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DR. RAHIM KARIM INSTALLED AS 10th PRESIDENT AND CEO OF THE CANADIAN COLLEGE OF NATUROPATHIC MEDICINE – Benzinga

New President signals an era of partnerships and global reach for CCNM

TORONTO, Sept. 23, 2022 /CNW/ - Today Dr. Rahim Karim, BSc, DC, MBA, CHE, ICD.D was installed as the tenth President and CEO of the Canadian College of Naturopathic Medicine (CCNM). The ceremony took place at the Toronto campus of CCNM.

Signaling a new era of partnerships and global reach for CCNM, Dr. Colleen McQuarrie, ND, Chair of the Board of Governors of CCNM said:

"CCNM is a truly pan-Canadian institution with global reach and is now the largest naturopathic institution in North America. The new President and CEO brings strong experience in partnerships and collaboration to CCNM at a critical moment in its growth."

As part of his installation address, new President and CEO Dr. Rahim Karim outlined a strategic direction building upon partnerships, programming, practice, participation and planning. In his remarks, to mark this occasion, he announced the creation of a lecture series in integrative care with a goal of showcasing and discussing global best practices in integrative care.

"Together, working collaboratively as a community, we will continue to grow this fine institution, build our global reputation and reach, and strengthen naturopathic medicine," said Dr. Karim.

The event was attended by government officials, other academic institutions, various community and professional organizations as well as CCNM employees and students.

About the Canadian College of Naturopathic Medicine (CCNM)

The Canadian College of Naturopathic Medicine (CCNM), established in 1978, isCanada'spremier, pan-Canadian academic institution for education and research in naturopathic medicine. CCNM has two campuses, one inTorontoand another in the Metro Vancouver area known as the Boucher Campus.Its graduates are eligible to write the licensing examinations for all regulated jurisdictions in Canada and the United States to become naturopathic doctors.

Visit http://www.ccnm.edufor more information.

SOURCE Canadian College of Naturopathic Medicine

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DR. RAHIM KARIM INSTALLED AS 10th PRESIDENT AND CEO OF THE CANADIAN COLLEGE OF NATUROPATHIC MEDICINE - Benzinga

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Deepak Chopra & Seva.Love Announce "ChopraVerse: House of Enlightenment," the Metaverse for Wellbeing in Collaboration with Utopia – PR…

LOS ANGELES, Sept. 21, 2022 /PRNewswire/ -- Deepak Chopra and SEVA.LOVE, a first-of-its-kind platform that is empowering a culture of wellbeing in the metaverse, today announced "ChopraVerse," the metaverse for wellbeing in collaboration with Utopia. Utopia is a Web3 ecosystem brought together by Alejandro Saez, Maria Bravo, Eva Longoria, and Javier Garcia. The ChopraVerse initiative is part of Seva.Love's ongoing mission to create a more conscious Web3 community for a peaceful, just, sustainable, healthier and joyful world. The House of Enlightenment, designed by Vera Iconica Architecture, is Deepak Chopra's personal home in the metaverse that was initially designed for the physical world incorporating eastern wisdom design principles and the latest in wellness architecture.

The Metaverse today is mostly about gaming. The ChopraVerse is about creating a world which enhances our wellbeing. A world that will be photorealistic and inhabited by human avatars and AI beings. A world where no one will feel alone one that offers infinite experiences and possibilities. As part of the initial launch, The ChopraVerse will make the "Deepak Chopra - House of Enlightenment" available for everyone to experience in the metaverse and also enable downloadable blueprints for build in the physical world via NFTs.

"ChopraVerse is creating homes for multidimensional living, nourishing the body, mind, spirit and environment as a unified experience in awareness. It will give everyone an opportunity to generate their own abode for the return to wholeness and healing," says Deepak Chopra, world-renowned pioneer in integrative medicine, NY Times best selling author and co-founder of Seva.Love.

