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Dr. Peat Right Again: Losartan And Covid-19 Evidence For Efficacy

Discussion in 'Scientific Studies' started by ecstatichamster, Mar 21, 2020.

  1. yoshiesque

    yoshiesque Member

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    U
    You need to make sure ur source has evidence behind it. Losartan can also increase ACE2, the very thing covid binds to. So that's likely their assumption. But it doesn't hold, because young ppl have high ACE2.
     
  2. schultz

    schultz Member

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    Yes, I think people are getting confused because they hear that the virus binds to ACE2 and so think that more ACE2 means worse outcome because it means more virus. The virus itself is a bit irrelevant here, it has more to do with the idea that there is less ACE2 available because the virus has deactivated it by attaching to it. ACE2 counters ACE by reducing the effects of angiotensin. When you don't have as much ACE2, then ACE is free to cause problems as it able to increase angiotensin without interference from ACE2.

    That's the gist of it, albeit incredibly over-simplified.

    People are too focused on the virus itself and are not thinking about the systems in the body. Don't worry about "killing" the virus, worry about improving the state of the organism so that it can deal with cascade of inflammatory events initiated by the virus. Anything that kills the virus but harms the organism is not an optimal treatment. Sort of like chemotherapy. We kill cancer by irradiating a person.... When the body is healthy it can deal with this stuff on its own no problem. War mentality.

    The study below shows what happens to lungs when ACE2 is downregulated.

    Angiotensin-converting enzyme 2 (ACE2) mediates influenza H7N9 virus-induced acute lung injury

    "Influenza A (H7N9) virus-induced ALI [acute lung injury] results in the significant downregulation of ACE2, which regulates the RAS."

    "The data presented here also demonstrated that ACE2 deficiency aggravated influenza A (H7N9) virus-induced ALI in mice."
     
  3. md_a

    md_a Member

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  4. ImprovingDaily

    ImprovingDaily Member

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    md_a 's writing explains it well. The virus binds to ACE2 effectively DECREASING its function, like an antagonist. So increasing ACE2 would be a good thing.
     
  5. Beastmode

    Beastmode Member

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    He could be wrong, but many here would take his research and take on it compared to the supposed "experts" out there. The ones that are potentially increasing virus activities are ACE inhibitors. Share the links that the "others" are saying. Best to hear this from all perspectives.
     
  6. GenericName86

    GenericName86 Member

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    Are there any alternatives to Losartan? I know peat mentioned prog but any other supplements that have similar effects?
     
  7. jb116

    jb116 Member

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    telmisartan should have same effects
     
  8. md_a

    md_a Member

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  9. OP
    ecstatichamster

    ecstatichamster Member

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    My theory is ACE inhibitors lower ACE2.

    Can someone smarter than me help interpret this animal study on the subject:
    Effect of angiotensin-converting enzyme inhibition and angiotensin II receptor blockers on cardiac angiotensin-converting enzyme 2. - PubMed - NCBI

    BACKGROUND:
    Angiotensin-converting enzyme 2 (ACE2) has emerged as a novel regulator of cardiac function and arterial pressure by converting angiotensin II (Ang II) into the vasodilator and antitrophic heptapeptide, angiotensin-(1-7) [Ang-(1-7)]. As the only known human homolog of ACE, the demonstration that ACE2 is insensitive to blockade by ACE inhibitors prompted us to define the effect of ACE inhibition on the ACE2 gene.

    METHODS AND RESULTS:
    Blood pressure, cardiac rate, and plasma and cardiac tissue levels of Ang II and Ang-(1-7), together with cardiac ACE2, neprilysin, Ang II type 1 receptor (AT1), and mas receptor mRNAs, were measured in Lewis rats 12 days after continuous administration of vehicle, lisinopril, losartan, or both drugs combined in their drinking water. Equivalent decreases in blood pressure were obtained in rats given lisinopril or losartan alone or in combination. ACE inhibitor therapy caused a 1.8-fold increase in plasma Ang-(1-7), decreased plasma Ang II, and increased cardiac ACE2 mRNA but not cardiac ACE2 activity. Losartan increased plasma levels of both Ang II and Ang-(1-7), as well as cardiac ACE2 mRNA and cardiac ACE2 activity. Combination therapy duplicated the effects found in rats medicated with lisinopril, except that cardiac ACE2 mRNA fell to values found in vehicle-treated rats. Losartan treatment but not lisinopril increased cardiac tissue levels of Ang II and Ang-(1-7), whereas none of the treatments had an effect on cardiac neprilysin mRNA.

