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Jag har tagit upp hur man kan använda bl.a. glutation och NAC om man drabbas av Covid-19. Både för att aktivera immunförsvaret (rätt delar) och för att dämpa de besvär som kan uppstå tex i form av cytokinstormar. En ny vetenskaplig sammanställning betonar just rollen i att dämpa inflammationen i sjukdomens senare skede. Det är just denna överdrivna immunrespons som gör att Covid-19 kan bli farligt.

Saxat ur artikeln:

“The Role of Glutathione in Protecting against the Severe Inflammatory Response Triggered by COVID-19

The novel COVID-19 pandemic is affecting the world’s population differently: mostly in the presence of conditions such as aging, diabetes and hypertension the virus triggers a lethal cytokine storm and patients die from acute respiratory distress syndrome, whereas in many cases the disease has a mild or even asymptomatic progression. A common denominator in all conditions associated with COVID-19 appears to be the impaired redox homeostasis responsible for reactive oxygen species (ROS) accumulation; therefore, levels of glutathione (GSH), the key anti-oxidant guardian in all tissues, could be critical in extinguishing the exacerbated inflammation that triggers organ failure in COVID-19. The present review provides a biochemical investigation of the mechanisms leading to deadly inflammation in severe COVID-19, counterbalanced by GSH. The pathways competing for GSH are described to illustrate the events concurring to cause a depletion of endogenous GSH stocks. Drawing on evidence from literature that demonstrates the reduced levels of GSH in the main conditions clinically associated with severe disease, we highlight the relevance of restoring GSH levels in the attempt to protect the most vulnerable subjects from severe symptoms of COVID-19. Finally, we discuss the current data about the feasibility of increasing GSH levels, which could be used to prevent and subdue the disease.”

“Among the many functions of GSH, some are worthy of mention in relation to their impact on the exacerbated inflammation taking place in COVID-19 and in relation to the symptoms developed in the disease.

1. GSH protects cells by neutralizing (i.e., reducing) ROS, which are key signaling molecules that play an important role in the progression of inflammatory disorders. The relationship between ROS production and proinflammatory cytokine activation is well established [22]. An enhanced ROS generation by polymorphonuclear neutrophils at the site of inflammation causes endothelial dysfunction and tissue injury [23].

2. The conjugation of GSH to xenobiotics is particularly abundant; glutathione S-transferase enzymes catalyze GSH conjugation to lipophilic xenobiotics, facilitating the excretion or further metabolism of many drugs. The conjugation process is illustrated by the metabolism of N-acetyl-p-benzoquinone imine (NAPQI). NAPQI is a reactive metabolite formed by the action of cytochrome P450 on paracetamol (acetaminophen). Glutathione conjugates to NAPQI and the resulting product is excreted [24].

3. Many enzymes use GSH as a cofactor or substrate. For example reactions requiring GSH as a key cofactor are catalyzed by the prostaglandin H synthase, the rate-limiting enzyme in the production of prostaglandins and thromboxane [25], which are essential regulators of vascular function. Moreover, the enzyme leukotriene C(4) synthase conjugates LTA(4) with GSH to form the leukotriene LTC(4), the parent compound of the cysteinyl leukotrienes [26]; these molecules are potent mediators of airway narrowing.

4. GSH is used to synthesize S-nitrosoglutathione (GSNO), an endogenous S-nitrosothiol that plays a critical role in nitric oxide (NO) signaling and is a source of bioavailable NO. The generation of GSNO can serve as a stable NO pool which can properly transduce NO signaling [27]. NO produced by nitric oxide synthase eNOS and nNOS, in the presence of GSH, can effectively modulate vessels and neuronal functions, regulating the blood flow according to the local calcium influx.

As a consequence of the competition between these and many other GSH-consuming pathways, on one hand, the raging inflammation and oxidative stress triggered by the viral infection steals GSH from core functions such as NO-dependent vasodilatation; on the other hand, when other biochemical pathways are consuming GSH, the patient is not protected from an inflammation that can prove fatal.”

