In 2022, it was the perfect pollen-fuelled storm; a nationwide shortage of hay fever drugs as everyone faced days of high allergen levels. Mid-May marks the crossover point where the tree pollen season ends, and the fall of grass pollen begins, making it one of the worst times of year for sufferers.
And that year, stocks of chlorphenamine maleate (the active ingredient in over the counter remedies like Piriton) were running low with retailers warning that shelves could remain bare when the UK’s 16 million sufferers need help most.
Taking medication early on in the season is a crucial first step, according to the UK’s NHS, which recommends that antihistamines are taken as a matter of course, rather than on days where symptoms are particularly troublesome.
Beginning two weeks ahead of when you’d typically start noticing a runny nose or itchy eyes yields most success; once the body’s production of histamine, a chemical response to pollen, begins, it can be harder to stop it. If you can’t get hold of over the counter remedies, here are six methods to try:
How to treat hayfever
1. Desensitise
High doses of the pollen you’re allergic to, administered via injections, tablets and sprays, can help the worst-affected sufferers, according to Dr Adam Fox, a paediatric allergist at the Evelina London Children’s Hospital. These are designed to reduce inflammation, which in turn “retrains your immune system to be less responsive to pollen”.
He warns that “while it’s not a cure, it’s a very effective treatment” – one more commonly doled out across other European countries. In the UK, NHS access to such treatment can be limited, but Fox says paying for it privately costs around £80 per month.
2. Avoid outdoor mornings
Pollen counts are highest in the mornings and at dusk, rising with the warming air at the outset of the day, and again when it cools down. Going outside in the middle of the day instead is, in the UK, the way to avoid aggravating symptoms.
3. Wash your hair at night
While research is yet to confirm its efficacy, “experts believe hair washing at night helps hay fever,” Fox says. This is because the pollen trapped in hair over the course of a day will, if unwashed, transfer to your pillow, which means “you’ll then rub your face in it during the night”. He also suggests wearing wraparound sunglasses during the day to act as a barrier towards pollen on the move.
4. Be beside the sea
“The air is better ventilated” at the seaside, according to Fox. Distance from trees and grass, the main distributors of pollen, means beaches are likely to make life easier for hay fever sufferers. Rain can also be beneficial, as it washes pollen away.
5. Relax
During periods of stress, the body releases hormones and chemicals including histamine, which can provoke allergy symptoms. Becoming stressed by the onset of hay fever can also worsen its effects; relax by taking a (daytime) walk, or reading a book.
6. Mask up
Experts warn this may require trial and error, but face masks may help limit the amount of pollen able to latch on. Recent research from Israel found that almost 40 per cent of severe allergy sufferers experienced fewer symptoms, such as sneezing and a stuffy nose, after wearing surgical or N95 masks over a two-week period.
For those with moderate symptoms, 30 per cent saw improvements when wearing a surgical mask, compared with 40 per cent who wore an N95. Just over half of those with mild symptoms said theirs improved when wearing either mask.
“Masks should be worn by all pollen allergics when outside,” says Dr Glenis Scadding, a consultant allergist and respiratory specialist. As well as protecting the wearer from pollen and pollution, they also “protect society from Covid, since asymptomatic Covid may be present in people with allergic rhinitis who are prone to sneezing.”
While COVID-19’s effects on the lungs and respiratory system are well known, there is growing research suggesting that the virus is also affecting the heart, with potentially lasting effects.
In a presentation at the annual meeting of the Biophysical Society, an international biophysics scientific group, Dr. Andrew Marks, chair of the department of physiology at Columbia University, and his colleagues reported on changes in the heart tissue of COVID-19 patients who had died from the disease, some of whom also had a history of heart conditions.
The team conducted autopsy analyses and found a range of abnormalities, particularly in the way heart cells regulate calcium. All muscles, including those in the heart, rely on calcium to contract. Muscle cells store calcium and open special channels inside of cells to release it when needed. In some conditions such as heart failure, the channel remains open in a desperate attempt to help the heart muscle contract more actively.
The leaking of calcium ultimately depletes the calcium stores, weakening the muscle in the end. “We found evidence, in the hearts of COVID-19 patients, abnormalities in the way calcium is handled,” says Marks. In fact, when it came to their calcium systems, the heart tissue of these 10 people who had died of COVID-19 looked very similar to that of people with heart failure.
Marks plans to further explore the heart changes that SARS-CoV-2 might cause by studying how the infection affects the hearts of mice and hamsters. He intends to measure changes in immune cells as well as any alterations in heart function in the animals both while they are infected and after they have recovered in order to document any lingering effects.
“The data we present show that there are dramatic changes in the heart,” Marks says. “The precise cause and long term consequences of those need to be studied more.” Previous studies have revealed a link between COVID-19 infections and heart-related problems. A large 2022 analysis of patients in the VA system—some of whom had recovered from COVID-19 and others who had never been diagnosed—showed those who had had COVID-19 had higher rates of a number of heart-related risks, including irregular heartbeats heart attack and stroke.
Dr. Susan Cheng, chair of women’s cardiovascular health and population science at Cedars-Sinai, is studying whether there are any associations between rates of heart attacks and surges of COVID-19 infections, in order to better understand how the virus might be affecting the heart.
There is also early evidence showing that people with hypertension may be at higher risk of heart events when they get COVID-19. What connects the viral infection to the heart isn’t known yet, but the body’s immune system is likely a major contributor.
“It’s been well documented that with SARS-CoV-2, the body responds with an inflammatory response that involves activating the immune system in a very dramatic way,” says Marks. “In the heart, it looks like the same inflammatory process is activating pathways that could be detrimental to heart function.” But more research needs to clarify that process, says Dr. Mariell Jessup, chief science and medical officer at the American Heart Association.
“If the assumption is that the infection causes inflammation, and the assumption is that the inflammation is precipitating more cardiovascular events, then how is it doing that?” It’s also possible that viruses can infect and adversely affect heart cells. “We’re still at the tip of the iceberg with respect to understanding how COVID-19 affects health,” says Cheng.
