Note from the author: I’ve always been interested in philosophy and have wanted to try and merge my philosophical readings with science writing for a while. The bold title gets its inspiration from an influential essay (Existentialism is a Humanism) by Jean Paul Sartre, which states, among other things, that individuals are responsible for themselves and that there is no core meaning or purpose without existing in the first place (existence precedes essence). The humanism here comes from the ability of a person, and only that person, to change their condition or situation in life. This calls into question what a person and their identity is, something that I think existentialists don’t do a clear job at answering, but psychology and biology can help. Nevertheless, philosophy can provide a different, perhaps deeper, sense of life’s meaning.

“Life is nothing until it is lived; but it is yours to make sense of and the value of it is nothing else but the sense that you choose.” -Sartre. (Header image “Make It Go Away” by Sabrina Irene)

“It is what it is:” a very simple definition of identity. But what a recognizable identity looks like is a trickier description is because it depends on the thing being identified. In terms of self-identification on a human level, truly recognizing our own identity without conflating that concept with the people and environment around us can be very complicated. In true existentialist fashion, this assignment is the responsibility of each individual to do on their own. The inability to identify the self leaves one vulnerable to being swept up by others and society, and existential crises.

On a microscopic scale, identity more explicitly comes from and is defined by the genetic content of a cell. The DNA constitutes a cell’s entire existence, coding for everything from organelles, to structural composition, and to communicative signaling to other cells. In a larger context within a whole organism, the cell is further defined by its role like neuron, muscle, or skin. But when there are over 200 types of cells within a human body, the whole organism needs to integrate and classify the concept of self and other, especially to buffer against infection from bacteria or viruses.

Where it’s the chore of your mind to choose who you-the-concept is, it’s the job of your immune system to decide who you-the-mass-of-cells is. The inability to self-identify on a cellular level leads to an autoimmune disease, when the body becomes misidentified as a foreign substance and the immune system rejects it, leading to an attack and destruction of healthy tissue.

Self-defense: a right and necessity

Due to the high level of complexity required to organize an entire cell or organism, a regulated system is necessary in order to keep all the processes working together smoothly. This is similar to a ruling government coordinating rules and laws across states within a nation. One of the more basic roles of a government is protection where cells must do the same or risk infection and disease, but what do these rules look like to enact that protection?

Thomas Hobbes, a 17th century English philosopher, sought to find principles that would lead to a functional government based on rationality. Starting with the state of nature, a condition without government, he came to the conclusion that the basal level of nature is a state of “war.” This war-like state runs without common authority, wherein individuals are completely free to decide what is best for them and act on their judgements, regardless of the potential anarchical and destructive outcome. In this world, people have both the right and obligation to self-defense to protect themselves against another’s harmful actions. The right of self-defense is the justification to use force for the purpose of defending one’s own life (or the lives of others).

Cells and organs may not have the high-level concept of ‘rights,’ but they certainly feel the obligation to self-defense and have a plan of attack to destroy infections and foreign agents. Providing the environment for life, organisms inadvertently create the ideal habitat for life of other organisms, sometimes competitively. This means that our cells are subject to infection from bacteria, viruses, and parasites that also love the warm nutrient rich area that our bodies have provided for us. Luckily, to counteract infections, our body has a mechanism of security: our immune system, a set of cells that serve as our self-defense (Figure 1).

To make sure that our bodies can be safe both in the short- and long- term, the immune system is broken up into two parts. The first line of protection comes from the innate response. Immediately upon contact with a foreign agent, or pathogen, the innate system has a knee-jerk response by causing inflammation – the swelling and temperature increase you experience when you are sick. During inflammation, important organelles and proteins get recruited for damage control and elimination of the foreign agent. Phagocytes, a type of defense cell, are the soldiers of the immune system and are the first line of attack. They swallow invading microbes, through phagocytosis, killing and digesting them inside. The purpose of the digestion is two-fold: to destroy the pathogen, and be able to display parts of the invader on the surface so it can be easily identified. Displaying the parts is not unlike a portrait of a bounty hunter picture put up across a town: be on the lookout for this bad guy.

