Dr. Weeks’ Comment: Vitamin B3 is very beneficial for arthritis and inflammation.
Synthesis and evaluation of the antiinflammatory activity of N-[2-(3,5-di-tert-butyl-4-hydroxyphenyl)-4-oxo-thiazolidin-3-yl]-nicotinamide.
Kalia R(1), Rao CM, Kutty NG.
A new molecule incorporating nicotinoyl moiety, thiazolidin-4-one ring and 3,5-di-tert-butyl-4-hydroxyphenyl group (a potent antioxidant moiety) was synthesized and evaluated for anti-inflammatory activity in acute as well as chronic phase models of inflammation. The compound exhibited significant anti-inflammatory activity in three experimental models of inflammation, comparable to the positive control drug, ibuprofen (CAS 15687-27-1). It is suggested that besides the hypolipidemic and anti-oxidant potential of the molecule, its anti-inflammatory action could possibly act as an additional mechanism of its hypothesized anti-atherosclerotic activity.
Niacinamide therapy for osteoarthritis–does it inhibit nitric oxide synthase induction by interleukin 1 in chondrocytes?
Med Hypotheses. 1999 Oct;53(4):350-60.
McCarty MF(1), Russell AL.
Fifty years ago, Kaufman reported that high-dose niacinamide was beneficial in osteoarthritis (OA) and rheumatoid arthritis. A recent double-blind study confirms the efficacy of niacinamide in OA. It may be feasible to interpret this finding in the context of evidence that synovium-generated interleukin-1 (IL-1), by inducing nitric oxide (NO) synthase and thereby inhibiting chondrocyte synthesis of aggrecan and type II collagen, is crucial to the pathogenesis of OA.
Niacinamide and other inhibitors of ADP-ribosylation have been shown to suppress cytokine-mediated induction of NO synthase in a number of types of cells; it is therefore reasonable to speculate that niacinamide will have a comparable effect in IL-1-exposed chondrocytes, blunting the anti-anabolic impact of IL-1. The chondroprotective antibiotic doxycycline may have a similar mechanism of action.
Other nutrients reported to be useful in OA may likewise intervene in the activity or synthesis of IL-1. Supplemental glucosamine can be expected to stimulate synovial synthesis of hyaluronic acid; hyaluronic acid suppresses the anti-catabolic effect of IL-1 in chondrocyte cell cultures, and has documented
therapeutic efficacy when injected intra-articularly. S-adenosylmethionine (SAM), another proven therapy for OA, upregulates the proteoglycan synthesis of chondrocytes, perhaps because it functions physiologically as a signal of sulfur availability. IL-1 is likely to decrease SAM levels in chondrocytes; supplemental SAM may compensate for this deficit. Adequate selenium nutrition may down-regulate cytokine signaling, and ample intakes of fish oil can be expected to decrease synovial IL-1 production; these nutrients should receive further evaluation in OA. These considerations suggest that non-toxic nutritional regimens, by intervening at multiple points in the signal transduction pathways that promote the synthesis and mediate the activity of IL-1, may provide a substantially superior alternative to NSAIDs (merely palliative and often dangerously toxic) in the treatment and perhaps prevention of OA.
Natural treatments for osteoarthritis.
Altern Med Rev. 1999 Oct;4(5):330-41.
Osteoarthritis (OA) is the most common form of joint disease. Although OA was previously thought to be a progressive, degenerative disorder, it is now known that spontaneous arrest or reversal of the disease can occur. Conventional medications are often effective for symptom relief, but they can also cause significant side effects and do not slow the progression of the disease. Several natural substances have been shown to be at least as effective as non-steroidal anti-inflammatory drugs at relieving the symptoms of OA, and preliminary evidence suggests some of these compounds may exert a favorable influence on the course of the disease.