Pueraria mirifica contains various [/url]phytoestrogens including
Deoxymiroestrol
Miroestrol or Deoxymiroestrol is a phytoestrogens , a plant-derived chemical that mimics the biological activity of the hormone estrogen
Study on Rats
Daidzin
(Binding of estrogen receptor (ER) to estrogen response element (ERE))
A natural organic compound phytoestrogen in the class of phytochemicals known as isoflavones
Daidzein
can be converted to its end metabolite S-equol in some humans based on the presence of certain intestinal bacteria. Based on several decades of research, S-equol has potential for significant health benefits.
(S)-Equol, or (S)-(–)-4',7-isoflavandiol, is the (S)-enantiomer of the naturally occurring isoflavandiol estrogen, equol.[1] It is a non-steroidal, selective agonist of ERβ (Ki = 16 nM), with 13-fold selectivity for ERβ over ERα.[1] Relative to (S)-equol, (R)-equol is less potent and, in contrast, binds to ERα (Ki = 50 nM) with 3.5-fold selectivity over ERβ.[1] Under the code name AUS-131, (S)-equol is under development for the treatment of menopausal symptoms such as hot flashes and benign prostatic hyperplasia.[2][3][1] Human intestinal bacteria metabolize the soy isoflavone daidzein into (S)-equol, and it has been determined that (S)-equol is exclusively produced.[4]
Genistein
Due to its structure similarity to 17β-estradiol (estrogen), genistein can compete with it and bind to estrogen receptors. However, genistein shows much higher affinity toward estrogen receptor β than toward estrogen receptor α.[47] Data from in vitro and in vivo research confirms that genistein can increase rate of growth of some ER expressing breast cancers. Genistein was found to increase the rate of proliferation of estrogen-dependent breast cancer when not cotreated with an estrogen antagonist.[48][49][50] It was also found to decrease efficiency of tamoxifen and letrozole - drugs commonly used in breast cancer therapy.[51][52] Genistein was found to inhibit immune response towards cancer cells allowing their survival.[53]
Coumestrol
Coumestrol is a phytoestrogen, mimicking the biological activity of estrogens. Phytoestrogens are able to pass through cell membranes due to their low molecular weight and stable structure, and they are able to interact with the enzymes and receptors of cells. Coumestrol binds to the ERα and ERβ with similar affinity to that of estradiol (94% and 185% of the relative binding affinity of estradiol at the ERα and ERβ, respectively), although the estrogenic activity of coumestrol at both receptors is much less than that of estradiol.[6] In any case, coumestrol has estrogenic activity that is 30 to 100 times greater than that of isoflavones.
Kwakhurin
Kwakhurin has recently been found to have oestrogenic potency comparable with that of daidzein (but much less than of either genistein, or then courmestan, coumestrol) as determined by it relative ability to promote growth of human breast cancer cells being cultured in the presence of the oestrogen antagonist toremifene ( Chansakaow et al., 2000a)
Mirificine
β-sitosterol
β-Sitosterol (beta-sitosterol) is one of several phytosterols (plant sterols) with chemical structures similar to that of cholesterol. Sitosterols are white, waxy powders with a characteristic odor.They are hydrophobic and soluble in alcohols.
Stigmasterol
(Study with Rats)
(Study About anti-osteoarthritic properties)
Stigmasterol is an unsaturated phytosterol occurring in the plant fats or oils of soybean, calabar bean, and rape seed, and in a number of medicinal herbs, including the Chinese herbs Ophiopogon japonicus (Mai men dong), in Mirabilis jalapa and American Ginseng.
Stigmasterol is also found in various vegetables, legumes, nuts, seeds, and unpasteurized milk. Pasteurization will inactivate stigmasterol. Edible oils contains higher amount than vegetables.[4]
Phytosterols normally are broken down in the bile.
Research has indicated that stigmasterol may be useful in prevention of certain cancers, including ovarian, prostate, breast, and colon cancers. Studies have also indicated that a diet high in phytoesterols may inhibit the absorption of cholesterol and lower serum cholesterol levels by competing for intestinal absorption. Studies with laboratory animals fed stigmasterol found that both cholesterol and sitosterol absorption decreased 23% and 30%, respectively, over a 6-week period. It also possesses potent antioxidant, hypoglycemic and thyroid inhibiting properties.
Campesterol
(Link to Extra Information)
Campesterol is a phytosterol whose chemical structure is similar to that of cholesterol.
