Curcumin Dosage recommendations

Further to 'curcumin chat' under "We stick to science and let the results speak" and Vicki's "I have confidence in me" - I've come across the 'Curcumin' web site of Dr Bharat Aggarwal of MD Anderson Cancer Center, with the info you need if interested in taking curcumin.

From the site:http://www.curcuminresearch.org/,
is this info on dosage:

Recommendations for Cancer:

If you have cancer, please consider curcumin for yourself as following regimen:

1 g/day for week one; if no side effects then,

2 g/day for week two; if no side effects then (can be split into three separate doses).

4 g/day for week three; if no side effects then (can be split into three separate doses).

8 g/day for week four; for eight weeks (can be split into three separate doses).

After 8 weeks, if no improvement is noted, curcumin is less likely to do anything for you.

If you do not have cancer, then one capsule (500 mg) per day is sufficient.

How should I take curcumin?

There are reports to indicate curcumin taken empty stomach is more effective than with the meals. Thus it is recommended that you take curcumin 1 h before meals. If you are taking curcumin powder (instead of capsule), you can mix it with milk, yogurt, coconut milk or other fluids.

Has there been any toxicity associated with curcumin?

Two Phase I studies have been published. These studies suggest that curcumin is safe in human subjects even when consumed up to 12 grams per day for three months. Inspite of it, one is recommended to take low dose (500 mg/day) and gradually increase dose if needed. Look for signs of both potential toxicity and improvement by talking to your body and to your doctor.
........................................................................... ....................
xxxGGC

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15 replies. Join the discussion

Wow, I was just going to ask for more info on curcumin. Thanks! Do you or anyone out there have recipes for cooking with turmeric? I'd like to incorporate more of it into my regular diet. Is there a place (other than mail order) where one can purchase good quality curcumin and tumeric? Which brands are best?

I did read the interview. Very interesting. I'm going to talk to my onc and nutritionist about it tomorrow, although since I am on chemo now I have a feeling my onc may not agree with it right now. He always says that anything in the form of food, as opposed to capsules, is okay to try.

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The interview was compelling and very thought provoking. This is also great follow up info. It is so empowering to get information that allows us to help
ourselves in this fight and not solely rely on doctors and toxic medications. Thanks for sharing!!

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Dr Kieth Block in his book Life Over Cancer (a good read) talks about Curcumin and recomends his patients take it. I have been taking the tablets but not very consistantly also add it to green juice (whch tasts terrible anyway) and try to go to the local Indian restaurant any chance I get!!! Thanks for the reminder!!!

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Thanks GGC - you are always such a great source of information for me!! lisa

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When I started thinking about taking curcumin I wanted to use exactly the same type they were using at MD Anderson. I discovered that the use the patented Curcumin C3 Complex made by Sabinsa Corp. You can reach a Sabinsa Corp. website at:

www.curcuminoids.com

They do not sell directly to the public but you can see on the home page a list of all the researchers using this product including Johns Hopkins, UCLA and MD Anderson. On the left side of the website page you can click on SABINSA's Curcumin C3 product users and on that page they give you a list of companies that use their proprietary formulation in their curcumin products. I used this list to research the various prices, and decided to buy the Doctor's Purest at Ageless Cures. You can't get to the various companies directly from Sabinsa's website but I found them just by googling the company names.

I just thought if I was going to do this I would use exactly the same thing they use in a lot of the research that is being done. Since the vitamin industry is not regulated I am sceptical of what's inside most vitamins. Using this list gives me the confidence to know I am getting what I want.

Terry

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Hey pbjgirl

I google-mapped where you live ( you DO learn something every day!), and found a health food store - which I think is not too far from you(?): Lebanon Health Foods http://www.lebanonhealthfoodstore.com/

You no doubt know where you're nearest health food store is any way, they do stock the NOW brand of curcumin, amongst others, but you could request they order in for you the brands mentioned by Terry/Shanti - with the C3 curcumin complex, used in the research and trials by the big institutions.

