Original Study Title: Phytate (myo-inositol hexaphosphate) and risk factors for osteoporosis.

Published In: Journal of Medicinal Food, Vol. 11(4), 2008, pp. 747–752

Authors: López-González AA, et al.

Summary:
This large human study looked at real-world diets and real bones. People eating more phytate (IP6) from whole-grain–rich foods had denser bones, while low phytate intake showed up as a clear risk factor. In other words: in this population, phytate wasn’t a problem for bones — it was part of the protection.

Study Design:

• Type: Human observational study (cross-sectional with validation cohort)
  
• Participants: 1,473 adults in the main cohort; 433 adults in a validation cohort
  
• 
  Duration: Single-time bone density assessment with repeated diet questionnaires 2–3 months apart
  
• Control/Comparison: Participants grouped by level of phytate intake and other osteoporosis risk factors
  

Key Results:

• Bone mineral density increased as phytate intake increased
  
• Low phytate intake and low body weight were the strongest risk factors for low bone density
  
• Findings were replicated in a second, independent group of subjects
  
• Authors concluded that low phytate intake should be considered a risk factor for osteoporosis in this population

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J Med Food.2008 Dec;11(4):747-52.

Original Study Title: A key role for phosphorylated inositol compounds in pancreatic beta-cell stimulus-secretion coupling.

Published In: Advances in Enzyme Regulation, Vol. 48, 2008, pp. 276–294

Authors: Berggren P-O, Barker CJ.

Summary:
This review maps out how inositol phosphates — including IP6 and related molecules — act as “traffic controllers” inside pancreatic beta cells. By shaping calcium flux, membrane dynamics, and signaling pathways, these compounds help beta cells sense glucose and release insulin appropriately.

Study Design:

• Type: Narrative scientific review
  
• Models: Cell culture, animal, and human beta-cell physiology data
  
• Duration: Not applicable (synthesis of existing work)
  
• Control: Not applicable
  

Key Results:

• Phosphorylated inositols are involved in calcium channel activity, exocytosis, and endocytosis in beta cells
  
• These molecules help couple glucose sensing to insulin secretion at multiple steps
  
• IP6 and related phosphates are highlighted as important intracellular regulators, not just dietary compounds
  
• The authors argue that inositol phosphates are central to normal beta-cell function and may be relevant in metabolic disease research

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Adv Enzyme Regul.2008;48:276-94

Original Study Title: Efficacy of IP6 + inositol in the treatment of breast cancer patients receiving chemotherapy: prospective, randomized, pilot clinical study.

Published In: (Pilot clinical study report, 2010 – Bacic et al., PDF)

Authors: Bašić I, Bašić M, et al.

Summary:
This small but important pilot trial followed women going through intensive breast cancer chemotherapy. Those taking IP6 plus inositol kept their white blood cells and platelets more stable and reported better quality of life, while the control group showed the typical chemo-related declines. The study doesn’t claim a cure — it suggests that IP6 + inositol may help patients stay stronger through treatment.

Study Design:

• Type: Prospective, randomized, controlled pilot trial
  
• Participants: 14 women with invasive ductal breast cancer receiving FEC chemotherapy
  
• Duration: Approximately 6 months, over the course of chemotherapy
  
• Control: Vitamin C (as comparator)
  

Key Results:

• IP6 + inositol group maintained leukocyte and platelet counts compared with significant declines in controls
  
• Quality-of-life and functional scores improved or remained stable in the IP6 + inositol group, but worsened in controls
  
• No negative impact on tumor markers or red blood cell counts was reported
  
• Authors conclude IP6 + inositol may support hematologic tolerance and quality of life during chemotherapy, warranting larger trials

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Bačić et al. Journal of Experimental & Clinical Cancer Research 2010, 29:12

Original Study Title: Enhanced killing of androgen-independent prostate cancer cells using inositol hexakisphosphate in combination with proteasome inhibitors.

Published In: British Journal of Cancer, Vol. 99(10), 2008, pp. 1613–1622

Authors: Diallo J-S, et al.

Summary:

This lab study looked at “hard-to-treat” androgen-independent prostate cancer cells. IP6 alone pushed the cells toward death. When combined with proteasome inhibitors — drugs already being explored in cancer therapy — the killing effect became much stronger, especially at the level of mitochondrial damage.

