11 replies to this topic

[sUper GeNius]

http://carcin.oxford...stract/bgp082v1

[tunt01]

man, that really sucks. i love my jarrow curcumin pills. i smoked 2 years in college and live in the city (practically makes me a smoker).

i guess i am gonna have to cut back a little bit at the very least. any idea how big their dosing was?

[ajnast4r]

the topic is misleading... what you probably meant was:

lung tumor promotion in mice by unknown amounts of curcumin when co-administered with doxycycline.

[AgeVivo]

I too add it to my meals, since the list of positive effects of curcumin (=curcuma; found in mustard and curry, or bought in powder) is large, with very few warnings (think of curry in India). Still, clinical trials would be appreciated.

http://chinese-schoo...min-cancer.html : so far the specific warnings/contrindications were some types of chemotherapy (cyclophosphamide), bile duct obstruction, gallstones, and GI disorders (including stomach ulcers and hyperacidity disorders). I'm not able to appreciate whether the very specific 'tumor promotion' described in the article you mention is relevant?

[tunt01]

i tried to look up a bit about K-Ras or Ki-Ras? tumors. it seems like one of the more rare genetic mutations associated with tumor progression, though more common in current and ex-smokers. i'm not much of a cancer aficionado.

if i'm taking sulforaphane and curcumin, hopefully they will cancel one another out !

[agwoodliffe]

Well, there's some evidence to suggest that, at the very least, piperine may counteract this risk (provided you stick to the low dose, of course):

Mol Cell Biochem. 2005 Mar;271(1-2):101-6.
Chemopreventive effect of piperine on mitochondrial TCA cycle and phase-I and glutathione-metabolizing enzymes in benzo(a)pyrene induced lung carcinogenesis in Swiss albino mice.
Selvendiran K, Thirunavukkarasu C, Singh JP, Padmavathi R, Sakthisekaran D.
Source
Department of Medical Biochemistry, Dr. ALM Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai 600 113, India. selvakphd@yahoo.com
Abstract
Piperine is a major component of black (Piper nigrum Linn) and long pepper (Piper longum Linn) used widely in various systems of traditional medicine. We have evaluated the effect of piperine on mitochondrial tricarboxylic acid cycle and phase I and glutathione-metabolizing enzymes in Benzo(a)pyrene induced experimental lung carcinogenesis in swiss albino mice. Lung cancer bearing mice showed a significant decrease in the activities of mitochondrial enzymes-isocitrate dehydrogenase (ICDH), -ketoglutarate dehydrogenase (KDH), succinate dehydrogenase (SDH), malate dehydrogenase (MDH) and significantly increased NADPH-Cytochorome reductase (NADPH-C reductase), cytochrome P450 (cyt-p450) and cytochrome b5(cyt-b5). The activities of glutathione-metabolizing enzymes glutathione peroxidase(GPx), glutathione reductase (GR) and glucose-6-phospho dehydrogenase(G6PDH) were significantly lowered in lung-cancer bearing mice when compared with control mice. Piperine supplementation to tumour-induced animals significantly lowered the phase-I enzymes (NADPH-C reductase, cyt-p450 and cyt-b5)) and there was a rise in glutathione-metabolizing enzymes (GPx, GR and G6PDH), which indicated an antitumour and anti-cancer effect. Comparison of normal control mice and mice administered piperine only as drug control showed no significant variations in enzyme activities. Piprine administration

Clin Exp Metastasis. 2002;19(8):703-8.
Effect of piperine on the inhibition of lung metastasis induced B16F-10 melanoma cells in mice.
Pradeep CR, Kuttan G.
Source
Amala Cancer Research Centre, Thrissur, Kerala, India.
Abstract
The effect of piperine on the inhibition of lung metastasis induced by B16F-10 melanoma cells was studied in C57BL/6 mice. Simultaneous administration of the compound with tumor induction produced a significant reduction (95.2%) in tumor nodule formation. Increased lung collagen hydroxyproline (22.37 microg/mg protein) in the metastasized lungs of the control animals compared to normal animals (0.95 microg/mg protein) was significantly reduced (2.59 microg/mg protein) in the piperine-treated animals. The high amount of uronic acid (355.83 microg/100 mg tissue) in the metastasized control animals was significantly reduced (65 microg/100 mg tissue) in the animals treated with piperine. Lung hexosamine content was also significantly reduced in the piperine-treated animals (0.98 mg/100 mg lyophilized tissue) compared to the untreated tumor-bearing animals (4.2 mg/100 mg lyophilized tissue). The elevated levels of serum sialic acid and serum gamma glutamyl transpeptidase activity in the untreated control animals was significantly reduced in the animals treated with piperine. The piperine-treated animals even survived the experiment (90 days). Histopathology of the lung tissue also correlated with the lifespan of the drug-treated animals. Our results demonstrate the antimetastatic activity of piperine, an alkaloid present in plants such as Piper nigrum and Piper longum.

