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To identify peri-conceptional diet patterns among women in Bangalore and examine their associations with risk of gestational diabetes mellitus (GDM).
BAngalore Nutrition Gestational diabetes LifEstyle Study, started in June 2016, was a prospective observational study, in which women were recruited at 5–16 weeks’ gestation. Peri-conceptional diet was recalled at recruitment, using a validated 224-item FFQ. GDM was assessed by a 75-g oral glucose tolerance test at 24–28 weeks’ gestation, applying WHO 2013 criteria. Diet patterns were identified using principal component analysis, and diet pattern–GDM associations were examined using multivariate logistic regression, adjusting for ‘a priori’ confounders.
Antenatal clinics of two hospitals, Bangalore, South India.
Seven hundred and eighty-five pregnant women of varied socio-economic status.
GDM prevalence was 22 %. Three diet patterns were identified: (a) high-diversity, urban (HDU) characterised by diverse, home-cooked and processed foods was associated with older, more affluent, better-educated and urban women; (b) rice-fried snacks-chicken-sweets (RFCS), characterised by low diet diversity, was associated with younger, less-educated, and lower-income, rural and joint families; and (c) healthy, traditional vegetarian (HTV), characterised by home-cooked vegetarian and non-processed foods, was associated with less-educated, more affluent, and rural and joint families. The HDU pattern was associated with a lower GDM risk (adjusted odds ratio (aOR): 0·80/sd, 95 % CI (0·64, 0·99), P = 0·04) after adjusting for confounders. BMI was strongly related to GDM risk and possibly mediated diet–GDM associations.
The findings support global recommendations to encourage women to attain a healthy pre-pregnancy BMI and increase diet diversity. Both healthy and unhealthy foods in the patterns indicate low awareness about healthy foods and a need for public education.
Adults who had non-edematous severe acute malnutrition (SAM) during infancy (i.e., marasmus) have worse glucose tolerance and beta-cell function than survivors of edematous SAM (i.e., kwashiorkor). We hypothesized that wasting and/or stunting in SAM is associated with lower glucose disposal rate (M) and insulin clearance (MCR) in adulthood.
We recruited 40 nondiabetic adult SAM survivors (20 marasmus survivors (MS) and 20 kwashiorkor survivors (KS)) and 13 matched community controls. We performed 150-minute hyperinsulinaemic, euglycaemic clamps to estimate M and MCR. We also measured serum adiponectin, anthropometry, and body composition. Data on wasting (weight-for-height) and stunting (height-for-age) were abstracted from the hospital records.
Children with marasmus had lower weight-for-height z-scores (WHZ) (−3.8 ± 0.9 vs. −2.2 ± 1.4; P < 0.001) and lower height-for-age z-scores (HAZ) (−4.6 ± 1.1 vs. −3.4 ± 1.5; P = 0.0092) than those with kwashiorkor. As adults, mean age (SD) of participants was 27.2 (8.1) years; BMI was 23.6 (5.0) kg/m2. SAM survivors and controls had similar body composition. MS and KS and controls had similar M (9.1 ± 3.2; 8.7 ± 4.6; 6.9 ± 2.5 mg.kg−1.min−1 respectively; P = 0.3) and MCR. WHZ and HAZ were not associated with M, MCR or adiponectin even after adjusting for body composition.
Wasting and stunting during infancy are not associated with insulin sensitivity and insulin clearance in lean, young, adult survivors of SAM. These data are consistent with the finding that glucose intolerance in malnutrition survivors is mostly due to beta-cell dysfunction.
To examine if smaller size at birth, an indicator of growth restriction in utero, is associated with lower cognition in late life, and whether this may be mediated by impaired early life brain development and/or adverse cardiometabolic programming.
Longitudinal follow-up of a birth cohort.
CSI Holdsworth Memorial Hospital (HMH), Mysore South India.
721 men and women (55–80 years) whose size at birth was recorded at HMH. Approximately 20 years earlier, a subset (n = 522) of them had assessments for cardiometabolic disorders in mid-life.
