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Victor C.
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   Posted 4/17/2001 4:56 AM (GMT -4)    Quote This PostAlert An Admin About This Post.
Inositol Hexaphosphate appears to be used by some as an iron chelating agent. Is there any experience on its use among the readers here? If you took it or take it currently, has it lowered Hemoglobin values?

::An iron chelating agent will only remove free iron (and many other minerals, since there are no pure one-element chelating agents). It will not generally lower hemoglobin.
Futhermore, while inositol hexaphosphate (phytic acid) combines with iron and prevents its absorption to that extent in the digestive tract, it has no effect on iron which is already absorbed.::

Any other information on its useful/uselessness?

::It will also inhibits absorption of many other useful minerals such as calcium, zinc, selenium, etc so its use for preventing iron absorption is very limited at best. The best way by far to lower systemic iron is to give blood 2-3 times per year. This will cause any excess iron to be taken up and made into hemoglobin from where it does not produce free radicals.::
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judy
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   Posted 4/17/2001 7:08 PM (GMT -4)    Quote This PostAlert An Admin About This Post.
Tom,

Reading the above: 1) is it unadvisable to take inositol hexaphosphate as in IP 6 due to its inhibiting the absorption of minerals? 2) What is the difference between inositol and inositol hexaphosphate? 3) Does inositol inhibit the absorption of minerals too?

::The amount of IP6 taken in supplements is quite small compared with the amounts which might be consumed in cereal brans, and will likely have little impact on minerals. However, if you are concerned it is best to consume the IP6 supplement separately from meals and mineral supplements.
Inositol is the basic chemical from which IP6 is built (there are IP1 - IP5 also), but by itself it does not inhibit mineral absorption.::


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Victor C.
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   Posted 4/18/2001 5:11 AM (GMT -4)    Quote This PostAlert An Admin About This Post.
The directions state to take it on an empty stomach, with no other materials (supplements or food). The Jarrow brand of IP6 also contains magnesium and calcium.

::That seems rather foolish since they will tend to combine with the IP6 and form unabsorbable residues.::

does taking it alone - and perhaps an hour later food and/or supplements resolve the issue?

::I am not sure what you are asking exactly. Any IP6 which combines with the magnesium and calcium will not be available to combine with iron, but without food there is no iron for it to combine with anyway.
What I have been trying to say is that IP6 is not an effective way to reduce dietary iron absorption, unless you take it with food (where the iron is) and also take supplements of all other things which it will absorb.::
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mikalra
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   Posted 4/21/2001 6:16 PM (GMT -4)    Quote This PostAlert An Admin About This Post.
All:

>Inositol Hexaphosphate appears to be used by some as an iron
>chelating agent....

>::Futhermore, while inositol hexaphosphate (phytic acid) combines with iron and prevents
>its absorption to that extent in the digestive tract, it
>has no effect on iron which is already absorbed.::

Evidence, tho limited, does exist for the use of IP6 as a systemic free iron chelator & hence antioxidant:

::The following abstract does not apply to what I was saying because it involves injection of IP6 rather then dietary intake. This forum is about Dietary Supplements not injectables. My objection was not that IP6 would not chelate free iron *if* it got into the blood, but that ingested IP6 would not get into the blood!::

Ann Thorac Surg 1991 Oct;52(4):908-12
Protection of ischemic heart from reperfusion injury by myo-inositol hexaphosphate, a natural antioxidant.
Rao PS, Liu XK, Das DK, Weinstein GS, Tyras DH.
Division of Cardiothoracic Surgery, Long Island Jewish Medical Center, New Hyde Park, New York

Myo-inositol hexaphosphate (phytic acid), a highly charged antioxidant, has been found to chelate metal ions such as iron and calcium and to scavenge hydroxyl radicals, .OH. This study examined the efficacy of this antioxidant and redox agent in attenuating myocardial reperfusion injury.

Sprague-Dawley rats were injected intravenously with three different doses of phytic acid (group 1, saline solution only, control; group 2, 1.5 mg/100 g; group 3, 7.5 mg/100 g; group 4, 15 mg/100 g) 30 minutes before excision of hearts. Isolated hearts were prepared by the Langendorff technique.

Global ischemia was induced for 30 minutes, followed by 30 minutes of reperfusion.

As expected, in group 1, reperfusion was associated with enhanced creatine kinase release, reduced coronary flow, poor recovery of ventricular function as evidenced by reduced left ventricular developed pressure and the first derivative of left ventricular pressure, and increased lipid peroxidation.

Groups 3 and 4, but not group 2, demonstrated myocardial protection as evidenced by reduced creatine kinase release, improved left ventricular function and coronary flow, and decreased lipid peroxidation compared with the control group.

These results suggest that potential use of this antioxidant in salvaging the heart from ischemic and reperfusion injury.
PMID: 1929656

::While the following abstract suggests that IP6 is a good antioxidant and a valuable addition to the diet, it says nothing about chelation of free systemic iron.::

J Biol Chem 1987 Aug 25;262(24):11647-50
Phytic acid. A natural antioxidant.
Graf E, Empson KL, Eaton JW.

The catalysis by iron of radical formation and subsequent oxidative damage has been well documented.

Although many iron-chelating agents potentiate reactive oxygen formation and lipid peroxidation, phytic acid (abundant in edible legumes, cereals, and seeds) forms an iron chelate which greatly accelerates Fe2 -mediated oxygen reduction yet blocks iron-driven hydroxyl radical generation and suppresses lipid peroxidation.

Furthermore, high concentrations of phytic acid prevent browning and putrefaction of various fruits and vegetables by inhibiting polyphenol oxidase.

These observations indicate an important antioxidant function for phytate in seeds during dormancy and suggest that phytate may be a substitute for presently employed preservatives, many of which pose potential health hazards.
PMID: 3040709

::Once again the IP6 administration in the following study was intravenous. Sure it is great for mixing with foods, but that was never in question.::

Toxicol Pathol 1995 Nov-Dec;23(6):689-95
Phytic acid, an iron chelator, attenuates pulmonary inflammation and fibrosis in rats after intratracheal instillation of asbestos.
Kamp DW, Israbian VA, Yeldandi AV, Panos RJ, Graceffa P, Weitzman SA.
Department of Medicine, Northwestern University Medical School, Chicago, Illinois 60611, USA.

Reactive oxygen species, especially iron-catalyzed hydroxyl radicals (.OH) are implicated in the pathogenesis of asbestos-induced pulmonary toxicity. We previously demonstrated that phytic acid, an iron chelator, reduces amosite asbestos-induced .OH generation, DNA strand break formation, and injury to cultured pulmonary epithelial cells (268[1995, Am. J. Physiol.(Lung Cell. Mol. Physiol.) 12:L471-480]).

