Scientific Studies DATABASE PAGE 6

CLICK AICI pentru  limba ROmana (traducerea „aproximativa”  utilizand google translate)

Hydroxycinnamic Acids

Dicaffeoyl-tartaric acid

Chicoric acid is a caffeic acid derivative, belonging to the group of polypfenols.

Chicoric acid is the most active compound in Echinacea pupurea. Chicoric acid is very stable in dry conditions but can be broken down by enzymes, which are found in the Echinacea, in moist conditions.

  • DistributionChicoric is only found in Echinacea purpurea.Health Benefits of Chicoric acidChicoric acid makes our immune cells more efficient in attacking intruders. In vivo en vitro studies have shown that chicoric acid promotes phagocytosis. This is the process whereby white blood cells and lymphocytes attack and destroy pathogens. Chicoric acid stimulates T-cell activation, stimulates healing of wounds and reduces the inflammation in arthritis. Chicoric acid increases the production of interferon, immunoglobulin and other chemicals important for the immune system.Studies have indicated that chicoric acid can inhibit the penetration of viruses in cells.Chicoric acid also acts as an antioxidant by preventing the oxidation of collagen and cells.

1,2-Benzopyrone, 2H-1-Benzopyran-2-one

Coumarin is a phytochemical with a vanilla like flavour. Coumarin is a oxygen heterocycle. Coumarin can occur either free or combined with the sugar glucose (coumarin glycoside).


Coumarin is found in several plants, including tonka beans, lavender, licorice, strawberries, apricots, cherries, cinnamon, and sweet clover. 

Health Benefits of Coumarin

Coumarin has blood-thinning, anti-fungicidal and anti-tumor activities.

Coumarin should not be taken while using anticoagulants. Coumarin increases the blood flow in the veins and decreases capillary permeability. Coumarin can be toxic when used at high doses for a long period

Facts about Coumarin

Coumarin seems to work as a pesticide in the plants that produce it. Coumarin is responsible for the sweet smell of new mown hay.


4-hydroxy-3-methoxycinnamic acid

Pure ferulic acid is a yellowish powder. Ferulic acid belong to the family of hydroxycinnamic acid. The chemical structure of ferulic acid is very similar to that of curcumin.

The phytochemical ferulic acid is found in the leaves and seeds of many plants, but especially in cereals such as brown rice, whole wheat and oats. Ferulic acid is also present in coffee, apple, artichoke, peanut, orange and pineapple.

Health Benefits of Ferulic acid

Ferulic acid is an antioxidant which neutralizes free radicals (superoxide, nitric oxide and hydroxyl radical) which could cause oxidative damage of cell membranes and DNA. Ferulic acid helps to prevent damage to our cells caused by ultraviolet light. Exposure to ultraviolet light actually increases the antioxidant potency of ferulic acid.…/88169_Protective_effects_of_a_topical_ antioxidant_mixture_containing_vitamin_C.html
 ferulic acid, and phloretin against ultraviolet induced photodamage in human skin. and chronic reactions, including premature skin aging and skin cancer.…/2559062_Protective_effect_of_ferulic_acid_on_ nicotine_induced_DNA_damage.html
Protective effect of ferulic acid on nicotine induced DNA damage and cellular  smoke and plays an important etiological role in the development of lung cancer.
FA15, a hydrophobic derivative of ferulic acid, suppresses Inflammatory responses and skin tumor promotion: comparison with ferulic acid. 2002 Cancer letters…/875229_Ferulic_acid_augments_angiogenesis_ via_VEGF_PDGF_and_HIF_1.html
Ferulic acid augments angiogenesis via VEGF, PDGF and HIF 1 alpha.  broad range of therapeutic effects on human diseases, including diabetes and cancer.…/1973049_Actions_of_ferulic_acid_and_vitamin_ E_on_prevention_of.html
Actions of ferulic acid and vitamin E on prevention of hypercholesterolemia and atherogenic lesion  Vitamin D is nutritional key for prevention of breast cancer.…/2144597_Protective_effect_of_ferulic_acid_on_ 712_dimethylbenzaanthracene_induced_skin.html
Protective effect of ferulic acid on 7,12 dimethylbenz[a]anthracene induced skin carcinogenesis in Swiss  List of Cancer-Causing Agents Grows (press release).

Ferulic acid is often added as ingredient of anti-aging supplements. Studies have shown that ferulic acid can decrease blood glucose levels and can be of help to diabetes patients.Ferulic acid seems to protect against cancer, bone degeneration, menopausal symptoms (hot flushes). Like many other antioxidants, ferulic acid reduces the level of cholesterol and triglyceride, thereby reducing the risk of hearth disease. Ferulic acid seems to reduce the risk of many cancers, including cancer of the stomach, colon, breast, prostate, liver, lung and tongue. A study by W Kuenzig et all Caffeic and ferulic acid as blockers of nitrosamine formation published in Carcinogenesis (Vol 5, 1984) showed that dietary caffeic acid and ferulic acid may play a role in the body’s defence against carcinogenesis by inhibiting the formation of N- nitroso compounds.

Ferulic acid can be converted into the flavour vanillin by biochemical reaction.

Isoprenoides :

Abscisic acid, Acorenone, Alloaromadendrene, Aromadendrene, Bergamotene, Bisabolene,Borneol, Bornyl acetate, Isoborneol, Cadinene, Camphene, Caranol, Carene, Carvacrol, Carvone,Pinocarvone, Caryophyllene, Cedrine, Cineole, Cinnamaldehyde, Cinnamate, Citral,Cinnamaldehyde, Cyclocitral, Citronella, Citronellyl acetate or butyrate or propionate, Copaene, Cresol, Cubebene, Cymene, Damascenone,Elemene, Estragol, Eugenol, Farnesene, Fencone, Geraniol, Germacrene, Hotrienol, Humulene, Ionol, Ionone, Isopinocamphone, Isopulegol, Linalool, Longifolene, Mentol, Neomenthol, Menthone, Isomenthone, Murolene, Myrcenol, Myrcene, Myrtenol, Neral, Nerol, Nerolidol, Nootkatone, Ocimene, Ocimenol, Perillaldehyde, Phellandrene, Pinene, Pinocamphone, Piperitol,Piperitone, Pristane, Pulegone, Sabinene, Sabinol, Santalol, Selinadiene, Selinene, Sinensal, Styrene, Terpinene, Terpineol, Terpinolene, Thymol, Tricyclene, Vanillin, Valencene, Verbenone, Vitispirane, etc.

  • Cinnamaldehyde

Sources:Cinnamon…/188629_Allyl_isothiocyanates_and_ cinnamaldehyde_potentiate_miniature_excitatory_postsynaptic_inp…
 Cancer Pathophysiology Division, National Cancer Center Reseach Institute,  Allyl Isothiocyanates (AITC) and cinnamaldehyde are pungent compounds…/1769088_Growth_inhibition_of_human_colon_ cancer_cells_by_plant_compounds.html
CONCLUSION : Cinnamaldehyde, piperine, and resveratrol offer significant in vitro anti-proliferative effects on cultured human colon cancer cells. While each…/1499711_Coumarin_and_cinnamaldehyde_in_ cinnamon_marketed_in_Italy_a_natural.html
Coumarin and cinnamaldehyde in cinnamon marketed in Italy: a natural  The Cure in the Kitchen: Honey and Cinnamon can Cure Cancer and Arthritis.

  • Elemene

Sources: (Curcuma zedoaria and another plants)

A significant effect on the treatment of glioma was reported using Elemene which is found in small

amounts in many essential oils: it prolonged quality survival time of 40 patients with glioma (1574)

(Tan P.: Clinical study on treatment of 40 cases of malignant brain tumor by Elemene emulsion injection, Chin. J.

Integ. Trad. Western Med, 20, pp.: 645-648, 2000)

OBJECTIVE: To investigate the effect of elemene emulsion injection (EEI) in treating malignant brain tumor.

METHODS: By conducting a retrospective study of 40 patients with brain tumor, 29 of malignant glioma and 11 metastatic tumor, who were treated with EEI from January 1994 to May 1998. EEI 0.4-1.2 g/d was given to each patient by intravenous dripping or/and intravenous infusion by pumps, and directly injected into carotid artery or infused through a carotid artery catheter with pumps. The total dosage of 6-12 g was given in 2-6 therapeutic courses with an interval of 1-1.5 months between courses. The effectiveness of treatment was accessed according to the changes of tumor size, Karnofsky Performance Status (KPS) and survival time of patients. The control group consisted of 29 cases of malignant brain tumor (22 of primary and 7 of metastatic) was treated with chemotherapy 2-3 therapeutic courses with an interval of 1-1.5 months between them.


(1) In the EEI treated group the mean tumor size was changed from 6.70 cm3 (before treatment) to 2.67 cm3 (after treatment), t = 3.02, P < 0.01, it was reduced by 61%;

(2) In the EEI treated group 4 cases was CR, 26 PR, the total effective rate being 75.0% (95% credibility interval +/- 13.4%), while in the control group, 2 of CR, 10 PR, and the total effective rate 41.4% (95% credibility interval +/- 17.9%), the difference between the two groups was significant, chi 2 = 3.867, P < 0.05;

(3) KPS decreased in the EEI group from 94.7 scores (before treatment) to 88.2 scores (after treatment), the decrement was 6.5 scores (t = 3.5313, P < 0.01); (4) The survival time in the EEI treated group was 25.4 months, and that in the control group was 17.4 months (t = 3.74, P < 0.01).

CONCLUSION: Elemene has significant effect on treatment of malignant brain tumor. It could prolong the high quality survival time of patients and is worthy of further investigation.

Elemene , induced apoptosis in leukaemia (1409).

  • Eugenol
2007 Molecular cancer. Pro-apoptotic effect of the landrace Bangla Mahoba of Piper betle on Leishmania donovani may be due to the high content of eugenol.
  • Limonene(see below)

Lecithins :…/2237506_Oral_carcinogenesis_induced_by_4_ nitroquinoline_1_oxide_in_lecithinretinol.html
Oral carcinogenesis induced by 4 nitroquinoline 1 oxide in lecithin:retinol  induced a higher incidence of oral cancer in LRAT knockout (LRAT(-/-)) than in 


  1. How lignans fight cancer? – NutraPro‎ Lignans are being studied for possible use in cancer prevention, particularly breast cancerLignans acts as anticancer compounds by blocking 
  2. Breast Cancer Survival and Lignan Intake | › Videos

    One teaspoon of flax seeds may double one’s daily production of lignans, phytonutrients that appear to play a role in both breast cancer prevention and survival.

  3. Lignans – Linus Pauling Institute at Oregon State foods are part of a healthful dietary pattern, but the role of lignans in the prevention of hormone-associated cancers, osteoporosis 
  4. PUBMED Dietary lignans: potential role in cancer prevention.‎Dietary lignans: potential role in cancer prevention. Webb AL, McCullough ML. Graduate Program in Nutrition and Health 
  5. Dietary intakes of total and specific lignans are associated with‎ – Dietary lignans may affect breast cancer by modifying tumor characteristics likely to affect prognosis. We investigated usual dietary intakes of 
  6. Fighting breast cancer with flaxseeds : Disease Proof › Breast Cancer‎- Anti-cancer effects of lignans. Enterolignans are structurally similar to estrogen and can bind to estrogen receptors – this capability allows 
  7. Higher lignan levels improve breast cancer survival – Life Extension…/0920_Higher-Lignan-Levels-Improve-Breast-Cancer-Sur…‎ In an article published online on September 6, 2011 in the Journal of Clinical Oncology, German researchers report that having high serum 
  8. Dietary Lignan Intake and Postmenopausal Breast Cancer Risk by‎ Studies conducted in Asian populations have suggested that high consumption of soy-based foods that are rich in isoflavone phytoestrogens is…/2632135_Estrogenic_activities_of_sesame_ lignans_and_their_metabolites_on_human.html
Estrogenic activities of sesame lignans and their metabolites on human breast cancercells. Publication: Journal of agricultural and food chemistry. Publication…/2602942_Cytostatic_inhibition_of_cancer_cell_ growth_by_lignan_secoisolariciresinol_diglucoside.html
Cytostatic inhibition of cancer cell growth by lignan secoisolariciresinol diglucoside.…/1558789_Spirocyclic_Lignans_from_Guaiacum_ Zygophyllaceae_Induce_Apoptosis_in_Human_Breast.html
Spirocyclic Lignans from Guaiacum (Zygophyllaceae) Induce Apoptosis in Human BreastCancer Cell Lines. Publication: Journal of natural products. Publication…/1311157_Extraction_of_lignans_from_flaxseed_ and_evaluation_of_their_biological.html
Our results show that lignans modulate development of breast cancer cells. The most intense effect was observed for anhydrosecoisolariciresinol, which…/1478913_Vitexins_nature_derived_lignan_ compounds_induce_apoptosis_and_suppress_tumor.html
Vitexins, nature derived lignan compounds, induce apoptosis and suppress tumor growth. Publication: Clinical cancer research : an official journal of the…/2157407_Inhibition_of_Akt_signaling_by_the_ lignan_matairesinol_sensitizes_prostate.html
Dietary lignans have shown cancer preventive and antitumorigenic activity, but the mechanisms behind these effects are poorly known. Here we observed that of…/1938497_The_effects_of_different_lignans_and _isoflavones_tested_as_aglycones.html
PURPOSE: Phytooestrogens are known to cause anti-cancer effects on mamma carcinoma cells. In this study, the effects of the lignan Secoisolariciresinol and…/2445678_Enterolactone_and_breast_cancer_ methodological_issues_may_contribute_to_conflicting.html
Enterolactone and breast cancer: methodological issues may contribute to conflicting Lignans found in plant foods are converted by the intestinal microflora to 

Lignans sources

Flaxseeds 1 oz
Sesame seeds 1 oz
Curly kale ½ cup, chopped
Broccoli ½ cup, chopped
Apricots ½ cup, sliced
Cabbage ½ cup, chopped
Brussels sprouts ½ cup, chopped
Strawberries ½ cup
Tofu ¼ block (4 oz)
Dark rye bread 1 slice

  • Silymarin
Identifying the differential effects of Silymarin constituents on cell growth and cell cycle regulatory molecules in human prostate cancer cells. 2008 International 

SOURCES :Milk thistle

See this article on milk Thistle click here


Hydroxytyrosol is believed to be the antioxidant with the highest free radical scavenging capacity: double that of quercetin and more than 3 times that of epicatechin.
Hydroxytyrosol is the main polyphenol found in olives.

The wastewaters generated during olive processing contain a high levels hydroxytyrosol, most of which can be recovered to produce hidroxytyrosol extracts. Studies by Visioli et al (2000) showed that a low dose of hydroxytyrosol reduces the consequences of sidestream smoke-induced oxidative stress in rats.

Health Benefits of Hydroxytyrosol

Hydroxytyrosol has the same health promoting properties than other polyphenols: prevention of atherosclerosis, promotion of intestinal and respiratory health and prevention of cancer. Hydroxytyrosol also reduces the oxidative stress caused by smoking.


