The Molecular Roots of Self-Identity
The roots of self-identity extend much deeper than conscious experience, down to the molecular level.
Links to related written content and the podcast episodes that informed them, can be found at the bottom of this post.
The ancient Greek maxim, “Γνῶθι σεαυτόν” (Know thyself), is inscribed in the Temple of Apollo at Delphi. The first of three maxims, it was meant to convey that life’s essence is not to be found in outside world, but within ourselves.
To know thyself is to have a clear sense of identity, a self-concept answering the question, “Who am I?” To know who you are, you must also know who you are not. The ability to distinguish self from non-self is a requirement of the maxim.
It’s natural to consider the subject of identity to be the province of philosophy or psychology. After all, to know yourself you must self-aware, using your mind to think about it. Philosophy is the field of study concerned with how to use your mind well. Psychology is the study of how the mind works. It makes sense that these fields would take identity as an object of study.
But the roots of identity extend much deeper, down to the molecular level. In fact, physical solutions to the problem of self-identification—how to distinguish self from non-self—arose long before the advent of humanity. Hundreds of millions of years ago, thoughtless molecular mechanisms evolved this ability, enabling our lineage to persist long enough to develop the mental capacity to ask the question, “Who am I?”
To understand “high level” psychological phenomena like identity, or psychiatric conditions like Dissociative Identity Disorder, we will work from the “bottom-up,” exploring how the problem of molecular self-identification is solved by ancient biological systems. Once we have a sense for how these brainless molecular systems work, we will build an intuition for how the brain’s wetware might construct a sense of self-identity, eventually tying it to the basic neuroscience concepts we used previously to understand perception.
The Molecular Roots of Self-Identity
“Every organism has a sense that we will call self. Not in terms of self-consciousness, [but that] they’re organized around the preservation of self.” —Terrence Deacon, M&M #20
The distinction between self and non-self runs deep and is not specific to the brain or humans. A healthy vertebrate immune system requires this kind of discernment. To neutralize infections, immune cells must recognize pathogens and infected cells as non-self, distinguishing them from your healthy cells. The immune system is a sensory system for parsing molecular identities into the categories of self and non-self.
When there is a failure to recognize harmful bodily invaders as non-self, the result is runaway infection. For example, the HIV virus infects cells of the immune system, diminishing its capacity to detect subsequent infections. This can eventually lead to the body being overrun by pathogens. Without a discerning self-identification mechanism, otherwise minor threats become deadly.
When there is failure to recognize healthy self cells, the result is autoimmunity. Autoimmune disease leads to damage or destruction of healthy tissue and systemic physiological dysregulation. Type I diabetes arises from the autoimmune destruction of specific cells of the pancreas, causing blood sugar dysregulation. Multiple sclerosis arises from the autoimmune damage of nerve fibers, causing sensory, cognitive, or motor dysregulation. There are many other examples, most of which are becoming more prevalent in modern cultures:
The consequence of autoimmunity is deterioration of the body’s natural means of self-preservation, culminating in a lower quality of life and truncated lifespan. An unhealthy immune system destroys things that work because it’s confused about what’s what.
A healthy immune system accomplishes the feat of self/non-self discrimination using molecular recognition mechanisms. The biology is beautiful and complex. In short, there are immune cells capable of recognizing specific molecular patterns found on cell surfaces. There are self proteins on nearly all of your cell surfaces. When your immune system “sees” these markers, it knows not to attack. There are also non-self molecules, called antigens, present on the surface of pathogens (e.g. bacteria), as well as infected self cells. When the immune system sees these markers, those cells are targeted for destruction.
How does the immune system—a “mindless” cellular system—know how to execute this form of self-recognition? Where does its knowledge come from?
Some knowledge is baked into the genome by evolution. Those organisms capable of mounting robust, automatic responses to common foreign invaders have better odds of survival. We are all descendants of people who did not die of disease before reproducing. From our ancestors, we inherit forms of molecular prejudice. Our body’s are reflexively intolerant of certain molecular identities. Innate immunity is the part of the immune system acting on these inherited assumptions.
