Epigenetics

You inherited a fixed set of genes and you cannot change them. What you can influence is which of them get read.

That is the whole idea behind epigenetics, and it is one of the more genuinely useful shifts in biology of the last thirty years. It is also one of the most oversold. Search this topic and you will be told your thoughts rewrite your DNA, that your grandmother’s trauma is sitting in your genome, and that the right supplement will optimise your methylation. Very little of that survives contact with the actual research.

At the Energetics Institute have practised somatic psychotherapy in Perth since 2005, and this page is our attempt to explain epigenetics properly, including where the evidence stops. We work with people whose nervous systems have been shaped by stress and early experience, so we have a professional interest in this field being described accurately rather than enthusiastically.

What Is Epigenetics?

Epigenetics is the study of changes in gene activity that do not involve any change to the underlying DNA sequence.

The National Human Genome Research Institute defines it as a field focused on changes in DNA that do not alter the sequence itself. Chemical tags sit on top of the genetic code and on the proteins packaged with it, and those tags govern how, where and when a gene is switched on. The full set of these tags across a genome is called the epigenome, and the field that maps it is epigenomics.

The prefix helps. Epi means above or on top of. Epigenetics is what sits above genetics and tells it what to do.

What Epigenetics Is Not

It is worth clearing two misunderstandings early.

Epigenetics does not mean your DNA sequence changes. The letters stay exactly as they were. What changes is accessibility, which genes the cell can reach and read at any given moment.

Epigenetics also does not mean you can consciously direct your own gene activity. Epigenetic marks respond to biology and environment, not to intention. The gap between “the environment influences gene activity” and “you can think your genes into a better state” is where most of the popular material on this subject goes wrong.

Epigenetics Versus Genetics

The simplest way to hold the difference is hardware and settings.

Your DNA sequence is the hardware. It is the same in a liver cell, a neuron and a skin cell, and it barely changes across your life. Genetic changes mean actual alterations to that sequence, and they are permanent.

Epigenetic changes are the settings. They determine which parts of the hardware are running. Unlike genetic mutations, epigenetic modifications are added and removed by enzymes, which means they can shift over a lifetime. That does not make them easy to shift on purpose, and many are extremely stable, which is the point of them.

What Epigenetics Explains That Genetics Cannot

Several ordinary observations make no sense if an organism’s genes are the whole story.

Identical twins diverge as they age. Two hundred cell types run one genome. Bee larvae fed differently become queens or workers carrying the same DNA. A condition appears in one sibling and not the other, in the same house, with the same parents. None of that follows from sequence alone.

Epigenetic influence accounts for it. The sequence sets what is possible and the epigenome sets what is currently happening, and the second is far more responsive to circumstance than the first. That is the explanatory gap the field was built to fill.

A Short History Of The Term

Epigenetics is older than the molecular biology that explains it.

The British developmental biologist Conrad Waddington introduced the term in a 1942 paper called The Epigenotype. He was not describing chemical tags, which nobody had found yet. He was describing the developmental processes that sit between genotype and phenotype and explain how one genome produces many different kinds of cells. His famous epigenetic landscape, a ball rolling down a hillside into one valley or another, came from a 1940 book and a 1957 follow up.

Earlier still, the Russian biologist Nikolai Koltsov had speculated as far back as 1915 that chemical modification of genes might create heritable variation. He was decades ahead of the evidence.

How The Definition Tightened

Modern definitions are narrower and more useful than Waddington’s.

In 1990 Robin Holliday defined epigenetics as the study of the mechanisms of temporal and spatial control of gene activity during the development of complex organisms. That version put control of gene activity at the centre, which is where it has stayed.

In December 2008 a meeting at Cold Spring Harbor produced an operational definition, published the following year by Berger, Kouzarides, Shiekhattar and Shilatifard. They defined an epigenetic trait as a stably heritable phenotype resulting from changes in a chromosome without alterations in the DNA sequence. That is the definition working scientists use.

How Does Epigenetics Work?

Three main epigenetic mechanisms do the work, and they interact constantly.

The first is DNA methylation, chemical tags placed directly onto the DNA. The second is histone modification, chemical changes to the histone proteins the DNA is wrapped around. The third is regulation by non coding RNA sequences, RNA molecules that never become protein but steer what does.

All three converge on the same outcome. They alter chromatin structure inside the cell nucleus, changing how tightly the DNA is packed, and therefore whether the machinery of transcription can physically reach a particular gene.

