3,924 research outputs found
The fetal and early life origins of adult disease
No full textThe fetal origins of adult disease (FOAD) hypothesis is based on the observation that men and women who were small at birth (low birthweight) have an increased risk of atherosclerotic cardiovascular disease (CVD) and the related diseases hypertension, type 2 diabetes and the Insulin Resistance Syndrome. Risk is increased further if they showed rapid weight gain in childhood or become obese. The hypothesis proposes that CVD is ‘programmed’ by under nutrition during critical periods of early development and that ‘poverty’ during early life creates a permanent vulnerability to ‘diseases of affluence’. This concept is arguably of greatest relevance to developing countries, where fetal growth restriction still affects large numbers of people, where economic progress is leading to the emergence of childhood and adult obesity, and where CVD and type 2 diabetes are rising rapidly. Its implication is that the prevention of adult disease should include strategies to improve maternal health and fetal growth. This paper reviews work leading to the FOAD hypothesis and the results of FOAD research in India. It also discusses some of the controversies surrounding the hypothesis, notably the debate as to whether the link between fetal growth restriction and adult CVD is mediated by environmental factors (such as maternal nutrition) or by genes
Maternal vitamin D deficiency and GDM risk: evidence for the case of investing more attention in antenatal clinics
No full textGestational diabetes mellitus (GDM) is a global public health problem, and in India, it affects about 20% of pregnancies. India, despite being a tropical country with abundant sunshine has a high prevalence (80%) of vitamin D deficiency (VDD) among reproductive-aged women. Global and Indian evidence links VDD with a higher risk of hyperglycaemia in pregnancy and GDM. VDD has also been implicated in gestational hypertension, preterm birth and poorer offspring health. Global scientific consensus acknowledges the need for maternal vitamin D screening and supplementation, but knowledge gaps exist about optimal blood levels (50-100 nmol/l), and the required vitamin D dosage (400-4000 IU). Diet can provide <10% of the vitamin D requirements, food fortification can deliver limited amounts, and hence optimal antenatal supplementation is key. Prenatal calcium supplements containing 400 IU of vitamin D may be sufficient for calcium absorption and bone health, but may not provide immunomodulatory benefits, including GDM prevention. Increasing evidence calls for higher maternal vitamin D requirements (2000-4000 IU) for skeletal, metabolic and immune health benefits. Current screening and supplementation for maternal VDD in India is low. We need to invest in future studies to determine optimal maternal vitamin D requirements and formulate policies for vitamin D supplementation to prevent GDM. Improving the maternal vitamin D status is an important nutritional priority for policymakers to reduce the large economic burden of non-communicable diseases (10% of India's gross domestic product), and eventually achieve the 2030 UN sustainable development goals.</p
Newborn size and body composition as predictors of insulin resistance and diabetes in the parents: Parthenon Birth Cohort Study, Mysore, India
No full textObjective: ee aimed to examine detailed neonatal measurements as predictors of later diabetes in both parents.Research Design and Methods: babies (n = 617) born to nondiabetic parents in Holdsworth Memorial Hospital, Mysore, India, were measured at birth for weight; crown-to-heel length (CHL), crown-to-rump length (CRL), and leg length; skinfolds (triceps and subscapular); and circumferences (head, abdomen, and mid-upper-arm circumference [MUAC]). Nine and a half years later, glucose tolerance and fasting insulin were measured in their parents (469 mothers and 398 fathers).Results: sixty-two (15.6%) fathers and 22 (4.7%) mothers had developed diabetes. There were linear inverse associations of the children's birth weight, CHL, CRL, MUAC, and skinfolds with paternal diabetes and insulin resistance (P < 0.05 for all). Offspring birth weight and adiposity (MUAC, abdominal circumference, and skinfolds) showed U-shaped associations with maternal diabetes (P for quadratic association <0.05 for all). These associations persisted after adjusting for the parents' current adiposity and maternal glucose concentrations and adiposity during pregnancy. Newborn adiposity was positively related to maternal insulin resistance; this association was nonsignificant after adjusting for maternal current adiposity.Conclusions: newborn size is a window into the future health of the parents. Small newborn size (especially soft-tissue body components) predicts an increased risk of later diabetes in both parents, suggesting a genetic or epigenetic link between parents' diabetes risk and reduced fetal growth in their children. The association of higher birth weight and newborn adiposity with later maternal diabetes suggests effects on fetal adiposity of the intrauterine environment in prediabetic mother
