DNA is the blueprint for life. It makes us unique individuals, from our appearance to our intelligence, to our risk of several diseases.
Exactly what shapes us into who we are has been debated for centuries in the “nature versus nurture” debate. Some believe we are products of our upbringing and our environment, whilst others would argue that we are born the way we are, encoded and fixed by the DNA we inherit from our parents.
This notion extends to how at risk we are of certain diseases.
The genes we inherit can predispose us to certain conditions like breast cancer, heart disease and Alzheimer’s disease 1. Some people believe that because they inherit an increased risk of disease from their parents, there’s nothing that can be done but sit and wait for their diagnosis to arrive.
But our genetics are not our fate.
Our genes and our environment are constantly interacting throughout our lifetime, to determine how our health gets better, or gets worse.
We can nurture our genes with nutrition and lifestyle to awaken the good ones and turn off the bad ones, protecting us from disease. Understanding this is key to gaining control of your health and not letting your genes decide your fate.
What are genes?
You might remember learning about DNA and genes at high school, perhaps you were taught that they’re pretty much the same thing.
In reality, only about 1-2% of our DNA makes up our genes, and these genes encode for proteins that have important functions within our bodies 2. Our genes are like instruction manuals that other molecules read and turn into something useful. Around 8% of our DNA controls which genes are turned on and off, and the other 90% has been given the term junk, dead, or unknown DNA, because we don’t really know what it does, some of it may do nothing at all 3.
We share our DNA with our biological parents. We get 50% of it from our mother and the other 50% from our father.
Some of the genes that you inherit can put you at risk of various diseases. For example, we all carry a gene encoding for a protein called apolipoprotein e (APOE). Your risk of Alzheimer’s disease is increased if you carry the apolipoprotein 4 (APOE4) type, compared to others who may inherit and carry APOE2 or APOE3. APOE4 has been implicated in the development of Alzheimer’s, whereas APOE2 may actually have a protective effect, but it’s luck of the draw which one you inherit 4(p4).
These kinds of genetic characteristics make you more likely to get a disease but don’t make it certain. Just because you carry APOE4 doesn’t mean you'll definitely get Alzheimer’s, many lifestyle factors also play an important role in determining your outcome 5. Similarly, if one parent dies of a heart attack, you know you’ve inherited some of that susceptibility, but it doesn’t mean a heart attack is your definite outcome.
How can we alter our genes with epigenetics?
Each of our cells contains the complete DNA recipe to make a human being. And whilst they contain the same DNA, many of our cells act differently. How does a skin cell behave differently to a heart cell, or to a brain cell, if they all have the same DNA?
That’s the power of epigenetics.
Epigenetics is the study of things that can change the way our genes are expressed, i.e. whether a gene is turned on or off.
Each cell has different genes turned on and off, making them act differently. DNA methylation is the process that often turns genes off, and histone modifications often turns genes on 6.
Cancer cells can use epigenetics against us to modify our DNA. They are able to turn off our tumor suppressor genes that could otherwise stop cancer in its tracks 7.
We know that diet, along with other lifestyle factors and our environment, influence epigenetics and the expression of our genes 8. This can reduce the risk of heart disease, type 2 diabetes and other chronic conditions 9 10.
We are not stuck with the risks that we inherit from our parents.
How can lifestyle modify gene expression?
Some of our genes are involved in causing chronic inflammation, which is a major driver of chronic diseases such as cardiovascular disease, cancer, type 2 diabetes, chronic kidney disease, non-alcoholic fatty liver disease, and autoimmune disorders 11.
We can control the expression of these genes with diet and lifestyle modifications, to either boost or suppress them. This can reduce chronic inflammation, and other mechanisms involved in chronic disease.
Scientists put this to the test in a group of individuals at risk of developing heart disease. The participants were placed on a 12 week lifestyle programme consisting of a low-fat vegetarian diet, stress management, exercise, and social support.
The results were incredible. After just 12 weeks, 26 genes were being expressed differently, and after 52 weeks the expression of 143 genes had been altered due to lifestyle changes 9.
With simple lifestyle changes these people actually changed the expression of their genes.
Genes involved in causing chronic inflammation, oxidative stress, angiogenesis, atherosclerosis, and cholesterol metabolism had all been suppressed. All of these processes are involved in the development of heart disease 9.
By the end of the study the participants had improved vascular health and a lower risk of heart disease.
For many, like myself, who have a history of heart disease in the family, this is a refreshing and inspiring view on how we can control our future. The way I live my life, the food I eat and the stress I experience, can change my outcomes for the better.
In another study, scientists put men with low-risk prostate cancer on a whole-food plant-based diet, along with stress management, moderate exercise, and psychosocial support without chemotherapy or radiotherapy. They took biopsies from the men before and 3 months after these changes to look at gene expression.
