3083 replies to this topic

[ta5]

Apigenin was mentioned a couple times, for inhibiting IL-6 and inhibiting the COVID-19 main protease (whatever that means).

Also, this:

 

Flavonoids: promising natural compounds against viral infections.

Zakaryan H, Arabyan E, Oo A, Zandi K.

Arch Virol. 2017 Sep;162(9):2539-2551. doi: 10.1007/s00705-017-3417-y. Epub 2017 May 25. Review.

PMID: 2854738

The antiviral activity of flavones is known from the 1990s, when it was showed that the simultaneous application of apigenin with acyclovir resulted in an enhanced antiviral effect on herpes simplex virus types 1 and 2 (HSV-1 and HSV-2) in cell culture [92]. Apigenin is most commonly isolated in abundance from the family Asteraceae. The organic and aqueous extracts from Asteraceae plants with apigenin as a major compound were found to be active against HSV-1, poliovirus type 2 and hepatitis C virus (HCV) [85, 127]. Apigenin isolated from sweet basil (Ocimum basilicum) showed a potent antiviral activity against adenoviruses (ADV) and hepatitis B virus in vitro [17]. Besides these DNA viruses, apigenin was found to exert antiviral effect against African swine fever virus (ASFV), by suppressing the viral protein synthesis and reducing the ASFV yield by 3 log [46]. Apigenin is also active against RNA viruses. For picronaviruses, it has been shown that apigenin is able to inhibit viral protein synthesis through suppressing viral IRES activity [82, 107]. Furthermore, apigenin affects enterovirus-71 (EV71) translation by disrupting viral RNA association with trans-acting factors regulating EV71 translation [153]. Shibata et al. [115] showed that apigenin has antiviral effect on HCV through the reduction of mature microRNA122, a liver-specific microRNA which positively regulates HCV replication.

 

Dried Parsely has 1.7% to 13.5% Apigenin.

Edited by ta5, 12 April 2020 - 01:55 AM.

[lancebr]

https://devinenews.c...seeing-results/

 

Medina County Texas Doctor Richard Neel announced this week that he is using high doses of Melatonin and Vitamin C to treat two patients for COVID-19 (both confirmed COVID cases), and it’s working.

He believes that high doses of Vitamin C and Melatonin (a powerful antitoxin and antioxidant) can treat the COVID-19 virus that has resulted in a global pandemic.

“I had one patient’s test come back positive this morning, (Monday, April 6). I was pretty sure he was going to be positive for COVID, so I started the patient on melatonin and vitamin C last week and he was much better within 24 hours,” Dr. Neel stated. “This patient in his late 40’s had several days of really high fever that wouldn’t break with Tylenol, a dry non-productive cough, worsening shortness of breath, and loss of taste and smell.”

“His symptoms started on a Sunday, and he talked to me on Wednesday afternoon. He began treatment that night, taking a high dose of melatonin around 8 pm, and he was fever-free when he woke up the next morning,” Neel said. “Then he began taking a high dose of Vitamin C as well as melatonin divided in 4 doses and continued improving, getting his sense of smell and taste back, and his cough got better and better on the 3rd and 4th day.”

“I have another patient who had strong direct exposure to COVID and developed symptoms. They began treatment of high doses of melatonin and Vitamin C and also started doing better in less than 24 hours,” Neel said. “This patient had called me the same day that symptoms began. She had 101.7 fever, body aches, cough increasing, said it really hit her hard. She took melatonin at 6:30, 8:30, and 10:30 pm and was fever free by the morning, and other symptoms continued improving to the point that she was almost totally well by the 3rd day.”

“Dosages are based on symptoms and age. I wish I could give a blanket recommendation on dosage, but I just can’t. So far, dosage of these patients has been ranging from 40 to 80 mg of melatonin divided in 4 doses during the day. Vitamin C dosage has been from 500 mg to 1000 mg 4 times per day. I want to be clear these high doses are only appropriate for people who actually have the virus, and you need to talk to a doctor first.”

Low doses 1 mg, 3 mg is more appropriate for preventative measures.

“If you want to take Melatonin and Vitamin C as a prophylaxis, a low dose might be helpful as a preventative measure,” Neel said. “I do have colleagues who believe that taking 5 mg daily is a good thing to do.”

 

With the recommendation to take 1,3 or 5 mg of melatonin daily as a prophylaxis would there be a concern about it shutting

down your body's own production of melatonin?

 

Is it true that taking too much melatonin or for too long of a period may permanently shut down your body's own production

or you become dependent on it?

 

Also, concerning this study would the relation of melatonin to the ACE be helpful or harmful with this virus?

 

"Melatonin and melatonin-mimicking agents inhibit B2 bradykinin receptors (B2Rs), as well as the dimerization of

angiotensin converting enzyme I (ACE) to inhibit ACE activity, thereby lowering blood pressure [30]. Melatonin and

its agonist stabilize ACE-B2R dimers [31] and angiotensin type II receptors (AT2R)."

 

https://www.tandfonl...12.2017.1315864

Edited by lancebr, 12 April 2020 - 04:25 AM.

[Kalliste]

With the recommendation to take 1,3 or 5 mg of melatonin daily as a prophylaxis would there be a concern about it shutting

down your body's own production of melatonin?

 

Is it true that taking too much melatonin or for too long of a period may permanently shut down your body's own production

or you become dependent on it?

 

Also, concerning this study would the relation of melatonin to the ACE be helpful or harmful with this virus?

 

"Melatonin and melatonin-mimicking agents inhibit B2 bradykinin receptors (B2Rs), as well as the dimerization of

angiotensin converting enzyme I (ACE) to inhibit ACE activity, thereby lowering blood pressure [30]. Melatonin and

its agonist stabilize ACE-B2R dimers [31] and angiotensin type II receptors (AT2R)."

 

https://www.tandfonl...12.2017.1315864

 

You don't get addicted to melatonin, and if I had Covid symtoms some addiction would be the least of my concerns.
If you want to dive deep then I'm not exactly qualified. There are lengthy melatonin threads on this forum.

However my memory of browsing many melatonin papers is that there rarely seem to be any adverse effects.

It often shows up with regards to viral and bacterial infections, influenza and cytokine storms. A part of the storm is the surge in intra-mitochondrial superoxide production. Melatonin goes in there and changes... something. Quenches superoxide or regulates something like what you mentioned. 

 

Most concerns seems to be theoretical.

I know Jack Kruse is a huge enemy of oral melatonin but even he went out and stated it could be used for Covid.

 

I used melatonin for sleep for many years, I NEVER noticed any feedback/feedforward problems. And I do notice those problems very acutely with other substances, e.g. if I try to stay away from coffee one day that day will be remarkably different. If I try to get drunk several days in a row my body rapidly adapts for that. If I stop MitoQ for more than a week my endurance and willingness to exercise changes profoundly.

