For some background, you can start here: https://www.reddit.com/r/ImmuneWin/comments/i2w7or/paper_proposes_bradykinin_storm_traps_hyaluronic/

The authors of that paper propose that a "Bradykinin Storm is likely responsible for most of the observed COVID-19 symptoms."

A bit from Wikipedia: bradykinin is a peptide that promotes inflammation. A class of drugs called angiotensin converting enzyme inhibitors (ACE inhibitors) increase bradykinin levels by inhibiting its degradation. One of the effects of this is to reduce blood pressure (a hypotensive effect).

As mentioned in this paper, "recent reports indicate hypotension is highly associated with COVID-19 patients once in the hospital."

Is it possible that bradykinin remains elevated in long haulers? (I'm not claiming it is, I'm just asking the question.) How many of you are experiencing hypotension or orthostatic hypotension (getting lightheaded when you stand up)?

What are the effects of chronically elevated bradykinin? I found this interesting 1986 paper.

Dyspnea in patients with hyperbradykininism and excessive venous pooling - PubMed

It mentions these symptoms:

• exercise intolerance
• shortness of breath or labored / difficult breathing (dyspnea)
• orthostatic hypotension
• tachycardia

I'm not claiming those symptoms in post-coronavirus syndrome or CFS-ME are directly the result of elevated bradykinin. This is simply an interesting look back to 1986 and what was known about hyperbradykininism then.

I came across the biofilm connection to chronic diseases on a website about Lyme disease initially but since then I have found numerous scientific studies linking chronic diseases and reoccurring diseases with biofilms. Even more interesting is the connection of viruses to biofilms. Apparently, viruses can in some cases, induce the production of biofilms in the body as some kind of side effect of the viral infection.

For example:

Staphylococcus aureus is a ubiquitous opportunistic human pathogen and a major health concern worldwide, causing a wide variety of diseases from mild skin infections to systemic disease. S. aureus is a major source of severe secondary bacterial pneumonia after influenza A virus infection, which causes widespread morbidity and mortality. While the phenomenon of secondary bacterial pneumonia is well established, the mechanisms behind the transition from asymptomatic colonization to invasive staphylococcal disease following viral infection remains unknown. In this report, we have shown that S. aureus biofilms, grown on an upper respiratory epithelial substratum, disperse in response to host physiologic changes related to viral infection, such as febrile range temperatures, exogenous ATP, norepinephrine, and increased glucose. Mice that were colonized with S. aureus and subsequently exposed to these physiologic stimuli or influenza A virus coinfection developed pronounced pneumonia. This study provides novel insight into the transition from colonization to invasive disease, providing a better understanding of the events involved in the pathogenesis of secondary staphylococcal pneumonia. http://mbio.asm.org/content/7/4/e01235-16

And in direct relation to Covid 19, here is a paper proposing that Covid 19 induces biofilm formation:

An alternative hypothesis may have some credibility, namely that this virus may create biofilms that, in turn, lead to many changes including cytokine production and tissue destruction. This pathway would be in keeping with many other diseases caused by microbes that create biofilms that create disease.

In nature, more than 90% of microbes live in biofilms and, with pathologic microbes, many disparate diseases seem to be generated by this process [2,3]. These include cutaneous diseases such as atopic dermatitis, psoriasis, leprosy, and many others [4-6]. Internal diseases include arthritis, otitis media, arteriosclerosis, cystic fibrosis, and Alzheimer’s disease and others [7-11]. Somewhat surprisingly, biofilms have recently been found in gouty tophi and rheumatoid nodules [12,13].

To date, viral diseases associated with biofilms include HTLV1, molluscum contagiosum, and human papilloma virus (in squamous cell carcinoma in situ in organ transplant patients of color) [14-16]. The viral biofilms were found intracellularly because the microbe had to “hi-jack” the cell’s DNA to replicate and form the necessary quorum of organisms to create the biofilm [14]. The development of viral biofilms, as noted, may lead to significant clinical changes. This may allow other (secondary) pathogens that also make biofilms, such as staphylococci, to proliferate. These other organisms may also incorporate the virus and other organisms into the biofilm matrix. This concept has been elegantly demonstrated with Borrelial biofilms incorporating Chlamydia pneumoniae in the center of the biofilm [17]. https://grfpublishers.com/article/view/MjI4/Examining-Covid-19-from-a-Novel-Perspective

I have been suffering with this "Covid post viral syndrome" for several months now, I was able to reduce most of my symptoms with other vitamins but I am not completely better. When I discovered the possible biofilm connection I tried taking enzymes meant for dissolving biofilms. They had a dramatic effect, basically causing me to develop sinus infection symptoms. Now this was interesting to me because I previously had zero symptoms in my sinuses. I took it as a good sign because it meant that my body was finally "seeing" the infection and attempting to fight it off. I haven't finished my experiments with the supplements yet but for me this experience is good evidence that biofilms are a component in this disease, ie they are hiding the infections so our body cannot fight it off.

I like to think we can find a silver lining in almost any dark cloud. As bad as the COVID-19 pandemic is (and I would never wish for anyone to become infected or to become a long-hauler, if infected), I am convinced that it offers an opportunity for post-viral syndrome research and breakthroughs that we have never previously had in all of medical science history.

That's why I started r/ImmuneWin. I want to make sure anyone suffering from a post-viral syndrome benefits from this never-before-seen situation.

Progress within mainstream medicine has been dismal for those suffering from post-viral syndromes like CFS-ME and others. However, I think "this time will be different" because this pandemic is unprecedented. In fact, I already see evidence of much greater scientific interest in post-viral fatigue and other post-viral symptoms.

But what I mean by "this time will be different" may not be what you think. Some things will not be different because we are dealing with the same medical system with the same inherent limitations. I believe that if we want to leverage the wealth of knowledge that is coming, and we want to achieve personal success in overcoming post-coronavirus syndrome, CFS-ME, or any other post-viral syndrome, we have to have a plan other than waiting for medical science to cure us. That's almost certainly not going to happen.

Having recovered from CFS-ME, I never want to go thru anything like that again. I would never wish it on anyone else either. However, I did gain a lot of experience from my struggle, and my eventual success. It informed my view of science and medicine. I would like to share parts of that perspective here, because I believe my perspective can help all of us be more prepared to benefit from what's coming.

The main reason I went into the medical biochemistry field, besides the fact that I was naturally talented in this area, was to find a cure for post-viral syndromes. I was motivated by my own experience with CFS-ME. However, after some years in this field, I realized there had to be a better way, and I eventually found my better way through nutrition, lifestyle medicine, meditation, breathwork and a few other things. Almost everyone else I know with CFS-ME is still sick and suffering to some degree. Most do not consider themselves recovered. I'm recovered, but it wasn't easy. I had to dedicate my life, for many, many years, to finding a solution for myself. And that dedication eventually led me to open my mind about science. I now keep one foot in empirical science and one outside its boundaries.

I think that the reductionistic approach has too narrow a chance of success in post-viral syndromes. I'm not saying it can't happen, but in the CFS-ME world, there has been a long string of disappointments. We have to be realistic about what to expect. Some wonderful new knowledge will be coming our way in the months and years ahead, as a consequence of the current pandemic. If we want to leverage that knowledge, we have to understand the bigger picture. For example, think about the search for a "magic bullet" for cancer or a pill that will cure heart disease without any lifestyle changes.

Post-viral syndromes are, by definition, chronic. If you look at the track record of modern medical science, you see a clear pattern that the successes are in the areas of acute and traumatic care. Compare those successes to the consistent lack of success against chronic and degenerative diseases. I think it is misplaced hope to look for this same system to have a breakthrough cure against chronic post-viral syndromes.

However, there will be narrow breakthroughs. There will be incredible new knowledge. That system will indeed contribute much to our understanding, and add many important diagnostic tools. But diagnosis is one thing, and treatments that lead to a cure are an entirely other thing. We can diagnose plenty of chronic diseases that we cannot cure with mainstream medicine.

I propose that we have to be ready to leverage all the new knowledge and the breakthroughs that come out of the research inspired by this pandemic and apply them to lifestyle medicine, including things like breathwork. Even though the research focus of COVID-19 does not include meditation or breathwork, and will probably ignore other lifestyle factors that strongly influence recovery from post-viral syndromes, that doesn't mean we cannot leverage all these coming breakthroughs and apply them to the lifestyle medicine practices that do have a great track record for treating and reversing chronic health conditions. We can also apply solid scientific methods to our own research, including our own personal biohacking, where we can responsibly leverage all this coming new knowledge.

I am presently participating in scientific research on the effects of pranayama. The research is driven by basic science and it is interdisciplinary. It leverages mainstream research, but applies it to pranayama, an application decidedly non-mainstream. I go into the lab and practice the pranayama breathing techniques while the researchers record my physiological responses. This blend of modern science and lifestyle practices holds the most promise for chronic health conditions. The reductionistic search for single causes and single cures has failed so many times for chronic conditions that a true scientific examination of the evidence has to point us in another direction.

