Written By: Kevin Cann
For those of you who have not read my original article on methylation and epigenetics, I encourage you to do so before continuing on, http://robbwolf.com/2013/04/10/epigenetics-methylation-gene-expression/ .
Epigenetics has been at the forefront of scientific research when looking at disease for roughly the last ten years. In that timeframe we have learned quite a bit about the topic, but still have much more to learn. With that said, every lifestyle choice we make has an effect on our gene expression. This all begins from the time we are in utero.
Studies have shown that nutrient deficiencies in utero can lead to the development of disease later on in life (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1885472/ ). During this time of fetal development, we are setting the stages for our metabolic processes later on in life. This whole idea that the stages of fetal development lay the groundwork for disease is known as the Barker Hypothesis. This is known still as a hypothesis because it is difficult to get solid research.
Most of the human research on this topic is epidemiological. The research is based upon observational data collected from large groups while they are pregnant. Of course we know this leaves the doors open for a number of variables to be used as an explanation for disease. With that being said, there has been some solid evidence to come out of animal studies that may explain the biological principles associated with the Barker Hypothesis.
Studies such as the Diet-Heart Hypothesis may have led to an increase in modern disease through epigenetics. The fear of animal fats led us to decrease our intake of them. With that decrease in animal meats, we consumed less protein. Studies have shown that low-protein diets in utero in rats led to an increase in hypertension, as well as an increase in glucocorticoids. The increase in glucocorticoids alters HPA axis function. Also, the kidneys were smaller compared to bodyweight, which may have led to alterations in the renal hormones (http://www.ncbi.nlm.nih.gov/pubmed/8942400/ ). This increase in glucocorticoids during fetal development may be of major concern.
An increase in glucocorticoids may down regulate leptin sensitivity and increase appetite (http://ajpendo.physiology.org/content/277/4/E708.full ). A low protein diet in utero might lead to a baby being born leptin resistant. This can lead to an increase in body fat and all the diseases that are associated with obesity.
The biological mechanism at play during gene expression is referred to as methylation. Our folate conversion and the ability to produce the major methyl donor, methionine, are important factors for the production of the gene silencing methyl groups. In utero, sheep that were deprived of B vitamins as well as methionine were heavier, more prone to autoimmunity, had elevated blood pressure, and were insulin resistant (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2148293/ ). This makes a female’s nutrition during pregnancy extremely important for the long term health of the offspring. Is this why some people can eat a bunch of junk food and not gain weight and others have a much smaller spectrum of what they can tolerate?
Does that mean we are doomed because of what our mothers ate? The answer to that question is: not necessarily. Methylation is constantly going on. This is what allows us to adapt to changing environments. This just may mean for some that they need to keep a tighter rope on their nutrition and lifestyle choices than others. If someone is preprogrammed at birth to be insulin resistant, it may be a bad idea to be overeating refined carbohydrates. This may explain why diets such as Weight Watchers work for some, and not so well for others.
This may explain why some do really well on a higher carbohydrate diet, and others like myself thrive off of a high fat diet. This makes it more important to keep in mind that nutrition is not always a one size fits all approach, but there are many confounding factors that go into it. This does not mean that you can just go out and overeat refined carbohydrates because you may not gain weight either. Remember methylation is constantly going on, and making those poor food choices can allow for unfavorable gene expression later in life regardless of what your mother ate while she was pregnant.
We want to make sure we are eating foods that are going to elicit positive gene expression (http://robbwolf.com/2012/08/23/antioxidants-pesky-free-radicals/ ). A diet following the paleo template is definitely a good start. From there some individual tinkering on macronutrients and food choices may be needed. Diet is not the only factor that effects gene expression. Our circadian rhythm is also a major player (http://robbwolf.com/2013/03/13/understanding-combating-oxidative-stress-huntingtons-disease/ ) so get your sleep and manage your stress!
Thank you for investing some time and effort into this topic, and thank you for this insightful article.
My own wish for the future is a desire for powers at work in the world and all of us to ensure an abundance of really healthy food and less stress to all pregnant women (and of course everybody thereafter). So many things start in utero and in our earliest lives.
I was so glad to see this line in your post:
“This makes it more important to keep in mind that nutrition is not always a one size fits all approach, but there are many confounding factors that go into it.”
I get really put off by people who claim that their way is the only way.
I think the genetics world is amazing, and even more so now with the discovery of the epigenome. I work in prenatal genetics so every day I talk with patients about their pregnancy and risks associated…typically this is limited to Down syndrome, family history of mental retardation, etc, or a genetic disease…I can’t wait until the day comes in which discussing prenatal methylation as it relates to fetal health is a normal topic of discussion!