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    Metadichol: An Effective Plant-Based Antiviral?


    Metadichol: An Effective Plant-Based Antiviral?
    The ongoing COVID-19 global pandemic and other pathogenic virus outbreaks have led scientists to explore new techniques to address treatment of
    trialsitenews.com


    The ongoing COVID-19 global pandemic and other pathogenic virus outbreaks have led scientists to explore new techniques to address treatment of SARS-CoV-2. With ongoing virus mutations, scientists are looking at approaches that hold promise for targeting the entire pathogen, rather than single variants. One such approach is targeting lipid membranes which are common to viruses and bacteria. Metadichol is a naturally derived supplement that targets lipid membranes, and recent research merited a review.


    Metadichol is a nano lipid formulation that consists of long-chain policosanol alcohols. It is made from renewable sources and has been commercially available for seven years.


    Also known as Nano Soma or Nano-Ojas, the preparation was developed in 2008 by Dr. Palayakotai Raghavan, CEO of NanoRx Inc. Raghavan has since obtained patents in the U.S. and worldwide. He has written several papers on the use of Metadichol for a range of diseases, some of which have been published in the Journal of Stem Cell Research and Therapy, and the Journal of Cytokine Biology.


    A Brief Review of Dr. Raghavan

    Dr. Raghavan originally earned his PhD from Oregon State University in “Organic Synthesis.” He went on to work as a scientist in big Pharma then launching a venture to develop biofuels. He launched his current venture, NanoRx, Inc., in 2008 which is a start-up in the field of nanomedicine.


    Developed from the waxes from sugar cane and rice, Metadichol has a range of effects in the body, including acting on Vitamin D receptors and nuclear hormone receptors that influence epigenetic regulation.


    While systematic reviews have shown policosanols to be “well tolerated and safe”, they have not received authorisation from the U.S. Food and Drug Administration (FDA) as of November 2021. As such, policosanol products such as Metadichol can currently only be marketed in the U.S. as dietary supplements and not as drugs for treating or preventing medical conditions.


    In a recent study, Raghavan tested the effect of Metadichol against COVID. As of November 2021, this study is still in print and has been peer-reviewed. The results, show hopeful signs for the use of Metadichol to fight COVID-19.


    The Theory: Metadichol’s Role in Fighting COVID

    Everyday substances, like soaps, alcohols, cleaning products, and anti-bacterial wipes target the lipid layer of viruses. Alcohols can also inactivate viruses by entering the lipid layer through a hydrophobic effect. This makes the lipid membrane permeable to other small molecules, and allows immune cells to recognize the virus.


    With properties of lipids and alcohols, Metadichol has been shown to be effective against a range of pathogens. In addition to this mechanism, the latest research focuses on the ability of Metadichol to inhibit specific host-cell receptors that play key roles in SARS-CoV-2 infection.


    The virus uses the human proteins TMPRSS2 and ACE2 to enter the host’s cells. The SARS-CoV-2 spike protein, located on its exterior, binds to ACE2 (angiotensin-converting enzyme 2) to gain entry into cells. While inhibiting ACE2 would prevent the virus entering cells, it is not a practical treatment: ACE2 plays a role in the body to regulate blood pressure and blood volume, so blocking this receptor completely would be fatal to the patient.


    However, the virus cannot bind to ACE2 without the help of TMPRSS2. TMPRSS2 is a serine protease, which cleaves the spike protein and enables it to bind to ACE2. When TMPRSS2 is inhibited, it stops the replication of viruses. Therefore, to fight COVID-19, a treatment that regulates TMPRSS2 would be ideal.


    Study Design and Methods

    In the study, Metadichol was tested for its suspected inhibitory actions against TMPRSS2, as well as its anti-viral effects against SARS-CoV-2.


    Commercially available testing kits were used to assess the in vitro effects of Metadichol on TMPRRSS2. Metadichol was also tested against the live virus in cell culture to assess its effects on the ability of the SARS-CoV-2 virus to replicate within cells.


    Results: How can Metadichol Fight COVID-19

    The results of the study indicated that Metadichol could be an effective therapy for COVID-19.


