Ohälsa & Sjukdomar

Inte alla har samma “helvetessyn” på den pågående coronapandemin som majoriteten av media. Länkat nedan är en artikel som uppdaterats regelbundet sedan mitten av mars, och är alldeles full av referenser till studier och statistik. I den står bl.a. att

• dödligheten i Covid-19 ligger på så lite som 0,1-0,4%, betydligt lägre än först förutspått av WHO
• 50-80% av de som testas positiva förblir symtomfria
• medianåldern för de som dör är 80 år i de flesta länder
• bara 1% av de som dör har ingen bakomliggande allvarlig sjukdom
• siffrorna av döda i Covid-19 förväxlas delvis med normal dödlighet. Tex dör normalt runt 8 000 dagligen i USA och dödlighet i influensa kan ligga på uppåt 80 000
• man gör inte en tillräckligt tydlig skillnad på om människor dör med eller av det nya Coronaviruset

Den är betydligt mer innehållsrik, men följande är en övergripande text från länken:

Overview

1. According to data from the best-studied countries such as South Korea, Iceland, Germany and Denmark, the overall lethality of Covid19 is between 0.1% and 0.4% and thus up to twenty times lower than initially assumed by the WHO.
2. A study in Nature Medicine comes to a similar conclusion even for the Chinese city of Wuhan. The initially significantly higher values for Wuhan were obtained because many people with only mild or no symptoms were not recorded.
3. 50% to 80% of test-positive individuals remain symptom-free. Even among the 70 to 79 year old persons about 60% remain symptom-free, many more show only mild symptoms.
4. The median age of the deceased in most countries (including Italy) is over 80 years and only about 1% of the deceased had no serious previous illnesses. The age and risk profile of deaths thus essentially corresponds to normal mortality. Up to 60% of all Covid19-related deaths have occurred in particularly vulnerable nursing homes.
5. Many media reports of young and healthy people dying from Covid19 have proven to be false upon closer inspection. Many of these people either did not die from Covid19 or they in fact had serious preconditions (such as undiagnosed leukaemia).
6. Normal overall mortality in the US is about 8000 people per day, in Germany about 2600 people and in Italy about 1800 people per day. Influenza mortality in the US is up to 80,000, in Germany and Italy up to 25,000, and in Switzerland up to 1500 people per winter.
7. Strongly increased death rates, as in northern Italy, can be influenced by additional risk factors such as very high air pollution and microbial contamination as well as a collapse in the care of the elderly and sick due to mass panic and lockdown measures.
8. In countries such as Italy and Spain, and to some extent Great Britain and the US, a serious overload of hospitals, notably by the flu, is not unusual. In addition, up to 15% of doctors and nurses currently have to self-quarantine, even if they develop no symptoms.
9. An important distinction concerns the question of whether people die with or indeed fromcoronaviruses. Autopsies show that in many cases the previous illnesses were an important or decisive factor, but the official figures usually do not reflect this.
10. Thus in order to assess the danger of the disease, the key indicator is not the often mentioned number of test-positive persons and deceased, but the number of persons who actually and unexpectedly develop or die of pneumonia.
11. The often shown exponential curves of “corona cases” are misleading, since the number of tests also increases exponentially. In most countries, the ratio of positive tests to total tests either remains constant between 5% to 25% or increases rather slowly.
12. Countries without lockdowns and contact bans, such as Japan, South Korea and Sweden, have not experienced a more negative course of events than other countries. This might call into question the effectiveness of such far-reaching measures.
13. According to leading lung specialists, invasive ventilation of Covid19 patients is often counterproductive and causes additional damage to the lungs. The invasive ventilation of Covid19 patients is partly done out of fear of spreading the virus through aerosols.
14. Contrary to original assumptions, however, the WHO determined at the end of March that there is no evidence of aerosol dispersal of the virus. A leading German virologist also found no aerosol and no smear infections in a pilot study.
15. Many clinics in Europe and the US have been lacking patients and some have had to introduce short-time work. Numerous operations and therapies were cancelled by clinics, even emergency patients sometimes stay at home out of fear of the virus.
16. Several media have been caught trying to dramatize the situation in clinics, sometimes even with manipulative pictures and videos. In general, many media outlets do not question even doubtful official statements and figures.
17. The virus test kits used internationally are prone to errors. Several studies have shown that even normal corona viruses can give a false positive result. Moreover, the virus test currently in use has not been clinically validated due to time pressure.
18. Numerous internationally renowned experts from the fields of virology, immunology and epidemiology consider the measures taken to be counterproductive and recommend a rapid natural immunisation of the general population while protecting risk groups.
19. The number of people suffering from unemployment, psychological problems and domestic violence as a result of the measures taken has exploded in the US and worldwide. Several experts believe that the measures may claim more lives than the virus itself.
20. NSA whistleblower Edward Snowden warned that the corona crisis is used for the massive and permanent expansion of global surveillance. The renowned virologist Pablo Goldschmidt spoke of a “global media terror” and “totalitarian measures”. Leading British virologist Professor John Oxford spoke of a “media epidemic”.

Mer via https://4health.se/?s=corona

https://swprs.org/a-swiss-doctor-on-covid-19/

Läkaren som publicerats i New York Times menar att Covid-19-patienter inte får symtom i lungorna förrän mycket sent i sjukdomsförloppet, vilket gör att de är svåra att rädda. Att om man testar patienter som inte har några andningsbesvär så uppvisar de trots allt lunginflammation. Du kan läsa hela hans text här nedan där han förklarar detta mer ingående. Men han skriver bl.a. att “These patients did not report any sensation of breathing problems, even though their chest X-rays showed diffuse pneumonia and their oxygen was below normal. How could this be?
We are just beginning to recognize that Covid pneumonia initially causes a form of oxygen deprivation we call “silent hypoxia” — “silent” because of its insidious, hard-to-detect nature.“

Vidare skriver han att “Normal oxygen saturation for most persons at sea level is 94 percent to 100 percent; Covid pneumonia patients I saw had oxygen saturations as low as 50 percent.
To my amazement, most patients I saw said they had been sick for a week or so with fever, cough, upset stomach and fatigue, but they only became short of breath the day they came to the hospital. Their pneumonia had clearly been going on for days, but by the time they felt they had to go to the hospital, they were often already in critical condition.

