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Food, Health, and Eco-news
Tea Blocks Path to Rheumatic Joint Damage

Cell study points to strong therapeutic potential of polyphenol abundant in green tea

by Craig Weatherby

Rheumatoid arthritis (RA) is an uncommon disease, affecting less than one percent of Americans. But it can be a painful, debilitating experience for its victimsmostly middle aged womenand leave crippled joints in its wake.

For reasons that remain mysterious, the antibodies and immune cells of people with rheumatoid arthritis and related diseases attack elements of connective tissues as though they were foreign invaders or harboring disease microbes.

RA drugs work by hindering the immune system's misguided attack on body tissues, but until recently, they were very blunt instruments, and not highly effective at preventing the serious joint damage that RA often wreaks.

Treatment got substantially better in the late 1990's, with approval of the first so-called biological response modifier (BMR) drugs. Examples include etanercept (Enbrel), Anakinra (Kineret), and adalimumab (Humira).

In comparison with older RA drugs, the BMR drugs' methods of action are more focused, and they do a better job of deterring joint damage and associated suffering.

Some of the new BMR-type drugs block pro-inflammatory immune-system proteins such as tumor necrosis factor and interleukin-1. They prevent these proteins from activating cell receptors that trigger rogue, joint-damaging inflammatory responses by immune system cells (including release of free radicals).

Other BMR drugs deplete or prevent pro-inflammatory activation of the B and T cells of the immune system.

Unfortunately, BMRs increase the risk of infection and weaken the response to them.

Thus, a safe alternative therapeutic agent that exerts complementary, additive effects might allow doctors to reduce BMR drug dosesor avoid prescribing them altogether.

It now appears that teaor concentrated tea extractsmight prove just such an alternative/complementary ally against RA. And because other auto-immune disorders, such as lupus and scleroderma, share RA's inflammatory mechanisms, tea's beneficial potential may extend more broadly.

Tea study in cells show promise

It's no secret that tea contains potent polyphenol antioxidants with anti-inflammatory effects at the cellular level. These compounds exert much of their anti-inflammatory impact via their effects on cellular genetic switches called transcription factors.

The new findings concern the most studied and seemingly most potent and beneficial polyphenol antioxidant in tea is called epigallocatechin-3-gallate or EGCG.

(One of the pro-inflammatory genetic transcription factors blocked by EGCG, called NF-kappaB, will be familiar to readers of the highly informative anti-aging-nutrition books by Nicholas Perricone, M.D.)

The new results, reported by researchers from the University of Michigan Health System indicate that EGCG in tea may inhibit production of the same pro-inflammatory cytokine proteins blocked by Enbrel, Humira, and other of the new biological-response-modifier (BMR) class of RA drugs.

Lead author Salah-uddin Ahmed told attendees at the Experimental Biology 2007 conference in Washington, D.C. that EGCG from tea may also suppress production of damaging inflammation byproducts in the connective tissue of people with rheumatoid arthritis.

As Dr. Ahmed told the press, “Our research is a very promising step in the search for therapies for the joint destruction experienced by people who have rheumatoid arthritis” (Ahmed S et al 2007).

The findings of their new study confirms and expands on the results of a similar one published last year by the same team (Ahmed S et al 2006).

The results add to the already ample evidence linking tea to health benefits ranging from weight control and enhanced heart, tooth, and gum health to reduced risk of Alzheimer's and certain cancers.

Green tea has three to 10 times more polyphenols than black tea, primarily the catechin-class flavanols EGCG, epigallocatechin, epicatechin gallate, and epicatechin.

When the leaves of green tea are fermented naturally to create black tea, portions of these potent catechin-class polyphenols get converted to related compounds called theaflavins, which have their own benefits but are probably not as strongly anti-inflammatory.

The researchers wanted to test the protective effects of EGCG on joint cells called fibroblasts, donated by patients with rheumatoid arthritis, which they exposed to interleukin-1 beta (IL-1beta): a pro-inflammatory cytokine believed to trigger much of the joint-damaging inflammation in RA patients.

When they added IL-1beta to cultured cells without also adding EGCG, the expected cascade of events occurred, resulting in production of the bone-destructive molecules interleukin-6 (IL-6) and cyclooxygenase-2 (COX-2).

In contrast, no IL-6 or COX-2 were created in joint-cell cultures that also contained EGCG.

The Michigan team is now conducting lab tests to measure the impact of EGCG on expression of inflammatory genes, via its effects on the aforementioned transcription factors.

The will also conduct animal studies to see whether EGCG might exert therapeutic or preventive effects against rheumatoid arthritis. Positive results should then prompt researchers to test EGCG from green tea in RA patients.


  • Ahmed S, Pakozdi A, Koch A. Oral presentation 101.7 - Epigallocatechin-3-gallate inhibits IL-1ß-induced IL-6 production and cyclooxygenase-2 expression in rheumatoid arthritis synovial fibroblasts in vitro. Session Title - Characterization of proteomic and metabolomic responses to dietary factors and supplements. Experimental Biology 2007, Washington, D.C. Sunday, April 29, 2007 (
  • Ahmed S, Anuntiyo J, Malemud CJ, Haqqi TM. Biological basis for the use of botanicals in osteoarthritis and rheumatoid arthritis: a review. Evid Based Complement Alternat Med. 2005 Sep;2(3):301-8.
  • Kim SJ, Jeong HJ, Lee KM, Myung NY, An NH, Mo Yang W, Kyu Park S, Lee HJ, Hong SH, Kim HM, Um JY. Epigallocatechin-3-gallate suppresses NF-kappaB activation and phosphorylation of p38 MAPK and JNK in human astrocytoma U373MG cells. J Nutr Biochem. 2007 Apr 17; [Epub ahead of print]
  • Ahmed S, Pakozdi A, Koch AE. Regulation of interleukin-1beta-induced chemokine production and matrix metalloproteinase 2 activation by epigallocatechin-3-gallate in rheumatoid arthritis synovial fibroblasts. Arthritis Rheum. 2006 Aug;54(8):2393-401.
  • Andriamanalijaona R, Kypriotou M, Bauge C, Renard E, Legendre F, Raoudi M, Boumediene K, Gatto H, Monginoux P, Pujol JP. Comparative effects of 2 antioxidants, selenomethionine and epigallocatechin-gallate, on catabolic and anabolic gene expression of articular chondrocytes. J Rheumatol. 2005 Oct;32(10):1958-67. Erratum in: J Rheumatol. 2005 Dec;32(12):2502.