But if I stop melatonin for a day or a week I barely even register. Sleep is virtually unchanged

Then I go back to it out of theoretical anti-cancer reasons: it's a bit deeper with my combo of 3mg Natrol melatonin/500mg aspirin an hour before bed.

 

 

Melatonin alleviates acute lung injury through inhibiting the NLRP3 inflammasome
Abstract

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are clinically severe respiratory disorders, and there are currently no Food and Drug Administration–approved drug therapies. Melatonin is a well‐known anti‐inflammatory molecule, which has proven to be effective in ALI induced by many conditions. Emerging studies suggest that the NLRP3 inflammasome plays a critical role during ALI. How melatonin directly blocks activation of the NLRP3 inflammasome in ALI remains unclear. In this study, using an LPS‐induced ALI mouse model, we found intratracheal (i.t.) administration of melatonin markedly reduced the pulmonary injury and decreased the infiltration of macrophages and neutrophils into lung. During ALI, the NLRP3 inflammasome is significantly activated with a large amount of IL‐1β and the activated caspase‐1 occurring in the lung. Melatonin inhibits the activation of the NLRP3 inflammasome by both suppressing the release of extracellular histones and directly blocking histone‐induced NLRP3 inflammasome activation. Notably, i.t. route of melatonin administration opens a more efficient therapeutic approach for treating ALI.

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[resveratrol_guy]

looks like avoiding ending up on a ventilator is the key:

 

Researchers in Wuhan, for instance, reported that, of 37 critically ill Covid-19 patients who were put on mechanical ventilators, 30 died within a month. In a U.S. study of patients in Seattle, only one of the seven patients older than 70 who were put on a ventilator survived; just 36% of those younger than 70 did. And in a study published by JAMA on Monday, physicians in Italy reported that nearly 90% of 1,300 critically ill patients with Covid-19 were intubated and put on a ventilator; only 11% received noninvasive ventilation. One-quarter died in the ICU; 58% were still in the ICU, and 16% had been discharged.

Older patients who do survive risk permanent cognitive and respiratory damage from being on heavy sedation for many days if not weeks and from the intubation

 

https://www.statnews...d-for-covid-19/

 

Funny how it all changed in just a month, no? A month ago some of us thought it could be better to get it sooner rather than later, while the resources were still available.

 

The problem is that this message isn't getting to the front lines very effectively, or more accurately to the policy makers. Docs are often trapped in protocols developed for bona fide pneumonia. It's like treating type 2 diabetes with insulin -- a "proven" practice that works well for a radically different disease with similar symptoms. Meanwhile we're expending massive industrial resources to ramp up ventilator production, when the money would be better spent fortifying the hospitals with promising drugs and supplements.

 

It might be wise to temporarily relocate to a place with docs who are allowed to read research, listen to experienced colleagues, and act accordingly with sufficient legal empowerment. Leaving one's country isn't generally feasible right now, but in the US, at least, there are wide disparities between jurisdictions in this regard. Arizona, Texas, and Florida stand out as some of the better destinations for patients seeking freedom of choice.
 

[resveratrol_guy]

The key here is "critically ill patients".  By definition, critically ill would indicate they were already at risk of dying no matter what.  Obviously ventilators didn't much improve outcome but likely it didn't make it worse either.  The vent was apparently reserved as a last ditch effort in an attempt to keep dying patients alive....which was apparently a lesson in futility.  It would appear these were dying patients no matter what.  And we've heard plenty of stories of people suddenly going down hill and dying before they can receive emergency medical care.

 

Vents are frankly harmful to the alveoli, and only less so at lower pressure. This is in addition to the morbid ramifications of sedating a patient for days to weeks. They're only justifiable if one has functioning hemoglobin and simply needs more oxygen. It's doubtful that that's the case with these patients, given the evolving evidence around heme iron detachment. A better strategy would probably be hyperbaric oxygen (which increases organ oxygen saturation simply by blood dissolution rather than enhanced hemoglobin binding). Unfortunately, those machines are huge and expensive, so perhaps ECMO would be more practical, even though it's designed as an end-stage rescue procedure.

[Dorian Grey]

My girlfriend has insomnia, & I looked at melatonin a couple years back.  I didn't find any alarming studies or even anecdotal reports about supplemental melatonin ruining anyone's ability to sleep without it (melatonin dependency).  Got her some low-dose stuff (1mg) & she loves it.  Says it sends her right to sleep, but with the low dose, she sometimes wakes up around 2-4:AM.  She's an RN, & is always worried about dependency, so we haven't tried higher doses or time release.  She likes to rotate melatonin, inositol, and an alcoholic beverage to avoid developing a habitual use of any one substance.  

 

I wouldn't be afraid of melatonin from what I've researched (sorry, no links) but I really didn't see any horror stories about melatonin putting the pineal gland into permanent dysfunction.  

[Hebbeh]

Another take on ventilators from somebody who's been there.  For some, it apparently is the choice between life and death:

 

https://www.washingt...e=pocket-newtab

 

I spent six days on a ventilator, in critical condition in the intensive care unit at New York University Langone medical center in New York City. I would not be here today without a ventilator.... A few days earlier, after my admission to the hospital, my physician father had warned me: “You better not get put on a ventilator. People don’t come back from that.”...

As a patient whose life was saved by a ventilator, I believe it is an outrage and an embarrassment that a nation as wealthy as ours is even discussing possible ventilator shortages. Thankfully the United States has managed to avoid widespread rationing partly due to ventilators being sent from places of low need to places of high need. We need to make sure that every patient who needs a ventilator can get one so that as many of them as possible can survive.

 

For those of us lucky enough to get off ventilators, our lives are not the same. Many patients who come off ventilators suffer lasting physical, mental and emotional issues, including cognitive deficits, lost jobs and psychological issues, such as depression and post-traumatic stress disorder.

 

For me, my lungs must rebuild their capacity. I experience breathlessness from even mild exertion. I used to run marathons; now I can’t walk across a room or up a flight of stairs without getting winded. I can’t go around the block for fresh air unless my husband pushes me in a wheelchair. When I shower, I can’t stand the entire time; I take breaks from standing to sit down on a plastic stool I have placed inside my bathtub.

Being on the ventilator for almost a week damaged my vocal cords, and now my voice is extremely hoarse. My speech pathologist expressed optimism that the damage is not permanent. Only time will tell

I’m not complaining. I am incredibly grateful to be alive. And for that, I have the ventilator to thank.

 

[Kalliste]

This is a paper I often remember when I think about antioxidants and cyto-storming. It should be read fully to see the problems also involved. The reserachers prefer injected antioxidants to some degree.

 

 

6. Conclusions

Considering the adverse effects of antioxidants, antioxidant drugs should be used carefully for chronic diseases, especially for diabetes and Alzheimer’s disease, when a certain level of ROS is required for normally cellular functions. However, for ROS-burst-mediated acute diseases, mitochondrion-permeable antioxidants should be used in the early stage.

