You’ve seen them discussed in newsrooms, the White House, and marketed in celebrity magazines, med spas, and social media feeds, breaking down which peptides you should consider for flawless skin, weight loss, and biohacking longevity. But how many people, scientists aside, know what a peptide actually is? What is the purported “magic potion” for health hacking and reverse aging?

Peptides are a broad class of molecules, some naturally occurring in the body. Some have become transformative medical treatments. But this “transformative” label has become synonymous with all peptides flooding social media feeds.

However, understanding what peptides are, how they work, and which peptides are supported by evidence offers more insight into peptides individually, rather than treating their boom as a whole as either a godsend or a scam.

There’s a Peptide for That!

If you’re anywhere near the health space, chances are, you’ve heard the word “peptide,” maybe even believed the generalization that all peptides are the new magic bullet. It’s not hard to fall for. The word “peptide” has become a catch-all for delivering on a multitude of promises. Depending on who you ask, or whose marketing you consume, peptides can help you lose weight, recover from an injury, improve skin, calm inflammation, build muscle, and even help you get a tan.

For people living with chronic illness, the appeal is not difficult to understand. When conventional treatments provide incomplete relief or come with significant side effects, a compound promising reduced inflammation, faster healing, and improved energy can sound less like a wellness upgrade and more like a possible way out. That makes the difference between promising research and proven treatment especially important.

In July of 2026, the FDA’s Pharmacy Compounding Advisory Committee considered whether several compounds should be added to a federal list of bulk substances that may be used in certain compounded drugs: BPC-157, KPV, TB-500, and MOTS-c. The committee ultimately recommended including the four substances on the list, but its recommendation was nonbinding. It did not amount to FDA approval or establish that the compounds were safe and effective treatments.

But before you decide that peptides are either revolutionary or suspicious, there’s one important question to ask, and ultimately learn the answer to: What exactly is a peptide?

The Peptides Already Inside You

Amino acids are biological building blocks that, when linked together, form peptides that generally become proteins. These chains perform a variety of functions in the body. Certain peptides serve as hormone regulators; others influence metabolism and insulin; some even serve immune defense functions and inflammation. The amino acid building blocks can be arranged in different ways to make new peptides with unique functions and specific biological targets.

Peptides may have been popularized as something to be taken from the outside, but these chains of amino acids are already made in the body. But not just the body. They exist almost everywhere, including in certain foods we eat, such as soybeans, beef, and potatoes.

What you see in Instagram feeds, wellness clinic ads, and FDA news coverage is the buzz around bioactive peptides- peptides capable of affecting biological processes such as metabolic signaling, inflammation, tissue repair, and oxidative stress.

The most popular peptide buzzword? GLP-1. Glucagon-like peptide 1 (GLP-1) is a naturally occurring peptide hormone, produced in the gut. This multifaceted peptide manages healthy insulin release, slows digestion, and signals to your brain that you’re full and satisfied.

Part of the peptide boom began with the drug Ozempic, a synthetic GLP-1 containing the active ingredient semaglutide, designed to mimic the naturally occurring GLP-1 in the body.

The results are generally positive for those in need of glycemic control, weight loss, or reduced risk of diabetes-related cardiovascular disease. But like any “wonder drug,” risks are being closely watched. Over the last decade since the drug’s release, adverse effects such as acute pancreatitis, kidney and gallbladder injury, and rare non-arteritic anterior ischemic optic neuropathy (NAION), or vision loss, have become associated with the drug.

But Ozempic, or rather semaglutide, is just one peptide on a long list of peptides with separate functions that have been popularized. The popularity of individual peptides has also fueled interest in “peptide stacking,” or using several peptides together.

Before peptide stacks, celebrity Ozempic allegations, and tanning without the sun (yes, really), there was a peptide less commonly thought to be a peptide that revolutionized medicine. Insulin.

A Century Before the Wellness Bros

Insulin is a peptide hormone, made up of two chains of amino acids. Produced in the pancreas, insulin helps regulate blood sugar and metabolism. In patients with Type 1 diabetes, an autoimmune disease, the immune system attacks the insulin-producing cells in the pancreas, leaving little to no insulin to help the body’s cells take up and use glucose.

In patients with Type 2 diabetes, although the pancreas produces insulin, the body’s cells no longer use it efficiently for glucose-to-energy conversion, leading to insulin resistance. But at the turn of the century, insulin was a medical mystery, yet to be identified as a driver of these conditions.

Before the discovery of insulin, Type 1 diabetes was often fatal due to rapid weight loss and cell starvation on top of inadequate treatment. Essentially, when cells in a patient’s body could no longer take up glucose due to a lack of insulin, they began to break down other tissues, such as fat and muscle, leading to the body wasting away.

At the turn of the 20th century, doctors turned to methods such as forced feeding or severe dietary restriction, sometimes referred to as “starvation treatment,” in an attempt to prolong patients’ lives.

Science eventually came to understand that the pancreas played a role in diabetes and explored using pancreatic tissue extracts to treat patients. But it was a long, tedious, and flawed process with little success and a high risk of toxicity.

In the early 1920s, a group of scientists at the University of Toronto revisited the pancreatic extracts, first testing them in diabetic dogs. After purifying the extracts, they turned to a 14-year-old boy, Leonard Thompson, to test the treatment. At first, there was little result, and an abscess formed around the injection site. But after biochemist James Collip further purified the extract, it was eureka: A second injection lowered Thompson’s blood glucose levels, and symptoms of his diabetes dissipated.

This purified extract would become what we know today as insulin, a potent peptide that underwent years of formulation, dosing, and clinical observation to achieve greater stability and longer-acting effects.

Insulin’s history was a medical breakthrough in experimental peptides, but unlike the miracle-peptide umbrella we see today, it underwent rigorous purification, testing, formulation, and clinical observation that spanned decades to prove its reliability as a treatment.

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Medicine Cabinets to Med Spas

A century after insulin, we are seeing a new revolution in the rapid adoption of GLP-1 medications. Similarly, a GLP-1 drug has astonishing effects on a patient’s metabolism and grand applications for populations with chronic illness that need such a drug to lower their risks. Other peptides, such as BPC-157, which claim to speed healing and reduce inflammation, are part of a new wave of synthetic peptides whose animal studies show these promising effects. But studies in humans remain extremely limited.

Somewhere along the way, the specificity of these effects got lumped into wellness and optimization culture, tied back to the broad term “peptides.” The promises of a better body, better skin, and better health as a whole catapulted widespread consumer access to these medications through online channels, whether or not a person needed them for their original intended use. What has happened is a widely believed assumption that because one or two peptides have been well researched and approved for use, all other peptides must be just as good and ready for consumption.

But the success of two peptides does not automatically prove the effectiveness of every other peptide. And their relationship to naturally occurring molecules does not mean they are safe at every dose.

Meet the Molecules

We know semaglutide (Ozempic) and tirzepatide (Zepbound). Their advertisements flash across your cable and streaming services, promising FDA-approved weight-loss results in X months. But here are some of the experimental peptides currently receiving regulatory and online attention:

• BPC-157: claimed to improve injury recovery, tendon healing, gut repair, and reduce inflammation.

• TB-500: claimed to rapidly repair damaged tissue, assist with muscle recovery, and promote efficient wound healing.

• KPV: claimed to lower inflammation, improve gut health, and promote efficient wound healing.

• MOTS-c: claimed to help with fat loss, improve metabolism, and increase longevity.

These peptides have different biological origins and structures; some are based on naturally occurring peptides or protein fragments, while others are synthetic derivatives synthesized in the lab.

Questions remain about their biological equivalency. Studies of these peptides have been ongoing, flagging concerns about their dosing, quality, and short- and long-term effects.

One such study tested intravenous BPC-157 injections in only two adults to assess adverse effects. While no short-term effects were reported, a study that small cannot establish safety, optimal dosing, or long-term risks, all characteristics key to determining if a specific BPC-157 product could be evaluated as a safe and effective treatment.

The Fine Print

When a fitness influencer or wellness junkie records a video dishing the details on their peptide stack, there’s a chance some of their stack consists of peptides that come from “gray-market” sources, sources that claim their peptides are safe and effective without a high degree of regulatory oversight.

The peptides sold on sites from polished and well-branded laboratories, even marked as “for research use only,” may not have undergone large-scale controlled studies, been evaluated for long-term effects over extended periods, or had their specific formulation and manufacturing processes assessed.

When they reach the hands of an individual who is hungry for the promises of better health, that consumer may not know the ins and outs of the “safety” they think they’re receiving.

And when these peptides are compounded, prepared as a customized medication by altering dose, ingredients, and form, it only raises more concerns about the purity and effectiveness, something the FDA has highlighted in its investigation into peptides. Although compounded drugs are not FDA-approved, they can serve legitimate medical needs, making the quality and oversight of the specific compound especially important.

Evidence that a molecule is effective in the body is not the same as evidence that its commercialized version produces a safe and meaningful clinical benefit.

The Right Question

The right question isn’t whether peptides are meaningful. We’ve seen the revolution of commercial insulin production, and now the widespread adoption of GLP-1 medications. These molecules are undoubtedly changing the way we look at medicine and the health of millions of individuals affected by the constraints of chronic illness or debilitating disease.

This is not to say that the popularized peptides you see online will not become useful treatments down the road. But the category itself does not establish safety and effectiveness for all. The right questions ask: Which peptide? For what condition? In what form and at what dose? Studied in whom and how many? Compared with what? And supported by how much human evidence?

Some peptides are medical breakthroughs. Others remain biologically interesting compounds in need of much more scrutiny. What matters is whether the promise being sold has moved beyond just promising science.

There was a day in my chronic illness journey that has stuck with me. It was 7:00 in the morning, and I had just checked in at a treatment clinic for my usual cocktail of drugs via IV infusion. The receptionists were friendly, and I knew their names; the nurses were kind, and I asked how they were. I sat in a leather lounge chair with a heating pad on my left arm, waiting for the “good” vein to pop up for use. The room was brightly lit; they gave me two pillows, per my request, and I sat, making small talk that, on the surface, felt good in light of what would be an exhausting day.

But as the plastic tube and catheter were taped down and the bag of fluid began to drip, even after the nurse asked me how I was feeling and I replied, “good,” deep down, I wasn’t fine at all. This became especially clear when I got into my car after the two-and-a-half-hour treatment and began to cry. It was not a surprising occurrence. Because even after the treatment, the review of my lab results, the lighthearted chatter with my rheumatologist, and the positive “everything looks good!”, I felt a crushing force of all the exhaustion, the dulled pain, all the grief, and the reality of living a life I hadn’t imagined, even just a year ago.

It was a force that was blurring the memories of my old life, dragging me into a painful reality that I’ll be some form of sick for the rest of my life. This is a feeling that conventional clinical measurements do not always adequately capture. This is the agonizing truth that many chronic illness patients experience. When good on paper doesn’t feel good at all, where do you go from there?

Good Numbers, Bad Days

The clinical classification of “improved” or “normal” does not necessarily reflect a patient’s lived experience. Feeling “well” is often a phantom we see in daydreams or recall in distant memories of who we used to be before disease crept in. But control on paper is like a long checklist that, once fulfilled, makes it difficult to measure the patient’s life outside the disease, a life that still feels unwell.

Laboratory values, in combination with examination findings and disease activity scores, stack up to show improvement. There are numbers, and then there are more numbers. Summaries and figures that define where the patient stands clinically. You get good numbers, and you can breathe a little. Your disease hasn’t gotten worse. But that doesn’t negate the chaos and greyness the disease still leaves in its wake.

My disease had been controlled, on paper. But I was frequently at a loss when it came to sleep, and the domino effect on function that followed. I averaged four to five hours of light sleep per night and woke stiff, like I had been hit by a truck, as I liked to describe it. What followed, depending on the day, was energy masked by lots of caffeine that would eventually make me feel worse, irritability and my unfortunate tendency to snap every now and then, and the uncontrollable inability to focus.

Some days it felt like I was moving through freshly poured cement. Other days, it felt like swimming with a heavy sweater on.

Days blurred together, tasks were left unfinished, and the constant existential weight of no longer recognizing myself, no longer seeing the energetic, social, and invincible girl I still mourn, would only seal the cycle to repeat all over again.

My rheumatologist had measured my disease’s activity, its progression, and the efficacy of the drugs I took to slow it down. What he had not measured was what the disease had done to me and my quality of life, a much more subjective measure.

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I Cannot Treat What I Cannot See.

Measurement of disease has undergone thousands of years of growing pains to accurately determine what’s plaguing a patient and to increase the likelihood of their survival.

When you look at the scale of how much science has changed, there was a stretch of centuries during which medical science shifted only slightly here and there, even as the world around people was growing increasingly modern.

Throughout history, particularly in ancient times, there were a few standards for diagnosing a patient based on the signs they presented: physical observations, pulse readings, uroscopy (examination of a patient’s urine), and listening to the patient’s narrative.

As different plagues swept across ancient and eventually medieval cities, herbal and botanical remedies were popular, and hygienic therapy- the practice of bathing regularly, among other practices - was a pillar that medicine leaned on for treatment. Bloodletting was especially common in response to determining that a patient had “too much” blood.

These practices continued alongside the work of scientists who invented microscopes, discovered germ theory, and pioneered surgeries over the next centuries.

For a long time, physicians developed theories of disease even when they couldn’t see it or understand its origin. And before empirical measurements came along, doctors and physicians relied on several theories about what was going on inside the diseased human body, the most popular being an imbalance in the four bodily humors, or fluids: blood, yellow bile, black bile, and phlegm. Each humor carried unique traits, and when imbalanced, it contributed to illness.

But the 19th century saw a boom in medical innovations and advancements, particularly in our understanding of disease and illness, paving the way for different standards of diagnosis and treatment. With the evolution of pathology, disease was finally understood to come not from bodily humors, but from cells and their pathological changes. Rudolf Virchow, a German-born scientist, helped establish the field of cellular pathology, urging other scientists to focus on microscopic and anatomical methods.

By the turn of the 20th century, laboratory testing had expanded to combat disease outbreaks and improve diagnostic precision. As research progressed, disease activity could be quantified more consistently, and various disease activity scores, such as scores for rheumatoid arthritis, were eventually standardized.

Disease was becoming increasingly easier to measure. As objective measurements became more successful and authoritative, personal experience received less clinical weight.

“Sickly” is the Word

I have frequently used the word “sickly” to describe myself and others, although it is used to describe a much more dramatic image. When someone of average health hears me use the word “sickly,” I can see their face change in a way that tells me they’re imagining I’m supposed to look frail, congested, clammy, and pale 24/7. Like I’m dying from some mysterious illness of which no one has found a cure.

Instead of a much more dramatic appearance than people tend to imagine, the word “sickly” describes someone as being often weak or feeling sick. When you put it like that, the definition sticks to chronic illness patients, but its measurement is not something doctors always address.

A patient can be improving on their medication, show few signs of disease activity, but still experience “sickly” symptoms, not always derived from the disease but from its effects that ebb and flow. For some, it could be structural damage from before the disease got wrangled under control; irreversible damage that eventually just becomes part of everyday life even though things look and feel different. For others it could be heightened sensitivity to pain, anemia or other nutritional deficiencies, or, in my case, sleep disorders.

Alongside these symptoms and changes are the gifts of being sickly that do not physically manifest like the others: depression, anxiety, and even medical or disease-related trauma — states of mind that are sometimes so naturalized that you begin to forget how you felt mentally before the disease came along.

A common denominator among many patients with chronic illness, one that eludes the science of measurement, is fatigue. Fatigue is the shapeshifting monster that never really comes from just one place, but from multiple. Not just a lack of sleep, but possibly a spike in unexplained inflammation, the pain that may follow, or even a side effect of a medication. Its intangible complexity is so frustrating, and even though it’s everybody’s concern in theory, it’s nobody’s responsibility in practice.

By the time you’re due for your next assessment, the difference in priorities may appear black and white. Medical care is often structured to focus on the numbers and data that string together results and progression, and on medication efficacy to tie things up in a bow.

Meanwhile, you’ve been so tired that the appointment was hard to go to in the first place. You can’t remember the last time you enjoyed a hobby or easily got through a full day of work. The numbers and data point to your disease being controlled. But they don’t point to getting your life back.

