3083 replies to this topic

[Kalliste]

 

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.”

He notes that he has only treated a small number of cases, but feels like the results he has seen need to be reported. Especially as the US death toll from the COVID-19 pandemic surpasses past 10,000 and doctors scramble for treatment.

“People are dying, and I’m asking other physicians if you’ve got nothing else, why not try this?” Dr. Neel said. “I know melatonin inside and out, and believe it is a safe and effective treatment for COVID-19. Melatonin can also be used safely in conjunction with other treatments.”

Russel J. Reiter, Ph.D, Professor of Cell Biology at UT Health Center (Graduate School of Biomedical Sciences) in San Antonio, Texas shared his thoughts on the matter. Reiter is one of the world’s leading melatonin researchers and the author of books and many research papers. He is the editor and chief of the Journal of  Pineal Research and on the editorial board of 7 other journals.  ” I understand Dr. Neel has treated two patients successfully with melatonin.  This is certainly newsworthy.  Likewise, his rationale for the use of melatonin as a potential treatment for COVID-19 is important.  A published report supports his rationale, COVID-19: Melatonin as a potential adjuvant treatment”, stated  Professor Russel J. Reiter, Ph.D in an interview. “Dr. Neel’s rationale for the use of melatonin as a potential treatment for COVID-19 is justified on the basis of the actions of this molecule”, said Reiter who was a part of this report that was published in February-March 2020 during the COVID-19 pandemic, co authored in conjunction with several medical professionals in China . (See footnote below).

“The likely efficacy of melatonin to treat COVID-19 stems from its actions as an antioxidant, as an anti-inflammatory agent and to its ability the reduce the effects of other viral agents in experimental models”, said Professor Reiter.

On a side note, Dr. Neel also stated that he did advise two middle-aged patients in Travis County to begin taking melatonin weeks ago after the healthcare worker and her spouse developed COVID symptoms as it hit Texas.

“That was weeks ago. However, they were not able to get tested for COVID-19 due to the shortage in testing, but they were experiencing all of those same symptoms and also reported being fever-free within 24 hours of starting melatonin and Vitamin C treatments,” Dr. Neel said.

He warns that high doses of melatonin are only to be used in cases where a doctor highly suspects COVID-19, and that you should always speak to a doctor for proper dosing.

“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.”

Neel is optimistic about what the powerful antitoxin and antioxidant Melatonin can do, as well as Vitamin C, and he hopes that the medical community will do the research that is needed for it to take foothold in daily practice of fighting many illnesses, including the COVID-19 pandemic.

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“The medical community needs to really start researching melatonin because I think it will be effective in treating so many other things as well including bacterial infections, heart attack, strokes, and more,” Dr. Neel. “Just look at what it did in the study of septic babies.”

In an article published March 20, Dr. Neel stated, “I believe doctors need to start using melatonin to treat patients now, today, to save lives, in conjunction with other treatment. I think it could keep a lot of people from having to go to the hospital as well. There’s enough research out there to prove it’s effective in fighting viruses like this. Further research could help tweak dosing, but melatonin is non toxic and available to everyone over the counter.”

The US death toll from COVID-19 surpassed 10,000 this week, with New York being hit the hardest so far. New York newspapers report “The state’s hospitals are inundated, morgues are overflowing, and many medical workers are forced to wear trash bags due to a lack of protective gear.”

Newspapers reported that New York Gov. called the coronavirus “truly vicious,” and described it as an “effective killer.”

To learn more about melatonin and medical studies that have been done, read our previous article here.

Editor’s note 4-9-20: Since this article’s publication, Dr. Neel has received confirmation that the patient whom he suspected had COVID-19 has tested positive for it. The article has been edited to reflect as much.

Dr. Richard Neel served on the team of chemical and biological weapons experts for the Pentagon from 1998-2003 and holds a Master’s Degree in Public Health from Harvard.  He is now a co-owner of The Little Alsace Urgent Care Clinic in Castroville and Uvalde, TX.

By Kayleen Holder & Kathleen Calame

Editor & Publisher, The Devine News

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

Edited by Kalliste, 10 April 2020 - 05:05 PM.

[Dallasboy]

40-80mg of melatonin would put me in a sleep-induced comma for a week!  Does anyone else have bad reactions to melatonin?  I've tried over the years, and I always wake up so groggy/foggy.  Even at 100mcg.  Last week I did try a 5mg extended release, and yes I slept for 9+ hours, but I was out of it all day.  But even these micro doses of 100-300mcg still affect me the next day.  Wonder why?

 

Nevertheless, that's good to hear on M & Vit C against Covid!! 

[zorba990]

Wondering about black seed oil (thymoquinone) :

