"UNFAIR," SHE SAYS, “that’s how it feels.” Her words are bathed in a deep certainty.
I wasn’t expecting that. Sandy and I have been friends for years, but we have never spoken like this before. Sitting in the small gray cubicle where she works, her words feel like stones—solid, cold. Outside it’s July. Trees full of leaves, lawns, children, pavement hot as griddles. Inside it is cool.
I wasn’t expecting “unfair,” and for a moment I can’t decide what to ask next. The silence grows prickly while I reach for something more.
“Has it changed you?” I ask finally, unable to think of anything more specific.
“Yes. For one thing, I’ve decided I won’t have children,” she says, shrugging off my stupidity. “It just isn’t worth the risk, no matter how small, that I might pass it on to my son or my daughter. I always wanted children. But not now.”
What a shame, I think, that a woman as beautiful as Sandy will never have children.
“Do people treat you differently?” I ask.
“Last week, one faculty member accused me of being drunk at nine o’clock in the morning. It’s true, I can’t walk a straight line anymore and sometimes I slur my words. But, drunk? I want people to know that it’s the disease, not me. I can’t help it.”
Sandy told me once before that anything that requires a consistent sense of balance is quickly moving beyond her abilities. But I cannot imagine Sandy drunk, even though she might have good cause.
Sandy is thirty-five years old, petite, brunette, with a face like a cameo, easy to like, and a smile that flickers as quickly and as brightly as flash bulbs. Seven years ago the doctors told her that her immune system had begun a relentless attack against her brain and spinal cord. They said it was called “multiple sclerosis,” this disease. The name seems a bit sterile to me, too easy to say out loud. I think they didn’t give the name much thought.
“When I was first diagnosed, the people I worked with worried that they might catch MS from me, that it was infectious. That was hard.”
“And though I try, sometimes I can’t help but believe that this is punishment for something I did.” For the first time she appears near tears.
“I believe, though, that everything happens for a purpose,” Sandy follows, her resolution glistening in her serious eyes, her smile again flickering at the corners of her lips. “I may not understand it now. I may never understand it. But I believe it.”
And it’s completely clear that she does. In spite of all the ways MS has changed her life—some so hard and hurtful no one else can even imagine them—she believes that something else is at work here. Something larger even than the mountain of human imagination.
“When I’m done with this, do you want to read it?” I ask her.
“I don’t read as easily as I used to.”
“I could read it to you.”
“No, I’ll have my S.O. read it to me. He’d like to read it, too.”
It took me a while to get “significant other” out of that and Sandy’s mischievous grin.
The tingling, the slurred speech, the angular gait, the accusations of drunkenness, the worried stares of the uninfected, and the revolt of her own body and mind arriving each day as wakefulness claims her—for a purpose?
But it isn’t like Sandy did nothing to deserve her disease, is it? Even Sandy knows better than that. Sandy is, after all, of German descent. And she was born a woman. And she did grow up in the state of Colorado.
Cancer and Capricorn
True insights into self don’t come cheaply. For twenty-seven years I studied the immunological nature of self. For the first twenty-five years, or so, I rummaged among the malignant diseases for insights into the chemical character of self—mine and others. I learned from cancer that nearly nothing about human beings is predictable, and that self has many faces. Some of those faces wear evil masks.
I finished my cancer work one night in front of a group of men and women with that disease. I had been asked by the local chapter of the American Cancer Society to speak on the role of the immune system in cancer therapy. Most of those present had been recently diagnosed with one form or another of cancer. Their heads were hairless, their bodies frail, their eyes gaunt. I spoke for two hours. About halfway through the arcane details of the immunological character of self and self-defense, though, I suddenly saw clearly that even if it were possible to share all that I had learned during the last twenty-five years, it would be less than they had learned in the past six weeks—less about themselves and their diseases. These people knew more than I did. So much more than I did about the elemental self—the one inside with coals for eyes. I knew then, it would have been best if I had quit talking, made some polite excuse, and left quietly. But I didn’t. I stumbled on for another hour or so squeezing out words that had lost their meaning, and even as I spoke, I knew that it was all over, all twenty-five years of it, finished—right there, right then.
