414 research outputs found
Recruitment into diabetes prevention programs : what is the impact of errors in self-reported measures of obesity?
BackgroundError in self-reported measures of obesity has been frequently described, but the effect of self-reported error on recruitment into diabetes prevention programs is not well established. The aim of this study was to examine the effect of using self-reported obesity data from the Finnish diabetes risk score (FINDRISC) on recruitment into the Greater Green Triangle Diabetes Prevention Project (GGT DPP).MethodsThe GGT DPP was a structured group-based lifestyle modification program delivered in primary health care settings in South-Eastern Australia. Between 2004–05, 850 FINDRISC forms were collected during recruitment for the GGT DPP. Eligible individuals, at moderate to high risk of developing diabetes, were invited to undertake baseline tests, including anthropometric measurements performed by specially trained nurses. In addition to errors in calculating total risk scores, accuracy of self-reported data (height, weight, waist circumference (WC) and Body Mass Index (BMI)) from FINDRISCs was compared with baseline data, with impact on participation eligibility presented.ResultsOverall, calculation errors impacted on eligibility in 18 cases (2.1%). Of n = 279 GGT DPP participants with measured data, errors (total score calculation, BMI or WC) in self-report were found in n = 90 (32.3%). These errors were equally likely to result in under- or over-reported risk. Under-reporting was more common in those reporting lower risk scores (Spearman-rho = −0.226, p-value < 0.001). However, underestimation resulted in only 6% of individuals at high risk of diabetes being incorrectly categorised as moderate or low risk of diabetes.ConclusionsOverall FINDRISC was found to be an effective tool to screen and recruit participants at moderate to high risk of diabetes, accurately categorising levels of overweight and obesity using self-report data. The results could be generalisable to other diabetes prevention programs using screening tools which include self-reported levels of obesity.<br /
Changes in Dietary Fat Intake and Projections for Coronary Heart Disease Mortality in Sweden: A Simulation Study.
OBJECTIVE: In Sweden, previous favourable trends in blood cholesterol levels have recently levelled off or even increased in some age groups since 2003, potentially reflecting changing fashions and attitudes towards dietary saturated fatty acids (SFA). We aimed to examine the potential effect of different SFA intake on future coronary heart disease (CHD) mortality in 2025. METHODS: We compared the effect on future CHD mortality of two different scenarios for fat intake a) daily SFA intake decreasing to 10 energy percent (E%), and b) daily SFA intake rising to 20 E%. We assumed that there would be moderate improvements in smoking (5%), salt intake (1g/day) and physical inactivity (5% decrease) to continue recent, positive trends. RESULTS: In the baseline scenario which assumed that recent mortality declines continue, approximately 5,975 CHD deaths might occur in year 2025. Anticipated improvements in smoking, dietary salt intake and physical activity, would result in some 380 (-6.4%) fewer deaths (235 in men and 145 in women). In combination with a mean SFA daily intake of 10 E%, a total of 810 (-14%) fewer deaths would occur in 2025 (535 in men and 275 in women). If the overall consumption of SFA rose to 20 E%, the expected mortality decline would be wiped out and approximately 20 (0.3%) additional deaths might occur. CONCLUSION: CHD mortality may increase as a result of unfavourable trends in diets rich in saturated fats resulting in increases in blood cholesterol levels. These could cancel out the favourable trends in salt intake, smoking and physical activity
Genome-wide meta-analysis uncovers novel loci influencing circulating leptin levels.
Leptin is an adipocyte-secreted hormone, the circulating levels of which correlate closely with overall adiposity. Although rare mutations in the leptin (LEP) gene are well known to cause leptin deficiency and severe obesity, no common loci regulating circulating leptin levels have been uncovered. Therefore, we performed a genome-wide association study (GWAS) of circulating leptin levels from 32,161 individuals and followed up loci reaching P<10(-6) in 19,979 additional individuals. We identify five loci robustly associated (P<5 × 10(-8)) with leptin levels in/near LEP, SLC32A1, GCKR, CCNL1 and FTO. Although the association of the FTO obesity locus with leptin levels is abolished by adjustment for BMI, associations of the four other loci are independent of adiposity. The GCKR locus was found associated with multiple metabolic traits in previous GWAS and the CCNL1 locus with birth weight. Knockdown experiments in mouse adipose tissue explants show convincing evidence for adipogenin, a regulator of adipocyte differentiation, as the novel causal gene in the SLC32A1 locus influencing leptin levels. Our findings provide novel insights into the regulation of leptin production by adipose tissue and open new avenues for examining the influence of variation in leptin levels on adiposity and metabolic health
Explaining the decline in coronary heart disease mortality in Turkey between 1995 and 2008.
BACKGROUND: Coronary heart disease (CHD) mortality rates have been decreasing in Turkey since the early 1990s. Our study aimed to determine how much of the CHD mortality decrease in Turkey between 1995 and 2008 could be attributed to temporal trends in major risk factors and how much to advances in medical and surgical treatments.
