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COVID Notes: Cardiolipin and Clotting

Published on October 23, 2020

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The text below came up on my Facebook book memories recently. It was from a project I worked on three years ago. I never did anything with this particular bit of insight, and apparently, completely forgot about it. Since it may have some bearing on COVID-related thrombosis, a quick search suggests that possibility (here, here, here), I thought I would publish the text so that others may follow up.

Cardiolipin: A Mitochondrial Response to Stress

I just learned something interesting. Am working on the project regarding testing women for clotting disorders prior to receiving a prescription for hormonal contraceptives, which induces clotting and thus exacerbate thrombosis risk. Antiphospholipid syndrome (APS) is a common contributor to clotting – think Lupus, RA, but many other disorders. One of the antibodies involved in APS is called anti-cardiolipin (aCL).

Cardiolipin is a mitochondrial antibody produced in by the inner membrane of the mitochondrion, involved in a bunch of functions, including complex IV of the electron transport chain (ETC), apoptosis, and other stuff. Cardiolipin moves to the outer mitochondrial membrane when the mitochondria are stressed (in response to pharmaceutical toxicants, nutrient deficiencies, etc). Once outside the membrane antibodies form to attack it because it is not supposed to be there, APS develops and all sorts of things go wrong.

First insight: APS is mitochondrial in origin and is a response to environmental cues. This suggests that what we call autoimmunity is mitochondrial in nature as well – inner membrane molecules displaced to the outer membrane and then recognized as threats or toxicants and acted upon accordingly. Second insight, the body is doing what it is supposed to do. It’s dealing with a threat. It is not autoimmunity in the sense of aberrant immune function (something I never bought anyway). The problem is that the threat never resolves. So if we were to resolve the threat – repair the mitochondria and remove the toxicant exposure, the immune response should resolve. The molecule should return to its appropriate home and immune cascades against it settle.

Unrecognized APS Cascades and COVID

Additionally, let me add a bit of background about APS. The text below is from our report, which is available on ResearchGate.

Antiphospholipid syndrome (APS), also called Hughes Syndrome, is an acquired autoimmune condition of unknown origins with hypercoagulability and a high rate of thrombosis. It affects predominantly women, increases with age and comorbid diseases such as systemic lupus erythematosus (SLE), Sjogren syndrome, and rheumatoid arthritis (RA). Up to 70% of SLE patients and 28%of RA patients respectively test positive for antiphospholipid antibodies. It should be noted that 1-5% of the general population also test positive for APS, but remain largely asymptomatic. This is likely attributable to the environmental reactivity of the antibodies. Common medications, including hormonal contraceptives, antibiotics, and vaccines induce APS chemistry. APS shows an elevated risk for both venous (70%) and arterial (30%) thrombosis. It is estimated that 30-40% of patients will develop thrombosis at some point in their lives and 15% of DVTs are attributable to APS. Myocardial infarction and CVTs are common among APS individuals. Of note, a study covered in the ‘cost of not testing’ section, found Lupus antibodies, one of the markers of APS, to be the most commonly identified thrombophilia in their hospital. APS may be among the more common causes of acquired thrombophilia, especially in women.

Diagnosis of APS is difficult, relying heavily on clinical acumen. Laboratory testing requires the measurement of antiphospholipid antibodies (anticardiolipin, lupus anticoagulant, beta 2 glycoprotein – B2GP1) done at repeat intervals 12 weeks apart. The tests are highly reactive to environmental factors, including acute phase thrombosis, infections, and medications. For these reasons, the indicated prevalence rate is likely inaccurate.

Connections to Explore

Given the environmental trigger of APS antibodies, including cardiolipin, and the apparently high but unrecognized prevalence of variables that predispose one towards APS reactions, I cannot help but wonder if a portion of the clotting seen in COVID patients is related to these pathways triggered by either virus itself and/or the medications used to treat the virus. Similarly, given the lack of diagnostic acuity with APS, is it possible that a percentage of the COVID patients have activated but latent APS cascades in advance of developing COVID? Finally, with cardiolipin antibodies identified in COVID patients, does that not tell us that tell us that we ought to be looking more closely at the mitochondria in our treatment protocols?

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Thiamine: A Missing Piece of the COVID-19 Treatment Puzzle?

by Jeffrey Lubell

Published on September 24, 2020

13813 views

Earlier this year, Hormones Matter published two posts suggesting that thiamine could be helpful in treating COVID-19, one by Dr. Lonsdale focused on the role of thiamine in facilitating the energy metabolism needed to fight disease and one by me focused on thiamine’s potential to increase oxygen levels through the inhibition of carbonic anhydrase isoenzymes. Since the publication of these posts, new evidence has emerged that further supports the potential benefits of thiamine for COVID-19. This post reviews the new evidence and argues for the accelerated execution of a randomized controlled trial to evaluate the potential of thiamine to slow the progression of COVID-19 in newly diagnosed outpatients.

