What the Mystery of the Tick-Borne Meat Allergy Could Reveal

Posted on July 30, 2018 by

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By Moises Velasquez-Manoff

Unraveling why tick bites are suddenly causing a strange reaction in some people who eat meat could help scientists better understand how all allergies work.

One spring evening in 2016, Lee Niegelsky’s underarm began to itch. An investment manager, he was doing housework around his condo, and he thought he’d been bitten by a chigger. But within 15 minutes, hives had erupted all over his body. He responded with what he calls a “typical man reaction” — if the hives didn’t clear up by the next day, he would have them checked. Fifteen minutes later, the itch had become unbearable. He needed help right away.

His wife wasn’t home, so he drove himself to the university hospital emergency room near where he lived in Chapel Hill, N.C. As he explained his symptoms at the check-in counter, he began to feel faint, then fell to one knee. An orderly offered a wheelchair. He sat down — and promptly lost consciousness.

When he came to, he was on the floor. He had rolled out of the wheelchair and hit his head. A gaggle of worried-looking medical staff stood over him. They asked if he was on drugs. Did he have heart problems? His blood pressure was extremely low, probably the reason he had passed out. Niegelsky, who was 58, told them that he was healthy and drug-free and had no heart condition. “I could see the concern on their faces in a way that did not help my confidence level at all,” Niegelsky says.

He felt as if insects were biting every inch of his hands, armpits and groin. A doctor asked if he had any food allergies. The hives and the low blood pressure suggested anaphylaxis, a severe allergic reaction. Again the answer was no, but Niegelsky did recall that he had a very bad allergic reaction a month earlier to a tick bite he got at a concert.

The E.R. doctor ordered two shots of epinephrine, a form of adrenaline that dampens the allergic reaction; the hives and itching began to subside about 25 minutes later. Now the doctor asked Niegelsky what he’d eaten that day. A hamburger for lunch, Niegelsky told him. In his recollection, the doctor’s eyes widened, and he said, “I think we know what you have” — a condition called mammalian-meat allergy.

Meat allergy was first observed in the 1990s and formally described in 2009, which makes it a relatively recent arrival to the compendium of allergic conditions. Its most curious quality may be that it is seemingly triggered by a tick bite. In America, the culprit, called the lone-star tick — females have a distinctive white splotch on their backs — is common in the warm and humid Southeast, where most cases of meat allergy have been diagnosed. Niegelsky had in fact heard about the allergy from friends. He remembers shaking his head and thinking that it sounded “made up.” He understood now, in a visceral way, how real it was. That bite from a month ago had primed his body for today’s hives and plummeting blood pressure.

Until meat allergy was recognized, the prevailing medical wisdom held that an allergic reaction to meat from mammals was extremely unusual. Unlike that from shellfish, say, meat from mammals was thought by some allergists to be too similar to human flesh for the immune system to attack it with the full fury of the allergic arsenal. In this and other respects, meat allergy is upending longstanding assumptions about how allergies work. Its existence suggests that other allergies could be initiated by arthropod bites or unexpected exposures. It also raises the possibility that other symptoms often reported by patients that clinicians might dismiss because they don’t fit into established frameworks — gluten intolerance, for example, or mucus production after drinking milk — could, similarly, be conditions that scientists simply don’t understand yet. Mammalian-meat allergy “really has the potential to revolutionize our understanding of food allergy, because it doesn’t fall under the umbrella of our paradigm,” Dr. Maya R. Jerath, a professor of medicine at Washington University School of Medicine, in St. Louis, told me. “Maybe our paradigm is wrong.”

