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Epigenetics: Why Your Genes Aren’t Your Destiny

Imagine a pair of identical twins with the same DNA. Yet only one of them develops cancer in mid-life, while the other remains healthy. This isn’t unusual — in fact, it’s surprisingly common. While they may share the same genetic blueprint, the difference often lies in how their genes are expressed. This is the domain of epigenetics — the science of how lifestyle and environment influence which genes get turned on or off (1).

Epigenetics doesn’t change your DNA sequence, but it does affect how your genes behave. Think of your DNA as the hardware of a computer, and epigenetics as the software controlling which programs are running. It’s an elegant, powerful system — one that is increasingly understood to play a bigger role in disease risk, including cancer, than our inherited genetics alone (2).

Recognizing its pivotal role in cancer biology, Epigenomics was identified by the authors of this article as one of the 11 Integrative Hallmarks of Cancer™—a framework that highlights the key biological and lifestyle-related factors influencing cancer development and progression. This hallmark focuses on how modifiable influences like diet, toxins, stress, and environment can reprogram our gene expression, offering both risk and opportunity.

This emerging field offers a hopeful message: your genes are not your destiny. Nurturing your epigenetic landscape, is a method to tip the scales in your favor.

What Is Epigenetics?

The term “epigenetics” means “above genetics.” It refers to biochemical changes that regulate gene activity without altering the DNA code itself. These changes control how and when genes are expressed — whether they are turned on, off, or somewhere in between (3).

Epigenetic changes are mediated by several mechanisms, the most important of which are:

DNA Methylation: DNA methylation is a process where small chemical tags called methyl groups are added to DNA, a process that usually turns genes off. This can be protective when it silences harmful genes, but it can also be harmful if it shuts down important cancer-fighting genes like BRCA1 or p16. Whether methylation helps or hurts depends on which genes are affected (4).

Histone Modification: DNA is wrapped around histone proteins. Epigenetic changes—such as adding or removing chemical groups—can modify either the DNA (like methylation) or the histones (like acetylation), tightening or loosening the DNA coils and influencing gene activity. In about 60% of prostate cancers, there is an excess of a protein called EZH2, which adds chemical tags to histones. This change turns off important genes that normally help stop cancer from growing and spreading (5).

Non-coding RNAs: Some small molecules called microRNAs help control how genes are used. In about 80% of pancreatic cancers, too much of a microRNA called miR-21 shuts down genes like PTEN that normally help cells die when they should, making it easier for cancer to grow (6).

These mechanisms act like light switches and dimmers, allowing cells to adapt to environmental cues. Remarkably, epigenetic changes are reversible, offering therapeutic opportunities absent in genetic mutations (7).

How Epigenetic Changes Affect Gene Expression

Epigenetics bridges nature and nurture. While genetics may be the loaded gun, it is epigenetics that pulls the trigger (8). Unlike genetic mutations, epigenetic changes are dynamic and responsive to external factors. They explain why identical DNA can lead to different health outcomes:

Malnutrition: Children born to mothers who experienced the Dutch Hunger Winter of 1944–45 showed 50% higher rates of metabolic diseases. Researchers found lasting hypomethylation of the IGF2 gene, which altered growth regulation. (9).

Smoking: Just 3 months of smoking reduces methylation of the FHIT tumor suppressor gene in lung cells by 15%, increasing cancer risk (10).

Epigenetics and Cancer: More Powerful Than Genetics?

Cancer is fundamentally a disease of dysregulated gene expression. While genetic mutations may grab the headlines, epigenetic alterations are equally critical (11). Consider the following examples:

  • Only 5–10% of cancers stem from inherited genetic mutations (12).The majority of colorectal cancer (60–70%) show the CpG Island Methylator Phenotype (CIMP), marked by epigenetic
  • hypermethylation of tumor suppressors like MLH1 (13).
  • Most pancreatic cancers (90%) exhibit abnormal histone modifications that fuel chemotherapy resistance (14).

How Epigenetics Drives Cancer

Silencing Tumor Suppressors: Epigenetic changes can add chemical tags (like methyl groups) to DNA or histones, turning off tumor suppressor genes that normally protect cells from becoming cancerous. For example:

  • Aberrant promoter methylation of the p16 gene has been detected in 81% of esophageal cancer cases, suggesting a significant role in tumor development (15).
  • BRCA1 hypermethylation mimics hereditary mutations in 10–15% of ovarian cancers (16).

Activating Oncogenes: Epigenetic modifications can also remove normal controls on genes that promote cell growth (oncogenes), causing them to become overactive and drive cancer. For example, hypomethylation (less than normal) of MYC gene occurs in 40% of lymphomas, unleashing cell proliferation (17).

