At OHS we feel that the benefits of CBD while suffering from inflammation induced dis-ease and anxiety could be profound. The regulating effects of a happy ECS (Endocannbinoid System) might be a game changer for some.
Excerpts from a brilliant article in The Atlantic by Meghan O'Rourke:
"Startlingly, most had had mild cases of COVID‑19—they had neither been hospitalized nor developed pneumonia. Before contracting the virus, many had had no known health issues. Yet they were reporting significant ongoing symptoms—“shortness of breath, heart palpitations, chest pain, fatigue, and brain fog,” Chen told me.
These tended to be the patients who had originally had mild to moderate symptoms. They were overwhelmingly women, even though men are typically hit harder by acute COVID‑19. (Acute COVID‑19 refers to the distinct period of infection during which the immune system fights off the virus; the acute phase can range from mild to severe.) And they tended to be young, between the ages of 20 and 50—not an age group that, doctors had thought, suffered the worst effects of the disease. Most of the patients were white and relatively well-off, raising concern among clinicians that many people of color with ongoing symptoms were not getting the care they needed.
These patients’ tests usually showed nothing obviously the matter with them. “Everything was coming back negative,” says Dayna McCarthy, a rehabilitation-medicine physician and a lead clinician at the center. “So of course Western medicine wants to say, ‘You’re fine.’ ”
An international survey by Patient-Led Research for COVID‑19, one of various groups drawing attention to persisting problems, asked nearly 3,800 patients with ongoing illness to describe their symptoms. A significant number—85.9 percent—reported having relapses in the months after their initial infection, usually triggered by mental or physical exertion. (Not all patients in this group had confirmed cases of COVID‑19, given that tests were hard to come by last March and April.) Many patients were experiencing severe fatigue and brain fog. Other patients suffered from chest tightness and tachycardia—a condition in which the heart beats more than 100 times a minute—when they stood up or walked. Others had diarrhea and lost their appetite; some had terrible bone pain. Nearly a quarter said they were still unable to work; many had gone on disability or taken medical leave. Patient groups of COVID‑19 “long-haulers” were springing up on Facebook and elsewhere online, where people shared data and compared notes about what they began to call “long COVID.”
Cohen began posting in a doctors’ group on Facebook, eager to find out whether any of her colleagues had patients whose symptoms resembled hers. On the afternoon of March 26, she sat up in bed, and her heart rate skyrocketed. “I had an epiphany,” she told me. “I thought, Wait a second. Oh my God. This is like POTS”—postural orthostatic tachycardia syndrome, one of the subtypes of dysautonomia. She began sleuthing—and turned up a paper that suggested a connection between POTS and an inflammatory immune response common in cases of COVID‑19.
“Most doctors don’t recognize dysautonomia as a real entity.”
“What we’re seeing is an entirely distinct syndrome,” Putrino told me, one that tends to be “way more debilitating and severe” than others like it, but similarly mysterious. No one knew exactly why the virus was throwing the autonomic nervous system out of whack—or causing all the other symptoms patients were reporting—but many suspected that the effect was likely to be “immune-incited,” as Dayna McCarthy put it. Based on preliminary evidence, some theories speculate that long COVID is a result of a powerful immune reaction unleashed by the virus, leaving widespread damage in the body; others posit that the immune response to the virus triggers autoimmune disease; and still other theories suggest that the virus itself causes hard-to-observe damage in the nervous system and other parts of the body. Or perhaps a combination of these factors is at play in different patients.
The patients’ symptoms were too varied to be lumped under an established label; in some ways the condition resembled dysautonomia, and POTS in particular—but it was not textbook. (Some clinicians began calling it post-COVID POTS.) In other ways, it closely resembled myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), in which people also demonstrate exercise intolerance and profound fatigue, but it was likewise not textbook. Same for autoimmune disorders. A commonality stood out: These are all poorly understood conditions that, evidence suggests, can be triggered by the body’s response to infections, with clusters of system-roaming symptoms that get grouped under one name.
