PubMed · 14959658
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Amanda Spake. 2004-02-09. Rethinking weight.. https://pubmed.ncbi.nlm.nih.gov/14959658/
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OBJECTIVE: The aim of the present study was to examine secular trends in major cardiovascular disease (CVD) risk factors, that is, obesity and dyslipidaemia, among Cretan children during 1982-2002. DESIGN: Epidemiological survey. SETTING AND SUBJECTS: A total of 528 boys in 1982 and 620 boys in 2002, aged 12.1+/-0.1 y, were randomly selected from urban and rural regions throughout the county of Iraklio, Crete, Greece. Care was taken so that all procedures in 2002 closely matched those in 1982. RESULTS: Mean height, weight, and body mass index (BMI) were 1.1, 9.6, and 8.4% higher, respectively, in 2002 vs 1982 (P<0.001). The prevalence of overweight and obesity has risen by 63 and 202%, respectively (P<0.001). Contemporary children were found to have 3.6% higher total cholesterol (TC), 24.9% lower high-density lipoprotein-cholesterol (HDL-C), 25.3% higher low-density lipoprotein-cholesterol (LDL-C), 19.4% higher triacylglycerol, 36.6% higher TC/HDL-C ratio, and 60.3% higher LDL-C/HDL-C ratio compared with their peers in 1982 (P<0.003). These differences persisted even when adjusting for BMI (P<0.02). The proportion of children having abnormal lipid values was much greater nowadays than in the 1980s, yielding odds ratios of 1.4-8.8 (P<0.005). CONCLUSIONS: Results are indicative of a largely deteriorated CVD risk profile in Cretan children since 1982, and predict an unfavourable CVD morbidity and mortality for this population in the foreseeable future.
One of the chief complexities of genetic influences on human obesity appears to be gene-gene interactions. Here, we employed model-free approaches to look for gene-gene interaction effects in human obesity using genome scan data from 260 European American families. We found consistent evidence for statistical interaction between 2p25-p24 (18-38 cM) and 13q13-q21 (26-47 cM). For discrete traits, the positive correlations were significant at P<0.0001 (P</=0.0023 after correction for multiple tests) in both IBD-based and NPL-based analyses for BMI>/=40 kg/m(2). Other analytic approaches gave consistent, supportive results. For quantitative traits, interaction effects were significant for BMI (P=0.0012), percent fat (P=0.0265) and waist circumference (P=0.0023) in a Haseman-Elston regression model, and for BMI (P=0.0043) in variance component analysis. Our findings suggest that obesity-susceptibility loci in chromosome regions 2p25-p24 and 13q13-21 may interact to influence extreme human obesity. The identification of gene-gene interactions may prove crucial to understanding the contributions of genes, which, by themselves, have relatively small effects on obesity susceptibility and resistance.
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