ve longitudinal cohort study of adults who purchased the Navigenics Health Compass , a commercially available genomic test . Web based assessment s were administered at baseline , short ( 3 months ) , and long term ( 1 year ) follow-up . Results 2240 participants completed either or both follow-ups and a subset of 1325 completed long term follow-up . There were no significant differences from baseline in anxiety ( p=0.50 ) , fat intake ( p=0.34 ) , or exercise ( p=0.39 ) at long term follow-up , and 96.8 % of the sample had no test related distress . Longitudinal linear mixed model analyses were consistent with results of cross-sectional analyses . Screening test completion was associated with sharing genomic test results with a physician ( 36.0 % shared ; p<0.001 ) and perceived utility of the test ( 61.5 % high perceived utility ; p=0.002 ) , but was not associated with the genomic risk estimate values themselves . Conclusions Over a third of DTC genomic test recipients shared their results with their own physician during an approximate 1 year follow-up period , and this sharing was associated with higher screening test completion . Genomic testing was not associated with long term psychological risks , and most participants reportedly perceived the test to be of high personal utility Objectives To assess the performance of a panel of common single nucleotide polymorphisms ( genotypes ) associated with type 2 diabetes in distinguishing incident cases of future type 2 diabetes ( discrimination ) , and to examine the effect of adding genetic information to previously vali date d non-genetic ( phenotype based ) models developed to estimate the absolute risk of type 2 diabetes . Design Workplace based prospect i ve cohort study with three 5 yearly medical screenings . Participants 5535 initially healthy people ( mean age 49 years ; 33 % women ) , of whom 302 developed new onset type 2 diabetes over 10 years . Outcome measures Non-genetic variables included in two established risk models — the Cambridge type 2 diabetes risk score ( age , sex , drug treatment , family history of type 2 diabetes , body mass index , smoking status ) and the Framingham offspring study type 2 diabetes risk score ( age , sex , parental history of type 2 diabetes , body mass index , high density lipoprotein cholesterol , triglycerides , fasting glucose)— and 20 single nucleotide polymorphisms associated with susceptibility to type 2 diabetes . Cases of incident type 2 diabetes were defined on the basis of a st and ard oral glucose tolerance test , self report of a doctor ’s diagnosis , or the use of anti-diabetic drugs . Results A genetic score based on the number of risk alleles carried ( range 0 - 40 ; area under receiver operating characteristics curve 0.54 , 95 % confidence interval 0.50 to 0.58 ) and a genetic risk function in which carriage of risk alleles was weighted according to the summary odds ratios of their effect from meta-analyses of genetic studies ( area under receiver operating characteristics curve 0.55 , 0.51 to 0.59 ) did not effectively discriminate cases of diabetes . The Cambridge risk score ( area under curve 0.72 , 0.69 to 0.76 ) and the Framingham offspring risk score ( area under curve 0.78 , 0.75 to 0.82 ) led to better discrimination of cases than did genotype based tests . Adding genetic information to phenotype based risk models did not improve discrimination and provided only a small improvement in model calibration and a modest net reclassification improvement of about 5 % when added to the Cambridge risk score but not when added to the Framingham offspring risk score . Conclusion The phenotype based risk models provided greater discrimination for type 2 diabetes than did models based on 20 common independently inherited diabetes risk alleles . The addition of genotypes to phenotype based risk models produced only minimal improvement in accuracy of risk estimation assessed by recalibration and , at best , a minor net reclassification improvement . The major translational application of the currently known common , small effect genetic variants influencing susceptibility to type 2 diabetes  is likely to come from the insight they provide on causes of disease and potential therapeutic targets Background Obesity rates in the United States have escalated in recent decades and present a major challenge in public health prevention efforts . Currently , testing to identify genetic risk for obesity is readily available through several direct-to-consumer companies . Despite the availability of this type of testing , there is a paucity of evidence as to whether providing people with personal genetic information on obesity risk will facilitate or impede desired behavioral responses . Purpose We describe the key issues in the design and implementation of a r and omized controlled trial examining the clinical