Inositol Hexaphosphate is derived from rice bran. Inositol is an essential component of cell membranes and plays an important role in cell growth and cellular function.
Recent research is showing that IP-6 might help:
- Fight cancer, possibly even shrinking tumor cells in some situations
- With diabetics
- Boost the immune system
- Prevent kidney and bladder stones
- Have a cardiovascular protective effect
The theory behind its anticancer properties is:
Since all cancers, irrespective of their type and origin, have a common defect of uncontrolled cell proliferation, and, since IP-3 is a key regulator of cell growth, and IP-6 & Inositol yield IP-3; therefore, IP-6 & Inositol should be effective against many different types of cancers across all species
In addition to reducing cell proliferation, IP6 increases differentiation of malignant cells, often resulting in a reversion to normal phenotype. Orally administered IP6 is rapidly taken into the cells and dephosphorylated to lower-phosphate inositol phosphates, which further interfere with signal transduction pathways and cell cycle arrest. Enhanced immunity and antioxidant properties can also contribute to tumor cell destruction. However, the molecular mechanisms underlying this anticancer action are not fully understood. Because it is abundantly present in regular diet, efficiently absorbed from the gastrointestinal tract, and safe, IP6 holds great promise in strategies for the prevention and treatment of cancer. IP6 enhances the anticancer effect of conventional chemotherapy, controls cancer metastases, and improves the quality of life.
IP-6 has been reported to have in vivo and in vitro anti- cancer activity against numerous tumors, such as colon cancer, prostate cancer, breast cancer, liver cancer, chronic myeloid leukemia, pancreatic cancer, and rhabdomyosarcomas.
IP6 has been introduced by mouth, by injection directly into tumors, intramuscular injection, intraperitoneal injection, etc. And regardless of how IP6 was given, it consistently had the same effects, whether it was tested on a colon-cancer model, a breast-cancer model, smooth-muscle cells, skeletal muscle tumors, liver cancers, etc.
In addition to animal studies, there are several human studies that have shown that IP6 inhibits growth of human prostate cancer cells and adenocarcinoma. Scientists have observed that cancer cells can revert back to normal cells in the presence of IP6. It should be pointed out that most of the research has been done with animals; in order for IP6 to gain greater support by the medical community, more human trials are needed.
Breast cancer
IP6 inhibits the growth of breast cancer cells; but it also acts synergistically with adriamycin or tamoxifen, being particularly effective against estrogen responsive alpha-negative cells and adriamycin-resistant cell lines.
Patients with invasive ductal breast cancer where polychemotherapy was indicated were monitored. Fourteen patients in the same stage of ductal invasive breast cancer were involved in the study, divided in two randomized groups. One group took IP6 + Inositol in the form of powder in the daily dosage of 6 g, divided in 2 doses, starting from the first postoperative day, every day until the end of treatment (6 months), while the other group took placebo. Patients receiving chemotherapy, along with IP6 + Inositol did not have cytopenia, drop in leukocyte and platelet counts. Red blood cell counts and tumor markers were unaltered in both groups. However, patients who took IP6 + Inositol had significantly better quality of life and functional status and were able to perform their daily activities. J Exp Clin Cancer Res. 2010. Efficacy of IP6 + inositol in the treatment of breast cancer patients receiving chemotherapy: prospective, randomized, pilot clinical study. Bacić I, Druzijanić N. Department of Surgery, General Hospital Zadar, Zadar, Croatia.
Pancreatic cancer benefit
Inositol hexaphosphate: a novel treatment for pancreatic cancer.
J Surg Res. 2005. Johnson VA Medical Center, Clarksburg, West Virginia; Department of Surgery, West Virginia University, Morgantown, West Virginia, USA.