To determine whether phytic acid diminishes pulmonaryinflammation and fibrosis in rats after a single intratracheal (it) instillation of amosite asbestos, Sprague-Dawley rats were given either saline (1 ml), amosite asbestos (5 mg; 1 ml saline), or amosite treated with phytic acid (500 microM) for 24 hr and then instilled. At various times after asbestos exposure, the rats were euthanized and the lungs were lavaged and examined histologically. A fibrosis score was determined from trichrome-stained specimens.

As compared to controls, asbestos elicited a significant pulmonary inflammatory response, as evidence by an increase (approximately 2-fold) in bronchoalveolar lavage (BAL) cell counts at 1 wk and the percentage of BAL neutrophils (PMNs) and giant cells at 2 wk (0.1 vs 6.5% and 1.3 vs 6.1%, respectively; p < 0.05). Asbestos significantly increased the fibrosis score at 2 wk (0 /- 0 vs 5 /- 1; p < 0.05). The inflammatory and fibrotic changes were, as expected, observed in the respiratory bronchioles and terminal alveolar duct bifurcations. The increased percentage of BAl PMNs and giant cells persisted at 4 wk, as did the fibrotic changes.

Compared to asbestos alone, phytic acid-treated asbestos elicited significantly less BAL PMNs (6.5 vs 1.0%; p < 0.05) and giant cells (6.1 vs 0.2%; p < 0.05) and caused significantly less fibrosis (5 vs 0.8; p < 0.05) 2 wk after exposure.

We conclude that asbestos causes pulmonary inflammation and fibrosis in rats after it instillation and that phytic acid reduces these effects.

These data support the role of iron-catalyzed free radicals in causing pulmonary toxicity from asbestos in vivo.
PMID: 8772254

Also, the binding of non-heme iron IN the GI is important to IP6s anticancer effects there, so even pre-absorption, the Fe-binding effects may be of benefit:

::This was already stated, but thanks for the abstract. ::

Mutat Res 1996 Feb 19;350(1):185-97
Dietary fiber and the chemopreventive modelation of colon carcinogenesis.
Alabaster O, Tang Z, Shivapurkar N.
Institute for Disease Prevention, George Washington University Medical Center, Washington DC, USA.

Comparative international epidemiological data indicate that the difference between the highest and lowest colon cancer incidence is approximately 10- fold. This suggests that the dominant causes of colon cancer are environmental rather than genetic in origin, with the dominant environmental cause being the typical diet of Western industrialized countries. Many epidemiological and experimental studies have suggested an important role for dietary fiber in the prevention of colon cancer. Using the Fischer-344 rat as the experimental model, data clearly demonstrate a strong protective effect of a diet that is low in fat, high in fiber and high in calcium (low-risk diet). Such a diet prevents the development of both preneoplastic aberrant crypt foci (ACF) and colon tumors. Recent experiments have also demonstrated a direct relationship between a ras point mutation in ACF at different stages of rat colon carcinogenesis, and a ras point
mutation that is subsequently present in colon tumors.

Using wheat bran as the model dietary fiber source, its effects were compared to the effects of psyllium, phytic acid, vitamin E, beta-carotene, folic acid, alone or in combination, for their ability to prevent colon cancer in rats on high-risk Western-style diets. Our studies clearly demonstrated the ability of wheat bran to reduce ACF and colon tumors in rats that consumed high-fat, Western-style diets.

Although phytic acid, which is a constituent of wheat bran, alone demonstrated strong cancer-preventive potential,

our experiments provided evidence for the cancer-preventive effect of the crude fiber fraction that is independent of the effect of phytic acid. The synergistic combination of wheat bran with the soluble fiber psyllium led to enhanced protection; while the combination of wheat bran with beta-carotene showed only an additive effect. Beta-carotene appeared to show higher protection than wheat bran at an intake level that is nutritionally relevant to humans, suggesting the possibility of using beta-carotene to enhance the effects of dietary fiber in high-risk Western populations. Using ACF as an intermediate endpoint, it was also shown that vitamin E and beta-carotene appear to inhibit progression of ACF to colon cancer, while wheat bran and folic acid appeared to have weak cancer-preventive potential at this late stage of carcinogenesis. In conclusion, wheat bran alone, or in combination with psyllium, appears to have greater potential to inhibit earlier phases of carcinogenesis, while beta-carotene and vitamin E may also inhibit later stages of carcinogenesis. Despite considerable epidemiological and experimental evidence that increasing the fiber and lowering the fat content of the Western diet could substantially reduce the risk of cancer and heart disease, the real challenge is to find effective ways to educate and motivate people to overcome their intrinsic cultural resistance to such changes in their eating habits.
PMID: 8657180


Proc Soc Exp Biol Med 1999 May;221(1):80-6
Dietary intrinsic phytate protects colon from lipid peroxidation in pigs with a moderately high dietary iron intake.
Porres JM, Stahl CH, Cheng WH, Fu Y, Roneker KR, Pond WG, Lei XG.
Department of Animal Science, Cornell University, Ithaca, New York 14853, USA.

High iron consumption has been proposed to relate to an increase in the risk of colon cancer, whereas high levels of supplemental sodium phytate effectively reduce iron-induced oxidative injury and reverse iron-dependent augmentation of colorectal tumorigenesis.

{This is the key point to supplement users, NB: I avoid dietary phytate, but supplement w/IP6}.

::This makes no sense unless you have something against other chemicals which come with food phytate sources since phytate and IP6 are chemically identical!::

However, the protective role of intrinsic dietary phytate has not been determined.

In this study, we examined the impact of removing phytate present in a corn-soy diet by supplemental microbial phytase on susceptibility of pigs to the oxidative stress caused by a moderately high dietary iron intake.

Thirty-two weanling pigs were fed the corn-soy diets containing two levels of iron (as ferrous sulfate, 80 or 750 mg/kg diet) and microbial phytase (as Natuphos, BASF, Mt. Olive, NJ, 0 or 1200 units/kg). Pigs fed the phytase-supplemented diets did not receive any inorganic phosphorus to ensure adequate degradation of phytate. After 4 months of feeding, liver, colon,
and colon mucosal scrapings were collected from four pigs in each of the four dietary groups.

Colonic lipid peroxidation, measured as thiobarbituric acid reacting substances (TBARS), was increased by both the high iron (P< 0.0008) and phytase (P< 0.04) supplementation.

Both TBARS and F2-isoprostanes, an in vivo marker of lipid peroxidation, in colonic mucosa were affected by dietary levels of iron (P< 0.03).

Mean hepatic TBARS in pigs fed the phytase-supplemented, high iron diet was 43%-65% higher than that of other groups although the differences were nonsignificant.

