My year of torment began with a brutal headache. The pain came on gradually over several weeks, as if some part of my brain were being slowly squeezed in a vise. Darkness lapped at the edge of my vision. Over-the-counter painkillers didn’t help. Occasionally, a dementia-like loss of vocabulary struck, often when I was talking to people over the phone. I found myself unable to recall easy things like “Washington, D.C.” or “George Clooney.” I’d end up staring at my computer without any inkling of what I’d sat down to do.Listen to This ArticleListen to this story in the New York Times Audio app on iOS.I suspected something was wrong with my sinuses because I had sinus infections in the past, and this headache was accompanied by a waterfall of mucus running down the back of my throat: postnasal drip, in medical parlance. I figured it wasn’t Covid, which a test eventually confirmed. When I went to the only ear, nose and throat doctor who could fit me into her schedule, she gently inserted a long, flexible rubber scope into my nose to examine my sinuses. As I sneezed and gagged, she pushed the scope farther, to peer down my throat. I might have reflux, she said — acid splashing up from my stomach into my esophagus. She could see “damage” in my pharynx. She seemed unconcerned, though. Some people have terrible reflux but don’t feel a thing, she said; others have a little reflux, and it causes intense discomfort. I must belong to the former group, if my throat looked like this and I wasn’t feeling pain there now. She prescribed a course of antibiotics to clear out whatever nasty microbes might have established themselves in my sinuses, the presumed source of my pain.Unfortunately, something was starting to disturb my insides. It began as a faint sensation of heat under my sternum and over several weeks grew stronger, until it felt as if some part of me had caught fire. The sensation reached an apogee one night following a meal of greasy quesadillas with hot peppers. After that, I changed my diet, abandoned coffee and avoided heavy foods, all said to aggravate reflux. But whatever was happening to me only got worse. Warmth began to rise in my throat soon after every meal, no matter how light or bland the food. To avoid the feeling of lava bubbling up within me, I ate as little as possible. I started to lose weight.I didn’t know it at the time, but I was embarking on a journey into territory I knew well. My ailment, it would turn out, was of a piece with a much larger development in affluent countries over the past 150 years or so. As improved sanitation, vaccines, antibiotics and other innovations beat back infectious diseases, some chronic diseases have been on the rise, including disorders in which the very immune system meant to protect us turns on us instead. A leading explanation for such self-sabotage involves the changes we have wrought on our microbiomes, the communities of microbes living in and on our bodies. As a science writer, I’d covered this phenomenon extensively. But despite having written a book about some of the diseases involved and the reasons for their increasing prevalence, I hadn’t ever considered how they could lead to the kind of unremitting pain that was making my life so miserable now at 47.I had to call several gastroenterology clinics to find a doctor who could perform an endoscopy reasonably soon. The procedure, which often involves sedation so that a thin tube with a tiny camera at the end can be pushed down the throat, revealed that my esophagus had abnormal rings — swellings — over its entire length, like a corrugated drainpipe. The doctor, my first gastroenterologist, said he couldn’t be certain, but those rings seemed to indicate a rare allergic condition called eosinophilic esophagitis (EoE).Eosinophils are specialized white blood cells that help repel intestinal parasites and bacteria. They can also play a role in various allergic diseases, including asthma and eczema. In my case, though biopsies showed elevated eosinophil numbers, they were below the cutoff used to diagnose EoE. But there was a confounding factor: To treat my presumed reflux, a week earlier I started taking Prilosec, an over-the-counter antacid drug that can also suppress eosinophils. It was impossible, in other words, to say whether I had an allergic condition obscured by the medication, or simply an unusual case of gastroesophageal reflux disease, or GERD.But a definitive diagnosis didn’t really matter, the doctor explained, because EoE and severe reflux are both treated with Prilosec or other drugs in the same class called proton pump inhibitors, or P.P.I.s. These medications suppress the production of the stomach acid that helps digest food. He recommended that I quadruple the dosage.Most people take the drug without