OBJECTIVES:To investigate the tracking of body mass index (BMI) during childhood. The effect of birth weight and family history of obesity on BMI development during childhood was also evaluated. METHODS: All children born during 1981-1982 in a rural community of eastern Finland were followed at ages 6 months, 7 and 15 y (-6 m, -7y, -15y). Out of 205 children, 138 completed the full follow-up period, of which 100 (45 girls) were included in the analysis with complete data. RESULTS: BMI-6 m was significantly associated with BMI-7y (r ¼ 0.320; P-value ¼ 0.001), but no longer with BMI-15y. BMI-7y was significantly associated with BMI-15y (r ¼ 0.686; P-value o0.001). Children in the highest tertile of BMI-6 m did not have a higher risk of being in the highest tertile of either BMI-7y or BMI-15y compared with children in other tertiles of BMI-6 m. Children in the highest tertile of BMI-7y had a significantly higher risk of being in the highest tertile of BMI-15y (relative risk ¼ 3.6 (2.0-6.3)) compared with children in other tertiles of BMI-7y. BMI-7y was predicted negatively by parents' education and male gender and positively by BMI-6 m. BMI-15y was predicted positively by BMI-7y, the difference in BMI between ages 7 y and 6 months and the mean of BMI between ages 6 months and 7 y. Birth weight was not a good predictor of BMI during childhood. Children with at least one obese parent seemed to have higher BMI during childhood; however, this association did not reach a significant level. CONCLUSION: The study confirmed the tracking of BMI during childhood. Neither birth weight nor family history of obesity was found a good predictor of BMI during childhood. The risk of obesity in adolescence can be determined during middle childhood and obese children may be targeted in lifestyle advice to reverse this trend. Parental education may have a key role in the prevention of obesity during childhood.

Blood pressure (BP) levels in the Finnish population are amongst the highest in the world, despite favourable changes at the national level in the past two decades. The study evaluates the familial aggregation of BP and the association of some environmental factors to the familial aggregation of BP as a primary epidemiological approach of the genetics of hypertension in a sample of families with young offspring from eastern Finland. Offspring aged 15 years were examined between 1996 and 1997 and their biological parents were examined between 1993 and 1994. A total of 224 children were invited, 184 families participated, from which 144 were included in the analysis with complete data. Systolic (SBP), diastolic (DBP) and mean (MAP) arterial BPs were the main outcome measurements. After the offspring's gender and body mass index (BMI) and the parent's age

In this study, we investigated the familial aggregation of body mass index (BMI) in a sample of families with young offspring from eastern Finland. 15-year-olds were examined from 1996 to 1997, and their biological parents were examined from 1993 to 1994. 224 children were invited; 184 families participated, and 144 were included in the analysis with complete data. Significant positive correlations were found for mother-offspring pairs (correlation [r] = 0.31, p < 0.001, n = 140), father-offspring (r = 0.23, p = 0.017, n = 107), mother-daughter (r = 0.26, p = 0.044, n = 63) and mother-son (r = 0.36, p = 0.001, n = 77). Adjustment for confounding variables did not alter these results. There was a higher proportion of children in the highest quartile of BMI when the mother was obese (odds ratio [OR] = 3.0, 95 % CI = 1.4 - 6.7, n = 140) and when one or both parents were obese (OR = 2.8, 95 % CI = 1.0 - 8.0 when one parent was obese; OR = 4.6, 95 % CI = 1.1 - 20.0 when both parents were obese; n = 103). The study confirmed familial BMI aggregation. The consistent obesity relationship between mother and offspring may indicate the key role of the mother in primary obesity prevention.

Aim: To investigate the tracking of serum total cholesterol (TC) during childhood. Methods: All children born during 1981–1982 in a rural community of eastern Finland were followed at 6 mo, 7 y and 15 y of age. The full follow‐up period was completed by 138 out of 205 children, of whom 82 (33 girls) had TC measured at 7 y and 15 y of age (–7 y, –15 y). The main outcome measurement was TC (mmol/L). Results: TC‐7 y was significantly associated with TC‐15 y (r= 0.655; p‐value <0.001). This correlation did not change significantly after accounting for confounders. Children in the highest tertile of TC‐7y had a significantly higher risk of being in the highest tertile of TC‐15y compared with children in other tertiles of TC‐7 y (relative risk = 6.4 (2.9–13.9)). TC‐15 y was predicted positively by TC‐7 y (linear regression beta = 0.63; p‐value <0.001) and parental high TC (TC ≥5.0 mmol/L in at least one parent) (beta = 0.58; p‐ value = 0.030). Birthweight had no significant association with TC during childhood. Conclusion: The study confirmed the tracking of TC during childhood. The identification of children at risk of developing high TC during adolescence should take into consideration the child's previous TC values during childhood and parental TC status.