OBJECTIVE: To examine body size and fat measurements of babies born in rural India and compare them with white Caucasian babies born in an industrialised country.
DESIGN: Community-based observational study in rural India, and comparison with data from an earlier study in the UK, measured using similar methods.
SUBJECTS: A total of 631 term babies born in six rural villages, near the city of Pune, Maharashtra, India, and 338 term babies born in the Princess Anne Hospital, Southampton, UK.
MEASUREMENTS: Maternal weight and height, and neonatal weight, length, head, mid-upper-arm and abdominal circumferences, subscapular and triceps skinfold thicknesses, and placental weight.
RESULTS: The Indian mothers were younger, lighter, shorter and had a lower mean body mass index (BMI) (mean age, weight, height and BMI: 21.4 y, 44.6 kg, 1.52 m, and 18.2 kg/m2) than Southampton mothers (26.8 y, 63.6 kg, 1.63 m and 23.4 kg/m2). They gave birth to lighter babies (mean birthweight: 2.7 kg compared with 3.5 kg). Compared to Southampton babies, the Indian babies were small in all body measurements, the smallest being abdominal circumference (s.d. score: −2.38; 95% CI: −2.48 to −2.29) and mid-arm circumference (s.d. score: −1.82; 95% CI: −1.89 to −1.75), while the most preserved measurement was the subscapular skinfold thickness (s.d. score: −0.53; 95% CI: −0.61 to −0.46). Skinfolds were relatively preserved in the lightest babies (below the 10th percentile of birthweight) in both populations.
CONCLUSIONS: Small Indian babies have small abdominal viscera and low muscle mass, but preserve body fat during their intrauterine development. This body composition may persist postnatally and predispose to an insulin-resistant state.
India is experiencing a rapidly escalating ‘epidemic’ of Type II diabetes1 and coronary heart disease (CHD).2,3,4 In a recent survey of adults in six cities, 12% were found to be diabetic and 14% had impaired glucose tolerance (IGT).5 This represents a more than five-fold increase over the last 30 y. Today, India has more diabetic patients (∼25 million) than any other single country, and the number is predicted to rise to 57 million by the year 2025.6 It is also predicted that CHD will become the leading cause of death by the year 2015.4 Indians as a group are insulin resistant compared to many other populations7 and manifest features of the ‘insulin resistance syndrome (IRS).8,9 This occurs on the background of a characteristic body composition: Indians are thin by conventional criteria (low body mass index (BMI)) but are centrally obese.10 Recent research suggests that adult Indians have more body fat and lower muscle volumes than white Caucasians, African Americans and other ethnic groups of comparable BMI.11,12,13,14 Thus, the Indian body composition could be described as adipose but muscle thin.
The current diabetes epidemic in India is traditionally attributed to ‘thrifty’ genes, which helped survival in the past when food supply was intermittent but have become detrimental in the modern context of plentiful food and reduced physical work.15 A recently proposed alternative explanation is the ‘thrifty phenotype’ (fetal origins) hypothesis,16,17 which proposes that persistent metabolic and structural changes caused by fetal under-nutrition increase the risk of type II diabetes and CHD. In the majority of studies, low birthweight is used as an indicator of fetal undernutrition. Indian babies are among the lightest in the world and might be expected to be at increased risk of type II diabetes and CHD.18 However, birthweight is a poor indicator of the complexities of intrauterine growth and does not provide information about body composition that may be relevant to subsequent morbidity and mortality. A better characterisation of the body composition at birth of Indian babies may improve our understanding of the ‘thrifty phenotype’ and fetal origins of adult disease. We, therefore, studied in detail the birth measurements of Indian babies and compared them with those of white Caucasian babies born in Southampton, UK, who were measured using similar methods. The babies in the UK belong to a population that is relatively well nourished, providing a ‘control’ population.