problems — P.P.I.s are widely used — but for me the side effects of such a high dose were horrendous. I couldn’t see straight or read very well. I couldn’t concentrate. Worst of all was a bone-crushing fatigue. Getting up from the couch became a groan-inducing ordeal of unsteadiness. My doctor said I’d have to be on this medicine for at least eight weeks. If everything was better, why did I still feel so miserable?Unable to work, I ended up spending the better part of two months lying in the hammock in my tiny backyard. I could no longer tolerate food with strong flavors, so I subsisted on brown rice, lentils, steamed vegetables and small amounts of chicken breast. At some point, my wedding band slipped off my thinning fingers, lost without my realizing it. One evening, my 10-year-old daughter, the eldest of my three children, burst into tears and said, “I just want you to get better!” But my condition worsened. Increasingly I felt as if I couldn’t breathe. I had severe asthma as a child, but the disease hadn’t troubled me greatly since then. Now, however, my breathing became more labored. The usual inhalers didn’t help. The bottom half of my lungs seemed to be filled with cement. And then, starting one morning in July 2021, the gasping attacks began. Every other day or so, an acute feeling of suffocation overwhelmed me. These attacks left me hot, panicked and sweaty. The fastest way to quell them, I discovered, was to sit in front of an air-conditioning unit going full blast and hold my breath for as long as I could. Somehow that calmed what I began to suspect was a problem with my nervous system.I live in the San Francisco Bay Area, and by now I had a new gastroenterologist, a doctor at Stanford Health Care, affiliated with the university and a specialist in EoE. The burning sensation had me convinced that I suffered from severe reflux. But she told me that all the acid-suppressing medicine I was taking — she’d advised me to add a few other types to the mix — meant my stomach probably wasn’t making much acid at all; acid in my esophagus was not causing the pain, most likely. Even so, she ordered tests to confirm her thinking. A pill-shaped gizmo inserted into my lower esophagus was used to measure acidity; another tube of sensors measured how well the sphincter that separated the stomach from the esophagus, which was essential in preventing stomach acid from splashing backward, squeezed shut. The results of these and other exams were both reassuring and baffling: Everything appeared to be working normally. The pressure of my lower esophageal sphincter was fine; the wavelike motion of swallowing, called peristalsis, was normal. There was no acid reflux. The ringlike swellings in my esophagus had faded. The number of allergic eosinophil cells had declined. I faced a conundrum: If everything was better, why did I still feel so miserable?During my years of interviewing doctors, I haven’t been able to help noticing the exasperation some of them feel toward patients who look for medical guidance online — what one of those physicians once called Dr. Google — and then come into the office making demands based on what is often incomplete information or outright misinformation. I tried to walk a fine line with my doctors, pointing out that I was a science writer (blank stares), and that I read a lot of scientific articles (more blank stares, now tinged with apparent dread). I wanted them to know they were the bosses. I just had lots of questions. Convinced that I had an extreme case of GERD, I compiled a list of surgeries and procedures used to tighten or repair the lower esophageal sphincter. I contacted specialists in the breathing problems associated with GERD. I looked into alternative treatments: the sleep aid melatonin; acupuncture; a new acid-suppressing drug first introduced in Japan. My research helped in some areas. It was because of what I had learned about EoE that I left my first gastroenterologist, who didn’t seem to know much about the condition.Yet the endless quest for answers also spiraled into a kind of madness. An ever-expanding decision tree paralyzed me. If it was X, then I’d do Y surgery. If it was A, then I’d take B drug. I was driving myself nuts with all that reading, my wife said. But if I didn’t do this research, I countered, who would? My new gastroenterologist had a theory to explain the all-consuming pain under my sternum. Sometimes patients develop a hypersensitivity syndrome, she told me. The original insult — in my case, inflammation of some kind — might be long gone, but the nerves that convey pain can become overactive and begin firing at the slightest provocation. When this happens, stimuli you normally wouldn’t even notice can cause extreme pain. I was skeptical. The pain felt exactly as if