Moderately high dietary iron induced hepatic glutathione peroxidase activity (P= 0.06) and protein expression, but decreased catalase (P< 0.05) in the colonic mucosa.

In conclusion, intrinsic phytate in corn and soy was protective against lipid peroxidation in the colon associated with a moderately high level of dietary iron.
PMID: 10320635


Nutr Cancer 1993;19(1):11-9
Suppression of colonic cancer by dietary phytic acid.
Graf E, Eaton JW.
Tastemaker, Cincinnati, OH 45216.

Large differences exist between human populations in the frequency of colonic cancer. Epidemiological evidence indicates that these differences are strongly influenced by country of residence, and a negative correlation has been found between the fiber content of the diet and frequency of colonic cancer. This has prompted the hypothesis that high-fiber diets are in some way protective. However, reanalysis of the dietary data provides equally strong support for the hypothesis that

the protective element may be phytic acid (inositol hexaphosphate). This heat- and acid-stable substance is present in high concentration in many food items, including cereal grains, nuts, and seeds.

Phytic acid forms chelates with various metals and suppresses damaging iron-catalyzed redox reactions.

Inasmuch as colonic bacteria have been shown to produce oxygen radicals in appreciable amounts, dietary phytic acid might suppress oxidant damage to intestinal epithelium and neighboring cells.

Indeed, rapidly accumulating data from animal models indicate that dietary supplementation with phytic acid may provide substantial protection against experimentally induced colonic cancer. Should further investigations yield additional support for this hypothesis, purposeful amplification of dietary phytic acid content would represent a simple method for reducing the risk of colonic carcinogenesis.
Publication Types:
Review
Review, tutorial
PMID: 8383315

::In opposition to the evidence for the benefits of fiber including phytates for reducing colon cancer risk is the following recent study, so the benefit of phytate specifically for colon cancer prevention is currently somewhat in question.

N Engl J Med 2000 Apr 20;342(16):1156-62
Comment in:
N Engl J Med. 2000 Apr 20;342(16):1206-7
N Engl J Med. 2000 Sep 7;343(10):737; discussion 737-8
Lack of effect of a high-fiber cereal supplement on the recurrence of colorectal adenomas. Phoenix Colon Cancer Prevention Physicians Network.
Alberts DS, Martinez ME, Roe DJ, Guillen-Rodriguez JM, Marshall JR, van Leeuwen JB, Reid ME, Ritenbaugh C, Vargas PA, Bhattacharyya AB, Earnest DL, Sampliner RE.
Arizona Cancer Center, Department of Medicine, University of Arizona, Tucson 85724-5024, USA. dalberts@azcc.arizona.edu

BACKGROUND: The risks of colorectal cancer and adenoma, the precursor lesion, are believed to be influenced by dietary factors. Epidemiologic evidence that cereal fiber protects against colorectal cancer is equivocal. We conducted a randomized trial to determine whether dietary supplementation with wheat-bran fiber reduces the rate of recurrence of colorectal adenomas. METHODS: We randomly assigned 1429 men and women who were 40 to 80 years of age and who had had one or more histologically confirmed colorectal adenomas removed within three months before recruitment began to a supervised program of dietary supplementation with either high amounts (13.5 g per day) or low amounts (2 g per day) of wheat-bran fiber. The primary end point was the presence or absence of new adenomas at the time of follow-up colonoscopy. Subjects and physicians, including colonoscopists, were unaware of the group assignments.
RESULTS: Of the 1303 subjects who completed the study, 719 had been randomly assigned to the high-fiber group and 584 to the low-fiber group. The median times from randomization to the last follow-up colonoscopy were 34 months in the high-fiber group and 36 months in the low-fiber group. By the time of the last follow-up colonoscopy, at least one adenoma had been identified in 338 subjects in the high-fiber group (47.0 percent) and in 299 subjects in the low-fiber group (51.2 percent). The multivariate adjusted odds ratio for recurrent adenoma in tile high-fiber group, as compared with the low-fiber group, was 0.88 (95 percent confidence interval, 0.70 to 1.11; P=0.28), and the relative risk of recurrence according to the number of adenomas, in the high-fiber group as compared with the low-fiber group, was 0.99 (95 percent confidence interval, 0.71 to 1.36; P=0.93).
CONCLUSIONS: As used in this study, a dietary supplement of wheat-bran fiber does not protect against recurrent colorectal adenomas.
Publication Types:
Clinical trial
Multicenter study
Randomized controlled trial
PMID: 10770980::

Fenton reactions appear to be a major source of free radical production in feces:

Gut 2000 Feb;46(2):225-32
Generation of reactive oxygen species by the faecal matrix.
Owen RW, Spiegelhalder B, Bartsch H.
Division of Toxicology and Cancer Risk Factors, German Cancer Research Center, Im Neuenheimer Feld 280, D-69120 Heidelberg, Germany.

BACKGROUND: Reactive oxygen species are implicated in the aetiology of a range of human diseases and there is increasing interest in their role in the development of cancer. AIM: To develop a suitable method for the detection of reactive oxygen species produced by the faecal matrix. METHODS: A refined high performance liquid chromatography system for the detection of reactive oxygen species is described. RESULTS: The method allows baseline separation of the products of hydroxyl radical attack on salicylic acid in the hypoxanthine/xanthine oxidase system, namely 2,5-dihydroxybenzoic acid,
2,3-dihydroxybenzoic acid, and catechol. The increased efficiency and precision of the method has allowed a detailed evaluation of the dynamics of reactive oxygen species generation in the faecal matrix.

The data show that the faecal matrix is capable of generating reactive oxygen species in abundance.

This ability cannot be attributed to the bacteria present, but rather to a soluble component within the matrix.

As yet, the nature of this soluble factor is not entirely clear but is likely to be a reducing agent.

CONCLUSIONS: The soluble nature of the promoting factor renders it amenable to absorption, and circumstances may exist in which either it comes into contact with either free or chelated iron in the colonocyte, leading to direct attack on cellular DNA, or else it initiates lipid peroxidation processes whereby membrane polyunsaturated fatty acids are attacked by reactive oxygen species propagating chain reactions leading to the generation of promutagenic lesions such as etheno based DNA adducts.
PMID: 10644317

Free Radic Biol Med 1990;8(1):61-9
Antioxidant functions of phytic acid.
Graf E, Eaton JW.
Pillsbury Company, Technology Center, Minneapolis, MN 55414.

Phytic acid is a natural plant antioxidant constituting 1-5% of most cereals, nuts, legumes, oil seeds, pollen and spores.