Och baserat på detta menar han att man borde screena patienter med pulsoximeter för att upptäcka lungsjukdom tidigare. En pulsoximeter är alltså en liten apparat som man sätter på fingret som mäter puls och syremättnad. Normalt är denna närmare 100%, men hos sjuka Covid-19-patienter sjunker den dramatiskt.

Han skriver också att rätt position av sjuka Covid-19-ptienter kan rädda liv. Att lägga dem omväxlande på mage och sidan: “Patient positioning maneuvers (having patients lie on their stomach and sides) open up the lower and posterior lungs most affected in Covid pneumonia. Oxygenation and positioning helped patients breathe easier and seemed to prevent progression of the disease in many cases. In a preliminary study by Dr. Caputo, this strategy helped keep three out of four patients with advanced Covid pneumonia from needing a ventilator in the first 24 hours.”

En snabb sökning efter pulosoximetrar visar dock att det är helt slutsålt överallt. Även sidor med erbjudanden som till synes är tillgängliga visar sig ha en leveranstid på fyra veckor. På någon sida stod det 18 dagar, men väl i kassan är det leveranstid i slutet av maj. Tänk också på att det kan vara lätt att få felaktiga resultat om man inte använder den helt rätt (https://www.dagensmedicin.se/artiklar/2008/10/06/staten-varnar-for-pulsoximeter/)
Informerar om att det går att testa för sars-cov-2 även i avföring. Dock får man då lägga en del pengar på det https://4health.se/covid-19

Det finns också läkare som motsätter sig hans slutsatser och skriver “once hypoxia is detected early with pulse oximeters, we don’t have treatment for COVID-19 pneumonia, whether we’re diagnosing it early or late. So what’s the point of detecting early signs of pneumonia in stable patients and bringing them to an already overwhelmed system if we can’t offer them anything other than supportive care.”

Mer via https://4health.se/?s=corona

“The Infection That’s Silently Killing Coronavirus Patients
This is what I learned during 10 days of treating Covid pneumonia at Bellevue Hospital.
By Richard Levitan. Dr. Levitan is an emergency doctor.

I have been practicing emergency medicine for 30 years. In 1994 I invented an imaging system for teaching intubation, the procedure of inserting breathing tubes. This led me to perform research into this procedure, and subsequently teach airway procedure courses to physicians worldwide for the last two decades.

So at the end of March, as a crush of Covid-19 patients began overwhelming hospitals in New York City, I volunteered to spend 10 days at Bellevue, helping at the hospital where I trained. Over those days, I realized that we are not detecting the deadly pneumonia the virus causes early enough and that we could be doing more to keep patients off ventilators — and alive.

On the long drive to New York from my home in New Hampshire, I called my friend Nick Caputo, an emergency physician in the Bronx, who was already in the thick of it. I wanted to know what I was facing, how to stay safe and about his insights into airway management with this disease. “Rich,” he said, “it’s like nothing I’ve ever seen before.”

He was right. Pneumonia caused by the coronavirus has had a stunning impact on the city’s hospital system. Normally an E.R. has a mix of patients with conditions ranging from the serious, such as heart attacks, strokes and traumatic injuries, to the nonlife-threatening, such as minor lacerations, intoxication, orthopedic injuries and migraine headaches.

During my recent time at Bellevue, though, almost all the E.R. patients had Covid pneumonia. Within the first hour of my first shift I inserted breathing tubes into two patients.

Even patients without respiratory complaints had Covid pneumonia. The patient stabbed in the shoulder, whom we X-rayed because we worried he had a collapsed lung, actually had Covid pneumonia. In patients on whom we did CT scans because they were injured in falls, we coincidentally found Covid pneumonia. Elderly patients who had passed out for unknown reasons and a number of diabetic patients were found to have it.

And here is what really surprised us: These patients did not report any sensation of breathing problems, even though their chest X-rays showed diffuse pneumonia and their oxygen was below normal. How could this be?

We are just beginning to recognize that Covid pneumonia initially causes a form of oxygen deprivation we call “silent hypoxia” — “silent” because of its insidious, hard-to-detect nature.

Pneumonia is an infection of the lungs in which the air sacs fill with fluid or pus. Normally, patients develop chest discomfort, pain with breathing and other breathing problems. But when Covid pneumonia first strikes, patients don’t feel short of breath, even as their oxygen levels fall. And by the time they do, they have alarmingly low oxygen levels and moderate-to-severe pneumonia (as seen on chest X-rays). Normal oxygen saturation for most persons at sea level is 94 percent to 100 percent; Covid pneumonia patients I saw had oxygen saturations as low as 50 percent.

To my amazement, most patients I saw said they had been sick for a week or so with fever, cough, upset stomach and fatigue, but they only became short of breath the day they came to the hospital. Their pneumonia had clearly been going on for days, but by the time they felt they had to go to the hospital, they were often already in critical condition.

In emergency departments we insert breathing tubes in critically ill patients for a variety of reasons. In my 30 years of practice, however, most patients requiring emergency intubation are in shock, have altered mental status or are grunting to breathe. Patients requiring intubation because of acute hypoxia are often unconscious or using every muscle they can to take a breath. They are in extreme duress. Covid pneumonia cases are very different.

A vast majority of Covid pneumonia patients I met had remarkably low oxygen saturations at triage — seemingly incompatible with life — but they were using their cellphones as we put them on monitors. Although breathing fast, they had relatively minimal apparent distress, despite dangerously low oxygen levels and terrible pneumonia on chest X-rays.