my esophagus were being burned by, yes, hydrochloric stomach acid. How could it be some kind of sensory hallucination?She explained it as “a headache of the esophagus.” And that “headache” might be treatable with an unlikely approach: neuromodulating drugs that were first developed to manage depression. Scientists don’t completely understand how antidepressants help pain syndromes, but certain ones seem to impede pain signals in the nervous system. There were two kinds on offer, she informed me: one that might give me diarrhea but also energy, or another that could make me tired and constipated.No contest: I requested diarrhea with energy. The drug, an antidepressant called duloxetine — one of its brand names is Cymbalta — increases in the brain levels of both serotonin and norepinephrine, chemical messengers that can help modulate pain signals. I didn’t get energy or diarrhea from the duloxetine, however. Instead, I became dizzy and nauseated. Food tasted off. Anything with a soft texture triggered a sense of revulsion. After a few weeks, those side effects faded. And that’s when things began to turn around. I could tolerate more and different kinds of food. Cheese and eggs. A tart apple. One day, after several weeks of feeling better, I ate so much that the burning pain came roaring back. My doctor recommended that I double my duloxetine dose. The improvements accelerated.After six months on the P.P.I.s that made me feel half dead, my gastroenterologist granted my wish to stop taking them. In early 2022, another endoscopy and another acidity study finally, almost a year after the ordeal began, yielded a conclusive diagnosis. Once I was off the P.P.I.s, the corrugated drainpipe-like swellings returned, just without the pain, thanks to the duloxetine. My eosinophil counts, detected in little plugs of flesh the doctor took from my esophageal lining, had skyrocketed. I had eosinophilic esophagitis. My food pipe had been chronically inflamed by an allergic reaction, most likely in response to some food I was eating.As many as one in every 1,000 Americans, according to recent studies, is afflicted with eosinophilic esophagitis, making it rare but not vanishingly so. Although the condition is somewhat obscure, I learned about it years earlier, while researching my 2012 book “An Epidemic of Absence,” which explores the reasons behind the rise of allergic and autoimmune diseases in affluent societies. I had seen it mentioned as one more example of the growing number and variety of allergic diseases we seem prone to developing. I was also, I knew by now, very likely predisposed to develop EoE: male, asthmatic and already allergic to two foods that I knew of (peanuts and sesame make me vomit), all conditions that occur more frequently in people with EoE than those without. In a way, the discovery that I had EoE felt like a diagnosis preordained, like a biological fate.The bigger issue, the one that inspired my book, was the question of where diseases like this came from. Hay fever, one of the most common allergic diseases, seemed to become more prevalent in the late 19th century, as did asthma in the mid-to-late 20th century. But EoE was first understood as a type of food allergy only in the 1990s, after which diagnoses began to increase. While this change probably stemmed in part from doctors’ greater awareness of the disease, research led by Evan S. Dellon, a gastroenterologist who specializes in EoE at the University of North Carolina School of Medicine, suggests that the disease has in fact become more common. When he and his colleagues analyzed Danish records of biopsies taken between 1997 and 2012, they did indeed find that the rate of biopsies — a signal of how often doctors were looking for EoE — doubled. Yet test results and symptoms indicative of EoE rose nineteenfold, far outpacing the jump in biopsies. More recent studies have reached a similar conclusion. When the incidence of a noninfectious disease changes so quickly — faster than our genomes can possibly accumulate new mutations that increase susceptibility — scientists suspect that changes in the environment are responsible. And studies involving twins point to an environmental trigger for EoE. According to one paper on both identical and fraternal twins, just 14.5 percent of the risk was attributable to genetics, with the rest determined by the twins’ surroundings. “We think it’s something in the prenatal environment,” says Amanda Muir, a pediatric gastroenterologist at the Children’s Hospital of Philadelphia, referring to in utero exposures.Other possible factors include common chemicals, like pesticides and food additives. For one Mayo Clinic study published earlier this year, scientists induced eosinophilic inflammation in the esophagi of mice merely by