In My DNA: How Our Lifestyle Impacts Our Genetic Code

April 23, 2020

by Jessica McAnulty 

Someone who loves to participate in marathons may say “running is in my blood”. Or someone who adores sweets (like myself) may claim “it’s in my DNA”. Individuals have tossed around this saying to help describe their interests. But what if our lifestyles or diets are actually affecting our DNA?

DNA, an abbreviation for deoxyribonucleic acid, is our genetic makeup. We have thousands of genes coding for proteins and cellular machinery that allow our bodies to function properly. However, it’s not just as simple as possessing the gene - the gene must be “turned on” or expressed to produce those proteins. 

The body knows what genes are on or off due to small chemical tags on the DNA or on the protein DNA wraps around, called a histone(Figure 1). The study of this phenomena is called epigenetics, meaning “on” or “above” the gene, and the tags on the genes are known as epigenetic modifications. A common epigenetic modification is methylation - the addition of a carbon surrounded by hydrogen atoms that typically (but not always) turns off gene expression. 

Illustration of DNA methylation. Genes are turned "off" when methyl groups attach to the histones
[Figure 1] TOP: Methyl groups can bind to DNA, affecting if the gene produces a protein product or not. BOTTOM: DNA (thin line) wraps around a protein called a histone (blue cylinder). When the histones are farther apart, DNA is accessible and can be expressed. However, when histones become methylated, the DNA may wrap closer around the histone, preventing the gene from being expressed. Methylation does not always result in turning a gene “off”.
These epigenetic modifications are reversible, will not alter the underlying genetic code, and may pass on to the next generation. Several studies suggest epigenetic modifications, such as methylation, may be altered due to environmental factors such as exercise, diet, and/or lifestyle.


A study completed in Stockholm in 2014 investigated the effects of short-term exercise on the epigenome. A group of 23 men and women acted as their own control by only exercising one leg for three months. At the end of the study, the trained leg was stronger and the skeletal muscle displayed different methylation patterns than the untrained leg. This study investigated short-term changes, but the Dutch famine, which will be discussed in the following section, is a classic example of long-term epigenetic changes. 

The Dutch Hunger Winter occurred 1944-1945 when food supply in the German-occupied Netherlands was blocked off during World War II. Food became scarce and all rations were meticulously recorded. Babies born during this period were unusually small and prone to develop coronary heart disease. Six decades later, scientists used archived data to reach out to survivors who were developing in the womb during the famine. Same-sex siblings born before or after the famine served as controls. Through blood sample analysis, scientists discovered that offspring developing in the womb during the famine had differences in methylation of certain genes compared to their siblings. Interestingly, these differences were associated with a higher body mass index (BMI). Additionally, another study on famine survivors found increased risks of obesity, type 2 diabetes, and schizophrenia. One theory on why the famine led to higher BMI levels and obesity risk is that genes that are thought to be involved with metabolism typically had higher methylation levels than the “nourished” siblings, which may result in a slower metabolic rate. 

These retrospective studies are an example of how scientists can better understand associations between health and the environment. In order to report causation, a controlled experiment must be conducted. One team conducted a controlled experiment in mice to mimic the Dutch famine and found similar results. More animal studies must be completed to better understand the long-term changes in epigenetics. So far, the data advocate that the environment in which the children grew was “remembered” through their epigenetic modifications, suggesting that epigenetic changes during development can have a lifelong impact. 

Use of specific products over time can also affect our DNA, even through multiple generations. For example, bisphenol-A (BPA) is a chemical that was used in several manufactured plastics, such as water bottles and food containers, and can enter the body through repeated use of these products. BPA is similar to estrogen, a hormone found naturally in the body. Therefore BPA can mimic estrogen and bind to similar receptors in the cell. These interactions have led to reproduction problems across two generations in mice and non-human primates, even though the second generation was never exposed to BPA. It is thought that this occurs through transgenerational epigenetic inheritance, in which the first generation is exposed through gestation and has lasting changes (similar to the Dutch famine prenatal exposure) that pass on to the second generation. It’s important to note the animal studies used much higher levels of BPA (up to >2000 times) than to which the average person would be exposed. The FDA states the low level of BPA that could be found in food from packaging containing BPA is safe.

The studies presented in this summary are some well-known examples of how environmental factors such as diet, exercise, and lifestyle affect the epigenome. This newer field of environmental epigenetics is expanding as scientists investigate the effects of cigarette smoke on our epigenome as well as whether epigenetic changes brought on by environmental factors may supplement disease progression. Even though scientists know the genetic code of thousands of species, there is more to learn regarding how the changing epigenome functionally impacts our genes. Our lifestyles may have a much larger impact on our health than previously imagined due to short- or long-term epigenetic changes. So, who knows, my love for sweets may be embedded in - er, rather on -  my DNA.


Jessica McAnulty headshotJessica McAnulty is a Ph.D. Candidate at the University of Michigan in Dr. Analisa DiFeo’s Lab investigating new treatments for ovarian cancer. She is an alumna of ComSciCon-MI 2018 and is passionate about science communication. Aside from learning, Jessica enjoys adding houseplants to her growing collection, exploring Michigan’s beautiful scenery, and driving her Mini Cooper. Twitter: @McAnultyJessica

See also: Life Science