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Cardiovascular Disease

Covid-19, Blood Pressure Medication, and Ibuprofen

One of the questions that shows up often in the comments to the various Covid-19 posts here (especially this one) and very often in my own emails is whether people who are taking hypertension medications should alter their drug therapy based on the coronavirus epidemic. Most of those questions are specifically about ACE inhibitors (all the -pril drugs) or angiotensin receptor blockers (all the -sartan ones). The advice given here starts out with, as usual, I Am Not a Physician, but points out that no professional society has yet recommended doing changing such a treatment regimen.

Today there’s a review of the field of all the renin-angiotensin-aldosterone system (RAAS) drugs and their possible interactions with the viral epidemic in the New England Journal of Medicine (open access article), and I wanted to highlight it as the most recent word on the subject. Here’s the key take-away: “Until further data are available, we think that RAAS inhibitors should be continued in patients in otherwise stable condition who are at risk for, being evaluated for, or with Covid-19” Note that this advice applies all the way to people who are positively infected with the coronavirus; there’s not enough evidence to say that even those people should change their blood pressure treatment.

The paper points out that the idea that one or another of these drugs might be harmful or increase the risk of infection is only a hypothesis, and that there are other (equally plausible) hypotheses that this might not be the case or that some of them might actually beneficial. And it also notes, absolutely correctly, that we do not have enough information yet to distinguish between these ideas. We’ll be getting some (whether it will help or not when we get it, who knows!) but what’s for sure is that we don’t have it yet. My guess is that if there were a big worrisome effect size in the data that we might have seen it pop up already, but the search has been underway for such things, at any rate.

So that’s the answer we have now: no one should be altering their blood pressure treatment regime based on coronavirus concerns, because we don’t know enough to say if that’s a good idea, and we do know enough to say that suddenly going off of these drugs or changing them up can be a bad one.

And since we’re on that drug-interaction topic, the related question of whether ibuprofen is safe to use during this epidemic is still going around. These two intersect, because one rationale that’s been advanced is that ibuprofen could upregulate the ACE2 protein that’s involved in the angiotensin system and is a known entry protein for the virus. But here’s the current situation: there is no overall evidence to suggest that ibuprofen increases the risk of coronavirus infection or its severity. The whole story was started off by a letter to The Lancet and accelerated by a tweet from a French minister of health, but these appear to have been based on early anecdotal reports that do not seem to have held up. The CDC, the WHO, and all other health authorities who have weighed in on the issue have come to the same conclusion: ibuprofen and the other NSAIDs do not appear to have bad effects in this epidemic. Nothing has shown up since those initial reports to confirm them; no association between coronavirus infection and anti-inflammatories has appeared in the data we have.

I definitely understand why these stories get a lot of attention and why people worry about them: these hypertension medications and NSAIDs are taken by huge numbers of people worldwide, and if there really were a heightened risk of infection or severity of disease with them, that’s something you would very much want to know. And people want to feel that there’s something that they can do, some concrete step they can take to minimize their risk. A lot of us humans also have a weakness for sudden-reversal stories and surprising explanations: under our noses all along! The very drugs we were taking to make us better are putting us at risk! And once in a while that happens (estrogen replacement therapy comes to mind). But doesn’t seem to be one of those times – fortunately.

38 comments on “Covid-19, Blood Pressure Medication, and Ibuprofen”

  1. colintd says:

    I’d be interested in your take on the relevance (or not) of this June 2019 (i.e. pre-COVID19) paper https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6617416/ on NSAIDs and lower respiratory tract infections, the conclusion of which was:

    “This should encourage experts and scientific societies to strongly advise against the use of NSAIDs in the management of lower respiratory tract infections.”

    1. Derek Lowe says:

      That does indeed seem to be what set off the French minister’s advice. Ibuprofen doesn’t seem to have been associated with different outcomes in upper respiratory tract infections, though (bronchitis): https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3790568/

    2. charlie says:

      Isn’t the clinical course of the disease that it starts in the upper respiratory tract, and then for some patients moves to the lower?

