[Tom]

Just me again. In a brief moment of clarity, I found the original article, and the link is posted below, as well as the body of text:

http://www.thehormoneshop.com/ip6.htm#Beneficial Effects of IP6 and Inositol

What is IP6 (Inositol Hexaphosphate)?
Possesses Broad Range of Bioactivities
Most abundantly found in rice bran, above all other cereals.
Long used as safe natural antioxidant in various food products in Japan.
In Japan it is known to remove active oxygen in the body, suppressing lipid peroxide production and absorbs excess iron ions, having an effect on heart disease, liver dysfunction, dermatitis and other pathologic conditions caused thereby.
In Japan it is known further to prevent kidney stone formation and cholesterol deposition.
In Japan there have recently been, an increasing number of papers available concerning its immunity-enhancing and anticancer actions.



Beneficial Effects of IP6 and Inositol


The symposium started with a discussion of chemistry and usage of rice
components. S. Ogawa (Keio University) presented an impressive overview
of chemical structures and uses of myo-inositol and its related
compounds. T. Osawa (Nagoya University) discussed the protective role of rice
antioxidants in oxidative stress and Y. Watanabe (Ehime University, Matsuyama)
reviewed the synthesis of inositol triphosphate and phospholipids.


A large portion of the symposium was devoted to IP6 and its parent
molecule, inositol. It is difficult to summarize all the studies
presented at the conference. This article will touch upon major
findings of relevance to disease prevention and treatment.

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Cancer


Let's consider the advances against cancer. A renowned epidemiologist
reviewed studies linking diet and life style to cancer (S.Sugano, Cancer
Institute, Tokyo). It's been known for sometime that consumption of whole
grains, vegetables and fruits is linked to reduced cancer risk. These foods
are rich in fiber which has been shown to protect against both colonic and
mammary cancer (reviewed by B.S. Reddy and L. A. Cohen, American Health
Foundation, New York). However, as it became apparent at the symposium, fiber
is not the sole anticarcinogen since other substances in fiber-containing
foods also exert protective influences on cancer. Thus, a multinational
epidemiologic study carried out in the mid 1980's had shown that foods rich in
phytate (IP6) but poor in fiber, such as cereals and grains, correlated better
with reduced risk of colon cancer than phytate-poor fiber foods such as fruits
and vegetables (Graf and Eaton, Cancer 1985; 56:717-718). IP6 is a strong
chelating agent and certain metals are known to promote cancer through
generationof reactive free radicals from oxidation of fats. IP6 also plays an
important role in regulating cell proliferation and differentiation.


In 1988, the first two studies were published, reporting inhibitory
effects of purified IP6 on tumor formation in experimental animals. One
study (Shamsuddin et al. Carcinogenesis 9:577-80) showed suppression of
cancer of the large bowel by IP6 and theother study (Jariwalla et al.
Nutr. Res. 8: 813-27) demonstrated reduction of the incidence and size
of soft-tissue tumors (fibrosarcomas) promoted by dietary factors.
Since then, a number of experimental studies have confirmed the
anti-cancer action of IP6 (reviewed by I. Vucenik and A.K.M. Shamsuddin, Univ.
of Maryland, Baltimore). The compound has been shown to inhibit various
rodent and human cancer cell lines in vitro and to protect against growth of
diverse cancers in vivo. Protective effects have been seen against cancers of
the breast, colon, pancreas, liver, skin and connective tissue. In vivo,IP6
not only prevents carcinogen-induced tumor development but it also interferes
with growth of pre-formed, transplanted tumors, suggesting that it may play a
role in both cancer prevention and treatment.


The step at which IP6 acts during tumor development varies depending
upon the type of cancer studied. In colon carcinogenesis, IP6 was shown to
suppress bowel cancer when given before, during and even several months after
carcinogen administration (Shamsuddin and colleagues, Univ. of Maryland).In
a multi-organ rat carcinogenesis model, IP6 administered (as phytic acid)
during the promotion stage suppressed hepatic tumors but had no influence on
development of esophagal, colonic, pancreatic, renal and thyroid tumor lesions
(M. Hirose, National Institute of Health Sciences, Tokyo). In a
two-stage model of carcinogenesis in mouse skin, IP6 inhibited tumor
formation when given during the initiation stage but not during tumor
promotion, indicating differential sensitivity of skin cancer (T. Ishikawa,
Univ. of Tokyo). Clinical studies in humans against different tumor types
would be useful. Awaiting such studies,
what can be said presently is that naturally-occurring salt forms of IP6
appear to be safe in animal studies even when used at higher than
physiologic dosages.


The role of myo-inositol as a chemopreventive agent was also discussed.
It is another phytochemical with low toxicity and ability to inhibit
carcinogenesis in various organs which include mammary gland, colon and
lung. In studies evaluating its chemopreventive activity in lung
carcinogenesis (L. W. Wattenberg, Univ. of Minneapolis, Minnesota), it
was reported that myo-inositol has unusual properties, manifesting a
capacity to prevent lung cancer when given during separate phases of the
carcinogenic process as well as throughout the entire course of the process.
When administered throughout the carcinogenic process, it's effects were found
to be additive. Another study reported on suppression of liver cancer by oral
administration of myo-inositol, thus adding to the diverse spectrum of tumors
affected by this naturally-derived plant constituent (H. Nishino, Kyoto Prefectual
University of Medicine). Myo-inositol has also been reported to enhance the
anti-cancer action of IP6 in other animal studies.

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Mechanism of Cancer Suppression
The mechanism by which IP6 or myo-inositol exert chemopreventive and
anti-cancer effects is not completely understood. IP6 is rapidly
absorbed by cells (in vitro and in vivo) and metabolized to lower
phosphates and inositol (reviewed by Shamsuddin). It has been suggested
that lower inositol phosphates may mediate cancer inhibition, although
direct evidence for this is lacking. Both IP6 and its lower phosphates have
metal chelating activity and may interfere with tumor formation by suppressing
metal catalyzed oxidation of fats. Alternatively, IP6 may block the activity
of key enzyme(s) affecting cell proliferation. One enzyme candidate is PI-3
kinase which plays a central role in signal transduction and cell
transformation triggered by growth factor or tumor promoter. IP6 has been
reported to inhibit PI-3 kinase activity in vitro (Z. Dong, Univ. of
Minnesota, Austin). While this enzyme inhibition may explain the
chemopreventive effect of IP6, it is not known whether it mediates IP6's
effect on pre-existing tumors or
established cancer cells. Other, as yet, unknown mechanism may be
involved in the anti-cancer effect of IP6.