Utopia, which recently acquired Virtual Voyagers, has carried out more than 230 projects related to the metaverse for major brands such as META and Vodafone, winning more than 20 awards for innovation and creativity. "The opportunity Web3 technology currently presents to creators, developers and businesses is exciting on many levels. Utopia is born from the dream, duty, and vision of achieving a connection between the tangible and virtual world - in which we will live in an ethical, inclusive, and responsible way," says Nino Saez, co-founder and CEO of Utopia.

"The ChopraVerse will transform how we interact and experience wellbeing in the digital and physical world. Our collaboration with Utopia will enable us to experience interoperable metaverse experiences in real-time, 3D virtual worlds that can be experienced synchronously, maintain presence and have a collaborative experience," says Poonacha Machaiah, co-founder and CEO of SEVA.LOVE. "While the NFT world is incredible, it is still evolving, and we saw a gap in the market to build a wellbeing community and make real social impact via the metaverse."

"The Utopia and ChopraVerse collaboration will enable an ecosystem in the digital world for impactful collaborations within the metaverse, where we aim to bring global action to educate the world, connecting philanthropists, embracing brands and businesses using the power of the blockchain to raise awareness on building a more ethical and transparent world, a community of philanthropreneur's, spreading kindness fast to where it's needed," says Maria Bravo, co-founder Utopia and Global Gift Foundation.

The ChopraVerse roadmap has planned NFT drops which will serve as access tokens to the ChopraVerse in Utopia. Additionally, there will also be a limited number of NFTs that will integrate blueprints and wellbeing design principles, by licensure through the Architect, Vera Iconica Architecture, that can be leveraged to build homes in the physical world. "The House of Enlightenment was designed both to be built in the physical world and to be experienced by many in the digital world as a home that optimizes health and wellbeing in harmony with nature. It is an education and awareness tool that anyone can go into to learn meditation or how your surroundings are impacting your health and behavior and what you can do to elevate your state of being," says Veronica Schreibeis Smith, CEO & Founding Principal, Vera Iconica Architecture.

The ChopraVerse platform has built on its partnership with Deepak Chopra and is collaborating with other global wellbeing experts, products and services within its own metaverse while also integrating with brands and experiences in the Utopia metaverse.

For more information please visit: http://www.chopraverse.io

About Seva.Love

Seva.Love is the metaverse for wellbeing initiative that has been founded by serial technology entrepreneur Pooancha Machaiah and world-renowned pioneer in integrative medicine, personal transformation and NY Times bestselling author Deepak Chopra, MD.

Seva.Love is championing wellbeing and social impact in Web3 by curating leading artists, influencers, wellbeing experts and creating conscious communities. Seva.Love has exclusive access to Deepak Chopra web3 content and the ChopraVerse will enable transmedia storytelling and engage communities in the metaverse and IRL. Access to the Seva ecosystem will be via NFTs and the Seva token. For more information please visit https://www.seva.love/ and follow us at twitter: @sevaislove instagram: @sevaislove discord: https://discord.seva.love/

About Utopia

Utopia Group is a Web3 ecosystem brought together by four founders, Alejandro Saez, Maria Bravo, Eva Longoria, and Javier Garcia - with the mission of disrupting how businesses operate and innovate using the power of blockchain technology.

The Utopia Group's vision is to focus on bridging the gap between the physical and digital worlds. Through Utopia's acquisition of Virtual Voyageurs, the group will offer strategic consulting services, particularly developing metaverse applications and experiences, as well as educational programs and initiatives in the world of Web3.

About Vera Iconica Architecture

Founded in 2010 in Jackson by Wyoming native and Wellness Architecture pioneer, Veronica Schreibeis Smith, Vera Iconica specializes in Architecture, Interior Design, and Real Estate Development and is known globally for its Wellness Kitchen. Based in the Mountain West with offices in Jackson and Denver, Vera Iconica's highly flexible, international team of experts merges cultural, spiritual, and qualitative elements with hard science to create highly customized solutions that elevate healthy, conscious living. For more information please visit https://veraiconica.com/ and follow at instagram: @veraiconicaarchitecture

SOURCE SEVA.LOVE

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Deepak Chopra & Seva.Love Announce "ChopraVerse: House of Enlightenment," the Metaverse for Wellbeing in Collaboration with Utopia - PR...