giving them drinking water with a small amount of detergent in it. The soap used in the study, sodium dodecyl sulfate, is an ingredient in some toothpastes and dish soaps. None of these possible explanations for EoE are mutually exclusive. Its causes are most likely multifactorial, Dellon says, with several simultaneous “hits,” as he calls them, required to induce the disease. Changes to the microbiome, which can occur for all sorts of reasons, also seem to be a major factor making people susceptible to EoE. Elizabeth Jensen, an associate professor of epidemiology at Wake Forest University School of Medicine, and her colleagues have found that having been breastfed — which, along with its other benefits, is thought to cultivate a healthier microbial garden in the infant gut — is protective against the disease, for example, but so far only in children with certain gene variants suspected of making the esophageal barrier more permeable. Jensen, who suffers from EoE herself, thinks that one explanation for this finding is that by nudging children’s microbiomes in a healthier direction, breastfeeding blunts their chances of developing EoE.Conversely, antibiotics taken early in life are associated with an increased risk of EoE later, according to Jensen’s research (a pattern also observed in studies of those with asthma, pediatric-onset inflammatory bowel disease and pediatric autoimmune arthritis). That’s probably for exactly the opposite reason: Along with the targeted pathogen, the medicine can kill off protective microbes. On the whole, Jensen’s findings suggest that it may not be some new environmental exposure alone that is driving the rise of EoE but also that we are peeling away layers of protection — and in some cases may never acquire that protection at all — by having changed what microbes live around, in and on our bodies.Here, Jensen’s research intersects with a much larger body of science that is sometimes misleadingly labeled the “hygiene hypothesis,” though it has nothing to do with personal hygiene. The research posits that the rise of allergic diseases over the past 150 years, and the apparent increase in many autoimmune disorders as well, may be evidence of a single phenomenon: a population-wide derangement of our microbial communities and the immune systems these communities train — a single problem, but one that expresses itself in many different ways. By late autumn in 2021, nine months into my ailment, I faced a new difficulty. The duloxetine never delivered on the promised energy (or diarrhea). But it did cause drenching night sweats and sleepiness. I was constantly yawning. And somewhere along the way, I lost all drive to do much of anything. The antidepressant was, I surmised, depressing me. I had to continue taking it, I knew, to keep the horrible pain at bay, but I yearned for an “upper,” some kind of stimulant. I asked my doctors to prescribe a drug that would animate me — Ritalin, perhaps. They were hesitant to prescribe a habit-forming medicine to counter the side effects of another drug and recommended evaluation by a psychiatrist instead. After much searching — the surge in mental-health troubles during the pandemic was keeping psychiatrists booked up — I found one who could see me over Zoom. He prescribed a drug called bupropion, which affects the dopamine pathways in the brain that underlie our sense of motivation and reward. (It’s also used to help people stop smoking.) Bupropion can cause dry mouth and insomnia, but I didn’t develop these side effects, thankfully, and the medicine ended up being miraculous. Very quickly, I could focus again. I cared about things. When I told my sister about this pill, she said, half-jokingly, “Can I have that psychiatrist’s number?”I saw disparate-seeming episodes that had distressed me going back decades in a new light.There were no F.D.A.-approved treatments for EoE itself. The available treatments were off-label, consisting of drugs primarily prescribed for other conditions. I hadn’t tolerated the high doses of P.P.I.s, the usual first treatment, so in February 2022, I began swallowing liquid steroids meant to be inhaled as an asthma treatment; I mixed the medicine with honey to help it stick to my esophageal wall. According to biopsies taken soon after, from the fourth endoscopy within a year’s time, the medicine did a good job of controlling the allergic inflammation.Steroids can cause cataracts, osteoporosis and other complications if used in excess or for too long. But the type I’ve been taking for over a year and a half, called budesonide, is formulated to be topical; supposedly only a minimal amount enters circulation. Eventually I hope to identify the food I’m allergic to so I can avoid it and stop the steroids completely. But because skin-prick