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Estro Performance

$83.97

ESTRO-PERFORMANCE-60

Promote healthy estrogen levels safely and naturally with Estro Performance.

Estro Performance is an anti-cancer, anti-estrogen product that promotes healthy estrogen levels in both men and women. The naturally occurring ingredients in Estro Performance convert toxic, carcinogenic estrogens (like xenoestrogens from plastics and pollution) into chemoprotective, anti-estrogenic forms. It is safe to take everyday and the ingredients in Estro Performance can be found in fruits and vegetables.

60 capsules/30 servings

Description

Ingredients

Calcium D-Glucarate: Supplemental calcium D-glucarate enhances the body’s detoxification of environmental toxins and metabolic wastes. It also helps eliminate excess estrogens that can cause estrogen-related diseases.

Indole-3-Carbinol (I3C): Found naturally in cruciferous vegetables (e.g., cauliflower, cabbage, broccoli), I3C is an anti-estrogen that has a positive effect on estrogen metabolism and is associated with a reduction in tumor growth. Labratory animal studies have demonstrated that I3C is effective against cancer, atherosclerosis, and systemic lupus erythematosus (SLE).

3,3′-Diindolylmethane (DIM): DIM is also an anti-estrogen and is a metabolite of I3C. In laboratory testing, DIM has proven to be a potent alternative cancer therapy, especially against breast cancer cells.

Dosage

Take 2 capsules once per day.

WARNING: Consult a medical professional before use if you are taking prescription medicine, are pregnant, or are nursing. Not intended for use by people under 18 years of age. It is highly recommended to have estrogen levels tested before using an anti-estrogen product.

KEEP OUT OF REACH OF CHILDREN.

References

Walaszek, Z., Szemraj, J., Narog, M., Adams, A. K., Kilgore, J., Sherman, U., & Hanausek, M. (1997). Metabolism, uptake, and excretion of a D-glucaric acid salt and its potential use in cancer prevention. Cancer detection and prevention,21(2), 178.

D-Glucaric acid (GA) is a nontoxic, natural compound. One of its derivatives is the potent beta-glucuronidase inhibitor D-glucaro-1,4-lactone (1,4-GL). The goal of this study was to demonstrate the in vivo formation of 1,4-GL from a D-glucarate salt and determine its metabolism, uptake by selected organs, and excretion following oral administration of potassium hydrogen D-[14C]glucarate to male and female Sprague-Dawley rats. 1,4-GL increases detoxification of carcinogens and tumor promoters/progressors by inhibiting beta-glucuronidase and preventing hydrolysis of their glucuronides. 1,4-GL and its precursors, such as potassium hydrogen D-glucarate and calcium D-glucarate, may exert their anticancer action, in part, through alterations in steroidogenesis accompanied by changes in the hormonal environment and the proliferative status of the target organ. Thus, GA derivatives may be useful as new or adjuvant cancer preventive and therapeutic agents. In our study, 1,4-GL was found to be formed from the D-glucarate salt in the stomach of rats. It was apparently absorbed from the gastrointestinal tract, transported with the blood to different internal organs, and excreted in the urine and to a lesser extent in bile. There were no significant differences in the metabolism of PHG between male and female rats. Thus, formation of 1,4-GL from D-glucaric acid derivatives may be prerequisite for their inhibition of chemical carcinogenesis in rodents and prevention of breast, prostate, and colon cancer in humans.

Singh, J., & Gupta, K. P. (2007). Induction of apoptosis by calcium D-glucarate in 7, 12-dimethyl benz [a] anthracene-exposed mouse skin. Journal of Environmental Pathology, Toxicology and Oncology, 26(1).

Calcium glucarate (Cag), a naturally occurring nontoxic compound, suppresses the DMBA-induced tumor development in mouse skin. In the process of understanding the mechanisms of tumor suppression by Cag, we investigated the effect of topical application of Cag on selective and critical events of apoptotic pathway in DMBA-exposed mouse epidermis. Varied doses of DMBA or Cag were used for the study. DMBA had an inhibitory effect on proteases in general and on caspases in particular. Cag tried to reverse the inhibitory effect of DMBA on 3, 8, or 9 caspase in a dose-dependent manner. Cag inhibited activity of Poly ADP-ribose polymerase enzyme, a substrate of caspses, after DMBA exposure. As indicated by western blotting, Cag treatment also inhibited PARP expression induced by DMBA at the level of protein. Cag induced the DMBA-inhibited Ca++/Mg++-dependent endonuclease, an enzyme responsible for the DNA fragmentation during apoptosis. DMBA induced the expression of mutant-p53 and Bcl-2. This induced expression of proteins was reversed when Cag was given along with DMBA. Cag showed a dose-dependent inhibition of DMBA-induced mutant-p53 expression. Similarly Bcl-2 overexpression by DMBA was also inhibited by topical treatment of Cag when given along with DMBA. Inhibition of mutant-p53 and Bcl-2 expression by Cag in DMBA-exposed mouse skin might contribute to the apoptogenic effect possibly exerted by Cag while suppressing the tumor development. The study indicates that Cag induces apoptosis in mouse epidermis, a possible mechanism for tumor suppression, and thus could be considered a promising anticancer agent.