Marks is hoping to get some of those answers with the animal experiments he plans to conduct. “We hope to optimize the animal model to best reflect what we think is going on in patients,” he says. “We want to study at a very, very detailed level what happens in the heart when the virus infects an animal.”
Ultimately, that knowledge will help to better treat people who might be at higher risk of heart-related problems from COVID-19, which could in turn reduce hospitalizations and deaths from the disease. Marks has already developed a potential drug that can address the leaking calcium if that proves to be a problem with COVID-19; he is ready and eager to test it if his animal studies justify the experiments.
Until more definitive studies clarify how the COVID-19 virus is affecting the heart, Jessup says she would advise her patients to “control the things we know how to control,” such as the risk factors that might put them at higher risk of heart disease to begin with, such as obesity, high blood pressure, and high cholesterol.
And with more data emerging, if people are getting repeat COVID-19 infections, it’s also probably worth seeing their doctor to get their heart disease risk factors checked as well. “We spend a lot of time telling people they should get vaccinated,” she says. “For people who have had COVID-19, we should also be making sure they know their heart numbers and make sure they know blood pressure. “We know how to prevent heart disease, so let’s do the things we know how to do.”
Immune cells infected with HIVPhotograph: BIOPHOTO ASSOCIATES/Science Source
An experiment tests whether the gene-editing technology can stop the virus from replicating, which would ultimately wipe out the infection.
In July, an HIV-positive man became the first volunteer in a clinical trial aimed at using Crispr gene editing to snip the AIDS-causing virus out of his cells. For an hour, he was hooked up to an IV bag that pumped the experimental treatment directly into his bloodstream. The one-time infusion is designed to carry the gene-editing tools to the man’s infected cells to clear the virus.
Later this month, the volunteer will stop taking the antiretroviral drugs he’s been on to keep the virus at undetectable levels. Then, investigators will wait 12 weeks to see if the virus rebounds. If not, they’ll consider the experiment a success. “What we’re trying to do is return the cell to a near-normal state,” says Daniel Dornbusch, CEO of Excision BioTherapeutics, the San Francisco-based biotech company that’s running the trial.
HIV attacks immune cells in the body called CD4 cells and hijacks their machinery to make copies of itself. But some HIV-infected cells can go dormant—sometimes for years—and not actively produce new virus copies. These so-called reservoirs are a major barrier to curing HIV.
“HIV is a tough foe to fight because it’s able to insert itself into our own DNA, and it’s also able to become silent and reactivate at different points in a person’s life,” says Jonathan Li, a physician at Brigham and Women’s Hospital and HIV researcher at Harvard University who’s not involved with the Crispr trial. Figuring out how to target these reservoirs—and doing it without harming vital CD4 cells—has proven challenging, Li says.
While antiretroviral drugs can halt viral replication and clear the virus from the blood, they can’t reach these reservoirs, so people have to take medication every day for the rest of their lives. But Excision BioTherapeutics is hoping that Crispr will remove HIV for good.
Crispr is being used in several other studies to treat a handful of conditions that arise from genetic mutations. In those cases, scientists are using Crispr to edit peoples’ own cells. But for the HIV trial, Excision researchers are turning the gene-editing tool against the virus. The Crispr infusion contains gene-editing molecules that target two regions in the HIV genome important for viral replication. The virus can only reproduce if it’s fully intact, so Crispr disrupts that process by cutting out chunks of the genome.
In 2019, researchers at Temple University and the University of Nebraska found that using Crispr to delete those regions eliminated HIV from the genomes of rats and mice. A year later, the Temple group also showed that the approach safely removed viral DNA from macaques with SIV, the monkey version of HIV.
That was an important step toward testing the treatment in people, says Kamel Khalili, a professor of microbiology at Temple University who led the work and is a cofounder of Excision Biotherapeutics. “You don’t want to eliminate the viral genome but at the same time cause any disruption in another part of the human genome and then create another set of problems for the patients,” he says. “We had to make sure that we identified a region within HIV that did not overlap with the human genome.”
Dornbusch thinks this strategy will spare patients from serious side effects and “off-target” edits—unintentional cuts elsewhere in the genome that could cause problems such as cancer.
The regions targeted by the company’s Crispr therapy are also in a part of the genome that tends to stay the same even when HIV evolves. That’s important because the virus mutates rapidly, and the researchers don’t want a moving target.
This isn’t the first time scientists have tried to use gene editing in the hope of curing people with HIV, but other efforts have focused on a protective mutation in a gene called CCR5. In the 1990s, scientists found that people with this naturally occurring mutation didn’t get HIV when exposed to it. The mutation—known as delta 32—thwarts the virus’s ability to get inside immune cells. In 2009, California-based Sangamo Therapeutics used an older editing technology called zinc finger nucleases to add that protective mutation into patients’ T cells—an important part of the immune system. Those trials have had limited success.
In 2017, Chinese scientists combined Crispr with a bone marrow transplant in an attempt to cure a patient with HIV and leukemia. In a typical transplant, donor stem cells are transferred to a recipient to replace their cancerous blood cells. These cells go on to form new, healthy blood cells. To also address the patient’s HIV, researchers edited the donor stem cells with Crispr to disable CCR5. But after the transplant, only a small percentage of the patient’s bone marrow cells ended up with the desired edit.
Then in 2018, Chinese scientist He Jiankui used Crispr to edit the CCR5 mutation into the genomes of twin baby girls to make them resistant to HIV. Fraught with ethical violations, the experiment was widely condemned by scientists. He’s research was suspended by the Chinese government, and he served a three-year prison sentence. While the twins were born healthy, only some of their cells were successfully edited, meaning the girls might in fact not be immune to HIV.
As of 2022, two people have now been cured of HIV after receiving bone marrow transplants from donors with the CCR5. Known as the Berlin patient and the London patient, both had cancer and received transplants to treat their disease. But these transplants aren’t a viable option for most people—they’re highly risky, and donors with the delta 32 mutation are scarce. But a third person was declared cured of HIV earlier this year after she received a new type of transplant involving umbilical cord blood.