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Allergic to the world: can medicine help people with severe intolerance to chemicals? – The Guardian

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 neighbours laundry detergent sailing through the air. When modern medicine failed to identify the cause of Sharons 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 Randolphs 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 Randolphs 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 Randolphs 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 Beards 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 USs 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 couldnt 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 Quebecs 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 theyd run a complete blood count and tell me I looked fine, that it must be stress, so theyd 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 Teichs 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 Teichs 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. Its 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 familys trailer home. A cardiac examination had produced no remarkable results, and Sharons 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 Teichs best friend). Rea diagnosed her with MCS secondary to mould toxicity. Mould is everywhere, Teich told me. Not just indoors. Mould grows on leaves. Thats 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 Ill 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 Marks 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 dont notice until its 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 dont need tests or blood work, he told me. I rarely ever order them. I can see with my eyes that he has mould, and thats enough. It was Teichs common practice to ask his patients to remove their socks to reveal the inevitable ridges and splits on their big toenails, and thats 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.

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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 Blacks 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 Randolphs idea of postindustrial toxicities leading to intolerance. The same has been said of the first responders and the World Trade Centres 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 MCS 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 youre on, she told me, theres 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 Randolphs 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 ORourke in the New Yorker in 2013 about her battle against Lyme disease, is that most people find what youre 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 cant 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 patients 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, Sharons 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 its 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 Sharons life. If anything, Covid-19 improved her situation. Sharons 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.

This essay was originally published in Aeon

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Allergic to the world: can medicine help people with severe intolerance to chemicals? - The Guardian

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Genetic footprints of assortative mating in the Japanese population – Nature.com

Study cohort description

We used data on a total of 172,270 individuals of Japanese and East Asian ancestry. Of these, data on 165,098 individuals were obtained from BBJ, which has enrolled 200,000 participants to date. BBJ is a multi-institutional hospital-based genome cohort that collected participants affected with at least one of 47 diseases20. We excluded (1) individuals with low genotyping call rates (<98%), (2) closely related individuals (PI_HAT0.125 by PLINK, v.1.90b4.4; https://www.cog-genomics.org/plink/) and (3) outliers from the Japanese cluster based on principal component analysis (PCA) using PLINK2 (v.2.00a2.3 and v.2.00a3; https://www.cog-genomics.org/plink/2.0/) with samples of the 1000 Genomes Projects. Further, we separated the BBJ individuals into two Japanese clusters22,27 the mainland cluster (n=156,151) and Ryukyu cluster (n=8,947), by visual inspection based on the PCA plot (Supplementary Fig. 1). All the participants provided written informed consent approved from ethics committees of RIKEN Center for Integrative Medical Sciences, and the Institute of Medical Sciences, the University of Tokyo.

The Japanese subjects in replication cohorts were collected from three Japanese population-based cohorts (the Nagahama cohort study, JBIC and the Osaka University healthy cohort). The Nagahama cohort study is a community-based cohort in Nagahama city, Shiga prefecture, Japan. The study recruited healthy individuals between the ages of 30 and 74 (ref. 46). JBIC consists of EpsteinBarr virus-transformed B lymphoblast cell lines of unrelated Japanese individuals47. Osaka University healthy cohort is a volunteer-based cohort study recruited from the Osaka University Graduate School of Medicine, the University of Tokyo and the University of Tsukuba48. For each cohort, we also excluded individuals with a low genotyping call rate, a high heterozygosity rate, closely related individuals (PI_HAT0.125) and PCA outliers from EAS populations28,48,49. In addition, we extracted the EAS individuals from UKB. UKB is a population-based cohort that recruited approximately 500,000 individuals between 40 and 69 years of age from across the United Kingdom50. We obtained EAS individuals from unrelated UKB individuals based on PCA visualization combined with the 1000 Genomes Projects (Supplementary Fig. 2). Finally, we included 16,119 individuals in the replication study (n=8,947 from BBJ Ryukyu, n=1,275 from Osaka University healthy cohort, n=2,945 from the Nagahama cohort study, n=1,110 from JBIC and n=1,842 from UKB EAS). This study was approved by the ethical committee of Osaka University Graduate School of Medicine.