What is Actually Living?

In the grand checklist of disease management, quality of life may become the last box. It often receives explicit attention to prevent organ damage, restore bodily functions, minimize risk, and return the patient to baseline. Quality of life improves, but something is still missing: a restored life.

The priorities of treating a disease can eclipse the priority of giving a patient their life back. Why can’t biological control and lived experience be balanced in the management of a disease? Because, after all, isn’t managing this disease managing the human who bears it? Including every aspect of how they think, feel, behave, and will see themselves for the rest of their lives.

But there still seems to be a gap between those who need support and the system with the means to provide it. Receiving support is not the same as having it offered without follow-through—a distinction often lost in completed doctor-patient questionnaires and 15-minute appointments.

The support only matters if offering it actually leads to tangible resources, change, and ongoing investigation.

Handing a patient a disease and quality-of-life survey and then filing it away sans investigation reinforces clinical measurement without humanized change.

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Two Birds, One Patient

Science and the study of how cells and medications interact are astonishing in their own right, but so is the patient’s life. The two should be measured distinctly but addressed together if living with chronic illness is ever to be considered more than doable.

A doctor’s language, the typical “things have improved!” often unintentionally envelops feelings and experiences as improved alongside disease activity. Instead, the language should be broken down into more specific terms to highlight exactly what has improved, rather than assuming everything has improved.

“You have less disease activity, and no new damage to your organs or tissues. However, you are still having trouble sleeping and functioning at work. Let’s come up with a treatment plan for that.”

Two different paths, two different experiences, one patient.

As the patient’s lived experiences gain recognition, those experiences should be tracked over time (put those questionnaires to good use!) so clinical encounters can assess them even without changes in the disease.

It is a lot to ask of a system that rewards volume and patient turnover while limiting prolonged patient conversations. That itself is an entirely separate issue worth discussing. But even in 15 minutes, imagine what could be done if we recorded quality of life as much as we record disease activity?

Imagine what could also be done if the system were changed so that quality of life is measured from the first diagnosis? If a patient is treated with equal parts scientific curiosity and humility, and asked: “What has your disease taken away from you?”, I imagine the journey of living with a chronic illness would be easier from the get-go.

Control as the Beginning, Not the End

I am sitting in my living room while I write this; my hands are able to move over my laptop’s keyboard quickly, like some sort of hacker. I can’t remember the last time my hands hurt enough to the point where I couldn’t move them like this. That is one of the little wins that reminds me to be grateful for my bottle of Rinvoq tablets upstairs.

I know the ins and outs of my disease and the medicine that works against it. I know my doctor’s name, first and last, and he doesn’t treat me like an idiot, which I appreciate. He knows the science, the biology, and the standard procedures for individuals like me.

But there is little acknowledgment that the questionnaires still reflect an increasingly blue mental state here and there, the lack of sleep, and the inability to focus at work, sometimes for days. But he still looks at me with his soft grin and a glow of happiness that he did it. He controlled my disease*.* The control I am grateful for. But it is not the same control that governs my life, thoughts, feelings, aspirations, energy, and strength.

They are two separate realities that, like me, leave many patients feeling adrift from wellness. Control is valuable and essential, but it must be treated as the beginning, not the end, of feeling well.

The immune system is arguably one of the most impressive systems in the human body, able to identify foreign invaders and destroy them while leaving the “self” alone. Its success depends on its ability to determine what belongs to the self in the first place: the cells and tissues that belong to the human it operates within, and the larger picture of organs, muscles, and nerves. Early immunologists considered this distinction so fundamental that an immune attack against the self appeared biologically impossible.

But the discovery of autoimmune diseases bulldozed that thinking and revealed an even more complex system of protection, one that is not inherent but constantly learning, tolerating, and fighting against self-destruction.

Impossible!

The immune system is built to protect the body from foreign invaders, pathogens, and cells that shouldn’t be there by seeking them out and destroying them, like the body’s greatest fleet of military missiles. Autoimmune disease begins when these missiles are turned inward to the self, and medicine has no simple switch to turn them away.

Patients today with rheumatoid arthritis (RA), systemic lupus erythematosus, and multiple sclerosis (MS), among others, frequently describe their diseases to the layperson as a result of their immune system mistakenly attacking their disease’s bodily structure of choice. In RA, the damage primarily affects the joints, although the disease can involve other organs. Lupus can affect nearly any part of the body, while MS damages structures within the central nervous system.

If I were to travel back in time with this same explanation and go to immunologists of the early 20th century, telling them my immune system is attacking myself, there’s a good chance I wouldn’t be believed. Why? In the early 20th century, scientists could not fathom that the immune system was capable of anything other than protecting the body in which it lived.

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A 20th Century House of Horrors

At the time, the immunology dogma was that the immune system was so innately fine-tuned to protect the body that it was impossible to think it could cause any harm to the self. This understanding was called ”horror autotoxicus,” a term coined by Paul Ehrlich. Ehrlich was a German-born scientist and physician who worked in the fields of hematology, antimicrobial chemotherapy, and immunology.

He came up with the term “horror autotoxicus,” the horror of self-toxicity, in 1906 in response to some scientists postulating the existence of autoimmune diseases. Ehrlich believed it went against nature for the body to cause self-injury. To prove this, Ehrlich and his assistant conducted experiments with animals, such as goats, injecting blood from a different animal or from the same animal into one animal and observing how the immune system would react. The result was that if an animal had been injected with blood from a different species, antibodies would swarm and attack those cells. Conversely, if they had been injected with the blood of the same animal, Ehrlich noted no change.

This experiment reinforced Ehrlich’s belief in the impossibility of the immune system attacking healthy cells, because why would it? It had no reason to. In Ehrlich’s book “Collected Studies on Immunity,” he wrote, “the organism possesses certain contrivances by means of which the immunity reaction, so easily produced by all kinds of cells, is prevented from acting against the organism’s own elements and so give rise to autotoxins.”

Just two years after he published that statement, Ehrlich shared the 1908 Nobel Prize in Physiology and Medicine with Élie Metchnikoff for their work on immunity.

Although Ehrlich had become one of immunology’s leading scientists and proposed the mechanics that govern antibody responses against foreign cells, Ehrlich had overestimated the reliability of these mechanics. But because of Ehrlich’s authority on the matter, it would take decades for the mechanics of autoimmune disease to be accepted, even with mounting evidence.

Autoimmunity without Autoimmune Disease

The mounting evidence came from some scientists who were discovering the very thing Ehrlich said was against nature. Just a few years before Ehrlich received praise for the biological safeguards that prevent antibodies from attacking one’s own cells, two scientists had discovered the opposite.

Julius Donath and Karl Landsteiner, two Austrian-born physicians, began studying a rare blood condition, later named paroxysmal cold hemoglobinuria (PCH). Patients presented with extreme red blood cell destruction and dark urine after being exposed to cold temperatures. Upon further investigation, Donath and Landsteiner found antibodies that bound to the red blood cells of these patients and destroyed them when the body was warmed back up.

PCH today is understood as a very rare form of autoimmune anemia, and one of the first known autoimmune diseases thanks to the Austrian physicians.

Across Asia, a similar discovery was unfolding in Japan. Dr. Hakaru Hashimoto had just graduated from medical school in Imperial Japan and, while studying thyroid tissue extracted from four thyroid glands of middle-aged women, noticed an unusual pattern. Each gland showed dense lymphocytic infiltration (white blood cells) and cellular degeneration of normal thyroid cells. In 1912, Hashimoto published his findings in a German medical journal, marking a landmark in the recognition of thyroid disease that would later be called Hashimoto’s disease. But the connection to the immune system was still missing.

Proof Against the Self

The 1950s were among the most decisive decades in the recognition of autoimmune disease. When it was still loosely recognized, scientists around the world were working to prove that the immune system was, in fact, attacking the body’s own cells in various experiments. Doctors Ernest Witebsky and Noel Rose started with rabbits. In 1956, Witebsky and Rose injected rabbits with thyroglobulin, a protein produced by the thyroid, to determine whether the rabbits would mount an immune response. They had already seen foreign thyroglobulin induce an immune response, so what would happen if the rabbit’s own thyroglobulin was injected?

The answer: an autoimmune response. The rabbits’ thyroids exhibited significant inflammation and tissue damage upon examination, and Witebsky and Rose continued even further. They tested human blood samples from patients with Hashimoto’s, looking for thyroglobulin-specific antibodies. They were found. Rose later recalled Whitebsky telling him, “You have fulfilled the postulates and proven that a human disease can be caused by autoimmunity.”

Meanwhile, Doctors Deborah Doniach and Ivan Roitt would produce complementary evidence with Hashimoto’s antibodies in patients with the condition. Alongside their own published research and the animal studies, the existence of autoimmunity was becoming clear. It was no longer an impossibility that the body could turn on itself, but it was scientifically provable. What was missing was the mechanisms.

Learning “Self”

What followed these scientific landmarks was decades of research into how the immune system knows not to attack the self, and what happens when that knowledge goes astray. The answer is not that the immune system automatically knows not to unleash havoc on the self (much like Ehrlich thought), but that it tolerates the self, a learned tolerance that requires multiple layers of security.

The immune system has layers of tolerance that prevent B and T cells from going AWOL and attacking self tissues. Central tolerance acts as a screening or exam for these cells. T cells undergo this screening in the thymus, while B cells are screened primarily in the bone marrow. Their receptors are partly generated at random, causing some cells to have a stronger reactivity to self than others. Cells that react too strongly undergo cell death or inactivity, and in the case of B cells, receptor editing to lessen self-reactivity. It is the first, and toughest, act of security for these cells before they’re released into the bloodstream.

What happens next is a long line of regulations constantly keeping the cells in check. Peripheral tolerance partly relies on regulatory immune cells (T-Regs) performing safety checks on other immune cells, ensuring they remain inactive or are suppressed in their responses. If those immune cells are found to be self-reactive, they are sent calming signals, or told to initiate cell death.

The prevention of autoimmune disease depends on overlapping systems of immune tolerance that monitor self-reactive cells throughout their development and after they enter circulation. This system, like a set of locks with specific keys, is meant to work down a chain of commands, signals, and ordered tasks. But what happens when something is unlocked, and you lose the key, leaving you unable to lock the mechanism back into safety?

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A Perfect Immunological Storm

The safety mechanisms that are supposed to keep the immune system a servant to the self have been uncovered and scrutinized with a fine-tooth comb, winning both the 1960 and 2025 Nobel Prizes and piecing together groundbreaking insights into how these systems contribute to autoimmune diseases.

All the science has led to the understanding that autoimmune diseases, no matter how they work mechanically because of these haywire systems, do not stem from a single cause. What has sent scientists down a rabbit hole for decades is the search for all the possible contributions that cause immune cells to turn on the self.

Combinations of triggers range from genetic susceptibility and infections to environmental exposures and disruptions of the gut microbiome, like different picks that can test different locks in the immune tolerance system.

The House Still Standing

Understanding, after over a century, the mechanisms by which the immune system turns on the self only goes so far. It still raises questions about why cells decide to attack an RA patient’s joints, versus an MS patient’s nerves, or a lupus patient’s kidneys, and why in that moment they chose to do so.

Knowing as much as we do, it feels as if we’re on the precipice of understanding, or solving, the immune system’s horror of itself, just barely able to reach out and tangibly grasp the underlying explanation for why a disease affects one person, organ, or stage of life.

There is much to be discovered. Ehrlich’s “horror autotoxicus” was not wrong. It still stands as the template for proper safeguards: what the immune system is supposed to do to avoid self-destruction. But those safeguards are not incontrovertible law. The immune system was never incapable of attacking us; it’s only learning every day not to.

Women experience higher rates of non-fatal chronic pain, autoimmune diseases, mental health conditions, and seek out healthcare services more, compared to men. Women arguably suffer more, and yet, are diagnosed less.

The barrier? Modern medicine was built by studying men, using men as the blueprint for physiology, and dangerously assuming that most scientific findings applied to women’s biology.

That arcane system affects millions of women when it comes to diagnosis, treatment, preventative and long-term care. It is a system that did not form overnight and has deep roots so tangled that the progression of modern medicine’s inclusivity toward women feels like a pity invite after we’re told we’re complaining too much.

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This Is a Man’s World

Imagine being handed a T-shirt that you need from a T-shirt salesman. You slip it over your head, and it completely swallows you in fabric.

“This doesn’t fit,” you say.

“Well, it fits everyone else. It’s all we have,” says the salesman. You’re left to figure out how to make it work on your own.

This is what happens in modern medicine, except not with T-shirts.

When a woman seeks medical treatment, more often than not, she encounters the age-old problem of sexism, maybe without even realizing it. In the pursuit of a remedy for pain, women are met with more skepticism about the severity, and even the existence of their pain, to begin with.

Say the skepticism is set aside; identifying the problem, or reaching a diagnosis, may not even happen at all because of female biology and the unfortunate “unknown” healthcare providers find themselves in when a woman presents a set of symptoms that are “off” compared to standard. The standard? A man’s symptoms.

A study conducted by the Journal of the American Heart Association found that women visiting the emergency room presenting symptoms of chest pain are more likely to experience longer wait times for heart attack assessments and are less likely to receive proper coronary medications in case of heart issues. The diagnosis and treatment of something as possibly fatal as a heart attack are amiss for women, due to how women present heart attack symptoms and how some healthcare providers think those symptoms aren’t heart attack-related at all.

And maybe a woman presents a set of symptoms with little standard at all, like predominantly female-affected autoimmune diseases, only to be given the run-around on exactly what she is suffering from because whatever it is doesn’t affect men, leaving little-to-no research to reference.

This is not because of secretly harbored malicious intentions by healthcare providers, nor is it due to isolated failures in women’s healthcare. It’s proof of something much older.

The Boy’s Club of Medicine

Men were considered “the standard” of physical perfection and ideals long before the words “chronic illness” were even uttered. The Ancient Greeks believed that women were less-than versions of men, or “deformed,” according to Aristotle in his work “Generation of Animals.”

Male physicians in ancient times, who began to dominate a once female stronghold of medical practice, so drastically separated men and women biologically that it seemed every ailment a woman encountered could only be solved by marriage or pregnancy. Female autonomy began to decline thousands of years ago, and the male-centric lens in medical study and practice only grew.

Andreas Vesalius, the “Founder of Modern Human Anatomy,” wrote one of the most famous and most referenced anatomical texts in history. It became the very basis of human anatomy. Vesalius wrote in extreme detail about the inner workings of human bodies, defying long-held anatomical beliefs, only possible due to his devotion to the dissection of male human cadavers. Although Vesalius improved anatomical science, his studies lacked detailed, fully accurate depictions of female anatomy.

By the Middle Ages and the rise of the Catholic Church, the education of women in medicine sharply fell. It became widely believed that women were biologically unable to practice medicine, and if they did, they were blamed for witchcraft. From the 13th to the 18th centuries, men took over all medical roles, including physicians, surgeons, and even midwives.

One Harvard Medical School professor stated that women who went through medical school would be left with “monstrous brains and puny bodies,” while American physician Horatio Storer thought menstruation caused “temporary insanity.”

Female anatomy was on the outs, and soon, so would be clinical trial inclusion.

Women Need Not Apply!

The thalidomide incident: an incident that arguably set female inclusion in the clinical landscape back decades.

Thalidomide was a drug widely prescribed in the 50s and 60s for the treatment of nausea in pregnant women. But when those pregnancies ended, the results were thousands of babies left with severe birth defects and a ban on the drug by multiple countries. It was a clinical explosion, leaving a mess for researchers and the FDA to clean up.

In a drastic response, in 1977, the FDA passed a policy recommending that women of childbearing age, 15 to 49, be excluded from Phase I and Phase II of clinical drug trials. It came across as the FDA doing women a favor, protecting them from harming themselves and their future children. The policy went as far as to also recommend that any woman who uses contraception, is single, or has a vasectomized husband be excluded as well. The result? Over half the population was excluded from the positive and negative effects of most medicine, and left subject to the unknown and indifferent treatment of medical professionals.