Thiamine and COVID-19: New Evidence

The most important new data are: (1) a study which found that high-dose thiamine lowers the Th17 cell proinflammatory response believed to be associated with the COVID-19 cytokine storm and (2) data on mortality rates from two medical centers using the MATH+ protocol to treat COVID-19 hospitalized patients. I summarize each in turn.

Modulation of Th17 proinflammatory response. Through a creative combination of in vivo and in vitro experiments, the authors of this study demonstrate that thiamine interrupts the cycle of inflammation believed to play a role in the cytokine storm associated with COVID-19, leading to reduced levels of IL-17 pro-inflammatory cytokines and increased levels of the anti-inflammatory IL-22 cytokines. They determined that a range of 74-474 mg daily of thiamine would achieve the desired response in COVID-19 patients. Notably, this study did not involve patients with COVID-19, but rather patients with alcohol use disorder, who also tend to experience a pro-inflammatory state characterized by elevated IL-17 levels. So thiamine’s effectiveness in preventing and treating COVID-19 still needs to be tested in a clinical setting. The study is in the pre-print phase only, and is currently under review by a peer-reviewed journal. This video by Dr. Mobeen Syed provides a helpful explanation of the study and its context.
Reduced COVID-19 mortality rates in two hospitals using the MATH+ protocol. The MATH+ protocol for COVID-19 combines a range of substances to treat hospitalized COVID-19 patients: Methylprednisolone (a steroid), Ascorbic Acid (Vitamin C), Thiamine, Heparin (a blood thinner) and several additional components, including melatonin, zinc, vitamin D, atorvastatin and famotidine. Grounded in the experience Dr. Paul Marik and his collaborators gained in treating patients with sepsis, and other emerging evidence, the protocol has been endorsed by a group of physicians known as the Front Line COVID-19 Critical Care Alliance. The protocol is intended to be used as soon as hospitalized COVID-19 patients meet the criteria for oxygen supplementation. Dr. Marik’s version of the protocol, the EVMS Critical Care COVID-19 protocol, also includes recommendations for treatment at earlier phases of the disease and for prevention.

The MATH+ protocol has not been evaluated through a randomized controlled trial, but the authors have published a detailed scientific review of the protocol as well as data on the mortality of patients treated with the protocol. According to their data, through July 20, 2020, the two hospitals using the protocol (United Memorial Medical Center, in Houston, TX, and Sentara Norfolk General Hospital, in Norfolk, Virginia) reported mortality rates for hospitalized COVID-19 patients of 4.4 and 6.1 percent, respectively. This compares with mortality rates for hospitalized COVID-19 patients of 15.6 to 32.0 percent reported in other studies. Since this is not a formal controlled study, it is possible that explanations other than the use of the MATH+ protocol could account for the sharply lower mortality rates at the Houston and Norfolk hospitals. Nevertheless, the comparatively low mortality rates of the hospitals using the MATH+ protocols represent very promising results.

Other recent articles suggesting a role for thiamine in treating COVID-19 include: an article on the potential role of B vitamins in treating COVID-19, a review of the potential of vitamins to treat COVID-19, and an article focused on famotidine, melatonin and thiamine. Many of the studies on the potential role of thiamine in treating COVID-19 are summarized in this review. This article focuses on the potential of the carbonic anhydrase inhibitor acetazolamide to prevent kidney damage from COVID-19. As noted in my earlier post, an in vitro study suggests that thiamine may be nearly as effective as acetazolamide in inhibiting carbonic anhydrase isoenzymes.

Potential Mechanisms Linking Thiamine Deficiency to COVID-19

The exact mechanism through which thiamine may be contributing to the results discussed above is unclear. One potential pathway is thiamine deficiency, which is fairly common in severely ill patients and discussed by the authors of both the Th17 research paper and the scientific review of the MATH+ protocol. As the scientific review of the MATH+ protocol observes:

The human adult can store around 30 mg of thiamine in muscle tissue, liver and kidneys, however, these stores can become depleted in as little as 18 days after the cessation of thiamine intake. A thiamine deficiency syndrome, beriberi, bears a number of similarities to sepsis, including peripheral vasodilation, cardiac dysfunction, and elevated lactate levels. In critical illness, the prevalence of thiamine deficiency is 10–20% upon admission and can increase up to 71% during ICU stay, suggesting rapid depletion of this vitamin.

