covid notes Archives - Hormones Matter

Covid Notes: Thiamine Reduces Thrombosis and Mortality

Published on August 30, 2021

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covid notes: thiamine reduces mortality and thrombosis

A recently published retrospective study showed ICU patients receiving thiamine therapy had a significantly reduced thrombosis and mortality rate compared to patients not treated with thiamine. The study, conducted in two hospitals in Saudi Arabia reviewed the cases of 738 critically ill Covid patients admitted to the ICU. As this was a retrospective study looking solely at electronic medical records, there was no determination of thiamine deficiency or clinical criteria to determine who received thiamine or at what dose. This was simply a review of all cases during a defined period of time that were admitted to the ICU and who, based upon clinical judgement of the treating physician, may have been prescribed thiamine.

Study Details

Among 738 patients, 83 had received IV or oral thiamine in doses ranging 50-200mg per day for an average of 7 days. This was in addition to whatever medical or pharmaceutical interventions provided. Using a statistical tool called a propensity score, the researchers then selected pair matches to those 83 patients for further analysis of several endpoints. The endpoints evaluated included:

Association between thiamine use as an adjunctive therapy with in-hospital and 30 day mortality
Duration of mechanical ventilation, length of stay and complications such as
- Acute kidney injury
- Thrombosis
- Respiratory failure
- Acute liver injury

Results

Across all variables, patients who received thiamine faired significantly better than those who did not. The most striking findings included mortality and thrombosis reduction. Thiamine reduced in-hospital and 30-day mortality by 61% and 63%, respectively compared to propensity matched controls. Additionally, critically ill ICU patients who received thiamine were 81% less likely to develop thrombosis, and non-significantly less likely to develop kidney damage or liver damage. Inasmuch as thrombosis is major contributor to mortality with COVID, this finding is huge.

Things to Consider

As this was a retrospective study and there were no determinations regarding deficiency or guidelines regarding dosing or other treatment protocols given concurrently, it is difficult to fully appreciate the role of thiamine in COVID recovery by traditional research parameters. Nevertheless, if we look at the role of thiamine in energy metabolism, in immune function, in controlling hypoxia, it makes sense that no matter what other confounding variables may detract from or enhance recovery prospects, thiamine, by its very mechanisms of action, would improve outcomes; something that we have been proposing since well before the pandemic began. Maybe now, more will listen.

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COVID Notes: The Blood Clot Problem

by Chandler Marrs, PhD

Published on April 20, 2020

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This is the second in a series of articles adapted from twitter threads where I explore different aspects of the COVID-19 pandemic. The first can be found here.

COVID and Blood Clots

Let’s talk about blood clots and COVID-19. It seems the latest of a long list of problems COVID is suspected of causing is hypercoagulation. Here is just one of the many articles that have come out recently.

The most telling sentence: “It’s not necessarily the virus killing people, it’s the organ failure that happens as a result of the viral infection,” Barrett said. “If you can support people through their organ failure… the immune system will eventually clear out the virus.”

One that seems to be summarily ignored or obfuscated by the fundamental presumptions of causation – what constitutes causation and the subsequent considerations of what constitutes acceptable treatments – something we will return to in a moment.

With each of these new realizations about the process of COVID deaths, we seem only ready to attribute these symptoms to either the virus or to the pre-existing ill-health of the patient.

Never in these discussion are questions regarding how medicine contributed to either variable. Pharmaceuticals, as all chemical toxicants, while sometimes necessary, also elicit damage capable of inducing a myriad of pathologies, including hypercoagulability.

Might it be the medications that we are hurling at humanity from birth to death, but especially in the rapid fire environment of the ED and in association with COVID that might be conspiring with an already altered coagulability profile to induce thrombogenesis? It might.

A good portion hypercoagulability is acquired and even when there are genetic variants that predisposed to clotting, they often are activated or induced by environmental variables – drugs included.

For background – thrombophilias affect 10-40% of the pop, varying by coagulation defect, race and region. Those that have both a genetic and acquired element are far more prevalent.

Which ones have both genetic and acquired components?

Hyperhomocysteinemia (MTHFRs); APS, antithrombin, protein C, protein S, dysfibrinogenemia, dysplasminogenemia all have environmental activations – read illness, medications, diet, lifestyles, sitting, immobility, etc. COVID could easily be a stressor capability of activating.

Immobility too.

However, and this is a big however, so too would all of the drugs given to patients to fight this virus.

Especially against a backdrop of longstanding polypharmacy.

Reports suggest viral, bacterial and fungal infections are linked to increased risk of clotting. Rarely however, do they dissociate the actions of the pathogen from that of the drugs used to quell the infection or reduce other symptoms.

For example: Environmental Triggers of Autoreactive Responses: Induction of Antiphospholipid Antibody Formation

From my own work – from which much of these data are shared.

Digging a little deeper. From 50% – 70% of patients who develop thrombosis carry one or more genetic and/or acquired thrombophilias.