Natural occurrences
Many vegetables, fruits, nuts,[1] and seeds contain campesterol, but in low concentrations. Banana, pomegranate, pepper, coffee, grapefruit, cucumber, onion, oat, potato, and lemon grass (citronella) are few examples of common sources containing campesterol at roughly 1–7 mg/100 g of the edible portion. In contrast, canola and corn oils contain as much as 16–100 mg/100 g. Levels are variable and are influenced by geography and growing environment. In addition, different strains have different levels of plant sterols. A number of new genetic strains are currently being engineered with the goal of producing varieties high in campesterol and other plant sterols.[2] It is also found in dandelion coffee.
It is so named because it was first isolated from the rapeseed (Brassica campestris).[3] It is thought to have anti-inflammatory effects. It was demonstrated that it inhibits several pro-inflammatory and matrix degradation mediators typically involved in osteoarthritis-induced cartilage degradation.[4]
Mirificoumestan
Mirificoumestan is a Coumestan which is a heterocyclic organic compound.
Coumestan forms the central core of a variety of natural compounds known collectively as coumestans. Coumestans are oxidation products of pterocarpan[2] that are similar to coumarin. Coumestans, including coumestrol, a phytoestrogen, are found in a variety of plants. Food sources high in coumestans include split peas, pinto beans, lima beans, and especially alfalfa and clover sprouts.[3]
Coumestrol has about the same binding affinity for the ER-β estrogen receptor as 17β-estradiol, but much less affinity than 17α-estradiol, although the estrogenic potency of coumestrol at both receptors is much less than that of 17β-estradiol.[4]
Because of the estrogenic activity of some coumestans, a variety of syntheses have been developed that allow the preparation of coumestans so that their pharmacological effects can be explored.[5][6]
There is contradictory evidence for the presence of miroestrol.
It also contains the cytotoxic non-phytoestrogen spinasterol (Phytosterol)
PLANT STEROLS AND ESTROGEN
[url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3635199/](PUB MED)
A number of studies have shown that dietary components can influence ER status [69,70,71,72]. The ER-α is necessary for the proliferative effects of estradiol in breast cancer cells and is overexpressed in the transformed state [73,74,75,76].
It has been shown that intake of β-sitosterol is associated with a greater likelihood of estrogen receptor positive (ER+) than estrogen receptor negative (ER−) tumors (OR 0.49; 95% CI 0.18–0.98) [77]. From the standpoint that the presence of the ER maintains cell responsiveness to endocrine therapy, such as with the selective ER modulator (SERM), tamoxifen, ER+ breast cancer itself represents a more treatable condition than the ER− phenotype. ER− breast cancer is not susceptible to such treatment [78]. This fact underlies the current rationale for ER+ breast cancer treatments, which are aimed at minimizing the utility of this hormone and its resulting stimulatory effects on cell growth and division. However, despite the causal role of estrogen in the progression of ER+ breast cancer, nearly 30%–40% of breast cancers do not exhibit ER+ status [79]. Therefore, newer treatments and/or adjuvant therapies, which do not solely rely upon the ER, are of great importance.
β-Sitosterol has been demonstrated to competitively bind with equivalent affinity to both the α and β-isoforms of the ER and with an affinity comparable to that of coumestrol [80], which itself has been found to moderately stimulate growth of the ER+ cell line, MCF-7 [81]. Despite exerting an affinity for the ER, in rat models of PS exposure, β-sitosterol failed to increase uterine weight, a marker of estrogenic activity [82]. Likewise, plant stanols and stanol esters failed to stimulate estrogen responsive growth in MCF-7 cells [83]. There is, however some evidence for the estrogenic effects of PS [84], with evidence from reporter gene array studies in human breast cancer cell lines suggesting a role for PS as weak SERMs [80]. Additionally, PS may affect levels of sterol 27 hydroxylase (CYP27A1), an endogenous SERM [85], as β-sitosterol has been shown to inhibit the activity of sterol 27 hydroxylase upwards of 50% [86]. Despite the potential for PS to exert some estrogenic effects, these compounds may still exert beneficial effects on breast cancer, considering that tamoxifen, for instance is also known to be a SERM [87].
While PS may bind the ER or even act as SERMs, there is also the potential for PS to attenuate de novo steroid synthesis through reductions in cholesterol levels. To this end, some evidence exists for a reduction in androgens as a result of statin treatment [88], however direct evidence of PS exerting this modality has, to date, not been demonstrated. As will be discussed, PS may indirectly affect estrogen levels through means other than ER binding.