utility of providing genetic risk information for obesity . Methods Participants are being recruited from the Coriell Personalized Medicine Collaborative , an ongoing , longitudinal research cohort study design ed to determine the utility of personal genome information in health management and clinical decision making . The primary focus of the ancillary Obesity Risk Communication Study is to determine whether genetic risk information added value to traditional communication efforts for obesity , which are based on lifestyle risk factors . The trial employs a 2 × 2 factorial design in order to examine the effects of providing genetic risk information for obesity , alone or in combination with lifestyle risk information , on participants ’ psychological responses , behavioral intentions , health behaviors , and weight . Results The factorial design generated four experimental arms based on communication of estimated risk to participants : ( 1 ) no risk feedback ( control ) , ( 2 ) genetic risk only , ( 3 ) lifestyle risk only , and ( 4 ) both genetic and lifestyle risk ( combined ) . Key issues in study design pertained to the selection of algorithms to estimate lifestyle risk and determination of information to be provided to participants assigned to each experimental arm to achieve a balance between clinical st and ards and method ological rigor . Following the launch of the trial in September 2011 , implementation challenges pertaining to low enrollment and differential attrition became apparent and required immediate attention and modifications to the study protocol . Although monitoring of these efforts is ongoing , initial observations show a doubling of enrollment and reduced attrition . Limitations The trial is evaluating the short-term impact of providing obesity risk information as participants are followed for only 3 months . This study is built upon the structure of an existing personalized medicine study wherein participants have been provided with genetic information for other diseases . This nesting in a larger study may attenuate the effects of obesity risk information and has implication s for the generalizability of study findings . Conclusions This r and omized trial examines value of obesity genetic information , both when provided independently and when combined with lifestyle risk assessment , to motivate individuals to engage in healthy lifestyle behaviors . Study findings will guide future intervention efforts to effectively communicate genetic risk information OBJECTIVE To examine whether diabetes genetic risk testing and counseling can improve diabetes prevention behaviors . RESEARCH DESIGN AND METHODS We conducted a r and omized trial of diabetes genetic risk counseling among overweight patients at increased phenotypic risk for type 2 diabetes . Participants were r and omly allocated to genetic testing versus no testing . Genetic risk was calculated by summing 36 single nucleotide polymorphisms associated with type 2 diabetes . Participants in the top and bottom score quartiles received individual genetic counseling before being enrolled with untested control participants in a 12-week , vali date d , diabetes prevention program . Middle-risk quartile participants were not studied further . We examined the effect of this genetic counseling intervention on patient self-reported attitudes , program attendance , and weight loss , separately comparing higher-risk and lower-risk result recipients with control participants . RESULTS The 108 participants enrolled in the diabetes prevention program included 42 participants at higher diabetes genetic risk , 32 at lower diabetes genetic risk , and 34 untested control subjects . Mean age was 57.9 ± 10.6 years , 61 % were men , and average BMI was 34.8 kg/m2 , with no differences among r and omization groups . Participants attended 6.8 ± 4.3 group sessions and lost 8.5 ± 10.1 pounds , with 33 of 108 ( 30.6 % ) losing ≥5 % body weight . There were few statistically significant differences in self-reported motivation , program attendance , or mean weight loss when higher-risk recipients and lower-risk recipients were compared with control subjects ( P > 0.05 for all but one comparison ) . CONCLUSIONS Diabetes genetic risk counseling with currently available variants does not significantly alter self-reported motivation or prevention program adherence for overweight individuals at risk for diabetes Flaws in the design , conduct , analysis , and reporting of r and omised trials can cause the effect of an intervention to be underestimated or overestimated . The Cochrane Collaboration ’s tool for assessing risk of bias aims to make the process clearer and more Background : Genetic information , typically communicated in-person by genetic counselors , can be challenging to comprehend ; delivery of this information online - as is becoming more common - has the potential of increasing these challenges . Methods : To address the impact of the mode of delivery of genomic risk information , 300 individuals were recruited from the general public and r and omized to receive genomic risk information for type 2 diabetes mellitus in-person from a board-certified genetic counselor or online through the testing company 's website . Results : Participants were asked to indicate their genomic risk and overall lifetime risk as reported on their test report as well as to interpret their genomic risk ( increased , decreased , or same as population ) . For each question , 59 % of participants correctly indicated their risk . Participants who received their results in-person were more likely than those who review ed their results on-line to correctly interpret their genomic risk ( 72 vs. 47 % , p = 0.0002 ) and report their actual genomic risk ( 69 vs. 49 % , p = 0.002 ) . Conclusions : The delivery of personal genomic risk through a trained health professional result ed in significantly higher comprehension . Therefore , if the online delivery of genomic test results is to become more widespread , further evaluation of this method of communication may be needed to ensure the effective presentation of results to promote comprehension Objective : There is considerable hope that genetic susceptibility testing will motivate behavior that can prevent or reduce the risk of complex conditions such as obesity . This study examined potential behavioral consequences of such testing . Methods : Participants ( n = 249 ) were r and omly assigned to review one of four vignettes that asked them to imagine that they had been tested for their risk of becoming overweight or obese . The experimental factors were test type ( genetic versus hormone test ) and risk level ( increased versus average risk for obesity ) . Study measures included  behavioral intentions and perceived behavioral control related to eating a healthy diet  , as well as  weight locus of control .  Results : Participants assigned to the increased risk conditions indicated greater intentions to eat a healthy diet compared with participants assigned to the average risk conditions ( P < 0.02 ) . There were significant interaction effects of risk × perceived behavioral control ( P < 0.02 ) and risk × weight locus of control ( P < 0.003 ) on dietary intentions . Individuals with low perceived behavioral control or an external weight locus of control who were told to imagine they were at average risk expressed significantly lower intentions to eat a healthy diet . A three-way interaction of body mass index , family history of overweight/obesity , and assigned risk level found the greatest effects of risk feedback among those who either had a family history or a higher body mass index ( P < 0.007 ) . Conclusion : This study provides preliminary evidence that testing for susceptibility to obesity may motivate healthier behavior . However , some individuals may be susceptible to a false reassurance effect after receiving test results indicating a lack of increased risk Background Proponents of consumer genetic tests cl aim that the information can positively impact health behaviors and aid in chronic disease prevention . However , the effects of disclosing genetic information on dietary intake behavior are not clear . Methods A double-blinded , parallel group , 2∶1 online r and omized controlled trial was conducted to determine the short- and long-term effects of disclosing nutrition-related genetic information for personalized nutrition on dietary intakes of caffeine , vitamin C , added sugars , and sodium . Participants were healthy men and women aged 20–35 years ( n = 138 ) . The intervention group ( n = 92 ) received personalized DNA-based dietary advice for 12-months and the control group ( n = 46 ) received general dietary recommendations with no genetic information for 12-months .  Food frequency question naires were collected at baseline and 3- and 12-months after the intervention to assess dietary intakes . General linear models were used to compare changes in intakes between those receiving general dietary advice and those receiving DNA-based dietary advice . Results Compared to the control group , no significant changes to dietary intakes of the nutrients were observed at 3-months . At 12-months , participants in the intervention group who possessed a risk version of the ACE gene , and were advised to limit their sodium intake , significantly reduced their sodium intake ( mg/day ) compared to the control group ( −287.3±114.1 vs. 129.8±118.2 , p = 0.008 ) . Those who had the non-risk version of ACE did not significantly change their sodium intake compared to the control group ( 12-months : −244.2±150.2 , p = 0.11 ) . Among those with the risk version of the ACE gene , the proportion who met the targeted recommendation