This historical turning point left innovative pharmacological pipelines skewed toward male biology, and the efficacy of drugs through a predominantly male lens. It didn’t matter that women were underrepresented or left out entirely; if a drug worked for men, surely it must work for women. It wasn’t until 1985 that the National Institutes of Health (NIH) published a policy that encouraged researchers to include women in clinical studies. But encouragement is far from a requirement.

By the early 90s, investigations into how well this policy was being upheld uncovered that clinical research had moved the needle very little in the analysis of study results by sex. The policy had barely even been acknowledged. Finally, in 1993, the NIH inclusion policy became federal law through a section in the NIH Revitalization Act of 1993. The “Women and Minorities as Subjects in Clinical Research” law mandates that women and minorities are included in all clinical research, among other requirements. But inclusion still does not mean equality. And equality arguably determines exactly how a drug affects men and women, and whether the difference is biologically beneficial or harmful.

One Size Does Not Fit All

Why does sex matter medically? If there was one thing the Ancient Greeks and Andreas Vesalius got right, it was that men and women are anatomically different, with differently shaped bones and even different reproductive organs. They acknowledged this. But did not apply it practically in science.

But in the modern medical landscape, the differences between men and women are of the utmost practical importance due to complex physiological differences. Hormones and genetics are two of the biggest differences, going as far as making women more susceptible to immune-related conditions and other diseases, compared to men.

And once a woman has disease symptoms, the clear path to diagnosis becomes foggy because she presents differently to doctors. Heart attacks, autoimmune diseases, mental health conditions, among others, can present differently in women. Recognition and diagnosis become a guessing game because clinicians expect a “typical” presentation, the presentation found in men. If symptoms are addressed, women even metabolize drugs differently than men, leaving another variable to be cautious of.

These biological differences, however important, do not mean one body is more important than the other. They also should not mean that one body as a textbook example should stand for every body thereafter.

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Stuck in the Past

As a woman attending a doctor’s appointment, it is not an unfamiliar experience to feel like a specimen in a jar for spectating. You may not fit “the usual” or the textbook example of symptoms and diagnosis. Instead, it’s left up to observation, which in turn can mean more harm than good.

You bounce between specialists and clinicians, hoping maybe they’ll take you out of the jar instead of just looking at you through the glass. Otherwise, symptoms come down to psychosomatic conditions, or the “condition” of being a woman. “Tough luck, you’re a woman,” they say, like it’s its own diagnosis. It has been, for thousands of years.

Any progress or treatment always comes with the grim realization that the medicine you take may not even work right, simply because of your biology that was haphazardly considered.

For many women, navigating healthcare still means wondering whether the problem is their body, or whether medicine simply wasn’t built with their body in mind. Collecting lab work, printouts of previous clinical charts and health history, previous prescription lists, and a barrage of questions feels less like getting the care you deserve, and more like being your own doctor.

Progress, Not Perfection

Progress has not been lost entirely. Although such an outdated system still stands, moves to chip away at it have been made. This year, a study was released highlighting higher rates of women’s inclusion in clinical drug trials for drugs that were eventually approved by the FDA. The study was especially promising for women’s inclusion in oncology drug trials, yet lacking in autoimmune and cardiovascular disease drug trial inclusion.

Sophie Zaaijer, the researcher behind the study, recently spoke at UC Irvine School of Medicine and challenged this movement of inclusion to keep moving forward. “Counting women in clinical trials is important, but we also need research methods and reporting standards designed to understand how women experience disease, treatment response, and toxicity,” said Zaaijer in an interview with UC Irvine School of Medicine.

As Zaaijer asserts, the progress can’t stop at just counting women and calling it a day. It also does not erase the history that brought us here. The American healthcare system dug a deep hole with very few ways out for women to receive “standard” care, beginning with the standard set against their biology that ripples into how they receive treatment, how the treatment affects them, and their outlook on their health.

The goal isn’t to replace one default with another; it’s to build a system that recognizes human biology as more than a single standard. It is not about treating everyone the same either. It is about recognizing individuality and complexity, beginning with biology, and using science to shape care onward.

Bryan Johnson, a pioneer in the biohacking space attempting to wind back the clock on his age and optimize his health, has been recently diagnosed with autoimmune gastritis. The more you think about that sentence, the more it smacks you with an ironic scientific truth: you can’t “out-hack” your immune system.

Johnson was not the first person to try to outrun disease by optimizing his health to the nth degree. You’ve seen it across micro chasms of the health and wellness industry, each with its own pole of extremism for “physical perfection.” From Arnold Schwarzenegger and bodybuilding to Liver King (whose name also happens to be Brian Johnson) and the consumption of raw meat. The extremism seems to plume larger and larger with each health optimization trend, as health figures and “influencers” attempt to outdo each other for what will actually save you from succumbing to disease. What will actually help you live longer?

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Johnson shot to the front of mainstream health optimization, not because he was relatable and offered average, replicable, and sound advice, but because of his extreme approach to longevity, doable only because of his tax bracket. With money as the catalyst for his extremism, driving his biohacking routine as an untouchable lifestyle, it simultaneously made him a science experiment that had the whole world watching.

“Protocol DON’T DIE” quickly gained recognition as both a genuine study into anti-aging efforts and a spectacle leaving viewers gobsmacked at just how a millionaire could spend his money. Because why is a 48-year-old man trying to reverse his age to nearly prepubescent?

Johnson describes the protocol as something he and his team have spent years and millions of dollars “researching, experimenting and measuring,” while labeling himself as “the most biologically measured person ever.” This viral human lab-rat protocol assesses whether you can change your biomarkers and increase your longevity. The biomarkers in question range from muscle and fat percentages, heart rate, sexual function and fertility, to sleep, grip strength, and blood glucose levels.

To be fair, Johnson generally framed Blueprint as an attempt to reduce disease risk and slow biological aging. Caring about such a laundry list of biomarkers is not futile. It provides a big-picture view of your health, stitched together by examining all the tiny working parts that cascade into physiological order. But it is not a guarantee against illness, even if his public image has inevitably become one of someone pursuing near-total physiological control. If measuring and altering such biomarkers were free and accessible, I could only imagine what state of health we’d all be in, and the disease and illness the majority of the population would be able to outlast.

To alter the markers of a chronologically 48-year-old man, Johnson rigidly subscribes to the “Blueprint Protocol,” another of his multimillion-dollar inventions, which outlines a strict no-red-meat diet, an intense exercise regimen, a precise sleep schedule, and even a hair, skin, and oral health system. While Johnson prescribes this blueprint, and a baseline of his own biomarkers and written advice, for free to his followers or the genuinely curious, Johnson’s level of optimization reaches far beyond a good grocery list and a gym membership.

Beyond a vast marketplace of Johnson’s branded supplements, nutrition aids, and personal care items, his dedication to peak physical perfection runs deep. Pockets deep. With millionaire money comes millionaire spending, so far out of reach for the rest of us. On top of the aforementioned “Blueprint Protocol,” Johnson bounces around a select list of “other advanced therapies,” therapies that perhaps fanned the flames of his notoriety in the last few years.

Mesenchymal Stem Cells (MSCs), gene therapy, cerebrolysin injections, and hyperbaric oxygen therapy (HBOT) are anything but cheap or easily accessible to the average health nut, but are crucial systems in Johnson’s biohacking and age-reversal quest. His use of these systems creates an unbridgeable gap between Johnson and his devoted followers, positioning him as the most radical biohacker to date who cannot be completely copied.

But just what exactly does radicalism get you? Johnson’s regimen may have improved many aspects of his health. Better cardio vascular fitness, metabolic health, and sleep and wake windows are all worthwhile goals. Add in news outlet coverage and a reported biological age of 18, and you have a success story.

After years, millions of dollars spent, lots of press, and a high-fashion runway appearance, Johnson claims to feel the best he’s ever felt, and, scientifically, the healthiest and most optimized. His new diagnosis does not erase those successes. Instead, it highlights a different reality: optimizing and “out-hacking” measurable health markers doesn’t necessarily prevent diseases rooted in immune function.

Most diseases that dominate conversations around longevity have clear lifestyle components. Take heart disease, for example. The number one cause of death of Americans is strongly rooted in lifestyle and adopted behaviors: diet, exercise, sleep, smoking, and alcohol use. Health optimization makes intuitive sense in this case because conditions like these are influenced by the choices we make over the course of our lives. But autoimmune diseases operate under a different set of biological rules.

Rather than arising from lifestyle-influenced organ damage or excess fat, autoimmune diseases begin when the immune system mistakes healthy tissues for something that shouldn’t be there. Why this happens remains layered in complexity in the world of immunology. There are genetic factors, possible environmental triggers, and infection-related alterations in immune signaling. In most cases, there isn’t a single behavior that causes an autoimmune disease, or one that guarantees it can be prevented. Supporting the immune system is not the same thing as controlling it.

Against that backdrop, Johnson’s diagnosis becomes less surprising than it first appears. If autoimmune disease is governed by a complex interplay of genetics, immune regulation, hormones, and environmental triggers, then even the world’s most meticulously optimized biomarkers cannot eliminate every possibility.

“My stomach is eating itself,” Johnson said in an X status post, post-news-break of his autoimmune gastritis (AIG) diagnosis. The rare disease, affecting an estimated 4% of people worldwide, characterized by the immune system attacking the cells of the stomach lining, recently befell Johnson but failed to break his biohacking spirit.

“I am going to try and solve it,” he posted in his announcement, along with a peek into his lifestyle, his previous iron deficiency, and the sugary, processed-food health habits he endured as a kid; theories of his as to why the disease sprang up. Perhaps the biggest working theory into Johnson’s new diagnosis was his history with autoimmune thyroiditis, something he also believes to be a key driver of this new condition.

Johnson’s view of his newfound health situation is not one of despair. Quite the opposite. His bound and determined nature, with a side of making a point to his followers, lifts out of his status update in the couple of hundred words he wrote. “My team and I are going to try and solve my AIG,” he wrote. It is simultaneously that Johnson warns his followers, “Had I not taken care of my health during the past five years, my situation could potentially be very serious. You too may have a lurking health issue that is undiagnosed and could increase in severity from unhealthy life choices, without your knowing. The absence of symptoms is not the presence of health.”

Whether autoimmune disease can ultimately be "solved" remains an open scientific question. For now, medicine focuses largely on managing disease rather than curing it. Even if Johnson never intended his millionaire lifestyle and Blueprint protocol to be fully replicable, his public persona has become symbolic of a broader belief: with enough data, discipline, and resources, we can dramatically increase control over our biology.

Autoimmune disease reminds us there are still limits to that control.

Perhaps that is the real lesson from Johnson’s diagnosis. It doesn’t mean health optimization is pointless; correcting bad lifestyle habits and undertaking preventative care undeniably matter. But it does remind us that biology has limits we cannot negotiate with. We can influence our health, sometimes profoundly, to the point where we’re biologically 18. We cannot engineer away every uncertainty.

Autoimmune diseases, no matter how abundant they may be, exist more in the world of women. In fact, the subset of chronic conditions is so skewed toward women that in the US, 4 out of 5 people affected by autoimmune disease are women.

In a frenzy to explain why this statistic exists, science has identified one key characteristic: hormones. Although the human immune system does not discriminate by gender and the possibility of most diseases, the complexity lies in how the immune system tangoes with sex hormones, influencing its behavior in ways that may increase autoimmune susceptibility, especially if you’re genetically predisposed.

The complexity can’t concretely explain every unique diagnosis, but it helps shed light on the question: Why women?

Adam and Eve, If Eve Had an Autoimmune Disease

Yes, men and women are created equal with regard to the presence of hormones. Both men and women have the same three sex hormones: estrogen, progesterone, and testosterone. These chemical messengers, responsible for reproduction, sexual function, and physical characteristics (hello, body hair!), circulate in men and women but differ in concentration.

Men produce higher levels of testosterone while women produce higher levels of estrogen, both stemming from gender-specific sex organs. When you hear the words “sex hormones,” your mind may go straight to the process of reproduction, or, if you’re a woman, you may think about when Aunt Flow is supposed to visit this month. But if you think these things are all that hormones are fit for, think again. Besides babies and body hair, sex hormones are in constant conversation with the immune system. It’s this communication that leaves women tangled in the prospect of developing an autoimmune disease.

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Ring Ring Hormones! It’s Your Immune Cells Calling!

The immune system is composed of a network of cells, such as B-cells, antibody factories; T-cells, the attackers; macrophages, the eaters of pathogens; and dendritic cells, the presenters of pathogens to other immune cells. Each of these cells has receptors, or lines of communication, for sex hormones. As your hormones circulate, they check in with your immune cells and hand off instructions for immune cell behavior and inflammatory responses.

As a woman, your estrogen is a highly influential factor in communication with your immune cells. The instructions that your estrogen hands off to your immune cells can change depending on how much estrogen you have, called a “dose-dependent” effect. Estrogen doesn’t always stimulate the immune system. Instead, it changes immune behavior depending on its concentration, the immune cells involved, and the stage of life. Depending on its concentration, estrogen can boost your immune cells, helping your B-cells and T-cells identify and attack pathogens more effectively. But there’s a catch.

When estrogen is high, although it is intended to be helpful, these levels may increase certain immune responses to the point where immune cells go into overdrive. When looking at autoimmune diseases, the immune system, no matter the disease, has been programmed to go overboard with response and attack bodily tissues. The link between this overdrive and estrogen is a link that science considers for why women are disproportionately affected by autoimmune disease.

In some people, estrogen appears to amplify immune pathways involved in antibody production and inflammation. If someone is already genetically susceptible to autoimmune disease, these hormonal signals may help tip the balance toward an immune system that begins recognizing the body’s own tissues as threats. In the presence of high estrogen, the body’s capabilities to stop auto-reactive immune cells become less effective, leaving the immune cells to mistakenly do unending damage. Unlike in women, researchers believe testosterone generally has more immunosuppressive effects, which may contribute to lower autoimmune disease rates in men.

Although the average age of an autoimmune disease diagnosis for a woman varies significantly across different diseases, there are possible reasons to believe that key ages in women’s lives contribute to when autoimmune disease diagnoses happen most.

Give Life, Get Sick

During pregnancy, a woman’s estrogen levels skyrocket to the highest levels that a woman will have throughout her entire lifetime. In this instance, not every autoimmune disease behaves the same.

In a fascinating scientific occurrence, some women’s bodies, surging with excess estrogen, do not go into hyperactive autoimmune chaos. Instead, their bodies will actually shift from a pro-inflammatory response to an anti-inflammatory response, focusing on tolerating and protecting the developing fetus. If a woman already has an autoimmune condition, such as rheumatoid arthritis (RA), she may actually go into remission. But if a woman has systemic lupus erythematosus (SLE), she may experience more pain and inflammation due to high antibody activity, in part because estrogen influences antibody-producing immune cells and immune signaling. It all depends on the woman, making estrogen’s dance with the immune system even more confounding.

But it’s what happens after pregnancy that can unleash havoc. In postpartum, estrogen levels plummet to low levels, often referred to as an “estrogen crash.” Research shows that the risk of developing several autoimmune diseases is highest in the first three years post partum. The state of immune tolerance and harmony that exists before a baby is born can quickly fall apart. Immune activity can rebound and trigger the onset of an autoimmune disease that a woman has never even thought possible to have.

And if women escape pregnancy and postpartum unscathed by a lurking autoimmune condition, there’s unfortunately still time.

Aging Problematically, Not Gracefully

After pregnancy, estrogen levels eventually level back out. But then you hit your 40s and 50s, and your estrogen levels drastically dip once again when the ovaries stop consistently producing estrogen. While research is still developing on how diminishing estrogen levels affect the development and occurrence of autoimmune diseases, there is an observed association between low estrogen levels and the onset or progression of rheumatic autoimmune diseases, like RA and lupus, in this age range.

Could this be why many autoimmune disease diagnoses range from 30 to 60? It’s a strong possibility. And yet, across a woman’s lifespan, with the ebbing and flowing of estrogen levels, a surprise autoimmune diagnosis can pop up, even when timing isn’t hormonally distinct. For myself, it doesn’t completely explain why I was diagnosed with RA at 21. In understanding why you’ve been struck down with a lifelong immune condition as a woman, it’s not just that the switch was flipped; your genetic code is mutated, or another sickness triggered it. There is a lot to consider, from just the standpoint of a woman’s biology. It begs science and researchers to keep attempting to untangle this web that seems to shapeshift as a woman ages.

