Research shows curcumin at therapeutic levels prevents cartilage erosion and inflammation.

Paul Clayton, Paul Clayton

October 14, 2019

3 Min Read
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Arthritis is shorthand for a group of around 120 diseases that affect the joints, muscles and ligaments, creating chronic inflammation and making movement painful and difficult. Globally, these affect an estimated 1.7 billion people, and among these, osteoarthritis (OA), rheumatoid arthritis (RA) and fibromyalgia are the most common, according to the World Health Organization (WHO).

Well-documented problems with pharmaceutical anti-inflammatories have created an interest in natural products, and a number of these have shown considerable promise. The omega-3s and the polyphenols in curcumin are well known, and palmitoylethanolamide (PEA) and prebiotic dietary fibers are also generating interesting data. It is logical to consider combinations of these ingredients, given their broad therapeutic indices and different mechanisms of action.

Until recently, curcumin’s diverse pharmacology has failed to transfer to clinical results due to its poor bioavailability.1 Several curcumin branded ingredients look to address bioavailability concerns. For instance, a dosage of 750 mg of HydroCurc curcumin (from Gencor) containing 85% curcuminoids produced peak plasma levels of 800 ng/ml, or roughly 2 uM.2 This is within the therapeutic range,3 where the curcuminoids exert multiple anti-inflammatory effects.

At these tissue levels, curcuminoids down-regulate the genes that code for matrix metallopeptidases (MMPs), inhibit those same enzymes and up-regulate the synthesis of tissue inhibitors of metalloproteinases (TIMPs),4,5, resulting in the prevention of cartilage attrition.6 A parallel inhibition of tumor necrosis factor (TNF)-alpha and activity of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB) reduces levels of pro-inflammatory cytokines,7 and the suppression of interleukin (IL)-1 beta signaling in particular chondrocytes through the down-regulation of mitogen-activated protein kinase (MAPK), activator protein 1 (AP-1) and NF- kappaB pathways9,8 provide further anti-inflammatory activity. The additional ability of curcuminoids to reduce the osteoclastogenic potential of peripheral blood mononuclear cells (PBMCs) of RA patients, shown by the inhibition of expression of receptor activator of nuclear factor kappaB (RANK), c-Fos and nuclear factor of activated T cells (NFATc1),9 provides yet more evidence of this spice’s ability to protect both articular and peri-articular tissues.

Learn more about curcumin and other ingredients that benefit joint health in the complete version of this article in INSIDER’s Joint health digital magazine.

Paul Clayton, Ph.D., chief scientific advisor, Gencor, is a fellow of the Institute of Food, Brain and Behaviour in Oxford and a visiting professor at the University of Pecs in Hungary. He is a former president of the Forum on Food & Health at the Royal Society of Medicine in London and is currently a fellow of both the Royal Society of Medicine and the Royal Society of Arts.

References

1. Ghosh S, Banerjee S, Sil P. “The beneficial role of curcumin on inflammation, diabetes and neurodegenerative disease: A recent update.” Food Chem Toxicol. 2015 Sep;83:111-24.

2. Briskey D, Rao A. “Curcumin Absorption – results of a parallel and cross-over randomized double-blind pharmacokinetic study.” Eur J Nutr. 2018 Jul 4. DOI: 10.1007/s00394-018-1766-2.

3. Henrotin Y, Priem F, Mobasheri A. “Curcumin: a new paradigm and therapeutic opportunity for the treatment of osteoarthritis.” SpringerPress 2013; 2: 56.

4. Tavakoli F et al. “Effects of nano-encapsulated curcumin-chrysin on telomerase, MMPs and TIMPs gene expression in mouse B16F10 melanoma tumour model.” Artif Cells Nanomed Biotechnol. 2018 Apr 1:1-12.

5. Guru S et al. “Comparative evaluation of inhibitory effect of curcumin and doxycycline on matrix metalloproteinase-9 activity in chronic periodontitis.” Indian J Dent Res. 2017 Sep-Oct;28(5):560-565.

6. Lay E et al. “Short- and long-term exposure of articular cartilage to curcumin or quercetin inhibits aggrecan loss.” J Nutr Biochem. 2012 Feb;23(2):106-12.

7. Kumar A et al. “Curcumin (Diferuloylmethane) inhibition of tumor necrosis factor (TNF)-mediated adhesion of monocytes to endothelial cells by suppression of cell surface expression of adhesion molecules and of nuclear factor-κB activation.” Biochem Pharmacol. 1998;55:775–783.

8. Kapil K. “Curcumin: A yellow magical spice of kitchen for treatment of rheumatoid arthritis.” Int Res J Pharm. 2011;2:29–31.

9. Shang W et al. “Curcumin inhibits osteoclastogenic potential in PBMCs from rheumatoid arthritis patients via the suppression of MAPK/RANK/c-Fos/NFATc1 signaling pathways.” Mol Med Rep. 2016;14:3620–3626.

 

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