tests and blood tests, the usual ways of identifying an allergy, do not work well for EoE — neither test really measures what eosinophils are specifically doing in your esophagus, the location of this disorder — the only reliable way to identify an allergen is to eliminate certain food groups and then examine the esophagus directly to see if the inflammation has improved, followed by additional endoscopies as you reintroduce each food group. The onerous process can require many months to complete, and depending on what foods turn out to trigger an allergy, they can be hard to avoid anyway. So my gastroenterologist and I decided that for the time being, I would continue treating the EoE with steroids.In May 2022, the F.D.A. approved the first drug for EoE. Called Dupixent, it inhibits two immune-signaling proteins that help drive the type of allergic inflammation underlying EoE. I was raring to get on the stuff; I’d been reading about it in journal articles and on medical news sites for months. But after learning about its potential downsides — including the activation of herpes virus infections, a rash, eye inflammation and the possibility that it might not be covered by insurance — I held off. With any new drug, my doctor pointed out, “you don’t want to be first. You want to be next.” Now that I knew what ailed me, and had a treatment regimen that was at least controlling the problem, I saw disparate-seeming episodes that had distressed me going back decades in a new light: a painful lump in my throat in my 20s that I attributed to stress; an occasional sensation of breathlessness, also in my 20s, that I thought was allergies. All along, some still unidentified food was probably inflaming my esophagus. The long lag time between the appearance of symptoms and a diagnosis wasn’t unusual, I learned. Evan Dellon of U.N.C.’s medical school told me that the lag time for diagnosing this condition typically ranges between five and eight years. People with EoE often have difficulty swallowing food years before they know what the cause is. They may develop unconscious coping mechanisms, reflexively avoiding mealy potatoes, say, or gristly steak. I had developed my own workarounds. After choking on a Tylenol pill years ago, for example, I started crushing all pills before swallowing them so they wouldn’t stick. Perhaps because of the constant fear of choking, esophagitis is closely linked with anxiety and depression. More than a quarter of adults with EoE take anti-anxiety or antidepressant drugs — a “really striking finding,” Dellon says. Food, he says, should never catch in your esophagus, a long flexible and muscular tube that extends down from the throat and that, when healthy, should be stretchy and well lubricated enough to pass large blobs of chewed-up stuff. “Nothing is normal about food sticking,” he says. The burning pain I felt wasn’t unusual, either, Dellon told me. He pointed to animal experiments that showed how an allergy could, over time, lead to a pain syndrome. Scientists induced EoE in guinea pigs and let it progress for a while. The chronic allergic inflammation in their esophagi eventually heightened the sensitivity of nearby nerve cells to painful stimuli. In Dellon’s experience with people, that sort of hypersensitivity can persist long after the inflammation has resolved. “That’s what I see relatively commonly in patients,” he said. Everything looks normal. No swelling. Biopsies show a reduction in eosinophils. But the patients complain of persistent pain. Doctors are increasingly aware of these kinds of pain syndromes in many disorders, including GERD. The condition, whose primary symptom is known colloquially as heartburn, is pervasive, afflicting an estimated one in five Americans. Some of these patients continue to feel intense pain even after their stomach acid has been reduced with antacids, a malady most likely caused by a hypersensitivity syndrome similar to mine. Ronnie Fass, the medical director of the Digestive Health Center at MetroHealth in Cleveland, argues that the treatment of GERD-like symptoms should accommodate this new understanding: Neuromodulators should be considered right away for those experiencing esophageal pain. “We should not wait until patients fail treatment to identify that esophageal hypersensitivity plays an important role,” he told me. Unfortunately, he adds, patients often refuse antidepressants because in their minds, using psychiatric medicine means they’re mentally ill. They tend to request opiates instead.As for the air hunger I experienced, my gastroenterologist rejected any connection to my esophageal problems. I’d sent her articles on how reflux disease could worsen asthma, trying to convince her that the two could be linked. Because the megadose of P.P.I.s I was