There is little doubt that Covid is an extremely deadly illness. However, simply put, and I will elaborate on these figures in a later post, Covid is around 10-100 times more deadly than the influenza virus which kills up to half a million people each year. Hence in a period of 18 months it has killed around 5million people. However, the risks to Covid are not equal. Many health professionals have been reported in the media saying that “for healthy younger people the risk is no more than the annual influenza virus”. Despite the media hyping up when a young person (under 50) dies from Covid, these are still around the same rates as influenza deaths. Young and so called healthy people die from the influenza virus every year. What is ignored by the media and politicians is that the elderly and in particular the sick elderly are disproportionately more vulnerable and much, much more than they are to the influenza virus. To put it in best guestimate figures if you are over 65-70 years and sick your risk is probably more than 100 times greater. The big difference largely depend upon how healthy the individual is and how many other pre-existing health conditions the person has. Susceptibility to all viruses increases with age and comorbid health conditions, however, this is exaggerated much more with Covid. Fortunately, we know what causes this increased vulnerability and we have known of it since Covid 1 back in 2003.
Based on hundreds of studies the susceptibility to the Covid virus appears to be governed largely by the ACE 2 (RAS) which closely linked with Alzheimer’s, obesity, hypertension, diabetes 2, metabolic syndrome and other diet and lifestyle diseases. This system called the RAS begins with Angiotensinogen (AGT) a protein produced by the liver and released into the blood when it is under some form of stress. Once angiotensinogen is released into the blood it is converted into a molecule called Angiotensin 1 which seems to be fairly inactive. However, if it is acted on the Angiotensin 2 converting enzyme (ACE2) it becomes Angiotensin II (AngII). AngII is a key mediator not only in blood pressure control and vascular tone regulation, but also involved in inflammation, endothelial dysfunction, atherosclerosis, hypertension and congestive heart failure.
Here is where it becomes really interesting and why you need to know some of these facts. The SARS-CoV-2 virus uses the angiotensin-converting enzyme 2 (ACE2) receptor to gain entry into the cells, especially in the respiratory system. During viral infection, entry of the virus into the host cell is the critical step that enable the virus to cause so much damage. Under normal circumstances a virus like influenza has to battle multiple defence mechanisms like your lung microbiota (yes you have protective microbiota in your lungs just like your gut), lung membrane and immune system to gain access into the cell. Because Covid can gain access through the ACE2 receptor it has quick and multiple levels of entry into the cells, a bit like the Trojan horse used by the Greeks to invade Troy. The Greeks could not get enough soldiers into Troy to defeat the city so they left behind the Trojan horse with elite soldiers inside. Once it was taken inside the city the soldiers were able to sneak out and begin to destroy the city from the inside. They snuck through the normal protective mechanisms. In a similar way the Covid virus is able to attach to the ACE2 to gain entry into the cell where the numbers quickly overwhelm the cells where they can begin viral replication. Once the viruses are able to gain entry, the infected cells recruit our own immune cells for viral clearance, which then causes hyperinflammation and as a result the damage done to our respiratory system. The common clinical symptoms of COVID-19 observed so far are fever, cough, breathlessness, and fatigue.
Imagine what would happen if we were able to block the entry of the Covid virus into the cell via ACE2. Because there are hundreds of studies that show the ACE2 is the reason Covid is so deadly, it would be sensible to try and stop or slow the virus from gaining such quick access into our cells like the Trojan horse. Even if a few Covid viral particles were able to get access into the cell it would not overwhelm the cells creating the hyper-inflammation and would dramatically improve the chances of our immune system destroying without the extra damage. Many drug companies are already working on drugs to reduce the ACE2. In contrast, the current vaccines all work by allowing the virus access to the cells then fighting them off.
Fortunately, we know many of the conditions linked with elevated ACE2 as well as many things we can do nutritionally to reduce the ACE2, whether you have taken the vaccine or not. This knowledge can benefit everyone as people with the vaccine can also get sick and die from Covid.
The main conditions linked with elevated ACE2 and risks from Covid are of course Alzheimer’s, metabolic syndrome, obesity diabetes 2, hypertension etc. Not to mention gut dysbiosis, malnutrition, vitamin D deficiency and the taking of some medications like proton pump inhibitors for reflux. Although there are many more I will report on later which can account for many of the so called young ones and healthy ones getting infected and seriously ill such as chronic stress. We also have lots of good research, hundreds and hundreds of papers on how to reduce the ACE2.
Unfortunately, this is not widely known and is not likely to get any media attention because it is not a pharmaceutical solution and as a result many more people will die vaccinated and unvaccinated.
Along with ACE2 a number of other factors are involved with increasing the risk from this virus. These can also help entry into the cells, replication and spread of the virus. This is important to know because the pharmaceutical companies are trying to retrofit other drugs to block the virus. It is also important to know because of the complexity of some nutraceuticals, like Withania, which I will highlight later, can reduce many of these at any one time. A real virus killer so to speak.
Transmembrane protease serine 2 (TMPRSS2) is also responsible for virus entry into the host cells by activating the viral S-proteins. Various studies have shown that inactivating the TMPRSS2 could facilitate inhibition of the viral infection.
The RNA dependent RNA polymerase (RdRp) is responsible for viral replication and transcription as is 3CL protease sometimes called as Mpro.
Papain-like proteinase (PLpro) is required for correction of viral replication and for viral immune evasion processes.
Cathepsin B and helps the virus to enter into cytoplasm and is also found in Nipah virus, Ebola virus, influenza virus etc.
Understanding the modes of entry and action of the virus gives us an amazing fighting chance and understanding of what we can do nutritionally.