PMID: 12553376 [PubMed - indexed for MEDLINE]

Biomed Pharmacother. 2004 May;58(4):264-7.
Chemopreventive effect of piperine on modulating lipid peroxidation and membrane bound enzymes in benzo(a)pyrene induced lung carcinogenesis.
Selvendiran K, Sakthisekaran D.
Source
Department of Medical Biochemistry, Dr. ALM Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai 600113, India.
Abstract
The current study was designed to evaluate the effects of oral supplementation of the piperine on lung tumour initiation by orally applied benzo(a)pyrene (B(a)p). To evaluate the effects of orally supplemented piperine on lung tumour initiation by B(a)p, its effects on ATPase enzymes were first evaluated. Lung cancer bearing mice showed an increase in erythrocyte membrane and tissues ATPase enzymes (Na(+)/K(+)-ATPases, Mg(2+)-ATPases and Ca(2+)-ATPases). Na(+) K-ATPase and Mg-ATPase enzyme activities were decreased and calcium ATPase increased (P < 0.05) in erythrocyte membrane and tissues of lung cancer bearing animals compared with control groups. The elevation of these enzyme activities in membrane and tissues were indicative of the persistent deteriorating effect of B(a)p in cancer bearing animals. These enzyme activities were reversed to near normal control values in animals treated with piperine (50 mg/kg body weight). It is apparent that the beneficial effect of piperine is primarily exerted on the during initiation phase and post-initiation stage of B(a)p induced lung carcinogenesis. Overall, these data indicative that piperine has chemopreventive effects when administered orally on lung cancer bearing animals.

PMID: 15183854 [PubMed - indexed for MEDLINE]

And of course, there is evidence to suggest that Curcumin does indeed INHIBIT lung-tumor cells:

Cancer Res. 2008 Sep 15;68(18):7428-38.
Curcumin inhibits lung cancer cell invasion and metastasis through the tumor suppressor HLJ1.
Chen HW, Lee JY, Huang JY, Wang CC, Chen WJ, Su SF, Huang CW, Ho CC, Chen JJ, Tsai MF, Yu SL, Yang PC.
Source
Department and Institute of Pharmacology, School of Medicine, National Yang-Ming University,Taipei, Taiwan.
Abstract
Curcumin (diferuloylmethane) is an active component of the spice turmeric and has a diversity of antitumor activities. In this study, we found that curcumin can inhibit cancer cell invasion and metastasis through activation of the tumor suppressor DnaJ-like heat shock protein 40 (HLJ1). Human lung adenocarcinoma cells (CL1-5) treated with curcumin (1-20 mumol/L) showed a concentration-dependent reduction in cell migration, invasion, and metastatic ability, and this was associated with increased HLJ1 expression. Knockdown of HLJ1 expression by siRNA was able to reverse the curcumin-induced anti-invasive and antimetastasis effects in vitro and in vivo. The HLJ1 promoter and enhancer in a luciferase reporter assay revealed that curcumin transcriptionally up-regulates HLJ1 expression through an activator protein (AP-1) site within the HLJ1 enhancer. JunD, one of the AP-1 components, was significantly up-regulated by curcumin (1-20 mumol/L) in a concentration- and time-dependent manner. Knockdown of JunD expression could partially reduce the curcumin-induced HLJ1 activation and diminish the anti-invasive effect of curcumin, indicating that JunD would seem to be involved in curcumin-induced HLJ1 expression. Curcumin was able to induce c-Jun NH(2)-kinase (JNK) phosphorylation, whereas the JNK inhibitor (SP-600125) could attenuate curcumin-induced JunD and HLJ1 expression. Activation of HLJ1 by curcumin further leads to up-regulation of E-cadherin and a suppression of cancer cell invasion. Our results show that curcumin induces HLJ1, through activation of the JNK/JunD pathway, and inhibits lung cancer cell invasion and metastasis by modulating E-cadherin expression. This is a novel mechanism and supports the application of curcumin in anti-cancer metastasis therapy.

