Most researchers agree that obesity is an important modulator of the metabolic syndrome, 1 2 which is a clustering of cardiovascular risk factors associated with insulin resistance-such as hypertension, hypertriglyceridaemia, a low concentration of high density lipoprotein cholesterol, abnormal glucose metabolism, and hyperinsulinaemia.3 Little is known, however, about the association between relative weight change from childhood to adulthood and the development of metabolic syndrome in adulthood. Material, methods, and resultsWe recently published data of a population study for the metabolic syndrome, performed during 1993-4 in Pieksämäki, Finland. All subjects (n = 1008) born in the years 1947, 1952, and 1957 were examined according to a protocol described elsewhere.4 Data on both weight and height at age 7 years (the start of primary school) were also collected.Altogether, 712/1008 (70.6%) subjects participated in the study. Weights and heights at age 7 were traced for 439/712 (61.7%) participants. Obesity was defined both in childhood and in adulthood as a sex specific highest third of the body mass index (weight(kg)/ (height (m) 2 )). The metabolic syndrome was defined as a cluster of (a) hypertension (a systolic blood pressure >140 mm Hg, a diastolic blood pressure >90 mm Hg, or treatment with antihypertensive drugs); (b) dyslipidaemia (hypertriglyceridaemia (>1.70 mmol/l) or a high density lipoprotein cholesterol concentration of < 1.00 mmol/l ( < 1.20 mmol/l in women), or both dyslipidaemia and hypertriglyceridaemia); and (c) insulin resistance (abnormal glucose metabolism according to the World Health Organisation's criteria or hyperinsulinaemia (>78 pmol/l), or both). 2-4Of the 439 subjects, 75 had been obese and 219 not obese in both childhood and adulthood; 71 had not been obese as children but were obese as adults; and 74 had been obese as children but were not obese as adults. The metabolic syndrome was present in 18/219 (8%) men and in 12/220 (5%) women. Of the 30 subjects having this syndrome, 28 were obese as adults; 21 of them had also been obese as children (table). In exact logistic regression analysis (LogXact), the risk of metabolic syndrome was 2.9 (95% confidence interval 1.1 to 7.6) for the subjects who had been obese as children and 26.7 (6.4 to 237) for the subjects who were obese as adults, compared with their non-obese controls. None of the 74 subjects who had been obese as children but who were not obese as adults had the metabolic syndrome. The increased risk of the metabolic syndrome was still present when the population was split into thirds for weight but not when it was split into thirds for height. CommentOur results show that half of the obese children had become obese adults with an especially high risk of the metabolic syndrome and that childhood obesity overall increases the risk for the metabolic syndrome in adulthood. The risk of the syndrome was lower among the obese adults who had not been obese as children than among the obese adults who had also been obese as childr...

PIHLAJAMÄ KI, JUSSI, MAUNO VANHALA, PASI VANHALA, AND MARKKU LAAKSO. The Pro12Ala polymorphism of the PPAR␥2 gene regulates weight from birth to adulthood. Obes Res. 2004;12:187-190. Objective: The Pro12Ala polymorphism in exon B of peroxisome proliferator-activated receptor ␥ 2 (PPAR␥2) gene has been related to obesity, insulin resistance, and risk of type 2 diabetes. In this study, the effect of the Pro12Ala polymorphism on long-term changes in weight and body composition was investigated. Research Methods and Procedures:The Pro12Ala polymorphism was genotyped in 311 subjects who participated in our previous population-based study. In that study, weight at birth, 7 years, 20 years, and 41 years, and ponderal index at birth and BMI and waist circumference at 41 years were recorded. Results: The Ala12 allele of the PPAR␥2 gene was associated with high ponderal index at birth (2.77 Ϯ 0.27 kg/m 3 in subjects with the Ala12Ala genotype, 2.79 Ϯ 0.29 kg/m 3 in subjects with the Pro12Ala genotype, and 2.63 Ϯ 0.25 kg/m 3 in subjects with the Pro12Pro genotype, p ϭ 0.007, adjusted for gender) and weight at 7 years (p ϭ 0.045) and tended to be associated with high birth weight (p ϭ 0.094). Subjects with this allele gained less weight between 7 and 20 years (p ϭ 0.043) and more weight between 20 and 41 years (p ϭ 0.001) and ended up having higher waist circumference (p ϭ 0.040) in adulthood than did subjects with the Pro12Pro genotype. Discussion: We conclude that the Pro12Ala polymorphism of the PPAR␥2 gene regulates weight and body composition from utero to adulthood.