Curcumin

Research & Evidence

Curcumin (diferuloylmethane) is the principal curcuminoid responsible for turmeric’s orange pigment and for much of the herb’s medicinal activity. The turmeric monograph in this database reports several well-studied actions:

• Anti-inflammatory — anti-inflammatory action is curcumin’s longest-standing reported use ^{3Reference 3Ammon HP · 1991Pharmacology of Curcuma longa}; it acts as a dual inhibitor of arachidonic acid metabolism ^{2Reference 2Bone K · 2013Principles and Practice of Phytotherapy} and inhibits TNF-induced NF-κB activation ^{4Reference 4Zambre AP et al. · 2006Novel curcumin analogs targeting TNF-induced NF-κB activation and proliferation in human leukemic KBM-5 cellsView study →}. This NF-κB activity has been a particular focus of synthetic curcumin analogue work targeting inflammatory and proliferative signalling ^{4Reference 4Zambre AP et al. · 2006Novel curcumin analogs targeting TNF-induced NF-κB activation and proliferation in human leukemic KBM-5 cellsView study →}.
• Antioxidant — curcumin reduces lipid peroxidation and primes the Nrf2/ARE pathway ^{2Reference 2Bone K · 2013Principles and Practice of Phytotherapy}, and its antioxidant activity (along with that of related enones) has been characterised directly ^{5Reference 5Weber WM et al. · 2005Anti-oxidant activities of curcumin and related enonesView study →}.
• Anticancer — curcumin has been found effective against leukemia ^{4Reference 4Zambre AP et al. · 2006Novel curcumin analogs targeting TNF-induced NF-κB activation and proliferation in human leukemic KBM-5 cellsView study →}, prostate cancer ^{6Reference 6Lin L et al. · 2006Antitumor agents}, and a range of inflammatory cascades ^{2,5Reference 2Bone K · 2013Principles and Practice of PhytotherapyReference 5Weber WM et al. · 2005Anti-oxidant activities of curcumin and related enonesView study →}. It is reported to influence transcription factors, cytokines, growth factors, kinases, and other enzymes, and has been used extensively in cancer treatment and prevention research ^{2Reference 2Bone K · 2013Principles and Practice of Phytotherapy}. Synthetic glucosyl-curcuminoids derived from Curcuma longa are being explored to improve on these activities ^{1,6Reference 1Saladini M et al. · 2009New synthetic glucosyl-curcuminoids, and their (1)H and (13)C NMR characterization, from Curcuma longa LView study →Reference 6Lin L et al. · 2006Antitumor agents}.

The central practical limitation is bioavailability: curcumin is poorly absorbed and rapidly conjugated in the liver before excretion in the faeces, which sharply limits the amount available systemically ^{7Reference 7Ireson C et al. · 2001AnimalCharacterization of metabolites of the chemopreventive agent curcumin in human and rat hepatocytes and in the rat in vivo, and evaluation of their ability to inhibit phorbol ester-induced prostaglandin E2 production}. Cooking the rhizome for long periods improves gut absorption somewhat (though it remains well under 50%), and combining turmeric with black pepper (piperine) has shown marked improvements in absorption ^{2Reference 2Bone K · 2013Principles and Practice of Phytotherapy}.

Monoamine oxidase (MAO) inhibition

Curcumin is frequently described as a MAO-B inhibitor, and animal studies link it to antidepressant-type effects that may run partly through monoamine oxidase. The commonly-quoted nanomolar potency figure for curcumin, however, comes from a source with internally inconsistent, garbled numbers and should not be trusted — so while a mild MAO-B effect is plausible, there is no reliable potency value to attach to it here. See the natural MAO inhibitors guide for why that figure is flagged.

Toxicity & Safety

Curcumin is considered very safe, including at high doses taken over long periods. In the source monograph, extensive toxicity testing of turmeric and its extracts consistently found low toxicity in both high-dose and long-term studies; the LD50 of an orally administered petroleum-ether extract was 12.2 g/kg in rats ^{2Reference 2Bone K · 2013Principles and Practice of Phytotherapy}. The main caveat is not toxicity but the compound’s poor systemic availability, which means large amounts of the parent herb are needed for systemic effects.

References

1. Saladini M, Lazzari S, Pignedoli F, Rosa R, Spagnolo F, & Ferrari E. (2009). New synthetic glucosyl-curcuminoids, and their (1)H and (13)C NMR characterization, from Curcuma longa L. Plant Foods For Human Nutrition (Dordrecht, Netherlands), 64(3), 224–9. doi:10.1007/s11130-009-0122-3
2. Bone K, Mills S. (2013). Principles and Practice of Phytotherapy. Elsevier Health, China. (Pg. 900–922).
3. Ammon HP, Wahl MA. (1991). Pharmacology of Curcuma longa. Planta Med, 57, 1–7.
4. Zambre AP, Kulkarni VM, Padhye S, Sandur SK, Aggarwal BB. (2006). Novel curcumin analogs targeting TNF-induced NF-κB activation and proliferation in human leukemic KBM-5 cells. Bioorg Med Chem, 14, 7196–7204. doi:10.1016/j.bmc.2006.06.056
5. Weber WM, Hunsaker LA, Abcouwer SF, Decka LM, Van der Jagbt DL. (2005). Anti-oxidant activities of curcumin and related enones. Bioorg Med Chem, 13, 3811–3820. doi:10.1016/j.bmc.2005.03.035
6. Lin L, Shi Q, Nyarko AK, Bastow KF, Wu CC, Su CY, Shih CCY, Lee KH. (2006). Antitumor agents. 250. Design and synthesis of new curcumin analogues as potential anti-prostate cancer agents. J Med Chem, 49, 3963–3972.
7. Ireson C, Orr S, Jones DJ, et al. (2001). Characterization of metabolites of the chemopreventive agent curcumin in human and rat hepatocytes and in the rat in vivo, and evaluation of their ability to inhibit phorbol ester-induced prostaglandin E2 production. Cancer Res, 61, 1058–1064.