      So treating it with ibuprofen for fever during that initial stage may prime it to move lower?

  2. luysii says:

    Speaking as someone taking Ramipril (an ACE inhibitor), I plan to continue. Here’s why. Drugs inhibiting enzymes, change the conformation of the active site. It stands to reason that COVID19 developed its affinity for ACE, when inhibitors were not around, so it seems the COVID19 would be less able to bind to the ACE/Ramipril complex.

    Without trying to be snarky, I must say it is interesting to see chemical minds wrestle with the type of data and situations that physicians routinely have to deal with. Not so easy is it?

    1. Steve says:

      To clarify, SARS-CoV-19 binds to ACE-2, not ACE-1, and most ACE-1 inhibitors to not have activity against ACE-2 (I don’t know about Ramipril in particular). Moreover, the binding site of the virus is not the active site of the ACE-2 enzyme. Crystal structures of ACE-2 do not show a large change in the viral binding site when inhibitors are bound. Although I would like know if there is actual data that viral spike protein binding affinity decreases in the presence of an ACE-2 active site ligand.

      1. Steve says:

        * SARS-CoV-2 (oops, confusing my acronyms!)

        1. luysii says:

          Steve: Thanks. Any conformation change almost anywhere, however small, produced by Ramipril even on ACE2 (it’s hard to believe there are none as the enzymes are so similar) would likely decrease viral spike protein binding. As you note, the crucial data is the binding affinity of the viral spike protein to ACE1, ACE2 in the presence and absence of drugs such as Ramipril.

          1. roger says:

            >Any conformation change almost anywhere, however small, produced by Ramipril >even on ACE2 (it’s hard to believe there are none as the enzymes are so similar) >would likely decrease viral spike protein binding.

            Hmm. Isn’t this assertion based on the assumption that the current conformation is somehow optimal, so that any change makes it less optimal? This seems like an overreach. A small conformation change could just as easily enhance the interaction. I’m in a different corner of science, but I don’t see how we have enough information about this particular binding to know that it is so optimal. What am I missing? Peace.

          2. Betty says:

            So dues that mean with the Covid 19 it is save to keep taking two low fuse rams prop every day. Must if the time so only take 2x per day. Thank you

  3. Kevin says:

    If you are taking requests (obnoxious, I know), I’d like to hear more about IL-6 receptor blockers. This tweet from UMich piqued my interest. I looked back and didn’t see them covered in your earlier overview of potential therapeutics. Lot’s ideas flowing around. It’s great to have someone reputable to help us make sense of it.

    https://twitter.com/vineet_chopra/status/1244998589366939651?s=20

    1. Alan Goldhammer says:

      @Kevin – there are a bunch of ongoing clinical trials of these drugs.

  4. JasonP says:

    A basic discussion of this excellent point can be found here:

    https://youtu.be/1vZDVbqRhyM

    Dr S reviews the mechanism of the ACE2 receptor on the cell wall and how the hypertension drugs effect ACE2, he shows and reviews the Lancet article, then provides a view from Cardiologists.

    Might be the same thing in a video form, for those who learn from hearing/seeing better than reading.

    1. KazooChemist says:

      Thanks for posting that link. I have read all this information many times, and I think I have a good grasp of the facts. The video does a great job of pulling things together in an easy to follow format. A good resource for those (like me) who are not experts in the field who want to have a better understanding.

  5. The curious one says:

    I would be interested to hear what you all think about another NSAID called Flurbiprofen to moderate Cytokine production down? Here is the link https://www.ncbi.nlm.nih.gov/pubmed/1404130 for the publication “Effect of flurbiprofen on cytokine production by human monocytes and U-937 and THP-1 cell lines”

    From the abstract “Flurbiprofen caused moderate inhibition of IL-1 beta and TNF alpha production by stimulated monocytes, but did not affect IL-6 production. In contrast, flurbiprofen completely abolished IL-6 production by both cell lines and substantially inhibited IL-1 beta and TNF alpha production.”