Deoxymiroestrol
Miroestrol or Deoxymiroestrol is a phytoestrogens , a plant-derived chemical that mimics the biological activity of the hormone estrogen
Study on Rats
Daidzin
(Binding of estrogen receptor (ER) to estrogen response element (ERE))
A natural organic compound phytoestrogen in the class of phytochemicals known as isoflavones
Daidzein
can be converted to its end metabolite S-equol in some humans based on the presence of certain intestinal bacteria. Based on several decades of research, S-equol has potential for significant health benefits.
(S)-Equol, or (S)-(–)-4',7-isoflavandiol, is the (S)-enantiomer of the naturally occurring isoflavandiol estrogen, equol.[1] It is a non-steroidal, selective agonist of ERβ (Ki = 16 nM), with 13-fold selectivity for ERβ over ERα.[1] Relative to (S)-equol, (R)-equol is less potent and, in contrast, binds to ERα (Ki = 50 nM) with 3.5-fold selectivity over ERβ.[1] Under the code name AUS-131, (S)-equol is under development for the treatment of menopausal symptoms such as hot flashes and benign prostatic hyperplasia.[2][3][1] Human intestinal bacteria metabolize the soy isoflavone daidzein into (S)-equol, and it has been determined that (S)-equol is exclusively produced.[4]
Genistein
Due to its structure similarity to 17β-estradiol (estrogen), genistein can compete with it and bind to estrogen receptors. However, genistein shows much higher affinity toward estrogen receptor β than toward estrogen receptor α.[47] Data from in vitro and in vivo research confirms that genistein can increase rate of growth of some ER expressing breast cancers. Genistein was found to increase the rate of proliferation of estrogen-dependent breast cancer when not cotreated with an estrogen antagonist.[48][49][50] It was also found to decrease efficiency of tamoxifen and letrozole - drugs commonly used in breast cancer therapy.[51][52] Genistein was found to inhibit immune response towards cancer cells allowing their survival.[53]
Coumestrol
Coumestrol is a phytoestrogen, mimicking the biological activity of estrogens. Phytoestrogens are able to pass through cell membranes due to their low molecular weight and stable structure, and they are able to interact with the enzymes and receptors of cells. Coumestrol binds to the ERα and ERβ with similar affinity to that of estradiol (94% and 185% of the relative binding affinity of estradiol at the ERα and ERβ, respectively), although the estrogenic activity of coumestrol at both receptors is much less than that of estradiol.[6] In any case, coumestrol has estrogenic activity that is 30 to 100 times greater than that of isoflavones.
Kwakhurin
Kwakhurin has recently been found to have oestrogenic potency comparable with that of daidzein (but much less than of either genistein, or then courmestan, coumestrol) as determined by it relative ability to promote growth of human breast cancer cells being cultured in the presence of the oestrogen antagonist toremifene ( Chansakaow et al., 2000a)
Mirificine
β-sitosterol
β-Sitosterol (beta-sitosterol) is one of several phytosterols (plant sterols) with chemical structures similar to that of cholesterol. Sitosterols are white, waxy powders with a characteristic odor.They are hydrophobic and soluble in alcohols.
Stigmasterol
(Study with Rats)
(Study About anti-osteoarthritic properties)
Stigmasterol is an unsaturated phytosterol occurring in the plant fats or oils of soybean, calabar bean, and rape seed, and in a number of medicinal herbs, including the Chinese herbs Ophiopogon japonicus (Mai men dong), in Mirabilis jalapa and American Ginseng.
Stigmasterol is also found in various vegetables, legumes, nuts, seeds, and unpasteurized milk. Pasteurization will inactivate stigmasterol. Edible oils contains higher amount than vegetables.[4]
Phytosterols normally are broken down in the bile.
Research has indicated that stigmasterol may be useful in prevention of certain cancers, including ovarian, prostate, breast, and colon cancers. Studies have also indicated that a diet high in phytoesterols may inhibit the absorption of cholesterol and lower serum cholesterol levels by competing for intestinal absorption. Studies with laboratory animals fed stigmasterol found that both cholesterol and sitosterol absorption decreased 23% and 30%, respectively, over a 6-week period. It also possesses potent antioxidant, hypoglycemic and thyroid inhibiting properties.
Campesterol
(Link to Extra Information)
Campesterol is a phytosterol whose chemical structure is similar to that of cholesterol.