    Metadichol is a powerful inhibitor of TMPRSS2 which is needed for helping the spike protein bind to ACE2. Metadichol also is an inhibitor of the androgen receptor which controls expression of TMPRSS2. Metadichol was found to have a mild inhibitory effect on ACE as well.


    Metadichol also demonstrated an anti-viral replication effect against the virus itself at a concentration of 0.00037 μM. Compared to Remdesivir and hydroxychloroquine, Metadichol has a 2100-fold and 3400-fold effectiveness respectively.


    From the results, it appears that high concentrations of Metadichol are able to behave similarly to soap. It was observed to disrupt the lipid membrane of the virus at these higher concentrations, while at lower concentrations it neutralized the virus through a different mechanism.


    Other properties of Metadichol

    Metadichol and Vitamin D


    It is thought that Metadichol acts on Vitamin D receptors (VDRs) as an inverse/protean agonist – the only one known in literature. VDRs are found throughout the body, including on immune cells. Bacteria and viruses can bind to VDRs, preventing the innate immune response. Metadichol is able to displace bacteria and viruses that attach to these VDRs, allowing for a normal immune response.


    Metadichol and Vitamin C


    Dr. Raghavan supplemented 30 people with Metadichol, and found it resulted in an increase in vitamin C levels – three times greater than the increase achieved with direct Vitamin C supplementation.


    Vitamin C is also required for a healthy immune response against pathogens and viruses. While Vitamin C is not an effective treatment against COVID-19, this vitamin still assists with wound healing, reducing the severity of symptoms of common viruses, and helps relieve lethargy.


    Effect on Other Pathogens


    As mentioned previously, the physical properties of Metadichol make it effective at interrupting the lipid envelopes of a range of pathogens, facilitating access of the immune system.


    Studies in the United States, Switzerland, and India have tested Metadichol against influenza, ebola, yellow fever, malaria, and tuberculosis in vitro, and have reported promising results in its efficacy. Clinical studies in TB patients are ongoing.


    Could Metadichol be the Next Game Changer?

    The in vitro results of Metadichol against SARS-CoV-2 are promising. TrialSite will continue to monitor this potential COVID treatment as the situation unfolds


    (PDF) Metadichol ® a novel nano lipid that inhibits In Vitro, SARS-COV-2 and a multitude of pathological viruses
    PDF | New pathogenic virus outbreaks with increasing regularity are leading us to explore novel approaches, which will reduce the reliance on a... | Find, read…
    www.researchgate.net

    Covid: Trigger of rare blood clots with AstraZeneca jab found by scientists


    Scientists find trigger for rare AstraZeneca clots - BBC News
    Researchers in Cardiff and the US work out how the Covid jab may be linked to the extremely rare clots.
    www.bbc.com


    The team - in Cardiff and the US - have shown in exquisite detail how a protein in the blood is attracted to a key component of the vaccine.


    They think this kicks off a chain reaction, involving the immune system, that can culminate in dangerous clots.


    The vaccine is thought to have saved about a million lives from Covid.

    However, concerns about rare blood clots shaped how the vaccine has been used around the world including an alternative being offered to the under-40s in the UK.


    It also started a scientific detective hunt to figure out what was going on and if it could be prevented. The Cardiff team were given emergency government funding to find the answers.


    AstraZeneca's own scientists also joined the research project after earlier results from the team were published.


    A spokeswoman for AstraZeneca stressed that clots were more likely to occur because of a Covid infection than the vaccine, and that the complete explanation for why they occur had not yet been established.


    "Although the research is not definitive, it offers interesting insights and AstraZeneca is exploring ways to leverage these findings as part of our efforts to remove this extremely rare side effect," she added.


    Graphic explaining how blood clots form

    There were two initial clues for the researchers investigating the rare blood clots:


    The greater risk of clots was seen only with some of the vaccine technologies

    People with clots had unusual antibodies that were attacking a protein in their blood called platelet factor four

    The vaccines used in the UK all try to deliver a snippet of the Covid-virus's genetic code into the body to train the immune system.


    Some package that code up inside spheres of fat, while the AstraZeneca one used an adenovirus (specifically a common cold virus from chimpanzees) as its microscopic postman.


    The researchers thought the adenovirus might be linked to the rare clots occurring in some people. So they used a technique called cryo-electron microscopy to take images of the adenovirus in molecular-level detail.