FYI this is my self-styled "anti cancer soup" with tumeric+extra virgin olive oil + black pepper to enhance absorption of the curcuminoids!

Ingredients

•1 tablespoon extra virgin olive oil
•2 tsps grated fresh ginger
•2 teaspoons curry powder
•2 heaped teaspoons tumeric
•approx ½ teaspoon black pepper
•1 onion, finely chopped
•2 cloves garlic, crushed
•4 – 6 dried shiitake mushrooms chopped,optional
•1 cup dried red lentils, washed in a sieve
•1/3 – ½ of a pumpkin chopped
•2 carrots, peeled and chopped
•1 cup frozen peas/green beans
•1 vegetable stock cube or liquid vege stock
•water to cover, salt to taste

** I generally add cumin, ground coriander, caraway seeds, cardamom pods, black mustard seeds, garam masala to the spice list – whatever comes to hand out of the spice storage container along with the curry powder and the tumeric!

*** Also I add whatever vegetable is lazing in the fridge crisper – red capsicum (that’s bell peppers to you : ), celery, broccoli, potato, tomato, asparagus – anything! In it goes – it all cooks up and tastes great!

Method

1.Add curry powder, turmeric and black pepper, and any other spices/herbs to olive oil in a large heavy-based saucepan/cookpot over a gentle heat for several minutes.

2.Add onion and garlic, ginger (celery/capsicum) and cook for 2 to 3 minutes until soft.

3.Add pumpkin and carrots, and cook for 5 minutes.

Add washed lentils, peas, shiitake mushrooms, stock cube and water to cover. Bring to the boil.

Reduce heat to medium-low. Cover and cook for about 30 minutes, stirring occasionally until carrot is soft and pumpkin mushy – that’s how I like it!

For the dairy inclined a ‘blob’ of Greek yoghurt on top to finish is yummo !

xxxGGC

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You're a good woman Miss Terry - I love it when someone's done the 'footwork'!!!

I'm ordering the Doctor's Best C3 complex (I had been looking and comparing the choices!) probably from 'iherb' as they seem to have the best price on int'l shipping.

Thanks for the links and the info - great stuff!

Also I purchased yesterday a 'boswellia complex'(Mediherbs brand), also with curcumin, ginger & 'apium graveolens' in it - Chloemom/Lorri put me onto it - the research on boswellia is fascinating.

It apparently stops "Osteoclastogenesis " which is the destructive action of bone mets - WITHOUT the side effects,and is reversible -AND induces apoptosis and is antiangiogenetic, etc. The last para in this article states (for those without the energy to read it all!!):


"Overall, our studies provide a detailed mechanism through which AKBA mediates its effects. The ability of AKBA to enhance apoptosis, suppress invasion, and inhibit osteoclastogenesis provides novel targets for cancer therapy."

http://www.jimmunol.org/cgi/content/full/176/5/3127

Acetyl-11-Keto- -Boswellic Acid Potentiates Apoptosis, Inhibits Invasion, and Abolishes Osteoclastogenesis by Suppressing NF- B and NF- B-Regulated Gene Exprssion1

Astract:
Acetyl-11-keto- -boswellic acid (AKBA), a component of an Ayurvedic therapeutic plant Boswellia serrata, is a pentacyclic terpenoid active against a large number of inflammatory diseases, including cancer, arthritis, chronic colitis, ulcerative colitis, Crohn’s disease, and bronchial asthma, but the mechanism is poorly understood.

We found that AKBA potentiated the apoptosis induced by TNF and chemotherapeutic agents, suppressed TNF-induced invasion, and inhibited receptor activator of NF- B ligand-induced osteoclastogenesis, all of which are known to require NF- B activation.

These observations corresponded with the down-regulation of the expression of NF- B-regulated antiapoptotic, proliferative, and angiogenic gene products. As examined by DNA binding, AKBA suppressed both inducible and constitutive NF- B activation in tumor cells.

