Covid 19: adjuvant approaches etc,

[P2Vaircrewman]

The science is settled, not. Once again another medical advise flip flop.


https://www.zerohedge.com/covid-19/a...horse-dewormer

[WillBrink]

New "Drug" To Test Long Covid

This new “drug” is simply amino acids (arginine, glutamine, isoleucine, leucine, and valine) and N-acetylcysteine (NAC). Not exactly cutting edge stuff, but ok. My position: If NAC and some other compounds were SOC with active covid infection, if not at as prophylaxis (even better...), as I have discussed in this thread and article linked in the OP, there may not be long covid.

Oxford to test potential treatment for fatigue in long COVID patients

The University of Oxford is leading a new a phase 2a clinical trial to investigate whether a drug could treat the fatigue and muscle weakness experienced by many patients who have recovered from COVID. The drug, AXA1125, is developed by the US-based biotechnology company Axcella Therapeutics.

Cont:

https://www.ox.ac.uk/news/2021-10-29...ovid-patients?

[P2Vaircrewman]

Deleted on request.

[WillBrink]

https://principia-scientific.com/gam...fe-shortening/

Not relevant to this thread. Please remove and start a thread, or post in existing threads on vaccine related issues. Thanx.

[WillBrink]

In the OP linked article, and all through this thread, I post on the importance of glutathione (GSH) and best ways to support it, via use of NAC and or whey. Just published, a study finding benefits of NAC on two the most important endpoints, not ending up on a vent or being dead:

N-acetyl-cysteine reduces the risk for mechanical ventilation and mortality in patients with COVID-19 pneumonia: a two-center retrospective cohort study

Abstract
Background

N-acetyl-cysteine (NAC) has been previously shown to exert beneficial effects in diverse respiratory diseases, through antioxidant and anti-inflammatory actions. Our aim was to evaluate NAC potential impact in hospitalised patients with COVID-19 pneumonia, in terms of progression to severe respiratory failure (SRF) and mortality.
Patients and Methods

This retrospective, two-centre cohort study included consecutive patients hospitalised with moderate or severe COVID-19 pneumonia. Patients who received standard of care were compared with patients who additionally received NAC 600 mg bid orally for 14 days. Patients’ clinical course was recorded regarding (i) the development of SRF (PO2/FiO2 <150) requiring mechanical ventilation support and (ii) mortality at 14 and 28 days.
Results

A total of 82 patients were included, 42 in the NAC group and 40 in the control group. Treatment with oral NAC led to significantly lower rates of progression to SRF as compared to the control group (p < .01). Patients in the NAC group presented significantly lower 14- and 28-day mortality as compared to controls (p < .001 and p < .01 respectively). NAC treatment significantly reduced 14- and 28-day mortality in patients with severe disease (p < .001, respectively). NAC improved over time the PO2/FiO2 ratio and decreased the white blood cell, CRP, D-dimers and LDH levels. In the multivariable logistic regression analysis, non-severe illness and NAC administration were independent predictors of 28-days survival.
Conclusion

Oral NAC administration (1200 mg/d) in patients with COVID-19 pneumonia reduces the risk for mechanical ventilation and mortality. Our findings need to be confirmed by properly designed prospective clinical trials.

https://www.tandfonline.com/doi/abs/...5.2021.1945675

[WillBrink]

Deleted on request.

Much appreciated sir.

[WillBrink]

Yet another possible benefit of whey!

Whey-Derived Peptides at the Heart of the COVID-19 Pandemic

2Int. J. Mol. Sci. 2021, 22(21), 11662; https://doi.org/10.3390/ijms222111662
Received: 21 September 2021 / Revised: 21 October 2021 / Accepted: 26 October 2021 / Published: 28 October 2021

Abstract
The renin–angiotensin system (RAS) is a key regulator of blood pressure and hypertension. Angiotensin-converting enzyme 2 (ACE2) and angiotensin-converting enzyme I (ACE) are two main components of the RAS that play a major role in blood pressure homeostasis. The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) uses ACE2 as a receptor to enter cells. Despite some controversies, numerous studies have reported a significant association between the use of ACE inhibitors and reduced risk of COVID-19. In our previous studies, we produced and identified peptide sequences present in whey hydrolysates exhibiting high ACE inhibitory activity.

Therefore, the aim of this work is to obtain an improved understanding of the function of these natural peptides as RAS inhibitors and investigate their potential therapeutic role in the COVID-19 pandemic. The molecular interactions between peptides IPP, LIVTQ, IIAE, LVYPFP, and human ACE2 were assessed by employing a molecular docking approach.

The results show that natural whey-derived peptides have a dual inhibitory action against both ACE and ACE2. This dual activity distinguishes these ACE inhibitory peptides from synthetic drugs, such as Captopril and Lisinopril which were not shown to inhibit ACE2 activity, and may represent a potential strategy in the treatment of COVID-19.

Full paper:

https://www.mdpi.com/1422-0067/22/21/11662/htm

[Waylander]

This seems interesting about Fenofibrate/Tricor possibly reducing c19 infection up to 70%

I had a physical a couple of months ago and the nurse called to let me know the doc put me on it for triglycerides. I looked it up and found the study from the UK/Italy.

https://www.eurekalert.org/news-releases/924448

[WillBrink]

This seems interesting about Fenofibrate/Tricor possibly reducing c19 infection up ts
I had a physical a couple of months ago and the nurse called to let me know the doc put me on it for triglycerides. I looked it up and found the study from the UK/Italy.

https://www.eurekalert.org/news-releases/924448

There seems to be a long list of drugs with other indented medical uses that may be of value with covid that are unexpected. Note that was an in vitro study (test tube) so while interesting, may or many apply to an in vivo (whole body) system. If you're already taking it, hopefully that's another potential benefit.

[WillBrink]

Study of interest:

WEST LAFAYETTE, Ind. — Scientists recently gained insights into how vitamin D functions to reduce inflammation caused by immune cells that might be relevant to the responses during severe COVID-19. In a study jointly published by Purdue University and the National Institutes of Health, scientists do just that.

https://www.purdue.edu/newsroom/rele...lammation.html

Study:

Autocrine vitamin D signaling switches off pro-inflammatory programs of TH1 cells
Nature Immunology (2021)

Abstract

The molecular mechanisms governing orderly shutdown and retraction of CD4+ type 1 helper T (TH1) cell responses remain poorly understood. Here we show that complement triggers contraction of TH1 responses by inducing intrinsic expression of the vitamin D (VitD) receptor and the VitD-activating enzyme CYP27B1, permitting T cells to both activate and respond to VitD. VitD then initiated the transition from pro-inflammatory interferon-γ+ TH1 cells to suppressive interleukin-10+ cells. This process was primed by dynamic changes in the epigenetic landscape of CD4+ T cells, generating super-enhancers and recruiting several transcription factors, notably c-JUN, STAT3 and BACH2, which together with VitD receptor shaped the transcriptional response to VitD. Accordingly, VitD did not induce interleukin-10 expression in cells with dysfunctional BACH2 or STAT3. Bronchoalveolar lavage fluid CD4+ T cells of patients with COVID-19 were TH1-skewed and showed de-repression of genes downregulated by VitD, from either lack of substrate (VitD deficiency) and/or abnormal regulation of this system.

https://www.nature.com/articles/s41590-021-01080-3