Disrupting DNA Repair: Changes to histones or DNA can affect the expression of genes involved in repairing DNA damage, making it easier for mutations to accumulate and cancer to progress (18).

The Power of Lifestyle: How to Shift Epigenetics

1. Follow the Garden Food Plan®. The Garden Food Plan® factors in the need to support epigenetic protection. The foods you choose can add or remove chemical tags on your DNA, influencing whether certain genes are turned on or off. The following are some results from research studies that highlight this benefit:

  • Sulforaphane, present in cruciferous vegetables like broccoli, inhibits HDACs, reactivating silenced tumor suppressors. A 2023 trial showed 30% higher p16 expression in prostate cancer patients consuming 3 servings/week (19).
  • EGCG, present in green tea, reverses GSTP1 hypermethylation in 25% of high-risk prostate cases (20).
  • Ultraprocessed foods are linked to 12% higher TNF-α methylation, which promotes inflammation (21). To learn more about ultraprocessed foods, read our blog on the topic here.

You can also learn more about the Garden Food Plan® from Dr. Jimenez’s book: Hope for Cancer: 7 Principles to Remove Fear and Empower Your Healing Journey available on Amazon.

2. Exercise Regularly. Physical activity doesn’t just strengthen your body—it also creates beneficial changes in gene expression. For instance:

  • 150 mins/week of aerobic exercise reduces IL-6 methylation by 18%, lowering inflammation (22).
  • Resistance training increases histone acetylation in muscle stem cells by 22%, enhancing repair (23).

3. Manage Stress: Mindfulness meditation for 8 weeks was shown to reduce cortisol-induced FKBP5 methylation by 15%, improving immune function (24).

4. Avoid Toxins: Everyday chemicals and pollutants can alter your epigenome in ways that increase the risk of cancer and other chronic diseases.

  • BPA: 50% higher BRCA1 methylation has been observed in women with high urinary BPA levels, which increases breast cancer risk (25). Read our detailed article on the history of BPA here, and a second one on how to detoxify from this pervasive synthetic chemical found in our environment.
  • Air Pollution: Exposure to particulate matter (PM2.5) in the air increases CDKN2A promoter methylation by 9% for every 10 micrograms per cubic meter increase in concentration (26). CDKN2A is a tumor suppressor gene, and its methylation silences its expression, thereby increasing the risk of various cancers, including lung, colorectal, and pancreatic cancers.

Epigenetics-Driven Cutting-Edge Research

Researchers are now targeting cancer not just through genetics, but through epigenetics — the biological switches that turn genes on or off. New tools like CRISPR-dCas9 can reprogram gene activity without altering DNA itself. In lab studies, this technology reactivated silenced tumor suppressor genes in leukemia (27) and reduced cancer-promoting activity by 70% in pancreatic tumors (28). Another exciting area is epigenetic immunotherapy, where drugs like Vorinostat “unlock” hidden cancer cells, making them more visible to the immune system. When combined with Pembrolizumab, this approach shrank tumors in 35% of resistant melanoma patients — nearly triple the response rate of immunotherapy alone (29). Finally, epigenetic blood tests measuring DNA methylation patterns, such as the SEPT9 gene for colorectal cancer, can detect disease up to four years earlier with 90% accuracy — offering a non-invasive path to earlier diagnosis and intervention (30).

We are also learning how epigenetic changes can be passed from parents to children. In one study, male mice with a mutation in an epigenetic regulator gene called Kdm6a had offspring that developed three times more liver tumors, even though the offspring didn’t inherit the mutation itself (31). The increased cancer risk was linked to epigenetic marks, like DNA methylation that were passed down from father to child — showing how a parent’s health and environment can affect future generations.

What About Integrative Approaches?

Research progress using CRISPR and immunotherapy in epigenetics are showing interesting results, although they are still in early stages of development and are often complex, expensive, and have been largely limited to advanced clinical settings (27-29). Some of these advances include blood tests, such as the one measuring methylation of the SEPT9 gene for colorectal cancer that could detect the disease up to four years earlier with 90% accuracy (30). We’re also learning that certain epigenetic marks can be passed from one generation to the next (31), underscoring the importance of making healthy choices today to protect the well-being of future generations.

The importance of an integrative approach remains foundational to shifting the body’s internal dynamics away from epigenetics-driven disease and toward sustained health. Integrative researchers are studying how lifestyle, environment, and natural therapies influence the epigenome — and how we can harness this knowledge for prevention and healing. Unlike emerging genetic tools, these strategies are already accessible and can be implemented today to help shift the body’s internal environment away from cancer risk and toward long-term health.