It also abrogated NF- B activation induced by TNF, IL-1 , okadaic acid, doxorubicin, LPS, H2O2, PMA, and cigarette smoke. AKBA did not directly affect the binding of NF- B to the DNA but inhibited sequentially the TNF-induced activation of I B kinase (IKK), I B phosphorylation, I B ubiquitination, I B degradation, p65 phosphorylation, and p65 nuclear translocation.
AKBA also did not directly modulate IKK activity but suppressed the activation of IKK through inhibition of Akt.

Furthermore, AKBA inhibited the NF- B-dependent reporter gene expression activated by TNFR type 1, TNFR-associated death domain protein, TNFR-associated factor 2, NF- B-inducing kinase, and IKK, but not that activated by the p65 subunit of NF- B. Overall, our results indicated that AKBA enhances apoptosis induced by cytokines and chemotherapeutic agents, inhibits invasion, and suppresses osteoclastogenesis through inhibition of NF- B-regulated gene expression.

Further in “Discussion”:

We also found that AKBA suppressed TNF-induced invasion by tumor cells, and this inhibition correlated with down-regulation of MMP-9 and adhesion proteins. The role of MMP-9 and adhesion molecules in invasion has been demonstrated (63, 64, 65). We also demonstrated for the first time that AKBA abolished the RANKL-induced differentiation of monocytes into osteoclasts. This result may explain the suppressive effect of AKBA on arthritis reported previously (13, 14, 16). The effect of AKBA on osteoclastogenesis was found to be reversible.


For the first time, we also found that AKBA inhibited NF- B activation induced by a wide variety of agents (e.g., TNF, IL-1 , PMA, LPS, and cigarette smoke condensate) that activate NF- B through different mechanisms (28, 37, 66, 67).

These results suggest that AKBA acts at a step common to all of these activators. In response to most of these stimuli, NF- B activation proceeds through sequential activation of IKK, phosphorylation at Ser32 and Ser36 of I B , and ubiquitination at Lys21 and Lys22 of I B , leading finally to degradation of I B and the release of NF- B (47).

We found that AKBA blocked NF- B activation by inhibiting IKK indirectly rather than directly. This result differs from those of Syrovets et al. (25, 26), who showed that AKBA blocks LPS-induced NF- B activation by direct inhibition of IKK.

AKBA affected neither the DNA binding of NF- B nor IKK activity directly. AKBA did, however, block TNF-induced activation of IKK, which led to suppression of I B phosphorylation, ubiquitination, and subsequent degradation. The phosphorylation and nuclear translocation of p65 were also abolished by AKBA. Because Akt has been shown to activate IKK (54), we examined its relation to AKBA activity.

We found that AKBA suppressed TNF-induced Akt activation as well as Akt-IKK association. These results indicate that AKBA may inhibit IKK activation through suppression of Akt activation.

We showed that AKBA inhibited NF- B-regulated gene transcription and NF- B-regulated gene products involved in cell proliferation (e.g., cyclin D1 and COX-2), antiapoptosis (e.g., survivin, IAP1, XIAP, Bcl-2, Bcl-xL, Bfl-1/A1, and FLIP), and invasion (MMP-9 and vascular endothelial growth factor).
To our knowledge, there is no other published report of the regulation of these gene products by AKBA. AKBA induction of cell cycle arrest (22, 23, 25) may be due to down-regulation of cyclin D1, as we have described. The down-regulation of the inflammatory cytokine TNF as reported previously (26) by AKBA could also be due to suppression of NF- B, as we have described.

AKBA has also been shown to reduce the incidence of Crohn’s disease, inflammatory bowel disease, and arthritis in animals and in humans (10, 11, 12, 13, 14). These effects may also be mediated through NF- B suppression because NF- B has been demonstrated to play a pivotal role in these diseases (43).