To treat ROS-accompanying diseases, no matter chronic or acute, antioxidants should be used combined with other therapeutic drugs. However, drug combinations may have additive or possible antagonistic effects on the disease development. And the dosage of the single compound should be adjusted according to the combination. Thus, carefully pharmaceutic studies should be done before certain antioxidant (e.g., astaxanthin injection) can really enter the clinical trial to oxidative-damage-related illnesses.

https://www.hindawi....l/2016/6859523/

 

 

SUMMARY

Melatonin (N‐acetyl‐5‐methoxytryptamine) is a multifunctional signaling molecule that has a variety of important functions. Numerous clinical trials have examined the therapeutic usefulness of melatonin in different fields of medicine. Clinical trials have shown that melatonin is efficient in preventing cell damage under acute (sepsis, asphyxia in newborns) and chronic states (metabolic and neurodegenerative diseases, cancer, inflammation, aging). The beneficial effects of melatonin can be explained by its properties as a potent antioxidant and antioxidant enzyme inducer, a regulator of apoptosis and a stimulator of immune functions. These effects support the use of melatonin in viral infections, which are often associated with inflammatory injury and increases in oxidative stress. In fact, melatonin has been used recently to treat several viral infections, which are summarized in this review. The role of melatonin in infections is also discussed herein. Copyright © 2012 John Wiley & Sons, Ltd.

 

 

 

 

Melatonin possesses an anti-influenza potential through its immune modulatory effect

Melatonin exhibits a therapeutic potential in influenza A H1N1 virus infection.

•

Melatonin elicits anti-inflammatory and immune modulatory effects.

•

The induction of IL-10 by melatonin occurs via the upregulation of IL-27 in DC.

•

Melatonin treatment exhibits a synergistic effect with an anti-viral drug.

Abstract

Influenza is an infectious disease caused by an RNA virus that affects birds and mammals. It is a leading cause of morbidity, mortality and economic loss worldwide. Under influenza A virus infection, an uncontrolled inflammatory response in the lungs frequently leads to severe pneumonia. The anti-inflammatory and immune modulatory effects of melatonin may provide a beneficial effect for this disease. In this study, we found that melatonin treatment significantly decreases the expression of TNF-α, IL-6 and IFN-γ, and increases the production of IL-10 and TGF-β. The induction of IL-10 by melatonin occurs via the upregulation of IL-27 expression in dendritic cells. Melatonin also significantly inhibits the production of TNF-α in CD8 T cells. Co-treatment of melatonin and ribavirin significantly increases the survival of virus-infected mice compared to ribavirin alone. Our study suggests that melatonin possesses a therapeutic potential in influenza-induced pneumonia as an adjuvant treatment with anti-viral drugs.

 

 

 

Inhibitory effect of melatonin on lung oxidative stress induced by respiratory syncytial virus infection in mice

Abstract

Abstract: Previous research has shown that antioxidant (butylated hydroxyanisole) treatment ameliorates respiratory syncytial virus (RSV)‐induced disease and lung inflammation. Melatonin has been reported to exhibit a wide varieties of biological effects, including antioxidant and anti‐inflammation, and has no evident toxicity and side effect. But it is not known whether melatonin would modify RSV‐induced lung disease and oxidative stress. The present study was to establish the involvement of oxidative stress in the pathogenesis of RSV‐induced lung inflammation, and to investigate the protective effect of administration of melatonin in mice with RSV‐induced oxidative pulmonary injury for 4 days. Malondialdehyde (MDA), an end product of lipid peroxidation, and glutathione (GSH) and superoxide dismutase (SOD) and nitric oxide (NO) levels were evaluated in lung tissue homogenates by spectrophotometry. Hydroxyl radical (˙OH), one of the indicators of free radical formation, was also detected in lung homogenates by Fenton reaction. Tumor necrosis factor‐a (TNF‐a) concentrations in mouse serum were measured with ELISA assay. The results demonstrated that the mice intranasally inoculated with RSV resulted in oxidative stress changes by increasing NO, MDA and ˙OH levels, and decreasing GSH and SOD activities, whereas administration of melatonin significantly reversed all these effects. Furthermore, melatonin inhibited production of proinflammatory cytokines such as TNF‐a in serum of RSV‐infected mice. These results suggest that melatonin ameliorates RSV‐induced lung inflammatory injury in mice via inhibition of oxidative stress and proinflammatory cytokine production and may be as a novel therapeutic agent in virus‐induced pulmonary infection.

 

Covid is a virus but we are seeing a lot of antibiotics being used co-administratively so this is interesting:

 

Melatonin as an antibiotic: new insights into the actions of this ubiquitous molecule

Abstract

Abstract: The incidence of serious infections caused by multidrug‐resistant gram‐positive and gram‐negative bacteria has been increasing rapidly worldwide despite advances in antibacterial therapy in the last two decades. Among multidrug‐resistant gram‐positive and gram‐negative bacteria, methicillin‐resistant Staphylococcus aureus, carbapenem‐resistant Pseudomonas aeruginosa and Acinetobacter baumannii are of great importance, because they have emerged as primary nosocomial pathogens in hospital outbreaks. In this study, we investigated whether melatonin has antibacterial effects against these microorganisms in vitro. The minimum inhibitory concentration of melatonin was determined using a standard microdilution method at 24 and 48 hr. Melatonin inhibited microbial growth at both 24 and 48 hr; but results showed that melatonin had antibacterial effects against these microorganisms after 48 hr of incubation in lower doses [concentrations between 31.25 to 125 μg/mL (0.13–0.53 mm)]. Also, it was determined that melatonin has a more potent antimicrobial effect on gram‐negative microorganism. Among possible mechanisms, it is concluded that melatonin showed antibacterial effects by reducing intracellular substrates.

 

 

 

Melatonin is an indoleamine with potent multifunctional biological and pharmacological effects, both receptor dependent and receptor-independent effects, including antioxidant, anticancer, antitumor, anti-inflammatory, anti-aging, anti-diabetic, antiviral, neuroprotective activities. Melatonin mitigates tissue injury via modification of abnormalities in redox status and other biochemical markers. At the molecular level, the biological and pharmacological activities of melatonin are attributed to the inhibition of nuclear factor-Κappa beta (NF-Κβ), c-Fos over expression and down-regulation of matrix metalloproteinases-3 (MMP-3), which are regulators of pro-inflammatory and pro-fibrotic cytokines. There are numerous scientific reports on the therapeutic potential of melatonin in treatment of asthma, respiratory diseases for infections, chronic obstructive pulmonary disease, lung cancer, pleural cavity diseases, as well as vascular pulmonary disease. In the present communication, we systematically review the therapeutic potential of melatonin in the treatment of respiratory diseases along with its molecular mechanism of actions.

https://www.ingentac...000004/art00011

 

I would like to see Covid patients injection-transfused with mitochondria and melatonin