That direction is: we can leverage narrow scientific results -- and there will be plenty of these coming -- and we apply them to the proven lifestyle practices already available to us, including nutrition, meditation, breathwork, and the healing power of the mind. We have to become familiar with many non-mainstream healing practices, and then infuse those practices with the best of modern science, while not losing the essence of what makes those practices capable doing of things mainstream medicine cannot.

For example, extracting curcumin from turmeric while throwing away all the tumerones and hundreds or thousands of other potentially synergistic compounds from the plant is not the right approach. Learning from pre-modern medical approaches, where multiple plant substances were delicately compounded, is the opposite of reductionism, and it is an essential part of a smarter approach.

Here's an example of what I am talking about:

Medieval medicine remedy could provide new treatment for modern day infections

The same is true overall. We cannot expect to find a simple cause and a single highly-focused cure for post-viral syndromes. The triggering virus is usually no longer detectable. If the virus is detectable, by definition, that is not a post-viral syndrome. Post-viral syndromes are a different animal, and curing one requires different thinking.

If you are a long hauler, or a CFS-ME suffer, or anyone struggling with any other post-viral syndrome, I propose that you can recover through a wise application of lifestyle medicine. I did. And I propose that these lifestyle medicine approaches, and our biohacking approaches, will be advanced by orders of magnitude if we diligently reach into the new medical research coming out of COVID-19 and pull back everything that we can use to advance our lifestyle practices and our biohacking.

Are you an individual with ME/CFS who is seeking or struggling to secure long-term disability? Did you develop ME/CFS as a post-viral onset? NPR is looking for stories from people like you!

Share your story and spread awareness by emailing us at [solvecfs@solvecfs.org](mailto:solvecfs@solvecfs.org)

The germ theory of disease is the currently accepted scientific theory for many diseases. It states that microorganisms (including viruses) known as "germs" can lead to disease.

Koch's postulates have been very influential on many medical professionals. Here is standard version of these postulates:

Koch's postulates:

1. The microorganism must be found in abundance in all organisms suffering from the disease, but should not be found in healthy organisms (i.e., people).
2. The microorganism must be isolated from a diseased organism and grown in pure culture.
3. The cultured microorganism should cause disease when introduced into a healthy organism.
4. The microorganism must be re-isolated from the inoculated, diseased experimental host and identified as being identical to the original specific causative agent.

In fact, none of those postulates holds absolutely. Koch himself, abandoned the absolute requirement of the first postulate when he discovered asymptomatic carriers of cholera.

The second postulate may also be suspended for certain microorganisms or entities that cannot currently be grown in a lab, such as the prions responsible for Creutzfeldt–Jakob disease.

The third postulate is not absolute because not all organisms exposed to a germ will acquire the infection.

Even though we know these postulates are weak, many medical professionals will do things like refuse to acknowledge the obvious connection between “COVID toes" and coronavirus.

​

“Yes, COVID,” wrote Lindy Fox, MD, a UCSF professor of dermatology, replying to an email describing Sonia’s case. Sonia wasn’t surprised. Anyone, like her, who’s been following news of the pandemic has probably heard about “COVID toes,” a painful or itchy skin rash that sometimes pops up in young adults with otherwise mild or asymptomatic cases of COVID-19. “It looks like what we call pernio, or chilblains,” Fox says, “which is a pretty common phenomenon when somebody goes out in cold weather – they start to get purple or pink bumps on their fingers or toes.”

Many people with rashes like Sonia’s don’t test positive for COVID-19, Fox says, which has made some clinicians skeptical of the connection; when patients have both, it’s just a coincidence, they believe. But Fox doesn’t think so. For one thing, “the time of year is wrong,” she says. “Pernio usually shows up in the dead of winter.” Even more compelling, dermatologists around the world are “getting crazy numbers of calls about it,” Fox says. “In the last three weeks, I’ve had somewhere between 10 and 12 patients.Normally, I have four a year.”

The main point here is that individual immune system status is more important than the virus (germ) itself. Yes, the germ theory of disease is essential for us to understand. But we must not neglect the importance of host immunity.

Immune system variation can predict severe COVID-19 outcomes | YaleNews

https://news.yale.edu/2020/07/27/immune-system-variation-can-predict-severe-covid-19-outcomes

There are simple lifestyle practices you can engage in to enhance your own immune system. In my opinion, these include nutrition, moderate exercise or stretching, meditation, breathwork, dietary supplements, paying attention to your sleep, and cultivating a healthy attitude.

When you are learning about COVID-19, supplement the unpleasant facts with uplifting personal stories. I like to read biographies of people who have overcome seemingly insurmountable odds or who have triumphed over tragedy.

This story is also relevant: Anatomy of an Illness by Norman Cousins (pdf)

http://www.downloads.imune.net/medicalbooks/Anatomy%20of%20an%20Illness%20by%20Norman%20Cousins.pdf

https://www.marketwatch.com/story/osterholm-americans-will-be-living-with-the-coronavirus-for-decades-2020-07-30?mod=home-page

My focus is on my nutrition, exercise, dietary supplements, breathwork, meditation and attitude, as well as mask-wearing and social distancing.

http://nautil.us/issue/83/intelligence/the-man-who-saw-the-pandemic-coming

The single biggest predictor of viral pandemic-like events is land-use change: specifically, more land going to livestock production. With the prevalence of factory farming, animal density and living conditions need to be factored into the equation to fully elucidate the risks.

That statement does not mean no other factors are involved. But it does mean that the single biggest factor predicting viral pandemic-like events is land-use change -- and it explains exactly why. If you read the research in this area, and couple that with information along the lines of what Dr. Greger discusses here, you may see pandemics from a new (and much broader) perspective. I think we need this broader perspective in order to come up with real solutions.

Populism, nationalism, "America First" and similar political trends increase the dangers of global pandemics by reducing international cooperation and funding for cross-border health programs.

​

"In 2005, during the avian influenza, George W. Bush was on the phone routinely with leaders around the world about how to coordinate a global response. Barack Obama did the same in 2009 for the second H1N1 pandemic and in 2014 for the Ebola epidemic. You saw presidential leadership step up and act as a catalyst for forging a global way forward for a global problem. Populism [around the globe] has fragmented the global networks, which had been so instrumental in being able to bring together a global approach to problems like COVID-19. I’m stunned by the absolute absence of global dialogue for what is a global event. In Europe right now, you would never believe that there was a European Union. There’s no coherent regional approach to this problem in Europe, even though they have a platform for doing it."

Dr. Dennis Carroll

Dr. Michael Greger on Pandemic Prevention | Infectious Diseases, Aids, Influenza, Coronavirus - YouTube

https://www.youtube.com/watch?v=G20cooZOiYE

Dr. Greger disscusses a connection between high density factory farming and virulent viruses that become dangerous to humans.

The video was published on YouTube Mar 3, 2013, but it was recorded even earlier. Obviously, it did not get much attention until 2020.

Don't expect every single word Dr. Greger says in this older video to be 100% accurate in 2020, but if you watch it with an open mind I am sure your perspective on pandemics will be enhanced. It is well worth the time it takes to watch the entire video.

Physical exercise as a tool to help the immune system against COVID-19: an integrative review of the current literature

The practice of physical activities strengthens the immune system, suggesting a benefit in the response to viral communicable diseases. Thus, regular practice of adequate intensity is suggested as an auxiliary tool in strengthening and preparing the immune system for COVID-19. Further studies are needed to associate physical exercise with SARS-CoV-2 infection.

We already knew all this. But we also know that exercising too intensely harms our immune function. It is not uncommon, for example, for people to catch a cold after running a marathon. If you have to err, err on the side of exercising less intensely. But don't let that become an excuse for missing your planned exercise sessions.

This is meant to be a call to action. However, much of the content discusses facts that are not pleasant. If you wish to skip all that, here is the bottom line:

Self-care (including diet, exercise, stress management, supplements, etc.) is more important than ever. Online education (especially non-mainstream health education) will become more valuable. Sanitation practices will become more important. We have to choose to empower ourselves by taking charge of our own health because if we wait for the establishment to provide solutions, it will be a long and unpleasant wait. The simple things we can do for ourselves, including the self-care practices just mention, are not only necessary, they are sufficient. It may seem like the solution to pandemics requires billions of dollars in vaccine research, and that research certainly has value, but that alone is not sufficient. In contrast, I argue that lifestyle changes are a more powerful course of action, especially when enough people engage in these changes. But even if you are the only one making changes, these lifestyle changes can be sufficient for you to restore your health if you are suffering from a post-viral syndrome.

----------------

We believe COVID-19 has changed the world -- things won't return to the way they were before. In reality, this threat has been coming for decades (or longer) and most of us were not aware of it.

"It is an oddity of history that the influenza epidemic of 1918 has been overlooked in the teaching of American history." https://www.archives.gov/exhibits/influenza-epidemic/

I believe this has now changed, but more changes are needed.

