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Are We Destined For Illness?

Updated: Sep 19, 2018

Are you destined to be sick? Is it written in your genes that you will have a specific disease? This line of thinking is known as genetic determinism. This line of thinking is what fueled the Human Genome Project. [1] It is possible to have specific genes or gene mutations that increase your likelihood of certain diseases. But this is not set in stone. Certain events must also occur for those genes to get switched ‘on’ or ‘off’ to actually make that susceptibility a reality. Actually, according to the CDC, only 10% of diseases are accounted for by genetics. [2]

What Are Genes?

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Genes are made of DNA and are the basic physical and functional units of heredity. We each have two copies of each gene. One we received from our mother and the other copy we received from our father. The Human Genome Project estimates that we have 20,000–25,000 genes. [3] A genome is the complete set of DNA for that organism. DNA has 4 bases that pair together. Guanine pairs with cytosine and adenine with thymine. Our genome consists of more than 3 billion of these DNA base pairs and a copy of the genome is contained in each cell that has a nucleus. [4]

The Human Genome Project began in 1990 to map the human genome. It was completed in 2003. [5] It was assumed that we had more genes than other species and that diseases all had a common genetic root. However, it turns out that a pinot grape has more genes than we do. It has nearly 30,000 genes. [6] Well, maybe there is a common genetic root for disease? Not exactly. Genes do play a part but they do not account for everything.

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Studies have been performed on identical twins to study the role of genes with disease. These studies have looked at schizophrenia, cancer, etc. Monozygotic twins are twins that come from the same zygote and therefore are identical. It seems logical to assume that if one twin has ‘X’ disease that the other twin will also have ‘X’ disease. After all, they are identical. However, this is not the case. In regards to schizophrenia, the risk of having it is higher if there is a family history of the disease. If one twin has it, the relative likelihood for the other twin to have it is 50%. [7] That is a high but it is the same change as a coin flip.

What Accounts For The Difference?

This difference has led to multiple fields of study. Two such fields are epigenetics and the exposome. The simplest definition of epigenetics is the study of biological mechanisms that will switch genes ‘on’ and ‘off’. [8] The exposome is the measure of all the exposures in an individual’s lifetime and how they relate to health. Exposures include the environment, diet, lifestyle, etc. [9] Often we think of exposures as only those things that occur outside of us in our environment. Yet this is only half of it. We are also exposed to chemicals on the inside of our bodies that are produced by inflammation, oxidative stress, infections and our gut microbiota to name only a few. [10]

Figure 1 from!po=37.5000 [10]


If we all have the same genes that comprise our genome, why do we all look and act differently? Genetic variation explains why we look and act differently. Single nucleotide polymorphisms (SNPs, pronounced ‘snips’) are the most common type of genetic variation. [11] These slight variations can increase our susceptibility for diseases like rheumatoid arthritis and may explain why some people are more prone to opioid addiction. [12, 13] SNPs are useful in determining our risk for disease.

Back To Epigenetics

The key word in the last sentence is “risk”. Just because you a SNP for a certain disease or other issue does not mean that you will definitely have that disease or issue. Why is that? Let’s return to epigenetics. Remember that you can turn genes ‘on’ or ‘off’ through biological mechanisms. If we reduce our exposures to know harmful chemicals, could this lead to improved health? Yes! There are numerous studies that show the health consequences of smoking.

Image from CDC [14]

If we limit our exposure or eliminate our exposure to smoking completely, we decrease our risk for many disease. Smoking has also been shown to be a critical factor in the epigenetic modification of DNA methylation. [15] Abnormal DNA methylation is related to the development of cancer, autoimmune disease, type I and type II diabetes and neurological conditions. [16] We can easily manage our exposure to smoking but we cannot as easily manage our exposure to other chemical and environmental factors.