    Since a “Cytokine Storm” supposedly is one major reason for a bad outcome https://link.springer.com/article/10.1007/s00134-020-05991-x I was wondering whether this might be useful especially in the late stage when it seems to go downhill fast and some of that perhaps being the own immune system going overboard.

    Thank you for some thoughts!

  6. Some idiot says:

    Just a quick typo warning: paragraph 4 you say:
    “ because we don’t know enough to saw if that’s a good idea”; I presume you mean “say”? That’s one I do too…

    Thanks for the nice summary!

  7. Tom Boyer says:

    Good to know the French minister tweet on ibu has not been borne out.

    But still — I wonder if there’s an argument for not taking ibu (or acetaminophen) at the first sign of fever – in theory the fever is helping your body’s immune response. Certain stages of the immune response operate more efficiently at higher temperatures.

    Dr. Roger Seheult has been doing a series of wonderful explanatory lectures on Covid-19 at the MedCram YouTube site. His focus this week has been the immune system and research that shows early stage response is boosted by raising (or lowering) body temperature. In the days before penicillin, the medical standard of care for flu patients was hot and cold baths.

    Seheult goes into the microbiology to explain why this might really work — it’s not a cure but it might boost the immune response and make the disease milder (which would certainly be helpful with this disease).

    The goal in 1918 was to prevent the flu from developing into pneumonia — and at some clinics they apparently got pretty good at it. Points out that might be a strategy with this disease because the death rate is so high once people reach ARDS.

    1. Sarah says:

      I would love to hear some more opinions about this

    2. Matt says:

      A fever also makes people feel bad so they get the rest they need. My purely anecdotal experience is that using ibuprofen to ignore a fever so that one can study for and take final exams seems to make it come back with a vengeance once you stop the ibuprofen.

  8. Alan Goldhammer says:

    With respect to NSAIDS, there is one registered French trial designed to look at the effect of naproxen on seriously ill SARS-CoV-2 patients. NIH Trial #: NCT04325633

  9. another idiot says:

    Hi Derek,

    I also use naproxen when I get aches and pains. I think that’s the same as Alieve but I’m not sure. And that’s ibuprofen because it’s for aches and pains just like what Alieve is for. What should I do? Does this interact with those enzymes and receptors everyone talks about?

    Maybe I should stop using condoms because if I get infected with HIV it will attack the COVID-19 virus? Right? I read it on a twitter account linked to a website linked to the government of some country so it’s probably true.

    Maybe I’ll go to the park and breathe in everyone’s farts because I heard farts contain thiols and they have antiviral activity. So that will make me safe.

    Just kidding……..and kind of where things are in my neck of the woods………..NY…….and the rest of the world

    Sarcasm aside……everyone keep safe. And I took my sartan this morning. And, after a lot of discussion, I convinced the nurse for my doctor today that it was unlikely that we could conduct a meaningful annual physical exam via Telehealth and perhaps, just maybe, they could just renew my script for that sartan. I was surprised that she didn’t want the copay for the visit.

  10. Zee Bendelstein says:

    Understood that coming off anti-hypertensive medicine on the basis of a spurious and likely false link is an unambiguously bad idea. But given that there are safe alternatives to ibuprofen that are not NSAIDs and (to my knowledge) few rely on ibuprofen for life-saving applications, would it not be wise to temper usage as a precaution? Or is that kind of thinking just a recipe to react to the slightest and most tenuous information…can’t make up my mind, but would probably just pop acetaminophen if I needed.

  11. Tom says:

    Wouldn’t the better argument against Ibuprofen be that is a stronger COX-1 than COX-2 inhibitor, a combination assumed to be detrimental in sepsis conditions as happening in late stage COVID-19. I’d like to see studies how it does in comparison to selective COX-2 inhibitors.