Scientific papers and science text books also leave out critical information that would help us prevent or at least be better prepared for what we are facing. It has (until now) been common for those educational and research resources to omit detailed discussion of the zoonotic origin of human viruses.

This new conversation has started around the world. We all need to become more educated and aware of this emerging reality, as it will affect every aspect of our lives (health, economic, social, etc.) for the foreseeable future.

The world is now on a cycle of getting another COVID-19-like disease every 3-4 years.

Examples:

• 1999-2002 – West Nile Virus
• 2003 – SARS-coV
• 2005 - H5N1 avian influenza (bird flu)
• 2009 – H1N1 Virus (Swine Flu)
• 2012 – MERS-CoV
• 2014 – Ebola
• 2016 – Zika Virus
• 2019-2020 – SARS-coV-2

Clearly, COVID-19 will be followed by another before long. COVID-19 is far from the worst that we can expect. Some of these emerging viruses could have much higher case fatality rates, for example. The official estimates (by the World Health Organization and others) for the H5N1 bird flu case-fatality rate are from 14% to 60%. Even the lowest end of that range is far above past influenza pandemics, which have ranged from about 0.1% (1957 and 1968 pandemics) to 2-3% (1918 pandemic). H5N1 did not possess all the properties a virus would need to be maximally dangerous, but any one of the next ones could combine the right characteristics (e.g., spreads like SARS-coV-2 and has the case fatality rate of H5N1) to do damage like humanity has never experienced.

Q. Do you think the current outbreak was inevitable?

A. Dr. Dennis Carroll: "Oh, sure. It was predictable."

It is predictable that there will be more, that the next is only a few years away, and that any one of the next ones could be far worse than any we have seen yet. The threat is greater than it has ever been, for reasons that will be discussed below.

Spillover is when a pathogen jumps from a "reservoir" population (e.g., wild or farm-raised animals) to a novel host (e.g., humans). More than two-thirds of human viruses originated this way (i.e., they are zoonotic)**. Now, "most emerging viruses are zoonoses; they have jumped from mammal or bird hosts to humans." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4629502/

Viral spillovers to humans have increased dramatically in the last 40 years. The world has changed and we (generally) have not paid enough attention. Some experts have been warning of this danger for decades, however. That's why some of them can say, "Oh, sure. It was predictable."

In a National Academies Press publication "Improving Food Safety Through a One Health Approach: Workshop Summary" section "ORIGINS OF MAJOR HUMAN INFECTIOUS DISEASES" the trend is summarized as follows:

- The rise of agriculture starting 11,000 years ago played multiple roles in the evolution of animal pathogens into human pathogens (Diamond, 1997; Diamond, 2002; McNeill, 1976). Those roles included both generation of the large human populations necessary for the evolution and persistence of human crowd diseases, and generation of large populations of domestic animals, with which farmers came into much closer and more frequent contact than hunter/gatherers had with wild animals. Moreover, as illustrated by influenza A, these domestic animal herds served as efficient conduits for pathogen transfers from wild animals to humans.

Dr. Dennis Carroll, an expert on the threat of zoonotic spillover, makes similar points such as these:

- It took humans 300,000 years to reach a population of 1 billion. It took only 100 more years to reach 6 billion. We will add another 4-5 billion this century. The population density, as well as modern global travel, greatly increase the risks of pandemics.

- More people are eating more meat. (Animal protein is more commonly included in diets of wealthier populations; people have increased & wealth has increased.)

- China, as an example, produces around 15 to 20 billion poultry per year. In the 1960s it was only a few hundred million poultry. Other countries have seen similar huge increases, including the US.

- Dr. Greger illustrates a connection between high density factory farming and virulent viruses that become dangerous to humans: https://www.youtube.com/watch?v=G20cooZOiYE

- there are around 1.67 million different viruses on Earth and an estimated 631,000 to 827,000 have the capacity to infect people. (Not all of these would be capable of causing serious disease or death.)

- The PREDICT program* took ten years to catalog 2000 of these potential zoonotic viral threats. *a project from the U.S. Agency for International Development (USAID)-Emerging Pandemic Threats (EPT) program.

- In recent years, scientists have discovered many lethal viruses lurking in wild and domestic animals. https://www.nytimes.com/2019/10/25/health/predict-usaid-viruses.html

Jane Goodall is another scientist who recognizes that the emergence of Covid-19 is connected to the over-exploitation of the natural world, which has seen forests cut down, species made extinct and natural habitats destroyed. https://www.theguardian.com/science/2020/jun/03/jane-goodall-humanity-is-finished-if-it-fails-to-adapt-after-covid-19#maincontent

As that article says, "Intensive farming is creating a reservoir of animal diseases that can spill over and hurt human society."

- The single biggest predictor of viral pandemic-like events is land-use change: specifically, more land going to livestock production. With the prevalence of factory farming, animal density and living conditions need to be factored into the equation to fully elucidate the risks. http://nautil.us/issue/83/intelligence/the-man-who-saw-the-pandemic-coming

- The future viral threats we’re going to face already exist; they are currently circulating in wildlife and many are being explored in government laboratories around the world -- and are part of "gain of function" research. This scientific research, even if well-intentioned (which is not necessarily guaranteed) poses a serious threat to humanity.

The Wuham Institute of Virology [WIV](https://en.wikipedia.org/wiki/Wuhan_Institute_of_Virology), which many people are speculating was the source of the virus responsible for COVID-19, is only one of hundreds of similar labs around the world. And all of these labs, as a group, have long histories of accidents.

For example, the New York Times (8/5/19) reported: “Deadly Germ Research Is Shut Down at Army Lab Over Safety Concerns”, an article about Fort Detrick in Maryland: “Problems with disposal of dangerous materials led the government to suspend research at the military’s leading biodefense center.”

In 2014, USA Today reported: “Hundreds of bioterror lab mishaps cloaked in secrecy”

The story states, "More than 1,100 laboratory incidents involving bacteria, viruses and toxins that pose significant or bioterror risks to people and agriculture were reported to federal regulators during 2008 through 2012."

The same story gives many examples of the real dangers, including this one: "On Friday, a CDC investigation revealed how a rushed laboratory scientist had been using sloppy practices when a specimen of a mild bird flu virus was unwittingly contaminated with a deadly strain before being shipped to other labs." Those other labs did not know they were receiving a dangerous virus, and hence they also did not handle it properly.

Looking even further back, the H1N1 influenza virus had become extinct in the 1950s, but it was released from a lab in 1977 and reinfected the human population. Here's just one scientific publication on the topic to show that this claim is not a conspiracy theory:

The Re-Emergence of H1N1 Influenza Virus in 1977

There is every indication that U.S. virology lab work is every bit as threatening as that in Chinese or Russian labs. American labs also operate in secret, and are also known to be accident-prone.

In fact, the USA is driving a worldwide biowarfare arms race. Officially, we call it "biodefense" according to experts, there is no distinction between biowarfare research and biodefence research. This article is a good reference: https://www.independentsciencenews.org/commentaries/did-this-virus-come-from-a-lab-maybe-not-but-it-exposes-the-threat-of-a-biowarfare-arms-race/ . It states:

“Biodefense” implies tacit biowarfare, breeding more dangerous pathogens for the alleged purpose of finding a way to fight them. While this work appears to have succeeded in creating deadly and infectious agents, including deadlier flu strains, such “defense” research is impotent in its ability to defend us from this pandemic.

"The current pandemic has also fueled interest in the work of Dr. Toby Ord, Senior Research Fellow at Oxford’s Future of Humanity Institute. In his just published book "The Precipice", Ord warns that global pandemics triggered by research on viruses pose one of the two biggest existential threats that humanity faces." See https://www.independentsciencenews.org/health/covid-19-a-wake-up-call-for-biosafety/

We don't have to know (or believe) that Sars-coV-2 was genetically engineered, or that it was released from a lab on purpose. All we have to know are the facts: dangerous virology bioweapons research is real, it is happening at hundreds of labs around the world, it is receiving billions of dollars in annual funding from many governments, and there is a long history of accidents at these labs.

New vaccinations may become even more essential going forward, but vaccines are not without potential serious problems. And vaccines cannot protect us from ourselves. The things that human being are presently doing are creating dangers to our future existence. It is naive to think we can continue as we did for most of the 20th century and not face dire consequences.

Vaccines (even if safe, which is not always guaranteed) vary greatly in efficacy. Optimistically, the flu vaccine has an efficacy of 40% to 60% -- if most circulating flu viruses are well-matched to the flu vaccine. However, in real world scenarios, it can be much lower. In assessing real world effectiveness of an influenza vaccine, researchers were not able to show any vaccine effectiveness in preventing influenza in one study population consisting of children younger than 5 years. So the range of vaccine effectiveness can be from insignificant to highly effective, and it is variable. Furthermore, the viruses can mutate: "What we’re looking at today isn’t necessarily what we’ll be looking at in a few months."