    Nobel prize awarded for imaging molecules

    Their study, published in the journal Science Advances, reveals the outer surface of the adenovirus attracts the platelet factor four protein to it like a magnet.


    Prof Alan Parker, one of the researchers at Cardiff University, told BBC News: "The adenovirus has an extremely negative surface, and platelet factor four is extremely positive and the two things fit together quite well."


    He added: "We've been able to prove the link between the key smoking guns of adenoviruses and platelet factor four.


    "What we have is the trigger, but there's a lot of steps that have to happen next."

    The researchers think the next stage is "misplaced immunity", but this needs to be confirmed in further research.


    It is thought the body starts to attack platelet factor four after confusing it for part of the foreign adenovirus to which it is stuck. So antibodies are released into the blood, which clump together with platelet factor four and trigger the formation of dangerous blood clots.


    However, this requires a series of unlucky events, which could explain why the clots are so rare.


    These clots, known as vaccine-induced immune thrombotic thrombocytopenia, have been linked to 73 deaths out of nearly 50 million doses of AstraZeneca given in the UK.


    "You could never have predicted it would have happened and the chances are vanishingly small, so we need to remember the bigger picture of the number of lives this vaccine has saved," said Prof Parker.


    AstraZeneca said the vaccine is thought to have saved more than a million lives around the world and prevented 50 million cases of Covid.


    The University of Oxford declined to comment on the research.


    Dr Will Lester, a consultant haematologist at University Hospitals Birmingham NHS Trust, praised the "very detailed" research saying it helps explain the "most likely initial step" in clotting.


    He added: "Many questions still remain unanswered, including whether some people may be more susceptible than others and why the thrombosis (clotting) is most commonly in the veins of the brain and liver, but this may come with time and further research."


    The Cardiff team hope their findings can be used to improve adenovirus-based vaccines in the future to reduce the risk of these rare events.

    Current POTUS Failing in Pandemic Response—No Mention of Natural Immunity Nor Available Drugs Like Fluvoxamine


    Current POTUS Failing in Pandemic Response—No Mention of Natural Immunity Nor Available Drugs Like Fluvoxamine
    Recently Dr. Mary Makary, MD, MPH, Chief, Islet Transplant Surgery and a Professor of Surgery with Johns Hopkins Medicine recently joined Fox’s Harris
    trialsitenews.com


    Recently Dr. Mary Makary, MD, MPH, Chief, Islet Transplant Surgery and a Professor of Surgery with Johns Hopkins Medicine recently joined Fox’s Harris Faulkner to discuss the Omicron variant and other matters associated with the pandemic. Dr. Makary who also serves as the Editor-in-Chief for MedPage Today enlightened the viewer, elucidating truthful points unfortunately not heard too often on other media. Sharing with the Fox news host that SARS-CoV-2 variants will probably be with us forever, Makary declared that perhaps the Biden’s administration’s biggest failure is to not acknowledge natural immunity to SARS-CoV-2, the virus behind COVID-19. Additionally, the surgeon and academic medical center investigator emphasized the critical importance of antivirals and other treatments that can work today against COVID-19. Notable among those was the importance of Fluvoxamine, an existing approved, thus repurposed drug that according to clinical study and subsequent peer-review can reduce COVID-19 deaths by 91%. Why isn’t the Biden administration, the National Institutes of Health or others in the so-called medical establishment advancing this drug to help people?


    Recently TrialSite published a letter authored by Dr. Michael Goodkin, part of the TrialSite advisory committee to the Infectious Disease Society of America asking the fundamental question why this influential medical society is shunning this important drug (Fluvoxamine).


    Dr. Makary had other points to share with the audience about travel bans, the importance of expedited analysis of Omicron as well as continuing standard healthcare such as elective surgeries. He declared that while the government announces that the testing and associate analysis of the Omicron mutation will take a couple weeks Makary believes this can be undertaken in one day. And declarations of emergencies, such as what just happened in the State of New York lead to bad outcomes for patients in dire need of care. For example, vital elective surgeries (cancer resection or hip replacements for example) are put off with real consequences. With each day it seems this current administration digs itself into a deeper hole.