Details of the Pune Maternal Nutrition Study have been reported.19,20 In brief, all married women (n=2675) of childbearing age living in six villages near the city of Pune (Maharashtra, India) who agreed to be studied were followed up every month to record their menstrual dates, and every 3 months for detailed anthropometry. A total of 797 women who became pregnant were studied twice during pregnancy for their nutritional status, biochemical parameters and fetal growth. Enrolment began in June 1994 and ended in April 1996. The babies in Southampton were measured as part of a student research project in 1987 that aimed to recruit all liveborn singleton babies without major congenital malformations born on weekdays between 19 January and 25 April 198721 (n=668) in the Princess Anne Hospital, the main maternity hospital in the city. In both populations, gestational age was derived from the LMP, unless it differed from that derived from an early ultrasound scan (<20 weeks gestation) by more than 2 weeks, in which case the latter was used. The analysis is limited to singleton, liveborn, full-term (gestational age ≥37 weeks) babies.
Measurement of the babies
In Pune, the babies were measured at birth by one of five trained fieldworkers. Birthweight was measured using a Salter spring balance; crown–heel length using a portable Pedobaby Babymeter (ETS JMB, Brussels, Belgium); occipito-frontal head circumference, mid-upper-arm circumference (MUAC) and abdominal circumference using a fibre glass tape (CMS Instruments, London, UK) and subscapular and triceps skinfold thicknesses using Harpenden skinfold callipers (CMS Instruments, London, UK). Abdominal circumference was measured immediately above the umbilical cord insertion, in expiration. In Southampton, birthweight was measured using a digital electronic weighing scale in the labour ward. Other measurements were made by one of two trained observers. The crown–heel length was measured using a Harpenden infant stadiometer (CMS instruments, London, UK), head circumference, MUAC and abdominal circumference using blank paper tapes that were marked and measured against a steel rule. Unlike in Pune, the abdominal circumference was measured at the level of the xiphisternum. Subscapular skinfold thickness was measured using Harpenden skinfold callipers (CMS instruments, London, UK). In both centres, a time limit of 72 h postdelivery was put on these measurements.
Ethical permission for the study was given by the respective Ethical Committees of both institutes and by village authorities in Pune.
Data are presented as means (s.d.) for normally distributed variables; skinfold thickness measurements and maternal weight and BMI were log transformed to satisfy assumptions of normality and are shown as the median and interquartile range. We compared Pune and Southampton babies using sex- and gestation-specific s.d. scores: Pune s.d. score=(Pune observation–Southampton mean)/Southampton s.d. Because abdominal circumference was measured at different levels in the two places, xiphisternum in Southampton and umbilicus in Pune, we subsequently measured 50 full-term Pune babies, at both levels, allowing us to calculate comparable regression-adjusted xiphisternum values for the Pune data. Both unadjusted and adjusted values are reported. We also examined within-population s.d. scores, (individual observation−whole cohort mean)/whole cohort s.d., to examine how different anthropometric measurements varied with birthweight within each population. Paired t-tests were used to compare s.d. scores for different measurements at different levels of birthweight (<10th centile, 10–90th centile and >90th centile) within each population. The data were analysed using the software package SPSS/PC v 5.0.
Of the 797 pregnant women enrolled in the Pune study, 12 had spontaneous abortions, 14 had late terminations and one died of pregnancy-induced hypertension. In all, 770 infants were delivered, of whom 71 were premature, eight were stillborn, nine had major anomalies and 51 did not have birth measurements within 72 h. Babies born to one woman with diabetes, and one with pregnancy-induced hypertension were excluded. Our analysis relates to 631 babies. Of 668 normal liveborn singleton babies born in Southampton, 235 were not measured within 72 h, a further 13 were premature, four were born to diabetic mothers and 35 were born to mothers with hypertension. Our analysis relates to 338 babies.