  12. Contagion says:

    Forsythia is the cure!

  13. Jim Palmef says:

    One concern is that the combination of multiple drugs (that could well include hypertensives, but which overall contribute to polypharmacy) could lead to increased Covid-19 susceptibility. The epidemiology on this is far from known, but the elder population of countries like the US and Italy might well be on a lot of drugs wherein one or two might be OK but five or more could radically muck up the balance of their immune systems.

    1. Chris Phoenix says:

      Here’s some anecdata against that: My father just turned 80, and isn’t taking any medicines for blood pressure or diabetes. He got COVID (test-confirmed). They put him on an oxygen mask (not a ventilator) because the highest flow rate cannula (15 L/min?) wasn’t keeping him oxygenated and gave him two(!) CT scans in 3 days.

      He’s back on a cannula now and past the 10-day mark from start of symptoms, so it looks like he’ll be OK. But prior to the mask, he was on a video call – thus, inhaling through his mouth while talking, not using the cannula enough. He started to get a bit out of breath, sat up in bed for 5 seconds to get his oximeter, put it on… it read 75%. A few minutes of quiet nose-breathing and he was back up near 90 again.

      COVID is no joke regardless of what medicines you aren’t taking.

  14. John Konopa says:

    As a plain old mechanical engineer with an affinity to chemistry I do enjoy (most) of your blog topics. As a consumer of these (as are many) I thank you for taking the time to comment on these studies and the surrounding hypotheses. I look forward to your posts.

  15. Rob says:

    I thought an issue with the ACE inhibitors was that their use resulted in an increase in the number of ACE-2 receptors, the entry point of the virus.

    1. Derek Lowe says:

      See today’s blog post – that may well not be the case.

  16. Mary says:

    Fresh ginger reduces both the vasoconstricting Angiotensin 2 ( which will become too high is ACE 2 is not working properly as affected by the virus) AND decreases inflammatory IL6
    …Also inhibits JAK 2 AND stimulates Beta Interferon
    All postulated to be beneficial in Covid 19

    [gingerol: a novel AT₁ antagonist for the treatment of cardiovascular disease.
    Liu Q1, Liu J, Guo H, Sun S, Wang S, Zhang Y, Li S, Qiao Y
    Abstract
    This study aimed to find novel compounds targeting the angiotensin II type 1 receptor, accepted as a therapeutic target in cardiovascular disease. Gingerol (ginger) was identified as a novel angiotensin II type 1 receptor antagonist, with an IC50 value of 8.173 µM. The major ingredient of ginger, [6]-gingerol, could inhibit angiotensin II type 1 receptor activation, which partially clarified the mechanism of ginger regulating blood pressure and strengthening heart in the cardiovascular system.

    Ginger reduces IL-6 https://www.ncbi.nlm.nih.gov/pubmed/22884532
    Effect of enteral feeding with ginger extract in acute respiratory distress syndrome.
    Results
    Patients fed enteral diet enriched with ginger had significantly lower serum levels of IL-1, IL-6, and tumor necrosis factor α and higher level of RBC glutathione on days 5 and 10 compared with control group (P < .05). Significant improvement in oxygenation was observed on day 5 (P = .02) and 10 (P = .003) in ginger group compared with control group. A significant difference was found in duration of mechanical ventilation (P = .02) and length of intensive care unit stay (P = .04) in favor of ginger group.
    CONCLUSIONS:
    An enteral diet supplemented with ginger in patients with ARDS may be beneficial for gas exchange and could decrease duration of mechanical ventilation and length of stay in intensive care unit.