To fill the void, I started sifting through the wreckage of neurological and immunological diseases, looking for clues, clues to where I had gone wrong with cancer, looking for insights into the biological and pathological character of self. I learned a lot. I learned that each of us is many things, all at once. And I learned that what we ultimately become may be completely out of our hands, may lie instead in the hands of those with whom we share our bodies—bacteria, parasites, viruses. That was more than even I expected when I began.
But it wasn’t enough.
I know many dead women. Too many. I know cemeteries full of dead women.
The day they buried Pat Brooks, I stayed home. It was wintertime, January maybe. But a nice enough day, as I recall. No obvious reason to stay away.
Pat and I had known one another for about fifteen years. I taught Pat immunology during her first year in vet school. And we got together regularly after that for as long as she was in school here in Fort Collins. When Pat graduated, she left Colorado and spent some time at the University of California at Davis. But two years later, I offered Pat a position as a graduate student in my laboratory. She accepted. For the next two years, we worked together as graduate student and mentor. And for all of that time, she was a good friend. Gina and I often shared meals with her and the man she lived with, times in the hot tub, music, even a bike ride or two. It was, in part, because of me and the job I offered her that Pat returned to Colorado State University and Fort Collins where she married Tom Spurgeon.
Unknown to either of us, during all of that time Pat had several things working against her, working against her in a way that would eventually kill her. Pat, too, was a woman, she, too, grew up in Colorado, and she, like Sandy, was of northern European descent. On top of that, during the course of her life, she had—like all the rest of us—been infected by simple things that could unlock the dark secrets buried inside men and women.
Because of all that, Pat was in danger. But none of us knew that. So we carried on as though each moment was exactly like the last one, as though there were a million moments yet to come, as though our lives would always be so easy.
In spite of all we had shared, I stayed away from Pat’s funeral because during the last couple of years, my relationship with Pat had deteriorated. It was, of course something trivial, and it seemed like we would get around to resolving it one of these days. We never did. Anyway, I figured because of our falling out that maybe she’d prefer I was somewhere else when her friends and family offered their last respects. I wanted to honor that perceived wish.
A few days before, Pat had purposely shot herself in the head with a pistol. She was thirty-two, maybe thirty-three years old. Pretty, young. Though no one could be sure, we all assumed that Pat had done that to herself because earlier the same day, her husband died in a car accident. A young man had run a stop sign at high speed and slammed into Tom’s car, crushing the little Toyota and splitting Tom’s aorta. He was dead before the last of the shattered glass hit the pavement. That seemed reason enough for Pat to choose to end her life, everyone felt certain. Nevertheless, that was not the reason Pat killed herself, or at least, not the only reason.
At Pat’s funeral, her brother read from a journal that Pat kept. A journal that no one had known existed until then. In Pat’s words, her brother revealed to everyone listening that Pat had been diagnosed with multiple sclerosis a few days before Tom’s death, a few days before her own death. None of us knew about that. But Pat and her brother told everyone at the funeral how devastated and confused she had been when she was told of the disease. And how she had kept all of that to herself. So the day Tom died, none of us knew that Pat’s immune system was quietly eating away at her spine and brain. Not even Tom knew about it. When the last of Pat’s friends left her that night, though, Pat remembered. She decided that that was enough for her, enough to know for one lifetime. And she put the final period into her story.
The First Self
Pat’s death did a lot of damage to my stories, punched a lot of holes into the birchbark of my arguments about who we are and why it matters. But I’m an immunologist. What immunologists do is make up stories about human selves—why we have them, how they fail, and why we should care.
We have selves, clearly—whether we wish to have them or not. And we have them only because we have immune systems, only because of self-defense. The one thing that keeps any one of us from becoming everyone else all at once is an immune system. Immune systems identify and destroy things that would, if they could, live in the space we already occupy, whether that something is a virus or another human being’s liver. Without immune systems there would be no selves. Self-perception (or deception, defense, destruction, or rescue) is only possible, because we have such things as selves, obviously. We have such things as selves only because we have immune systems. An especially vivid demonstration of this occurs when HIV destroys a human being’s immune system. Suddenly, where one of us once stood, there lies a community of living things—bacterial, fungal, parasitic, viral, human, maybe. The individual, the self, has evaporated, and in his or her place lies a murky mixture of living things that resembles a human being less each day.