Inositol hexaphosphate (IP6) is a naturally occurring polyphosphorylated carbohydrate found in food sources high in fiber content. IP6 has been reported to have significant inhibitory effects against a variety of primary tumors including breast and colon. The effects of IP6 have not been evaluated in pancreatic cancer. We hypothesized that IP6 would significantly inhibit cell growth and increase the apoptotic rate of pancreatic cancer in vitro. Treatment of pancreatic cancer with the common dietary polyphosphorylated carbohydrate IP6 significantly decreased cellular growth and increased apoptosis. Our findings suggest that IP6 has the potential to become an effective adjunct for pancreatic cancer treatment. Further in vivo and human studies are needed to evaluate safety and clinical utility of this agent in patients with pancreatic cancer.
Prostate cancer and inositol hexaphosphate IP6 : efficacy and mechanisms.Anticancer Res. 2005.
Department of Pharmaceutical Sciences, School of Pharmacy, University of Colorado Health Sciences Center, Denver, CO, USA.
Inositol hexaphosphate is a major constituent of most cereals, legumes, nuts, oil seeds and soybean. Taken orally as an over-the-counter dietary/nutrient supplement, and is recognised as offering several health benefits without any known toxicity. In vitro anticancer efficacy of IP6 has been observed in many human, mouse and rat prostate cancer cells. Completed studies also show that oral feeding of IP6 inhibits human prostate cancer xenograft growth in nude mice without toxicity. In a recently completed pilot study, we observed similar preventive effects of IP6 on prostate tumorigenesis in the TRAMP model. Mechanistic studies indicate that IP6 targets mitogenic and survival signaling, as well as cell cycle progression, in prostate cancer cells. IP6 is also shown to target molecular events associated with angiogenesis. Moreover, IP6 has pleiotropic molecular targets for its overall efficacy against prostate cancer and, therefore, could be a suitable candidate agent for preventive intervention of this malignancy in humans.
Rhabdomyosarcoma
Novel anticancer function of inositol hexaphosphate IP6 : inhibition of human rhabdomyosarcoma in vitro and in vivo.
Anticancer Res. 1998.
The objective of this study was to investigate whether IP6 inhibits growth of rhabdomyosarcoma, a tumor of mesenchymal origin, which is the most common soft tissue sarcoma in children. Our results show that IP6 suppresses growth of rhabdomyosarcoma cell line (RD) in vitro in a dose-dependent fashion. However, the removal of IP6 from the media, after 72 hours of treatment, allowed cells to recover their logarithmic growth. Exposure of RD cells to IP6 led to differentiation; cells became larger with abundant cytoplasm, expressing higher levels of muscle-specific actin. Consistent with in vitro observation, IP6 suppressed rhabdomyosarcoma cell growth in vivo, in a xenografted nude mice model. When compared to controls, IP6-treated mice produced a 25 fold smaller tumors, as observed after a two weeks treatment. In a second experiment, wherein the treatment period was extended to five weeks, a 49 fold reduction in tumor size was observed in mice treated with IP6. Histologically no evidence of tumor cell necrosis was observed.
IP6: a novel anti-cancer agent.
Source
University of Maryland School of Medicine, Baltimore 21201-1192, U.S.A.
