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Obesity is the 5th leading cause of global death, and is major risk factors for many chronic diseases, such as type 2 diabetes, cardiovascular diseases, hypertension and cancer. Obesity is caused by an imbalance between energy intake and energy expenditure, and it is widely agreed to be a consequence of a gene by environment interaction. Although on average obesity rates are increasing, the shape of the distribution of adiposity is changing: it is becoming more right skewed. This is because there is a population of very lean subjects that has remained almost unchanged by the epidemic. The investigators have called these very lean individuals that are resistant to the epidemic and sustain a BMI < 18.5 kg/m2 'super lean' subjects. We have very little understanding of the lifestyles of these individuals and how they are able to maintain their super lean phenotype, and whether the basis of their leanness is primarily genetics.
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In this study, the investigators will recruit a sample of 150 super lean healthy volunteers with a BMI >15 and < 18.5 kg/m2 aged 20-40 years, in parallel with an age matched group of 150 healthy subjects with a BMI ≥22 and < 25 kg/m2 as the control group. The investigators will screen out any individuals with eating disorders. In both groups, the investigators will study their lifestyles in particular focusing on their physical activity patterns and their food intake choices (monitored via food intake diaries and supported by metabolomics analyses of their urine to detect biomarkers of different food groups). Saliva samples will be collected for genotyping. The investigators will SNP genotype the individuals for 30 known polymorphic loci previously linked to obesity to establish if they have a particular genetic profile linked to their lean phenotype.
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300 participants in 2 patient groups
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John Speakman, PhD; Sumei Hu, PhD
Data sourced from clinicaltrials.gov
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