Benefits of Hydroxytyrosol

In Vivo Studies about Antioxidant Properties of Hydroxytyrosol

In Vitro Studies about Antioxidant Properties of Hydroxytyrosol

Cancer and Hydroxystyrosol

Cancer chemoprevention by hydroxytyrosol isolated from virgin olive oil through G1 cell cycle arrest and apoptosis.European Journal of Cancer Prevention. 2002 August;11(4):351-8Epidemiologic studies and animal studies show that olive oil may reduce the risk of several diseases such as cancer and heart disease. The aim of this study was to determine the effect of the main polyphenol in virgin olive oil, hydroxytyrosol, on tumor growth. The in vitro test were carried out in human colon cancer and leukemia cell lines. They found that hydroxytyrosol inhibited proliferation of both cancer cell lines. human promyelocytic leukaemia cells HL60 and colon adenocarcinoma cells HT29 and HT29 clone 19A. Hydroxytyrosol induced cell apoptosis and reduced cancer cell proliferation was reduced up to 50 percent. Hydroxytyrosol caused no such effects on non-cancer human cells, such as lymphocytes and polymorphonuclear cells. The study concluded that hydroxytyrosol may protect against cancer by arresting cell cycle and inducing apoptosis in cancer cells.
Hydroxytyrosol, a natural molecule occurring in olive oil, induces cytochrome c-dependent apoptosisBiochemical and Biophysical Research Communications. 2000 November 30;278(3):733-9Hydroxytyrosol is a natural phenolic antioxidant found in olive oil. It has many claimed biological and pharmacological activities. The aim of this study was to investigate the effect of hydroxytyrosol on the proliferation and survival of a leukemia cell line. The researchers found that hydroxytyrosol caused a complete arrest of leukemia cell proliferation and even induced apoptosis. This apoptotic effect was not observed with tyrosol, suggesting that presence of two ortho-hydroxyl groups is required. The study concluded that hydroxytyrosol reduces the immunological response, resulting in antinflammatory and chemopreventive effects.…/2378205_Oleuropein_and_hydroxytyrosol_ inhibit_MCF_7_breast_cancer_cell_proliferation.html
Oleuropein and hydroxytyrosol inhibit MCF 7 breast cancer cell proliferation interfering with ERK1 2 activation.…/606773_Anti_proliferative_and_apoptotic_ effects_of_oleuropein_and_hydroxytyrosol_on.html
In this study, oleuropein and hydroxytyrosol, major phenolic compound of olive oil, was studied for its effects on growth in MCF-7 human breast cancer cells
Aug 15, 2013  The Journal of nutritional biochemistry. Anti-proliferative and apoptotic effects of oleuropein and hydroxytyrosol on human breast cancerMCF-7…/2577390_Hydroxytyrosol_inhibits_growth_and_ cell_proliferation_and_promotes_high_expression.html
The aim of this study was to investigate, for the first time in an animal model of experimental mammary carcinoma, the anti-cancer ability of Hydroxytyrosoland to…/2561646_Synthesis_of_a_novel_ester_of_ hydroxytyrosol_and_a_lipoic.html
Synthesis of a novel ester of hydroxytyrosol and a lipoic acid exhibiting an antiproliferative effect on human colon cancer HT 29 cells.…/945006_Hydroxytyrosol_from_laboratory_ investigations_to_future_clinical_trials.html
Hydroxytyrosol: from laboratory investigations to future clinical trials.  lower rates of mortality from Cardiovascular disease and cancer than Northern European…/1518292_Hydroxytyrosol_inhibits_the_ proliferation_of_human_colon_adenocarcinoma_cells_through.htm…
Hydroxytyrosol inhibits the proliferation of human colon adenocarcinoma cells  many pathological processes, including the development of colon cancer.
Aug 15, 2013  Hydroxytyrosol studies.  Neuroprotective effect ofhydroxytyrosol and hydroxytyrosol acetate in rat brain slices subjected breast cancer (27)…/1150773_A_concise_synthesis_of_glucuronide_ metabolites_of_urolithin_B_resveratrol.html
Finally, three O-beta-D-glucuronides of hydroxytyrosol 6, 7, and 8 have been  Has Anti-aging and Anti-Cancer Properties, Linked to Cardiovascular Health.…/1423703_Protective_effect_of_hydroxytyrosol_ and_tyrosol_against_oxidative_stress_in.html
Protective effect of hydroxytyrosol and tyrosol against oxidative stress in kidney cells. New Study Finds Olive Oil Effective against HER-2 Breast Cancer.…/2501663_Effect_of_the_olive_oil_phenol_ hydroxytyrosol_on_human_hepatoma.html
Effect of the olive oil phenol hydroxytyrosol on human hepatoma HepG2 cells. Protection  New Study Finds Olive Oil Effective against HER-2 Breast Cancer.

Influence of Hydroxystyrol on Heart Disease


Lemonol, beta-Geraniol, trans-3,7-Dimethyl-2,6-octadien-1-ol

Geraniol is acyclic monoterpene-alcohol. Pure geraniol is a colourless oily liquid, with a sweet rose-like scent. When oxidized, geraniol becomes geranial or citral.

Bergamot, carrot, coriander, lavender, lemon, lime, nutmeg, orange, rose, blueberry and blackberry.

Health Benefits of Geraniol

Geraniol is a natural antioxidant. Geraniol has been suggested to help prevent cancer. Carnesecchi S. et al demonstrated in his study „Geraniol, a component of Plant Essential Oils, Inhibits Grwoth and Polyamine Biosyntehsis in Human Colon Cancer Cells”, (Pharmacology, July 2001) that geraniol caused a 50% increase of ornithine decarboxylase activity, which is enhances during cancer growth. Geraniol inhibits DNA synthesis.

Burk YD concluded in his study „Inhibition of Pancreatic Cancer Growth by the dietary isoprenoids farnesol and geraniol” (Lipids, February 1997) that geraniol, farnesol and perilll alcohol suppress pancreatic tumor growth.

Other animal studies have also demonstrated the anticancer effects of geraniol.…/287047_Geraniol_inhibits_prostate_cancer_ growth_by_targeting_cell_cycle_and.html
Geraniol inhibits prostate cancer growth by targeting cell cycle and apoptosis pathways.

Methyl-4-isopropenyl cyclohexene, Cajaputene, Carvene, Cinene, Dipentene, Efchole

Pure limonene is a clear liquid. Limonene is a monoterpene, made up of two isoprene units. Limonene occurs in two optically active forms, l-limonene and d-limonen. Both isomers have different odours: l-limonene smells piney and turpentine like and d-limonene has a pleasing orange scent.

Limonene is found in the essential oils of citrus fruits and many other plant species.

Limonene, found in lemons (Citrus limonum), oranges (Citrus aurantium), juniper (Juniperus communis) Foeniculum vulgare, Mentha pulegium, Mentha spicata, Verbena officinalis, Hyssopus officinalis, and in sage (Salvia officinalis), induces  apatosis in leukaemia cells (693).

Health Benefits of Limonene

Studies have shown that limonene have anti- cancer effects.

Limonen increase the levels of liver enzymes involved in detoxifying carcinogens. The Glutathione S-transferase (GST) is a system which eliminates carcinogens. Limonene seems to promote the GST system in the liver and small bowel, thereby decreasing the damaging effects of carcinogens. Animal studies demonstrated that dietary limonene reduced mammary tumor growth.

Limonene induces the formation of apoptotic bodies on BCG-823 gastric cancer cells in a dose-and time –dependent manner (1565) and induced significant reductions of hepatocellular carcinomas (1566).

Limonene showed anti-angiogenic and pro-apoptotic effects on human gastric cancer implanted in nude mice, thus inhibiting tumor growth and metastasis (1577).

At least 6-7 lemons a day should be taken, possibly fresh, because lemons help eliminate the acid wastes from the body, increasing the reserves of alkaline substances in the blood and helping the urinary apparatus to expel uric acids. One lemon a day should be taken in the first week, to reach 7 lemons a day by the seventh week of the treatment; this should be continued this throughout the illness until the hoped-for cure. The honey from lemon flowers is currently under evaluation.

The essential oil of Citrus limonum is extremely nutritious both for its K-cals and for the phytochemicals found in it. N.B. the pressing of the oil must be done cold and without solvents.

Industrial limonene is produced by by alkali extraction of citrus residues and steam distillation. This distillate contains more than 90% d-limonene.

for studies cited above SEE LAST PAGE of DATABASE


Allicin is an unstable compound that is strongly antibacterial and mainly responsible for garlic’s characteristic odor.

In vitro studies show that allicin inhibits the invasion and metastasis of human colon carcinoma cells. The phytochemical also exhibits antigenotoxic action. But the anticancer effect of allicin in humans remains uncertain, because of its low stability and poor bioavailability.

A study conducted at the Nanjing Medical University, China, concluded that allicininhibited the invasion and metastasis of human colon carcinoma cells in vitro at non-cytotoxic concentration through down-regulating the expression of vascular endothelial growth factor (VEGF), urokinase receptor (uPAR) and heparanase mRNA [1]. The researchers tested the effect of allicin on invasion and metastasis of human colon cancer cell line LoVo in vitro by using migratory test, adhesion test and Transwell chamber experiment. Allicin showed an inhibitive effects on growth of the cells in a dose and time-dependent manner. The phytochemicals suppressed the movement, adhesion and invasive capability of carcinoma cells.

A study by the Weizmann Institute of Science, Israel, demonstrated the antiproliferative function of allicin on two leukemia cell lines (HL60 and U937) [2]. They found that allicin showed anticancer effect by inducing growth inhibition, apoptotic events such as blebbing, mitochondrial membrane depolarization, cytochrome c release into the cytosol, activation of caspase 9 and caspase 3 and DNA fragmentation. Allicin reduced glutathione in the cytosol and mitochondria and changed the intracellular redox status.

Siddique and Afzal of the Aligarh Muslim University, India, investigated the antigenotoxic potential of allicin in cultured human lymphocytes using chromosomal aberrations and sister chromatid exchanges induced by the genotoxic methyl methanesulphonate [3]. They found that allicin treatment reduced the damage caused by the genotoxin, as illustrated by lower levels of chromosomal aberrations and sister chromatid exchanges.

[1] Effects of allicin on invasion and metastasis of colon cancer LoVo cell line in vitro. Zhonghua Yi Xue Za Zhi. 2009 May 26;89(20):1382-6.

[2] Allicin inhibits cell growth and induces apoptosis through the mitochondrial pathway in HL60 and U937 cells. J Nutr Biochem. 2008 Aug;19(8):524-35.

[3] Antigenotoxic effect of allicin against methyl methanesulphonate induced genotoxic damage. J Environ Biol. 2005 Jul;26(3):547-50.

See this extensive article on garlic  click here


Glutathione is a sulfur-containing amino acid that is composed of three amino acids: cysteine, glutamic acid and glycine.

Although glutathione is produced by our body is can be beneficial to consume extra glutathione through the diet.

Glutathione is mainly in animal products but also in many plants including avocado, asparagus, broccoli, grapefruit, potato, strawberries, orange, tomato, peach and spinach.

Health Benefits of Glutathine

Glutathione is an important antioxidant. Glutathione neutralizes toxic peroxide which could otherwise damage our DNA and cell membranes. As we get older the glutathione level decreases in intracellular fluids. Dietary intake of glutathione can be important for older individuals which have reduced capabilities to detoxify free radicals. Glutathione also reacts with some toxins and helps to break them down, such as the pain reliever acetaminophen.

Glutathione improves the stability of other antioxidants including vitamin C and vitamin E. Glutathione supports our immune system and stimulates the production of lymphocyte immune cells.

Studies on Glutathione and cancer

I3C, 3-hydroxymethyl indole, 3-indole methanol

The phytochemical indole-3-carbinol is found in cruciferous vegetables such as cabbage, cauliflower, broccoli, kale and brussels sprouts. Indole-3-carbinol is made from indole-3-glucosinolate by the enzyme myrosinase. This enzyme is only activated after maceration of the vegetables.Pure indole-3-Carbinol is an off-white solid belonging to the group of indoles. Indole-3-carbinol is only formed in these vegetable after crushing or during cooking

Health Benefits of Indole-3-Carbinol

Indole-3-carbinol and its main metabolite diindoylmethane modulates several nuclear transcription factors resulting in a variety of biological and biochemical effects. Indole-3-carbinol works as a strong antioxidant, thereby protecting the DNA and other cell structures.Chemopreventive

Indole-3-carbinol has chemopreventive activity and stimulates the production of detoxifying enzymes. The phytochemical protects against carcinogenic effect of pesticides and other toxins.Anticancer

The anticancer effects of indole-3-carbinol and its metabolite diindoylmethane are the result of specific activities: inducing enzymes that metabolize carcinogens, enhancing DNA repair, inducing G1 cell cycle arrest and apoptosis.

Diets high in vegetables, especially cruciferous vegetables provide protection against cancer. Cruciferous vegetables provide the only source of glucosinolates, which breaks down in indole-3-carbinol and sulforaphane. The anticancer effects of indole-3-carbinol and diindoylmethane are the result of specific activities: inducing phase I and phase II enzymes that metabolize carcinogens, enhancing DNA repair, inducing G1 cell cycle arrest and apoptosis.

Most studies have focused on the effects on endometrial cancerbreast cancer and prostate cancer.Tumor progression relies on the upregulation of signaling pathways relevant to cell proliferation and increased resistance against chemotherapeutic agents. Indole-3-carbinol and its metabolite diindoylmethane target different aspects of carcinogenesis, such as estrogen metabolism, estrogen receptor signaling, Akt-NF kappa B signaling, caspase activation, cyclin-dependent kinase activities, endoplasmic reticulum stress, and expression of tumor suppression genes [1].

Many in-vitro results have demonstrated the anticancer effect of indol-3-carbinol, but these favorable results should be treated with extra care because of its low biological availability in humans. A phase I trial demonstrated that after a oral intake of up to 1200 mg indol-3-carbionol did not result in detectable plasma levels of the phytochemical [2].

The researchers could only detect diindolylmethane , a metabolite of indole-3-carbinol, which reached max plasma level 2 hours after the administration on indole-63-carbinol, but disappeared almost completely after 12 hours. The pharmaceutical industry has already developed and patented anti-cancer chemicals with structure similar to that of diindolyl)methane, a metabolite of indole-3-carbinol.

[1] Indole-3-carbinol as a chemopreventive and anti-cancer agent. Cancer Lett. 2008 Apr 18;262(2):153-63.

[2] Single-dose and multiple-dose administration of indole-3-carbinol to women: pharmacokinetics based on 3,3′-diindolylmethane. Cancer Epidemiol Biomarkers Prev. 2006 Dec;15(12):2477-81.[3] The natural chemopreventive compound indole-3-carbinol: state of the science. In Vivo. 2006 Mar-Apr;20(2):221-8.