DNA Methylation Explained

DNA methylation is the best understood epigenetic modification and the one most research measures.

DNA methylation involves attaching a methyl group, a small cluster of one carbon and three hydrogen atoms, to the fifth carbon position of a cytosine base. The result is 5-methylcytosine. This cytosine methylation happens overwhelmingly where a cytosine sits immediately next to a guanine, a pairing written as CpG.

The consequence depends on where it lands. Methyl groups change DNA protein interactions, either by physically blocking transcription factors from binding or by recruiting repressive proteins that shut the region down. Dense methylation across a gene’s control region is associated with stable transcription repression.

CpG Islands And Promoter Regions

Methylation is not scattered evenly. It clusters, and where it clusters matters enormously.

Stretches of DNA unusually rich in CpG pairs are called CpG islands. They average around a thousand base pairs long, and the human genome contains roughly twenty five thousand of them. Crucially, about seventy per cent of human gene promoters are associated with a CpG island, which makes this the most common promoter type in vertebrates.

In healthy tissue these island promoter regions are mostly kept free of methylation, leaving the genes available. When methylation arrives at one of them, gene silencing usually follows. This is the single most important relationship in the whole field.

The Enzymes That Write The Marks

A family of enzymes called DNA methyltransferases does the writing.

They split into two jobs. DNMT3A and DNMT3B perform de novo DNA methylation, laying down new patterns from scratch during early development as cells commit to becoming one tissue rather than another. DNMT1 performs maintenance, and it is the reason methylation patterns survive.

The distinction matters for anyone trying to understand epigenetic control. De novo work establishes an identity. Maintenance work defends it. Both are carried out by DNA methyltransferase enzymes, and both can go wrong.

How Marks Survive When Cells Divide

This is the mechanism that makes epigenetic marks heritable at the cellular level.

During DNA replication each double helix is copied into two, and each new pair has one old strand carrying the methylation and one freshly built strand carrying none. That state is called hemimethylated. DNMT1 recognises it and copies the pattern onto the new strand.

The result is that when cells divide, their progeny cells inherit the same methylation patterns and therefore the same identity. Block DNMT1 and the marks are simply diluted away across successive rounds of division, which is precisely how some cancer drugs work.

Histone Modification And Chromatin Structure

The second mechanism works on packaging rather than on the DNA itself.

Two metres of DNA fits inside every cell nucleus because it is wound around spools of histone proteins. The basic unit is the nucleosome, roughly 147 base pairs of DNA wrapped around an octamer of eight histone proteins, two each of H2A, H2B, H3 and H4. DNA plus histones plus associated proteins is chromatin.

Protruding from each nucleosome is a flexible histone tail built from amino acids. These tails are chemically decorated, and histone modification of those tails is what loosens or tightens the packaging around any given stretch of sequence.

Histone Acetylation And Gene Activation

Acetylation is the clearest example of chromatin modification, because the physics is easy to picture.

Histone tails carry positive charge, largely from lysine residues, and DNA carries negative charge. Opposites attract, so the packaging is tight. Lysine acetylation neutralises that positive charge, the grip loosens, chromatin opens, and transcription activation becomes possible.

Enzymes called histone acetyltransferases add the acetyl groups and histone deacetylases remove them. As a rough rule that holds well enough for general purposes, acetylation goes with transcriptional activation and deacetylation goes with silencing.

Histone Methylation And Other Marks

Not all epigenetic methylation happens on DNA. Histones get methylated too, and here the rule of thumb breaks down.

Histone methylation can activate or repress depending entirely on which residue is marked and how many methyl groups it carries. Trimethylation of lysine 4 on histone H3 sits at active promoters. Trimethylation of lysine 9 or lysine 27 on the same histone marks regions that are shut down. The same chemical modification, opposite meanings.

Histone phosphorylation adds another layer, particularly during cell division and DNA damage response. Histone variants, alternative versions of the standard histone proteins, are swapped in at sites of active transcription.

Non Coding RNA And Gene Silencing

The third mechanism was the last to be taken seriously and is now among the most active areas of research.

Most of the human genome is transcribed into RNA that never codes for protein. Current annotations list around nineteen thousand protein coding genes against nearly thirty six thousand long non coding RNA genes. Far from being noise, many of these act as scaffolds, recruiting chromatin modifying enzymes to specific addresses on the genome.

