Your DNA sequence, the genetic code you were born with, is remarkably stable. But it’s not completely fixed. Your genes can change in two distinct ways: the DNA sequence itself can pick up permanent mutations over your lifetime, and your body can change how it reads and uses your existing genes without altering the underlying code. The first type of change is permanent. The second is often reversible.
Two Kinds of Genetic Change
When most people ask whether genes can change, they’re really asking about two different things that often get blurred together. The first is a mutation: a physical change to the letters of your DNA code. These happen constantly. Every time a cell divides and copies its DNA, there’s a small chance of an error. UV radiation, cigarette smoke, and certain chemicals can also damage DNA directly, leaving behind permanent alterations in the affected cells. Specific mutational “signatures” have been identified in the lung tissue of smokers, for example, showing that tobacco leaves a distinct fingerprint on DNA.
The second type of change is epigenetic. Your body attaches small chemical tags to DNA and to the proteins that DNA wraps around. These tags act like dimmer switches, turning genes up or down without changing the code itself. Your diet, physical activity, stress levels, and chemical exposures all influence these tags. The critical difference: epigenetic changes are reversible. Mutations typically are not.
How Your Body Accumulates Mutations
You are not working with the same pristine DNA you had at birth. As you age, your cells accumulate what scientists call somatic mutations, changes that arise in ordinary body cells (as opposed to egg or sperm cells). These mutations build up from a combination of copying errors during cell division, exposure to environmental damage, and the gradual decline of your body’s DNA repair machinery.
Most somatic mutations are harmless. They land in stretches of DNA that don’t code for anything important, or they’re in cells that won’t divide again. But some mutations land in genes that control cell growth. When enough of these “driver” mutations accumulate in the same cell lineage, the result can be cancer. Oncogenes, which are genes that promote cell growth, can be switched into overdrive by a single mutation. Tumor suppressor genes, which normally keep cell division in check, can be knocked out. Cancer cells typically carry one to two orders of magnitude more genetic alterations than normal cells.
Specific environmental exposures have been linked to specific cancer-driving mutations. Sun exposure in melanoma has been connected to a particular mutation in the BRAF gene. An aflatoxin signature has been linked to a mutation in TP53, a key tumor suppressor. A mutation in the KRAS gene in lung cancer has been tied to tobacco-related damage. These are permanent, irreversible changes to the DNA code in those cells.
Epigenetic Changes From Lifestyle and Environment
Your daily habits reshape how your genes behave. Smoking reduces DNA methylation (one of those chemical dimmer switches) on certain genes, effectively turning them on when they should be quiet. But here’s the encouraging part: after quitting smoking, methylation levels at those genes can return to the levels seen in people who never smoked. In some cases, this recovery happens in less than a year, though it depends on how long and how heavily someone smoked.
Exercise leaves its own epigenetic marks. Resistance training reduces methylation on genes involved in muscle growth and repair, essentially priming those genes for greater activity. Sprint and aerobic exercise affect different gene pathways, altering signals related to energy metabolism and insulin sensitivity. Perhaps most interesting is the concept of “epigenetic memory” in skeletal muscle. Researchers identified a cluster of genes that become hypomethylated (turned on) during a training period, return to baseline when training stops, and then show even greater activation when training resumes. Your muscles, on a molecular level, remember having been trained before.
Diet matters too. What you eat can influence the availability of methyl groups, the chemical building blocks your body uses to tag DNA. A deficiency in key nutrients like the amino acid methionine can reduce your body’s ability to maintain normal methylation patterns.
Changes That Start Before Birth
Some of the most dramatic evidence for environmental effects on gene expression comes from the Dutch Hunger Winter of 1944-45. Researchers studied people whose mothers experienced severe famine during pregnancy, then compared them to their unexposed siblings six decades later. Those exposed to famine around the time of conception had about 5.2% lower methylation on a growth-related gene called IGF2 compared to their siblings. The effect was specific to very early pregnancy: people exposed to famine only in late gestation did not show the same methylation changes, though they did have significantly lower birth weights (averaging about 300 grams less than reference births).
This was the first evidence that a temporary environmental condition during early human development could leave a lasting epigenetic mark detectable more than 60 years later. The finding reinforced that the earliest weeks of pregnancy are a critical window for establishing the chemical tags that govern gene activity throughout life.
Which Changes Can You Pass to Your Children
Only changes in reproductive cells, eggs and sperm, can be inherited. These are called germline mutations. If a mutation occurs in a sperm or egg cell, the resulting child will carry that mutation in every cell of their body, and they can pass it on to their own children.
Somatic mutations, the ones that accumulate in your skin, lungs, liver, and other body cells throughout life, cannot be passed to the next generation. A mutation caused by sun damage to your skin cells stays in your skin. It doesn’t travel to your reproductive cells. This is why a lifetime of sun exposure doesn’t give your children a genetic predisposition to the specific mutations in your skin.
Whether epigenetic changes can be inherited across generations in humans remains a more complicated question. The Dutch Hunger Winter data shows that a mother’s environment during pregnancy can directly affect the developing embryo’s epigenetic programming. But that’s technically still a direct exposure, not true multi-generational inheritance, since the embryo itself experienced the famine environment.
Your Biological Age vs. Your Actual Age
One practical consequence of epigenetic change is that your genes age at a rate that doesn’t always match your birthday. Researchers have developed what’s known as an epigenetic clock: a tool that reads methylation patterns across your DNA and estimates your biological age. Developed using over 8,000 tissue samples from 51 different tissue types, these clocks can predict chronological age with a correlation of 0.96 and an average error of about 3.6 years across tissues.
The accuracy varies by tissue. Blood samples are predicted within about 1.9 to 3.7 years. Brain tissue falls within about 5.9 years. Muscle tissue is harder to read, with an error of about 18 years. The key insight is that when your epigenetic age runs ahead of your chronological age, it’s associated with worse health outcomes. Lifestyle factors that shift epigenetic marks, like exercise, diet, and avoiding tobacco, can influence where your biological clock lands relative to your actual age.
Deliberately Editing Genes
For the first time in history, it’s now possible to intentionally change a person’s DNA as a medical treatment. In December 2023, the FDA approved Casgevy, a therapy that uses CRISPR gene-editing technology to treat sickle cell disease. The treatment works by removing a patient’s own blood stem cells, editing a specific gene to boost production of healthy hemoglobin, and infusing the modified cells back. It’s approved for patients 12 and older with severe sickle cell disease, and it was also approved for a related blood disorder called transfusion-dependent thalassemia. The European Medicines Agency followed with approval in February 2024.
This is a one-time treatment that makes a permanent, targeted change to the DNA in a patient’s blood-forming stem cells. It represents a fundamentally different kind of genetic change: deliberate, precise, and designed to correct a disease-causing mutation rather than introduce one.