Too often, a woman walks into a doctor’s office with a long list of symptoms and a high rating of pain, but walks out after hearing the same few blanket statements. “It’s just stress.” “You’re probably just depressed.” “It’s probably your anxiety.” Throughout history, women have been ignored, dismissed, or gaslit medically for nearly every medical ailment they’ve experienced. It didn’t matter the symptoms, the pain, or the gut feeling that something was very wrong. All roads of dismissal of women in clinical settings often led back to one thing: that any medical concern was imagined or all in the woman’s head.

Roads as far back as the ancient Greeks documented how a woman’s biological differences made her more prone to hysteria than men. Throughout his career, famed psychoanalyst Sigmund Freud perpetuated hysteria as a mental condition more likely to affect women. It wasn’t until 1980 that “hysteria neurosis” was removed from the Diagnostic and Statistical Manual of Mental Disorders (DSM), a mere 46 years ago. And while that seems like a very old-fashioned way of thinking, unsurprisingly, for women, even in the 21st century, they are still placed into a “hysterics” box in the desperate attempts to address their health, especially with chronic illness.

You’re Being Dramatic

The road to dismissal begins before a doctor even lays eyes on a female patient. Even in our impressive modern age, equality in a hospital waiting room eludes men and women. Not only do women often wait longer to be seen by a doctor, but according to the Proceedings of the National Academy of Sciences in a 2024 report, women’s pain is perceived to be less intense than a man’s. The unfortunate reason for this perception is the “gender-pain exaggeration bias,” or the belief that women are exaggerating their reported pain, notably in chronic pain reports. Even if a woman reports the same number on a pain scale of one to ten as a man, their scores are more likely to be judged as lower. The root of this bias? The long-held historical belief that women are just too dramatic, emotional, or hysterical.

Remember the Greeks? It’s fair to point a finger at ancient Greek physicians for cementing the dismissal of women in medical settings, even thousands of years later. After all, the word “hysteria” is derived from the Greek word “hystera” or “uterus,” going back to the Greeks’ belief that women were naturally more neurotic simply because of their reproductive organs.

By the 19th century, hysteria was an undefeatable, catch-all diagnosis for women experiencing any type of physical pain or mental distress. Women were often diagnosed with hysteria as a disease of the mind, no matter their symptoms, and were subjected to harsh and isolating treatments, such as being locked away in an attic, thrown into an asylum, or undergoing forced surgery on various bodily systems.

By the 20th century, hysteria was thought to affect any part of the body and cause an array of symptoms. The harsh focus began to shift away from just women, as the World Wars raised the observation of men experiencing hysteria and mental disorders brought on by severe trauma. But even as the focus shifted, bias against women remained entrenched, too far ahead for equality to catch up, even today.

In it for the Long, Unnecessary Haul

Imagine you rush to the hospital with symptoms of a heart attack. When you finally see a doctor, instead of performing careful, necessary tests to ensure a positive, healthy outcome, the doctor says your symptoms aren’t “heart-related.” And you’re sent on your less-than merry way. This was the experience of more than half of the women engaged in a study back in 2018. Less than half of the men in the study experienced the same dismissal.

As of 2024, a report detailed that women are more likely to receive a misdiagnosis, as well as hold the fear of being misdiagnosed when receiving medical care. This only adds to women’s overall distrust and avoidance of doctors and healthcare providers. But in the desperation for answers for why you feel crappy, sometimes you don’t have a choice. Unfortunately, that doesn’t mean you’ll reach an immediate answer.

Not only are medical research and previous clinical trials dominated by male representation, but even diagnostic criteria for various chronic illnesses are based on how symptoms present in men. Only in the last few decades has the National Institute of Health (NIH) mandated that women and minority groups be well represented in clinical research and clinical trials. Because of this gap that is only just now being attempted to be closed, women reaching a swift and accurate diagnosis is a rare experience. In a recent study, researchers examined time-to-diagnosis and diagnostic delays in men and women and found that women take significantly longer to receive a formal diagnosis, even when symptoms are the same in each gender.

What happens during this delay is disease progression, irreversible damage, and mental deterioration, three things that make the search for answers ultimately exhausting.

Chronic conditions such as heart disease, the number one killer of women in the United States, endometriosis, and varying autoimmune diseases are some of the worst offenders for misdiagnosis and diagnostic delays in women. Take renowned author and journalist Meghan O’Rourke’s experience on medical gaslighting and the long road to diagnosis. In her memoir, The Invisible Kingdom: Reimagining Chronic Illness, O’Rourke details the harrowing, over-a-decade-long journey to reach not just one, but three chronic illness diagnoses, including autoimmune thyroiditis. Like many women, O’Rourke was thrust into becoming her own medical researcher, turned over every option she could think of, and spoke with almost any kind of doctor or specialist that would listen.

Like O’Rourke, women are consistently brushed aside or labeled as “normal” in their experience. They just need to “rest more,” or “wait for things to pass.” But when you hear this repeatedly and nothing changes, what then? “Maybe I am just being dramatic,” we all say woefully.

More often than not, many women take their troubles elsewhere, hoping their experiences will not fall on another set of deaf ears. Second opinions and specialists are a common part of a woman’s investigation into the mysteries of her health. Women and those with a chronic condition are more likely to seek a second opinion compared to other demographics. But the outcome of the second opinions is a slippery slope. If a diagnosis is not reached, then a woman is put right back at square one. If a diagnosis different than the first is reached, treatment, resources, insurance, and overall costs could change significantly. Not to mention the confusion and mental toll of differing conclusions.

As the medical landscape is slowly being rebuilt around the mandate to not only include women, but also consider them and their experiences as entirely separate from years of derogatory perceptions and “catch-all” diagnoses, the world of women’s pain demands to be recognized. Although the ancient Greeks fundamentally got it wrong, they were also painfully close to getting it right. Had they stopped at recognizing a woman’s biology as different from a man’s, instead of continuing on to label said biology as a “problem,” it is possible that in 2026, it wouldn’t take more than three doctors to acknowledge a woman’s pain.

As a patient, the American medical system feels like rolling the dice, blindfolded, unsure of which numbers are even the best numbers, when you walk in and out of a clinic or hospital. What follows is a unique anxiety that comes with opening a medical bill. But if you are chronically ill, that anxiety doesn’t happen once; it happens monthly.

It is unsurprising that most people are on the edge of their seats waiting for medical bills. That’s because the cost of healthcare far exceeds the average American’s income, with no signs of slowing down or meeting a rate of affordability. The United States spends around $4.9 trillion annually on total health care spending, encompassing doctor visits, hospital stays, and prescription drugs.

If you have a chronic illness, your spending makes up a whopping 90% of the U.S. healthcare costs, according to the Centers for Disease Control (CDC). Once diagnosed with a chronic illness, such as type 1 diabetes, heart disease, or cancer, it is as if you have signed up for a lifetime subscription to medical bills that are not so easily dealt with by a stable source of income.

Illness as an Inescapable System

Unlike a one-and-done emergency room visit, patients with chronic illness are required to revisit medical settings over long periods of time, leading to recurring expenses. In 2023, the average annual cost for a patient with a chronic illness was $6,032, five times the cost of those without a chronic illness.

If an individual with a complex disease or diseases needs specialized treatment, the number of obstacles and bills only grows. Types of providers or specialists can be costly, along with the travel time to get there, bills for routine bloodwork pour in, and specialized medications and refills add up over time. The cost of medications alone is dizzying, with U.S. prescription drug spending at $915 billion in 2025. In 2021, Americans spent $1,147 per year on prescription drugs. Throw in a chronic illness diagnosis, and the figure is likely higher. And when you hone in on individuals diagnosed with an autoimmune disease, a subset of chronic diseases, affording treatment is priced as a luxury.

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Autoimmune Disease: A Luxury Item

Over 50 million Americans have an autoimmune disease, a chronic, lifelong disease characterized by the immune system attacking the body’s own tissues. Patients with diseases such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and multiple sclerosis (MS) cost the American healthcare system an estimated $100 billion dollars each year. As autoimmune diseases rapidly rise in the U.S., the cost will surely follow.

But reaching an autoimmune diagnosis is not incredibly straightforward or inexpensive. For some patients, it can take months, even years, to come to a definite autoimmune diagnosis. Rounds upon rounds of bloodwork and imaging scans are often necessary, but only at the discretion of a doctor who believes a patient’s experience. Depending on diagnosis, total costs can significantly skyrocket.

These costs contain one of the most important and unavoidable costs of living with an autoimmune disease: treatment costs. Autoimmune disease treatments, such as disease-modifying antirheumatic drugs (DMARDs) and biologics, are significantly more expensive than average drug costs in the U.S., with biologics among the most expensive.

Biologics, such as injections or infusions, are complex drugs made of living cells, requiring advanced technology and manufacturing that significantly spike costs for consumers who need them. Biologics for certain arthritic diseases can cost anywhere between $10,000 and $30,000 per year, a price to be paid for the millions of dollars spent in research, testing, and development of the drug.

And once a patient no longer responds to a drug, they are forced to jump ship to a new, possibly more expensive drug, just to get their symptoms back under control. The cycle of medical bills never stops, while a patient is left to navigate insurance premium nightmares and jump through the hoops of specialty pharmacies to hopefully get their medication delivered on time. If it sounds exhausting to manage, imagine how exhausting it is to keep up with work to afford treating your disease, if you can even keep up at all.

Ghost Costs

Some of the most expensive parts of chronic illness never appear on a medical invoice. Yet, they collect over time through sick days, low energy and productivity, and your emotional bandwidth is stretched thin. Before you even realize it, your paycheck that you desperately need to cover medical expenses begins to reflect these “ghost costs.”

It shouldn’t come as a shock that when you are sick, you are less productive or have called out of work entirely. For those without a chronic illness, an occasional sick day is no big deal. Time and money can be made up; productivity can be recovered. But patients with chronic illness find sick days to be less of a one-in-a-while occurrence, and more of a frequent necessity to take care of themselves. A 2016 study found that full-time employees are regularly absent from their jobs, costing their employers 28.2 million workdays annually, and $4.95 billion in lost income.

Another study found that an individual with a chronic illness can expect their earnings to drop by 12% at the time of their diagnosis, and increase to 18% long-term, due to work limitations. Combine the loss of wages and the rise in medical costs, and you get a nasty, highly prevalent case of medical debt amongst patients with chronic illness.

A poll conducted by the Patient Advocate Foundation’s Center for Patient Research found that one in three adults with a chronic illness has medical debt, as of 2025. The average amount of debt a patient with a chronic illness has, according to the poll, totaled at $3,480, with the majority coming from emergency care and hospital stays. It is an unfortunate and bitter truth that the accumulated debt for many chronic illness patients is nearly inescapable, as long as they have their disease. And for most, they always will.

Reminder! Payment Due Today…and Tomorrow…and the Day After…

The cost of healthcare in America has always been an unsightly can of worms that nobody wants to open or deal with. For patients with chronic illness, although they make up 90% of the medical spending in the U.S., the slow battles to address the costs and debt make way for a domino effect that only perpetuates the cycle further. Like me, patients worry about the cost of their medications, maybe even to the point of skipping them altogether. And suddenly, the cost of groceries seems more important than scheduling a routine doctor’s visit, knowing the bill that will come with it later. For millions of Americans, chronic illness is not just a diagnosis. It is a recurring charge. It trickles down into poor symptom management and poor disease outcomes, landing patients right back at square one of trying to find a solution.

This is the cycle that many with chronic illnesses will be trapped in for the rest of their lives, reducing them to a very important cog in the machine of the American healthcare system that keeps on going.

If Only a Nap Could Cure Me

Fatigue, a word loosely thrown around, used to describe many people’s everyday tiredness or sleepiness. Most average people will use the word to describe a poor night’s sleep or a tough workout. Although the word often loses its more complex, medical meaning through casual use, in chronic illness and autoimmune disease (AD) patients, the word is anything but casual. It is a word that describes a debilitating symptom that is rarely resolved.

Fatigue is the most commonly experienced symptom of a chronic illness, such as cancer, chronic obstructive pulmonary disease, and autoimmune diseases. In fact, those with a chronic illness experience more chronic fatigue compared to healthy subjects, according to one study.

The diagnostic criteria for myalgic encephalomyelitis, or chronic fatigue syndrome (CFS), include profound, extreme exhaustion that lasts for at least six months, with no improvement despite adequate rest or sleep. And although CFS was previously thought to be a “fake” or “made up” illness or symptom for many decades, it is extremely common, with over 3.3 million Americans diagnosed with CFS by medical professionals, according to the CDC.

With casual use of the word often comes casual proposed solutions, thought to easily cure one of the most debilitating symptoms of a chronic illness. If you stop taking a drug with fatigue as a side effect, rest up from a busy day or tough workout, or lounge in bed for a few extra hours, the problem of fatigue should be solved.

But for those with chronic illness or an AD, fatigue is a never-ending experience. Ask any chronic illness or AD patient, and they’ll tell you just how different fatigue feels from casual tiredness. More often than not, fatigue acts like a vampire that never stops draining your energy, severely impacting your productivity and the daily tasks that come easily to others. It doesn’t matter how many naps you take or how many days you call in sick. Fatigue is an all-consuming fog that is difficult to escape.

But what makes fatigue so different from just feeling behind on a few hours of sleep or tired from a long and busy day? There’s science to it, biology behind it, and it’s a lot more complex for chronic illness patients than you may think.

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Real, or Not Real?

Although a large percentage of the population experiences fatigue, it is not a highly studied subject. In fact, it has never been an easy task to measure fatigue. Fatigue can be both tangible and intangible, or examined in one of two ways: “The first is the diminution of muscular force. The second is fatigue as a sensation,” said Angelo Musso, an Italian physiologist, who over 100 years ago described fatigue as being seen in two ways, but only measured in one.

It’s as if fatigue is a two-headed beast. Except that one head can be studied in detail, and the other is highly figurative, almost imaginative. And to make measurement more difficult, fatigue is often self-reported by patients, leaving medical examination to rely on a sensation that cannot be seen, examined, or touched by a doctor.

While fatigue manifests like a ghostly medical presence, leaving healthcare professionals and scientists scratching their heads about its existence, there are still solid understandings of the biological mechanisms behind fatigue. Chronic illnesses are conditions characterized by persistent, often high levels of inflammation.

Scientists theorize and often attempt to measure that inflammation, resulting from the production of inflammatory proteins, could be a major contributor to fatigue. One study found that participants with multiple sclerosis (MS) who had chronic fatigue had higher levels of inflammatory proteins in circulation than healthy participants.

It is highly likely that immune dysfunction, which aids the presence of inflammatory proteins, is one root cause of chronic fatigue. It is no wonder that many patients with autoimmune diseases, victims of their own immune dysfunction, constantly feel like they are dragging themselves through freshly poured concrete.

But if you zoom in even closer, chronic fatigue is likely a ghastly byproduct of a breakdown in cell function. Persistent levels of inflammation can cause what’s called mitochondrial dysfunction, essentially when the “powerhouse” of the cell stops efficiently releasing ATP, or energy, that is essential for all bodily functions. This lack of energy throughout the body can contribute to the severe exhaustion and brain fog that patients with chronic illnesses know all too well. And it is this brain fog that is even more perplexing.

Bad Weather on the Brain

If, as a chronic illness patient, you’ve ever been unable to remember something, find your thought process extremely hazy, or struggle to focus on even the simplest of tasks, you have experienced what has been casually coined “brain fog.”

Many descriptions of brain fog mention not just these ailments, but also confusion, lack of concentration, and overall slow thinking. Although fog on the brain is one of the most recorded aspects of chronic fatigue, there is no distinct, concrete definition. This is because brain fog, much like fatigue, is often viewed as an intangible experience, rather than something that can be measured.

However, what scientists can measure are the cognitive processes that may contribute to a patient’s so-called “brain fog.” These processes, when impaired, can be strongly linked to fatigue’s brain-fog experience. One of the most well-studied cognitive impairments related to fatigue is cerebral blood flow (CBF), the delivery of oxygen and energy to the brain.

