Newborn size, infant and childhood growth, and body composition and cardiovascular disease risk factors at the age of 6 years: the Pune Maternal Nutrition Study

Abstract

Objective: To study associations of size and body proportions at birth, and growth during infancy and childhood, to body composition and cardiovascular disease (CVD) risk factors at the age of 6 years. Design: The Pune Maternal Nutrition Study, a prospective population-based study of maternal nutrition and CVD risk in rural Indian children. Methods: Body composition and CVD risk factors measured in 698 children at 6 years were related to body proportions and growth from birth. Measurements: Anthropometry was performed every 6 months from birth. At 6 years, fat and lean mass (dual X-ray absorptiometry) and CVD risk factors (insulin resistance, blood pressure, glucose tolerance, plasma lipids) were measured. Results: Compared with international references (NCHS, WHO) the children were short, light and thin (mean weight oÀ1.0 s.d. at all ages). Larger size and faster growth in all body measurements from birth to 6 years predicted higher lean and fat mass at 6 years. Weight and height predicted lean mass more strongly than fat mass, mid-upper arm circumference (MUAC) predicted them both approximately equally and skinfolds predicted only fat mass. Neither birthweight nor the 'thin-fat' newborn phenotype, was related to CVD risk factors. Smaller MUAC at 6 months predicted higher insulin resistance (Po0.001) but larger MUAC at 1 year predicted higher systolic blood pressure (Po0.001). After infancy, higher weight, height, MUAC and skinfolds, and faster growth of all these parameters were associated with increased CVD risk factors. Conclusions: Slower muscle growth in infancy may increase insulin resistance but reduce blood pressure. After infancy larger size and faster growth of all body measurements are associated with a more adverse childhood CVD risk factor profile. These rural Indian children are growing below international 'norms' for body size and studies are required in other populations to determine the generalizability of the findings.

Early growth and markers of cardiovascular risk in Keralan children in the Integrated Child Development Scheme

“…Rapid infant growth appeared protective, but rapid later childhood growth (between 6 and 8 years of age) weakly predicted adverse WHR and systolic blood pressure. These trajectories have been identified in other studies (12)(13)(14)(15)(16)(17)(18)(19)(20) . Those in the lowest birth weight tertile remained at higher risk of a high WHR but this was attenuated by faster overall growth.…”

Bases biológicas e evidências epidemiológicas da contribuição do crescimento fetal e pós-natal na composição corporal: uma revisão

“…Assim, constitui-se a aceleração compensatória do crescimento, que pode provocar graves efeitos em longo prazo, dentre estes a alteração da composição corporal, quando se observa uma desproporção entre massa magra e tecido adiposo, 8 resistência à insulina, 10 síndrome metabólica e as doenças crônicas não transmissíveis. 11…”

“…51 Para Reilly et al, 52 um aumento em cada 100 g do peso ao nascer é um fator de risco relacionado à obesidade na infância apresentando associação independente e linear com uma maior prevalência de obesidade aos sete anos. Contudo, Joglekar et al, 10 não encontraram associação entre o peso ao nascer e o peso na infância, o mesmo sendo observado por Botton et al, 53 e Singhal et al, 22 em relação ao índice de massa corporal e a massa gorda em adolescentes. Para Amorim et al, 54 o estado nutricional de crianças na idade escolar foi pouco influenciado pelo peso ao nascimento.…”

Early Life Influences and Type-2 Diabetes – A Review

“…Poor intrauterine growth affecting weight at birth has been linked to adverse outcomes later in life [15][16][17][18][19][20] . This 'developmental programming' hypothesis propounded by David Barker and colleagues posits that a stimulus or insult during a critical period of foetal growth and development that causes perturbations of the maternal-placental-foetal unit can cause permanent changes in metabolism, structure and function of foetal organs and systems 15,21 .…”

“…This mismatch can result in unhealthy patterns of postnatal growth, some of which can result in greater levels of risk factors for chronic diseases, including diabetes. Birth weight has been used as a proxy marker of intrauterine growth and in turn, lower weight at birth has been linked to increased propensity of adverse outcomes later in life 15,16,18 . This paradigm, at the centre of the 'developmental origins' hypothesis, has been the focus of research for nearly four decades, in assessing mechanistic pathways for metabolic and lifestyle disorders like T2D and cardiovascular disease [23][24][25] .…”