If we wish to hear what the fossils are telling us, we must find out how they came to be what they were (and how their descendants came to be what they are today). For generations, scientists have looked to Darwinian evolution (natural selection acting on random mutations) almost exclusively to account for all that. Questions were considered settled if a Darwinian account could be provided.
That was not because any law of nature shows that Darwinism must be the correct explanation. Rather because, as Richard Dawkins put it, “Darwinism is the only known theory that is in principle capable of explaining certain aspects of life” (p. 287, Blind Watchmaker, 1986).
But when we looked at horizontal gene transfer (HGT), we found that Dawkins’ claim is incorrect.
To recap, Darwinism entails vertical transfer of genes from a common ancestor to descendants. Horizontal gene transfer means transfer of genes from one organism to another on contact, irrespective of the ancestry of either life form. HGT is a form of evolution, yes. But it drastically weakens the status of Darwinism as the “only known theory.” Any Darwinian claim about evolution must first rule out HGT as a possible explanation. And, as we shall shortly see, it must rule out epigenetics as well.
Why does this historic shift in the burden of proof receive comparatively little attention? Probably it’s due to the overwhelming acceptance of Darwinism as a cultural metaphor and philosophy of life. One thinks, for example, of Amazon citing “purposeful Darwinism” and taking Darwinian Theory to the max as a defense against a recent expos� of the firm’s labor conditions. The concepts Amazon advances are scientifically meaningless but culturally meaningful. And culture drowns out science.
Thus, when talking to fossils (or current living forms), our challenge is to listen to what they have to say, not what the Darwinian interpreters of the fossils (and of almost everything else) have to say.
Which brings us to epigenetics. Jean-Baptiste Lamarck (1744-1829) was an early evolutionist who proposed that life forms could acquire information from their environment and pass it on in their genes. He was dismissed, when not ridiculed, by Darwinists for many decades (though not, as it happens, by Darwin). But the basic thrust of his idea has recently resurfaced in epigenetics.
There is an irony in the way the resurgence came about. A key science achievement of the 1990s was the mapping of the human genome. Those were the days when Nobelist Walter Gilbert, extolling the Human Genome Project, would hold up a data CD and inform his audience, “Here is a human being; it’s me!”
But what if it isn’t? What if it is just a CD containing important information about Gilbert but by no means the whole story? What if the rest of the story is created in the continuous stream of life? Scientists are just now beginning to learn about the hitherto unrecognized “second genetic code,” the epigenome, which greatly increases both the complexity and the uniqueness of the information in living systems.
Epigenetics is the study of the systems and processes by which genes’ expression can be altered, not randomly as in Darwinism, but by specific, predictable, repeatable, and researchable events — and then inherited in the altered state. Research has shown methylation to be a key mechanism. It is described thus:
Not all genes are active at all times. DNA methylation is one of several epigenetic mechanisms that cells use to control gene expression…. a common epigenetic signaling tool that cells use to lock genes in the “off” position. In recent decades, researchers have learned a great deal about DNA methylation, including how it occurs and where it occurs, and they have also discovered that methylation is an important component in numerous cellular processes, including embryonic development, genomic imprinting, X-chromosome inactivation, and preservation of chromosome stability.
Epigenetic changes like methylation do not change a cell’s DNA, but they do change how the DNA functions. In rodent studies, for example, stress can trigger a series of chemical reactions that dictate how active some genes will be in passing on the effects of parental stress.
Such inheritance of acquired traits is gradually gaining acceptance in academic science, but we are still in an early stage of understanding the mechanisms. Or, as one researcher put it, “… we’re all having a hell of a time figuring out how they work.” And another: “Although many are scratching their heads over the holes in the proposed mechanism, few are suggesting that the underlying phenomenon is a fairy tale.”
Most genes, it turns out, are not so much selfish as willing to hang out with the wrong crowd and learn bad habits. You’d think so, to read this in a special issue of Science:
The molecular legacy extends beyond gene transfer to include mitochondria and epigenetics (Lane et al., p. 756). Finally, the gestation and birthing processes also shape offspring, and preterm birth is now a focus of research (Romero et al., p. 760).