    Ginger reduces IL-6 https://www.ncbi.nlm.nih.gov/pubmed/22884532

    Identification of a Dual Inhibitor of Janus Kinase 2 (JAK2) and p70 Ribosomal S6 Kinase1 (S6K1) Pathways.
    Byun S1, Lim S2, Mun JY3, Kim KH4, Ramadhar TR5, Farrand L6, Shin SH7,
    Abstract
    Bioactive phytochemicals can suppress the growth of malignant cells.. Ginger has been reported to exhibit potent anti-cancer effects, although previous reports have often focused on a narrow range of specific compounds. Through a direct comparison of various ginger compounds, we determined that gingerenone A selectively kills cancer cells while exhibiting minimal toxicity toward normal cells. Kinase array screening revealed JAK2 and S6K1 as the molecular targets primarily responsible for gingerenone A-induced cancer cell death. The effect of gingerenone A was strongly associated with relative phosphorylation levels of JAK2 and S6K1.

    Fresh ginger of high concentration could stimulate mucosal cells to secrete IFN-β that possibly contributed to counteracting viral infection.
    Fresh ginger (Zingiber officinale) has anti-viral activity against human respiratory syncytial virus in human respiratory tract cell lines.
    Chang JS1, Wang KC, Yeh CF, Shieh DE, Chiang LC

    https://www.ncbi.nlm.nih.gov/pubmed/23123794
    Conventional Med study Beta Interferon stimulating Drug Trial Southampton University
    UK biotech Synairgen has started dosing patients in its phase 2 trial of SNG001, an inhaled formulation of interferon beta-1a that aims to treat coronavirus infections.
    Interferon beta orchestrates the body’s response to a viral infection, and there is some evidence to suggest that people who get dangerously sick after being infected with SARS-CoV-2 – the virus that causes COVID-19 – have lower than usual levels of interferon beta in the lungs.
    Synairgen also says viruses – including coronaviruses such as SARS-CoV-2 and MERS-CoV – have evolved mechanisms which suppress the production of interferon beta in the body, helping them evade the immune system.
    The drug is already widely used in an injectable form for multiple sclerosis, and Synairgen has already tested its inhaled version in clinical trials involving more than 200 asthma patients with a cold or flu infection, showing improvements in lung function.

  17. Mary says:

    Fresh ginger reduces vasoconstrictor Angiotensin 2 ( which will be raised if ACE 2 is not working properly as affected by being the virus entry point). Ginger also lowers inflammatory IL6 , acts as a JAK inhibitor and increases Beta Interferon.
    ALL thought to be positive in Covid 19.

    Ginger reduces IL-6 https://www.ncbi.nlm.nih.gov/pubmed/22884532
    Effect of enteral feeding with ginger extract in acute respiratory distress syndrome.
    Results
    Patients fed enteral diet enriched with ginger had significantly lower serum levels of IL-1, IL-6, and tumor necrosis factor α and higher level of RBC glutathione on days 5 and 10 compared with control group (P < .05). Significant improvement in oxygenation was observed on day 5 (P = .02) and 10 (P = .003) in ginger group compared with control group. A significant difference was found in duration of mechanical ventilation (P = .02) and length of intensive care unit stay (P = .04) in favor of ginger group.
    CONCLUSIONS:
    An enteral diet supplemented with ginger in patients with ARDS may be beneficial for gas exchange and could decrease duration of mechanical ventilation and length of stay in intensive care unit.

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4440027/
    The effect of Zingiber officinale R. rhizomes (ginger) on plasma pro-inflammatory cytokine levels in well-trained male endurance runners
    Conclusions
    Our findings indicate that prolonged intense training for 6 weeks in well-trained male endurance runners can significantly elevate post-exercise plasma levels of several pro-inflammatory cytokines and that a ginger using period of 6 weeks will essentially reverse these elevations. Therefore, it may be better if coaches apply approximately 6 weeks’ ginger using periods prior to important competitions in order to properly prepare endurance athletes of optimal performance and recovery.

    COVID-19: consider cytokine storm syndromes and immunosuppression

    https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)30628-0/fulltext
    All patients with severe COVID-19 should be screened for hyperinflammation using laboratory trends (eg, increasing ferritin, decreasing platelet counts, or erythrocyte sedimentation rate) and the HScore
    There is a subgroup of patients for whom immunosuppression could improve mortality. Therapeutic options include steroids, intravenous immunoglobulin, selective cytokine blockade (eg, anakinra or tocilizumab ( blocks IL-6) ) and JAK inhibition.