of 1500 mg/day increased from 19 % at baseline to 34 % after 12 months ( p = 0.06 ) . Conclusions These findings demonstrate that disclosing genetic information for personalized nutrition results in greater changes in intake for some dietary components compared to general population -based dietary advice . Trial Registration Clinical Trials.gov Objective To test the hypothesis that adding obesity gene feedback ( FTO ) to simple weight control advice at a life stage with raised risk of weight gain ( university ) increases readiness to control weight . Methods Individually r and omized controlled trial comparing the effect of : ( i ) simple weight control advice plus FTO feedback ( FA ) and ( ii ) simple weight control advice only ( AO ) on readiness to engage with weight control . Differences in stage of change by genotype and differential weight control behaviors were secondary outcomes . Results Of 1,016 participants r and omized , only 279 completed follow-up , yielding 90 % power to detect a small effect for readiness to control weight . As predicted , FA participants were more likely to be in the contemplation stage than AO participants ( P = 0.023 ) . Participants receiving higher-risk genetic results were at a higher stage of change than controls ( P = 0.003 ) , with a trend toward a higher stage of change than those getting lower-risk results ( P = 0.051 ) . Lower-risk results did not decrease weight control intentions compared with controls ( P = 0.55 ) . There were no group differences in adherence to recommended weight control behaviors ( P = 0.87 ) . Conclusions Adding FTO feedback to weight control advice enhanced readiness to control weight , without evidence for genetic determinism , but had no more effect on behavior than weight control advice alone Elevated postpr and ial blood glucose levels constitute a global epidemic and a major risk factor for prediabetes and type II diabetes , but existing dietary methods for controlling them have limited efficacy . Here , we continuously monitored week-long glucose levels in an 800-person cohort , measured responses to 46,898 meals , and found high variability in the response to identical meals , suggesting that universal dietary recommendations may have limited utility . We devised a machine-learning algorithm that integrates blood parameters , dietary habits , anthropometrics , physical activity , and gut microbiota measured in this cohort and showed that it accurately predicts personalized postpr and ial glycemic response to real-life meals . We vali date d these predictions in an independent 100-person cohort . Finally , a blinded r and omized controlled dietary intervention based on this algorithm result ed in significantly lower postpr and ial responses and consistent alterations to gut microbiota configuration . Together , our results suggest that personalized diets may successfully modify elevated postpr and ial blood glucose and its metabolic consequences . VIDEO ABSTRACT Abstract Improving lifestyle behaviours has considerable potential for reducing the global burden of non-communicable diseases , promoting better health across the life-course and increasing well-being . However , realising this potential will require the development , testing and implementation of much more effective behaviour change interventions than are used conventionally . Therefore , the aim of this study was to conduct a multi-centre , web-based , proof-of-principle study of personalised nutrition ( PN ) to determine whether providing more personalised dietary advice leads to greater improvements in eating patterns and health outcomes compared to conventional population -based advice . A total of 5,562 volunteers were screened across seven European countries ; the first 1,607 participants who fulfilled the inclusion criteria were recruited into the trial . Participants were r and omly assigned to one of the following intervention groups for a 6-month period : Level 0—control group — receiving conventional , non-PN advice ; Level 1—receiving PN advice based on dietary intake data alone ; Level 2—receiving PN advice based on dietary intake and phenotypic data ; and Level 3—receiving PN advice based on dietary intake , phenotypic and genotypic data . A total of 1,607 participants had a mean age of 39.8 years ( ranging from 18 to 79 years ) . Of these participants , 60.9 % were women and 96.7 % were from white-European background .  