COVID-19 And The Cardiovascular System

Discussion in 'Articles & Scientific Studies' started by Mito, Mar 16, 2020.

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  1. Mito

    Mito Member

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    “Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infects host cells through ACE2 receptors, leading to coronavirus disease (COVID-19)-related pneumonia, while also causing acute myocardial injury and chronic damage to the cardiovascular system. Therefore, particular attention should be given to cardiovascular protection during treatment for COVID-19.”

    Conclusions
    “SARS-CoV-2 is thought to infect host cells through ACE2 to cause COVID-19, while also causing damage to the myocardium, although the specific mechanisms are uncertain. Patients with underlying CVD and SARS-CoV-2 infection have an adverse prognosis. Therefore, particular attention should be given to cardiovascular protection during treatment for COVID-19.”

    COVID-19 and the cardiovascular system
     
  2. sugarbabe

    sugarbabe Member

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    Yeah Ray just brought this up on one radio network about half an hr ago. You are two steps ahead! He said those dieing already have pre-existing conditions as far as heart disease and circulatory disease, they are INFLAMED.
     
  3. charlie

    charlie The Law & Order Admin

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  4. OP
    Mito

    Mito Member

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    Did he talk about angiotensin-converting enzyme (ACE) inhibitors? Wonder if they increase or decrease vulnerability?
     
  5. sugarbabe

    sugarbabe Member

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    Starts at around 17:00 here is some of it I transcribed during the livestream:
    "The people dieing at a very high rate of the virus are already suffering from circulatory disease, heart disease, hypertension and stroke, they already have an active angiotensin system and the virus finds an environment already going in that direction. It happens that the ace angiotensin converting enzyme #2 its a dereceptor for the virus the virus attaches to that and in the process entering the cell and becoming infective and ace2 is the enzyme that undoes the work of ace in the cells and ace produce angiotensin and ace2 then destroys angiotensin so what the virus does in binding to ace2 seems to be inactivating the inactivator of angiotensin that leaves ace free to make angiotensin which then doesn't have any way out and it accumulates causing all of the dry cough high fever and increased hypertension and stroke and so on. "

    Young people have more ACE2 making them less susceptible to the virus and to age related degenerative disease.
     
  6. nad

    nad Member

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    Not so well educated so still didn't get it - should one keep to take (ACE) inhibitors or start it?
     
  7. sugarbabe

    sugarbabe Member

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    Honestly that whole ace thing was really confusing to me too. Some are saying the inhibitors promote this virus, and then Peat said the inhibitors work, but I need more info.
     
  8. OP
    Mito

    Mito Member

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    Mainstream medical prospective....people taking ACE inhibitors might be more susceptible but it seems to me like this is all speculation at this point.

    https://peterattiamd.com/covid-19-update-03152020/
    Potential drug therapies [22:00]

    Angiotensin II receptor blocker
    • Originally, it was though that Angiotensin II receptor blockers could be an effective treatment
      • ARBs block the receptor to which the virus binds
      • But now it seems that individuals on hypertensive medication are actually more susceptible to the virus
      • Current thinking is that those already on ARBs should remain on the medication
      • Research team is continuing to look at case-control reports looking at hypertensive cohorts
    Kaletra and Chloroquine
    • Studies didn’t show clinical endpoints but did show a decrease in viral load
      • Mechanistically virus may be susceptible to chloroquine (changes lysosomal PH)
      • Viral proteases is similar to HIV replication so HIV medications may be avenues in conjunction with Chloroquine with no obvious harm
    Remdesivir
    • Repurposed from Ebola clinical trial
    • Used in treatment and as IV only
     
  9. Noodlz2

    Noodlz2 Member

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    I would bet the confusion stems from how these researchers define "susceptible". People who test positive for the virus are "susceptible", but the researchers should really focus on keeping symptoms from manifesting. Excess ACE2 may make you more likely to harbor the virus, but probably also more likely to not feel bad effects from it, like Peat says.
     
  10. sugarbabe

    sugarbabe Member

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    Yes exactly. And explains why the elderly die and not the young people.
     
  11. RealNeat

    RealNeat Member

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    Could this effect be because serotonin decrease as opposed to melatonin increase?

    Her articles are very interesting but Im not sure of the validity.

    COVID-19, Pneumonia & Inflammasomes - The Melatonin Connection - EvolutaMente.it

    [Source: Grivas TB, Savvidou OD. Melatonin the “light of night” in human biology and adolescent idiopathic scoliosis. Scoliosis. 2007;2:6. Published 2007 Apr 4. doi:10.1186/1748-7161-2-6]

    What does this chart measure? An ancient and powerful molecule that everyone is familiar with – melatonin. What does melatonin have to do with SARS-CoV-2?

    Melatonin Inhibits NLRP3 Inflammasomes
    Melatonin is well known for its chronobiotic effects, regulating biological functions tied to circadian rhythms. Numerous studies have revealed that melatonin exerts effects beyond the control of circadian oscillators. The NLRP3 inflammasome is now recognized as a target for melatonin!

    The fact that the pro-inflammatory cytokine storm effects are induced by the activation of NLRP3 inflammasomes, the ability of melatonin to INHIBIT NLRP3 inflammasome elevates this powerful molecule to a truly unique position in the fight against COVID-19. This also means that if a patient, regardless of age, has adequate melatonin, the infectiousness of COVID-19 will be greatly reduced, and the chances of developing ARDS/ALI significantly diminished.

    Melatonin is the reason why children under the age of 9 seldom exhibit severe symptoms. In fact, children may exhibit mild or even no symptoms at all, even though they have been infected by SARS-CoV-2 [73]. How significant is the difference in melatonin production between children, adults and the elderly?