Many studies over decades have found that individuals with chronic fatigue have decreased CBF, which can contribute to brain fog through a lack of energy in the brain. Where there’s a lack of energy, there’s a lack of efficient, proper cognitive processes, such as concentration, memory recall, and more.

There’s a lot of discussion on the role inflammatory proteins play in the experience of brain fog in those with chronic fatigue and chronic illness. Neuroinflammation is commonly examined as a cause of brain fog, specifically through neuroimmune reactions.

Surrounding the brain is a layer of cells that acts as a protective blanket, or shield, guarding it against toxins, pathogens, and changes in the blood. This is known as the blood-brain barrier, or BBB. When you are exposed to prolonged, chronic inflammation due to a disease or condition, inflammatory proteins begin to seep through this barrier and enter the brain. Once inside brain tissue, the proteins can cause extensive damage and activate brain immune cells (microglia), leading to cognitive impairments closely associated with brain fog.

The “brain on fire,” or neuroinflammation, is an unfortunate casualty in the domino effect of chronic illness and severe inflammation levels. But it can look different from person-to-person.

What makes fatigue, and the measurement of brain fog, more complex is its case-by-case nature. Because some chronic illnesses and autoimmune diseases have episodic courses or are prone to “flares,” measuring the severity of fatigue across patient populations becomes difficult, especially when you throw other conditions into the mix.

“How Fatigued Are You?”

Although fatigue is now medically recognized as both a syndrome and a symptom that accompanies most, if not all, chronic illnesses, it is a complex experience and symptom that is highly variable amongst chronic illness patients. For example, some patients with chronic illness experience fatigue to varying degrees, depending on factors such as secondary conditions or symptoms already present.

Say, a rheumatoid arthritis (RA) patient experiences more severe fatigue due to also managing depressive symptoms, versus a lupus patient experiencing mild to moderate fatigue with no other present conditions or symptoms. While some autoimmune or chronic illness patient populations have varying percentages of fatigue, some studies have shown that MS patient populations experience high rates of fatigue, with over 80% reporting fatigue as the most common symptom of the disease.

Fatigue and brain fog, as its sinister sidekick, continue to be some of the most complex ailments of patients with chronic illnesses. There is a science behind it, a science that distinguishes fatigue and its exhausting effects from mere general sleepiness. Although understood, to a degree, there is still much about the two that is murky, or one could say foggy, which is perhaps why concrete diagnostic or medical definitions continue to be up in the air. Even with vast amounts of the American population experiencing a condition that feels like living with the flu for several months, it is only just now, in the last five to ten years, that the word “fatigue” is being taken seriously and treated with concern, over the advice to get some extra sleep. If only it were that simple.

The First Line of Defense

Methotrexate. “MTX.” The drug that many autoimmune patients fear, and the drug that many doctors always prescribe first. You ask any autoimmune disease patient if they’ve taken the drug, or even heard of it to begin with, chances are high that they have. It is often the first drug that doctors prescribe, the beginning of throwing spaghetti at a wall to see what sticks in the treatment of an autoimmune disease. And although it is widely successful for most, and incredibly affordable, it has assumed a bad rap.

With this “starter drug’s” name comes an often touchy reputation and subject of argument amongst patients and even scientists. “It’s toxic.” “It’s outdated.” “It’s chemotherapy.” And yet, it remains the “anchor drug” for clinicians in treating certain autoimmune diseases. Its long-term efficacy, or effectiveness, in combination with its low cost, keeps the drug at the top of the leaderboard in treatment practices, even with emerging treatments like biologics. In fact, the drug is so effective that it’s used in combination with newer drugs to further enhance the response to the disease. But rave reviews aside, not all patients are convinced that this drug is superior, particularly given its chemotherapeutic nature.

Love it or hate it, methotrexate is one of the most commonly prescribed autoimmune drugs, with over 900,000 users in the United States, and one of the least understood. And it all goes back much further than most patients realize.

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An Answer for Cancer

Methotrexate, available in an oral pill or injection, is commonly prescribed for the treatment of a handful of autoimmune diseases: rheumatoid arthritis (RA), psoriatic arthritis, lupus (SLE), and sometimes Crohn’s disease. It is a disease-modifying antirheumatic drug, or DMARD, that suppresses the immune system to reduce inflammation and damage. And while biologics and newer DMARDs have grown in use due to their revolutionary mechanisms of action and high rates of remission, methotrexate is revolutionary in its own right, holding a prominent place in medical history for decades.

Methotrexate burst into medical popularity during a time when the general public and scientists were desperate for answers in the treatment of cancer, specifically, childhood leukemia. A scientist, Sidney Farber, released a report in 1948 on the successful use of a new immunosuppressant drug to treat leukemia, called aminopterin. The drug was a huge success in the treatment of the aggressive blood cancer commonly found in children at the time, acting as a chemotherapy that drastically reduced the growth of cancer cells. It quickly became the gold-standard for cancer treatment in the United States. But rheumatologists got a bright idea.

A Curious Crossover

By the 50s, the drug was closely studied for its effects on cell growth in connective tissue, which can lead to abnormalities in the cartilage and bone of patients with RA. RA patients commonly develop thickened, tumor-like tissue around their joints, a hallmark of the immune system attacking these areas.

In 1951, a study on the administration of aminopterin to patients with RA, psoriatic arthritis, and psoriasis was conducted, with successful results. More than half the patients treated reported rapid improvement and the disappearance of symptoms after several weeks of using the drug. Only when the patients stopped using the drug did their symptoms return. But the manufacture and use of aminopterin came with difficulties. Naturally, there were side effects and concerns about the absorption and toxicity of the drug, since its potency was strong and originally intended for cancer treatment. And so, methotrexate, a slightly more moderate child of aminopterin, was born.

With its birth came even more studies, both on its use in cancer patients at higher doses and in RA patients at much lower doses. Scientists conducted specific studies on methotrexate’s effects on RA patients, but pushback grew. During this time, corticosteroids, such as prednisone, were the preferred drug of choice in the treatment of RA patients, cemented with great enthusiasm. A Nobel Prize was awarded to Philip Hench et al. in 1950 for their study of the treatment of RA with corticosteroids, contributing to most rheumatologists turning a blind eye to the idea of using methotrexate to treat RA patients. They went as far as calling it a “benign disease” compared to cancer. Imagine that. But as decades went on, studies continued, exploring the growing success in the use of methotrexate against RA.

By the early 70s, methotrexate’s success in treating RA was becoming increasingly obvious with each study, with long-term follow-up studies highlighting marked success and even complete remission in some patients. But methotrexate was still unapproved for use in treating patients with RA, and considered an unconventional, unimaginable method of treatment. It simply wasn’t concrete enough. It wasn’t until 1988, after numerous placebo-controlled studies, trials where certain participants were given the drug, and others were not, that the US Food and Drug Administration (FDA) finally approved methotrexate as a therapeutic drug for RA. And as treatment guidance marched on into the 2000s, the drug settled as the “top dog,” the gold standard, and oncology’s best crossover drug into rheumatology.

At its core, methotrexate is a low-dose chemotherapeutic drug for RA patients. An incredibly effective first-line DMARD. But how do the mechanics of this drug cross over from oncology to rheumatology? Like its mechanisms in cancer patients, methotrexate unfolds similarly in the bodies of RA patients.

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Case-by-Case Mechanics

Methotrexate is an antimetabolite drug, meaning it belongs to a class of chemotherapeutic agents that inhibit cell division by binding to cell division-specific enzymes. These enzymes instruct cells to divide and reproduce, but when cells go haywire, they divide at a rapid rate, leading to the formation of cancer cells. Enter methotrexate, the drug that turns off this rapid cell division rate and destroys cancer cells. When we think of chemotherapy, we think of a drug so toxic that it often turns humans into walking, usually bald, corpses. Methotrexate is one of those villains, with high toxicity but only when taken in high, frequent doses, either orally or through an IV.

Although it is the same drug, it is not nearly as toxic for autoimmune patients. In the treatment of autoimmune diseases, at low doses (from 7.5mg to 25mg), methotrexate produces a chemical called adenosine, a potent anti-inflammatory substance that lowers the body’s inflammation and blocks inflammatory proteins, or cytokines (TNF-ɑ, IL-6), essentially halting an overactive immune system and reducing damage to the joints or affected areas. Patients diagnosed with RA, psoriatic arthritis, juvenile idiopathic arthritis, or psoriasis, among other conditions, are all candidates for this orally administered pill, taken once a week, or an injectable form. For many, this drug is a simple, cheap miracle that has proven effectiveness, only after six to eight weeks, or three to six months to see full benefits. A “one and done” medication.

However, for some autoimmune patients, methotrexate may not be enough to treat their disease on its own. Over the last decade, exploring methotrexate’s effectiveness in combination with other drugs has been popular when the singular use, or monotherapy, of the drug fails. Specifically, many studies have examined combining methotrexate with other FDA-approved DMARDs, demonstrating that this approach is a viable “step-up” from methotrexate alone. Even though it is prescribed before other drugs, if a patient moves on to biologic DMARDs, administered via injections or IV infusions, methotrexate has been shown to act as a booster for these medications, improving their effectiveness.

As an in-tandem super drug, this effectiveness falls on a case-by-case basis. Not everyone who takes methotrexate benefits from it, or benefits from it long enough to use it with another drug. In fact, methotrexate resistance occurs in 30-50% of its autoimmune users, where patients show little-to-no response to the drug after prolonged use, paving the way for a return of disease symptoms. Other patients experience methotrexate intolerance. This intolerance, an extremely underreported condition, specifically in rheumatic patients, is developed through the experience of gastrointestinal symptoms, such as nausea, vomiting, and abdominal pain, as well as a rise in behavioral issues. In one cross-sectional study, approximately 34.5% of observed adult RA patients experienced this intolerance. This intolerance, especially of the gastrointestinal sort, seems to be the most commonly experienced side effect of the drug, while developing mouth sores comes a close second. And as most commonly associated with chemotherapy, some methotrexate users do report hair loss. And if that isn’t enough, “methotrexate fog,” a state of extreme fatigue, difficulty concentrating, or headaches, is another usual complaint.

But it’s good to know that just because you take methotrexate doesn’t mean you’ll be stuck with a collection of bodily issues. The drug is almost always taken with a folic acid supplement to aid in the reduction of these eerie side effects. Folic acid is the synthetic form of folate, a key vitamin whose levels are often reduced during methotrexate use. It can be taken daily, or at the same time as the once-per-week methotrexate dose. When taken regularly, folic acid has been shown to provide significant benefits and reduce methotrexate side effects compared with not taking it. In cases of gastrointestinal issues, folic acid helps soothe the GI tract following folate depletion caused by methotrexate. If experiencing pesky mouth sores or hair loss, folic acid helps rebuild the lining of the mouth and strengthen hair follicles, both of which are victims of folate depletion. A little vitamin B9 never hurt!

An Oldie and Sometimes Still a Goodie

With a treasure trove of advances in autoimmune treatment, methotrexate still serves as the entry-point, an onboarding experience, for autoimmune patients. It was my onboarding experience for my own autoimmune disease treatment, unfortunately, leading to an undesired intolerance and infuriating side effects. I quickly jumped ship from methotrexate, leading me down the path to subscribe to its bad rap and toxic nature. However, I have since discovered it is better to view the drug as a successful foundation for treating autoimmune diseases, effective for some, or a useful “sidekick,” rather than a universal “cure-all.” Thanks to Sidney Farber and the early curiosity of rheumatologists, methotrexate initiated the beginning of revolutionary autoimmune treatment. While not the most modern drug in autoimmune medicine, methotrexate is still, and forever will be, one of the most important.

The Absence

There may come a moment in the journey of an autoimmune patient when they stumble upon information never given to them, never informed of, yet crucial to their understanding of their condition. Information you’d think would be covered in a simple doctor’s visit. But the reality is that the patient has to find out for themselves, either through a deep dive into the internet or through word of mouth. Between the white walls of doctors’ offices, a diagnosis, a textbook recitation of the disease, is often mistreated as a complete and total understanding, and the patient is sent on their merry way. Cookie-cutter clinical information only summons questions or experiences that the afflicted patient takes to Google. Or, in many patients’ cases, the questions seep into Reddit communities.

In my own experience, I was left with a grey fog over the deeper implications of my autoimmune disease after quick and surface-level rheumatology visits, not lasting more than 20 minutes. Surely, I was informed of the disease’s aggressive mechanics and the mechanics of the drugs used to treat it, but as time passed, I was left with more and more fog that I attempted to navigate through Google searches. Until I found a Reddit group. Post after post, almost hourly, populated the group’s feed, revealing other individuals cast out into their own fog. It wasn’t just me who was searching for more information on something I’ll be stuck with for life. So I asked the group: What do you wish doctors told you but didn’t? What came back wasn’t answers, but a harsh spotlight on the absence of effective doctor-patient communication.

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All the Things You Never Said

Diagnosis is often delivered like a conclusion. Questions or nuance are often brushed over with clinicians evaporating before answers are provided. One Reddit user, a member of a rheumatoid arthritis (RA) page, described this as being “shoved into a box” by their rheumatologist. And with a conclusion-like diagnosis comes the usual treatment plan for patients: standard immunosuppressants, standard steroids, with little to no explanation.

One Reddit user wished there had been a more “thorough discussion” on infection risk and management, highlighting a glossed-over approach to understanding the effects of common immunosuppressant drugs commonly prescribed to autoimmune patients. Those who replied to the Reddit commenter only doubled down on this frustration, detailing brutal sickness after sickness or infection, easily caught due to their suppressed immune system, but entirely unknown to them as a side effect.

Another Reddit commenter expressed their frustration with a lack of communication about their prescribed RA medications clashing with their anxiety medication, as a result of their own obsessive research into drug interactions due to their doctor not telling them entirely. In response, another user laid out the reality of many: “You need to bone up, read, and try and become an expert on it yourself.”

But infections and medication clashing are only the tip of a horrifying iceberg into the risks and complications of an autoimmune disease. Some patients had to find out for themselves about the seemingly impending, deadlier risks of their own disease and its treatments.

Silent, But Deadly Risks

Perhaps many doctors aren’t comfortable laying it all out on the table for their patients when they embark on complex treatments or drugs with significant power. But this power is a double-edged sword, while patients are only informed of one side.

Cancer, a malicious and often voracious disease, is a risk that has smacked some Reddit commenters square in the face as a very real risk. One user described a clinical encounter with pure shock after her rheumatologist nonchalantly informed a med student that certain medications can cause cancer, information completely left in the dark to the user. “I had no idea that some medications can cause cancer,” the user posted, with other commenters equally shocked.

Accumulating diseases, or other serious conditions, is another dark room that users feel themselves thrashing around in. “Biologics can [sometimes] lead to brain inflammation,” such as meningitis and encephalitis, said one user. “I wish I had been told that RA medication would negatively affect my organs,” said another, with the liver being one of the most commonly affected organs from methotrexate use. One user, after cycling through multiple rheumatologists, typed their surprise to learn that even RA itself can affect the lungs.

Autoimmunity itself is another sinister, looming possibility, uncovered through one user’s self-directed search for answers. “Many people develop as many as 6 autoimmune [diseases] over time,” the user commented. “I wish everyone understood just how many different conditions are related through autoimmunity.” But alas, even with all the pieces in front of experts and the self-determined patients eager to unravel the complexities and comorbidities of their own disease, nobody, according to the user, can ever connect the dots.

Now imagine finding all of this out on your own, your doctor’s voice absent from the conversation, transparency a lucid dream. On top of the diagnosis itself, the emotional weight of the medical eggshells patients have to walk on can be crushing. And it seems they only pile up after every new self-informed surprise. Where does this leave patients emotionally in the face of their care providers? For many, it leaves them abandoned, or with the rug pulled out from under them.

Emotional Blind Spots

A never-ending life preserver, cast out to patients by their doctors as rafts of emotional support and resources, should theoretically fall under the umbrella of the “care” patients receive. Beyond the medicine they throw at the disease, nothing is thrown at the emotions that come with it. The emotional buildup can be isolating for many, with almost no preparation or warning for the mental turmoil that can follow the physical diagnosis.