By virtue of forming a unique iron chelate it suppresses iron-catalyzed oxidative reactions and may serve a potent antioxidant function in the preservation of seeds. By the same mechanism dietary phytic acid may lower the incidence of colonic cancer and protect against other inflammatory bowel diseases.

Its addition to foods inhibits lipid peroxidation and concomitant oxidative spoilage, such as discoloration, putrefaction, and syneresis.

A multitude of other industrial applications are based on the antioxidant function of phytic acid.
Publication Types:
Review
Review, tutorial
PMID: 2182395

Broader reviews:

Crit Rev Food Sci Nutr 1995 Nov;35(6):495-508
Phytic acid in health and disease.
Zhou JR, Erdman JW Jr.
Division of Nutritional Sciences, University of Illinois, Urbana 61801, USA.

Phytic acid (PA), a major phosphorus storage compound of most seeds and cereal grains, contributes about 1 to 7% of their dry weight. It may account for more than 70% of the total kernel phosphorus. PA has the strong ability to chelate multivalent metal ions, especially zinc, calcium, and iron. The binding can result in very insoluble salts that are poorly absorbed from the gastrointestinal tract, which results in poor bioavailability (BV) of minerals.

Alternatively, the ability of PA to chelate minerals has been reported to have some protective effects, such as decreasing iron-mediated colon cancer risk and lowering serum cholesterol and triglycerides in experimental animals.

**Data from human studies are still lacking.** ::Emphasis mine.::

PA is also considered to be a natural antioxidant and is **suggested** to have potential functions of reducing lipid peroxidation and as a preservative in foods.

Finally, certain inositol phosphates, which **may** be derived from PA, have been noted to have a function in second messenger transduction systems.

::Instead, they are mostly derived from inositol or lower inositol phosphates, IP1-IP5 which are also derived from inositol not IP6.::

The potential nutritional significance of PA is discussed in this review.
Publication Types:
Review
Review, academic
PMID: 8777015

Mol Cell Biochem 1996 Apr 12-26;157(1-2):229-32
Inositolpolyphosphates and their binding proteins--a short review.
Huisamen B, Lochner A.
Department of Medical Physiology and Biochemistry, Faculty of Medicine, University of Stellenbosch, Tygerberg; Republic of South Africa.

Since 1983, when it was discovered that inositol 1,4,5-trisphosphate can act as second messenger to release Ca2 from the endoplasmic reticulum, widespread research has focused on the phosphatidylinositol signalling transduction pathway and

**the host of inositolphosphates formed intracellularly after stimulation therof.**

Although the polyphosphates, inositoltetrakisphosphate (InsP4) and inositolhexakisphosphate (InsP6), have received their share of attention, a definite physiological role has not been ascribed to them as yet.

**Different binding proteins for these two polyphosphates have been demonstrated,**

::Emphasis mine. They are different chemicals and a value for IP4 or IP6 after formation by intracellular stimulation does not imply a value for ingestion of IP6.::

especially in brain tissue, indicating their possible importance in the cell.

InsP6 is known as one of natures most powerful antioxidants and has already been demonstrated to possess the abilities to be of use in the industry as well as in the medical profession.

As its natural actions are poorly understood and its possible side-effects have not been widely investigated, basic research regarding its cellular and subcellular activities is urgently called for.
Publication Types:
Review
Review, tutorial
PMID: 8739251


-Michael
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mikalra
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   Posted 4/26/2001 7:01 PM (GMT -4)    Quote This PostAlert An Admin About This Post.
All:

>>Inositol Hexaphosphate appears to be used by some as an iron
>>chelating agent....
>
>>::Futhermore, while inositol hexaphosphate (phytic acid) combines with iron and prevents
>>its absorption to that extent in the digestive tract, it
>>has no effect on iron which is already absorbed.::
>
>Evidence, tho limited, does exist for the use of IP6 as
>a systemic free iron chelator & hence antioxidant:
>
>::The following abstract does not apply to what I was saying
>because it involves injection of IP6 rather then dietary intake.
>This forum is about Dietary Supplements not injectables. My objection
>was not that IP6 would not chelate free iron *if*
>it got into the blood, but that ingested IP6 would
>not get into the blood!::

The fact that ingested IP6 prevents skin and mammary cancer:

Anticancer Res 1999 Sep-Oct;19(5A):3749-52
Inhibition of skin cancer by IP6 in vivo: initiation-promotion model.
Ishikawa T, Nakatsuru Y, Zarkovic M, Shamsuddin AM.
Department of Pathology, Faculty of Medicine, University of Tokyo, Japan.

A two-stage mouse skin carcinogenesis model was used to examine the effects of IP6 on initiation and promotion phases of tumorigenesis. Seven week old ICR female mice were divided into 6 groups, each consisting of 20 animals.

Initiation was performed by a single application of the carcinogen 7,12-dimethyl benz(a)anthracene (DMBA) (50 micrograms) to the back skin.

Three weeks later, local application of the promoter TPA was started (2.5 micrograms, 2 x/week) and continued up to the end of the experiment (22 weeks).

Mice were also administered 2% IP6 in drinking water over the entire duration of the experiment, or during the initiation (initial 3 weeks) or promotion (final 19 weeks) periods only.

The animals consuming IP6 during the initiation stage showed an approximately 50% reduction in the mean number of papillomas per animal, as well as in the number of tumor bearing mice.

However, no such inhibition was observed when IP6 was given during the tumor promotion stage.

In a separate experiment the effects of IP6 on epithelial cell growth were assessed by BrdU labeling at several time points. Statistically significant inhibition of cell proliferation was observed during the initiation stage (one week after DMBA treatment) in the group given IP6. No inhibition was evident during the promotion stage.
PMID: 10625952

Cancer Lett 1993 Dec 10;75(2):95-102
Inhibition of rat mammary carcinogenesis by inositol hexaphosphate (phytic acid). A pilot study.
Vucenik I, Sakamoto K, Bansal M, Shamsuddin AM.
Department of Medical and Research Technology, University of Maryland School of Medicine, Baltimore 21201-1192.

Since phytic acid (inositol hexaphosphate, InsP6) and inositol (Ins) have been demonstrated to have anti-tumor and anti-cell proliferative action in several experimental models of carcinogenesis, in a pilot study we have examined their effect on 7,12-dimethylbenz(a)anthracene (DMBA)-induced rat mammary tumor model.

Starting a week prior to induction with DMBA, the drinking water of female Sprague-Dawley rats was supplemented with either: 15 mM InsP6, 15 mM Ins, or 15 mM InsP6 15 mM Ins; a control group received no inositol compounds. Animals (55-day-old) were given a single dose of DMBA (20 mg) in 1 ml of sesame oil by oral intubation.