Comparison between Pune and Southampton mothers and babies
The characteristics of the mothers and their babies are shown in Table 1. Pune mothers were younger and smaller in all respects than the UK mothers. Maternal weight and height were lower by 2.09 (95% CI: −2.15 to −2.03) and 1.68 (95% CI: −1.74 to −1.62) standard deviations, respectively (Figure 1a). Gestational age at delivery was lower in Pune by an average of 4.7 days. Even after allowing for their smaller gestational age, the Indian babies were smaller in all measurements than the babies born in Southampton (Figure 1a). Birthweight, placental weight, and neonatal head and mid-arm circumferences were reduced to a degree comparable to maternal measurements (s.d. scores: −1.74 (95% CI: −1.81 to −1.68); −1.43 (95% CI: −1.50 to −1.37), −1.68 (95% CI: −1.76 to −1.61) and −1.82 (95% CI: −1.89 to −1.75), respectively). There was a larger deficit in abdominal circumference (s.d. score: −2.99; 95% CI: −3.09 to −2.89), even after adjustment for the different measurement technique in Southampton (s.d. score: −2.38; 95% CI: −2.48 to −2.29). In contrast, neonatal length was relatively spared (s.d. score: −1.01; 95% CI: −1.09 to −0.93), and subscapular skinfold thickness markedly so (s.d. score −0.53; 95% CI: −0.61 to −0.46). Low birthweight Pune babies (<2500 g) also demonstrated fat preservation relative to birthweight when compared to the Southampton babies (Figure 1b). When we compared neonatal measurements of babies with comparable birthweight (2800–3300 g) in Pune and Southampton, Pune babies were longer and more adipose (subscapular skinfold), although Southampton babies were larger in other measurements (Table 2). A conventional measure of neonatal ‘thinness’ is the ponderal index (PI). A comparison of the relationship between subscapular skinfold and PI in the two populations revealed that at any subscapular skinfold thickness, the Indian babies have a lower PI (thinner) than that of the white Caucasian babies (Figure 2).
Figure 3 shows s.d. scores for the anthropometric measurements, with the babies divided into three groups: <10th percentile, 10th–90th percentile and >90th percentile, in this case calculated within each of the two populations. A similar pattern was seen in both places, such that at low birthweights (<10th percentile) there was relative sparing of body fat (Pune subscapular s.d. score: −1.00, 95% CI: −1.23 to −0.78; Southampton subscapular s.d. score: −0.92, 95% CI: −1.17 to −0.68) compared with birthweight (Pune birthweight s.d. score: −1.57, 95% CI: −1.71 to −1.43; Southampton birthweight s.d. score: −1.39, 95% CI: −1.53 to −1.25). The difference between subscapular s.d. score and birthweight s.d. score was statistically significant (P<0.001 in both centres). In both Pune and Southampton, the only other body measurement similarly preserved was the head circumference (Figure 3, Pune head circumference s.d. score: −0.94, 95% CI: −1.18 to −0.70; Southampton head circumference s.d. score: −0.96, 95% CI: −1.22 to −0.70).
To our knowledge, this is the first population-based study in which detailed anthropometric measurements have been made in a large number of rural Indian women and their newborn babies. Consistent with other Indian data,18,22 the babies had low birthweights. We have gone beyond birthweight, however, to define the detailed phenotype of Indian babies. There was a pattern in their smallness (Figure 1), with relative sparing of subcutaneous fat. In contrast, abdominal circumference, which reflects visceral size, was markedly reduced, as was MUAC, which reflects muscle bulk.