Standardized measurement of cognitive function, depression, sociodemographic, and lifestyle factors; blood tests and assessments for cardiometabolic disorders
Participants who were heavier at birth had higher composite cognitive scores (0.12 SD per SD birth weight [95% CI 0.05, 0.19] p = 0.001) in late life. Other lifecourse factors independently positively related to cognition were maternal educational level and participants’ own educational level, adult leg length, body mass index, and socioeconomic position, and negatively were diabetes in mid-life and current depression and stroke. The association of birth weight with cognition was independent cardiometabolic risk factors and was attenuated after adjustment for all lifecourse factors (0.08 SD per SD birth weight [95% CI −0.01, 0.18] p = 0.07).
The findings are consistent with positive effects of early life environmental factors (better fetal growth, education, and childhood socioeconomic status) on brain development resulting in greater long-term cognitive function. The results do not support a pathway linking poorer fetal development with reduced late life cognitive function through cardiometabolic programming.
Prenatal low vitamin D may have consequences for bone health. By means of a nationwide mandatory vitamin D fortification programme, we examined the risk of fractures among 10–18-year-old children from proximate birth cohorts born around the date of the termination of the programme. For all subjects born in Denmark during 1983–1988, civil registration numbers were linked to the Danish National Patient Registry for incident and recurrent fractures occurring at ages 10–18 years. Multiplicative Poisson models were used to examine the association between birth cohort and fracture rates. The variation in fracture rates across birth cohorts was analysed by fitting an age-cohort model to the data. We addressed the potential modification of the effect of vitamin D availability by season of birth. The risk of fractures was increased among both girls and boys who were born before the vitamin D fortification terminated in 1985 (rate ratio (RR) exposed v. non-exposed girls: 1·15 (95 % CI 1·11, 1·20); RR exposed v. non-exposed boys: 1·11 (95 % CI 1·07, 1·14). However, these associations no longer persisted after including the period effects. There was no interaction between season of birth and vitamin D availability in relation to fracture risk. The study did not provide evidence that prenatal exposure to extra vitamin D from a mandatory fortification programme of 1·25 µg vitamin D/100 g margarine was sufficient to influence the risk of fractures in late childhood, regardless of season of birth. Replication studies are needed.
We aimed to test the fetal overnutrition hypothesis by comparing the associations of maternal and paternal adiposity (sum of skinfolds) with adiposity and cardiovascular risk factors in children.
Children from a prospective birth cohort had anthropometry, fat percentage (bio-impedance), plasma glucose, insulin and lipid concentrations and blood pressure measured at 9·5 years of age. Detailed anthropometric measurements were recorded for mothers (at 30 ± 2 weeks’ gestation) and fathers (5 years following the index pregnancy).
Holdsworth Memorial Hospital, Mysore, India.
Children (n 504), born to mothers with normal glucose tolerance during pregnancy.
Twenty-eight per cent of mothers and 38 % of fathers were overweight/obese (BMI ≥ 25·0 kg/m2), but only 4 % of the children were overweight/obese (WHO age- and sex-specific BMI ≥ 18·2 kg/m2). The children's adiposity (BMI, sum of skinfolds, fat percentage and waist circumference), fasting insulin concentration and insulin resistance increased with increasing maternal and paternal sum of skinfolds adjusted for the child's sex, age and socio-economic status. Maternal and paternal effects were similar. The associations with fasting insulin and insulin resistance were attenuated after adjusting for the child's current adiposity.
In this population, both maternal and paternal adiposity equally predict adiposity and insulin resistance in the children. This suggests that shared family environment and lifestyle, or genetic/epigenetic factors, influence child adiposity. Our findings do not support the hypothesis that there is an intra-uterine overnutrition effect of maternal adiposity in non-diabetic pregnancies, although we cannot rule out such an effect in cases of extreme maternal obesity, which is rare in our population.