Four additional groups not receiving DMBA, but drinking tap water, InsP6, Ins, or InsP6 Ins of the same molarity as experimental groups were observed for the duration of the study to monitor for any putative toxicity following this long-term treatment.

As opposed to the DMBA-only group, rats treated with InsP6 /- Ins showed a 48% reduction in the number of tumors/tumor bearing animal (tumor multiplicity) and a 40% reduction in the number of tumors/rat. In contrast to 20% rats in DMBA-only group, only 0-8% animals in the treatment group had 5 or more tumors.

Likewise, the tumor incidence was reduced by 19% in InsP6 /- Ins as compared to control untreated animals. The tumors in the treated groups were also 16% smaller in size. Data from this pilot study suggest that in addition to being effective against colon cancer, InsP6 /- Ins may be protective against mammary carcinoma as well; additional studies are however warranted.
PMID: 8293426

... suggests to me that it is absorbed from the GI & distributed from there to the skin & breasts thru the blood.

::You have still missed the point! IP6 forms insoluble and unabsorbable compounds *when* it absorbs minerals in the intestines. That is how it inhibits mineral absorption. If/when it does so, it will not get into the body. Very little, if any IP6 taken with meals will get into the blood. Finally, these abstracts show an *effect* of dietary IP6, but they do not show that it either enters the body intact nor that it chelates iron there.::

>{This is the key point to supplement users, NB: I avoid
>dietary phytate, but supplement w/IP6}.
>
>::This makes no sense unless you have something against other chemicals
>which come with food phytate sources since phytate and IP6
>are chemically identical!::
>
>::In opposition to the evidence for the benefits of fiber including
>phytates for reducing colon cancer risk is the following recent
>study, so the benefit of phytate specifically for colon cancer
>prevention is currently somewhat in question.
>
>N Engl J Med 2000 Apr 20;342(16):1156-62
>Lack of effect of a high-fiber cereal supplement on the recurrence
>of colorectal adenomas ::

In answer to both of these objections, this study found supplemental IP6 superior to equal amounts of IP6 from wheat bran in preventing chemoinduced mammary cancer. Note that the dose of bran is a much higher % of the diet than 13.5 g in a human diet would be, & that much of the phytate would be insolubly bound to minerals in the meal, & thus not absorbed (my point above).

::The dosage given was 13.5 grams of wheat bran fiber not wheat bran itself. Since even crude wheat bran contains only 42.8% fiber (according to http://www.nal.usda.gov/fnic/cgi-bin/nut_search.pl ) this is equivalent to 31.5 grams of crude wheat bran which is a subtantial daily dose.::

Anticancer Res 1999 Sep-Oct;19(5A):3671-4
Nutr Cancer 1997;28(1):7-13
Comparison of pure inositol hexaphosphate and high-bran diet in the prevention of DMBA-induced rat mammary carcinogenesis.
Vucenik I, Yang GY, Shamsuddin AM.
Department of Medical and Research Technology, University of Maryland School of Medicine, Baltimore 21201, USA.

Inositol hexaphosphate (IP6), abundant in cereals and legumes, has been demonstrated to be a promising anticancer agent in different in vivo and in vitro models. Because IP6 is particularly abundant in the bran part of certain mature seeds such as wheat, we investigated whether a high-fiber bran diet containing high IP6 shows a dose-response inhibition of 7,12-dimethylbenz[a]anthracene (DMBA)-induced rat mammary carcinogenesis.

Starting at two weeks before DMBA intubation, rats were divided into five groups and fed AIN-76A diet only or AIN-76A diet containing 5%, 10%, or 20% Kelloggs All Bran; the fifth group received 0.4% IP6 given in drinking water, an amount equivalent to the IP6 content in 20% bran. After carcinogen administration, the rats remained on these regimens for 29 weeks.

Compared with the carcinogen control, at 29th week, tumor incidence was reduced by 16.7%, 14.6%, and 11.4% in rats fed 5%, 10%, and 20% bran, respectively (not statistically significant).

However, rats given 0.4% IP6 in drinking water, equivalent to that in 20% bran, had a 33.5% reduction in tumor incidence (p < 0.02) and 48.8% fewer tumors (p < 0.03).

These data show that supplemental dietary fiber in the form of bran exhibited a very modest, statistically nonsignificant inhibitory effect, which was also not dose dependent. In contrast, animals given IP6 showed significant reduction in tumor number, incidence, and multiplicity. Thus IP6 an active substance responsible for cereals beneficial anticancer effect, is clearly more effective than 20% bran in the diet. In practical terms, intake of IP6 may be a more pragmatic approach than gorging enormous quantities of fiber for cancer prophylaxis.

PMID: 9200144

::Once again your abstracts are largely irrelevant to what I was saying. I was not saying that insoluble fibers or IP6 are not beneficial. All that I was and am denying is that:
1) there is no evidence that IP6 chelates iron inside the body, and
2) the evidence that fiber it beneficial for colon cancer is somewhat equivocal.
FYI, I take eat high fiber foods and take IP6 as a supplement also. If I did not think they were beneficial, I would not be doing so.::

On a related point, Victor C said:

The directions state to take it on an empty stomach, with no other materials (supplements or food). The Jarrow brand of IP6 also contains magnesium and calcium.

Tom replied: That seems rather foolish since they will tend to combine with the IP6 and form unabsorbable residues. ... Any IP6 which combines with the magnesium and calcium will not be available to combine with iron, but without food there is no iron for it to combine with anyway.

AFAIK, all available IP6 supplements contain some Ca & Mg phytate salts. I buy IP6 as the powder, which is quite gritty for just the reason you mention, & have observed that it become significantly more soluble (& hence pleasant to drink) in ascorbic acid solution. I therefore expect that, if taken on an empty stomach, the stomach acidity should significantly liberate the phytate.

::Thats a good point. However, it is then a question of whether the metal ions would keep separate or again be absorbed (chelated) by the high metal ion affinity of the phytic acid (higher than ascorbic acid) in the less acidic conditions of the small intestine after leaving the stomach. I think it is here where mineral chelations in fact take place. Thus, the liberted phytic acid may well simply recombined with the liberated minerals in the small intestine.::

>Crit Rev Food Sci Nutr 1995 Nov;35(6):495-508
>Phytic acid in health and disease.
>Zhou JR, Erdman JW Jr.
>PMID: 8777015

>Alternatively, the ability of PA to chelate minerals has been reported
>to have some protective effects, such as decreasing iron-mediated colon
>cancer risk and lowering serum cholesterol and triglycerides in experimental
>animals.
>
>**Data from human studies are still lacking.** ::Emphasis mine.::

The same can be said for any other putative anti-cancer supplement, excepting Se and (sort of) I3C and lycopene.