The most spectacular example is XIST, a long non coding RNA that coats an entire chromosome and recruits the machinery that silences it. We will come back to that one.

Chromatin Modifying Enzymes And Open Chromatin

Everything above is carried out by a large cast of enzymes, and researchers group them by function.

Writers add marks. Erasers remove them. Readers, such as methyl-CpG binding proteins, recognise marks and translate them into an outcome. Chromatin modifying enzymes and remodelling complexes then physically reposition nucleosomes to expose or bury regulatory sequences.

The practical question is always the same. Is this stretch of chromatin open or closed? A technique called ATAC-Seq, introduced in 2013, maps regions of open chromatin across the whole genome, and it has become one of the standard tools for reading a cell’s regulatory state.

How The Epigenome Is Measured

Reading epigenetic state requires different tools from reading sequence.

The standard method for methylation is bisulfite conversion, which chemically alters unmethylated cytosines but leaves methylated ones untouched, so sequencing afterwards reveals DNA methylation patterns base by base. Array based versions measure hundreds of thousands of sites at once, and they are what most large human studies rely on.

Histone marks are mapped differently, by pulling chromatin down with antibodies raised against one specific modification and sequencing whatever DNA came with it. Together these methods reveal which regulatory proteins are in position and which regions are accessible, which is how researchers work out what is set to regulate gene expression in a given tissue at a given moment.

Why One Genome Makes Two Hundred Cell Types

This is the problem epigenetics was invented to solve, and the answer is still the field’s best argument.

Every cell in your body carries the same DNA sequence. A neuron and a pancreatic cell are radically different objects running identical code. The difference is entirely a matter of which genes are available, and that is set by epigenetic regulation.

Cell differentiation works by progressively narrowing options. Genes for other lineages are marked for silencing, genes for the chosen lineage are opened up, and once established the pattern is defended through every subsequent round of division. Cellular differentiation is, at the molecular level, a story about what gets switched off.

Stem Cells And Cell Fates

Stem cell biology is where this becomes visible.

A stem cell is defined by keeping its options open. Many of its key developmental genes sit in what is called a bivalent state, carrying both an activating and a repressing histone mark at once, poised for a decision. Stem cell differentiation resolves that ambiguity, and cell fates are locked in.

This is why the field matters far beyond mental health. Regenerative medicine, cancer biology and developmental disorders all turn on the same question of how epigenetic marks assign and defend cell identity.

Genomic Imprinting And Imprinted Genes

Most genes come in two working copies, one from each parent. A small number do not.

Genomic imprinting silences one parental copy so that only the maternal or only the paternal version is active. Imprinted genes carry a mark established in the egg or sperm that survives into the next generation, which makes them the clearest case of genuine epigenetic inheritance in humans.

The consequences are visible in disease. Prader-Willi syndrome and Angelman syndrome both arise from faults in the same region of chromosome 15, but which condition develops depends on whether the fault is on the copy inherited from the father or the mother. Same address, different parent, entirely different outcome.

X Chromosome Inactivation

Chromosome inactivation is epigenetics operating at the largest scale it ever does.

Females carry two X chromosomes and males carry one, so a dosage problem arises. X chromosome inactivation solves it. Early in development each cell randomly shuts down one of its two X chromosomes, coats it in XIST RNA, and packs it into dense silent chromatin. Every progeny cell of that cell keeps the same choice.

The result is that every woman is a mosaic. Tortoiseshell and calico cats make it visible, because the coat colour gene sits on the X and the patches show which chromosome was silenced where.

Are Epigenetic Changes Reversible?

Yes in principle, and this is where careful language matters most.

Epigenetic marks have erasers as well as writers. The TET enzymes, discovered in 2009, oxidise 5-methylcytosine through a series of intermediates and feed it into active demethylation. Before that discovery, methylation was thought to be removable only by dilution during replication. It is now clear that epigenetic marks are more dynamic than anyone expected.

But reversible in principle is not the same as reversible on demand. Many marks are extraordinarily stable, and they need to be, because that stability is what keeps a liver cell a liver cell for eighty years. Nothing in the literature supports the idea that you can decide to reverse an epigenetic mark.

Environmental Factors That Leave Marks

Certain environmental factors genuinely and measurably alter epigenetic markers, and some of the evidence is very strong.