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    Nothing exceptional from South Africa:


    https://www.nicd.ac.za/wp-content/uploads/2021/12/Datcov19_National_Export-20211201.pdf


    The Data exactly follows last years November Raise. So the increase is seasonal. Hospitals had a strong increase two weeks ago but already lower last week. So still no trend is visible.

    As said RSA has the largest AIDS infected population that makes them somehow different. These folks may host the virus for ever...and if e.g. V-D3 gets low it will break out again.


    Omicron is endemic in almost all parts in world as the scanning of old probes shows. So travel restrictions are simply a part of the world wide vaccine terror game.


    On the other side Age 70+ should get a Ziverdo kit at home to allow for early treatment.


    But as long as the world wide big pharma NAZI mafia (FM/R/JJJ/B) sees a chance to make mega tons of money this will not happen.


    We here DE/CH/AU see a strong increase in mafia public relation in the news papers. These folks use "Neusprech" vaccine for gene therapy and claim profit for people age <50 with a mortality as low as 0.001% from CoV-19. The risk to slip to death on soap - shower gel - is higher!!!! Same for car accidents.

    Most people that died age < 50 where on cancer therapy. So a real loss for big pharma...

    Covid-⁠19 Schweiz | Coronavirus | Dashboard
    Covid-⁠19 Pandemie Schweiz und Liechtenstein: Fallzahlen, Virusvarianten, Hospitalisationen, Re-⁠Wert, Spitalkapazitäten, internationale Lage, Zahlen zu Tests,…
    www.covid19.admin.ch


    Here the Swiss death/hospital rates for the last 9 months.


    The figures clearly show age 80+ dies 400x more often than age < 50. Hospitalization is 10x larger for age > 50 than age < 50. Age < 50 is < 50% vaccinated age > 50 is > 80% vaccinated.


    This clearly shows that the pandemic is driven by the the age > 70 with a moderate risk for age > 50 < 70 and no risk for age < 50.


    So restrictions should only exist for age > 50. The rest is fascists terror.

    Quote from Wyttenbach

    This clearly shows that the pandemic is driven by the the age > 70 with a moderate risk for age > 50 < 70 and no risk for age < 50.


    So restrictions should only exist for age > 50. The rest is fascists terror.

    Incorrect. See:


    Cases, Data, and Surveillance
    Cases, data, and surveillance to track and analyze COVID-19.
    www.cdc.gov


    Furthermore, the vaccines reduce risk in all age groups:


    https://www.axios.com/age-coronavirus-risk-vaccines-2e1391b0-5d0e-4fa9-894b-4b894dc017c9.html


    The most important thing you are overlooking is that death is not the only bad outcome. Hundreds of thousands of people, including young people, are suffering long-haul symptoms. Many have lost jobs, livelihood, the ability to live on their own without nursing help. In some cases their lungs are ruined and they will never fully recover. In nearly every case, a vaccine would have prevented this.

    Quote from Wyttenbach

    ...and if e.g. V-D3 gets low it will break out again.

    An interesting note...

    I had my annual blood work up done last week and specifically asked that V-D levels be included.

    The result came back that I was curiously very low in VD!


    I state curious in that I have been taking 2500 IU's a day for the past 18 months! I guess I will have to bump up to 5000. It was not just low, but very low. (I am traveling at the moment and do not have the exact numbers with me)


    I wonder how many people "think" their levels are OK since they eat a fairly healthy diet? I would have sworn my levels would be OK as well since I eat balanced and take supplements as well.... but I was proven wrong... or the tests were inaccurate which I would not think the case.


    I have seen multiple articles about the benefits of VD lately and not from this forum. I believe this information is starting to get around some and perhaps might do some good.

    Quote from JedRothwell

    See:


    https://www.lenr-canr.org/acrobat/RothwellJreviewofth.pdf


    And see the papers linked to this in the References.

    Thank you.


    The vacuum jacket and part-silvered dewar is an interesting rig. And critical to testing boil-offs.


    I get their reasoning for it. I wonder if it actually accomplishes it actually. It seems to have worked OK, but radiation at such low temperatures is pretty weak compared to convection.