Innate immunity is fast and automatic, but limited in scope. It isn’t possible to genetically encode every non-self molecular identity. Pathogens are simply too numerous, diverse, and quick to evolve new forms. In response to this moving target, the capacity for learning—the ability to acquire knowledge through experience—evolved in the ancestor of all vertebrates. This component of the immune system is called adaptive immunity. It takes time to learn new molecular identities, but the adaptive immune system can learn to recognize almost any novel pathogen.
When you get sick from infection, it means some kind of non-self cellular identity got into the body and caused problems. Like bouncers at a nightclub, your white blood cells eventually remove the perpetrator. Upon subsequent encounters, the reaction is swift—we generally don’t get sick from the same bug twice. For this effective action to occur, the perpetrator’s identity had to be stored in memory and integrated with prior knowledge. Once a bug is on the molecular shitlist, it’s hard to get back into the club. Your white blood cells are born with a pre-populated list of offenders (innate immunity), which grows over time (adaptive immunity).
The immune system’s molecular shitlist roughly corresponds to a suite of pattern recognition receptors enabling recognition of specific molecular motifs associated with pathogens. A distinct set is associated with self. Accurate self-identification is a game of pattern recognition.
Practice is required to effectively manage and grow the molecular shitlist to protect the self. Without exposure to adversity, the immune system will not realize its full potential. No pain, no gain.
The Development of Molecular Self-Identity
When exposure to novel pathogens results in more effective future action, the immune system has been trained. A analogous process occurs in machine learning. Computer algorithms can be trained to identify distinct classes of objects, achieved by exposing them to datasets labelled with categorical identifiers (e.g. images tagged “hotdog” or “not hotdog”). In both cases, the system is pre-ordained by its basic structure to execute a discriminatory function, but will only become proficient with adequate training.
In order to effectively discriminate self from not self, the immune system’s training dataset must be sufficiently diverse, allowing it to generalize across a wide range of pathogens. As with the brain, training often must occur within specific windows of development. In newborns, both the innate and adaptive immune response are immature. As a result, infections that would pose no serious threat later in life may be damaging or deadly during infancy or early childhood.
As post-natal development proceeds, different components of the immune system mature at different rates, reaching peak capacity at some point between infancy and early adulthood. Some of this is passive—the unfolding of pre-programmed developmental processes. Some is active, requiring exposure to training data in the form of pathogens or the microbiome. These exposures “program” the adaptive immune response, giving it the pattern recognition capabilities it will need throughout life.
When the immune system is exposed to a sufficient diversity of non-self molecular identities at the appropriate phases of development, it’s perceptual abilities are trained in ways that maximize self-preservation—defense systems are able to recognize and neutralize threats without being overzealous (autoimmunity).
When the immune system is not adequately trained, self-preservation is compromised. This can happen when an animal is coddled. Without exposure to real challenges, the ability to distinguish self from non-self may become developmentally retarded. The result of retarded development is retarded behavior—an immune system with poor acuity, apt to misclassify cellular identities. It may then attack healthy tissue, resulting in type I diabetes, multiple sclerosis, or other autoimmune disease.
Defective self-identification leads to self-degradation. This is the essence of autoimmunity. It is most prevalent and on the rise in the “developed world,” a trend likely driven by socio-technological factors preventing the immune system from developing a clear sense of self-identity.
Modernity’s Molecular Identity Crisis
Antibiotics are a crowning jewel of modern medicine. They have played a critical role in treating infectious disease, having saved an astronomical number of lives. But humans are indulgent creatures, quick to forget the second maxim inscribed at the Temple of Apollo: “Μηδὲν ἄγαν” (Nothing in excess).
Overuse of antibiotics has had at least two major negative consequences for humanity. First, the evolution of antibiotic-resistant microbes. In the worst cases, deadly “superbugs” with resistance to all available drugs evolve. Second, antibiotics kill not only harmful pathogens, but beneficial inhabitants of our microbiome—the ecology of microbes living on the external and internal surfaces of the body.