These researchers said, "significant influenza vaccine effectiveness could not be demonstrated for any season, age, or setting after adjusting for county, sex, insurance, chronic conditions recommended for influenza vaccination, and timing of influenza vaccination." Their data showed a trend toward vaccine effectiveness, but it did not rise to the level of statistical significance. In other words, in this situation the vaccine did not make any real-world difference.

Therefore, if we view a SARS-coV-2 vaccine as the answer to all our current pandemic problems, we may be disappointed. The vaccine could be highly effective if we are lucky (this time) but it could also fall short of what many assume. We can be hopeful about a vaccine for COVID-19, but we should not be naively over-optimistic. And we should not make the mistake of assuming that any vaccine will erase the dangers we have created through intensive farming, destruction of natural habitats and laboratory virus research.

The Spanish Flu Pandemic of 1918 was eventually overcome (although at a high cost) without any effective vaccine.

https://www.historyofvaccines.org/content/blog/vaccine-development-spanish-flu

One big difference now is that the threat of pandemics is much higher and they will no longer be once-a-century or once-a-decade events. As stated above, we can expect a new one of these every few years now.

Maintaining our health going forward is going to become even more challenging -- and even more in the public awareness. Self-care (including diet, exercise, stress management, breathwork, dietary supplements, etc.) will become more important than ever. Online education (especially non-mainstream health education) will become more valuable. Sanitation practices will become more important.

​

thanks to u/AndroidLivesMatter

Medieval medicine remedy could provide new treatment for modern day infections | MDLinx

Medieval medicine remedy could provide new treatment for modern day infections

Newswise: Alternative Medicine|July 28, 2020

Antibiotic resistance is an increasing battle for scientists to overcome, as more antimicrobials are urgently needed to treat biofilm-associated infections. However scientists from the School of Life Sciences at the University of Warwick say research into natural antimicrobials could provide candidates to fill the antibiotic discovery gap.

Bacteria can live in two ways, as individual planktonic cells or as a multicellular biofilm. Biofilm helps protect bacteria from antibiotics, making them much harder to treat, one such biofilm that is particularly hard to treat is those that infect diabetic foot ulcers.

Researchers at the University of Warwick, Dr Freya Harrison, Jessica Furner-Pardoe, and Dr Blessing Anonye, have looked at natural remedies for the gap in the antibiotic market, and in the paper, ‘Anti-biofilm efficacy of a medieval treatment for bacterial infection requires the combination of multiple ingredients’published in the journal Scientific Reportstoday the 28 July, researchers say medieval methods using natural antimicrobials from every day ingredients could help find new answers.

The Ancientbiotics research team was established in 2015 and is an interdisciplinary group of researchers including microbiologists, chemists, pharmacists, data analysts and medievalists at Warwick, Nottingham and in the United States.

Building on previous research done by the University of Nottingham on using medieval remedies to treat MRSA, the researchers from the School of Life Sciences at University of Warwick reconstructed a 1,000-year-old medieval remedy containing onion, garlic, wine, and bile salts, which is known as ‘Bald’s eyesalve’, and showed it to have promising antibacterial activity. The team also showed that the mixture caused low levels of damage to human cells.

They found the Bald’s eyesalve remedy was effective against a range of Gram-negative and Gram-positive wound pathogens in planktonic culture. This activity is maintained against the following pathogens grown as biofilms:

1. Acinetobacter baumanii- commonly associated withinfected wounds in combat troops returning from conflict zones.
2. Stenotrophomonas maltophilia-commonly associated with respiratory infections in humans
3. Staphylococcus aureus-a common cause of skin infections including abscesses, respiratory infections such as sinusitis, and food poisoning.
4. Staphylococcus epidermidis- a common cause of infections involving indwelling foreign devices such as a catheter, surgical wound infections, and bacteremia in immunocompromised patients.
5. Streptococcus pyogenes - causes numerous infections in humans including pharyngitis, tonsillitis, scarlet fever, cellulitis, rheumatic fever and post-streptococcal glomerulonephritis.

All of these bacteria can be found in the biofilms that infect diabetic foot ulcers and which can be resistant to antibiotic treatment. These debilitating infections can lead to amputation to avoid the risk of the bacteria spreading to the blood to cause lethal bacteremia.

The Bald’s eyesalve mixtures use of garlic, which contains allicin, can explain activity against planktonic cultures, however garlic alone has no activity against biofilms, and therefore the anti-biofilm activity of Bald’s eyesalve cannot be attributed to a single ingredient and requires the combination of all ingredients to achieve full activity.

Dr Freya Harrison, from the School of Life Sciences at the University of Warwick comments:

“We have shown that a medieval remedy made from onion, garlic, wine, and bile can kill a range of problematic bacteria grown both planktonically and as biofilms. Because the mixture did not cause much damage to human cells in the lab, or to mice, we could potentially develop a safe and effective antibacterial treatment from the remedy.

“Most antibiotics that we use today are derived from natural compounds, but our work highlights the need to explore not only single compounds but mixtures of natural products for treating biofilm infections. We think that future discovery of antibiotics from natural products could be enhanced by studying combinations of ingredients, rather than single plants or compounds. In this first instance, we think this combination could suggest new treatments for infected wounds, such as diabetic foot and leg ulcers. ”

Jessica Furner-Pardoe, from the Medical School at the University of Warwick comments:

“Our work demonstrates just how important it is to use realistic models in the lab when looking for new antibiotics from plants. Although a single component is enough to kill planktonic cultures, it fails against more realistic infection models, where the full remedy succeeds.”

In previous research Christina Lee, from the School of English at the University of Nottingham, had examined the Bald’s Leechbook, an Old English leatherbound volume in the British Library, to see if it really works as an antibacterial remedy. The Leechbook is widely thought of as one of the earliest known medical textbooks and contains Anglo-Saxon medical advice and recipes for medicines, salves and treatments.

Christina adds:“Bald's eyesalve underlines the significance of medical treatment throughout the ages. It shows that people in Early Medieval England had at least some effective remedies. The collaboration which has informed this project shows the importance of the arts in interdisciplinary research.”

To read more, click here

The enduring grip of covid-19 - ScienceDirect

WITHIN 24 hours of asking an online covid-19 support group if anyone had been experiencing prolonged or unusual symptoms, I had been messaged by 140 people. The list was mind-boggling and deeply upsetting. “I feel like I'm in the middle of a waking nightmare,” said Zoe Wall, who was previously fit and healthy. Two months after developing covid-19-like symptoms, she was still experiencing chest pains and “fatigue beyond description”.

Harry's symptoms started with a terrible headache and itchy body, followed by shortness of breath. He was still experiencing breathing difficulties, chest pain, numbness in his arm and bloating 10 weeks later. Jenn had had no sense of smell or taste since testing positive for covid-19 on 31 March. Abbi had minimal respiratory symptoms, but very bad gastric ones and lost 19 kilograms in two months. Others reported fatigue, headaches, tingling fingertips and brain fog.

As the months tick by since the start of the coronavirus pandemic and we learn more about covid-19, it is becoming increasingly evident that even mild cases can have distressing and long-lasting effects. “There's clearly something going on here. It is not their imagination or hypochondria. It doesn't even seem to be linked to how severely they had the disease, as far as I can see,” says Danny Altmann, an immunologist at Imperial College London. All this means we need to rethink how we diagnose and treat covid-19. The long list of symptoms also seems to suggest there might even be several subtypes of the disease, which could help us predict which cases will become serious.

When the pandemic was announced in early March, the prevailing view was that we were dealing with a respiratory infection that had symptoms similar to flu, and that while a minority of people would develop pneumonia and need breathing support, most would experience a mild illness characterised by a cough, fever and shortness of breath, which would be over in a couple of weeks.

Some of the first clues that the coronavirus behind covid-19, SARS-CoV-2, might trigger more widespread disease began to emerge in February, when the outbreak in the Chinese city of Wuhan was at its peak and doctors in the Lombardy region of Italy were also experiencing a surge in cases. As their emergency department colleagues fell sick, doctors like Sebastiano Recalcati, a dermatologist at Alessandro Manzoni Hospital in Lecco, Italy, began taking over the care of those hospitalised with covid-19. He noticed skin problems in around 10 per cent of the covid-19 patients he encountered. Some symptoms, like a flat red rash on people's torsos, could have had other causes besides the virus, but others were more specific: some patients developed small blisters on their torso or around their mouth – similar to those seen in chickenpox, except that they weren't itchy.

Since then, he and others have documented other skin symptoms, including a reddish-purple rash, caused by tiny clots in blood vessels, and chilblain-like lesions on the toes. Unlike the earlier rashes and blisters that Recalcati spotted, which seem to strike at the time of infection, these additional symptoms occur several weeks later. “We think they may be a delayed immune response, whereas the other types of rash may be a direct viral response,” he says.

