(Word of warning. Long post)
I was sent an article by a number of people discussing a new theory about how and why Covid does what it does and found it very interesting with many factual and other very plausible points. I took the liberty of editorializing it, adding some information for clarification.
In a nutshell, bradykinins, one of many cytokines in our body, builds up leading to many of the unexplained symptoms we are seeing with Covid-19. The virus impairs how this molecule is broken down and how the receptor for the virus is changed and amplified. All very scientifically sound. This theory even points to new potential treatments of the disease.
Although this is a very interesting, plausible and even actionable theory, it does not change the basics.
Don’t get sick and you won’t have to worry about it.
WEAR A MASK.
DISTANCE.
WASH YOUR HANDS.
DON’T ToUCH YOUR FACE.
GET HEALTHY.
VENTILATE.
VACCINATE.
Stay safe and be well.
AC 😎✌️🌱❤🐖🏃🏻🧘🏻♂️🌎😷
The Summit supercomputer at Oak Ridge National Lab in Tennessee, the second fastest computer in the world, analyzed more than 40,000 genes from 17,000 genetic samples of Covid-19 looking to find patterns of behavior, mutation, symptoms…
The computer revealed a new theory about how Covid-19 impacts the body. The “bradykinin hypothesis” provides a model that explains many aspects of Covid-19, including some of its most bizarre symptoms like rashes, headaches, heart arrhythmias… The analysis also provided a number potential treatments, many of which are already FDA approved.
A Covid-19 infection begins when the virus enters the body and attaches to ACE2 receptors (Angiotensin Converting Enzyme 2) in the nose since they are abundant there. THAT, by the way, is why covering your nose is so important when wearing a mask! The virus starts to replicate there. As we inhale, it also attaches to the ACE2 receptors in the lungs. It then proceeds through the body, entering cells in other places where ACE2 is also present like the intestines, kidneys, brain and heart. This likely accounts for at least some of the disease’s cardiac, neuro and GI symptoms.
At that point, the virus actively hijacks the body’s own systems, tricking it into upregulating, increasing the number and the sensitivity of ACE2 receptors in places where they’re usually expressed. This includes not only the lungs, but also just about every other organ system.
The renin–angiotensin system (RAS) controls many aspects of the circulatory system, including the body’s levels of a chemical called bradykinin, one of many cytokines (compounds made up of chains of amino acids , like proteins). Bradykinin is a potent vasodilator (it opens up arteries) and mild diuretic (causes removal of extra fluid through the kidneys), both contributing to lowering blood pressure. It also causes contraction of smooth muscle in the lung airways and gut, increases vascular permeability (ability for things to cross in and out of the walls) and it is also involved in the mechanism of pain.
When the virus tweaks the RAS, it causes the body’s mechanisms for regulating bradykinin to go haywire. Bradykinin receptors are stimulated to be more sensitive, and the body also stops effectively breaking down bradykinin. The enzyme ACE normally degrades bradykinin, but when the virus downregulates it, it can’t do this as effectively. The end result is a “bradykinin storm”, a massive, runaway buildup of bradykinin in the body. According to the bradykinin hypothesis, it’s this storm that is ultimately responsible for many of Covid-19’s deadly effects.
As bradykinin builds up in the body, it dramatically increases vascular permeability, making your blood vessels leaky. This aligns with recent clinical data, which increasingly views Covid-19 primarily as a vascular disease, rather than a respiratory one. But Covid-19 still has a massive effect on the lungs. As blood vessels start to leak due to a bradykinin storm, the lungs fill with fluid. Immune cells also leak out into the lungs, causing inflammation. It also makes this fluid thick, like a gel. Through another pathway, it increases production of hyaluronic acid (HLA) in the lungs. HLA is often used in soaps and lotions for its ability to absorb more than 1,000 times its weight in fluid. When it combines with fluid leaking into the lungs, the results are disastrous as it forms a hydrogel, which can fill the lungs in some patients. It’s like trying to breathe through Jell-O. This may explain why ventilators have proven less effective in treating advanced Covid-19 than doctors originally expected. It reaches a point where regardless of how much oxygen you pump in, it doesn’t matter, because the alveoli in the lungs are filled with this hydrogel. Patients can suffocate even while receiving full breathing support. Techniques like continuously repositioning patients snad doing pulmonary therapy can be helpful, to clear the gel.