The clearest example in all of human epigenetics is tobacco smoke. A 2016 consortium meta-analysis pooled thirteen cohorts and 6,685 newborns and found more than six thousand sites differentially methylated in babies whose mothers smoked sustainedly during pregnancy. The signal was still detectable in the same children years later.

Diet, chemical exposure, infection, sleep loss and chronic stress have all been linked to epigenetic alterations. The quality of that evidence varies enormously, which we will get to.

The Dutch Hunger Winter

The most cited human study in the field deserves both its fame and its caveats.

Between November 1944 and April 1945 the western Netherlands endured a severe famine under German blockade. In 2008 Heijmans and colleagues examined sixty people who had been conceived during it, comparing each against their own unexposed same sex sibling. Six decades later, those exposed around conception still showed measurably lower methylation at a control region of the IGF2 gene.

Two things to hold. The effect was small, around five per cent. And this is prenatal exposure, not inheritance. These people were in the womb during the famine. Their own bodies were exposed.

Identical Twins And Epigenetic Differences

If genes were destiny, identical twins would stay identical. They do not.

Fraga and colleagues published a study in 2005 examining forty monozygotic twin pairs, eighty individuals in total, aged from three to seventy four. Young pairs were epigenetically close to indistinguishable. Older pairs were clearly distinct, with around a third showing substantial epigenetic differences in methylation and histone acetylation.

The divergence was greatest in pairs who had spent less of their lives together and had different medical and lifestyle histories. It is a cross sectional study rather than a follow up of the same twins over time, so read it as suggestive rather than conclusive. It remains the most intuitive demonstration that identical genetic code does not produce identical outcomes.

Epigenetics And Disease

Epigenetic errors contribute to a wide range of illness, and cancer is where the evidence is strongest.

Two opposite things happen at once in tumours. The genome as a whole loses methylation, which destabilises it. At the same time, specific promoters gain it. Comparing cancer cells with normal cells, promoter regions of tumour suppressor genes that are unmethylated in healthy tissue are frequently heavily methylated in tumours.

The effect is epigenetic silencing of exactly the genes that would otherwise apply the brakes. No mutation is required. The gene is intact and simply unreadable, which is why epigenetic abnormalities can both initiate and accelerate the disease.

Cancer Metastasis And Epigenetic Plasticity

The same flexibility that lets a stem cell choose a fate lets a cancer cell change one.

Metastasis requires tumour cells to loosen their attachments, migrate, survive in circulation and re-establish elsewhere. That sequence demands changes in gene function far faster than mutation can supply. Epigenetic mechanisms provide them, because they are stable enough to persist and reversible enough to be undone at the destination.

Silencing of the E-cadherin gene through promoter hypermethylation is one well documented step in that process. Cancer metastasis is, in part, a failure of epigenetic control rather than a purely genetic event.

Treating Disease Through The Epigenome

This is where the science has moved from laboratory curiosity into actual disease control.

Because these marks are enzyme dependent, they are druggable. Azacitidine and decitabine inhibit DNA methyltransferases and are approved for myelodysplastic syndromes. Vorinostat and romidepsin inhibit histone deacetylases and are approved for cutaneous T-cell lymphoma. Newer agents target other chromatin modifying enzymes.

These are serious oncology drugs with serious side effects, not wellness interventions. But they are proof of principle. Epigenetic modifications can be therapeutically altered in living people.

Epigenetic Errors And Genetic Disease

Beyond cancer, several conditions sit at the boundary between genetic disease and epigenetic error.

Beckwith-Wiedemann syndrome results from faulty regulation of a region on chromosome 11, and about half of cases involve a methylation fault at an imprinting control centre. Prader-Willi and Angelman syndromes, described earlier, can also arise from imprinting defects rather than from missing DNA.

Two conditions often listed here need a correction. Fragile X syndrome and Rett syndrome are caused by genetic changes to the DNA sequence. They are worth mentioning because both act through epigenetic machinery, but they are mutations, not epimutations.

Epigenetics And Mental Health

This is the section most readers came for, and it needs the most care.

The proposition is appealing. Early adversity shapes the nervous system, the nervous system is built by gene expression, and epigenetic marks govern gene expression, so adversity should leave a readable epigenetic signature. Something like this is almost certainly true in outline.

The problem is that the human evidence for the specific version of the story is much weaker than the popular coverage suggests. We are going to lay out what is solid, then what is not, because we think you are better served by that than by encouragement.

What The Animal Research Shows

The foundational work is genuinely impressive, and it was done in rats.

