Curcumin is a yellow colouring agent found in the spice turmeric. It is curcumin that is responsible for the colour of curry. In Asia, extracts of turmeric have been used for centuries to treat inflammatory conditions such as arthritis. In the 1990s, researchers found that curcumin had anti-HIV activity in lab experiments with cells. As well, curcumin is supposed to have antioxidant properties and may impair the growth of lymphoma.
A closer examination of the data associated with curcumin suggests that, although this extract may have anti-HIV activity, its prolonged use in large doses (far greater than those found in curry recipes!) may not be appropriate in people with HIV/AIDS for a number of reasons.
First, curcumin appears to suppress the chemical messengers needed by the immune system (cytokines) to fight HIV and many of the infections seen in AIDS. At the same time, this plant extract appears to stimulate production of cytokines that further weaken the immune system.
Second, curcumin can block the growth of B-cells and, more important, T-cells. In people with HIV/AIDS, CD4+ and CD8+ cells appear to die faster than normal. Compounds that therefore impair the growth of T-cells - and possibly cause them to die prematurely - may accelerate HIV's destruction of the immune system.
Third, curcumin has historically been used to suppress inflammatory conditions such as arthritis. Drugs such as corticosteroids and low-dose cyclosporin can also produce similar benefits. However, prolonged use of corticosteroids can weaken the immune system's ability to fight infections. Indeed, in some experiments, curcumin's anti-inflammatory activity has been compared to that of the immune-suppressing drug cyclosporin. Clinical trials of cyclosporin in people with HIV/AIDS have not produced beneficial results.
Fourth, curcumin has antioxidant activity. This feature may make it attractive to people with HIV/AIDS because of their need for an increased intake of antioxidants. It appears, however, that curcumin should not be the antioxidant of first choice. The reason for this is that the body has specific biochemical needs for certain antioxidants such as vitamins C and E. As well, the body can make its own antioxidant enzymes using the amino acid cysteine and the minerals selenium, zinc, copper and manganese. Finally, some people may choose to take supplements of alpha-lipoic acid, an expensive antioxidant. Fulfilling the basic nutritional needs with antioxidants and the substances to make them should take priority over a compound for which there is no daily requirement.
In this issue of TreatmentUpdate we examine the impact of curcumin on the following:
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2. Imami N, Antonopoulos C, Hardy GAD, et al. Assessment of Type 1 and Type 2 cytokines in HIV Type-1-infected individuals: impact of Highly Active Antiretroviral Therapy. AIDS Research and Human Retroviruses 1999;15(17):1499-1508.
3. Dockrell DH, Badley AD, Algeciras-Schimnich A, et al. Activation-induced CD4+ T cell death in HIV-positive individuals correlates with Fas susceptibility, CD4+ T cell count, and HIV plasma viral copy number. AIDS Research and Human Retroviruses 1999;15(17):1509-1518.
4. Badley AD, Parato K, Cameron WD, et al. Dynamic correlation of apoptosis and immune activation during treatment of HIV infection. Cell Death and Differentiation 1999;6:420-243.
5. Pietrella D, Monari C, Retini C, et al. HIV type 1 envelope glycoprotein gp120 induces development of a T helper type 2 response to Cryptococcus neoformans. AIDS 1999;13(16):2197-2207.
6. Shankar P, Xu Z and Lieberman J. Viral-specific cytotoxic T lymphocytes lyse Human Immunodeficiency Virus-infected primary T lymphocytes by the granule excytosis pathway. Blood 1999;94(9):3084-3093.
7. Kaufman RJ. Double-stranded RNA-activated protein kinase mediates virus-induced apoptosis: a new role for an old actor. Proceedings of the National Academy of Sciences USA 1999;96(21):11693-11695.
8. Han S-S, Chung S-T, Robertson DA, et al. Curcumin causes the growth arrest and apoptosis of B cell lymphoma by downregularion of egr-1, C-myc, Bcl-X L , NF-kB, and p53. Clinical Immunology 1999;93(2):152-161.
9. Jobin C, Bradham CA, Russo MP, et al. Curcumin blocks cytokine-mediated NF-kB activation proinflammatory gene expression by inhibiting inhibitory factor I-kB kinase activity. Journal of Immunology 1999;163:3474-3483.
10. Gupta B and Ghosh B. Curcuma longa inhibits TNF- -induced expression of adhesion molecules on human umbilical vein endothelial cells. International Journal of Immunopharmacology 1999;21:745-757.
11. DeKruyff RH, Fang Y and Umetsu DT. Cortiocosteroids enhance the capacity of macrophages to induce Th2 cytokine synthesis in CD4+ lymphocytes by inhibiting IL-12 production. Journal of Immunology 1998;160(5):2231-2237.
12. Lane BR, Markovitz DM, Woodford NL, et al. TNF- inhibits HIV-1 replication in peripherial blood monocytes and alveolar macrophages by inducing the production of RANTES and decreasing C-C chemokine receptor 5 (CCR5) expression. Journal of Immunology 1999;163:3653-3661.
13. Haskó G and Szabó C. IL-12 as a therapeutic target for pharmacologic modulation in immune-mediated and inflammatory diseases: regulation of T helper 1/T helper 2 responses. British Journal of Pharmacology 1999;127:1295-1304.
14. Griffith OW. Biologic and pharmacologic regulation of mammalian glutathione synthesis. Free Radical Biology and Medicine 1999;27(9/10):922-35.
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Disclaimer: The editors have taken all such care as they consider reasonable in preparing this database, but they cannot be held responsible for any inaccuracies or mis-statements of fact contained herein. Inclusion in this database of any information on any treatment, therapy, or clinical trial in no way represents an endorsement of that treatment, therapy, or trial by ÆGiS or any of its sponsors. This data should always be used in conjunction with professional medical advice.