We have compared Indian babies with those born in Southampton 10 y ago and, importantly, measured using similar anthropometric techniques. There are few other data sets with such detailed measurements of the baby. The UK represents an affluent industrialised country where mean birthweight has changed only modestly over many decades: there has been an increase in percentage of heavier birthweights as well as very low birthweights, the distribution shifting towards heavier birthweights.23 Analysis in Scotland suggested that the increase in birthweight is contributed by increased maternal height and age, by a decrease in the proportion of induced births and also by a reduction in maternal smoking.24
Our findings suggest that in these underweight Indian babies, fat deposition continues, while abdominal viscera and muscle are ‘sacrificed’. Although apparently ‘thin’, these babies are relatively adipose. This is clearly seen in Table 2, which shows that at comparable birthweights Indian babies have higher subscapular fat compared to the white babies and Figure 2, which shows that for a given subcutaneous fat, Indian babies are thinner as measured by PI. Our findings are consistent with studies of aborted fetuses from undernourished Indian mothers, who were deficient in protein, calcium and iron, but had more fat than UK fetuses.25 The smallest Indian babies (<10th centile of birthweight for the population) also showed a fat-preserving tendency compared to normal weight (10–90th centile) babies, in addition to the well-known brain-preserving tendency. This was true even for Southampton babies. Fat preservation in growth-retarded fetuses has been shown in studies of animals. Widdowson26 reported 20 y ago that growth-retarded newborn guinea pigs had a higher percentage of body fat compared with controls. Relative fat preservation has also been described in small for gestational age (SGA) babies in the USA27 and in the smaller of twins in later life.28 A comparison of birthweights in Australian Aboriginal and non-Aboriginal neonates showed the former to be 450 g lighter and had smaller triceps skinfold thickness, subscapular skinfolds were not measured.29 Late gestation is a period of rapid fat gain for the fetus because of differentiation and hyperplasia of adipocytes.30 We have reported that maternal pre-pregnant size, weight gain during pregnancy and intake of fats and micronutrient-rich foods (green leafy vegetables, fruits and milk) are significant determinants of neonatal size.19,31 Neonatal skinfold thicknesses are specifically predicted by maternal pre-pregnant fat mass, head circumference, and her fat intake and the frequency of consumption of green leafy vegetables during pregnancy. Thus, the nutritional his-tory of the mother in the distant past as well as during preg-nancy may influence fetal adiposity and body composition. Genetic polymorphisms (eg PPAR-γ) may also influence adipogenesis through nutrient–gene interactions.32,33
Fat stores have an advantage for neonatal survival, acting as a store of energy, insulation to maintain body temperature and a depot of precursors for the rapidly developing brain. Sociobiologists believe that fat also makes the baby more attractive to the mother and thus promotes feeding.34 A tendency to lay down fat may continue into adult life and lead to obesity, as seen in offspring of diabetic mothers.35,36 Birthweight is a strong predictor of body size in Indian children.37 The only Indian study to report on the association between birth measurements and adult diabetes showed that higher PI (‘obesity’) at birth predicted later diabetes.38
Neonatal triceps skinfold measurements were not done in Southampton; therefore, we do not know if the ‘fat-sparing’ tendency of the Indian babies is generalised or specific to the subscapular region. We have shown, however, that the ratio of subscapular to triceps skinfold thickness is increased in 8-year-old Indian children who were born with low birthweight.37 Subscapular fat, is a well-recognised depot of ‘central’ fat, which is associated with an increased risk of insulin resistance and cardiovascular disease. Adult Indians show a tendency to excess central fat deposition, which is linked to the IRS, diabetes and CHD.7,8,9,10,13 We propose that this phenotype results from persistence of central fat laid down in utero. Adiposity, especially with central distribution, is also associated with elevated circulating levels of glucocorticoids, cytokines IL-6 and TNF-α, which contribute to insulin resistance.39,40,41 A reduced muscle mass could compound insulin resistance by a tendency to poor physical activity and promoting obesity. Compromised abdominal visceral development (hepatic, pancreatic and renal) could predispose to lipid and coagulation abnormalities, disturbances of insulin secretion and abnormalities of salt handling, thus increasing cardiovascular risk.