    Dr John Campbell posted a video on vit D and all mortality in its conclusion the researchers recommended 4,000- 10,000 units per day from fall to summer to raise levels above 50Ng/mL . The NIH recommendation is 20Ng/mL so yours is probably below even that minimum . By the way that level was established for rickets.

    Quote from JedRothwell

    Simplicity, Fig. 6, leading up to the boil-off phase.

    No. In the "Simplicity Paper" (1), the first calorimetric method was used to calculate the excess enthalpy Qf during the heating up phase, well before the onset of boiling conditions. These calculated values are reported on the Figs. 6A to 6D, but they are always a small fraction of the corresponding enthalpy input.


    The output enthalpy during the boil-off phase was calculated by using the second calorimetric method. F&P calculated a value of about 4 times the input enthalpy, but this value is absolutely wrong because they didn't considered that at that point the fluid in the cells was mostly foam.


    (1) http://www.lenr-canr.org/acrobat/Fleischmancalorimetra.pdf

    Some experts suggest Omicron variant may have evolved in an animal host


    Some experts believe Omicron variant may have evolved in an animal host
    The theory goes that some type of animal, potentially rodents, was infected with the SARS-CoV-2 virus sometime in mid-2020.
    www.statnews.com


    When Covid-19 variants arise, the accepted wisdom is that the constellation of mutations they contain developed in an immunocompromised person who contracted the virus and couldn’t shake the infection. But some scientists have an alternative theory for where the latest variant of concern, Omicron, may have acquired the unusual mutations that stud its spike protein.


    They speculate the virus could have evolved in another animal species.


    The theory goes that some type of animal, potentially rodents, was infected with the SARS-CoV-2 virus sometime in mid-2020. In this new species, the virus evolved, accumulating roughly 50 mutations on the spike protein before spilling back over into people

    Kristian Andersen, an immunologist at the Scripps Research Institute, is among those who has been raising the idea that Omicron may have emerged from a reverse zoonotic event.


    (A zoonotic event is when an animal pathogen starts to infect and spread among people. A reverse zoonosis is when such a virus passes back into an animal species.)

    “I know that most people think that these [come from] immunocompromised individuals, and I do think that that’s plausible, but to be perfectly honest, I actually think this reverse zoonosis followed by new zoonosis seems more likely to me given just the available evidence of the really deep branch, and then the mutations themselves, because some of them are quite unusual,” Andersen told STAT.


    “I don’t think we should dismiss that possibility, because I think it’s definitely on the table.”


    A number of other scientists who study the evolution of viruses have told STAT they think the idea isn’t out of the question. Some place more weight on the theory that variants develop in immunocompromised people, while others feel there isn’t enough evidence at this point to favor one option over the other.


    “Personally, I think it’s probably more likely it was circulating undetected, in an immunocompromised individual,” Emma Hodcroft, a molecular epidemiologist at the Institute of Social and Preventive Medicine in Bern, Switzerland, said via email. Having said that, though, Hodcroft insisted that it is important to explore the hypothesis.


    “I would certainly consider it a plausible alternative hypothesis to the evolution during a persistent infection in a human,” said Andrew Rambaut, a professor of molecular evolution at the Institute of Evolutionary Biology in Edinburgh. He cautioned that coming up with a definitive answer won’t be quick.


    “I am not sure we will be in a position to say for sure for a while,” Rambaut wrote in an email.


    One of the peculiar traits of SARS-2 underpins this thinking. It is what virologists describe as a promiscuous virus; it is capable of infecting a number of species. Dogs and house cats. Large cats. Mink. White-tailed deer. Given how easily the virus seems to jump from species to species, people studying it assume this list will grow.

    The original virus that came out of Wuhan, China, in early 2020 did not infect rodents. But as variants — Alpha, Beta, Delta — started to emerge, those viruses could infect rodents.


    Robert Garry, a professor of microbiology and immunology at Tulane Medical School, has been tracking the SARS-2 mutations that have arisen. Seven are associated with rodent adaptation — the changes that seemed to allow the virus to infect mice, rats, and related species. All seven of those mutations are in Omicron, Garry noted. He believes it’s a toss-up whether the variant developed in an animal or a human host, but if it’s the former, his bet would be on rodents.