The mean BMI for all r and omised participants was 25.5 kg m−2 , and 44.8 % of the participants had a BMI ≥ 25.0 kg m−2 . Food4Me is the first large multi-centre RCT of web-based PN . The main outcomes from the Food4Me study will be su bmi tted for publication during 2015 Background Cardiovascular disease ( CVD ) remains the leading cause of death globally . Primary prevention of CVD requires cost-effective strategies to identify individuals at high risk in order to help target preventive interventions . An integral part of this approach is the use of CVD risk scores . Limitations in previous studies have prevented reliable inference about the potential advantages and the potential harms of using CVD risk scores as part of preventive strategies . We aim to evaluate short-term effects of providing different types of information about coronary heart disease ( CHD ) risk , alongside lifestyle advice , on health-related behaviours . Methods / Design In a parallel-group , open r and omised trial , we are allocating 932 male and female blood donors with no previous history of CVD aged 40–84 years in Engl and to either no intervention ( control group ) or to one of three active intervention groups : i ) lifestyle advice only ; ii ) lifestyle advice plus information on estimated 10-year CHD risk based on phenotypic characteristics ; and iii ) lifestyle advice plus information on estimated 10-year CHD risk based on phenotypic and genetic characteristics . The primary outcome is change in objective ly measured physical activity . Secondary outcomes include : objective ly measured dietary behaviours ; cardiovascular risk factors ; current medication and healthcare usage ; perceived risk ; cognitive evaluation of provision of CHD risk scores ; and psychological outcomes . The follow-up assessment takes place 12 weeks after r and omisation . The experiences , attitudes and concerns of a subset of participants will be also studied using individual interviews and focus groups . Discussion The INFORM study has been design ed to provide robust findings about the short-term effects of providing different types of information on estimated 10-year CHD risk and lifestyle advice on health-related behaviours . Trial registration Current Controlled Trials IS RCT N17721237 . Registered 12 January 2015 This trial tests the hypothesis that confirming a clinical diagnosis of familial hypercholesterolemia ( FH ) by finding a genetic mutation reduces patients ' perceptions of control over the disease and adherence to risk‐reducing behaviors . Three hundred forty‐one families , comprising 341 hypercholesterolemia prob and s and 128 adult relatives , were r and omized to one of two groups : ( a ) routine clinical diagnosis ; ( b ) routine clinical diagnosis plus genetic testing ( mutation search ing in prob and s and direct gene testing in relatives ) . The main outcome measures were perceptions of control over hypercholesterolemia , adherence to cholesterol‐lowering medication , diet , physical activity , and smoking .  There was no support for the main hypothesis : finding a mutation had no impact on perceived control or adherence to risk‐reducing behavior ( all P‐values > 0.10 ) . While all groups believed that lowering cholesterol was an effective way of reducing the risk of a heart attack , participants in whom a mutation was found believed less strongly in the efficacy of diet in reducing their cholesterol level ( P = 0.02 at 6 months ) and showed a trend in believing more strongly in the efficacy of cholesterol‐lowering medication ( P = 0.06 at 6 months ) . In conclusion , finding a mutation to confirm a clinical diagnosis of FH in a previously aware population does not reduce perceptions of control or adherence to risk‐reducing behaviors . The pattern of findings leads to the new hypothesis that genetic testing does not affect the extent to which people feel they have control over a condition , but does affect their perceptions of how control is most effectively achieved . Further work is needed to determine whether similar results will be obtained in population s with little previous awareness of their risks . © 2004 Wiley‐Liss , Objective We examined the clinical utility of supplementing  type 2 diabetes mellitus ( DM )  risk counseling with DM genetic test results and counseling . Research Design and Methods In this r and omized controlled trial , non-diabetic overweight/obese veteran out patients aged 21 to 65 years received DM risk estimates for lifetime risk , family history , and fasting plasma glucose , followed by either genetic test results ( CR+G ; N = 303 ) or control eye disease counseling ( CR+EYE ; N = 298 ) . All participants received brief lifestyle counseling encouraging weight loss to reduce the risk of DM . Results The mean age was 54 years , 53 % of participants were black , and 80 % were men . There was no difference between arms in weight ( estimated mean difference between CR+G vs. CR+EYE at 3 months = 0.2 kg , 95 % CI : −0.3 to 0.7 ; at 6 months = 0.4 kg , 95 % CI : −0.3 to 1.1 ) , insulin resistance , perceived risk , or physical activity at 3 or 6 months . Calorie and fat intake were lower in the CR+G arm at 3 months ( p ’s ≤ 0.05 ) but not at 6 months ( p ’s > 0.20 ) . Conclusions Providing patients with genetic test results was not more