“ACE expression and activity are modulated by glutathione; in fact, the oxidized form GSSG shows an activating effect on ACE activity, whereas the reduced GSH provides an inhibitory effect [28]. Finally, the boosted ANGII production can be due to decreased ACE2 expression and activity; this is the case with coronavirus infection, which recognizes ACE2 as its extracellular binding site [29]. Compared to SARS-COV-1, SARS-CoV-2 has about 4-fold higher affinity for ACE2 [30]. Infection of cells by SARS viruses that bind ACE2 results in two effects: inhibition of ACE2 activity and decrease of ACE2 expression in infected cells”

“By reducing ROS production, GSH inhibits NF-kB activation and consequently keeps the cytokine storm under control.”

Tidigare om glutation bl.a. i podcastavsnitt om Covid-19 https://4health.se/259-dr-cecilia-furst-covid-19 och här https://4health.se/sa-kan-glutation-boosta-ditt-immunforsvar och här https://4health.se/?s=glutation och här https://4health.se/?s=corona

https://www.mdpi.com/2076-3921/9/7/624

Apropå den svenska modellen och T-cellssvar (som jag skrev om igår https://4health.se/t-cellsskydd-mot-coronavirus-sa-funkar-det Missa inte den!! En så funkar det-text ) Här är ett intressant inlägg från en svensk läkare (se länk nedan för hela hans text). Den svenska modellen har ju blivit smutskastad på många håll i världen för att vi haft höga dödstal. Men nu kommer ju andra vågen i alla länder som varit nedslängda, medan Sverige verkar vara på väg ut ur krisen.

Igår kväll rapporterades t.ex. från Folkhälsomyndigheten att inga nya dödsfall till följd av covid-19 har inrapporterats i Region Stockholm, vilket innebär att det har gått en vecka sedan det senaste dödsfallet i Stockholm.

Vi ska nog inte säga att faran är över, men det går ju helt klart åt rätt håll – sen får vi se om kyla för med sig en andra våg även i Sverige eller om vi faktiskt börjar få flockimmunitet pga både T-cellssvar och antikroppar.

Så här skriver läkaren Sebastian Rushworth:

“How bad is covid really? (A Swedish doctor’s perspective)

“As many people know, Sweden is perhaps the country that has taken the most relaxed attitude of any towards the covid pandemic. Unlike other countries, Sweden never went in to complete lockdown. Non-essential businesses have remained open, people have continued to go to cafés and restaurants, children have remained in school, and very few people have bothered with face masks in public.

Covid hit Stockholm like a storm in mid-March. One day I was seeing people with appendicitis and kidney stones, the usual things you see in the emergency room. The next day all those patients were gone and the only thing coming in to the hospital was covid. Practically everyone who was tested had covid, regardless of what the presenting symtom was. People came in with a nose bleed and they had covid. They came in with stomach pain and they had covid.

Then, after a few months, all the covid patients disappeared. It is now four months since the start of the pandemic, and I haven’t seen a single covid patient in over a month. When I do test someone because they have a cough or a fever, the test invariably comes back negative. At the peak three months back, a hundred people were dying a day of covid in Sweden, a country with a population of ten million. We are now down to around five people dying per day in the whole country, and that number continues to drop. Since people generally die around three weeks after infection, that means virtually no-one is getting infected any more. If we assume around 0.5 percent of those infected die (which I think is very generous, more on that later), then that means that three weeks back 1,000 people were getting infected per day in the whole country, which works out to a daily risk per person of getting infected of 1 in 10,000, which is miniscule. And remember, the risk of dying is at the very most 1 in 200 if you actually do get infected. And that was three weeks ago. Basically, covid is in all practical senses over and done with in Sweden. After four months.

In total covid has killed under 6,000 people in a country of ten million. A country with an annual death rate of around 100,000 people. Considering that 70% of those who have died of covid are over 80 years old, quite a few of those 6,000 would have died this year anyway. That makes covid a mere blip in terms of its effect on mortality.

That is why it is nonsensical to compare covid to other major pandemics, like the 1918 pandemic that killed tens of millions of people. Covid will never even come close to those numbers. And yet many countries have shut down their entire economies, stopped children going to school, and made large portions of their population unemployed in order to deal with this disease.

The media have been proclaiming that only a small percentage of the population have antibodies, and therefore it is impossible that herd immunity has developed. Well, if herd immunity hasn’t developed, where are all the sick people? Why has the rate of infection dropped so precipitously? Considering that most people in Sweden are leading their lives normally now, not socially distancing, not wearing masks, there should still be high rates of infection.

