3 ms·

I wonder if this may be related to Aspirin's effect on inflammation. Long term inflammation is supposed to be "bad thing". Taking low doses of Aspirin for long

by bd 16y ago

I wonder if this may be related to Aspirin's effect on inflammation. Long term inflammation is supposed to be "bad thing". Taking low doses of Aspirin for long time may help with silent inflammations throughout the body. This should be testable by comparing effects of Aspirin with other anti-inflammatory drugs (taken in similar regime).

Alex3917 16y ago
That's what I was thinking when I read this. I'd bet you would get even more benefit from taking a low dose of hemp oil, because not only is that a stronger (and less toxic) anti-inflammatory, but it's also anti-angiogenic. In any event though total morbidity is much more interesting than cancer risk.
pygy_ 16y ago
I don't think so, low dose aspirin has little effect on inflammation. Aspirin (ASA)is special WRT NSAID, in that it inhibits the Cyclo-oxygenase (COX) enzymes irreversibly. COX are a family of enzymes that transform arachidonic acid to various inflamatory mediators called the prostaoids (comprising prostaglandins, prostacyclin and thromboxanes). There are two subtypes, present in different tissues, but since ASA inhibits both kinds. Platelets contain COX and uses it produce Thromoxane A2, a potent vasoconstrictor and platelet activator. Since platelets don't have a nucleus, the effect inhibitory effect is permanent in them. New platelets have to be produced in order to restore a normal clotting activity. Since the platelet have an half life of more than a week, the effect is long lasting. Other cells can synthesize COX as needed. Low dose aspirin has thus little effect on them. You need a much higher dose to get a clinically noticeable anti-inflamatory response. In blood vessels, activated platelets use COX to synthesize Thromoxane A2 (TXA). TXA further promotes vasoconstriction, platelet activation and aggregation, leading to the formation of a blood clot [1]. On the other hand, endothelial cells (the inner layer of blood vessels) use COX to synthesize a prostaglandin (PGI2), which antagonizes TXA (vasodilatation, platelet inhibition). ASA disrupts the TXA2/PGI2 equilibrium in favor of PGI2, inhibiting platelet activation. Other NSAID also have an anti-aggregation activity, but it is far more short lived, and requires anti-inflammatory doses to do so. That said, I can't prove that a chronic, subclinical anti-inflammatory effect isn't at play here too. EDIT: A Google scholar search confirms that TXA2 is involved in carcinogenesis [2-3]. -- [1] Such a clot is fragile. It is then stabilized by the coagulation process: the irreversible binding of fibrinogen into a fibrine mesh. [2] http://scholar.google.be/scholar?hl=nl&q=pgi2+neoplasm&btnG=Zoeken&lr=&as_ylo=&as_vis=1 http://scholar.google.be/scholar?hl=nl&q=pgi2+neoplasm&#... [3] http://scholar.google.be/scholar?hl=nl&q=txa2+neoplasm&btnG=Zoeken&lr=&as_ylo=&as_vis=1 http://scholar.google.be/scholar?hl=nl&q=txa2+neoplasm&#...

by bd 16y ago

Alex3917 16y ago

That's what I was thinking when I read this. I'd bet you would get even more benefit from taking a low dose of hemp oil, because not only is that a stronger (and less toxic) anti-inflammatory, but it's also anti-angiogenic. In any event though total morbidity is much more interesting than cancer risk.

pygy_ 16y ago

I don't think so, low dose aspirin has little effect on inflammation. Aspirin (ASA)is special WRT NSAID, in that it inhibits the Cyclo-oxygenase (COX) enzymes irreversibly. COX are a family of enzymes that transform arachidonic acid to various inflamatory mediators called the prostaoids (comprising prostaglandins, prostacyclin and thromboxanes). There are two subtypes, present in different tissues, but since ASA inhibits both kinds. Platelets contain COX and uses it produce Thromoxane A2, a potent vasoconstrictor and platelet activator. Since platelets don't have a nucleus, the effect inhibitory effect is permanent in them. New platelets have to be produced in order to restore a normal clotting activity. Since the platelet have an half life of more than a week, the effect is long lasting. Other cells can synthesize COX as needed. Low dose aspirin has thus little effect on them. You need a much higher dose to get a clinically noticeable anti-inflamatory response. In blood vessels, activated platelets use COX to synthesize Thromoxane A2 (TXA). TXA further promotes vasoconstriction, platelet activation and aggregation, leading to the formation of a blood clot [1]. On the other hand, endothelial cells (the inner layer of blood vessels) use COX to synthesize a prostaglandin (PGI2), which antagonizes TXA (vasodilatation, platelet inhibition). ASA disrupts the TXA2/PGI2 equilibrium in favor of PGI2, inhibiting platelet activation. Other NSAID also have an anti-aggregation activity, but it is far more short lived, and requires anti-inflammatory doses to do so. That said, I can't prove that a chronic, subclinical anti-inflammatory effect isn't at play here too. EDIT: A Google scholar search confirms that TXA2 is involved in carcinogenesis [2-3]. -- [1] Such a clot is fragile. It is then stabilized by the coagulation process: the irreversible binding of fibrinogen into a fibrine mesh. [2] http://scholar.google.be/scholar?hl=nl&q=pgi2+neoplasm&btnG=Zoeken&lr=&as_ylo=&as_vis=1 http://scholar.google.be/scholar?hl=nl&q=pgi2+neoplasm&#... [3] http://scholar.google.be/scholar?hl=nl&q=txa2+neoplasm&btnG=Zoeken&lr=&as_ylo=&as_vis=1 http://scholar.google.be/scholar?hl=nl&q=txa2+neoplasm&#...