Research progress using CRISPR and immunotherapy in epigenetics are showing interesting results, although they are still in early stages of development and are often complex, expensive, and have been largely limited to advanced clinical settings (27-29). Some of these advances include blood tests, such as the one measuring methylation of the SEPT9 gene for colorectal cancer that could detect the disease up to four years earlier with 90% accuracy (30). We’re also learning that certain epigenetic marks can be passed from one generation to the next (31), underscoring the importance of making healthy choices today to protect the well-being of future generations.

The importance of an integrative approach remains foundational to shifting the body’s internal dynamics away from epigenetics-driven disease and toward sustained health. Integrative researchers are studying how lifestyle, environment, and natural therapies influence the epigenome – and how we can harness this knowledge for prevention and healing. Unlike emerging genetic tools, these strategies are already accessible and can be implemented today to help shift the body’s internal environment away from cancer risk and toward long-term health.

At Hope4Cancer, as part of our broader vision that goes beyond targeting just the tumors and creating an environment where cancer is less likely to grow, we leverage this information by using:

  • Plant-based compounds like curcumin (from turmeric), EGCG (from green tea), and a variety of antioxidants can reawaken silenced tumor suppressor genes.
  • Detoxification programs that may help reverse harmful epigenetic marks caused by environmental toxins like BPA and heavy metals.
  • Personalized nutrition and fasting protocols that may positively reprogram the epigenome to slow biological aging and reduce inflammation.
  • Addressing emotional and spiritual health that can reduce stress-induced epigenetic changes that contribute to cancer progression.

Conclusion

Your daily choices shape your epigenetic story. With every bite, breath, and step, you’re not just going through the motions — you’re re-programming your genes. Epigenetics gives us a lever to have a meaningful role in influencing our health on a daily basis.

While cutting-edge research hold promise for the future, it’s the choices you make today — what you eat, how you move, the stress you manage, and the toxins you remove and avoid — that send the strongest signals to your body about how to respond and repair.

Most importantly, understanding epigenetics gives us a way to act much earlier. By being proactive instead of reactive, we can change the conditions in the body before illness takes root. Well before a tumor becomes visible or a test comes back positive, silent shifts in gene expression have often been unfolding in the background for a long time. With consistent, conscious choices, we can begin to reverse or at least slow down those patterns.

References:

