Curcumin, Diabetes and Heart Failure
Jacob Schor ND, FABNO
May 11, 2008
Regular readers will think I’ve become obsessed with curcumin. It isn’t just me. The scientific community is also enchanted with this chemical extracted from turmeric root. As of this writing, a PubMed search lists 376 papers related to curcumin published in this last year alone. Without the time limit, the search turns up 2,317 papers related to curcumin. A search limited to ‘curcumin and cancer,’ turns up 806 papers.
A paper set for publication this coming July in the International Journal of Cancer is typical of many others on cancer. The title, “Curcumin induces cell-arrest and apoptosis in association with the inhibition of constitutively active NF-kappaB and STAT3 pathways in Hodgkin's lymphoma cells”
Curcumin given to cancer cells causes cell-arrest, that is, it paralyzes the cells and prevents further division, and it persuades the cancer cells to commit suicide through apoptosis, but this isn’t what this paper is about. Cell cycle arrest and apoptosis due to curcumin are old news. This paper is taking it three steps down the line attempting to explain the chemical mechanisms.
But this isn’t what spurred me to write. Instead, I chanced upon a paper suggesting that curcumin might be useful in treating type 2 diabetes, the first I’ve seen on this topic. It was published a month ago. In the April 10 issue of Endocrinology, Dr Drew Tortoriello of Columbia University in New York, reported on his experiments feeding curcumin to obese mice. The mice were put on high fat diets, got obese and developed diabetes. Adding curcumin to their food reversed their diabetes as, “determined by glucose and insulin tolerance testing and hemoglobin A1c percentages.” Equally interesting was that the, “Curcumin treatment also significantly reduced macrophage infiltration of white adipose tissue, increased adipose tissue adiponectin production, and decreased hepatic nuclear NF-kappaB activity, hepatomegaly, and markers of hepatic inflammation.”
In other, simpler words, the curcumin calmed down the hot, swollen and inflamed livers associated with diabetes in these mice.
The bottom line for Tortoriello and colleagues,
“We therefore conclude that orally ingested curcumin reverses many of the inflammatory and metabolic derangements associated with obesity and improves glycemic control in mouse models of type 2 diabetes. This or related compounds warrant further investigation as novel adjunctive therapies for type 2 diabetes in man.”
Curcumin is not commonly suggested for treating diabetes, at least it has not been up to now. It may be used in the future.
Full text of the diabetes article is available for free at:
There’s another paper around here somewhere on curcumin and heart disease that is also worth mentioning.
In the March issue of the Journal of Clinical Investigation, Moriomoto and his colleagues in Kyoto, Japan report on experiments they performed on rats. They induced high blood pressure in one group of rats by overly salting their food. In another group of rats, they performed surgery to mimic a heart attack. Both of these experimental interventions should have put the rats on a direct path to heart failure. Yet according to the authors,
“In both models, curcumin prevented deterioration of systolic function and heart failure-induced increases in both myocardial wall thickness and diameter. From these results, we conclude that inhibition of p300 HAT activity by the nontoxic dietary compound curcumin may provide a novel therapeutic strategy for heart failure in humans.”
Or to in English, feeding the rats curcumin prevented their hearts from failing.
People aren’t rats of course and until this is tested in humans, (or a drug company figures out how to patent an herb,) we don’t know if curcumin will prevent heart attacks in people. Given the human trials for cancer and Alzheimer’s Disease that show curcumin is safe to use, what is it going to hurt to take some of this while waiting for a heart transplant while dying of heart failure?
Full text of the heart failure article is free at: http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=18292809
Past newsletters on curcumin:
Alzheimer’s Disease: http://denvernaturopathic.com/curcuminandAlzheimers.htm
Int J Cancer. 2008 Jul 1;123(1):56-65.
Curcumin induces cell-arrest and apoptosis in association with the inhibition of constitutively active NF-kappaB and STAT3 pathways in Hodgkin's lymphoma cells.
Mackenzie GG, Queisser N, Wolfson ML, Fraga CG, Adamo AM, Oteiza PI.
Department of Nutrition, University of California, Davis, CA 95616, USA.
