http://www.nutricentre.com/articlearchive/article.aspx?catid=0&aid=756

Inositol Hexaphosphate (IP6): Fiber-Derived Support for Mutagenic,
Cardiovascular and Immune Concerns

Kimberly Pryor
Dated: July 2005

We live in a delicate state of balance. Ironically, we depend on our
cells' ability to commit suicide in order for us to continue living.
This process is called apoptosis and it's the body's way of weeding out
once healthy cells that have turned cancerous. When our state of
balance is disrupted, the body loses its ability to block the malignant
transformation of normal cells by sentencing them to die before they
become cancerous.

Once a cell has become cancerous, it's virtually unheard of for it to
revisit its previous state of normalcy. However, a substance derived
from dietary fiber known as inositol hexaphosphate (IP6) or phytic
acid, forces malignant cells to revert to a non-cancerous state, a
phenomenon observed in human colon cancer cells and other cell lines.

Scientists discovered IP6's novel ability to turn back the clock on
cancer cells through looking at a tumor marker expressed on malignant
and premalignant cells. This marker, however, is absent on normal
cells. Following IP6 treatment of cancer cells, the tumor marker was
significantly suppressed, and in most IP6-treated cells the marker was
completely absent. IP6 also caused a decreased rate of cell
proliferation.[1-2] It also has been suggested that IP6 can regulate
heart rate and blood pressure and keep platelets from clumping
together.[3-6]

Dietary IP6
IP6 occurs in fiber-rich foodsparticularly cereals and wheat bran,
along with corn, soy beans, nuts (especially peanuts), oats, seeds and
rice. Scientists have recently discovered that IP6 is a powerful
antioxidant and cancer-modulating agent,[7-9] but when administered in
the diet, IP6 binds with proteins, forming insoluble complexes less
readily metabolized and absorbed compared to when it is taken alone. In
fact, one group of researchers stated: Thus, IP6, an active substance
responsible for cereal's beneficial anticancer effect, is clearly more
effective than 20 percent bran in the diet.... Intake of IP6 may be a
more pragmatic approach than gorging enormous quantities of fiber for
cancer prophylaxis.[10-11]

Proposed Anticancer Mechanisms
IP6 exerts its effects on the body by controlling cell division. IP6
reduces the rate of cellular proliferation, both in vivo and in vitro,
and has exhibited an ability to reduce DNA synthesis.[12-14]

Scientists have suggested that one way IP6 may exert this cellular
control is by interfering with mineral absorption, since iron and other
minerals are important in gene regulation.[15] Studies have shown a
possible link between excess iron and an increased risk of cancer in
animals and humans, particularly colon cancer.[16] IP6 has been shown
to interfere with iron absorption and reverse iron-dependent
augmentation of colorectal tumor initiation. IP6 also suppresses
iron-caused oxygen generation, and almost totally inhibits iron-caused
lipid peroxidation, the process where lipids turn rancid.[17-18]

A concern in this regard is the possibility that IP6 may deplete the
body's mineral stores. Yet, in numerous studies, researchers have noted
no significant differences in the level of serum or bone minerals in
rats, even after lengthy treatment with IP6 and inositol.[19]

AbulKalam Shamsuddin, MD, PhD, a researcher who has extensively studied
IP6 and the author of IP6: Nature's Revolutionary Cancer Fighter,
stated that Certainly, its [IP6's] hypothetical harm connected to
chelation is far less than that of other compounds of similar usage
(e.g., cancer chemotherapeutic and chemopreventive agents) and are far
outweighed by the plethora of benefits.[20]

The questions that arise in regard to IP6's ability to chelate minerals
suggest that other anticancer actions are at play. These actions
include boosting natural defense mechanisms through the augmentation of
natural killer (NK) cells that defend the body against tumor
initiation;[21] blocking PI-3 Kinase, an enzyme necessary for tumor
promotion;[22-23] altering cellular communication necessary for tumor
growth;[24-25] and stimulating tumor suppressor gene p53.[26] New
animal and cell culture experiments also have indicated that IP6 works
primarily by inhibiting metastases and blocking angiogenesis, the
process of forming new blood vessels that feed tumors.

Angiogenesis depends on the interaction between endothelial cells
(cells that line the blood vessel walls) and tumor cells. For
angiogenesis to occur, endothelial cells on the blood vessel walls must
multiply or proliferate. Consequently, Shamsuddin and colleagues
investigated IP6's effect on both endothelial and tumor cells.

