Professor (and Doctor) Prescott has given us a remarkable book that summarizes research on the sensitivity of human health to diet, lifestyle and the environment, from womb to tomb. She writes engagingly for a lay broad audience, but also cites evidence in depth for biomedical insiders. The synthesis and coverage is wide and insightful, ranging from studies of mummies that show atherosclerosis is an ancient disease to modern environmental toxic influences on the fetus from tobacco. The clinical examples are illuminated by citations of examples from the animal literature – for example, that captive marmosets also show the impact of maternal obesity on their offspring. Environmental influences begin at least as early with the health and exposures of each of our parents, and conceivably back into our grandmothers, where our natal eggs formed in our mothers’ ovaries before her birth.

Early exposure to infections can lower allergies, as shown by Prescott’s landmark Lancet paper in 1999,Reference Prescott, Macaubas and Smallacombe ¹ proposing the fetal programming of allergic disease. Remarkable developments in this frontier field are summarized in her widely cited 2011 book, The Allergy Epidemic, a Mystery of Modern Life.Reference Prescott ² Prescott’s analysis of inflammatory processes is further extended here as the core of most chronic conditions of aging, from adult obesity to atherosclerosis.

The present book begins with a concise history of the ‘developmental origins of adult disease’, a theory identified with David Barker and the MRC labs in Southampton, England. She describes the momentous meeting in Mumbai in 2001 organized by Barker, with Caroline Fall and Mark Hanson, which I also attended. We all perceived that a scientific frontier was being advanced. A decade later in 2011, these concepts were reified by the UN General Assembly in the Shanghai declaration on non-communicable diseases (NCDs), which the UN Secretary General Ban-Ki Moon described as ‘a public health emergency in slow motion’. This global imperative seeks to improve early nurture as a pragmatic approach to costly interventions for premature chronic diseases. Not all first world governments are on board.

In the face of today’s obesity epidemic, it is worth pondering the major nutritional improvements from a century ago. Even in 1900, hunger was rampant within the industrialized nations. Hear from London in 1903, when the British Empire was at a pinnacle of wealth, where a poor man tells, ‘… Look at my scrawny arm … it’s too late to make up for what I didn’t eat when as a kiddy. Mother died and there were six of us and dad. Older children starve more. By the time the younger ones come along, the older ones are starting to work, and there is more money coming in, and more food to go around’.Reference London ³ The illustrated monograph this comes from³ gives first-hand observations of human misery in the East End of London; the author is the Jack London, best known for novels, whose keen and quantitative observations on the London poor can be ranked with Henry Mayhew’s of fifty years before.Reference Mayhew ⁴ The parents and grandparents in Barker’s seminal studies of Hertfordshire may have transmitted such privations to the low birth weights during 1911–1930, which was linked to proportionately more coronary disease.Reference Barker, Winter, Osmond, Margetts and Simmonds ⁵

Back to the 21st century, Prescott notes the new developmental hazards from air pollution that were derived from automotive traffic. Not available when her book went to press are associations of air pollution with childhood obesity. The Southern California Children’s Health Study showed that children living close to freeways were more obese, moreover, with additive effects of household tobacco smoke.Reference McConnell, Shen and Gilliland ⁶ Exposure to traffic pollution and tobacco is more prevalent in poor households, as Prescott discussed. Despite the decrease in adult smoking during the past decade, in 2011–2012, 40.6% of US children aged 3–11 were exposed to secondhand smoke.Reference Homa, Neff and King ⁷

In a work of this scope, minor errors can creep in such as overstating the benefits of caloric restriction ‘… Rodents generally live 50% longer with caloric restriction’ (p. 255). In fact, most studies of inbred rodents find <20% increase, with major differences by genotype and sex.Reference Swindell ^{8 ,} Reference Liao, Rikke and Johnson ⁹ Caloric restriction shortened lifespan of some genotypes, particularly those with the greatest fat reduction. A QTL analysis identified loci for fat maintenance during caloric restriction that favored longevity,Reference Liao, Rikke and Johnson ⁹ whereas wild-derived mice (true wild-type!) had minimal increase of lifespan.Reference Harper, Leathers and Austad ¹⁰ Intriguingly, the long-lived Ames dwarf mouse, which lives beyond most calorically restricted mice, is on the chubby side, with benefits to insulin signaling that depend on its visceral fat.Reference Menon, Zhi and Hossain ¹¹ Although early-life obesity remains a risk factor for NCD, we know little about the role of specific fat depots in later life health.

Another recent book merits mention: Laura Dawes’ Childhood Obesity in America Reference Dawes ¹² covers the social and political history of obesity, which was even a target of psychoanalysis. Both books discuss the politics of government and industry in food production and marketing that continue the toxic engorgement of sugary, fatty foods. The global scourge of obesity is likely to persist for several generations.

C. E. Finch

Davis School of Gerontology, University of Southern California Los Angeles, CA, USA