We provide food and shelter to our resident microbes. In exchange, they buffer us against infection and produce nutrients we cannot otherwise obtain. The microbiome also teaches us something—literally. It plays an instructive role in training the pattern recognition abilities of our immune system. Without a healthy microbiome present at key phases of development, the immune system receives a poor education, compromising its sense of self-identity.
Germ-free rodents are one way scientists assess the impact of the microbiome on immunity. Raised under tightly controlled, sterile conditions, these animals can be studied in detail. In the absence of microbes, they exhibit numerous immune system abnormalities. Introducing the right microbial populations later in life can restore some, but not all, of these deficiencies. For the immune system to develop properly, a healthy microbiome likely needs to be present during a window of opportunity early in life. If the microbiome is absent or depleted within this window, there may be potentially irreversible negative consequences.
The health and composition of the early microbiome depends on maternal factors present in utero, within the birth canal, and in breast milk. Various modern practices limit our exposure to these maternal factors, including antibiotic use in mothers and infants, birth by cesarean section, and artificial baby formula. Such practices have become more common and are associated with increased susceptibility to autoimmune and metabolic ailments. Examples include allergy, asthma, inflammatory bowel disease, obesity, and diabetes.
As with most aspects of development, timing is critical. A deficient environment can lead to irreversible defects as physiological systems get locked in to a stable configuration (“canalization”). Autoimmune diseases are typically chronic. Once triggered, they tend to persist for life. Miseducated about molecular identity early on, the immune system can settle into a permanent state of confusion.
The social and technological advancements of modern civilization have created much abundance—more facts, medicines, choice, and convenience. But there is much else in abundance: confusion, mental illness, and autoimmunity. Many hunter-gatherer societies have diets that violate the official, “fact-based” edicts of modern institutions like the US Department of Agriculture. And yet, by many measures, they are often healthier than us, with little chronic disease. Compared to Westerners, the microbiomes of hunter-gatherers display much more diversity. Diet is likely a key driver of this and related to the near absence of autoimmunity, obesity, and diabetes among these peoples.
Traditional societies lack our oversupply of hyper-novelty and appetitive desire. Their variable diets, daily routines, and stable cultural traditions seem to render them less confused about who they are, right down to the molecular level.
The Biological Self
Death occurs when self-preservation fails—when the self-sustaining patterns of life are disrupted and dissolve into the surrounding physical patterns of the nonliving world. If we didn’t embalm the dead, they would become soil.
Every organism is a set of special patterns, physically encapsulated to protect it from the entropic forces of the external environment. To sustain itself, life must constantly do work to battle the second law of thermodynamics. This work is done by ingesting raw materials, extracting the energy held within molecular bonds, and using it to power the mechanisms of self-preservation.
The sum total of these bioenergetic processes is what we call metabolism. The various metabolic mechanisms employed by life tend to be homeostatic, using negative feedback loops to keep physiological parameters within the narrow ranges required for life. Temperature, pH, blood sugar levels and even aspects of psychology are regulated in this manner. Not too much, not too little—a biological Goldilocks principle. When these homeostatic mechanisms break, lifespan is truncated.
When healthy, the immune system recognizes as self all of the cells required to maintain the full set of homeostatic patterns contained within the organism. It learns to recognize as non-self any cellular identities that can disrupt these patterns. The ‘biological self’ is the set of cellular identities that generate and maintain the preservative patterns of life.
Lifespan is the time window in which these patterns are in operation. One way or another, these patterns are inevitably disrupted by the relentless march of entropy. Our mechanisms of self-preservation decay over time, a process which is accelerated when the immune system is confused about cellular identity. But the process can be reset through reproduction. With each new generation the problem of self-identification is revivified, providing a fresh opportunity to battle the forces of physical decay.
For humans, identity formation isn’t limited to the cellular level. We also form a sense of psychological identity—conscious awareness of who we are as an individual. This motivates us to behave in certain ways, including our tendency to affiliate with people we perceive to share the same general sense of psychological identity.
