Our study confirms that BW in isolation would minimally affect the metabolic abnormalities related to NCD in children. Consequently, children with optimum body composition (children belonging to middle BW and BMI-Z score tertiles) were found to be metabolically healthier, denoting the role of both BW and post-natal growth on subsequent metabolic derangements. However, more importantly and contrary to the Barker hypothesis, the study further shows that, if a child is born with a lower BW but tend to have a lower BMI-Z score during childhood, they are protected from adverse metabolic derangements. This contrasts with children born with a lower BW, followed by a higher weight gain during childhood (those belonging to lower BW and higher BMI-Z score tertiles) showing the worst metabolic outcomes. This highly suggests that BW is not the only risk factor that determines a poorer metabolic profile in children, but the weight gain during the first few years of life has a significant contribution to the development of an adverse metabolic profile.
Blood pressure appears to track from a younger age and the 1970 British birth cohort showed an inverse relationship between SBP at 10 years of age and BW [17]. This study showed that the highest mean SBP was observed among those belonging to the lowest BW and highest current weight tertile, while the lowest mean SBP was seen in the highest BW and lowest bodyweight tertile. In comparison, the best mean SBP-Z score and DBP-Z score observed in our study were among children belonging to the mid BW and lowest current BMI-Z score tertiles. This reflects that both poor growth during fetal period as well as excess growth during post-natal period could be risk factors for development of high BP later in life. Furthermore, Barker and co-workers showed an inverse relationship of SBP with mothers’ height, which could be considered as an indirect measure of uterine size that may contribute to birth size of her offspring [17]. Although we have not looked at this relationship, our data shows that optimum birth size provides protection from future metabolic derangements. Therefore, could postulate that the control of NCDs could even be a generation long process, where a healthy girl child with good uterine size would give birth to a well-grown healthy baby.
FBS and RBS 2 h after a glucose load failed to show a clinically relevant relationship, highlighting its poor applicability as a routine screening test to detect impaired glycaemic control. A previous study showed that fasting and 2-h post glucose serum insulin levels as well as insulin resistance measured using HOMA-IR had a strong relationship with BW and BMI [18]. Hales and co-workers studying a group of 59–70 year old men from Hertfordshire UK, showed that adults with a low BMI, helped in protecting those with poor prenatal growth against dysglycaemia [19].
It is shown that children with “catch-up growth” have a greater risk of dying from coronary heart diseases (CHD) later in life [20]. The Helsinki study showed that the highest death rates were seen in children who were thin at birth but caught up their weight to the level of average child or above at 7 years of age [20]. Similarly, Harvard growth study showed the effect of high BMI at childhood on CHD in later life, which was independent of adult BMI [21]. In comparison, our data also showed that low BW children achieving a higher BMI in early life would have an adverse metabolic profile. As to the cause underlying this, accumulation of fat was strongly implicated. Prader and co-workers originally defined ‘catch up growth” as a phenomenon that occurs after slowing of growth following illness or starvation, that recovers after correction of the insult [22], Loose application of this on low birth weight babies, would have had led to dire consequences. However more clear knowledge at present day had differed the use of this practice on feeding to achieve a “catch up” growth for low birth weight children as it would lead to harmful effects of “accelerated growth” [4].
Reports suggest that fetal nutrition, as denoted by BW, may have an inverse programing effect on abdominal adiposity in later life, which could contribute to the development of insulin resistance [6]. This indicates that one’s body composition during fetal and early life is associated with adult disease risk [23].
It is shown that rapid weight gain during infancy in SGA children is associated with increased FM rather than FFM [6, 24]. Early “catch-up growth” following SGA birth has been noted as a CVD risk factor in later life rather than SGA alone [25]. However, the tendency of SGA children to assimilate intra-abdominal fat is not yet clear; whether due to low BW itself, rapid postnatal “catch-up” growth or a combination of both [6, 26]. During recovery from wasting or protein-energy malnutrition in children and adults, FM is shown to accumulate much faster than the muscle mass. This phenomenon could partly explain the adverse outcomes in SGA children during “catch-up” growth [6]. Therefore, although “catch-up” growth explicitly confers several benefits in relation to improved neurodevelopment, enhanced immune function, and achieving adult height, there are certain adverse metabolic consequences as well, such as the insulin resistance, metabolic syndrome, DM, CVD, increased fat mass and obesity. As such, it is imperative that early feeding of SGA children requires close growth monitoring to achieve an optimum body composition.
This paper highlights the importance of improving the clinical practice related to children in early life, especially in developing countries where poor prenatal growth of a child is still a grave issue. In such clinical settings, measures should be in place to prevent excess weight gain during early childhood in SGA children. Length/height of a baby, which is usually parallel to weight gain, should be assessed regularly at 3–6-month intervals, so growth could be evaluated in a manner where weight is standardize to height (use of length/height for weight or BMI for age charts).