The meat-allergy story begins somewhat obliquely, with a new drug for metastatic colon cancer called cetuximab. In 2006, Thomas Platts-Mills, an allergist at the University of Virginia School of Medicine, received a phone call from a colleague. Oncologists testing cetuximab were baffled to find that nearly one in four patients had severe anaphylactic reactions to the drug. A few patients even died. The caller urged Platts-Mills to look into the mystery. He agreed and began by comparing the blood from those who had an allergic response to cetuximab with the blood from those who didn’t. The patients who reacted, he discovered, had allergic antibodies to a complex sugar called galactose-alpha-1,3-galactose, or alpha-gal for short. Most mammals produce alpha-gal; it’s a component of their cell membranes. The exceptions are African and Asian apes and monkeys. As primates of African origin, we do not produce alpha-gal, either. That makes the human immune system unusual: It can learn to see alpha-gal, present in the beef and pork and other mammalian meat we eat, as foreign and threatening, thereby allowing for an allergic response. Cetuximab contained alpha-gal, it turned out; the sugar came from the genetically modified mice used to manufacture the drug.

While Platts-Mills had identified the molecule in the drug causing these severe allergic reactions, he didn’t yet know why those patients were allergic to it. How had their immune systems become sensitized to it? Humans aren’t born allergic to anything; allergy is like a bad habit the immune system needs to learn. Many scientists suspect that our allergic machinery — the swelling of tissues, mucus production, the coughing and sneezing — served an important purpose in our evolutionary past. It probably helped us to fight off parasites. But in allergic disorders, the body unleashes this ancient anti-parasite response inappropriately against molecules that aren’t obviously dangerous (beyond their role in causing a reaction) — against cat dander or pollens or peanuts. The mystery of any allergy is how and why the immune system is first led to make this mistake.

Until meat allergy was recognized, the prevailing medical wisdom held that an allergic reaction to meat from mammals was extremely unusual. Unlike that from shellfish, say, meat from mammals was thought by some allergists to be too similar to human flesh for the immune system to attack it with the full fury of the allergic arsenal. In this and other respects, meat allergy is upending longstanding assumptions about how allergies work. Its existence suggests that other allergies could be initiated by arthropod bites or unexpected exposures. It also raises the possibility that other symptoms often reported by patients that clinicians might dismiss because they don’t fit into established frameworks — gluten intolerance, for example, or mucus production after drinking milk — could, similarly, be conditions that scientists simply don’t understand yet. Mammalian-meat allergy “really has the potential to revolutionize our understanding of food allergy, because it doesn’t fall under the umbrella of our paradigm,” Dr. Maya R. Jerath, a professor of medicine at Washington University School of Medicine, in St. Louis, told me. “Maybe our paradigm is wrong.”

The meat-allergy story begins somewhat obliquely, with a new drug for metastatic colon cancer called cetuximab. In 2006, Thomas Platts-Mills, an allergist at the University of Virginia School of Medicine, received a phone call from a colleague. Oncologists testing cetuximab were baffled to find that nearly one in four patients had severe anaphylactic reactions to the drug. A few patients even died. The caller urged Platts-Mills to look into the mystery. He agreed and began by comparing the blood from those who had an allergic response to cetuximab with the blood from those who didn’t. The patients who reacted, he discovered, had allergic antibodies to a complex sugar called galactose-alpha-1,3-galactose, or alpha-gal for short. Most mammals produce alpha-gal; it’s a component of their cell membranes. The exceptions are African and Asian apes and monkeys. As primates of African origin, we do not produce alpha-gal, either. That makes the human immune system unusual: It can learn to see alpha-gal, present in the beef and pork and other mammalian meat we eat, as foreign and threatening, thereby allowing for an allergic response. Cetuximab contained alpha-gal, it turned out; the sugar came from the genetically modified mice used to manufacture the drug.

While Platts-Mills had identified the molecule in the drug causing these severe allergic reactions, he didn’t yet know why those patients were allergic to it. How had their immune systems become sensitized to it? Humans aren’t born allergic to anything; allergy is like a bad habit the immune system needs to learn. Many scientists suspect that our allergic machinery — the swelling of tissues, mucus production, the coughing and sneezing — served an important purpose in our evolutionary past. It probably helped us to fight off parasites. But in allergic disorders, the body unleashes this ancient anti-parasite response inappropriately against molecules that aren’t obviously dangerous (beyond their role in causing a reaction) — against cat dander or pollens or peanuts. The mystery of any allergy is how and why the immune system is first led to make this mistake.