Consequences of poor maternal micronutrition before and during early pregnancy
No full textIn developing countries, micronutrient deficiencies are common and associated with poor pregnancy outcomes, which may in turn have longer-term effects on human health. The peri-conceptional period represents a particularly sensitive window of feto-placental development, during which suboptimal maternal micronutrition may have far-reaching consequences. The effects of targeted interventions during this period have been little studied in humans
A principal components approach to parent-to-newborn body composition associations in South India
No full textBackground: size at birth is influenced by environmental factors, like maternal nutrition and parity, and by genes. Birth weight is a composite measure, encompassing bone, fat and lean mass. These may have different determinants. The main purpose of this paper was to use anthropometry and principal components analysis (PCA) to describe maternal and newborn body composition, and associations between them, in an Indian population. We also compared maternal and paternal measurements (body mass index (BMI) and height) as predictors of newborn body composition.Methods: weight, height, head and mid-arm circumferences, skinfold thicknesses and external pelvic diameters were measured at 30 ± 2 weeks gestation in 571 pregnant women attending the antenatal clinic of the Holdsworth Memorial Hospital, Mysore, India. Paternal height and weight were also measured. At birth, detailed neonatal anthropometry was performed. Unrotated and varimax rotated PCA was applied to the maternal and neonatal measurements.Results: rotated PCA reduced maternal measurements to 4 independent components (fat, pelvis, height and muscle) and neonatal measurements to 3 components (trunk+head, fat, and leg length). An SD increase in maternal fat was associated with a 0.16 SD increase (?) in neonatal fat (p < 0.001, adjusted for gestation, maternal parity, newborn sex and socio-economic status). Maternal pelvis, height and (for male babies) muscle predicted neonatal trunk+head (? = 0. 09 SD; p = 0.017, ? = 0.12 SD; p = 0.006 and ? = 0.27 SD; p < 0.001). In the mother-baby and father-baby comparison, maternal BMI predicted neonatal fat (? = 0.20 SD; p < 0.001) and neonatal trunk+head (? = 0.15 SD; p = 0.001). Both maternal (? = 0.12 SD; p = 0.002) and paternal height (? = 0.09 SD; p = 0.030) predicted neonatal trunk+head but the associations became weak and statistically non-significant in multivariate analysis. Only paternal height predicted neonatal leg length (? = 0.15 SD; p = 0.003).Conclusion: principal components analysis is a useful method to describe neonatal body composition and its determinants. Newborn adiposity is related to maternal nutritional status and parity, while newborn length is genetically determined. Further research is needed to understand mechanisms linking maternal pelvic size to fetal growth and the determinants and implications of the components (trunk v leg length) of fetal skeletal growt
Evidence for the intra-uterine programming of adiposity in later life
No full textAim: Research in animals has shown that altering foetal nutrition by under-nourishing or over-nourishing the mother or rendering her diabetic or foetal exposure to glucocorticoids and toxins can programme obesity in later life. The increased adiposity is mediated by permanent changes in appetite, food choices, physical activity and energy metabolism. In humans, increased adiposity has been shown in people who experienced foetal under-nutrition due to maternal famine or over-nutrition due to maternal diabetes. Lower birth weight (a proxy for foetal under-nutrition) is associated with a reduced adult lean mass and increased intra-abdominal fat. Higher birth-weight caused by maternal diabetes is associated with increased total fat mass and obesity in later life. There is growing evidence that maternal obesity, without diabetes, is also a risk factor for obesity in the child, due to foetal over-nutrition effects. Maternal smoking is associated with an increased risk of obesity in the children, although a causal link has not been proven. Other foetal exposures associated with increased adiposity in animals include glucocorticoids and endocrine disruptors.Conclusions: Reversing the current obesity epidemic will require greater attention to, and better understanding of, these inter-generational (mother-offspring) factors that programme body composition during early development.<br/
