• Key epigenetic mechanisms include DNA methylation (adding a chemical tag to DNA) and histone modification (changing proteins around which DNA is wound).

• These chemical tags can turn genes on or off, or dial their activity up or down.

• What's fascinating is that these epigenetic bookmarks can be influenced by environmental factors like diet, stress, exercise, and even exposure to toxins.

• This means your experiences can leave marks on your epigenome that affect gene expression. In a few animal studies such marks are passed to offspring; whether this happens in humans is still debated.

• If one identical twin develops schizophrenia, there's only a 50% chance their twin will too. Why not 100% if their DNA is identical?

• Part of the answer may lie in epigenetics – changes to gene expression that don't involve alterations to the underlying DNA sequence.

• Think of it like this: identical twins start with the same "recipe book" (DNA). However, epigenetics introduces "sticky notes" or "bookmarks" that can tell certain genes to be read more often, less often, or not at all.

• Identical twins already differ epigenetically at birth, and these differences grow with age, especially in twins who have lived apart for a long time. Chance events in early development, as well as different environments, contribute.

• Epigenetic differences may account for some of the differences in health between identical twins, but much of the evidence is still correlation rather than proven cause.

• Normally the agouti gene switches on only briefly in each hair-growth cycle, producing a yellow band in an otherwise dark hair. In viable yellow (Avy) mice, a retrotransposon (an IAP 'jumping gene') inserted just upstream of agouti keeps the gene switched on all the time, in almost every tissue. The result is yellow fur together with obesity, high insulin and diabetes.

• The key discovery was that a mother's diet could move this switch. When pregnant mothers were fed extra methyl donors (folic acid, vitamin B12, choline and betaine), a larger share of their genetically identical offspring had brown, mottled-to-agouti coats and fewer were fully yellow.

• The extra methylation silenced the retrotransposon in more embryos, without any change to the DNA sequence. The effect was a shift in proportions, not a guarantee for each pup, and in these experiments the diet effect was not passed on to the following generation.

• The orange and black patches of tortoiseshell cats are a direct result of X-inactivation: each patch grows from cells that switched off the same X chromosome.

• This "cellular roulette" beautifully demonstrates epigenetics: how gene expression can be altered without changing the underlying DNA sequence.

• Male tortoiseshells are rare. Most that have been examined carry an extra X chromosome (an XXY make-up, comparable to Klinefelter syndrome in humans), and almost all of them are sterile.

• Near the end of World War II, from November 1944 to May 1945, a German blockade caused severe famine in the occupied western Netherlands. At times people had only about 30 per cent of normal daily calories, and more than 20,000 died.

• Excellent Dutch medical records allowed researchers to follow, for decades, children who were in the womb during the famine. What mattered was not only that the famine happened, but when in pregnancy it happened:

• Researchers propose that famine in early pregnancy 'programmed' the developing baby's metabolism for scarcity. One influential explanation for such links is the 'thrifty phenotype' hypothesis: poor nutrition early in life produces permanent changes in how the body handles glucose and insulin.

• When these children later lived with plenty of food, that early programming may have raised their risk of obesity and metabolic disease. Studies of famine survivors have found changes in DNA methylation at key metabolic genes, but these findings show correlation, not proven cause.

• This work suggests that maternal care acts as biological information, not only affection: during a short window after birth it sets how strongly the brain will respond to stress for the rest of the animal's life.

• These changes alter how genes are expressed without changing the DNA sequence. Post-mortem studies of human brain tissue have found a similar pattern, with more methylation of the cortisol receptor gene in people who suffered abuse or neglect in childhood. This is a correlation, not yet proof of cause.

• These 'stickers' are vital for proper fetal development, especially for regulating growth, brain function, and metabolism.

• A healthy baby needs a balanced set of instructions from both parents. If a child inherits two active copies of a paternally expressed imprinted gene, or two inactive copies of a maternally expressed one, it can lead to severe developmental disorders.

• Conditions like Prader-Willi syndrome and Angelman syndrome are classic examples of what happens when these delicate epigenetic tags go awry, often due to an imbalance or error in the parental origin of these crucial imprinted genes.

• This experiment showed that specialised cells still contain all the genetic information needed to make a whole animal. Later, nuclei from adult skin cells also produced swimming tadpoles.

• It was initially believed that as cells differentiated, they permanently lost or switched off genes they no longer needed. Gurdon's work demonstrated that the "storybook" of life, the full set of genetic instructions, remains intact in all body cells.

• It also showed that the epigenetic marks that keep a cell specialised can be largely erased and rewritten by the egg. The process is inefficient: hundreds of transfers were needed for each success, and cloned animals often have abnormalities, probably because the reset is incomplete.

• For too long, genetic determinism suggested our DNA was an immutable, fixed blueprint—our destiny written in stone from conception. This view presented a fatalistic outlook, where the script of our lives was entirely pre-written.

• But our understanding of biology revealed a revolutionary truth: our genes are not the sole arbiters of our fate. We discovered the epigenome, a dynamic, responsive layer "above" the genome that orchestrates how our genes are expressed—which ones are turned on, which are turned off, and how strongly they influence our cellular functions. It's about changing how the DNA code is read, not the code itself.

The epigenome is a responsive layer linking our genes to our development and environment.

• This dynamic interplay makes our biological narrative far more flexible. Acting like a complex dimmer switch, the epigenome responds to internal and external cues. Mechanisms like DNA methylation add chemical tags to silence genes, while histone modification can make genes more or less accessible. These crucial epigenetic marks influence cell differentiation, tissue development, and our ongoing adaptation to life.

• The Cloned Toad: John Gurdon showed that a specialised cell's nucleus keeps all its genes and can be reprogrammed by an egg.

• Identical Twins: Despite identical DNA, twins differ epigenetically from birth, and the differences grow with age.

• Bees: Genetically identical queens and workers differ because of diet; royal jelly acts at least partly through DNA methylation.

• Cats: Tortoiseshell (calico) cats' distinct fur patterns arise from random X-chromosome inactivation, an epigenetic process that silences one X chromosome in each cell, expressing different color genes.

• The Dutch Famine: Famine early in pregnancy was followed by higher obesity rates in adult children, with possible effects in grandchildren.

• Maternal Nurturing in Rats: A mother's licking and grooming in the first week of life sets the pup's adult stress response through methylation of the cortisol receptor gene.