Here are some other findings that give some sense of the scope of the changes epigenetics brings to our understanding of the history of life:
— Bacteria rewrite their DNA epigenetically. Carl Zimmer notes in Quanta:
For students of the history of biology, this kind of heredity echoes a largely discredited theory promoted by the naturalist Jean-Baptiste Lamarck in the early 19th century. Lamarck argued for the inheritance of acquired traits. … The advent of genetics seemed to crush this idea. There didn’t appear to be any way for experiences to alter the genes that organisms passed down to their offspring. But CRISPR revealed that microbes rewrite their DNA with information about their enemies — information that Barrangou showed could make the difference between life and death for their descendants.
New analysis techniques will help define the role that bacterial epigenetics plays in creating antibiotic resistance.
Male rats fed a high-fat diet, for example, beget daughters with abnormal DNA methylation in the pancreas. Male mice fed a low-protein diet have offspring with altered liver expression of cholesterol genes. And male mice with pre-diabetes have abnormal sperm methylation, and pass on an increased risk of diabetes to the next two generations.
Epigenetic stress effects found in rats can last for generations. Similarly, in a recent mouse study, reported in Nature, sperm RNA showed heritable signs of trauma for two more generations. And starved mice produced pups whose offspring risked diabetes. In another mouse study, it was found that “Without any change to DNA at all, methyl groups could be added or subtracted, and the changes were inherited much like a mutation in a gene.”
— Epigenetics can influence animal behavior in later generations as well. “Transgenerational epigenetic inheritance is not a solved field — it’s very much in flux,” one researcher admits, but it seems that epigenetic memory of experienced stress can cross generations and travel from cell to cell during early development: “It does not change the sequence of genes but rather how the DNA is packaged and how genes are expressed.” Recent rodent studies suggest that “an animal parent’s exposure to drugs, alcohol, and stress can alter brain development and behavior in their offspring.”
For example, from one study on how mice can inherit fear of a smell from their male parent, we learn:
Somehow, the information about the frightening smell gets into a mouse’s testes and results in lower methylation of the Olfr151 gene in sperm DNA. The researchers even ran experiments using in vitro fertilization to make sure that the father was not in some way passing on a fear of acetophenone through interactions with the mother. The epigenetic tweak in the sperm is perpetuated in the offspring’s DNA, leading to increased expression of the receptor in the animals’ noses and, ultimately, enhanced sensitivity to the smell.
Much more work remains, of course, and this finding was questioned, as “too good to be true.” But the authors pointed out that they had not cherry picked the data; they had included in the supplemental materials experiments that did not yield statistically significant results.
If The Scientist isn’t hanging the epigenetics study authors out to dry, it’s most likely because the editors think there is something to be said for their model. It may help resolve longstanding questions, for example, about how animals appear to “know” things they did not learn by experience. To say that their knowledge is an “instinct” just means we don’t know how they know. Epigenetic studies, by contrast, may identify a specific mechanism by which the information is transmitted.
— Epigenetics may influence human health too. It’s fine to inherit “good genes” (we heard plenty about that from the eugenicists for over a century!). But what if a package of “good genes” gets damaged in transit and arrives that way? Genes can be inherited in an awakened state, and may influence metabolism, behavior, and proneness to disease, including heart disease and diabetes. From one researcher:
According to Ishii, the take-home message is this: “I hope that people understand that various stresses can change gene expression without DNA sequence change.” He says the youngest among us — developing embryos and infants — may be especially sensitive to that kind of stress-induced epigenetic change and “we should be more careful about stresses on them.”
In another study, traumatized pregnant women who had been near 9-11 not only had significantly lower cortisol levels in their saliva but so did their children, measured after birth. Researchers noted that the effect was most obvious when the exposed children were in the third trimester. Subsequent studies on stressed rats identified differences in DNA methylation, the way that DNA is chemically modified.
Similarly, Project Ice Storm found “a distinctive ‘signature’ in the DNA of children born in the aftermath of the massive Quebec ice storm” (1998):
Thirteen years later, the researchers found that DNA within the T cells — a type of immune system cell — of 36 children showed distinctive patterns in DNA methylation. The researchers concluded for the first time that maternal hardship, predicted the degree of methylation of DNA in the T cells. The “epigenetic” signature plays a role in the way the genes express themselves. This study is also the first to show that it is the objective stress exposure (such as days without electricity) and not the degree of emotional distress in pregnant women that causes long lasting changes in the epigenome of their babies.
