I recently wrote about hypercoagulation, which is the phenomenon of increased activation of blood clotting and decreased activation of clot dissolution, and how it’s connected to aging. I showed how iron is involved in hypercoagulation. There’s likely another player in hypercoagulation, also connected to iron, and that’s bacteria. Do bacteria cause hypercoagulation and aging?
Consider that there’s lots of evidence both that healthy people have bacteria in sites normally considered sterile, such as the blood, and that numbers of bacteria are increased in unhealthy people, for instance those with cardiovascular disease. People with cardiovascular disease have as much as 40 to 70 times more bacteria in their blood than healthy people, and bacteria, fungi, and viruses have been found in the brains of Alzheimer’s patients.
Gram negative bacteria, which are the most numerous and important gut bacteria, have an endotoxin, called lipopolysaccharide (LPS), very toxic stuff.
So, we have the sequence:
Aging -> increased iron -> bacterial growth supported by iron -> shedding of LPS by bacteria -> hypercoagulation.
If hypercoagulation is characteristic of aging, and caused by bacteria, are bacteria the cause of aging?
In theory, bacterial invasion could account for many of the manifestations of aging.
Bacteria require iron to grow and reproduce. Most of them produce molecules called siderophores that grab iron from their milieu and sequester it for use by the bacteria.
The bacterial genus Pseudomonas, an ubiquitous organism that causes infections, uses salicylate as a siderophore.
Salicylate is the metabolic end-product of aspirin and is responsible for its pain-killing anti-inflammatory action. It goes like this: aspirin -> salicylate -> iron chelation. In Pseudomonas, the sequence goes like this: salicylate -> iron chelation -> use of iron for growth.
Humans and other mammals use the protein called transferrin to transport iron within the body. (Ferritin is used for safe iron storage.)
Transferrin and the iron it transports are at the center of an evolutionary arms race between bacteria and humans.
The frontline of host-pathogen coevolution
Pathogens have to subvert a host’s innate defenses to avoid being killed. Barber and Elde now show that this principle extends to nutrient-transporting proteins, such as transferrin, which binds iron. Without iron, invading pathogens cannot replicate, but iron is sequestered in transferrin, which stops pathogens using it. So pathogens have evolved a succession of transporters that can hijack transferrin’s iron. Over time, the primate transferrin binding surface has coevolved to wrestle iron back from the grip of pathogens.
By following the logic of everything I’ve written above, aspirin prevents blood clots which leads to less heart disease, and it prevents the growth of clot-causing, LPS-shedding bacteria by preventing them from getting iron.
As heart disease is mainly a disease of old people, once again we see how iron and bacteria promote aging.
Scientists avidly search for the causes of aging.
They’re overlooking iron and the bacteria that it enables.
Most aging experts insist that aging has nothing to do with the passage of time.
Yet humans have a mechanism for acquiring iron, but no mechanism to get rid of it. Since evolution doesn’t care about what happens to us after reproduction, iron accumulates into older age.
Iron feeds bacterial growth, which leads to hypercoagulation, and perhaps many of the other manifestations of aging.
Iron alone also causes increased fibrin clots, and slower fibrin degradation.
Iron and bacteria are a double whammy causing disease and aging.