Development from early conceptus to a complex, multi-cellular organism is a highly ordered process that is dependent on an adequate supply of nutrients. During this process, the pattern of organ growth is robust, driven by a genetic blueprint and matched to anticipated body mass with high precision and with built-in physiological reserve capacity. This apparent canalisation of the developmental process is particularly sensitive to variation in environmental stimuli, such as inappropriate drug or hormone exposure, or pattern of nutrient delivery. Significant variation in any of these factors can profoundly affect fetal and neonatal growth patterns, with later detriment for physiological function and/or reserve capacity of the resultant adult, with potential health impact. This paradigm shift in science has become known as the Developmental Origins of Health and Disease (DOHaD). Over the last 30 years, many animal and clinical studies have vastly expanded our fundamental knowledge of developmental biology, particularly in the context of later effects on health. In this horizons article, we discuss DOHaD through the lens of nutritional quality (e.g. micronutrient, amino acid, NSP intake). The concept of ‘Quality’ was considered undefinable by Robert Persig in his book, ‘Zen and the Art of Motorcycle Maintenance’. Here, development and the art of nutritional maintenance will define quality in terms of the pattern of nutrient intake, the quality of development and how each interact to influence later health outcomes.

Extensive marine terraces along the North Canterbury coast of the South Island of New Zealand record uplift in this tectonically active area. Although the terraces have been studied previously, applications of Quaternary geochronological techniques to the region have been limited. We use infrared-stimulated luminescence (IRSL), amino acid racemization (AAR), and radiocarbon to determine ages of terraces at three locations—Glenafric, Motunau Beach, and Haumuri Bluff. We develop an AAR calibration curve for the mollusk species Tawera spissa from sites of known age, including the sedimentary sequence of the Whanganui Basin. Bayesian model averaging of the results is used to estimate ages of marine shells from the North Canterbury terraces. By using both IRSL and AAR, we are able to confirm ages using two independent dating methods and to identify one IRSL result that is likely in error. We develop new age estimates for the marine terraces of North Canterbury and propose correlations between sites. This terrace chronology differs significantly from most previous studies, highlighting the importance of numerical dating. The most extensive terraces are from marine isotope stages (MISs) 5a and 5c, with partial reoccupation of one terrace during MIS 3, whereas MIS 5e terraces are notably lacking among those dated.

Genetically engineered varieties of creeping bentgrass, resistant to glyphosate, have been developed. Studies were initiated in 2000 and 2001 to examine the relative competitive lateral spread of several transformed lines of creeping bentgrass, nontransformed controls, and cultivar standards. Five-centimeter-diameter vegetative plugs of creeping bentgrass were transplanted into a 1-yr-old stand of perennial ryegrass in Columbus, OH, and 10-yr-old bermudagrass or 10-yr-old St. Augustinegrass in Loxley, AL. Plots were watered to prevent moisture stress to either the bentgrass plugs or surrounding turf swards. Monthly average diameter of the creeping bentgrass was determined by measuring the longest spread and shortest spread. At the end of the experiment, no differences (P = 0.05) in lateral spread were observed between individual lines of transgenic bentgrass, standard cultivars, and nontransformed control lines. Lateral spread of transgenic lines was similar to or less than their nontransformed parent and the standard cultivars tested. Results indicate that glyphosate-resistant creeping bentgrass lines do not spread laterally more than nontransgenic lines. Therefore, if the glyphosate-resistant creeping bentgrass escaped into surrounding turfgrass swards, the potential for spread would not be greater than other creeping bentgrass cultivars currently in use.

The Western diet is typically high in salt and fructose, which have pressor activity. Maternal diet can affect offspring blood pressure, but the extent to which maternal intake of excess salt and fructose may influence cardiovascular function of the offspring is unknown. We sought to determine the effect of moderate maternal dietary intake of salt and/or fructose on resting and stimulated cardiovascular function of the adult male and female offspring. Pregnant rats were fed purified diets (±4 % salt) and water (±10 % fructose) before and during gestation and through lactation. Male and female offspring were weaned onto standard laboratory chow. From 9 to 14 weeks of age, cardiovascular parameters (basal, circadian and stimulated) were assessed continuously by radiotelemetry. Maternal salt intake rendered opposite-sex siblings with a 25-mmHg difference in blood pressure as adults; male offspring were hypertensive (15 mmHg mean arterial pressure (MAP)) and female offspring were hypotensive (10 mmHg MAP) above and below controls, respectively. Sex differences were unrelated to endothelial nitric oxide activity in vivo, but isolation-induced anxiety revealed a significantly steeper coupling between blood pressure and heart rate in salt-exposed male offspring but not in female offspring. MAP of all offspring was refractory to salt loading but sensitive to subsequent dietary fructose, an effect exacerbated in female offspring from fructose-fed dams. Circadian analyses of pressure in all offspring revealed higher mean set-point for heart rate and relative non-dipping of nocturnal pressure. In conclusion, increased salt and fructose in the maternal diet has lasting effects on offspring cardiovascular function that is sex-dependent and related to the offspring’s stress–response axis.

