Mom’s pregnancy diet linked to DNA changes, child's obesity.

Jun 20, 2011

Godfrey, KM, A Sheppard, PD Gluckman, KA Lillycrop, GC Burdge, C McLean, J Rodford, JL Slater-Jefferies, E Garratt, SR Crozier, BS Emerald, CR Gale, HM Inskip, C Cooper and MA Hanson. 2011. Epigenetic gene promoter methylation at birth Is associated with child’s later adiposity. Diabetes http://dx.doi.org/10.2337/db10-0979.



Synopsis by Renee Gardner and Wendy Hessler

2011-0614pregnanteating
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What a woman eats when she is pregnant can influence her child's genetics in ways that have long-lasting effects on their weight, finds research published in the journal Diabetes. This is the first study to show that maternal diet is linked to epigenetic changes in people and that these changes are related to body fat in children years later.

The moms who ate diets lower in vegetables, fruits, grains and ohter carbohydrates were more likely to have babies with subtle changes in their DNA markers that dictate how genes are read and expressed.

These children were more likely to be heavier and have higher body fat at age nine. The findings reinforce how important it is for women of childbearing age and pregnant women to eat a balanced, nutritous diet, the researchers conclude.


Context

The environment a baby is exposed to in the nine months before birth can affect health in childhood and even throughout life. Events before birth can increase the risk of health problems – such as cardiovascular disease and obesity – 40 or more years later, studies find. But, it is not entirely clear how prenatal events can have such long-lasting health effects. 

Most of the work in this rapidly developing field of prenatal origins of adult disease has focused on a mother’s diet and the subsequent risk of cardiovascular disease, diabetes and obesity later in life. The idea is that if moms do not have adequate nutrition, the fetuses will be programmed to conserve nutrients. If well fed after birth, they are more likely to store nutrients and become overweight adults. Weight gain can lead to obesity, which can be accompanied by other health complications, including diabetes, heart disease and high blood pressure. Some studies even indicate that these changes can be passed on from generation to generation. 

Based on animal studies, researchers now think that changes to the control switches of DNA in the epigenome may be one key to understanding these long-term health effects of the prenatal environment. Epigenetic markers on DNA function to turn the expression of the gene up or down.

To picture epigenetic changes to DNA, think of radio dials that control the station and the volume. The sequence of the genes – their order and position – is akin to the radio station. The epigenetic markers – the chemical groups attached to those genes – will determine if the volume is high or low.

Changes made to epigenetic markers in response to conditions in the womb may be carried throughout life. These changes may affect risk of certain diseases. They  can also be passed on to the next generation.

Animal studies have shown that an unbalanced diet during pregnancy can lead to epigenetic changes in the offspring that cause the animals to become obese. Researchers suspect similar actions occur in people and look to epigenetic changes to the DNA as the most likely culprit in explaining how a grandparent's diet may affect their grandchild's health. 

What did they do?

A team of researchers from the United Kingdom, New Zealand and Singapore collected umbilical cord samples and compared the epigenetic patterns in the DNA to the mothers' diets and their children's body fat levels at age nine.

In the first part of the study, 78 healthy British women in the early second trimester of their pregnancies filled out a questionnaire to describe what they normally ate. From these, the researchers determined key nutrients – such as, protein, fat and carbohydrates – and how much of them were in the women's diets. The general category of carbohydrates included vegetables, fruits, pasta, breads and grains.

At birth, the researchers extracted DNA from umbilical cord samples and analyzed them, looking for areas with a lot of variation in the epigenetic pattern. Nine years later, the researchers measured the children's weight and body fat. They then tested if epigenetic patterns in those areas were related to children’s body fat measurements.

The researchers repeated the same study in a separate group of 239 mothers and children.

What did they find?

The epigenetic pattern at a specific site on a specific gene was related to children’s body fat at nine years of age and to the mother's diet in early pregnancy.

The researchers found that changes at a location on the retinoid X receptor-α (RXR-α) gene were most strongly related to children’s body fat. 

RXR-α interacts with the proteins that act as cell gatekeepers to determine fat and sugar metabolism. Because of this action, the results support that epigenetic changes to this gene may influence children’s body fat later in life.