During the in vitro experiment, IP6 inhibited the proliferation and
growth of endothelial cells. The combination of IP6 and an agent with
anti-angiogenic activity was even more powerful in reducing cell
growth. IP6 also inhibited the proliferation of endothelial cells
derived from human umbilical veins. In addition, IP6 significantly
reduced the action of a growth factor involved in vessel formation. In
human liver cancer cells, exposure to IP6 for eight and 24 hours
resulted in a dose-dependent inhibition of another growth factor
involved in vessel growth (vascular endothelial growth factor or VEGF).
Thus, IP(6) has an inhibitory effect on induced angiogenesis, the
researchers wrote.[27]

In two other studies, Shamsuddin and his fellow researchers also showed
that IP6 influences key events that stop the spread of cancer
cells.[28-29] These potential mechanisms of actions explain the outcome
of a number of studies showing IP6's anti-mutagenic potential in a
number of different cancers.

Colon Cancer
In 1988, Shamsuddin first reported in the journal Carcinogenesis the
stunning effect IP6 had on large intestinal cancer in rats. Researchers
fed 1 percent sodium inositol hexaphosphate (Na-IP6) to one group of
animals one week prior to inducing cancer, and to another group two
weeks after the last dose of a carcinogen was administered. Rats who
took the IP6-laced drinking water prior to carcinogen treatment
exhibited a 35 percent decrease in large intestinal cancer compared to
the control carcinogen group. The group fed IP6 after receiving the
carcinogen showed a similar reduction.[30]

Phytic acid (IP6) was also effective at reducing the incidence of colon
tumors in conjunction with a high-risk, high-fat diet. Colon tumor
incidence in carcinogen-treated rats plummeted from up to 70 percent in
the control groups to 30 percent in the groups fed a high-risk diet
(HRD) plus phytic acid (IP6).[31] IP6 may also increase its ability to
inhibit colon cancer when combined with green tea.[32]

Liver Cancer
In the January-March 2005 issue of the Asian Pacific Journal of Cancer
Prevention , researchers in Seoul, Korea investigated the effect of IP6
and/or inositol on liver cancer in mice. The researchers gave the
animals either inositol or IP6 or a combination of both, starting one
week prior to administration of a chemical carcinogen to induce liver
cancer.

Supplementation with IP6, inositol or both resulted in a significant
decrease in the size and the number of a precancerous marker for liver
cancer.[33] Patients suffering from Hepatocellular carcinoma (HCC), a
common liver cancer, usually have an extremely poor prognosis. In the
first of two experiments, Shamsuddin and colleagues compared the in
vitro effects of IP6 on HepG2, a human liver cancer cell line. Compared
to other cancer cell lines, HepG2 cells were extremely sensitive to
IP6, experiencing a dose-dependent, 50 percent inhibition of cell
growth. IP6 also weakened HepG2's ability to form colonies.

The sequel to the experiment demonstrated that IP6 regressed
pre-existing human liver cancer cells transplanted in mice back to
their normal, non-cancerous state, when IP6 was injected into the
transplanted tumor cells. In addition, the tumor weight in IP6-treated
mice was 86 percent to 1180 percent less than that in control
mice.[34-35]

Prostate Cancer
In the last several years, a number of in vitro and animal studies have
explored IP6's potential role in supporting a healthy prostate. In the
September-October 2004 issue of the journal Neoplasia , University of
Colorado researchers investigated the growth-inhibitory effect of IP6
in androgen-dependent human prostate carcinoma cells. IP6 treatment
strongly inhibited cancer cell growth and triggered apoptosis in the
cancer cells.

According to the researchers, whose 2003 study on IP6 and
androgen-independent prostate cancer also showed similar results, this
latest study using androgen-dependent prostate cancer cells indicates
IP6 has promise and potential to be effective against prostate
cancer.[36,37]

Breast Cancer
IP6 has been shown to inhibit carcinogenesis in all types of mammary
cancer cellsthose that require estrogen for growth and those whose
growth is independent of the female sex hormone. It accomplishes this
by inhibiting DNA synthesis and cell growth, and inducing
differentiation of the cancer cell lines.[38-40] IP6 also enhances the
anti-cancer effects of the drugs tamoxifen and adriamycin. In a study
published in 2003, Shamsuddin and colleagues investigated IP6's ability
to inhibit cancer growth in vitro in combination with adriamycin or
tamoxifen. The researchers tested the three substances against an
estrogen dependent human breast cancer cell line, an estrogen
independent human breast cancer cell line, and an adriamycin-resistant
breast cancer cell line.