“I wish the conversation had been more centered around, ‘you have a chronic illness, and you’ll [most] certainly be dealing with it for the rest of your life,’” one Reddit commenter described after a meeting with their rheumatologist, who had instilled false hope in them. “I would have appreciated an honest discussion more than false hope,” another said, after 10 years of trying and failing numerous drugs to get pain under control. Desires for honesty, support, and other care specialists were lamented across dozens of comments, all united by the stark fact that, mentally, it can all be very dark.

“Please consider grief counseling,” one user responded.

“I knew I found the right RA doctor when he actually [asked] about my mental health,” said another.

Another user detailed the day of their diagnosis and how they broke down as a result of their doctor’s lackluster bedside manner when delivering a life-altering diagnosis. “You have a touch of rheumatism! We’re starting you on chemo! You will get sick!” said the user, describing their doctor’s delivery of the diagnosis. “I wish that [rheumatologists] also came with free therapy,” the user continued. “It’s so hard to wrap your head around the idea of having a chronic illness.” A diagnosis can only explain the effects of the disease in the body, but not much about living with those effects. “It would be great if they had therapists that worked with [rheumatologists] and helped [us] process what it’s like to live with an illness,” the user concluded.

With physical hoop after hoop to jump through, performing mental gymnastics at the same time begs the question, as one user wrote, “What is improvement? What can be better? What do I have to [do] to live with it?”

As patients, like myself, tie themselves in knots with this question, it zooms out on the systemic shortcomings we encounter, and are likely to encounter for the rest of our diseased lives.

Speaking in the Silence

These lived experiences are not entirely the fault of the collective of rheumatologists and clinicians who perform the balancing act of delivering harsh diagnoses while gently providing the necessary resources for all kinds of care. Rather, these are the result of a larger picture riddled with holes in translative communication that makes space for what patients actually need to hear, and how they hear it. The endpoint of diagnosis and a means to treat it is a doctor’s job. By some measure, this execution of information and the following plan of attack is all well and good and can be seen as “care.” This is the training that doctors are meticulously provided.

But the gaps lie in the breakdown and tailoring of cold, hard, clinical information to fit a human with a life outside a doctor’s office, and in their comprehension of all that is important and relevant to the disease, without having to find it out on their own. Authenticity. Compassion. Two things that aren’t so easily taught or covered in lectures, maybe, but instead are innate in some and absent in others.

Patients aren’t asking for just the sugar coating. We’re not asking for complete perfection in communication. It is understandable that dropping a bomb of “here is everything that is horrible and possible with your diagnosis” is not entirely productive and can lead to a patient avoiding treatment and doctors altogether. So what’s the middle ground? It’s not what doctors say, but how they say it, but only if they’re saying it at all.

In the clinical world, where time is fleeting and case numbers climb, the delivery of life-altering news sits at a fork in the road, with one path abruptly ending in conclusion and the other stretching out with an offer of support and full transparency. A ten-minute diagnosis can be followed by a simple “You won’t navigate this alone,” and “I am here if you have questions,” which could mean the difference between less emotional, uninformed megatons of weight on a patient’s shoulders and a frenzy of internet searches and online communities banding together, navigating the silence.

Exercise is a key part of staying healthy. Many of us, one in five adults to be exact, often don’t get enough of it. We either can’t find a space to squeeze it into our schedules or let it drift into a not-so-necessary status that can be replaced with something less tedious. Despite our excuses, the U.S. Department of Health and Human Services recommends 150 minutes of moderate-intensity aerobic activity, such as running, biking, or swimming, per week for good health. In addition, moderate-intensity resistance training is recommended. These guidelines are based on current scientific evidence on what it takes to be healthy, improve quality of life, and prevent disease. There’s just one grey area. What does it mean to be physically healthy through exercise when you already have a disease?

For patients with autoimmune diseases, the concept of what “healthy” looks like can become blurry. Most patients are less concerned about their physical activity levels and more concerned about their immune system’s fragility and the symptoms they experience. Being healthy physically seems more complex than straightforward in the body of someone with a chronic disease. And the activity of exercising, although meant to be beneficial to health, can appear more dreadful due to physical limitations or the thought of worsening inflammation. It is as if autoimmune patients are faced with a high-wire tightrope they must navigate. To exercise or not to exercise? And will it actually benefit the health of someone whose health is already struggling?

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A Balancing Act

Exercise can end up in the back seat of many autoimmune patients’ lives, not because they want it to, but because it is seen as a daunting physical task when they already endure so much. Their bodies are already plagued by a variety of symptoms, all damaging to their energy levels, so working out and expending even more energy seems more hurtful than helpful, or just downright impossible. The balancing act between exercise’s benefits and harms comes down to intensity and frequency for anyone, not just autoimmune patients.

At a cellular level, exercise can either help or cause more harm than good to the body, whether diseased or not. Depending on how much and how intensively you exercise, damage can occur.

This damage can result from hard, heavy, and intense training or exercise that occurs more frequently than it should and outpaces recovery time. Overtraining syndrome, or overexertion during workouts or other intense training, can cause a variety of issues, not just for the average aerobic participant but also for patients with autoimmune diseases. Beyond causing more fatigue, or “energy crashes,” overtraining syndrome can increase inflammatory markers, such as tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6), which are commonly elevated in autoimmune patients. Chronic oxidative stress, a condition in which free radicals, or unstable molecules, outnumber antioxidants and cause cellular damage, can also result from overtraining syndrome. Once the body enters a state of oxidative stress, immune function is impaired, making autoimmune patients especially at risk.

To spot overtraining, symptoms often manifest as extreme fatigue, extreme muscle soreness, muscles feeling “heavy,” and an inability to train at a previous, comfortable level. If you get sick more often, have poor sleep, or feel generally low on energy and motivation, you’re likely exercising too much, too often. But how do you spot overtraining in someone with already elevated fatigue levels? How much is too much exercise for an autoimmune patient to avoid making things worse?

Push it, Feel good

In a perfect world, autoimmune patients would be able to manage their symptoms and get back to physical activity and exercise with little concern about how exercise would affect them or their fatigue. But it’s still an intimidating task, especially if you are not familiar with different types of physical activity or what’s most comfortable for you.

Some may ask, “What’s the point?” If your health is already compromised, if you are already tired, how could it get any better? It is a vicious cycle that many autoimmune patients fall into. The more fatigue you experience, the less likely you’ll want to try, and the more deconditioned your body will become. By the time you try to reason with yourself, it feels too late. It’s hard to believe there’s any sunny side to physical activity as an autoimmune disease patient when physical activity squeezes every last drop of energy out of you.

But as science says the average person needs physical exercise for health benefits, there’s plenty of evidence suggesting that autoimmune patients should still exercise for their own benefit. At the cellular level, exercise can significantly benefit patients with autoimmune diseases. Studies have repeatedly shown that regular exercise can reduce markers of inflammation and pro-inflammatory cytokines. In patients with autoimmune disease, this means milder symptoms and an overall more manageable disease. Exercise can also increase regulatory T cells, the immune system’s regulatory cells. These T cells are vital for the overwatch of autoimmune disease activity. With more T-cells, an autoimmune disease can be better regulated, leading to more balance, less inflammation, and better symptom management.

Past cells and cytokines, it’s all about how an autoimmune disease patient feels symptomatically. While some autoimmune patients may think exercise can worsen their fatigue, one of the most common autoimmune symptoms around, science says it can actually do the opposite. Studies have been ongoing to examine how exercise can benefit patients with autoimmune conditions. And one such study surveyed lupus patients who reported feeling less fatigued after a set amount of treadmill exercise over 12 weeks. Scientists recognized that this was due to increased cellular output, which raised energy levels for all participants, significantly reducing fatigue.

As exercise is recommended for disease prevention, it remains useful for preventing other diseases in patients with autoimmune disease. Some autoimmune patients, such as those with rheumatoid arthritis (RA), who engaged in mild to moderate exercise were found to have a lower risk of cardiovascular disease, on top of having much milder disease courses. Regular exercise can also drastically improve and prevent mental health disorders of an autoimmune patient, an area often severely impacted by an autoimmune disease. Exercise boosts serotonin and dopamine levels in the brain, which can lower symptoms of depression and anxiety and boost overall mood.

With reduced inflammation, increased T-cells, less fatigue, and greater cognitive and neurological benefits, exercise can clearly improve an autoimmune patient’s quality of life. Undoubtedly, exercise is an effective way to manage the effects of an autoimmune disease. But just as there is a perfect amount of medication to manage autoimmune symptoms, there is a perfect amount of exercise, and a type of exercise, to engage in alongside autoimmune symptoms.

The Perfect Dose

Not all types of exercise are created equal for patients with autoimmune conditions. Some choices are better than others, depending on disease severity, and can help reduce inflammation rather than worsen it. The key to exercising with an autoimmune disease without overdoing it or falling into overtraining is low-impact types of movement. Low-impact movement involves physical activities that place little stress on joints, bones, and muscles. These movements still provide cardiovascular and strength benefits without increasing risk of injury, stress, or inflammation. So what does the “right dose” actually look like in practice? There are several options of low-impact exercise that autoimmune patients can engage in:

• Walking: improves circulation and flexibility.

• Swimming or Water Aerobics: water reduces joint stress while still providing a full-body workout.

• Yoga: gentle movement that promotes relaxation and decreases stress while promoting flexibility.

• Cycling or Elliptical: great for cardiovascular health without high impact on joints.

• Strength training: can be done with light weights, resistance bands, or body weight to support joints and maintain muscle mass.

Mobility can also be an issue, depending on the severity of the disease in an individual. There may be only so much movement you can execute given your mobility, making it difficult to adopt many traditional forms of exercise. Taking the plunge to start exercising as someone with limited mobility may actually increase your mobility and strength over time, paving the way for more exercise for your benefit.

As life progresses with an autoimmune disease, and the disease can also progress, it is important to monitor how your body responds to activity in conjunction with treatment. Individuality should always be considered when engaging in exercise type and intensity. Adapt physical activity intensity, types, and duration to meet your body’s needs and current symptoms or inflammation. Try swimming one day, and yoga the next! Recognize day-to-day symptoms and adjust your movement as necessary. Even some exercise is better than none.

While the definition of health may seem like an ever-evolving equation with no single right answer for patients with autoimmune disease, it is undeniable that exercise can contribute to improved health and reduced symptoms. The immune system may be unpredictable, but movement does not have to be. When approached intentionally, exercise is not a threat to autoimmune patients; it is a tool for moving your body, even to the best of its tired, achy ability.

Disease collectors

Many patients with autoimmune diseases report developing symptoms of another disease a few years after their initial diagnosis of a distinct disease, such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), or multiple sclerosis (MS). When a secondary disease develops alongside the primary disease, the patient’s condition is referred to as a comorbidity. For patients, this often feels like betrayal layered upon betrayal.

Comorbidity is defined as the presence of two or more medical conditions coexisting at the same time, typically another chronic illness or disease. Usually, a secondary disease follows a few years after the initial diagnosis, or the primary diagnosis. Once diseases coexist, the life of an autoimmune patient becomes significantly more complex.

Approximately 25% of patients with autoimmune diseases will develop another disease at some point. This overlap is not coincidental. Once diagnosed with the primary autoimmune disease, the risk of comorbidities increases significantly, as autoimmune diseases are commonly known to be comorbid. Patients diagnosed with RA, MS, SLE, or other autoimmune conditions are at higher risk of developing secondary diseases, specifically, other autoimmune diseases, such as thyroiditis, celiac disease, and psoriasis, among others. When a patient develops more than three distinct autoimmune diseases, this is known as multiple autoimmune syndrome, or MAS, a rare condition. The real question is not whether autoimmune diseases cluster together, but why.

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Bad genes, mechanical dysfunction, and poor environments

To understand why patients with autoimmune diseases are at high risk of developing secondary, even tertiary, diseases, it is essential to grasp the concept of shared susceptibility. Shared susceptibility is the phenomenon in which specific gene variants, biological mechanisms, or environmental factors increase an individual’s risk of developing multiple, distinct diseases and conditions.

In patients with autoimmune diseases, there is a higher risk of developing a second autoimmune disease because many autoimmune diseases share genetic material, particularly genes that regulate disease risk or autoimmunity. Once you have one autoimmune disease, you are more genetically likely to develop a second since many autoimmune diseases share the same genetic dysfunctions that allow their existence in the body.

But shared DNA is only part of the puzzle. Another piece of shared susceptibility is immune dysfunction, a key biological mechanism. Patients with autoimmune diseases are already immunocompromised, meaning their immune systems are weakened by the primary disease and its self-inflicted attacks. This leaves room for a secondary disease to be triggered. When immune regulation falters, whether by intrinsic dysfunction or medication-induced suppression, self-reactive immune cells can target new tissues, expanding into a new disease.

Even after genetic predispositions and immune dysfunction, disease often requires an environmental trigger. These triggers, such as viral exposure or infection, stress, toxins, or poor lifestyle choices (e.g., smoking and poor diet), can cause a short circuit in the immune system, leading to the initiation of another disease.

These shared mechanisms do not operate in an abstract way. They manifest in real, recognizable patterns.

Two’s company, three’s a crowd

Some comorbidities are more commonly linked to certain primary diseases than others. For example, many studies and observations have revealed that the following primary autoimmune diseases are more commonly linked to their respective secondary diseases than others:

• Autoimmune thyroiditis is most commonly linked to → RA, celiac disease, or pernicious anemia

• RA is most commonly linked to → Sjögren’s Syndrome

• Type 1 Diabetes (T1D) is most commonly linked to → autoimmune thyroiditis, RA, gastrointestinal diseases

But the immune system’s ripple effects extend beyond autoimmunity.

Although autoimmune patients are at high risk of developing another autoimmune disease, specifically, they are also at risk of developing other diseases or chronic illnesses that are non-autoimmune. Similar to shared susceptibility, non-autoimmune comorbid conditions can share genetic material, but can also appear as a result of chronic inflammation or medication side effects. Common non-autoimmune comorbidities can include cardiovascular disease (CVD), diabetes, chronic infections, and even mental health conditions.

Much like the commonly linked primary-to-secondary autoimmune comorbidities, certain autoimmune diseases have a higher risk for certain non-autoimmune conditions. For example, RA patients have a 1.5 times higher risk of developing cardiovascular disease, or conditions such as heart failure, stroke, and heart attacks, than the general population.

Because autoimmune patients often experience chronic inflammation, they are at increased risk of non-autoimmune inflammation-related comorbidities, such as insulin resistance, obesity, and diabetes. But comorbidities are not just limited to organs below the neck. The brain can also develop a comorbidity as a result of chronic inflammation, such as depression, anxiety, bipolar disorder, or schizophrenia.

Often, patients with autoimmune diseases are monitored closely, depending on the medications they are taking, such as immunosuppressants and corticosteroids, due to the increased risk of comorbidities developing from medication side effects or long-term use. Patients are more prone to infections due to immunosuppressant drugs, and in some cases, are more prone to osteoporosis due to long-term corticosteroid use.

In some cases, the consequences of chronic immune disruption become even more serious. Certain immunosuppressants taken by patients with autoimmune diseases also carry the risk of creating a pro-tumor environment, leading to the development of certain cancers. Due to long-standing chronic inflammation and suppressed immune function, malignancies or abnormal cell growth have room to multiply and develop into various lymphomas.

Understanding these risks is only part of the equation. Managing them is another challenge entirely.

Proceed with treatment caution

Treatment becomes more complicated once a second or third disease coexists with the primary disease. Many factors of the second or third disease must also be considered alongside those of the primary disease and the current treatment being administered. In some cases, the primary disease treatment may worsen the secondary disease, and a patient may need to switch medications entirely. There are medications that can be used to treat multiple diseases, but risk assessment is necessary. Monitoring and safety are of the utmost importance to make sure new immune disorders aren’t triggered, or medications do not worsen pre-existing conditions

When it comes to cancer as a comorbidity, there is a treatment paradox, where an immunotherapy meant to boost the immune system will conflict with an immunosuppressant for an autoimmune disease, and vice versa. If a patient is taking an immunosuppressant, the cancer can grow and worsen. If a patient is receiving immunotherapy to enhance immune function, their autoimmune disease may worsen.