https://pharmacology...NL007_Molla.pdf

A REVIEW ON ANTIVIRAL EFFECTS OF NIGELLA SATIVA L.
Shamim Molla1, Md. Abul Kalam Azad1, Md Ali Azam Al Hasib1, M. Monayem Hossain1, Md.
Sohel Ahammed1, Shohel Rana1, Muhammad Torequl Islam1*
1Department of Pharmacy, Life Science Faculty, Bangabandhu Sheikh Mujibur Rahman Science and Technology University, Gopalgang-8100, Bangladesh dmt.islam@bsmrstu.edu.bd.
Abstract
Nigella sativa seeds have wide therapeutic effects and have been reported to have significant effects against many ailments such as skin diseases, jaundice, gastrointestinal problems, anorexia, conjunctivitis, dyspepsia, rheumatism, diabetes, hypertension, intrinsic hemorrhage, paralysis, amenorrhea, anorexia, asthma, cough, bronchitis, headache, fever, influenza and eczema. Thymoquinone (TQ) is one of the most active constituent and has different beneficial properties. Focus on antimicrobial effects, different extracts of N. sativa as well as TQ, have a broad antimicrobial spectrum, including Gram-negative, Gram-positive bacteria, viruses, parasites, schist soma and fungi. The effectiveness of N. sativa seeds and TQ is variable and depends on species of target microorganisms. The present review paper tries to describe some antiviral activities of N. sativa. Such as murine cytomegalo virus infection, avian influenza (H9N2), Chistosoma Mansoni Infection, PPR virus, Broad bean mosaic virus, HIV virus, Hepatitis C Virus, Zucchini Yellow Mosaic Virus, and Papaya Ring Spot Virus.
Keywords: Nigella sativa; antiviral effects; HIV; thymoquinone
August 30, 2019
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Introduction
Nigella sativa, a dicotyledon of the Ranunculaceae family, has been employed for thousands of years as a spice and food preservative, as well as a protective and curative remedy for numerous disorders, and is known to have many medicinal properties in traditional medicine (Chopra et al., 1956, Nadkarni et al., 1976). It is the black seed referred to by the prophet Mohammed (PBUH) as having healing powers. Black seed is also identified as the curative black cumin in the Holy Bible, and is described as the Melanthion of Hippocrates and Discroides and as the Gith of Pliny (Attar-ur-Rahman et al.,1985).
Most of studies on biological effect of N. sativa have dealt with its crude extracts in different solvents, however, some studies used its active principles. Haq et al. (1999) fractionated whole N. sativa seeds using SDS-PAGE, which showed a number of protein bands ranging from 94 to 10 kDa molecular mass. Quinones thymoquinone and dithymoquinone are also important constituents of N. sativa (Daba et al.,1998; Nagi et al.,1999).
N. sativa has been reported to have various biological activities (Islam et al., 2019). It exhibited antioxidant properties by suppressing chemiluminescence (Daba et al., 1998; Nagi et al.,1999). Black seed preparations have also demonstrated significant in vivo antineoplastic activity against Erlich ascites carcinoma (Worthen et al.,1998), and in vitro against murine Dalton's ascites lymphoma and sarcoma, and human pancreatic ade- nocarcinoma, uterine sarcoma and leukemic cell lines (Salomi et al., 1991). The active components of black seed also showed antihel-minthic effects against nematodes, cestodes, tapeworms and earthworms (Agarwal et al.,1979; Akhtar et al., 1991). Extracts of N. sativa also showed antimicrobial activity against Escherichia coli, Bacillus subtitles, Streptococcus faecalis, Staphylococcus aureus, Pseudomonas aeruginosa and the pathogenic yeast Candida albicans (Saxena et al.,1986; Hanafy et al.,1991). Black seed has also been evaluated in clinical and animal studies for its choleretic and cytotoxic action (Mahfouz et al., 1962; Tennekoon et al., 1991).
In this review, we have sketched a current scnario on the anti-viral effects of N. sativa and its
derived compounds on the basis of database information.
Methods
An up to date (May 2019) search was made in the following databases: PubMed, Science direct and google scholar with the key word ‘Nigella sativa’ and/or ‘Virus’ and ‘Anti-virus effect’.
Findings
N. sativa against murine cytomegalovirus infection N. sativa oil was found to act against murine cytomegalovirus (Messerle et al., 1992; Reynolds et al., 1993; Smith et al., 1994). In another study, N. sativa oil was also found to act against cytomegalovirus, where an increase in macrophage number and function, and interferon gamma (IFN-γ) production was also reported (Salem et al., 2000).
N. sativa against avian influenza (H9N2)
Avian influenza virus (AIV) subtype H9N2 is becoming a serious threat to poultry birds. H9N2 AIV is an emerging respiratory problem, isolated from different birds from a number of countries and has been reported to have zoonotic potential (Swayne, 2012; Ahad et al., 2013; Umar et al., 2016a,b). Currently, the feed industry is focusing on various substitutes for antimicrobial drugs (Al- Mufarrej, 2014). Antimicrobial agents of plant origin, such as essential oils, plant extracts, and complete plant substances are considered as alternatives to the traditional antimicrobial feed additives. N. sativa oil is one of such alternatives that could be used as feed additives in order to reduce the pathogen load in poultry. Thymoquinone (TQ) has been found as the main bioactive constituent of the volatile oil of N. sativa seeds. In a study, N. sativa was found to exert an anti-influenza virus activity (Umar et al., 2016).
N. sativa against PPR virus
Peste des petits ruminants (PPR), is an acute, highly contagious and economically important transboundary viral disease of sheep and goats associated with high morbidity and mortality (Balamurugan et al., 2014). It is caused by PPR virus, a morbillivirus of the Paramyxoviridae family. Disease severity depends on species infected, breed