The Excision trial will eventually enroll nine participants and test three dosage amounts to determine which is most effective. Investigators will measure each person’s viral load and CD4 count before receiving the therapy and after they stop taking antiretroviral drugs. The ultimate goal is to get viral loads down to an undetectable level—that is, less than 200 copies of HIV per milliliter of blood. At this level, HIV can’t be passed on through sex.
The challenge for Excision will be getting Crispr to enough cells to bring HIV down to undetectable levels. The company is using an engineered virus to shuttle the gene-editing components to patients’ HIV-infected CD4 cells. But so far, there’s little human data on how well Crispr works when it’s delivered directly to the body. “It’s possible that you get the virus to such low levels that if a person’s immune system were intact, they might be able to keep the virus at bay such that they don’t have to take antiretroviral therapy anymore,” says Rowena Johnston, vice president and director of research for amfAR, the Foundation for AIDS Research.
And even though these drugs are very effective, Johnston says, many people would rather be completely free of the virus. A single Crispr infusion—if it works—would eliminate the need for daily pills. “People with HIV still live with a lot of stigma and internalized shame,” she says. “I think a cure is something that addresses that much better than lifelong therapy, regardless of how easy that therapy becomes.”
Emily Mullin is a staff writer at WIRED, covering biotechnology. Previously, she was an MIT Knight Science Journalism project fellow and a staff writer covering biotechnology at Medium’s OneZero. Before that, she served as an associate editor at MIT Technology Review, where she wrote about biomedicine. Her stories have also… Read more
Human immunodeficiency virus infection and acquired immunodeficiency syndrome (HIV/AIDS) is a spectrum of conditions caused by infection with the human immunodeficiency virus (HIV), a retrovirus. Following initial infection an individual may not notice any symptoms, or may experience a brief period of influenza-like illness .Typically, this is followed by a prolonged incubation period with no symptoms.
If the infection progresses, it interferes more with the immune system, increasing the risk of developing common infections such as tuberculosis, as well as other opportunistic infections, and tumors which are otherwise rare in people who have normal immune function. These late symptoms of infection are referred to as acquired immunodeficiency syndrome (AIDS).This stage is often also associated with unintended weight loss.
While there is no broadly available cure or vaccine, antiretroviral treatment can slow the course of the disease and may lead to a near-normal life expectancy. Treatment is recommended as soon as the diagnosis is made.[17] Without treatment, the average survival time after infection is 11 years. In 2021, about 38 million people worldwide were living with HIV and 650,000 deaths had occurred in that year.
An estimated 20.6 million of these live in eastern and southern Africa. Between the time that AIDS was identified (in the early 1980s) and 2021, the disease has caused an estimated 40 million deaths worldwide. HIV/AIDS is considered a pandemic—a disease outbreak which is present over a large area and is actively spreading. HIV made the jump from other primates to humans in west-central Africa in the early-to-mid 20th century.
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MMWR. Recommendations and reports : Morbidity and mortality weekly report. Recommendations and reports / Centers for Disease Control. 54 (RR-2): 1–20. PMID15660015.Kripke C (August 1, 2007). “Antiretroviral prophylaxis for occupational exposure to HIV”. American Family Physician. 76 (3): 375–6. PMID17708137. Dosekun O, Fox J (July 2010). “An overview of the relative risks of different sexual behaviours on HIV transmission”. Current Opinion in HIV and AIDS. 5 (4): 291–7. doi:10.1097/COH.0b013e32833a88a3. PMID20543603.
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Sharon calls herself a universal reactor. In the 1990s, she became allergic to the world, to the mould colonising her home and the paint coating her kitchen walls, but also deodorants, soaps and anything containing plastic. Public spaces rife with artificial fragrances were unbearable. Scented disinfectants and air fresheners in hospitals made visiting doctors torture. The pervasiveness of perfumes and colognes barred her from in-person social gatherings.
Even stepping into her own back garden was complicated by the whiff of pesticides and her neighbour’s laundry detergent sailing through the air. When modern medicine failed to identify the cause of Sharon’s illness, exiting society felt like her only solution. She started asking her husband to strip and shower every time he came home. Grandchildren greeted her through a window. When we met for the first time, Sharon had been housebound for more than six years.
When I started medical school, the formaldehyde-based solutions used to embalm the cadavers in the human anatomy labs would cause my nose to burn and my eyes to well up – representing the mild, mundane end of a chemical sensitivity spectrum. The other extreme of the spectrum is an environmental intolerance of unknown cause (referred to as idiopathic by doctors) or, as it is commonly known, multiple chemical sensitivity (MCS).
An official definition of MCS does not exist because the condition is not recognised as a distinct medical entity by the World Health Organization or the American Medical Association, although it has been recognised as a disability in countries such as Germany and Canada.
Disagreement over the validity of the disease is partially due to the lack of a distinct set of signs and symptoms, or an accepted cause. When Sharon reacts, she experiences symptoms from seemingly every organ system, from brain fog to chest pain, diarrhoea, muscle aches, depression and odd rashes. There are many different triggers for MCS, sometimes extending beyond chemicals to food and even electromagnetic fields. Consistent physical findings and reproducible lab results have not been found and, as a result, people such as Sharon not only endure severe, chronic illness but also scrutiny over whether their condition is “real”.
The first reported case of MCS was published in the Journal of Laboratory and Clinical Medicine in 1952 by the American allergist Theron Randolph. Although he claimed to have previously encountered 40 cases, Randolph chose to focus on the story of one woman, 41-year-old Nora Barnes. She had arrived at Randolph’s office at Northwestern University in Illinois with a diverse and bizarre array of symptoms.
A former cosmetics salesperson, she represented an “extreme case”. She was always tired, her arms and legs were swollen, and headaches and intermittent blackouts ruined her ability to work. A doctor had previously diagnosed her with hypochondria, but Barnes was desperate for a “real” diagnosis.
