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October 16, 2020 at 07:30PM Wellness Mama® https://ift.tt/2hMTHxr https://ift.tt/eA8V8JThe gastrointestinal (GI) tract is a remarkable organ: it resides on the inside of our bodies, but is regularly in contact with the outside world by virtue of what we ingest. It is quite incredible that the immune cells of the GI tract are not activated more regularly by the many foreign products it encounters every day. Only when the GI tract encounters an intruder that risks causing disease do the immune cells of the GI tract spring into action.
That is, of course, under normal circumstances. In people with Crohn’s disease, the normally tolerant immune cells of the GI tract are activated without provocation, and this activation leads to chronic or relapsing — but ultimately uncontrolled — inflammation.
First described by Dr. Burrill B. Crohn and colleagues in 1932, Crohn’s disease is a complex inflammatory disorder that results from the misguided activity of the immune system. It can involve any part of the GI tract from the mouth to the anus, but most commonly involves the end of the small intestine.
Depending on the precise location of GI inflammation, Crohn’s disease may cause any number of symptoms including abdominal pain, diarrhea, weight loss, fever, and sometimes blood in the stool.
Treatment options for Crohn’s disease have evolved dramatically since Dr. Crohn and colleagues first described the condition, but the basic principle has remained the same: reduce the uncontrolled inflammation. Early approaches to treatment involved nonspecific anti-inflammatory medications such as corticosteroids, which have many potentially serious side effects outside the intestines.
Today, a number of newer therapies exist that act more specifically on the immune system to target inflammatory pathways known to be active in Crohn’s disease. These newer drugs, termed biologics, are antibodies that block proteins involved in specific inflammatory pathways relevant to Crohn’s disease. Since we don’t fully understand which pathways are involved in which patients, however, choosing a medication for a given patient is as much an art as it is a science.
Early approaches to treatment of Crohn’s disease followed a step-up algorithm in which the newer medications would only be used if the patient did not benefit from established therapies. This sequential approach — termed step therapy — has more recently been called into question, as studies have repeatedly shown that the newer drugs for Crohn’s disease are more effective than the old standards, and have preferable side effect profiles. Research also indicates that early, aggressive intervention and treatment, targeting not just symptoms but objective evidence of inflammation (as assessed through blood work, stool tests, imaging, and endoscopy), lead to better health and quality of life, at least in the short term.
Researchers recently published a study in the journal Gastroenterology on the longer-term benefits of treating Crohn’s patients to reduce both symptoms and inflammation. Specifically, they analyzed follow-up data from patients enrolled in the CALM study — a multicenter trial that compared two approaches to the treatment of early, moderate to severe Crohn’s disease. In the first approach, the decision to escalate therapy was based on symptoms alone; in the other approach, the decision was based on both symptoms and objective evidence of inflammation (found in blood work or a stool test, for example). This second approach is called tight control. A patient under tight control might feel well, but therapy would be escalated if there was objective evidence of inflammation. The primary end point of the original CALM study was healing the inflamed lining of the intestines, and the data showed that the tight control approach to treatment was more effective at reaching this goal.
The Gastroenterology study took the results of the original CALM study one step further. The researchers looked at how the patients who achieved healing of their intestinal lining are doing several years later. To this end, the researchers looked at the rates of various adverse outcomes (including the need for surgery and hospitalization for Crohn’s disease) in the CALM study patients since the trial ended.
They found that patients who were both feeling well and had demonstrated healing of the intestinal lining (called deep remission) had a significantly decreased risk of Crohn’s disease progression. Healing of the intestinal lining without feeling well, and feeling well without healing of the intestinal lining, were also associated with a lower risk of disease progression when compared to patients with active symptoms and inflammation, but to a lesser extent.
The recent study lends strength to a growing body of evidence in support of a treatment approach that emphasizes early intervention aimed at healing the lining of the intestines and resolving symptoms. Can we generalize the findings to most patients with Crohn’s disease? Not necessarily.
Enrolled patients had never been treated with a newer biologic drug, or with a drug called an immunomodulator that affects the way the immune system functions, before enrolling in the CALM study. Immunomodulators have been used to treat inflammatory bowel disease (IBD) since the 1960s, and they are often one of the first drug classes used for treatment of IBD. As a result, these study results may not generalize to the many people who have had a Crohn’s diagnosis for long enough to have already been treated with an immunomodulator.
Furthermore, those who received escalation of therapy were treated with increasingly optimized doses of a single biologic, adalimumab (Humira). It remains to be seen whether we would see the same results in patients already exposed to a biologic or with the use of another biologic.
In my practice, I regularly encourage using highly effective therapies early to pursue tight control. For some, the decision to follow this approach is easy. For others, the idea of escalating therapy, perhaps in the absence of symptoms, and to target something they may not feel, is more difficult to be convinced of. Concerns about side effects and the need for frequent monitoring are paramount among the roadblocks.