At the same time, however, the authors noted that “[b]ased on limited data, no association was detected between thiamine levels, markers of oxidative stress and mortality” in two studies.^”

There could also be benefits in using thiamine as part of a combination protocol with other agents. For example, the authors of the MATH+ scientific review note that the combined administration of thiamine and steroids may help to enhance the anti-inflammatory properties of steroids. “In experimental rheumatoid arthritis, thiamine increased the ability of corticosteroids to suppress production of TNF-á and IL-6.”

An intriguing role for thiamine in countering the inflammation associated with some viruses is raised by the authors of the paper on the Th17 proinflammatory response. They cite in vitro research which found, using feline models that some viruses rely on a thiamine transport protein in the disease cycle. In theory, occupying the thiamine transporter by providing thiamine to thiamine-deficient individuals could inhibit a virus which relied on this same transporter. While not specifically addressed in the paper, this raises the question of whether the use of high doses of thiamine in individuals without a deficiency could have a similar effect in interrupting the disease cycle of a virus that depends on the thiamine transporter.

Neither the Th17 study nor the scientific review of the MATH+ protocol mention thiamine’s role as a carbonic anhydrase inhibitor, but it is noted in two of the other articles referenced above as potentially contributing to reduced hypoxia. This pathway needs further study. Carbonic anhydrase inhibitors produce carbon dioxide, which can help to reduce the hypoxic conditions that produce inflammation. One way is through increased respiration. Several other mechanisms for carbon dioxide’s protective effects are summarized in this article:

Numerous other mechanisms potentially exist whereby CO2 protects the tissues from hypoxic-ischemic damage. An increase in blood pCO2 shifts the oxygen hemoglobin dissociation curve to the right (Bohr effect), the result of which is a decrease in the affinity of hemoglobin for oxygen. Therefore, at the capillary level, CO2 would tend to raise pO2, increase the gradient for any given oxyhemoglobin saturation, and facilitate transfer of O2 to the tissue for oxidative processes. CO2 might also preserve cardiac function during systemic hypoxia. The inhibition of systemic lactate production by CO2 inhalation during hypoxia would serve to maintain optimal cardiovascular function.

Research Needed

Given the severity of the COVID-19 pandemic, and the expected challenges associated with the combined burden of flu and COVID-19 on hospitals this fall and winter, it is important to test all plausible treatment avenues for COVID-19. The data reviewed in this post add to the evidence base supporting a randomized controlled trial (RCT) to test whether thiamine – alone or in combination with other agents – could help to slow the progression of COVID-19 and/or mitigate the cytokine storm associated with some of its worst effects.

Cognizant of the prevailing view that RCTs are the best way to build evidence about the effects of medical treatment, the authors of the scientific review of the MATH+ protocol specifically discuss their decision to forgo an RCT. They argue that the clinical value of each of the treatments included in their protocol has been well established and that they therefore do not have the clinical equipoise (“the belief by the investigator that neither intervention in the control or experimental group is more effective”) necessary to justify a trial. In essence, they argue that it would be unethical to deprive patients facing a deadly disease of treatments they believe to be effective. Instead, they are pursuing a different research approach: “the formation of a patient registry to measure and compare the outcomes of patients treated with MATH+, not only against the prevailing ‘supportive-care only’ strategy, but also against other novel proposed treatment approaches employed throughout the country and world.”

Even if the necessary clinical equipoise is not available to justify an RCT in hospitalized patients, I would argue that there IS sufficient clinical equipoise to justify an RCT testing the effects of thiamine and other agents in slowing the progression of COVID-19 in newly diagnosed outpatients. While there is a theoretical basis for believing thiamine could be helpful, we won’t know whether and to what extent it is helpful in a real-world setting until a trial is done. One approach would be to test a combination therapy that relies on oral versions of many of the substances used in the MATH+ protocol, such as vitamin C, thiamine, heparin or another blood thinner such as aspirin, vitamin D, melatonin, famotidine, and zinc. Due to concerns about possible harms resulting from the administration of a steroid too early in the progression of COVID-19, it would likely be advisable to omit a steroid from the earliest stages of treatment. The rationale for avoiding steroids in non-critically ill COVID-19 patients is discussed in the September 2, 2020 World Health Organization guidelines on the use of corticosteroids for COVID-19.