Study Design:

• Type: In vitro mechanistic study in prostate cancer cell lines
  
• Models: Human androgen-independent PC3 and DU145 prostate cancer cell lines
  
• Duration: Short-term cell culture experiments (hours to 1–2 days)
  
• Control: Vehicle-treated cells; proteasome inhibitor alone; IP6 alone
  

Key Results:

• IP6 altered expression of several BCL-2 family proteins (↑ PUMA, BIK/NBK, NOXA; ↓ MCL-1, BCL-2) consistent with pro-apoptotic signaling
  
• Blocking protein degradation with proteasome inhibitors (MG-132, ALLN) significantly increased IP6-induced loss of metabolic activity and mitochondrial depolarization
  
• Blocking protein synthesis (cycloheximide) partially protected cells, implicating newly synthesized proteins in the cell death process
  
• Authors conclude that combining IP6 with proteasome inhibitors might be a promising pre-clinical strategy for androgen-independent prostate cancer

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Br J Cancer.2008 Nov 18;99(10):1613-22. Epub 2008 Oct 21.

Original Study Title: Protection against cancer by dietary IP6 and inositol.

Published In: Nutrition and Cancer, Vol. 55(2), 2006, pp. 109–125

Authors: Vucenik I, Shamsuddin AK.

Summary:
This comprehensive review pulls together decades of data on IP6 and inositol. Across many models, these nutrients slow abnormal cell growth, support differentiation back toward a more normal state, and show striking anticancer activity — especially in combination. Early human work suggests they may also help standard therapies work better and improve quality of life.

Study Design:

• Type: Narrative review of preclinical and early clinical evidence
  
• Models: Multiple animal tumor models, cell lines, and preliminary human data
  
• Duration: Not applicable (summary of existing studies)
  
• Control: Not applicable
  

Key Results:

• IP6 regulates cell signaling, proliferation, differentiation, and apoptosis in many tumor models
  
• Combination IP6 + inositol often outperforms either compound alone
  
• Reported benefits include reduced tumor growth, slower progression, less metastasis, and improved immune and antioxidant status in experimental systems
  
• Early human data suggest potential to enhance chemotherapy, limit metastasis, and improve quality of life, prompting calls for larger clinical trials

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Nutr Cancer.2006;55(2):109-25.

Original Study Title: Prostate cancer and inositol hexaphosphate: efficacy and mechanisms.

Published In: Anticancer Research, Vol. 25(4), 2005, pp. 2891–2903

Authors: Singh RP, Agarwal R.

Summary:
Here the authors focus specifically on prostate cancer. They review evidence that IP6 can slow tumor growth, reduce angiogenesis (new blood vessel formation), disrupt survival signals, and push cancer cells toward cell cycle arrest. The big picture: IP6 hits multiple “wires” in the circuitry that prostate tumors use to grow.

Study Design:

• Type: Mechanistic and efficacy review
  
• Models: Prostate cancer cell lines, xenograft models, and a transgenic mouse model (TRAMP)
  
• Duration: Not applicable (summary of prior experiments)
  
• Control: Not applicable
  

Key Results:

• Oral IP6 inhibited prostate tumor growth in mouse xenograft and TRAMP models without observed toxicity
  
• IP6 targeted mitogenic and survival pathways, interfered with cell cycle progression, and impacted angiogenesis-related mechanisms
  
• The authors argue IP6 is a strong candidate for prostate cancer chemoprevention based on its pleiotropic actions and safety profile

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Anticancer Research, Vol. 25(4), 2005, pp. 2891–2903

Original Study Title: Inositol hexaphosphate (IP6) inhibits key events of cancer metastasis: I. In vitro studies of adhesion, migration and invasion of MDA-MB 231 human breast cancer cells.

Published In: Anticancer Research, Vol. 23(5A), 2003, pp. 3671–3679

Authors: Tantivejkul K, Vucenik I, Shamsuddin AM.

Summary:
Metastasis isn’t just about tumor size — it’s about how well cancer cells stick, move, and break through tissue barriers. In this lab study, IP6 made aggressive breast cancer cells less “sticky,” less mobile, and less able to invade, while also reducing enzymes that help tumors chew through surrounding tissue.

Study Design:

• Type: In vitro cell culture study
  
• Models: Human MDA-MB-231 breast cancer cells
  
• Duration: Short-term assays following IP6 exposure
  
• Control: Untreated cells (vehicle only)
  

Key Results:

• 65% reduction in adhesion to fibronectin and 37% reduction to collagen after IP6 treatment (both statistically significant)
  
• ~72% reduction in migration into wounded (denuded) areas and significant decreases in migration on fibronectin, collagen, and laminin
  
• ~72% reduction in invasive capacity through Matrigel
  
• Significant inhibition of matrix metalloproteinase-9 (MMP-9) secretion, an enzyme linked to tissue breakdown and metastasis
  
• Authors conclude that IP6 can inhibit multiple key steps in the metastatic process in vitro

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Anticancer Res.2003 Sep-Oct;23(5A):3671-9.