BBJ collected baseline clinical information and dietary and activity habits information through interviews and reviews of medical records using a standardized questionnaire. We selected 81 traits (57 anthropometric traits and biomarkers, 11 dietary habits, six behavioural traits, six diseases and one dummy; Supplementary Tables 24). We used these data from participants above the age of 18, and drinking and smoking traits from those above the age of 20. We normalized each anthropometric trait and biomarker traits by applying rank-based inverse normal transformation as previously reported (Supplementary Table 8)51,52,53. For each dietary habit, the participants were asked to clarify the frequency of consumption on a four-point scale, and we assigned the corresponding values to their responses as previously described26, where almost every day=7, 34 days per week=3.5, 12 days per week=1.5 and rarely=0. Behavioural traits included ever versus never drinking and ever versus never smoking54 as binary traits, and the frequency of four PAs (light-PA, gymnastics, walking and sports). For each PA, participants were also asked for the frequency and the length of time per week on a seven-point scale, and we quantified the activity by converting the responses to total minutes of activity time per week (minweek1), where 30 (15) minday1=210 (105), <30 (15) minday1=140 (70), three to four times a week for 30 (15) min=105 (52.5), three to four times a week for <30 (15) min=70 (35), one to two times a week for 30 (15) min=45 (22.5), one to two times a week for <30 (15) min=30 (15) and rarely=0 (the number in parentheses indicates gymnastics time).

For disease phenotypes, cases with myocardial infarction, stable angina and unstable angina were reclassified as CAD. We then selected six diseases from the target disease of BBJ (T2D, dyslipidaemia, cataract, CAD, arrhythmia and ischaemic stroke), where the number of cases exceeded 10,000 individuals55.

In addition, we set a dummy phenotype as a negative control. We generated a phenotype with heritability (h2=0.5) from 10,000 causal variants randomly sampled from BBJ GWAS data using GCTA GWAS simulation56. The phenotype followed the model yj=gj+ej, where gj=i(Wiji) and Wij=(xij2pi)[2pi(1pi)]1/2, where xij is the genotype for the ith causal variant of the jth individual, pi is the allele frequency of the ith causal variant within a population and ej is the residual effect generated from a normal distribution with mean 0 and variance Var(gj)(1h2)/h2. i is the effect size of the ith causal variant generated from a normal distribution with mean 0 and variance 1 (ref. 57). The values were normalized by applying a rank-based inverse normal transformation.

The BBJ GWAS data were genotyped using the Illumina HumanOmniExpressExome BeadChip or a combination of the Illumina HumanOmniExpress and HumanExome BeadChips. The quality control of the genotypes was described elsewhere51. In brief, we excluded variants satisfying the following criteria: (1) call rate <99%, (2) P value for HWE<1.0106, (3) number of heterozygotes <5 and (4) a concordance rate <99.5% or a non-reference concordance rate between the GWAS array and whole genome sequencing. The genotype data were phased by Eagle (v.2; https://alkesgroup.broadinstitute.org/Eagle/), and imputed with the 1000 Genomes Project Phase3 (v.5) and BBJ1K using Minimac3 software (v.2.0.1; https://genome.sph.umich.edu/wiki/Minimac3). After imputation, we excluded variants with an imputation quality of R-square (Rsq)<0.7 and those with a minor allele frequency (MAF)<1%.

