OBJECTIVE:To examine whether early anthropometric measures and reproductive factors were associated with body mass index (BMI), overweight, and obesity. DESIGN: Cross-sectional, observational study. SUBJECTS: In all, 18 109 healthy women who participated in the Swedish Mammography Cohort aged 49-83 y. MEASUREMENTS: Early anthropometric (birthweight and body shape at age 10 y) and reproductive (age at menarche, age at the birth of the first child, and parity) variables were our predictors and current BMI, overweight (BMI 25-29.99 kg/m 2 ), and obesity (BMI Z30 kg/m 2 ) were our outcomes. RESULTS: In multivariate-adjusted polytomous logistic regression analysis, risk of overweight and obesity increased with increasing body shape at age 10 y and decreased with increasing age at menarche and age at first birth (P for trend o0.0001). A U-shaped relation with birthweight was observed. In our tests for effect modification of the relation with overweight/obesity (ow/ob; BMI Z25 kg/m 2 ), we detected significant interactions between body shape at 10 y and age (Po0.0001); body shape at 10 y and physical activity (Po0.0001); age at first birth and smoking (P ¼ 0.02); and parity and physical activity (P ¼ 0.004). The increased risk of ow/ob among women who reported a larger childhood body shape was reduced as women moved from the lowest to highest quartile of physical activity in adulthood. Likewise, the increasing risk of ow/ob among women with greater parity was reduced with increased physical activity. CONCLUSION: Early anthropometric measures and reproductive factors are significantly associated with BMI, overweight, and obesity among older women. The effects of childhood body weight, age at first birth, and parity may be modified by adult lifestyle choices, as well as age.

IL1-RN is an important anti-inflammatory cytokine that modulate the inflammation response by binding to IL1 receptors, and as a consequence inhibits the action of proinflammatory cytokines IL1a and IL1b. In this study, we hypothesise that sequence variants in the IL1-RN gene are associated with prostate cancer risk. The study population, a population-based case -control study in Sweden, consisted of 1383 prostate cancer case patients and 779 control subjects. We first selected 18 sequence variants covering the IL1-RN gene and genotyped these single-nucleotide polymorphisms (SNPs) in 96 control subjects. Gene-specific haplotypes of IL1-RN were constructed and four haplotype-tagging single-nucleotide polymorphisms (htSNPs) were identified (rs878972, rs315934, rs3087263 and rs315951) that could uniquely describe 495% of the haplotypes. All study subjects were genotyped for the four htSNPs. No significant difference in genotype frequencies between cases and controls were observed for any of the four SNPs based on a multiplicative genetic model. Overall there was no significant difference in haplotype frequencies between cases and controls; however, the prevalence of the most common haplotype (ATGC) was significantly higher among cases (38.7%) compared to controls (33.5%) (haplotype-specific P ¼ 0.009). Evaluation of the prostate cancer risk associated with carrying the 'ATGC' haplotype revealed that homozygous carriers were at significantly increased risk (odds ratio (OR) ¼ 1.6, 95% confidence interval (CI) ¼ 1.2 -2.2), compared to noncarriers, while no significant association was found among subjects heterozygous for the haplotype (OR ¼ 1.0, 95% CI ¼ 0.8 -1.2). Restricting analyses to advanced prostate cancer strengthened the association between the 'ATGC' haplotype and disease risk (OR for homozygous carriers vs noncarriers 1.8, 95% CI ¼ 1.3 -2.5). In conclusion, the results from this study support the hypothesis that inflammation has a role of in the development of prostate cancer, but further studies are needed to identify the causal variants in this region and to elucidate the biological mechanism for this association.

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