 

Systemic combined melatonin–mitochondria treatment improves acute respiratory distress syndrome in the rat Abstract

Despite high in‐hospital mortality associated with acute respiratory distress syndrome (ARDS), there is no effective therapeutic strategy. We tested the hypothesis that combined melatonin–mitochondria treatment ameliorates 100% oxygen‐induced ARDS in rats. Adult male Sprague‐Dawley rats (n = 40) were equally categorized into normal controls, ARDS, ARDS‐melatonin, ARDS with intravenous liver‐derived mitochondria (1500 μg per rat 6 hr after ARDS induction), and ARDS receiving combined melatonin–mitochondria. The results showed that 22 hr after ARDS induction, oxygen saturation (saO₂) was lowest in the ARDS group and highest in normal controls, significantly lower in ARDS‐melatonin and ARDS‐mitochondria than in combined melatonin–mitochondria group, and significantly lower in ARDS‐mitochondria than in ARDS‐melatonin group. Conversely, right ventricular systolic blood pressure and lung weight showed an opposite pattern compared with saO₂ among all groups (all P < 0.001). Histological integrity of alveolar sacs showed a pattern identical to saO₂, whereas lung crowding score exhibited an opposite pattern (all P < 0.001). Albumin level and inflammatory cells (MPO+, CD40+, CD11b/c+) from bronchoalveolar lavage fluid showed a pattern opposite to saO₂ (all P < 0.001). Protein expression of indices of inflammation (MMP‐9, TNF‐α, NF‐κB), oxidative stress (oxidized protein, NO‐1, NOX‐2, NOX‐4), apoptosis (mitochondrial Bax, cleaved caspase‐3, and PARP), fibrosis (Smad3, TGF‐β), mitochondrial damage (cytochrome C), and DNA damage (γ‐H2AX+) exhibited an opposite pattern compared to saO₂ in all groups, whereas protein (HO‐1, NQO‐1, GR, GPx) and cellular (HO‐1+) expressions of antioxidants exhibited a progressively increased pattern from normal controls to ARDS combined melatonin–mitochondria group (all P < 0.001). In conclusion, combined melatonin–mitochondrial was superior to either treatment alone in attenuating ARDS in this rat model.

https://onlinelibrar....1111/jpi.12199

 

 

Lots of pulmonary fibrosis going on with Covid

 

Melatonin: the dawning of a treatment for fibrosis?

Fibrosis is a common occurrence following organ injury and failure. To date, there is no effective treatment for this condition. Melatonin targets numerous molecular pathways, a consequence of its antioxidant and anti‐inflammatory actions that reduce excessive fibrosis. Herein, we review the multiple protective effects of melatonin against fibrosis. There exist four major phases of the fibrogenic response including primary injury to the organ, activation of effector cells, the elaboration of extracellular matrix (ECM) and dynamic deposition. Melatonin regulates each of these phases. Additionally, melatonin reduces fibrosis levels in numerous organs. Melatonin exhibits its anti‐fibrosis effects in heart, liver, lung, kidney, and other organs. In addition, adhesions which occur following surgical procedures are also inhibited by melatonin. The information reviewed here should be significant to understanding the protective role of melatonin against fibrosis, contribute to the design of further experimental studies related to melatonin and the fibrotic response and shed light on a potential treatment for fibrosis.

https://onlinelibrar....1111/jpi.12302

 

Early immune activation seems to be important for Covid, but does this paper actually say T cells will be upregulated?

 

Melatonin provides signal 3 to unprimed CD4⁺ T cells but failed to stimulate LPS primed B cells

Abstract

Growing evidence has supported the conclusion that melatonin, a pineal hormone, modulates the immune function. In our previous study, we evaluated in vivo the potential role of melatonin in the regulation of the antigen specific T and B cells. In the present study, we observe that melatonin down‐regulated the expression of the co‐stimulatory molecule B7‐1 but not B7‐2 on macrophages. Further, melatonin encouraged the proliferation of anti‐CD3 antibody activated CD4⁺ T cells only in the presence of antigen‐presenting cells and promoted the production of Th2‐like cytokines. Furthermore, it failed to influence the activity of B cells in a T‐independent manner. Melatonin suppressed the release of TNF‐α by LPS or IFN‐γ activated macrophages but failed to inhibit nitric oxide (NO) release. Thus the study shows that melatonin can engineer the growth of unprimed CD4⁺ T cells if both the signals are provided by antigen‐presenting cells. However, it could not regulate the function of B cells.

https://onlinelibrar...49.2001.01519.x

 

 

Melatonin increases antigen presentation and amplifies specific and non specific signals for T-cell proliferation

Abstract

Our preceding results have shown that melatonin administration to normal and immunodepressed mice increases significantly the antibody response. We also found that melatonin is able to restore the impaired T-helper cell activity in immunodepressed mice. The present study shows that melatonin enhances antigen presentation by splenic macrophages to T-cells. This effect is concomitant with an increase in the expression of MHC class II molecules and production of IL-1 and TNF-α. Considering the role of antigen presentation and cytokine production in the initiation of the immune response, the present findings provide evidence for relevant mechanisms that may account for the regulatory role of the pineal gland in immunoregulation.

 

 

• Published: 04 May 2010

Blocking of melatonin synthesis and MT₁ receptor impairs the activation of Jurkat T cells

Abstract

Melatonin has been proposed as regulating the immune system by affecting cytokine production in immunocompetent cells, enhancing the production of several T helper (Th)1 cytokines. To further investigate the melatonin’s role in IL-2/IL-2R system, we established an inducible T-REx expression system in Jurkat cells in which the protein levels of HIOMT enzyme or MT₁ receptor were significantly down-regulated upon tetracycline incubation. We found that T-REx Jurkat cells with lower levels of HIOMT activity, and consequently lower content of endogenous melatonin, showed IL-2 production decrease after activation with lectin. Likewise, tetracycline-inducible stable cell line expressing MT₁ antisense produced decreased amounts of IL-2 (mRNA and protein levels) after stimulation. Moreover, in T-Rex-MT₁ cells incubated with tetracycline, a sub-optimal PHA dose failed to induce the early activation marker CD25 on the cell surface. The results shown here support the relevance of endogenous melatonin and its signaling in T cell activation.

 

[Hebbeh]

Vents are frankly harmful to the alveoli, and only less so at lower pressure. This is in addition to the morbid ramifications of sedating a patient for days to weeks. They're only justifiable if one has functioning hemoglobin and simply needs more oxygen. It's doubtful that that's the case with these patients, given the evolving evidence around heme iron detachment. A better strategy would probably be hyperbaric oxygen (which increases organ oxygen saturation simply by blood dissolution rather than enhanced hemoglobin binding). Unfortunately, those machines are huge and expensive, so perhaps ECMO would be more practical, even though it's designed as an end-stage rescue procedure.