A number of other physiologic peculiarities observed in Indians may be explained by intrauterine programming of metabolism and structure. Thus, a tendency to synthesise fat even in adverse conditions may explain the phenomenon of ketosis resistance in varieties of diabetes peculiar to developing countries.42 Poor muscle mass in Indians reflects in poor work capacity and in reduced energy expenditure.43,44
In summary, we have studied neonatal size and body measurements in a rural Indian population. Compared with UK babies, Indian babies were small. There was a substantial deficit in nonfat soft tissues, while subcutaneous fat was preserved. Thus, abdominal viscera and muscle suffered the most, while subscapular fat was the most preserved. Genetic factors undoubtedly influence body size and composition of a developing fetus.45,46 We have shown that maternal nutrition before and during pregnancy also plays an important role in determining fetal body composition. The adult Indian phenotype of excess total and central body fat in a relatively ‘thin’ individual may originate in utero and predispose Indian men and women to IRS. Serial follow-up of our children will indicate the importance of body fat at birth in relation to adult disease. Further research will clarify whether fetal body composition is modifiable by nutritional interventions in the mother and thus influence the risk of disease in the offspring.
Ramachandran A, Snehalatha C, Latha E, Vijay V, Viswanathan M . Rising prevalence of NIDDM in an urban population in India. Diabetologia 1997; 40: 232–237.
Reddy KS . Cardiovascular diseases in India. World Health Stat Q 1993; 46: 101–107.
Gupta R, Gupta VP . Meta-analysis of coronary heart disease prevalence in India. Indian Heart J 1996; 48: 241–245.
Bulatao RA, Stephens PW . Global estimates and projections of mortality by cause, 1970–2015. Working Paper Series No.1007: Population and Human Resources Department, The World Bank: October 1992. Washington, DC.
Ramachandran A, Snehalatha C, Kapur A, Vijay V, Mohan V, Das AK, Rao PV, Yajnik CS, Prasanna Kumar KM, Nair JD, the Diabetes Epidemiology Study Group in India (DESI). High prevalence of diabetes and impaired glucose tolerance in India: National Urban Diabetes Survey. Diabetologia 2001; 44: 1094–1101.
King H, Aubert RE, Herman WH . Global burden of diabetes, 1995–2025; prevalence, numerical estimates and projections. Diabetes Care 1998; 21: 1414–1431.
McKeigue PM, Shah B, Marmot MG . Relation of central obesity and insulin resistance with high diabetes prevalence and cardiovascular risk in South Asians. Lancet 1991; 337: 382–386.
Yajnik CS, Naik SS, Bhat DS, Joshi VM, Shelgikar KM, Alberti KGMM, Hockaday TDR . The relationship between obesity, plasma immunoreactive insulin concentration and blood pressure in newly diagnosed Indian Type 2 diabetic patients. Diabetic Med 1993; 10: 146–151.
Shelgikar KM, Naik SS, Khopkar M, Bhat DS, Raut KN, Joglekar CV, Gerard ME, Yajnik CS . Circulating lipids and cardiovascular risk in newly diagnosed non-insulin-dependent diabetic subjects in India. Diabetic Med 1997; 14: 757–761.
Shelgikar KM, Hockaday TDR, Yajnik CS . Central rather than generalised obesity is related to hyperglycaemia in Asian Indian subjects. Diabetic Med 1991; 8: 712–717.
Chowdhury B, Helen Lantz, Lars Sjostrom . Computed tomography - determined body composition in relation to cardiovascular risk factors in Indian and matched Swedish males. Metabolism 1996; 45: 634–644
Banerji MA, Faridi N, Atluri R, Chaiken RL, Lebovitz HE . Body composition, visceral fat, leptin and insulin resistance in Asian Indian men. J Clin Endocrinol Metab 1999; 84: 137–144.
Chandalia M, Abate N, Garg A, Stray-Gundersen J, Grundy SM . Relationship between generalized and upper body obesity to insulin resistance in Asian Indian men. J Clin Endocrinol Metab 1999; 84: 2329–2335
Vaz M, Ukyab TT, Padmavathi R, Kuriyan R, Muthayya S, Diffey B, Kurpad AV . Body fat topography in Indian and Tibetan males of low and normal body mass index. Indian J Physiol Pharmacol 1999; 43: 179–185.