As for the other Japanese datasets, JBIC was genotyped using Illumina HumanCoreExome Beadchip. As stringent quality control filters, we excluded the variants that satisfied (1) call rate<0.99, (2) MAF<1% and (3) HWE P<1.0107 (ref. 47). Osaka University healthy cohort was genotyped using Illumina Infinium Asian Screening Array. We excluded the variants that satisfied (1) call rate<0.99, (2) minor allele count<5 and (3) HWE P<1.0105 (ref. 48). The Nagahama cohort study was genotyped using six genotype arrays. We then selected two platforms (Illumina Human610-Quad Beadchip and Illumina HumanOmni2.5-4v1 Beadchip) with a large number of samples. For each of the two datasets, we excluded variants with (1) call rate<0.98, (2) MAF<1% and (3) HWE P<1.0106 (ref. 28). Genotype data were phased by Shapeit (v.2; https://mathgen.stats.ox.ac.uk/genetics_software/shapeit/shapeit.html) or Eagle, and imputed with the reference panel from the 1000 Genomes Project Phase3 (v.5) and BBJ1K using Mimimac3. After imputation, we excluded variants with an imputation quality of Rsq<0.7 and MAF<1%.

The UKB project was genotyped using either Applied Biosystems UK BiLEVE Axiom Array or Applied Biosystems UKB Axiom Array. The genotypes were imputed using the Haplotype Reference Consortium, UK10K and the 1000 Genomes Phase 3 reference panel by IMPUTE4. The detailed characteristics of the cohort and genotypephenotype data were described elsewhere50. We extracted EAS individuals and excluded variants with INFO score 0.8 and MAF1%.

As independent external reference GWASs or genotype data of Japanese ancestry were not publicly available, we adopted a tenfold LOGO meta-analysis to maintain both the accuracy of the GWAS statistics and the statistical power in PGS21. We first randomly split the BBJ mainland samples into the 10 target subsets. GWAS was performed on 81 complex traits for samples excluding the target subset using GCTA-fastGWA (v.1.93.3beta2; https://cnsgenomics.com/software/gcta/#Overview) as a MLM approach with 7,401,847 autosomal variants23,24. For GCTA-fastGWA, we computed a sparse genetic relationship matrix (GRM) for BBJ participants (n=182,961) using slightly LD-pruning variants (LD-pruning parameters in PLINK: indep-pairwise 1000 100 0.9, and MAF1%, sparse GRM parameter: make-bK-sparse 0.05). Regarding the 57 anthropometric traits and biomarkers, the 11 dietary traits, the four PA traits and the two binary traits in the behavioural traits, we fitted age, age-squared, sex, the top 20 PCs and 47 disease status as covariates. For the six diseases, we also fitted age, age-squared, sex and the top 20 PCs as covariates. We also performed GWAS using GCTA-fastGWA for all individuals in the BBJ mainland cluster to apply to other Japanese or EAS datasets. LD score regression (LDSC, v.1.0.0; https://github.com/bulik/ldsc) was applied to the summary statistics of the whole-sample GWAS to estimate potential population stratification. We adopted the HapMap3 SNPs, excluding the human leukocyte antigen region, using precomputed LD scores from 1KG EAS downloaded from the LDSC software website (Supplementary Table 5)58.

To estimate phenotypic variances explained by imputed data for some of the traits, we applied GREML-LDMS using GCTA (v.1.93.2beta; https://cnsgenomics.com/software/gcta/#Overview)57. We created the GRM using all variants for BBJ mainland samples. We estimated LD scores using default parameters in GCTA, and stratified SNPs into LD score quartiles. Next, we divided the SNPs within each LD score quartile into six MAF groups (MAF<5%, 5%MAF<10%, 10%MAF<20%, 20%MAF<30%, 30%MAF<40%, 40%MAF) and generated 24 GRMs. We calculated the phenotypic variance for each GRM and summed them to derive the total phenotypic variance (Supplementary Table 7). In the calculations, we randomly sampled 50,000 unrelated individuals (GRM<0.05) randomly downsampled from BBJ mainland individuals to avoid computational burden and used the same normalized values for quantitative traits and covariates for binary traits as used in the GWAS analysis.