Natural occurrences
Many vegetables, fruits, nuts,[1] and seeds contain campesterol, but in low concentrations. Banana, pomegranate, pepper, coffee, grapefruit, cucumber, onion, oat, potato, and lemon grass (citronella) are few examples of common sources containing campesterol at roughly 1–7 mg/100 g of the edible portion. In contrast, canola and corn oils contain as much as 16–100 mg/100 g. Levels are variable and are influenced by geography and growing environment. In addition, different strains have different levels of plant sterols. A number of new genetic strains are currently being engineered with the goal of producing varieties high in campesterol and other plant sterols.[2] It is also found in dandelion coffee.
It is so named because it was first isolated from the rapeseed (Brassica campestris).[3] It is thought to have anti-inflammatory effects. It was demonstrated that it inhibits several pro-inflammatory and matrix degradation mediators typically involved in osteoarthritis-induced cartilage degradation.[4]
Mirificoumestan
Mirificoumestan is a Coumestan which is a heterocyclic organic compound.
Coumestan forms the central core of a variety of natural compounds known collectively as coumestans. Coumestans are oxidation products of pterocarpan[2] that are similar to coumarin. Coumestans, including coumestrol, a phytoestrogen, are found in a variety of plants. Food sources high in coumestans include split peas, pinto beans, lima beans, and especially alfalfa and clover sprouts.[3]
Coumestrol has about the same binding affinity for the ER-β estrogen receptor as 17β-estradiol, but much less affinity than 17α-estradiol, although the estrogenic potency of coumestrol at both receptors is much less than that of 17β-estradiol.[4]
Because of the estrogenic activity of some coumestans, a variety of syntheses have been developed that allow the preparation of coumestans so that their pharmacological effects can be explored.[5][6]
There is contradictory evidence for the presence of miroestrol.
It also contains the cytotoxic non-phytoestrogen spinasterol (Phytosterol)
PLANT STEROLS AND ESTROGEN
[url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3635199/](PUB MED)
A number of studies have shown that dietary components can influence ER status [69,70,71,72]. The ER-α is necessary for the proliferative effects of estradiol in breast cancer cells and is overexpressed in the transformed state [73,74,75,76].
It has been shown that intake of β-sitosterol is associated with a greater likelihood of estrogen receptor positive (ER+) than estrogen receptor negative (ER−) tumors (OR 0.49; 95% CI 0.18–0.98) [77]. From the standpoint that the presence of the ER maintains cell responsiveness to endocrine therapy, such as with the selective ER modulator (SERM), tamoxifen, ER+ breast cancer itself represents a more treatable condition than the ER− phenotype. ER− breast cancer is not susceptible to such treatment [78]. This fact underlies the current rationale for ER+ breast cancer treatments, which are aimed at minimizing the utility of this hormone and its resulting stimulatory effects on cell growth and division. However, despite the causal role of estrogen in the progression of ER+ breast cancer, nearly 30%–40% of breast cancers do not exhibit ER+ status [79]. Therefore, newer treatments and/or adjuvant therapies, which do not solely rely upon the ER, are of great importance.
β-Sitosterol has been demonstrated to competitively bind with equivalent affinity to both the α and β-isoforms of the ER and with an affinity comparable to that of coumestrol [80], which itself has been found to moderately stimulate growth of the ER+ cell line, MCF-7 [81]. Despite exerting an affinity for the ER, in rat models of PS exposure, β-sitosterol failed to increase uterine weight, a marker of estrogenic activity [82]. Likewise, plant stanols and stanol esters failed to stimulate estrogen responsive growth in MCF-7 cells [83]. There is, however some evidence for the estrogenic effects of PS [84], with evidence from reporter gene array studies in human breast cancer cell lines suggesting a role for PS as weak SERMs [80]. Additionally, PS may affect levels of sterol 27 hydroxylase (CYP27A1), an endogenous SERM [85], as β-sitosterol has been shown to inhibit the activity of sterol 27 hydroxylase upwards of 50% [86]. Despite the potential for PS to exert some estrogenic effects, these compounds may still exert beneficial effects on breast cancer, considering that tamoxifen, for instance is also known to be a SERM [87].
While PS may bind the ER or even act as SERMs, there is also the potential for PS to attenuate de novo steroid synthesis through reductions in cholesterol levels. To this end, some evidence exists for a reduction in androgens as a result of statin treatment [88], however direct evidence of PS exerting this modality has, to date, not been demonstrated. As will be discussed, PS may indirectly affect estrogen levels through means other than ER binding.
Very interesting, but I believe Lotus posted most of this months ago. I could be wrong?
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