Indole-3-carbinol blocks estrogen receptor sites on the membranes of breast and other cells, thereby reducing the risk of cervical and breast cancer.
Recent results from epidemiology, in vitro cell culture and in vivo studies have suggested the benefits of indole-3-carbinol for the prevention of many types of cancer, including breast cancer. Oral administration of indole-3-carbinol has been shown to influence our estrogen metabolism in humans in a beneficial manner. It increases the ratio of 2-hydroxyestrone to 16alpha-hydroxyestrone.
Experimental and clinical evidence suggests that 16alpha-hydroxylated estrogen metabolites react as strong estrogens, and are associated with breast cancer risk, while 2-hydroxylated metabolites have a lower estrogenic activity and are weakly related to this disease. Indole-3-carbinol is a good candidate for clinical trial in women at increased risk of developing breast cancer. Fan S and co-workers of the Georgetown University (New York) reported that both indole-3-carrbinol and genistein target the breast cancer susceptibility genes in both prostate and breast cancer cells [4].
The breast cancer susceptibility genes are responsible for the suppression of tumor growth, not only of breast cancer cells but also ovarian and prostate cancer cells. This in-vitro study showed that the phytochemicals induced the expression of these genes.An in-vitro study with cultured human breast cancer cells demonstrated that indole-3-carbinol directly inhibited elastase enzymatic activity and concluded that this phytochemicals, or similar compounds, should be further investigated as drug for the treatment of human breast cancers where high elastase levels are correlated with poor prognosis [2].
More specifically they found that indole-3-carbinol shifted the stable accumulation of cyclin E protein from the lower molecular mass form, that is associated with cancer cell proliferation and poor clinical outcomes, to its higher molecular mass form, that is typically produced in normal cells. A Taiwanese study found that indole-3-carbinol reduced the invasion and migration of breast cancer cells [3].
The phytochemical inhibited matrix metalloproteinases expression by blocking the ERK/Sp1-mediated gene transcription.Indole-3-carbinol might improve the effect of tamoxifen according to an experiment with rats carried out by the University of Minnesota [4].
Tamoxifen is a selective estrogen receptor modulator that is used in the treatment of breast cancer. The scientists induced tumors in rats by dosing the carcinogen dimethylbenz-a-anthracene and then treated the rats with tamoxifen, indole-3-carbionol or a combination of both. All three types of treatment resulted in a significant increased latency and decreased mass of malignant mammary tumors, but also treatment with indole-3-carbinol, although the effect of indole-3-carbinol alone was weaker.A study by scientists of the University of California concluded that indole-32-carbinol had an influence on the function and expression of estrogen receptor-alpha (ERA) and estrogen receptor-beta (ERB) [6].
By increasing the ratio of ERA to ERB indole-3-carbinol could reduce the proliferation of human breast cancer cells. The tests were conducted on breast cancer cells that expressed both ERA and ERB. Treatment of these breast cancer cells with indole-3-carbinol strongly inhibited ERB protein production, without that of ERA.Indole-3-carbinol selectively induced apoptosis in breast cancer cells, but not in nontumorigenic breast cells, suggesting the potential therapeutic benefit of I3C against breast cancer [7]. Low levels of indole-3-carbinol inhibited the growth of the tumor cells more than that of normal breast cells. The phytochemical upregulated Bax/Bcl-2 ratio and downregulated Bcl-xL expression only in the breast cancer cells.
[1] Prevention and treatment of cancer with indole-3-carbinol. Altern Med Rev. 2001 Dec;6(6):580-9.
[2] The dietary phytochemical indole-3-carbinol is a natural elastase enzymatic inhibitor that disrupts cyclin E protein processing. Proc Natl Acad Sci U S A. 2008 Dec 8.
[3] Indole-3-carbinol Inhibits Sp1-Induced Matrix Metalloproteinase-2 Expression To Attenuate Migration and Invasion of Breast Cancer Cells. J Agric Food Chem. 2008 Dec 5.
[4] BRCA1 and BRCA2 as molecular targets for phytochemicals indole-3-carbinol and genistein in breast and prostate cancer cells. Br J Cancer. 2006 Feb 13;94(3):407-26.
[5] Suppression of mammary gland carcinogenesis by post-initiation treatment of rats with tamoxifen or indole-3-carbinol or their combination. Eur J Cancer Prev. 2007 Apr;16(2):130-41.
[6] Indole-3-carbinol selectively uncouples expression and activity of estrogen receptor subtypes in human breast cancer cells. Mol Endocrinol. 2006 Dec;20(12):3070-82. Epub 2006 Aug 10.
[7] Indole-3-carbinol (I3C) induces apoptosis in tumorigenic but not in nontumorigenic breast epithelial cells. Nutr Cancer. 2003;45(1):101-12.
Indole-3-carbinol increases the ratio of 2-hydroxyestrone to 16 alpha-hydroxyestrone and inhibits the 4-hydroxylation of estradiol. This is a favourable action of indole-3-carbinol because 16 alpha-hydroxyestrone and 4-hydroxyestrone have carcinogenic action.
The estrogen metabolite 2-hydroxyestrone has protective against several types of cancer. Studies with animals have demonstrated that indole-3-carbinol reduced the carcinogenic affects of aflatoxins. The influence of indole-3-carbinol on the development of prostate cancer is less clear. Most studies report protective effects but a few studies indicate that indole-3-carbinol may promote prostate cancer formation.
In the USA prostate cancer is one of the most common cancers in men and the second leading cause of cancer-related deaths. Epidemiological and dietary studies have shown a link between high dietary intake of cruciferous vegetables and decreased prostate cancer risk. A study conducted by Technion Israel Institute of Technology (Haifa) showed that indole-3-carbinol had a significant inhibitory effect on prostate cancer cells in vitro and in vivo and concluded that this phytochemicals is a potential candidate as both preventive and therapeutic agent for humans [1].
The researchers tested the effect of indole-3-carbinol on the growth of prostate cancer cells inoculated subcutaneously in mice. They found that the administration of indole-3-carbinol significantly reduced cells proliferation and promoted the apoptosis of the prostate cancer cells. Fan S and co-workers of the Georgetown University (New York) reported that both indole-3-carrbinol and genistein target the breast cancer susceptibility genes in both prostate and breast cancer cells [2].
The breast cancer susceptibility genes are responsible for the suppression of tumor growth, not only of breast cancer cells but also ovarian and prostate cancer cells. This in-vitro study showed that the phytochemicals induced the expression of these genes.Another study found that injected indole-3-carbinol has anti-prostate cancer activity in rats [3].
Both intraperitoneal (in the body cavity) and intravenous injection of the phytochemical inhibited the growth, incidence and metastases of prostate cancer cells which were injected in rats.A study conducted at the Wayne State University School of Medicine, Detroit, concluded that indole-3-carbinol and its metabolite diindolylmethane are candidates for the prevention and the treatment of prostate cancer [4].
The researchers confirmed that indole-3-carbinol and diindolylmethane upregulate the expression of phase I and phase II enzymes, which are involved in the detoxification and inhibition of carcinogens. Both phytochemicals regulate many genes that are important for the control of cell cycle, cell proliferation, signal transduction, and other cellular processes.A study conducted by the Long Island Jewish Medical Center, New York, suggested that indole-3-carbinol may be an effective sensitizer of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) treatment against TRAIL-resistant prostate cancer cell lines [5].
TRAIL is a ligand molecule which induces the process apoptosis in a variety of transformed cells including prostate cancer cells but has no effect on normal cells. The researchers, led by Jeon KI, tested the potential sensitizing effects of indole-3-carbinol on TRAIL-mediated apoptosis in a prostate cancer cell line. They found that the phytochemical enhanced TRAIL-mediated apoptosis and that the apoptosis was the result of increased levels of two trail death receptors.
[1] Indole-3-carbinol (I3C) exhibits inhibitory and preventive effects on prostate tumors in mice. Food Chem Toxicol. 2008 Mar;46(3):863-70.
[2] BRCA1 and BRCA2 as molecular targets for phytochemicals indole-3-carbinol and genistein in breast and prostate cancer cells. Br J Cancer. 2006 Feb 13;94(3):407-26.
[3] Anti-carcinogenic and anti-metastatic properties of indole-3-carbinol in prostate cancer. Oncol Rep. 2005 Jan;13(1):89-93.
[4] Indole-3-carbinol and prostate cancer.J Nutr. 2004 Dec;134(12 Suppl):3493S-3498S.Sarkar FH, Li Y.
Treatment of skin cancer cells with ultraviolet-B results in the apoptosis of their apoptosis, a favorable effect that seems to be stimulated by indole-3-carbinol. Some studies also show a beneficial effect on the treatment of skin cancer.Every year more than 1 million new cases of ultraviolet radiation-induced non-melanoma skin cancers occur in the USA. Although exposure to sun and specifically ultraviolet radiation increases the risk of skin cancers, treatment of skin cancer cells with ultraviolet-B also results in their apoptosis, a favorable effect that seems to be stimulated by indole-3-carbinol.
That is what scientist of the Seoul National University found in an experiment with cultured human melanoma cells [1].
They investigated the effect of indole-3-carbinol on the sensitization to ultraviolet-B-induced apoptosis . They found that a combined treatment with the indole-3-carbinol and ultraviolet-B synergistically reduced melanoma cell viability, whereas the phytochemical or ultraviolet-B alone had little effect. Indole-3-carbinol acted by down-regulating pro-apoptotic protein Bcl-2.
Another study also demonstrated the protective action of indol-3-carbinol on ultraviolet-induced carcinogenic process on skin cells of mice [2]. They conducted tests on groups of 20 mice exposed ultraviolet radiation and to fed with respectively chlorophyllin, indole-3-carbinol or placebo. The scientists found that rats fed with chlorophyllin should a significant increase in tumor multiplicity, whereas those supplemented with indol-3-carbinol has significant lower tumor multiplicity.[
1] Indole-3-carbinol enhances ultraviolet B-induced apoptosis by sensitizing human melanoma cells. Cell Mol Life Sci. 2006 Nov;63(22):2661-8.
[2] Ultraviolet radiation-induced non-melanoma skin cancer in the Crl:SKH1:hr-BR hairless mouse: augmentation of tumor multiplicity by chlorophyllin and protection by indole-3-carbinol. Photochem Photobiol Sci. 2006 May;5(5):499-507.Indol-3-carbinol, and OTHER (Brassica vegetables); conversion to isothiocyanates.

Indole 3 Carbinol (See also Di-indole methane) I3C, as it is frequently called, has been tested and documented in humans and results are highly promising. Indole-3-carbinol reduced or halted the formation of precancerous lesions (papillomas) in 12 out of 18 people with recurrent respiratory tract papillomas. In addition, in a small double-blind trial, supplementation with 200 or 400 mg of indole-3-carbinol per day for 12 weeks reversed early-stage cervical cancer in 8 of 17 women. Preliminary studies have also shown indole-3-carbinol has significantly increased the conversion of estrogen from cancer-producing forms to nontoxic breakdown products. Indole-3-carbinol is found in highest concentrations in broccoli, but is also found in other cruciferous vegetables, such as cauliflower, cabbage, and kale. This treatment would be indicated for those with hormonal related cancers. Note: Di-indole methane is considered a stronger metabolite of I3C.
  1. Pretreatment of Indole-3-Carbinol augments TRAIL-induced apoptosis in a prostatecancer cell line, LNCaP.
    2003 FEBS letters
  2. Indole-3-Carbinol and prostate cancer.
    2004 The Journal of nutrition
  3. Indole-3-Carbinol (I3C) induced cell growth inhibition, G1 cell cycle arrest and apoptosis in prostate cancer cells.
    2001 Oncogene
  4. Inactivation of akt and NF-kappaB play important roles during indole-3-carbinol-induced apoptosis in breast cancer cells.
    2004 Nutrition and cancer
  5. Indole-3-Carbinol prevents cervical cancer in human papilloma virus type 16 (HPV16) transgenic mice.
    1999 Cancer research
  6. Therapeutic intervention of experimental breast cancer bone metastasis by Indole-3-Carbinol in SCID-human mouse model.
    2006 Molecular cancer therapeutics
  7. The effect of Indole-3-Carbinol and sulforaphane on a prostate cancer cell line.
    2003 ANZ journal of surgery
  8. A potent Indole-3-Carbinol derived antitumor agent with pleiotropic effects on multiple signaling pathways in prostate cancer cells.
    2007 Cancer research
  9. Indole-3-Carbinol as a chemopreventive and anti-cancer agent.
    2008 Cancer letters
  10. 1-Benzyl-indole-3-carbinol is a novel Indole-3-Carbinol derivative with significantly enhanced potency of anti-proliferative and anti-estrogenic properties in human breastcancer cells.
    2010 Chemico-biological interactions
  11. Indole-3-Carbinol prevents PTEN loss in cervical cancer in vivo.
    2005 Molecular medicine (Cambridge, Mass.)
  12. Gender differences in gemcitabine (Gemzar) efficacy in cancer cells: effect of indole-3-carbinol.
    2010 Anticancer research
  13. BRCA1 and BRCA2 as molecular targets for phytochemicals Indole-3-Carbinol and genistein in breast and prostate cancer cells.
    2006 British journal of cancer
  14. Indole-3-Carbinol and tamoxifen cooperate to arrest the cell cycle of MCF-7 human breast cancer cells.
    1999 Cancer research
  15. Anti-carcinogenic and anti-metastatic properties of Indole-3-Carbinol in prostate cancer.
    2005 Oncology reports
  16. Bax translocation to mitochondria is an important event in inducing apoptotic cell death by Indole-3-Carbinol (I3C) treatment of breast cancer cells.
    2003 The Journal of nutrition
  17. A new Indole-3-Carbinol tetrameric derivative inhibits cyclin-dependent kinase 6 expression, and induces G1 cell cycle arrest in both estrogen-dependent and estrogen-independent breast cancer cell lines.
    2003 Cancer research
  18. Indole-3-Carbinol stimulates transcription of the interferon gamma receptor 1 gene and augments interferon responsiveness in human breast cancer cells.
    2004 Carcinogenesis
  19. Anti-estrogenic activities of Indole-3-Carbinol in cervical cells: implication for prevention of cervical cancer.
    1999 Anticancer research
  20. Indole-3-Carbinol (I3C)-induced apoptosis in nasopharyngeal cancer cells through Fas/FasL and MAPK pathway.
    2010 Medical oncology (Northwood, London, England)
  21. Direct inhibition of elastase activity by Indole-3-Carbinol triggers a CD40-TRAF regulatory cascade that disrupts NF-kappaB transcriptional activity in human breastcancer cells.
    2010 Cancer research
  22. Putative mechanisms of action for Indole-3-Carbinol in the prevention of colorectal cancer.
    2008 Expert opinion on therapeutic targets
  23. Indole-3-Carbinol inhibits MDA-MB-231 breast cancer cell motility and induces stress fibers and focal adhesion formation by activation of Rho kinase activity.
    2009 International journal of cancer. Journal international du cancer
  24. Indole-3-Carbinol inhibits Sp1-induced matrix metalloproteinase-2 expression to attenuate migration and invasion of breast cancer cells.
    2009 Journal of agricultural and food chemistry
  25. Indole-3-Carbinol selectively uncouples expression and activity of estrogen receptor subtypes in human breast cancer cells.
    2006 Molecular endocrinology (Baltimore, Md.)
  26. Indole-3-Carbinol mediated cell cycle arrest of LNCaP human prostate cancer cells requires the induced production of activated p53 tumor suppressor protein.
    2006 Biochemical pharmacology
  27. Modulation of the constitutive activated STAT3 transcription factor in pancreaticcancer prevention: effects of Indole-3-Carbinol (I3C) and genistein.
    2004 Anticancer research
  28. Indole-3-Carbinol and 3,3′-diindolylmethane induce apoptosis in human prostatecancer cells.
    2003 Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
  29. Inhibition of proliferation of a colon cancer cell line by indole-3-carbinol.
    2002 Colorectal disease : the official journal of the Association of Coloproctology of Great Britain and Ireland
  30. The Indole-3-Carbinol cyclic tetrameric derivative CTet inhibits cell proliferation via overexpression of p21/CDKN1A in both estrogen receptor positive and triple negative breast cancer cell lines.
    2011 Breast cancer research : BCR
  31. Indole-3-Carbinol triggers aryl hydrocarbon receptor-dependent estrogen receptor (ER)alpha protein degradation in breast cancer cells disrupting an ERalpha-GATA3 transcriptional cross-regulatory loop.
    2010 Molecular biology of the cell
  32. Cancer chemotherapy with indole-3-carbinol, bis(3′-indolyl)methane and synthetic analogs.
    2008 Cancer letters
  33. Ultraviolet radiation-induced non-melanoma skin cancer in the Crl:SKH1:hr-BR hairless mouse: augmentation of tumor multiplicity by chlorophyllin and protection by indole-3-carbinol.
    2006 Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology
  34. Indole-3-carbinol-induced modulation of NF-kappaB signalling is breast cancer cell-specific and does not correlate with cell death.
    2008 Breast cancer research and treatment
  35. Indole-3-Carbinol inhibition of androgen receptor expression and downregulation of androgen responsiveness in human prostate cancer cells.
    2005 Carcinogenesis
  36. N-Alkoxy derivatization of Indole-3-Carbinol increases the efficacy of the G1 cell cycle arrest and of I3C-specific regulation of cell cycle gene transcription and activity in human breast cancer cells.
    2008 Biochemical pharmacology
  37. Synthetic dimer of indole-3-carbinol: second generation diet derived anti-cancer agent in hormone sensitive prostate cancer.
    2006 The Prostate
  38. Indole-3-Carbinol and 3-3′-diindolylmethane antiproliferative signaling pathways control cell-cycle gene transcription in human breast cancer cells by regulating promoter-Sp1 transcription factor interactions.
    2003 The Journal of nutrition
  39. Indole-3-Carbinol (I3C) inhibits cyclin-dependent kinase-2 function in human breastcancer cells by regulating the size distribution, associated cyclin E forms, and subcellular localization of the CDK2 protein complex.
    2005 The Journal of biological chemistry
  40. Indole-3-Carbinol inhibits CDK6 expression in human MCF-7 breast cancer cells by disrupting Sp1 transcription factor interactions with a composite element in the CDK6 gene promoter.
    2001 The Journal of biological chemistry
  41. Multiple molecular targets of indole-3-carbinol, a chemopreventive anti-estrogen in breast cancer.
    2002 European journal of cancer prevention : the official journal of the Europeancancer Prevention Organisation (ECP)
  42. Targets for Indole-3-Carbinol in cancer prevention.
    2005 The Journal of nutritional biochemistry
  43. Inhibition of lung carcinogenesis and critical cancer-related signaling pathways by N-acetyl-S-(N-2-phenethylthiocarbamoyl)-l-cysteine, Indole-3-Carbinol and myo-inositol, alone and in combination.
    2010 Carcinogenesis
  44. Targeting of aryl hydrocarbon receptor-mediated activation of cyclooxygenase-2 expression by the Indole-3-Carbinol metabolite 3,3′-diindolylmethane in breastcancer cells.
    2009 The Journal of nutrition
  45. Review. Indole-3-Carbinol as a chemoprotective agent in breast and prostate cancer.
    2008 In vivo (Athens, Greece)
  46. Indole-3-Carbinol enhances anti-proliferative, but not anti-invasive effects of oxaliplatin in colorectal cancer cell lines.
    2008 Biochemical pharmacology
  47. Molecular targets and anticancer potential of Indole-3-Carbinol and its derivatives.
    2005 Cell cycle (Georgetown, Tex.)
  48. Inhibition of MUC1 expression by indole-3-carbinol.
    2004 International journal of cancer. Journal international du cancer
  49. Indole-3-Carbinol (I3C) induces apoptosis in tumorigenic but not in nontumorigenic breast epithelial cells.
    2003 Nutrition and cancer
  50. A novel mechanism of Indole-3-Carbinol effects on breast carcinogenesis involves induction of Cdc25A degradation.
    2010 Cancer prevention research (Philadelphia, Pa.)
  51. Indole-3-Carbinol is a negative regulator of estrogen.
    2003 The Journal of nutrition