Overall, our studies provide a detailed mechanism through which AKBA mediates its effects. The ability of AKBA to enhance apoptosis, suppress invasion, and inhibit osteoclastogenesis provides novel targets for cancer therapy.
........................................................................... ....................

God bless you Terry and Lorri - we'll cure ourselves yet!!

xxxGGC

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Hey Groovygirl,
Thanks SO much for the soup recipe!! Can't wait to try it. You are amazing and have a ton of energy...how do you do it???
Love ya girl!
PJ

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Just found this article Published Oct. 2009 in Medical News Today taken from British Journal of Cancer.

Curry Powder Ingredient Kills Cancer Cells

28 Oct 2009

Researchers from Ireland and Poland found that curcumin, a compound found in the popular Indian spice turmeric that gives curry powder its distinct yellow colour, killed oesophageal cancer cells in the lab via an unexpected cell-death mechanism that did not involve apoptosis or cell suicide.

Moreover, they found that the compound started killing cancer cells within 24 hours and the cells began to digest themselves.

The study was the work of lead author Dr Sharon McKenna at the Cork Cancer Research Centre, University College Cork (UCC) in Ireland, and colleagues, and appears in the 28 October issue of the British Journal of Cancer.

McKenna told the press that:

"These exciting results suggest that scientists could develop curcumin as a potential anti-cancer drug to treat oesophageal cancer."

She explained that scientists have long known that natural compounds have potential therapeutic value in treating cancerous cells and they suspected that curcumin was one of them.

First author and UCC medical researcher Dr Geraldine O'Sullivan-Coyne, had been looking for new ways of killing resistant oesophageal cancer cells explained McKenna, and when she started using curcurmin she found the cells started to die using a cell signalling system that unexpectedly did not go via the apoptosis or cell suicide path.

Apoptosis is the most usual route by which faulty cells die: it is a cell suicide path triggered by proteins called caspases. But O'Sullivan-Coyne, McKenna and colleagues found that not only did the cells show no evidence of suicide, when they added a molecule that stops the caspases triggering apoptosis, it made no difference to the number of cells that died.

This strongly suggests that curcumin killed the cancer cells via another cell signalling path, said the researchers.

Oesophageal cancer is the seventh most common cause of death from cancer in Ireland, where it accounts for 350 deaths a year, around 4 per cent of all cancer deaths in Ireland. In the UK it kills around 7,800 people a year.

Fewer than 20 per cent of patients with oesophageal cancer live more than 5 years after diagnosis.

Professor Gerald O'Sullivan, who heads the Cork Cancer Research Centre at UCC said that this study opens the door to developing natural chemicals in turmeric as new treatments for oesophageal cancer.

"The incidence of oesophageal cancer has gone up by more than a half since the 70s, particularly in the Western world and this is thought to be linked to rising rates of obesity, alcohol intake and reflux disease, so finding ways to both treat and prevent this disease is extremely important," he said, adding that:

"The development of natural compounds as chemo-preventative agents is also a very promising area of research."

Dr Lesley Walker, director of cancer information at Cancer Research UK expressed a similar view to the BBC.

"Curcumin induces apoptosis-independent death in oesophageal cancer cells."
G O'Sullivan-Coyne, G C O'Sullivan, T R O'Donovan, K Piwocka, S L McKenna
British Journal of Cancer, Published 28 October 2009.
DOI:10.1038/sj.bjc.6605308

Sources: UCC, BBC.

Written by: Catharine Paddock, PhD
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today

Article URL: http://www.medicalnewstoday.com/articles/168987.php

Main News Category: Cancer / Oncology

Also Appears In: GastroIntestinal / Gastroenterology, Nutrition / Diet, Biology / Biochemistry,


Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

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Amazing information Lorri -

Mother Nature is quite a woman, is she not?! Father Time will catch up eventually : )

xxxGGC

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GGC and others:

Have any clinical trials investigated curcumin in women with metastatic breast cancer? I noticed the references for all the other types of cancer but couldn't find a reference for breast cancer. thx, Julie

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Hi 'B/S'dinNY'

I don't have any info (I think) on human MBC trials, only on mice - but that is good enough for me!

