A Golden Wonder: Turmeric Compounds Trigger Apoptosis in Lymphoma, Lower LDL Cholesterol

Turmeric powder. Photo: Sivanagk; Agency: Dreamstime.com.

PHILADELPHIA—Long valued for its tangy culinary appeal, turmeric is proving to be a cornucopia of medicinal substances with potential for treatment of some of the most common and deadly disorders.

Curcuma longa, the powdered rhizome of which gives curry its golden zing, contains a number of anti-inflammatory compounds, including some that regulate the cyclooxygenase enzyme pathways, suggesting that turmeric could be a valuable botanical remedy for inflammatory conditions including arthritis.

Studies at Columbia University’s Center for Holistic Urology have shown that Zyflamend, a multi-herb anti-inflammatory product of which turmeric is a cornerstone, can inhibit the growth of human prostate cancer cell lines (visit www.holisticprimarycare.net and read, “Plant Medicines Offer Multiple Mechanisms Against Prostate Cancer,” Spring 2006). Turmeric and compounds derived from it have recently become a hot topic among researchers interested in botanical therapies for various forms of cancer.

Induces Apoptosis

New data presented at the annual meeting of the Society for Investigative Dermatology show that turmeric rhizomes contain compounds that can induce apoptosis in T-cells and Sezary cells from patients with cutaneous T-cell lymphoma (CTCL). According to Chunlei Zhang, MD, of the MD Anderson Cancer Center, Houston, the new findings are the first to suggest curcumin, one of the major biochemical constituents of turmeric, may have a role in controlling lymphoma.

“Defective T-cell apoptosis and constitutive activation of Stat3 and NF-κB are implicated in the pathogenesis of CTCL, and pharmacologic modulation of apoptosis and related signaling pathways may provide a novel therapeutic approach for CTCL,” said Dr. Zhang. Curcumin appears to affect these signaling pathways.

The MD Anderson researchers looked at the effect of curcumin at concentrations ranging from 0–20 μM, on CTCL cell lines and peripheral blood lymphocytes taken from three Sezary syndrome patients who had circulating malignant T-cell levels in the range of 44% to 96%. They incubated the CTCL cells with the curcumin for 24, 48 or 72 hours.

They found that the curcumin triggered apoptosis in a time and concentration-dependent fashion in all of the cell lines. Curcumin-treated peripheral blood monocytes also showed the same pattern of apoptosis.

Considerable further research will be needed to determine exactly how curcumin triggers the observed malignant cell die-off, but the current experiment has pointed out certain key clues. Curcumin seems to down-regulate expression of Stat3 and phospho-Stat3 proteins, as well as genes that encode anti-apoptotic signals. In other words, it inhibits cellular signals that under ordinary circumstances prevent malignant cells from going into apoptosis. It also suppresses the binding of NF-κB, a strong inflammatory signal, in two of the three peripheral blood samples.

Dr. Zhang said the current data rightfully raise hope that curcumin could play a role in treatment of CTCL, Sezary syndrome, and other hematologic malignancies. But at this point, it is too soon to draw a firm conclusion based on in vitro work like this. Dr. Zhang and colleagues hope to use this promising data as a springboard to develop a clinical trial with the objective of assessing the impact of curcumin in people with various forms of lymphoma.

Cardiovascular Risk Reduction

The zippy cancer-fighting spice appears to be currying favor (sorry, we couldn’t resist) with cardiologists as well as cancer researchers. Several previous studies have indicated that turmeric, or compounds extracted from it, can reduce LDL and improve lipid profiles.

Researchers at the Martin Luther University, Halle-Wittenberg, Germany, believe they have discovered mechanisms by which turmeric exerts its cholesterol-lowering effect. Norbert Nass, MD, and his team looked at the impact of curcumin at doses ranging from 2–50 micromoles on gene expression in human hepatic cells.

They found that once the dose exceeds 10 micromoles, curcumin exposure induces an up to seven-fold increase in expression of LDL-receptor mRNA, which, from a functional viewpoint, means a marked increase in hepatic uptake of LDL. The greater the hepatic uptake, the lower the circulating levels of LDL will be, thus reducing potential for atherosclerotic buildup (Peschel D, Koerting R, Nass N. J Nutr Biochem. 2007; 18 (2): 113–119).

Dr. Nass also observed increases in expression of two other important genes: one coding for what is known as the liver X receptor (LXR), which binds oxidized cholesterol fragments; and another coding for the retinoic acid receptor (RXR) which in turn activates other genes involved in cholesterol metabolism. Interestingly, the upregulation of the LXR and RXR genes occurs at curcumin concentrations in the 2–10 micromolar range. He noted that these levels are easily obtained by oral consumption of supplemental curcumin. The investigators saw no changes suggestive of hepatic toxicity associated with curcumin exposure.

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