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Multivitamins may not slow colon cancer

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HuckleB Donating Member (1000+ posts) Send PM | Profile | Ignore Sun Sep-12-10 02:47 PM
Original message
Multivitamins may not slow colon cancer
http://www.reuters.com/article/idUSTRE6883I220100909

"Taking a multivitamin is unlikely to help colon cancer patients in battling the disease, suggests a new study.

"There is widespread belief among cancer patients that taking multivitamins will help to treat their cancer and prolong life," lead researcher Dr. Kimmie Ng of the Dana-Farber Cancer Institute, in Boston, told Reuters Health in an e-mail.

Because 26 to 77 percent of cancer survivors report using the supplements, Ng and her colleagues wanted to see what impact, if any, these multivitamins really had on colon cancer recurrence and survival.

The team followed more than 1,000 individuals who had recently undergone surgery for advanced (stage III) colon cancer, which, combined with rectal cancer, is the third most diagnosed cancer in both men and women in the U.S.

..."



-----------------------


It's just a single study, but, you know, FYI.

:)
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napi21 Donating Member (1000+ posts) Send PM | Profile | Ignore Sun Sep-12-10 02:52 PM
Response to Original message
1. Dr. Edell talked about that on his program the other day.
The results of several studies have shown that there is NO BENEFIT from vitamines on colon cancer patients and CAN interfere with radiation therapy if the patient is treated with that.
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HysteryDiagnosis Donating Member (1000+ posts) Send PM | Profile | Ignore Sun Sep-12-10 03:45 PM
Response to Reply #1
3. Indole three carbinol with DIM is not a "vitamin". Docosahexanoic
acid is not a "vitamin". Lipoic acid is not a "vitamin".


I find it highly unusual that these favorable scientific research results came from Japan, Norway and Germany. Funny that.

A combination of indol-3-carbinol and genistein synergistically induces apoptosis in human colon cancer HT-29 cells by inhibiting Akt phosphorylation and progression of autophagy.
Nakamura Y, Yogosawa S, Izutani Y, Watanabe H, Otsuji E, Sakai T.
Department of Molecular-Targeting Cancer Prevention, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kawaramachi-Hirokoji, Kyoto 602-8566, Japan. nakamura@koto.kpu-m.ac.jp
Abstract
BACKGROUND: The chemopreventive effects of dietary phytochemicals on malignant tumors have been studied extensively because of a relative lack of toxicity. To achieve desirable effects, however, treatment with a single agent mostly requires high doses. Therefore, studies on effective combinations of phytochemicals at relatively low concentrations might contribute to chemopreventive strategies.

RESULTS: Here we found for the first time that co-treatment with I3C and genistein, derived from cruciferous vegetables and soy, respectively, synergistically suppressed the viability of human colon cancer HT-29 cells at concentrations at which each agent alone was ineffective. The suppression of cell viability was due to the induction of a caspase-dependent apoptosis. Moreover, the combination effectively inhibited phosphorylation of Akt followed by dephosphorylation of caspase-9 or down-regulation of XIAP and survivin, which contribute to the induction of apoptosis. In addition, the co-treatment also enhanced the induction of autophagy mediated by the dephosphorylation of mTOR, one of the downstream targets of Akt, whereas the maturation of autophagosomes was inhibited. These results give rise to the possibility that co-treatment with I3C and genistein induces apoptosis through the simultaneous inhibition of Akt activity and progression of the autophagic process. This possibility was examined using inhibitors of Akt combined with inhibitors of autophagy. The combination effectively induced apoptosis, whereas the Akt inhibitor alone did not.

CONCLUSION: Although in vivo study is further required to evaluate physiological efficacies and toxicity of the combination treatment, our findings might provide a new insight into the development of novel combination therapies/chemoprevention against malignant tumors using dietary phytochemicals.