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or virus strain (Wernike et al., 2014). As PPR is a viral disease, there exists no particular treatment for the disease and post-exposure therapeutic approaches for infection are not described much in the literature (Balamurugan et al., 2014). Numerous studies report the use of N. sativa as liver tonics, anti-diarrheal, analgesics, and anti-bacterial. Extensive studies on the herb have explored a wide spectrum of its pharmacological actions, including immunomodulatory, antimicrobial and antiinflammatory, properties, etc. Because of its miraculous power of healing, N. sativa has got the place among the top ranked evidence based herbal medicines (Ahmad et al., 2013). Current story describes the immunomodulatory and therapeutic effect of this herb against the PPR virus in experimentally infected goats. N. sativa prevented the occurrence of clinical signs and significant decrease in clinical signs, gross and histopathological abnormalities.
N. sativa against broad bean mosaic virus
Broad bean (Vicia faba L.) is one of the major legumes crops. Broad bean mottle disease is one of the world's main virus diseases in broad bean producing areas. Broad bean mottle virus (BBMV) has spread worldwide wherever broad bean plants are grown. Broad bean mottle virus (BBMV) was classified as a member of the bromovirus group (Hashim and El-Kiey, 1962; El-Alfy et al., 1975). N. sativa is also found to act against MCMV (Nafez et al., 2009; Mehdi et al., 2010).
N. sativa against human immunodificency virus (HIV)
Since 1980’s when the human immunodeficiency virus (HIV) was isolated from patients with opportunistic infections and Kaposi sarcoma, there aremillions of people living with this dreadful virus (Barre-Sinoussi et al, 1983; Gallo et al, 1983; UNAIDS, 2010). It was estimated that no infectious organism has claimed more lives in history than HIV (UNAIDS, 2010). Although the prevalence of HIV infection is reducing globally, many factors had been associated with this gain. The advent of highly active antiretroviral therapy (HAART) and vigorous campaign on sexual behavior considerably have reduced the loss of lives to HIV infection. However, HIV infection is still believed to be incurable and can
only be managed with HAART. N. sativa was found to act against HIV in a number of reports (Onifade 2011,2012,2013).
N. sativa against hepatities C virus
Acute hepatitis C virus (HCV) infection is rarely associated with life-threatening disease, with 15–45% of infected persons recovering within 6 months without any treatment (WHO, 2015). However, chronic infection develops in the remaining 55-85% out of which 15-30% eventually progress to liver cirrhosis after many years of persistent virus carriage. Persistent HCV infection has been a major risk factor for hepatocellular carcinoma (HCC) development (about 2-6% per year) in patients with cirrhosis, mainly through indirect pathways, which include chronic inflammation, cell death, cell proliferation, and induction of free radicals (Sangiovanni et al., 2004; Farinati et al., 2007). Treatment of hepatitis C for virus eradication and non-progression to decompensated liver diseases is achievable and highly recommended for all with chronic infection. The recovery rate however is determined by the strain of the infecting virus, the type of treatment and its early institution (WHO, 2015). An earlier treatment for hepatitis C which combined interferon and ribavirin effectively resolved the infection leading to a cure in 50% of the treated individuals; though frequently associated with life threatening adverse reactions (WHO, 2015). N. sativa was found to act against HCV (Olufunmilayo et al., 2016).
N. sativa against Zucchini yellow mosaic virus Watermelon (Citrullus lanatus L.; family Cucurbitaceae) crop is infected by a dozen of viruses of which Zucchini yellow mosaic virus (ZYMV) that belongs to the genus Potyvirus (family: Potyviridae), is regarded as one of the most destructive viruses. Watermelon infected plants exhibit symptoms that vary from mild to server mosaic, mottling and bubbling followed by leaf deformation and blister (Lisa et al.,1984). ZYMV has a positive single- stranded RNA and flexuous filamentous particles. The antiviral activity of the products including plant extracts, and synthetic chemicals is connected to their components which may act directly by interaction with virus particles in the early stage of infection and block the liberation of its nucleic acid
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that could finally lead to stopping the virus multiplication (Abdel-Shafi et al., 2013). Nigella decoction was found to act against ZYMV (Essam et al., 2017).
N. sativa against Newcastle disease virus
Newcastle disease virus (NDV) has different strains viz, lentogenic less virulent, velogenic and intermediate virulent mesogenic. The disease has high morbidity and mortality with marked decrease in eggs production in laying birds (Alexander, 2000). N. sativa is also found to act against NDV (Al-Garib et al., 2003). The velogenic NDV strains kill the embryo within 48 hours, while lentogenic take 5 to 7 days to affect the embryos (Lam et al., 1995). The active component is crystalline nigellone and thymoquinone that has potent anti-bacterial, anti- inflammatory immune stimulator, anti-parasitic, anti- histamine and anti-hypertensive are the main effects of these seeds (Sultan et al., 2009; Umar et al., 2017). The antiviral drug Ribavirin is well known for the treatment of different diseases like hepatitis. But high dosage produced different types of organ toxicity and was also one the causes of death. Ethanolic extract of the N. sativa is markedly effective against NDV in term of decreased viral load and mortality in embryonated chicken eggs (Khan et al., 2017).
In summary, N. sativa and its derived compounds have been seen to act against a number of human, animals, birds and plant pathogenic viruses. N. sativa may be one of the best sources of anti-viral drugs.
Conflict of Interest
None declared.
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[albedo]