NOTE: Di-Indole Methane

Di-Indole Methane is the direct metabolite of I3C (Indole-3-Carbinol) and twice as strong. This naturally occurring extract of the cabbage (cruciferous) family vegetables has proven effective in studies worldwide against hormonal related cancers. It’s mechanism is to decrease high estrogen levels in both men and women, an issue which usually leads to cancer or other illnesses often associated with aging. Included are prostate disease, breast and uterine cancers, and weight gain. Supplementing the diet with DIM and eating cruciferous vegetables increases the specific aerobic metabolism for estrogen, multiplying the chance for so-called bad estrogen to be broken down into beneficial, or good estrogen metabolites. These good estrogen metabolites are known as the 2-hydroxy estrogens.

DIM (diindolylmethane) DIM is a phytochemical that is found in broccoli, cabbage, turnip and mustard greens, kale, brussel sprouts, collards, etc. „The first development in this research using chemically altered [sic] DIM from broccoli came when the growth of breast cancer cells was inhibited in laboratory studies. Subsequent research showed these compounds also inhibited growth of pancreatic, colon, bladder and ovarian cancer cells in culture, Safe said. Limited trials on lab mice and rats have produced the similar results, he noted.”  „Researchers from the University of California at Berkeley looked at the effects of broccoli on human breast cancer cells. According to findings, compounds in broccoli known as indoles are digested and broken down in the stomach to a compound called 3,3′-diindolylmethane (DIM). This compound may be the key to keeping cancer at bay.” 

Isothiocyanates are sulphur-containing phytochemicals with the general formula R-NCS. Different molecules belong to this group. Isothiocyanates with the stongest anticancer effects are phenylethylisothiocyanate, benzylisothiocyanate and 3-phenylpropylisothiocyanate. Isothiocyanates occur naturally as glucosinolate conjugates in cruciferous vegetables. Isothiocyanates are also responsible for the typical flavour of these vegetables.

Isothiocyanates can be found in cruciferous vegetables such as broccoli, cauliflower, kale, turnips, collards, Brussels sprouts, cabbage, radish, turnip and watercress. Glucosinolates are precursors of isothiocyanates. When the raw vegetables are chewed the plant cells are broken and an enzyme (myrosinase) hydrolyses the glucosinolates into isothiocyanates.

Health Benefits of Isothiocyanates

Isothiocyanates combat carcinogens by neutralizing them, reducing their poisonous effect and stimulating the secretion of carcinogens of carcinogens. Isothiocyanates act by inhibition of cell proliferation and induction of apoptosis.

The isothiocyanates with the stongest anticancer effects are phenylethylisothiocyanate, benzylisothiocyanate and 3-phenylpropylisothiocyanate. Studies have shown that isothiocyanates help to prevent lung cancer and esophageal cancer. Isothiocyanates can also lower the risk of other cancers, including gastrointestinal cancer.…/1947743_Dietary_isothiocyanates_glutathione_S _transferase_M1_GSTM1_and_lung_cancer.html
Dietary isothiocyanates, glutathione S transferase M1 (GSTM1), and lung cancer risk in African Americans and Caucasians from Los Angeles County, California.…/132691_Selective_Depletion_of_Mutant_p53_by _Cancer_Chemopreventive_Isothiocyanates_and.html
Isothiocyanates (ITCs) derived from cruciferous vegetables induce apoptosis in cancercells. We demonstrate that certain naturally occurring ITCs selectively…/568279_Cancer_preventive_isothiocyanates_ induce_selective_degradation_of_cellular_alpha_.html
Cancer preventive isothiocyanates induce selective degradation of cellular alpha and beta tubulins by proteasomes.…/1314059_Isothiocyanates_glutathione_S_ transferase_M1_and_T1_polymorphisms_and_gastric.html
Isothiocyanates, glutathione S transferase M1 and T1 polymorphisms and gastric cancerrisk: a prospective study of men in Shanghai, China.…/786957_Chemoprevention_of_cancer_by_ isothiocyanates_and_anthocyanins_mechanisms_of_action.html
Chemoprevention of cancer by isothiocyanates and anthocyanins: mechanisms of action and structure activity relationship.…/2410_Isothiocyanate_exposure_glutathione_S_ transferase_polymorphisms_and_colorectal_cancer_risk.html
Isothiocyanate exposure, glutathione S transferase polymorphisms, and colorectal cancerrisk. Publication: The American journal of clinical nutrition. Publication…/27163_Urinary_isothiocyanates_glutathione_S_ transferase_M1_T1_and_P1_polymorphisms.html
The present study examined the associations among urinary isothiocyanates, Glutathione S-transferase (GST) polymorphisms, and colorectal cancer risk in a…/1265130_Isothiocyanates_induce_oxidative_ stress_and_suppress_the_metastasis_potential_of.html
However, the effect of isothiocyanates on lung cancer cell metastasis has not been studied. In the present study, we investigated the inhibitory effects of BITC…/3294354_Head_and_neck_cancer_a_case_for_ inhibition_by_isothiocyanates.html
Head and neck cancer: a case for inhibition by isothiocyanates and indoles from cruciferous vegetables.…/1569614_Prostate_cancer_chemopreventive_ activity_of_phenethyl_isothiocyanate_through_epigenetic_regulatio…
Consumption of cruciferous Vegetables has been reported to be associated with reduced incidence of prostate cancer cases. The isothiocyanates, including…/3381294_Repression_of_androgen_receptor_in_ prostate_cancer_cells_by_phenethyl.html
Repression of androgen receptor in prostate cancer cells by phenethyl isothiocyanate. Publication: Carcinogenesis Publication Date: 2006. Study Author(s):…/629276_Isothiocyanates_sensitize_the_effect_of_ chemotherapeutic_drugs_via_modulation_of.html
Isothiocyanates sensitize the effect of chemotherapeutic drugs via modulation of protein kinase C and telomerase in cervical cancer cells.…/125542_Anti_NF_kappaB_and_anti_ inflammatory_activities_of_synthetic_isothiocyanates.html
Of the natural compounds, the Isothiocyanates (ITCs) found in cruciferous Vegetables have received particular attention because of their potential anti- cancer…/1338610_ABC_transporters_and_isothiocyanates _potential_for_pharmacokinetic_diet_drug_interactions.html
Isothiocyanates, a class of anti-cancer agents, are derived from cruciferous Vegetables such as broccoli, cabbage and watercress, and have demonstrated…/209522_New_biomarkers_for_monitoring_the_ levels_of_isothiocyanates_in_humans.html
Isothiocyanates (ITCs) found in cruciferous vegetables have demonstrated cancerpreventive activity in animals, and increased dietary intake of ITCs has been…/2587875_Urinary_isothiocyanate_levels_and_ lung_cancer_risk_among_non_smoking.html
Urinary isothiocyanate levels and lung cancer risk among non smoking women: A prospective investigation.…/1538721_Metabolism_of_isothiocyanates_in_ individuals_with_positive_and_null_GSTT1.html
BACKGROUND & AIMS : Isothiocyanates (ITCs) derived from cruciferous vegetables have been shown to be promising agents against cancer in human cell 

Researchers at the Johns Hopkins University School of Medicine in Baltimore studied the metabolism of isothiocyanates and found that isothiocyanates were about six times more bioavailable than glucosinolates.

Sulforaphane is a phytochemical belonging to the family of isothiocyanates, which means it contains the typical NCS group.

(R)-1-isothiocyanto-4-methyl-sulfonyl butane

Sulforaphane occurs in plants bound to a sugar molecule: sulforaphane glucosinolate. Only after eating will the sulforaphane by released. Sulforaphane glucosinolate is found in cruciferous vegetables such as broccoli, cauliflower, cabbage and kale. The richest source of sulforaphane are broccoli sprouts.

Health Benefits of Sulforaphane

Sulforaphane is an antioxidant and stimulators of natural detoxifying enzymes. Sulforaphane may reduce the risk of breast, bladder and prostate cancer.

Anti-cancer effect

Epidemiological studies show that people who eat a lot of cruciferous vegetables have reduces incidences of cancer. In-vitro and animals studies have confirmed the anti-cancer effects and have demonstrated that the phytochemical reduces the frequency, size, and number of tumors.

During the fight against cancer cells our body produces special enzymes, called phase 2 enzymes. Sulforaphane is a phase 2 enzyme inducer, thereby neutralizing carcinogens before they can damage DNA. Sulforaphane inhibits benzo[a]pyrene-DNA and 1,6-dinitropyrene-DNA adducts formation. A study by James D. Brooks et al entitled Potent Induction of Phase 2 Enzymes in Human Prostate Cells by Sulforaphane has shown that sulforaphane induces phase 2 enzyme expression and activity in human prostate cells [1]. This study may help to explain the lower prostate cancer risk with men who consume more cruciferous vegetables.A team of scientists lead by B. Abbouit at the Ohio State University investigated the effect of isothiocyanates (sulforaphane and erucin) in primary or secondary bladder cancer prevention. Both phytochemicals showed inhibition of bladder cancer cells, which was associated downregulation of survivin, epidermal growth factor receptor and human epidermal growth factor receptor 2 and apoptosis.

A 2012 study by the Texas Children’s Hospital suggested a potential role of sulforaphane as an adjunctive agent to improve the therapeutic response in acute lymphoblastic leukemia patients [3]. This type of cancer is the most common hematological cancer in children. The scientists found that purified sulforaphane had anticancer properties in a broad range of leukemic cells. More specifically they found that sulforaphane caused dose-dependent apoptosis and cell cycle arrest, mainly by activation of caspases. While sulforaphane killed cancer cells, it did not affect healthy cells. It should be noted that the levels of sulforaphane used in this study were quite high and can not be obtained by eating cruciferous vegetables, such as broccoli.

[1] Potent induction of phase-2-enzymes in human prostate cells by sulforaphane.. Cancer Epidemiology Biomarkers and Prevention, Vol. 10, 949-954, September 2001

[2] Inhibition of bladder cancer by broccoli isothiocyanates sulforaphane and erucin: characterization, metabolism, and interconversion. Mol Nutr Food Res. 2012 Nov;56(11):1675-87

[3] Sulforaphane induces cell cycle arrest and apoptosis in acute lymphoblastic leukemia cells. PLoS One. 2012;7(12):e51251

Heart health

The antioxidant action of sulforaphane helps to fight high blood pressure. A study by the Tokyo University of Agriculture has shown that persons who eat about 100 g of broccoli sprouts daily during one week had reduces levels of cholesterol.

Research Reviews

Potent induction of phase-2-enzymes in human prostate cells by sulforaphane.

Sulforaphane inhibits extracellular, intracellular, and antibiotic-resistant strains of Helicobacter pylori and prevents benzo-a-pyrene-induced stomach tumors

Phenolic Acids

trans-8-methyl-N-vanillyl-6-nonenamide, N-(4-Hydroxy-3-methoxyphenyl)-8-methyl-non-trans-6-enamide

Capsaicin is the phytochemical in chilli peppers that causes the typical heat. Pure capsaicin is a white crystalline powder. Capsaicin is a capsaicinoid which belongs to the alkaloid family. It is very heat stable and keeps its activity despite cooking. Capsaicin is only slightly soluble in water, but very soluble in ethanol and vegetable oil. Other capsaicinoid are dihydrocapsaicin, nordihydrocapsaicin, homocapsaicin and homodihydrocapsaicin.