What had primed the patients to be allergic to the alpha-gal sugar? The oncologists did have one clue: They noticed that allergic patients tended to come from the Southeast. Initially Platts-Mills thought that maybe intestinal parasites or even a mold from the region was sensitizing patients to alpha-gal. But a technician in his lab pointed out that the geographical distribution of cases matched the reported distribution of a tick-borne disease called Rocky Mountain spotted fever. That got Platts-Mills thinking about ticks.

At the same time, he was seeing a growing number of patients in his allergy clinic, many of them hunters and outdoorsy types, complaining about what was apparently a strange reaction to eating meat. They suffered stomach pains and rashes hours later. When Platts-Mills analyzed their blood, he found that, like the cancer patients who had an allergic reaction to cetuximab, they also had allergic antibodies for alpha-gal. And when he and his colleague Scott P. Commins surveyed the patients, they found that more than 80 percent of them reported having had strong reactions to tick bites.

Independent of the research Platts-Mills was doing, in 2007 an Australian allergist named Sheryl van Nunen described 24 cases of meat allergy associated with tick bites. Colleagues were skeptical of her claims, she told me. They didn’t think an allergy to meat from mammals was very likely. And she hadn’t identified what the immune system was specifically attacking, the molecule in meat that was attracting the onslaught. That discovery fell to Platts-Mills, Commins and their colleagues. They posited that alpha-gal was the allergen that made people sick hours after eating hamburgers (or, in Australia, kangaroo steaks). And they proposed tick bites as the trigger. Ticks could explain the two seemingly disparate phenomena: why people who reacted to cetuximab came from the Southeast and why most cases of meat allergy occurred in the same region. The Southeastern lone-star tick was exposing and thus sensitizing people to the sugar through its bites. Some subset of the ectoparasite’s victims would thereafter react to alpha-gal whenever they encountered it, including in meat and cetuximab.

Platts-Mills still lacked definitive proof that a tick bite initiated the allergy. He hadn’t conducted an experiment in which, for example, he deliberately induced meat allergy in human volunteers. But one day in August 2007, he took a hike in the nearby Blue Ridge Mountains. When he got home, he discovered hundreds of larval-stage ticks feeding on his ankles. (He spent the evening removing them with a knife and Scotch tape.) Platts-Mills doesn’t eat red meat often — he had a heart attack in 2005 — but a few months after that hike, on a trip to Europe, he ate two lamb chops and had a glass of red wine. “Six hours later I was in a hotel, covered in hives, itching like crazy and laughing at myself,” he told me. By then, he thought he knew what was happening: The ticks had made him allergic to those chops.

In 2013, on a hike and a picnic with some friends in the Blue Ridge Mountains, Platts-Mills was again swarmed by larval ticks. By this time he was already monitoring his alpha-gal antibody levels, so he was able to compare how much antibody he had circulating before and after these ticks fed on him. Post-picnic, the allergic antibodies directed at alpha-gal in his bloodstream surged more than tenfold, direct evidence that tick bites had provoked the allergic response to alpha-gal. It seemed he had cracked the case, and others around the world took note. Sheryl van Nunen, now at the University of Sydney, told me this understanding of the precise cause of mammalian-meat allergy makes it unique. “This is really allergy in a kit — how to get it and how to lose it,” van Nunen said. “There’s really nothing else like it.

Another unusual aspect of meat allergy is that it can emerge after a lifetime spent eating meat without problems. In other food allergies, scientists think that children’s immune systems may never learn to tolerate the food in the first place. But in meat allergy, the tick seems to break an already established tolerance, causing the immune system to attack what it previously ignored. One way to understand how the parasite pulls this off is to consider its bite as a kind of inadvertent vaccine. A vaccine teaches an immune system to pursue a pathogen it otherwise wouldn’t by exposing it to weakened versions of that pathogen — an attenuated measles virus, say — or bits and pieces of dead pathogen. Vaccines also often contain a substance called an adjuvant, which is designed to spur the immune system into action.