Neel JV . Diabetes mellitus: a ‘thrifty’ genotype rendered detrimental by ‘progress’? Am J Hum Genet 1962; 14: 353–362.
Hales CN, Barker DJP . Type 2 (non-insulin-dependent) diabetes mellitus: the thrifty phenotype hypothesis. Diabetologia 1992; 35: 595–601.
Barker DJP . Mothers, babies and health in later life. Churchill Livingstone: London, 1998.
Gopalan C . Low birth weight: significance and implications. In: Sachdev HPS, Chaudhury P, (eds). Nutrition in children; developing country concerns. Imprint: New Delhi, 1994.
Rao S, Yajnik CS, Kanade A, Fall CHD, Margetts BM, Jackson AA, Shier R, Joshi S, Rege S, Lubree H, Desai B . Intake of micronutrient-rich foods in rural Indian mothers is associated with the size of their babies at birth: Pune Maternal Nutrition Study. J Nutr 2001; 131: 1217–1224.
Kinare AS, Natekar AS, Chinchwadkar MC, Yajnik CS, Coyaji KJ, Fall CHD, Howe DT . Low midpregnancy placental volume in rural Indian women: a cause for low birth weight? Am J Obstet Gynaecol 2000; 182: 443–448.
Dewar AL . The ponderal index of the newborn infant. Dissertation for 4th year medical student research project. Department of Reproduction, University of Southampton, May 1987.
Mohan M, Shiv Prasad SR, Chellani HK, Kapani V . Intrauterine growth curves in North Indian babies: weight, length, head cir-cumference and ponderal index. Indian Pediatr 1990; 27: 43–51.
Power C . National trends in birth weight: implications for future adult disease. BMJ 1994; 308: 1270–1271.
Bonellie SR, Raab GM . Why are babies getting heavier? Comparison of Scottish births from 1980 to 1992. BMJ 1997; 35: 1205
Apte SV, Iyengar L . Composition of the human fetus. Br J Nutr 1972; 27: 305–317.
Widdowson E . Immediate and long-term consequences of being large or small at birth: a comparative approach. In: Elliot K, Knight J (eds). Size at birth. Ciba Foundation No. 27; Elsevier: Holland; 1974.
Hediger ML, Overpeck MD, Kuczmarski RJ, McGlynn A, Maurer KR, Davis WW . Muscularity and fatness of infants and young children born small or large for gestational age. Pediatrics 1998; 102: 1–6.
Loos RJF, Beunen G, Fagard R, Derom C, Vlietinck R . Birth weight and body composition in young adult men—a prospective twin study. Int J Obes Relat Metab Disord 2001; 25: 1537–1545
Humphreys MD, Holzheimer DJ . Differing influences on Aboriginal and non-Aboriginal neonatal phenotypes: a prospective study. Med J Aust 2001; 21: 503–506.
Flynn M, Goldberg G, Prentice A, Cole T . Aetiology of obesity III: critical periods for the development of obesity. In: Obesity, the report of the British Nutrition Foundation Task Force, Chapter 7. Blackwell Science: UK; 1999, pp 45–59.
Fall CHD, Yajnik CS, Rao S, Coyaji KJ . The effects of maternal body composition before pregnancy on fetal growth; The Pune Maternal Nutrition Study. In: Shaughn O'Brien PM, Wheeler T, Barker DJP (eds). Fetal programming influences on development and disease in later life, Chapter 21, RCOG: London; 1999, pp 231–245.
Auwerx J . PPARγ-the ultimate thrifty gene. Diabetologia 1999; 42: 1033–1049.
Luan J, Brownw P, Harding AH, Halsall D, O'Rahilly S, Chaterjee VK, Wareham NJ . Evidence for gene-nutrient interaction at the PPARγ locus. Diabetes 2001; 50: 686–689.
Hardy SB . Mother nature. Vintage: London, UK; 2000.