>Finally, certain inositol phosphates, which **may** be derived from PA, have
>been noted to have a function in second messenger transduction
>systems.
>
>::Instead, they are mostly derived from inositol or lower inositol phosphates,
>IP1-IP5 which are also derived from inositol not IP6.::
>
>::... They are different chemicals and a value for IP4
>or IP6 after formation by intracellular stimulation does not imply
>a value for ingestion of IP6.::

This study, which I have not read, is referenced as indicating that IP6 rapidly elevates lower IPs, including IP3, in vitro:

Cole KE, Smith MS, Xu JF, Vucenik I, Shamsuddin AM. Modulation of the intracellular signal in human colon cancer cells by the anticancer agent inositol hexaphosphate. Anticancer Res. 1997 Nov-Dec;17(6A):4000.

As it APPEARS,from the above, to be systemically absorbed, the authors expectation that certain inositol phosphates ... may be derived from PA seems reasonable, tho I agree not proven. In any case, I did not intend to make any specific assertions re: intracellular signalling as a mechanism; I would in fact have snipped the sentences in question out, as not being relevant to the subject of my previous post, but I know that you (Tom) prefer that abstracts be left completely intact.

-Michael
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Victor C.
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   Posted 4/27/2001 7:54 AM (GMT -4)    Quote This PostAlert An Admin About This Post.
fascinating stuff :-)

::I take eat high fiber foods and take IP6 as a supplement also. ::

tom - I understand your side of the argument, so permit a totally non-combative inquiry: how do you take IP6? I mean, how do you schedule it so as to maximize its benefits, yet avoid it from interfering with nutrient intake? I assume you also take it on an empty stomach, how many hours after or before eating or other supplement intake?

thanks!

::Probably the best benefit would be obtained by eating fiber with meals (it is part of many foods anyway), and taking IP6 on an empty stomach (ie. about 3 hours after a meal or one hour before a meal). The IP6 that I take also contains inositol. The two together are supposed to be more effective (from what I understand this it because of the IP1-5 which can be produced). I confess that I have not being doing this, however, there are a growing number of nutrients that I really should be taking on an empty stomach, so I am seriously considering changing my daily regimen to contain one between meals dose of pills and another which I will take with my current nighttime nutrients, in addition to those things I take on rising and with meals. This will not mean more nutrients overall, but merely that several of the things that I currently take with meals (the easiest way for me) will then be taken on an empty stomach.::
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mikalra
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   Posted 4/29/2001 4:57 PM (GMT -4)    Quote This PostAlert An Admin About This Post.
::Note: Extensive quoting from previous messages is unnecessary with this forum arrangement because (unlike newsreaders) the previous message are all on the same page as the reply and can thus be easily referenced.
Finally, I think this discussion has long ago lost any benefit relative to the effort involved, so but I am posting this message with only minor comment. If anyone else wishes to comment please do.::

Thee following abstracts show that IP6 from the diet increases urinary excretion of same, that removing IP6 from the diet eliminates its urinary excretion, that IP6 per se is absorbed into gastric cells after oral administration, that it is present in the blood, & that oral IP6 reduces tissue calcification. Hence, even if one takes the extremely skeptical position that oral IP6 may be degraded & then resynthesized (which is no doubt at least PARTLY true -- NB the finding in the BJU study that Adding inositol (with no InsP6) to the liquid diet caused only a slight increase in the urinary excretion of InsP6), the results from the injection studies, re: chelating free iron & protecting from oxidative stress, also apply to oral IP6.

BJU Int 2000 Jan;85(1):138-42
Inositol hexakisphosphate in urine: the relationship between oral intake and urinary excretion.
Grases F, Simonet BM, March JG, Prieto RM.
Laboratory of Renal Lithiasis Research, University of the Belearic Islands, Palma de Mallorca, Spain. dqufg0@ps.uib.es

OBJECTIVE: To study the relationship between the oral intake of inositol hexakisphosphate (InsP6, phytic acid, an inhibitor of urinary crystallization) and its urinary excretion, to establish their possible mutual influence. MATERIALS AND METHODS: Two groups of male Wistar rats (six animals each) received either; tap water and normal rat food pellets (controls); or a liquid diet in which InsP6 was absent and which then received gradually increasing amounts of InsP6. The urinary levels of InsP6 were then assessed regularly in both groups.

RESULTS: When InsP6 was absent from the diet, urinary excretion declined to undetectable levels after 22 days.

The addition of increasing amounts of InsP6 to the liquid diet caused an increase in its urinary excretion after about 10 days. Adding InsP6 in amounts > 425 mg/L caused no further increases in urinary excretion.

Adding inositol (with no InsP6) to the liquid diet caused only a slight increase in the urinary excretion of InsP6.

CONCLUSION: These results showed that InsP6 urinary levels were related to its oral intake;

consequently, a low consumption of InsP6 would cause a urinary deficit of this crystallization inhibitor and thus an increase in the risk of
developing urinary calcium stones.

Although urinary excretion was dose-dependent, there was an ingested amount (20.9 mg/kg) above which there was no increase in the amount excreted. This intake is easily obtained by consuming a normal diet (rich in InsP6) indicating that to maintain appropriate urinary levels of InsP6, the consumption of InsP6 supplements is only necessary when the diet is particularly poor in InsP6.
PMID: 10619962

{Of course, a person eating a fanatically low-grain diet (like me ;) -- & I believe Tom, tho correct me if Im wrong, here) has a poor IP6 diet}.

::I am not fanatical about low-grains, but I mostly eat whole rye bread. However, phytates are also plentifully found in legumes and vegetables, so I dont expect that either of us have a poor IP6 diet.::

Scand J Urol Nephrol 2000 Jun;34(3):162-4
Urinary phytate in calcium oxalate stone formers and healthy people--dietary effects on phytate excretion.
Grases F, March JG, Prieto RM, Simonet BM, Costa-Bauza A, Garcia-Raja A, Conte A.
Laboratory of Renal Lithiasis Research, University of Balearic Islands, Palma de Mallorca, Spain. dqufgf0@ps.uib.es

The phytate urinary levels in a group of active calcium oxalate stone formers were studied and compared with those found in healthy people. Urinary phytate was significantly lower for stone formers. If deficit of the capacity to inhibit crystallization of calcium salts is considered an important factor related to calcium stone formation, the excretion of low phytate amounts could be an important risk factor in the development of this type of renal calculi.

The influence of dietary phytate on urinary excretion was also studied. Clearly maintenance of a phytate-free diet significantly decreased the urinary excretion of phytate (about 50% after 36 h).