Randolph noted that the drive into Chicago from Michigan had worsened her symptoms, which spontaneously resolved when she checked into her room on the 23rd floor of a hotel where, Randolph reasoned, she was far away from the noxious motor exhaust filling the streets. In fact, in his report Randolph listed 30 substances that Barnes reacted to when touched (nylon, nail polish), ingested (aspirin, food dye), inhaled (perfume, the “burning of pine in fireplace”) and injected (the synthetic opiate meperidine, and Benadryl).
He posited that Barnes and his 40 other patients were sensitive to petroleum products in ways that defied the classic clinical picture of allergies. That is, rather than an adverse immune response, such as hives or a rash where the body is reacting to a particular antigen, patients with chemical sensitivities were displaying an intolerance. Randolph theorised that, just as people who are lactose-intolerant experience abdominal pain, diarrhoea and gas because of undigested lactose creating excess fluid in their gastrointestinal tract, his patients were vulnerable to toxicity at relatively low concentrations of certain chemicals that they were unable to metabolise.
He even suggested that chemical sensitivity research was being suppressed by “the ubiquitous distribution of petroleum and wood products”. MCS, he believed, was not only a matter of scientific exploration, but also of deep-seated corporate interest. Randolph concludes his report with his recommended treatment: avoidance of exposure.
In that one-page abstract, Randolph cut the ribbon on the completely novel but quickly controversial field of environmental medicine. Nowadays, we hardly question the ties between the environment and wellbeing. The danger of secondhand smoke, the realities of climate change and the endemic nature of respiratory maladies such as asthma are common knowledge. The issue was that Randolph’s patients lacked abnormal test results (specifically, diagnostic levels of immunoglobulin E, a blood marker that is elevated during an immune response). Whatever afflicted them were not conventional allergies, so conventional allergists resisted Randolph’s hypotheses.
Randolph was in the dark. Why was MCS only now rearing its head? He also asked another, more radical question: why did this seem to be a distinctly American phenomenon? After all, the only other mention of chemical sensitivities in medical literature was in the US neurologist George Miller Beard’s 1880 textbook A Practical Treatise on Nervous Exhaustion (Neurasthenia).
Beard argued that sensitivity to foods containing alcohol or caffeine was associated with neurasthenia, a now-defunct term used to describe the exhaustion of the nervous system propagated by the US’s frenetic culture of productivity. Like Beard, Randolph saw chemical sensitivities as a disease of modernity, and conceived the origin as wear-and-tear as opposed to overload.
Randolph proposed that Americans, propelled by the post-second world war boom, had encountered synthetic chemicals more and more in their workplaces and homes, at concentrations considered acceptable for most people. Chronic exposure to these subtoxic dosages, in conjunction with genetic predispositions, strained the body and made patients vulnerable. On the back of this theory, Randolph developed a new branch of medicine and, with colleagues, founded the Society for Clinical Ecology, now known as the American Academy of Environmental Medicine.
As his professional reputation teetered, his popularity soared and patients flocked to his care. Despite this growth in interest, researchers never identified blood markers in MCS patients, and trials found that people with MCS couldn’t differentiate between triggers and placebos. By 2001, a review in the Journal of Internal Medicine found MCS virtually nonexistent outside western industrialised countries, despite the globalisation of chemical use, suggesting that the phenomenon was culturally bound.
MCS subsequently became a diagnosis of exclusion, a leftover label used after every other possibility was eliminated. The empirical uncertainty came to a head in 2021, when Quebec’s public health agency, the INSPQ, published an 840-page report that reviewed more than 4,000 articles in the scientific literature, concluding that MCS is an anxiety disorder.
In medicine, psychiatric disorders are not intrinsically inferior; serious mental illness is, after all, the product of neurological dysfunction. But the MCS patients I spoke to found the language offensive and irresponsible. Reducing what they felt in their eyes, throats, lungs and guts to anxiety was not acceptable at all.
As a woman I will call Judy told me: “I would tell doctors my symptoms, and then they’d run a complete blood count and tell me I looked fine, that it must be stress, so they’d shove a prescription for an antidepressant in my face and tell me to come back in a year.” In fact, because MCS is so stigmatising, such patients may never receive the level of specialised care they need.
In the wake of her “treatment”, Judy was frequently bedbound from crushing fatigue, and no one took her MCS seriously. “I think a lot of doctors fail to understand that we are intelligent,” she said. “A lot of us with chemical sensitivities spend a good amount of our time researching and reading scientific articles and papers. I probably spent more of my free time reading papers than most doctors.”
Judy grew up in Texas, where she developed irritable bowel syndrome and was told by doctors that she was stressed. Her 20s were spent in Washington state where she worked as a consultant before a major health crash left her bedbound for years (again, the doctors said she was stressed). Later, after moving to Massachusetts, a new paint job at her home gave her fatigue and diarrhoea.
She used to browse the local art museum every Saturday, but even fumes from the paintings irritated her symptoms. She visited every primary care doctor in her city, as well as gastroenterologists, cardiologists, neurologists, endocrinologists and even geneticists. Most of them reacted the same way: with a furrowed brow and an antidepressant prescription in hand. “Not one allopathic doctor has ever been able to help me,” Judy said.
Morton Teich is one of the few physicians who diagnoses and treats patients with MCS in New York. The entrance to his integrative medicine private practice is hidden away behind a side door in a grey-brick building on Park Avenue. As I entered the waiting room, the first thing to catch my eye was the monstrous mountain of folders and binders precariously hugging a wall, in lieu of an electronic medical record.
I half-expected Teich’s clinic to resemble the environmental isolation unit used by Randolph in the 1950s, with an airlocked entrance, blocked ventilation shafts and stainless-steel air-filtration devices, books and newspapers in sealed boxes, aluminium walls to prevent electromagnetic pollution, and water in glass bottles instead of a cooler. But there were none of the above. The clinic was like any other family medicine practice I had seen before; it was just very old. The physical examination rooms had brown linoleum floors and green metal chairs and tables. And there were no windows.
