“The Minnesota twin study raised questions about the depth and pervasiveness of qualities specified by genes: Where in the genome, exactly, might one find the locus of recurrent nightmares or of fake sneezes? Yet it provoked an equally puzzling converse question: Why are identical twins different? Because, you might answer, fate impinges differently on their bodies. One twin falls down the crumbling stairs of her Calcutta house and breaks her ankle; the other scalds her thigh on a tipped cup of coffee in a European station. Each acquires the wounds, calluses, and memories of chance and fate. But how are these changes recorded, so that they persist over the years? We know that the genome can manufacture identity; the trickier question is how it gives rise to difference.”
~Siddhartha Mukherjee, Same But Different
If genetics are the words in a dictionary, then epigenetics is the creative force that forms those words into a library of books. Even using the same exact words in the genomic code from identical twins, they can be expressed in starkly different ways. Each gene’s expression is dependent on it’s relationship to numerous other genes, potentially thousands, and all of those genes together are moderated according to epigenetics.
The epigenome itself can be altered by individual and environmental factors (type of work, exercise, and injuries; traumatic abuse, chronic stress, and prejudice; smoking, drinking, and malnutrition; clean or polluted air, water and soil; availability of green spaces, socioeconomic class, and level of inequality; etc). Then those changes can be passed on across multiple generations (e.g., the grandchildren of famine victims having higher obesity rates). This applies even to complex behaviors being inherited (e.g., the grandchildren of shocked mice, when exposed to cherry blossom scent, still jumping in response to the shock their grandparents experienced when exposed to the same scent).
What is rarely understood is that heritability rates don’t refer directly to genetics alone. It simply speaks to the entire package of influences. We don’t only inherit genes for we also inherit epigenetic markers and environmental conditions, all of the confounders that make twin studies next to useless. Heritability is only meaningful at a population level and can say nothing directly about individual people or individual factors such as a specific gene. And at a population level, research has shown that behavioral and cultural traits can persist over centuries, and they seem to have been originally caused by distant historical events of which the living memory has long since disappeared, but the memory lingers in some combination of heritable factors.
Even if epigenetics could only last several generations, though at least in some species much longer, the social conditions could continually reinforce those epigenetic changes so that they effectively become permanently set. And the epigenetics, in predisposing social behaviors, would create a vicious cycle of feeding back into the conditions that maintain the epigenetics. Or think of the centuries-long history of racism in the United States where evidence shows racism remains pervasive, systemic, and institutional, in which case the heritability is partly being enforced upon an oppressed underclass by those with wealth, privilege, and power. That wealth, power, and privilege is likewise heritable, as is the entire social order. No one part can be disentangled from the rest for none of us are separate from the world that we are born into.
Now consider any given disease, behavior, personality trait, etc might be determined by thousands of genes, thousands of epigenetic markers, and thousands of external factors. Change any single part of that puzzle might mean to rearrange the the entire result, even leading to a complete opposite expression. The epigenome determines not only if a gene is expressed but how it is expressed because it determines how which words are used in the genomic dictionary and how those words are linked into sentences, paragraphs, and chapters. So, one gene might be correlated as heritable with something in a particular society while correlated to something entirely else in a different society. The same gene could potentially have immense possible outcomes, in how the same word could be found in hundreds of thousands of books. Many of the same words are found in both Harry Potter and Hamlet, but that doesn’t help us to understand what makes one book different from the other. This is a useful metaphor, although an aspect of it might be quite literal considering what has been proven in the research on linguistic relativity.
There is no part of our lives not touched by language in shaping thought and affect, perception and behavior. Rather than a Chomskyan language organ that we inherit, maybe language is partly passed on through the way epigenetics ties together genes and environment. Even our scientific way of thinking about such issues probably leaves epigenetic markers that might predispose our children and grandchildren to think scientifically as well. What I’m describing in this post is a linguistically-filtered narrative upheld by a specific Jaynesian voice of authorization in our society. Our way of speaking and understanding changes us, even at a biological level. We are unable of standing back from the very thing about which we speak. In fact, it has been the language of scientific reductionism that has made it so difficult coming to this new insight into human nature, that we are complex beings in a complex world. And that scientific reduction has been a central component to the entire ruling paradigm, which continues to resist this challenging view.
Epigenetics can last across generations, but it can also be changed in a single lifetime. For centuries, we enforced upon the world, often violently and through language, an ideology of genetic determinism and race realism. The irony is that the creation of this illusion of an inevitable and unalterable social order was only possible through the elite’s control of environmental conditions and hence epigenetic factors. Yet as soon as this enforcement ends, the illusion drifts away like a fog dissipated by a strong wind and now through clear vision the actual landscape is revealed, a patchwork of possible pathways. We constantly are re-created by our inheritance, biological and environmental, and in turn we re-create the social order we find. But with new ways of speaking will come new ways of perceiving and acting in the world, and from that a different kind of society could form.
