re: Covid: outside the box thinking - hemoglobin/ Vit D/ “host-centric” (and why that matters)

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But some of y’all act as if Trump is in a lab studying this stuff and that he is the only expert. Let the docs and researchers figure it out. I have faith that they will get it done.

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what a strange response to a thread that has nothing to do with Trump

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So if I am understanding your logic correctly,

We should not speculate as we are because the information presented suggested that all bilateral pneumonia associated with covid where not really pneumonias?

Your position is that because atypical pneumonia can present with bilateral infiltrates that it is what is accounting for the covid patients clincial picture? All of them ?(as it is a pretty consistent finding)

Is it not possible for us to both be correct (some patient may not have covid, but instead have an atypical pneumonia unrelated to covid???) or both be incorrect (other mechanisms in play still evading us)?

Either way, your feedback has not definitively made the case to "end speculation". The cocksure "we got this figured out but don't have enough information to do anything" mindset is not sitting well with most people in the lay public if you have not noticed...

Your input adds to the discussion, but dismissing other points suggested here wholesale is being willing obtuse (or you just want to be "right"...)

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I said your sources use false information as well as botches basic concepts of pneumonia. sources that include inaccurate info and misrepresent the basics is significant cause to call into question the entire source.



typical vs atypical is named based off presentation and a set of causal organisms. typical is caused by a handful of microbes, it is contained in 1-2 lobes of 1 lung.
atypical is caused by many more types of organisms than typical pne. Atypical pne IS BILATERAL. these are the differences in pneumonias relevant to imaging and causal pathogen.

your source says bilateral pne is rare which is very false, more organisms/virus/fungi cause atypical than cause typical. influenza is an example of something that causes atypical pne.

the process/distribution of infiltrate, is important and accounts for the clinical picture. diffuse immune response to both lungs (atypical), or a more localized response contained to 1-2 lobe (typical). its why people link influenza and pneumonia deaths. its why influenza is a good comparison with COVID. when people die from pneumonia, its due to the intensity of their immune system reaction not the infective pathogen itself.

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I said your sources use false information as well as botches basic concepts of pneumonia. sources that include inaccurate info and misrepresent the basics is significant cause to call into question the entire source.

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Fair enough

How then do we reconcile the growing reports of providers having success using chloroquine?

If your mechanism is the predominant method in covid patients, why are people reporting successes using therapuetics that have mechanisms of actions not directly linked to what you are proposing? Are they lying? Random/coincidence?

The speculation here is considering all of these factors in an attempt to explain why people are doing so poorly with traditional therapy while consistently reporting some symptoms not typical of traditional viral pathogens. Thoughts?

When I first saw some of the initial diabetes comorbidity stats, the first thing I thought was glycated hemoglobin. I'm not a doctor or scientist but I read enough to have some vague understanding of metabolism and pulmonary function.

And with the poor vent success rate, this is all starting to make some sense.

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How then do we reconcile the growing reports of providers having success using chloroquine?

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pneumonia is caused by your immune system response as it fights an infection, not due to the pathogen directly.
if HCQ depresses your bodies immune response, it makes sense there would be potential benefit from something that would be decrease damage from pneumonia. this is why physicians may want to use HCQ for COVID.

the question is are there other mechanisms COVID causes damage? are there other consequences for immune suppression during the infection? what if COVID gains resistance to drugs like HCQ easily and we cause a super resistant strain by throwing it around like candy because theres a small amount of anecdotal evidence that it helps? We dont know the exact mechanisms of COVID or HCQ so there are obvious potential pitfalls which is why Dr. Fauci recommends caution.


truth is we wont know until we get the rigorous studies Dr. Fauci advocates for.

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we wont know until we get the rigorous studies Dr. Fauci advocates for.

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they will come

but in the meantime, given the choice of death or something that seems to be helping

I'll take the HCQ

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It’s an analogous potential for unintended consequence given HCQ use for COVID hasn’t been thoroughly investigated although it seems to help right now. Fauci has cause for caution, while clinicians have cause to want to use HCQ.

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I will choose Ivermectin because I have used it many times in the past and it has been safe even though I wasn't always being careful. It is appproved for human use and if it works in the lab in Australia I am willing to try it here.