Within just 12 weeks of diet and lifestyle changes, the expression of 501 genes had been beneficially altered. The expression of disease-preventing genes were boosted whilst oncogenes (genes that have the ability to cause cancer) were suppressed.
Specifically, researchers saw a significant downregulation of the RAS family of oncogenes, which promote prostate cancer and breast cancer 12.
We can also influence the epigenetics involved in obesity and type 2 diabetes.
A high-fat western style diet can negatively affect the expression of genes involved in our metabolism, in skeletal muscle and fat tissue, increasing the risk of developing obesity and type 2 diabetes 10. Particularly, high levels of saturated fat, found in meat, dairy products, and processed foods, can adversely affect gene expression in these tissues and increase the risk of type 2 diabetes 13.
The authors of the study said “This fundamental knowledge suggests that the unhealthy diet of many obese and diabetic people may affect their epigenome and thereby disease pathogenesis.”
Exercise can also impact the processes that turn genes on and off, changing gene expression in skeletal muscle and fat tissue.
So whilst you may initially be at higher risk of developing type 2 diabetes, exercise and a healthy diet can change your gene expression and protect you from ever developing the disease.
Epigenetics is a hot new topic in science and continues to advance. As more research emerges, we’ll discover more about the role of diet and lifestyle, and how this affects our risk of disease.
Various genes that we inherit can increase our likelihood of developing a disease. But our health is not decided by our parents, it’s decided by us.
A plant based diet, along with stress management, sufficient sleep, and exercise has the ability to boost the expression of good genes and suppress the bad ones. This can increase our body’s ability to fight chronic inflammation, cancer, heart disease, and type 2 diabetes.
If we have the power to choose our lifestyle and diet, we have the power to turn on the good genes, turn off the bad ones, and decide our own fate.
1. Power RA, Pluess M. Heritability estimates of the Big Five personality traits based on common genetic variants. Transl Psychiatry. 2015;5(7):e604-e604. doi:10.1038/tp.2015.96
2. International Human Genome Sequencing Consortium, Whitehead Institute for Biomedical Research, Center for Genome Research:, Lander ES, et al. Initial sequencing and analysis of the human genome. Nature. 2001;409(6822):860-921. doi:10.1038/35057062
3. Kellis M, Wold B, Snyder MP, et al. Defining functional DNA elements in the human genome. Proc Natl Acad Sci. 2014;111(17):6131-6138. doi:10.1073/pnas.1318948111
4. Safieh M, Korczyn AD, Michaelson DM. ApoE4: an emerging therapeutic target for Alzheimer’s disease. BMC Med. 2019;17(1):64. doi:10.1186/s12916-019-1299-4
5. Lourida I, Hannon E, Littlejohns TJ, et al. Association of Lifestyle and Genetic Risk With Incidence of Dementia. JAMA. 2019;322(5):430. doi:10.1001/jama.2019.9879
6. Tiffon C. The Impact of Nutrition and Environmental Epigenetics on Human Health and Disease. Int J Mol Sci. 2018;19(11):3425. doi:10.3390/ijms19113425
7. Wang LH, Wu CF, Rajasekaran N, Shin YK. Loss of Tumor Suppressor Gene Function in Human Cancer: An Overview. Cell Physiol Biochem. 2018;51(6):2647-2693. doi:10.1159/000495956
8. Sapienza C, Issa JP. Diet, Nutrition, and Cancer Epigenetics. Annu Rev Nutr. 2016;36(1):665-681. doi:10.1146/annurev-nutr-121415-112634
9. Ellsworth DL, Croft DT, Weyandt J, et al. Intensive Cardiovascular Risk Reduction Induces Sustainable Changes in Expression of Genes and Pathways Important to Vascular Function. Circ Cardiovasc Genet. 2014;7(2):151-160. doi:10.1161/CIRCGENETICS.113.000121
10. Ling C, Rönn T. Epigenetics in Human Obesity and Type 2 Diabetes. Cell Metab. 2019;29(5):1028-1044. doi:10.1016/j.cmet.2019.03.009
11. Furman D, Campisi J, Verdin E, et al. Chronic inflammation in the etiology of disease across the life span. Nat Med. 2019;25(12):1822-1832. doi:10.1038/s41591-019-0675-0
12. Ornish D, Magbanua MJM, Weidner G, et al. Changes in prostate gene expression in men undergoing an intensive nutrition and lifestyle intervention. Proc Natl Acad Sci. 2008;105(24):8369-8374. doi:10.1073/pnas.0803080105
13. Malmgren S, Spégel P, Danielsson APH, et al. Coordinate Changes in Histone Modifications, mRNA Levels, and Metabolite Profiles in Clonal INS-1 832/13 β-Cells Accompany Functional Adaptations to Lipotoxicity. J Biol Chem. 2013;288(17):11973-11987. doi:10.1074/jbc.M112.422527