    Identification of a Dual Inhibitor of Janus Kinase 2 (JAK2) and p70 Ribosomal S6 Kinase1 (S6K1) Pathways.
    Byun S1, Lim S2, Mun JY3, Kim KH4, Ramadhar TR5, Farrand L6, Shin SH7,
    Abstract
    Bioactive phytochemicals can suppress the growth of malignant cells.. Ginger has been reported to exhibit potent anti-cancer effects, although previous reports have often focused on a narrow range of specific compounds. Through a direct comparison of various ginger compounds, we determined that gingerenone A selectively kills cancer cells while exhibiting minimal toxicity toward normal cells. Kinase array screening revealed JAK2 and S6K1 as the molecular targets primarily responsible for gingerenone A-induced cancer cell death. The effect of gingerenone A was strongly associated with relative phosphorylation levels of JAK2 and S6K1.

    GINGER is a JAK inhibitor – related to IL 6 and IL 10

    ===========================================================================
    https://www.healio.com/rheumatology/rheumatoid-arthritis/news/online/%7B1957db6e-f7a2-4e5d-939e-d4b5964b2dd3%7D/sarilumab-enters-clinical-trial-for-covid-19-spotlighting-key-role-for-il-6
    Conventional Med study Sarilumab enters clinical trial for COVID-19, spotlighting 'key role' for IL-6

    It appears that IL-6 may play a key role in driving the inflammatory response that leads to morbidity in patients with COVID-19 who develop acute respiratory distress syndrome. There have been reports of increasing experience using tocilizumab, another IL-6 inhibitor, to treat these patients with severe COVID-19 infection, including a non-peer-reviewed retrospective Chinese experience describing 21 COVID-19 positive patients with severe illness who received tocilizumab. They observed improvement in oxygenation and other clinical outcomes.”
    In that Chinese study, conducted by Xiaolong Xu, MD, , tocilizumab was given to 21 patients with severe COVID-19, in addition to routine therapy, between Feb. 5 and Feb. 14. According to the researchers, fevers returned to normal and all other symptoms “improved remarkably” within a few days. Additionally, 75% of patients had lowered their oxygen intake and one patient no longer needed oxygen therapy.

    TH17 responses in cytokine storm of COVID-19: An emerging target of JAK2 inhibitor Fedratinib
    https://www.sciencedirect.com/science/article/pii/S1684118220300657
    In a mouse model, H1N1 causes acute lung injury in an IL-17-dependent manner.8 Taken together, the TH17 type response contributes to the cytokine storm in pulmonary viral infection including SARS-CoV-2, which results in tissue damage and likely promotes pulmonary edema; targeting the TH17 pathway may benefit the patients with TH17 dominant immune profiles.

    Ginger Extract Reduces the Expression of IL-17 and IL-23 in the Sera and Central Nervous System of EAE Mice.
    https://www.ncbi.nlm.nih.gov/pubmed/26714420

    Beta Interferon- thought to be beneficial
    Ginger stimulates it
    https://www.ncbi.nlm.nih.gov/pubmed/23123794
    Conventional Med study Beta Interferon stimulating Drug Trial Southampton University
    UK biotech Synairgen has started dosing patients in its phase 2 trial of SNG001, an inhaled formulation of interferon beta-1a that aims to treat coronavirus infections.
    Interferon beta orchestrates the body’s response to a viral infection, and there is some evidence to suggest that people who get dangerously sick after being infected with SARS-CoV-2 – the virus that causes COVID-19 – have lower than usual levels of interferon beta in the lungs.
    Synairgen also says viruses – including coronaviruses such as SARS-CoV-2 and MERS-CoV – have evolved mechanisms which suppress the production of interferon beta in the body, helping them evade the immune system.
    The drug is already widely used in an injectable form for multiple sclerosis, and Synairgen has already tested its inhaled version in clinical trials involving more than 200 asthma patients with a cold or flu infection, showing improvements in lung function.
    The Southampton-based company says the first patient with COVID-19 has now been given SNG001 at the University Hospital Southampton NHS Foundation Trust
    Investigators aim to enroll 100 patients in the pilot phase.