PMID: 18794131 [PubMed - indexed for MEDLINE] Free full text

This is merely speculation, but I would assume that dosage is the key here. Lower doses tend to possess greater cancer-preventive effects, whereas higher doses seem to possess cancer-promoting effects.

[agwoodliffe]

Well, there's some evidence to suggest that, at the very least, piperine may counteract this risk (provided you stick to the low dose, of course):

Mol Cell Biochem. 2005 Mar;271(1-2):101-6.
Chemopreventive effect of piperine on mitochondrial TCA cycle and phase-I and glutathione-metabolizing enzymes in benzo(a)pyrene induced lung carcinogenesis in Swiss albino mice.
Selvendiran K, Thirunavukkarasu C, Singh JP, Padmavathi R, Sakthisekaran D.
Source
Department of Medical Biochemistry, Dr. ALM Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai 600 113, India. selvakphd@yahoo.com
Abstract
Piperine is a major component of black (Piper nigrum Linn) and long pepper (Piper longum Linn) used widely in various systems of traditional medicine. We have evaluated the effect of piperine on mitochondrial tricarboxylic acid cycle and phase I and glutathione-metabolizing enzymes in Benzo(a)pyrene induced experimental lung carcinogenesis in swiss albino mice. Lung cancer bearing mice showed a significant decrease in the activities of mitochondrial enzymes-isocitrate dehydrogenase (ICDH), -ketoglutarate dehydrogenase (KDH), succinate dehydrogenase (SDH), malate dehydrogenase (MDH) and significantly increased NADPH-Cytochorome reductase (NADPH-C reductase), cytochrome P450 (cyt-p450) and cytochrome b5(cyt-b5). The activities of glutathione-metabolizing enzymes glutathione peroxidase(GPx), glutathione reductase (GR) and glucose-6-phospho dehydrogenase(G6PDH) were significantly lowered in lung-cancer bearing mice when compared with control mice. Piperine supplementation to tumour-induced animals significantly lowered the phase-I enzymes (NADPH-C reductase, cyt-p450 and cyt-b5)) and there was a rise in glutathione-metabolizing enzymes (GPx, GR and G6PDH), which indicated an antitumour and anti-cancer effect. Comparison of normal control mice and mice administered piperine only as drug control showed no significant variations in enzyme activities. Piprine administration

Clin Exp Metastasis. 2002;19(8):703-8.
Effect of piperine on the inhibition of lung metastasis induced B16F-10 melanoma cells in mice.
Pradeep CR, Kuttan G.
Source
Amala Cancer Research Centre, Thrissur, Kerala, India.
Abstract
The effect of piperine on the inhibition of lung metastasis induced by B16F-10 melanoma cells was studied in C57BL/6 mice. Simultaneous administration of the compound with tumor induction produced a significant reduction (95.2%) in tumor nodule formation. Increased lung collagen hydroxyproline (22.37 microg/mg protein) in the metastasized lungs of the control animals compared to normal animals (0.95 microg/mg protein) was significantly reduced (2.59 microg/mg protein) in the piperine-treated animals. The high amount of uronic acid (355.83 microg/100 mg tissue) in the metastasized control animals was significantly reduced (65 microg/100 mg tissue) in the animals treated with piperine. Lung hexosamine content was also significantly reduced in the piperine-treated animals (0.98 mg/100 mg lyophilized tissue) compared to the untreated tumor-bearing animals (4.2 mg/100 mg lyophilized tissue). The elevated levels of serum sialic acid and serum gamma glutamyl transpeptidase activity in the untreated control animals was significantly reduced in the animals treated with piperine. The piperine-treated animals even survived the experiment (90 days). Histopathology of the lung tissue also correlated with the lifespan of the drug-treated animals. Our results demonstrate the antimetastatic activity of piperine, an alkaloid present in plants such as Piper nigrum and Piper longum.