    Getting a firm answer might require enormous luck. Scientists are looking at various animal species to see if they can be infected with SARS-2; were they to find viruses like Omicron in any, that would swing the needle.


    But Michael Worobey, a professor of evolutionary biology at the University of Arizona, thinks one could do some experiments on selected species of wild animals to see if they can be infected and if, when infected, similar patterns of viral evolution occur.


    Studying the molecular clock of viruses that spread in animals — looking at the speed at which they evolve and comparing it to SARS-2 evolution in humans — could also provide some clues, said Worobey, who initially thought Andersen’s idea was not impossible, but not the likeliest of explanations for Omicron. After hearing details of the explosive outbreak in white-tailed deer, he’s rethinking the idea.


    For Worobey, the question is whether any animal species can become chronically infected with SARS-2 — in effect, whether there are animal species in which SARS-2 lingers in the way it does in immunocompromised people. That could put positive selective pressure on the virus — in other words give it an incentive to mutate to stay ahead of the animal’s immune response.


    “It does move my thinking in terms of Omicron possibly having come from a reservoir, if there are [animal] reservoirs that do chronic infections,” he said.


    Part of what leads Andersen to wonder about an animal source is the fact that the variant traces back to viruses that were spreading over a year ago. “That in itself you need to be able to explain,” he said.


    Angela Rasmussen, a coronavirus virologist at the University of Saskatchewan’s Vaccine and Infectious Disease Organization, agreed.


    “I think it’s pretty obvious to everybody … that this virus has been on an independent evolutionary track for quite some time and it’s very surprising, which to me just kind of goes back to say well, the idea that this could be … plausible,” she said.


    Regardless of whether this variant emerged in another species or not, given SARS-2’s ability to jump species, it is possible the world will face animal-derived variants in the future, Garry warned. The upshot of that? “We’re going to have to keep tweaking the vaccines.”

    Quote from Paradigmnoia

    It seems to have worked OK, but radiation at such low temperatures is pretty weak compared to convection.

    Convection and conduction are minimal because there is a vacuum between the electrolyte and the water bath. Radiation dominates. There is a vacuum even in the "window" at the bottom with no silver (no mirror).


    Miles measured a little conduction with a cell that was made some years before his experiment. A little air had leaked into the vacuum portion of the cell. See p. 12.

    Quote from Ascoli65

    No. In the "Simplicity Paper" (1), the first calorimetric method was used to calculate the excess enthalpy Qf during the heating up phase, well before the onset of boiling conditions.

    Incorrect. It was used right up the moment boiling began. Furthermore, the method was used in many other experiments, described in other papers, in which high heat was measured. Furthermore, this method (and methods very similar to it) has been used in many other cold fusion experiments by other researchers in which high heat was measured, and in countless other experiments going back to J. P. Joule in the 1840s.


    Basically, you are saying that one of the oldest, most reliable and widely used experimental techniques does not work. You are wrong. That fact that you think you are right and every scientist in the last 180 years is wrong tells us that you are an egomaniac, you have no grasp of reality, and you suffer from an extreme case of the Dunning Kruger effect.

    Quote from JedRothwell

    Convection is minimal because there is a vacuum between the electrolyte and the water bath. Radiation dominates. There is a vacuum even in the "window" at the bottom with no silver (no mirror).


    Miles measured a little convection with an cell that was made some years before his experiment. A little air had leaked into the vacuum portion of the cell.

    Right, it would mostly try to convect near the cap.

    I would have to look at the emissivity of the glass at that temperature so see how well it radiates heat out, but obviously all of the heat gets out somewhere and the assembly functioned.

    40% of Hong Kong People Show Gut Dysbiosis Comparable to that of COVID-19 Patients CUHK Microbiome Immunity Formula Hastens Recovery of COVID-19 Patients and Offers Hope to Boost Immunity


    40% of Hong Kong People Show Gut Dysbiosis Comparable to that of COVID-19 Patients CUHK Microbiome Immunity Formula Hastens Recovery of COVID-19 Patients and Offers Hope to Boost Immunity
    A recent study by CU Medicine revealed a worrying fact that 40% of Hong Kong people appeared to have significant gut dysbiosis comparable to that of COVID-19…
    www.med.cuhk.edu.hk


    Gut microbiota plays an important role in regulating immunity against infections. People who suffer from imbalance in gut microbiota (dysbiosis) are more susceptible to viral infection and other complications. An earlier study by the Faculty of Medicine of The Chinese University of Hong Kong (CU Medicine) has highlighted that severe gut dysbiosis exists in COVID-19 patients.