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The French are conducting a study using hemoglobins from sea worms. Their hemoglobin load can hold more than 40X oxygen than that of humans.

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Interesting, but sounds strained from a feasibility stance on a number of fronts.

The 40X load is impressive, but characteristics of its oxyhemoglobin dissociation curve in vivo would be critical. In other words, effective transport involves (A) efficient loading of freight cars at one end, and (B) efficient unloading at the other.

A second issue involves containment, or a containment vehicle for the hemoglobin. Free floating Hb in the body is bad kimchi.

I wonder if you took drugs that increase hemoglobin would one with Covid 19 recover faster?

Shared by a friend...

Disclaimer:

These are correlations
Covid requires complex systems based thinking (see next post). This is 1 input
Reframe African Americans being disproportionately impacted. Darker pigmented individuals absorb sun/ produce vit D poorly...

https://docs.google.com/document/u/0/d/1jffdZOSuIA64L_Eur8qyCQ12T7NXrHSKPxtMe134C0Y/mobilebasic

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Covid-19 and Vitamin D Information Dr Gareth Davies (PhD), Dr Joanna Byers (MBChB), Dr Attila R Garami (MD, PhD)

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TL;DR Summary

Vitamin D deficiency is common during winter in northern latitudes above 20 degrees and southern latitudes 20 degrees below the equator. Severe Covid-19 outbreaks have only happened above 20 degree latitudes (23rd March 2020). Outbreaks in the southern summer hemisphere have been mild so far. SARS-Cov-2 virus enters cells via ACE2 receptors. Viral replication downregulates ACE2 dysregulating the renin-angiotensin system and leads to a cytokine storm in the host, causing Acute Respiratory Distress Syndrome (ARDS). Vitamin D deficiency is strongly associated with ARDS, poor mortality outcomes as well as being associated with the majority of comorbidities associated with Covid-19 case fatalities. Vitamin D acts to rebalance RAS and attenuates lung injury. Vitamin D supplementation reduces the risk of acute respiratory tract infection. Vitamin D is a steroid hormone naturally produces in the skin in summer exposure to UVB light. It is considered safe to take as cholecalciferol (D3) oral supplements in doses up to a maximum of 4,000iu/d for short periods. For healthy young individuals, NICE recommendations advise “all adults living in the UK, including people at increased risk of vitamin D deficiency, should take a daily supplement containing 400 international units (IU [10 micrograms]) of vitamin D throughout the year, including in the winter months”. Young people with known Vitamin D deficiency and those older than 60 and should supplement with 2,000iu/d during winter. The Scientific Advisory Committee on Nutrition (SACN, 2016) does not recommend routine monitoring of serum vitamin D levels during long-term supplementation with vitamin D. Furthermore, expert opinion in the National Osteoporosis Guideline Group 2017 (NOG 2017) is that routine monitoring of serum 25(OH)D levels is unnecessary for people on long-term maintenance doses of vitamin D (up to 2000 IU a day). Please note prolonged supplementation at higher levels carries a risk of hypercalcaemia (Contraindications, British National Formulary) and should only be undertaken with professional advice. If you are able to get exposure to natural sunlight then your body will synthesize Vitamin D and you are less likely to need supplements to maintain healthy levels.

Supporting Evidence

Coronavirus Seasonality and Correlation with Latitude Summary of findings in this section Coronaviruses and influenza viruses in the past have displayed very strong seasonality with winter appearances. Covid-19 severe outbreaks have so far only happened north of the 20º latitude line in the current winter hemisphere. Vitamin D deficiency occurs during winter since Vitamin D is synthesised in the skin during summer exposure to UVB rays. Italy has one of the worst Vitamin D deficiency rates in Europe and has paid the highest death toll. Italy found serum levels of Vitamin D lower than 12 ng/ml (<30 nmol/L) in as many as 76% of 700 women tested between the ages 60-80 yrs. Japan is an outlier in the north, with only a very mild outbreak and has the lowest incidence of Vitamin D deficiency thanks to its high fish-content diet. (No doubt other factors also contribute in both countries). Prevalence of hypovitaminosis D (<30 nmol/L) in women over 30 years old in Japan is only 10.3% and in active elderly (25(OH)D <75 nmol/L) is below 5%. [Social, cultural and behavioural differences account for slower spread but not lower case fatality rates.]

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