PMID: 12553376 [PubMed - indexed for MEDLINE]

Biomed Pharmacother. 2004 May;58(4):264-7.
Chemopreventive effect of piperine on modulating lipid peroxidation and membrane bound enzymes in benzo(a)pyrene induced lung carcinogenesis.
Selvendiran K, Sakthisekaran D.
Source
Department of Medical Biochemistry, Dr. ALM Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai 600113, India.
Abstract
The current study was designed to evaluate the effects of oral supplementation of the piperine on lung tumour initiation by orally applied benzo(a)pyrene (B(a)p). To evaluate the effects of orally supplemented piperine on lung tumour initiation by B(a)p, its effects on ATPase enzymes were first evaluated. Lung cancer bearing mice showed an increase in erythrocyte membrane and tissues ATPase enzymes (Na(+)/K(+)-ATPases, Mg(2+)-ATPases and Ca(2+)-ATPases). Na(+) K-ATPase and Mg-ATPase enzyme activities were decreased and calcium ATPase increased (P < 0.05) in erythrocyte membrane and tissues of lung cancer bearing animals compared with control groups. The elevation of these enzyme activities in membrane and tissues were indicative of the persistent deteriorating effect of B(a)p in cancer bearing animals. These enzyme activities were reversed to near normal control values in animals treated with piperine (50 mg/kg body weight). It is apparent that the beneficial effect of piperine is primarily exerted on the during initiation phase and post-initiation stage of B(a)p induced lung carcinogenesis. Overall, these data indicative that piperine has chemopreventive effects when administered orally on lung cancer bearing animals.

PMID: 15183854 [PubMed - indexed for MEDLINE]

And of course, there is evidence to suggest that Curcumin does indeed INHIBIT lung-tumor cells:

Cancer Res. 2008 Sep 15;68(18):7428-38.
Curcumin inhibits lung cancer cell invasion and metastasis through the tumor suppressor HLJ1.
Chen HW, Lee JY, Huang JY, Wang CC, Chen WJ, Su SF, Huang CW, Ho CC, Chen JJ, Tsai MF, Yu SL, Yang PC.
Source
Department and Institute of Pharmacology, School of Medicine, National Yang-Ming University,Taipei, Taiwan.
Abstract
Curcumin (diferuloylmethane) is an active component of the spice turmeric and has a diversity of antitumor activities. In this study, we found that curcumin can inhibit cancer cell invasion and metastasis through activation of the tumor suppressor DnaJ-like heat shock protein 40 (HLJ1). Human lung adenocarcinoma cells (CL1-5) treated with curcumin (1-20 mumol/L) showed a concentration-dependent reduction in cell migration, invasion, and metastatic ability, and this was associated with increased HLJ1 expression. Knockdown of HLJ1 expression by siRNA was able to reverse the curcumin-induced anti-invasive and antimetastasis effects in vitro and in vivo. The HLJ1 promoter and enhancer in a luciferase reporter assay revealed that curcumin transcriptionally up-regulates HLJ1 expression through an activator protein (AP-1) site within the HLJ1 enhancer. JunD, one of the AP-1 components, was significantly up-regulated by curcumin (1-20 mumol/L) in a concentration- and time-dependent manner. Knockdown of JunD expression could partially reduce the curcumin-induced HLJ1 activation and diminish the anti-invasive effect of curcumin, indicating that JunD would seem to be involved in curcumin-induced HLJ1 expression. Curcumin was able to induce c-Jun NH(2)-kinase (JNK) phosphorylation, whereas the JNK inhibitor (SP-600125) could attenuate curcumin-induced JunD and HLJ1 expression. Activation of HLJ1 by curcumin further leads to up-regulation of E-cadherin and a suppression of cancer cell invasion. Our results show that curcumin induces HLJ1, through activation of the JNK/JunD pathway, and inhibits lung cancer cell invasion and metastasis by modulating E-cadherin expression. This is a novel mechanism and supports the application of curcumin in anti-cancer metastasis therapy.

PMID: 18794131 [PubMed - indexed for MEDLINE] Free full text

This is merely speculation, but I would assume that dosage is the key here. Lower doses tend to possess greater cancer-preventive effects, whereas higher doses seem to possess cancer-promoting effects.