The reason we test for antibodies is because it is easy and cheap. Antibodies are in fact not the body’s main defence against virus infections. T-cells are. But T-cells are harder to measure than antibodies, so we don’t really do it clinically. It is quite possible to have T-cells that are specific for covid and thereby make you immune to the disease, without having any antibodies. Personally, I think this is what has happened. Everybody who works in the emergency room where I work has had the antibody test. Very few actually have antibodies. This is in spite of being exposed to huge numbers of infected people, including at the beginning of the pandemic, before we realized how widespread covid was, when no-one was wearing protective equipment.

I am not denying that covid is awful for the people who do get really sick or for the families of the people who die, just as it is awful for the families of people who die of cancer, or influenza, or an opioid overdose. But the size of the response in most of the world (not including Sweden) has been totally disproportionate to the size of the threat.

Sweden ripped the metaphorical band-aid off quickly and got the epidemic over and done with in a short amount of time, while the rest of the world has chosen to try to peel the band-aid off slowly. At present that means Sweden has one of the highest total death rates in the world. But covid is over in Sweden. People have gone back to their normal lives and barely anyone is getting infected any more. I am willing to bet that the countries that have shut down completely will see rates spike when they open up. If that is the case, then there won’t have been any point in shutting down in the first place, because all those countries are going to end up with the same number of dead at the end of the day anyway. Shutting down completely in order to decrease the total number of deaths only makes sense if you are willing to stay shut down until a vaccine is available. That could take years. No country is willing to wait that long.

Covid has at present killed less than 6000 in Sweden. It is very unlikely that the number of dead will go above 7,000. An average influenza year in Sweden, 700 people die of influenza. Does that mean covid is ten times worse than influenza? No, because influenza has been around for centuries while covid is completely new. In an average influenza year most people already have some level of immunity because they’ve been infected with a similar strain previously, or because they’re vaccinated. So it is quite possible, in fact likely, that the case fatality rate for covid is the same as for influenza, or only slightly higher, and the entire difference we have seen is due to the complete lack of any immunity in the population at the start of this pandemic. 

This conclusion makes sense of the Swedish fatality numbers – if we’ve reached a point where there is hardly any active infection going on any more in Sweden in spite of the fact that there is barely any social distancing happening then that means at least 50% of the population has been infected already and have developed immunity, which is five million people. This number is perfectly reasonable if we assume a reproductive number for the virus of two: If each person infects two new, with a five day period between being infected and infecting others, and you start out with just one infected person in the country, then you will reach a point where several million are infected in just four months. If only 6000 are dead out of five million infected, that works out to a case fatality rate of 0.12 percent, roughly the same as regular old influenza, which no-one is the least bit frightened of, and which we don’t shut down our societies for.”

Läs hela hans text här. https://sebastianrushworth.com/2020/08/04/how-bad-is-covid-really-a-swedish-doctors-perspective/

Mer via https://4health.se/?s=corona

Här beskrivs hur det kommer sig att personer med ohälsa, och särskilt metabolt syndrom, lättare insjuknar i allvarlig Covid-19.

Jeffrey Bland, känd som grundaren av funktionsmedicin, har skrivit en lång intressant artikel om Covid-19 (se länk nedan). Jag kommer särskilt att lyfta ut en intressant mekanism han tar upp i artikeln, men läs gärna hela via länken.

ACE2 som jag skrivit om tidigare (https://4health.se/?s=ACE2) är ju det nya coronavirusets inkörsport i cellerna. Det visar sig att viruset lättare binder till ACE2 i närvaro av inflammation.

CoV-SARS-2-viruset har proteiner på sin yta som ser ut som taggar. Det är dessa som gör att det kan binda in till ACE-2-receptorer, och även dessa som skiljer det nya coronaviruset från andra Coronavirus.

Taggarna på viruset har hög affinitet till ett enzym som kallas furin (high affinity furin binding sites). Furin är ett enzym i blodet som ska aktivera särskilda proteiner.

Det nya coronaviruset kan kidnappa furin, vilket tillåter det att binda till ACE2-receptorerna enklare och bättre, och underlättar för viruset att ta sig in i våra celler.

Furinnivåerna i vårt blod spelar alltså stor roll för hur lätt vi infekteras, och hur mycket vi insjuknar.