In 2004 Weaver, Meaney and colleagues showed that rat pups raised by mothers who licked and groomed them frequently developed less methylation at the promoter of the glucocorticoid receptor gene in the hippocampus, more histone acetylation there, higher receptor expression and a calmer stress response. Cross fostering reversed it, so this was maternal care rather than maternal genes.

They then reversed the pattern pharmacologically in adult animals, in both directions. This is the strongest evidence anywhere that early caregiving alters the epigenetic regulation of the stress system. It is also rats, with drugs infused directly into the brain.

What The Human Research Shows

Here the picture becomes considerably murkier, and honesty requires saying so.

A 2009 post mortem study found higher methylation of the same glucocorticoid receptor promoter in suicide victims with histories of childhood abuse. It is cited constantly. It also had twelve people per group. Similar candidate gene findings around FKBP5 and BDNF followed.

Then the large studies arrived. A 2018 analysis of 1,658 twins found effects under one per cent that largely vanished once smoking was accounted for, and none of the classic candidate genes held up. A 2024 meta-analysis of 5,077 people with PTSD did not find the expected genes reaching genome wide significance. Australian work through the Barwon Infant Study, with 481 mother and baby pairs, likewise urged caution about earlier findings.

What This Means In Practice

None of this means early experience does not matter. It means we cannot currently read it off a blood test.

Adversity in childhood is one of the most robust predictors of adult mental health difficulty in all of psychology. That finding does not depend on epigenetics being the mechanism. What is under dispute is whether the mechanism is measurable methylation at particular genes, not whether the effect is real.

We think this distinction matters clinically. Effective treatment for early trauma does not require anyone to know which gene was marked, and no reputable therapist should be selling epigenetic testing as a guide to psychological care.

Epigenetic Clocks And Biological Ageing

One area where the measurement side has advanced is ageing.

Methylation patterns change with age reliably enough that algorithms can estimate biological age from a blood sample. The best current version, DunedinPACE, was built from a New Zealand cohort of over a thousand people tracked from twenty six to forty five, and estimates the pace at which someone is ageing rather than a single age.

Threat related childhood adversity is associated with modest acceleration on these measures. Deprivation and low socioeconomic status, treated separately, are not. Effect sizes are small, most studies are cross sectional, and smoking confounds the picture heavily. Nobody has yet shown that an intervention slows these clocks.

Stress, Gene Activity And Inflammation

This is the mechanism story that is actually well supported, and it is not primarily about methylation.

Steve Cole’s research group has documented a consistent pattern under chronic social stress, isolation, threat and low status, which they call the conserved transcriptional response to adversity. Pro-inflammatory genes are upregulated, antiviral interferon genes and antibody genes are downregulated. It has been reproduced across bereavement, loneliness, low socioeconomic status, cancer diagnosis and in primate studies where the stressor could be experimentally imposed.

The driver is largely the sympathetic nervous system acting on beta-adrenergic receptors and driving inflammatory transcription factors, rather than cortisol alone. Cole is explicit that epigenetic marks correlate only weakly with this gene expression pattern. Stress changing gene activity and stress changing the epigenome are two different claims.

Loneliness And The Immune System

The loneliness research is among the most solid work connecting social experience to gene regulation.

Cole’s 2007 study compared people at the extremes of chronic loneliness and found around 144 genes differentially expressed, with a near threefold enrichment of inflammatory signalling elements in the promoters of overexpressed genes. A 2015 follow up tracked 141 adults over years and found the gene expression pattern predicted loneliness a year later, suggesting a self reinforcing loop, with a matched primate arm supplying causal evidence.

For a therapy practice this is the most clinically relevant finding in the whole literature. Social disconnection is not merely unpleasant. It is measurably biological.

Epigenetics And Happiness

Now to the second question people bring here, and to a claim we are not going to make.

A widely publicised 2013 study reported that meaning based wellbeing was associated with a healthier gene expression profile than pleasure based wellbeing. It was heavily criticised, it failed the authors’ own attempted replication in 2015, and a reanalysis showed the result flipped sign when a single participant was removed. Later genetic work found the two kinds of wellbeing are barely distinguishable anyway.

We mention it because you will find it quoted everywhere as established fact. It is not. There is no credible evidence that one flavour of happiness is better for your genes than another.

Is Happiness Inherited?

The heritability question has a much better evidence base, and the answer is nuanced.

