When we think about what we pass on to our children, we think of genes: eye colour, height, susceptibility to disease. But over the last twenty years, biology has uncovered a second channel of inheritance — quieter, less studied, and possibly more significant than we imagined.
In 2013, neuroscientists Brian Dias and Kerry Ressler at Emory University published results that initially struck many colleagues as impossible. They conditioned mice to fear the scent of acetophenone — a cherry-like compound — by pairing it with a mild electric shock. A classic conditioned reflex. Nothing new.
What was new came next. The offspring of these mice — who had never encountered either the scent or the shock — showed a fear response the very first time they smelled acetophenone. The same happened in the third generation. The fear had passed not through learning, but through biology.
To rule out maternal behaviour as an explanation, the researchers transferred embryos from the “fearful” mice into calm surrogates who had no history with the scent. The result was unchanged. The fear was encoded in the father’s sperm — specifically in epigenetic marks on the olfactory receptor gene Olfr151. Methylation of this gene was reduced, increasing the number of receptors and making the offspring hypersensitive to that particular odour.
The trauma was written not in memory but in molecules. And those molecules passed to children and grandchildren.
The paper triggered an intense debate. Some scientists pointed to methodological limitations and difficulties of replication. But several independent labs confirmed the basic effect, and transgenerational epigenetic transmission is now considered a real phenomenon — though the precise mechanisms in humans are far less well understood than in mice.
Classical genetics transmits information through the nucleotide sequence of DNA — the “code” that does not change over a lifetime. Epigenetic inheritance works differently: what is transmitted is not the letters of the code but its “annotations” — methyl groups, histone modifications, small RNAs.
For a long time it was assumed that epigenetic marks are completely “erased” during the formation of reproductive cells and in early embryogenesis — a kind of biological factory reset guaranteeing that each new generation starts with a blank slate. It turns out the reset is incomplete. Some marks — particularly at specific genomic loci — survive and are passed to offspring.
Three main channels through which this occurs:
Sperm and eggs — carry not only DNA but also histone proteins with chemical modifications, small non-coding RNAs (miRNA, piRNA, tRNA fragments), and specific methylation patterns. All of this influences how the genome is read in the embryo.
The intrauterine environment — the hormonal background, nutrition, stress levels and inflammation in the mother’s body during pregnancy directly affect foetal epigenetics. This is not inheritance in the strict sense, but it is a biological transmission of experience.
The early postnatal period — the quality of care in the first months of life shapes epigenetic patterns that influence the stress response system and immunity. This was demonstrated in Michael Meaney’s experiments with rats, covered in more detail in the epigenetics article.
Direct experiments on humans are ethically impossible, but history has provided several “natural experiments” with large enough samples to draw from.
The most cited example. Children conceived during the Nazi blockade of the Netherlands were significantly more likely as adults to suffer from obesity, type 2 diabetes and cardiovascular disease — even if they themselves had grown up in comfort. Their grandchildren also showed elevated risk of metabolic disorders. The epigenetic profile of cord blood from “famine-conceived” children differed from the control group in specific genes linked to insulin regulation and fat metabolism.
Swedish epidemiologist Lars Olov Bygren studied harvest and mortality records from the isolated parish of Överkalix (Sweden) across several generations in the nineteenth and twentieth centuries. He found something unexpected: years of overeating in the paternal grandfather during his prepubertal growth period were associated with elevated cardiovascular mortality in grandsons — but not granddaughters. And nutritional deficiency in the maternal grandmother was associated with elevated risk in granddaughters.
This sex- and lineage-specific pattern is difficult to explain by chance. The study has been criticised for its small sample size, but the core effect has been reproduced in other cohorts.
Rachel Yehuda’s group at Mount Sinai studied the epigenetic profile of adult children of Holocaust survivors and compared it with a control group of Jewish families without that history. Descendants of survivors showed a specific pattern of methylation of the FKBP5 gene — involved in regulating the cortisol stress response — resembling the pattern observed in veterans with PTSD. The descendants themselves had no direct traumatic history.
Biology appears capable of transmitting not only the structure of the body, but something resembling a “memory of the world” — a representation of how safe or dangerous it is.
The unseen inheritance is not a reason for anxiety and not a verdict. It is an invitation to greater intentionality: in how we live during the preparation for a child’s birth, in what questions we ask a potential partner or donor, in what environment we create for a child in the first years of life.
Genes are the possibilities and constraints set at birth. Epigenetics is what happens to them afterwards. The second layer is open to influence. And that is good news.
The Epigenetics article in the Learn section explains DNA methylation mechanisms in detail and what can concretely be done in the 90 days before conception. Module 1 (Matching & Co-Parenting) provides a framework for conversations with a potential partner — including questions about family history and lived experience that now have biological grounding.
the transmission of epigenetic marks to offspring that survive the partial “reset” occurring during reproductive cell formation and early embryogenesis.
short RNA molecules that regulate gene activity. Present in sperm and eggs and capable of influencing embryonic development.
a gene involved in regulating the cortisol stress response. Altered methylation of this gene has been found in descendants of people who experienced severe traumatic events.
an epidemiological study of an isolated Swedish parish providing some of the earliest human evidence for transgenerational effects of nutrition on descendants’ health.