Sometimes, the right combination is better than stuff with far more side effects. People never understand why I like coffee that much. But then, maybe some of you all also want to improve pain control at less side effects and less cost.
What really seems to matter here is the correct ratio more than dosing high to begin with. That means that for each cup of coffee (100-200 mg caffeine), about 4-5 times that amount of ibuprofen (that is, Ibuprofen 400 or 800) appears to work best according to that study.
Read this from http://www.ncbi.nlm.nih.gov/pubmed/16872598:
Eur J Pharmacol. 2006 Aug 21;544(1-3):31-8. Epub 2006 Jun 27.
Enhancement of antinociception by co-administration of ibuprofen and caffeine in arthritic rats.
Departamento de Sistemas Biológicos, UAM-Xochimilco, México D.F., México.
School of Physiology and Pharmacology, University of NSW, 2052, Sydney, Australia.
There is much uncertainty about the mechanism of action of paracetamol (acetaminophen). It is commonly stated that, unlike the non-steroidal anti-inflammatory drugs (NSAIDs), it is a weak inhibitor of the synthesis of prostaglandins. This conclusion is made largely from studies in which the synthesis of prostaglandins was measured in homogenized tissues. However, in several cellular systems, paracetamol is an inhibitor of the synthesis of prostaglandins with IC(50) values ranging from approximately 4 microM to 200 microM. Paracetamol is not bound significantly to plasma proteins and therefore the concentrations in plasma can be equated directly with those used in in vitro experiments. After oral doses of 1 g, the peak plasma concentrations of paracetamol are approximately 100 microM and the plasma concentrations are therefore in the range where marked inhibition of the synthesis of prostaglandins should occur in some cells. Paracetamol is metabolized by the peroxidase component of prostaglandin H synthase but the relationship of this to inhibition of the cyclooxygenase or peroxidase activities of the enzyme is unclear. Paracetamol is also metabolized by several other peroxidases, including myeloperoxidase, the enzyme in neutrophils which is responsible for the production of hypochlorous acid (HOCl). The metabolism of paracetamol by myeloperoxidase leads to the decreased total production of HOC1 by both intact neutrophils and isolated myeloperoxidase, even though the initial rate of production of HOC1 is increased. The IC(50) value, derived from inhibition of the total production of HOC1 by isolated myeloperoxidase, is 81 microM. Several NSAIDs inhibit functions of neutrophils in media containing low concentrations of protein but their effects, in contrast to that of paracetamol, are generally produced only at concentrations greater than those of the unbound drug in plasma during treatment with the NSAIDs. However, neutrophils isolated during treatment with NSAIDs, such as piroxicam, ibuprofen and indomethacin show decreased function. Paracetamol has little or no anti-inflammatory activity by itself but may potentiate the clinical activity of NSAIDs in the treatment of rheumatoid arthritis.
Disclaimer: Generally it is probably best to discuss all matters related to health with your doctor. Always ask your doctor and pharmacist. Never exceed limits, requirements or prescriptions. Always follow the orders. What works for me may not work for you or even get you killed.