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Q: Why do the different blood groups have different gut flora? Can you explain this for all blood groups?
Krishna: Sure!
In humans, the gut microbiota has the highest numbers and species of bacteria compared to other areas of the body. The complex communities of microbes that constitute the human microbiome are influenced by host and environmental factors.
Image source: iStock
Gut microbiota, gut microbiome, or gut flora are the microorganisms, including bacteria, archaea, fungi, and viruses, that live in the digestive tracts of animals.
They need food to survive. Right?
The bacteria in our gut not only extract energy from the food we eat, but also from our blood sugars.
People with different blood groups have different metabolic sugars (called glycans) attached to the surfaces of their red blood cells. These surface sugars determine whether your blood type is A, B, AB, or O.
For many microbes, success in the host begins with the ability to adhere, and host glycans are ideal receptors. The diversity of blood glycan structures likely arose as a means to inhibit the binding of pathogens to host cells, but these molecules also present a scaffold for commensals.
The secretion of these glycans also evolved as a strategy to bind up pathogens before they encounter infectable cells . These evolutionary skirmishes have resulted in differential disease risk based on host blood type.
Different blood groups have different gut flora (the bacteria living in your intestines) because your blood type genes create specific sugars in your body. These sugars line your digestive tract and act as an all-you-can-eat buffet. Certain bacteria are really good at eating specific blood sugars, so they thrive in that blood type.
It is like a restaurant menu. The body puts out different sugars (menus) depending on the blood type. Bacteria that like that specific menu will move in and grow. This causes different bacterial communities in each blood type:
Type A: The body secretes a specific sugar called the A-antigen. Bacteria like Ruminococcus gnavus have special tools to break down and eat this sugar, giving them an advantage to grow.
Type B: The body secretes the B-antigen in the gut mucus. This creates a unique environment where the overall clustering and amount of certain bacterial families differ from non-B types.
Type AB: These individuals produce both A and B antigens. Because they have both food sources available, their gut often hosts a blended mix of the bacteria typically found in both Type A and Type B people.
Type O: These individuals do not produce A or B antigens. Instead, they produce an "H antigen." Without A or B sugars to feed on, their gut often harbours a higher abundance of generalist bacteria like Bacteroides, which are very good at digesting a wide variety of plant fibres and starches.
Our genetic makeup itself determines which bacteria are in our gut, this seems to help explain variations we see in how people respond to nutrition and therapy.
Enterotoxigenic Escherichia coli expresses an adhesion molecule that specifically targets the A blood glycan which results in children with type A or AB blood being disproportionately affected by the diarrheal disease caused by this pathogen. Helicobacter pylori binds to fucosylated blood antigens on the gastric epithelium and while H. pylori can be found in healthy individuals of all blood types, it can better access this receptor in type O individuals, putting them at greater risk for the overgrowth and pathogenesis of H. pylori . The commensal Lactobacilli have diversified and target A, B, and H antigens in a strain specific manner; with L. gasseri OLL2827 targeting the H-antigen, L. gasseri OLL2755, OLL2877 the B-antigen, and L. brevis OLL2772 the A antigen. An indirect benefit of our commensal bacteria adhering to these receptors is that they prevent pathogens from getting a foothold via adhesion exclusion. (1)
The treatment should also be based on these blood types.
What is good for people with one blood group may not be good for people with other blood groups.
Footnotes:
1. https://pmc.ncbi.nlm.nih.gov/articles/PMC10104170/
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