Overnutrition or undernutrition during all or part of the reproductive cycle predisposes sows to metabolic consequences and poor reproductive health which contributes to a decrease in sow longevity and an increase in perinatal mortality. This represents not only an economic problem for the pig industry but also results in poor animal welfare. To maximise profitability and increase sustainability in pig production, it is pivotal to provide researchers and practitioners with synthesised information about the repercussions of maternal obesity or malnutrition on reproductive health and perinatal outcomes, and to pinpoint currently available nutritional managements to keep sows’ body condition in an optimal range. Thus, the present review summarises recent work on the consequences of maternal malnutrition and highlights new findings.

This essay uses a specific example—proposals to exclude sugary drinks from the Supplemental Nutrition Assistance Program (SNAP)—to explore some features of the contemporary U.S. administrative state. Dating back to the Wilsonian origins of the U.S. administrative state there has been uncertainty about whether we can and should separate politics and administration. On the traditional view, the agencies are to be kept separate from politics—technocratic and value-neutral—although they are indirectly accountable to the president and Congress. The SNAP exclusions example shows, however, that agencies often must make complex and controversial decisions on their own, decisions that go beyond value-neutral technocratic administration. When authorizing legislation has multiple goals, as we’ll argue is the case in the SNAP example, an agency will have to choose between conflicting statutory mandates. Moreover, as the SNAP example shows, agencies often face complex normative questions of ethics and justice that go beyond the question of how to balance competing aims. The appropriate response to the SNAP exclusions example is not to keep politics out of administrative decision-making, but to develop procedures that allow ethical and political questions to be addressed in agency policy-making, consistent with overarching commitments to fairness and democracy.

The double burden of overnutrition and undernutrition is rapidly becoming a public health concern in low- and middle-income countries. We explored the occurrence of mother−child pairs of over- and undernutrition and the contributing factors using the 2014 Kenya Demographic and Health Survey data. A weighted sample of 7830 mother−child pairs was analysed. The children's nutritional status was determined using the WHO 2006 reference standards while maternal nutritional status was determined with BMI. Descriptive statistics, bivariate and multivariate logistic regression analysis were conducted. The proportion of overweight and obese mothers was 26 % (18·8 % overweight and 7·2 % obese). The prevalence of child stunting, underweight and wasting was 26·3, 12·8 and 5·1 %, respectively. Out of the overweight/obese mothers (weighted n 2034), 20 % had stunted children, 5·4 % underweight children and 3·1 % wasted children. Overweight/obese mother−stunted child pairs and overweight/obese mother−underweight child pairs were less likely to occur in the rural areas (adjusted OR (aOR) = 0·43; P < 0·01) in comparison with those residing in the urban areas (aOR = 0·54; P = 0·01). Children aged more than 6 months were more likely to be in the double burden dyads compared with children below 6 months of age (P < 0·01). The double burden mother−child dyads were more likely to be observed in wealthier households. Mother−child double burden is a notable public health problem in Kenya. Household wealth and urban residence are determinants of the double burden. There is need for target-specific interventions to simultaneously address child undernutrition and maternal overweight/obesity.

An infant's early developmental environment plays a pivotal role in the programming of its physiological phenotype. The identification of the factors in the maternal environment that mediate the effects of maternal obesity and diet is essential to the development of clinical intervention strategies. Maternal hyperglycaemia, hyperinsulinaemia, hypertriglyceridaemia, hyperleptinaemia and altered inflammatory cytokines concentrations are potentially important predictive factors of her future offspring's susceptibility to metabolic disease. Using a diet-induced obese mouse model, we have investigated which of these maternal factors could induce adverse metabolic programming in the offspring. Female C57Bl/6 mice were fed either laboratory chow (10% fat) or high fat diet (42% fat) for 10 weeks before mating and throughout gestation. At day 18 of pregnancy, maternal body weight, body composition and glucose tolerance were measured, as well as plasma insulin, adiponectin, RBP4, leptin, resistin and the inflammatory cytokines (IL6, IL10, IL12, IL1β, IFNγ, KC, TNF-α). At day 18 of pregnancy, high fat-fed dams were significantly heavier than the chow dams and had increased fat mass. High fat-fed dams had higher 5 h fasting blood glucose than chow dams and elevated plasma insulin. Although the obese dams had both reduced plasma adiponectin and resistin levels compared with lean dams, their plasma IL6, IL10 and IFNγ levels were all increased. High fat feeding in pregnancy leads to altered plasma concentrations of both adipokines and adipocytokines in the dam that may directly pass to the fetus and affect their development.

Before about 1750 there was no substantial secular fall in protein–energy malnutrition (PEM) over large areas, nor reason to expect it. We have since learned that sufficient economic advance (poverty reduction) plus scientific advance (in medicine and food production) are achievable to eliminate mass PEM. The two advances are linked via increased demand for labour, and hence wages and employment, for those formerly too poor to afford adequate food. The extra employment income arises first from smallholder and employee food production, and later, as labour is released, from a wide range of specialised, increasingly non-farm, production, with employment income traded for food. This process eliminated mass hunger in Europe in 1750–1960. Only by 1975 had PEM in the developing world retreated to (very high) 1936–8 levels, but it fell sharply in Asia and Latin America in 1975–1990, due to unprecedented growth in staples yields, smallholder and farm employment income, and hence the poor's purchasing power over food. However, since 1990, poverty reduction has slowed (before reaching most of Africa), alongside much slower-staples yield growth, increasing water shortages, and big shifts of grain and land from man to farm animals. These trends prefigure declining progress against PEM in coming decades, unless there is renewed, employment-intensive food-staples-yield growth. That process requires reorienting crop biotechnology and water science towards the needs of small tropical farmers and their staple food crops, and shifting land towards them. Mass PEM is indeed largely due to inadequate ‘food entitlements’ by the hungry, but will not be remedied without growth in their employment, based on further advances in food-staples yields per unit land and water. Recent evidence suggests that early PEM may increase lifelong risks of infection and/or degenerative disease. This factor would increase the ‘squeeze’ on health resources in low-income countries, between the diseases of poverty and those of old age. That situation increases the need to readdress PEM by renewed progress in food production and land distribution.