[agwoodliffe]

Well, there's some evidence to suggest that, at the very least, piperine may counteract this risk (provided you stick to the low dose, of course):

Mol Cell Biochem. 2005 Mar;271(1-2):101-6.
Chemopreventive effect of piperine on mitochondrial TCA cycle and phase-I and glutathione-metabolizing enzymes in benzo(a)pyrene induced lung carcinogenesis in Swiss albino mice.
Selvendiran K, Thirunavukkarasu C, Singh JP, Padmavathi R, Sakthisekaran D.
Source
Department of Medical Biochemistry, Dr. ALM Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai 600 113, India. selvakphd@yahoo.com
Abstract
Piperine is a major component of black (Piper nigrum Linn) and long pepper (Piper longum Linn) used widely in various systems of traditional medicine. We have evaluated the effect of piperine on mitochondrial tricarboxylic acid cycle and phase I and glutathione-metabolizing enzymes in Benzo(a)pyrene induced experimental lung carcinogenesis in swiss albino mice. Lung cancer bearing mice showed a significant decrease in the activities of mitochondrial enzymes-isocitrate dehydrogenase (ICDH), -ketoglutarate dehydrogenase (KDH), succinate dehydrogenase (SDH), malate dehydrogenase (MDH) and significantly increased NADPH-Cytochorome reductase (NADPH-C reductase), cytochrome P450 (cyt-p450) and cytochrome b5(cyt-b5). The activities of glutathione-metabolizing enzymes glutathione peroxidase(GPx), glutathione reductase (GR) and glucose-6-phospho dehydrogenase(G6PDH) were significantly lowered in lung-cancer bearing mice when compared with control mice. Piperine supplementation to tumour-induced animals significantly lowered the phase-I enzymes (NADPH-C reductase, cyt-p450 and cyt-b5)) and there was a rise in glutathione-metabolizing enzymes (GPx, GR and G6PDH), which indicated an antitumour and anti-cancer effect. Comparison of normal control mice and mice administered piperine only as drug control showed no significant variations in enzyme activities. Piprine administration

Clin Exp Metastasis. 2002;19(8):703-8.
Effect of piperine on the inhibition of lung metastasis induced B16F-10 melanoma cells in mice.
Pradeep CR, Kuttan G.
Source
Amala Cancer Research Centre, Thrissur, Kerala, India.
Abstract
The effect of piperine on the inhibition of lung metastasis induced by B16F-10 melanoma cells was studied in C57BL/6 mice. Simultaneous administration of the compound with tumor induction produced a significant reduction (95.2%) in tumor nodule formation. Increased lung collagen hydroxyproline (22.37 microg/mg protein) in the metastasized lungs of the control animals compared to normal animals (0.95 microg/mg protein) was significantly reduced (2.59 microg/mg protein) in the piperine-treated animals. The high amount of uronic acid (355.83 microg/100 mg tissue) in the metastasized control animals was significantly reduced (65 microg/100 mg tissue) in the animals treated with piperine. Lung hexosamine content was also significantly reduced in the piperine-treated animals (0.98 mg/100 mg lyophilized tissue) compared to the untreated tumor-bearing animals (4.2 mg/100 mg lyophilized tissue). The elevated levels of serum sialic acid and serum gamma glutamyl transpeptidase activity in the untreated control animals was significantly reduced in the animals treated with piperine. The piperine-treated animals even survived the experiment (90 days). Histopathology of the lung tissue also correlated with the lifespan of the drug-treated animals. Our results demonstrate the antimetastatic activity of piperine, an alkaloid present in plants such as Piper nigrum and Piper longum.

PMID: 12553376 [PubMed - indexed for MEDLINE]

Biomed Pharmacother. 2004 May;58(4):264-7.
Chemopreventive effect of piperine on modulating lipid peroxidation and membrane bound enzymes in benzo(a)pyrene induced lung carcinogenesis.
Selvendiran K, Sakthisekaran D.
Source
Department of Medical Biochemistry, Dr. ALM Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai 600113, India.
Abstract
The current study was designed to evaluate the effects of oral supplementation of the piperine on lung tumour initiation by orally applied benzo(a)pyrene (B(a)p). To evaluate the effects of orally supplemented piperine on lung tumour initiation by B(a)p, its effects on ATPase enzymes were first evaluated. Lung cancer bearing mice showed an increase in erythrocyte membrane and tissues ATPase enzymes (Na(+)/K(+)-ATPases, Mg(2+)-ATPases and Ca(2+)-ATPases). Na(+) K-ATPase and Mg-ATPase enzyme activities were decreased and calcium ATPase increased (P < 0.05) in erythrocyte membrane and tissues of lung cancer bearing animals compared with control groups. The elevation of these enzyme activities in membrane and tissues were indicative of the persistent deteriorating effect of B(a)p in cancer bearing animals. These enzyme activities were reversed to near normal control values in animals treated with piperine (50 mg/kg body weight). It is apparent that the beneficial effect of piperine is primarily exerted on the during initiation phase and post-initiation stage of B(a)p induced lung carcinogenesis. Overall, these data indicative that piperine has chemopreventive effects when administered orally on lung cancer bearing animals.

