This is a repost of an article from Health Rising about specific concerns ME/CFS patients should have about coronavirus. To summarize the article, take care of yourself and avoid the virus since we have immune system abnormalities. These abnormalities need to be considered with respect to coronavirus, since it may reduce our resistance to Covid-19. We need to be aware of the limitations ME imposes on us and adapt accordingly. Anyway, the article has suggestions for self care for ME patients during this time of Covid-19 pandemic.
Coronavirus Pt. II: Scary Models, 8 Reasons People with ME/CFS and Fibromyalgia Should Be Careful, How to Stop an Epidemic, Why You Should Trust No One and More
by Cort Johnson | Mar 15, 2020
Eight Reasons People with Chronic Fatigue Syndrome (ME/CFS) and/or Fibromyalgia Should Take Care
Please note, if it’s not obvious, that I’m not a doctor – I’m a patient. Take these musings as you will. We don’t know if people with ME/CFS or FM are more at risk of: a) getting COVID-19; or b) coming down with a severe case of it they do. Because both appear to be quite heterogenous diseases, it’s possible that some people will be at lowered risk while others will be at higher risk.
It’s hard to tell how much risk people with ME/CFS and FM are from COVID-19. Elderly people with a serious disease are at the highest risk.
Thus far, the studies coming out of China suggest that having diseases like hypertension, cardiovascular diseases and diabetes, particularly in combination with older age (>65), increase the risk of mortality. Note that diseases thought to have more in common with ME/CFS or FM such as multiple sclerosis, rheumatoid arthritis and migraine are not on the list.
There are some broad factors, however, which suggest people with ME/CFS and/or FM might want to take extra care.
1. Infectious Onset – the most obvious one; if a nasty infection started off your illness – what might a possibly nastier infection do?
2. Poor Sleep – Studies indicate that people getting reduced levels of sleep (<6 hours) are far more likely to come down with a cold than those getting normal amounts of sleep.
During sleep, pathogen-fighting immune cells move to the lymph nodes where they search for evidence of a pathogen. If they find it, those immune cells mount a furious (and metabolically expensive) immune response. Unfortunately, poor sleep also reduces the metabolic reserves our immune cells need to fight off infections!
Plus, having insomnia or late bedtimes reduces hormones that are produced during early sleep which enhance T-cell activity and promote pathogen defense. All in all, now is a good time, if you haven’t, to implement some sleep hygiene protocols.
4. Activated Stress Response – The low heart rate variability (HRV), common in both ME/CFS and FM, suggests hyperactivation of the sympathetic nervous system (SNS) (fight or flight system) has occurred. Activated SNS responses are associated with Th2 dominance in the immune system which translates into a reduced ability to fight pathogens such as viruses (and increases risk of autoimmunity). They’ve also been associated with poor sleep in ME/CFS.
5. Immune Exhaustion / Altered Immune Networking – The Hornig/Lipkin cytokine studies in the blood and cerebral spinal fluid suggest a state of immune exhaustion may be present. Dr. Klimas’s immune networking studies – showing odd and blunted networking – back that idea up as well. Dr. Klimas reported that ME/CFS patients are “modestly immunocompromised” and are “a little more” at risk than others.
6. Brainstem Issues – Several Australian studies suggest that damage to the brainstem has occurred in ME/CFS. A recent COVID-19 study (thanks Helen!) demonstrates that the virus can invade the brainstem, in particular, and the brain as well. Invasion of the brainstem could be contributing to the breathing problems found in severe cases. (The virus can also apparently invade the gut at times.)
7. Lack of Exercise – It turns out that exercise is darn good for your immune system. Studies indicate that regular exercise improves immune health and enhances our ability to fight off infections.
8. Bedrest – increased bed rest is associated with reduced levels of the IL-2 cytokine which tells our T and B lymphocytes and NK cells to go out and fight off invaders; i.e. possibly reducing the immune system once again.
All in all – lots of reasons to limit your contacts, rest as much as possible, do things that are relaxing and calming and take care of yourself.
On the brighter side, Dr. Teitelbaum urges people with ME/CFS and FM not to panic. He stated that he’s never seen people with these diseases die from the flu, and he doesn’t expect, as nasty as this bug can be, that they will from COVID-19.
Scary Models and Super Freaks
COVID-19 may be as contagious and nearly as lethal as the HINI flu that sparked the 1918 pandemic but there’s no reason to believe it will have the same effects.