People who were small at birth have been shown to have an increased risk of CHD and chronic bronchitis in later life. These findings have led to the fetal origins hypothesis that proposes that the fetus adapts to a limited supply of nutrients, and in doing so it permanently alters its physiology and metabolism, which could increase its risk of disease in later life. The Dutch famine — though a historical disaster — provides a unique opportunity to study effects of undernutrition during gestation in humans. People who had been exposed to famine in late or mid gestation had reduced glucose tolerance. Whereas people exposed to famine in early gestation had a more atherogenic lipid profile, somewhat higher fibrinogen concentrations and reduced plasma concentrations of factor VII, a higher BMI and they appeared to have a higher risk of CHD. Though the latter was based on small numbers, as could be expected from the relatively young age of the cohort. Nevertheless, this is the first evidence in humans that maternal undernutrition during gestation is linked with the risk of CHD in later life. Our findings broadly support the hypothesis that chronic diseases originate through adaptations made by the fetus in response to undernutrition. The long-term effects of intrauterine undernutrition, however, depend upon its timing during gestation and on the tissues and systems undergoing critical periods of development at that time. Furthermore, our findings suggest that maternal malnutrition during gestation may permanently affect adult health without affecting the size of the baby at birth. This gives the fetal origins hypothesis a new dimension. It may imply that adaptations that enable the fetus to continue to grow may nevertheless have adverse consequences for health in later life. CHD may be viewed as the price paid for successful adaptations to an adverse intra-uterine environment. It also implies that the long-term consequences of improved nutrition of pregnant women will be underestimated if these are solely based on the size of the baby at birth. We need to know more about what an adequate diet for pregnant women might be. In general, women are especially receptive to advice about diet and lifestyle before and during a pregnancy. This should be exploited to improve the health of future generations.
This chapter uses new epidemiological data to examine the role of materno-placental interactions in initiating chronic disease in the offspring. The size, weight and shape of the placenta are all subject to wide variations. Its size reflects its ability to transfer nutrients. In humans, placental growth responds to maternal influences. Maternal anemia and high maternal body mass index are associated with a high placental weight to birth weight ratio. The observations on hypertension established that the relation between placental size/shape and fetal programming depend on the mother. There are similar materno-placental interactions in the programming of coronary heart disease. Growth of the placental surface is polarized from the time of implantation. The human fetus may attempt to compensate for undernutrition by expansion of the placental surface along its minor axis. The maternal/ placental programming of chronic disease differs in boys and girls.
Both intra-uterine and early childhood development contribute to the risk of developing CVD in adult life. We therefore evaluated the maternal, placental, fetal, birth, infant and childhood determinants of cardiovascular risk in a cohort of Afro-Jamaican children. The Vulnerable Windows Cohort is a longitudinal survey of 569 mothers and their offspring recruited from the first trimester. The offspring's anthropometry was measured at birth, at 6 weeks, every 3 months to 1 year and then every 6 months. At mean age 11·5 years, fasting blood was sampled for glucose, insulin and lipids. Analyses were confined to 296 women and their offspring who had complete data. Waist circumference (WC) was related to maternal weight and BMI, placental weight and to the size of the offspring in utero, at birth and the rate of growth in childhood (P < 0·05). Total cholesterol, TAG and glucose concentrations were unrelated to maternal, placental, fetal, neonatal and childhood measurements. Fasting insulin and homeostasis model assessment of insulin resistance were related to maternal weight and BMI (P < 0·05), but not after adjusting for WC. HDL-cholesterol was inversely related to placental and birth weight, and inversely related to weight and BMI throughout childhood (P < 0·001), but not after adjusting for WC. Systolic blood pressure was directly related to maternal weight, child's height, weight and BMI (P < 0·05), but not after adjustment for WC. Systolic blood pressure and fasting glucose concentration were inversely related to birth weight in boys but directly associated in girls. We concluded that maternal anthropometry during pregnancy, fetal size, and childhood growth rate contribute to cardiovascular risk factors in childhood.
