What Doctors Are Learning From Autopsy Findings of Coronavirus (COVID-19) Patients - And Why You Should Care

I'm not a medical professional, but I've been fascinated with the study of biochemistry and how the body works in general since I can remember. I'm on a quest to distill as much factual, well-researched information about the novel COVID-19 virus as possible. Here, I share my findings with you. Together, we can maneuver the noise and misinformation floating about, and seek the truth. Even if that truth is a bit scary and not necessarily what we want to hear. We cannot fix something or protect ourselves from it until we know and face the truth about it.

Notes on “What Doctors Are Learning From Autopsy Findings of Coronavirus (COVID-19) Patients.”
https://www.youtube.com/watch?v=KzKvIYwqQkE

TL;DR Version:
- COVID damages the body by directly attacking the ACE2 receptors on cells found throughout the body, as well as indirectly through inflammation and blood clots
- This combination of clotting and immune response can cause all kinds of symptoms and lead to organ failure, gangrene, and ruptured veins (COVID toes, purpura, Nick Cordero needing to have his leg amputated, poor guy)
- Unlike most illnesses that cause blood clots, COVID causes clots in the arteries AND veins
- The only other illness known to clot both is APS/CAPS
- This is an autoimmune disease that occurs when your body's immune system attacks phospholipids
- Phospholipids provide barriers in cellular membranes to protect the cell, and they make barriers for the organelles within those cells - which means if they go AWOL, our bodies fall apart at the cellular level!
- Viral infectious diseases, especially those of the respiratory tract, have been reported as being the trigger for CAPS
- The risk factors for APS/CAPS are the same as for COVID: Being Male, Smoking, Obese, High Blood Pressure, Diabetes, Age, Chemotherapy, & Immunocompromised
- Considering all these factors, COVID seems to trigger APS/CAPS by triggering the immune system’s platelet activating factor (PAF)
- More studies need to be done to confirm these findings, and to learn more about how viral infections play a role in causing the body to start attacking its own cell walls, but we seem to be getting an idea of how COVID works

Full Version:
Clots have been found in the lungs and brain (stroke). Also associated with seizures & Guillian-Barr Syndrome. These variabilities make it very difficult to treat (like any disease that attacks the immune system). There’s never been a disease in the history of mankind that’s presented itself with this much variability. Holy fuck, that is terrifying.

We're about to go deep into the inner workings of the body, time to strap on our Science Hats!

What we know:
- Spike proteins bind to ACE2 receptors via the nose, eyes, or mouth.
- These receptors are found in many parts of the body.
- Once in the body, the virus invades cells to make copies of itself, while also disabling the cell’s ability to “call for help.” Like if a home invasion was taking place but the electricity was cut off.
- Once deeply embedded in our bodies, the virus starts attacking organs with ACE2 receptors. These organs include: Heart, Kidneys, Brain, Liver, & Blood Vessels (easy to forget those are organs too)
- Viral particles have been found in not only the nasal passages and throat, but also: Tears, Stool, Kidneys, Liver, Pancreas, Heart, & Cerebral Spinal Fluid (holy fuck!)
- So yeah, this virus also causes meningitis (inflammation of the membranes that encapsulate the brain and spinal cord)
- So, the virus invades the body by attaching itself to ACE2 receptors. But, that’s only part of the whole COVID story. At this point, the immune system finally reacts, causing a cytokine storm.

The Cytokine Storm:
- “Disruption of the CCL5/RANTES/CCR5 pathway restores immune homeostasis and reduces plasma viral load in critical COVID-19”
- This RANTES cytokine is thought to play a large role in the COVID cytokine storm
- It binds to the CCR5 receptors on CD4+ and CD8+ lymphocytes (T cells) - essentially propagating further inflammation, and possibly further clotting as well (that’s fucked up, so it causes a cytokine storm and uncontrollable clotting as well!)
- When the virus invades the alveolar cells (tiny air sacs in the lungs that help them exchange air), it replicates rapidly and then goes on to invade more cells. The cells closest the alveolar are the capillaries (the thinnest blood vessels in our bodies).
- Capillaries are lined with cells called endothelium, which also have ACE2 receptors (these also line the intestines if I’m not mistaken too - hmm is Leaky Gut related to this?) (apparently so! https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5846192/ ) - it’s a crazy domino effect that reminds me SO very much of autoimmune diseases and chronic illnesses like mine
- Once the virus attacks those capillaries, the immune system goes PAF - Platelet Activating Factor, aka Acetyl-Glycerol-Ether-Phosphorylcholine
- It’s a “big deal” because it’s a potent phospholipid activator
- Pause to research: https://sciencing.com/primary-functions-phospholipids-7349125.html
“Phospholipids” are molecules that have hydrophilic phosphate heads and hydrophobic lipid tails. Aka, water loving heads that repel from fat, and fat loving tails that repel from water. They are a genius way of comprising cell walls, and other things that need to keep the inside of something separate from the outside, especially when keeping water and fat based molecules separate. Basically, these are the “wall molecules” of the cells of our body. And if those get fucked with, and the inside of our cells become vulnerable to the outside, that will wreak all kinds of havoc, and cause all kinds of health problems.
- Back to the video: This means the cells in our body undergo massive inflammation, AND clotting. One study has shown that a third of patients got clots even when already on blood thinners. The real number is probably higher because most doctors haven’t been checking patients with a “respiratory illness” for blood clots. Until now.