How immune systems establish and protect selves is one of the most remarkable stories biologists have ever unraveled—even though much of the text remains untranslated.
That story begins inside of human blood. All of the elements of human blood arise in bone marrow—the pink stuff that fills the insides of femurs and ribs. The thymus is a little organ about the size of a large marble at birth and sits directly above the heart. Near the end of the third trimester of a human pregnancy, billions of lymphocytes (one type of white blood cells) leave the baby’s newly formed bone marrow and head for the fetal thymus. Inside the thymus, during the last three months of fetal development, individual men and women learn how to distinguish self from all the rest of this hungry world.
This process of self-definition is called thymic selection. Ultimately it will be the job of those newly arrived T cells to defend the child from all of the bacteria, viruses, parasites, and funguses that would like to occupy the space he or she will learn one day to call “me.” But before T cells can do all of that, a lot has to happen. And the way it happens places us all at risk for darker possibilities.
When the T cells from the bone marrow arrive inside the infant thymus, the thymus forces them to start dividing and to begin expressing a particular set of proteins called T cell receptors. T cell receptors will one day enable these T cells to identify and attack infectious microorganisms. But no one begins fetal life with a set of T cell receptors. All of us generate all of our T cell receptors de novo. On our own, that is, after the thymus and the bone marrow have formed inside of the fetus. And the way we do this is remarkable.
As the new T cells divide, they begin to rearrange portions of their DNA. For a biologist, imagining that rearranging DNA would be a good idea is akin to a Baptist imagining that rearranging the language of the Bible would be a good idea. The DNA that was passed to us by our parents tells a story that is over three billion years old. And that story has been refined during all of those years into a very fine and fiercely accurate tale of what it means to be a living thing on this planet. Because of that, for any one of us to dare change even a single word of this story is dangerous. It is not easy to improve on what it took us three billion years to write and revise. So most changes in human DNA are bad, often fatal. Things like phenylketonuria, sickle cell anemia, breast cancer, Lesch-Nyan disease, cretinism, and retinoblastoma involve changes in human DNA. So we have evolved a whole series of neat tricks to prevent changes from creeping into these DNA molecules anywhere.
But not inside the thymus. Inside the thymus, we treat our DNA as if it was a deck of cards. Under the influence of triggering chemicals produced by the thymus, T cells pick up their decks of DNA and, in spite of billion of years of warnings, the T cells start to shuffle and reshuffle and reshuffle, until they have generated something like 1015 different T cell receptor proteins. That’s a lot of T cell receptor proteins. But we are going to need a lot of T cell receptor proteins before we’re done with this septic life—nearly one for every piece of every molecule on every microorganism that might infect us. And through this nearly magical process, we are able to generate all of the T cell receptors we will ever need using very little of our total gift of DNA.
That’s nearly miraculous. But it is also dangerous.
With a deck of cards, after honest shuffling, there is no way to control what hands will be dealt from that deck. That’s why some people lose everything they own playing cards. Same with T cells. After all the rearranging that goes on in the thymus, there is no way to control what sort of T cell receptors will be made. That’s why some people lose their lives to their T cells.
Random rearrangement, shuffling, of T cell receptor genes leads to three kinds of T cell receptors—those that don’t work at all (the most common and useless outcome of this process), those that bind to pieces of human beings (the most dangerous outcome of all), and those that bind to pieces of the microbial world that may some day threaten us (the most important of all T cell receptors). The thymus’ job is to sort through the new T cell receptors and destroy those T cells that might destroy us, as well as get rid of those T cells that have no receptors at all or receptors that can’t do anything.
And the thymus is pretty good at what it does. More than ninety percent of all the T cells inside the thymus die before they get a shot at anything outside the thymus. And that’s good. But it isn’t good enough.