It’s early days yet, but there is also some evidence that parents’ poverty can promote children’s obesity. Privation may reprogram DNA in the womb to turn certain genes involving appetite up or down. “Whenever you find food, eat all you can,” perhaps? This may continue into adulthood, when no shortage actually exists. As one researcher explains, “If genetics is the alphabet, epigenetics is the spelling that guides the activity of our cells.”
So the role epigenetics may play in obesity generally, some immunities, chronic diseases, and even cancer is now actively studied. With respect to cancer, some researchers have found that epigenetic regulation is required to ensure the correct number of chromosomes in daughter cells after division, and “tumor cells frequently have either too few or too many chromosomes, leading to the incorrect expression of a number of genes.”
Many of these findings may need modification or replacement, but we can no longer rule out the possibility that modifications in great-grandparents’ diet or environment affect later generations’ health or life span. These changes are not Darwinian genetic inheritance; the parent did not have a randomly mutated “gene” for, say, obesity, but rather an experience (chronic hunger, perhaps) that altered the way genes controlling appetite are expressed. The alterations are passed on, at least for a generation or so. Thus, epigenetics is not to be confused with genetic or any other kind of determinism; it is not a prophecy, merely a tool for assessing sources of risk.
— Can epigenetics influence human behavior as well as human health? Possibly; for example, early abuse can change gene expression in children:
The researchers found an association between the kind of parenting children had and a particular gene (called the glucocorticoid receptor gene) that’s responsible for crucial aspects of social functioning and health.
If such findings hold up, they may shed light on “broken adoptions,” where rescued children continue to behave as if they were living in a low trust/high threat environment. In any event, “born bad” just doesn’t cut it any more, by way of explanation. If epigenetics provides valid insights, we can at least hope for more realistic rehabilitation strategies.
As epigenetics slowly achieves acceptance in science culture, medical genomicist Stephan Beck thinks that epigenomic epidemiology is “at the same stage genomic epidemiology was at eight years ago, when most studies were small and rarely identified the same genetic variants for any one disease.” The workshop material for a conference in Sweden in March 2015, “Epigenetics as the Meeting Point Between Nature and Nurture,” offers a challenge, “There are obstacles in terms of a suspicion of biological explanations among some scholars and simplifications of social and philosophical problems among some scientists. The two cultures must be bridged and the bridge, we suggest, is epigenetics.”
Yes indeed. Consider the controversial revisit of Darwinian race theory in science writer Nicholas Wade’s recent book, Troublesome Inheritance. Epigenetics makes such theories irrelevant as well as divisive. The question isn’t whether certain characteristics show up more often in one group than another, but what is the mechanism? As Michael Behe would say, how exactly?
Epigenetics should lead to revisions in textbooks, some European researchers say, perhaps unaware of the Darwin followers camped outside the offices of education authorities, protecting their tax-funded domain. That said, epigenetics coverage did increase in the most recent edition of Darwinian evolutionist Ken Miller‘s popular university text. The book now features a definition of epigenetics, cross-referenced to a paragraph on the subject.
Some, nonetheless, stand athwart epigenetics and yell STOP!! It is, after all, very new and is not settling in with ease. A “key concept” quote from The Scientist reads: “The concept of cellular memory passed onto offspring may not be as crazy as it appears.” There is nothing crazy about epigenetics, unless one is committed to genetic fatalism, featuring the “fat gene,” the “gay gene,” the “infidelity gene,” the “violence gene,” etc., that supposedly “make” people do things.
“End the Hype over Epigenetics & Lamarckian Evolution,” Real Clear Science demands, noting that “mammals are completely different beasts” from worms and plants, where epigenetic inheritance has been demonstrated:
Therefore, be very skeptical of studies which claim to have detected health effects due to epigenetic inheritance. The hype may soon fade, and the concept of Lamarckian evolution may once again return to the grave.