To derive PGSs of individuals in each of the target subsets, we applied PRS-CS (https://github.com/getian107/PRScs) to construct PGSs that included genome-wide HapMap3 variants. PRS-CS is one of the beta shrinkage methods, which applies a Bayesian regression framework to identify posterior variant effect sizes based on continuous shrinkage before using both GWAS summary data and the external LD reference panel25. When the training sample size was large enough and the casecontrol imbalance was small, the automated optimization model (PRS-CS-auto) had the same precision as the grid model59,60. Therefore, for each of the target folds, we estimated the posterior mean effects of SNPs from the MLM-GWAS summary data of all training samples using PRS-CS-auto with the precomputed HapMap3 SNP LD reference panel from 1KG EAS downloaded from the PRS-CS website. We calculated PGSodd and PGSeven of individuals within the target subset using the estimated posterior effect of SNPs by PLINK2 score function. We normalized the calculated PGSs for each trait in each target subset to compare the effect sizes across the phenotypes.

We quantified the trait variance explained by the derived PGSs in individuals within one withheld subgroup. Each trait was modelled as a combination of PGS and all covariates. The null hypothesis used the same model without the PGS term. We calculated the adjusted R2 for quantitative traits and the Nagelkerkes R2 for binary traits (Supplementary Table 5).

For GPD estimation, we performed PCA of even and odd number chromosomes for each of the target subsets. We then estimated GPD using a linear regression method following the formula based on the original study18:

$${mathrm{PGS}_{rm{odd}}}approx theta _{mathrm{{even}}_{mathrm{to}}_{mathrm{odd}}}{mathrm{PGS}_{rm{even}}} + 20{mathrm{PCs}_{rm{even}}}$$

$${mathrm{PGS}_{rm{even}}}approx theta _{mathrm{{odd}}_{mathrm{to}}_{mathrm{even}}}{mathrm{PGS}_{rm{odd}}} + 20{mathrm{PCs}_{rm{odd}}}$$

where PGS is the scaled polygenic score, PCs are the results of the PCA and is the estimate of GPD. We further meta-analysed the GPD estimate from each of the ten subsets using the fixed effect method using metafor (v.1.9-9; http://www.metafor-project.org/doku.php/metafor) implemented in R (v.3.4.0; https://www.r-project.org/). We also estimated the GPD for the other Japanese and EAS datasets using the summary results of the whole BBJ sample GWASs by PRS-CS-auto. Finally, we performed a meta-analysis on the GPD estimates from the BBJ and other Japanese and EAS datasets by the fixed effect method using metafor. We estimated the P value of meta-analysed GPD using the Wald test.

To assess the robustness of our analysis to the chosen grouping of chromosomes, we altered the combinations of chromosomes such that the number of SNPs was the same in the two groups: (1) first half and second half; chromosomes 18 versus chromosomes 922, and (2) pseudo-random chromosomes; chromosomes 1, 3, 5, 6, 9, 10, 13, 14, 17 and 18 versus chromosomes 2, 4, 7, 8, 11, 12, 15, 16, 19, 20, 21 and 22. Using the two alternative combinations, we estimated the GPD for each cohort and meta-analysed the results.

We also calculated the theoretical GPD derived in the original study18. The theoretical value () followed the formula,

$$theta = frac{{rho f_0}}{{2 - rho (2 - f_0)}}left[ {1 + frac{{M(1 - rho )}}{{nh_{mathrm{{eq}}}^2}}left{ {1 + frac{{rho f_0}}{{2(1 - rho )}}} right}^{ - 3}} right]^{ - 1}$$

where (rho = rh_{mathrm{{eq}}}^2), r is a phenotypic correlation between spouses, (h_{mathrm{eq}}^2) is an equilibrium heritability of the phenotype, (f_0 approx f_{mathrm{{eq}}}/(1 - rho )), (f_{{rm{eq}}} = h_{{rm{snp}}}^2/h_{{rm{eq}}}^2,) (h_{{rm{snp}}}^2) is a SNP-based heritability, M is the number of causal variants and n is the sample size of the GWAS.