We are only just beginning to understand why this is so. The coronavirus attacks lung cells that make surfactant. This substance helps the air sacs in the lungs stay open between breaths and is critical to normal lung function. As the inflammation from Covid pneumonia starts, it causes the air sacs to collapse, and oxygen levels fall. Yet the lungs initially remain “compliant,” not yet stiff or heavy with fluid. This means patients can still expel carbon dioxide — and without a buildup of carbon dioxide, patients do not feel short of breath.

Patients compensate for the low oxygen in their blood by breathing faster and deeper — and this happens without their realizing it. This silent hypoxia, and the patient’s physiological response to it, causes even more inflammation and more air sacs to collapse, and the pneumonia worsens until oxygen levels plummet. In effect, patients are injuring their own lungs by breathing harder and harder. Twenty percent of Covid pneumonia patients then go on to a second and deadlier phase of lung injury. Fluid builds up and the lungs become stiff, carbon dioxide rises, and patients develop acute respiratory failure.

By the time patients have noticeable trouble breathing and present to the hospital with dangerously low oxygen levels, many will ultimately require a ventilator.

Silent hypoxia progressing rapidly to respiratory failure explains cases of Covid-19 patients dying suddenly after not feeling short of breath. (It appears that most Covid-19 patients experience relatively mild symptoms and get over the illness in a week or two without treatment.)

A major reason this pandemic is straining our health system is the alarming severity of lung injury patients have when they arrive in emergency rooms. Covid-19 overwhelmingly kills through the lungs. And because so many patients are not going to the hospital until their pneumonia is already well advanced, many wind up on ventilators, causing shortages of the machines. And once on ventilators, many die.

Avoiding the use of a ventilator is a huge win for both patient and the health care system. The resources needed for patients on ventilators are staggering. Vented patients require multiple sedatives so that they don’t buck the vent or accidentally remove their breathing tubes; they need intravenous and arterial lines, IV medicines and IV pumps. In addition to a tube in the trachea, they have tubes in their stomach and bladder. Teams of people are required to move each patient, turning them on their stomach and then their back, twice a day to improve lung function.

There is a way we could identify more patients who have Covid pneumonia sooner and treat them more effectively — and it would not require waiting for a coronavirus test at a hospital or doctor’s office. It requires detecting silent hypoxia early through a common medical device that can be purchased without a prescription at most pharmacies: a pulse oximeter.

Pulse oximetry is no more complicated than using a thermometer. These small devices turn on with one button and are placed on a fingertip. In a few seconds, two numbers are displayed: oxygen saturation and pulse rate. Pulse oximeters are extremely reliable in detecting oxygenation problems and elevated heart rates.

Pulse oximeters helped save the lives of two emergency physicians I know, alerting them early on to the need for treatment. When they noticed their oxygen levels declining, both went to the hospital and recovered (though one waited longer and required more treatment). Detection of hypoxia, early treatment and close monitoring apparently also worked for Boris Johnson, the British prime minister.

Widespread pulse oximetry screening for Covid pneumonia — whether people check themselves on home devices or go to clinics or doctors’ offices — could provide an early warning system for the kinds of breathing problems associated with Covid pneumonia.

People using the devices at home would want to consult with their doctors to reduce the number of people who come to the E.R. unnecessarily because they misinterpret their device. There also may be some patients who have unrecognized chronic lung problems and have borderline or slightly low oxygen saturations unrelated to Covid-19.

All patients who have tested positive for the coronavirus should have pulse oximetry monitoring for two weeks, the period during which Covid pneumonia typically develops. All persons with cough, fatigue and fevers should also have pulse oximeter monitoring even if they have not had virus testing, or even if their swab test was negative, because those tests are only about 70 percent accurate. A vast majority of Americans who have been exposed to the virus don’t know it.

There are other things we can do as well to avoid immediately resorting to intubation and a ventilator. Patient positioning maneuvers (having patients lie on their stomach and sides) open up the lower and posterior lungs most affected in Covid pneumonia. Oxygenation and positioning helped patients breathe easier and seemed to prevent progression of the disease in many cases. In a preliminary study by Dr. Caputo, this strategy helped keep three out of four patients with advanced Covid pneumonia from needing a ventilator in the first 24 hours.

To date, Covid-19 has killed more than 40,600 people nationwide — more than 10,000 in New York State alone. Oximeters are not 100 percent accurate, and they are not a panacea. There will be deaths and bad outcomes that are not preventable. We don’t fully understand why certain patients get so sick, or why some go on to develop multi-organ failure. Many elderly people, already weak with chronic illness, and those with underlying lung disease do very poorly with Covid pneumonia, despite aggressive treatment.

But we can do better. Right now, many emergency rooms are either being crushed by this one disease or waiting for it to hit. We must direct resources to identifying and treating the initial phase of Covid pneumonia earlier by screening for silent hypoxia.

It’s time to get ahead of this virus instead of chasing it.

Huvudkommentaren som motsätter sig hans argument lyder:

I’m an emergency room physician, a pulmonologist intensivist, and I agree with your observation but not with your conclusion. This is a form of atypical pneumonia. None of the pneumonia symptoms or signs are 100% sensitive, so the absence of “typical” symptoms is not necessarily that unusual. And then, once hypoxia is detected early with pulse oximeters, we don’t have treatment for COVID-19 pneumonia, whether we’re diagnosing it early or late. So what’s the point of detecting early signs of pneumonia in stable patients and bringing them to an already overwhelmed system if we can’t offer them anything other than supportive care. Once we have better understanding of therapeutics and what’s a good treatment in the early phases, perhaps this will be warranted. Where we stand today, I worry, we’re only adding to the mass hysteria and getting people to purchase pulse-ox they don’t know how to use, to then outpour into hospitals already strapped for resources on all fronts.

https://www.nytimes.com/2020/04/20/opinion/coronavirus-testing-pneumonia.html

Det är mycket som tynger i mediaflödet kring covid-19. Men trots vad jag skrev om felbehandlingar (https://4health.se/behandlas-de-sjukaste-covid-19-patienterna-fel) så överlever 80% av de som får intensivvård i Sverige (åtminstone på Karolinska, där ju många hamnat) och överlag så överlever ju de allra flesta. Hittills har minst 400.000 människor i världen tillfrisknat från covid-19.