Although several of Teich’s patients were chemically sensitive, MCS was rarely the central focus of visits. When he introduced me, as a student writing about MCS, to his first patient of the day, a petrol-intolerant woman whose appointment was over the phone because she was housebound, she admitted to never having heard of the condition. “You have to remember,” Teich told me, “that MCS is a symptom. It’s just one aspect of my patients’ problems. My goal is to get a good history and find the underlying cause.” Later, when I asked him whether he had observed any patterns suggesting an organic cause of MCS, he responded: “Mould. Almost always.”
Many people with MCS I encountered online also cited mould as a probable cause. Sharon told me about her first episode in 1998, when she experienced chest pain after discovering black mould festering in her family’s trailer home. A cardiac examination had produced no remarkable results, and Sharon’s primary care physician declared that she was having a panic attack related to the stress of a recent miscarriage. Sharon recognised that this contributed to her sudden health decline, but also found that her symptoms resolved only once she began sleeping away from home.
She found recognition in medical books such as Toxic (2016) by Neil Nathan, a retired family physician who argued that bodily sensitivities were the product of a hyper-reactive nervous system and a vigilant immune system that fired up in reaction to toxicities, much as Randolph had said. The conditions that Nathan describes are not supported by academic medicine as causes of MCS: mould toxicity and chronic Lyme disease are subject to the same critique.
Sharon went to see William Rea, a former surgeon (and Teich’s best friend). Rea diagnosed her with MCS secondary to mould toxicity. “Mould is everywhere,” Teich told me. “Not just indoors. Mould grows on leaves. That’s why people without seasonal allergies can become chemically sensitive during autumn.” When trees shed their leaves, he told me, mould spores fly into the air. He suspected that American mould is not American at all, but an invasive species that rode wind currents over the Pacific from China. He mentioned in passing that his wife recently died from ovarian cancer. Her disease, he speculated, also had its roots in mould.
In fact, Teich commonly treats patients with nystatin, an antifungal medication used to treat candida yeast infections, which often infect the mouth, skin and vagina. “I have an 80% success rate,” he told me. I was dubious that such a cheap and commonplace drug was able to cure an illness as debilitating as MCS, but I could not sneer at his track record. Every patient I met while shadowing Teich was comfortably in recovery, with smiles and jokes, miles apart from the people I met in online support groups who seemed to be permanently in the throes of their illness.
However, Teich was not practising medicine as I was taught it. This was a man who believed that the recombinant MMR vaccine could trigger “acute autism” – traditionally an anti-science point of view. When one of his patients, a charismatic bookworm I’ll call Mark, arrived at an appointment with severe, purple swelling up to his knees and a clear case of stasis dermatitis (irritation of the skin caused by varicose veins), Teich reflexively blamed mould and wrote a prescription for nystatin instead of urging Mark to see a cardiologist.
When I asked how a fungal infection in Mark’s toes could cause such a bad rash on his legs, he responded: “We have candida everywhere, and its toxins are released into the blood and travel to every part of the body. The thing is, most people don’t notice until it’s too late.” Moulds and fungi are easy scapegoats for inexplicable illnesses because they are so ubiquitous in our indoor and outdoor environments. A great deal of concern over mould toxicity (or, to use the technical term, mycotoxicosis) stems from the concept of “sick-building syndrome”, in which visible black mould is thought to increase sensitivity and make people ill.
This was true of Mark, who could point to the demolition of an old building across the street from his apartment as a source of mould in the atmosphere. Yet in mainstream medicine, diseases caused by moulds are restricted to allergies, hypersensitivity pneumonitis (an immunologic reaction to an inhaled agent, usually organic, within the lungs) and infection.
Disseminated fungal infections occur almost exclusively in patients who are immunocompromised, hospitalised or have an invasive foreign body such as a catheter. Furthermore, if “clinical ecologists” such as Teich are correct that moulds such as candida can damage multiple organs, then it must be spreading through the bloodstream. But I have yet to encounter a patient with MCS who reported fever or other symptoms of sepsis (the traumatic, whole-body reaction to infection) as part of their experience.
Teich himself did not use blood cultures to verify his claims of “systemic candidiasis”, and instead looked to chronic fungal infection of the nails, common in the general population, as sufficient proof.
“I don’t need tests or blood work,” he told me. “I rarely ever order them. I can see with my eyes that he has mould, and that’s enough.” It was Teich’s common practice to ask his patients to remove their socks to reveal the inevitable ridges and splits on their big toenails, and that’s all he needed.
Through Teich, I met a couple who were both chemically sensitive but otherwise just regular people. The wife, an upper-middle-class white woman I will call Cindy, had a long history of allergies and irritable bowel syndrome. She became ill whenever she smelled fumes or fragrances, especially laundry detergent and citrus or floral scents. Teich put both her and her husband on nystatin, and their sensitivities lessened dramatically.
What struck me as different about her case, compared with other patients with MCS, was that Cindy was also on a course of antidepressants and cognitive behavioural therapy, the standard treatment for anxiety and depression. “It really helps to cope with all the stress that my illness causes. You learn to live despite everything,” she said.
In contemporary academic medicine, stress and anxiety cause MCS, but MCS can itself cause psychiatric symptoms. Teich later told me, unexpectedly, that he had no illusions about whether MCS is a partly psychiatric illness: “Stress affects the adrenals, and that makes MCS worse. The mind and the body are not separate. We have to treat the whole person.”
To understand this case, I also spoke to Donald Black, associate chief of staff for mental health at the Iowa City Veterans Administration Health Care. He co-authored a recent article on idiopathic environmental intolerance that took a uniform stance on MCS as a psychosomatic disorder. In 1988, when Black was a new faculty member at the University of Iowa, he interviewed a patient entering a drug trial for obsessive-compulsive disorder.
He asked the woman to list her medications, and watched as she started unloading strange supplements and a book about environmental illness from her bag. The woman had been seeing a psychiatrist in Iowa City – a colleague of Black’s – who had diagnosed her with systemic candidiasis. Black was flummoxed. If that diagnosis was true, then the woman would be very ill, not sitting calmly before him.