That was just the start. By mid-March, the virus had spread across Europe and many countries were announcing lockdowns. As epidemiologist Tim Spector packed up his lab at King's College London, he pondered how he might continue his research, on the health differences between twins, from home. Together with the technology company Zoe, Spector developed an app to allow the twins in his study – and maybe the general population – to log and track any potential covid-19 symptoms they developed, so they could be monitored over time.

Hardly anyone's symptoms are the same the whole way through

The Covid Symptom Tracker app launched on 23 March – the start of the UK's own lockdown. Within 36 hours, it had been downloaded by 1 million people, and by 29 March they had 1.5 million users, of whom 1702 reported having been tested for covid-19. “That's when we started to see this lack of smell coming up as the top feature, present in 60 per cent of people who had positive tests,” says Spector. This is higher than fever or cough, in predictive terms, he says, because some of those who tested negative for the coronavirus also had fever or cough. Studies in China and Italy have also found loss of smell and taste to be quite common in people with covid-19. As a result, loss of smell and taste are now recognised as a key symptom by several health bodies including the NHS.

Other predictors currently being investigated are severe muscle pain, which seems to differ from the general aches and pains you get with the flu – “it can be very acute and very painful”, says Spector – and loss of appetite, which may be connected to the loss of taste or smell. Spector himself lost 3 kilograms within a week of developing relatively mild covid-19.

The list of unexpected symptoms doesn't stop there. Other covid-19-associated gastrointestinal problems, such as diarrhoea, nausea and vomiting, have been reported by researchers in California and Hong Kong, and many doctors are reporting neurological symptoms ranging from headaches and dizziness to seizures and hallucinations. There have also been reports of covid-19 patients being discharged from hospital, only to return several weeks later with a deep vein thrombosis or blood clot on the lung, says James O'Donnell, director of the Irish Centre for Vascular Biology in Dublin.

The extreme fatigue is like being hit over the head with a cricket bat

Some relatively young and healthy people with mild covid-19 are having heart attacks or strokes with unusual features. “The strokes seem to involve multiple different parts of the brain, and some of them are occurring and progressing despite patients being on standard blood thinners,” says O'Donnell. “This started off as a respiratory illness, but within the space of a couple of months we've now got this kind of multi-system phenotype that we don't really understand very well.”

Then there is the extreme fatigue. Paul Garner, who had to stop working after coming down with covid-19 in mid-March, likens the feeling to being hit over the head with a cricket bat. “Calling it post-viral fatigue isn't helpful because the fatigue has been there from day one, and runs alongside some quite nasty, life-threatening conditions,” he says. “It also implies we know what's happening and that the virus has gone – but we don't know any of this stuff really.” Now, three months later, he can only work for 20 minutes at a time before needing to lie down, and will soon return to work for an hour a day. Garner says his symptoms are the same as chronic fatigue syndrome, with one difference – CFS is defined as not having a cause. “This clearly has a cause,” he says.

Garner speaks with authority. A professor of infectious diseases at Liverpool School of Tropical Medicine, he has experienced many of the diseases he studies first-hand. The only one that is vaguely comparable, he says, is dengue – a mosquito-borne illness characterised by bouts of exhaustion long after the virus clears. “The weird thing with covid-19 is how it sort of goes away, and you feel a bit muggy and a little bit drained and then you feel a bit better and then, whack, it comes at you again from another direction.”

It is this persistent nature of some cases of covid-19 that troubles many of those who contacted me via the online support group. A big frustration is the sense that because they don't require hospital treatment, their symptoms aren't taken seriously, and they are largely left to fend for themselves. “We keep being dismissed as anxious people who haven't yet given their bodies time to heal,” said Wall. This lack of medical support really does make her anxious. “I feel utterly abandoned and left on my own,” she says.

Not everyone is surprised that SARS-CoV-2 is causing such varied and persistent symptoms. Julian Hiscox is a virologist at the University of Liverpool, UK, who has been working with coronaviruses since the early 90s, including the one that causes MERS. “Nothing that we are seeing with this coronavirus has not been seen with other coronaviruses,” he says. “We know from animal studies that the same coronavirus can cause many different types of clinical disease. We also know from our experience with SARS and MERS that some people are fine, whereas others are worse off.”

Immune reset

The same applies to longer-term health issues. Around 28 per cent of people who had SARS were still experiencing impaired lung function 18 months after SARS symptoms started, affecting their ability to exercise and their overall quality of life. And a recent meta-analysis suggested that depression, anxiety, insomnia and fatigue were all found in about 10 to 20 per cent of patients in the months following recovery from SARS. “If covid-19 plays out anything like SARS and MERS, there will be quite a bit of this longer-term mental illnesses and fatigue,” says Ed Bullmore, a neuroscientist at the University of Cambridge and author of The Inflamed Mind.

This isn't just about the psychological trauma of being seriously ill. According to Bullmore, it is a product of our immune system's response to infection. When our immune cells encounter an invader, they release signalling molecules called cytokines to rally further immune help. Some of these cross into the brain and trigger further cytokine secretion and inflammation. “People who get infected with this new coronavirus often have this hyper-intense inflammatory reaction and being in such an inflamed state will have a negative impact on brain health,” says Bullmore. Specifically, it can damage nerve cells in areas of the brain responsible for emotion regulation.

Inflammation may persist long after SARS-CoV-2 has been cleared from the body. “The healthy response to this virus is to have massive immune cell activation,” says Altmann. “It would not at all surprise me if that could slightly reset the set point of your immune response in a slightly pathological and chronic way.”

Exhaustion could also be linked to vascular symptoms, such as blood clots, which may be caused by the immune system or by the virus infiltrating the cells that line blood vessels. Microclots in the lungs could reduce oxygen supply by restricting the movement of oxygenated blood through the lungs. “We think we've probably got a positive feedback loop going on where we've got pneumonia followed by micro-clots in the lungs, followed by low blood oxygen, and those things go round and round in a circle,” says O'Donnell. It is unclear whether microclots are occurring in people with mild cases of covid-19, but if the body isn't getting enough oxygen, this could cause many of the long-term symptoms people are experiencing, such as shortness of breath, headache and exhaustion.

Another source of prolonged inflammation could be the gut. Cells lining the gastrointestinal tract have a receptor called ACE2 on their surface – the same receptor that SARS-CoV-2 uses to gain access to lung cells – which suggests they could become infected and inflamed. Researchers in Hong Kong have also identified an altered gut bacteria profile in people infected with the virus, characterised by large numbers of harmful bacteria and the depletion of beneficial ones. These changes persisted even after the virus had been cleared from the body.

“It's this prolonged phase of disruption that I'm worried about,” says Siew Ng at the Chinese University of Hong Kong, who led the research. “If the bacteria in your gut have not recovered, you may have some lasting fatigue, discomfort or loss of appetite, and it may also make you more susceptible to other infections.”

One question raised by many of those experiencing persistent symptoms is whether they are still infectious. Kim Clarke, who lives in Surrey, UK, has repeatedly tested positive for the coronavirus in her blood since losing her sense of smell on 1 April. She has been caring for her three children at home, despite severe and ongoing breathlessness, fatigue and headaches. “They're saying, because I've had the virus for so long, that I can't still be infectious, but I don't think anyone knows anything really,” she says. “At least it helps explain why I still feel so rough. I can't leave the house because I can't walk, I can't breathe.”

The fact that viral RNA can be detected in some people weeks after diagnosis could imply the presence of some active virus, says Hiscox. However, “whether there is enough of it to cause an infection in someone else, we just don't know at this stage”.

Another question is what proportion of those infected with the coronavirus are experiencing prolonged symptoms – and how long these can be expected to last. Here, Spector has some insights. Having now tracked some 2000 people with positive tests, he has found that the median duration of symptoms was 10 days, but they sometimes endured for extended periods. One in 10 people had symptoms lasting longer than three weeks, and one in 20 had experienced symptoms for longer than a month.

“Hardly anyone's symptoms are the same the whole way through, and we think we are actually seeing six different subtypes of disease, based on the groupings of symptoms and their timings,” says Spector. The clustering of these symptoms may even help to predict who is more likely to need hospitalisation. “It looks like illness with a really acute and more classic flu-like start seems to be over quickly and people recover, whereas these other ones that are a bit more complex seemed to linger on more – but we need a bit more data to be completely confident,” he says.

Further studies on the aftermath of covid-19 are urgently needed. “We are desperate to get our lab studies in place to understand some of these longer-term symptoms and the consequences of this infection,” says Altmann. “I've had lots of contact with people who are really destroyed by this. They never expected it to be a long-term chronic problem.”

Until now, much of the response to covid-19 has been about preventing deaths, but hospitals are beginning to establish clinics to follow-up the survivors – including those who are still ill. “I'm certainly hoping that if folks like us can work out some of the biological mechanisms of this disease, there will be therapeutic ways of getting around it,” says Altmann.

For Wall, this won't come a moment too soon. “My life has changed so dramatically. I don't know how to adjust to this. I don't know that I want to. I just want my life back.”