[This post is based on what is emerging in this area of research. But some of it remains speculative. Epigenetics, specifically, is still a young field. It’s difficult to detect and follow such changes across multiple generations. If and when someone proves that linguistic relativity can even reach to the level of the epigenome, a seeming inevitability (considering it’s already proven language alters behavior and behavior alters epigenetics), that could be the death blow to the already ailing essentialist paradigm (Essentialism On the Decline). According to the status quo, epigenetics is almost too radical to be believed, as is linguistic relativity. Yet we know each is true to a larger extent than present thought allows for. Combine the two and we might have a revolution of the mind.]
* * *
The Ending of the Nature vs Nurture Debate
Heritability & Inheritance, Genetics & Epigenetics, Etc
Identically Different: A Scientist Changes His Mind
Epigenetic Memory and the Mind
Inherited Learned Behavior
Epigenetics, the Good and the Bad
Trauma, Embodied and Extended
Facing Shared Trauma and Seeking Hope
Society: Precarious or Persistent?
Plowing the Furrows of the Mind
But Evan Boyle, Yang Li, and Jonathan Pritchard from Stanford University think that this framework doesn’t go far enough.
They note that researchers often assume that those thousands of weakly-acting genetic variants will all cluster together in relevant genes. For example, you might expect that height-associated variants will affect genes that control the growth of bones. Similarly, schizophrenia-associated variants might affect genes that are involved in the nervous system. “There’s been this notion that for every gene that’s involved in a trait, there’d be a story connecting that gene to the trait,” says Pritchard. And he thinks that’s only partly true.
Yes, he says, there will be “core genes” that follow this pattern. They will affect traits in ways that make biological sense. But genes don’t work in isolation. They influence each other in large networks, so that “if a variant changes any one gene, it could change an entire gene network,” says Boyle. He believes that these networks are so thoroughly interconnected that every gene is just a few degrees of separation away from every other. Which means that changes in basically any gene will ripple inwards to affect the core genes for a particular trait.
The Stanford trio call this the “omnigenic model.” In the simplest terms, they’re saying that most genes matter for most things.
More specifically, it means that all the genes that are switched on in a particular type of cell—say, a neuron or a heart muscle cell—are probably involved in almost every complex trait that involves those cells. So, for example, nearly every gene that’s switched on in neurons would play some role in defining a person’s intelligence, or risk of dementia, or propensity to learn. Some of these roles may be starring parts. Others might be mere cameos. But few genes would be left out of the production altogether.
This might explain why the search for genetic variants behind complex traits has been so arduous. For example, a giant study called… er… GIANT looked at the genomes of 250,000 people and identified 700 variants that affect our height. As predicted, each has a tiny effect, raising a person’s stature by just a millimeter. And collectively, they explain just 16 percent of the variation in heights that you see in people of European ancestry.
Over the past five years, Benjamin has been part of an international team of researchers identifying variations in the human genome that are associated with how many years of education people get. In 2013, after analyzing the DNA of 101,000 people, the team found just three of these genetic variants. In 2016, they identified 71 more after tripling the size of their study.
Now, after scanning the genomes of 1,100,000 people of European descent—one of the largest studies of this kind—they have a much bigger list of 1,271 education-associated genetic variants. The team—which includes Peter Visscher, David Cesarini, James Lee, Robbee Wedow, and Aysu Okbay—also identified hundreds of variants that are associated with math skills and performance on tests of mental abilities.
The team hasn’t discovered “genes for education.” Instead, many of these variants affect genes that are active in the brains of fetuses and newborns. These genes influence the creation of neurons and other brain cells, the chemicals these cells secrete, the way they react to new information, and the way they connect with each other. This biology affects our psychology, which in turn affects how we move through the education system.
This isn’t to say that staying in school is “in the genes.” Each genetic variant has a tiny effect on its own, and even together, they don’t control people’s fates. The team showed this by creating a “polygenic score”—a tool that accounts for variants across a person’s entire genome to predict how much formal education they’re likely to receive. It does a lousy job of predicting the outcome for any specific individual, but it can explain 11 percent of the population-wide variation in years of schooling.
That’s terrible when compared with, say, weather forecasts, which can correctly predict about 95 percent of the variation in day-to-day temperatures.
Complex grammar of the genomic language
from Science Daily
Each gene has a regulatory region that contains the instructions controlling when and where the gene is expressed. This gene regulatory code is read by proteins called transcription factors that bind to specific ‘DNA words’ and either increase or decrease the expression of the associated gene.
Under the supervision of Professor Jussi Taipale, researchers at Karolinska Institutet have previously identified most of the DNA words recognised by individual transcription factors. However, much like in a natural human language, the DNA words can be joined to form compound words that are read by multiple transcription factors. However, the mechanism by which such compound words are read has not previously been examined. Therefore, in their recent study in Nature, the Taipale team examines the binding preferences of pairs of transcription factors, and systematically maps the compound DNA words they bind to.
Their analysis reveals that the grammar of the genetic code is much more complex than that of even the most complex human languages. Instead of simply joining two words together by deleting a space, the individual words that are joined together in compound DNA words are altered, leading to a large number of completely new words.
“Our study identified many such words, increasing the understanding of how genes are regulated both in normal development and cancer,” says Arttu Jolma. “The results pave the way for cracking the genetic code that controls the expression of genes. “