This demonstrated the importance of dietary phytate in maintaining adequate urinary levels to permit effective crystallization inhibition of calcium salts and consequently preventing renal stone development.
PMID: 10961468

Biofactors 2000;11(3):171-7
Phytate prevents tissue calcifications in female rats.
Grases F, Prieto RM, Simonet BM, March JG.
Laboratory of Renal Lithiasis Research, University of Balearic Islands, Palma de Mallorca, Spain. dqufgf0@ps.uib.es

The AIN-76 A, a purified rodent diet, has a propensity to cause kidney calcifications in female rats which is not observed with non-purified rodent diets, suggesting a nutritional factor that avoids these calcifications. One candidate is phytate, which inhibits crystallisation of calcium salts and is practically absent in purified diets. Therefore, the effects on calcification of kidney tissue of phytate addition to the AIN-76 A diet using female Wistar rats were studied.

The rats were assigned to three groups: AIN-76 A, AIN-76 A 1% phytate and standard nonpurified chow.

Urinary phytate of the AIN-76 A fed group was undetectable.

Urinary phytate of AIN-76 A 1% phytate and standard fed groups did not differ and was significantly higher than in the AIN-76 A group.

The concentrations of calcium and phosphorus in kidneys were greater in the
AIN-76 A group than in AIN-76 A 1% phytate and standard groups.

Only rats of the AIN-76 A group displayed mineral deposits at the corticomedullary junction.

These findings demonstrated that the absence of phytate in the AIN-76 A diet is one of the causes of renal calcification in female rats.
PMID: 10875304

Anticancer Res 1999 Sep-Oct;19(5A):3733-6
Metabolism and cellular functions of IP6: a review.
Shamsuddin AM.
Department of Pathology, University of Maryland at Baltimore, USA.

Inositol hexaphosphate (IP6) has a demonstrably effective anti-cancer action against a variety of experimental tumors. However, the mechanisms of its actions are yet to be completely discerned.

Studies in my laboratory have shown that IP6 is rather rapidly absorbed by rats in vivo.

Ion exchange chromatography demonstrates the presence of inositol and IP1-6 in gastric epithelial cells as early as within 1 h of intragastric 3H-IP6 administration.

The metabolized IP6, in the form of inositol and IP1 is transported via plasma and reaches distant organs as well as tumors. In rats, the urinary metabolites of IP6 are inositol and IP1 {see above: not exclusively}.

However, in humans 1-3% of total administered IP6 is excreted in the urine as IP6; the level shows a normal oscillation between 0.5-6 mg/L {F. Grases
et al}.

Investigations of the uptake and metabolism by a variety of cancer cell lines in vitro also demonstrate an instantaneous absorption of IP6. The rate and pattern at which IP6 is metabolized by cancer cells varies depending on the cell type.

Intracellular inositols accumulated mostly (80-97%) in the cytosol as inositol and IP1-6. IP6 treatment of all the cell lines tested so far demonstrates that it is cytostatic and not cytotoxic. Along with inhibition of cell proliferation, there is enhanced differentiation of malignant cells to a more mature phenotype, often resulting in reversion to normal. Studies of the expression of tumor suppressor gene demonstrate up-regulation of wild type p53 and down-regulation of the mutant form. Since p53-mediated cell cycle arrest may be the direct result of induction of WAF-1 gene (p21WAF-1/CIP1), our studies demonstrate that IP6 up-regulates the expression of p21WAF-1/CIP1 in a dose-dependent manner. 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.
Publication Types:
Review
Review, tutorial
PMID: 10625949

>The fact that ingested IP6 prevents skin and mammary cancer:
>
>Anticancer Res 1999 Sep-Oct;19(5A):3749-52
>Inhibition of skin cancer by IP6 in vivo: initiation-promotion model.
>Ishikawa T, Nakatsuru Y, Zarkovic M, Shamsuddin AM.
>PMID: 10625952
>
>Cancer Lett 1993 Dec 10;75(2):95-102
>Inhibition of rat mammary carcinogenesis by inositol hexaphosphate (phytic acid). A
>pilot study.
>Vucenik I, Sakamoto K, Bansal M, Shamsuddin AM.
>PMID: 8293426
>
>... suggests to me that it is absorbed from the GI
>& distributed from there to the skin & breasts thru
>the blood.
>
>::You have still missed the point! IP6 forms insoluble and unabsorbable
>compounds *when* it absorbs minerals in the intestines. That is
>how it inhibits mineral absorption. If/when it does so, it
>will not get into the body. Very little, if any IP6 taken with meals will get into the blood.::

I agree. My position, to be clear, is that IP6 should be taken between meals on an empty stomach to avoid precisely these outcomes, & also to ensure the maximum systemic antioxidant effect via chelation of free iron. You seem, here, to think that I was counselling taking the stuff with food; I cant see where this miscommunication occurred, esp. as I had said:

>>{This is the key point to supplement users, NB: I avoid
>>dietary phytate, but supplement w/IP6}.

... but apologies, in any case, for confusion on your or anyone elses part.
>
>>{This is the key point to supplement users, NB: I avoid
>>dietary phytate, but supplement w/IP6}.
>>
>>::This makes no sense unless you have something against other chemicals
>>which come with food phytate sources since phytate and IP6
>>are chemically identical!::
>>
>>::In opposition to the evidence for the benefits of fiber including
>>phytates for reducing colon cancer risk is the following recent
>>study, so the benefit of phytate specifically for colon cancer
>>prevention is currently somewhat in question.
>>
>>N Engl J Med 2000 Apr 20;342(16):1156-62
>>Lack of effect of a high-fiber cereal supplement on the recurrence
>>of colorectal adenomas ::
>
>In answer to both of these objections, this study found supplemental
>IP6 superior to equal amounts of IP6 from wheat
>bran in preventing chemoinduced mammary cancer. Note that the dose
>of bran is a much higher % of the diet
>than 13.5 g in a human diet would be, &
>that much of the phytate would be insolubly bound to
>minerals in the meal, & thus not absorbed (my point
>above).
>
>::The dosage given was 13.5 grams of wheat bran fiber not
>wheat bran itself. Since even crude wheat bran contains only
>42.8% fiber (according to http://www.nal.usda.gov/fnic/cgi-bin/nut_search.pl ) this is equivalent to
>31.5 grams of crude wheat bran which is a subtantial daily dose.::

OK, but that is still only a 3% wheat bran diet, assuming a 1 kg food intake. The study I cited showed no significant protective effect from fiber, too, at much higher doses, but that equivalent IP6 was protective:
>
>Anticancer Res 1999 Sep-Oct;19(5A):3671-4
>Nutr Cancer 1997;28(1):7-13
>Comparison of pure inositol hexaphosphate and high-bran diet in the prevention
>of DMBA-induced rat mammary carcinogenesis.
>Vucenik I, Yang GY, Shamsuddin AM.