The process of psychological self-identification occurs at the level of the brain. Vast neural networks ingest sensory information from the world, using it to construct distinct objects of perception in order to guide behavior. When this process is healthy, a stable sense of identity develops, allowing us to be psychologically content and productively engaged with others. When this process is unhealthy, our sense of identity can become destabilized or even fractionated. There may even be forms of psychological “autoimmunity” in which identity confusion results in self-harm.
As we saw with the immune system, autoimmune disease tends to be chronic. Once confusion sets in, it’s hard to reverse. With the nervous system, there may be more room to repair broken self-identification mechanisms and undergo “rebirth” into a healthier state. Throughout history, humans have discovered various ways to catalyze psychological resets, enabling us to abandon self-harming patterns of behavior. One way is through the intentional use of psychedelics. There are also religious rituals, rites of passage, or other acts of discipline. All involve identity dissolution and reformation.
As with autoimmune disease, psychological identity becomes problematic when confusion about self-identity settles into a chronic, recurring pattern of self-harm—a system that is mistaken, yet certain. To avoid this, we would do well to remember the third and final maxim inscribed at the Temple of Apollo: “Ἐγγύα πάρα δ Ἄτα” (Certainty brings insanity).
To learn more about the topics covered in this essay, try these episodes of the Mind & Matter podcast:
Brian Muraresku: Psychedelics, Civilization, Religion, Death & Plant Medicine | #1
Emeran Mayer: Microbiome, Gut Health, Probiotics, Dieting & Fasting | #24
Lee Cronin: Life's Origins, Alien Biochemistry, Assembly Theory, Discovering Life Beyond Earth | #28
Heather Heying & Bret Weinstein: Culture, Consciousness, Diet, Medicine, Sleep, Dating, Civilization & Evolution | #36
Read other parts of the ‘What is Psychological Identity?’ series:
Dr Jikomes, first let me say that I have enjoyed several of your interviews, and I hope you will take my comments as a form of gratitude and respect.
Responding to the third part of your essay:
Much of it is aimed at describing the simplest forms of self-identity, taking it down to the molecular level – i.e. identifying what belongs to the cell and what doesn’t. Of course that was foiled, and thankfully so, by the first mitochondrial cells.
Also, I am surprised you did not refer to your interview with Terrance Deacon, in which he takes the idea of self-identity to be the defining characteristic of all living organisms: “Every organism has a sense that we will call self. Not in terms of self-consciousness like we’re talking about, but they’re organized around the preservation of self. Even viruses, I can talk about viruses, they’re not alive in the sense that a bacterium is alive, but we know that they’re organized around the persistence of themselves and the transmission of themselves. We know that getting a vaccine is working against the virus’s self-interest, so to speak, so there’s a very very primitive notion of self that we wouldn’t ascribe to just chemistry. Viruses are not just chemicals. They’re chemicals organized with respect to maintaining that organization, preserving that organization against being disrupted.”
After your discussion of self at a cellular level, your last three paragraphs, starting with, “The process of psychological self-identification occurs at the level of the brain…” seem to deny the social component of identity. But can there be any human self-identity without culture? That is, without social interaction, without language and its cognitive outcomes? I let Helen Keller answer:
“BEFORE my teacher came to me, I did not know that I am. I lived in a world that was a no-world. I cannot hope to describe adequately that unconscious, yet conscious time of nothingness. I did not know that I knew aught, or that I lived or acted or desired. I had neither will nor intellect. I was carried along to objects and acts by a certain blind natural impetus. I had a mind which caused me to feel anger, satisfaction, desire. These two facts led those about me to suppose that I willed and thought. ”
“My inner life, then, was a blank without past, present, or future, without hope or anticipation, without wonder or joy or faith.”
Then you continue: “When this process is healthy, a stable sense of identity develops, allowing us to be psychologically content and productively engaged with others.” That is, the process of self-identification. Maybe that’s how it happens with you, but personally, not being from the US, and being the inheritor of European, African and Asian genes, and coming from an even more polyglot society, I feel I can choose my identity as the mood suits me. I am African, I am European, I am Chinese, I am Indian, I am Native American, and I refuse to allow anyone to deny me what I consider to be my cultural DNA.