Intensivvården på Karolinska sjukhuset i Stockholm klarar än så länge av belastningen av coronapatienter bättre än förväntat, och i söndags fanns 177 intensivvårdsplatser öppna på Karolinska, och de är redo att gå upp till 216 om det skulle behövas.

Andra ljuspunkter är att i de hårt drabbade länderna Italien och Spanien minskar nu antalet dödsfall.

I Sverige är det för tidigt att dra några slutsatser om utvecklingen. Men ett tydligt tecken på att vi svenskar i alla fall har ändrat vårt beteende för att minska smittspridningen, är att spridningen av vinterkräksjukan redan avstannat, vilket normalt inte brukar ske förrän framåt midsommar.

I skrivande stund verkar antalet dödsfall i Sverige klinga av. Om det beror på mindre rapportering under påskhelgen eller en faktiskt minskning lär utvisas under dagen idag.

På skärtorsdagen rapporterades 106 nya dödsfall. Sedan dess har den siffran gått stadigt ned. Ytterligare 12 personer har rapporterats avlidna i covid-19 det senaste dygnet, uppgav Folkhälsomyndigheten på påskdagen. Det var fem färre än vad som rapporterades in under föregående dygn och mönstret känns igen från de senaste dagarna. Men siffrorna bör tolkas försiktigt. Riktigt facit får vi inte förrän allt går tillbaks som vanligt igen efter påskhelgen.

Jag skrev också om effekten på miljön när det gäller luftföroreningar https://4health.se/minskade-luftfororeningar-raddar-fler-liv-an-corona-tar och dessutom verkar mer återvinnas nu i coronatider. T.ex. så har återvinningscentralerna i Helsingborg, Höganäs och Ängelholm fått dubbelt så många besökare sedan coronautbrottet.

Mer handfasta saker som du kan göra själv för att stärka dig mentalt https://4health.se/253-stark-din-mentala-halsa-konkreta-enkla-forklaringar-och-tips-med-markus-greus och fysiskt https://4health.se/252-corona-covid-19-vad-fungerar-mot-viruset

Mer: https://4health.se/?s=corona

https://coronavirus.jhu.edu/map.html

https://www.worldometers.info/coronavirus/#countries

https://www.svt.se/nyheter/inrikes/over-80-procent-overlever-intensivvarden

https://www.svt.se/nyheter/vetenskap/analys-fler-ljusglimtar-i-coronamorkret-1

https://www.dn.se/nyheter/sverige/battre-luft-och-mer-atervinning-sa-har-samhallet-forandrats-under-krisen/

https://www.svt.se/nyheter/lokalt/helsingborg/hogt-tryck-pa-atervinningen-i-coronatider

https://www.dn.se/nyheter/sverige/tegnell-om-dodstal-facit-kommer-pa-tisdag/

I forskning från Sverige (Karolinska) och Kanada ser man att det inte bara är lungor, utan även andra organ som direkt drabbas av sars-cov-2, det nya coronaviruset.

Forskningen visar bl.a. att det nya viruset använder samma inkörsport som det gamla SARS-viruset när det ska ta sig in i cellerna. ACE2 är en receptor i båda fallen, enligt mina tidigare inlägg https://4health.se/?s=corona.

Försöken visar också att det inte bara är lungvävnad som angrips. Viruset förökar sig också i bland annat njurar och blodkärl, vilket kan vara en förklaring till att vissa covid-19-patienter drabbas av skador på flera organ än lungorna.

Forskarna i nämnda studie tror också att en behandling som togs fram under sars-epidemin 2003 kan bli ett vapen mot det nya coronaviruset.

I kampen mot den befarade sars-epidemin 2003 upptäckte kanadensiska forskare att viruset binder till ACE2-molekylen på cellernas yta. Utan den inkörsporten kan det inte ta sig in i till exempel lungvävnad och börja massföröka sig. Forskarna framställde sedan ett läkemedel med hjälp av en kopia av ACE2, som drog till sig viruset och band fast det utan att det kunde börja göra kopior av sig självt inne i människokroppen. Detta kom aldrig till användning mot sars, eftersom utbrottet 2003 aldrig utvecklades till den pandemi man först befarade. I stället har den vidareutvecklats som en medicin mot lungsjukdom.

När det nya coronaviruset, som är närbesläktat med sars, började spridas tog forskningen fart igen. Forskarna har isolerat sars-cov-2 från en patient i Stockholm, och sedan testat läkemedlet på mänskliga celler i laboratorium.

KI-forskarna infekterade både celler och miniatyrkopior av mänskliga organ som odlats fram i provrör med sars-cov-2, och effekten blev densamma: Försöken visar att mängden virus i cellerna minskade med en faktor 1 000 till 5 000. Man hoppas på att det ska leda till ett läkemedel mot covid-19.

En första pilotstudie har redan genomförts på covid-19-patienter i Kina. Ett drygt 20-tal personer fick ACE-kopian injicerad i blodet. Redan inom ett par veckor ska läkemedlet testas på ytterligare 200 covid-19-patienter i Tyskland, Österrike och Danmark. Först därefter kan det bli frågan om att få det godkänt för användning i sjukvården. Om resultaten håller vad de lovar skulle det skulle kunna finnas på marknaden redan efter ett par månader.

https://www.svt.se/nyheter/vetenskap/sars-lakemedel-mot-corona-ger-positiva-resultat

Här är två spännande länkar som beskriver hur man kanske tänker och gör helt fel när det gäller intensivvården av de sjukaste i det nya coronaviruset.