Health Benefits of Capsaicin


Capsaicin is used in many topical ointments used to relieve the pain of peripheral neuropathy (treatment of pain in the nerve endings near the surface of the skin). Capsaicin is then applied on the skin and removed when the patient starts feeling the burning sensation. The nerves seem to become insensitive to pain. The burning sensations of capsaicin is caused by its interaction with the nerve cells. Capsaicin binds with special receptor cells (vanilloid receptor subtype 1) and produces the same effect as physical heat. Consumption of capsaicin can also create a euphoric sensation caused by the release endorphins.

Studies have shown that capsaicin can relieve arthritic symptoms and improve flexibility of the joints. Capsaicin seems to inhibit the activity of DSP (Decapeptide Substance P), which the painful feeling of arthritis.

Capsaicin might protect against gastric ulcers. Studies have shown that capsaicin protects the stomach membrane by increasing the blood flow.

Capsaicin seems to reduce the symptoms of psoriasis. A study by Ellis CN et al., „A double-blind evaluation of topical capsaicin in pruritic psoriasis” (Journal of the American Academy of Dermatology, Sept 1993) showed that patients with psoriasis who took capsaicin cream had reduced itching, scaling and redness compared with patients who used a placebo.

Why do plants contain capsaicin? By producing the burning capsaicin the pepper plant prevents animals from eating its fruits. Birds don?t feel the burning sensation of capsaicin so they eat the fruits and are responsible for the spreading of seeds. The chilli seeds survive the digestion process. Capsaicin is also a component of pepper spray, used as chemical riot control agent.


Capsaicin and Health

Benzoaric acid, eleagic acid, elagostasine, gallogen

Ellagic acid is a fused four-ring polyphenol.

Ellagic acid is present in many red fruits and berries, including raspberries, strawberries, blackberries, cranberries, pomegranate and some nuts including pecans and walnuts. The highest levels of ellagic acid are found in raspberries. In plants ellagic acid is present in the form of ellagitannin, which is ellagic acid bound to a sugar molecule.

Pure ellagic acid is a cream to light yellow crystalline solid.

Health Benefits of Ellagic Acid

Ellagic acid has antioxidant, anti-mutagen and anti-cancer properties. Studies have shown the anti-cancer activity on cancer cells of the breast, oesophagus, skin, colon, prostate and pancreas. More specifically, ellagic acid prevents the destruction of P53 gene by cancer cells. Ellagic acid can bind with cancer causing molecules, thereby making them inactive. In their studie The effects of dietary ellagic acid on rat hepatic and esophageal mucosal cytochromes P450 and phase II enzymes. Ahn D et al showed that ellagic acid causes a decrease in total hepatic mucosal cytochromes and an increase in some hepatic phase II enzyme activities, thereby enhancing the ability of the target tissues to detoxify the reactive intermediates. Ellagic acid showed also a chemoprotective effect against various chemically induced cancers.

Studies on Ellagic Acid and cancer –

A study by Thresiamma KC and Kuttan R.Indian (Indian Journal Physiology and Pharmacology, 1996 October) indicate that oral administration of ellagic acid by rats can circumvent the carbon tetrachloride toxicity and subsequent fibrosis of the liver.

Ellagic acid has also antiviral and antibacterial activities.

Plants produce ellagic acid to protect themselves from microbiological infection and pests.

Research Reviews

Pomegranate Juice Ellagitannin Metabolites Are Present in Human Plasma and Some Persist in Urine for Up to 48 Hours

Chemoprevention of esophageal tumorigenesis by dietary administration of lyophilized black raspberries.


3,4,5-Trihydroxybenzoic acid

Gallic acid occurs as a freemolecule or as part of a tannin molecule.

Gallic acid is found in almost all plants. Plants known for their high gallic acid content include gallnuts, grapes, tea, hops and oak bark. Pure gallic acid is a colourless crystalline organic powder.

Health Benefits of Gallic acid

Gallic acid seems to have anti-fungal and anti-viral properties. Gallic acid acts as a antioxidant and helps to protect our cells against oxidative damage. Gallic acid was found to show cytotoxicity against cancer cells, without harming healthy cells.

Gallic acid is used a remote astringent in cases of internal haemorrhage. Gallic acid is also used to treat albuminuria and diabetes. Some ointment to treat psoriasis and external haemorrhoids contain gallic acid.

Rosmarinic acid is found in big quantities in oregano, lemon balm, sage, marjoram, rosemary.

Rosmarinic acid has antioxidant, anti-inflammatory and antimicrobial activities.

The antioxidant activity of rosmarinic acid is stronger than that of vitamin E. Rosmarinic acid helps to prevent cell damage caused by free radicals, thereby reducing the risk for cancer and atherosclerosis.

Rosmarinic acid has anti-inflammatory properties. Perilla, rich in rosmarinic acid, is used for its anti-allergic activity. A study by Sanbongi C and colleagues (Clinical and Experimental Allergy, June 2004) have shown that the oral administration of rosmarinic acid is an effective intervention for allergic asthma. Another study by Youn J and colleagues (Journal of Rheumatology, June 2003) demonstrated that rosmarinic acid suppressed synovitis in mice and that it may be beneficial for the treatment of rheumatoid arthritis. Unlike antihistamines, rosmarinic acid prevents the activation of immune responder cells, which cause swelling and fluid formation.

Rosmarinic acid is also used for food preservation. In Japan the perilla extracts, rich in rosmarinic acid, is used the garnish and improve the shelf life of fresh seafood.

Rosmarinic acid is used to treat peptic ulcers, arthritis, cataract, cancer, rheumatoid arthritis and bronchial asthma.

Studies on Rosmarinic acid and cancer…/2186820_Rosmarinic_acid_antagonizes_activator _protein_1_dependent_activation_of_cyclooxygenase.html
Rosmarinic acid antagonizes activator protein 1 dependent activation of cyclooxygenase 2 expression in human cancer and nonmalignant cell lines.…/1022843_Inhibitory_effects_of_rosemary_ extracts_carnosic_acid_and_rosmarinic_acid.html
Subsequently, six extracts and the active compounds, carnosic acid, andRosmarinic acid were applied to various human cancer cell lines including NCI- H82…/1331077_Rosmarinic_acid_sensitizes_cell_death _through_suppression_of_TNF_alpha.html
Rosmarinic acid sensitizes cell death through suppression of TNF alpha  of RA have not been well elucidated in TNF-alpha-mediated anti-cancer therapy.
Aug 15, 2013  Rosmarinic acid antagonizes activator protein-1-dependent activation of cyclooxygenase-2 expression in human cancer and nonmalignant cell
Rosmarinic acid antagonizes activator protein-1-dependent activation of cyclooxygenase-2 expression in human cancer and nonmalignant cell lines. 2008 The…/264528_Inhibition_of_bone_metastasis_from_ breast_carcinoma_by_rosmarinic_acid.html
Our study showed that Rosmarinic acid (RA) could inhibit the migration of MDA- MB-231BO human bone-homing breast cancer cells dose-dependently.…/2450932_Combination_of_active_components_ enhances_the_efficacy_of_Prunella_in.html
 enhances the efficacy of Prunella in prevention and treatment of lung cancer caffeic acid, rosmarinic acid, rutin, quercetin, Oleanolic acid and Ursolic Acid.

Gallotanic acid, digallic acid, allotannin, tannimum.Tannic acid is a polymer of gallic acid molecules and glucose. It the example there are 3 gallic acid molecules, but normally there are about 8. Because there are different molecular structures for tannic acid it would have been better to speak about tannic acids (in plural). Tannic acid will hydrolyze into glucose and gallic or ellagic acid units. Tannic acid is odourless but has a very astringent taste. Pure tannic acid is a light yellowish and amorphous powder.

Tea, nettle, wood, berries, Chinese galls. Oak wood is very rich in tannic acid. When wine is kept in oak kegs some tannic acid will migrate into the wine. High levels of tannic acid are found in some plant galls. These are formed by plants when they are infected by certain insects. These insects pierce the plant leaves and when the egg hatches out into a larva the plant produces a gall which surrounds the larva.

Health Benefits of Tannic Acid

Tannic acid has anti-bacterial, anti-enzymatic and astringent properties. Tannic acid has constringing action upon mucous tissues such as tongue and inside of mouth. The ingestion of tannic acid caused constipation and can be used to treat diarrhoea (in the absence of fever or inflammation). The anti-oxidant and anti-mutagenic properties of tannic acid are beneficial.

Studies on Tannic Acid and cancer

However, tannic acid should not be used continuously or in high quantities ad it slows down the absorption of iron and possibly other trace minerals. A study by Afsana K et al entitled Reducing effect of ingesting tannic acid on the absorption of iron, but not of zinc, copper and manganese by rats. published by Bioscience, Biotechnology, and Biochemistry (March 2004) concluded that the usual intake of polyphenols is relatively safe, but that a high intake by supplementation or by dietary habit of tannin affects only the iron level. Tannic acid can also reduce the effectiveness of digestive enzymes.


(3beta)-stigmast-5-en-3-ol, 22:23-dihydrostigmasterol, alpha-dihydrofucosterol, cinchol, cupreol, rhamnol, quebrachol and sitosterin.

Beta-sitosterol is a phytosterols or plant sterol. The structure of beta-sitosterol is similar to that of cholesterol. Beta-sitosterol differs from cholesterol by the presence of an extra ethyl group.

There are many plant sources of beta-sitosterol, but the most important are wheat germ, rice bran, flax seeds, peanuts, soybeans, pumpkin seeds and corn oil. Muli and co-workers showed that a plant-based diet, rich in fibre, soy and flax seed, can increase serum levels of beta-sitosterol.

Health Benefits of Beta-Sitosterol

Beta-sitosterol is mainly known and used for its cholesterol lowering property. But studies have shown that the phytochemical may have other health benefits: easing symptoms of benign prostatic enlargement, reducing risk of cancer and prevention of oxidative damage through its antioxidant activity.


Epidemiological and experimental studies have suggested a protective role of beta-sitosterol in the development of some types of cancer such as breast, colon and prostate cancer. In-vivo studies have shown that the phytochemical inhibited proliferation and induce apoptosis in human solid tumors such as colon and breast cancers.

Beta-sitosterol is mainly studied for its cholesterol-lowering properties but many studies also find that the phytochemical may help to prevent cancer. Epidemiological and experimental studies have suggested a protective role of beta-sitosterol in the development of some types of cancer such as breast, colon and prostate cancer. In-vivo studies have shown that the phytochemical inhibited proliferation and induce apoptosis in human solid tumors such as colon and breast cancers.

A Japanese study led by Imanaka demonstrated that the oral intake of beta-sitosterol, encapsulated in a liposome, was able to prevent tumour metastasis in rats, although the phytochemical was not absorbed in the serum. The researchers believed that beta-sitosterol works by stimulating the gut immune surveillance systems, as indicated by an increase in natural killer cell activity and production of immune response cytokines [1]. Park and co-workers concluded in their study that „beta-sitosterol potently induces apoptosis in U937 cells (these are leukemia cells) and that beta-sitosterol-induced apoptosis is related to the selective activation of caspase-3 and induction of Bax/Bcl-2 ratio.” Beta-sitosterol induced apoptosis in the leukemia cells in a dose-dependent manner [2].

Beta-sitosterol seems to induce apoptosis of cancer cells through two pathways: the extrinsic and intrinsic pathways, which are catalyzed by by the initiator caspases 8 and 9 respectively. Both pathways result in the activation of caspase 3, which is an effector caspases that cleaves protein substrates within the cell resulting in the apoptotic process. Korean study lead by Moon also found this effect of beta-sitosterol on caspase activation on cultured fibrosarcoma cells: treatment of the cells with an caspase-3 inhibitor inhibited the beta-sitosterol induced apoptosis. Treatment of the fibrosarcoma cells with beta-sitosterol also induced activation (phosphorylation) of extracellular-signal regulating kinase and blocked protein kinase B, which inhibits apoptotic processes [3]. Nakamura and co-workers found that beta-sitosterol restored the impaired gap junctional intercellular communication of transfected rat liver epithelial cells. The beta-sitosterol used in this experiment was extracted from the husks of psyllium seeds. Beta-sitosterol and also stigmasterol increased the level of gap junction proteins and restored their level of phosphorylation to levels similar to nontransfected cells [4].

Epidemiological evidence has shown that men consuming high amounts of plant products have a lower risk of prostate cancer. Von Holtz and colleagues investigated the possible effect of the plant sterol, beta-sitosterol, on cancer cells. They found that beta-sitosterol decreased the numbers of prostate cancer cells and increased apoptosis. Beta-sitosterol the production of ceramide, which is cellular signaling molecule regulating the differentiation, proliferation, programmed cell death and apoptosis of cells [5]. An in-vitro experiment with bone marrow cells showed that beta-sitosterol reduced the genotoxic damage caused by doxorubicin [6]. Beta-sitosterol significantly reduced the frequency of sister chromatid exchanges, which are exchange of genetic material between two identical sister chromatids. When the frequency of chromatid exchange is too high, cell damage can occur.

[1] Imanaka H, Koide H, Shimizu K, Asai T, Kinouchi Shimizu N, Ishikado A, Makino T, Oku N. ” Chemoprevention of tumor metastasis by liposomal beta-sitosterol intake” Biol Pharm Bull. 2008 Mar;31(3):400-4.

[2] Park C, Moon DO, Rhu CH, Choi BT, Lee WH, Kim GY, Choi YH. ” Beta-sitosterol induces anti-proliferation and apoptosis in human leukemia U937 cells through activation of caspase-3 and induction of Bax/Bcl-2 ratio.” Biol Pharm Bull. 2007 Jul;30(7):1317-23.

[3] Moon DO, Lee KJ, Choi YH, Kim GY. „Beta-sitosterol-induced-apoptosis is mediated by the activation of ERK and the downregulation of Akt in MCA-102 murine fibrosarcoma cells.” Int Immunopharmacol. 2007 Aug;7(8):1044-53.

[4] .Nakamura Y, Yoshikawa N, Hiroki I, Sato K, Ohtsuki K, Chang CC, Upham BL, Trosko JE. „Beta-sitosterol from psyllium seed husk (Plantago ovata Forsk) restores gap junctional intercellular communication in Ha-ras transfected rat liver cells.” Nutr Cancer. 2005;51(2):218-25.

[5]Von Holtz RL, Fink CS, Awad AB. ” beta-Sitosterol activates the sphingomyelin cycle and induces apoptosis in LNCaP human prostate cancer cells.” Nutr Cancer. 1998;32(1):8-12.

[6] Paniagua-Pérez R, Madrigal-Bujaidar E, Reyes-Cadena S, Alvarez-González I, Sánchez-Chapul L, Pérez-Gallaga J, Hernández N, Flores-Mondragón G, Velasco O. ” Cell protection induced by beta-sitosterol: inhibition of genotoxic damage, stimulation of lymphocyte production, and determination of its antioxidant capacity. ” Arch Toxicol. 2008 Feb 6.

The studies about the protective effect of beta-sitosterol on breast cancer only involved in-vitro experiments using cultured breast cancer cells. These studies clearly show that the phytochemicals kills breast cancer cells and is not toxic to normal cell. Clinical studies linking beta-sitosterol and breast cancer are still missing but some scientists suggest that it may improve the efficiency of tamoxifen, a drug often used to treat breast cancer.