In similar fashion, when the lone-star tick feeds, alpha-gal leaks from its mouth into the wound, exposing the victim’s immune system to the sugar, prompting the immune system to remember and pursue alpha-gal. But exposure to alpha-gal alone probably doesn’t achieve this feat. Commins, who is at the University of North Carolina, at Chapel Hill, has identified a candidate, an enzyme in the tick’s saliva called dipeptidyl-peptidase that works as an adjuvant. It’s also common in bee and wasp venom. This enzyme, Commins argues, is what tells your immune system to see alpha-gal as the type of threat that warrants the itching and swelling of the allergic response.

Once sensitized, some victims find that they can no longer tolerate beef, pork, lamb — even milk or butter, foodstuffs with only very small amounts of alpha-gal. Several factors can also affect the severity of the allergic reaction, or if there is an allergic reaction at all. Grilled meat is less allergenic than other methods of preparation that preserve more of its fat. Fatty meat leads to more alpha-gal crossing a person’s gut barrier into his or her circulatory system, triggering a stronger immune reaction than leaner cuts. A study of German patients also found that alcohol imbibed with meat can push people toward an allergic reaction, as can exercise; both actions make the gut more permeable, exposing the immune system to more alpha-gal.

As it happens, an immune response to alpha-gal is also what drives, in part, the rejection of tissue transplanted from animals to people. Scientists have developed genetically modified pigs meant to supply parts that can be grafted onto human bodies without eliciting an anti-alpha-gal immune reaction. Now, as awareness of the meat allergy spreads, there has been talk of using such alpha-gal-free pigs for food — pork chops your doctor can prescribe if you find yourself allergic to meat.

A recent study by scientists at the National Institutes of Health, which included Commins and Platts-Mills as co-authors, linked allergic sensitization to alpha-gal with a greater risk of arterial plaques, a hallmark of heart disease. It’s unclear whether having alpha-gal antibodies specifically increases your risk of developing plaques or whether some other factor increases a person’s risk of heart disease and sensitization to alpha-gal. But if it turns out that meat allergy pushes people toward cardiac arrest, it would imply that encounters with the lone-star tick contribute to the leading cause of death in the United States.

The big, unanswered question is why meat allergy is on the rise today. Commins estimates that at least 5,000 cases have been diagnosed in the United States, and many more probably remain undiagnosed. In some tick-heavy regions, the prevalence of meat allergy is estimated to be at least 1 percent of the population. Ticks are not new. Neither is the human consumption of meat. Why the sudden problem for so many? One possibility is that the ticks have changed somehow. Maybe they’ve acquired a pathogen we don’t understand yet, and this infection is causing the allergy. Or perhaps, Commins says, changes to the insect’s microbiome, the collection of symbiotic microbes that it carries in its body, have somehow made its bites more allergenic.

The idea is plausible and could nicely explain how an arachnid that has been around for a long time could begin causing a new set of complications. Scientists have long debated where the alpha-gal in the tick originates: Does it come from the blood a tick sucks from other mammals and then regurgitates as it feeds on people, or does it come from the tick itself? Shahid Karim, a vector biologist at the University of Southern Mississippi, in Hattiesburg, told me that the answer might be neither; the sugar probably comes from the microbes that the tick carries within it. So it’s entirely possible, he said, that changes in its microbiome could, by increasing the amount of alpha-gal humans are exposed to in tick bites, make the lone-star tick more likely to induce meat allergy.

What such an account fails to address, however, is why the meat allergy has increased in other parts of the world, like Australia and Europe. (Van Nunen says that in the tick country around Sydney, people are now more likely to carry EpiPens, which contain a shot of adrenaline, for meat allergy than for better-known peanut allergies.) Other tick species are linked with meat allergy in those regions, not the lone-star tick. And it seems very unlikely that the microbiomes of all these ticks on different continents have changed in similar ways at the same time. “I don’t for the life of me have a unifying hypothesis for why it’s happening everywhere,” Commins told me, although he added that pesticides could be one factor changing tick microbiomes globally.

