AbstractWhen governments and healthcare providers offer people cash rewards for weight loss, an assumption is that cash rewards are versatile, working equally well for everyone – for example, for all genders. No research to date has tested for gender difference in response to financial incentives for weight loss. We show in an randomized controlled trial (RCT) (n = 472) that cash incentives for weight loss only worked for males. The RCT consisted of a 3-month, self-administered online weight loss program. Offering a US$150 incentive for a 5% weight loss more than tripled the proportion of males who were successful, compared with a no-incentive Control arm (20.9% vs. 5.9%). On average, males in the incentive arm lost 2.4% of weight over 3 months, compared with 0.9% in the Control arm. The same incentive had no such effect on females: The average weight loss in the incentive arm was not significantly different than in the Control (1.03% and 1.44%, respectively), nor was the proportion of participants meeting the 5% weight loss goal (8.6% and 8.7%, respectively). This study shows that males respond better than females to financial incentives for weight loss.
BACKGROUND: In recent years, behaviourally driven policies such as nudges have been increasingly implemented to steer desired outcomes in public health. This study examines the different nudges and the socio-demographic characteristics and lifestyle behaviours that are associated with public acceptance of lifestyle nudges. METHODS: The study used data from the nationwide Knowledge, Attitudes and Practices study (KAP) on diabetes in Singapore. Three types of nudges arranged in increasing order of intrusiveness were examined: (1) information government campaigns, (2) government mandated information and (3) default rules and choice architecture. Acceptance was assessed based upon how much respondents 'agreed' with related statements describing heathy lifestyle nudges. Multivariable linear regressions were performed with socio-demographics and lifestyle behaviours using scores calculated for each nudge. RESULTS: The percentage of respondents who agreed to all statements related to each nudge were: 75.9% (information government campaigns), 73.0% (government mandated information), and 33.4% (default rules and choice architecture). Respondents of Malay/Others ethnicity (vs. Chinese) were more likely to accept information government campaigns. Respondents who were 18 – 34 years old (vs 65 years and above), female, of Malay/Indian ethnicity (vs Chinese), were sufficiently physically active, and with a healthier diet based on the DASH (Dietary Approach to Stop Hypertension) score were more likely to accept nudges related to government mandated information. Respondents of Malay/Indian ethnicity (vs Chinese), and who had a healthier diet were more likely to accept default rules and choice architecture. CONCLUSION: Individuals prefer less intrusive approaches for promoting healthy lifestyle. Ethnicity and lifestyle behaviours are associated with acceptance of nudges and should be taken into consideration during the formulation and implementation of behaviourally informed health policies. SUPPLEMENTARY INFORMATION: The online ...
To access publisher's full text version of this article. Please click on the hyperlink in Additional Links field. ; To extend understanding of the genetic architecture and molecular basis of type 2 diabetes (T2D), we conducted a meta-analysis of genetic variants on the Metabochip, including 34,840 cases and 114,981 controls, overwhelmingly of European descent. We identified ten previously unreported T2D susceptibility loci, including two showing sex-differentiated association. Genome-wide analyses of these data are consistent with a long tail of additional common variant loci explaining much of the variation in susceptibility to T2D. Exploration of the enlarged set of susceptibility loci implicates several processes, including CREBBP-related transcription, adipocytokine signaling and cell cycle regulation, in diabetes pathogenesis. ; Academy of Finland 77299 102318 110413 118065 123885 124243 129680 129293 129494 136895 139635 141005 213506 251217 Agence Nationale de la Recherche (France) American Diabetes Association 7-08-MN-OK Association Francaise des Diabetiques Association de Langue Francaise pour l'Etude du Diabete et des Maladies Metaboliques (France) Association Diabete Risque Vasculaire (France) British Diabetic Association (BDA) Research (UK) British Heart Foundation RG/98002 RG2008/08 Cancer Research UK Central Norway Health Authority Central Finland Hospital District Center for Inherited Disease Research (CIDR) (USA) Chief Scientist Office, Scotland CZB/4/672 City of Kuopio (Finland) City of Leutkirch (Germany) Department of Health (UK) Deutsche Forschungsgemeinschaft ER1 55/6-2 Diabetes UK Doris Duke Charitable Foundation (USA) Estonian government SF0180142s0 European Commission: ENGAGE HEALTH-F4-2007-201413 EXGENESIS LSHM-CT-2004-005272 245536 QLG1-CT-2002-00896 2004310 European Commission (Marie Curie: FP7-PEOPLE-IEF) European Regional Development Fund Faculty of Medicine at the Norwegian University of Science and Technology Finnish Diabetes Association Finnish Diabetes Research Foundation Finnish ...