    CONCLUSIONS:
    Selective blockade of either Ang II synthesis or activity induced increases in cardiac ACE2 gene expression and cardiac ACE2 activity, whereas the combination of losartan and lisinopril was associated with elevated cardiac ACE2 activity but not cardiac ACE2 mRNA. Although the predominant effect of ACE inhibition may result from the combined effect of reduced Ang II formation and Ang-(1-7) metabolism, the antihypertensive action of AT1 antagonists may in part be due to increased Ang II metabolism by ACE2.
     
  10. OP
    ecstatichamster

    ecstatichamster Member

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    I think the key is here:

    ACE inhibitor therapy caused a 1.8-fold increase in plasma Ang-(1-7), decreased plasma Ang II, and increased cardiac ACE2 mRNA but not cardiac ACE2 activity. Losartan increased plasma levels of both Ang II and Ang-(1-7), as well as cardiac ACE2 mRNA and cardiac ACE2 activity.

    --

    So ARBs can increase ACE2. ACE inhibitors increase ACE2 mRNA, which may cause a down regulation of ACE2 in some way.
     
  11. OP
    ecstatichamster

    ecstatichamster Member

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  12. Gone Peating

    Gone Peating Member

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    The Chinese used these drugs to treat people effectively and Peat commented about it. It’s not like he told them to use those drugs
     
  13. OP
    ecstatichamster

    ecstatichamster Member

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    Patients treated with ACEIs displayed in comparison with untreated controls increased intestinal mRNA levels of ACE2,

    in a gut study of ACE and ACE inhibitors. So again, what does it mean when mRNA levels are increased?
     
  14. Beastmode

    Beastmode Member

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    I haven't heard of alternatives, but cyproheptadine and aspirin are "global" approaches to consider according to him. Keeping PTH very low (via high calcium intake) and vitamin D up are other general approaches that will help avoid "sickness!"
     
  15. md_a

    md_a Member

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    Angiotensin-converting enzyme 2 protects from severe acute lung failure.
    Imai Y1, Kuba K, Rao S, Huan Y, Guo F, Guan B, Yang P, Sarao R, Wada T, Leong-Poi H, Crackower MA, Fukamizu A, Hui CC, Hein L, Uhlig S, Slutsky AS, Jiang C, Penninger JM.
    Author information

    Abstract
    Acute respiratory distress syndrome (ARDS), the most severe form of acute lung injury, is a devastating clinical syndrome with a high mortality rate (30-60%) (refs 1-3). Predisposing factors for ARDS are diverse and include sepsis, aspiration, pneumonias and infections with the severe acute respiratory syndrome (SARS) coronavirus. At present, there are no effective drugs for improving the clinical outcome of ARDS. Angiotensin-converting enzyme (ACE) and ACE2 are homologues with different key functions in the renin-angiotensin system. ACE cleaves angiotensin I to generate angiotensin II, whereas ACE2 inactivates angiotensin II and is a negative regulator of the system. ACE2 has also recently been identified as a potential SARS virus receptor and is expressed in lungs. Here we report that ACE2 and the angiotensin II type 2 receptor (AT2) protect mice from severe acute lung injury induced by acid aspiration or sepsis. However, other components of the renin-angiotensin system, including ACE, angiotensin II and the angiotensin II type 1a receptor (AT1a), promote disease pathogenesis, induce lung oedemas and impair lung function. We show that mice deficient for Ace show markedly improved disease, and also that recombinant ACE2 can protect mice from severe acute lung injury. Our data identify a critical function for ACE2 in acute lung injury, pointing to a possible therapy for a syndrome affecting millions of people worldwide every year.