Joint growth hormone and cortisol spontaneous secretion is more asynchronous in older females than in their male counterparts
No full textIn humans, cortisol and GH are secreted in a pulsatile manner, and an interaction between GH and the hypothalamic-pituitary-adrenal axis has been established. In view of the sexually dimorphic pattern in GH secretion, we investigated the GH-cortisol bihormonal secretory dynamics in male and female healthy older individuals. We studied the GH and cortisol secretory patterns in 83 healthy subjects (45 men and 38 women; age range, 59.4–73.0 yr) by determining serum GH and cortisol concentrations at 20-min intervals for 24 h. The irregularity of GH and cortisol secretion was assessed using approximate entropy (ApEn), a scale- and model-independent statistic. The synchrony of joint GH-cortisol spontaneous secretion was quantified using the cross-ApEn statistic. Cross-correlation analysis of GH and cortisol patterns was computed at various time lags covering the 24-h period. Mean 24-h serum GH concentrations were significantly higher in females (mean, 1.31 mU/L; SD, 0.87) than in males (mean, 0.88 mU/L; SD, 0.42; P = 0.009), whereas mean 24-h serum total cortisol concentrations were higher in males (mean, 9.0 µg/dL; SD, 1.4) than in females (mean, 7.3 µg/dL; SD, 1.4; P = 0.0001). GH secretion was more irregular in females (mean ApEn, 0.81; SD, 0.23) than in males (mean ApEn, 0.60; SD, 0.20; P < 0.001). No significant difference in the regularity of cortisol secretion was noted between sexes. Cross-ApEn values of paired GH-cortisol were higher in females (mean, 1.15; SD, 0.18) than in males (mean, 1.01; SD, 0.16; P = 0.0003). Stepwise multiple linear regression analysis indicated that estradiol and insulin-like growth factor-binding protein-3 concentrations were independently related to GH ApEn values (r2 = 0.14; P = 0.01), whereas cross-ApEn values of paired GH-cortisol were best predicted by FSH concentrations (r2 = 0.37; P = 0.003). Cross-correlation analysis revealed a significant positive correlation between GH and cortisol, peaking at lag time of 4.7 h in males (r = 0.30; P < 0.0001) and 4.3 h in females (r = 0.14; P < 0.0001), with GH leading cortisol by these time intervals. In addition, a significant negative correlation between the two hormones was noted over time, peaking at 4.7 h in males (r = -0.21; P < 0.0001) and 6.3 h in females (r = -0.25; P < 0.0001), with cortisol leading GH by these time intervals. The above results indicate that in the elderly, females have a more disordered GH secretory pattern and a more asynchronous joint GH-cortisol secretion than their male counterparts. These observations most likely reflect bidirectional interactions between the GH and hypothalamic-pituitary-adrenal axis in humans as well as diminution of subsystem integrity and synchronous control of interconnected hormonal systems with advancing age. <br/
Intergenerational change in anthropometric indices and their predictors among children in New Delhi Birth Cohort
No full textObjective: to evaluate intergenerational change in anthropometric indices of children and their predictors.Design: prospective cohortParticipants: New Delhi Birth Cohort participants (F1), born between 1969 and 1972, were followed-up for anthropometry at birth and 6-monthly intervals until 21 years. Their children (F2) below 10 years were evaluated anthropometrically.Outcome measure: intergenerational change (F2-F1) in height, weight and body mass index (BMI) of children in comparison to their parents at corresponding ages.Results: 432 F2-F1 pairs were analyzed in age-groups of 0-5 (26.9%) and 5-10 (73.1%) years. Children were considerably taller (0-5 years 0.99 SD; 5-10 years 1.17 SD) and heavier (0-5 years 0.77 SD; 5-10 years 1.52 SD) while only those aged 5-10 years were broader (had a higher BMI; 1.03 SD), than their