It may simply be that an increase in the number of ticks has turned a problem once so rare that it went scientifically unnoticed into an observable epidemic. “I think we’ve got far more tick bites today than people had as recently as 35 years ago,” Platts-Mills told me. He lays the blame for the growing spread of ticks on newly abundant deer. In Virginia, he thinks new laws requiring dogs to remain on leashes have emboldened deer, which then bring ticks closer to people. People aren’t necessarily venturing deeper into the forests than in the past, he says. More than half the patients he sees with the allergy were bitten on their own lawns.

His leash theory is anecdotal, but it’s certainly true that the current ecological state of Eastern forests is probably encouraging ticks to multiply. After having been cleared in the Colonial era, the forests have partly grown back. Deer and turkey, which the lone-star tick likes to feed on, are abundant again. They thrive in the new-growth forests, now fragmented by roads and suburbs. Large predators are mostly absent. And the rise of tick-borne disease generally has been linked with the decline (or absence) of predators that eat the animals ticks feed on. In Australia, for example, van Nunen points to the eradication of foxes, an introduced species there, as one factor in the increase of ticks and the rise of meat allergy.

We might label this the disturbed ecosystem theory of meat allergy. Forests ecosystems have recovered partially — lots of animal hosts for ticks but not enough predators to keep those hosts in check — and this imbalance has fostered an exponential growth in the number of ticks. In some ways, this is the most probable explanation for the rise of meat allergy. Climate change may be aiding the lone-star tick’s move northward too, Rick Ostfeld, a disease ecologist at the Cary Institute of Ecosystem Studies, told me. Hundreds of cases of meat allergy have been diagnosed on Long Island in recent years, which wasn’t part of the tick’s range in recent history. The tick has been spotted as far north as Maine.

But what’s happening in the American East can’t account for the full extent of the phenomenon elsewhere in the world. In Northern Europe, ticks are proliferating as forests recover and the climate becomes warmer. But in Spain and Southern Europe, the rising incidence of meat allergy has not been accompanied by an increase in tick numbers, according to José de la Fuente, a professor at the Institute of Game and Wildlife Research in Ciudad Real, Spain. For him, the mystery of meat allergy is captured in one question: If a tick bites two genetically similar people, why might only one develop the meat allergy?

Onyinye Iweala, an assistant professor who works with Scott Commins’s lab at the University of North Carolina, echoes this uncertainty. Why are some people sensitized to alpha-gal — meaning they have allergic antibodies directed at the sugar in their blood stream — but never have an allergic reaction to it? This can happen in all allergies. You can have antibodies to, say, cat dander, yet never wheeze or sneeze around cats. Iweala suspects that sensitization to alpha-gal isn’t new. What’s changing is the proportion of people who, after sensitization, proceed to overt allergy. Something else in the environment, she told me, is likely pushing people toward full-blown meat allergy. Perhaps shifts in the microbes that live within us have somehow made us more easily sensitized by tick bite. As a model of how this might work, Iweala points to intriguing research on the interaction between malaria and the human microbiome that centers on alpha-gal.
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Our distant ancestors once made alpha-gal. Understanding why humans don’t could shed light on the meat-allergy mystery. Like other mammals, South American monkeys produce alpha-gal. Only Old World monkeys and apes (and humans) have lost the ability to make the sugar. Hence scientists deduce that the change most likely happened after New and Old World primates diverged from each other around 40 million years ago. One explanation for the disappearance of alpha-gal is that it was driven by some catastrophe, a deadly infection that afflicted Old World primates, perhaps, and as a result maybe these distant relatives of ours stopped being able to produce the sugar because doing so conferred an evolutionary advantage. The mutation that eliminated alpha-gal could have improved a primate’s ability to fight off an infection by enabling its immune system to more easily distinguish between its own body and some pathogen with alpha-galWhat could this pathogen have been? In the late 2000s, Miguel Soares, a scientist at the Instituto Gulbenkian de Ciência in Oeiras, Portugal, began to suspect the plasmodium parasite that causes malaria. Because the protozoan is so deadly and has historically been so widespread in warmer climes, geneticists often say that malaria has been the single greatest force shaping the human genome in our recent evolutionary history. The parasite remains a leading cause of death in the developing world. And it’s coated in alpha-gal.

