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.
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.
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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