School of Public Health and Health Professions at the University at Buffal investigated the effects of beta-sitosterol and tamoxifen on the cultured breast cancer cells. The study led by Awad concluded that „these results suggest that the combination regimen of dietary beta-sitosterol and tamoxifen chemotherapy may be beneficial in the management of breast cancer patients”[1]. Tamoxifen is drug used for the treatment of breast cancer and works as a selective estrogen receptor modulator. Therefore it only works on estrogen receptor positive breast cancer cells. They tested the effect of beta-sitosterol and tamoxifen, separately and combined, on the growth of estrogen receptor positive breast cancer cells and estrogen receptor negative breast cancer cells. They found that a treatment with beta-sitosterol inhibited the growth of both type of cells whereas tamoxifen only inhibited of estrogen receptor positive breast cancer cells. A combined treatment further inhibited the growth of both cell types. Both beta-sitosterol and tamoxifen modulated the ceramide metabolism. Ceramides act as a signaling molecule, regulating differentiation, proliferation, programmed cell death and apoptosis. Beta-sitosterol increased ceramide levels by stimulating ceramide production whereas tamoxifen tamoxifen increased ceramide levels by inhibting ceramide glycosylation.

A study conducted by the State University of New York concluded that beta-sitosterol is an effective apoptosis-promoting phytochemical and more dietary phytosterols may protect against breast cancer. The scientists studied the effect of beta-sitosterol on cultured breast cancer cells and adenocarcinoma cells. Beta-sitosterol concentrated in the cell membranes and significantly inhibited tumor cell growth. It increased the Fas levels and caspase-8 activity [2]. Beta-sitosterol seems to induce apoptosis of cancer cells through two pathways: the extrinsic and intrinsic pathways, which are catalyzed by by the initiator caspases 8 and 9 respectively. Both pathways result in the activation of caspase 3, which is an effector caspases that cleaves protein substrates within the cell resulting in the apoptotic process. Awad and his team found that beta-sitosterol treatment of cultured breast cancer cells increased the activities of caspases 8 and 9 by 39% and 80% respectively, resulting in a a three-fold increase in the activity of caspase 3 [3].

In another in-vivo experiment conducted by Awad also showed that beta-sitosterol inhibited the growth of breast cancer cells by up to 80%, caused a six-fold increase in apoptosis cells but showed no cytotoxicity. The found no effect of beta-sitosterol on the level of protein phosphatase 2A in the tumor cells [4].

A study by Ju et al investigated the estrogenic effects of the plant sterols beta-sitosterol, beta-sitosterol glucoside and Moducare (mixture of beta-sitosterol, beta-sitosterol glucoside). The test was carried out on estrogen dependent human breast cancer cells in vitro and in vivo. The researchers concluded that beta-sitosterol and Moducare stimulated cancer cells in vitro and that dietary beta-sitosterol and Moducare protected against estrogen stimulated tumor growth. These findings suggest that beta-sitosterol could have potential benefits for women with a risk for estrogen-dependent breast cancer [5].

[1] Awad AB, Barta SL, Fink CS, Bradford PG. ” beta-Sitosterol enhances tamoxifen effectiveness on breast cancer cells by affecting ceramide metabolism.”Mol Nutr Food Res. 2008 Apr;52(4):419-26.

[2] Awad AB, Chinnam M, Fink CS, Bradford PG. ” beta-Sitosterol activates Fas signaling in human breast cancer cells.” Phytomedicine. 2007 Nov;14(11):747-54.

[3] Awad AB, Roy R, Fink CS. „Beta-sitosterol, a plant sterol, induces apoptosis and activates key caspases in MDA-MB-231 human breast cancer cells. „Oncol Rep. 2003 Mar-Apr;10(2):497-500

[4] Awad AB, Downie AC, Fink CS. „Inhibition of growth and stimulation of apoptosis by beta-sitosterol treatment of MDA-MB-231 human breast cancer cells in culture.” Int J Mol Med. 2000 May;5(5):541-5.

[5] Ju YH, Clausen LM, Allred KF, Almada AL, Helferich WG. „Beta-sitosterol, beta-sitosterol glucoside, and a mixture of beta-sitosterol and beta-sitosterol glucoside modulate the growth of estrogen-responsive breast cancer cells in vitro and in ovariectomized athymic mice.” J. Nutr. 134: 1145-1151.


Beta-sitosterol is an antioxidant able to reduce DNA damage, reduce the level of freeradical in our cells and to increase the level of typical antioxidant enzymes.


Regular intake of beta-sitosterol may reduce blood cholesterol levels by directly inhibiting the absorption of cholesterol. Beta-sitosterol also prevents the oxidation of LDL cholesterol thereby reducing the risk of atherosclerosis.

Prostate enlargement

Clinical studies have confirmed the beneficial effects of beta-sitosterol in patients withprostate enlargement. The phytochemical decreases post-void residual urinary volume and increases urinary flow rate in these patients.


Saponins are glucosides with foaming characteristics. Saponins consist of a polycyclic aglycones attached to one or more sugar side chains. The aglycone part, which is also called sapogenin, is either steroid (C27) or a triterpene (C30). The foaming ability of saponins is caused by the combination of a hydrophobic (fat-soluble) sapogenin and a hydrophilic (water-soluble) sugar part. Saponins have a bitter taste. Some saponins are toxic and are known as sapotoxin.

Saponins are phytochemicals which can be found in most vegetables, beans and herbs. The best known sources of saponins are peas, soybeans, and some herbs with names indicating foaming properties such as soapwort, saoproot, soapbark and soapberry. Commercial saponins are extracted mainly from Yucca schidigera and Quillaja saponaria.

Health Benefits of Saponins

Saponinshave many health benefits. Studies have illustrated the beneficial effects on blood cholesterol levels, cancer, bone health and stimulation of the immune system. Most scientific studies investigate the effect of saponins from specific plant sources and the results cannot be applied to other saponins.

Cholesterol reduction

Saponins bind with bile salt and cholesterol in the intestinal tract. Bile salts form small micelles with cholesterol facilitating its absorption. Saponins cause a reduction of blood cholesterol by preventing its re-absorption.

Reduce cancer risk

Studies have shown that saponins have antitumor and anti-mutagenic activities and canlower the risk of human cancers, by preventing cancer cells from growing. Saponins seem to react with the cholesterol rich membranes of cancer cells, thereby limiting their growth and viability. Roa and colleagues found that saponins may help to prevent colon cancer and as shown in their article „Saponins as anti-carcinogens” published in The Journal of Nutrition (1995, 125, 717s-724S).

Antitumor activity of Pulsatilla koreana saponins and their structure-activity relationship. 

Chemical & Pharmaceutical Bulletin. 2005 November;53(11):1451-4

The aim of this study was to determine the antitumor properties of saponins from the root of Korean pasque flower (Pulsatilla koreana). The researchers measured the in-vitro cytotoxic activity against cultured human solid cancer cells and the in-vivo antitumor activity in mice bearing lung carcinoma. The saponins with a free acidic group at C-28 of aglycon showed moderate to considerable in-vitro cytotoxic activity. In the in-vivo test hederagenin saponins showed stronger antitumor effect than the taxol and doxorubicin saponins. The precense of a hederagenin aglycones and a special sugar sequence at C-3 are essential factors for the antitumor activity of saponins.

Protective effect of Astragalus corniculatus saponins against myeloid graffi tumor in hamsters.

Phytother Research. 2004 March;18(3):255-7

This study investigated the antitumor effect of a saponin rich extract from Astragalus corniculatus Bieb, a garden plant originating from Eastern European, against myeloid Graffi tumors in hamsters. The researchers found that an injection of extract in the peritoneal cavity decreased tumor transplantability, inhibited tumor growth in the early stages of tumor progression, increased survival time and reduced mortality. The study concluded that the saponin extract of Astragalus corniculatus should be further investigated as a antitumor treatment of myeloid Graffi tumour.

Protective effect of soybean saponins and major antioxidants against aflatoxin B1-induced mutagenicity and DNA-adduct formation. 

Journal of Medicinal Food. 2002 Winter;5(4):235-40.

Previous studies have suggested that saponins have possible anti-cancer effect. The main dietary sources of saponins are legumes, including soybeans. The aim of this study was to determine the effect of soybean saponins mutagenic activity of aflatoxin B1 on Salmonella typhimurium and human liver cells. The anti-mutagenic effect of saponins was compared to those of other typical antioxidants such as vitamin C, vitamin E including L-ascorbic acid, alpha-tocopherol, vitamin A and butylated hydroxytoluene. The researchers found that the anti-mutagenic activity of saponins was between those of butylated hydroxytoluene and vitamin E. Soybean saponins reduced the muitagenic effect of aflatoxin B1 up to 81%. The preincubation of human liver cells with saponins reduced the amount of DNA adducts significantly. The study concluded that soybean saponins possess a significant anti-mutagenic activity. More studies are required to determine the exact mechanism but soybean saponins seems to block the initial stages of carcinogenesis.

Environmental influences on isoflavones and saponins in soybeans and their role in colon cancer.

Journal of Nutrition. 2005 May;135(5):1239-42

Soybeans are not only an important source of high quality proteins but contain also health promoting phytochemicals such as isoflavones and saponins. The aim of this study was to quantify isoflavone and saponin levels in soybean cultivars grown under different conditions and to determine the influence of isoflavones and saponins on carcinogenic process of cultured human colon cancer cells. The researchers found an inhibitive effect of soy isoflavones and saponins on the colon cancer cells. There were no adverse effects of the intake of pure saponins on growth, organ weight or intestinal morphology, even when the diet contained 3% saponins. The study concluded that soy isoflavones and saponins may protect against colon cancer and are well tolerated.

Soy saponins and the anticancer effects of soybeans and soy-based foods. 

Current Medicinal Chemistry – Anti-Cancer Agents. 2004 May;4(3):263-72

There are indications that the consumption of soy products help to protect against cancer but the exact constituents, which are responsible for this action, remain elusive. The aim of this review was to summarize epidemiological studies linking saponins to cancer risk. Recents studies have shown that soy saponins have a direct effect on cancer cells but may also influence carcinogenesis in alternative mechanisms. The anti-cancer action of saponins may result in the discovery of new anticancer agents.

Soybean saponins suppress the release of proinflammatory mediators by LPS-stimulated peritoneal macrophages.

Cancer Letters. 2005 December 18;230(2):219-27

Pro-inflammatory mediators play also a role in cancer development. Phytochemicals with anti-inflammatory properties may help to reduce the risk of cancer. The aim of this study was to investigate the effects of soybean saponins on the production of proinflammatory mediators peritoneal macrophages stimulated with liposaccharides. The researchers found that soybean saponins reduced the levels of pro-inflammatory indicators such as cyclooxygenase-2, nitric oxide synthases and Nuclear Factor kappa B. The study concluded that soybean saponins may be useful for ameliorating inflammatory diseases and suppressing tumor progression.

Some studies have shown that saponins can cause apoptosis of leukemia cells by inducing mitotic arrest.

Cytotoxic and apoptogenic effect of tea (Camellia sinensis var. assamica) root extract (TRE) and two of its steroidal saponins TS1 and TS2 on human leukemic cell lines K562 and U937 and on cells of CML and ALL patients.

Leukemia Research. 2006 April;30(4):459-68

Not only tea leaves but also tea roots contain phytochemicals with potential health benefits. The aim of this study was to investigate the anti-cancer properties of tea root extract and two specific steroidal saponins found in the tea root on human cancer cells. The study showed that the tea root extract and the two steroidal saponins induced apoptosis of leukemia cells. Consumption of the tea root extract by healthy volunteers caused an insignificant reduction in cell count.

The mitotic-arresting and apoptosis-inducing effects of diosgenyl saponins on human leukemia cell lines.

Biological and Pharmaceutical Bulletin. 2004 July;27(7):1059-65

Previous studies have shown that diosgenyl saponins could induce cytotoxicity and apoptosis in human leukemia cells. The aim of this study was to investigate mechanisms of action. The researchers found that diosgenyl saponins activated some caspases (caspases are essential in cells for apoptosis, one of the main types of programmed cell death) and down-regulated anti-apoptotic proteins. Dioscin treatment of leukemia cells inhibited cell mitosis. The study concluded that diosgenyl saponins may act by inducing mitotic arrest and apoptosis. Diosgenyl saponins might be used antimitotic agents.…/693_Cancer_chemopreventive_and_therapeutic_ effects_of_diosgenin_a_food_saponin.html
Food saponins have been used in complimentary and traditional medicine against a variety of diseases including several cancers. Diosgenin, a naturally…/2005340_Dimeric_antioxidant_and_cytotoxic_ triterpenoid_saponins_from_Terminalia_ivorensis_A.html
Dimeric antioxidant and cytotoxic triterpenoid saponins from Terminalia ivorensis A.  and further for their Cytotoxic activity against four human cancer cell lines.…/432621_Chemical_and_pharmacological_studies _of_saponins_with_a_focus_on.html
It is believed that the ginseng saponins called ginsenosides are the major  and central Nervous system as well as the antidiabetes and anti-cancer effects.…/270524_Cytotoxic_saponin_against_lung_cancer _cells_from_Dioscorea_birmanica_Prain.html
Cytotoxic saponin against lung cancer cells from Dioscorea birmanica Prain & Burkill.

Immunity booster

Plants produce saponins to fight infections by parasites. When ingested by humans, saponins also seem to help our immune system and to protect against viruses and bacteria.

Reduce bone loss

Studies with ovariectomized induced rats have shown that some saponins, such as the steroidal saponins from Anemarrhena asphodeloides, a Chinese herb, have a protective role on bone loss.


The non-sugar part of saponins have also a direct antioxidant acitivity, which may results in other benefits such as reduced risk of cancer and heart diseases.


What’s more, several recent animal-based studies and studies on human cells have found that pterostilbene may be effective for protection against breast cancerprostate cancer, andcolon cancer.


Resveratrol is a flavonol belonging to the group of flavonoids.

Resveratrol is present in many plants and fruits, including red grapes, eucalyptus, spruce, blueberries, mulberries, peanuts, giant knotweed. Also red wine contains a lot of it. The longer the grape juice is fermented with the grape skins the higher the resveratrol content will be. It is produced by the plant as a defence against diseases.

Health Benefits of Resveratrol

Resveratrol is an antioxidant but its antioxidant properties are weaker that those of quercetin and epicatechin. It has anticancer properties and inhibits lipid peroxidation of low-density lipoprotein and prevents the cytotoxicity of oxidized LDL. Resveratrol also increases the activity of some antiretroviral drugs in vitro.


In vitro studies have shown that resveratrol inhibits the oxidative damage caused by the heavy metal cadmium. The antioxidant activity of resveratrol reduces damage to endothelial cells exposed to nitrite radicals and protects skin cells against damage caused by UV radiation.


The antioxidant action of resveratrol helps to prevent damage to DNA but it also influences the transcriptions of genes responsible for redox metabolism and inhibits proliferartion of cancer cells. Resveratrol appears to decrease tumor promotion activity by inhibiting the enzyme cyclooxygenase-1, which converts arachidonic acid to substances that promote tumor growth. In vitro experiments provide support for resveratrol to serve as a candidate preventive agent against prostate cancer, but in vivo effects of resveratrol and the mechanisms of action of resveratrol on prostate cancer prevention remain largely unknown.