    A recent study by CU Medicine revealed a worrying fact that 40% of Hong Kong people appeared to have significant gut dysbiosis comparable to that of COVID-19 patients, suggesting they have potentially impaired immunity. CU Medicine has developed a microbiome immunity formula that targets gut dysbiosis. Compared with patients who had standard care, our research team found that more COVID-19 patients who received the microbiome immunity formula achieved complete symptom resolution, showed significantly reduced proinflammatory markers in their blood, had increased favourable bacteria in their stool; and developed neutralising antibody. Data also suggested that the formula can restore the balance of gut microbiota and boosts immunity.


    CU Medicine Develops a Probiotic Formula to Target Imbalance in Gut Microbiota in COVID-19

    CU Medicine Develops a Probiotic Formula to Target Imbalance in Gut Microbiota in COVID-19
    CU Medicine Develops a Probiotic Formula to Target Imbalance in Gut Microbiota in COVID-19
    www.med.cuhk.edu.hk



    40% of people in HK have moderate to severe gut dysbiosis related to impaired immunity


    To evaluate the extent of dysbiosis in the general population, CU Medicine studied 1,000 subjects in Hong Kong aged between 18 and 83, and found that almost 40% of them had significant dysbiosis (i.e., impaired immunity) comparable to that of COVID-19 patients.



    Professor Francis KL CHAN, Dean of Medicine and Director of the Centre for Gut Microbiota Research at CUHK remarked, “Gut dysbiosis is an important marker of impaired immunity. Our study findings showed 40% of Hong Kong people had evidence of significant dysbiosis comparable to that of COVID-19 patients which is alarming to us. We should take immediate action to restore the balance in gut microbiota and hence to help the public boost immunity against the threats of emerging infections such as COVID-19.”



    CUHK’s microbiome immunity formula enhances recovery of COVID-19 patients

    Using big data analysis and metagenomics derived from COVID-19 patients, researchers in CU Medicine has developed a unique oral microbiome formula that targets gut dysbiosis. Clinical data showed the recovery of COVID-19 patients who received the microbiome immunity formula outperformed those with standard care in many aspects. These include the achievement of complete symptom resolution; significant reduction of proinflammatory markers in their blood, increase in favourable bacteria in their stool and development of neutralising antibody.

    Amid the third wave of COVID-19 outbreak in Hong Kong, the CU Medicine team recruited 55 hospitalised patients with COVID-19; 25 patients were treated with the microbiome immunity formula and 30 received standard care. Key findings are as follow:

    100% of patients treated with the microbiome immunity formula achieved complete resolution of symptoms compared with half in the control group by week 2.

    88% of patients in the microbiome immunity formula group developed neutralizing antibody compared with 63% in the control group.

    The blood level of pro-inflammatory cytokines was significantly reduced in the microbiome immunity formula group, indicating that inflammation was under control.

    The levels of favourable bacteria recovered from stool in patients receiving the microbiome immunity formula was significantly increased, suggesting that the formula could restore gut dysbiosis.

    This study demonstrated that the microbiome immunity formula is effective in replenishing a series of good bacteria missing in the gut of COVID-19 patients. Restoration of gut dysbiosis could hasten symptom resolution, enhances host immunity and increases neutralising antibody. These data support the use of microbiome therapy as a potential strategy to restore gut dysbiosis to fight against COVID-19,” Professor Siew Chien NG, Associate Director of the Centre for Gut Microbiota Research at CUHK, explained.

    Professor Francis KL CHAN concluded, “The imbalance of gut microbiota is common among Hong Kong people, indicating that many are suffering from impaired immunity. While there are many products in the market claiming that they could boost immunity, such claims need further scientific evidence. The development of this unique microbiome immunity formula was backed up by science and its benefits are supported by clinical evidence against COVID-19. The formula not only has the potential to hasten the recovery of COVID-19 patient, but also helps boost immunity of the public.”

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