Covid-19 Causing Irreversible Lung Fibrosis

Discussion in 'Society' started by Kingpinguin, Mar 9, 2020.

  1. Momentum

    Momentum Member

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    Going back to earlier in the thread regarding CoV19 causing pulmonary fibrosis, wouldn't a good treatment be using Systemic Enzymes also known as Proteolytic Enzymes? These are "officially" used in other countries to thin blood and dissolve clots. I'm not sure if they use them "official" to dissolve fibroids, but they do. Things like natto, bromelain, protease, etc.
     
  2. Momentum

    Momentum Member

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    Going back to the OP and lung fibrosis. Wouldn't taking Systemic or Proteolytic enzymes be helpful? These are used medicinally in other countries as blood thinners and dissolve blood clots. They also reduce or remove fibroids. And post much earlier in this thread seemed to indicate that protease would be bad, but that doesn't make sense to me as it is used to dissolve fibrin.
     
  3. md_a

    md_a Member

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    Old people have a decreased expression of ACE2 (Angiotensin-converting enzyme 2), and increased expression of AT-1 receptors compared to the young.

    If young people have higher ACE2, and that was the factor allowing faster viral inoculation, then it would be worse in the young, but it is not.

    Cancer, hypertension, diabetes, chronic obstructive pulmonary disease are all conditions that are associated with higher levels of the AT-1 receptor (Angiotensin II receptor type 1), with greater age or severity related to higher levels.

    In patients with low ACE2 by age, sickness or virus binding to ACE2 means that it leaves the ACE1 which produces angiotensin.

    ACE2 is capable in inactivating angiotensin breaking down to the first seven amino acids, they call it angiotensin 1-7, and this is a defensive anti-inflammatory peptide, so if your ACE2 is knocked out, angiotensin has a free range to cause damage, so the virus increases the inflammatory reaction by sticking to the defensive enzyme ACE2, and that enzyme combined with the virus, than acts to enter the cell by way of the Angiotensin II receptor type 1 which is called the AT1, that are two known receptors by which angiotensin can do damage, with stimulation of the larger population of AT-1 receptors within the local tissue eliciting further edema, leading to hypoxia witch upregulates the expression and function of AT1 receptor, with a whole range of destructive processes, nitric oxide production, pulmonary hypertension, acute lung injury and lung fibrosis.

    Endotoxin (LPS) induced an increase in the AT1 subtype of the angiotensin II receptors.


    ACE2 has been shown to be the entry point into human cells for some coronaviruses, including SARS-CoV, the virus that causes SARS. A number of studies have identified that the entry point is the same for SARS-CoV-2, the virus that causes COVID-19.

    This might lead some to believe that decreasing the levels of ACE2, in cells, might help in fighting the infection. On the other hand, ACE2 has been shown to have a protective effect against virus-induced lung injury by increasing the production of the vasodilator angiotensin 1–7.

    In fact, the interaction of the spike protein of the virus with the ACE2 induces a drop in the levels of ACE2 in cells.



    Angiotensin signalling in pulmonary fibrosis.
    Uhal BD1, Li X, Piasecki CC, Molina-Molina M.
    Author information

    Abstract
    A large body of evidence demonstrates that angiotensin II and angiotensin receptors are required for the pathogenesis of experimental lung fibrosis. Angiotensin has a number of profibrotic effects on lung parenchymal cells that include the induction of growth factors for mesenchymal cells, extracellular matrix molecules, cytokines and increased motility of lung fibroblasts. Angiotensin is also proapoptotic for lung epithelial cells, and is synthesized by a local system (i.e., entirely within the lung tissue) after lung injury by a variety of agents of both xenobiotic and endogenous origins. Recent evidence shows that the counterregulatory molecule angiotensin 1-7, the product of the enzyme ACE-2, inhibits epithelial cell apoptosis and thus acts as an antifibrotic epithelial survival factor. This manuscript reviews the evidence supporting a role for angiotensin in lung fibrogenesis and discusses the signalling mechanisms underlying its action on lung parenchymal cells important in the pathogenesis of pulmonary fibrosis.

    Angiotensin signalling in pulmonary fibrosis. - PubMed - NCBI
     
  4. blob69

    blob69 Member

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    Actually I don't know of anyone who was rescued by them. Symptoms do abate sometimes, but again, at what price? I would say at a big one, because you kill a part of yourself as well when you take any poison. Perhaps permanently.

    I used to have a chronic sore throat when younger and my doctor prescribed antibiotics a few times. The sore throat abated for a while, but in some weeks it was back same as before. So basically the drugs didn't work because the pathology came right back in a short time.

    Then there's epidemiology showing that infectious diseases were mostly gone already before the advent of antibiotics and vaccines. And in China we have epidemiology done on a large scale showing that in the last decades infectious diseases and deaths from infectious diseases rose markedly (together with autism, allergies, mental problems, autoimmunity etc. going up too).

    "China has achieved great development in economy, hygiene, and public health since the SARS outbreak [3]. Thus, the increase, not decrease, in the overall incidence of a total of 39 notifiable infectious diseases from 3 906 566 cases (7248 deaths) in 2004 to 6 944 240 cases (18 237 deaths) in 2016 is difficult to understand (Fig. 1 and Fig. 2). These released numbers were public data accessible from the new web-based reporting system for notifiable infectious diseases established in 2004 [4], and this system is so far the largest infectious disease surveillance tool equipped with modern information technology [5] and covering the largest populations in the world."

    "The assumption that infectious diseases will diminish with improvement in economy, quality of water, food, housing, and nutritional status is incorrect and even misleading. China has achieved great development in economy, and the government has invested heavily in managing infectious diseases after SARS. However, the incidence of overall notifiable infectious diseases was not even reduced but in the rising trend."

    Landscape of emerging and re-emerging infectious diseases in China: impact of ecology, climate, and behavior. - PubMed - NCBI

    So, explain that if you can! ;)

    As for parasites that people mentioned here, I heard once that in poorer countries it's common for everyone to have parasites without having any symptoms. I suspect that Westerners may be unable to deal with parasites because of their deranged and allergic immune systems, caused by antibiotics and other toxins.

    As for promiscous sex, I also had a lot of that in my younger years and not once any trouble.

    And in any case I'm not afraid of HIV in the least because the whole thing is one very ugly scam: Beware of Hoaxes Involving Viruses
     
  5. Wilfrid

    Wilfrid Member

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    Thyroid hormones and especially T3 may have some effective therapeutic effects.
    Thyroid hormones inhibit TGF-β signaling and attenuate fibrotic responses
    " In their study, they showed the potential therapeutic (anti-inflammatory and anti-fibrotic) effects of triiodothyronine in experimental models of ventilator-induced lung injury, skin, and hepatic fibrosis. Their results suggest that binding of triiodothyronine to its nuclear receptors could be beneficial in blocking progression of pulmonary fibrosis." from : Autoimmune Hypothyroidism As a Predictor of Mortality in Chronic Hypersensitivity Pneumonitis
     
  6. ecstatichamster

    ecstatichamster Member

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    This is very timely and helpful — I was going to find out about T3 and you’ve beat me to it. Thank you.
     
  7. Wilfrid

    Wilfrid Member

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    There is no doubt in my mind that underlying hypothyroidism must be investigate in all critical ill peuple from the coronavirus.
    Hypertension, obesity and diabetes ( the most co-morbidity factors ) are all features of low thyroid activity.
     
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