Many of these substances are already being evaluated in trials to assess their effectiveness in treating COVID-19, as reflected in the ClinicalTrials.gov database. But not thiamine.

What are we waiting for?

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COVID Notes: Medications and Mitochondrial Damage

by Chandler Marrs, PhD

Published on May 6, 2020

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The following article came up on one of my feeds recently: Antibiotics Against COVID-19 and Mitochondria? Urgent Thinking Out of the Box. I hope it is one of the first of many articles questioning damage done to mitochondrial function by medications. Below is the twitter thread where I contemplated this topic. This is the fourth in a series of short posts adapted from my writings on twitter. The other three can be found here, here, and here.

Medications and Mitochondrial Damage

Not sure that it should be considered out-of-the-box, but here we are, so entrenched in the benefits of all meds for all disease processes that we forget to even question their utility or their mechanisms. Yes, the data presented here are preliminary and merely correlational but the questions the report poses are valid, particularly when one knows that these and other drugs severely damage the mitochondria; making a bad situation infinitely worse.

Everything about the COVID crisis speaks to broader crisis in medicine; namely that we cannot medicate our way out of bad health. Indeed, much of the ill-health is sadly iatrogenic. Medications damage mitochondria.

This is just for starters – but there are hundreds of articles on this topic. [See below for a few more articles.]

We tend to think these effects are rare, mainly because we pay them no heed, but also, because we rarely connect the dots and go deeply enough into the chemistry to recognize that this mitochondrial damage is not merely a rare ‘adverse’ effect of the drug in question, but simply an effect of the drug itself. It is a mechanism of its chemistry, something it was designed to do. We only call them adverse effects and think of them as rare because we want to believe in the controllability of drug mechanisms; that we can target these medications specifically, that we can compartmentalize, much like we have compartmentalized organ systems and medical specialities.

This is bolstered, of course, by the fact that some folks seemingly resist such ‘adverse’ reactions. I say seemingly, because the chemistry of the drug is the chemistry of drug no matter into whom it is placed.

Just because someone doesn’t appear to suffer ill-effects from a medication does not deny that the chemistry induced them. It means only that the individual had sufficient mitochondrial reserves to withstand the damage of the drug. That’s it.

Everything we see with the COVID crisis points not just to the strength of the virus, but to our weaknesses metabolically, medically, and intellectually.

We believed for so long that we could medicate our way out of poor lifestyles, that the answer to everything was more medication, more chemicals, and more technology, that we completely forgot the most fundamental aspects of health depend entirely upon the mitochondria and all that the mitochondria require are nutrients. They do not require chemical toxicants. Those are stressors that must be withstood. Even those medications deemed necessary are mito-toxicants. Every single one of them.

COVID is bringing that into full relief. The multi-organ failure, the panoply of seemingly random symptoms attributed to COVID – that is mitochondrial failure – brought on by chronic ill health, initiated and/or exacerbated by drug induced mitochondrial damage.

The virus has simply expedited that process in a way that none of us were prepared for. So is it out of the box to consider antibiotic induced mitochondrial damage leading to COVID death? No. It is finally placing the mitochondria into the ‘medical’ box where they belong.

The question is whether any of us is ready to consider the depth of our folly and ignorance regarding medication effects. Do we really want to know what damage we might have done to ourselves and others?

Postscript: Diet and Chemically Induced Mitochondrial Damage

There are a few points to note with medication-induced mitochondrial damage that I did not cover in the thread above. First, mitochondria require nutrients to function properly. See Figure 1. below. To the extent any of those nutrients are insufficient in the diet makes one more susceptible to the damage by chemical toxicants. A diet full of processed foods, though fortified, is often nutrient deficient while simultaneously full of chemical additives that increase the burden on mitochondria (here, here, here). Similarly, conventionally grown agriculture and livestock, while healthier than their highly processed counterparts, contain fewer nutrients today than they did in decades past and than their organic counterparts. And once again, because of current agricultural practices, carry a higher toxicant load which must be dealt with by the mitochondria (here). Achieving nutrient sufficiency with a typical western diet is difficult at best and many individuals suffer from what we call high calorie malnutrition.

Second, pharmaceuticals leach nutrients and thus both short term, but especially, long term usage of common medications is likely to leave one in a precarious state of nutrient insufficiency and even outright deficiency. This imperils mitochondrial function. The mitochondria require lots of nutrients to function. Insufficiency in any one of the micronutrients listed below elicits negative compensatory reactions that become the hallmarks of the metabolic disease processes plaguing modernity.

mitochondrial nutrients — Figure 1. Mitochondrial Nutrients from: Thiamine Deficiency Disease, Dysautonomia and High Calorie Malnutrition

Third, chemical toxicants, whether of the pharmaceutical or environmental persuasion, damage the mitochondria both by leaching those nutrients, as mentioned above, but also, by blocking or overriding various enzymes and functions within the mitochondria. So even if one had a pristine diet, and who among us does, exposure to these toxicants demands a surplus of nutrients to withstand the effects of these chemicals.