PMID: 15183854 [PubMed - indexed for MEDLINE]

And of course, there is evidence to suggest that Curcumin does indeed INHIBIT lung-tumor cells:

Cancer Res. 2008 Sep 15;68(18):7428-38.
Curcumin inhibits lung cancer cell invasion and metastasis through the tumor suppressor HLJ1.
Chen HW, Lee JY, Huang JY, Wang CC, Chen WJ, Su SF, Huang CW, Ho CC, Chen JJ, Tsai MF, Yu SL, Yang PC.
Source
Department and Institute of Pharmacology, School of Medicine, National Yang-Ming University,Taipei, Taiwan.
Abstract
Curcumin (diferuloylmethane) is an active component of the spice turmeric and has a diversity of antitumor activities. In this study, we found that curcumin can inhibit cancer cell invasion and metastasis through activation of the tumor suppressor DnaJ-like heat shock protein 40 (HLJ1). Human lung adenocarcinoma cells (CL1-5) treated with curcumin (1-20 mumol/L) showed a concentration-dependent reduction in cell migration, invasion, and metastatic ability, and this was associated with increased HLJ1 expression. Knockdown of HLJ1 expression by siRNA was able to reverse the curcumin-induced anti-invasive and antimetastasis effects in vitro and in vivo. The HLJ1 promoter and enhancer in a luciferase reporter assay revealed that curcumin transcriptionally up-regulates HLJ1 expression through an activator protein (AP-1) site within the HLJ1 enhancer. JunD, one of the AP-1 components, was significantly up-regulated by curcumin (1-20 mumol/L) in a concentration- and time-dependent manner. Knockdown of JunD expression could partially reduce the curcumin-induced HLJ1 activation and diminish the anti-invasive effect of curcumin, indicating that JunD would seem to be involved in curcumin-induced HLJ1 expression. Curcumin was able to induce c-Jun NH(2)-kinase (JNK) phosphorylation, whereas the JNK inhibitor (SP-600125) could attenuate curcumin-induced JunD and HLJ1 expression. Activation of HLJ1 by curcumin further leads to up-regulation of E-cadherin and a suppression of cancer cell invasion. Our results show that curcumin induces HLJ1, through activation of the JNK/JunD pathway, and inhibits lung cancer cell invasion and metastasis by modulating E-cadherin expression. This is a novel mechanism and supports the application of curcumin in anti-cancer metastasis therapy.

PMID: 18794131 [PubMed - indexed for MEDLINE] Free full text

This is merely speculation, but I would assume that the key here is 'dosage'. Lower doses tend to protect against tumor-cells, whereas higher doses seem to promote them.

Edited by agwoodliffe, 10 July 2011 - 09:39 PM.

[hav]

http://carcin.oxford...stract/bgp082v1

Here's what's mentioned about the curcumin dosage used in this study in the full-text:

Separate groups of
mice were fed either the chemopreventive agent sulindac at a dose of 80 ppm or 4,000
ppm of curcumin starting 2 days after the initiation of DOX. The dose of curcumin that
we employed is twice that utilized in a previous lung chemoprevention study [28] and
well within the range of doses employed in other in vivo models and human clinical trials
as reviewed recently in Goel et al. [37]

... but the fact that they administered DOX and curcumin at the same time makes me wonder if the study's conclusion necessarily follows. Could be the curcumin merely enhanced the bio availability of the DOX (as it apparently does with resvertrol) in a way that might not necessarily model what would happen with a smoker. Much less with an ex-smoker.

Howard

[Renegade]

Any more info on curcumin safety?

[Nootropic Cat]

Sigh, confusing. When I quit smoking several months ago and did research as to appropriate supps to be taking, curumin was on the list and I've been taking it since...

[Mind]

The study had confounding variables, and was done in mice. From what I have through the years, mouse studies do not have strong correlations with human health.