The thymus tries to identify all the T cells that might react with and destroy pieces of self. But all the thymus has to work with are the tissues of the thymus itself. So the thymus pretty effectively destroys all of the T cells that react with anything found in the thymus. And that covers a lot of stuff—maybe as much as ninety-nine percent of everything that might be found in or on most human cells is found inside a human thymus. But not one-hundred percent. Everything that makes up a man or a woman isn’t inside of human thymuses. So some self-reactive cells get out of the thymus, always. Because of that, even though the human immune system is one of the finest defenses ever devised, each of us carries in his or her blood the means for self-destruction.
That is the price we pay for having selves. Our thymuses, at some considerable risk to us, create a certain sense of self. A powerful sense we could not survive without. A sense unlike anything our parents ever felt, a set of genes unlike any our parents ever held, a piece of the story that no one else has ever heard or told. Without that, that thymic sense of self, none of us would walk the face of this sweet world. An image of self held at once by trillions of T cells coursing through our veins and arteries and our tissues. 1015 possibilities, maybe more. If you counted seconds on a clock, it would take you thirty million years to get to 1015. That is the power of human immunity. However, it doesn’t come without a price. For that kind of power we all must risk of self-destruction.
We might wish that it were otherwise. But whether we would choose to accept the power or the risk makes no difference, because it is only from that power and those risks that human beings are born.
We should care because these bits of physiology make us human.
Born inside the human thymus, the first self—rife with possibility
The Second Self
If we are to truly appreciate this first self, we must have a second self—one given to us by our brains, a self with eyes and ears and taste buds and fingers for touching our selves and one another.
In most ways, this aspect of self is much less well understood. Clearly, though, biology also bestows upon each of us a clot of mental and neurological processes that allow us to distinguish our bodily selves from all that surrounds us. Even organisms as simple as crabs or clams know better than to eat their own bodies, see clearly at least one of the barbed boundaries of self. And everyone agrees that this “sight” involves neurons and all the other cells that make up an animal’s nervous system.
Nerves, neurons, and the signals they transmit are essential to even the simplest manifestations of self and self-perception.
Most nerves send signals by rapidly changing the concentrations of sodium and potassium inside and outside of the neuron. Neurons have a cell body, which houses the nucleus and the chromosomes, and processes or arms that radiate off the cell body called dendrites and axons. The axons are sometimes very long and carry the nerve impulses. There are two obviously different forms of neurons. Those in which the axon is naked and those in which the axon is wrapped inside of layers of myelin.
Myelin allows nerves to conduct signals much faster. In one sense myelin serves to insulate the axons, but not in the same way as the plastic wrapping insulates wires in our homes. Myelin accelerates the nerve impulse by forcing the electrical signal (the change in sodium and potassium concentrations) to leap from point to point along the axon. As a result the nerve impulse moves much more quickly down myelinated axons than they do down unmyelinated axons. Much of what makes us human and keeps us alive in a predatory world would be impossible without myelinated axons.
Inside the brain and spinal cord, these two types of neurons are responsible for the distinct appearance of the white and the gray matter. White matter consists almost entirely of myelinated axons, while the gray matter is made up mostly of the unmyelinated dendrites and cell bodies of the neurons that have spawned the myelinated axons of the white matter. The deep centers of the brain are mostly white matter. The outer cortex mostly gray matter.
Transmission of most signals from brain to body or even within the brain involves two or more neurons. Interestingly, those neurons are not attached directly to one another like the wires between our homes and the power plant that supplies our electricity. Instead, at the point where two nerves meet, there is a gap, an empty space, called a synapse. The signal from the first nerve causes chemicals to be released into the synapse. These chemicals are called neurotransmitters—things like serotonin, norepinephrine, glutamine, dopamine, GABA—and they carry the nerve signal across the synapse to the next nerve.