Hypertension is a major risk factor for the development of CVD. Epidemiological studies have shown that low birth weight increases the risk of developing hypertension in adulthood. Hypertension increases the risk of suffering IHD and early findings provide evidence that hearts from prenatally protein-restricted, hypertensive, male offspring are more susceptible to cardiac dysfunction following ischaemic events. Hypertension and abnormalities in cardiac function following ischaemia–reperfusion in the human population are treated therapeutically with β-adrenergic antagonists. We hypothesised that increased susceptibility to myocardial ischaemia–reperfusion injury in prenatally programmed offspring may be due to sympathetic hyperactivity. Pregnant Wistar rats were fed control or low-protein (maternal low protein; MLP) diets throughout gestation. At age 6 months, hearts were rapidly excised and retro-perfused using the Langendorff apparatus, to assess isolated cardiac function following stimulation with increasing doses of the non-specific β-agonist isoproterenol. Baseline heart rates were similar in control and MLP-fed offspring. With significant diet × sex interactions (P < 0·01) maximum heart rate response following isoproterenol infusion was significantly longer in MLP than control. Prenatal diet had no effect on maximal left ventricular developed pressure (LVDP) response, but the LVDP isoproterenol response was significantly longer in duration in MLP-exposed male offspring (diet × sex P < 0·001). Myocardial mRNA expression of β2-adrenergic receptors was increased in 2-week-old female MLP offspring only (P < 0·049). In conclusion, maternal protein restriction programmes cardiac sympathetic activity in a sex-specific manner, and may explain increased susceptibility to ischaemia–reperfusion injury in males subject to fetal undernutrition.

Rats exposed to protein restriction as fetuses develop hypertension as adults. Hypertension increases the risk of myocardial ischaemia and infarction. We investigated whether rats exposed to low-protein diets in utero are more susceptible to myocardial ischaemia–reperfusion (IR) injury. Pregnant Wistar rats were fed control or low-protein (MLP) diets throughout pregnancy. At 4 and 8 weeks postnatal age systolic blood pressure was determined in the offspring using tail-cuff plethysmography. At 6 months of age, rats were treated with saline or N-acetylcysteine (NAC) for 48 h. Rapidly excised hearts were retro-perfused (Langendorff) to assess isolated cardiac function before (baseline), during 30 min ischaemia (no coronary perfusion) and for 60 min after reinstating coronary perfusion (reperfusion). Hearts were then harvested and treated appropriately for analysis of infarct size. Exposure to the MLP diet in utero significantly increased systolic blood pressure at 4 and 8 weeks of age (6–13 mmHg increase; P < 0·001) and significantly impaired recovery of left ventricular developed pressure after ischaemia at 6 months of age in male offspring only (P < 0·003). Pre-treatment with NAC prevented this impairment of recovery in MLP male offspring and improved recovery in all females. Myocardial infarct size was not different between dietary groups after IR, but NAC pre-treatment significantly reduced the degree of infarction (P < 0·001). In conclusion, an MLP diet throughout gestation significantly impairs recovery of the 6-month-old adult rat heart to IR-induced injury in a sex-specific manner. Undernutrition during development may increase susceptibility to CHD by impairing recovery from coronary events.

It is apparent from epidemiological studies that the timing of maternal nutrient restriction has a major influence on outcome in terms of predisposing the resulting offspring to adult obesity. The present review will consider the extent to which maternal age, parity and nutritional restriction at defined stages of gestation can have important effects on fat deposition and endocrine sensitivity of adipose tissue in the offspring. For example, in 1-year-old sheep the offspring of juvenile mothers have substantially reduced fat deposition compared with those born to adult mothers. Offspring of primiparous adult mothers, however, show increased adiposity compared with those born to multiparous mothers. These offspring of multiparous ewes show retained abundance of the brown adipose tissue-specific uncoupling protein 1 at 1 month of age. A stimulated rate of metabolism in brown fat of these offspring may act to reduce adipose tissue deposition in later life. In terms of defined windows of development that can programme adipose tissue growth, maternal nutrient restriction targetted over the period of maximal placental growth results in increased adiposity at term in conjunction with enhanced abundance of mRNA for the insulin-like growth factor-I and -II receptors. In contrast, nutrient restriction in late gestation, coincident with the period of maximal fetal growth, has no major effect on adiposity but results in greater abundance of specific mitochondrial proteins, i.e. voltage-dependent anion channel and/or uncoupling protein 2. These adaptations may increase the predisposal of these offspring to adult obesity. Increasing maternal nutrition in late gestation, however, can result in proportionately less fetal adipose tissue deposition in conjunction with enhanced abundance of uncoupling protein 1.