Gunsmith AMEN for your quote in your sig
. Low dose aspirin is like knife to a gun fight. The elevated RBC (red blood cell) is what really thickens your blood. If you are on EQ this is even more so amplified. AAS increases Hematocrit, which is the proportion level of blood occupied by cells (rbc, wbc, platelets). So thinning the blood doesn't make it any less dense as the aspirin does not impact size or stickiness of cells. Giving blood is the only thing to put you at less risk.
Here is something I found that explains how aspirin helps to prevent blood clots. It says it better than I could.
"How does aspirin work?
Aspirin helps to prevent blood clots forming. A blood clot may form in an artery (blood vessel) if a lot of platelets stick onto some atheroma. A clot in an artery may stop blood flowing to the tissues 'downstream'. If a blood clot forms in an artery in the heart or brain, it may cause a heart attack or stroke.
Atheroma patches are like fatty lumps that develop in the inside lining of some arteries. This mainly occurs in older people and is sometimes called 'hardening of the arteries'.
Platelets are tiny particles in the blood that help the blood to clot when a blood vessel is cut. Platelets sometimes stick onto atheroma inside an artery.
Low dose aspirin reduces the 'stickiness' of platelets. This helps to stop platelets sticking to a patch of atheroma and forming a blood clot..
.What is the dose of aspirin to prevent blood clots?
The usual dose to prevent blood clots is 75 mg each day. This is a lot less than the dose for pain relief. Taking more than the recommended dose does not make aspirin work any better to prevent blood clots, but increases the risk of side-effects developing. Therefore, stick to the dose recommended by your doctor which is usually 75 mg daily.
If you take low-dose aspirin to prevent blood clots and you need to take painkillers (for example, for headaches) it is best to take paracetamol rather than a higher dose of aspirin.."
Here is more off antoher site, and this is more detailed"
"Thrombin formation
Thrombin (activated Factor II [IIa]), a serine protease, converts fibrinogen into insoluble strands of fibrin. Fibrin, a protein, crosslinks with Factor XIII enzyme (fibrin stabilizing Factor FXIII) and combines with platelets to form a clot.
Studies of microvascular injury models have demonstrated that aspirin at a daily dose of 30 mg administered for one week decreased thrombin formation in healthy patients. Aspirin at higher doses (75 mg and 300 mg) decreased concentrations of thrombin markers similarly, as did a single dose of 500 mg following a period of aspirin therapy. This thrombin-lowering effect was found in healthy individuals and patients with increased risk for coronary artery disease.
A seven-day course of low-dose (75 mg) aspirin was associated with slower prothrombin consumption (by 29%), thrombin formation (by 27.2%) and prothrombinase formation (by 29%) at the site of microvascular injury."
" Polymorphisms and fibrin
When aspirin inhibits thrombin generation, it subsequently inhibits the creation of fibrin on arterial walls, thus interrupting hemostasis. Upon introduction into fibrin, aspirin may interfere with FXIII activation and function because fibrinogen and fibrin enhance FXIII activation approximately 100-fold. Genetic polymorphisms influenced by aspirin may consequently alter the stability of the fibrin network.
The Val34Leu polymorphism in the A chain of FXIII is in close proximity to the thrombin cleavage site at Arg37-Glyl38. It has been suggested that this mutation may influence FXIII activation due to its relative position. The researchers showed that a seven-day administration of 75 mg aspirin per day inhibits FXIII activation to a greater degree in LEU34–positive healthy patients compared with patients with the Val34Val genotype.
Mann and colleagues cited a study of fibrin clot properties in healthy individuals with three allelic variants of the FXIII Val34Leu mutation before and after they received 300 mg aspirin. After four hours, patients with the LEU34 allele exhibited significantly greater clot permeability, although permeability increased in association with the Val34Leu polymorphism to some degree in all patients.
The researchers suggested that aspirin alters fibrin cross-linking to a greater degree in individuals with the LEU34 allele compared with individuals with the Val34Val genotype. Therefore, a pharmacogenetic association might exist between aspirin’s antithrombotic effects and the presence of the FXIII LEU34 allele, according to the researchers.
A common polymorphism of the B3-integrin gene, PIA1A2, may modulate the effect of aspirin-related alterations in thrombin formation. Studies have found impaired platelet aggregation in patients with the PI*A2 allele who were treated with aspirin. "
"Aspirin and cholesterol
The researchers noted a positive correlation between total cholesterol or low-density lipoprotein cholesterol and the amount of thrombin generated after aspirin administration. Studies showed that 75 mg aspirin daily reduced thrombin formation only in patients whose total cholesterol level was below 200 mg/dL. In patients with total cholesterol levels between 200 mg/dL and 250 mg/dL, low-dose aspirin did not appear to impair thrombin formation. However, 300 mg aspirin daily has shown to inhibit thrombin generation in patients with a total cholesterol less than 240 mg/dL and LDL cholesterol less than 155 mg/dL. "
That last part is something that i just learned about aspirin. So keeping your total cholesterol low is very influential in how well aspirin lowers thrombin levels. Thrombin is what I have trouble with indirectly becuase of my trait-prothrombin disorder. Luckily my total cholesterol last time was about 105 and its been nice and low even when I had my heart attack. I was also taking an adult aspirin per day when i had the heart attack. Back then I was still thinking "more is better". I now know that just a baby aspirin is actually better for you.
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