But is avoidance of exposure the only way to improve our genes and health as well as decrease our risk for disease? Remember from earlier in the article that our internal environment also plays a big role in exposure. We can modify this environment through stress management, diet and other lifestyle factors. By using meditation, prayer and other forms of stress management, we help to decrease overall inflammation in our bodies and the allostatic load that has been placed on our bodies. This helps to modify our internal environment in our favor.

photo by Anemone123 from

Even social integration can affect our risk. Studies have shown that people with low to moderate social integration are twice as likely to be readmitted to the hospital after having a heart attack and people who live alone are have increased mortality after a heart attack. It has also been shown that getting support and providing support have positive health outcomes like decreased blood pressure and can decrease stress. [17] These are just a few examples of how lifestyle exposures can benefit our health.

Risk vs. Destiny

Our genes do not hold our destiny. They hold our risk….”But risk is not destiny.” [18] We have discussed how epigenetics can help to turn genes ‘on’ or ‘off’ so that our risk is never expressed. We also talked about how each cell with a nucleus has a copy of our genome. These cells have to divide to make new cells as we age and develop. According to Molecular Geneticist, Shiva M. Singh, “these cells may lose or acquire additional DNA. The genome is not static.” [7] While we cannot get rid of all risk, this shows that we have much more control over our health destiny than genetic determinism would have had us believe!

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This article is for educational use only. Nothing contained in this article should be considered, or used as a substitute for, medical advice, diagnosis or treatment. This article does not constitute the practice of any medical, nursing or other professional health care advice, diagnosis or treatment. Always seek the advice of a physician or other qualified health care provider with any questions regarding personal health or medical conditions. Never disregard, avoid or delay in obtaining medical advice from your doctor or other qualified health care provider because of something you have read in this article. If you have or suspect that you have a medical problem or condition, you should contact a qualified health care professional immediately. If you are in the United States and are experiencing a medical emergency, you should dial 911 or call for emergency medical help on the nearest telephone.


  1. Zwart H. (2014) Genetic Determinism. In: ten Have H. (eds) Encyclopedia of Global Bioethics. Springer, Cham





  6. Bland, Jeffrey. The Disease Delusion: Conquering the Causes of Chronic Illness for a Healthier, Longer, and Happier Life. HarperWave, an Imprint of HarperCollinsPublishers, 2015.




  10. Rappaport, S. M., & Smith, M. T. (2010). Environment and Disease Risks. Science (New York, N.Y.), 330(6003), 460–461.


  12. Ann B. Begovich, Victoria E.H. Carlton, Lee A. Honigberg, Steven J. Schrodi, Anand P. Chokkalingam, Heather C. Alexander, Kristin G. Ardlie, Qiqing Huang, Ashley M. Smith, Jill M. Spoerke, Marion T. Conn, Monica Chang, Sheng-Yung P. Chang, Randall K. Saiki, Joseph J. Catanese, Diane U. Leong, Veronica E. Garcia, Linda B. McAllister, Douglas A. Jeffery, Annette T. Lee, Franak Batliwalla, Elaine Remmers, Lindsey A. Criswell, Michael F. Seldin, Daniel L. Kastner, Christopher I. Amos, John J. Sninsky, Peter K. Gregersen. A Missense Single-Nucleotide Polymorphism in a Gene Encoding a Protein Tyrosine Phosphatase (PTPN22) Is Associated with Rheumatoid Arthritis. The American Journal of Human Genetics, Volume 75, Issue 2, 2004, Pages 330–337, ISSN 0002–9297,

  13. Bond, C., LaForge, K. S., Tian, M., Melia, D., Zhang, S., Borg, L., … Yu, L. (1998). Single-nucleotide polymorphism in the human mu opioid receptor gene alters β-endorphin binding and activity: Possible implications for opiate addiction. Proceedings of the National Academy of Sciences of the United States of America, 95(16), 9608–9613.


  15. Xu Gao, Min Jia, Yan Zhang, Lutz Philipp Breitling and Hermann Brenner. Clinical Epigenetics The official journal of the Clinical Epigenetics Society 2015 7:113

  16. Zelin Jin and Yun Liu. DNA methylation in human diseases. Genes & Diseases, Volume 5, Issue 1, 2018, Pages 1–8, ISSN 2352–3042,

  17. Reblin, M., & Uchino, B. N. (2008). Social and Emotional Support and its Implication for Health. Current Opinion in Psychiatry, 21(2), 201–205.


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