Environmental perturbations during early mammalian development can affect aspects of offspring growth and cardiovascular health. We have demonstrated previously that maternal gestational dietary protein restriction in mice significantly elevated adult offspring systolic blood pressure. Therefore, the present study investigates the key mechanisms of blood pressure regulation in these mice. Following mating, female MF-1 mice were assigned to either a normal-protein diet (NPD; 18 % casein) or an isocaloric low-protein diet throughout gestation (LPD; 9 % casein), or fed the LPD exclusively during the pre-implantation period (3·5 d) before returning to the NPD for the remainder of gestation (Emb-LPD). All offspring received standard chow. At 22 weeks, isolated mesenteric arteries from LPD and Emb-LPD males displayed significantly attenuated vasodilatation to isoprenaline (P = 0·04 and P = 0·025, respectively), when compared with NPD arteries. At 28 weeks, stereological analysis of glomerular number in female left kidneys revealed no significant difference between the groups. Real-time RT-PCR analysis of type 1a angiotensin II receptor, Na+/K+ ATPase transporter subunits and glucocorticoid receptor expression in male and female left kidneys revealed no significant differences between the groups. LPD females displayed elevated serum angiotensin-converting enzyme (ACE) activity (P = 0·044), whilst Emb-LPD males had elevated lung ACE activity (P = 0·001), when compared with NPD offspring. These data demonstrate that elevated offspring systolic blood pressure following maternal gestational protein undernutrition is associated with impaired arterial vasodilatation in male offspring, elevated serum and lung ACE activity in female and male offspring, respectively, but kidney glomerular number in females and kidney gene expression in male and female offspring appear unaffected.
The present study aimed to investigate weight retention and body composition in the postpartum period between adolescent girls and older women.
A prospective cohort study. Anthropometry and skinfold thickness measurements were performed at the first antenatal visit and at 6 weeks postpartum. An FFQ was administered at 6 weeks postpartum to explore the relationship between diet and postpartum weight retention.
Clinics at the University of the West Indies, Kingston, Jamaica.
Recruitment included women aged 19 years and younger (adolescent girls) and 20 years and older (older women).
Three hundred and forty women were studied. Adolescent girls had significantly lower measurements compared with the older women at the first antenatal visit and at 6 weeks postpartum. Dietary intakes of energy and macronutrients were similar in both groups. Postnatal assessments showed that adolescent girls retained more weight (P = 0·003) and a greater percentage of body fat (P < 0·002) than older women. In multiple regression analyses, 0·982 kg more fat mass was retained postpartum in the adolescent group compared with the older women, while there was no significant difference in lean body mass retained between the two groups.
Adolescent girls retained more weight postpartum and this was predominantly fat mass as opposed to lean body mass.
A non-optimal foetal environment, reflected in smaller birth size and shorter duration of gestation, is a risk factor for compromised health later in life.
To examine whether smaller birth size and shorter gestation predict depressive symptoms.
A total of 1371 members of a cohort born between 1934 and 1944 at term (259–294 days' gestation) in Helsinki, Finland, completed the Beck Depression Inventory (BDI) and the Center for Epidemiological Studies Depression scale (CES–D) at an average age of 61.5 years (BDI) and 63.4 years (BDI and CES–D).
Gestational length predicted depressive symptoms linearly and independently of gender and birth weight: per day decrease in gestational length, depressive symptoms scores increased by 0.8-0.9% (95% CI 0.2-1.4, P<0.009). Weight, length and head circumference at birth showed no linear association with depression, adjusted for gender and gestational length. The results did not change when further controlled for socioeconomic characteristics at birth and in adulthood, age and body mass index in adulthood.
Susceptibility to depressive symptoms may relate to shorter length of gestation.
Low birth weight is a risk factor for coronary heart disease, diabetes, stroke and hypertension. Depression is highly associated with these conditions.
To examine the association between birth weight and depression in late life.
A total of 882 singleton term births in the 1920s had contemporary records of birth weight and weight at 1 year. At 68 years all completed the Geriatric Depression Scale and 867 completed the Geriatric Mental State Examination. A logistic regression was used to analyse the associations between depression, birth weight and weight at 1 year while adjusting for known risk factors.
Current social class, social class at birth, recent bereavement, social isolation and physical illness increased the risk of depression. After adjusting for these and weight at 1 year, the odds ratios for depression among men, but not women, rose incrementally with decreasing birth weight (1.0, 12.8; for continuous variable, P < 0.007).
Foetal undernutrition predisposes men to depression in late adult life. If replicated, these results would suggest a neurodevelopmental aetiology of depression, possibly mediated by programming of the hypothalamic–pituitary–adrenal axis.
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