taking at the time meant my stomach probably hadn’t been producing enough acid to irritate my esophagus, my breathing difficulties more likely stemmed from an allergic reaction to something in the environment, she said, because I was clearly an allergy-prone fellow. I didn’t press her on this, but I didn’t completely agree with that reasoning. To my mind, it didn’t matter whether irritation was actually occurring. What mattered was whether my nervous system thought it was. That had been the great lesson of my pain syndrome: The burning sensation persisted even when the disease that caused it had quieted down.Indeed, the breathing problems began to improve only once I started the duloxetine, suggesting (to me, at any rate) that the issues with my lungs, like the pain syndrome, emanated from a nervous system at cross purposes with itself. Yet when I began asking experts how these things might be related, several of them noted that reflux could exacerbate asthma or cause a sensation of breathlessness, but there wasn’t enough data to say the same about EoE. When I brought up my episodes of feeling suffocated, the scientists waffled. I got the sense that they thought I was really having panic attacks. It wasn’t until I called Brendan Canning, a professor of medicine at Johns Hopkins, that I found someone willing to speculate how an allergy in the esophagus might lead to the terrifying sensation of drowning. Canning, a self-described “science nerd,” is not a physician but a researcher who focuses on allergies and airways. He explained to me that the nerves that transmit pain, air hunger and other information from our organs lead, like telegraph lines, to very primitive parts of the brain that are physically near one another. Because of this proximity, the neurons receiving signals sometimes have a hard time determining precisely where the message is coming from. It might be that any irritation in the esophagus, whether from an upward surge of acid or inflammation spurred by a food allergy, could be interpreted as originating in the lungs — or even the heart — and a body might respond, as mine apparently did, with the panic of someone who’s drowning. “It’s not surprising that this could happen,” Canning said, given “the tremendous overlap that exists in the brain stem.” Why has there been no moonshot program to conquer allergic disease? Eosinophilic esophagitis is rare, but allergic diseases as a group include the itchy skin of eczema, the hives and vomiting of food allergies, the runny noses of hay-fever season, the breathing problems of allergic asthma and more. They afflict nearly one in three Americans, making life miserable for vast swaths of the population. And if the microbiome has been implicated for so long in these ailments — and now in EoE — why is it taking so long for a microbiome-targeting therapy to become available? “We’re wondering about that, too,” Alkis Togias, the chief of the Allergy, Asthma and Airway Biology Branch at the National Institute of Allergy and Infectious Diseases, told me. In recent years, the institute has fielded only a few applications for microbiome-related studies, he says — far fewer than anticipated. Scientists aren’t convinced that they have identified the right microbes, he suspects. But Togias says that the agency is taking the allergy problem seriously and that funding for the study of food allergies, for example, has risen to between $60 million and $80 million per year now from $1.3 million in 2003. “It’s a very big jump,” he says. “But I totally agree with you. It should be more.” Much of the science on the microbiome suggests that what you encounter early in life sets the tone for how your immune system works later, so many in the field understandably focus on prevention, rather than on how to correct an already-dysfunctional community of microbes. But a few researchers have been pursuing the prospect of changing those adult microbiomes as well. A few years ago, Rima Rachid, the director of the Allergen Immunotherapy Program at Boston Children’s Hospital, and her colleagues gave 10 adult volunteers with peanut allergies microbes from nonallergic donors. The subjects ingested, in capsule form, carefully screened feces from healthy people in order to see if the microbes it contained could give them relief from nut allergies. After four months, three subjects could tolerate at least three times the amount of peanut protein compared with amounts that originally triggered reaction. That translated to a little more than one peanut. Three out of five other patients who, before swallowing the capsules, took antibiotics, presumably clearing out their own distorted microbiomes and making it easier for the new ones to establish themselves, could tolerate more than two peanuts’ worth of