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Early years research

Lifestyle choices during preconception, pregnancy and in infancy are now known to affect the metabolic, physiological and neurological development of a baby. These choices: - either protect a baby from the risk of obesity, heart disease or diabetes; - or increase a baby's risk of developing these conditions later in life. These factors also influence the ongoing health of the mother. Simple healthy choices in pregnancy and hte infant years can make a big difference to life-long health.

 

Early years research is a fascinating area of science which looks at how environmental influences affect the growth and development of the embryo, the fetus, the infant, the child and the impact these have on adult they become. 

 

There has already been much focus on the effect of environmental toxins such as smoking, drugs and alcohol during pregnancy on an unborn infant’s physiology and neurological development and these have been the subject of health promotion campaigns for many years.

 

Now understanding is growing about the influence of other environmental factors such as nutrition, physical activity and stress on the life-long health of the mother and her baby.

 

A groundswell of research shows us that healthy lifestyles during pregnancy and the early years can affect the metabolic, physiological and neurological development of a child, in particular their risk of developing non-communicable diseases later in life such as:
 

  • Diabetes
  • Cardiovascular disease
  • Obesity
  • Asthma 
  • Some cancers.

 

In addition, these environmental factors may also influence the development of neurological pathways in the child's brain that control appetite regulation and taste preferences.

 

Further evidence also shows us that pregnancy complications and outcomes may be used as markers to predict a mother’s own future risk of metabolic or non-communicable diseases.14,15

 

Importantly, a growing body of evidence shows that a heathy lifestyle, particularly good nutrition and moderate physical activity during pregnancy and the early years, may help to improve or reverse certain diseases or conditions. 

 

This developing area of research means that health practitioners now have a greater role in helping to prevent long-term disease by encouraging healthy lifestyle choices in discussions with their clients.  Taking steps to ensure that mothers and infants benefit through healthy lifestyle choices is a vital strategy to help combat the world-wide growth in non-communicable diseases such as, obesity, diabetes and cardiovascular disease1.

 

Find out how you can make a difference - join our workforce development programmes.

 

Research background

 

Early Beginnings 

Early years’ research has developed over the past 30 years and the field is commonly known as the Developmental Origins of Health and Disease.

 

Much of the research in this field draws on the meticulous birth and postnatal records kept by midwives in Hertfordshire and throughout England between 1911 and 1948.16

 

In the 1980s, academics at the University of Southampton in the UK, notably Professor David Barker, examined these records and discovered that low birth weight and poor growth in the first year of life correlated with adult death rates from cardiovascular disease.2, 3  Barker’s work was the first to make the link between health and growth in early life and the development of a non-communicable disease in later life.     This work subsequently led to a focus on the critical role of maternal nutrition (both under and over-nutrition) during pregnancy on the later health of a baby.

 

The scope of Developmental Origins of Health and Disease now examines the impact of a range of different environmental factors on lifetime health.  Some key research areas include:
 

  • The impact of  lifestyle factors around the time of conception on the expression of genes which affect future disease risk 
  • The influence of nutrition during pregnancy on a child’s future risk of developing obesity and/or Type 2 Diabetes
  • The effect of exercise during pregnancy on a child’s future risk of developing Type 2 Diabetes and/or obesity
  • The role of paternal influences on the developing embryo 4, 6
  • The impact of nutrition in the post-partum period, including the effects of breastfeeding7, on the mother’s lifetime health and the child’s appetite control, taste preferences, and gut bacteria
  • The influence of environmental factors on health across generations.

 

Consensus has now grown for a “life course approach” which recognises that the influence of environmental factors, such as nutrition and exercise, on future health spans an individual’s life.  In particular, this approach acknowledges that lifestyle changes made during the periods of pre-conception, conception, pregnancy and the early years of childhood have the greatest impact on lifetime health.

Environmental influences such as nutrition can help to programme the human body. This is known as plasticity. Just like plasticine, a person's DNA can be shaped to take on different characteristics and health traits. It can also be moulded back again. The period of greatest plasticity in a person's life is at conception, in-utero and early childhood.

 

The complex interplay between our genes and our environment

Today, researchers around the world continue to try to understand how the complex bodily processes  that occur during the first 1,000 days of life affect a person’s health.

 

This involves an examination of “epigenetics” which looks at how environmental factors, such as nutrition, can affect the expression of genes. Environmental influences do not alter a person’s DNA, but they can determine which genes are switched “on or off”.

 

Animal and epidemiological studies in this  emerging area of science have resulted in the development of theories  which suggest that a mother’s diet during pregnancy can influence epigenetic mechanisms which will affect a child’s future metabolism and risk of developing obesity, Type 2 Diabetes and other diseases.

 

Researchers are now trying to unravel the specific inherited and environmental factors which influence epigenetic processes. 10, 11

 

This work has led to a wave of discoveries about the impact of environmental factors on gene expression.  Scientists have already identified epigenetic mechanisms in early life which may affect the development of obesity and Type 2 Diabetes, but are now also exploring associations with taste preference, appetite control and the role of gut bacteria, among other things. 

 

Our understanding of the intricate interplay between environmental factors and genetics will continue to strengthen as this research consolidates and develops with further discoveries.