Just learned two major Cantonal university hospitals in Switzerland (HUG in Geneva and CHUV in Lausanne) are treating at 45-50% hospitalized patients with Covid-19 and pneumonia with a treatment including hydroxychloroquine in a pragmatic approach which often characterizes this Federal Country.

[Mr Serendipity]

@Jesus is King: in the other thread you said your wife turned rather pale with infection. I wonder if you have methylene blue and if a very weak solution of it (in water) would bring some color to her cheeks and make her feel better. Or! better yet, you can add a tinny drop to the drinking bowl of your sneezing cat -- how about that?

 

We don’t have any methylene blue.

 

She got her colour back but then turned pale again today (but has regained some of her colour now), and her headaches are also back, and feeling lethargic. Also this morning she was saying it felt it spread to the top of her head, a tingling pressure. She seems to be suffering from recurring symptoms like me, some days she feels fine and thinks there’s nothing wrong with her, and then they pop back up again days afterward. She’s always suffered with irregular heartbeat, low blood pressure, cold hands & feet, and getting dizzy at times, so I think that’s the reason she might be going pale at times. But she’s always had a better immune system than I have.

 

The cats been sleeping more than usual, I haven’t heard him sneeze today.

 

I just feel lethargic and have some headaches. Also we both still don’t have a sense of smell or taste.  

 

Here’s what I’ve been taking everyday:

 

Morning

 

2 x Vitamin C [1g] (Any brand is fine as long as it’s ascorbic acid)

2 x Vitamin E (Healthy Origins - E400)

1 x B-Complex (Higher Nature - B-Vital)

1 x Borage Oil [1g] (Supplemented) 

1 x Vitamin A [3,300 I.U.] + Vitamin D [400 I.U.] (Holland & Barrett)

1/2 x Vitamin D [5000 I.U.] (Natures Aid)

1 x Vitamin K2 [5mg MK4] (Carlson)

1 x Pycnogenol [30mg] (Natures Aid)

1 x Ginger [500mg = 4mg gingerols/shogaols] (Natures Aid)

1 x Garlic extract (Higher Nature)

1 x Turmeric/Curcumin extract (Nature’s Aid)

1 x NAC [500mg] (ProFrontal)

 

Before Bed

 

2 x ZMA [Zinc 10mg, Vitamin B6 3.5mg, Magnesium 150mg] (Supplemented/Amazon)

1 small cap (or 1/2 a big cap) of Ionic Magnesium (Good State)

 

 

To be honest I’ve been slack on the supplements before bed, but I’ve taken my morning supplements everyday bar 2 days, and also the garlic extract was only added a couple of days ago. So since March 29th (13 days ago) when I first got symptoms, 11 of those days I’ve been taking the morning stack, with many pro immune boosting supplements, and still haven’t recovered.

 

Also note, bar the turmeric (added 1st April) and garlic extracts (added a couple of days ago), this has been my stack I’ve been taking prior to getting any of the symptoms, so it really didn’t protect me or prevent the virus in my case, so I think my immune system is generally weak.

 

The only thing that prevented me from getting ill regularly, was when I added Vitamin D to my stack last June, and I hadn’t been sick again since then, until this coronavirus.

Edited by Jesus is King, 10 April 2020 - 06:52 PM.

[Dorian Grey]

OK, umm Viagra?  Was reading about some docs using INHALED nitric oxide to dilate blood vessels in the lung, & thought of Viagra.  

 

Sildenafil, a treatment for erectile dysfunction, is a specific phosphodiesterase type 5 (PDE 5) inhibitor that enhances nitric oxide (NO)-mediated vasodilation in the corpus cavernosum by inhibiting cyclic guanosine monophosphate breakdown.

 

Then I saw this: https://www.pnas.org/content/93/6/2448

 

"The role of nitric oxide (NO) in the pathogenesis of influenza virus-induced pneumonia in mice was investigated...   In vivo spin trapping with dithiocarbamate-iron complexes indicated that a significant amount of NO was generated in the virus-infected lung. Furthermore, an NO-hemoglobin ESR signal appeared in the virus-infected lung, and formation of NO-hemoglobin was significantly increased by treatment with superoxide dismutase and was inhibited by N(omega)-monomethyl-L-arginine (L-NMMA) administration.

 

Immunohistochemistry with a specific anti-nitrotyrosine antibody showed intense staining of alveolar phagocytic cells such as macrophages and neutrophils and of intraalveolar exudate in the virus-infected lung. These results strongly suggest formation of peroxynitrite in the lung through the reaction of NO with O2-, which is generated by alveolar phagocytic cells and xanthine oxidase. In addition, administration of L-NMMA resulted in significant improvement in the survival rate of virus-infected mice without appreciable suppression of their antiviral defenses.

 

On the basis of these data, we conclude that NO together with O2- which forms more reactive peroxynitrite may be the most important pathogenic factors in influenza virus-induced pneumonia in mice."

 

https://www.medicaln...t-is-L-arginine

"In addition to building protein, L-arginine releases nitric oxide in the blood."

 

Now I'm confused!  Is NO bad & arginine good?  Both good?  NO only good with added arginine?  Is inhalation the only way to get the NO effect in pulmonary capillaries?  

Edited by Dorian Grey, 10 April 2020 - 09:12 PM.

[bladedmind]

in the end data wins:

 

both poor clinical and virological outcomes were associated to the use of selective beta-blocking agents and angiotensin II receptor blockers (P<0.05)

 

https://www.mediterr...042020_vD1v.pdf
 

So far only the abstract is available. Would be interesting to see the details when the full text is published.

 

Yes, data win, and alas here are data pointing in another direction.  