 

There is no evolving evidence of "heme iron detachment".  And even if there was (which there isn't), there would be no cure for massive hemoglobin failure.  That would be automatic death without massive transfusions and there wouldn't be enough blood supply to transfuse near that number of patients.

 

And in my case, as my doctor advised that it takes 6 months to recover from simple hemoglobin deficiency, I experienced that it was exactly a full six months for bone marrow to produce enough hemoglobin to recover just into the normal range.

 

If the critical COVID-19 patients were actually suffering that level of damage to their hemoglobin, there would be no way to keep them alive long enough to recover.  No, the lack of oxygen is due to lungs filling with fluid and the damage that causes.  And as brutal as a vent is, that is why ventilating can at least save some until the lungs began to clear.  Destroyed hemoglobin would be an entirely different animal and there would be no recovery from something that massive.

 

Certainly there have been 1000's of complete blood workups with 1000's of COVID-19 patients and not a single doctor in any country has mentioned any kind of hemoglobin failure issue.  It's never been witnessed.

Edited by Hebbeh, 12 April 2020 - 06:27 AM.

[Dorian Grey]

The problem is that this message isn't getting to the front lines very effectively, or more accurately to the policy makers. Docs are often trapped in protocols developed for bona fide pneumonia. It's like treating type 2 diabetes with insulin -- a "proven" practice that works well for a radically different disease with similar symptoms. Meanwhile we're expending massive industrial resources to ramp up ventilator production, when the money would be better spent fortifying the hospitals with promising drugs and supplements.

 

It might be wise to temporarily relocate to a place with docs who are allowed to read research, listen to experienced colleagues, and act accordingly with sufficient legal empowerment. Leaving one's country isn't generally feasible right now, but in the US, at least, there are wide disparities between jurisdictions in this regard. Arizona, Texas, and Florida stand out as some of the better destinations for patients seeking freedom of choice.
 

 

Agree...  I worked in healthcare for 35 years, & have watched medicine solidify from independent doctors doing what they think is best for their patient in a given situation, to very ridged protocols often based largely on dogma.  The inpatient "hospitalist" actually practice the most dogmatic medicine of all.  "Insert tab A into slot B".  Respiratory distress with low O-sat?  Vent him! 

 

I actually read both doctors & nurses love to get an infectious patient on a vent as soon as possible, as this greatly reduces infectious aerosols (the exhaled air from the vent is filtered).  The last thing you want is a COVID patient awake and coughing in an ICU!  

 

This is why I'm staying HOME as long as possible.  Bought an O-sat monitor for $45 a month ago as this is the best indicator of when you're in deep doo-doo.  When O-sat starts trending down towards 90 or below, it's time to call 911.  It would be great if doc's would send an oxygen tank to patients treating at home, but lots of luck with that.  

 

I noticed Boris Johnson got blow-by O2 rather than a vent, and...  Got better!  I would insist on this (refuse a vent / blow-by O2 only) if I went into hospital for at least a trial period.  

 

Regarding "open minded doctors" and freedom to practice, I've heard Mayo & Cleveland Clinics still have doc's who consider what's best for each patient, and do not practice cookie-cutter medicine.   This said, after working with doctors for 35 years, I believe the best medicine (for me) is to avoid them if you can! 

Edited by Dorian Grey, 12 April 2020 - 06:33 AM.

[Iporuru]

On Covid-19 and bradykinin

 

Kinins and Cytokines in COVID-19: A Comprehensive Pathophysiological Approach

"We propose that blocking the B1 and B2 receptors might have an ameliorating effect on disease caused by COVID-19. This kinin-dependent pulmonary edema is resistant to corticosteroids or adrenaline and should be targeted as long as the virus is present. In addition, this pathway might indirectly be responsive to anti-inflammatory agents or neutralizing strategies for the anti-S-antibody induced effects, but by itself is likely to be insufficient to reverse all the pulmonary edema. ?

[lancebr]

On Covid-19 and bradykinin

 

Kinins and Cytokines in COVID-19: A Comprehensive Pathophysiological Approach

"We propose that blocking the B1 and B2 receptors might have an ameliorating effect on disease caused by COVID-19. This kinin-dependent pulmonary edema is resistant to corticosteroids or adrenaline and should be targeted as long as the virus is present. In addition, this pathway might indirectly be responsive to anti-inflammatory agents or neutralizing strategies for the anti-S-antibody induced effects, but by itself is likely to be insufficient to reverse all the pulmonary edema. ?

 

If I am reading this right it seems as if melatonin inhibits B2 receptors:

 

"Melatonin and melatonin-mimicking agents inhibit B2 bradykinin receptors (B2Rs)"

 

https://www.tandfonl...12.2017.1315864

[Mind]

Am I being a little too conspiratorial? It seems like this is kind-of a hit piece on hydroxychloroquine (for political reasons): https://www.bloomber...omoted-by-trump

 

It is something to keep an eye on of course. They reported 4 deaths linked to "treatments for coronavirus", but the article suspiciously doesn't specifically say what the treatments were in those 4 incidents.

 

Were the heart incidents or death's even from Raoult's trial? It is not clear from the article. Raoult himself reports no cardiac toxicity.

 

Also, it would be expected that people with severe COVID-19 and low on oxygen would be at greater risk to having "heart incidents", right?

 

In addition they say there was a total of 82 "serious" incidents, that were split between hydroxychloroquine and other anti-retroviral drugs, but again don't give a number (although one might suspect it was 43, mentioned earlier in the article)

 

They also randomly throw in the fact that there were cases of hydroxychloroquine poisoning in Nigeria. Overdoses probably. From negligent use?

 

It is from "Bloomberg" news, and people in the U.S. might recall Mike Bloomberg is a bitter enemy of President Trump.

 

I guess I am just suspicious that a couple of days after Raoult shows some encouraging results, a news service run by the president's political rival brings forth this negative story with a blaring political headline.

 

If Raoult's treatment lowers the elderly fatality rate from 20% down to 0.5%, it still seems like a huge win, even if there were a small number of "heart incidents".

 

 

[Kalliste]

Every day I wonder what it is about those asymtomatic cases? What did they do right? Are they for the most part people with good metabolic health and a good circadian rhythm exposed to the sun so their internal D3/K2 status is great? Perhaps people with a natural diet rich in some plants with substances like Vit D/ECEG/Vit C/Bromelain/Quercetin/Curcumin... People whose thymus have not been atrophied so their immunesystem kicks in?

 

I hope so. Have still not heard any generalizing comment on what these people have in common. Whatever they got I hope I have it.

 

 

Am I being a little too conspiratorial? It seems like this is kind-of a hit piece on hydroxychloroquine (for political reasons): https://www.bloomber...omoted-by-trump

 

It is something to keep an eye on of course. They reported 4 deaths linked to "treatments for coronavirus", but the article suspiciously doesn't specifically say what the treatments were in those 4 incidents.