Children who are obese are more likely to: - develop non-communicable diseases as adults, have breathing difficulties, suffer fractures, develop hypertension, and show early markers of cardiovascular disease, insulin resistance and psychological problems. Quoted from the World Health Organisation Overweight and Obesity Fact Sheet

 

From research lab to public health initiatives 

Policy makers around the world, including the World Health Organisation (WHO), are now pushing for public health initiatives that focus on clinical interventions and healthy lifestyle advice for mothers, babies and children in order to address the growing burden of non-communicable diseases.1

 

In a 2013 paper published in the journal Nature, Professor David Barker and his team passionately urged today’s researchers, public health professionals, politicians and commercial companies to use the evidence gathered in the field of Developmental Origins of Health and Disease to promote change and education. Criticism or un-contextualised information-giving is not the way ahead, Professor Barker and his team wrote:

 

“Our work and that of others strongly suggests that a better strategy would be to support women to identify the barriers they face and, where possible, to empower them to generate their own solutions…People working in public health must support girls and young women …to help them to feel more in control of their lives and so better able to prioritize healthy eating. Today, we have the knowledge to readily prevent chronic diseases, had we but the will to do so.” 7

 

To that end, a range of clinical intervention trials are already underway in maternity care, hospitals and neo-natal intensive care units in New Zealand and around the world.

 

In addition, new public health and education programmes, including this one, are being rolled out, accompanied by robust evaluation programmes to ensure that key learnings can be passed on.

 

All those working in the field are driven by a heartfelt desire to improve the health outcomes and quality of life of all mothers and children.
 

Their message is echoed in the Healthy Start Professional Development tagline for our workforce initiative: 
“A healthy start to life… starts with all of us ”.

 

 

 

References:

 

The references for this page are part of a wide literature review undertaken by the Healthy Start Workforce Project  for the basis of its education curriculum. The review cites more than 350 academic papers and is updated annually. Students of our programmes have access to the range of references.

1. W.H.O. Preventing Chronic Diseases: a vital investment. Geneva: World Health Organisation; 2005. and W.H.O. The Interim Report of the Commission on Ending Childhood Obesity. Geneva: World Health Organisation; 2015.
2. Barker DJP, Osmond C. Infant mortality, childhood nutrition, and ischaemic heart disease in England and Wales. The Lancet. 1986;327(8489):1077-81.
3. Barker DJP, Godfrey KM, Gluckman PD, Harding JE, Owens JA, Robinson JS. Fetal nutrition and cardiovascular disease in adult life. The Lancet. 1993;341(8850):938-41.
4. Bygren LO, Kaati G, Edvinsson S. Longevity determined by paternal ancestors' nutrition during their slow growth period. Acta Biotheor. 2001 Mar;49(1):53-9.
5. Barker DJ. The origins of the developmental origins theory. Journal of Internal Medicine. 2007;261(5):412-7.
6. Binder NK, Hannan, N. J., and Gardner, D. K. . Paternal diet-induced obesity retards early mouse embryo development, mitochondrial activity and pregnancy health. PLoS One 7. 2012;e52304. .
7. Barker B, Barker M, Fleming T, Lampl M. Developmental biology: Support mothers to secure future public health Nature. 2013;504(7479):209-11.
8. Gluckman PD, Hanson MA, Cooper C, Thornburg KL. Effect of In Utero and Early-Life Conditions on Adult Health and Disease. New England Journal of Medicine. 2008;359(1):61-73.
9. Gluckman PD, Hanson MA, Beedle AS. Non‐genomic transgenerational inheritance of disease risk. Bioessays. 2007;29(2):145-54.
10. Guilloteau P, Zabielsk iR, Hammon H, Metges C. Adverse effects of nutritional programming during prenatal and early postnatal life, some aspects of regulation and potential prevention and treatments. Journal of Physiology and Pharmacology. 2009;60(3):17-35.
11. Wadhwa PD, Buss C, Entringer S, Swanson JM, editors. Developmental origins of health and disease: brief history of the approach and current focus on epigenetic mechanisms. Seminars in reproductive medicine; 2009: NIH Public Access.
12. Gillman MW, Ludwig DS. How Early Should Obesity Prevention Start? New England Journal of Medicine. 2013;369(23):2173-5.
13. Macaulay EC, Donovan EL, Leask MP, Bloomfield FH, Vickers MH, Dearden PK, et al. The importance of early life in childhood obesity and related diseases: a report from the 2014 Gravida Strategic Summit. Journal of Developmental Origins of Health and Disease. 2014;5(06):398-407.
14. Fraser, A., Nelson, S.M., Macdonald-Wallis, C., Cherry, L., Butler, E., Sattar, N. and Lawlor, D.A., Associations of pregnancy complications with calculated CVD risk and cardiovascular risk factors in middle age: the Avon Longitudinal Study of Parents and Children. 2012 CIRCULATIONAHA.111.044784
15. Sattar, N., & Greer, I. A. (2002). Pregnancy complications and maternal cardiovascular risk: opportunities for intervention and screening?. BMJ: British Medical Journal.2002; 325(7356), 157.
16. Barker, D., 2003. The midwife, the coincidence, and the hypothesis. British Medical Journal. 2003; 327: 1428-1430.


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