Resveratrol modulates mRNA transcripts of genes related to redox metabolism and cell proliferation in non-small-cell lung carcinoma cells.

Journal of Biological Chemistry. 2007 February;388(2):207-19

Previous studies have shown that phytochemical resveratrol has antioxidant properties and influences the cellular redox reactions in eukaryotic cells. The researchers investigated the effects of resveratrol on the transcription of genes and activity of enzymes involved with the redox metabolism and cell cycle regulation in lung cancer cells. They found that resveratrol significantly increased the transcription of glutathione peroxidase resulting in lower glutathione levels. Glutathione also increased the transcription of many genes involved in the cell cycle, differentiation and apoptosis. The researchers concluded that resveratrol increased the expression of genes responsible for cell survival, differentiation, proliferation inhibition and apoptosis. Resveratrol may therefore have a chemopreventive and anticancer effect.

Effect of resveratrol and mixtures of resveratrol and mitomycin C on cancer cells under irradiation.

Anticancer Research. 2006 November-December;26(6B):4403-8

This study investigated the antitumor and radiation protective effects of resveratrol in combination with mitomycin-C, an antibiotic that is also used as chemotherapeutic agent because of its antitumour activity. The in-vitro tests were carried out on human breast cancer cells in aerated and anaerobic media. In the aerated media resveratrol showed anti-tumor and antioxidant activities, which were enhanced by mitomycin-C. Under anaerobic conditions, resveratrol acted as a radiation-protecting agent and at high concentration it stopped cell growth. The study concluded that resveratrol has both radiation protective and anticancer activity. Resveratrol acts by ejection of electrons and by reacting on primary radicals, such as hydroxyl radical.

Resveratrol Inhibits Pancreatic Cancer Cell Proliferation through Transcriptional Induction of Macrophage Inhibitory Cytokine-1.

Journal of Surgical Research. 2007 January 24

Resveratrol is a phytochemical found in many mainly in red grape skins, mulberries and some nuts. Previous studies have shown that resveratrol has potential antitumorigenic and anti-inflammatory activities. It is known that macrophages produce a cytokine (MIC-1) which has antitumorigenic activity. The aim of this in-vitro study was to determine the effect resveratrol on the activity of MIC-1 and the regulation the growth of lines human pancreatic cancer cells. The researchers found that resveratrol upregulated the expression of the MIC-1 gene. When the cells were first treated with a transcriptional inhibitor the effect of resveratrol was reduced, confirming that resveratrol works expression of genes. The study concluded that resveratrol increases MIC-1 gene expression in pancreatic cancer cells.

Resveratrol inhibits proliferation, induces apoptosis and overcomes chemoresistance through downregulation of STAT3 and nuclear factor-{kappa}B-regulated antiapoptotic and cell survival gene products in human multiple myeloma cells.

Blood, 15 March 2007, Vol. 109, No. 6, pp. 2293-2302

This study investigated the effect of resveratrol, a phytochemical found in red grapes, red berries and peanuts on the growth of human multiple myeloma cells. Multiple myeloma is cancer of immune system cells in bone marrow. Bhardwaj and his colleagues found that resveratrol inhibited the proliferation of human multiple myeloma cell lines. Resveratrol also increased the apoptotic affect of bortezomib and thalidomide. They concluded that resveratrol may have a potential in the treatment of multiple myeloma cancer.

Resveratrol interferes with AKT activity and triggers apoptosis in human uterine cancer cells.

Molecular Cancer. 2006 October 17;5:45

Endometrial cancers (cancer of the lining of the uterus) are the most common gynecologic cancers in the Western world. Studies have shown that resveratrol, an anti-oxidant found in high quantities in red wine, has anticancer activity and acts by inhibiting the proliferation and inducing apoptosis of cancer cells. The aim of this study was to investigate the antiproliferative and apoptotic activity of resveratrol in six different endometrial cancer cell lines. The researchers found that resveratrol caused apoptosis apoptosis in five out of six uterine cancer cell lines and decreased cell proliferation. They found that resveratrol acts by regulating the cyclooxygenase expression.

Benefits for diabetes

Resveratrol may be benificial for diabetes. Administration of resveratrol may protect against oxidative damage caused by high glucose levels. It also reduces diabetic neuropathic pain.

Heart health

Resveratrol protects our heart and blood vessels by directly scavenging oxidants, which could cause oxidation of lipids, and by preventing apoptosis of endothelial cells. It may also help to prevent heart damage after a cardiac arrest. Reduced platelet aggregation has been attributes to resveratrol, thereby reducing the risk of atherosclerosis.

Increase of lifespan

Tests with animals have shown that that high food intake reduces lifespan. One study showed that resveratrol was able to able to increase the life span of mice on a high calorie diet.


Many studies on animals have shown antitoxic effects of resveratrol. Resveratrol was able to reverse damages caused by the administration of the chemotherapeutic drug bleomycin. Resveratrol also helped to reduce brain damage and oxidative damage of the liver during ethanol intoxication. It also reduced kidney damage of rats treated with the antibiotic gentamicin.

Facts about Resveratrol

Resveratrol explains partly the French Paradox: the low incidence of heart disease among French people, who eat relatively a lot of unhealthy fat but drink resveratrol containing red wine.

Research Reviews

Resveratrol Promotes Clearance of Alzheimer’s Disease 

Resveratrol Inhibits TNF-alpha?Induced Proliferation and Matrix Metalloproteinase Expression in Human Vascular Smooth Muscle Cells

Resveratrol in cancer management

Studies on Resveratrol and cancer

Studies on Resveratrol and colon cancer  (MANY STUDIES)

Studies on Resveratrol and ovarian cancer ( MANY STUDIES)

Studies on Resveratrol and Anti-Tumor

Studies on Resveratrol and Apoptotic

Studies on Resveratrol and Chemotherapeutic

Oxindole alkaloids:

Pteropodin, Specrofillin, Hystopteropodin, Uncaria F, Uncaria Tomentosa, Isomitrofillin, etc.

  1. Cytotoxic effect of the pentacyclic oxindole alkaloid mitraphylline

    Sep 1, 2009 – In this study, the pentacyclic oxindole alkaloid mitraphylline was isolated  on human Ewing’s sarcoma MHH-ES-1 and breast cancer MT-3 cell 

  2. Cat’s Claw Oxindole Alkaloid Isomerization Induced by Cell

    Aug 23, 2013 – Cat’s Claw Oxindole Alkaloid Isomerization Induced by Cell Incubation and Cytotoxic Activity against T24 and RT4 Human Bladder Cancer Cell 

  3. Mitraphylline – Wikipedia, the free encyclopedia

    „Cytotoxic effect of the pentacyclic oxindole alkaloid mitraphylline isolated from Uncaria tomentosa bark on human Ewing’s sarcoma and breast cancer cell lines” 

  4. Cat’s Claw – American Cancer Society

    Sep 12, 2011 – Thanks to American Cancer Society volunteers, cancer patients receive…. Cytotoxic effect of the pentacyclic oxindole alkaloid mitraphylline 

  5. Oxindole alkaloids from Uncaria tomentosa induce apoptosis in  Nov 9, 2005 – increasing survival rates amongst cancer patients. However, mutations purified oxindole alkaloids, namely isopteropodine (A1), pteropodine 
  6. cancer | Naturopathy by Savvas Ioannides N.D.

    Jul 10, 2013 – Posts about cancer written by Naturopathy by Savvas Ioannides. minimal traces of immune-suppressing tetracyclic oxindole alkaloids (TOAs) 

  7. Cat’s Claw: A Rainforest Herb Quells Inflammation, Supports  www

    He improved remarkably, and one year later was apparently free of cancer of cat’s claw to compounds called oxindole alkaloids;1 more recently, however, 

    see this article Cat’s Claw click here

Styryl-lactones :

Altholactone, Goniothalamin,etc


A group of polyhenols; tannins are divided into 2 chemically distinct groups:

1) the condensed tannins (Proanthocyanidin)

2) the hydrolysable tannins (as hydrolysable Ellagitannins, such as Woodfordin C (macrocyclic ellagitannin dimmer), Oenotheietc.

NOTE: Anthocyanins: Peonidine-3-glucoside, Cyanidin-3-glucoside , etc.

see Tannic acid above


Alisol B acetate, Atractylon, Atractylenolides, Betulinic acid, Bisabolol, Boswellic acid, Carnosic acid,

Ferutidin, Ferutinin, Myristicin, Oleanolic acid, Parthenolide, Pomolic acid, Tymoquinone, …etc…

See Myristicin,above

Vanillys-phenols :

a group of polyhenols; share structural similarities possessing both the vanillyl (4-hydroxy

3-methoxyphenyl) moiety and the ketone functional group in their structure; Paradols, Gingerols, Yakuchinone B,

Curcumin (diferuloyl methane), Capsaicin (homo-vanillic acid derivative : 8 methyl-N-Vanillyl-6-nonenamide),etc.

See  Capsaicin,above

  • Curcumin

Turmeric(cucurmin) : ,

See also:



SPICES – more spices and herbs.plants in the book .


Malol, micromerol, urson, prunol, (3b)-3-hydroxyurs-12-en-28-oic acid

Ursolic acid is a is a pentacyclic triterpenoid.

Ursolic acid is present in many plants, including apples, bilberries, cranberries, elder flower, peppermint, lavender, oregano, thyme, hawthorn, prunes.

Ursolic acid has medicinally action, both topically and internally. Ursolic acid is used in many cosmetic preparations for its anti-inflammatory, antitumor and antimicrobial properties.Ursolic acid has antibacterial and antifungal activity. Tests have shown that Ursolic acid inhibits the growth of Candida albicans and Microsporium lenosum.Ursolic acid has anti-inflammatory properties and is used in ointments to treat burns.Topical application of ursolic acid inhibited TPA-induced initiation and promotion of tumor growth. important for preventing inflammation (i.e:used  in conjunction with CESIUM treatment)

Other Phytochemicals


In plants phytic acid is the principal store of phosphate. Phytic acid is a natural plant antioxidant.

Phytic acid can be found in most grains, seeds and beans. Rich sources of phytic acid are wheat bran and flaxseed (3 % phytic acid).

Health Benefits of Phytic acid

Phytic acid has been considered as an anti-nutritional component in cereals, seeds and beans. Research has traditionally focused on its structure that gives it the ability to bind minerals, proteins and starch, and the resulting lower absorption of these elements. However, resent research have shown that phytic acid has many health benefits. Phytic acid has antioxidant, anticancer, hypocholesterolemic and hypolipidemic effects.

Anticancer effect of phytic acid

In animal studies phytic acid showed a protective action in carcinogenesis. This action could be explained by its mineral chelating potential. Some studies suggest that phytic acid acts as anti-cancer agent by reversing the proliferative effects of carcinogens.

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

Journal of Nutrition. 2003 November;133:3778S-3784S.

Phytic acid seems only to affect cancer cells and not normal cells. Phytic acid and inositol improves the effectiveness of chemotherapy. More studies are required to determine optimal dosage, effectiveness and safety of phytic acid.

The biochemical changes associated with phytic Acid on induced breast proliferative lesions in rats: preliminary findings. 

Cancer Biology and Therapy. 2006 September;5(9):1129-33

Previous studies shown that phytic acid inhibits or prevents the growth of neoplasms. The aim of this study was to investigate if phytic acid has an effect on tumorigenesis by inducing apoptosis and inhibiting of oxidative stress. The in-vivo test was carried out on rats which were treated with the carcinogen dimethylbenz(a)anthracene (DMBA). The researchers found that the administration of phytic removed the benign proliferative breast changes. Phytic acid significantly decreased trichostatin A and nitric oxide levels and increased apoptosis. The study concluded that the administration of phytic acid reversed the proliferative effects of the carcinogen DMBA, and could have a protective effect.

Interactive suppression of aberrant crypt foci induced by azoxymethane in rat colon by phytic acid and green tea. 

Carcinogenesis. 1997 October;18(10):2023-6

Epidemiological studies show a relation between diet and the incidence of colon cancer. Both phytic acid and phytochemicals in green tea seems to act as anticancer agents and have been linked wit reduced risk of cancer. The aim of this in vivo study with rats was to determine the possible synergistic effect of phytic acid and green tea on the inhibition of colonic preneoplastic lesions formations and the enzyme glutathione S-transferase. The rats were treated with the carcinogen azoxymethane and received different combinations of phytic acid and green tea. The researchers found that green tea alone had only marginal effect whereas phytic acid significantly reduced the incidence of aberrant crypt foci. The combination of phytic acid and green tea showed a significant and synergistic anticancer effect.

Protective effect of phytic acid on oxidative DNA damage with reference to cancer chemoprevention. 

Biochemical and Biophysical Research Communications. 2001 November 2;288(3):552-7

According to K Midorikawa and colleagues, phytic acid is one of the most promising cancer chemopreventive agents. The aim of this study was the determine the anticancer mechanism of phytic acid. They found that phytic acid inhibited the oxidative damage of hydrogen peroxide, but that phytic acid did not directly scavenge hydrogen peroxide. Phytic acid did not cause damage to DNA. They concluded that phytic acid acts as an antioxidant and anticancer agent by chelating metals.

Antitumor activity of phytic acid (inositol hexaphosphate) in murine transplanted and metastatic fibrosarcoma, a pilot study.

Cancer Letters. 1992 July 31;65(1):9-13

In vivo tests have shown that phytic acid exerts a antitumor effect on experimental colon cancer. The purpose of this study was to determine the antitumor activity of phytic acid on other experimental tumor models, such as murine fibrosarcoma. The researchers found that the intraperitoneal injection of mice with phytic acid reduced the growth of subcutaneously transplanted fibrosarcoma and prolonged survival. Phytic acid could have a potential use in the therapy of cancer.
2008 Acta poloniae pharmaceutica
2008 Acta poloniae pharmaceutica
Anticarcinogenic efficacy of phytic acid extracted from rice bran on azoxymethane-induced colon carcinogenesis in rats.2010 Experimental and toxicologic pathology : official journal of the Gesellschaft für Toxikologische Pathologie

Benificial for diabetic patients

Phytic acid may have health benefits for diabetes patients. It lowers blood glucose response by reducing the rate of starch digestion and slowing the gastric emptying.

Other effects

Phytic acid releases inositol that during digestion. Although inositol is not an essential nutrient it might reduce depressions. Studies also show that phytic acid may reduceinflammation.