 

Were the heart incidents or death's even from Raoult's trial? It is not clear from the article. Raoult himself reports no cardiac toxicity.

 

Also, it would be expected that people with severe COVID-19 and low on oxygen would be at greater risk to having "heart incidents", right?

 

In addition they say there was a total of 82 "serious" incidents, that were split between hydroxychloroquine and other anti-retroviral drugs, but again don't give a number (although one might suspect it was 43, mentioned earlier in the article)

 

They also randomly throw in the fact that there were cases of hydroxychloroquine poisoning in Nigeria. Overdoses probably. From negligent use?

 

It is from "Bloomberg" news, and people in the U.S. might recall Mike Bloomberg is a bitter enemy of President Trump.

 

I guess I am just suspicious that a couple of days after Raoult shows some encouraging results, a news service run by the president's political rival brings forth this negative story with a blaring political headline.

 

If Raoult's treatment lowers the elderly fatality rate from 20% down to 0.5%, it still seems like a huge win, even if there were a small number of "heart incidents".

 

I'm a member of a left wing forum with a big Corona thread and I noticed how they polarized like an array of magnets against HCQ the same instant that Trump started talking about it as a possible cure. He is hated with passion and I don't have a hard time seeing how they would discount a useful medicine in order to attack him. From their minds own secret internal dialogue it would probably be justified as saving many lives because an effective medicine endorsed by Trump could help him become re-elected so he can continue his mass-killings.

 

Lucky for us Asia and Russia both have big trouble with Corona so they will look into HCQ with more open eyes. This shared concurrent disaster is very interesting in that way.

[Kalliste]

 

Our results demonstrated that NO specifically inhibits the replication cycle of SARS CoV, most probably during the early steps of infection, suggesting that the production of NO by iNOS results in an antiviral effect. However, the production of NO should be adjusted to exert antiviral rather than damaging effects. At present, there is no information concerning the levels of NO in SARS patients. Previous studies have shown that NO plays a role in the pathogenesis of influenza virus pneumonia in mice (2, 17). This pathological effect, however, has been suggested to be associated with the mouse model of pneumonia, since the peak of NO in infected humans was not associated with clinical symptoms (23). Thus, the role of NO during SARS infection in animal models and the level of NO in SARS patients constitute important areas for future studies.

 

https://jvi.asm.org/content/79/3/1966

 

Abstract

Increasing evidence regarding positive effects of exposure to sunlight has led to suggestions that current advice may be overly weighted in favour of avoidance. UV-A has been reported to lower blood pressure, possibly through nitric oxide (NO) production in skin. Here, we set out to investigate effects of UV-A and solar-simulated radiation on the potential source of dermal NO, the effective doses and wavelengths, the responsiveness of different human skin cells, the magnitude of inter-individual differences and the potential influence of age. We utilised isogenic keratinocytes, microvascular endothelial cells, melanocytes and fibroblasts isolated from 36 human skins ranging from neonates to 86 years old. We show that keratinocytes and microvascular endothelial cells show greatest NO release following biologically relevant doses of UV-A. This was consistent across multiple neonatal donors and the effect is maintained in adult keratinocytes. Our observations are consistent with a bi-phasic mechanism by which UV-A can trigger vasodilatory effects. Analyses of NO-production spectra adds further evidence that nitrites in skin cells are the source of UV-mediated NO release. These potentially positive effects of ultraviolet radiation lend support for objective assessment of environmental influence on human health and the idea of “healthy sun exposure”.

https://www.ncbi.nlm...les/PMC5593895/

 

I have several UV-B lights. One 300w Philips UV lamp, one Exo-Terra 13w UVB, one Exo Terra Solar-Glo 160w Sun imitation lamp, also got some pure Infrared lights. Will light them all in a well ventilated room and fry myself to a sizzle at first sign of Covid.

[Iporuru]

In vitro, but still...

Scutellaria baicalensis extract and baicalein inhibit replication of SARS-CoV-2 and its 3C-like protease in vitro

COVID-19 has become a global pandemic that threatens millions of people worldwide. There is an urgent call for developing effective drugs against the virus (SARS-CoV-2) causing this disease. The main protease of SARS-CoV-2, 3C-like protease (3CLpro), is highly conserved across coronaviruses and is essential for the maturation process of viral polyprotein. Scutellariae radix (Huangqin in Chinese), the root of Scutellaria baicalensis has been widely used in traditional Chinese medicine to treat viral infection related symptoms. The extracts of S. baicalensis have exhibited broad spectrum antiviral activities. We studied the anti-SARS-CoV-2 activity of S. baicalensis and its ingredient compounds. We found that the ethanol extract of S. baicalensis inhibits SARS-CoV-2 3CLpro activity in vitro and the replication of SARS-CoV-2 in Vero cells with an EC50 of 0.74 μg/ml. Among the major components of S. baicalensis, baicalein strongly inhibits SARS-CoV-2 3CLpro activity with an IC50 of 0.39 μM. We further identified four baicalein analogue compounds from other herbs that inhibit SARS-CoV-2 3CLpro activity at microM concentration. Our study demonstrates that the extract of S. baicalensis has effective anti-SARS-CoV-2 activity and baicalein and analogue compounds are strong SARS-CoV-2 3CLpro inhibitors.

[Iporuru]

Does Zinc Supplementation Enhance the Clinical Efficacy of Chloroquine/Hydroxychloroquine to Win Todays Battle Against COVID-19?

"Currently, drug repurposing is an alternative to novel drug development for the treatment of COVID-19 patients. The antimalarial drug chloroquine (CQ) and its metabolite hydroxychloroquine (HCQ) are currently being tested in several clinical studies as potential candidates to limit SARS-CoV-2-mediated morbidity and mortality. CQ and HCQ (CQ/HCQ) inhibit pH-dependent steps of SARS-CoV-2 replication by increasing pH in intracellular vesicles and interfere with virus particle delivery into host cells. Besides direct antiviral effects, CQ/HCQ specifically target extracellular zinc to intracellular lysosomes where it interferes with RNA-dependent RNA polymerase activity and coronavirus replication. As zinc deficiency frequently occurs in elderly patients and in those with cardiovascular disease, chronic pulmonary disease, or diabetes, we hypothesize that CQ/HCQ plus zinc supplementation may be more effective in reducing COVID-19 morbidity and mortality than CQ or HCQ in monotherapy. Therefore, CQ/HCQ in combination with zinc should be considered as additional study arm for COVID-19 clinical trials."

 

Can Zinc Correction in SARS-CoV-2 Patients Improve Treatment Outcomes?