Somewhere inside of synapses, there are large pieces of human beings. If we change the concentration of the chemicals inside of synapses—especially serotonin and norepinephrine—we change people and their behavior. Prozac and Paxil, Remeron and Serzone, Celexa and Effexor change the concentrations of serotonin and or norepinephrine inside of synapses. Because of this, these drugs sometimes lift people form severe depression, or stop them from compulsively washing their hands, or make it possible for people to leave their homes—people who haven’t seen the out of doors except through a window for years.
Part of who we are, parts of human selves, are living in our synapses and our neurotransmitters, our neurons, and our brains. One self is locked up inside of our nervous systems.
Out of the mind’s idea of self and the thymus’ portrait of self come human selves and self-awareness. Human existence and human persistence. Science, poetry, religion, philosophy, song, hatred, war, love, bigotry, brotherhood. All things human.
And so similar are the neurological and immunological processes that are involved, so close is the communication between lymphocytes and neurons, between thymus and lymph node and brain, that I and others have proposed that these are not (as we have been told for so long) two unrelated systems, but a single functioning unit. A single system—neuroimmune—whose primary task is to speak the words of the only stories that are truly ours, the story of self and self-defense. To name us and to defend us from things as varied as viruses and vodka, parasites and patriarchs, bacteria and Buicks.
Inside of us are the words, and inside of the words are our stories. Those stories are all that can save us. Sometimes, those stories are all that we have.
That is our gift from those who came before us. The gift of self and the power to defend it. But there is a curse as well, a curse laid upon the gift by the evil goddess of necessity. The curse states that in return for our precious selves and their defense, we must, at once, acquire inside both our immune and our nervous systems the weapons for the destruction of those selves. And further, that any control we exert over these weapons is tenuous, at best. Illusory, at worst.
The power of immunological self would be impossible without the formidable force of random gene rearrangement. It is only through that process that we can attain the unimaginable diversity that is the true force behind human immunity. But that same process assures each of us of our share of T cells that may someday attack us.
And the complexity of neurological self speaks a tale so fanciful, so lurid, that we may never understand what separates the whole from the pieces, the firm from the infirm, the sane from the insane, or what takes human beings down any of the paths that we so willingly follow, or why some of those paths end so well and some so poorly. The gifts of imagination, courage, resolve, strength of will, and vision carry with them the inherent risks of depression, delusion, anxiety, insanity, and suicide—unavoidably.
There are flaws inside of each of us, potentially fatal flaws. Within our nervous systems, of necessity, there are the seeds of psychoses. Within our immune systems, of necessity, there are the roots of autoimmunity.
Self, healthy self, depends absolutely on both systems and insists, as well, on the flaws.
There are holes yet, lots of them. Holes in my story, holes in our thymuses, holes in our heads, holes in our pictures of selves. But in spite of the holes, that’s my best story yet, and for the moment, I’m sticking with it.
The Disease at the Seam
Multiple sclerosis is about the purity of our two selves and about their flaws. It is the mystery in the middle of the pool. Among all the autoimmune diseases, multiple sclerosis is, at once, one of the most remarkable and one of the most sinister—because this disease works in between the two selves. But as it does that, as it pries the two selves apart, MS opens a window on the human self.
Inside of people with MS the immune system believes the nervous system is the enemy. Because of that, the immune self lashes out at the nervous self. All the while, the nervous system is, of course, manning the controls of the immune system, orchestrating its own destruction. All the while the immune system is mucking with the dials and levers that regulate the nervous system. The immune system strips a neuron of its myelin. The nervous system, in its turn, raises the voltage. The immune system reaches a little deeper. And the whole thing ratchets up a notch. Self versus self. A state of being quite unlike any other.
