FOR SIX CONSECUTIVE SEMESTERS in the early 1990s, I taught a seminar on Charles Darwin to nonscience majors at an urban community college. We read Darwin’s writings closely — often out loud to each other — along with commentary by scholars. We looked at the evidence that Darwin amassed for his theory of natural selection, and we looked at the evidence amassed in subsequent years.
At the beginning and end of each semester, I asked students if they themselves accepted Darwin’s ideas, and every semester, predictably, about half said they did, and half said they did not — a ratio that did not budge much over the course of the term. Mostly, those who had come into the class believing that humans had evolved continued to so believe, and those who came in hewing to a biblical account of the origins of life still hewed to it when they left.
One hundred fifty years have now gone by since the 1859 publication of On the Origin of Species by Means of Natural Selection, an anniversary that has prompted new scholarly reflections on Darwin’s legacy. Many of these speeches and papers have focused on the bombshell elements of his theory — how it blew the human race away from the center of creation, generating psychic aftershocks that reverberated for decades. Even the Victorian novelist Thomas Hardy marveled at the consequences to ethics and altruism posed by “the establishment” of a common origin of species.
That was 1910. And yet there are still plenty of people blithely walking around in a pre-Darwinian world, admitting shared origins with no one whose last name is not sapiens. According to the Pew Research Center, polls conducted over twenty years reveal little movement in the percentage of the public who accept evolution. In a one-to-one ratio that echoes my own classroom findings, about 40 to 50 percent of Americans say they believe in it, and a slightly smaller percentage say they do not. Those who believe that natural selection is the driver of evolution (Darwin’s keynote point) are firmly in the minority at 14 to 26 percent.
With numbers like these, I am unsurprised that the findings emerging from an obscure field of study called epigenetics have not yet rocked the world. They are rocking my world, though, and they are also mounting a profound challenge to the traditional systems of environmental regulation, which presume that toxic chemical exposures create health risks primarily through the accumulation of genetic damage (mutations) and that people can be categorized as inherently vulnerable or resistant. (“Genetics loads the gun; environment pulls the trigger.”) Moreover, in the way that it upends our understanding of heredity, epigenetics offers a whole new way of appreciating Darwin.
Epigenetics is the study of gene expression. Genes, of course, are made of DNA and are strung like beads along the chains of our chromosomes. Each cell in our bodies has a complete set. We humans have more than two hundred distinct kinds of cells, and they all contain the same number of genes. What makes a prostate gland cell so different in form and function from, say, a salivary gland cell is not the genes contained within them but the activity of those genes. During prenatal life and infancy — and again in puberty — immature cells become differentiated when long strings of genes that are not needed for the specific tasks of, say, semen production or saliva production are silenced. The rest are allowed to express themselves. Epigenetic regulation of the genome is what makes development possible.
Unlike the human genome, which has been exhaustively sequenced and mapped, plans to decode the human epigenome are still in the planning stage. What we know about it now is that the epigenome exists, in part, within various bobbles attached to our chromosomes. Previously ignored by cell biologists, these ornaments play a key role in regulating genetic activity. Some are simple methyl groups and others are proteins called histones. Together, they hush the genes whose messages are not needed at the moment. Methyl groups and histones are highly sensitive to messages streaming in from the outside world. In other words, the epigenome guides the genome and, in turn, responds to environmental signals.
Consider this: identical twins are epigenetically unique; attached to their identical chromosomes are nonidentical patterns of methyl groups and histones. Moreover, in a phenomenon called epigenetic drift, twins become more different with time. As revealed in a 2005 study, younger twins are more alike than older twins. As twins age and have different environmental experiences, their genetic expression diverges. Twins who spend more of their lives together in the same environment have gene-expression portraits that are more similar than twins who go their separate ways.
As an adoptee, I can’t help wondering if the reverse process might also be true. Growing up together in the same environment, do adopted siblings experience epigenetic convergence? Is this why, as girls, my genetically unrelated sister and I suffered from the same allergies, developed identical digestive problems, and wore the same eyeglass prescription? More generally, might it be possible that the longer people share a common environment, the more their genes act like each other? Do we carry on our chromosomes a kind of extra-genetic memory of all of our past habitats?
There is reason to think so. Environmental epigenetics examines how environmental exposures influence gene expression. What the results of this nascent field of study reveal is the vulnerability of early life. When epigenetic regulation is disrupted early on, the process of differentiation can be thrown off course in ways that may raise the risk for many diseases, including cancer. We already know that Inuit people in Greenland who acquire high body burdens of persistent pollutants have fewer methyl groups attached to their chromosomes than their lesser-exposed compatriots. This is not good. In the laboratory, hypomethylation is associated with chromosomal instability. We know from lab experiments that certain chemical exposures in prenatal life can alter developmental pathways and lead to altered architecture of adult structures (such as breasts). But our current system of environmental regulation — with its narrow focus on identifying chemicals that cause mutations — does not screen for chemicals that trigger changes in development. And our current system of genetic testing — with its narrow focus on identifying carriers of certain genes that bestow notably higher cancer risks — does not consider the regulation of genes by environmentally mediated signals either.
Perhaps most astonishing of all, epigenetic changes can be inherited. This means that the environmental exposures we experienced as children can have consequences not just for us but also for our descendants. More philosophically, it means that, contrary to current biological dogma, the nineteenth-century idea that acquired traits can be passed down the generations may not be so wrong-headed after all. And this brings us back to Darwin, who developed his ideas before we had a working understanding of genes and who was agnostic on the subject of the heritability of acquired characteristics. The reality of epigenetic inheritance hardly overturns natural selection — indeed it shows us another route by which species can adapt. Finally, it shines a spotlight on one of Darwin’s lesser-appreciated insights: that all of life is interrelated — not only by our common origins but also by our common ecology.