The ongoing severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic for which there is no established treatment available yet, has caused more than 68,000 deaths so far. Following the SARS-CoV outbreak in 2003, an Italian group described a hypothesis about the efficacy of two old drugs: Chloroquine (CQ) and Hydroxychloroquine (HCQ), against SARS-CoV and its future emergents. Later, this hypothesis was shown to be relevant in-vitro. Due to the high genetic similarity of SARS-CoV-2 and SARS-CoV, the hypothesis introduced by Savarino et al. and the further supportive in-vitro evidence served a rational ground for three different Chinese groups to test the efficacy of CQ or HCQ against SARS-CoV-2 in-vitro. These studies showed promising in-vitro efficacy of CQ and HCQ against SARS-CoV-2. Unfortunately, in the absence of sufficient clinical data on the (in)efficacy of CQ and HCQ in SARS-CoV-2 patients, the compassionate and off-label use of these medications is becoming politicized. Herein, we underline some critical features of the CQ/HCQ mechanism of action concerning SARS-CoV-2. Moreover, we put forward a hypothesis based on three lines of evidence on a probable link between zinc-deficiency/zinc correction and response to CQ/HCQ- and possibly other SARS-CoV-2 treatments.

Edited by Iporuru, 12 April 2020 - 11:29 AM.

[Izan]

so, based on science and what we gathered so far: 

 

melatonin + bromelain +(liposomal) quercetin +  zinc (picolinate)/zinc gluconate lozenges + add some of Dorian's Delicious quinine water = you're all set? 

 

(just don't take zinc and bromelain at the same time, because zinc can inhibit bromelain's activity).

 

Any thoughts on this guys?

 

[Rosanna]

Just me posting back with a description of my experience of what I think was Covid-19  (sorry to say I can't get a test yet to say for sure).  In case this is helpful to anyone.

  

 

Seemed to be these stages:

 

 

Day 1 - 4 - itchy eyes, itchy back of throat, slight sniffle, slight sore throat, shivery legs.......but generally feeling normal and thinking this was allergies (apart from the legs)

 

 

(then a 5 day break where feel back to normal, during which come out of isolation and resume normal activities)

 

 

Day 9 or 10 - 12  - viral type headache, very sore throat as if it's going to swell up (thankfully it didn't), shivery legs return, feel it's the same thing hitting harder, high temperature

 

 

Day 12 - 15 - extreme fatigue, remnants of sore throat, weakness, flu - like feeling and mild cough, intermittent high temperature

 

 

Day 15 onwards (where I'm at around now........productive cough, hoping its just infection clearing, feel the viral aspect is over)

 

 

 

I took Elderberry and Echinacea until Day 9, as I thought perhaps I'd exacerbated things.  Stopped then and increased green tea, vitamin C, Co Q10 and zinc.  On the days I've been

ok I've gone out for a walk but seem to have a bit of a 'set back' the next day (can't be more specific than that, just 'off'), so will take things even slower.  Feel almost fine doing nothing in the house.  Will get tested asap.

 

 

I don't know if this is helpful info, not very scientific.  Wondering on what to do for lungs now, although symptoms are mild and would welcome thoughts on that.  More concerned about lungs now, post virus for obvious reasons.

 

 

 

 

 

 

[resveratrol_guy]

Certainly there have been 1000's of complete blood workups with 1000's of COVID-19 patients and not a single doctor in any country has mentioned any kind of hemoglobin failure issue.  It's never been witnessed.

 

I see. What do you make of this and this and this and this?

 

Most of all, why do you think some of those blood tests show sky high ferritin, if not to perform its usual job of mopping up loose iron ions?

 

I should also note that there's no reason to assume that hemoglobin destruction is necessarily fatal. It's all a question of rate.

Edited by resveratrol_guy, 12 April 2020 - 01:27 PM.

[resveratrol_guy]

so, based on science and what we gathered so far: 

 

melatonin + bromelain +(liposomal) quercetin +  zinc (picolinate)/zinc gluconate lozenges + add some of Dorian's Delicious quinine water = you're all set? 

 

(just don't take zinc and bromelain at the same time, because zinc can inhibit bromelain's activity).

 

Any thoughts on this guys?

 

Good start. Just watch it on the zinc dose, which can get toxic at low multiples of RDA.

 

For people unable to obtain bromelain, it's abundant in pineapple cores. Likewise, capers are a great source of quercetin (but you might want to rinse out the salt and vinegar additives first).

 

Vitamin C, vitamin D, and beta glucan (from shiitake, perhaps) seem wise as well, but I'm not sure as to the optimal dose.

 

Hydrogen water also seems like a no-brainer, especially during active infection. AquaH2 pills, machine, or DIY, whichever. My only concern is heavy metal impurities in the magnesium source, but I don't think it's enough to care about during a few weeks of illness. In any case, I've used it on and off for years, and have noticed rigorous correlation between drinking 400 mL or more before bed, and better sleep quality.

Edited by resveratrol_guy, 12 April 2020 - 01:15 PM.

[resveratrol_guy]

Agree...  I worked in healthcare for 35 years, & have watched medicine solidify from independent doctors doing what they think is best for their patient in a given situation, to very ridged protocols often based largely on dogma.  The inpatient "hospitalist" actually practice the most dogmatic medicine of all.  "Insert tab A into slot B".  Respiratory distress with low O-sat?  Vent him! 

 

I actually read both doctors & nurses love to get an infectious patient on a vent as soon as possible, as this greatly reduces infectious aerosols (the exhaled air from the vent is filtered).  The last thing you want is a COVID patient awake and coughing in an ICU!  

 

This is why I'm staying HOME as long as possible.  Bought an O-sat monitor for $45 a month ago as this is the best indicator of when you're in deep doo-doo.  When O-sat starts trending down towards 90 or below, it's time to call 911.  It would be great if doc's would send an oxygen tank to patients treating at home, but lots of luck with that.  

 

I noticed Boris Johnson got blow-by O2 rather than a vent, and...  Got better!  I would insist on this (refuse a vent / blow-by O2 only) if I went into hospital for at least a trial period.  

 

Regarding "open minded doctors" and freedom to practice, I've heard Mayo & Cleveland Clinics still have doc's who consider what's best for each patient, and do not practice cookie-cutter medicine.   This said, after working with doctors for 35 years, I believe the best medicine (for me) is to avoid them if you can! 

 

Yeah it's both fortunate and informative that Johnson recovered with passive O2. I wonder how many of the resolved cases in the UK, 96% of which having exited hospital in body bags (Worldometer), were on vents.

 

FYI I've noticed lots of variance among SpO2 meters. It's probably wise to have 2 different brands and mutually calibrate them.

[albedo]

America Guidelines on the Treatment and Management of Patients with COVID-19 Infection

Published ,

4/11/2020

COVID-19 Guideline, Part 2: Diagnostics - Coming Soon

COVID-19 Guideline, Part 3: Infection Prevention - Coming Soon

https://www.idsociet...and-management/

[lancebr]

In vitro, but still...

