It is common knowledge that we inherit our parents’ genes. Some DNA from mom combines with some DNA from dad, and that makes us. However, did you know that what your parents ate during their lifetime affects the genes that they pass on to you? To find out how that works and what we know so far about the consequences of that, keep on reading. To listen to this article, click here.
You are what you eat - and what your parents ate.
Alright, let’s talk about epigenetics.
What is epigenetics?
The reason that your parents’ food habits can affect you over the course of your life is due in large part to epigenetics. Epigenetics is the study of how changes in our environment, including what we eat, can change the way that our genes express themselves. These changes, in turn, can be passed from one generation to the next.
While our unique set of genes, also called our genome, stays the same, the way that our genes get expressed can vary. This is thanks to the molecules that attach themselves like puzzle pieces on top of our genome to make the epigenome. These molecules can either turn genes off or turn them on. Quick side note - molecules attaching to and detaching from the genome like puzzle pieces are just one mode of changing the way that our genes get expressed. Histone modifications and micro RNAs are two other pathways, but you can put those on the back burner for now (or stop reading and Google them) while we focus on the attach/detach method, more formally known as methylation.
Epigenetics in animals: The agouti mouse
Having ways of turning genes on and off is essential for normal growth and development. This type of mechanism allows stem cells to differentiate into different cell types, like skin cells, blood cells, and so on. As a practical example of the impact of methylation on the genome, let’s look at the agouti mouse.
Siblings with similar genes, but very different epigenetics (Wikimedia Commons 2021).
In this study, pregnant female mice were either fed a diet full of those puzzle piece methyl groups, or one that did not include methyl groups. When there were methyl groups in the diet, the agouti gene was bound and silenced, causing most of the offspring to be slender with a brown coat. Without those methyl groups in the diet, the agouti gene was left in the "on" position and most of the offspring were like the mom - overweight with a yellow coat.
The diet of the mom impacted not only the appearance of her children, but also their weight (HudsonALPHA institute for biotechnology).
Epigenetics in humans: The Dutch Famine Birth Cohort Study
Like mice, what we humans eat can affect the genes that are switched on or off in our offspring. I am going to first be looking at pregnancy, but dads, please know that you are not off the hook – the epigenome of sperm cells affects the baby’s epigenome too.
Fathers DO matter - more on that later.
One of the most significant studies that has contributed to our collective understanding of how a mother’s diet affects her baby’s health comes from the Dutch Famine Birth Cohort Study. The Dutch famine of 1944-1945, referred to as the Hongerwinter (hunger winter) in the Netherlands, took place during the German Nazi occupation of the Netherlands during World War II. While this is not the first nor the last famine to occur in the world, the Dutch famine represents a particularly interesting event from a scientific standpoint, because it occurred in a developed country where the food supply had previously been abundant. It also helps that detailed medical records were kept. This was a rare case where people who were previously well-nourished suddenly had to deal with the stressors of war, a more severe winter than usual, no electricity – meaning no gas, heat, or light - and seemingly interminable hunger. Meal rations for adults were reduced from 1800 calories a day to 400-800 calories a day at the peak of the famine.
Children eating meal rations during the famine (Wikimedia Commons 2021).
Decades after the war ended, a group of researchers decided to study how the famine had affected children born and conceived during this harsh period in Dutch history. This led to the Dutch Famine Birth Cohort Study. The 2,414 study participants were contacted at age 50 and again at age 58 – well into adulthood. What the researchers found was that maternal nutrition played a significant role not just in the baby’s health at birth, but over the course of their entire lifespan! Even more noteworthy is that they were able to detect specific gestational periods when certain adverse health outcomes were more likely to be triggered.
Let’s get into the major findings of this study.
Maternal undernutrition early on in gestation was linked to:
A greater likelihood of developing coronary heart disease,
A more atherogenic lipid profile, i.e. high triglycerides and low HDL levels,
Problems with blood coagulation (aka clotting),
Increased stress responsiveness,
Schizophrenia,
Antisocial personality disorder,
Congenital neural defects,
Obesity, and
Breast cancer in women.
Maternal undernutrition during mid-gestation was linked to:
Microalbuminuria, which is a potential sign of kidney and heart problems, and
Obstructive airways disease.
Maternal undernutrition late in gestation was linked to:
High blood pressure, particularly if the mom ate little protein relative to carbohydrate.
Finally, maternal undernutrition during any stage of gestation was linked to glucose intolerance, which is associated with a greater likelihood of developing type 2 diabetes.
The results of this study show us that how our bodies function as adults has a lot to do with what our mothers ate and lived through during pregnancy. This occurrence is termed the “fetal origins of adult disease.” It has been suggested that these adaptations – due to epigenetics - help the baby to make it to term, but can have harmful consequences later on in their life span.
The diseases that a baby develops when they reach adulthood may have origins in the womb.
Can our health be affected by our fathers' and grandfathers' diets, too?
As I mentioned previously, dads are not off the hook here – their diets also affect the health outcomes of their progeny. This idea is supported by a study that was done in the Overkalix parish of Sweden.
The researchers found that fathers who were exposed to food shortages during their prepubescent years of slow growth produced children that were less likely to develop cardiovascular disease later in life. What is even more fascinating is that the researchers were able to find a connection to the grandfathers, too. If, as a boy, grandfathers ate excessively, their grandchildren were more likely to die of diabetes.