Saxat från första länken där John Whyte, MD, intervjuar Cameron Kyle-Sidell, MD

“You’ve been talking a lot about the number of patients, the percentage of patients dying on ventilators.”

“Kyle-Sidell: When I initially started treating patients, I was under the impression, as most people were, that I was going to be treating acute respiratory distress syndrome (ARDS), similar in substance to AIDS, which I saw as a fellow. And as I start to treat these patients, I witnessed things that are just unusual. And I’m sure doctors around the country are experiencing this. In the past, we haven’t seen patients who are talking in full sentences and not complaining of overt shortness of breath, with saturations in the high 70s. It’s just not something we typically see when we’re intubating some of these patients. That is to say, when we’re putting a breathing tube in, they tend to drop their saturations very quickly; we see saturations going down to 20 to 30. Typically, one would expect some kind of reflexive response from the heart rate, which is to say that usually we see tachycardia, and if patients go too low, then we see bradycardia. These are things that we just weren’t seeing. I’ve seen literally a saturation of zero on a monitor, which is not something we ever want and something we actively try to avoid. And yet we saw it, and many of my colleagues have similarly seen saturations of 10 and 20. We try to put breathing tubes in to avoid this very situation. Now, these patients tend to desaturate extremely quickly, so these situations have occurred. Still, what we’re seeing—that there was no change in the heart rate—is just unusual. It’s just something that we are not used to seeing.”

“You get used to seeing certain patterns, and the patterns I was seeing did not make sense. This originally came to me when we had a patient who had hit what we call our trigger to put in a breathing tube, meaning she had displayed a level of hypoxia of low oxygen levels where we thought she would need a breathing tube. Most of the time, when patients hit that level of hypoxia, they’re in distress and they can barely talk; they can’t say complete sentences. She could do all of those and she did not want a breathing tube. So she asked that we put it in at the last minute possible. It was this perplexing clinical condition: When was I supposed to put the breathing tube in? When was the last minute possible? All the instincts as a physician—like looking to see if she tires out —none of those things occurred. It’s extremely perplexing. But I came to realize that this condition is nothing I’ve ever seen before. And so I started to read to try to figure it out, leaving aside the exact mechanism of how this disease is causing havoc on the body, but instead trying to figure out what the clinical syndrome looked like.”

“in my reading, I came upon decompression, pulmonary sickness, which is essentially the bends—when divers dive and come up too quickly—which seemed to mirror the clinical picture of these patients. And in discussions of other people, it came up that they do appear similar clinically. This is not to say that the pathophysiology underlying it is similar, but clinically they look a lot more like high-altitude sickness than they do pneumonia.”

“what Gattinoni was saying, which is that really what we’re seeing in ARDS are two different phenotypes: one in which the lungs display what you call high compliance, low elastance; and one in which they have low compliance and high elastance. To say it simply for people who are not pulmonologists, if you think of the lungs as a balloon, typically when people have ARDS or pneumonia, the balloon gets thicker. So not only do you lack oxygen, but the pressure and the work to blow up the balloon becomes greater. So one’s respiratory muscles become tired as they struggle to breathe. And patients need pressure. What Gattinoni is saying is that there are essentially two different phenotypes, one in which the balloon is thicker, which is a low-compliance disease. But in the beginning they display high compliance. Imagine if the balloon is not actually thicker but thinner, so they’d suffer from a lack of oxygen. But it is not that they suffer from too much work to blow up the balloon. As far as how we’re going to switch, we’re going to take our approach differently from the traditional ARDSnet protocol in that we are going to do an oxygen-first strategy: We’re going to leave the oxygen levels as high as possible and we’re going to try to use the lowest pressures possible to try to keep the oxygen levels high. That’s the approach we’re going to do, so long as the patients continue to display the physiology of a low elastance, high-compliance disease.”

“then you can accept the idea that perhaps all the studies on ARDS in the 2000s and 2010s, which were large, randomized, well-performed, well-funded studies, perhaps none of those patients in those studies had COVID-19 or something resembling it. It allows you to move away from a paradigm in which this disease may fit and, unfortunately, walk somewhat into the unknown.”

Saxat från andra länken (ingen studie, ingen läkare). “Covid-19 had us all fooled, but now we might have finally found its secret.”

“In the last 3–5 days, a mountain of anecdotal evidence has come out of NYC, Italy, Spain, etc. about COVID-19 and characteristics of patients who get seriously ill. It’s not only piling up but now leading to a general field-level consensus backed up by a few previously little-known studies that we’ve had it all wrong the whole time. “

“There is no ‘pneumonia’ nor ARDS. At least not the ARDS with established treatment protocols and procedures we’re familiar with. Ventilators are not only the wrong solution, but high pressure intubation can actually wind up causing more damage than without,”

“The past 48 hours or so have seen a huge revelation: COVID-19 causes prolonged and progressive hypoxia (starving your body of oxygen) by binding to the heme groups in hemoglobin in your red blood cells. People are simply desaturating (losing o2 in their blood), and that’s what eventually leads to organ failures that kill them, not any form of ARDS or pneumonia. All the damage to the lungs you see in CT scans are from the release of oxidative iron from the hemes, this overwhelms the natural defenses against pulmonary oxidative stress and causes that nice, always-bilateral ground glass opacity in the lungs. Patients returning for re-hospitalization days or weeks after recovery suffering from apparent delayed post-hypoxic leukoencephalopathy strengthen the notion COVID-19 patients are suffering from hypoxia despite no signs of respiratory ‘tire out’ or fatigue.“

“Your red blood cells carry oxygen from your lungs to all your organs and the rest of your body. Red blood cells can do this thanks to hemoglobin, which is a protein consisting of four “hemes”. Hemes have a special kind of iron ion, which is normally quite toxic in its free form, locked away in its center “

“When the red blood cell gets to the alveoli, or the little sacs in your lungs where all the gas exchange happens, that special little iron ion can flip between FE2+ and FE3+ states with electron exchange and bond to some oxygen, then it goes off on its little merry way to deliver o2 elsewhere.”