A 2015 meta-analysis of thirty twin and family studies put the heritability of wellbeing at around thirty six per cent and of life satisfaction at around thirty two per cent. Later summaries settle near forty per cent. Genetic studies have found hundreds of associated variants, each with a tiny effect.

Read that the right way around. Roughly sixty per cent of the variation in how satisfied people are with their lives is not genetic. Temperament is real and it is not destiny, which is roughly what any experienced therapist would tell you anyway.

The Set Point Is Not Fixed

The popular version of this research is more fatalistic than the research itself.

The old claim was that everyone returns to a fixed happiness baseline no matter what happens. The current position, set out by Diener and colleagues, revises that in five ways. Baselines are positive rather than neutral, most people sit above the midpoint, they differ between individuals, positive mood and negative mood and life satisfaction move independently, and baselines do change. In one long running German panel, twenty four per cent of people shifted significantly from their early baseline.

The well known pie chart assigning forty per cent of happiness to intentional activity has been retired by its own authors, who accepted the figure was an overestimate.

What Actually Shifts Gene Activity

If you want interventions with real evidence behind them, they are unglamorous.

Stopping smoking is the cleanest demonstration in the field. Methylation at the AHRR gene tracks tobacco exposure closely and reverts measurably after quitting, over years rather than weeks. Exercise produces rapid demethylation at metabolic gene promoters in skeletal muscle, shown in a 2012 study, though the effect is local and transient. Sleep restriction alters the expression of hundreds of genes and flattens circadian rhythms, demonstrated in a study where twenty six people ran a week at under six hours a night.

Randomised trials of acts of kindness directed at other people, in samples of 159 and 182 adults, reduced the inflammatory gene expression pattern described earlier. Meta-analysis of forty eight mindfulness trials across 4,683 people found small reductions in inflammatory markers, mainly in people who were already medically unwell.

What Does Not Work

Two popular recommendations are not supported and we would rather say so.

Methyl donor supplements, meaning folate, B12, choline and betaine, do not measurably change DNA methylation levels in humans. A systematic review including eighteen human randomised trials found no significant effect against placebo. The animal data at high doses looks different, which is where the marketing comes from.

Commercial epigenetic testing sold as a guide to lifestyle or psychological treatment has no clinical validation. Being able to measure something is not the same as knowing what to do about it.

The Everyday Version Of All This

Strip the terminology out and a short, unexciting list remains.

Sleep enough that your circadian rhythm holds. Move your body hard enough to matter, regularly. Do not smoke. Treat chronic stress as a physiological problem rather than a character flaw. Stay socially connected, because isolation shows up in immune gene activity more clearly than almost anything else that has been measured. Deal with unresolved trauma rather than managing around it.

None of that is new, and none of it needed epigenetics to justify it. What the field adds is mechanism, an account of how a way of living gets under the skin and stays there. Knowing the mechanism does not change the advice. It does make it considerably harder to dismiss.

Where Psychotherapy Fits

We are a psychotherapy practice writing about epigenetics, so this is where we could reasonably be expected to overreach.

A handful of small studies have looked at methylation before and after therapy. Sixteen veterans through prolonged exposure. A hundred and fifteen people through intensive dialectical behaviour therapy. A hundred and eleven through exposure based cognitive behavioural therapy. All found methylation differences that tracked with who responded well.

They also disagreed with each other about direction, the methylation changes did not correspond to gene expression changes, and none established that therapy caused anything. The honest summary is that this is interesting, preliminary, and not yet a reason to choose one therapy over another.

How We Work With This

Our approach is Integrative Body Mind Psychotherapy, and epigenetics has not changed what we do. It has changed how we explain it.

What the biology supports is that chronic threat states are physiological, not merely mental. A nervous system held in sympathetic activation for years is running a different pattern of gene activity than one that stands down regularly. That is well documented, and it is why we work with the body directly rather than through conversation alone.

What we work with is the input rather than the genome. Sleep, safety, social connection, unresolved trauma and the habitual bracing that keeps someone in a defensive state. Change those and physiology follows. Our body mind psychotherapy is aimed squarely at that layer.

What We Tell Clients About Their Genes

People arrive with strong beliefs about inherited fate, and they run in both directions.

Some are convinced they are doomed because depression runs in the family. Others have read that their grandmother’s suffering is encoded in them. Both beliefs do damage, and neither is supported. Family patterns transmit through behaviour, attachment, modelling and shared circumstance far more demonstrably than through any epigenetic channel.