    Angiotensin-converting enzyme 2 protects from severe acute lung failure. - PubMed - NCBI
     
  16. md_a

    md_a Member

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    [Lessons from SARS: a new potential therapy for acute respiratory distress syndrome (ARDS) with angiotensin converting enzyme 2 (ACE2)].
    [Article in Japanese]
    Imai Y1, Kuba K, Penninger JM.
    Author information

    Abstract
    During several months of 2002, severe acute respiratory syndrome (SARS) caused by SARS-coronavirus (SARS-CoV) spread rapidly from China throughout the world causing more than 800 deaths due to the development of acute respiratory distress syndrome (ARDS). Interestingly, a novel homologue of angiotensin converting-enzyme (ACE), termed angiotensin converting enzyme 2 (ACE2) has been identified as a receptor for SARS-CoV. ACE and ACE2 share homology in their catalytic domain and provide different key functions in the renin-angiotensin system. ACE cleaves angiotensin I to generate angiotensin II that is a key effector peptide of the system and exerts multiple biological functions, whereas ACE2 reduces angiotensin II levels and thus is a negative regulator of the system. Importantly, our recent studies using ACE2 knockout mice have demonstrated that ACE2 protects murine lungs from ARDS. Furthermore, SARS-CoV infections and the Spike protein of the SARS-CoV reduce ACE2 expression. Notably, injection of SARS-CoV Spike into mice worsens acute lung failure in vivo that can be attenuated by blocking the renin-angiotensin pathway, suggesting the activation of pulmonary RAS influences the pathogenesis of ARDS and SARS.

    A crucial role of angiotensin converting enzyme 2 (ACE2) in SARS coronavirus-induced lung injury. - PubMed - NCBI
     
  17. md_a

    md_a Member

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    Angiotensin II receptor 1 blocker (losartan) restores the ability of the lung to clear edema in rats
    Reem Ismael-Badarneh, Julia Guetta, Niroz Abu-Saleh, Geula Klorin, Gidon Berger, Zaid Abassi, Zaher Azzam
    European Respiratory Journal 2013 42: P3921; DOI:
    Abstract
    Alveolar fluid clearance (AFC) is important in keeping the airspaces free of edema, mainly due to alveolar epithelial Na,K-ATPase pump and Na channels (ENaC). Angiotensin II (AngII) stimulates a variety of physiologic responses that supports arterial blood pressure and renal function. We previously showed that AngII impairs AFC (AFC in control rats was 0.44±0.04 ml/h (Mean ± SEM) and decreased by 40% in AngII treated rats (P = 0.003)). AngII effects are mediated by two specific receptors; AT1 and AT2. The localization of these two receptors in the lung was recently discovered, specifically in alveolar epithelial cells type II (ATII), but no studies investigated whether they play a role in AFC. In order to understand AngII mechanism, we investigated the effect of AT1 specific blocker (Losartan) using the isolated perfused lung model. Losartan administration, followed by AngII restored the inhibitory effect of AngII, indicating an AT1 mediated effect of AngII on AFC.

    Furthermore, Oubain (Na,K-ATPase ihhibitor) and Amiloride (ENaC ihibitor) reduced AFC to 5.9±0.4 ml/hr and 5.8±0.11 ml/hr respectively. The administration of either Oubain or Amiloride with AngII tended to have more inhibitory effect on AFC (4.41±0.2 ml/hr or 5.29±0.08ml/hr respectively), suggesting that AngII signaling may target more than one protein. In ATII cells treated with AngII the expression of AT1 levels was upregulated. Notably, there was no significant change in αNa,K-ATPase and αENaC abundance after AngII treatment.

    We herein provide a new mechanism of clinical relevance by which angiotensin adversely impairs the ability of the lungs to clear edema.
    Angiotensin II receptor 1 blocker (losartan) restores the ability of the lung to clear edema in rats
     
  18. OP
    ecstatichamster

    ecstatichamster Member

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    I'm looking for harm from ACE inhibitors. My thesis is that they are causing a lot of deaths. ARBs would be helpful, ACEi are harmful.

    That's a question for ya.
     
  19. Lollipop2

    Lollipop2 Member

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    What a fantastic post - clear and explanatory! Very helpful. Thank you for taking the time.
     
  20. Seeweed65

    Seeweed65 Member

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