What is epigenetics and can you influence your genes?
Epigenetics determines which genes are active and is in principle open to influence. In medicine, epigenetic mechanisms are already being successfully targeted in some blood cancers, but evidence for self-directed modification through lifestyle remains limited in humans.
DNA methylation, histone modification and microRNA are the three principal epigenetic mechanisms. They determine which genes are switched 'on' or 'off', without the DNA sequence itself changing. Think of it as sticky notes on a book: the text stays the same, but the markings decide which passages are actually read. This kind of regulation is largely heritable and applies to every cell in your body.
Epigenetic abnormalities have a demonstrated role in the development of disease. Dysregulation of these systems contributes to autoimmune diseases, cancer and other conditions. In breast cancer, for example, shifts in the epigenome can cause tumour cells to become resistant to hormonal treatment. In asthma, cell-specific methylation patterns have been found that are associated with lung function, although it is not yet fully clear whether those patterns cause the disease or are a consequence of it.
The good news is that epigenetic abnormalities are, in principle, reversible. That is a crucial difference from genetic mutations, which permanently alter your DNA. This reversibility makes epigenetics an attractive target for medicines. Drugs that inhibit epigenetic mechanisms have already been proven clinically effective in certain lymphomas and a precursor to leukaemia. In solid tumours the picture also looks promising, but the evidence there is still thinner.
Ageing is accompanied by measurable shifts in the epigenome, particularly in DNA methylation patterns. These changes are associated with how quickly someone ages biologically and how long they remain healthy. Researchers are testing interventions that might slow this process, such as removing senescent cells or making metabolic adjustments. Those results come largely from animal studies and early-stage clinical research in humans for the time being. It is therefore too early to say that you can steer your own epigenetic ageing.
Claims are based on five to nine PMIDs, including review articles on the basic biology of epigenetics, clinical studies on epigenetic drugs in blood cancer, and early mechanistic research into epigenetic ageing. Strongest evidence: the basic workings of the mechanisms and their clinical use in blood cancer. Weakest evidence: rejuvenating interventions in humans.
Can you repair DNA damage, or can you only prevent it?
Your body actively repairs DNA damage through multiple well-studied mechanisms, but that repair is not always perfect and becomes less effective when the cell is under excessive strain or grows older.
Can you counteract DNA damage from ageing through your lifestyle?
Quitting smoking, exercising regularly and eating plenty of vegetables demonstrably reduce DNA damage; antioxidant supplements are unlikely to help with this.
Can diet protect your DNA from damage?
Diet has a real effect on DNA protection: a plant-based eating pattern and adequate folate and selenium demonstrably help, while heavily heat-processed meat and mouldy grains cause DNA damage. High antioxidant supplements are not a safe shortcut and can even be counterproductive.
Can DNA damage in your cells repair itself?
Your cells repair DNA damage constantly and on a large scale, but this capacity is not unlimited: complex or repeated damage can lead to errors that accumulate and drive diseases such as cancer.
Can you tell from your DNA which diseases you are at greater risk of, and how is that measured?
Your DNA and certain proteins in your blood provide a useful picture of your predisposition to heart disease and other common conditions, but in people of non-European ancestry those scores are less reliable.
Can smoking permanently damage your DNA?
Smoking damages your DNA in multiple ways simultaneously and leaves recognisable mutation patterns in at least 17 types of cancer. Quitting smoking demonstrably reduces the risk, as no association between smoking-related DNA damage and cancer has been found in former smokers.