Surprisingly, the opposite was true for mothers and grandmothers. If a mother had plenty to eat during her prepubertal years (i.e., the years before hitting puberty), that protected her future kids from heart disease. Additionally, if grandma did not have enough to eat during that same phase of life, her future grandchildren were not protected against diabetes. It seems like adequate nutrition may be slightly more important for females compared to males. Why do you think that these sex differences exist? Feel free to share your theories in the comments!
As a researcher, I must also mention that these studies were not free of limitations. In the examples that I have given so far, the progenitors were in famine or starvation scenarios. You can imagine that if food is hard to come by, then there are other risk factors that are likely to also be present (like the stress of war) which may have also affected the epigenome. Therefore, while diet is very likely to have played a key role in the findings, we cannot say with certainty that these results were solely due to diet.
What about other diet patterns?
But enough about famine. Here in the US, we have the opposite problem – obesity affects about 42% of adults in this country, increasing their risk for type 2 diabetes, some forms of cancer, stroke, and heart disease.
Animal studies support the theory that when a mother overeats, her offspring have a greater chance of being obese and having liver dysfunction, metabolic syndrome, and cardiovascular disease. Experimental evidence demonstrates that feeding both male and female mice a high fat diet causes them to have larger babies with a predisposition towards insulin resistance, which is better known as diabetes. Levels of the hormone leptin, which tells our brain when we have had enough to eat, increase, and adiponectin levels, which is inversely correlated with obesity, decrease.
If parents have a diet that is high in fat, this can have negative consequences on their baby's health.
But, hope is not all lost. From these studies, we also know that you are not doomed to pass on the same epigenome that you are given. After two generations of normal feeding, it was found that the epigenetic changes caused by the high fat diet went away, and adiponectin and leptin function returned to normal.
Furthermore, including more nutrient-dense foods in the diet may also lead to favorable changes in the epigenome. Phytochemicals from green tea, turmeric, soy and other foods have been shown to alter gene expression in a way that promotes decreased inflammation, inhibited cancer cell proliferation, and inhibited fat synthesis.
The food choices that you make each day can literally affect how your genes get expressed! (Shankar et al 2013).
All in all, the data is clear – lifestyle affects gene expression, and changes in gene expression can be passed from both parents to their children. If you are planning to have children, this may give you extra motivation to make those healthy changes to your life that you have been thinking about.
You never know how the choices you make today could positively affect your child’s life when they themselves reach old age!
If you learned anything new or think that someone you care about could benefit from this information, share this article, and subscribe to the blog for regular updates on commonly asked nutrition questions.
Enjoy today!
References:
Barrès, R., Zierath, J. (2016). The role of diet and exercise in the transgenerational epigenetic landscape of T2DM. Nature Reviews Endocrinology,12, 441–451. https://doi.org/10.1038/nrendo.2016.87
Centers for Disease Control and Prevention. (2021, February 11). Adult Obesity Facts. Centers for Disease Control and Prevention. https://www.cdc.gov/obesity/data/adult.html
Dunn, G. A., & Bale, T. L. (2009). Maternal high-fat diet promotes body length increases and insulin insensitivity in second-generation mice. Endocrinology, 150(11), 4999–5009. https://doi.org/10.1210/en.2009-0500
HudsonALPHA institute for biotechnology. (n.d.). Epigenetics - Flipping the genetic switch. Retrieved May 4, 2022, from https://hudsonalpha.org/wp-content/uploads/2014/04/epigenetics.pdf
Kaati, G., Bygren, L. O., Edvinsson, S. (2002). Cardiovascular and diabetes mortality determined by nutrition during parents' and grandparents' slow growth period. European Journal of Human Genetics, 10(11):682-8. doi: 10.1038/sj.ejhg.5200859. PMID: 12404098.
Masuyama, H., Hiramatsu, Y. (2012). Effects of a high-fat diet exposure in utero on the metabolic syndrome-like phenomenon in mouse offspring through epigenetic changes in adipocytokine gene expression. Endocrinology, 153(6):2823-30. doi: 10.1210/en.2011-2161. Epub 2012 Mar 20. PMID: 22434078.
Ng, SF., Lin, R., Laybutt, D. et al. (2010). Chronic high-fat diet in fathers programs β-cell dysfunction in female rat offspring. Nature, 467, 963–966. https://doi.org/10.1038/nature09491
Pembrey, M., Bygren, L., Kaati, G. et al. (2006). Sex-specific, male-line transgenerational responses in humans. European Journal of Human Genetics, 14, 159–166. https://doi.org/10.1038/sj.ejhg.5201538
Roseboom, T., de Rooij, S., Painter, R. (2006). The Dutch famine and its long-term consequences for adult health. Early Human Development,v82(8):485-91. doi: 10.1016/j.earlhumdev.2006.07.001. Epub 2006 Jul 28. PMID: 16876341.
Shankar, S., Kumar, D., Srivastava, R. K. (2013). Epigenetic modifications by dietary phytochemicals: implications for personalized nutrition. Pharmacology & Therapeutics, 138(1):1-17. doi: 10.1016/j.pharmthera.2012.11.002. Epub 2012 Nov 16. PMID: 23159372; PMCID: PMC4153856.
Wikipedia Contributors. (2021, August 19). Agouti-signaling protein. Wikipedia. https://en.wikipedia.org/wiki/Agouti-signaling_protein
Wikipedia Contributors. (2022, March 22). Dutch famine of 1944–1945. Wikipedia; Wikimedia Foundation. https://en.wikipedia.org/wiki/Dutch_famine_of_1944%E2%80%931945
Comments