The media was awash with reports of a preprint (not-peer reviewed) report that individuals who are blood type A might be at more risk of Covid19 infection than those who are type O. The study was conducted by scientists and doctors from cities across China including Beijing, Wuhan, Shanghai and Shenzhen. Medical researchers in China took blood group patterns of more than 2,000 patients infected with the virus in Wuhan and Shenzhen and compared them to local healthy populations. They found that blood type A patients showed a higher rate of infection and they tended to develop more severe symptoms.
While the researchers said the study was preliminary and more work was needed, they did urge governments and medical facilities to consider blood type differences when planning mitigation measures or treating patients with Sars-CoV-2.
“People of blood group A might need particularly strengthened personal protection to reduce the chance of infection,” wrote the researchers led by Wang Xinghuan with the Centre for Evidence-Based and Translational Medicine at Zhongnan Hospital of Wuhan University.
There is a long evidence-based history that linking the ABO blood types (A, B, AB and O) with specific differences in susceptibility to a wide range of infectious illnesses, including smallpox, plague, cholera and influenza. Although most speculation calls research to identify some aspect of the difference between the cell antigens that characterize the physical manifestation of ABO blood type, it is much more likely that the cause behind the blood type differences lay instead with the opposing blood group antibodies and not the antigens.
The science behind the relationships between the ABO blood groups is simple enough:
- Blood type A has the ‘A’ antigen (a sugar known as GalNac) and makes an antibody against blood type B
- Blood type B has the ‘B’ antigen (a sugar known as Gal) and makes an antibody against blood type A
- Blood type AB has the ‘A’ antigen and the ‘B’ antigen; they do not make antibodies against any other blood types (universal receiver)
- Blood type O does not have a recognizable antigen (think of ‘O’ as ‘zero‘); they make antibodies against both A and B blood types (universal donor)
A study published in 2008 in the journal Glycobiology, ‘Inhibition of the interaction between the SARS-CoV spike protein and its cellular receptor by anti-histo-blood group antibodies.’ looked at the SARS virus and observed that the S (‘spike’) protein’s ability to adhere to cells expressing angiotensin-converting enzyme 2 (ACE2) was specifically inhibited by either monoclonal or human natural anti-A antibodies. This indicated that these antibodies may block the interaction between the virus and its receptor, thereby providing protection. They concluded that ‘the ABO polymorphism could contribute to substantially reduce the virus transmission, affecting both the number of infected individuals and the kinetics of the epidemic.’
Although these finding might be somewhat sobering for individuals (including myself) who are type A blood, I don’t think it’s time for drawing too many conclusions from the base observations.
- There are other reasons and factors that influence susceptibility to Covid19, including age, and other comorbidities, (hypertension, diabetes, cardiovascular disease, etc.)
- There is a great degree of variation between type O individuals with regard to the level (‘titer’) of their anti-A antibodies
and in their class and quality
- Opposing blood type antibodies can come in two classes: the long-term ‘memory’ antibodies, known as IgG, and the ‘early’ antibodies, known as IgM.
- Of the two, IgM is the more powerful. It is a large molecule that floats in the bloodstream as a snowflake, then attaches to some microbial invader and changes shape to a ‘crab’. This crab shape allows the IgM antibody to clump (‘agglutinate’) pathogens directly, unlike IgG which acts more like a tagging signal to attract the immune system to the invader
- The reason that the protective effect was observed in type O and not type B (who after all also make anti-A antibodies) is that type B typically makes only the IgG class anti-A, which is probably less effective.
- Being type O on its own is not cause for wild celebration. In type O anti-A levels vary widely. They go down with age and are lower in urban dwellers when compared to rural dwellers, so just being type O in itself does not mean much
However, like any discovery with a true basis in reality, deep inside there is an engineering solution.
Many of you know, that I’ve researched lectins for many years. These are proteins that are made by many plants and invertebrates that react with sugars typically found in living organisms. My interest in lectins stemmed from the fact that many of these are in common foods and quite a few are specific for one blood type or another. For example, a lectin found in lima beans can agglutinate cells of a person who is either blood type A or AB but will not react with the cells of those who are B or O. In a way lectins are primitive antibodies, made by nature to protect delicate seeds, beans and other delicate ’embryos’ from fungi and other parasites until they can germinate and protect themselves. It’s at least possible to consider using food lectins to impart a somewhat ‘anti-A’ defense, even in people who are blood type A.
This is because lectins are extraordinarily specific molecules (the word ‘lectin’ was coined by its similarity to the Latin legere, which connotes a lock and key and translates into ‘I choose’.) We’ve known that certain lectins are ‘A like’ (have a preference for type A) but don’t actually clump type A cells. This is due to subtle differences in the structural specificity of their choice in the sugars they react with. For example, sugars can be the same with regard to their chemical structure, but differ in the spacial structure (ie in one sugar a hydrogen might ‘bend’ to the left, but in another might go to the right.) Same molecular structure; different shape.
These differences in lectin specificity are extraordinarily discreet. Let’s do something with this knowledge.
Readers of my books know that for type A I advocate a diet comprised of many plant based foods. These include:
- Mushrooms (the supermarket ‘Silver Dollar’ type)
- Soy beans, tofu, tempeh, miso
- Fava and Great Northern Beans
It’s no coincidence that these foods all contain ‘A-like lectins,’ agglutinins that can act as pseudo anti-A antibodies. Also, as I wrote in a prior post, an entirely different class of lectins, known as as the ‘mannose-monocot class’ lectins have also been shown to block ACE2, the tethering dock for novel coronavirus. This class, which contains most of the Allium species (garlic, onion, shallots, leeks) also provide some pseudo-antibody support for type A, but can also be used by other blood types as well. The aforementioned lima beans would not be workable because they actually do clump type A cells, and in this case we want a near miss; a case of slightly mistaken identity.
Even type O can hot-rod their anti-A defenses, to hedge their defense a bit.
I were type O, I’d go into the closet and try to find that chondroitin sulphate I bought for my friend’s bum knee last year that didn’t work. chondroitin sulphate is actually polymerized GalNac which is the type A epitope (antigen). Stomach acid hydrolysis should yield free GalNac, which theoretically should induce an increase in anti-A antibodies. Sort of like using your gut to trick your immune system into thinking it received the wrong blood type in a transfusion, but the dose does make the poison I guess. The type O tips might even pimp up the antibodies for type B as well. Type AB should follow the tips for type A.
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