Regleringen av furin påverkas bl.a. av immunsystemet och inflammation. Vid inflammation och höga nivåer av triglycerider i blodet så är furin mer känsligt för att kidnappas av viruset (notera att lågkolhydratkost vanligen ger mycket låga nivåer av triglycerider, mer i avsnitt 139 och 140 av podcasten). Detta kan troligen bidra till det som kallas “comorbidity”, dvs att personer med inflammatoriska sjukdomstillstånd, i synnerhet metabola syndrom (högt blodtryck, diabetes, hjärt- och kärlsjukdom, övervikt osv), har ökad dödlighet i Covid-19.

Man har sett i studier att personer med metabolt syndrom har avvikande nivåer av furin. En studie (som bl.a. utförts av forskare i Lund) visade att personer med metabola syndrom och diabetes har förhöjda nivåer av furin i blodet. Och man har i andra studier sett att de gener som styr furinproduktion påverkas av metabola syndrom. Man vet också att personer med inflammatoriska autoimmuna sjukdomar har förhöjda nivåer av furin.

Furin verkar alltså vara en länk mellan metabolt syndrom, inflammation och Covid-19-komplikationer.

Saxat ur artikeln

Först bakgrund om Covid-19 och metabolt syndrom:

Why do some people fare so poorly while others have only mild symptoms? The answer may be tied to the functional status of an individual’s immune system.

how comorbidities (preexisting health conditions) might increase the risk for COVID-19 complications. The researchers noted that older age, hypertension, obesity, and diabetes were all associated with increased disease severity.

Certain chronic conditions, including the comorbidities mentioned above, result in altered immune system function, which can include unhealthy forms of inflammation.

As it turns out, there is a condition called metabolic syndrome which is characterized by altered immune function. In fact, it overlaps with the comorbidities that contribute to COVID-19 severity, and has been steadily rising in frequency over the last several decades. What happens when the world’s most prevalent non-communicable health condition and a highly infectious viral disease collide? We find ourselves in our new reality: a COVID-19 pandemic within a pandemic of metabolic syndrome.

I believe these comorbidities result from the complex interaction of individual genetics, lifestyle, environment, diet, and the social determinants of disease.

all of the comorbidities linked to both metabolic syndrome and COVID-19 severity are associated with altered immune function and a chronic state of inflammation.[13] “Inflammaging” is a term that has come to be used as a descriptor for chronic inflammation related to aging or chronic non-communicable conditions such as hypertension, insulin resistance, and obesity.

Technically, metabolic syndrome is not a disease. It is probably better described as a state of lowered resilience to disease, as is evidenced by the number of associated comorbidities. People with metabolic syndrome are at increased risk to both non-communicable and infectious diseases such as COVID-19.

Och så om den fysiologiska mekanismen:

COVID-19 is a new virus within the coronavirus family. As we all know now, it has a very high infection rate. Additionally, COVID-19 has some unusual infectivity features: it can be transmitted by asymptomatic individuals, plus the severity and clinical manifestations of the infection can vary widely (from mild to life-threatening). Seemingly, all body systems can be impacted by a COVID-19 infection; serious cases of respiratory, cardiovascular, immunological, kidney and liver, gastrointestinal, and neurological crises have all been reported.[21] In the organ systems affected by COVID-19, cells have been found to express the angiotensin-converting enzyme 2 (ACE2) receptor. The ACE2 receptor is thought to represent a target for the virus which allows it to bind to and enter our cells.[22] Recent studies show that the virus binds to the ACE2 receptor more easily in the presence of inflammation.[23]

The COVID-19 virus has spike-like proteins on its surface. These give the virus the unique ability to bind tightly to the ACE2 receptors. The spike-like proteins are also what differentiate the COVID-19 virus from other coronaviruses. These spikes have what are called high affinity furin binding sites (furin is an enzyme in human blood that activates specific proteins).[24] Researchers believe a slight change in the genetic architecture of the virus resulted in a modification at the furin binding site in the spike proteins. This is what makes COVID-19 such a formidable foe. How? It enables the virus to hijack furin, which allows it to attach to the ACE2 receptors on tissues more readily and facilitate penetration into cells. Given that so many tissues express the ACE2 receptor, this mutation and sequence of events makes COVID-19 uniquely more infective than other coronaviruses.[25]

Regulation of furin levels in the blood is influenced, in part, by the immune system and inflammation. When cholesterol in the blood is elevated, furin is more vulnerable to being hijacked by the virus, and there is a greater opportunity for COVID-19 to convert to its more infective form. It is speculated that this can contribute to the comorbidity-related priming of COVID-19 in people with elevated cholesterol who are at risk to cardiovascular problems.[26] The ability of this virus to impact furin and increase infectivity is unique to COVID-19 (SARS-COV-2); it does not occur (to the same extent) with other coronaviruses, including SARS-COV-1.