Hanausek, M., Walaszek, Z., & Slaga, T. J. (2003). Detoxifying cancer causing agents to prevent cancer. Integrative Cancer Therapies, 2(2), 139-144.

Different vitamins and other micronutrients in vegetables, fruits, and other natural plant products may prevent cancer development (carcinogenesis) by interfering with detrimental actions of mutagens, carcinogens, and tumor promoters. The goal of current studies in cancer prevention is to determine the mechanisms of synergistic action of the natural source compounds known to inhibit one or more stages of carcinogenesis, that is, initiation and promotion/progression. Many natural cancer preventive agents are effective inhibitors of tumor initiation, promotion, and/or progression. The mechanism of action is related to their abilities to prevent critical carcinogen metabolism and to increase detoxification of carcinogens and tumor promoters. The authors review here the potential role of the detoxification system and, in particular, the roles of D-glucaric acid and the enzyme β-glucuronidase in early detection and prevention of cancer. There is now growing evidence for the possible control of different stages of the cancer induction by inhibiting β-glucuronidase with D-glucaric acid derivatives, especially with its salts (D-glucarates). D-Glucaric acid has been found in many vegetables and fruits. Therefore, the consumption of fruits and vegetables naturally rich in D-glucaric acid or self-medication with D-glucaric acid derivatives such as calcium D-glucarate offers a promising cancer prevention approach.

Jellinck, P. H., Gekforkert, P., Riddick, D. S., Okey, A. B., Michnovicz, J. J., & Bradlow, H. L. (1993). Ah receptor binding properties of indole carbinols and induction of hepatic estradiol hydroxylation. Biochemical pharmacology, 45(5), 1129-1136.

The effect of route of administration on the ability of indole-3-carbinol (I3C), an anticarcinogen present in cruciferous vegetables, to induce estradiol 2-hydroxylase (EH) in female rat liver microsomes was investigated and compared to that of its main gastric conversion product, 3,3′-diindolylmethane (DIM). This dimer was more potent than I3C after either oral or intraperitoneal administration and was also a better in vitro inhibitor of EH in control and I3C-induced hepatic microsomes. The induction of both CYP1A1 and 1A2 in about equal amounts by I3C and DIM as well as of CYP2B1/2 was demonstrated using monoclonal antibodies. DIM, isosafrole, β-naphthoflavone, 3-methylcholanthrene and naringenin added in vitro inhibited EH strongly in induced microsomes but gestodene was a better inhibitor of estrogen 2-hydroxylation in liver microsomes from untreated female rats. The binding affinities of I3C and DIM to the Ah receptor were compared to that of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) by competition studies, and the IC50 values were shown to be 2.0 × 10−9 M, 5.0 × 10−5 M and 2.3 × 10−3 M for TCDD, DIM and I3C, respectively. The ability of I3C or DIM to cause in vitro transformation of the Ah receptor to a form able to bind to the dioxinresponsive element-3 (DRE3) was compared to that of TCDD and shown to parallel their abilities to compete for binding of [3H]TCDD to the Ah receptor. These experiments confirm and extend the proposals that dietary indoles induce specific cytochrome P450s in rat liver by a mechanism possibly involving the Ah receptor. The induced monooxygenases, in turn, increase the synthesis of 2-hydroxylated estrogens in the competing pathways of 2- and 16α–hydroxylation which decreases the levels of 16α-hydroxyestrone able to form stable covalent adducts with proteins including the estrogen receptor. Such steroid-protein interaction has been correlated with mammary carcinogenesis.

Parkin, D. R., YONGJIAN, L., Bliss, R. L., & Malejka-Giganti, D. (2008). Inhibitory effects of a dietary phytochemical 3, 3′-diindolylmethane on the phenobarbital-induced hepatic CYP mRNA expression and CYP-catalyzed reactions in female rats. Food and chemical toxicology, 46(7), 2451-2458.