DHA alters expression of target proteins of cancer therapy in chemotherapy resistant SW620 colon cancer cells.
Slagsvold JE, Pettersen CH, Størvold GL, Follestad T, Krokan HE, Schønberg SA.
Norwegian University of Science and Technology, Trondheim, Norway.
Abstract
Diets rich in n-3 polyunsaturated fatty acids (PUFAs) have been associated with a reduced risk of several types of cancer. Recent reports have suggested that these PUFAs enhance the cytotoxic effect of cancer chemoradiotherapy. The effect of docosahexaenoic acid (DHA) on key cell cycle regulators and target proteins of cancer therapy was investigated in the human malign colon cancer cell line SW620. Cell cycle check point proteins such as p21 and stratifin (14-3-3 sigma) increased at mRNA and protein level, whereas cell cycle progression proteins such as cell division cycle 25 homolog and cyclin-dependent kinase 1 decreased after DHA treatment. Protein levels of inhibitors of apoptosis family members associated with chemotherapy resistance and cancer malignancy, survivin and livin, decreased after the same treatment: likewise the expression of NF-kappaB. Levels of the proapoptotic proteins phosphorylated p38 MAPK and growth arrest-inducible and DNA damage-inducible gene 153/C/EBP-homologous protein (CHOP) increased. The results indicate that DHA treatment causes simultaneous cell cycle arrest in both the G1 and G2 phase. In conclusion, DHA affects several target proteins of chemotherapy in a favorable way. This may explain the observed enhanced chemosensitivity in cancer cells supplemented with n-3 PUFAs and encourage further studies investigating the role of n-3 PUFAs as adjuvant to chemotherapy and radiotherapy in vivo.
PMID: 20574922


Apoptosis. 2005 Mar;10(2):359-68.
alpha-Lipoic acid induces apoptosis in human colon cancer cells by increasing mitochondrial respiration with a concomitant O2-*-generation.
Wenzel U, Nickel A, Daniel H.
Molecular Nutrition Unit, Department of Food and Nutrition, Technical University of Munich, Hochfeldweg 2, D-85350, Freising, FRG. uwenzel@wzw.tum.de
Abstract
The antioxidant alpha-lipoic acid (ALA) has been shown to affect a variety of biological processes associated with oxidative stress including cancer. We determined in HT-29 human colon cancer cells whether ALA is able to affect apoptosis, as an important parameter disregulated in tumour development. Exposure of cells to ALA or its reduced form dihydrolipoic acid (DHLA) for 24 h dose dependently increased caspase-3-like activity and was associated with DNA-fragmentation. DHLA but not ALA was able to scavenge cytosolic O2-* in HT-29 cells whereas both compounds increased O2-*-generation inside mitochondria.

Increased mitochondrial O2-*-production was preceded by an increased influx of lactate or pyruvate into mitochondria and resulted in the down-regulation of the anti-apoptotic protein bcl-X(L). Mitochondrial O2-*-generation and apoptosis induced by ALA and DHLA could be prevented by the O2-*-scavenger benzoquinone. Moreover, when the lactate/pyruvate transporter was inhibited by 5-nitro-2-(3-phenylpropylamino) benzoate, ALA- and DHLA-induced mitochondrial ROS-production and apoptosis were blocked. In contrast to HT-29 cells, no apoptosis was observed in non-transformed human colonocytes in response to ALA or DHLA addition.

In conclusion, our study provides evidence that ALA and DHLA can effectively induce apoptosis in human colon cancer cells by a prooxidant mechanism that is initiated by an increased uptake of oxidizable substrates into mitochondria.
PMID: 15843897
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BuddhaGirl Donating Member (1000+ posts) Send PM | Profile | Ignore Sun Sep-12-10 04:41 PM
Response to Reply #3
5. great info - thanks!
n/t
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HysteryDiagnosis Donating Member (1000+ posts) Send PM | Profile | Ignore Sun Sep-12-10 05:59 PM
Response to Reply #5
6. Then there's this... but you can't trust them people "over there".