There's no mega-money in these things, so drug companies and their mega-money (for trials) don't want to know about it at all.

Personally, I'm very convinced by all the research I've read on it to try curcumin (&boswellia).

I like a tag line I read last night, on someone's post (elsewhere): "I'd rather be anecdotely alive, than statistically dead" - Good one!!

Maybe someone else may have info for you, xxxGGC

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Hey GGC - you can call me Julie - "B/S'd" has a funny ring to it - ha!

I don't know much about clinical trials but it might not just be about money. Curcumin is not expensive and Dr. Aggarwal and others would be able to find funding from sources other than pharmaceutical companies. Plus, human clinical trials of curcumin have been done with other types of cancer so why not metastatic bc?

Maybe it has to do with experimental controls and requiring that patients be off all other forms of treatment (hormonal and chemo)? I'm not sure but it's frustrating given the astronomical amount of money raised for breast cancer and the fact that bc is the leading cause of death for young adult women.

The next time you chat with Dr. Aggarwal, would you mind asking him the question? Maybe we could help "lobby" certain groups (Komen, Live Strong, etc.) for funding for a clinical trial. Who wouldn't love an effective treatment with no toxicity?? Plus, I would love to invest my time and effort into something so promising.

Thanks for all the links and the good info and keep us up to date on your treatment!

Best, Julie

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GGC - check it out - just published. Abstract doesn't give results but says from encouraging efficacy results they're onto Phase II trials in women with mbc!


Cancer Biol Ther. 2010 Jan 21;9(1). [Epub ahead of print]

Phase I dose escalation trial of docetaxel plus curcumin in patients with advanced and metastatic breast cancer.
Bayet-Robert M, Kwiatkowski F, Leheurteur M, Gachon F, Planchat E, Abrial C, Mouret-Reynier MA, Durando X, Barthomeuf C, Chollet P.

Centre Jean Perrin, Division de Recherche Clinique, EA4231, Université d'Auvergne, Centre d'Investigation Clinique, Clermont-Ferrand, France.

Background: Since the improvement of chemotherapy with safe molecules is needed for a better efficacy without supplementary toxicity, we investigated the feasibility and tolerability of the combination of docetaxel and curcumin, a polyphenolic derivative extracted from Curcuma longa root. Results: Fourteen patients were accrued in this open-label phase I trial. At the last dose level of curcumin, 3 dose-limiting toxicities were observed and 2 out of 3 patients at this dose level refused to continue treatment, leading us to define the maximal tolerated dose of curcumin at 8,000 mg/d. Eight patients out of 14 had measurable lesions according to RECIST criteria, with 5 PR and 3 SD. Some improvements as biological and clinical responses were observed in most patients. Patients and methods: Patients with advanced or metastatic breast cancer were eligible. Docetaxel (100 mg/m(2)) was administered as a 1-hour i.v. infusion every 3 weeks on d1 for 6 cycles. Curcumin was orally given from 500 mg/d for 7 consecutive days by cycle (from d-4 to d+2) and escalated until a dose-limiting toxicity should occur. The primary endpoint of this study was to determine the maximal tolerated dose of the combination of dose-escalating curcumin and standard dose of docetaxel chemotherapy in advanced and metastatic breast cancer patients. Secondary objectives included toxicity, safety, vascular endothelial growth factor and tumor markers measurements, and assessment of objective and clinical responses to the combination therapy. Conclusion: The recommended dose of curcumin is 6,000 mg/d for 7 consecutive days every 3 weeks in combination with a standard dose of docetaxel. From the encouraging efficacy results, a comparative phase II trial of this regimen plus docetaxel versus docetaxel alone is ongoing in advanced and metastatic breast cancer patients.

http://www.ncbi.nlm.nih.gov/pubmed/19901561?dopt=Abstractplus

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