Nutritional geometry (NG) is a novel dietary analysis approach that considers nutrient balance, rather than single nutrient effects, on health and behaviour. Through NG, recent animal experiments have found that lifespan and reproduction are differentially altered by dietary macronutrient distribution. Epidemiological research using NG reports similar findings for human ageing. Yet, the relation of macronutrient balance to human reproduction, especially reproductive maturation, remains undefined. We studied the impact of childhood macronutrient intake on pubertal maturation, by applying NG to an Australian longitudinal adolescent dataset. Food records, collected at age 8 years from 142 pre-pubertal children (females, 92; males, 50), were analysed for absolute energy, percentage energy and energy-adjusted residuals from protein, carbohydrate and fat. Pubertal stage change (assessed at 8, 13 and 15 years) was modelled to obtain individual mathematical estimates of pubertal timing and tempo. Timing of menarche was recorded. The association of macronutrients to pubertal timing/tempo was assessed via NG, involving generalised additive models and heat maps to aid interpretation. Results showed lower dietary protein (relative to carbohydrate and fat) in girls consistently predicted earlier pubertal timing and menarche, and was related to faster pubertal tempo (all P < 0·05). No significant associations were identified in boys for both timing and tempo. Results suggest a role of non-protein macronutrients in facilitating female maturation; corroborating feeding and reproductive behaviour patterns observed in earlier NG studies of primates. Application of NG to other adolescent datasets is required to confirm the present findings. Such work would advance understanding of how nutrient balance shapes human development and health.

We apply nutritional geometry, a framework for modelling the interactive effects of nutrients on animals, to help understand the role of modern environments in the obesity pandemic. Evidence suggests that humans regulate the intake of protein energy (PE) more strongly than non-protein energy (nPE), and consequently will over- and under-ingest nPE on diets with low or high PE, respectively. This pattern of macronutrient regulation has led to the protein leverage hypothesis, which proposes that the rise in obesity has been caused partly by a shift towards diets with reduced PE:nPE ratios relative to the set point for protein regulation. We discuss potential causes of this mismatch, including environmentally induced reductions in the protein density of the human diet and factors that might increase the regulatory set point for protein and hence exacerbate protein leverage. Economics – the high price of protein compared with fats and carbohydrates – is one factor that might contribute to the reduction of dietary protein concentrations. The possibility that rising atmospheric CO2 levels could also play a role through reducing the PE:nPE ratios in plants and animals in the human food chain is discussed. Factors that reduce protein efficiency, for example by increasing the use of ingested amino acids in energy metabolism (hepatic gluconeogenesis), are highlighted as potential drivers of increased set points for protein regulation. We recommend that a similar approach is taken to understand the rise of obesity in other species, and identify some key gaps in the understanding of nutrient regulation in companion animals.

It is a well-appreciated fact that in many organisms the process of ageing reacts highly plastically, so that lifespan increases or decreases when the environment changes. The perhaps best-known example of such lifespan plasticity is dietary restriction (DR), a phenomenon whereby reduced food intake without malnutrition extends lifespan (typically at the expense of reduced fecundity) and which has been documented in numerous species, from invertebrates to mammals. For the evolutionary biologist, DR and other cases of lifespan plasticity are examples of a more general phenomenon called phenotypic plasticity, the ability of a single genotype to produce different phenotypes (e.g. lifespan) in response to changes in the environment (e.g. changes in diet). To analyse phenotypic plasticity, evolutionary biologists (and epidemiologists) often use a conceptual and statistical framework based on reaction norms (genotype-specific response curves) and genotype × environment interactions (G × E; differences in the plastic response among genotypes), concepts that biologists who are working on molecular aspects of ageing are usually not familiar with. Here I briefly discuss what has been learned about lifespan plasticity or, more generally, about plasticity of somatic maintenance and survival ability. In particular, I argue that adopting the conceptual framework of reaction norms and G × E interactions, as used by evolutionary biologists, is crucially important for our understanding of the mechanisms underlying DR and other forms of lifespan or survival plasticity.