    For most people, peak melatonin production is between the hours of 2 am to 3 am. The maximum melatonin levels measured in healthy adults between the ages of 65 to 70 years appeared to be around 49.3 picograms/ml (pg/ml). Adults more than 75 years of age only have maximum production levels of 27.8 pg/ml [74].

    Young children, on the other hand, have extremely high melatonin levels, compared to adults. The maximum levels recorded for children showed a decline as age increased. Children between the ages of 1 to 5 had peak melatonin at 325 pg/ml, while those between the ages of 5 to 11 already declined to 133 pg/ml [76].

    Compared to healthy adult seniors, a young child can easily have TEN TIMES the amount of peak melatonin levels. But even then, the actual physiological concentration is extremely low. How much is one picogram, exactly?

    To give you some perspective, most melatonin supplements are around 3 to 5 mg per capsule or tablet. One milligram equals 1,000,000,000 picograms. That is why the physiological dosage generally recommended for melatonin supplementation is around 0.3 milligram [75].

    The fact that young children have such high melatonin levels explains why they show very mild symptoms after COVID-19 infections.
     
  12. schultz

    schultz Member

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    I would think so. Melatonin sort of protects against serotonin as far as I understand it. In higher amounts though I think it's stress promoting.
     
  13. boris

    boris Member

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    The problem is they don‘t use the sartans in the hospitals. They only use ACE inhibtors that don‘t block ACE2.
    These ACE inhibitors promote ACE2 creation, ACE2 is the entryway for the virus. Once it‘s inside it downregulates ACE2. ACE2 is the balancing factor for ACE. So then without enough ACE2, ACE is free to cause cell damaging effects without opposition. (This is the theory how ACE inhibitors promote the virus)

    ACE2 blockers[corrected: Angiotensin II receptor blockers] like Peats recommended Losartan are thought to be beneficial.

    SARS-CoV-2: Begünstigen ACE-Hemmer schwere Verläufe?
    ACE inhibitors are being heavily used in italy and there is speculation they are responsible for the high death rate. They are still being used and are a recommended treatment. In germany too.
     
  14. jb116

    jb116 Member

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    I don't think so. I think it's mostly related to good thyroid function, which most young kids have.
    Melatonin is to be looked at as a serotonin neutralizer and anti-oxidant insofar it is regulated by high thyroid function. It is mostly why supplementing melatonin in large amounts or even what's considered physiological amounts, doesn't really work and can act as a hibernation hormone. I think they are narrowingly looking at the picture by suggesting this byproduct of good thyroid function is also the thing to protect one from "the virus" where really it is the thyroid optimizing structure and function and naturally the body's defenses.
     
  15. jb116

    jb116 Member

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    I think this has confused people because Peat's corollary has to do ultimately with the fact it doesn't matter that ACE 2 is a so-called entry way, what matters is what ACE 2 does for the body overall. Losartan doesn't block ACE2. It is a angiotensin II receptor blocker.
     
  16. boris

    boris Member

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    Thanks for the clarification.

    In the german article they differentiate between ACE inhibitors and Sartans, with the ACE inhibitors being the ones creating more of the extra entry ways.

    So the theory of those medications kickstarting the condition is bunk?
     
  17. RealNeat

    RealNeat Member

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    So then Losartan ultimately prevents docking of the virus?
     
  18. jb116

    jb116 Member

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    It's good they distinguish better, that small detail can create confusion. What is ultimately and absolutely needed is Peat's perspective on the organism and energy metabolism. Understanding what viruses are from that prism, we then realize it isn't so much the "virus entered the body" but that the body is energized enough to deal with it. I think the idea of "kickstarting the condition" is bunk, since from their view it's removing the organism/organism's status from the picture. That's key.

    It should be less about the "docking" idea in and of itself but the idea is to keep energy production up and block an aging/stress cascade such as the RAAS. So Losartan directly acts on angiotensin and the receptor protein, that can only be helpful.
     
  19. nad

    nad Member

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    Just put it in another treat but need more people to see:
    Just read this in news: a new study reveals possible connection between BP meds. and worse case of Covid-19.
    Dr Gregory Mishkel a NorthShore University HealthSystem cardiologist -
    It's ACE-2 inhibitors!
    WGN-TV
     
  20. OP
    Mito

    Mito Member

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    ACE2 receptor
    SARS-CoV and SARS-CoV-2 both use the same keyhole to enter cells, the ACE2 receptor. There’s an abundance of this receptor in cells in the lower lung, which may explain the high incidence of pneumonia and bronchitis in those with severe COVID-19 infection. A recent study showed that ACE2 is also highly expressed in the mouth and tongue, granting the virus easy access to a new host. ACE2 receptor abundance goes down in the elderly in all these tissues, but, counterintuitively, this might place them at a greater risk of severe illness.

    This is because the ACE2 enzyme is an important regulator of the immune response, especially inflammation. It protects mice against acute lung injury triggered by sepsis. And a 2014 study found that the ACE2 enzyme offers protection against lethal avian influenza. Some patients with better outcomes had higher levels of the protein in their sera, and turning off the gene for ACE2 led to severe lung damage in mice infected with H5N1, while treating mice with human ACE2 dampened lung injury.

    A fall in ACE2 activity in the elderly is partly to blame for humans’ poorer ability to put the brakes on our inflammatory response as we age, according to emailed comments from Hongpeng Jia of Johns Hopkins Medicine. Reduced abundance of ACE2 receptors in older adults could leave them less able to cope with SARS-CoV-2, says Baric, though the hypothesis still needs more research.
    Possible Biological Explanations for Kids’ Escape from COVID-19
     
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