Fourth, battling a serious virus or any illness or serious stressor requires exponentially more ‘energy’ than is required for everyday living, even without the added stressor of the medication induced damage. This increase in demand necessitates efficient mitochondrial function and the continued supply of both macro- (carbs, fat, and protein especially) and micro- (vitamins and minerals) nutrients. Absent that supply, damage is incurred. In other words, to survive an illness, any illness, the body requires fuel. When that fuel is insufficient or absent, as is so often the case with serious illness, mitochondrial collapse and significant morbidity, and eventually, death become imminent. So when we consider how to treat the illnesses associated with the COVID virus, it is incumbent upon us to remember that the health and fitness of the mitochondrial response will determine success or failure.

Mitochondrial Damage via Nutrient Depletion

Below are additional articles on nutrient depletion by medication and environmental exposure. These depletions are recognized, but few make the connection between nutrient depletion and mitochondrial damage unless one understands the chemistry and the nutrients involved in the various pathways leading to, through, and from the mitochondria (see Figure 1. above). Then, it becomes clear just how easily mitochondria can become impaired. This is not a complete list. It is just a sampling. I have included a few articles of my own on common drugs for the pre-existing conditions most commonly presenting with COVID where associated research articles are hyperlinked within.

Environmental Chemicals, Pharmaceuticals, and Mitochondrial Damage

The research above involves illustrates the mitochondrial damage precipitated by individual toxicants. In reality, no one is ever exposed to just one toxicant. Polypharmacy is rampant and environmental exposures are broad. How those combine to affect mitochondrial function no one really knows. We don’t study combined exposures. What we do know, however, is that much of the population is not as healthy as we consider them to be.

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COVID Notes: Random Thoughts On Brain and Immune Function

by Chandler Marrs, PhD

Published on April 28, 2020

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This is the third in a series of short posts adapted from Twitter threads contemplating various aspects of the COVID-19 pandemic. The first two posts can be found here and here, and of course, on Twitter.

COVID, the Brain, and Immune Function

The neuroinvasive potential of SARS‐CoV2 may play a role in the respiratory failure of COVID‐19 patients.

“The most characteristic symptom of patients with COVID‐19 is respiratory distress, and most of the patients admitted to the intensive care could not breathe spontaneously…”
…where the brainstem was heavily infected…”

Key sentence: could not breathe spontaneously and brainstem involvement. Reading further we get thalamic involvement – as was reported in COVID-19–associated Acute Hemorrhagic Necrotizing Encephalopathy: CT and MRI Features.

As soon as I see this pattern, brainstem degradation>thalamic involvement, I immediately think dysautonomia>beriberi>thiamine deficiency>mito-hypoxia>disrupted immune function>inflammation overkill>leaky BBB >leaky junctions.

Then a few, more philosophical questions, niggle in the background. I have long had this theory that these pathogens have always already been with us and are just ‘activated’ when the circumstances align. I have no real basis for this and certainly much evidence against it.

But the idea remains – what if everything was already there? That the threats that we face are not entirely external but internal as well. This doesn’t mean that there are not external pathogens to which we fall prey, there absolutely are, but what if we constitutionally mirror those pathogens – they exist in us already but remain quiescent, mostly, until some confluence of events activates them.

If that were the case, then the potential for any pathogen to ‘reach’ any part of the body, the brain included, would not be so much about the uniqueness of the pathogen, although that would play a role certainly, but more about the uniqueness of the ‘host’.

This would then bring us back to Matzinger’s danger theory, where the immune system has advanced beyond the overly simplistic self vs non-self model – because everything is self, the pathogens were always already a part of us, and it is our response to them that engenders danger.

That brings us back to host response being the key variable to address with any illness. And with that, two questions. 1) what does the individual need to survive/be healthy and 2) are they getting it?

Reframed for this pandemic. 1) What molecular resources does the patient require to mount an effective immune response, with the appropriate amount of inflammation at the appropriate time? 2) Are they getting them? Likely they are not, because they are ill, sometimes seriously.

Reframed one more time. 1) What are the molecular resources one needs to beat this illness altogether – to be an asymptomatic carrier? 2) Are they getting them?