While medication and treatment plans are central to the management of comorbidities, they are not the only strategies. Certain lifestyle changes can be implemented to manage the presence and severity of comorbidities in patients with autoimmune diseases. Engaging in low-impact exercise, such as yoga, adopting an anti-inflammatory diet, and reducing environmental exposure to toxins can help manage symptoms and inflammation associated with comorbid diseases and reduce their burdens over time.

The Current State of Treatment

For decades, only two treatment options have been available to patients with autoimmune diseases. The first path is the overall approach to lowering their immune system. Drugs such as methotrexate are used to broadly suppress the immune system’s activity and manage symptoms. The second path is the injection or infusion of biologics, a more targeted approach that targets specific causes of inflammation, such as certain proteins.

Oftentimes, when methotrexate fails, biologics are the next step for autoimmune patients to take. But the options stop there, beyond drug hopping, and for a long time, innovation did too. Biologics were once the newest and coolest collection of laboratory-engineered treatments, thought to be revolutionary, yet they still only managed symptoms and reduced disease activity. Nothing could be cured, only turned dormant. The treatment landscape of autoimmune diseases lacked something stronger, something that would modify the existence of the disease entirely, something that would send a patient into a long, sustained, and drug-free remission.

Momentum in revolutionary treatments for autoimmune disease has quietly crawled forward until the last few years, when an outpouring of new developments has occurred, with numerous medications slowly making their way through the research, trial, and development pipelines.

As a patient, following new developments is like swimming in the sea during a storm. There’s so much going on, you can’t figure out how to navigate it all, and is there any hope at all? While treatment for the incurable feels hopeless, there’s one development worth holding out hope for.

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Modern Engineering

Chimeric Antigen Receptor T-cell therapy, or CAR-T for short, is among the most promising treatments under development for patients with autoimmune diseases.

Unlike current autoimmune treatments, which only suppress the immune system’s attack on the body’s healthy tissues or focus on symptom management, CAR-T cell therapy is a novel treatment that not only suppresses but also modulates the immune system, completely redirecting or stopping its attacks. In some cases, such as in patients with lupus, treatment can completely deplete disease activity to the point of drug-free remission, when patients no longer need to rely on immunosuppressant drugs.

CAR-T cell therapy is a specialized type of lab-engineered treatment that uses a patient’s own T cells to treat a disease. A patient’s cells are collected through blood, genetically re-engineered in a laboratory, and then returned to the body through an infusion. From there, the new cells get to work attacking cells that shouldn’t be there.

In the early development of CAR-T cell therapy, in the 90s and well into the 2000s, its primary aim was to eliminate cancer cells in patients. A cancer patient’s T cells were extracted, modified, and returned to the body, carrying new genes that bind to cancer cells and kill them.

In recent years, engineered CAR-T cells have been effective at targeting pathogenic B cells, a cell type largely responsible for producing inflammatory proteins in autoimmune diseases such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and multiple sclerosis (MS), among others. When engineered for use in patients with autoimmune diseases, CAR-T cells bind to these malfunctioning B cells, effectively wiping them out and causing an immune system “reset.”

The success of CAR-T cell therapy is clear for patients with autoimmune diseases. One trial showed that all participants achieved drug-free remission, their immune systems effectively reset, and they practically returned to normal. For almost all patients with autoimmune diseases, this is “the dream” they cling to: a life returned to normal. While CAR-T therapy carries risks, such as cytokine release syndrome (CRS), in which recipients may experience fever, low blood pressure, or body aches, recipients are closely monitored and treated for any post-infusion complications. Long-term risks, such as developing a secondary cancer, are being studied.

CAR-T therapy is an especially exciting development for those with treatment-resistant autoimmune diseases, or refractory disease, a condition in which a patient fails to respond to conventional immunosuppressants that are widely available. With a new engineered therapy, such as CAR-T therapy, those with refractory autoimmune disease have a chance for a more intense treatment that could result in response and remission.

Approval: A Waiting Game

Although CAR-T cell therapy shows great promise for treating autoimmune diseases, it has not yet been approved for this use. To date, the U.S. Food and Drug Administration (FDA) has approved only CAR-T cell therapies for various cancers, such as lymphomas and leukemias. As of 2024, there are six CAR-T therapies approved by the FDA for use in the U.S. CAR-T therapy for autoimmune disease remains in the experimental stage and is only available through clinical trials. However, certain biopharmaceutical companies, such as Kyverna, are developing CAR-T therapies specifically for the treatment of patients with autoimmune diseases, advancing them through the pipeline from trials to approval.

The cost of CAR-T therapy will be another major consideration for patients with autoimmune diseases, given the high cost of current CAR-T therapies for cancer patients. The drugs alone can cost anywhere between $370,000 to $475,000. In addition to hospital admission, treatment administration, and monitoring, the total cost of CAR-T therapy can exceed $1 million per patient. But various organizations are pushing for CAR-T therapy costs to come down.

It’s only a matter of a few years before this revolutionary therapy is approved beyond just treating cancer and for the treatment of autoimmune diseases. This is a hopeful dawn for many living with day-to-day symptoms or treatment-resistant autoimmune diseases, with a chance for drug-free remission, the absolute best-case-scenario for autoimmune patients.

Chronic Illness and Depression: Not all in your head.

The physical toll of living with an autoimmune disease is usually the first downside addressed. The way your symptoms appear in everyday life, the difficulties they cause, the drawbacks, and the limitations are among the top reasons to pursue treatment. The physical symptoms are such large, unavoidable traits of autoimmune diseases to address that we often forget or completely overlook one crucial aspect that may be affected by an autoimmune disease, way worse than we think: the psychological aspect.

There are over 80 autoimmune diseases, such as lupus, rheumatoid arthritis, type 1 diabetes, and Crohn’s disease, each causing inflammation in its own special way. Each one, a life-long condition with little end in sight; no cure available. The way these diseases affect patients physically is often the most-discussed topic, whether from doctors and healthcare providers, friends and family, or even strangers. “How does your disease affect you physically?” someone may ask. Or, “Here’s how we can manage your physical symptoms,” a doctor may say. Life with an autoimmune disease goes on with every physical avenue explored, often leaving the psychological and mental avenues completely unchecked.

Double the risk.

The fact is, autoimmune patients are a bright red target for depression and anxiety to hit. One study found that over half of autoimmune patients have depression and anxiety, and even worse, many never report their mental health symptoms to a healthcare provider at all. But why are autoimmune patients such an easy target for poor mental health conditions? The reason isn’t just because living with an autoimmune disease sucks, to put it bluntly. It’s far more scientific and nearly unavoidable than that.

Autoimmune diseases, conditions in which the immune system attacks the body’s healthy tissues and cells, drive elevated inflammation. This inflammation, driven by pro-inflammatory proteins called cytokines, can occur anywhere in the body in certain autoimmune diseases. For rheumatoid arthritis (RA) and lupus, it’s the joints. For Crohn’s disease, it’s the intestines. But although we often think of inflammation as only affecting these targeted areas, depending on the disease, some studies have shown that inflammation from an autoimmune disease can be connected to the occurrence and cause of depression.

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Breaking down the brain.

Here’s how it works. When subjected to chronic inflammation, or inflammation that is ongoing for a long period of time, the parts of the body first targeted by an autoimmune disease are no longer the only ones to worry about. The brain is a sneaky but alarming character worth considering. That’s because the inflammation can expand and directly start to mess with the brain, leading to depression or a host of other psychiatric disorders. Pro-inflammatory proteins, the cytokines, can enter the brain, triggering a domino effect on its function. It starts off with the cytokines triggering the brain’s microglia, or the brain’s own brand of immune cells. These immune cells begin to damage healthy brain cells and disrupt the production of new cells in important areas of the brain that regulate mood and memory.

Beyond damaging healthy brain cells, inflammation can also affect the production of neurotransmitters responsible for feelings of happiness, such as serotonin and dopamine. When inflammatory proteins enter the brain, they can bind to neurotransmitter receptors, completely blocking or altering neurotransmitter function and production. Without these essential neurotransmitters being produced and functioning properly, depression becomes a problem. Symptoms like fatigue, persistent sadness, loss of interest in life or activities, irritability, or feelings of worthlessness can begin to affect an individual mentally.

Further breakdown in brain function and optimal recovery are more likely when neuroplasticity, or the brain’s ability to bounce back and adapt, is limited by these attacks. This means that individuals often find themselves unable to pull themselves out of depression or overcome their symptoms, leading to an ongoing low mental state that can be long-term.

A different approach to treatment.

With an extremely heightened risk of developing depression, if that development happens, what does treatment look like? It turns out that treating depression rooted in chronic inflammation has more roadblocks compared to those without chronic inflammation. Due to ongoing exposure to inflammation and its long-term effects on the brain, traditional approaches, like prescription antidepressants, may not be as effective. Some studies have shown that patients with high levels of inflammation respond poorly to antidepressant drugs.

Part of the reason is how pro-inflammatory proteins and brain immune cells attack neurotransmitter pathways and healthy brain cells. Antidepressants like selective serotonin reuptake inhibitors (SSRIs), meant to help the brain’s neurotransmitter pathways, essentially become useless in the face of these attacks on the pathways. The attacks on these pathways are too strong and ongoing for these antidepressants to do anything.

Instead of more mainstream antidepressant treatment, autoimmune patients experiencing depression or anxiety could try a different approach that begins with lowering their overall inflammation. Studies have shown that nonsteroidal anti-inflammatory drugs (NSAIDs), such as over-the-counter ibuprofen or prescription-strength diclofenac, have successful antidepressant effects. Furthermore, cytokine inhibitors, such as certain brands of biologics, a class of medications that autoimmune patients take, have also been shown to boost mood. Many of these drugs are already used as treatment for autoimmune patients, but if a low mood still persists, there are other lifestyle changes patients can make, beyond talking to their doctor about other medications.

Changes such as undertaking an anti-inflammatory diet, consuming more omega-3 fatty acids, or participating in various therapies can reduce feelings of depression and make life more manageable for those with chronic inflammation.

Mentally in check.

It is important to recognize not only the physical limitations that come with an autoimmune disease, but also the sneaky and under-addressed psychological limitations as well. Many patients often believe that being depressed is just one of those abstract things that come with a lifelong, incurable chronic illness, and many patients do not know they’re more likely to develop psychological issues at all. The truth is, there is more of a biological cause and effect than you may think, with the brain a perfectly open target for inflammation and its breakdown a straight shot for depression. But managing the inflammation and making certain lifestyle changes can keep the low or anxious moods at bay. And it’s important for patients to realize you’re not alone.

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I am sitting across from Deanna Hoover in a Starbucks on a gloomy Sunday morning. She gently runs a fingertip across a scar on another finger, a reminder of the pain she’s endured up to this point. The scar came from an operation that left her with a fused joint, a product of “the only” proposed solution by her doctor to fix a joint so swollen that it was frozen. Hoover has rheumatoid arthritis (RA), an autoimmune disease characterised by the body’s nasty self-inflicted attacks on joints and surrounding tissues, primarily in the fingers and toes, but really, it can spread anywhere.

Hoover’s diagnosis was anything but swift. Hoover’s journey to diagnosis was a confusing one, a classic uphill battle, like knocking on hundreds of closed doors, begging for one to open with answers. When her joints began to swell and stiffen, especially in the mornings, RA was her immediate “bingo.” Her best friend had RA, and Hoover’s knew the ins and outs of all the symptoms. And at her age, well into her sixties, the boxes had been ticked. But a visit to a rheumatologist quickly unravelled into frustration after none of her blood test results supported her beliefs. “[My rheumatologist] wouldn’t even diagnose me as having RA,” she said. And when she begged for something to help bring down the swelling and inflammation, her doctor begrudgingly relented. “It’s like he really didn’t believe I had RA. He gave me the lowest dose because he knew it wouldn’t work. He gave it to me just to get me out the door.”

Nothing was working for Hoover. None of the basic immunosuppressant drugs worked, nor corticosteroids, which made her face puffy. The one joint was so bad, so painful and frozen, she gave in to having it fused. Hoover later discovered she had a rare form of RA, seronegative RA, a form that doesn’t show up in blood tests due to a lack of disease-specific antibodies, and a form where most drugs don’t do a thing. After bouncing from doctor to doctor, Hoover was finally diagnosed through a collection of exams and imaging revealing the extent of joint damage and swelling she had accumulated. Now, as I sit across from her, her hands flat on the table, the joints in her fingers still appear slightly bulbous, like knots in a tree, but not as bad as they used to be.

Hoover’s story is a relatable experience for many people suffering from autoimmune diseases across the United States. Hoover’s body, much like the bodies of millions of people affected by an autoimmune disease in the United States, doesn’t know any better. The immune system’s key function of regulation and protection, which guards against invaders and foreign entities, can turn against the body and cause harm, leading to an autoimmune disease. For decades, science and medicine have fumbled around in the dark, trying to explain the root cause of these diseases and why this malfunction occurs, with concrete answers eluding them. Although research has revealed the mechanisms behind how the body attacks its own healthy tissues, without an idea of a root cause, treatment could only be developed to manage symptoms and suppress the immune system. Autoimmune diseases were only ever labeled as “incurable.” Until 2025.

After piecing together autoimmune mechanisms and avenues for symptom management that still left experts scratching their heads, a light came on, worthy of this year’s Nobel Peace Prize in Physiology or Medicine. The light, turned on by three immunologists, put a spotlight on the possible source of autoimmune diseases, a long-believed grey area. In 1995, Japanese scientist Shimon Sakaguchi discovered a previously unknown class of immune cells, known as regulatory T cells (Tregs), the peacekeepers of the immune system that guard our healthy cells, and instruct other cells to kill invaders. This discovery pushed the field of immunology a few steps forward.

Then, in 2001, scientists Mary Brunkow and Fred Ramsdell discovered a gene, FOXP3, that was linked to autoimmune disease in mice when the gene had issues. Even more steps forward were taken when, two years later, Sakaguchi linked the gene as the governor of the Treg cells, the cells that ensure our immune system does not turn on our own bodies. But when this gene is mutated, the cells go haywire, and an autoimmune disease is activated.

Melanie Matheu, an immunologist and co-founder of the biotech laboratory LYRIC BIO, emphasizes the importance of the FOXP3 gene in instructing regulatory T cells to behave correctly.

“If you have a mutation in the FOXP3 gene, which is critical for establishing and maintaining a regulatory T cell’s identity, you develop immediate autoimmune disease that attacks everything in your body,” Matheu said in a TikTok reaction to the awarded research. Matheu explained that, when normal, Tregs always recognize the body as they are supposed to.

“What’s special about regulatory T cells is they recognize self-protein, and they protect against other T cells responding to that self-protein.” But when these cells no longer have proper instructions, this recognition falls apart. The peacekeepers of the immune system turn into fighter jets, no longer recognizing self-proteins or the body’s own tissues, spurring autoimmune disease attacks.

Before Brunkow, Ramsdell, and Sakaguchi’s discoveries, autoimmune diseases were thought to result from a range of factors, including environmental factors such as air quality or pollution, infections, chemicals, or certain lifestyle choices such as smoking or poor diet. Genetic predisposition was another explanation for the origin of autoimmune diseases. But after a diagnosis, there is little concrete understanding of exactly what triggers an autoimmune disease, despite all those factors. But now, with a clear view of how the body’s regulatory T cells are instructed to act, and what happens when those instructions are wrong, scientists can piece together a road map for the future of autoimmune treatment that is not just suppressive, but possibly curative.

Current treatments widely available to autoimmune patients only go as far as suppressing the immune system and managing symptoms. In recent years, the frontier of autoimmune treatment has shifted from suppressing the immune system as a whole to targeting specific aspects of the immune system via injections or IV infusions.

“There’s a lot of different types of drugs [that are] meant to target different parts of the immune system,” said Lindsay Sweet, an executive medical science liaison in rheumatology for Sanofi, with a background as a medical director in U.S. rheumatology for Pfizer. “A lot of the drugs are aimed at targeting the pro-inflammatory aspect of the immune response,” Sweet continued, highlighting how current drug options modify disease activity by blocking very specific inflammatory proteins and cells.

These drugs, which act like a brick wall to inflammatory responses, were revolutionary at the time of their conception, going beyond simply suppressing the immune system as a whole and offering a more targeted approach. “These have been very efficacious,” said Sweet, particularly praising the safety of these drugs. “But they don’t always work forever.” And when that happens, another path must be explored.