A more long-term system of immunity comes from the adaptive immune system, where in this case each pathogen is remembered. Unlike the innate response, adaptive immune system works against specific pathogens rather than general foreign agents. From the phagocyte wanted poster, B cells make and secrete antibodies that help identify the foreign agents, or antigens. Once the antibody on the B cell contacts the antigen, the B cell turns into an “antibody factory” to increase the immune response, creating more and more antibodies to scavenge and identify antigens. Another type of adaptive immune cell called T cells scan the body looking for infected or foreign cells. Unlike B cells that use antibodies, T cells instead interact directly with other cells with cell-surface receptors. Different T-cell types have different roles and interactions, for example cytotoxic T-cell (called “killer T-cell”) will kill the cell that it’s told to like an assassin.

The combination of B- and T- cells work to make sure that our bodies are protected from threats. Their immune response is the basis for the success of the flu shot, where a small amount of the prevalent flu strain is injected into your system. Your immune response is able to recognize this usually harmless virus within the vaccine and make antibodies against it, so if you ever come in contact with it again, your body is ready for a counterattack.

Back to basics: defining self and other

So far, only a handful of cell types have been discussed here, but there are in total over 200 different cells in a human body. In order for the whole organism to know its boundaries, there must be signifiers or markers that distinguish self and other. With over 7 billion people on the planet, likewise we have to be able to carve a space for ourselves. On an experiential level, an other is another person, someone else, or more simply, something other than oneself. This identification requires the individual, says philosopher Robert Nozick, to have the ability for self-reference and the capacity to self-identify. This raises the question “how do I identify myself distinguish myself from others?”

To begin to answer this question, American sociologist G. H. Mead focused on the role of an individual in groups. Looking at social roles derived from experienced interactions in large groups, on a very basic level, by the process of elimination having characteristics that are not found in others. His theory was that the self is constructed in the process of social activity, where the self comes from both external expectations and individuality. This suggests that self-concept is what makes one different than others and is based on the unique role one has within a group. However, this structure runs the risk of reducing people to becoming flat or one-dimensional by reducing individuals to a single trait with the intension to simplifying society. Framed this way, a multifaceted individual can be boiled down to their role in society: a man who is a violin player in a band, leads a community group, and works on a farm becomes only The Farmer, for example.

But even with expected roles based on unique characteristics, being within a society has an additional component of sameness or fitting in. An early psychoanalyst Erik Erikson, known for bringing ‘identity’ and ‘identity crisis’ into popular culture, described the self as having a need for security and feeling the need to be a part of the community along with the desire for freedom, individuality, and autonomy. These needs unmet throws a person into an existential crisis, unable to identify himself within the context of his life.

As we are able to integrate the many facets of the violinist-leader-farmer into a whole person, our body too is able to recognize the different types of cells and combine these units and attributes into a full distinguishable organism. Likewise, cells can have a difficult time performing this balancing act between self and society, and security and autonomy, especially during the early development.

The immune system, again, helps establish a larger organismal identity. It distinguishes between your body’s own cells and foreign cells by reading protein markers that each cell has, like the antigens before. A protein complex called the MHC (major histocompatibility complex) helps immune cells be able to discriminate between normal and foreign markers on the surface of all cells (Figure 2). Initially, both B and T cells are actually reactive against self-markers but typically these self-reactive cells are eliminated before becoming reactive and initiating an immune response. The MHC presents these self-markers to B and T cells so that they can learn what self looks like and not cause an immune response.

Again at a human level, we feel this strain of self-identification and making our own markers to know who we are and have others be able to know us. This is likely most difficult at its peak during puberty, a time where one is becoming responsible for one’s own character and actions. Where some people seem to always know what makes them them, for many there’s a sometimes continuous discovery period to identify that marker and feel confident in our self-identification.

Misidentification: disease of body and mind

While the growing pains of maturation are uncomfortable and identity-crisis inducing, your cells do not have that luxury of a temporary laps in self-identification. When a cell has “an existential crisis,” it loses the ability to tell self from other and assumes that everything is a threat. This makes the body start to attack its own healthy tissue, turning on the very thing it is supposed to protect, known as an autoimmune disease. A person’s immune system in this diseased state is activated by and works against the body’s own proteins causing significant damage.

