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Epigenetic Effects of Mom’s Diet

Molecular markers of a mother’s nutrition around the time of conception can be found in her child’s DNA.

By | April 29, 2014

HENNIG ET AL.

Maternal nutrition around the time of conception can affect the regulatory tagging of her child’s DNA from the earliest embryonic stages, according to a study published today (April 29) in Nature Communications, which focused on a population of women and children in Gambia.             

The West African country has distinct rainy and dry seasons that dictate its inhabitants’ diets, making nutrition easy to track. Branwen Hennig from the London School of Hygiene & Tropical Medicine and her colleagues sought to determine whether Gambian women’s nutrition at conception affected their infants’ patterns of DNA tags, or methyl groups. The researchers profiled maternal blood samples, looking for nutrients linked to methylation, and examined methylation patterns of infant hair and blood DNA, homing in on specific sites called metastable epialleles—sequences where methyl groups appear to be added randomly, compared with the more-predictable patterning of much of the rest of the genome.

Because Hennig’s team found similar methylation patterns in the blood and hair samples from the same individuals, and because these patterns varied among individuals, “the authors demonstrate that these loci properly fulfill the criteria of metastable epialleles,” Gavin Kelsey, an epigeneticist with the Babraham Institute and the University of Cambridge, told The Scientist in an e-mail. “This is clearly an interesting paper,” said Kelsey, who was not involved in the work, adding that the study extends upon previous reports linking maternal nutrition with epigenetic tagging in both mouse and human offspring.

“The real advance of this study is that we nailed it that these regions in the human genome are bona fide metastable epialleles,” said study coauthor Robert Waterland, a nutritional epigeneticist at Baylor College of Medicine in Houston, Texas. “Not only does [the variation] occur stochastically and is influenced by maternal nutrition before and during pregnancy, but also it occurs systemically,” throughout the early embryo, he added.

The team enrolled 167 women in a prospective study. Of these, 84 women conceived during the peak rainy season and 83 became pregnant during the peak dry season. The investigators then evaluated concentrations of methylation-related chemicals such as homocysteine, folate, and B vitamins in maternal blood samples correlated with conception season and methylation patterns of infant blood and hair sample DNA. They found associations between maternal biomarkers and increased or decreased methylation in infant DNA, and that all of the maternal biomarkers together explained about 10 percent of the variation in these infant DNA methylation patterns.

Hints at a maternal dietary influence beyond the offspring’s gene sequence first came from the Hungerwinter study of the Dutch Famine Birth Cohort, which included mothers who lived through the Dutch famine in World War II and their children born during that period. While that study focused on later development of diabetes and heart disease, other studies in mice and humans have pointed to specific mechanisms involving methylation and methylation-related nutrients in maternal diet and offspring health.

According to coauthor Andrew Prentice, director of the MRC International Nutrition Group at the School of Hygiene & Tropical Medicine, for the present study, his team did something the Hungerwinter study could not. Because he and his colleagues recruited mothers prospectively and focused on metastable epialleles, they were able to “identify the critical period when maternal diet has affected this process.” That time, he wrote in an e-mail, is “either occurring in the mother’s ovary some two weeks prior to conception or within the first two days or so of conception.”

Prentice noted the advice for women to take folic acid supplements before conceiving to prevent fetal neural tube defects. But, he said, “our results suggest that a cocktail of nutrients in addition to folic acid is needed.”

Kevin Mitchell, an associate professor of genetics and neuroscience at Trinity College Dublin who was not involved in the study, was more cautious about interpreting the study’s results. “It does seem like there are seasonal differences in serum levels of various biomarkers,” he wrote in an e-mail, but “an exploratory study like this should really have a separate replication sample,” he said.

Waterland agreed that the effects are “relatively subtle.” But he pointed to mouse studies showing that “a relatively large phenotypic effect was explained by a rather modest increase in DNA methylation.”

Prentice noted that this study replicates a previous result from their group in a separate population of women in Keneba, “so we feel very secure that it is a genuine finding,” he said.

P. Dominguez-Salas et al., “Maternal nutrition at conception modulates DNA methylation of human metastable epialleles,” Nature Communications, doi: 10.1038/ncomms4746, 2014.

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Avatar of: James V. Kohl

James V. Kohl

Posts: 194

April 29, 2014

Nutrient-dependent/pheromone-controlled adaptive evolution: a model is also an open access article

It links the epigenetic landscape to the physical landscape of DNA in the organized genomes of different species via ecological variation and nutrient-dependent DNA methylation that enables ecological adaptations. The adaptations are manifested in individual differences in cell types and in species diversity of morphological and behavioral phenotypes.

More recent published works by others link specific vitamins to Tet-mediated biophysically constrained cell type differentiation associated with 5 hmcs -- in mammalian embryos and throughout life.

Avatar of: James V. Kohl

James V. Kohl

Posts: 194

April 30, 2014

P. Dominguez-Salas et al., write: "... DNA methylation is predictably influenced by periconceptional maternal plasma biomarker concentrations of key micronutrients involved in one-carbon metabolism. This represents a demonstration in humans that a mother’s nutritional status at the time of conception can influence her child’s epigenome, with likely lifelong implications." 

This brings forward the entirety of experimental evidence that refutes popular theories and replaces ideas about mutations, natural selection, and evolution with facts. For example: "Folate and other dietary methyl donors (betaine, choline, vitamin B12, and methionine) are vital for methylation of DNA, proteins, phospholipids, and neurotransmitters..."

Mutations, which perturb protein folding, cannot create new genes. Therefore, ecological variation and nutrient-dependent pheromone-controlled methylation-dependent ecological adaptations have replaced mutation-driven evolution with the concept of biophysically constrained species diversification.

The concept of biophysically constrained species diversity can be compared to the theory that "...genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world." (p. 199)

Avatar of: mightythor

mightythor

Posts: 44

April 30, 2014

If, I say if, the changes in DNA methylation are real and reproducible, supplementation studies are needed to show that vitamin levels are the causative variable.

Avatar of: James V. Kohl

James V. Kohl

Posts: 194

Replied to a comment from mightythor made on April 30, 2014

April 30, 2014

Did someone show mutations are the causitive variable, or do you think there is no need to supply experimental evidence to support the null hypothesis of species diversity, which is not biologically plausible?

See the comment section at Understanding and accounting for relational context is critical for social neuroscience for more information on how Bredy's works on Tet-mediated biophysically constrained cell-type differentiation associated with 5hmcs pertain to the works of others that link nutrient-dependent DNA methylation to pheromone-controlled species diversity.

The refutations of pseudoscientific nonsense touted by evolutionary theorists have been accumulating during the past few decades. I mention this because we've just seen how uninformed some people continue to remain: "...show that vitamin levels are the causative variable"

It's as if they are deliberately ignoring the fact that  "If you learnt evolutionary biology and genetics a decade or more ago you need to be aware that those debates have moved on very considerably, as has the experimental and field work on which they are based." (p 1014)

See also, from The Scientist: Unmasking Secret Identities A tour of techniques for measuring DNA hydroxymethylation By | February 1, 2014

Articles like hers make me wonder what kind of nonsense is still being taught to students today, when serious scientists -- like those who look here for information -- have long since dispensed with the ridiculous theories of those who Dobzhansky referred to as bird watchers and butterfly collectors (i.e., in 1964).

Fifty years later, and they still haven't learned about the birds and the bees.

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