Silverman BL, Metzger BE, Cho NH, Loeb CA . Impaired glucose tolerance in adolescent offspring of diabetic mothers. Relationship to fetal hyperinsulinism. Diabetes Care 1995; 18: 611–617.
Metzger BE, Silverman BL, Freinkel N, Dooley SL, Ogata ES, Green OC . Amniotic fluid insulin concentration as a predictor of obesity. Arch Dis Childhood 1990; 65: 1050–1052.
Bavdekar A, Yajnik CS, Fall CHD, Bapat S, Pandit AN, Deshpande V, Bhave S, Kellingray SD, Joglekar C . The insulin resistance syndrome (IRS) in eight-year-old Indian children: small at birth, big at 8 years or both? Diabetes 2000; 48: 2422–2429.
Fall CHD, Stein CE, Kumaran K, Cox V, Osmond C, Barker DJP, Hales CN . Size at birth, maternal weight, and type 2 diabetes in South India. Diabetic Med 1998; 15: 220–227.
Bjorntorp P . Adipose tissue distribution and function. Int J Obes Relat Metab Disord 1991; 15: 67–81.
Mohamed-Ali V, Goodrick S, Rawesh A, Miles JM, Katz D, Yudkin JS, Coppack SW . Human subcutaneous adipose tissue secretes interleukin-6 but not tumour necrosis factor-α in vivo. J Clin Endocrinol Metab 1997; 82: 4196–4200
Hotamisligil GS, Spiegelman BM . Tumour necrosis factor-α: a key component of the obesity-diabetes link. Diabetes 1994; 43: 1271–1278.
Yajnik CS, Sardesai BS, Bhat DS, Naik SS, Raut KN, Shelgikar KM, Orskov H, Alberti KGMM, Hockaday TDR . The ketosis- resistance in fibro-calculous pancreatic diabetes. 2. Hepatic ketogenesis after oral medium chain triglycerides. Metabolism 1997; 46: 1–4.
Kulkarni RN, Kurpad AV, Shetty PS . Reduced postexercise recovery oxygen consumptions: an adaptive response in chronic energy deficiency?. Metabolism 1993; 42: 544–547.
Kulkarni RN, Shetty PS . Net mechanical efficiency during stepping in chronically energy-deficient human subjects. Ann Hum Biol. 1992; 19: 421–425.
Hattersley A, Beards F, Ballantyne et al. Mutations in the glucokinase gene in the fetus result in reduced birthweight. Nat Gene 1998; 19: 268–270.
Klebanoff MA, Mednick BR, Schulsinger C, Secher NJ, Shiono PH . Father's effect on infant birth weight. Am J Obstet Gynecol 1998; 178: 1022–1026.
We are grateful to the community, in particular the pregnant women and their families, for taking part in this study. We would also like to thank Dr Mrs Banoo Coyaji, Director of the KEM Hospital, Pune, and initiator 25 years ago of the rural primary healthcare programme in the study area. We acknowledge the major contributions made to the study by Dr Arun Kinare, Dr Monesh Shah, Dr Asit Natekar, Dr Manoj Chinchwadkar, Dr Binu John, Dr Anuja Bisht, Dr Mahananda Bhavikatti, Dr Asawari Kanade, Mrs Punam Gupta, Mrs Parveen Bharucha, Miss Vanessa Cox and Dr Barrie Margetts. We also thank Mr Tim Wheeler, Reader in Obstetrics and Gynaecology, Princess Anne Hospital, Southampton, UK, for the Southampton data. The study was funded by the Wellcome Trust, London, UK, the Medical Research Council, UK and SNEHA, India.
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Cite this article
Yajnik, C., Fall, C., Coyaji, K. et al. Neonatal anthropometry: the thin–fat Indian baby. The Pune Maternal Nutrition Study. Int J Obes 27, 173–180 (2003). https://doi.org/10.1038/sj.ijo.802219
- Indian babies
- body size
- body fat
- insulin resistance syndrome
- thrifty phenotype
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