Collaborating with my patients so that they can make medical decisions that are in line with their values but still informed by evidence is critical for success, as is a commitment to regularly revisit and rethink the approach over time.
The post Early, tight control of Crohn’s disease may have lasting benefits appeared first on Harvard Health Blog.
A few years ago, Jaime Seltzer was helping coordinate research projects, grant applications and funding for a Stanford research group studying a condition called myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). Up to 2.5 million Americans, including Seltzer, have ME/CFS, and yet it felt like almost no one paid attention to her group’s research. “What is it going to take for researchers to take ME seriously?” she and her colleagues often wondered aloud.
The morbid answer, they hypothesized, was a pandemic. Since ME/CFS often follows viral infections, they feared it would take something as destructive as mass illness for the larger scientific community to take notice.
Unfortunately, this year they were proven right. As the COVID-19 pandemic presses on, doctors are increasingly worried about the significant subset of coronavirus patients—estimated to be somewhere around 10%—who are suffering symptoms like fatigue, brain fog and chronic pain for months on end. Many of them will soon fit the diagnostic criteria for ME/CFS, which is characterized by debilitating exhaustion lasting six months or longer. This flood of potential new ME/CFS patients has, just as Seltzer predicted, thrust her once little-known condition into the spotlight.
No one, least of all Seltzer, would argue that thousands of people becoming chronically ill at once is anything but tragic. The question is whether any good can come from that tragedy. ME/CFS has for decades existed outside the margins of mainstream medical knowledge, historically drawing only a few million research dollars each year—pennies, compared to conditions like breast cancer and Alzheimer’s disease. Many doctors know next to nothing about ME/CFS. Nearly every ME/CFS patient has a story about not being believed, or someone trying to convince them their often debilitating symptoms are psychological.
With the world’s attention, and the medical community’s research dollars, directed toward COVID-19, the conversation around long-haul coronavirus could finally change that—if clinicians are ready to take long-haulers and ME/CFS patients seriously, and get to the root of why a viral illness that’s supposed to clear in weeks can linger for decades.
On Christmas Eve 2009, Christina Cooper, 62, developed a flu-like illness. Eleven years later, the registered nurse and once-avid cyclist from Canby, Ore. still suffers symptoms that sound awfully similar to those now associated with long-haul coronavirus. Virtually any amount of physical exertion—even showering—leaves her with a bone-deep, sometimes days-long exhaustion unlike any she experienced before she got sick. Her brain is always foggy, her thoughts always jumbled. She has a chronic sore throat and constant pain. Even her voice changed, weakening into one that sounds frail and sick. She feels like she inherited the body of a 100-year-old, half a century early.
After she got sick in 2009, it took two years of feeling deathly ill for Cooper to find a doctor willing and able to help; several dismissed her outright or had no clue what was wrong with her. That experience isn’t uncommon.
ME/CFS is what’s known in the medical community as a “contested illness”—in other words, an illness some people think is fake. Patients’ lab tests often come back clean despite their debilitating symptoms. And though it often (but not always) follows a viral illness, there’s no agreed-upon cause of ME/CFS. As a result, it’s easy to dismiss as psychological. It takes a certain amount of medical savvy and determination—which is challenging to muster when you’re bedridden—just to get an ME/CFS diagnosis. People of color with symptoms of the condition often have an especially difficult time getting doctors to take them seriously.
Because the condition is so often dismissed, many sufferers reject the name “chronic fatigue syndrome.” Likening the illness to fatigue minimizes it, some patients argue. Fatigue is what you feel after a busy day; ME lands you in bed for a week after going to a doctor’s appointment. Instead, they refer to the condition only as myalgic encephalomyelitis or ME.
Many coronavirus long-haulers have endured similar mistreatment. In long-hauler support groups, there are countless stories of doctors who were skeptical, rude or unhelpful, if not baldly disbelieving. America’s slipshod coronavirus testing system also means many long-haulers can’t prove they had COVID-19 at all—a whole new headache when it comes to securing treatment.
But there is, at least, a critical mass of long-haulers getting sick and speaking out all at once, enough to draw attention from scientists, the media and the general public. Enough of these patients tested positive for COVID-19 or its antibodies to make a strong case that coronavirus is turning into ME/CFS.
“You had it. It’s documented. No one can doubt that. That makes it credible,” says Dr. Anthony Komaroff, a physician at Brigham and Women’s Hospital in Boston who has treated ME/CFS patients since the 1980s. “If you add that it may affect, ultimately, millions of people in this country alone, I think it certainly should generate new interest and I hope it will.”
For decades, most ME/CFS patients didn’t have that kind of group support. It took until 2015 for the Institute of Medicine to publish a substantial report describing the condition and its diagnostic criteria. According to the IOM’s definition, someone can be diagnosed with ME/CFS if they experience fatigue extreme enough to impair normal activity for at least six months; develop more severe symptoms after exertion; feel little relief from sleep; and suffer either cognitive changes or difficulty sitting or standing upright.
