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ive read some studys on how curcumin can modulate certain genetic pathways and protein expression, and can stop cancerous tumors, but the doseges used were 200-600mg/kg so thats alot.

the way it does this could also help acne, i was wondering if anyone had any knowledge on the subject or have tried it for their acne in large dosages like anywhere near 13 grams a day

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Well, it's what makes turmeric yellow. I used to drink turmeric tea. I didn't notice too much of a difference. There's turmeric in the milk thistle supplement I take now (dandelion root too, all of which are great for the liver), but I don't know if it is what specifically helps, but the combination of that milk thistle supplement and papaya/pineapple enzymes / other anti-parasitic supplements seems to do worlds of good for my skin and allows me to eat whatever, even drink coffee like a fish. I still eat healthy foods everyday too though, like omega-3 eggs, salads, fruits, nuts, kefir, berries, etc.

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Well, it's what makes turmeric yellow. I used to drink turmeric tea. I didn't notice too much of a difference. There's turmeric in the milk thistle supplement I take now (dandelion root too, all of which are great for the liver), but I don't know if it is what specifically helps, but the combination of that milk thistle supplement and papaya/pineapple enzymes / other anti-parasitic supplements seems to do worlds of good for my skin and allows me to eat whatever, even drink coffee like a fish. I still eat healthy foods everyday too though, like omega-3 eggs, salads, fruits, nuts, kefir, berries, etc.

have you taken anywhere near 13 grams a day?

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this is alot of crap but heres why curcumin could help, ive compared it to the genetic effects of isotretinoin.

there was one other study i read about curcumin being administered to rats with tumors at a dosage of 200-600mg/kg both of which reduced the tumors in the rats but i cant find that one yet.

13-cis Retinoic acid induces apoptosis and cell cycle arrest in human SEB-1 sebocytes.

J Invest Dermatol. 2006 Oct;126(10):2154-6.

The Jake Gittlen Cancer Research Foundation, The Pennsylvania State University College of Medicine, Hershey, 17033, USA.

Isotretinoin (13-cis retinoic acid (13-cis RA)) is the most potent inhibitor of sebum production, a key component in the pathophysiology of acne, yet its mechanism of action remains largely unknown. The effects of 13-cis RA, 9-cis retinoic acid (9-cis RA), and all-trans retinoic acid (ATRA) on cell proliferation, apoptosis, and cell cycle proteins were examined in SEB-1 sebocytes and keratinocytes. 13-cis RA causes significant dose-dependent and time-dependent decreases in viable SEB-1 sebocytes. A portion of this decrease can be attributed to cell cycle arrest as evidenced by decreased DNA synthesis, increased p21 protein expression, and decreased cyclin D1 . Although not previously demonstrated in sebocytes, we report that 13-cis RA induces apoptosis in SEB-1 sebocytes as shown by increased Annexin V-FITC staining, increased TUNEL staining, and increased cleaved caspase 3 protein. Furthermore, the ability of 13-cis RA to induce apoptosis cannot be recapitulated by 9-cis RA or ATRA, and it is not inhibited by the presence of a retinoid acid receptor (RAR) pan-antagonist AGN 193109. Taken together these data indicate that 13-cis RA causes cell cycle arrest and induces apoptosis in SEB-1 sebocytes by a RAR-independent mechanism, which contributes to its sebosuppressive effect and the resolution of acne.

PMID: 16575387 [PubMed - indexed

Curcumin selectively induces apoptosis in deregulated cyclin D1-expressed cells at G2 phase of cell cycle in a p53-dependent manner.Choudhuri T, Pal S, Das T, Sa G.

Bose Institute, P-1/12 Calcutta Improvement Trust Scheme VII M, Kolkata, India.

Biol Chem. 2005 May 20;280(20):20059-68. Epub 2005 Feb 28. Links

Curcumin (diferuloylmethane) is known to induce apoptosis in tumor cells. In asynchronous cultures, with time-lapse video-micrography in combination with quantitative fluorescence microscopy, we have demonstrated that curcumin induces apoptosis at G(2) phase of cell cycle in deregulated cyclin D1-expressed mammary epithelial carcinoma cells, leaving its normal counterpart unaffected. In our search toward delineating the molecular mechanisms behind such differential activities of curcumin, we found that it selectively increases p53 expression at G(2) phase of carcinoma cells and releases cytochrome c from mitochondria, which is an essential requirement for apoptosis. Further experiments using p53-null as well as dominant-negative and wild-type p53-transfected cells have established that curcumin induces apoptosis in carcinoma cells via a p53-dependent pathway. On the other hand, curcumin reversibly inhibits normal mammary epithelial cell cycle progression by down-regulating cyclin D1 expression and blocking its association with Cdk4/Cdk6 as well as by inhibiting phosphorylation and inactivation of retinoblastoma protein. In addition, curcumin significantly up-regulates cell cycle inhibitory protein (p21Waf-1) in normal cells and arrests them in G(0) phase of cell cycle. Therefore, these cells escape from curcumin-induced apoptosis at G(2) phase. Interestingly, these processes remain unaffected by curcumin in carcinoma cells where cyclin D1 expression is high. Similarly, in ectopically overexpressed system, curcumin cannot down-regulate cyclin D1 and thus block cell cycle progression. Hence, these cells progress into G(2) phase and undergo apoptosis. These observations together suggest that curcumin may have a possible therapeutic potential in breast cancer patients.

Curcumin inhibits cell cycle progression of immortalized human umbilical vein endothelial (ECV304) cells by up-regulating cyclin-dependent kinase inhibitor, p21WAF1/CIP1, p27KIP1 and p53.Park MJ, Kim EH, Park IC, Lee HC, Woo SH, Lee JY, Hong YJ, Rhee CH, Choi SH, Shim BS, Lee SH, Hong SI.