The bradykinin hypothesis also extends to many of Covid-19’s effects on the heart. About 20% of hospitalized Covid-19 patients have damage to their hearts, even if they never had cardiac issues before. Some of this is likely due to the virus infecting the heart directly through its ACE2 receptors. But the RAS also controls aspects of cardiac contractions and blood pressure. Arrhythmias and low blood pressure are common in Covid-19 patients.
The bradykinin hypothesis also accounts for Covid-19’s neurological effects, which include dizziness, seizures, delirium and stroke, present in as 50% of hospitalized Covid-19 patients. Using MRI studies, many Covid-19 patients have evidence of leaky blood vessels in their brains. Bradykinin can also lead to a breakdown of the blood-brain barrier which acts as a filter between your brain and the rest of your circulatory system. It lets in the nutrients and small molecules that the brain needs to function, while keeping out toxins and pathogens and keeping the brain’s internal environment tightly regulated.
If the blood-brain barrier is broken, this could allow harmful cells and compounds into the brain, leading to inflammation, potential brain damage, and many of the neurological symptoms Covid-19 patients experience.
Increased bradykinin levels could also account for other common Covid-19 symptoms. ACE inhibitors, a class of drugs used to treat high blood pressure, have a similar effect on the RAS system as Covid-19, increasing bradykinin levels. By essentially acting like a natural ACE inhibitor, Covid-19 may be causing the same effects that hypertensive patients sometimes get when they take blood pressure–lowering drugs. ACE inhibitors are known to cause a dry cough and fatigue, two textbook symptoms of Covid-19. And they can potentially increase blood potassium levels, which has also been observed in Covid-19 patients. I routinely evaluate patients for chronic coughing and they are often on ACE inhibitors. Furthermore, the symptoms can persist as long as 2-3 months after switching to a different blood pressure medication. In addition the majority of the airway swelling emergencies, including emergency tracheostomies, what we in the business call “slash-trachs”, I deal with occur in patients who take ACE inhibitors.
ACE inhibitors are also known to cause a loss of taste and smell. Although, this symptom is more likely due to the virus affecting the supporting cells surrounding olfactory nerve cells, than the direct effects of bradykinin.
Though still an emerging theory, the bradykinin hypothesis explains several other of Covid-19’s seemingly bizarre symptoms. “Covid toes,” a condition involving swollen, bruised toes that some Covid-19 patients experience. This could be a result of the blood vessel leakiness caused by bradykinins. The thyroid gland can also be affected by bradykinins leading to the thyroid symptoms recently observed in some patients. Thyroid inflammation can cause excessive amounts of hormone to be produced (thyrotoxicosis) resulting in palpitations, sweats and election in blood pressure. In other forms of viral thyroid issues, as many as 20% may have permanent effects on their thyroid function. It’s still not clear what the long term impact on thyroid function will be from Covid-19.
The bradykinin theory can also explain why women have a lower rate of complications since certain aspects of the RAS are linked to the X chromosome. Women have 2 X chromosomes, hence more ability to break down bradykinin. Men are XY, so they have a less active RAS.
As far as potential treatments are concerned, several drugs target aspects of the RAS that are already FDA approved to treat other conditions. They could arguably be applied to treating Covid-19. Several of these drugs reduce bradykinin production and could potentially stop a deadly bradykinin storm. Others reduce bradykinin signaling and could blunt its effects once it’s already in the body.
Vitamin D is involved in the RAS system and could prove helpful by reducing levels of another compound, known as REN. Again, this could stop potentially deadly bradykinin storms from forming. The researchers note that vitamin D has already been shown to help those with Covid-19. The vitamin is readily available over the counter, and around 20% of the population is deficient. Keep in mind that Vitamin D has only been shown to be helpful if patients are deficient to begin with.
Other compounds could treat symptoms associated with bradykinin storms. The drug hymecromone, for reduces hyaluronic acid levels, potentially stopping deadly hydrogels from forming in the lungs. Another drug, timbetasin could mimic the mechanism that is thought to protect women from more severe Covid-19 infections. All of these potential treatments are speculative, of course, and would need to be studied in a rigorous, controlled environment before their effectiveness could be determined and they could be used more broadly.
https://elemental.medium.com/a-supercomputer-analyzed-covid-19-and-an-interesting-new-theory-has-emerged-31cb8eba9d63