Aspirin in Presence of Endotoxins In the Blood is Pro-Inflammatory
The information in the title of this post is one of the most important things you should know if you are interested in health, medicine or maybe you just have psoriasis.
Aspirin is an over-the-counter drug popular all over the world. Less known fact is that aspirin (acetylsalicylic acid) causes kidney failure and renal necrosis in rats.
Aspirin treatment even at mini-dosages like 75mg per day causes significant changes in uric acid and creatinine clearance. So keep in mind the fact that Aspirin has really bad effects on kidneys!
Aspirin is sometimes a pro-inflammatory drug
The easiest explanation of the information below is that if you took Aspirin for:
- headache caused by inflammation due to poor posture = Aspirin would be probably anti-inflammatory
- psoriasis caused by endotoxins from small intestine due to low bile flow = Aspirin would be probably pro-inflammatory
Sadly, Aspirin is often used as treatment for rheumatoid arthritis which is strongly suspected to be caused by endotoxins just like psoriasis.[6, 7]
Aspirin may act as an anti-inflammatory drug in some ways but when it comes to lipopolysaccharide (endotoxin) induced inflammation then aspirin acts more as pro-inflammatory substance.
In study from 2000 the researchers proved that aspirin “induced a concentration dependent increase (2.5-5-fold at 5 mM aspirin) in LPS-induced appearance of TNF-alpha and fibrinopeptide A (FPA) in plasma”.
Addition of exogenous PGE2 before incubation nearly abrogated the effect of aspirin on TNF-alpha, substantiating the role of PGE2 as a regulator of TNF-alpha synthesis, whereas the effect on FPA was small. Thus, in the presence of LPS in this whole blood model, aspirin apparently had a pro-inflammatory rather than an anti-inflammatory effect.
The proof of prostaglandin E2 (PGE2) as controller of inflammation is the fact that gel with this prostaglandin applied to the psoriatic lesions improved the skin even though complete clearing of the lesions was not achieved.
However, for the truth to be told the other study performed on murine laboratory animals says that aspirin is anti-inflammatory as it is generally accepted.
We now report that therapeutic doses of aspirin suppress lipopolysaccharide-inducible NF-kappaB binding to an NF-kappaB binding site in the TNF-alpha promoter, lipopolysaccharide-induced TNF-alpha mRNA accumulation, and protein secretion.
It is really a very complex issue and many factors may significantly affect the study results.
For now I think that Turmeric (active ingredient Curcumin) is generally one of the best ways how to target the inflammation. Turmeric especially when combined with Black Pepper also thins the blood via its anti-inflammatory properties.
You will find more about the effects of Turmeric and Curcumin in my future posts.
1) D’Agati V. Does aspirin cause acute or chronic renal failure in experimental animals and in humans? Am J Kidney Dis. 1996 Jul;28(1 Suppl 1):S24-9.
2) Caspi D, Lubart E, Graff E, Habot B, Yaron M, Segal R. The effect of mini-dose aspirin on renal function and uric acid handling in elderly patients. Arthritis Rheum. 2000 Jan;43(1):103-8.
3) Osnes LT, Haug KB, Joø GB, Westvik AB, Ovstebø R, Kierulf P. Aspirin potentiates LPS-induced fibrin formation (FPA) and TNF-alpha-synthesis in whole blood. Thromb Haemost. 2000 Jun;83(6):868-73.
4) Int J Dermatol. 1986 May;25(4):266-8. Prostaglandin E2 gel improvement of psoriatic lesions. Remy W, Sigl I, Leipold B.
5) Shackelford RE, Alford PB, Xue Y, Thai SF, Adams DO, Pizzo S. Aspirin inhibits tumor necrosis factoralpha gene expression in murine tissue macrophages. Mol Pharmacol. 1997 Sep;52(3):421-9.
6) Lorenz W, Buhrmann C, Mobasheri A, Lueders C, Shakibaei M. Bacterial lipopolysaccharides form procollagen-endotoxin complexes that trigger cartilage inflammation and degeneration: implications for the development of rheumatoid arthritis. Arthritis Res Ther. 2013;15(5):R111.
7) Gyurcsovics K, Bertók L. Pathophysiology of psoriasis: coping endotoxins with bile acid therapy. Pathophysiology. 2003 Dec;10(1):57-61.