The useful message is narrower and more hopeful. Your genes set a range. Where you sit in it responds to how you live, what you resolve and who you are close to. That is not a slogan, it is what the evidence actually supports.

A Note On Inherited Trauma

Transgenerational epigenetic inheritance is the most misused idea in this entire field.

The technical definition is strict. True transgenerational inheritance requires the first generation that was never exposed, meaning the great grandchild for an exposure during pregnancy, because the pregnant woman, the foetus and the germ cells that will become the next generation are all directly exposed. Almost every human study described as transgenerational is actually intergenerational.

In plants and worms the phenomenon is well demonstrated. In mammals it is contested. A 2018 review in Nature Communications concluded the human evidence is not conclusive, and a 2024 review found robust mammalian evidence absent. The mammalian germline strips most methylation twice during development, which is a serious obstacle for any inherited signal.

Why We Are Careful With That Claim

There is an ethical dimension here that matters in Australia specifically.

Australian scholars have argued that epigenetic framings of intergenerational trauma, applied to Aboriginal and Torres Strait Islander peoples, risk turning the consequences of colonisation into an inherited biological condition. That framing can entrench the damage narrative it was meant to explain.

We raise it because “it is in your DNA” sounds compassionate and lands as a life sentence. Intergenerational patterns are real and we work with them constantly. Attributing them to inherited epigenetic marks is neither necessary nor currently supportable.

What This Looks Like In Practice

These are composite examples drawn from our clinical work, with identifying details changed.

A man in his forties arrived certain that depression was genetic in his family and therefore fixed. Three generations had it, which he read as proof. What emerged over several months was a family where nobody had ever named a feeling and where withdrawal was the only modelled response to distress. That is transmitted, but it is transmitted through learning.

A woman in her thirties had read extensively about inherited trauma and had concluded her anxiety belonged to her grandmother rather than to her. It was a comfortable position because it required nothing of her. The work was returning ownership of a nervous system that had learned its settings in her own childhood.

A woman in her fifties had spent significant money on epigenetic and methylation testing before she reached us, and arrived with reports she could not act on. She had chronic insomnia, an isolating job and a marriage she had not spoken honestly in for a decade. None of that appeared on the test.

Frequently Asked Questions

The questions people ask us most often about this, and our honest answers.

Can You Change Your Epigenetics?

Indirectly and partially. Behaviours with real evidence behind them include stopping smoking, exercise, sleep and treating chronic stress. What you cannot do is direct specific epigenetic changes deliberately, and anything promising that is overselling.

Is Epigenetics Real Science Or Pseudoscience?

The science is entirely real and central to modern biology. The popular wellness version, where thoughts rewrite genes and supplements optimise methylation, is not. Both use the same word, which causes most of the confusion.

Can Trauma Be Inherited Through Genes?

Not in the way the phrase implies. Trauma reliably transmits between generations through parenting, attachment and environment. Evidence for transmission through inherited epigenetic marks in humans is not established.

Does Epigenetics Mean Genes Do Not Matter?

No. Genetic factors matter a great deal, and heritability for most psychiatric conditions is substantial. Epigenetics explains how the same genome produces different outcomes, not that the genome is irrelevant.

Should You Get Epigenetic Testing?

Not for mental health. Research grade methylation analysis is a scientific tool, and consumer versions marketed as lifestyle guidance are not clinically validated. Money is better spent on sleep, treatment and connection.

How Long Do Epigenetic Changes Last?

It varies enormously. Some marks turn over within hours. Others, including imprinted genes and the marks defining cell identity, last a lifetime and are copied faithfully every time cells divide.

Where To Go From Here

The genuine finding at the centre of epigenetics is worth holding onto. Your DNA sequence is fixed, but a great deal about how it is read is not, and environment and experience influence gene activity throughout life in ways nobody suspected forty years ago.

What that does not license is the claim that you can think your way to a new genome, or that your difficulties are chemically inherited and therefore fixed. The first is wishful and the second is fatalistic, and the evidence supports neither. Chronic stress, isolation and unresolved trauma have measurable biological consequences. Those things respond to being addressed, and the mechanism was never the point.

If you recognise yourself in the stress patterns described here, that is worth working with directly. We see individuals and couples at our Inglewood rooms and online, and no referral is needed.

Book a session with us, or read more about our counselling services today.