“Here’s where COVID-19 comes in. Its glycoproteins bond to the heme, and in doing so that special and toxic oxidative iron ion is “disassociated” (released). It’s basically let out of the cage and now freely roaming around on its own. This is bad for two reasons:

1) Without the iron ion, hemoglobin can no longer bind to oxygen. Once all the hemoglobin is impaired, the red blood cell is essentially turned into a Freightliner truck cab with no trailer and no ability to store its cargo.. it is useless and just running around with COVID-19 virus attached to its porphyrin. All these useless trucks running around not delivering oxygen is what starts to lead to desaturation, or watching the patient’s spo2 levels drop. It is INCORRECT to assume traditional ARDS and in doing so, you’re treating the WRONG DISEASE. Think of it a lot like carbon monoxide poisoning, in which CO is bound to the hemoglobin, making it unable to carry oxygen. In those cases, ventilators aren’t treating the root cause; the patient’s lungs aren’t ‘tiring out’, they’re pumping just fine. The red blood cells just can’t carry o2, end of story. Only in this case, unlike CO poisoning in which eventually the CO can break off, the affected hemoglobin is permanently stripped of its ability to carry o2 because it has lost its iron ion. The body compensates for this lack of o2 carrying capacity and deliveries by having your kidneys release hormones like erythropoietin, which tell your bone marrow factories to ramp up production on new red blood cells with freshly made and fully functioning hemoglobin. This is the reason you find elevated hemoglobin and decreased blood oxygen saturation as one of the 3 primary indicators of whether the shit is about to hit the fan for a particular patient or not.

2) That little iron ion, along with millions of its friends released from other hemes, are now floating through your blood freely. As I mentioned before, this type of iron ion is highly reactive and causes oxidative damage. It turns out that this happens to a limited extent naturally in our bodies and we have cleanup & defense mechanisms to keep the balance. The lungs, in particular, have 3 primary defenses to maintain “iron homeostasis”, 2 of which are in the alveoli, those little sacs in your lungs we talked about earlier. The first of the two are little macrophages that roam around and scavenge up any free radicals like this oxidative iron. The second is a lining on the walls (called the epithelial surface) which has a thin layer of fluid packed with high levels of antioxidant molecules.. things like abscorbic acid (AKA Vitamin C) among others. Well, this is usually good enough for naturally occurring rogue iron ions but with COVID-19 running rampant your body is now basically like a progressive state letting out all the prisoners out of the prisons… it’s just too much iron and it begins to overwhelm your lungs’ countermeasures, and thus begins the process of pulmonary oxidative stress. This leads to damage and inflammation, which leads to all that nasty stuff and damage you see in CT scans of COVID-19 patient lungs. Ever noticed how it’s always bilateral? (both lungs at the same time) Pneumonia rarely ever does that, but COVID-19 does… EVERY. SINGLE. TIME.”

“Once your body is now running out of control, with all your oxygen trucks running around without any freight, and tons of this toxic form of iron floating around in your bloodstream, other defenses kick in. While your lungs are busy with all this oxidative stress they can’t handle, and your organs are being starved of o2 without their constant stream of deliveries from red blood cell’s hemoglobin, and your liver is attempting to do its best to remove the iron and store it in its ‘iron vault’. Only its getting overwhelmed too. It’s starved for oxygen and fighting a losing battle from all your hemoglobin letting its iron free, and starts crying out “help, I’m taking damage!” by releasing an enzyme called alanine aminotransferase (ALT). BOOM, there is your second of 3 primary indicators of whether the shit is about to hit the fan for a particular patient or not.

Eventually, if the patient’s immune system doesn’t fight off the virus in time before their blood oxygen saturation drops too low, ventilator or no ventilator, organs start shutting down. No fuel, no work. The only way to even try to keep them going is max oxygen, even a hyperbaric chamber if one is available on 100% oxygen at multiple atmospheres of pressure, just to give what’s left of their functioning hemoglobin a chance to carry enough o2 to the organs and keep them alive. Yeah we don’t have nearly enough of those chambers, so some fresh red blood cells with normal hemoglobin in the form of a transfusion will have to do.

The core point being, treating patients with the iron ions stripped from their hemoglobin (rendering it abnormally nonfunctional) with ventilator intubation is futile, unless you’re just hoping the patient’s immune system will work its magic in time. The root of the illness needs to be addressed.”

“Best case scenario? Treatment regimen early, before symptoms progress too far. Hydroxychloroquine (more on that in a minute, I promise) with Azithromicin has shown fantastic, albeit critics keep mentioning ‘anecdotal’ to describe the mountain, promise and I’ll explain why it does so well next. “

“How does chloroquine work? Same way as it does for malaria. You see, malaria is this little parasite that enters the red blood cells and starts eating hemoglobin as its food source. The reason chloroquine works for malaria is the same reason it works for COVID-19 — while not fully understood, it is suspected to bind to DNA and interfere with the ability to work magic on hemoglobin. The same mechanism that stops malaria from getting its hands on hemoglobin and gobbling it up seems to do the same to COVID-19 (essentially little snippets of DNA in an envelope) from binding to it. On top of that, Hydroxychloroquine (an advanced descendant of regular old chloroquine) lowers the pH which can interfere with the replication of the virus. Again, while the full details are not known, the entire premise of this potentially ‘game changing’ treatment is to prevent hemoglobin from being interfered with, whether due to malaria or COVID-19.”