So, COVID causes organ damage by:
- Directly attacking organs via their ACE2 receptors
- Indirectly attacking organs by way of collateral damage from the cytokine storm
- Indirectly cause damage to organs by causing blood clots
- Indirectly cause damage as a result of low oxygen levels, improper ventilator settings, drug treatments, and/or all of these factors combined
- Damn son, that’s fucked up.

Whew, that was a lot of technical information! We have more to get through yet, let's pause and enjoy the simple cuteness of these kittens before we go on!

APS may be the key:
- Antiphospholipid Syndrome is an autoimmune disorder that occurs when your body's immune system makes antibodies that attack phospholipids. It may be why so many patients with COVID are getting clots.
- The lining of the blood capillaries in the lungs are called endothelium. These are destroyed by inflammation from the cytokine storm along with COVID itself. This causes people to not be able to get oxygen.
- COVID is more destructive to endothelial cells that are already compromised. Populations with compromised endothials tend to be: Male, Smokers, Obese, High Blood Pressure, and Diabetes - the same associated risk factos for worse outcomes in COVID
- Blood clots can not only cause organ failure, but gangrene and purpura! Hence the COVID toes and people having to get their legs amputated!
- We still don’t know 100% if APS is responsible for all the clotting with COVID
- Some patients with COVID exhibit Catastrophic APS aka CAPS
- They experience more severe symptoms like strokes, seizures, heart attacks, kidney failure, ARDS (Acute respiratory distress syndrome), skin changes like covid toes and purpura -- which makes doctors wonder if CAPS is what’s going on with severe COVID cases

Based upon existing evidence, it seems likely that APS/CAPS is the root result of COVID:
- Viral infectious diseases, especially those of the respiratory tract, have been reported as being the trigger for CAPS
- The pathogenesis is complex and might involve the activation of TLR4 (Toll Like Receptor 4), which triggers a cytokine storm, followed by the alterations to the endothelium cells in the lung capillaries, which serves as the trigger for the cytokine storm

Let’s talk about arterial thrombosis:
- Blood clots that develop in an artery, usually due to plaque. These can travel downstream and cause blockages in organs, limbs, the gut, and the brain.
- Risk factors for AT: High BP, Hypertension, High Levels of Cholesterol, smoking, diabetes, age, chemotherapy, and the degree of infection. All the same factors as for COVID.
- So yes, there does seem to be a link. There’s really only one other illness known to affect veins and arteries, and that’s APS. BOOM. Other conditions known to cause abnormal clotting, such as Factor V Leiden, HITT, and PNH, aren’t known to cause clots in arteries. They almost always form clots in just veins.
- So all the factors seem to point to APS as the key. Which makes this novel indeed.
- Plus, studies are showing that patients with COVID and clots also test positive for APS. (“Coagulopathy and Antiphospholipid Antibodies in Patients With COVID-19”)
- This very well may be the reason some COVID patients are dying
- We need more studies and he will be releasing a video on APS and CAPS soon

It’s hard to diagnose APS because it’s easily confused with “DIC”:
- DIC = Disseminated Intravascular Coagulation
- Certain labs resemble DIC, such as: increased PT/INR, increased PTT, increased platelet levels.
- But we know patients with COVID don’t have DIC for two reasons: they weren’t suffering extensive bleeding, and they don’t have low fibrinogen levels.

This is why it’s so hard to properly diagnose. It’s very complicated and we still have so much to learn.

We did it! We got through all the science together! Don't you feel empowered now that you're armed with a bit more knowledge?