Scientists often look for crossovers in other areas of treatment, such as cancer treatment, which has led to new trials using engineered cells to target and eradicate cancer cells. These engineered cell therapies have already shown success in treating autoimmune patients with lupus. “We’ve been able to do these types of cell therapies in lupus patients to totally knock out the bad cells and reset the immune system,” said Sweet. “The patients were totally free of the disease.”

In the context of engineered cell therapies and restorative treatments, the Nobel-awarded discoveries from Brunkow, Ramsdell, and Sakaguchi could pave the way for drug development for autoimmune patients seeking a complete reset of their immune systems and the eradication of their diseases, as if they had never been diagnosed in the first place. But the road ahead is long and not without its challenges.

“It takes so many years to get FDA approval, so hopefully in the next five years we’ll see more data and safety,” said Sweet. But it’s the distribution and monetary factors that still have to be considered. The expenses of targeted drugs alone can cost Americans between $10,000-$50,000 per year. “Just getting them approved, and the regulatory considerations are still working out,” said Sweet. “How are people going to pay for it? How is insurance going to cover it? And will all patients even have access?”

But the need and care for these treatments are a movement, Sweet believes, that has grown. “With the people who won the Nobel Prize, that’s a huge advancement because it looks at a different aspect of the immune system. They’re demonstrating that there’s still a lot we don’t know and there’s still a lot to learn. There are ways to apply these learnings to potential future treatment.”

As much as we take steps forward, the complexities of the immune system and scientists’ ever-growing understanding challenge the idea of an end-all solution for every autoimmune disease, each different and each patient’s experience unique. “There’s no one answer,” said Sweet. “But that’s what makes it exciting.”

This turning point in research and subsequent developments paints a picture of hope for anyone living with a disease and those working around it. “I am hopeful because the technology has progressed so much and continues to progress,” said Sweet. And those who work directly with patients share a similar hope in the progression of technology. Dr. Perry Fuchs, a rheumatologist at the Denver Arthritis Clinic, shared his outlook on what it means for patients on the cusp of answers to their mysterious diseases and the prospective solutions.

“My biggest hope is for curative therapies that are safe and less risky to be developed. There have been a lot of studies in Europe that are now coming to America; that is great to see,” said Fuchs. These studies, and award-winning research such as the Nobel Prize, have put a spotlight on autoimmune diseases, offering long-awaited, stronger recognition for patients who fight what others see as invisible. And this year’s Nobel Prize in Physiology or Medicine is worthy of a standing ovation, and it’s not the final bow.

When I asked Hoover her thoughts on the progress toward curative therapies, expecting either an elated whoop of surprise or a barrage of questions, she casually replied, “That would be nice,” as if grabbing a blanket to cover years of only manageable torment. Something easy, something simple, two things not usually associated with the art of living with an autoimmune disease. And although future treatments may not be one-size-fits-all, the current understanding of autoimmune diseases has opened closed doors, entirely new ones, to answers that were once thought impossible, paving the way back to peace in the immune system.

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“You’re in remission.” These are the words that many people with an autoimmune disease dream of hearing. The three words are enough to bring people to tears and are a reason for doctors and researchers to celebrate. Although the words do not mean that the disease is gone, it’s just inactive, the upside outshines the chances of the disease coming back: no more pain, no more symptoms.

But remission is incredibly nuanced. It does not just mean the disease is inactive; it means it’s inactive in addition to other factors to make it so. Unfortunately, remission is as far as the treatment will go. Autoimmune diseases cannot be completely reversed; they are lifelong conditions. Most autoimmune diseases, such as lupus, rheumatoid arthritis, or Crohn’s disease, can be treated to the point where they enter remission, a state of incredibly low activity, the best-case scenario for any patient struggling with their symptoms.

When many people hear the word “remission,” they think of cancer. Similar to the way a cancer patient can go into remission, patients diagnosed with an autoimmune disease can go into remission with the assistance of treatment. Often, when remission is discussed for autoimmune diseases, it is best described as an outcome thanks to long-term, routine symptom management. Symptom management, addressing the inflammation that causes aches, pains, fatigue, and other features of the disease, is achieved through various medications and treatments that patients can explore with their healthcare providers.

The most common form of treatment with the highest likelihood of remission in autoimmune patients is immunosuppressant drug therapy, which lowers the body’s immune response and slows the attack on the body’s healthy tissues and cells. Because the immune system is suppressed, or “turned down,” inflammation is reduced, and symptoms become less severe or even go away altogether. This is where the patient enters remission.

Immunosuppressants: A Wide Selection

One of the most common types of immunosuppressants is corticosteroids, usually in prescription pill form, which patients can take at home for a set amount of time to manage their inflammation, or in combination with another immunosuppressant. These “steroids” have significant short-term effects and can be adjusted in dosage, but are usually not meant for long-term solo use due to poor side effects. While this type of drug is excellent for short-term, temporary inflammation and symptom management, it does little to alter the activity of the autoimmune disease being treated.

Not all immunosuppressants are created equal, nor do they all do the same thing. There are different categories of immunosuppressants that do different things at different intensities. To alter the activity of an autoimmune disease at a cellular level or change how the immune system attacks the body, patients are often advised to take a disease-modifying antirheumatic drug (DMARD).

IMDH inhibitors (inosine monophosphate dehydrogenase), a class of DMARDs, are another immunosuppressant most commonly prescribed. These inhibitors are just that: they inhibit the activity of an autoimmune disease at the cellular level by suppressing the growth of specific cells or the production of inflammatory proteins. Although these drugs alter cellular growth and reduce inflammation associated with the disease, they broadly affect the immune system and can cause undesirable side effects.

For a more targeted approach to treating an autoimmune disease, patients can consider biologic therapy, another class of drugs that systematically target key parts of the immune system to reduce inflammation. Unlike the oral route, these immunosuppressants are administered only by injection or IV infusion. The most significant difference between biologic drugs and drugs like IMDH inhibitors is that biologics are made from living cells, unlike their synthetic counterparts. These highly targeted therapies are designed to bind to specific proteins and cells in the body and alter their activity, thereby reducing inflammation. These drugs, although very effective, are costly, costing an average of $10,000 to $30,000 per year.

Every drug comes with a downside. Because these drugs suppress the body’s immune system, they leave room for adverse side effects, such as short-term effects like headaches, nausea, dizziness, and changes in appetite, and even long-term effects such as bacterial or viral infections, bone thinning, and cancer. But for most autoimmune patients, these are risks they are willing to take to live a life more pain-free and enter remission.

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Remission: Life somewhat returned to normal

The broad definition of remission states that the disease is inactive and that a patient has little to no inflammation. However, remission can look different for everyone, and can even be categorized differently depending on the nature of the disease and the individual.

Clinical remission is the most commonly experienced form of remission, in which an individual experiences mild or nearly undetectable symptoms that don’t interfere with daily life. This type of remission is usually drug-induced, meaning the patient takes some form of drug to keep their symptoms mild or unnoticeable. If a patient stops taking the drug, there is a chance the symptoms could come back. Then there’s laboratory remission, where, although a patient still experiences some symptoms, their blood tests show that their inflammation has decreased and the disease is under control.

The rarest form of remission is immunological remission. This type of remission is characterized by the body stopping the production of disease-specific cells and proteins, a complete vanishing of the disease to the point where the patient no longer needs drugs. Immunological remission is nothing short of a medical anomaly or miracle. A patient can return to life as if they never had their autoimmune disease in the first place.

Most individuals will still rely on drugs for the rest of their lives in order to stay in remission, even if they have flares in their disease where symptoms reappear for short periods of time. For many, remission is subjective beyond doctor definitions and laboratory markers. Many people define remission as a return to normal everyday activities or an improved quality of life. But like most diseases, relapse is always a concern.

Relapse: When the disease comes back.

Autoimmune disease relapse out of remission can occur for several reasons. The immune system is incredibly delicate; even the slightest thing can throw off its response. Much like when you catch a cold or other virus, certain factors can trigger your immune system to overreact even if you’ve been in remission. The most common triggers include infections, physical or mental stress, hormonal changes, and environmental factors or seasonal changes. Tapering drug treatments or lowering dosage can also cause a relapse.

When these relapses happen, individuals will often talk to their doctors about their treatment dosages and frequencies, take pain management drugs like corticosteroids, or make specific lifestyle changes to get back to a state of remission.

Although relapses happen, autoimmune diseases are incredibly cyclical; states of remission and relapse come and go across the life of an autoimmune disease patient, known as relapsing-remitting.

The hard truth is that there are no cures for autoimmune diseases, at least not yet. For now, patients around the world rely on the journey to reach remission and stay in remission as long as possible.

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Sugar is one of the most well-studied food compounds in science, and for good reason. Lots of health issues all trace back to diet, primarily the diets of individuals with high sugar intake, such as obesity and diabetes. Autoimmune diseases, a collection of conditions in which the immune system attacks the body, such as rheumatoid arthritis (RA), Crohn’s disease, lupus, and others, can be particularly affected by sugar intake.

Inflammation levels, an ongoing battle in those with autoimmune diseases, have a direct link with sugar consumption. Research has shown that consuming sugar causes higher inflammation levels in autoimmune disease patients, worsening their pain levels and disease activity.

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Image source: Frontiers

So how does it work? When you eat excess sugar, simply put, your body produces advanced glycation end products (AGEs), a type of harmful chemical that can lead to more inflammation. The more of these harmful chemicals there are, the more pro-inflammatory proteins are released in the body, creating a vicious cycle of chronic inflammation.

One way sugar triggers this inflammatory response in the body is through the gut. Consuming sugar can disrupt, and even decrease, the good bacteria in your gut, leading to increased inflammation and a weaker immune system.

When your immune system is already attacking the wrong parts of your body, like it does in patients with RA, sugar can make the disease much worse. Alongside higher inflammation levels, physical symptoms such as swelling, stiffness, and burning can be much more intense with a higher-sugar diet.

At the microscopic level, research has shown how sugar can completely alter autoimmune cells, such as the destruction of colon tissue in mice with Crohn’s disease when given sugar water.

Destruction of colon tissue due to sugar water (bottom image) versus tissue from mice that drank regular water (top image). Source

But is all sugar created equal? Not exactly. You may know that there are a few different names of sugars thrown around in diet talk: processed, added, or refined sugar, and natural sugar. Natural sugars are what they sound like: they occur naturally in whole foods such as fruits, vegetables, and even dairy products. Added, processed, and refined sugars are sugars added to foods and beverages during processing and manufacturing, increasing their sugar nutritional content.

One such processed sugar we all hear about is high-fructose corn syrup (HFCS), found in sugary snacks and beverages, as well as in breads and cured meats. While naturally occurring sugars are low in concentration, have antioxidant properties,and may not have the same inflammatory effects as their processed counterparts, HFCS and other processed sugars are linked to spiking inflammation through improper absorption in the body and the disruption of healthy gut bacteria.

Image Source: MD Anderson Cancer Center

“But I can’t live without sugar!” While one sweet treat per day may only slightly keep the doctor away, there are ways to live a sugar-free life to keep inflammation and health concerns to a minimum. In fact, swapping refined sugars for natural sugar concentrates, such as honey, coconut sugar, sorghum, and even natural sugar cane, can have health benefits, including aiding weight loss.

Natural sugar substitutes, such as stevia and monk fruit, derived from plants, offer sweetness levels similar to table sugar when added to foods and meals and have zero calories, reducing the risk of weight gain.

The reality of sugar intake is anything but sweet when considering your inflammation levels. At least, it’s not as sweet for processed sugar. However, you don’t have to cut out sugar from your life completely to reap any benefits. Natural sugar substitutes consumed in healthy moderation are a sure-fire replacement for the sweetness we all know and crave in our diets. And they may even offer additional health benefits while keeping chronic inflammation low. So put down the processed, and go for au naturale. Your inflammation will thank you.

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Health jargon is all around us. We all encounter health and medical terminology or language at one point in our lives. From prescription labels, medication packets, doctor’s forms, bloodwork results, and more, understanding it all is daunting. From a patient’s perspective, understanding medical language is important. Still, it can be impossible, creating a barrier to learning more about a diagnosis, a medication, or a medical situation that requires action.

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Health literacy is defined as an individual’s “capacity to obtain, process and understand basic health information and services needed to make appropriate health decisions.” (Nielsen-Bohlman et. al., National Academies Press (US), 2004). Health jargon, technical words, and terminology that are complex and difficult to understand at the average level make healthy literacy less accessible. As a consequence, individuals are more likely to end up hospitalized, go to the emergency room, misinterpret prescription labels, and have higher mortality rates and health care costs (Berkman, Nancy D et al.).

When a doctor walks a patient through a life-altering diagnosis, using medical jargon like “malignant neoplasm” to describe a cancer diagnosis, the patient may be left scared, confused, and most importantly, uninformed about their serious condition. When an individual reads the prescription label on a bottle of pills and doesn’t know what a “corticosteroid” is, they are left uninformed about the medication’s purpose and possible side effects.

In both scenarios, healthcare professionals can approach the jargon differently. Instead of using medical terminology to describe a cancer diagnosis, a doctor should say that it’s cancer. When prescribing a corticosteroid to an individual, the doctor should explain that the medication is an anti-inflammatory drug and could cause high blood pressure, not hypertension.

Had medical jargon not been used in these situations, a cancer patient could go forward without receiving proper treatment, and an individual with a history of high blood pressure would not be monitored for poor side effects from an anti-inflammatory drug. These are the outcomes related to poor health literacy and misunderstanding of medical jargon.

The outcomes of health illiteracy affect Americans disproportionately. In the United States, senior citizens, who have a greater need for health services, conversely have the lowest health literacy rates out of any age group. When an individual, especially those in older age, lives in a U.S. county with high rates of health literacy, they are more likely to receive positive healthcare, such as more flu shots, and avoid hospitalizations, hospital readmissions, ER visits, and incur lower health-related costs (UnitedHealth Group, 2020).

To move forward in ensuring health literacy is more accessible and that medical jargon is understood, resources and practices must be implemented in all settings, from doctor visits to media presentations and beyond. A key foundation for accessible health literacy is the use of plain language, which involves breaking down technical terms into easily understood words and phrases. Medical and healthcare professionals must also consider culture and language barriers between themselves and the individuals they serve to ensure that no confusion or misunderstandings occur. Research into the audience they are serving is important for accessing health literacy effectively (CDC, 2024).

The push to have nationally recognized resources for health literacy is a momentous step in the right direction toward understanding medical jargon. Sources such as the U.S. Department of Health and Human Services, the U.S. Department of Education, and the National Assessment of Adult Literacy all present findings and solutions to the lack of health literacy amongst American adults. These resources should be referred to frequently to expand healthcare professionals' knowledge of how they can assist with accessibility (CDC, 2024).

As writers and editors in the health and medical writing space, it is our responsibility to ensure that medical topics and terminology are written in plain and simple language for all audiences. Whether you are a writer, editor, or healthcare professional, there are clear ways to make a positive impact on the health of individuals by allowing easy access to health literacy.

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Sources:

Berkman, Nancy D et al. “Low health literacy and health outcomes: an updated systematic review.” Annals of internal medicine vol. 155,2 (2011): 97-107. doi:10.7326/0003-4819-155-2-201107190-00005

CDC. “Understanding Health Literacy.” Health Literacy, 16 Oct. 2024, www.cdc.gov/health-literacy/php/about/understanding.html CDC. “What Is Health Literacy?” Health Literacy, 8 Oct. 2024, www.cdc.gov/health-literacy/php/about/?CDC_AAref_Val=www.cdc.gov/healthliteracy/learn/index.html

Institute of Medicine (US) Committee on Health Literacy. Health Literacy: A Prescription to End Confusion. Edited by Lynn Nielsen-Bohlman et. al., National Academies Press (US), 2004. doi:10.17226/10883

UnitedHealth Group. “Improving Health Literacy Could Prevent Nearly 1 Million Hospital Visits and Save over $25 Billion a Year,” UnitedHealth Group, Oct. 2020, www.unitedhealthgroup.com/content/dam/UHG/PDF/About/Health-Literacy-Brief.pdf.