The “scary model” was the Institute for Disease Modeling study which calculated that COVID-19 is as contagious and almost as lethal as the HINI flu virus that sparked the 1918 flu pandemic. The “super freak” was that COVID-19 is as contagious and almost as lethal as the HINI flu virus that sparked the 1918 flu pandemic and killed more people than the bubonic plague and HIV/AIDS has to date.
The Institute’s model also asserts that after HINI, COVID-19 is the most transmissible and severe flu virus the world has encountered over the past 100 years.
That’s scary but it’s clear that whatever happens with COVID-19, it’s not going to be anything like the Spanish Flu. While we travel more and are more connected (a minus), the Spanish Flu took place during wartime when the movements of huge numbers of soldiers across the U.S. exacerbated the epidemic, the health care system was a joke compared to what it is now, we have many more tools, we’re better informed, and we’re starting to take the precautions needed to ward off the worst effects.
One of the most disturbing aspects of the “Spanish flu” – which incidentally appears to have originated in the U.S. – was how devastating it was for young people. That is not happening with COVID-19.
Trying Not to Be Seattle
Two weeks ago “I probably would have said that there’s a possibility that this will become endemic.” Now, “I think given our government’s public health response, I’m much more alarmed that this probably will become endemic.” Angela Rasmussen, a Columbia virologistSeattle is one city we know COVID-19 got in early (mid-January) and has spread. Genetic analyses indicated that, as of late February, the virus had been spreading for at least six weeks. Statistical modeling done in early March suggested that 500 to 600 cases of COVID-19 were probably present in the Seattle area.
Washington’s health care system began reeling early. Two weeks ago, Tom Staiger, UW Medical Center’s medical director, wrote, “We are currently exceptionally full and are experiencing some challenges with staffing” and asked staff to expedite discharges; i.e. open up more beds.
Later modelling efforts suggested that unless strong social distancing measures were taken, Washington was looking at 400 deaths and 25,000 infections by early April. Another model projected that social distancing — limiting contacts with others — could reduce deaths caused by infections acquired in the next month in the Seattle region (one of the hardest hit regions) by 75 percent (from 400 to 100).
Since then, schools have been closed, large gatherings banned, farmer’s markets shuttered, and small groups discouraged. Yesterday, the New York Times reported 421 confirmed cases in Washington and 34 deaths. If the earlier modeling was correct, the authorities are still missing hundreds and hundreds of cases. It’ll be very interesting for the rest of us to see how Washington does.
Are We Already Seattle?
“What we should be doing is absolutely much different. Not business as usual.” Anthony FauciThe United State’s big problem – and we are not alone is this – is that we won’t know how much coronavirus is out there until testing ramps up. Arizona’s Director of Health, Dr. Cara Christ, reported yesterday that the CDC’s models suggest that 70,000 people in Arizona are now infected with the virus. That’s an incredible number given that only 12 people in the state have been diagnosed with it, but that’s what ABC news is reporting, Dr. Christ said. To date, Arizona, population 7.2 million, has only tested about 150 people.
Dr. Amy Acton, Director of the Ohio Department of Health, believes a similar scenario is happening in Ohio:
“We know now, just the fact of community spread says that at least 1%, at the very least, 1% of our population is carrying this virus in Ohio today. We have 11.7 million people.”Let’s hope those numbers are an exaggeration. If they’re anywhere close to being accurate, the cat truly is out of the bag and every major city is basically, or soon will be, where Seattle is. The virus is everywhere.
It might not be that surprising. We know, after all, that COVID-19 is a very impressive traveler. Consider that it was just January 19th, that first documented case of COVID-19 showed up in the U.S. in the form of a 35-year-old man with a cough and subjective fever at an urgent care clinic in Snohomish County, Washington. (He’d returned from Wuhan city.)
Less than 2 months later, even with our very limited testing regimen, the virus is not just in California, New York and Texas; it’s in North Dakota, Alaska, Idaho and Montana as well. In fact, it’s been found in every state of the union except one. A couple of days ago, a person on the Navajo Indian Reservation, a large but rather remote reservation in northern Arizona, tested positive. Think what it took for the virus to get there.
The missing state – West Virginia, population 1.86 million – has tested a grand total of 31 people. (It’s there.)
The Chinese timeline indicates demonstrates the explosive growth the virus can achieve. The number of infections in China jumped from 550 on January 22nd, to 2,000 by January 26th, to 6,500 by January 27th, to almost 12,000 on February 1st. (As Peyo points out, some of the jump is due to increased testing.) The U.S. went from 15 cases on February 29th to 2,500 on March 14th – and that’s, again, with quite restricted testing.
- Check out the simulations in this Washington Post article – to really get how rapidly an infection can spread. (Thanks Pat!)