protein. The study was tiny, lacked a control group and was hardly conclusive. (A follow-up study is underway with children.) And EoE doesn’t work exactly like these more common nut allergies. But the research gives people like me, adults with established allergic disease, reason to hope. “I don’t think you can say that once your microbiome is formed, you’ve lost hope,” Rachid told me. “There is a possibility of changing the microbiome.”There may also be a new class of microbe-inspired medicine on the horizon, a drug that doesn’t even have a name, just a number: ‘1104. Early studies suggest it reduces eosinophils in patients with EoE, as well as other white blood cells that contribute to the disease. It also increases patients’ own “regulatory” T cells and B cells, which are thought to be crucial in preventing the inappropriate immune aggression that underlies many allergic diseases. The drug is based on a molecule derived from Mycobacterium tuberculosis, the pathogen that causes tuberculosis. The bacterium can establish long-term infection in the body by suppressing the immune system. Some studies have observed that people carrying latent TB infections appear to have a lower risk of developing asthma, as do those who have been vaccinated against TB. Revolo Biotherapeutics, the company developing ‘1104, is seeking to leverage the bacterium’s ability to “reset” the immune system. If further human trials pan out, maybe we’re headed toward a new generation of drugs derived from our interactions with microbes that inhabit our bodies.In June 2022, I decided I’d had enough of duloxetine. It proved pivotal to my recovery, but after 10 months of constant exhaustion — I’d stopped the bupropion, which turned out to irritate my esophagus — I was ready to be weaned off it. My psychiatrist warned me about possible withdrawal symptoms, including “zapping” sensations akin to electric shocks. The warning didn’t quite prepare me. The “electric” shocks were more like being struck unconscious for a millisecond while cold, blue flames rushed up my backbone.For about a week, the side effects were intense enough that I considered resuming the duloxetine. (As it happens, Eli Lilly, the company that first manufactured duloxetine, has been repeatedly sued by patients claiming that it hadn’t given them full warning about the difficulty of discontinuing the antidepressant.) Happily though, the worst of the symptoms began to fade after about two weeks. And I no longer felt as if I was constantly fighting the urge to nap, which was encouraging. My mind felt less enveloped in cobwebs. And the burning pain remained quiescent. I was not cured, just much better. I occasionally felt nagging pain under my sternum. I still couldn’t eat certain foods, particularly the spicy cuisine I used to adore, and the heavy, greasy foods loved by many. My breathing still felt off sometimes, as if I couldn’t fully inhale. But there were periodic moments when I felt better than I had in a long time, presumably because I was finally treating a disease that had been on a slow burn for years, maybe decades.And then this past February, about seven months after my last dose of duloxetine, the burning returned. The paradox was that even though I was now treating the EoE with steroids, I felt pain as if the disease were raging uncontrolled. Evidently my nervous system could be easily reactivated to produce this burning sensation. I went back on the duloxetine, although this time a much lower dose did the trick.I often remind myself how fortunate I’ve been. Because of my work as a science writer, I already had some familiarity with EoE and I was relatively comfortable navigating the byzantine medical system and advocating for myself. My wife has a well-paying job that allowed me to stop working for a year and not worry too much about finances or health insurance. New treatments are either available or in development for a disorder doctors barely understood just three decades ago. Still, any disease in which the body overreacts (allergy) or turns against itself (autoimmunity) is bound to inspire a unique kind of desperation. Those of us in this club we never asked to join have bodies that are, in ways both literal and figurative, self-lacerating. Our magnificent and complicated bodily defenses, our immune systems, instead torment us. What we yearn for is a single treatment that can, once and for all, correct this wayward tendency toward self-destruction.Moises Velasquez-Manoff is a writer based in California. His last article for the magazine was on vaccine hesitancy in the wake of the Covid-19 pandemic. He is also the author of the book “An Epidemic of Absence: A New Way of Understanding Allergies and Autoimmune Diseases.”
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