Updated: Apr 5, 2020
As of this writing there have been 856,955 confirmed cases of the virus worldwide, with 42,089 deaths. While the death rate reported from the virus is accurate, and will continue to be, the deadliness of the virus, calculated by how many have been affected and how many have died, will not be accurate. We will likely never know how deadly the virus actually was in the end.
This is because we have not been testing, nor do we have the capacity to test, anywhere near enough people. Therefore, since many people become infected and have no symptoms or very little symptoms, the number of actual people infected will be substantially underestimated. The people most likely to have been tested are those who have the worst symptoms and actually seek medical care. Many of the mild cases among the general population will be missed from a reporting point-of-view and if we do not know the true total of people who have been infected, then we cannot know the true deadliness of the virus. Deaths, divided by number of those who have been infected, is the death rate. We have a good idea of the top number, but since everyone infected will not have been tested, we will not know the true bottom number.
Statistics aside, this whole thing is far from over, and we do not know what the final effects from it will be. Up to this point, I want to discuss some of the observations I have seen as well as their implications. First, I want to briefly go over what the virus is and how it affects our bodies. Coronaviruses are a class of viruses that are transmitted, initially, from animals to people. They are called “corona” because under a microscope each viral strand seems to have a crownlike ring on it. Historically, there have been several types of coronaviruses, some have been shown to cause more mild symptoms:
- 229E (alpha coronavirus)
- NL63 (alpha coronavirus)
- OC43 (beta coronavirus)
- HKU1 (beta coronavirus)
and others have proven more serious:
- MERS-CoV (beta coronavirus that causes Middle East Respiratory Syndrome, or MERS)
- SARS-CoV (beta coronavirus that causes severe acute respiratory syndrome, or SARS)
- SARS-CoV-2 (novel coronavirus that causes coronavirus disease 2019, or COVID-19)
A virus works by gaining access to the cells of its host in some way. This is usually by hijacking a receptor on the cell (think of it like a little gate in the cell wall). In the case of SARS-CoV-2, it gains access via the ACE-2 receptor. (1,2) This is a receptor used by the body to increase blood pressure when it is needed. Therefore, the relationship between SARS-CoV-2 and the ACE-2 receptor has implications for those with high blood pressure. When the body wants to increase blood pressure it releases various proteins and hormones that eventually end up stimulating the ACE-2 receptor and triggering the increase in blood pressure. If someone has chronically high blood pressure, they are likely to have an increase in the amount of ACE-2 receptors on their cells. You can see that this creates more of an opportunity for SARS-CoV-2 to gain access to cells in those people.
Because of its action on the ACE-2 receptor, it makes sense that SARS-CoV-2 gains access through the lungs and small intestine as these tissues have been shown to have ample amounts of ACE-2 receptors. (3) Also, with SARS-CoV-2, it seems that people who suffer more severely also have co morbidities relating to the vascular system of the body, this is logical considering the effects that the ACE-2 receptor has on the vascular system. Obviously, the studies on this virus are in their infancy because it a new virus, but in one study, the most prominent co morbidities of 32 non-survivors from a group of 52 intensive care unit patients with the virus were cerebrovascular diseases (22%) and diabetes (22%). (4)
As more information comes out, it seems that people with conditions like high blood pressure, diabetes, and heart disease are at much higher risk of being severely affected by, and/or dying from, the virus than those who do not have these preexisting conditions. More and more doctors on the front lines are reporting this observation. Another study out of China looked at 191 patients with diagnosed Coronavirus and found that almost half had a co morbidity, of which hypertension, diabetes, and heart disease were the most common. They also found that among those with a co morbidity, the older they were the more risk of death they had. (5)
While it does seem that these diseases, which are driven by dysfunctional metabolism, are contributing to the poor outcomes, I think that the treatments being given to people for these pre-existing conditions may also be predisposing them to poor outcomes. For example, people with hypertension are often given an ACE inhibitor or another blood pressure lowing medication. These medications have been shown to increase the amount of ACE-2 receptors on cells. (6) It is plausible to think that this effect would make it more likely that the virus could take hold in someone taking these medications. This is exactly what authors of one early research paper thought, they stated:
“These data suggest that ACE2 expression is increased in diabetes and treatment with ACE inhibitors and ARBs increases ACE2 expression. Consequently, the increased expression of ACE2 would facilitate infection with COVID-19. We therefore hypothesize that diabetes and hypertension treatment with ACE2-stimulating drugs increases the risk of developing severe and fatal COVID-19.” (7)
So not only does having high blood pressure make someone more susceptible to the virus, but taking the medications offered by western medicine to treat high blood pressure could make someone more vulnerable as well.
As for people with diabetes having worse outcomes with this virus, research has shown that higher blood sugars make people more susceptible to viral infection, and diabetes is characterized by higher blood sugars. When looking at glucose and susceptibility of cells to viral infection, one study found that, “cells normally grown in a high glucose medium (4–6 mg/ml glucose), when switched to a low glucose medium (1 mg/ml) were much less susceptible to infection”. (8) Another study, that detailed the mechanisms by which higher blood sugar, and more significant oscillations in blood sugar, can make someone more susceptible to a virus, stated that, “diabetes increases susceptibility to severe infections”. (9) The higher blood sugars associated with diabetes seem to give viruses an advantage when they are trying to gain access to the cells of a host.
Lastly, people who have hypertension, diabetes, and heart disease are often told that they should lower their intake of saturated fat, and many are told to take a cholesterol lowering medication. If you follow my blog, you know that the idea that eating cholesterol, or having high cholesterol, is the cause of heart disease does not make sense and is not backed up in the research. You also know that cholesterol plays a very important role in the immune system. (see this post on cholesterol) This is especially true for viruses.
Studies have shown that when the viral antibodies of our immune system are made, they can team up with cholesterol molecules to become much more potent virus killers. (10) One study stated that, “C34 derivatized with cholesterol (C34-Chol) shows dramatically increased antiviral potency”. (11) Another study found that cholesterol conjugated peptides could halt the merging of a viral and cellular membrane, they stated that this had “broad implications for antiviral development” and that, “applicable targets include influenza A and B viruses as well as arenaviruses (Junin), human metapneumoviruses, filoviruses (Ebola), flavivirus, and coronaviruses (severe acute respiratory syndromes)”. (12) Clearly, cholesterol can be a powerful ally in the fight against viral infection. By not eating it, or decreasing it with a drug, we could hinder these viral defense mechanisms.
Curiously, some studies have found loose associations with cholesterol lowering drug use and lower rates of infection, but these are association studies and cannot prove that the drug caused the lower infection rate. These studies often end with the authors saying that the findings were not statistically significant and that no mechanism could be identified. On the other hand, one study found that in patients who were in the hospital recovering from stroke, those who were taking a cholesterol lowering medication had increased rates of infection. (13) Another study found that cholesterol lowering drugs increased the amount of what are called regulatory T cells, the authors pointed out that a reduction in these cells made people more susceptible to a number of viral infections. (14)
What does all this mean? Well, given that there seems to be a correlation between these diseases, as well as the western medical treatments for them, and worse outcomes with the coronavirus, I think it would be wise to understand how to correct these pre-existing conditions by correcting their root cause. Research has shown that high blood pressure is largely driven by insulin resistance, (15) that diabetes is also caused by insulin resistance, (16) that cholesterol in the diet is not the cause of heart disease and that those with higher cholesterol live longer, (17,18) and that a high saturated fat/ketogenic diet has been shown to correct insulin resistance. (19,