Original Study Title: Cancer inhibition by inositol hexaphosphate (IP6) and inositol: from laboratory to clinic.

Published In: Journal of Nutrition, Vol. 133(11 Suppl 1), 2003, pp. 3778S–3784S

Authors: Vucenik I, Shamsuddin AK.

Summary:

This paper bridges the gap between bench and bedside. It reviews how IP6 and inositol work inside cancer cells, and then points to early human data suggesting that the same combination may enhance standard treatments and support patients’ quality of life — all with a strong safety profile as dietary constituents.

Study Design:

• Type: Translational review (mechanistic + preclinical + early clinical)
  
• Models: Multiple tumor cell lines, animal models, and a pilot clinical trial
  
• Duration: Not applicable
  
• Control: Not applicable
  

Key Results:

• IP6 reduces proliferation and increases differentiation of malignant cells, sometimes shifting them toward a more normal phenotype NCBI
  
• IP6 is taken up by cells and converted to lower inositol phosphates, which interfere with key signaling and cell cycle pathways
  
• Combination IP6 + inositol showed the most consistent anticancer effects across models
  
• A pilot clinical trial reported improved quality of life and better tolerance of conventional therapy with IP6 + inositol, prompting calls for larger trials

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J Nutr.2003 Nov;133(11 Suppl 1):3778S-3784S.

Original Study Title: Suppression of DMBA-induced mouse skin tumor development by inositol hexaphosphate and its mode of action.

Published In: Nutrition and Cancer, Vol. 46(1), 2003, pp. 66–72

Authors: Gupta KP, Singh J, Bharathi R.

Summary:
In this classic carcinogenesis model, mouse skin is exposed to a potent chemical carcinogen. Topical IP6 significantly cut down tumor formation and turned key cellular switches toward healthier behavior — less DNA synthesis and more normalization of differentiation.

Study Design:

• Type: Animal chemocarcinogenesis study
  
• Models: Mouse skin tumors induced by DMBA (7,12-dimethylbenz[a]anthracene)
  
• Duration: Tumor development followed over the course of DMBA exposure and topical IP6 treatment
  
• Control: DMBA alone vs. DMBA + topical IP6
  

Key Results:

• IP6 significantly inhibited skin tumor development in a dose-dependent manner
  
• IP6 restored DMBA-suppressed transglutaminase activity, a marker of differentiation
  
• DNA synthesis and thymidine kinase activity were reduced, indicating decreased proliferation
  
• Authors conclude that IP6 inhibits tumor development by modulating proliferation, differentiation, and apoptosis pathways

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Nutr Cancer.2003;46(1):66-72.

Original Study Title: Effect of inositol hexaphosphate (IP(6)) on human normal and leukaemic haematopoietic cells.

Published In: British Journal of Haematology, Vol. 118(1), 2002, pp. 255–264

Authors: Lambertenghi Deliliers G, et al.

Summary:
This study asked a critical question: what does IP6 do to normal blood-forming cells versus leukemic cells? In the lab, leukemic cells were clearly more sensitive — showing dose-dependent growth inhibition and cell cycle arrest — while normal bone marrow progenitors were largely spared at similar concentrations.

Study Design:

• Type: In vitro cellular and molecular study
  
• Models: Human leukemic cell lines and primary CD34+ progenitor cells from chronic myelogenous leukemia (CML) vs. normal marrow
  
• Duration: Short-term culture assays
  
• Control: Untreated cells and normal vs. leukemic comparisons
  

Key Results:

• IP6 produced dose-dependent cytotoxic effects in multiple leukemic cell lines, with G2/M phase accumulation in some lines
  
• Gene expression analysis showed down-regulation of transcription and cell-cycle–promoting genes with up-regulation of cell-cycle inhibitors
  
• IP6 significantly reduced CFU-GM (granulocyte-macrophage colony) formation in CML progenitors, but not in normal progenitors
  
• Authors suggest IP6 selectively targets malignant hematopoietic cells while sparing normal ones at tested doses

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Br J Haematol.2002 Jun;117(3):577-87.