Furin belongs to a family of nine proteins that are called proprotein convertases (PCSKs). The function of these proteins is to regulate various biochemical processes, both in times of good health and when a disease state is present. Furin is produced by a number of different cell types, including some within immune cells.[27] In people who have comorbidities that are associated with metabolic syndrome (hypertension, obesity, elevated triglycerides, impaired insulin sensitivity, and inflammation), furin levels have been found to be abnormal.[28],[29] Interestingly, David Harrison, MD, who leads a research team at Vanderbilt University School of Medicine, published work in 2015 indicating that hypertension is related to inflammation derived from an activated immune system.[30]

In 2018, researchers at the Department of Clinical Sciences at Lund University in Sweden and the School of Pharmacology at Helsinki University in Finland collaboratively reported the results of a study involving 4678 individuals with metabolic syndrome and diabetes that revealed elevated levels of furin in the blood.[31] Prior to that, a group representing several clinical and academic institutions in Japan had reported that certain variations in the genes that control furin production were related to metabolic syndrome.[32] This work suggests that the influence of furin on the comorbidities associated with COVID-19 may have a genetic connection. Finally, it’s well established that furin levels are elevated in people with inflammatory autoimmune disorders.[33] In sum, this research shows furin may be a key link between metabolic syndrome, inflammation, and COVID-19 complications.

Summerat:

Let’s now draw a straight line between the non-infectious pandemic of metabolic syndrome pandemic and the infectious pandemic of COVID-19. Metabolic syndrome dramatically increases our risk of developing comorbidities like hypertension and diabetes. These in turn predispose us to contracting COVID-19 and for developing more severe systems after infection. This is likely due to the chronic inflammatory state (altered immunity) associated with metabolic syndrome. Furthermore, the comorbidities associated with metabolic syndrome may compromise our immune function through increased levels of furin in the blood. Let’s put this together. When an individual with metabolic syndrome is exposed to COVID-19, the virus gets the benefit of a compromised immune system and extra furin to facilitate binding to our cells. This is a mechanistic explanation of the situation that the world now finds itself in: a pandemic (COVID-19) within a pandemic (metabolic syndrome).

Om lösningen:

Food as medicine? A recent article suggests that it’s a valid concept to consider for the prevention of coronavirus disease.[38]Emerging evidence even shows that dietary intervention could potentially reduce the probability of infection with COVID-19 or the severity of symptoms in infected individuals.[39] Recently, a multinational research consortium published work indicating that a diet associated with lowering the incidence of metabolic syndrome both improves immune system function and reduces inflammation, which — as already noted — are important considerations in minimizing the severity of COVID-19.[40]

Vegetables and fruits contain a class of nutrients called phytochemicals that play important dietary roles in reducing the comorbidities associated with metabolic syndrome.[41] Certain phytochemicals, such as the flavonoids quercetin and luteolin, have been found to bind to the ACE2 receptor on COVID-19, which can potentially help to protect against infection.[42],[43] A recent study evaluated how quercetin and vitamin D may contribute to the mitigation of COVID-19 through their impact on immune system function and the reduction of chronic inflammation.[44] It is clear that improvement in the lifestyle, environmental, and dietary factors associated with the comorbidities that are linked to both metabolic syndrome and COVID-19 can have a positive impact on enhancing immunity.[45] Studies have shown that improved physical fitness, reduction in obesity, and increased quality of sleep can all positively influence immunity and reduce the severity of viral infections like COVID-19.[46],[47],[48]

In a sense, COVID-19 represents an alarm bell — “a tocsin to our aging and unfit society,”

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

https://medium.com/@jeffreyblandphd/covid-19-a-pandemic-within-a-pandemic