We have a new series of publications reporting discoveries about three GWAS success stories: obesity, smoking, and asthma. These three conditions are known to accelerate physical ageing. Because we have traced these phenotypes in the Dunedin Study as they unfold from birth to midlife, we were ideally situated to ask the following: exactly when in the course of human development does genomic risk ascertained in GWAS hits first come on line? We reported that genes detected in GWAS of obese adults are unrelated to birth weight, but they influence rapid growth from birth to age 3. The link from genes to adult obesity is accounted for by this rapid infant growth [48, 49]. We found that genes detected in GWAS of adult smokers are unrelated to cigarette initiation, but they influence rapid progression from first cigarette to addiction. The link from genes to failure of adult smoking cessation is explained by this initial fast progression in teenagers. We further found that ‘chippers’ who can smoke without becoming addicted carry less-than-normal genetic risk [50]. In asthma, genes detected in GWAS of