Besides, it was not up to a psychiatrist to treat a fungal infection. How did he make the diagnosis? Did he do a physical or run blood tests? No, the patient told him, the psychiatrist just said that her symptoms were compatible with candidiasis. These symptoms included chemical sensitivities. After advising the patient to discard her supplements and find a new psychiatrist, Black made some phone calls and discovered that, indeed, his colleague had fallen in with the clinical ecologists.
Black was intrigued by this amorphous condition that had garnered an endless number of names: environmentally induced illness, toxicant-induced loss of tolerance, chemical hypersensitivity disease, immune dysregulation syndrome, cerebral allergy, 20th-century disease, and mould toxicity. In 1990, he solicited the aid of a medical student to find 26 subjects who had been diagnosed by clinical ecologists with chemical sensitivities and to conduct an “emotional profile”.
Every participant in their study filled out a battery of questions that determined whether they satisfied any of the criteria for psychiatric disorders. Compared with the controls, the chemically sensitive subjects had 6.3 times higher lifetime prevalence of major depression, and 6.8 times higher lifetime prevalence of panic disorder or agoraphobia; 17% of the cases met the criteria for somatisation disorder (an extreme focus on physical symptoms – such as pain or fatigue – that causes major emotional distress and problems functioning).
In my own review of the literature, it was clear that the most compelling evidence for MCS came from case studies of large-scale “initiating events” such as the Gulf war (where soldiers were uniquely exposed to pesticides and pyridostigmine bromide pills to protect against nerve agents) or the terrorist attacks on the US of 11 September 2001 (when toxins from the falling towers caused cancers and respiratory ailments for years).
In both instances, a significant number of victims developed chemical intolerances compared with populations who were not exposed. From a national survey of veterans deployed in the Gulf war, researchers found that up to a third of respondents reported multi-symptom illnesses, including sensitivity to pesticides – twice the rate of veterans who had not deployed.
Given that Gulf war veterans experienced post-traumatic stress disorder at levels similar to those in other military conflicts, the findings have been used to breathe new life into Randolph’s idea of postindustrial toxicities leading to intolerance. The same has been said of the first responders and the World Trade Centre’s nearby residents, who developed pulmonary symptoms when exposed to “cigarette smoke, vehicle exhaust, cleaning solutions, perfume, or other airborne irritants” after 9/11, according to a team at Mount Sinai.
Black, who doubts a real disease, has no current clinical experience with MCS patients. (Apart from the papers he wrote more than 20 years ago, he had seen only a handful of MCS patients over the course of his career.) Despite this, he had not only written the article about MCS, but also a guide in a major online medical manual on how to approach MCS treatment as a psychiatric disease. When I asked him if there was a way for physicians to regain the trust of patients who have been bruised by the medical system, he simply replied:
“No.” For him, there would always be a subset of patients who are searching for answers or treatments that traditional medicine could not satisfy. Those were the people who saw clinical ecologists, or who left society altogether. In a time of limited resources, these were not the patients on which Black thought psychiatry needed to focus. It became clear to me why even the de facto leading professional on MCS had hardly any experience actually treating MCS.
In his 1990 paper, Black – then a young doctor – rightly observed that “traditional medical practitioners are probably insensitive to patients with vague complaints, and need to develop new approaches to keep them within the medical fold. The study subjects clearly believed that their clinical ecologists had something to offer them that others did not: sympathy, recognition of pain and suffering, a physical explanation for their suffering, and active participation in medical care.”I wondered if Black had given up on these “new approaches” because few CS patients wanted to see a psychiatrist in the first place.
Physicians on either side of the debate agreed that mental illness is a crucial part of treating MCS, with one I spoke to believing that stress causes MCS, and another believing that MCS causes stress. To reconcile the views, I interviewed another physician, Christine Oliver, a doctor of occupational medicine in Toronto, where she has served on the Ontario Task Force on Environmental Health. Oliver believes that both stances are probably valid and true. “No matter what side you’re on,” she told me, “there’s a growing consensus that this is a public health problem.”
Oliver represents a useful third position, one that takes the MCS illness experience seriously while sticking closely to medical science. As one of few “MCS-agnostic” physicians, she believes in a physiological cause for MCS that we cannot know and therefore cannot treat directly due to lack of research. Oliver agrees with Randolph’s original suggestion of avoiding exposures, although she understands that this approach has resulted in traumatising changes in patients’ abilities to function. For her, the priority for MCS patients is a practical one: finding appropriate housing.
Often unable to work and with a limited income, many of her patients occupy public housing or multi-family dwellings. The physician of an MCS patient must act like a social worker. Facilities such as hospitals, she feels, should be made more accessible by reducing scented cleaning products and soaps. Ultimately, finding a non-threatening space with digital access to healthcare providers and social support is the best way to allow the illness to run its course.
Whether organic or psychosomatic or something in between, MCS is a chronic illness. “One of the hardest things about being chronically ill,” wrote the American author Meghan O’Rourke in the New Yorker in 2013 about her battle against Lyme disease, “is that most people find what you’re going through incomprehensible – if they believe you are going through it. In your loneliness, your preoccupation with an enduring new reality, you want to be understood in a way that you can’t be.”
A language for chronic illness does not exist beyond symptomatology, because in the end symptoms are what debilitate “normal” human functioning. In chronic pain, analgesics can at least deaden a patient’s suffering. The same cannot be said for MCS symptoms, which are disorienting in their chaotic variety, inescapability and inexpressibility. There are few established avenues for patients to completely avoid triggering their MCS, and so they learn to orient their lives around mitigating symptoms instead, whether that is a change in diet or moving house, as Sharon did. MCS comes to define their existence.
As a housebound person, Sharon’s ability to build a different life was limited. Outside, the world was moving forward, yet Sharon never felt left behind. What allowed her to live with chronic illness was not medicine or therapy, but the internet. On a typical day, Sharon wakes up and prays in bed. She wolfs down handfuls of pills and listens to upbeat music on YouTube while preparing her meals for the day: blended meats and vegetables, for easier swallowing.