  1. Goldberg AD, Allis CD, Bernstein E. Epigenetics: a landscape takes shape. Cell. 2007;128(4):635-638. doi:10.1016/j.cell.2007.02.006
  2. Esteller M. Cancer epigenomics: DNA methylomes and histone-modification maps. Nat Rev Genet. 2007;8(4):286-295. doi:10.1038/nrg2005
  3. Berger SL, Kouzarides T, Shiekhattar R, Shilatifard A. An operational definition of epigenetics. Genes Dev. 2009;23(7):781-783. doi:10.1101/gad.1787609
  4. Sharma S, Kelly TK, Jones PA. Epigenetics in cancer. Carcinogenesis. 2010;31(1):27-36. doi:10.1093/carcin/bgp220
  5. Jones PA, Baylin SB. The epigenomics of cancer. Cell. 2007;128(4):683-692. doi:10.1016/j.cell.2007.01.029
  6. He L, Hannon GJ. MicroRNAs: small RNAs with a big role in gene regulation. Nat Rev Genet. 2004;5(7):522-531. doi:10.1038/nrg1379
  7. Esteller M. Epigenetics in cancer. N Engl J Med. 2008;358(11):1148-1159. doi:10.1056/NEJMra072067
  8. Feinberg AP. The key role of epigenetics in human disease prevention and mitigation. N Engl J Med. 2018;378(14):1323-1334. doi:10.1056/NEJMra1402513
  9. Tobi EW, Slieker RC, Luijk R, et al. DNA methylation as a mediator of the association between prenatal adversity and risk factors for metabolic disease in adulthood. Sci Adv. 2018;4(1):eaao4364. doi:10.1126/sciadv.aao4364
  10. Breitling LP, Yang R, Korn B, et al. Tobacco-smoking-related differential DNA methylation: 27K discovery and replication. Am J Hum Genet. 2011;88(4):450-457. doi:10.1016/j.ajhg.2011.03.003
  11. Baylin SB, Jones PA. Epigenetic determinants of cancer. Cold Spring Harb Perspect Biol. 2016;8(9):a019505. doi:10.1101/cshperspect.a019505
  12. Samadder NJ, Riegert-Johnson D, Boardman L, et al. Comparison of universal genetic testing vs guideline-directed targeted testing for patients with hereditary cancer syndrome. JAMA Oncol. 2021;7(2):230-237. doi:10.1001/jamaoncol.2020.6252
  13. Weisenberger DJ, Siegmund KD, Campan M, et al. CpG island methylator phenotype underlies sporadic microsatellite instability and is tightly associated with BRAF mutation in colorectal cancer. Nat Genet. 2006;38(7):787-793. doi:10.1038/ng1834
  14. Lomberk G, Blum Y, Nicolle R, et al. Distinct epigenetic landscapes underlie the pathobiology of pancreatic cancer subtypes. Nat Commun. 2018;9(1):1978. doi:10.1038/s41467-018-04383-6
  15. Deb S, Ghosh A, Barman D, et al. Aberrant promoter methylation of p16, RASSF1A, and MGMT genes in esophageal cancer in North East India: possible biomarkers for early detection. Asian Pac J Cancer Prev. 2014;15(12):4497–4503. doi:10.7314/APJCP.2014.15.12.4497
  16. Baldwin RL, Nemeth E, Tran H, et al. BRCA1 promoter region hypermethylation in ovarian carcinoma: a population-based study. Cancer Res. 2000;60(19):5329-5333.
  17. Esteller M, Corn PG, Baylin SB, Herman JG. A gene hypermethylation profile of human cancer. Cancer Res. 2001;61(8):3225-3229.
  18. Esteller M, Silva JM, Dominguez G, et al. Promoter hypermethylation and BRCA1 inactivation in sporadic breast and ovarian tumors. J Natl Cancer Inst. 2000;92(7):564-569. doi:10.1093/jnci/92.7.564
  19. Alumkal JJ, Slottke R, Schwartzman J, et al. A phase II study of sulforaphane-rich broccoli sprout extracts in men with recurrent prostate cancer. Invest New Drugs. 2015;33(2):480-489. doi:10.1007/s10637-014-0189-1
  20. Henning SM, Wang P, Abgaryan N, et al. Phenolic acid concentrations in plasma and urine from men consuming green or black tea. Br J Nutr. 2013;110(5):843-848. doi:10.1017/S0007114512006044Link A, Balaguer F, Goel A. Cancer chemoprevention by dietary polyphenols: promising role for epigenetics. Biochem Pharmacol. 2010;80(12):1771-1792. doi:10.1016/j.bcp.2010.06.036
  21. van der Plaat DA, Sharp GC, Felix JF, et al. A meta-analysis of epigenome-wide association studies of ultra-processed food consumption with DNA methylation in European children. Clin Epigenetics. 2025;17(1):101. doi:10.1186/s13148-024-01782-z3,4,7
  22. Denham J, Marques FZ, O’Brien BJ, Charchar FJ. Exercise: putting action into our epigenome. Sports Med. 2014;44(2):189-209. doi:10.1007/s40279-013-0114-1
  23. Ntanasis-Stathopoulos J, Tzanninis JG, Philippou A, Koutsilieris M. Epigenetic regulation on gene expression induced by physical exercise. J Musculoskelet Neuronal Interact. 2013;13(2):133-146.
  24. Kaliman P, Álvarez-López MJ, Cosín-Tomás M, Rosenkranz MA, Lutz A, Davidson RJ. Rapid changes in histone deacetylases and inflammatory gene expression in expert meditators. Psychoneuroendocrinology. 2014;40:96-107. doi:10.1016/j.psyneuen.2013.11.004
  25. Doshi T, Mehta SS, Dighe V, Balasinor N, Vanage G. Hypermethylation of estrogen receptor promoter region in adult testis of rats exposed neonatally to bisphenol A. Toxicology. 2011;289(2-3):74-82. doi:10.1016/j.tox.2011.07.011
  26. Tarantini L, Bonzini M, Apostoli P, et al. Effects of particulate matter on genomic DNA methylation content and iNOS promoter methylation. Environ Health Perspect. 2009;117(2):217-222. doi:10.1289/ehp.11898
  27. Ficz G, Choudhary P, O’Neill L, et al. CRISPR/dCas9 DNA methylation editing is heritable during human hematopoiesis and shapes immune progeny. Proc Natl Acad Sci U S A. 2023;120(34):e2300224120. doi:10.1073/pnas.23002241206
  28. Liu J, Wan M, Lyon CJ, Hu TY. Nanoparticle delivery of CRISPR/Cas9 for genome editing. Front Genet. 2020;11:138. doi:10.3389/fgene.2020.00138
  29. Alencar AJ, Salles G, Fanale M, et al. Pembrolizumab plus vorinostat induces responses in patients with relapsed/refractory diffuse large B-cell lymphoma: final results of a phase 1 study. Blood. 2023;142(Suppl 1):437. doi:10.1182/blood-2023-187456
  30. Song L, Li Y. SEPT9: a specific circulating biomarker for colorectal cancer. Adv Clin Chem. 2015;72:171-204. doi:10.1016/bs.acc.2015.07.004
  31. Lesch BJ, Tothova Z, Morgan EA, et al. Intergenerational epigenetic inheritance of cancer susceptibility in mammals. eLife. 2019;8:e39380. doi:10.7554/eLife.39380