parents. These increases for 0-5 and 5-10 years, respectively corresponded to 3.9 and 6.4 cm for height, 1.3 and 5.4 kg for weight and 0.2 and 1.9 kg/m2 for BMI. Lower parents’ anthropometric indices and poor water supply and sanitation facilities; higher age of parents at child birth and of children when measured (for height and weight); and more parental education (for weight and BMI), were associated with greater intergenerational gains in children.Conclusion: over one generation in an urban middle-class population, whose general living conditions had improved, underfive children have become considerably taller and heavier, and 5- 10 year old children have additionally become broader, than their parents at corresponding ages. Child populations probably ‘grow up’ before ‘growing out’
A review of adolescent nutrition in South Africa: transforming adolescent lives through nutrition initiative
No full textObjective: In South Africa, urbanisation is associated with substantial burdens of adolescent overweight and obesity, making teenagers vulnerable to longer-term non-communicable diseases. In addition, as potential future parents, the nutritional status of adolescents is increasingly recognised as a key driver of health and well-being in the next generation. This review reported on the available literature examining nutritional status and dietary intakes and practices, as well as their determinants, in South African adolescents. Study design and methods: Medline (Pubmed), Web of Science and EMBASE were searched for relevant articles published between 1994 and May 2018. Applicable search terms and phrases were identified in study titles and/or abstracts and full-text articles were reviewed according to inclusion/exclusion criteria. Data were extracted according to specific review objectives. Results: A total of 67 relevant studies were identified. Only one study used a biochemical marker to describe adolescent nutritional status (vitamin D status; 25(OH)D). Overweight and obesity prevalence increased in South African adolescents over the reference period, with national increases of 6% in boys and 7% in girls between 2002 and 2008. Girls and urban-dwellers were particularly vulnerable to excess adiposity. Dietary intakes demonstrated a transition towards energy-dense, processed foods high in sugar and fat, but low in essential micronutrients. Food choices were driven by the adoption of obesogenic behaviours in the teenage years, including irregular breakfast consumption and fewer family meals, increased snacking and low levels of physical activity. Conclusion: South African adolescents—particularly girls—are increasingly burdened by obesity as a result of urbanisation-associated shifts in dietary intake and eating behaviours. However, the implications for micronutrient status and long-term nutritional health are not known. Additionally, more data on the clustering of diet, activity and sedentary behaviours in adolescent boys and girls is needed, as well as on behaviour patterns to facilitate healthy growth and reduced adiposity.</p
Evidence of sexual dimorphism in relationships between estrogen receptor polymorphisms and bone mass: the Hertfordshire study
No full textObjective: to examine the relationship between estrogen receptor (ER) a and ß gene polymorphisms and bone mass.Methods: bone mineral density (BMD) was measured at the lumbar spine and proximal femur twice, 4 years apart, in a cohort of 147 men and 125 women aged 61-73 years. Genomic DNA was extracted from whole blood samples, and genotyping for the ER (PvuII, XbaI, and AluI) was undertaken.Results: there were no significant associations between either the XbaI or PvuII polymorphisms and bone mass, or bone loss in the cohort as a whole. However, men homozygous for the aa ß receptor polymorphism had higher BMD at the lumbar spine (p = 0.05), femoral neck (p = 0.01), and total femur (p = 0.01). Women homozygous for aa had lower femoral neck and total femoral BMD than women of the AA or Aa genotypes (p = 0.01 and p = 0.02). Gender*ERß interaction terms were statistically significant (p = 0.02 for lumbar spine BMD, p = 0.0004 for femoral neck BMD, and p = 0.0003 for total femoral BMD, each test with 2 degrees of freedom unadjusted). Adjustment for sex hormone concentration and lifestyle factors made little difference to our results.Conclusion: we found relationships between the ERß gene and the determination of bone mass among men and women in their seventh decade
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