 

https://www.medrxiv....3.31.20038935v1

April 4, 2020 preprint

 

Angiotensin II Receptor Blockers and Angiotensin-Converting Enzyme Inhibitors Usage is Associated with Improved Inflammatory Status and Clinical Outcomes in COVID-19 Patients With Hypertension

 

Abstract

With the capability of inducing elevated expression of ACE2, the cellular receptor for SARS-CoV-2, angiotensin II receptor blockers or angiotensin-converting enzyme inhibitors (ARBs/ACEIs) treatment may have a controversial role in both facilitating virus infection and reducing pathogenic inflammation. We aimed to evaluate the correlation of ARBs/ACEIs usage with the pathogenesis of COVID-19 in a retrospective, single-center study. 126 COVID-19 patients with preexisting hypertension at Hubei Provincial Hospital of Traditional Chinese Medicine (HPHTCM) in Wuhan from January 5 to February 22, 2020 were retrospectively allocated to ARBs/ACEIs group (n=43) and non-ARBs/ACEIs group (n=83) according to their antihypertensive medication. 125 age- and sex-matched COVID-19 patients without hypertension were randomly selected as non-hypertension controls. In addition, the medication history of 1942 hypertension patients that were admitted to HPHTCM from November 1 to December 31, 2019 before COVID-19 outbreak were also reviewed for external comparison. Epidemiological, demographic, clinical and laboratory data were collected, analyzed and compared between these groups. The frequency of ARBs/ACEIs usage in hypertension patients with or without COVID-19 were comparable. Among COVID-19 patients with hypertension, those received either ARBs/ACEIs or non-ARBs/ACEIs had comparable blood pressure. However, ARBs/ACEIs group had significantly lower concentrations of CRP (p=0.049) and procalcitonin (PCT, p=0.008). Furthermore, much lower proportion of critical patients (9.3% vs 22.9%; p=0.061), and a lower death rate (4.7% vs 13.3%; p=0.216) were observed in ARBs/ACEIs group than non-ARBs/ACEIs group, although these differences failed to reach statistical significance. Our findings thus support the use of ARBs/ACEIs in COVID-19 patients with preexisting hypertension.

 

 

Whether or not to continue an ARB is the only unresolved question in my defense plan.  Right now I am continuing.  Any and all new info on this question is welcome.

[joelcairo]

So is the mortality rate of 0.5% in elderly a good thing or bad thing based upon this study?

 

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.

 

 

Edited by joelcairo, 11 April 2020 - 01:07 AM.

[joelcairo]

Forgot to mention Raoult is associated with various personal scandals and misrepresentations, so I don't necessarily trust what he claims no matter how many co-authors he has. I'll wait for experts to pass judgment.

[yz69]

Another HCQ success story, Sacramento CA

https://www.youtube....Vathrs218&t=32s

[resveratrol_guy]

Another HCQ success story, Sacramento CA

https://www.youtube....Vathrs218&t=32s

 

It's important to point out that Dr. Truong combined HCQ with vitamin D, vitamin C, zinc, and copper. Unfortunately he didn't give the dosages of those additional components. He also mentioned that this isn't his first such result, although he neglected to mention the numbers.

 

Copper mineral salts are not suitable for prophylaxis, on account of their fueling of Alzheimer's. But of course I have no problem with emergency use, as in this case.

[Heisok]

He had also been on Azithromycin which they continued with Vitamin C, D, Zinc and Copper.

 

(Sorry poster above was also writting their reply.)

 

On another note, the 70 year old man I knew who was already intubated did not recover with Azithromycin and HCQ treatment. Passed away. They ended up having a hole in a lung which might have been from the intubation. I do not know.

 

Edited by Heisok, 11 April 2020 - 02:59 AM.

[resveratrol_guy]

The risks that we're willing to assume, in addition to economic cost and societal cost, need to be informed by death rate. But do we know what it is? I've heard numbers below 1%, but exit statistics run as high as 94%. Both might be true, depending on the country in question. It seems to hinge on:

 

* How much freedom do doctors have, in a given country, to react to what they see in a manner informed by research and medical social networking? (Lots of freedom produced the South Korean 3% death rate vs. 94% in the UK under the rigid NHS.)

 

* Do recoveries lag deaths, or the other way round? It seems that overburdened countries will have lagging deaths because they want to keep the hospitals as available as possible, so they evict the healthy as soon as possible; while undercapacity ones will have lagging recoveries, as they have the ability and desire to keep recovered patients isolated for the sake of public safety. This tradeoff then governs the forecast of the death rate. No doubt the UK will improve, for instance, as recoveries finally start to exit the system.

 

* What is the asymptomatic rate? I read one estimate of one third, which wouldn't affect the numbers much. But others have suggested that China, for one, has already had half its population infected. I haven't seen a single random testing study which might shed light on this. And this is all complicated by uncertainty as to whether we've already identified all possible antibodies, and the latency until they're detectable.

 

* How are deaths being counted? Is it true that Italian deaths spiked by 4X as much as official COVID19 deaths would account for, during the peak of their outbreak, indicating that most victims died at home? If so, how were those deaths labelled? And what about Dr. Birx' promise that anyone who died while positive would be counted as a COVID19 death, regardless of the major cause? (And now the US government has created a financial incentive for hospitals to report deaths as due to the virus.)

 

The bottom line is that I don't think we have a clue, and the answer likely varies by orders of magnitude among countries. We might be making horrible policy decisions as a result.

 

I want to see a robust estimate in at least one country informed by random sampling with minimum bias.

 

At some point, this information should inform the criminal prosecution of health officials who continue to force their staff to adhere to rigid protocols developed prior to the discovery of any information about the peculiarities of COVID19.

 

[Dorian Grey]

This guy's affect is a bit tedious, but I did learn a few things about how HCQ (and perhaps quinine!) might work against COVID.  

 

 

Interesting he says these quin meds can get into red blood cells.  The theory on COVID damaging hemoglobin came to mind.

 

The immune suppression is a bit concerning regarding prophylactic use, but I've read the "ground glass opacities" seen on CT typically occur very early on, often before advanced disease develops.  If lungs are damaged early in the disease process, perhaps this is a rationale for prophylactic quins?  