http://www.jacn.org/cgi/content/full/24/1/16


In another study, thirty-two ‘high risk’ breast cancer patients, aged 32–81 years, were given adjuvant nutritional intervention (a combination of Vitamins C, E, beta-carotene, Selenium, essential fatty acids and Coenzyme Q10) and followed for 18 months <25>. None of the patients died during the study period or showed signs of distant metastases. The quality of life of these patients was improved and six patients showed apparent partial remission. Antioxidant supplementation (beta-carotene 45 mg, alpha-tocopherol 825 mg and ascorbic acid 450 mg daily for three weeks) before conditioning therapy in bone marrow transplant patients led to no difference in relapse rates <26>. In another study with 65 patients of bladder carcinoma treated with BCG immunotherapy, supplementation with mega-dose combination of vitamin A (40,000 units), vitamin B6 (100 mg), vitamin C (2000 mg), vitamin E (400 units) and Zinc (90 mg) led to decreased recurrence rates at 10 months of follow up (40% vs. 80%) compared to patients receiving RDA values of these agents <27>. These variations in clinical studies may be due to differences in doses, type and number of antioxidants. Therefore, it is essential to define the optimal number, type and dose of antioxidants for a maximal benefit when used as an adjunct to standard therapy.

Pre-clinical data showed that antioxidant vitamins reduce the frequency and severity of toxicity associated with (x)-irradiation and chemotherapeutic agents. For instance, vitamin E has been shown to decrease adriamycin-induced toxicity in rabbits <28>; vitamin E in combination with pentoxifyllin has been reported to significantly regress the radiation-induced fibrosis <29>. In the current study, however, no such protection was seen when we used paclitaxel and carboplatin. It would thus appear that the protective effect of antioxidants on normal cells might not be against all anticancer agents.

There are certain limitations in the present study that should be considered while interpreting the findings. The antioxidants (beta carotene, vitamin E and vitamin C) could not be used in their biologically active forms due to constraints of commercial availability. For example, the 9-cis isomer of beta-carotene found in natural preparations may be a more potent antioxidant <30> compared to the all-trans isomer used by us. Similarly, d-{alpha}-tocopherol succinate is considered more active form than the synthetic form (dl)-alpha-tocopherol succinate used by us <31>. Thus, there is a possibility that the results might improve if more active forms of antioxidant vitamins are used. Also, the antioxidant preparation used by us contained other compounds like copper sulfate, manganese sulfate, zinc sulfate and selenium, which might have affected the results. For instance, selenium has its own antioxidant properties, which might have confounded the results <32>. Another limitation of the present study is that the serum levels of the antioxidants were not estimated. In order to establish an optimal dose response relationship, it is essential that future studies utilizing antioxidant preparations be based on pharmacokinetic data.

Large-scale phase III clinical trials in relatively homogeneous patient populations receiving well-specified conventional treatment regimen alone and in combination with high-dose multiple antioxidants are needed to clarify the true potential of antioxidants in the management of human malignancies.


CONCLUSION
TOP
FOOTNOTES
ABSTRACT
INTRODUCTION
PATIENTS AND METHODS
RESULTS
CONCLUSION
ACKNOWLEDGMENTS
REFERENCES

In conclusion, antioxidant supplementation during paclitaxel/carboplatin containing chemotherapy in NSCLC appears to be safe and the results of the present study do not support the hypothesis that antioxidant vitamins could compromise the efficacy of standard chemotherapy. There is a possibility that these agents could be potentially useful in the management of NSCLC. Larger controlled trials are required to ascertain their exact role.
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BuddhaGirl Donating Member (1000+ posts) Send PM | Profile | Ignore Sun Sep-12-10 04:39 PM
Response to Reply #1
4. Dean Edell is extremely biased against the benefits of vitamins
just an FYI -
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HuckleB Donating Member (1000+ posts) Send PM | Profile | Ignore Sun Sep-12-10 10:46 PM
Response to Reply #1
7. It's good to know that at least one of the TV docs is looking at actual research.
Even if it's only some of the time.
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yellerpup Donating Member (1000+ posts) Send PM | Profile | Ignore Sun Sep-12-10 03:05 PM
Response to Original message
2. It is always better to get as many of your vitamins
as possible from the food you eat. There are foods that can protect you from cancer, such as leafy greens coming from the cabbage family such as bok choy, brocolli, collard greens, kale, and chard. Bok Choy along with tomatoes, flounder, artichokes also can prevent blood vessels from developing to feed tumors. Oatmeal and whole grains are protective of the colon. All of the elements of nutrition come into play, including herbs and spices. A vitamin pill might not be much help if you are eating junk food every day. If you take vitamins to supplement to a diet of wholesome food, then the vitamin may have a better chance of making a difference.
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