We analysed individuals of white British ancestry determined by PCA (n=337,139) from UKB by adopting the tenfold LOGO approach to the six available traits (adult height, BMI, T2D, CAD, duration of light-PA and yoghurt consumption)50. When adult height and BMI were measured multiple times, we adopted the mean value to obtain a single value per participant and normalized the values using the rank-based inverse normal transformation method. Regarding T2D, the case was defined following the ICD-10 codes and probable T2D and possible T2D in a T2D inference algorithm based on Eastwood et al.61. We also defined individuals without any diabetes status as the T2D control based on ICD-10 and the inference algorithm. As for CAD, the case was extracted following ICD-10 codes, surgical procedure recodes, self-reported illness codes and self-reported operation codes based on Fall et al.62. Regarding the duration of light-PA (Data-Field 104920), we extracted the data from instance 0 (n=70,692) and converted the coding to categorical values. Regarding the consumption of yoghurt, we extracted data from instance 0 within consumers of yoghurt/ice cream as binary traits (n=70,692 and Data-Field 102080). From the imputed GWAS data, we excluded the variants that satisfied MAF1% and INFO score 0.8, and fastGWA conducted generalized MLM approaches for nine subset samples with adjustment for age, age-squared, sex, top 20 PCs, ascertainment centre information and batch information as covariates. For the six phenotypes, we estimated the PGSs for odd and even chromosomes by PRS-CS-auto using genome-wide HapMap SNPs and the 1KG EUR LD reference panel, and the GPD was estimated in the same way as described in the Japanese study. We further meta-analysed the GPD estimate from each of the ten subgroups by the fixed effect method using metafor.

Further information on research design is available in the Nature Research Reporting Summary linked to this article.

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Jefferson doctors publish new book, ‘Tapestry of Health,’ with tips on wellness – On top of Philly news – Billy Penn

Note: This article is a paid placement and does not necessarily reflect the views or opinions of Billy Penn at WHYY.

With the United States long at the forefront of medical breakthroughs, why do so many Americans still get sick with preventable illnesses?

Around 60% of adults in the U.S. have a chronic disease, according to the CDC, and over 40% have more than one.

The fast-growing field of integrative medicine looks to address that problem. Its practitioners are trained to consider the whole patient the person instead of just the symptoms or the disease. Its the driving philosophy behind the Marcus Institute of Integrative Health Jefferson Health in Philadelphia, where doctors just published a book with insights and tips on how you can use this thinking to further your own health.

Called Tapestry of Health: Weaving Wellness into Your Life through the New Science of Integrative Medicine (Kales Press), the book is by Marcus Institute founding director and CEO Daniel Monti, MD, and Medical Director Anthony Bazzan, MD.

It presents a step-by-step plan of evidence-based restorative approaches and emerging cutting-edge strategies. Its been well-received by readers, rocking a 4.4-star rating on Amazon, and by other experts in the field,

This book is so incredibly timely and important, writes Sara Gottfried, a doctor with four NYT best-sellers who provided the new books forward, because it helps you understand this new paradigm of health a massive shift that affects healthcare providers and patients alike,

As its currently structured, the authors say, the medical field suffers from an overemphasis on acute care, which is a reactionary approach. Under this model, when a person gets sick, medical care is sought and a standard treatment be it drugs or surgery is prescribed. Theres no doubt this approach has saved many lives. But it is not enough.

Heart disease, cancer, stroke, and diabetes are leading causes of death and disability in the U.S., accounting for the majority of the nations $4.1 trillion a year in health care costs.

In many cases, these illnesses are significantly exacerbated by key lifestyle risk factors. Some, such as tobacco use, are straightforward and easy to understand. Others, including the vital role of diet and specific nutrients, physical inactivity, and stress effects on immunity, are more complex.

In the case of immune resilience, the pandemic is a perfect example of how acute care medicine dominated the conversation.

Everyone understandably became very focused on the COVID-19 pathogen. However, what got lost was the state of the host i.e. people! For example, we know nutritional status affects the immune response to the virus, and that stress in general affects the immune system in very measurable ways. So while we very much needed an effective vaccine, we also needed tools to maximize immune wellness to maximize the host response to infection. That largely did not happen.

Some in medicine have begun to recognize the gap, which is why a new paradigm is emerging that integrates the best of modern medicine with proactive, holistic and preventive care.