 

We've heard the theory of the alkalizing effect on lysosomes inhibiting viral replication before, but seeing his visual made me think YES, this is what I want!  Protect my lungs from the early stage damage...  Protect my hemoglobin from being compromised...  Inhibit viral replication...  A triple whammy therapy!  

 

Sipping my second gin & tonic now and feeling fine.  Have accumulated a couple dozen 4-packs of light/low sugar tonic water lined up under my book case. Gather ye quinine while ye may! 

 

Look for: Fever-Tree Refreshingly Light Premium Indian Tonic Water with Natural Quinine @ 30 calories per 200ml bottle; and “Q Spectacular Tonic Water” @ 45 calories per 222ml.

 

If my doc won't prescribe HCQ early on if/when I get sick, I'll be drinking 8-12 of these per day (sans the gin).  Until then, its 2 G & T's per night, before bed prophylaxis.  Medicine never tasted so good!  

Edited by Dorian Grey, 11 April 2020 - 06:57 AM.

[Izan]

Very interesting.

 

Dutch scientists believe they discovered the essential mechanism of COVID-19 and found a way to counter it with success (icatibant).

 

I google translated it for you guys:

 

 

 

Researchers at Radboud Hospital in Nijmegen think they have discovered an essential mechanism in the covid-19 disease process that has been overlooked so far.

 

"If the insight is correct, it probably has important consequences for the treatment of the disease," says a press statement from the hospital.

 

Leaky blood vessels

Doctors always see three stages of serious infections with the coronavirus: shortness of breath due to fluid on the lungs, an inflammatory reaction in the lungs and the development of thrombosis and scarring in the lungs due to the fluid.

 

"The first phase, in which the lungs fill up with fluid, CT scans of the lungs look serious and patients quickly become short of breath when administering fluid, is very characteristic," says Frank van de Veerdonk, internist-infectiologist at Radboud university medical center. "This picture cannot be explained only by the infection of the lungs. We had the idea that during this process the very small blood vessels in the lungs also leak. That leakage causes problems for the lungs, because they partly fill up."

 

This was previously seen with SARS, the virus infection that claimed many lives in 2003. However, a good explanation was never found.

 

Possible leakage explanation

The researchers at Radboud university medical center now come up with a possible explanation for the leak. Covid-19 is known to enter the lungs through the so-called ACE2 receptor. ACE2 is an enzyme found on organs, including the lungs. It is also the receptor, the 'receiver', for the coronavirus in the human body.

 

"The virus binds to the receptor and is withdrawn by the receptor into the lung cell, where the virus can multiply," says Van de Veerdonk. "In a massive infection, those ACE2 receptors disappear from the outside of the cell. Their function also disappears."

 

Until now, doctors have known that ACE2 plays a role in maintaining blood pressure throughout the body. But it has another function, according to the researchers, which has been left out of the picture in covid-19 infections. "ACE2 keeps the substance bradykinin under control. Bradykinin makes blood vessels leak. We have good reason to believe that with these covid-19 infections we see exactly this effect: ACE2 receptors disappear from the lung cells by the introduction of the virus , which gives bradykinin free rein and causes the small blood vessels to leak en masse at the site of infection. "

 

Therapy

The researchers believe that this is an essential mechanism in the disease process of Covid-19. While most covid-19 treatments are now aimed at inhibiting inflammation, this research focuses on the phase before that: the leak that is causing the lungs to get into trouble.

 

That is why the researchers are already setting up treatments with icatibant, a drug that can inhibit the effects of bradykinin. "The beauty is: every patient is the same," says Van de Veerdonk. "They all have no defenses and everyone is leaking. We have now started the treatment with five patients and I can be cautiously positive. But of course we are not there yet."

 

International research must show whether the new insights and treatments do indeed have an effect. If that is the case, then this has major consequences, according to Van de Veerdonk. "The moment a patient enters the hospital, the whole process can be stopped within a few days and they will have an opportunity to clear the virus in the next two weeks. People can go home faster and because we asked patients no longer end up in intensive care. "

 

The researchers' new insights have yet to be assessed and commented by colleagues. Van de Veerdonk chose to publish the research as soon as possible and not wait for publication in a highly regarded magazine. "Because if what we think is right, it can make all the difference."

 

https://nos.nl/artik...lootgelegd.html

 

[OP2040]

 

Very interesting.

 

Dutch scientists believe they discovered the essential mechanism of COVID-19 and found a way to counter it with success (icatibant).

 

Leaky blood vessels

Doctors always see three stages of serious infections with the coronavirus: shortness of breath due to fluid on the lungs, an inflammatory reaction in the lungs and the development of thrombosis and scarring in the lungs due to the fluid.

 

"The first phase, in which the lungs fill up with fluid, CT scans of the lungs look serious and patients quickly become short of breath when administering fluid, is very characteristic," says Frank van de Veerdonk, internist-infectiologist at Radboud university medical center. "This picture cannot be explained only by the infection of the lungs. We had the idea that during this process the very small blood vessels in the lungs also leak. That leakage causes problems for the lungs, because they partly fill up."

 

This was previously seen with SARS, the virus infection that claimed many lives in 2003. However, a good explanation was never found.

 

Possible leakage explanation

The researchers at Radboud university medical center now come up with a possible explanation for the leak. Covid-19 is known to enter the lungs through the so-called ACE2 receptor. ACE2 is an enzyme found on organs, including the lungs. It is also the receptor, the 'receiver', for the coronavirus in the human body.

 

"The virus binds to the receptor and is withdrawn by the receptor into the lung cell, where the virus can multiply," says Van de Veerdonk. "In a massive infection, those ACE2 receptors disappear from the outside of the cell. Their function also disappears."