RXR-α encodes a protein that senses the levels of retinoic acid – a product of vitamin A metabolism – in the cells. It responds by interacting with many other genes to control their expression. Other similar proteins that sense different aspects of the cell environment control how RXR-α influences the expression of other genes. 

This specific epigenetic marker was also related to the mother’s diet in early pregnancy. The fewer carbohydrate foods that a women consumed during early pregnancy, the more likely it was that her child had the epigenetic marker associated with greater body fat.

The researchers confirmed the same relationships between mother’s diet, the epigenetic marker and children’s body fat in the second, separate group of children.

What does it mean?

A women's diet during early pregnancy can influence specific DNA regions that tell genes how to perform throughout life. In this study, these same epigenetic patterns were associated with their children's weight and body fat at age nine.

The study is the first to show in people that changes in epigenetic markers in response to the prenatal environment can have lasting consequences. The results suggest developmental factors may have a bigger influence on lifetime health than previously thought.

A major strength of the study is that the researchers found the same results in two separate population groups. Overall, the findings align with what has been learned from animal studies.

The study is also the first to identify which specific genes on the epigenome were affected by differences in prenatal nutrition. This points to one possible avenue for the long-term health effects. 

The diets and foods eaten were within a normal range for women of this age group. Importantly, diet during early pregnancy was most tightly linked to the child's weight and fat levels.  Based on this, the researchers conclude that it is very important for pregnant women and those who might become pregnant to eat a balanced diet. Pregnant women should also receive appropriate nutrition and health support throughout their pregnancy.

While the mother’s diet is clearly important in determining the health of her baby, many scientists suspect other factors – including chemical exposures – may also influence the developing fetus' epigenetic patterns. Exposure to such chemicals while in the womb may cause lasting changes that can affect health for years to come.

Animal studies show that exposure to chemicals – such as endocrine disrupting compounds (EDCs) – and certain metals – such as arsenic and cadmium – before birth influence epigenetic patterns in the offspring. For instance, rats exposed to the synthetic estrogen diethylstilbestrol (DES) can develop rare cancers of the reproductive tract not only in offspring exposed in the womb but also in the unexposed next generation. Altered epigenetic patterns have been observed in the reproductive tissues of DES-exposed mice.

A similar pattern is emerging in humans. Young women and men whose mothers were exposed to DES while in the womb are now developing similar reproductive abnormalities identified in animal studies. However, no studies to date have looked for associations with epigenetic changes in the exposed populations.

It is a good possibility that other aspects of the fetal environment may operate via epigenetic changes to cause lasting effects on health, though this has yet to be shown conclusively in people.  


Resources

Barker DJ. 1997. Maternal nutrition, fetal nutrition, and disease in later life. Nutrition http://dx.doi.org/10.1016/S0899-9007(97)00193-7.

 

Bollati V and A Baccarelli. 2010. Environmental epigenetics. Heredity http://dx.doi.org/10.1038/hdy.2010.2.

Crews, D and JA McLachlan. 2006. Epigenetics, evolution, endocrine disruption, health, and disease. Endocrinology http://dx.doi.org/10.1210/en.2005-1122.

DES Update. Centers for Disease Control.

Gluckman, PD, KA Lillycrop, MH Vickers, AB Pleasants, ES Phillips, AS Beedle, GC Burdge, and MA Hanson. 2007. Metabolic plasticity during mammalian development is directionally dependent on early nutritional status. Proceedings of the National Academy of the Sciences http://dx.doi.org/10.1073/pnas.0705667104.

Gluckman, PD, MA Hanson, C Cooper, and KL Thornburg. 2008. Effect of in utero and early-life conditions on adult health and disease. The New England Journal of Medicine http://dx.doi.org/10.1056/NEJMra0708473.

Kaati, G, L-O Bygren, M Pembrey, and M Sjöström. 2007. Transgenerational response to nutrition, early life circumstances and longevity. European Journal of Human Genetics http://dx.doi.org/10.1038/sj.ejhg.5201832.

Remacle, C, F Bieswal, V Bol, and B Reusens. 2011. Developmental programming of adult obesity and cardiovascular disease in rodents by maternal nutrition imbalance. The American Journal of Clinical Nutrition http://dx.doi.org/10.3945/ajcn.110.001651.

 

 

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