I believe the pneumonia and the cerebral symptoms of COVID 19 could be a result of some type of Fat Embolism. Fat Embolism is caused by any trauma to the cell, physical or chemical, that causes fat globules to form that can lodge in the lungs and even the brain. It was believed that fat embolism was caused by physical injury to the body, but I believe that it is also chemical and only takes mild cellular trauma to cause the calcium ions to increase and ultimately form fat and plaques.
My hypothesis is that the cells in the body are traumatized by the virus, which result in calcium ions exiting the reticulum of the mitochondria and entering the bloodstream. The calcium ions act like little soldiers that come out of the cell when the cell is traumatized. Similarly, when you put blood into a centrifuge, the plasma rises to the surface. I believe the ions try to defend our bodies against any potential harm and the result is lipids that turn into plaques. Considering the end result of all disease is some type of plaque, and considering calcium ions are a catalyst for plaque, it’s not impossible to believe this could be a piece of a very complex puzzle. Heart disease causes plaque in the coronary arteries. Strokes can be caused by plaques that break off and lodge in the cerebral vessels. Alzheimer’s is caused by amyloid plaques. Parkinson’s is scattered plaques. Multiple sclerosis results in sclerotic plaques. Diabetes is a systemic disease of plaque. And even in death, your body tries to protect you by forming plaques, which lead to rigor mortis.
The hard part is that the calcium ions that are the key to trying to defend us from cellular trauma, are ultimately what ends up killing us. My assumption, which I believe can be investigated through post mortem lung and brain studies, is that some patients that have died from pneumonia have higher than normal levels of fat in their lungs and brain. My assumption is that the volume of calcium ions exiting the reticulum of the cell are higher than normal because the virus is attacking the cells at a rapid pace. The fat/lipids that normally pass through the capillary network, are now too large to pass through and can lodge in the lungs forming sticky fats and can pass to the brain causing confusion and even seizures. Fat embolism looks exactly like pneumonia on X-ray. Perhaps pneumonia is some form of fat embolism.
A while ago I presented this abstract at an ultrasound conference as a guide to help physicians and clinicians determine if a patient had a blood clot (Deep Vein Thrombosis) or a fat clot (Fat Embolism). Looking at the symptoms of the COVID 19 patients, it seems they are experiencing some level of fat embolism in addition to the cytokine storm. Patients are demonstrating petechial rashes, ARDS, confusion, thrombocytopenia, etc. as in the FES Clinical Scoring Chart. Is it possible that this is happening? Can this information help?
I’ve heard that a vaccine for the corona virus might not work because the virus uses the antibodies to grow. I’ve heard that we can‘t all receive prophylactic antiviral medicines. What is left is trying to prevent people from being on a respirator when they go into what seems to be like ARDS, acute respiratory distress syndrome, by preventing the ARDS symptoms in the first place. If it is ARDS or is similar to ARDS, then we need to understand that ARDS occurs in patients with trauma approximately 24-72 hours after injury. A patient will be talking, eating and acting normal and then suddenly feel they can’t breathe. When the fat/insult reaches a point where it can’t pass through the capillaries, ARDS is what occurs. If something similar is happening with COVID patients, we should be researching this now. I don’t have the capacity or a lab to do this. I am hoping someone else does that can see the benefit of this information.
I am not trying to gain anything by posting this. Posting something like this certainly isn’t what I had ever hoped or planned. I am an educator and I feel that I have this point of view and feel compelled to share it. Even if I’m wrong, or way off or not even close, I hope that it helps lead to other research for the future and greater thinking around the mitochondria and the phospholipid bilayer and the mathematical dilemma of the calcium ions and if there is a way the ions can be controlled to reduce plaque. I have been studying fat embolism, plaques and microbiology for almost 20 years, but am in no way an expert. I have beliefs about the calcium ions in the sarcoplasmic and endoplasmic reticulum and hope that further studies can be done to ultimately control the plaque formation. If by some small miracle there is even some slight benefit of posting this, I am glad I did.
I ask that you please do not attack me for posting this in any way, as I am only trying to provide information. I don’t know how to slow calcium ions. I don’t know how to slow lipids from forming. I don’t know how to stop plaque. I don't know how to stop blood from clotting rapidly. This has been the study of lifetimes. But maybe there is a pharmaceutical company or a scientist or a doctor that does know how and maybe they will see this post and maybe it will trigger something in them and maybe it will lead to a way to stop the lipids and the insults that is causing the respiratory issues. If this hypothesis and this information can’t help patients with COVID, then perhaps it can lead to helping people in other ways.