    Fresh ginger of high concentration could stimulate mucosal cells to secrete IFN-β that possibly contributed to counteracting viral infection.
    Fresh ginger (Zingiber officinale) has anti-viral activity against human respiratory syncytial virus in human respiratory tract cell lines.
    Chang JS1, Wang KC, Yeh CF, Shieh DE, Chiang LC
    Abstract:
    Ginger has been proved to have antiviral activity against human respiratory syncytial virus (HRSV). However, it is unknown whether ginger is effective against HRSV.
    RESULTS:
    Fresh ginger dose-dependently inhibited HRSV-induced plaque formation in both HEp-2 and A549 cell lines (p<0.0001). In contrast, dried ginger didn't show any dose-dependent inhibition. 300 μg/ml fresh ginger could decrease the plaque counts to 19.7% (A549) and 27.0% (HEp-2) of that of the control group. Fresh ginger was more effective when given before viral inoculation (p<0.0001), 300 μg/ml fresh ginger could decrease the plaque formation to 12.9% when given before viral inoculation. Fresh ginger dose-dependently inhibited viral attachment (p<0.0001) and internalization (p<0.0001). Fresh ginger of high concentration could stimulate mucosal cells to secrete IFN-β that possibly contributed to counteracting viral infection.

  18. mary says:

    Fresh Ginger reduces levels of vasoconstricting Angiotensin 2 ( which may be raised if Ace 2 is not working properly as the virus attaches to it) . Ginger Reduces inflammatory cytokine IL6, inhibits JAK and increses levels of Interferon B.
    – All suggested to be of benefit in Covid 19

  19. Mary says:

    Ginger reduces IL-6 https://www.ncbi.nlm.nih.gov/pubmed/22884532
    Effect of enteral feeding with ginger extract in acute respiratory distress syndrome.

    https://www.healio.com/rheumatology/rheumatoid-arthritis/news/online/%7B1957db6e-f7a2-4e5d-939e-d4b5964b2dd3%7D/sarilumab-enters-clinical-trial-for-covid-19-spotlighting-key-role-for-il-6 enters clinical trial for COVID-19, spotlighting ‘key role’ for IL-6

    TH17 responses in cytokine storm of COVID-19: An emerging target of JAK2 inhibitor Fedratinib
    https://www.sciencedirect.com/science/article/pii/S1684118220300657

    Identification of a Dual Inhibitor of Janus Kinase 2 (JAK2) and p70 Ribosomal S6 Kinase1 (S6K1) Pathways.
    Byun S1, Lim S2, Mun JY3, Kim KH4, Ramadhar TR5, Farrand L6, Shin SH7,
    The effect of gingerenone A was strongly associated with relative phosphorylation levels of JAK2 and S6K1.

    Beta Interferon stimulating Drug Trial Southampton University
    UK biotech Synairgen has started dosing patients in its phase 2 trial of SNG001, an inhaled formulation of interferon beta-1a that aims to treat coronavirus infections.
    Interferon beta orchestrates the body’s response to a viral infection, and there is some evidence to suggest that people who get dangerously sick after being infected with SARS-CoV-2 – the virus that causes COVID-19 – have lower than usual levels of interferon beta in the lungs.