Soares and his colleagues investigated a rural Malian population that was naturally exposed to malaria. As it happens, humans produce some antibodies to alpha-gal all the time. They’re not allergic antibodies like those responsible for Lee Niegelsky’s anaphylactic experience, but antimicrobial ones that give rise to a different, less drastic immune response. Between 1 and 5 percent of all the antibodies circulating in any person, a remarkably large quantity, are directed at alpha-gal, Soares estimates. The target of these antibodies is not the alpha-gal in the steak you may have eaten for dinner but the alpha-gal that leaks into circulation from the microbes dwelling in your gut. There are natural variations in the amount of these antibodies any individual produces; some people make more, some less. Soares wanted to know if this variability influenced the villagers’ susceptibility to malaria.

What he discovered may yet change how malaria is combated. Villagers who produced the greatest quantity of alpha-gal antibodies, he found, weren’t immune to infection by the parasite, but they were less likely to be infected after exposure.

What was different about those with more alpha-gal antibodies? They had more gut microbes that produced the sugar, Soares speculated. By priming their immune response against alpha-gal, these individuals’ microbiomes probably helped shield them against malaria. Soares showed as much using mice. Rodents colonized by a strain of E. coli found in the human microbiome that contains alpha-gal produced antibodies to the sugar and were protected from malaria. Rodents that harbored an E. coli strain that didn’t produce the sugar, on the other hand, were not protected. (Other scientists later observed a connection between resistance to malaria and the composition of Malian villagers’ microbiomes.) This research highlights one reason we probably have a few pounds of microbes in us: Friendly microbes can help protect us against unfriendly ones.

Soares is currently working on a vaccine to spur the immune system to attack alpha-gal more actively, thereby conferring greater protection against malaria. His findings also raise the prospect, at least theoretically, of an antimalarial probiotic. In the context of meat allergy, his work underscores the fact that our microbes may affect how we respond to alpha-gal from other sources, including, perhaps, tick bites.

How might this work? You can envision antibodies as arrows that have Velcro on the front instead of arrowheads. Depending on their targets, that Velcro sticks only to a particular substance, like alpha-gal or peanut protein. The back end of the arrow displays a signal that tells the immune system what to do. Allergic antibodies, called immunoglobulin-E, or IgE for short, call for an allergic response. But the antibodies that humans typically have in circulation directed at alpha-gal are antimicrobial antibodies like IgM and IgG, not allergic ones
A question central to the meat-allergy mystery is how, if we’re always exposed to alpha-gal from our gut microbes, and we’re constantly mounting a nonallergic response against it, the lone-star tick prompts what’s called “class switching,” spurring the immune system to pump out allergic antibodies instead of antimicrobial ones?

The microbes we host may, by stimulating the immune system and guiding its response to alpha-gal, make this class switching more or less likely, Onyinye Iweala told me. But scientists don’t yet know how the relationship works. Perhaps if your microbiota have more species that produce alpha-gal, these microbes stimulate your immune system in a way that protects you from allergic sensitization to the sugar when a tick bites. Or maybe the relationship works the other way around: If you host fewer alpha-gal-producing species and your immune system is less exposed to alpha-gal on a daily basis, that relative lack of stimulation might prevent alpha-gal allergy from developing when you’re bitten by a tick. These interactions can be tested — as Iweala is doing — with mice that, like humans, don’t produce alpha-gal.

What scientists do know is that if you treat a baboon with antibiotics, reducing the amount of alpha-gal-producing microbes in its gut, and thus lessening the stimulation they provide, the quantity of alpha-gal antibodies in its bloodstream also declines. This suggests that altering a primate’s gut microbes may change its immune response to alpha-gal. People living in developed countries, where most cases of meat allergy have been diagnosed, have been doing something very similar to themselves. “We keep changing the microbiome with antibiotics and what we eat,” Iweala says. By tweaking the microbes that live inside us, we may have inadvertently changed how our immune system responds to alpha-gal, making us more vulnerable to tick-induced meat allergy. It’s also possible, however, that the microbes that determine the general tone of our immune function have shifted, altering how we respond to all potential allergens, not just alpha-gal.