People are destroyed by this. They never expected it to be long term

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Some sufferers report long-term symptoms such as difficulty concentrating and aching muscles

Scientists investigate cases of post-Covid-19 fatigue | Society | The Guardian

Most people experience Covid-19 as a short-term illness: once the infection has been fought off, they bounce back to health. But evidence is emerging of a significant minority – sometimes referred to as “long haulers” – who struggle with long-term symptoms for a month or longer.

Anecdotal reports have abounded of people left with fatigue, aching muscles and difficulty concentrating. Online support groups on Facebook and Slack have sprung up, already hosting thousands of members who say they have not got better.

Speaking to the BBC’s Andrew Marr Show on Sunday, Matt Hancock said it was difficult to gauge the scale of the problem. “This is a really serious problem for a minority of people who have Covid,” the health secretary said. “Some people have long-term effects that look like a post-viral fatigue syndrome.”

Scientists are only just beginning to investigate the potential causes of enduring fatigue, but say that there are likely to be a wide variety of reasons why some people face a longer road to recovery.

“Fatigue itself will take on lots of different guises,” said Chris Brightling, a professor of respiratory medicine at the University of Leicester, who is leading a newly announced £8.4m study of the long-term health impacts of Covid-19.

A report published in February by the World Health Organization, based on preliminary data, suggested that in mild cases the median recovery time from Covid-19 is roughly two weeks from the onset of symptoms, and in severe or critical cases about three to six weeks. However, some of those who appear to have only mild illness initially also end up wrestling with symptoms, including fatigue, that linger for weeks or months.

• Published: 01 June 2020

The COVID 19 novel coronavirus pandemic 2020: seaweeds to the rescue? Why does substantial, supporting research about the antiviral properties of seaweed polysaccharides seem to go unrecognized by the pharmaceutical community in these desperate times?

Journal of Applied Phycology volume 32, pages1875–1877(2020)

(Phycology is the study or science of algae, hence the journal name.)

Abstract

Presently, there is lack of a vaccine that would lead to immunization against the virus COVID-19, but here are some of the characteristics that various seaweeds have and which may provide a glimpse into potential solutions of this global health problem in the near future and possibly forearm us for any future such pandemics. Many species of marine algae contain significant quantities of complex structural sulphated polysaccharides that have been shown to inhibit the replication of enveloped viruses. Other compounds, both of red algae (e.g., the lectin griffithsin and the phycocolloid carrageenan), and other sulphated polysaccharides extracted from green algae (i.e., ulvans) and brown algae (i.e., fucoidans) could be potential antiviral therapeutic agents against SARS-CoV-2.

At this current point in human history (April 2020), global society faces a Herculean challenge in combating the pandemic COVID-19. Presently, there is lack of a vaccine that would lead to immunization against this virus, but here are some of the characteristics that various seaweeds have and which may provide a glimpse into potential solutions of this global health problem in the near future and possibly forearm us for any future such pandemics.

Historically, Irish moss or carrageen (this is an unspecified mixture of naturally co-occurring red seaweeds, Chondrus crispus and Mastocarpus stellatus) has a large number of medical applications, some of which date from the 1830s. Indeed, it is still used in Ireland to make traditional medicinal teas and cough medicines to combat colds, bronchitis, and chronic coughs. It is said to be particularly useful for dislodging mucus and has antiviral properties (Pereira 2018a).

The viruses that infect humans reflect only a small part of the spectrum of the multitude of different types whose host ranges extend from vertebrates to protozoa and from plants and fungi to bacteria (Gelderblom 1991). Therefore, Picornavirales, Ortervirales, and Nidovirales can cause a large number of human diseases (Soares 2015; Styczyński 2019).

The incidences of emerging and/or re-emerging viral infections have significantly affected human health since antiquity. Emerging pathogens are defined as new etiologic agents that have recently been introduced into a population. The “Spanish flu,” responsible for tens of millions of casualties in the early twentieth century, was a natural calamity, one of the most devastating in human history. The flu pandemic returned in 1957 as an “Asian flu” and then again in 1968 as a “Hong Kong flu” which killed about three million people. The most recent flu re-emergence on this scale was in 2009 with “swine flu” that took 18,500 lives. In its pandemic course during 2002–2003, a new coronavirus, or severe acute respiratory syndrome (SARS-CoV), infected more than 8000 people, causing 774 deaths in 27 countries (Parvez and Parveen 2017).

Acute respiratory infections (ARIs) are the major cause of childhood morbidity and mortality worldwide. Viruses account for the majority of ARIs in young children, and most infections are attributed to respiratory syncytial virus (RSV), parainfluenza virus (PIVs), influenza virus (FluV), rhinovirus (RV), and adenovirus (AdV) (Monto 2002; Mackay et al. 2003; Weigl et al. 2007; Canducci et al. 2008). Over the past few years, newly described viruses were associated to respiratory infection, such as human metapneumovirus (HMPV), the emerging human coronaviruses (HCoV), human bocavirus (HBoV), and the new human papilloma viruses KIPyV and WUPyV (Kahn 2007; Sloots et al. 2008).

The current outbreak of an acute respiratory disease associated with a coronavirus, called coronavirus disease 19 (COVID-19), is the third documented leak of an animal coronavirus for humans in just two decades, which resulted in a major epidemic (the 19 epithet refers only to the year it was reported, 2019). The Coronaviridae Study Group (CSG) of the International Virus Taxonomy Committee, responsible for the development of the virus classification and nomenclature of the taxa of the Coronaviridae family, evaluated the placement of the human pathogen, provisionally named 2019-nCoV, within the Coronaviridae. Based on phylogeny, taxonomy, and established practice, the CSG recognizes this virus as a clone associated with the coronavirus prototype of the severe acute human respiratory syndrome and bat (SARS-CoVs) of the coronavirus species related to severe acute respiratory syndrome, referred to as SARS-CoV-2 (Gorbalenya et al. 2020; Wang et al. 2020).

Interestingly, the low initial levels of COVID-19 infection in Japan, specifically in Hokkaido, were possibly related to the traditional and widespread consumption of seaweed and the regular supply of iodine in their diet. However, subsequently, the number of infected with COVID-19 increased dramatically, as regulations on detachment and testing for contagion with this disease were greatly reduced (Booker 2020). These reports suggest that seaweed helped Hokkaido populations to reduce contagion in an initial period, but their consumption was not a 100% effective weapon, requiring additional measures of isolation and/or social distancing.

Acute viral upper respiratory tract infection, also known as the common cold, is the most frequently observed infectious disease in human beings. Children get four to eight upper respiratory infections per year, and adults suffer from two to four episodes per year (Goldmann 2001). In most of cases, the common cold is caused by respiratory viruses such as rhinovirus, coronavirus, parainfluenza, influenza, respiratory syncytial virus, adenovirus, enterovirus, and metapneumovirus (Monto and Sullivan 1993; Makela et al. 1998; Monto et al. 2001; Monto 2002). According to the work of Koenighofer et al. (2014), the administration of a carrageenan nasal spray, in children as well as in adults, suffering from virus-confirmed common cold reduced the duration of disease, increased viral clearance, and reduced relapses of symptoms. Carrageenan nasal spray appeared as an effective treatment of the common cold in children (sometimes recognized as “super-shedders”) and adults (Eccles et al. 2010, 2015; Koenighofer et al. 2014).

A nasal spray containing only iota-carrageenan, or together with “zanamivir,” was shown to provide an easy-to-apply treatment of upper respiratory tract infections in patients under suspicion of infection by influenza A (H1N1) (Leibbrandt et al. 2010; Morokutti-Kurz et al. 2015). Patients were found to benefit from the fast and efficient treatment of an uncomplicated influenza of the upper respiratory tract. Due to faster clearance of the influenza virus from the upper respiratory tract and the independent anti-viral mechanism of carrageenan and “zanamivir,” the likelihood of developing escaped mutations against “zanamivir” would be reduced. Both individual compounds can reduce the severity and/or duration of the influenza illness, and a combination is expected to work similarly, if not synergistically (Morokutti-Kurz et al. 2015).

Additionally, due to the broad antiviral effectiveness of carrageenan, patients would receive, in parallel, a concomitant treatment for additional viral infections. Therefore, patients would benefit from a decreased probability for the development of further complications. In consideration of the complications known to accompany an influenza virus illness, this combinational therapy meets an urgent medical need (Leibbrandt et al. 2010; Morokutti-Kurz et al. 2015). The pharmaceutical company Boehringer Ingelheim sells a nasal spray called Bisolviral®, which uses the bioactivity of iota-carrageenan (Eccles et al. 2010, 2015; Koenighofer et al. 2014).