Some of the most common types of autoimmune diseases are rheumatoid arthritis, an inflammatory disorder that affects joints, multiple sclerosis, where the protective ends of nerves are degraded, and lupus, when the immune system attacks its own tissues. All of these are characterized by the body being unable to recognize a part of itself, where the self-antigens will activate the immune response and killer T-cells will initiate an attack, all leading to the eventual painful break down of the body (Figure 3).

Autoimmune disease research is as relevant today as it has always been, largely because the underlying causes are still unknown. A long-standing hypothesis is that viral or bacterial infections can instigate autoimmune defects by remaining in the body and keeping the immune system on hyper alert. There is also evidence that having loose junctions in the intestine can also trigger a response, where food particles and microbes specific for the GI tract escape and get to other parts of the body, instigating immune responses there. Because adrenaline and cortisol, hormones released due to stress, activate immune cells, long-term stress can also cause chronic inflammation and induces autoimmune disease-like conditions. Autoimmune diseases additionally can run in families, suggesting a genetic or inherited component. Some genetic factors have been identified that can increase the production of T-cells leading to hyper active immune responses.

Regardless of cause, because autoimmune diseases are not diseases of the immune system as a whole, it means that they are difficult to treat. Additionally, the treatments that do exist aim at suppressing the immune system as a whole. These aggressive therapies aim to modulate the immune system, but either leave patients vulnerable to infections or become ineffective over time. New therapies aimed to support or remodel the immune system are hypothesized to be more effective, but more research needs to be done to develop them.

This loss of organismal identity was tied closely to existential identity for Meghan O’Rourke who had Hashimoto’s disease, an autoimmune response attacking the thyroid, the organ responsible for producing hormones. She describes:

“Loss of intact sense of self… My mental sensation of no longer being a Person had a correlating physical symptom: my eyes no longer seemed like transparent lenses onto the world. They seemed, rather, to be distinct parts of my body, as perceptible as fingers—oddly distant, protuberant, like old-fashioned spectacles. My face felt the same way—like a mask I was disorientingly conscious of at all times. It made me feel categorically fraudulent. I could feel the fat in the cheeks and the weight of bones as I spoke. I felt a mounting anxiety: everything was wrong, and that wrongness was inside me; only I wasn’t sure anymore what that “me” was.”

In many cases, the disease becomes an identity replacing personalized nuances of individuality with sickness and physical pain. This loss or replacement of personal identity happens over a period of months or years, or suddenly following a major change or trauma. It leaves an empty space and a notable abyss in one’s life resulting in increased anxiety, low self-esteem, and depression. Danish existentialist Sören Kierkegaard claimed that “the biggest danger, that of losing oneself, can pass off in the world as quietly as if it were nothing; every other loss, an arm, a leg, five dollars, a wife, is bound to be noticed.” Even though the self is incredibly important, not tending to its needs can unobtrusively lead to its degradation. This autoimmune disease of the psychological self could also be termed as an identity crisis.

Turning toward others to recover a sense of self can be helpful, but any reassurance depends on how others see you and how accurate that ever was to your authentic self. A better treatment of a loss of identity requires, perhaps paradoxically and not without significant effort, self-reflection to re-identify with one’s body, mind, social roles, and interests. Where autoimmune therapies hope to retrain the immune system through administered drugs, in times of existential crisis we have to retrain our brain to find and identify the “being which we ourselves are” with attention and mindfulness.

Additional thank yous to Attabey for making Figures 1-3, Sabrina for letting me use images of her paintings, and the many people who provided edits and feedback.

Working towards getting her Ph.D. in Chemical Biology at the University of Michigan, Sarah studies the molecular roads of the cell using a bunch of microscopes. Outside of research, she is active in science communication by writing for her blog Annotated Science, editing and serving as Communication’s Director for MiSciWriters, and having chaired the inaugural ComSciCon-Michigan 2018. Sarah also loves to bake bread, take photos, make playlists, and drink lots of coffee. Connect with her on Twitter or LinkedIn.