Although treatment of Hodgkin's lymphoma (HL) with a multi-drug approach has been very successful, its toxicity becomes evident after several years as secondary malignancies and cardiovascular disease. Therefore, the current goal in HL treatment is to find new therapies that specifically target the deregulated signaling cascades, such as NF-kappaB and STAT3, which cause Hodgkin and Reed-Sternberg (H-RS) cell proliferation and resistance of apoptosis. Based on the above information, we investigated the capacity of curcumin to inhibit NF-kappaB and STAT3 in H-RS cells, characterizing the functional consequences. Curcumin is incorporated into H-RS cells and acts inhibiting both NF-kappaB and STAT3 activation, leading to a decreased expression of proteins involved in cell proliferation and apoptosis, e.g. Bcl-2, Bcl-xL, cFLIP, XIAP, c-IAP1, survivin, c-myc and cyclin D1. Interestingly, curcumin caused cell cycle arrest in G2-M and a significant reduction (80-97%) in H-RS cell viability. Furthermore, curcumin triggered cell death by apoptosis, as evidenced by the activation of caspase-3 and caspase-9, changes in nuclear morphology and phosphatidylserine translocation. The above findings provide a mechanistic rationale for the potential use of curcumin as a therapeutic agent for patients with HL. (c) 2008 Wiley-Liss, Inc.
Endocrinology. 2008 Apr 10 [Epub ahead of print]Click here to read Links
Dietary Curcumin Significantly Improves Obesity-Associated Inflammation and Diabetes in Mouse Models of Diabesity.
Weisberg SP, Leibel R, Tortoriello DV.
Diabetes and Endocrinology Research Center, Columbia University, New York, New York; Sher Institute for Reproductive Medicine, New York, New York.
Obesity is a major risk factor for the development of type 2 diabetes, and both conditions are now recognized to possess significant inflammatory components underlying their pathophysiologies. We tested the hypothesis that the plant polyphenolic compound curcumin, which is known to exert potent anti-inflammatory and anti-oxidant effects, would ameliorate diabetes and inflammation in murine models of insulin-resistant obesity. We found that dietary curcumin admixture ameliorated diabetes in high-fat diet induced obese (DIO) and leptin-deficient ob/ob male C57BL/6J mice as determined by glucose and insulin tolerance testing and hemoglobin A1c percentages. Curcumin treatment also significantly reduced macrophage infiltration of white adipose tissue, increased adipose tissue adiponectin production, and decreased hepatic nuclear NF-kappaB activity, hepatomegaly, and markers of hepatic inflammation. We therefore conclude that orally ingested curcumin reverses many of the inflammatory and metabolic derangements associated with obesity and improves glycemic control in mouse models of type 2 diabetes. This or related compounds warrant further investigation as novel adjunctive therapies for type 2 diabetes in man.
J Clin Invest. 2008 Mar;118(3):868-78.Click here to read Click here to read Links
J Clin Invest. 2008 Mar;118(3):850-2.
The dietary compound curcumin inhibits p300 histone acetyltransferase activity and prevents heart failure in rats.
Morimoto T, Sunagawa Y, Kawamura T, Takaya T, Wada H, Nagasawa A, Komeda M, Fujita M, Shimatsu A, Kita T, Hasegawa K.
Division of Translational Research, Kyoto Medical Center, National Hospital Organization, Kyoto, Japan.
Hemodynamic overload in the heart can trigger maladaptive hypertrophy of cardiomyocytes. A key signaling event in this process is nuclear acetylation by histone deacetylases and p300, an intrinsic histone acetyltransferase (HAT). It has been previously shown that curcumin, a polyphenol responsible for the yellow color of the spice turmeric, possesses HAT inhibitory activity with specificity for the p300/CREB-binding protein. We found that curcumin inhibited the hypertrophy-induced acetylation and DNA-binding abilities of GATA4, a hypertrophy-responsive transcription factor, in rat cardiomyocytes. Curcumin also disrupted the p300/GATA4 complex and repressed agonist- and p300-induced hypertrophic responses in these cells. Both the acetylated form of GATA4 and the relative levels of the p300/GATA4 complex markedly increased in rat hypertensive hearts in vivo. The effects of curcumin were examined in vivo in 2 different heart failure models: hypertensive heart disease in salt-sensitive Dahl rats and surgically induced myocardial infarction in rats. In both models, curcumin prevented deterioration of systolic function and heart failure-induced increases in both myocardial wall thickness and diameter. From these results, we conclude that inhibition of p300 HAT activity by the nontoxic dietary compound curcumin may provide a novel therapeutic strategy for heart failure in humans.