In this regard, everything comes back to host resources availability. That places the determinants of health versus illness squarely onto host health or more specifically, host mitochondrial health because the question always comes back to mitochondrial fitness, to the energy/ATP needed to either stave off illness altogether or fight it and survive if this fails.

Then where the pathogen attacks becomes an equation that includes equal parts pathogen to host variability e.g. host genetics/epigenetics/diet/lifestyle/environment etc., which is moderated by energy availability.

And from that perspective, as meandering and incompletely argued as it was, maybe it still provides a clue to how we fight this – bolster host defenses. Maybe that’s too simple in the age of technology. Maybe not.

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COVID-19 and Thiamine: An Interview with Dr. Derrick Lonsdale

by Kristi Wees

Published on April 27, 2020

9910 views

In the summer 2013, a geneticist we were seeing for my daughter ordered a test. Little did I know that test would contribute to a change in the course of my daughter’s life as well as a new area of study and advocacy for my career. This is my first time to write for Hormones Matter, so let me start by introducing myself. I am Kristi Wees and I am a pediatric patient advocate with EmpoweredAdvocacy.com as well as a national consultant for patient advocacy, empowerment, and engagement in the field of pediatric genetics. I was trained as a chemist at Penn State University with graduate training at UCLA. It was the journey that my daughter’s health took our family on that made me realize exactly why I had studied chemistry.

Fast forward to 2020, nearly 7 years later and now a pandemic with COVID-19, and I again realize how that 2013 test has sent us on an incredible journey. That 2013 test was for transketolase, which is a blood test to determine a vitamin (thiamine, B1) insufficiency. At the time, my daughter was struggling with autistic-like behaviors, severe fatigue, suspected mitochondrial disease, gastrointestinal concerns, severe food intolerances, and chemical sensitivities. The future looked bleak and hopeless.

After this test result came back, I began to search the literature about thiamine and found the work of Dr. Derrick Lonsdale. With guidance and a prescription from our medical team, we began our daughter on thiamine supplementation. In 2016, I had the distinct honor of meeting Dr. Lonsdale in person. In 2019, I had the honor of interviewing him with Patricia Lemer for an episode called, “I Have A Child Who…Has Tantrums”.

A few weeks ago, I was reading the medical literature (here, here, and here) and watching anecdotal reports (here) regarding COVID-19 and began to see some clues that made me think of Dr. Lonsdale’s work on thiamine. I reached out to him via email and he shared with me that he too was seeing similar red flags and that he was frustrated because at 96 years old, and having dedicated his life to research on this vitamin, he believed it could be helping so many critically ill patients. He asked if I had any ideas about how to help him get the word out.

Here is the idea we came up with: a recorded interview. Dr. Lonsdale is a gentleman with whom I have come to know as a friend, mentor, and researcher and whose body of work helped my child thrive. I believe he possesses wisdom that has been forgotten and largely ignored by modern medicine. Listen to the interview, you won’t be disappointed.

Interview With Dr. Derrick Lonsdale: Thoughts on COVID-19

Dr. Derrick Lonsdale’s thoughts on COVID19 from Empowered Advocacy on Vimeo.

Shortly after releasing the video last week I came across this study: Intravenous Thiamine Is Associated With Increased Oxygen Consumption in Critically Ill Patients With Preserved Cardiac Index. Which again confirms Dr. Lonsdale’s conviction that thiamine can greatly improve the current situation in many ICU’s nationwide.

After treatment with thiamine, and many dietary, environmental and lifestyle changes, plus a whole lot of answered prayers, my daughter is thriving today with no residual behavioral, medical, neurological, developmental or learning challenges. Could thiamine also help overcome COVID-19? Possibly.

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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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COVID Notes: The Blood Clot Problem

by Chandler Marrs, PhD

Published on April 20, 2020

3825 views

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

5057 views

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.

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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We’re On Our Own With COVID-19

by Chandler Marrs, PhD

Published on April 14, 2020

3526 views

Over the last several weeks, like many of you, I have been gripped by news of the coronavirus (COVID-19) pandemic. I spend hours reading the medical research, reviewing the statistical models, and following the first hand accounts of doctors and patients. Normally, I am not one disposed to anxiety, panic, or overreaction, but I have to admit, this virus scares the crap out of me. It’s not just that this is a novel virus to which none of us has immunity or that there are no treatments, or that it disrupts an absolutely critical physiological system, the renin-angiotensin aldosterone system (RAAS), or that it is highly contagious, those variables alone make COVID-19 dangerous. That would be sufficient to induce panic in anyone under normal circumstance, but these are not normal circumstances. The virus seems to have timed its appearance perfectly so as to exert the most damage; when population ill-health is soaring and world economic, political, and health systems are crumbling. We are fundamentally ill-prepared to confront such a threat. And this is terrifying.