effective in changing patient behavior to reduce the risk of DM compared to conventional risk counseling . Trial registration : Clinical Trials.gov NCT01060540 http:// clinical Aims /hypothesisAdvances in type 2 diabetes genetics have raised hopes that genetic testing will improve disease prediction , prevention and treatment . Little is known about current physician and patient views regarding type 2 diabetes genetic testing . We hypothesised that physician and patient views would differ regarding the impact of genetic testing on motivation and adherence . Methods We surveyed a nationally representative sample of US primary care physicians and endocrinologists ( n = 304 ) , a r and om sample of non-diabetic primary care patients ( n = 152 ) and patients enrolled in a diabetes pharmacogenetics study ( n = 89 ) . Results Physicians and patients favoured genetic testing for diabetes risk prediction ( 79 % of physicians vs 80 % of non-diabetic patients would be somewhat/very likely to order/request testing , p = 0.7 ) . More patients than physicians ( 71 % vs 23 % , p < 0.01 ) indicated that a ‘ high risk ’ result would be very likely to improve motivation to adopt preventive lifestyle changes . Patients favoured  genetic testing to guide therapy ( 78 % of patients vs 48 % of physicians very likely to request/recommend testing , p < 0.01 ) and reported that genetic testing would make them ‘ much more motivated ’ to adhere to medications ( 72 % vs 18 % of physicians , p < 0.01 ) . Many physicians ( 39 % ) would be somewhat/very likely to order genetic testing before published evidence of clinical efficacy . Conclusions /interpretationDespite the paucity of current data , physicians and patients reported high expectations that genetic testing would improve patient motivation to adopt key behaviours for the prevention or control of type 2 diabetes . This suggests the testable hypothesis that ‘ genetic ’ risk information might have greater value to motivate behaviour change compared with st and ard risk information Genetic testing for obesity risk is increasingly available to the public but few studies have examined motivational or affective reactions . Here we report findings from a " vignette " study investigating reactions to " higher-risk " and " average-risk " results for the obesity-related FTO gene in two groups : a panel sample of individuals with weight concerns , for whom testing may have treatment implication s ( n = 306 , mean age = 45 years , mean BMI = 35 ) and a student sample ( n = 395 , mean age = 25 years , mean BMI = 23 ) , for whom testing would have implication s for obesity prevention . Participants were given FTO gene information that described higher-risk alleles as linked with modest weight gain and slightly higher risk of obesity . They responded to both higher- and average-risk vignettes , with order r and omized . Interest in genetic testing was high overall , and higher in panel respondents than students ( 93 % vs. 78 % would " probably " or " definitely " have the test ; P < 0.001 ) . In students , a higher-risk result generated higher motivation to change ( d = 0.15 ; P < 0.001 ) , but also slightly higher negative affect ( d = 0.03 , P < 0.001 ) and fatalism ( d = 0.05 , P < 0.001 ) than an average-risk result . Panel respondents also had higher motivation to change ( d = 0.17 , P < 0.001 ) as well as relief about having an explanation for their body weight ( d = 0.02 , P = 0.013 ) in the higher-risk condition , but no increase in fatalism or depression . These results suggest that at the level of anticipated responses to FTO gene feedback , higher-risk results had positive motivational effects with minimal changes in negative affect or fatalism . Genetic testing has the potential to be a useful clinical or preventive tool when combined with appropriate information Prospect i ve registration of systematic review s promotes transparency , helps reduce potential for bias and serves to avoid unintended duplication of review s. Registration offers advantages to many stakeholders in return for modest additional effort from the research ers registering their review
target: This review found no clear or consistent evidence that genetic risk communication alone either raises motivation or translates into actual change in dietary intake or physical activity to reduce the risk of cardiometabolic disorders in adults .
background: Genetic risk prediction of chronic conditions including obesity , diabetes and CVD currently has limited predictive power but its potential to engage healthy behaviour change has been of immense research interest .
  We aim ed to underst and whether the latter is indeed true by conducting a systematic review and meta- analysis investigating whether genetic risk communication affects motivation and actual behaviour change towards preventative lifestyle modification .