New meta-analysis [1] below.
Seems to me that there must be more meta-analyses than primary studies by now. PubMed returns 389 hits for <aspirin[title] "meta-analysis">. Perhaps someone should do a meta-analysis of meta-analyses & put the subject to bed for ever.
Aspirin is odd for two reasons. As a pain-killer it is a non-specific COX inhibitor, but unlike other COX inhibitors, it also inhibits platelet aggregation. It is used at therapeutic doses for pain management, but also chronically, at low doses as a prophylactic against clotting.
Clotting involves a number of stages. An early stage is the aggregation of platelets. A later stage involves the accretion of fibrin. Both are attractive targets in preventing/treating inappropriate clotting.
Aspirin inhibits platelet aggregation at low doses. Those who use low doses are unlikely to be addressing unsuspected inflammation. Chronic usage of regular/high dose aspirin might result in inflammation control as well as platelet control. Two quite different populations, which complicates the interpretation of study results.
But I'm inclined to view the major benefit in PCa as being clot reduction. This should reduce metastasis, & therefore PCa-specific mortality. From the new study:
The inclusion of 8 of the PCa studies "led to acceptable homogeneity ... and an overall HR {hazard ratio} = 0.89" i.e. a 11% drop in PCa mortality.
"Two studies of breast cancer, two of prostate and one of both cancers together with colon, give evidence of a reduction in {metastatic} spread by aspirin. A combined estimate gives a relative risk for aspirin of 0.77."
"Data in three reports of prostate cancer suggest that the effect of aspirin may be greater in advanced disease. Thus Daugherty et al describe an effect of aspirin in ‘advanced’ prostate cancer (HR 0.37 ...) which is greater, than in localized disease (HR 0.86 ...) Similarly Jacobs, Newton et al report an HR of 0.60 ... in ‘high-risk’ patients, contrasted with the effect of aspirin in the total cohort (HR 0.98 ...) in the total series of patients. Neither of these differences are however significant, nor is a result reported by Jacobs, Chun et al who selected ‘high risk’ patients and reported a reduction by aspirin HR 0.44 ..."
"Several authors state that an effect of aspirin {becomes} apparent only after 3–5 years of therapy. Goh et al state that they found evidence of benefit only after 5 years, Stock et al who reported no benefit to prostate cancer overall (HR 1.03 ...) states that after five years of aspirin taking there was benefit (HR 0.54 ...)"
For inflammation control & normalization of coagulation factors, NF-kB is the proper target. Plant polyphenols are known to inhibit NF-kB.
For coagulation control, I use nattokinase & have never tried aspirin. As a COX-1 inhibitor there are stomach & kidney issues in some. But low-dose aspirin beats nattokinase on price. I would monitor D-dimer & add nattokinase to aspirin if necessary.
-Patrick
Effects of Curcumin and Lactoferrin to Inhibit the Growth and Migration of Prostatic Cancer Cells
Stimulants for ADT fatigue?