    Fresh ginger of high concentration could stimulate mucosal cells to secrete IFN-β that possibly contributed to counteracting viral infection.
    Fresh ginger (Zingiber officinale) has anti-viral activity against human respiratory syncytial virus in human respiratory tract cell lines.
    Chang JS1, Wang KC, Yeh CF, Shieh DE, Chiang LC

    [gingerol: a novel AT₁ antagonist for the treatment of cardiovascular disease.
    Liu Q1, Liu J, Guo H, Sun S, Wang S, Zhang Y, Li S, Qiao Y
    Abstract
    This study aimed to find novel compounds targeting the angiotensin II type 1 receptor, accepted as a therapeutic target in cardiovascular disease. Gingerol (ginger) was identified as a novel angiotensin II type 1 receptor antagonist, with an IC50 value of 8.173 µM.

  20. mary says:

    TH17 responses in cytokine storm of COVID-19: An emerging target of JAK2 inhibitor Fedratinib
    https://www.sciencedirect.com/science/article/pii/S1684118220300657

    Identification of a Dual Inhibitor of Janus Kinase 2 (JAK2) and p70 Ribosomal S6 Kinase1 (S6K1) Pathways.
    Byun S1, Lim S2, Mun JY3, Kim KH4, Ramadhar TR5, Farrand L6, Shin SH7,
    The effect of gingerenone A was strongly associated with relative phosphorylation levels of JAK2 and S6K1.

  21. mary says:

    Beta Interferon stimulating Drug Trial Southampton University
    UK biotech Synairgen has started dosing patients in its phase 2 trial of SNG001, an inhaled formulation of interferon beta-1a that aims to treat coronavirus infections.
    Interferon beta orchestrates the body’s response to a viral infection, and there is some evidence to suggest that people who get dangerously sick with C19 have lower than usual levels of interferon beta in the lungs.

    Fresh ginger of high concentration could stimulate mucosal cells to secrete IFN-β that possibly contributed to counteracting viral infection.
    Fresh ginger (Zingiber officinale) has anti-viral activity against human respiratory syncytial virus in human respiratory tract cell lines.
    Chang JS1, Wang KC, Yeh CF, Shieh DE, Chiang LC

  22. mary says:

    [gingerol: a novel AT₁ antagonist for the treatment of cardiovascular disease.
    Liu Q1, Liu J, Guo H, Sun S, Wang S, Zhang Y, Li S, Qiao Y
    Abstract
    This study aimed to find novel compounds targeting the angiotensin II type 1 receptor, accepted as a therapeutic target in cardiovascular disease. Gingerol (ginger) was identified as a novel angiotensin II type 1 receptor antagonist, with an IC50 value of 8.173 µM.

  23. mary says:

    Areas to investigate further –
    1 Ace 2 receptors normally act on Angiotestin 2 ( a vasoconstrictor) converting it to Angiotestin (1-7) ( vasodilators) but if ACE 2 not working properly (as taken over by virus) there could be an increase in Angiotestin 2 which could cause an increase in blood pressure and oedema.
    2 Inflammatory Cytokines – IL1 IL6 IL17 – of benefit to reduce – Ginger, Vit c and Citrus flavanoids antioxidents, Quercin , Hesperidin,
    3 Beta interferon ( possibly beneficial if increased ) – ginger increases
    4 Hydroxychloroquine – Zinc Ionaphore – Natural substitute = Quercetin ( a flavonoid)

  24. GerryD says:

    I am on ramipril. I read that investigations for possible effects on covid-19 are under way, but results will be available after 1 year!!! Why don’t they inverstigate the huge numbers of already affected people, like in Italy, and establish if there is a strong (or weak) correlation of covid-19 mortality with ramipril taking?

  25. LimboLlama says:

    Ramipril causes a dry persistent cough in up to 1/3 of those that take it. Can also cause a rash. my mother took ramipril and lost her sense of taste, developed a persistent cough and eventually ended up in hospital after suspected heart attack, fluid in lungs and needed blood thinning medication……..? sound familiar?
    I’m wondering if there is a link between those that develop Ramipril cough and susceptibility to Covid-19 i.e.developing the hyper-reaction. Possibly a genetic sub group for which the Ramipril cough is a marker?
    What do you think ?

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