A philosophy may underlie this outburst, if we go by the article in Cell referenced at RCS: “Since the human genome was sequenced, the term ‘epigenetics’ is increasingly being associated with the hope that we are more than just the sum of our genes.”
It’s not a “hope,” it’s a fact. And the accusation of “hype” sounds odd, considering the widespread Darwinian hype about all things gene, attributing to “genes” every phenomenon from bad driving to wonder at the universe.
Real Clear Science goes on to worry that the epigenome oppresses women:
Epigenetics is the next big field that the media, fearmongers, and political hacks will attempt to exploit. … The authors worry, perhaps rightly so, that the media hype surrounding epigenetics will once again turn its focus on mothers. Will the government once again regulate what pregnant women can eat, drink, and do? And if so, why not regulate the behavior of men, as well? Epigenetics, after all, can affect sperm quality.
The authors referred to had published an op-ed in Nature which advises, “Society: Don’t blame the mothers – Careless discussion of epigenetic research on how early life affects health across generations could harm women.” That’s an odd concern, as most mothers would gladly avoid passing on a chronic disorder, if they had the correct information. And epigenetics is principally about establishing the correct information.
Meanwhile, the onetime chief lobbyist for Darwin in American schools has been heard to say:
It was almost a relief when an antievolutionist contended that the books should be rejected because they don’t include epigenetics. At least the epigenetics argument is relatively recent (perhaps only 5-8 years old). In creation-think, including epigenetics in biology textbooks will weaken evolution because epigenetics is evidence against evolution.
Note the curious term “the epigenetics argument,” as if everyone agrees that epigenetics’ only potential is as a political strategy.
But life goes on… Some quibble over whether epigenetics is truly “Lamarckian.” Quibbles aside, ours is not the world of the “This Is You” CD.1 Some acknowledged experts even say, “Epigenetics can drive genetics” and that it “appears to be one of the main drivers of intergenerational changes, not simply a passive component.” Meanwhile, epigenomics is making its debut, courtesy a decade’s worth of data analysis program development.
So, far from heading to the grave, epigenetics has invested in bigger equipment.
Many epigenetics findings, like many findings in horizontal gene transfer may be revised or replaced, but the direction is not likely to change. So how does epigenetics feature in evolution? There are two opinions about that. The epigenome is said to evolve faster than the genome, but most of its changes don’t last for more than a few generations. Perhaps that is because they are overridden by further changes due to new conditions: In a pioneer study, researchers concluded that “epigenetic changes are many orders of magnitude more frequent than conventional DNA mutations, but also often short lived.”
Yet epigenomic diversity, according to other research, allows plants to adapt to adapt to a variety of environments worldwide. Changes in plant habitats may massively impact animal evolution. So it may come down to a question of what kind of change we are looking for. What counts as a change?
To the extent that epigenetics casts doubt on simplistic Darwinian or other schemes of evolution, its main role may be that of “spoiler.” For example, recently, Swedish researchers found that epigenetics, not Darwinian evolution, is the cause of wide variation in domestic chicken types. They say their findings explicitly disagree with “[t]he traditional Darwinian explanation,” which is interesting in view of the fact that Darwin’s own pigeon breeding is often used as a way of introducing his theory to the public.
So what can we now say about evolution, the history of life?: Provided we are not looking for miraculous transformations, we have indeed seen some evolution. We have seen that life forms can progress toward the same target without common ancestry (convergent evolution). Sharing genes (horizontal gene transfer) can result in new features in a life form. Epigenetics can result in offspring inheriting features from their parents that were created in their parents’ own lifetime, rather than inherited from a previous common ancestor.
But another possibility arises as well: Can a life form evolve by losing instead of gaining features (devolution)? We shall see.
(1) Quoted in Dorothy Nelkin, “Less Selfish than Sacred? Genes and the Religious Impulse in Evolutionary Psychology,” in Hilary Rose and Steven Rose, eds., Alas, Poor Darwin: Arguments Against Evolutionary Psychology (London: Random House, Vintage, 2001), p. 18.
See the rest of the series to date at “Talk to the Fossils: Let’s See What They Say Back.”
Image: Jean-Baptiste de Monet Chevalier de Lamarck, by Charles Th�venin [Public domain], via Wikimedia Commons.