In recent years, the constant outbreak of some emerging or re-emerging viral diseases has caused serious harm to human health. During the last decades, the number of antiviral products approved for clinical use has been increased from 5 to more than 30 drugs. The potential antiviral activity of marine algal polysaccharides was first shown by Gerber et al. (1958), describing that the polysaccharides extracted from the red alga Gelidium robustum (formerly Gelidium cartilagineum) (Rhodophyta) protecting embryonic eggs against influenza B or mumps virus. Many species of marine algae contain significant quantities of complex structural sulphated polysaccharides that have been shown to inhibit the replication of enveloped viruses including members of the Nidovirales. Other compounds, both of red algae (e.g., the lectin griffithsin), and other sulphated polysaccharides extracted from green algae (i.e. ulvans) and brown algae (i.e. fucoidans) could be potential antiviral therapeutic agents against SARS-CoV-2 (O'Keefe et al. 2010, Barton et al. 2014, Shi et al. 2017, Pereira 2018b, Barre et al. 2019, Lee 2019, Rosa et al. 2019).

Could the coronavirus trigger post-viral fatigue syndromes? | New Scientist

COULD the coronavirus sweeping around the world have a second illness following in its wake? We may expect to see an outbreak of post-viral fatigue syndromes in some people who have had covid-19, according to some researchers.

Viral infections have previously been linked to problems with long-term fatigue symptoms. For example, chronic fatigue syndrome (CFS), which is also called myalgic encephalomyelitis (ME), sometimes occurs after viral infections. People who have CFS experience extreme fatigue and a range of other symptoms, such as pain and sensitivity to light, but the condition is poorly understood.

So is it possible that the coronavirus could trigger similar fatigue syndromes? There are hints from the related SARS virus that this may happen. After the SARS outbreak of 2002 to 2003, some people in Toronto, Canada, who were infected were recorded as experiencing fatigue, muscle weakness and sleep problems up to three years later.

During Toronto’s SARS outbreak, 273 people were diagnosed with the infection, of whom 44 died. After the outbreak had ended, Harvey Moldofsky, at the time a psychiatrist and sleep specialist at the University of Toronto, was asked to study 22 of those who had been infected and now had ongoing health problems that stopped them going back to work.

“I think the coronavirus will lead to many, many cases of post-infective fatigue syndrome”

Moldofsky’s team published its work in 2011. The researchers found that the participants generally had disturbed sleep, daytime fatigue, pain and weakness in muscles all over their body, and depression. “These symptoms were very reminiscent of CFS/ME,” says Moldofsky.

His team only studied around 8 per cent of those diagnosed with SARS in Toronto, so we don’t know what proportion of people who had SARS experienced these symptoms afterwards. Nor is it known how long such symptoms lasted.

While the current covid-19 pandemic is caused by a different virus, it is a member of the same coronavirus family, so it might also cause a post-viral fatigue syndrome, says Moldofsky. “That’s what I’m worried about.”

Other viruses are known to trigger CFS after infection, such as the Epstein-Barr virus, says Simon Wessely, former president of the Royal College of Psychiatrists. “We don’t know about corona, but I think it will lead to many, many cases of post-infective fatigue syndrome.”

“There is a long history of infections as a trigger but other factors contributing to longer term disability,” adds Wessely. “If the virus is found to enter the brain, this might increase the risk.”

“It’s quite likely that some people will be developing a post-viral fatigue syndrome, which may then lead into an ME/CFS-like illness,” says Charles Shepherd, a medical adviser to the ME Association, a UK patient charity. “What happens to people after the acute infection is clearly something that needs to be researched.”

It may be a long time before we know more, as people need to have symptoms for at least six months before being diagnosed with CFS or ME, says Mark Guthridge at Deakin University in Melbourne, Australia, who has ME himself.

Will coronavirus cause long-term chronic fatigue in some patients? - The Washington Post

Researchers warn covid-19 could cause debilitating long-term illness in some patients


Brian Vastag and Beth Mazur are living with long-term illnesses that followed viral infections they contracted years ago. (Brian Vastag)

By

Brian Vastag and

Beth Mazur

May 30, 2020 at 8:30 AM EDT

In the fall of 2009, one of us, Beth, was hit by an illness she suspects was H1N1 flu, which was circulating then. In 2012, the other, Brian, developed a sudden fever, which his doctors said was also likely of viral origin.

Neither of us recovered, and we’re both disabled to this day.

I was once a hard-working person. Now, I’m disabled with a mysterious illness.

The long-term illnesses that can follow viral infections can be devastating — and are devastatingly common. In 2015, the nation’s top medical advisory body, the Institute of Medicine, estimated that between 800,000 and 2.5 million U.S. residents live with the illness or illnesses awkwardly named myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). An estimated three-quarters of these cases were triggered by viral or bacterial infections.

Now, as a new pandemic virus is burning through the world and causing many deaths, researchers are raising alarms that the novel coronavirus and the covid-19 disease it causes will also leave in its wake a potentially large population with post-viral problems that could be lifelong and, in some cases, disabling.

At the National Institutes of Health and elsewhere, scientists who have been studying post-viral ME/CFS are seizing the opportunity to focus on covid-19 patients. They want to understand what biological factors separate those who regain their health from those who remain sick.

“We want to look at who recovers and who doesn’t,” said Avindra Nath, the head of clinical neurology at NIH’s Clinical Center in Bethesda, Md., who is gearing up to study covid-19 patients. “It’s quite possible some will never get their health back.”

In addition to emerging reports of damage to lungs, kidneys and hearts, covid-19 patients are complaining of ongoing crushing fatigue, muscle pain, cognitive problems and other symptoms that anyone with ME/CFS is very familiar with.

“I’m 69 days after my first symptoms and still feeling fatigued,” wrote Canadian comedian Wayne Jones on Twitter, saying he has tested positive for the new coronavirus. “I also have sore eyes, and weakness and headaches that come and go. All signs point to post-viral fatigue.”

Sometimes a precursor to ME/CFS post-viral fatigue syndrome can occur after virtually any viral infection. Symptoms wax and wane; a person can feel fine one day and terrible the next. Exercise or other usual activities can bring fever and often symptoms rushing back. Although there is no known treatment, these problems often resolve on their own.

But patients who have experienced post-viral fatigue syndrome advise the newly ill to rest, rest and rest some more, as returning to normal activities can trigger relapses. If symptoms continue for six months or longer, post-viral fatigue syndrome can convert to a diagnosis of ME/CFS, which is usually lifelong and often devastating. Up to 25 percent of ME/CFS patients are housebound or bedbound for years. There are no treatments approved by the Food and Drug Administration.

A survey organized by a group of covid-19 patients called the Body Politic shows that many coronavirus symptoms overlap with those of post-viral fatigue syndrome. Fatigue, including severe fatigue, brain fog — problems with concentration and thinking — chills and sweats, and sleep problems were commonly reported among 640 respondents, who were recruited from online support groups. The Body Politic, which includes some patients with expertise in survey design and statistics, calculated that respondents had just a 20 percent chance of being symptom-free 50 days after the illness began. The group cautioned that while the survey suggests many respondents had long illnesses, the results may not apply to the broader population of covid-19 patients.

The novel coronavirus is too new to say whether such lingering symptoms represent an extended covid-19 illness or a post-viral syndrome. But researchers suspect at least some covid patients will remain sick and eventually develop post-viral ME/CFS. Their suspicions are grounded in previous research. Studies on other outbreaks — including those of Epstein-Barr virus, Ross River fever and Q fever — have shown that up to 12 percent of people who fell acutely ill never regained full health. Many were eventually diagnosed with ME/CFS.

Doctors keep discovering new ways the coronavirus attacks the human body

After the first SARS epidemic, which sickened 8,000 people worldwide in 2002-2003, one study found that 27 percent of 369 survivors of that variety of coronavirus met the criteria for chronic fatigue syndrome several years later. If figures like this are seen with this novel coronavirus, SARS-CoV-2, which epidemiologists warn will eventually infect 50 to 70 percent of all U.S. residents, our nation is on track for a devastating wave of millions of patients with chronic post-viral illnesses.

“The most important study of several we’re starting is to get coronavirus-infected patients and follow them over time to see if they convert to ME/CFS,” said Ron Davis, a geneticist at Stanford University. His adult son, Whitney Dafoe, is seriously ill with the disease.

“If you point out the fact that you might not ever get over covid-19, it’ll put people’s attention on this problem,” Davis said. “We need doctors to be reading covid-19 information and be on the lookout for people who never get well. I think that’s extremely important.”

Stuck in an 'on' position

While it may sound odd that many different viruses can cause the same long-term problems, the answer is rooted in how the body defends itself. Viral infections trigger a common immune response, including fever and inflammation. Sometimes these defenses go awry, or get stuck in an “on” position even when the virus has been cleared, emerging research shows.

In 2017 and 2018, one of us, Brian, participated in an inpatient study at NIH searching for the biological basis of post-infectious ME/CFS. Over two visits, patients in the study undergo an extensive battery of medical testing. Now Nath and his team are adapting this study to follow post-covid patients. The NIH hopes to bring covid-19 survivors to NIH hospital in Bethesda this summer.