 

Until now, doctors have known that ACE2 plays a role in maintaining blood pressure throughout the body. But it has another function, according to the researchers, which has been left out of the picture in covid-19 infections. "ACE2 keeps the substance bradykinin under control. Bradykinin makes blood vessels leak. We have good reason to believe that with these covid-19 infections we see exactly this effect: ACE2 receptors disappear from the lung cells by the introduction of the virus , which gives bradykinin free rein and causes the small blood vessels to leak en masse at the site of infection. "

 

Therapy

The researchers believe that this is an essential mechanism in the disease process of Covid-19. While most covid-19 treatments are now aimed at inhibiting inflammation, this research focuses on the phase before that: the leak that is causing the lungs to get into trouble.

 

That is why the researchers are already setting up treatments with icatibant, a drug that can inhibit the effects of bradykinin. "The beauty is: every patient is the same," says Van de Veerdonk. "They all have no defenses and everyone is leaking. We have now started the treatment with five patients and I can be cautiously positive. But of course we are not there yet."

 

International research must show whether the new insights and treatments do indeed have an effect. If that is the case, then this has major consequences, according to Van de Veerdonk. "The moment a patient enters the hospital, the whole process can be stopped within a few days and they will have an opportunity to clear the virus in the next two weeks. People can go home faster and because we asked patients no longer end up in intensive care. "

 

The researchers' new insights have yet to be assessed and commented by colleagues. Van de Veerdonk chose to publish the research as soon as possible and not wait for publication in a highly regarded magazine. "Because if what we think is right, it can make all the difference."

 

https://nos.nl/artik...lootgelegd.html

 

 

 

wow, this is very interesting izan82, at least to me.  Angiodema and even (more rarely) edema are side effects of ACE inhibitors and Bradykinin has been implicated in it for some time.

 

I've done a bit of research on this in the past.  Once again, the pharma drug does nothing for us.  However, Bromelain is known as an bradykinin inhibitor.  And the best part last, Bromelain is very often combined with Quercetin in supplements, for reasons that escape me right now.  So that Q/B combo supplement just took a huge leap toward the top of the list since Q is already known to be beneficial for other reasons.

[Iporuru]

Treatment with ACE-inhibitors is associated with less severe disease with SARS-Covid-19 infection in a multi-site UK acute Hospital Trust

Abstract: Background:​ The SARS-Cov2 virus binds to the ACE2 receptor for cell entry. It has been suggested that ACE-inhibitors, which are commonly used in patients with hypertension or diabetes and which raise ACE2 levels, may increase the risk of severe COVID-19 infection. Methods:​ We evaluated this hypothesis in an early cohort of 205 acute inpatients with COVID-19 at King's College Hospital and Princess Royal University Hospital, London, UK with the primary endpoint being death or transfer to a critical care unit for organ support within 7-days of symptom onset. Findings:​ 53 patients out of 205 patients reached the primary endpoint. Contrary to the hypothesis, treatment with ACE-inhibitors was associated with a reduced risk of rapidly deteriorating severe disease. There was a lower rate of death or transfer to a critical care unit within 7 days in patients on an ACE-inhibitor OR 0​.​29 (CI 0​.​10-0​.​75, p<0​.0​1), adjusting for age, gender, comorbidities (hypertension, diabetes mellitus, ischaemic heart disease and heart failure). Interpretation:​ Although a small sample size, we do not see evidence for ACE-inhibitors increasing the short-term severity of COVID-19 disease and patients on treatment with ACE-inhibitors should continue these drugs during their COVID-19 illness. A potential beneficial effect needs to be explored as more data becomes available.

 

Possible weaknesses: small sample size, competing interest

[albedo]

Great recap from Clinicaltrials.gov by Jesse Burk-Rafel:

 Trials April 2020.jpg   232.46KB   0 downloads

https://pbs.twimg.co...C6-XgAEnHmz.jpg

[joelcairo]

Identification of Dietary Molecules as Therapeutic Agents to Combat COVID-19 Using Molecular Docking Studies

https://assets.resea.../Manuscript.pdf

 

Notably EGCG. Why is it always EGCG? Other suggested compounds are curcumin, myricetin, genistein, myricetin, beta-glucan, quercetin and diadzein.

 

The authors selected phytonutrients that have previously been shown to have antiviral properties, not necessarily against COVID-19. The assumption is that having one of these molecules bind to the virus would be a good thing, but I wonder if there isn't a scenario where EGCG or whatever could help the virus cross the cell membrane and thus be harmful.

 

[joelcairo]

Another docking study FWIW.

 

Potential Inhibitor of COVID-19 Main Protease (Mpro) From Several Medicinal Plant Compounds by Molecular Docking Study

https://www.research...r_Docking_Study

 

The phytonutrients suggested as meriting further study were (from best to worst in order of binding energy) were kaempferol, quercetin, luteolin-7-glucoside, demethoxycurcumin, naringenin, apigenin-7-glucoside, oleuropein, catechin, curcumin,and  epicatechin-gallate.

 

[OP2040]

wow, this is very interesting izan82, at least to me.  Angiodema and even (more rarely) edema are side effects of ACE inhibitors and Bradykinin has been implicated in it for some time.

 

I've done a bit of research on this in the past.  Once again, the pharma drug does nothing for us.  However, Bromelain is known as an bradykinin inhibitor.  And the best part last, Bromelain is very often combined with Quercetin in supplements, for reasons that escape me right now.  So that Q/B combo supplement just took a huge leap toward the top of the list since Q is already known to be beneficial for other reasons.