COVID Exposes Our Weaknesses

As a way to slow the infection rate and spare hospital demand, social isolation and quarantine policies have been implemented around the world. All but essential industries have shut down, including non-essential healthcare e.g, non-emergency or non-COVID related healthcare. Governmental response, in the US at least, and in some other countries, has been unorganized at best, and blinded by malice, incompetence and corruption at worst. Inasmuch as healthcare systems here in the US were already at capacity and frequently more aligned with economics than health, this crisis will overwhelm even the best of them.

With poor infectious disease capabilities, the risk to the health and life of frontline practitioners is high. This will be magnified by skewed economic interests of hospital financiers. We are likely also to lose a substantial number of primary care physicians to this crisis, not necessarily to the illness itself, but to the economic restructuring that is inevitable. Medical practices whose economic stability rely on complicated, services-based billing, will become financially infeasible when those services cannot be ministered and they will shutter. Given that here in US we already have fewer per capita physicians than many other countries, this becomes an increasingly risky prospect for a population that has learned to rely on these services.

We are seeing hints of this economic collapse already in the hospitals including those not yet hit by the COVID wave. In anticipation of lost revenue from elective procedures, hospitals are canceling contracts with their employees, including those who will risk their lives to care for COVID patients. In the hospitals where COVID is building or has already hit, where the financial output required to treat this virus is enormous, especially with supply profiteering encouraged the administration, and where once again, elective procedures have been canceled, insolvency is close (here, here, here). Of course, the hospitals and the healthcare industry are not blameless in this impending financial fiasco. For decades now, unethical and outright corrupt medical billing practices have padded revenue streams by upcharging and upselling every single aspect of healthcare. Does a single aspirin really need to cost $25? It does indeed, if one’s financial wherewithal rests on a convoluted reimbursement system that more closely aligns with grift than legitimate cost accounting.

This is, of course, on top of the very real risk of morbidity and mortality facing all healthcare personnel on the frontlines of this pandemic. Everyone from the cleaning staff to the physicians is at risk and yet, the solution reached by many seems more skewed towards protecting the bottom line rather than employees (here, here, here). While the costs of this pandemic are staggering, they are made infinitely worse by the economics of our current model of for-profit medicine. This does not bode well for the future of American healthcare, and perhaps, if there is an upside to this crisis, that is it. When we reach the other side, perhaps we can create a healthier and more sustainable model of healthcare, but we must survive this crash first.

We Are On Our Own With COVID

To survive, we must recognize that we are very much on our own with this pandemic, not just for our response to COVID but for general health as well. That is, we will be mostly left to treat ourselves in isolation unless or until we either come through to the other side or require hospitalization. We cannot simply go to our primary physicians for assistance, not only because there are no known medically effective treatments available for COVID, though many have been proposed, but primarily because many physicians are no longer available. Some have switched to telehealth, but the overwhelming demand posed by this virus has severely constricted already inundated practices. Considering that it took anywhere from 6 – 66 days to see a family care physician prior to COVID, it should not be surprising that a pandemic of this scale would further limit physician availability.

There is also the risk we present to everyone who might care for us should we seek out medical attention early in the disease process. Everyone whom we would come contact with would be exposed, particularly in the US where protective gear is limited. Finally, if we require hospitalization, the outcome is not always positive, especially if we require mechanical ventilation. According to the current data from New York, COVID related hospitalization corresponds with an approximately 18% mortality rate. The mortality rate relative to all cases, is much lower of course. Drilling down a bit, if the disease process progresses to the need for mechanical ventilation, the mortality rate skyrockets. Those data are not available yet here, but one report from China found 97% of COVID patients requiring ventilation died. In general, mechanical ventilation outcomes are not good, with mortality rates ranging from 30-40%.

In addition to the increased patient mortality associated with mechanical ventilation, it is here where physicians and other healthcare personnel are most at risk to contract COVID. From other pandemics, we know that risk of contracting the viral contagion ranged from 2.8-6.6X higher in practitioners involved in intubation and subsequent care for these patients. Given the lack of protective gear in the US, along with the higher transmissibility rate of COVID compared to some other viral pandemics, the risk to all healthcare personnel is much higher. And yet, the employers of these institutions are cutting contracts, reducing pay, refusing hazard pay of their frontline personnel, and in many cases, have yet to provide sufficient protective gear, with some hospitals even preventing staff from wearing self-purchased protective gear. This is unconscionable, and yet, not completely unexpected given the perverted financial and ethical mores of the American healthcare industry.