After 96 hours of treatment, much lower concentrations of IP6 were
required to inhibit the growth of adriamycin-resistant breast cancer
cells than to inhibit the estrogen-dependent human breast cancer cells.
The estrogen independent human breast cancer cells were also highly
sensitive to IP6. Cancer growth was markedly suppressed when IP6 was
administered prior to the addition of adriamycin. This inhibition of
cancer cell growth was especially notable in the estrogen-dependent
breast cancer cells. In all three cell lines studied, IP6 acted
synergistically with tamoxifen.

According to the researchers, Our data not only confirm that IP6 alone
inhibits the growth of breast cancer cells, but it also acts
synergistically with adriamycin or tamoxifen and is particularly
effective against estrogen-independent breast cancer cells and
adriamycin-resistant cells.[41]

Leukemia
In a study published in 2002, researchers analyzed IP6's effects on
human leukemia cell lines and leukemia cells originating in bone
marrow. IP6 dose-dependently triggered cancer cell death in all of the
leukemia cell lines tested. IP6 exposure caused an extensive down
modulation of genes involved in leukemia development and an
upregulation of genes that inhibited leukemia's cell cycle. IP6
treatment of fresh bone marrow samples where the leukemia cells
originated decreased proliferation of the cancerous cells, but had no
effect on the normal bone marrow specimens. Taken together, our results
confirm the antiproliferative activity of IP6, wrote the researchers,
and suggest that it may have a specific antitumour effect also in
chronic myeloid leukemias, via active gene modulation.[42]

Skin Cancer
When we first reported on IP6 in 2000, a study of mouse skin cancer
indicated that IP6 prevented skin papillomas when given during cancer
initiation. After initiation however, IP6 exerted little effect.[43]
Since then, a study published in 2003 showed that topical application
of IP6 to the skin of mice with induced skin cancer had a dramatic
effect. Topical IP6 inhibited skin tumor development significantly in a
dose-dependent manner.[44]

Lung Cancer and Asbestos-Induced Fibrosis
Scientists have also received positive results with IP6 in regards to
lung cancer and asbestos-induced fibrosis and carcinoma. Studies have
shown that fibrosarcoma cells in mice treated with IP6 resulted in a
significant inhibition of tumor and size as well as improvement of
survival over the untreated controls. In addition, IP6 treatment of
mice with experimental lung metastasis resulted in a significant
reduction in the number of metastatic lung colonies.[45]

Due to its antioxidant properties and its ability to chelate iron, in
another study IP6 diminished the asbestos-induced oxidative damage that
results in inflammation and fibrosis in the lungs of exposed animals,
from six- to 30-fold less than in control groups.[46]

Rhabdomyosarcoma
IP6 has suppressed the growth of rhabdomyosarcoma, the most common soft
tissue sarcoma in children. Cell line growth was reduced by 50 percent
in vitro in a dose-dependent fashion. After two weeks, IP6-treated mice
experienced 25-fold smaller tumors and a 49-fold reduction in tumor
size after five weeks.[47]

Kidney Stones, Platelet Aggregation, Heart Attacks and HIV
IP6 has been shown to support a number of other conditions. Researchers
at the Harvard Medical School and Massachusetts General Hospital in
Boston successfully used pure Na-InsP6 to treat idiopathic
hypercalciuria, which is associated with a high incidence of kidney
stones.[48]

Other research points to IP6's usefulness in preventing platelet
aggregation (sticky platelets), a prime cause of heart attacks and
strokes. In one in vitro study by the same researchers, stickiness was
induced in human whole blood taken from healthy volunteers. IP6 reduced
clotting by 50 percent, or eliminated it altogether.[49]

IP6's role may also extend to controlling the damage inflicted upon the
myocardium (heart muscle) during heart attacks. After a heart attack,
doctors reperfuse (fill) the heart area with oxygenated blood. This
poses its own set of risks, because the oxygen can churn out free
radicals, damaging the blood vessels and heart muscle. Researchers
successfully used IP6 to protect the heart muscle from superoxide
damage during reperfusion.[50-51]

As more studies unfold, additional properties of IP6 have been
revealed. Otake and colleagues demonstrated that IP6 inhibited the cell
destruction induced by HIV as well as the HIV specific antigen
expression.[52]

Synergistic Effect
In his book, IP6: Nature's Revolutionary Cancer Fighter, Shamsuddin,
calls IP6 combined with inositol, an anticancer cocktail. IP6 combined
with inositol exerts an even more powerful suppression of cell
proliferation and colorectal cancer than with either agent alone. This
potent cocktail has also been used to suppress carcinogenesis in
mammary and metastatic tumor models.[53]

Shamsuddin and colleagues wrote in an IP6 review published in the
November 2003 Journal of Nutrition. The data strongly argue for the use
of IP6 plus inositol in our strategies for cancer prevention and
treatment.

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