No one knows what makes men’s and women’s selves turn on themselves. But people who get multiple sclerosis disease have some things in common. Caucasians get MS more than any other ethnic group. Caucasian women are two to three times more likely than Caucasian men to develop MS. In general, women who live at or above the fortieth parallel north (a line that, in this country, runs from about Newport News, Virginia to Santa Cruz, California along the northern borders of North Carolina and Arizona and the southern border of Colorado) are twice as likely as those living south of this line to develop MS. Similarly, people south of the fortieth parallel south—places like southern Australia and New Zealand—have a higher incidence of multiple sclerosis. Except for native peoples. Native peoples north of the fortieth parallel in North America and south of the fortieth parallel in Australia and New Zealand rarely get multiple sclerosis and some groups, such as the Inuit of North America appear immune to MS. But, interestingly and inexplicably, women who grow up in the state of Colorado are ten times more likely to develop the disease than women living in southern states. Girls and boys under the age of fifteen who move to Colorado become as likely as those born in the state to contract MS But people who move to Colorado after age fifteen are no more likely than their southern neighbors to contract MS. Most people with MS have descended from northern European peoples, especially Scandinavians, and many with MS have been infected by human herpes virus 6 (the virus that causes roseola in children), or measles virus, or EBV, and some have been vaccinated for hepatitis B. Bacteria, such as Chlamydia pneumoniae have also been found in much greater numbers in people with MS. The difficulty, of course, lies in distinguishing causes from effects in MS.
Occasionally there have even been outbreaks of MS and groups of people have simultaneously developed the disease. Such outbreaks are call “clusters.” Between 1943 and 1989, four separate clusters of multiple sclerosis outbreaks occurred in the Faroe Islands. This group of islands rises between Iceland and Scandinavia and was occupied by British troops during the Second World War. Since that occupation, the number of cases of MS increased each year for twenty years. Other clusters have been reported among people living in the same neighborhood or people working in the same office.
That’s what we know. What we don’t know is what causes MS.
A lot of evidence supports the notion that an infectious agent, specifically a virus, plays a role in the development of multiple sclerosis. The geographic differences, the association with HHV-6, the clusters of MS, the report by many women that diagnosis of the disease was preceded by a flu-like episode, suggest that an infectious agent is involved, as does the immunological character of the disease. But it is not clear what the infectious agent might be—things as diverse as typhoid and mumps have been investigated. But no “smoking gun” has been found. And how an infectious microorganism could cause a human autoimmune disease is murky at best.
In other systems, particularly animal model systems, though, there is evidence that some viruses have proteins on their surfaces that are very similar to proteins in their animal hosts. When these animals are infected by one of these viruses, their immune systems respond and produce T cells and antibodies that will bind to and destroy the virus. But some of the antibodies and T cells that were stimulated by the virus, also, apparently, bind to normal human tissues and begin the destructive process known as autoimmunity. Immunologists have called this process “molecular mimicry,” because the molecules on the virus mimic similar molecules on host cells. The name seems too benign.
When such a virus infects an animal, human or otherwise, self-reactive T cells that escaped the thymus may be activated in an attempt to produce a self-protective immune response. But as the immune response evolves, there is an unexpected cross-reaction between these T cells and normal kidney, or pancreas, or myelin sheath, and things quickly get out of hand. Suddenly, what was intended as protection becomes destruction, and our T cells and our antibodies begin to destroy our own cells. That may be how people get insulin-dependent diabetes and rheumatoid arthritis when they begin to destroy their own pancreatic islet cells or connective tissues. It may also be the way people get multiple sclerosis. But unlike these other autoimmune diseases, in MS, the self itself is quickly at risk.
And the higher incidence of MS among people of northern European descent suggests that a person’s genes may play a role in determining whether or not that person gets MS. Interestingly, one of the candidate genes is a gene within the major histocompatibility complex, or MHC, a gene called DR2. Only about twenty percent of the human population at large have this gene. But about sixty percent of people with MS have DR2. The major histocompatibility complex is called that because it contains the genes that are major factors in determining whether or not an allograft—like a kidney or a liver—will survive when transplanted between two people. These genes have a major effect on allograft survival because the proteins produced from the MHC genes govern the process of self-definition, the process that goes on inside every human thymus. Inside the thymus, MHC-derived proteins present self to the T cells there, and depending on their response, the T cells are either destroyed in the thymus or allowed to emigrate into the blood. They are either marked as self-responsive and dangerous or allowed to escape the regulatory confines of the thymus.
Other MHC molecules very similar in size and shape to DR2 are known to be involved in the normal development of mammalian brains and the processes of memory and learning.