Scutellaria baicalensis extract and baicalein inhibit replication of SARS-CoV-2 and its 3C-like protease in vitro

COVID-19 has become a global pandemic that threatens millions of people worldwide. There is an urgent call for developing effective drugs against the virus (SARS-CoV-2) causing this disease. The main protease of SARS-CoV-2, 3C-like protease (3CLpro), is highly conserved across coronaviruses and is essential for the maturation process of viral polyprotein. Scutellariae radix (Huangqin in Chinese), the root of Scutellaria baicalensis has been widely used in traditional Chinese medicine to treat viral infection related symptoms. The extracts of S. baicalensis have exhibited broad spectrum antiviral activities. We studied the anti-SARS-CoV-2 activity of S. baicalensis and its ingredient compounds. We found that the ethanol extract of S. baicalensis inhibits SARS-CoV-2 3CLpro activity in vitro and the replication of SARS-CoV-2 in Vero cells with an EC50 of 0.74 μg/ml. Among the major components of S. baicalensis, baicalein strongly inhibits SARS-CoV-2 3CLpro activity with an IC50 of 0.39 μM. We further identified four baicalein analogue compounds from other herbs that inhibit SARS-CoV-2 3CLpro activity at microM concentration. Our study demonstrates that the extract of S. baicalensis has effective anti-SARS-CoV-2 activity and baicalein and analogue compounds are strong SARS-CoV-2 3CLpro inhibitors.

 

Scutellariae baicalensis (skullcap) was one of the main herbs the Chinese supposedly used to treat

some of their patients. 

 

It also seems that scutellariae baicalensis has a flavanoid that is an inhibitor of bradykinin.

 

http://modernscienti...l 9cTPI5N02DGwm

 

"literature has shown that skullcapflavone II, a flavonoid from S. baicalensis, is a potential bradykinin antagonist."

 

[lancebr]

so, based on science and what we gathered so far: 

 

melatonin + bromelain +(liposomal) quercetin +  zinc (picolinate)/zinc gluconate lozenges + add some of Dorian's Delicious quinine water = you're all set? 

 

(just don't take zinc and bromelain at the same time, because zinc can inhibit bromelain's activity).

 

Any thoughts on this guys?

 

A majority of the quercetin supplements already contain bromelain since it supposedly makes

the bioavailability of quercetin better.

 

Since the quercetin is suppose to be a zinc ionophore does anyone know if the quercetin and zinc

have to be taken within a certain amount of time to provide the zinc ionophore?

 

And if you have to take the two in close proximity of time will the added bromelain cause problems

with the zinc?

 

 

[Hebbeh]

I see. What do you make of this and this and this and this?

 

A bunch of reddit and twitter threads discussing hypoxia?  The hypoxia develops when the fluid filled lungs can no longer exchange oxygen.  This is well established.  Creating conspiracy theories isn't helping.

[BlueCloud]

 

I'm a member of a left wing forum with a big Corona thread and I noticed how they polarized like an array of magnets against HCQ the same instant that Trump started talking about it as a possible cure. He is hated with passion and I don't have a hard time seeing how they would discount a useful medicine in order to attack him. From their minds own secret internal dialogue it would probably be justified as saving many lives because an effective medicine endorsed by Trump could help him become re-elected so he can continue his mass-killings.

 

Lucky for us Asia and Russia both have big trouble with Corona so they will look into HCQ with more open eyes. This shared concurrent disaster is very interesting in that way.

I’m not surprised at all. This is what i said in a post a couple of pages back ( that was heavily downvoted), except it was about the right-wing  . Whether left or right, politics work by a contrarian attitude : ” if our opponent says X is good, then we must say that X is bad, and vice-versa” . Politics and politicians should stay away from science. 
 

The point of view on HCQ still varies among countries. Sweden has stopped its use in all their hospitals recently ( except for research) claiming lack of results, while France has cautiously endorsed it for widespread use in hospitals as well as individual prescriptions by doctors, and started various studies on it. Despite it, there are various criticisms concerning the way Raoult conducted his study, but even those criticizing his methodology ( he does have a reputation for  sloppiness ) do accept that HCQ has real potential. 

Edited by BlueCloud, 12 April 2020 - 04:37 PM.

[Dorian Grey]

A majority of the quercetin supplements already contain bromelain since it supposedly makes

the bioavailability of quercetin better.

 

Since the quercetin is suppose to be a zinc ionophore does anyone know if the quercetin and zinc

have to be taken within a certain amount of time to provide the zinc ionophore?

 

And if you have to take the two in close proximity of time will the added bromelain cause problems

with the zinc?

 

Zinc is absorbed in the jejunum, so peak blood levels probably occur 2-6 hours after dropping a supp with a meal.  This would be prime time to add the ionophore.  Bromelain with lunch, zinc with dinner, & tonic ionophore before bed.  Alternately I expect zinc with lunch & quercetin/bromelain with dinner would work fine.  

[xEva]

A bunch of reddit and twitter threads discussing hypoxia?  The hypoxia develops when the fluid filled lungs can no longer exchange oxygen.  This is well established.  Creating conspiracy theories isn't helping.

 

those are firstresponders discussing the fact that their covid-19 patients generally do not fit the profile of ARDS. To begin with, in some hospitals, intubated covid-19 patients have 80% mortality after staying on the ventilator often for 2 and even 3 weeks -- while a 'regular' ARDS patient has a much better survival rate and needs ventilation on average for 4-5 days. 

 

There is a strong suspicion of a dysglobulinemia associated with this disease -- which, I have been googling, is not that easily diagnosed. Apparently, an unusual test is called for. I don't feel like digging it deeper, at least not at the moment. The key to surviving this is not to need to go to the hospital in the first place.

 

you sound like the issue you had with hemoglobin, its levels were too low (-? and then you write how long it took for you to bring it up). With covid-19, hemoglobin levels are normal or high. And yet the patients are hypoxic. Often, they are hypoxic, while their lungs are still 'compliant'. They breathe on their own, talk "in full sentences" and even text, while their O2 saturation levels imply that they should be comatose. This observation alone is what the MDs find most perplexing.

 

 

Btw, re hydroxychloroquine and azithromycin, that frustrated doc on reddit puts his patients on both drugs right away, without apparent benefit -- too late? In the end of the thread he is asked about zinc, no answer so far.

Edited by xEva, 12 April 2020 - 05:05 PM.

[BlueCloud]

The abstract says the mean age of the patients was 43.6 years old, so not elderly at all. I suppose when they say "with a mortality rate of 0.5%, in elderly patients", they mean the mortality was mainly limited to elderly patients.

 

I don't think there was a control group, but IF the number of cases can be compared to France's official figures, than a 0.5% mortality rate looks pretty good. France's raw figures show a crazy high mortality rate of ~10%. But it would be better if there was a control group so we could be sure the selection process was resulting in an apples to apples comparison.

France has been doing very little testing. In comparison, Germany has been testing massively from day one, almost as much as South Korea, and therefore has one of the lowest mortality/infection ratios in Europe. This explain ( partly) the difference in ratios.