Publisher's version (útgefin grein). ; Heavy alcohol consumption is an established risk factor for hypertension; the mechanism by which alcohol consumption impact blood pressure (BP) regulation remains unknown. We hypothesized that a genome-wide association study accounting for gene-alcohol consumption interaction for BP might identify additional BP loci and contribute to the understanding of alcohol-related BP regulation. We conducted a large two-stage investigation incorporating joint testing of main genetic effects and single nucleotide variant (SNV)-alcohol consumption interactions. In Stage 1, genome-wide discovery meta-analyses in ≈131K individuals across several ancestry groups yielded 3, 514 SNVs (245 loci) with suggestive evidence of association (P < 1.0 × 10-5). In Stage 2, these SNVs were tested for independent external replication in ≈440K individuals across multiple ancestries. We identified and replicated (at Bonferroni correction threshold) five novel BP loci (380 SNVs in 21 genes) and 49 previously reported BP loci (2, 159 SNVs in 109 genes) in European ancestry, and in multi-ancestry meta-analyses (P < 5.0 × 10-8). For African ancestry samples, we detected 18 potentially novel BP loci (P < 5.0 × 10-8) in Stage 1 that warrant further replication. Additionally, correlated meta-analysis identified eight novel BP loci (11 genes). Several genes in these loci (e.g., PINX1, GATA4, BLK, FTO and GABBR2) have been previously reported to be associated with alcohol consumption. These findings provide insights into the role of alcohol consumption in the genetic architecture of hypertension. ; The following authors declare commercial private and/or governmental affiliations: Bruce M. Psaty (BMP) serves on the DSMB of a clinical trial funded by Zoll Lifecor and on the Steering Committee of the Yale Open Data Access Project funded by Johnson & Johnson. Barbara V. Howard (BVH) has a contract from National Heart, Lung, and Blood Institute (NHLBI). Brenda W.J.H. Penninx (BWJHP) has received research funding (non-related to the work reported here) from Jansen Research and Boehringer Ingelheim. Mike A. Nalls (MAN) is supported by a consulting contract between Data Tecnica International LLC and the National Institute on Aging (NIA), National Institutes of Health (NIH), Bethesda, MD, USA. MAN also consults for Illumina Inc., the Michael J. Fox Foundation, and the University of California Healthcare. MAN also has commercial affiliation with Data Tecnica International, Glen Echo, MD, USA. Mark J. Caulfield (MJC) has commercial affiliation and is Chief Scientist for Genomics England, a UK government company. Oscar H Franco (OHF) is supported by grants from Metagenics (on women's health and epigenetics) and from Nestlé (on child health). Peter S. Sever (PSS) is financial supported from several pharmaceutical companies which manufacture either blood pressure lowering or lipid lowering agents, or both, and consultancy fees. Paul W. Franks (PWF) has been a paid consultant in the design of a personalized nutrition trial (PREDICT) as part of a private-public partnership at Kings College London, UK, and has received research support from several pharmaceutical companies as part of European Union Innovative Medicines Initiative (IMI) projects. Fimlab LTD provided support in the form of salaries for author Terho Lehtimäki (TL) but did not have any additional role in the study design to publish, or preparation of the manuscript. Gen‐info Ltd provided support in the form of salaries for author Ozren Polašek (OP) but did not have any additional role in the study design to publish, or preparation of the manuscript. The specific roles of these authors are articulated in the 'author contributions' section. There are no patents, products in development, or marked products to declare. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. ; Peer Reviewed