Laboratory of Cell Biology, Korea Cancer Center Hospital, 139-706 Seoul, Korea.

Int J Oncol. 2002 Aug;21(2):379-83. Links

To elucidate possible mechanisms of anti-angiogenic activity by curcumin, we performed cDNA microarray and found that curcumin modulated cell cycle related gene expression. For further confirmation, DNA contents and expression levels of cyclins, cyclin-dependent kinases (CDKs), and CDK inhibitors (CDKIs) were examined by FACS analysis and Western blotting, respectively. Curcumin was found to induce G0/G1 and/or G2/M phase cell cycle arrest, up-regulate CDKIs, p21WAF1/CIP1, p27KIP1, and p53, and slightly down-regulate cyclin B1 and cdc2 in ECV304 cells. However, expression level of other cyclins and CDKs were not changed by curcumin. We, therefore, conclude that the up-regulation of CDKIs by curcumin plays a critical role in the regulation of cell cycle distribution in these cells, which may have a major role in anti-angiogenic activity of curcumin.

Curcumin-induced apoptosis of human colon cancer colo 205 cells through the production of ROS, Ca2+ and the activation of caspase-3.Su CC, Lin JG, Li TM, Chung JG, Yang JS, Ip SW, Lin WC, Chen GW.

School of Chinese Medicine, Department of Microbiology, China Medical University, No 91, Hsueh-Shih Road, Taichung City 404, Taiwan, ROC.

Anticancer Res. 2006 Nov-Dec;26(6B):4379-89. Links

Curcumin (diferuloylmethane), the yellow pigment in turmeric (Curcuma longa), is known to inhibit proliferation of cancer cells by arresting them at various phases of the cell cycle and to induce apoptosis in tumor cells. Curcumin-induced apoptosis mainly involves the activation of caspase-3 and mitochondria-mediated pathway in various cancer cells of different tissue origin. In the present study, the induction of apoptosis and cytotoxicity by curcumin in colon cancer colo 205 cells was investigated by using flow cytometry. The results demonstrated that curcumin induced cytotoxicity and apoptosis dose- and time-depedently. Curcumin induced the production of reactive oxygen species (ROS) and Ca+2, decreased the levels of mitochondria membrane potential and induced caspase-3 activity . Curcumin also promoted the expression of Bax, cytochrome C, p53 and p21but inhibited the expression of Bcl-2. These observations suggest that curcumin may have a possible therapeutic potential in colon cancer patients.

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maybe using it topically would help acne.

Biol Chem. 2007 Mar 2;282(9):6707-15. Epub 2006 Dec 5. Links

Curcumin Suppresses AP1 Transcription Factor-dependent Differentiation and Activates Apoptosis in Human Epidermal Keratinocytes.Balasubramanian S, Eckert RL.

Departments of Physiology and Biophysics, Dermatology, Biochemistry, Reproductive Biology, and Oncology, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106-4970.

The diet-derived cancer preventive agent, curcumin, inhibits skin cancer cell proliferation and tumor formation. However, its effect on normal human keratinocyte differentiation, proliferation, and apoptosis has not been adequately studied. Involucrin (hINV) is a marker of keratinocyte differentiation and a useful model for the study of chemopreventive agent action. We show that curcumin suppresses the differentiation agent-dependent activation of hINV gene expression and that an AP1 transcription factor DNA binding site in the hINV gene is required for this regulation. A protein kinase C, Ras, MEKK1, MEK3 signaling cascade controls hINV expression by regulating AP1 factor level. Curcumin treatment inhibits the novel protein kinase C-, Ras-, and MEKK1-dependent activation of hINV promoter activity and reduces the differentiation agent-dependent increase in AP1 factor level and DNA binding. This reduction requires proteasome function. In addition, curcumin treatment reduces cell number, which is associated with a reduced cyclin and cdk1 levels. Curcumin treatment also suppresses the Bcl-xL level, leading to reduced mitochondrial membrane potential and increased cleavage of procaspases and poly(ADP-ribose) polymerase. These studies provide important insights regarding the mechanism whereby curcumin acts as a chemopreventive agent in normal human epidermis.

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Looks interesting, but the dosages used are pretty heavy. At 600mg/kg i'd need over 54g a day =|

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I've taken curcumin for cystic breakouts before by ingesting one teaspoon of turmeric (from the spice isle in the grocery store) three times daily. To increase it's effects, take bromelain simultaneously, in between meals. I cannot tell you how amazing it is for killing infections. There are lots of reports of turmeric ingestion even treating MRSA (drug resistant staph infection) effectively. Taking this three times a day completely flattened (but did not fade) all inflammations on my body within two days. To take it (this takes practice, as turmeric is strong tasting), I mixed a teaspoon of turmeric in a glass (8oz or so) of milk and heated it in the microwave until it mixed more consistently and was lukewarm. I would then take a deep breath and down it as quickly as possible and chase it with some fresh milk. I know this sounds disgusting, but it is way better than mixing it with water. Trust me. I tried. I have also purchased giant empty capsules from my local heath foods store and filled them with turmeric, but something about the milk mixture (a recipe recommended on the internet by those more than experienced than I) is just really effective. I have treated cysts that I have foolishly poked at, spreading the painful inflammation throughout my cheek (or wherever), and yet turmeric has been able to flush such infections out of my system literally within hours. Turmeric has a poweful effect as a liver cleanser and thus blood cleanser, it is amazing. Look it up. And if you take the already-made supplements (usually listed as Turmeric) from the health store, make sure it is made with standardized 95% curcumins to ensure potency. This stuff works miracles, especially in emergencies.

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