Does what you eat affect your baby during pregnancy?
Have you wondered if what you eat affects your baby during pregnancy? The complicated interplay of environment and genetics has been the subject of much research and debate. While folic acid supplementation has been advised for decades to prevent against certain birth malformations, there are now thoughts that there could be too much of a good thing. I’ll talk about how the foetal nutritional environment might affect your baby’s future risk of long term chronic disease such as high blood pressure. In addition, I’ll explain what genomic imprinting and foetal programming are, how they relate to eating during pregnancy and why they matter.
What is Foetal Programming?
In every cell we have DNA that codes all our genes. The expression of these genes can be modulated and changed without altering the genes, almost like a remote control. This works by adding compounds like methyl groups to the surface of the DNA, and winding the DNA round different proteins called histones. This is termed epigenetic modification and is the basis of the theories of foetal programming. It used to be thought that only genes were passed on between generations, but now we know that epigenetic modifications can also be inherited. Our interactions with the environment from eating, smoking, our lifestyle, infectious diseases, and toxins can all contribute to epigenetic modification of our genes. Disruption of epigenetic mechanisms can result in an increased risk of oxidative stress, obesity, insulin resistance, diabetes, and vascular dysfunction.
Folate supplementation – a double edged sword?
During pregnancy most women take folate supplements, because too little folate supplementation is associated with neural tube defects (NTD). NTD such as spina bifida affect more than 320,000 live births worldwide per year, while the incidence rate ranges from 0.03 to 20 per 1000 births depending on geographical location (1).
Evidence is now emerging that there might be a link between too much folate supplementation with increased risk of autoimmune disease, and autism in offspring via DNA methylation (epigenetic modification) (1).
Foetal Origins Hypothesis
During pregnancy and early life, alterations of the DNA by these epigenetic switches are now thought to lead to a higher susceptibility to complex diseases later in life such as high blood pressure, cholesterol metabolism, and insulin resistance (2). This is termed the Foetal Origins Hypothesis first proposed by Barker (3,4).
While for most genes, when they are inherited from your mother and father, both copies are active and turned on. However, some genes undergo ‘genomic imprinting’ via epigenetic modification so that they are turned off. Which copy of the gene is active depends on whether it was inherited from the mother or father. Some genes are only active when they are inherited from their mother, while others from their father. In these genes which undergo genomic imprinting, the parent of origin is marked on the DNA at the time of formation of the ovum and sperm cells via methylation. Methylation is the process of adding small methyl groups to certain sections of the DNA that act like switches and identify from whom the gene was inherited. Only a small percentage of human genes undergo genomic imprinting, and it isn’t known why this happens to some genes and not others.
In genes that undergo genomic imprinting, the parent of origin is often marked, or “stamped,” on the gene during the formation of egg and sperm cells. This stamping process, called methylation, is a chemical reaction that attaches small molecules called methyl groups to certain segments of DNA. These molecules identify which copy of a gene was inherited from the mother and which was inherited from the father. The addition and removal of methyl groups can be used to control the activity of genes.
Often random events during early foetal development can mean that two normal genes are inherited from one parent and none from the other. Most of the time, this will not have a noticeable effect, because it doesn’t matter from whom the genes are inherited. However, if this happens to a gene that undergoes genomic imprinting, this can have significant implications if during replication 2 normal copies of the gene are inherited from just one parent. If a stamped copy of the gene is not inherited from a specific parent, it can lead to a number of different syndromes such as Angelman syndrome, despite having two otherwise ‘normal’ copies of the gene. Epigenomic modulation has powerful and far ranging repercussions, although the full effects remain unknown.
One study followed up the offspring of women enrolled in a folic acid supplementation trial in the 1960s, 47 years later. They found that there were differences in their epigenome that were associated with folic acid supplementation, however, more research is needed to understand significance of these findings for the offspring (5).
Incredibly, the epigenomic modulation may affect timing of sexual maturation, reproductive success and even birth weight of the offspring’s future children (6). Additionally, low foetal weight during pregnancy, may be associated with an increased risk of accelerated weight gain during childhood, which may contribute to a relatively higher risk of coronary heart disease, hypertension and type 2 diabetes (7). It is thought that this foetal programming might enable the baby to be prepared for different predicted nutrient environments (7). In utero nutrient states of significant over or under nutrition appear to have a higher likelihood epigenetic modification. So while some women struggle with eating due to severe sickness, it is still important to ensure you optimise your nutrition as much as possible. In contrast, over nutrition and gaining too much weight during pregnancy, and also lead to epigenetic modification. This highlights the need to eating healthily and aim for a healthy weight gain during pregnancy.
However, while epigenomic modulation may occur during pregnancy, these switches are plastic and are constantly influenced by the environment. Therefore future risk of disease depends not only on the DNA that you inherit from your parents, the epigenetic modifications and genomic imprinting of these genes, but also how they combine with environmental factors and subsequent changes through further epigenetic modulation. But optimising the nutritional environment of the mother, and therefore her baby, could have far reaching implications for public health and prevention of chronic diseases.
Summary – how this affects me
It is very important to take folic acid or folate supplementation during pregnancy to reduce the chance of neural tube defects in your baby. However, taking more than the recommended dose (unless directed by your doctor in specific circumstances), is not advised. More research is needed to better understand the role of maternal diet and foetal programming. Healthy eating during pregnancy and a healthy weight gain (not too little, but not too much) is important, as there could be long term impacts on your baby.
If you are currently pregnant, you might find my FREE meal planner and micronutrient checklist helpful. I designed this planner and checklist, so that you don’t have to hunt for reliable information. Instead you will have a summary to hand in an accessible format, to help you eat well during breastfeeding.
If you are looking for more science backed information about eating during pregnancy, then check out my new ebook, written to answer all your questions.
If you are looking for more information about what to eat after a baby and beyond, check out my book ‘Postpartum Nutrition: An Expert’s Guide to What to Eat After a Baby‘.
Have you seen my articles on bacteria in breastmilk, starting weaning, and vitamins for children.
1. Liu H-Y, Liu S-M, Zhang Y-Z. Maternal Folic Acid Supplementation Mediates Offspring Health via DNA Methylation. Reprod Sci. Springer International Publishing; 2020 Apr;27(4):963–76.
2. Chmurzynska A. Fetal programming: link between early nutrition, DNA methylation, and complex diseases. Nutr Rev. 2010 Feb;68(2):87-98.
3. Almond D, Currie J. Killing Me Softly: The Fetal Origins Hypothesis. Journal of Economic Perspectives. 2011 Sep 1;25(3):153–72.
5. Richmond RC, Sharp GC. The long-term impact of folic acid in pregnancy on offspring DNA methylation: follow-up of the Aberdeen Folic Acid Supplementation Trial (AFAST). Int J Epidemiol. 2018 Jun 1;47(3):928-937.
6. Burdge GC, Lillycrop KA. Nutrition, Epigenetics, and Developmental Plasticity: Implications for Understanding Human Disease. Annual Reviews; 2010 Jul 20;30(1):315–39.
7. Gluckman PD, Hanson MA, Cooper C, Thornburg KL. Effect of In Utero and Early-Life Conditions on Adult Health and Disease. N Engl J Med 2008; 359:61-73