The rest of the day is spent on her laptop computer, checking email and Facebook, watching YouTube videos until her husband returns home in the evening. Then bed. This is how Sharon has lived for the past six years, and she does not expect anything different from the future. When I asked her if being homebound was lonely, I was taken aback at her reply: “No.”
In spite of not having met most of her 15 grandchildren (with two more on the way), Sharon keeps in daily contact with all of them. In fact, Sharon communicates with others on a nearly constant basis. “Some people are very much extroverts,” Sharon wrote. “I certainly am. But there are also people who need physical touch … and I can understand why they might need to see ‘real people’ then … but it’s very possible to be content with online friends. This is my life!”
The friendships that Sharon formed online with other housebound people with chronic illnesses were the longest-lasting and the most alive relationships she had ever known. She had never met her best friend of 20 years – their relationship existed completely through letters and emails, until two years ago, when the friend died. That “was very hard for me”, Sharon wrote.
The pandemic changed very little of Sharon’s life. If anything, Covid-19 improved her situation. Sharon’s local church live-streamed Sunday service, telehealth doctor appointments became the default, YouTube exploded in content, and staying indoors was normalised. Sharon saw her network steadily expand as more older adults became isolated in quarantine.
People within the online MCS community call themselves “canaries”, after the birds historically used as sentinels in coalmines to detect toxic levels of carbon monoxide. With a higher metabolism and respiratory rate, the small birds would theoretically perish before the less-sensitive human miners, providing a signal to escape. The question for people with MCS is: will anyone listen?
“Us canaries,” said a woman named Vera, who was bedbound from MCS for 15 years after a botched orthopaedic surgery, “we struggle and suffer in silence.” Now, in the information age, they have colonised the internet to find people like themselves. For our part, we must reimagine chronic illness – which will become drastically more common in the aftermath of the pandemic – where what matters to the patient is not only a scientific explanation and a cure, but also a way to continue living a meaningful life.
This calls into action the distinction between illness and disease that the psychiatrist and anthropologist Arthur Kleinman made in his 1988 book The Illness Narratives. Whereas a disease is an organic process within the body, illness is the lived experience of bodily processes. “Illness problems,” he writes, “are the principal difficulties that symptoms and disability create in our lives.”
By centring conversations about MCS on whether or not it is real, we alienate the people whose illnesses have deteriorated their ability to function at home and in the world. After all, the fundamental mistrust does not lie in the patient-physician relationship, but between patients and their bodies. Chronic illness is a corporeal betrayal, an all-out assault on the coherent self. Academic medicine cannot yet shed light on the physiological mechanisms that would explain MCS. But practitioners and the rest of society must still meet patients with empathy and acceptance, making space for their narratives, their lives, and their experience in the medical and wider world.
After two years of wrangling, false starts and disappointments, it finally happened: America has passed its first-ever climate legislation, moving the country closer to its goal of a decarbonized future and taking a significant step toward helping the planet avert the worst scenarios of climate catastrophe.
But it’s not a time to rest. We have always held power to account – on climate and every other major issue – from the fossil fuel companies responsible for heating the planet to the politicians representing their interests. The country responsible for the most greenhouse gas emissions in history has indicated it will change course; we will relentlessly report on what comes next, who will benefit and the remaining obstacles to progress.
With daily reporting and analysis on the climate emergency, we aim to ensure that even more people are made aware of the dangers – and opportunities – of this moment.
Your immune system is your main line of defense against illness, so it only makes sense that you’d want to keep it in top shape. That’s especially true during cold and flu season—and with continued outbreaks of novel coronavirus (COVID-19) sweeping the country.
You’re born with your immune system and everyone’s is slightly different, but there are certain things you can do to try to bolster it, says Julia Blank, M.D., family medicine physician at Providence Saint John’s Health Center in Santa Monica, CA. “Maintaining a healthy immune system requires that you take good care of your body,” she says.
How does the immune system work, exactly?
Your immune system is actually made up of “multiple layers of defense,” Dr. Blank says. This includes physical barriers like your skin, cilia (tiny, hair-like structures) that line your airways, and specialized cells that recognize and attack foreign substances like viruses and bacteria, she explains.
“Some of these immune cells are nonspecific and destroy anything that appears foreign. Other cells produce antibodies that recognize and target protein markers (called antigens) on the surface of germs,” Dr. Blank says.
Your immune system also has the ability to recognize pathogens you’ve come into contact with before and mount a quick response. “This is why we don’t usually get sick after being exposed to a germ we’ve already encountered and fought off in the past,” Dr. Blank says.
How to Boost Your Immune System
There are a few science-backed approaches you can take to boost your immune system, most of which are recommended for overall wellness:
1. Keep your alcohol intake in check.
“High alcohol intake has been shown to suppress immune function,” says Jessica Cording, M.S., R.D., author of The Little Book of Game-Changers. Plus, booze “can be dehydrating, and hydration is really important for protecting yourself from illness.” When you’re dehydrated, your cells aren’t able to function at their optimal level—and that can open up the door for you to get sick, Cording explains.
If you don’t want to cut out booze completely, sip in moderation. That means having up to one drink a day for women and two drinks a day for men, according to the U.S. Dietary Guidelines for Americans.
2. Reduce your stress levels.
Stress seems harmless enough once you get over whatever it is you’re anxious about, but studies show it can “compromise or suppress the immune system and make us more vulnerable to infection,” Dr. Blank says.
Specifically, research has found that stress causes a release of the hormone cortisol, which can boost inflammation, a precursor to many diseases, in your body. Chronic stress may also interfere with the infection-fighting ability of your white blood cells, making you more susceptible to contracting illnesses. (Can’t unwind? Check out these science-backed ways to relieve stress.)
3. Eat plenty of fruits and vegetables.
Putting a rainbow of fruits and vegetables on your plate can do your immune system a solid, says Beth Warren, R.D., founder of Beth Warren Nutrition and author of Secrets of a Kosher Girl. “Fruits and veggies help arm your body with antioxidants it needs to fight oxidative stress, which includes contracting a sickness, in your body,” she says.