Thomas Jefferson University is at the forefront of this movement. The Philly institution recently created the first-ever Department of Integrative Medicine & Nutritional Sciences at Sidney Kimmel Medical College. The new department includes the clinical programs of Jefferson Healths Marcus Institute of Integrative Health. These programs have introduced an approach to care that is a multifaceted partnership, connecting all aspects of well-being, including the physical, emotional, intellectual, spiritual, social, and nutritional.

To learn more about the book and other resources, visit the Tapestry of Health website.

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Sure Signs Your Immune System Isn’t as Strong as it Should Be Eat This Not That – Eat This, Not That

Your immune system works hard to fight off forein invaders like infections and germs to keep you healthy and it never gets a break. It works around the clock everyday to protect you, so helping your immune system stay strong is vital to your overall well-being. So how can you help strengthen your immunity? Eat This, Not That! Health spoke with Dr. Michael Hirt, a Board Certified Nutrition from Harvard University and Board Certified in Internal Medicine and is with The Center for Integrative Medicine in Tarzana California who shares what to know about your immune system, signs it's too weak and how to help boost it. As always, please speak with your physician for medical advice. Read onand to ensure your health and the health of others, don't miss these Sure Signs You've Already Had COVID.

Dr. Hirt tells us, "You know exercise can make your heart stronger. You know puzzles can make your brain smarter. However, even after two years of pandemic health lessons, people are still puzzled as to how to reliably make their immune system stronger. Like your cardiovascular and nervous systems, the immune system is subject to the same lifestyle choices that affect the rest of your body. Eat too much sugar, drink too much liquor, shorten your sleep hours, and you should not be surprised that you are going to wake up with your heart pounding, brain fogged in, and the start of a sore throat. You are the sum of your choices, and a robust immune system is no exception to your cumulative health investments (or lack thereof)."

"The innate programming of your immune system is only to attack microbial threats and coordinate repairs ranging from skin scrapes to broken bones," says Dr. Hirt. "Under the influence of environmental toxins, intestinal imbalances (from diet and bacteria), and genetic tendencies, some parts of your immune system can go 'rogue' and attack the body it was sworn to only defend. This is called an auto-immune condition because the immune system is attacking parts of self like joints, skin, or internal organs. This is never supposed to happen, serves no evolutionary benefit, and requires major lifestyle changes, detoxification, and medical interventions to stop the attack and remove the triggers of self-attack. Without a coordinated healing effort, the immune system will likely continue to attack itself and require strong, immune-suppressive measures."

Dr. Hirt shares, "If you're thinking of trying to boost your immune system, consider how you would boost the effectiveness of your nation's defense forces. To have a stronger, more effective military, you would feed them healthy food, ensure they are well rested, avoid unnecessary stress, house them on clean bases, provide cutting edge equipment, and have plenty of munitions so they never run out of bullets and missiles. Same with your immune system. Eat the healthiest food you can, in the cleanest environment you can, under the least stress you can, having had the most restful sleep you can, and taking the best vitamins you can including zinc, vitamin C, and vitamin D. Just like our military, your immune system never gets to take a collective break from defending you from all threats, both foreign and domestic."6254a4d1642c605c54bf1cab17d50f1e

Dr. Hirt states, "Most adults get a cold or flu 2 3 times yearly. If you're calling in sick on a monthly basis, you could have a more significant immune deficiency that needs testing and treatments."

"When you cut your self, superficial wounds typically take seven days to heal," Dr. Hirt tells us. "If you are watching your skin take weeks to heal, then your immune system may be compromised."

According to Dr. Hirt, "When you get an upper respiratory infection, most people with healthy immune systems can fully recover in ten days. If your symptoms go on for most of the month, then there may be issues with the strength of your immune responsiveness."

"There are many reasons to be tired," Dr. Hirt says. "Many people are surprised to learn that one of them is a weak immune system, or low white blood cell count. If you are experiencing unusual fatigue, make sure your healthcare provider includes a screening test for your immune system."

Heather Newgen

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