METHODS: The validated IMPACT CHD mortality model was used to combine and analyse data on uptake and effectiveness of CHD treatments and risk factor trends in Turkey in adults aged 35-84 years between 1995 and 2008.Data sources were identified, searched and appraised on population, mortality and major CHD risk factors for adults those aged 35-84 years. Official statistics, electronic databases, national registers, surveys and published trials were screened from 1995 onwards.
RESULTS: Between 1995 and 2008, coronary heart disease mortality rates in Turkey decreased by 34% in men and 28% in women 35 years and over. This resulted in 35,720 fewer deaths in 2008.Approximately 47% of this mortality decrease was attributed to treatments in individuals (including approximately 16% to secondary prevention, 3% angina treatments, 9% to heart failure treatments, 5% to initial treatments of acute myocardial infarction, and 5% to hypertension treatments) and approximately 42% was attributable to population risk factor reductions (notably blood pressure 29%; smoking 27%; and cholesterol 1%). Adverse trends were seen for obesity and diabetes (potentially increasing mortality by approximately 11% and 14% respectively). The model explained almost 90% of the mortality fall.
CONCLUSION: Reduction in major cardiovascular risk factors explained approximately 42% and improvements in medical and surgical treatments explained some 47% of the CHD mortality fall. These findings emphasize the complimentary value of primary prevention and evidence-based medical treatments in controlling coronary heart disease
The contribution of psychological distress to socio-economic differences in cause-specific mortality: a population-based follow-up of 28 years
<p>Abstract</p> <p>Background</p> <p>Psychological factors associated with low social status have been proposed as one possible explanation for the socio-economic gradient in health. The aim of this study is to explore whether different indicators of psychological distress contribute to socio-economic differences in cause-specific mortality.</p> <p>Methods</p> <p>The data source is a nationally representative, repeated cross-sectional survey, "Health Behaviour and Health among the Finnish Adult Population" (AVTK). The survey results were linked with socio-economic register data from Statistics Finland (from the years 1979-2002) and mortality follow-up data up to 2006 from the Finnish National Cause of Death Register. The data included 32451 men and 35420 women (response rate 73.5%). Self-reported measures of depression, insomnia and stress were used as indicators of psychological distress. Socio-economic factors included education, employment status and household income. Mortality data consisted of unnatural causes of death (suicide, accidents and violence, and alcohol-related mortality) and coronary heart disease (CHD) mortality. Adjusted hazard ratios were calculated using the Cox regression model.</p> <p>Results</p> <p>In unnatural mortality, psychological distress accounted for some of the employment status (11-31%) and income level (4-16%) differences among both men and women, and for the differences related to the educational level (5-12%) among men; the educational level was associated statistically significantly with unnatural mortality only among men. Psychological distress had minor or no contribution to socio-economic differences in CHD mortality.</p> <p>Conclusions</p> <p>Psychological distress partly accounted for socio-economic disparities in unnatural mortality. Further studies are needed to explore the role and mechanisms of psychological distress associated with socio-economic differences in cause-specific mortality.</p
Children as urbanites: mapping the affordances and behavior settings of urban environments for Finnish and Japanese children
© 2018, © 2018 The Author(s). Published by Informa UK Limited, trading as Taylor & amp; Francis Group. Increasingly, children are residing in urban environments, yet little is known about the urban affordances for children. A place-based approach was employed to map the urban experiences of over 1300 children residing in Helsinki (Finland) and in Tokyo (Japan) in terms of meaningful places (affordances), travel mode and accompaniment to these places. Shared affordances were considered behavior settings, and audited on-site by trained experts for their main function, land use, openness, and communality. Significant differences were found between countries for all affordance categories. Although differences in behavior settings were observed between countries, a number of patterns emerged: outdoor settings and those with shared communality were the most prevalent behavior settings, traffic settings were predominantly evaluated negatively and commercial and indoor settings most positively. Findings suggest that although the context is important, independent mobility and the possibility to actualize environmental affordances seem to be fundamental in both contexts as the key criteria for environmental child-friendliness
Increased genetic vulnerability to smoking at CHRNA5 in early-onset smokers
Recent studies have shown an association between cigarettes per day (CPD) and a nonsynonymous single-nucleotide polymorphism in CHRNA5, rs16969968.Objective: To determine whether the association between rs16969968 and smoking is modified by age at onset of regular smoking.Data Sources: Primary data.Study Selection: Available genetic studies containing measures of CPD and the genotype of rs16969968 or its proxy.DataExtraction: Uniform statistical analysis scripts were runlocally. Starting with 94 050 ever-smokers from 43 studies, we extracted the heavy smokers (CPD >20) and light smokers (CPD 16 years), and a logistic regression of heavy vs light smoking with ther s16969968 genotype was computed for each stratum. Meta-analysis was performed within each age-at-onset stratum.Data Synthesis: Individuals with 1 risk allele at rs16969968 who were early-onset smokers were significantly more likely to be heavy smokers in adulthood (odds ratio [OR]=1.45; 95% CI, 1.36-1.55; n=13 843) than were carriers of the risk allele who were late-onset smokers (OR=1.27; 95% CI, 1.21-1.33, n=19 505) (P=.01).Conclusion: These results highlight an increased genetic vulnerability to smoking in early-onset smokers
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