https://www.medscape.com/viewarticle/928156 och http://web.archive.org/web/20200405061401/https://medium.com/@agaiziunas/covid-19-had-us-all-fooled-but-now-we-might-have-finally-found-its-secret-91182386efcb NOTERA: detta är inte några studier, utan personer som uttrycker tankar och erfarenheter

Mer: https://4health.se/?s=corona

I coronatider vill vi göra allt för att stärka vårt immunförsvar. Men visste du att glutation, det ämne som är så viktigt för att ta hand om gifter och fria radikaler i våra kroppar, även kan stimulera vårt immunförsvar? (Mer om glutation: https://4health.se/?s=glutation )

Forskare från Luxemburg upptäckte 2017 hur glutation också stimulerar T-cellernas energimetabolism. T-celler är ju immunsystemets celler. Glutation instruerar T-celler att föröka sig och bekämpa inkräktare, och även att rensa upp det metaboliska avfall som skapas som biprodukt.

Tidigare troddes glutation bara konjugera toxiner (läs mer via taggen detox: https://4health.se/tag/detox ) och ta hand om fria radikaler / reaktiva syreföreningar (ROS).

T-celler avvärjer attack när de uttrycker Gclc-genen. Gclc-genen kodar ett protein som hjälper till att producera glutation.

Vår kropp måste hålla vårt immunsystem i en mycket balanserad jämvikt. T-celler befinner sig i ett tillstånd av energibesparing, ett slags “varningsläge”. T-celler vaknar upp i närvaro av främmande molekyler. Detta uppvaknande skapar ett överskott av ROS (fria radikaler) som i sin tur tas omhand av glutation. Denna aktivitet kan bara hända när Gclc-genen uttrycks.

I studien använde forskarna genetiskt modifierade möss där mössens T-celler saknade Gclc-genen. Därför kunde inte cellerna producera glutation. Hos dessa möss upptäckte man att kontrollen av virus är försämrad – möss som saknar Gclc-genen har en immunbrist. Studien avslöjade hur cellmetabolism och immunsystemet är mer komplicerat kopplade än tidigare trott.

“Scientists have discovered an unknown molecular mechanism promoting the activation of the human immune system. The team has been studying the glutathione molecule known for its role in cleaning the body from harmful metabolic wastes and revealed that glutathione also stimulates T cells energy metabolism. This discovery offers perspectives to develop new therapeutic strategies for targeting cancer and autoimmune diseases.”

Mer om Corona / COVID-19 : https://4health.se/?s=corona

https://www.sciencedaily.com/releases/2017/04/170418120923.htm

Immunförsvaret kan överreagera mot det nya coronaviruset och skapa så kallade cytokinstormar i kroppen. Cytokinstormarna angriper våra organ.

Immunförsvaret och cytokinstormar

Många som blir smittade av SARSCov-2 har milda symptom. Men för många av dem som ligger på intensivvården så är det inte själva viruset, utan immunförsvarets överdrivna reaktion på infektionen, som har lett till att de har blivit svårt sjuka.  

När immunförsvaret känner av en inkräktare i kroppen, som ett virus eller bakterie, producerar den proteiner som kallar för cytokiner. Cytokiner kan sägas vara immunförsvarets signalmolekyler. Dessa små proteiner skickar signaler till cellerna att agera mot inkräktaren. I normala fall stannar signalerna upp när viruset eller bakterien inte längre utgör ett hot för kroppen.

Men i vissa fall händer det motsatta. Det som då händer är att immunförsvarets reaktion på viruset övergår i en överdriven respons. Utan någon broms så fortsätter immunförsvaret att skicka ut cytokiner, som i ett försök att skydda kroppen i stället skadar den. Fenomet kallas för cytokinstorm. Symptomen kan bryta ut tio till tolv dagar efter det att man blivit sjuk i en virusinfektion, och märks av när patienten plötsligt blir mycket sjuk. Cytokinstormen påverkar blodcirkulationen och man får hög feber och Acute Respiratory Distress Syndrome, ARDS, vilket också är det som karaktäriserar covid-19.

Slutstadiet av virusinfektioner korrelerar ibland med påbörjan av en cytokinstorm. Denna okontrollerade frisättning av proinflammatoriska cytokiner från kroppens immunsystem involverar mer än 150 kända inflammatoriska mediatorer. Det är många faktorer som är involverade i utvecklingen av vad som börjar som ett friskt immunsvar, men sen går emot ett tillstånd av förstärkt cytokinproduktion.

Cytokiner signalerar till immunceller som T-celler och makrofager att ta sig till infektionsstället när immunsystemet kämpar mot en patogen (sjukdomsframkallande mikrob). Denna signalering aktiverar de här immuncellerna och stimulerar dem att producera mer cytokiner. Återkopplingsslingan hanteras normalt effektivt av kroppen, men i vissa fall blir processen oreglerad, med för många immunceller som aktiveras på en enda plats.

Cytokinstormar kan orsaka betydande skador på olika vävnader och organ. Om en cytokinstorm t.ex. inträffar i lungorna, kan makrofager och vätskor ansamlas, vilket så småningom hindrar luftvägarna.

Varför uppstår cytokinstormar

Detta överdrivna immunsvar förstår vi ännu inte helt, men kan tillskrivas att kroppen möter en ny, mycket patogen angripare.

Det finns flera teorier till varför immunsystemet får en sådan kraftig reaktion. Studier visar att personer som utsätts för en stor mängd virus riskerar att drabbas hårdare. Därför har läkare och sjuksköterskor utan tillräcklig skyddsutrustning blivit svårt sjuka, trots att de tidigare var friska.  

I regel far inte de som är unga och friska lika illa av COVID-19. Men just personer inom vården som exponerats för väldigt många virus svarar i större utsträckning med en sådan här kraftig reaktion som till och med leder till att de kan dö.  