Not since the early frontier days have we Americans required medical self-sufficiency, or any self-sufficiency. We like to portray ourselves as rugged individualists, bootstrappers and the like, but in reality, we are deeply dependent upon each other. Recognizing our fundamental interdependence with each other is not such a bad thing. Where it becomes problematic is when we place our faith and our health into the hands of those whose primary interest is financial. This is what COVID is teaching us. The question is, are we listening?

If We Are On Our Own, We Need A Plan

With the current state of politics in the US, it seems likely that many of us will have to face this crisis without external assistance. The question is how do we do this? Or more importantly, how are you going to prepare for your survival. It sounds like I am being overly dramatic, and I hope I am, but in the event things continue to go south, we all need a plan. So these are the questions I pose. First, how are you going to minimize infection rates – yours, your family’s and your community’s. Second, if you become infected, what is your survival plan? Simply hoping that you will have one mild cases may not work. If you get lucky, sure, but if not, how do you plan to survive this illness? Think about it. What will you need? Do you have supplies in storage for the quarantine? If you have a family, have you decided how to tackle possible co-infection? What is the plan? Third, if you should become severely ill and require hospitalization, what is the plan then? How will you get there? Knowing that if it progresses to that point that you will put into isolation at the hospital, and you may or may not recover, have you made the appropriate arrangements for yourself and/or your family? If you recover, what is the plan then? And finally, considering the impact of this pandemic on the structure of healthcare in general, what is the plan to manage existing conditions, now and going forward? Are there things you might do differently because you might not have access to physicians? These are questions we must all ask ourselves. And who knows, maybe if we do this right, we’ll come out of this crisis, healthier and happier than before. Please share your plans below.

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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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Image by Mabel Amber from Pixabay

Hormones Matter

Where health, hormones, and a whole bunch of other stuff, make sense.

COVID - Page 3

COVID Notes: Cardiolipin and Clotting

Cardiolipin: A Mitochondrial Response to Stress

Unrecognized APS Cascades and COVID

Connections to Explore

We Need Your Help

Thiamine: A Missing Piece of the COVID-19 Treatment Puzzle?

Thiamine and COVID-19: New Evidence

Potential Mechanisms Linking Thiamine Deficiency to COVID-19

Research Needed

We Need Your Help

COVID Notes: Medications and Mitochondrial Damage

Medications and Mitochondrial Damage

Postscript: Diet and Chemically Induced Mitochondrial Damage

Mitochondrial Damage via Nutrient Depletion

Environmental Chemicals, Pharmaceuticals, and Mitochondrial Damage

We Need Your Help

COVID Notes: Random Thoughts On Brain and Immune Function

COVID, the Brain, and Immune Function

We Need Your Help

COVID-19 and Thiamine: An Interview with Dr. Derrick Lonsdale

Interview With Dr. Derrick Lonsdale: Thoughts on COVID-19

We Need Your Help

COVID Notes: The Blood Clot Problem

COVID and Blood Clots

We Need Your Help

COVID Notes: Reconsidering Death, Oxygen, and ATP

Reconsidering Death, Oxygen, and ATP

A few articles that influenced my thinking:

We Need Your Help

We’re On Our Own With COVID-19

COVID Exposes Our Weaknesses

We Are On Our Own With COVID

If We Are On Our Own, We Need A Plan

We Need Your Help

COVID - Page 3

Cardiolipin: A Mitochondrial Response to Stress

Unrecognized APS Cascades and COVID

Connections to Explore

We Need Your Help

Related posts:

You might be interested in

Thiamine and COVID-19: New Evidence

Potential Mechanisms Linking Thiamine Deficiency to COVID-19

Research Needed

We Need Your Help

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Medications and Mitochondrial Damage

Postscript: Diet and Chemically Induced Mitochondrial Damage

Mitochondrial Damage via Nutrient Depletion

Environmental Chemicals, Pharmaceuticals, and Mitochondrial Damage

We Need Your Help

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COVID, the Brain, and Immune Function

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Interview With Dr. Derrick Lonsdale: Thoughts on COVID-19

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COVID and Blood Clots

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Reconsidering Death, Oxygen, and ATP

A few articles that influenced my thinking:

We Need Your Help

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We Are On Our Own With COVID

If We Are On Our Own, We Need A Plan

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