Inositol hexaphosphate (InsP6 or IP6) ubiquitous in plants and animals
is not only a natural antioxidant, but may also be the precursor/storage
of intracellular inositol phosphates, important for various cellular
functions. A novel anti-tumor action of InsP6 was demonstrated in models
of experimental colon and mammary carcinogenesis in vivo. We now show
its effects on growth and differentiation of HT-29 human colon carcinoma
cells in vitro. A dose- and time-dependent (0.33-20 mM InsP6 and 1-6
days treatment) growth inhibition was observed as tested by MTT-
incorporation assay. The inhibition was statistically significant (p
< 0.05) at 1 mM concentration as early as first day after treatment
and continued up to 6 days. DNA-synthesis was also suppressed by InsP6
and significantly inhibited as early as 6 h after treatment at 1 mM
concentration (p < 0.05) and continued to 48 h (p < 0.01). The
expression of proliferation marker PCNA was down-regulated (p < 0.05)
by InsP6 (1 and 5 mM) after 48 h of treatment. To investigate the
mechanism of action of InsP6 the intracellular phosphatases (including
phytase) were inhibited by F to slow down the dephosphorylation of
InsP6. Ion-exchange chromatographic separation of intracellular inositol
phosphates demonstrated a 84-98% decrease of Ins, InsP1 and InsP2 InsP3
was reduced by 39% and InsP4 and InsP5 by 21% and 13% respectively,
whereas intracellular InsP6 was increased by 24.6% at 5 min following
3H-InsP6. Since neither the rate of uptake of 3H-InsP6 was unaffected,
nor was the efficacy of growth inhibition altered by F inhibition of
phytase, data suggest that contrary to the popular misconception,
phytase plays no role in influencing the anti-neoplastic action of
InsP6. Alkaline phosphatase activity (brush border enzyme, associated
with absorptive cell differentiation), increased following 1 and 5 mM
InsP6 treatment for 1-6 days. The expression of a mucin antigen
associated with goblet cell differentiation and defined by the
monoclonal antibody CMU10 was augmented (p < 0.0001) by InsP6. The
tumor mucin marker Gal-GalNAc, expressed by precancer and cancer of
colon, but not by the normal cells showed a time-dependent biphasic
change by InsP6; an increased expression after 1 day of treatment
followed by suppression after 2 days suggest progression of mucin
synthesis and differentiation of cancer cells with reversion to normal
phenotype. Because the tumor marker Gal-GalNAc is a) easily detected in
rectal mucin of patients with colonic cancer and precancer with high
sensitivity and specificity, and b) suppressed by InsP6 treatment, it
can be used to monitor the efficacy of chemoprevention by InsP6 or other
such agents. Since InsP6 a natúral dietary ingredient of cereals and
legumes, inhibits growth and induces terminal differentiation of HT-29
cancer cells, it is an excellent candidate for adjuvant chemotherapy and
prevention of cancer.
Inositol hexaphosphate (InsP6 or IP6) is ubiquitous. At 10 microM to 1 mM concentrations, IP6 and its lower phosphorylated forms (IP(1-5)) as well as inositol (Ins) are contained in most mammalian cells, wherein they are important in regulating vital cellular functions such as signal transduction, cell proliferation and differentiation. A striking anti-cancer action of IP6 has been demonstrated both in vivo and in vitro, which is based on the hypotheses that exogenously administered IP6 may be internalized, dephosphorylated to IP(1-5), and inhibit cell growth. There is additional evidence that Ins alone may further enhance the anti-cancer effect of IP6. Besides decreasing cellular proliferation, IP6 also causes differentiation of malignant cells often resulting in a reversion to normal phenotype. These data strongly point towards the involvement of signal transduction pathways, cell cycle regulatory genes, differentiation genes, oncogenes and perhaps, tumor suppressor genes in bringing about the observed anti-neoplastic action of IP6.
Inositol hexaphosphate (InsP6 or IP6) is ubiquitous. At 10 microM to 1 mM concentrations, IP6 and its lower phosphorylated forms (IP(1-5)) as well as inositol (Ins) are contained in most mammalian cells, wherein they are important in regulating vital cellular functions such as signal transduction, cell proliferation and differentiation. A striking anti-cancer action of IP6 has been demonstrated both in vivo and in vitro, which is based on the hypotheses that exogenously administered IP6 may be internalized, dephosphorylated to IP(1-5), and inhibit cell growth. There is additional evidence that Ins alone may further enhance the anti-cancer effect of IP6. Besides decreasing cellular proliferation, IP6 also causes differentiation of malignant cells often resulting in a reversion to normal phenotype. These data strongly point towards the involvement of signal transduction pathways, cell cycle regulatory genes, differentiation genes, oncogenes and perhaps, tumor suppressor genes in bringing about the observed anti-neoplastic action of IP6.
I give Lucy 1 capsule in her PM dinner.
