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Early origins of health and disease

We are what we eat. But what happens when we eat for two?

It is common knowledge that maternal nutrition plays a fundamental role in the baby’s development. We are aware of the importance of folic acid intake in the prevention of neural tube defects, the risk of developmental defects associated with increased intake of vitamin A and the beneficial role of omega-3 fatty acids in the development and maturation of the optic system and the brain. But how can malnutrition or obesity during pregnancy influence the offspring later in life?

Critical developmental windows and environmental influences during fetal and early life are considered to underpin the early life origins of health and disease in later life. These periods are characterised by plasticity because of rapid cell proliferation and organ development; therefore the developing child is particularly vulnerable to environmental exposures [1].

The first epidemiological evidence showing an influence of early nutritional status on the risk of disease in later life was provided by retrospective studies in Norway and UK. Different geographical regions showed that increased incidence of cardiovascular disease was positively linked with early infant mortality and low birthweight [2-4]. In addition evidence form the Dutch famine have shown that malnutrtion during pregnancy resulted in glucose intolerance and obesity in the children [5]. Interestingly, the incidence of obesity in adulthood in the offspring was increased if the mother was exposed to famine in the first half of pregnancy [6].

Based on these evidence the theory of thrifty phenotype was suggested [7]. This hypothesis suggests that a fetus exposed to a nutritionally poor environment during pregnancy, undergoes permanent changes in glucose-insulin metabolism, which would facilitate survival if nurtured in a similar environment of nutritional deprivation; subsequently this would provide it with an evolutionary advantage. However, if after birth the child gets exposed to a nutritionally rich postnatal environment then, the risk of developing obesity and other chronic diseases increases [8]. This theory, has since been tested, proven and improved upon.

Considering the increasing prevalence of maternal obesity and gestational diabetes, it was later suggested that over-nutrition might also have an impact on fetal development, as a result of hormonal imbalance in the uterus [9, 10].

Plethora of studies has shown a link between increased gestational weight gain and maternal obesity with the risk of the children developing obesity. For instance, in a study including 13,188 3-years old, it was demonstrated that 23% of children were obese if their mother was overweight in the beginning of pregnancy. Moreover, a meta-analysis of 45 studies has shown that if the mother was obese in the beginning of pregnancy the risk of the child becoming obese was double [11].

TThe ROLO (Randomised cOntrol trial of LOw glycaemic index) dietary intervention, from Dublin, targeted women who have previously delivered infants with macrosomia (birth weight > 4kg). The women included in the intervention did gain less weight and improved their glucose metabolism [12, 13]. It was, also, reported that neonatal infants from the intervention group had reduced thigh circumference, indicative of reduced adiposity [13]. The LIMIT study is an intervention in obese and overweight women providing dietary and lifestyle advice to the intervention group [14]. Recently it was reported that the prevalence of macrosomia among children was reduced [15]. The UPBEAT study [16], from King’s College London introduces an exercise intervention together with a low glycaemic index dietary intervention in pregnant women. The aim of the study is to examine how the maternal intervention influences the development of obesity and cardiovascular dysfunction in children 3 and 5 years old. The principle investigators of these three studies are now working together to standardise protocols for follow up of the children.

In order to be able to design effective health intervention for the public we first need to understand fully how maternal exposures influence the risk of developing chronic diseases in the offspring. In the meantime, every pregnant woman would benefit from foods that have been shown to be beneficial for her, the pregnancy outcome and the child in later life. Food that will provide nourishment for two (or more)…


1. Symonds, M.E., et al., Nutritional programming of the metabolic syndrome. Nat Rev Endocrinol, 2009. 5(11): p. 604-10.

2. Forsdahl, A., Living conditions in childhood and subsequent development of risk factors for arteriosclerotic heart disease. The cardiovascular survey in Finnmark 1974-75. J Epidemiol Community Health, 1978. 32(1): p. 34-7.

3. Forsdahl, A., Are poor living conditions in childhood and adolescence an important risk factor for arteriosclerotic heart disease? Br J Prev Soc Med, 1977. 31(2): p. 91-5.

4. Barker, D.J., et al., Weight in infancy and death from ischaemic heart disease. Lancet, 1989. 2(8663): p. 577-80.

5. Ravelli, A.C., et al., Glucose tolerance in adults after prenatal exposure to famine. Lancet, 1998. 351(9097): p. 173-7.

6. Ravelli, A.C., et al., Obesity at the age of 50 y in men and women exposed to famine prenatally. Am J Clin Nutr, 1999. 70(5): p. 811-6.

7. Hales, C.N. and D.J. Barker, Type 2 (non-insulin-dependent) diabetes mellitus: the thrifty phenotype hypothesis. Diabetologia, 1992. 35(7): p. 595-601.

8. Barker, D.J.P., Mothers, babies, and health in later life. 2nd ed. 1998, Edinburgh ; New York: Churchill Livingstone. ix, 217 p.

9. Gluckman, P.D. and M.A. Hanson, The developmental origins of the metabolic syndrome. Trends Endocrinol Metab, 2004. 15(4): p. 183-7.

10. Gluckman, P.D. and M.A. Hanson, Living with the past: evolution, development, and patterns of disease. Science, 2004. 305(5691): p. 1733-6.

11. Yu, Z., et al., Pre-pregnancy body mass index in relation to infant birth weight and offspring overweight/obesity: a systematic review and meta-analysis. PLoS One, 2013. 8(4): p. e61627.

12. Walsh, J.M., et al., Low glycaemic index diet in pregnancy to prevent macrosomia (ROLO study): randomised control trial. BMJ, 2012. 345: p. e5605.

13. Donnelly, J.M., et al., Impact of maternal diet on neonatal anthropometry: a randomized controlled trial. Pediatr Obes, 2014.

14. Dodd, J.M., et al., Limiting weight gain in overweight and obese women during pregnancy to improve health outcomes: the LIMIT randomised controlled trial. BMC Pregnancy Childbirth, 2011. 11: p. 79.

15. Dodd, J.M., et al., Antenatal lifestyle advice for women who are overweight or obese: LIMIT randomised trial. BMJ, 2014. 348: p. g1285.

16. Poston, L., et al., Developing a complex intervention for diet and activity behaviour change in obese pregnant women (the UPBEAT trial); assessment of behavioural change and process evaluation in a pilot randomised controlled trial. BMC Pregnancy Childbirth, 2013. 13(1): p. 148-164.

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