Not sure how much you need? The U.S. Dietary Guidelines for Americans recommends that people who eat 2,000 calories a day have 2 cups of fruit and 2.5 cups of vegetables a day. Some solid options: leafy greens, bell peppers,citrus fruits, sweet potatoes, and berries.
4. Load up on vitamin D.
Vitamin D plays an important role in supporting the immune system by helping your body produce antibodies, which can then fight illness, Cording says.
“Active vitamin D gets sent to different areas of your body, including your bones, intestines, colon, brain, and immune cells, where it binds with the receptors on these cells and ultimately turns them on,” adds Warren.
The kicker: Most people don’t get enough of it. Your body primarily produces vitamin D from the sun’s UV rays (it’s called the sunshine vitamin for a reason!), but you can also load up on vitamin-D rich foods to boost your intake, including fatty fish and seafood, mushrooms, eggs (don’t skip the yolk), and fortified foods, Cording says. If you suspect your vitamin D intake is low and would like to take a supplement, be sure to talk to your doctor. He or she can do a blood test to determine the appropriate dosage for you.
5. Prioritize sleep.
Spending more time snoozing is key, Dr. Blank confirms. “Getting enough sleep helps our bodies recover from everyday stress—both physical and mental—and promotes better functioning of our immune system,” she says.
When you don’t get enough shut-eye, your body may decrease the production of protective proteins called cytokines, which your immune response needs more of when it’s dealing with an infection or inflammation while under stress.
So just how much sleep are we talking about? The National Sleep Foundation says adults up to age 64 should snooze between seven and nine hours per night for, while adults 65 and up should aim between seven and eight hours. (Tossing and turning? Check out our full guide on how to sleep better every night.)
6. Wash your hands often.
Washing your hands regularly will help keep viruses and bacteria away from your eyes, nose, and mouth, which can do your immune system a solid, Dr. Blank says. “This reduces the variety and number of germs we are exposed to and keeps our immune system from getting overwhelmed,” she explains.
The Centers for Disease Control and Prevention (CDC) specifically recommends washing your hands with soap and water for at least 20 seconds, or the amount of time it takes to hum the “Happy Birthday” song from beginning to end twice.
7. Keep up with a regular exercise routine.
Being physically active can help keep pathogens out of your lungs and airways, according to the National Library of Medicine, which can minimize your odds of getting a cold, the flu, or other illnesses. Exercise can also give antibodies and white blood cells a boost, causing them to circulate more widely throughout your body, where they might detect illnesses better than they would if you didn’t get moving.
8. Finally, quit smoking if you haven’t already.
You already know smoking is bad for your health in so many ways, but it can also wreak havoc and “cause direct damage” to parts of your immune system, Dr. Blank says.
For example, smoking immobilizes cilia, the hair-like structures in your airways that help “sweep” out bacteria. “These cilia form the first line of defense against respiratory infections,” Dr. Blank says. When they’re immobilized, germs have “much easier access” to your lungs, she explains. Cue the coughing and sneezing.
Adopting certain lifestyle habits can strengthen your immune system. Of course, you can do everything right and still get sick. But doing your best to boost your immune system now means your body will be that much more prepared for tackling whatever bugs may come your way later.
You may have noticed you’re more likely to catch a cold or other infection when you’re not getting enough sleep. Studies help bear out that well-rested people who received the flu vaccine developed stronger protection against the illness. Not getting enough sleep can lead to higher levels of a stress hormone. It may also lead to more inflammation in your body.
Although researchers aren’t exactly sure how sleep boosts the immune system, it’s clear that getting enough – usually 7 to 9 hours for an adult – is key for good health. Try to get regular, moderate exercise, like a daily 30-minute walk. It can help your immune system fight infection. If you don’t exercise regularly, you’re more likely to get colds, for example, than someone who does. Exercise can also boost your body’s feel-good chemicals and help you sleep better. Both of those are good for your immune system.
Eating or drinking too much sugar curbs immune system cells that attack bacteria. This effect lasts for at least a few hours after downing a couple of sugary drinks. Eat more fruits and vegetables, which are rich in nutrients like vitamins C and E, plus beta-carotene and zinc. Go for a wide variety of brightly colored fruits and vegetables, including berries, citrus fruits, kiwi, apples, red grapes, kale, onions, spinach, sweet potatoes, and carrots.
Other foods particularly good for your immune system include fresh garlic, which may help fight viruses and bacteria, and old-fashioned chicken soup. If you do come down with a cold or the flu, a bowl of chicken soup can help you get well faster, one study shows. Some mushroom varieties — such as shiitake — may also help your immune system.
Everyone has some stress; it’s part of life. If stress drags on for a long time, it makes you more vulnerable to illness, from colds to serious diseases. Chronic stress exposes your body to a steady stream of stress hormones that suppress the immune system. You may not be able to get rid of your stress, but you can get better at managing it.
Learn to meditate.
Slow down.
Connect with other people.
Work out to blow off steam.
Counseling is a big help, too. Easing stress lowers levels of a stress hormone. It also helps you sleep better, which improves immune function. People who meditate regularly may have healthier immune system responses, some studies show. In one experiment, people who meditated over an 8-week period made more antibodies to a flu vaccine than people who didn’t meditate. And they still showed an increased immune system response 4 months later.
Having strong relationships and a good social network is good for you. People who feel connected to friends – whether it’s a few close friends or a large group – have stronger immunity than those who feel alone, studies show. In one study, lonely freshmen had a weaker immune response to a flu vaccine than those who felt connected to others. Although there are many other things that affect your health, making meaningful connections with people is always a good idea.
Laughing is good for you. It curbs the levels of stress hormones in your body and boosts a type of white blood cell that fights infection. Just anticipating a funny event can have a positive effect on your immune system. In one study, men were told 3 days in advance that they were going to watch a funny video. Their levels of stress hormones dropped.