Behandla en cytokinstorm

Behandlingar mot cytokinstormen fokuserar på att dämpa immunförsvarets aktivitet och det pågår just nu studier om hur behandlingen ska gå till vid just covid-19. I en studie har man behandlat en coronapatient i Kina med läkemedelet Tocilizumab, som har en lugnande effekt av immunsystemet. Det visade sig att läkemedlet hade positiva effekter på den virussmittade patienten.

Det finns även andra sätt att behandla cytokinstormarna. I Sverige har man gett patienter med influensa bland annat cellgifter och kortison. Men immunförsvaret är ett komplext och kraftfullt system, och därför är det viktigt förstå vad som krävs för åtgärder vid just covid-19. Det pågår försök i Italien, Kina och andra länder där man försöker förstå vad den optimala måltavlan och tidpunkten är vid covid-19. Man vill kunna styra immunförsvaret så att skyddet mot virusinfektionen behålls utan att man får den överreaktion som kan bli livsfarlig.

Örtpreparat mot cytokinstormar

En studie tittade på hur kurkumin från gurkmeja påverkar cytokinfrisättning och cytokinstorm. Artikeln rapporterade om effekterna av kurkumin på cytokinuttryck i en musmodell av virusinducerat ARDS (acute respiratory distress syndrome). Författarna konkluderade att “Curcumin blocks cytokine release, most importantly the key pro-inflammatory cytokines, interleukin-1, interleukin-6 and tumor necrosis factor-α. The suppression of cytokine release by curcumin correlates with clinical improvement in experimental models of disease conditions where a cytokine storm plays a significant role in mortality.” Forskningsteamet drog slutsatsen att kurkumin kan vara av nytta för dem som upplever cytokinstormar. I det här fallet fokuserade man på Cytokinstormar som följd av Ebola-

En utmaning när man använder kurkumin är att det absorberas dåligt ur tarmen. Studieförfattarna föreslår användning av kurkumin intravenöst.

Kurkumin var också ett av de ämnen som, in vitro, hade effekt mot SARS-COV2-viruset enligt mitt tidigare inlägg https://4health.se/studie-fytonaringsamnena-i-mat-som-skyddar-mot-corona

Kurkumin och ACE2

Men det finns också indikationer på att kurkumin skulle kunna ha en oönskad effekt på COVID-19 eftersom det kan stimulera ACE2. Jag skrev om ACE2 här https://4health.se/coronamyter-naturliga-preparat-och-tillskott-fungerar-de men i korthet så handlar det om att ACE2 (angiotensin-converting enzyme) är Coronavirusets inkörsport in i våra celler. En del immunstimulerande preparat kan stimulera just ACE2 eller ACE2-receptorer. Det finns alltså de som tror att ämnen som stimulerar ACE2, inklusive kurkumin/gurkmeja, också kan öka risken att infekteras av det nya coronaviruset. Men det vetenskapliga stödet för att så skulle var fallet är inte tillräckligt starkt. Bl.a. eftersom studier som visat att kurkumin ökar ACE2 är gjorda på hjärtat, och inte på lungorna.

Det vi däremot har mer forskning på är hur gurkmeja, ingefära mfl växter både kan ha en immunförstärkande och antiinflammatorisk effekt, och vara effektiva mot patogener.

Återigen, kanske ska man göra det här med måtta. Att fortsätta äta gurkmeja för dess olika hälsoeffekter och eventuella effekt mot det nya coronaviruset, men undvika stora mängder extraherad kurkumin. Om man däremot insjuknar i COVID-19 kan kurkumin potentiellt börja användas efter ett antal dagar med symtom, när immunförsvaret sannolikt har själva viruset under kontroll, men vi vill motverka att en cytokinstorm tar vid. Och detta sista är såklart bara funderingar från min sida. Vad tror du? Kommentera gärna.

Uppdatering: passande nog har Chris Masterjohn skrivit än mer ingående om Cytokinstormar precis idag. Och om Cytokinstormar i förhållande till att använda fläder Läs här: https://chrismasterjohnphd.com/covid-19/2020/04/06/could-elderberry-cause-a-cytokine-storm-in-covid-19-extremely-unlikely

Mer: https://4health.se/?s=kurkumin och https://4health.se/?s=corona

http://iv.iiarjournals.org/content/29/1/1.full

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3294426/

http://news.unair.ac.id/en/2020/03/20/studying-the-benefits-of-turmeric-and-curcuma-unair-expert-they-improve-immune-system/

https://www.svt.se/nyheter/vetenskap/covid-19-darfor-blir-aven-unga-och-friska-allvarligt-sjuka

Här är en bra sida från Emergency Medicine News som ska hållas uppdaterad ang behandling av det nya Coronaviruset (riktad till vårdpersonal): https://journals.lww.com/em-news/blog/BreakingNews/pages/post.aspx?PostID=508

Uppdatering: Läs dock även detta https://4health.se/behandlas-de-sjukaste-covid-19-patienterna-fel

Uppdatering: Här är IFM:s (The Institute for Functional Medicine) rekommendationer runt COVID-19 https://www.ifm.org/news-insights/the-functional-medicine-approach-to-covid-19-virus-specific-nutraceutical-and-botanical-agents/
Deras särskilda råd riktade mot patienter:
https://www.ifm.org/news-insights/top-6-strategies-managing-stress-around-infectious-disease/ och https://www.ifm.org/news-insights/good-sleep-hygiene-may-help-protect-infectious-diseases/

Imorgon publicerar jag ett längre spännande inlägg om så kallade Cytokinstormar, en av de saker som kan inträffa i kroppen och som kan göra det nya coronaviruset farligt. Där tar jag också upp vad som potentiellt kan hjälpa mot cytokinstorm. Hörs imorgon!

https://4health.se/?s=corona