Since at least the late 20th century, and probably earlier, we’ve been living in the midst of what’s often called the allergy epidemic, an era that has seen an increase in the prevalence and severity of food allergies generally and, before that, a rise in the prevalence of respiratory allergies and asthma. The forces driving this trend may help account for meat allergy as well. A leading explanation holds that we develop more allergies now because our immune systems have become more sensitive to what they encounter, not because they are exposed to more pollens or allergenic foods than in the past. The reason the modern immune system errs this way, the thinking goes, is that it’s not receiving the right kind of education.

The news media have taken to calling this explanation the “hygiene hypothesis,” which is unfortunate and misleading; personal hygiene has little to do with what’s at issue. More accurate terms coined by researchers include the microbial-deprivation hypothesis, the disappearing-microbiota hypothesis and even the “old friends” hypothesis (the implication being that we’ve lost contact with once-ever-present friendly organisms).

Whatever you call it, the idea is that the rising tide of allergic diseases comes from changes to the type and quantity of microbes we encounter in our environment, particularly in our early life, as well as from changes to the microbes that live on and in us. Improved sanitation, antibiotics and the junk-food-ification of our diet, among other factors, may have shifted our microbial communities, giving us an immune system that’s overly jumpy, unable to reliably distinguish friend from foe and prone to diseases of overreaction, like allergies.

Studies on populations that have bucked the increase in allergies support the idea. Nearly 20 years of research on European children who grow up on farms with animals, for example, indicates that they are less likely to have respiratory allergies, asthma and eczema compared with other children in the same rural areas. The abundant microbial stimulation of the farm environment, scientists have proposed, tunes farming children’s immune system in a way that prevents allergic disease. The cowshed has thus become a stand-in for premodern conditions and the immune system that that environment produces — lightly stimulated but less likely to react to allergens — a model of how the human immune system might have worked in a more microbially enriched pastSo here is the question as it relates to meat allergy: If a lone-star tick bit a Bavarian farm-raised child, would she be less likely to develop an allergy to alpha-gal compared with her nonfarming counterparts? Put another way, if the tick bit someone 150 years ago when the whole world was more like a cowshed, would that person be less or more likely to develop a food allergy than someone from modern-day Chapel Hill?

It’s pure speculation at this point, but gradual, intergenerational changes to our microbes may have altered our immunological tenor, shifting it from cool, calm and collected toward restless and irritable and increasing the odds of developing allergy from a tick bite. Today we may encounter more ticks than in times past, but they may also be interacting with an immune system that’s more sensitive to their bites than ever before. “It’s the ‘perfect storm,’ as you would say in America,” Sheryl van Nunen told me.

For Lee Niegelsky, who had eaten hamburgers his entire life, the allergy forced him to constantly scrutinize his diet. You don’t realize how many foods have meat-derived products in them, he told me — especially in the South, where pork fat and bacon are widely used as flavoring — until you have to avoid meat for fear of passing out. Not long ago, for example, he fell ill after eating clam chowder, which he attributes to meat broth that he suspects was in the soup.

The good news is that, provided you’re not bitten by a tick again, sometimes the meat allergy fades on its own. A year after his visit to the emergency room, under Scott Commin’s supervision, Niegelsky began introducing small amounts of lean meat into his diet. The idea is to test the possibility that his allergic alpha-gal antibodies have subsided to the point that his immune system no longer attacks the sugar. It took Niegelsky about a week to muster the courage to take his first bite of pork tenderloin. He waited anxiously for six hours. When nothing happened, he moved on to steak.

Moises Velasquez-Manoff is a contributing Op-Ed writer for The Times and the author of ‘‘An Epidemic of Absence: A New Way of Understanding Allergies and Autoimmune Diseases.’’ He last wrote for the magazine about carbon farming.


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