A disease at the very center of self. A disease in between.
In people with multiple sclerosis, something causes the T cells (the heart and soul of immunological self-consciousness) to recruit macrophages and microglia cells (the macrophage-like cells of the brain and spinal cord) and inflame these cells to wage war on the myelin sheath that surrounds the neurons of the central nervous systems (the heart and soul of neurological self-consciousness). Self vs. self. In the ensuing battle, the myelin sheath is stripped from the neurons of the brain spinal cord (sometimes the optic nerve, sometimes olfactory nerves, sometime the nerves that enable us to walk and speak normally) and then the oligodendrocytes (the cells that make the myelin sheath) and some of the neurons underneath their myelin sheaths are also destroyed by the immune system.
When that happens, people change. Suddenly nothing is as it was. Things no longer sound the same. Things no longer look the same. Gait may change, swallowing may be more difficult. Sometimes there is an incessant tingling in hands or feet, dizziness, loss of memory, or even a wish to have no children. Self, itself, changes.
Early on, some of the time, the damage to the myelin sheath is repaired and then things return to normal for a time. But sometimes, especially later in the disease, the oligodendrocytes cannot repair the damage. Then, nerve transmission slows. Plaques—demyelinated patches of white matter turned gray in the brain and spine—appear in radiographs and magnetic resonance images. Missteps appear on the way from an office door to a classroom, speech curls in odd and unpredictable ways around familiar vowels and consonants, sometimes legs give out, sometimes eyes, ears, sometimes noses just quit working.
Then the war between nervous and immune selves becomes so fierce that the line between what we are and what we are not can blur. Inside of my story, this is the worst possible mistake—self vs. self.
Imagine that. Imagine what it must feel like to have the two most intimate parts of ourselves—parts most of us take completely for granted every day, parts we never even think about, but the parts that make us who we are—warring with one another. Imagine self, itself, at risk. Imagine such a sudden and searing insight into the elemental fire of our individuality. An image uncluttered by all the confabulations of life, unobstructed by the nonessential. An immaculate vision into our heart of hearts. How that must feel?
“Unfair,” Sandy says unhesitatingly.
I’ve explained my fascination with self to Sandy. My belief that true self-knowledge always comes at very high price. And my sense that because of the nature of the disease, MS offers an insight into self that is inaccessible to everyone else. As an immunologist I am nearly overwhelmed by the simple idea of it. Sandy seems little interested in my rambling.
“Unfair,” she says once more. But, for a purpose, perhaps, an important and invisible purpose. One Sandy’s certain of in her mind. One she’s willing to wait for, even if it takes forever.
Sandy’s courage frightens me. She is human, like us all. But she has found another story—one with fewer words and fewer reasons. And inside of that tale, in there with the anger and the hope, the courage and the fear, there are words of encouragement for others like me still placing and removing commas, still striking verbs, still searching for the one right sound to begin with.
The only road left open to the two us is the roughest road of all, the road that leads inside. Sandy, with her slender hands and her gentile smile, is leading me a little farther down that road just now. All that I have learned in my books and my laboratories is useless now. This is not an intellectual struggle. This is a fight for survival.
“Has it changed the way you see yourself?”
“I’ve thought a lot about that. And yes, it has changed things. I feel like a piece of me is missing. I don’t feel like a whole person anymore. I’m not like everyone else, anymore,” Sandy says with her unflinching honesty.
We learn quickly what it means to be diseased. How it sets us apart from others, others with their self-confidence, their health, their corrosive innocence. We learn that nothing is the same anymore, and we notice that people look at us differently, if they choose to look at us at all.
But disease does open windows, windows that frame sights no one else has ever seen, delivers us onto ships that carry us to places our health denied us. Pictures visible only to weakened eyes, places and people touchable only with tingling or broken fingers, thoughts plausible only to demyelinated or crushed neurons. A passage, paid for with human flesh.
Sandy is showing me that way.
“Does it hurt?” I ask.
“Big time,” Sandy says. “Big Time.”