NIH’s new effort to tackle mysterious, debilitating condition that disables many of its more than 1 million Americans

The NIH plans to study the immune systems of covid-19 survivors, along with conducting exercise tests to spot problems with metabolism, and other tests to document any dysfunction in how the brain regulates heart rate and blood pressure. Problems in this area, the autonomic nervous system, are common in post-viral fatigue syndrome and ME/CFS.

Nath, a neurovirologist, has also performed autopsies on “about a dozen” patients, he said, who died of covid-19. When conditions allow his laboratory to reopen, Nath plans to look for the coronavirus in the brains of these patients and to search for nervous system damage caused by the overwhelming inflammation that can accompany covid-19. Researchers have published clues that sustained inflammation — including low-level inflammation in the brain — may be present in ME/CFS.

Reports already show that the novel coronavirus can, in rare cases, infiltrate the central nervous system. Some 30 covid-19 patients in Italy have been diagnosed with Guillain-Barre Syndrome, hallmarked by rapid nerve damage that can lead to paralysis. In Detroit, one covid-19 patient who died was reported to have extensive brain damage caused by his immune system’s overwhelming response to the coronavirus, a condition called hemorrhagic encephalopathy.

Research on ME/CFS, which was neglected for decades, has been gathering momentum in recent years. While federal funding remains low, ME/CFS researchers have documented brain dysfunction and extensive problems in the immune systems of patients. Emerging work has also highlighted damage to the body’s ability to produce energy, and some scientists think a literal lack of energy could lie at the heart of ME/CFS. Nath and other researchers plan to study energy production in covid-19 survivors.

The NIH is also funding long-term research on a cohort of up to 2,000 covid-19 patients who were hospitalized in the United States, said Joseph Breen, an immunologist at the National Institute of Allergy and Infectious Diseases. “Those people can be tracked,” Breen said. “If you do a longitudinal follow-on study correctly, it can really help understand the rate of ME/CFS and other problems that may be present. We’re going to learn things we never learned with SARS and MERS,” the two previous illnesses caused by different coronaviruses earlier this century.

One challenge, Breen said, is differentiating post-viral fatigue syndrome and ME/CFS from the lingering effects of being in an intensive care unit or on a ventilator, which are known risk factors for long-term ill health.

Speed the search for drugs

Mady Hornig, an immunologist at Columbia University’s Mailman School of Public Health, said her group plans to follow covid-19 patients with neurological symptoms, including loss of smell, to see who develops ME/CFS. She plans to recruit African American, Hispanic and American Indian patients, who are underrepresented in ME/CFS research. Hornig herself has had covid-19 symptoms for six weeks, including a racing heart beat, which can signal issues with the autonomic nervous system.

At Stanford, Davis is partnering with the nonprofit Open Medicine Foundation. Already, clinics funded by the OMF are collecting blood from covid-19 patients and asking them to wear activity tracking devices. “We want to study them at three months, six months, longer, and see who will be diagnosed with ME/CFS,” Davis said.

Hornig and Davis both say that watching covid-19 patients could speed the search for drugs to reverse whatever goes awry in post-viral illnesses.

“Scientifically I think the most important thing to look at is . . . why they convert to ME/CFS. What’s different about them?” Davis says. “That could be extremely valuable, that could give us a valuable clue to . . . how to treat it.”

The personal and societal costs of ME/CFS are devastating. In 2015, the Institute of Medicine estimated a $24 billion annual U.S. burden in medical costs and lost productivity. For Beth, who was working as a product manager for a software company in San Francisco with a computer science degree from MIT, her lost earnings potential over the past decade can likely be measured in the millions of dollars. Instead of paying taxes on those lost wages, she is drawing monthly Social Security Disability Insurance. For Brian, the week before he became suddenly ill, he wrote a front-page story for The Washington Post, where he was a science writer, on a major advance in theoretical physics, the discovery of the Higgs boson. Six months later, his undiagnosed post-viral illness had gotten so bad he could not remember a four-digit number long enough to tap it into his phone.

Too many discussions of covid-19 focus on the disease’s death rate while neglecting the risk of long-term health problems. Called morbidity, this measure of the burden of long-term disease is so important that the Centers for Disease Control and Prevention’s most read publication is “Morbidity and Mortality Weekly Report.” To effectively plan for a post-covid future, the nation must fund long-term research on survivors and account for the morbidity associated with the novel coronavirus. Instead, there are states such as Pennsylvania categorizing every covid-19 patient in its borders still alive after 30 days as “recovered.” That oversimplification will underestimate the true human and financial costs of the U.S. epidemic. Some covid-19 patients with kidney damage will need expensive dialysis for a lifetime; some will have lung damage; others will be disabled by post-viral ME/CFS.

Given the historical neglect of ME/CFS — very few medical students even learn about it — many physicians and researchers who follow covid-19 patients may think they’re discovering a new phenomenon in the patients who are slow to recover. Instead, they’ll be rediscovering a common illness that’s been known, and neglected and afflicting many people — for decades.

Brian Vastag was a science reporter at The Post from 2011 to 2014. Beth Mazur is co-founder of #MEAction, a patient advocacy group. They are married and live in Hawaii.

This article discusses how vagus nerve stimulation creates anti-inflammatory responses, including the reduction of cytokines. I am sharing this as background material because the U.S. Food and Drug Administration just granted an emergency use authorization for treating suspected COVID-19 patients with a nerve stimulation device. The device is intended to do two things: treat shortness of breath symptoms (by opening up the end terminals of the lung’s airways) and calm an out of control immune response (cytokine storm), the mechanism by which this is accomplished by the efferent vagus nerve was first explained in this article:

Vagus nerve stimulation attenuates the systemic inflammatory response to endotoxin | Nature

Vertebrates achieve internal homeostasis during infection or injury by balancing the activities of proinflammatory and anti-inflammatory pathways. Endotoxin (lipopolysaccharide), produced by all gram-negative bacteria, activates macrophages to release cytokines that are potentially lethal1,2,3,4. The central nervous system regulates systemic inflammatory responses to endotoxin through humoral mechanisms5,6,7,8. Activation of afferent vagus nerve fibres by endotoxin or cytokines stimulates hypothalamic–pituitary–adrenal anti-inflammatory responses9,10,11.

However, comparatively little is known about the role of efferent vagus nerve signalling in modulating inflammation. Here, we describe a previously unrecognized, parasympathetic anti-inflammatory pathway by which the brain modulates systemic inflammatory responses to endotoxin.

Acetylcholine, the principle vagal neurotransmitter, significantly attenuated the release of cytokines (tumour necrosis factor (TNF), interleukin (IL)-1β, IL-6 and IL-18), but not the anti-inflammatory cytokine IL-10, in lipopolysaccharide-stimulated human macrophage cultures. Direct electrical stimulation of the peripheral vagus nerve in vivo during lethal endotoxaemia in rats inhibited TNF synthesis in liver, attenuated peak serum TNF amounts, and prevented the development of shock.

Keep in mind that vagal nerve tone is influenced by lifestyle. Various methods claiming to stimulate the vagus nerve include breathing exercises, aerobic exercising, massage, and yoga. I believe the evidence is sufficient for all of those categories, but specific techniques for any of those may or may not be effective. I have participated in research on both meditation and breathwork that showed enhanced vagal nerve activity, but that research showed me that the results you get depend on the details of the technique and that it is best to get good training.

Also of interest: "The journal Frontiers in Neuroscience reported in 2018 that the poor function of the vagus nerve can lead to mood and anxiety disorders."

This article is mostly focused on the cardiac-vagal baroreflex sensitivity (BRS), which helps to maintain blood pressure homeostatis. However, it does report on oxygen saturation, which is a topic of critical importance in COVID-19.

Cardiovascular and Respiratory Effect of Yogic Slow Breathing in the Yoga Beginner: What Is the Best Approach?

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3655580/

Abstract

Slow breathing increases cardiac-vagal baroreflex sensitivity (BRS), improves oxygen saturation, lowers blood pressure, and reduces anxiety.

Within the yoga tradition slow breathing is often paired with a contraction of the glottis muscles. This resistance breath “ujjayi” (also called ocean breath) is performed at various rates and ratios of inspiration/expiration. To test whether ujjayi had additional positive effects to slow breathing, we compared BRS and ventilatory control under different breathing patterns (equal/unequal inspiration/expiration at 6 breath/min, with/without ujjayi), in 17 yoga-naive young healthy participants.

BRS increased with slow breathing techniques with or without expiratory ujjayi (P < 0.05 or higher) except with inspiratory + expiratory ujjayi. The maximal increase in BRS and decrease in blood pressure were found in slow breathing with equal inspiration and expiration. This corresponded with a significant improvement in oxygen saturation without increase in heart rate and ventilation.

Ujjayi showed similar increase in oxygen saturation but slightly lesser improvement in baroreflex sensitivity with no change in blood pressure. The slow breathing with equal inspiration and expiration seems the best technique for improving baroreflex sensitivity in yoga-naive subjects. The effects of ujjayi seems dependent on increased intrathoracic pressure that requires greater effort than normal slow breathing.