The issue of blood clotting and what exactly triggers it (even in healthy people) remains a “mystery” for medicine. There are many factors that have been discovered in past studies, and many of them are inconvenient truths. For example, clotting events in young people without coronary disease (CVD) has been blamed on everything from lack of exercise to recreational drug use. However, the fact that it is much more prevalent in young women, suggesting an endocrine cause, is a topic that pharma companies do not ever want to seriously investigate as it would directly implicate their multi-billion hormonal contraceptive market, consisting mostly of synthetic estrogens and synthetic progestins (most of which are estrogenic and with pro-cortisol effects). Be that as it may, it is clear that estrogen is not the only cause given that women taking high-dose aromatase inhibitors (AI) for conditions such as breast cancer only reduce their blood clotting risk by 30%-40%. So, that means a major non-hormonal clotting factor is present in both males and females and likely explains the majority of the clotting events. Oh, and there is also the “minor” issue of endotoxin boosting the production of serotonin (5-HT) and nitric oxide (NO), with both of the latter being also known clotting promoters.
The study below demonstrated that endotoxin/LPS from the gut is perhaps that major factor. Even minor increases in endotoxin/LPS in the bloodstream led to activation of all four (4) plasma clottign factors within minutes of endotoxin exposure and the effect persisted for hours. According to the study, the higher clotting driven by endotoxin may explain the high mortality in sepsis, which is the most common cause of death in hospitalized people. It may also explain why current remedies for sepsis, consisting mostly of glucocorticodi therapy, is largely ineffective resulting in a mortality rate of up to 40% in such patients. Glucocorticoids not only do not address the endotoxin angle, some of them further promote clotting. Putting sepsis aside, which is usually a concern mostly for critically ill people already in the hospital, the study also has great relevance for chronic conditions such as heart diasease (CVD), which also ultimately manifests in a deadly clotting event such as a heart attack or ischemic stroke. Given that most people have at least partially compromised gut barrier and significant increases in blood endotoxin after each meal, the study suggests that our risk of an ischemic event is higher after each meal, which has already been confirmed by multiple human studies. The good news is that there are some easy remedies. Rather than taking aspirin (which is still a good method for general health maintenance), which acts downstream of the endotoxin/LPS cascade, it would likely be more prudent to limit the amount of endotoxin/LPS produced and entering the blood. That can be achieved by eating easily digestible food, and especially by avoiding the so-called “resistant” starches as the letter make it to the gut relatively intact and boost endotoxin production. The carrot salad or some charcoal (just 2-3 times weekly, but not daily) can absorb a great deal of the generated endotoxin even if the diet is suboptimal and promotes endotoxin synthesis. Substances such as niacinamide and vitamin E have been shown by multiple studies to help restore the gut barrier, which would limit endotoxin absorption into the bloodstream. Finally, pregnane steroids (and especially bioidentical progesterone) have been shown to directly bind endotoxin in the bloodstream and render it inactive. Finally, increasing the metabolic rate has been shown to reduce or even eliminate bacteria presence in the small intestine (a condition now known as SIBO) by increasing the production of stomach acid. Elimination of SIBO should help keep the upper/middle portion of the GI tract mostly sterile and thus allow more food to be absorbed into the blood instead of serving as food for our endotoxin-producing microbiome.
https://doi.org/10.1016/j.jbc.2024.108110
“…A team of US scientists has uncovered how a molecule found on certain bacteria may drive blood clotting in sepsis — a life-threatening condition that causes about eight million deaths per year. The findings may pave the way for enhancing treatments for critically ill patients. They found that lipopolysaccharide, or LPS — a molecule found on the surface of certain bacteria like E. coli — can directly activate proteins in the blood that trigger clotting.”
“…This process can both block blood flow and damage vital organs in a chain reaction where proteins in the blood work together to form clots. The researchers found a specific type of LPS, called O26:B6, that is particularly good at setting off this reaction, making it more likely to cause clotting problems. The research, published in the Journal of Biological Chemistry, is based on a study conducted in nonhuman primates. The team found that when bacteria containing LPS entered the bloodstream, it quickly activated the clotting system.”