Other things:

Melatonin( night sleep between 22 pm – 3am) -VERY IMPORTANT  – IMPORTANT article  ,


1.  „Melatonin is a potent immune-enhancing hormone produced by the human pineal gland and appears to have substantial cancer-repelling power. In addition to boosting the activity of key immune cells called T helper cells, melatonin stimulates the tumor-killing action of natural killer cells (NK) by increasing the white blood cell production of the cytokine Interleukin-2 (IL-2) [Excerpt from the Definitive Guide to Cancer, by John Diamond, M.D. and Lee Cowden, M.D]

2.  „Researchers at Brigham and Women’s Hospital (BWH), led by Eva Schernhammer, MD, DrPH, (Assistant Professor of Medicine at Harvard Medical School) were among the first to report that nightshift workers may have an increased risk of developing breast cancer. Decreased levels of melatonin – a hormone closely linked to sleep patterns – is believed to be a possible cause. Now, in the next phase of this research, Schernhammer reports that lower melatonin levels are associated with a higher risk of breast cancer. The findings are published in the July 20, 2005 issue of the Journal of the National Cancer Institute (JNCI). The hormone melatonin is typically released from the brain during the night. It is the reason people get sleepy. Nightshift workers, exposed to bright light during the evenings, produce less melatonin. Laboratory studies have shown that melatonin production can put tumor cells “to sleep” by stunting growth. A recent report indicated that in constant light, tumors grew seven times faster than they did in the dark. In this study, the researchers measured urinary melatonin in 147 women who developed invasive breast cancer and 291 matched women who did not develop breast cancer. They found that women with the lowest levels of the melatonin metabolite in their urine were 70 percent more likely to develop breast cancer.” [Press Release – Brigham and Women’s Hospital Research Unit]

3.  On October 17 2001, the Journal of the National Cancer Institute (Vol. 93, No. 20, pp. 1557-1568) published two papers reporting a significant increase in the risk of breast cancer among women who frequently did not sleep during the period of the night, about 1:30am, when melatonin levels are typically at their highest.

4.  Research presented recently at the 94th Annual Meeting of the American Association for Cancer Research in Washington, D.C., shows evidence that the night-time production of the hormone melatonin (produced during deep sleep) inhibits the growth of human breast cancer by blocking the tumor’s uptake of dietary linoleic acid. [Bassett Research Institute – Preclinical Study supported by the National Cancer Institute]

5.  Studies at the University of Texas Medical Branch showed that „melatonin significantly increased the latency period of the tumor, by delaying the appearance of the tumor”.

6.  According to the University of Maryland Medical Center: „Women with breast cancer and men with prostate cancer tend to have lower levels of melatonin than those without the disease. Low levels of melatonin stimulate the growth of certain types of cancer cells and adding melatonin to these cells inhibits their growth. Meditation appears to be a valuable addition to the treatment of cancer due to a rise in levels of melatonin in the body.”

7.  According to the University of Massachusetts Medical Center: „Melatonin has been shown by a number of studies to significantly inhibit breast cancer in animals and tissue culture.” In a separate study performed at the University a higher level of melatonin was found in meditators than in non-meditators.

8.  According to the American Cancer Society: „A National Institute of Health panel found evidence that regular meditation can also reduce symptoms of post-traumatic stress syndrome, and increase longevity and quality of life. The same study found that those who meditated had a better immune response than those who did not meditate.”

9.  „Melatonin can kill directly many different types of tumour cells. It is a naturally produced cytotoxin, which can induce tumor cell death (apoptosis). In instances where the tumour has already established itself in the body, melatonin has been shown to inhibit the tumour’s growth rate. Melatonin exhibits natural oncostatic activity and inhibits cancer cell growth. In patients in whom cancer has become a noticeable physical burden and produces overt symptoms, melatonin has been shown to alleviate numerous cancer symptoms and to inhibit development of new tumour blood vessels (tumour angiogenesis), which in turn inhibits the cancer from spreading further (mestastasis). Radiation therapy usually induces anemia. Melatonin stimulates platelet production and has been shown to effectively treat cancer patients with low platelet counts and anemia. Melatonin reduces chemotherapy-induced cardiotoxicity, neurotoxicity, thrombocytopenia (reduced platelet counts), stomatitis (inflammation of mouth), and asthenia (weakness), and improves the overall response in cancer patients.” [Clinical Study, The Life Extension Foundation]

10.  “Results from a new study in laboratory mice show that night-time exposure to artificial light stimulated the growth of human breast tumors by suppressing the levels of a key hormone called melatonin. The study also showed that extended periods of night-time darkness greatly slowed the growth of these tumors.” [US Department of Health and Human Services – National Institute of Health]

11.  „Experienced meditators practicing either TM-Sidihi or another internationally well known form of yoga meditation showed significantly higher melatonin levels in the period following meditation.” [School of Psychology, La Trobe University, Australia]




Scientific Publications

  • Bicher, James Haim, MD., Wolfstein, Ralf, M.D. Thermoradiotherapy with curative intent – breast, head and neck and prostate tumors. Deutsche Zeitschrift für Onkologie (German Journal of Oncology) 2006, 38: 116-122.
  • Bicher HI, McLaren JR, Pigliucci GM, (eds). Consensus on Hyperthermia for the 1990s.Clinical Practice in Cancer Treatment. Plenum Press, New York and London, 1990.
  • Bicher HI, Hetzel FW, Sandhu TS. Physiology and Morphology of Tumor Microcirculation on Hyperthermia. Chapter 9. Ed. K Storm, K Hall Publisher, New York, 1982.
  • Bicher HI, Hetzel FW, D’Agostino L, Johnson RJ. Changes in tumor tissue oxygenation induced by microwave hyperthermia. Int J. Radiat Oncol Biol Phys 1977, S2:157.
  • Bicher HI, Hetzel FW, Mitagvaria N, O’hara M. Reoxygenation induced by localized microwave hyperthermia as an adjuvant to radiation therapy. 6th International Congress of Radiation Research, 1979, 5:171-175.
  • Bicher HI, Hetzel FW, Sandhu TS, Frinak S, Vaupel P, O’Hara MD, O’Brien T. Effects of hyperthermia on normal and tumor microenviroment. Radiology 1980, 137:523530.
  • James Haim Bicher, M.D. The physiological effects of hyperthermia. Radiology; 1980:511513.
  • Sandhu TS, Bicher HI, Hetzel FW. A thermal dosimetry system with blood flow simulation. Journal of National Cancer Institute, 6:361-363.
  • Bicher HI, Sandhu TS, Vaupel P, Hetzel FW. The effect of localized microwave hyperthermia on physiological responses. Journal of National Cancer Institute, 6:375-377.
  • Bicher HI, Sandhu TS, Hetzel FW. Inhomogenities in oxygen and pH distributions in tumors. Radiat Res 1980, 83376.
  • Hetzel FW, Kaufman N, Brown M, Bicher HI. Indirect sensitization by drug induced reoxygenation in spheroids. Radiat Res 1980, 83:375376.
  • Bicher HI, Sandhu TS, Vaupel P, Hetzel FW. Physiological mechanisms of action of localized microwave hyperthermia. Presented at the Third International Symposium on Cancer Therapy by Hyperthermia, Drugs and Radiation. Fort Collins, Colorado, June 1920, 1980.
  • Bicher HI, Sandhu TS, Hetzel FW, Matvia F. An effective fractionation protocol for the clinical use of hyperthermia with adjuvant radiation. Presented at the Second Meeting of the European Group on Hyperthermia in Radiation. Rome, Italy, September 1920, 1980.
  • Bicher HI, Vaupel P, O’Hara MD, O’Brien T, Mitagvaria N. Tissue oxygenation in normal and hyperthermic conditions. In proceedings of the XXVIIIth International Congress of Physiological Sciences. Budapest, Hungary, July 1318, 1980. Akademial Kiado Publishers: Adv. Physiol Sci. 1981, 25:215233.
  • Bicher HI, Hetzel FW, Vaupel P, Sandhu TS. Microcirculation modification by localized microwave hyperthermia and hematoporphyrin phototherapy. Bibl Anat 1981, 20:628632.
  • James Haim Bicher, M.D., Nodar Mitagvaria Circulatory responses of malignant tumors during hyperthermia. Microvascular Research 1981, 21:1926.
  • Bicher HI, Sandhu TS, Vaupel P, Hetzel FW. Effect of localized microwave hyperthermia on physiological responses. Natl Inst Drug Abuse Res Monogr Ser 1982, 61:217219.
  • Vaupel P, Frinak S, MuellerKlieser W, Bicher HI. Impact of localized hyperthermia on the cellular microenvironment in solid tumors. Natl Inst Drug Abuse Res Monogr Ser 1982, 61:207209.
  • Bicher HI. Impact of microcirculation and physiologic considerations on clinical hyperthermia. Proceedings 13th International Cancer Congress, 235245, Alan R Liss Inc., New York, 1983.
  • Bicher HI, Mitagvaria NP. Changes in tumor tissue oxygenation during microwave hyperthermia clinical relevance. Advances in Experimental Medicine and Biology, 180: 190905, 1985.
  • Mitagvaria NP, Bicher HI. Effect of microwave radiation on local blood flow and tissue oxygenation in the brain. Bulletin of Experimental Biology and Medicine, 98:895897, 1984.
  • Bicher HI, Shani J, Reesman KJ. Use of non perturbing thermocouples (NPT’s) for hyperthermia clinical thermometry. Int. J. Hyperthermia, 3:550551, 1987. (Abst) and J. Microwave power 22: 173, 1987, (Abst).
  • Bicher HI, Wolfstein RS. Local Hyperthermia of tumors at moderate depth using POPAS: Results by site (Abstract). 36th Annual Meeting of the Radiation Research Society, 4:1621, 1988.
  • Bicher HI, Shani J, Reesman KJ. Use of nonperturbing thermocouple for clinical hyperthermia thermometry (Abstract). 36th Annual Meeting of the Radiation Research Society, 4:1621, 1988.
  • Bicher HI, Wolfstein RS. Treatment of intratoracic lesions. Preliminary results (Abstract). 37th Annual Meeting of the Radiation Research Society. 3:1823, 1989.
  • Bicher HI, Reesman KJ, Afuwape SA. A target triapplicator system with nonperturbing thermocouples thermometry. Hyperthermic Oncology 1988, Taylor and Francis, 1:778779, 1989.
  • Bicher HI, Mitagvaria, N. Oxygen and pH in Human Tumors During Hyperthermia (Abstract). Proceeding of the 1991 International Society on Oxygen Transport to Tissue Meeting (ISSOT). Willemstad, Curaco, Netherlands Antilles, August 24-30, 1991.
  • Mitagvaria, N., Bicher HI. Local Blood Flow and PO2 in Rat’s Brain During Maze Behavior (Abstract). Proceeding of the 1991 International Society on Oxygen Transport to Tissue Meeting (ISSOT). Willemstad, Curaco, Netherlands Antilles, August 24-30, 1991.
  • Bicher HI, Wolfstein RS. Transcranial Treatment of Brain Tumors with Microwave Hyperthermia (Abstract). Proceeding of the 8th Annual Conference of the American Society for Clinical Hyperthermic Oncology (ASCHO). Chicago, Illinois, October 31-November 2, 1991.
  • Bicher HI, Mitagvaria N. Oxygen and pH in Human Tumors During Hyperthermia (Paper presented as a poster). Proceeding of the 6th International Congress on Hyperthermic Oncology. Tucson, Arizona, April 26- May 1, 1992.
  • Surowiec, A. Bicher HI, Caridad, C. A Comparison of Heating Characteristics of Two Hyperthermia Systems Used for Deep Seated Malignancies BSD-2000 and Tripas (Abstract). Proceeding of the 16th International Symposium on Clinical Hyperthermia (ISCHO). Kyoto, Japan, June 13-16, 1993.
  • Bicher HI, Yarmonenko S, Wainson A, Swrowiec I, Metagvaria N. Specific inhibition of L-Glucose cell proliferation. Potentiation of Hyperthermia, Radiation and Chemotherapy effects (Abstract). Proceeding of the 10th Annual Meeting of the American Society Of Clinical Hyperthermic Oncology (ASCHO). Memphis, Tennessee; November 28-30, 1993.
  • Surowiec, A, Bicher HI, Intercomparison of Heating Patterns of the BSD-2000 and the Tripas System (Abstract). Proceeding of the 14th Annual Meeting of the North American Hyperthermia Society (NAHS), Nashville, Tennessee, April 29- May 4, 1994.
  • Bicher HI, Yarmonenko, S. Wainson, A. Surowiec, I. Mitagvaria, N. Anticancer Effect of L-Glucose In-Vivo Potentiation of Hyperthermia (Abstract). Proceeding of the 17th International Symposium on Clinical Hyperthermia (ISCH). Pavia, Italy, May 1-5, 1994.
  • Bicher HI MD., Eva H. Barker, Patrick J. Bolan, Lance delabarre, Hellmuth Merkle, Lenore I. Everson, Michael Garwood. In VIVO Monitoring to Treatment for Breast Cancer Using 4T H MRS. Center for Magnetic Resonance Research, University of Minnesota, 2021 Sixth street SE, Minneapolis, MN. USA;
  • H. Bicher, Mitagvaria, I. Kvachadze , T. Khetsuriani, A. Shukakidze, I. Lazrishvili, M. Arabuli, TS.T. Khomeriki, Main factors in development of local hyperthermia-induced morphological changes in cerebral tissue of the rat In Press, Proceedings of Tbilisi State Medical University.


Here are part of the extended bibliography and enormous amount of studies that exist about natural substances and their effective effect against cancer( I say part as most of them are cited from NaturalNews website, website I also write for; fpr example, see my article on scientific studies on chemo/radiation:


1.Take your nutrients from ORGANIC WHOLE FOODS rather than supplements

2.The impoverishment of vitamin and pro-vitamin complexes no longer present in food, with the consequent increase in degenerative and deficient diseases such as cancer. The deliberate attempt to deactivate the natural substances contained in the plants is very serious: in this way fresh fruit and vegetables – greatly impoverished of many vitamins – can be carried over long distances and long periods of time because their oxidation does not take place.This vitamin impoverishment will ensure commercial

profits and represents a serious act of deliberate damage inflicted on the Ecosystem by means of GMOs.

It’s heavy the possible disappearance of anti-cancer vitamins, that induce apoptosis (suicide) of the

tumors (Anthocyanin, Flavonoids (1122), Polyphenols (1123), sesquiterpene lactone Parthenolide (701), penta-acetyl

Geniposide (1061), Camelliin B (698), beta-Cryptoxantin (1063), Hesperidin (1063), Emodin (247,333,715), ursolic acid (700),

allyl Sulfur (694,696), Eriodictoyol (693), hibiscus protocatechin acid (692), Indoles (809), Isothiocyanates (809), Resverarol

(695), Elemene (690), Acutiaporberine (711), Capsaicin (719), Wagonin (713), Fisetin (713), carnosic acid (1062), Germanium

sesquioxide (269), epigallocatechin Gallate (173,1124), Axerophthol palmitate, alpha and beta Carotene, trans-Retinoic acid,

Tocopherols, Limonene (693), Cynaropicrin, Lycopene (633,1359), Proanthocyanidin, Damnacanthal (1043), Baicalin (718),

Baicalein (718), hydrocinnamic acid (693), sesquiterpenoids as Atractylon (704), as Atractylenolides I, II, III (704),

gelsemium alkaloids (699), tartary buckwheat flavonoid (1064), Sinigrin, ferulic acid, ellagic acid, cumarinic acid, …)

SEE: http://www.erbeofficinali/dati/nacci/allpdf.php

The disappearance of these natural anti-cancer vitamins is a grave threat.

See also a FREE EBOOK detailing Thousand Plants against Cancer without Chemo-Therapy ,May 2010 ,650 pages

EVIDENCE BASED MEDICINE:  2,050 official scientific publications ,2,100 various bibliographical references BONUS in my book, next to other 4 free ebooks(Dr. W .Kelley Dr. Binzel, Dr. Matias Rath , Johanna Brandt. )

In this book the plants are identified by their Latin names – according to the modern scientific classification (see Chapter 20)

– and 2,050 official scientific publications are quoted (out of 2,100 various bibliographical references (see Chapter 21), useful to in depth studies, which confirm the various arguments indicated there.

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