Up to 2.5 million Americans fit that description—as will many coronavirus survivors as their symptoms approach the six-month mark. “The coronavirus pandemic is very likely over time to create almost a pandemic of ME,” says Dr. Ron Tompkins, a surgeon from Massachusetts General Hospital who also researches ME/CFS. Long-haulers who have persistent symptoms related to specific organ damage won’t fit that diagnosis, but thousands of people who now have inexplicable symptoms likely will.
The influx of new patients could go a long way toward figuring out why, exactly, a viral illness can last forever. Though there are multiple theories in the ME/CFS research world, Komaroff believes the cause of the condition can be traced back to a part of the brain that kicks on when you’re sick—the part that saps your energy and appetite so your body can focus all its energy on clearing an infection. “This center in the brain gets flicked on, but for whatever reason it never gets switched off,” Komaroff says. New research efforts spurred by the pandemic could help determine if that’s really happening, and why.
“You need a lot of patients to study anything,” Komaroff says. “We will have enough patients to study at least that kind of ME/CFS that develops following COVID.” Catching people early, relatively speaking, could also help researchers understand why and how a viral illness turns into ME/CFS. Many ME/CFS patients have been sick for years by the time they find a qualified doctor, which makes it hard to work backward and look for biomarkers or inflammatory signals that could offer clues about the disease. In COVID long-haulers, researchers might have a better shot at learning about the condition’s origins, says Dr. Avindra Nath, a researcher at the National Institutes of Health (NIH) who studies ME/CFS.
Already, there’s a registry called You + ME where long-haulers can volunteer for studies. Researchers from the NIH, the Open Medicine Foundation and other groups are also studying the relationship between long-haul coronavirus and ME/CFS. And in May, Maryland Representative Jamie Raskin introduced a bill that would channel NIH funding toward studies examining the connection between ME/CFS and coronavirus. The bill has yet to clear either the House of Representatives or the Senate.
This burst of activity could have a significant impact, not only for ME/CFS patients but for people with other contested illnesses, like chronic Lyme disease and fibromyalgia. “The big issue diseases always overshadow the smaller ones,” says Dr. John Aucott, a chronic Lyme disease expert at Johns Hopkins University. “All the focus of everything is now on COVID”—but with that focus now extended to include long-haul coronavirus, there may be a ripple effect for similar chronic fatigue conditions that historically get little attention. Belief in long-haul coronavirus could translate to belief in other contested illnesses.
But for people who have been in the ME/CFS community for a long time, it’s hard to get too optimistic. Seltzer, who now directs scientific and medical outreach for the advocacy group Myalgic Encephalomyelitis Action Network, has seen flurries of interest in ME/CFS before. One came after the National Academy of Medicine’s report on the condition in 2015. Over the next five years, little changed. Research moves slowly, especially when there’s minimal money attached. Even with new studies underway, treatments may be years off in a best-case scenario.
The medical system also isn’t ready for an influx of ME/CFS patients. Already, there aren’t enough knowledgeable doctors to treat the country’s ME/CFS patients. (Treatment mostly consists of symptom relief, since there’s no known cure.) If the number of patients doubles, Komaroff isn’t sure what will happen.
Tompkins adds that any progress for ME/CFS patients will hinge on doctors definitively determining that coronavirus can turn into ME/CFS, rather than making post-coronavirus syndrome a separate diagnosis. “It would be a disservice to make post-COVID something special,” he says, because ME/CFS patients wouldn’t share the benefits. “I don’t think there’s a nickel of difference between the two,” he adds.
Already, Seltzer says, she’s seen some long-haulers reject the idea that they’re developing ME/CFS. It’s hard to understand how a new virus leads to an old condition, for one thing. And with all the stigma attached to ME/CFS, and its long history of doubt and disbelief, Seltzer says some long-haulers don’t want it to be their diagnosis. “Who would want to inherit the history of this disease?” she says.
Cooper, the ME/CFS patient from Oregon, finds herself thinking of that history often when she reads about coronavirus long-haulers. She can’t help but feel conflicted, in some moments, by all the attention thrown their way when there was none for her. “What happened to me?” she wonders. “Why wasn’t I believed?”
There’s no way to go back and time and make Cooper’s doctors believe her, nor any way to reclaim the last decade of her life. But there is reason to believe the sudden interest in long-haul coronavirus will help provide answers and legitimacy for the millions of people out there with ME/CFS, and the millions more who will develop it in the coming years. And that, Cooper says, makes the bitter pill easier to swallow. “I’m very hopeful that this opens the door to more research,” she says, “and [vindication for] all of us who got the flu and had a door closed on our lives.”
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