3,3′-Diindolylmethane (DIM), derived from indole-3-carbinol (13C), is used as a dietary supplement for its putative anticancer effects that include suppression of mammary tumor growth in female rats. The mechanism of action DIM may involve its interaction(s) with hepatic cytochromes P450 (CYPs) catalyzing oxidations of 17p-estradiol (E2). Our study showed that DIM added to hepatic microsomes of female Sprague-Dawley rats was primarily a competitive inhibitor of β-naphthoflavone (β-NF)- or 13C-induced CYP1A1 probe activity, and a potent mixed or uncompetitive inhibitor of phenobarbital (PB)-induced CYP2B1 or CYP2B2 probe activity, respectively. Microsomal metabolites of DIM were tentatively identified as two mono-hydroxy isomers of DIM, each formed preferentially by CYP1A1- or CYP2B1 /2-catalyzed reaction. Evaluation of the effects of co-treatment of rats with PB and DIM by a full factorial ANOVA showed that DIM decreased the PB-induced CYP2B1 and CYP2B2 mRNA expression levels, and the rates of 2- and 4-hydroxylation of E2, and total E2 metabolite formation. The results suggest that interactions of DIM, and/or its mono-hydroxy metabolites, with CYP2B1 and CYP2B2 found to occur in hepatic microsomes upon addition of DIM or co-treatment of rats with DIM affect the rates of relevant oxidations of E2, and potentially protect against estrogen-dependent tumorigenesis.

Hsu, J. C., Dev, A., Wing, A., Brew, C. T., Bjeldanes, L. F., & Firestone, G. L. (2006). Indole-3-carbinol mediated cell cycle arrest of LNCaP human prostate cancer cells requires the induced production of activated p53 tumor suppressor protein. Biochemical pharmacology, 72(12), 1714-1723.

Indole-3-carbinol (13C), a dietary compound found naturally in cruciferous vegetables of the Brassica genus such as broccoli and brussels sprouts, induces a G1 growth arrest of human reproductive cancer cells. We previously reported that in LNCaP prostate cancer cells, I3C down-regulated cyclin-dependent kinase (CDK) 2 activity. In our current study, Western blotting and quantitative RT-PCR demonstrated that I3C treatment increased both the transcripts and protein levels of the CDK2 inhibitor p21waf1/cip1 (p21). Transfection of luciferase reporter plasmids containing wild-type and mutated p21 promoter fragments revealed that I3C induced p21 gene transcription through a p53 DNA binding element. Oligonucleotide precipitation showed that I3C increased the level of activated p53 nuclear protein that is competent to bind its DNA target site on the p21 promoter. Ablation of p53 production using short interfering RNA (siRNA) prevented that the I3C induced G1 arrest and up-regulation of p21 expression. Western blots using p53 phospho-specific antibodies revealed that I3C treatment increased the levels of three phosphorylated forms of p53 (Serl5, Ser37, Ser392) that are known to contribute to p53 protein stability and greater transactivation potential. Taken together, our results establish that the I3C induced G1 arrest of human prostate cancer cells requires the induced production of the activated phosphorylated forms of p53, which stimulate transcription of the CDK2 inhibitor p21.

Safe, S., Papineni, S., & Chintharlapalli, S. (2008). Cancer chemotherapy with indole-3-carbinol, bis (3′-indolyl) methane and synthetic analogs. Cancer letters,269(2), 326-338.

Indole-3-carbinol (I3C) conjugates are phytochemicals expressed in brassica vegetables and have been associated with the anticancer activities of vegetable consumption. I3C and its metabolite bis(3′-indolyl)methane (DIM) induce overlapping and unique responses in multiple cancer cell lines and tumors, and these include growth inhibition, apoptosis and antiangiogenic activities. The mechanisms of these responses are complex and dependent on cell context. I3C and/or DIM activate or inactivate multiple nuclear receptors, induce endoplasmic reticulum stress, decrease mitochondrial membrane potential, and modulate multiple signaling pathways including kinases. DIM has been used as a template to synthesize a series of 1,1-bis(3′indolyl)-1-(substituted aromatic)methanes (i.e. C-DIMs) which are also cytotoxic to cancer cells and tumors. Some of the effects of C-DIMs resemble those reported for DIM analogs; however, structure–activity studies with the aromatic ring has resulted in generation of highly unique receptor agonists. For example, p-trifluoromethylphenyl, p-t-butylphenyl and p-biphenyl analogs activate peroxisome proliferator-activated receptor γ (PPARγ), and p-methoxyphenyl and p-phenyl compounds activate nerve growth factor-induced-Bα (NGFI-Bα, Nur77) orphan nuclear receptor. The effects of C-DIMs on PPARγ and Nur77 coupled with their receptor-independent activities has resulted in the development of a novel group of multi-targeted anticancer drugs with excellent potential for clinical treatment of cancer.

*These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.

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