>Starting at two weeks before DMBA intubation, rats were divided into
>five groups and fed AIN-76A diet only or AIN-76A diet
>containing 5%, 10%, or 20% Kelloggs All Bran; the fifth
>group received 0.4% IP6 given in drinking water, an amount
>equivalent to the IP6 content in 20% bran. After carcinogen
>administration, the rats remained on these regimens for 29 weeks.
>
>
>Compared with the carcinogen control, at 29th week, tumor incidence was
>reduced ... in rats fed ... bran ... (not statistically significant).
>
>However, rats given 0.4% IP6 in drinking water, equivalent to that
>in 20% bran, had a 33.5% reduction in tumor incidence
>(p < 0.02) and 48.8% fewer tumors (p < 0.03).
>
>These data show that supplemental dietary fiber in the form of
>bran exhibited a very modest, statistically nonsignificant inhibitory effect, which
>was also not dose dependent. In contrast, animals given IP6
>showed significant reduction in tumor number, incidence, and multiplicity.
>
>PMID: 9200144
>
>::Once again your abstracts are largely irrelevant to what I was
>saying. I was not saying that insoluble fibers or IP6
>are not beneficial. All that I was and am denying
>is that:
>1) there is no evidence that IP6 chelates iron inside the
>body, and::

Do you agree that the evidence here posted (of cellular uptake, blood circulation, & urinary excretion of phytate per se) demonstrates that dietary IP6, directly or indirectly, elevates systemic IP6, which thus makes the op cit studies on IP6 INJECTION as a protectant vs. oxidative damage relevant to dietary IP6? I ask these questions with genuine interest: despite our disagreements on a variety of subjects & consequent bickering, I do genuinely respect your knowledge & judgement on l-e issues.

::Yes, from the evidence you have presented, I do agree.::

>::2) the evidence that fiber is beneficial for colon cancer is somewhat equivocal. ::

I was not advocating consuming more IP6 from fiber (ie. grains); as I have said, I avoid dietery phytates, but take the supplement.

>::FYI, I take eat high fiber foods and take IP6 as
>a supplement also. If I did not think they were
>beneficial, I would not be doing so.::

Thanks for this: as youve counselled others to drop the stuff in the past,

::I remember doing so and I dont think that I did.::

& as you rejected this PARTICULAR benefit, I was assuming you thought it useless.

::All that I was arguing against was that IP6 would chelate iron internally.::

Also, of course, I knew that you ate a lot of FIBER, from fruits & veggies, but I take it that your GRAIN (& hence DIETARY IP6) intake is fairly low.

::I dont think it is low, but this is hard to say since the phytate content of food is not available AFAIK.::

>On a related point, Victor C said:
>
>The directions state to take it on an empty stomach, with
>no other materials (supplements or food). The Jarrow brand of
>IP6 also contains magnesium and calcium.
>
>Tom replied: That seems rather foolish since they will tend to
>combine with the IP6 and form unabsorbable residues. ... Any
>IP6 which combines with the magnesium and calcium will not
>be available to combine with iron, but without food there
>is no iron for it to combine with anyway.
>
>AFAIK, all available IP6 supplements contain some Ca & Mg phytate
>salts. I buy IP6 as the powder, which is quite
>gritty for just the reason you mention, & have observed
>that it become significantly more soluble (& hence pleasant to
>drink) in ascorbic acid solution. I therefore expect that, if
>taken on an empty stomach, the stomach acidity should significantly
>liberate the phytate.
>
>::Thats a good point. However, it is then a question of
>whether the metal ions would keep separate or again be
>absorbed (chelated) by the high metal ion affinity of the
>phytic acid (higher than ascorbic acid) in the less acidic
>conditions of the small intestine after leaving the stomach.
>think it is here where mineral chelations in fact take
>place. Thus, the liberted phytic acid may well simply recombine
>with the liberated minerals in the small intestine.::

I agree that some of it will -- but of that which does so, not all will recombine w/ the SAME minerals. My ASSUMPTION is that some of it will -- but that in addition to that which gets taken up systemically, some of it will also re-affiliate with unbound Fe2 . As most divalent minerals are taken up fairly high in the intestines, but food passes thru the GI more slowly than an IP6 drink, I further REASON that unabsorbed IP6 will also reach the fecal matrix, depleted of absorbable minerals, & also possibly reassociate there with any free iron there.

I agree that this is all unproven, except inasmuch as simple, insoluble Ca & Mg salts of IP6 per se are clearly not elevating systemic IP6 or fighting cancer. Do you agree with this reasoning, with this caveat?

::It seems reasonable.::

-Michael
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Paul Wakfer [was:Tom]
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   Posted 5/6/2001 8:27 AM (GMT -4)    Quote This PostAlert An Admin About This Post.
Here is a review of the various IPs.

Nature Reviews Molecular Cell Biology 2, 327 -338 (2001)

BACK IN THE WATER: THE RETURN OF THE
INOSITOL PHOSPHATES

Robin F. Irvine & Michael J. Schell

There has been great progress recently in our knowledge of potential
functions for inositol phosphates (other than inositol-1,4,5-trisphosphate
Ins(1,4,5)P3), as well as in our understanding of the enzymes that
metabolize them, although we still remain uncertain about many of the
details of the metabolic pathways.
Inositol-1,3,4,5-tetrakisphosphate (Ins(1,3,4,5)P4) has several
functions in animal cells, where it is synthesized from Ins(1,4,5)P3 by a
family of 3-kinases that have evolved quite recently in animals.
Inositol-3,4,5,6-tetrakisphosphate (Ins(3,4,5,6)P4) functions as a
negative regulator of chloride efflux in epithelial cells. Although the
molecular details are not all clear, the implications for cystic fibrosis have a
possible clinical relevance.
Inositol-1,4,5,6-tetrakisphosphate (Ins(1,4,5,6)P4) might also have a
physiological role, indicated by its unusual metabolism, but we do not yet
know what that role is.
Inositol-1,3,4,5,6-pentakisphosphate (Ins(1,3,4,5,6)P5) is a metabolic
'hub' in inositol phosphates, but has no clearly defined function other than
its suggested role as a modulator of haemoglobin in erythrocytes of a few
animal species, a role that might be more complex than has previously
been suspected.
Inositol hexakisphosphate (InsP6) has been suggested to fulfill many
functions, and recently there have been several new possibilities
proposed. These include K+ channel regulation in plant guard cells,
controlling messenger RNA transport from the nucleus, regulating DNA
repair and a role in endocytosis (possibly involving an InsP6-regulated
protein kinase).
InsP7 and InsP8 are the newest members of the physiological inositol
phosphate repertoire, which might function as drivers of
membraneprotein interactions by acting as a localized energy source.
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