That is a huge proportion of the population that is at risk for developing clots given the right circumstances.

Current estimates suggest that 7-10% of the population carry genetic thrombophilias and up to 60% develop factors that may lead to an acquired state of hypercoagulability.

Again – 60% of the population carries factors that may lead to hypercoagulability.

Just how common are clots? Very common.

Consider: according to US. Hospital discharge records (2007-2009) show 548,000 annual hospitalizations related to peripheral blood clots or venous thromboemboli (VTE).

Among those, 349,000 were deep vein thromboemboli (DVT) and 278,000 were pulmonary emboli (PE).

These numbers, may be underestimated.

Another study, that included both hospital and community events, showed annual rate of 909,793 clotting events (378,623 DVT; 531,170 PE), and fully a third were fatal.

The rate of annual VTEs has been steadily increasing over the last decade and researchers project that by 2050, the US healthcare system may be burdened with a staggering 1.82 million VTEs annually.

Mind you, not only are these numbers underestimated, they reflect late stage clotting – clotting that causes death directly or at least noticeably and where someone noticed. These numbers do not reflect the widespread mini-clots that don’t yet cause death and go unnoticed.

Autopsy reports of women who die from birth control related blood clots report widespread clotting, not just the clots that lead to fatality.

That is because hypercoagulability is systemic and only becomes noticeable when it blocks something fully.

It is not unreasonable to assume those dying of COVID with clots observed, didn’t also develop coagulation problems long before and/or concurrent with the illness but not necessarily relative to the illness itself, but rather to the drugs given to treat the illness.

So, maybe COVID is only indirectly involved. It may be our treatments that are causing the clots and the multi-organ failures observed with these cases.

Before jumping on the COVID-causes-X bandwagon, consider other culprits. It might just reframe treatment possibilities.

References for above cited statistics are included within: Testing for Thrombophilia Before Contraceptives Are Prescribed: Background, Laboratory Tests, and Economics.

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COVID Notes: Reconsidering Death, Oxygen, and ATP

by Chandler Marrs, PhD

Published on April 17, 2020

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I have had some difficulty finishing full research articles during this crisis. In lieu of full articles, and in order to more fully understand some connections, I have been tweeting thoughts and hypotheses – yes, tweeting. Eventually, these snippets will become articles, but in the meantime, I thought I would share them here. I have cleaned them up a bit and added a few links where relevant, but they remain largely as they were posted on Twitter.

Reconsidering Death, Oxygen, and ATP

I was contemplating death last night, not my own per se, but the notion of death. What is death or what constitutes death? And you know what? I still land squarely at the mitochondria.

Oxygen (O2) is fundamental for life and we like to think that its absence constitutes death. While its diminishment sure makes living difficult and its absence makes life impossible, there is something more fundamental required. There is one more step below the necessity of O2.

Without ATP – O2 cannot be used.

Sit with that for a moment.

We can mechanically ventilate and force-feed O2, but if there is insufficient ATP, it will not matter.

The relationship is reciprocal, of course, without O2, there can be no ATP.

But yet still, ATP is key.

Making fueling the mitochondria the single most important thing we can do to prevent death for any disease process, but especially something like COVID.

Unfortunately, virtually every treatment in the medical armament damages mitochondria (yes that includes all pharmaceuticals) – even or perhaps especially – forced ventilation (here, here, here). That is not to say that sometimes meds or mechanical ventilation are not necessary, but only that we could do better if we considered how O2 is used and what is required for O2 saturation beyond just the mechanics.

And that we could do better if we considered the damage drugs do to that process. [For that matter, we should also be considering the damage environmental chemicals do as well.]

For O2 to be used — we need ATP.

For ATP – we need functional mitochondria.

For functional mitochondria – we need micronutrients, thiamine especially. Thiamine drives the mitochondrial processing plant.

Mitochondrial nutrients — Nutrients required for mitochondrial production of ATP.

Thiamine deficiency — by itself, absent any other variables, causes hypoxia. They call it pseudohypoxia because it doesn’t match our current conceptualization of obstructive hypoxia, but it is hypoxia just the same. The only difference – it originates in the mitochondria.

From a lack of ATP, we get the inability of the mitochondria to utilize the readily available O2, which leads to more hypoxia and a crap ton of other negative sequelae. All of which we are seeing in full relief with COVID patients.

If only there was a simple solution…

Oh, that’s right, there is.

No heroics needed, just give folks IV thiamine, an IV banana bag when they come in, continue until they improve.

If they are still able to eat, throw in some protein, fat, a few carbs, and perhaps, some fat-soluble vitamins (A, D,K, for example).

To reframe – what do mitochondria need to create ATP? Nutrients plus O2.

What do mitochondria need to use O2? ATP.

So what do mitochondria need to ‘breathe’? Nutrients.

Nutrients are the missing piece in the puzzle.

Feed the mitochondria >>> prevent mitochondrial collapse >>> prevent death.

A few articles that influenced my thinking:

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More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

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