 

Someone wanted references for this.  I think the Ace inhibitor Bradykinin part of it is just common knowledge so I'll just cite a random study for that one:

 

https://www.ncbi.nlm...pubmed/27260014

 

 

Historically, the first described effect of an angiotensin converting enzyme (ACE) inhibitor was an increased activity of bradykinin, one of the substrates of ACE.

 

 

And then the connection from there to angiodema or vessel leakage is also well known, since these are known effects of too much bradykinin.

 

https://en.wikipedia...wiki/Bradykinin

 

 

Currently, bradykinin inhibitors (antagonists) are being developed as potential therapies for hereditary angioedema. Icatibant is one such inhibitor. Additional bradykinin inhibitors exist. It has long been known in animal studies that bromelain, a substance obtained from the stems and leaves of the pineapple plant, suppresses trauma-induced swelling caused by the release of bradykinin into the bloodstream and tissues.^[15] Other substances that act as bradykinin inhibitors include aloe^[16][17] and polyphenols, substances found in red wine and green tea.^[18]

 

 

I guess that Aloe is another one aside from Bromelain that has potential.  My interest in this is with other forms of edema which are very numerous in disease and one of the hallmarks of inflammation.  Potentially combine with lots of fish oil to get the pro-resolving factors going and you have a mini-protocol that makes sense, and accessible/cheap enough that many people are already taking one or two of these things.

[Dorian Grey]

Brilliant work izan82 & OP2040!  I'll share some of my tonic water with you if there is a run on the market once early results of the HCQ studies start coming out. 

 

The discoveries on COVID regarding substantial pulmonary damage occurring early on, patients who've cleared the virus becoming reinfected, the failure of ventilation therapy, the vaccine disasters with original SARS (antibody enhanced disease), and new mutations popping up have been so depressing.  

 

I'm starting to think we may never be able to beat this bug and effective prophylaxis & treatment is our only hope.  I now have new hope we'll be able to live with this virus.  

 

To all on this thread...  We Salute You!  

Edited by Dorian Grey, 11 April 2020 - 03:45 PM.

[OP2040]

haha, thanks Dorian same to you.  I'm at a state now where I'm not worried at all about the people here nor my family and friends that are taking similar precautions.  I do NOT believe in giving up on people just because they are old, or placing blame or dismissing those struggling with obesity and chronic illness.  Wanted to write a long screed about it, but suffice it to say we are all in this together and we got this!

[BlueCloud]

There is something odd going on with tobacco/nicotine and covid. This was an interview on radio, so no link sorry, but according to Prof. Delfraissy, head of the scientific council on covid in France, the overwhelming majority of cases with severe symptoms are all non-smokers. In the main hospital of Besançon ( east of France with highest number of cases along with the Paris region ) , Almost none of the cases in ICU are smokers

 

Now, consider that France is among the biggest smokers in Europe, maybe less than China, but probably the same or slightly less than Italy, Spain and Greece. Definitely more than the rest of western european countries. Also, there are more female smokers than men there.

 

We’re pretty sure non-smokers have healthier lungs than smokers, so what could it be in nicotine that acts as antiviral in this case ?

 

 

Edited by BlueCloud, 11 April 2020 - 04:16 PM.

[joelcairo]

There is something odd going on with tobacco/nicotine and covid. This was an interview on radio, so no link sorry, but according to Prof. Delfraissy, head of the scientific council on covid in France, the overwhelming majority of cases with severe symptoms are all non-smokers. In the main hospital of Besançon ( east of France with highest number of cases along with the Paris region ) , Almost none of the cases in ICU are smokers

 

Now, consider that France is among the biggest smokers in Europe, maybe less than China, but probably the same or slightly less than Italy, Spain and Greece. Definitely more than the rest of western european countries. Also, there are more female smokers than men there.

 

We’re pretty sure non-smokers have healthier lungs than smokers, so what could it be in nicotine that acts as antiviral in this case ?

 

If this study has not been subsequently discredited, the carbon monoxide inhaled due to smoking cigarettes is anti-inflammatory by inhibiting production if IL-12. That's one possible mechanism.

 

https://www.scienced...60103084934.htm

[joelcairo]

... Also smoking induces expression of ACE2 in lung cells, with possible mixed effects.

[xEva]

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.

[Hebbeh]

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.

[Mind]

Is it just me, or does Raoult's recent paper look pretty encouraging.

 

1,061 patients

 

So far only 5 died (16 still in the hospital)

 

Mortality rate of 0.5% in the "elderly" patients. Given this mortality rate, does that mean there were 200 "elderly" and only 1 died.

 

From the article, there is no breakdown of how many there were in each age cohort, only a mean age of people in the study.

 

https://techstartups...1-success-rate/

 

The article also said he was using zinc with hydroxychloroquine and azithromycin. Can anyone else confirm this?

Edited by Mind, 11 April 2020 - 11:35 PM.

[xEva]

Is it just me, or does Raoult's recent paper look pretty encouraging.
 
1,061 patients
 
So far only 5 died (16 still in the hospital)
 
Mortality rate of 0.5% in the "elderly" patients. Given this mortality rate, does that mean there were 200 "elderly" and only 1 died.
 
From the article, there is no breakdown of how many there were in each age cohort, only a mean age of people in the study.
 
https://techstartups...1-success-rate/
 
The article also said he was using zinc with hydroxychloroquine and azithromycin. Can anyone else confirm this?

There is only abstract available at the moment. It was posted above by BlueCloud. No mention of zinc though: https://www.mediterr...042020_vD1v.pdf