A missing piece of the puzzle, the Mount Sinai teams soon found, was right in front of them: breathing. Everyone knew, of course, about severely sick COVID‑19 patients on ventilators. What the researchers and doctors at Mount Sinai hadn’t realized was that even mild cases might be affecting respiration after the acute phase of the disease. Evidence began to accrue that long-COVID patients were breathing shallowly through their mouths and into their upper chest. By contrast, a proper breath happens in the nose and goes deep into the diaphragm; it stimulates the vagus nerve along the way, helping regulate heart rate and the nervous system. Many of us breathe through our mouths, slightly compromising our respiration, but in patients with post-acute COVID syndrome, lung inflammation or another trigger appeared to have profoundly affected the process. In these cases, patients’ breathing “is just completely off,” McCarthy told me.
Dayna McCarthy at the Center for Post-COVID Care laid out the group’s theories about why the treatment is so helpful. Through breathwork, patients can consciously control their heart rate, she noted. In addition, modulating the nervous system’s fight-or-flight response may help regulate the immune system. (Studies have shown that elevated stress hormones can lead to chronic inflammation.) And proper breathing is crucial to circulation in the lymphatic system, often described as the body’s highway for immune cells, which plays a role in eliminating toxins and waste.
Medicine’s history with hard-to-identify chronic illnesses, particularly those that mainly affect women, has not been a good one. For decades now, marginalized patients who have felt mysteriously unwell—with ME/CFS, with post-treatment Lyme disease syndrome, with Ehlers-Danlos syndrome, and more—have banded together into activist groups to try to legitimize their suffering. The same is happening online in the long-hauler groups, which are full of patients who have been met with disbelief by local physicians. But the Mount Sinai doctors (along with collaborative teams in various other academic centers) have responded promptly to the problem. Recently, the NIH and the World Health Organization recognized long COVID as a syndrome that warrants more research.
COVID‑19 seems like a test case for this new model of thinking about infection as a trigger of immune dysfunction: One of the disease’s great mysteries is why some 30-year-olds die from it while others barely notice they have it, and still others initially have a mild acute case but end up unable to manage a flight of stairs. This pandemic has vividly dramatized the variability—and lingering complexity—of the human host’s response to a pathogen.
“This is something that has been going on forever,” said Craig Spencer, the director of emergency medicine at Columbia University Irving Medical Center. Spencer understands something about postviral conditions, because he contracted Ebola while working in Guinea and fell ill upon his return to New York City, where he then also struggled with its aftereffects.
“I wouldn’t be surprised if people are walking about with long Epstein-Barr virus, or long influenza. We all know someone who is low energy, who’s told to work harder. We have all heard about chronic-Lyme sufferers, and those with ME/CFS. But they get written off,” Spencer told me. The difference now is that it is happening “on such a huge scale—unlike anything we’ve seen before. It is harder for the medical community to write off.” Indeed, many researchers I spoke with believe that the race to understand long COVID will advance our understanding of chronic conditions that follow infection, transforming medicine in the process.
A great deal remains to be discovered about long COVID—about why more women than men seem to suffer from it (estrogen, genetics, and differences in the immune response are all being explored); about why some men experience erectile dysfunction; about how it affects taste and appetite, as well as mental health; about why some people respond to exercise-based rehab and others don’t. Proof of the virus’s destructive power keeps accumulating. One study found that a significant number of hospitalized COVID‑19 patients developed antibodies to their own tissue. Some research suggests that the virus persists in immunocompromised patients for many weeks. Evidence is also mounting that the virus infiltrates and damages not just the lungs and the heart, and possibly the vagus nerve, but also the brain, vocal cords, esophagus, and more. Doctors are experimentally treating long-COVID patients with a variety of pharmaceuticals, among them antihistamines, Pepcid AC, and an antiparasitic drug called ivermectin."
At OHS we feel that the benefits of CBD while suffering from inflammation induced dis-ease and anxiety could be profound. The regulating effects of a happy ECS (Endocannbinoid System) might be a game changer for some.
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