Nice, it's funny as men we're actually better off eating less starch than sugar but for women it's different. So that'd make sense, starch and oil yield bigger boobs. I have some astonishing news. Remember that time you said Bee Pollen made boobs bigger, I saw a story that said Bee Vitality makes them grow bigger. So I need to see about experimenting with that.
I found this video of a doctor reviewing Bee Vitality
https://www.youtube.com/watch?v=V0VvQ68K8AM. I also found this video of a nutrition and health coach talking about Bee Vitality
https://www.youtube.com/watch?v=HpnB3W_WG2k. They said that there is no proof that bee products have any effect on the breasts including increasing breast size. The coach mentioned that it seems that bee products such as pollen have phytoestrogens. Apparently there have been products in the past that also contain pollen that have had no effects. There are many cultures that eat phytoestrogen-rich foods yet not many of these cultures have big or bigger breasts because of these phytoestrogens.
The doctor stated that while there are no health benefits there are nutritional benefits, however, someone would have to be eating the minimum required intake to have those benefits. The supplement contains a few hundred milligrams of bee products and not a few hundred milligrams of nutrients so it is highly likely that the supplement has no nutritional value. There are other nutrition-rich superfoods with similar benefits such as Flaxseeds, Chia Seeds, Bee Pollen (in regular form), Spirulina, Chlorella, and Bee Bread (in regular form). If you want an alternative that resembles bee bread you should consider other bee products such as Honey, Propolis, Royal Jelly, Bee Venom (Bee Sting Therapy), Bee Pollen, and Bee Bread. Royal Jelly in particular has hormonal effects and may alleviate menopausal symptoms. Propolis may balance blood-sugar levels. Just because there is nutrition essential to breast growth does not mean that the nutrients will increase breast growth.
The coach stated that bee products have traditionally been used for medicinal purposes. Pollen contains protein, amino acids, and fatty acids, carbohydrates, antioxidants, vitamins (A, B1, B2, B5, B6, B7, C, D, and E), minerals (magnesium, calcium, zinc, potassium, iron, and selenium), Inositol. Inositol is a sugar that has been proven to help improve insulin sensitivity, and is a popular supplement for insulin resistance in PCOS. Bee Pollen may protect against metabolic syndrome disorders by helping to regulate blood pressure, blood sugar, cholesterol, visceral fat, and healthy ovarian function. It may help to decrease androgen and increase female hormones to achieve balanced hormone levels. It may also have neuroprotective and apoptogenic properties. Pollen, maybe because of its B vitamin content, can improve blood supply to the nervous tissue and support the nervous system.
I am impressed by the product because it exists, it contains honey, pollen, royal jelly, and propolis, but I don't know how effective this Bee Vitality product is. In general, bee products have not yet been proven to have particular health benefits including increasing breast size. However, that is part of the point. Bee Pollen seems plausible when it comes to increasing breast size because it has the nutrients, hormonal / nervous effects, and inositol. Pollen and other bee products may actually have breast growth properties, its just that no one has tested that in the past, so someone should be testing this now and into the future.
Recently I found a map of China for bust size on a website. It is a Korean blog for breast enhancement. I looked around the blog and found a page for breast enhancement herbs.
https://blog.naver.com/iiyo492/220360962952
It lists all of the herbs they have discovered according to their purposes. Some of these herbs were discovered by the blog's followers. One of them was very interesting. Hops, which contains 8-prenylnaringenin (8-PN). This is just the kind of thing we have been looking for when it comes to phytoestrogens or substances that affect Estrogen Receptor Alpha. It is stronger than the strongest phytoestrogen source, soy products, and is the next best thing to estrogen or synthetic estrogen created from wild yam, while remaining relatively safe. However, it has not been tested for therapeutic purposes although it is sometimes sold in menopause and breast growth products.
8-prenylnaringenin (8-PN) is a prenylflavonoid, a type of flavanone, which is a subclass of flavonoids. It has a basic flavonoid structure with a prenyl group attached to the flavonoid nucleus. It is primarily found in hop cones, the female flowers of the hop plant (Humulus lupulus), which are used in brewing beer.
8-prenylnaringenin (8-PN) estrogenic activity is approximately 0.6 to 150 times stronger than genistein, 8 to 150 times stronger than daidzein, and 50 to 1500 times stronger than coumestrol. In general, 8-prenylnaringenin (8-PN) is 5 to 250 times weaker in terms of estrogenic activity relative to endogenous estrogen, 17β-estradiol (E2). Additionally, 8-prenylnaringenin (8-PN) has a 3-fold higher affinity for ERα compared to ERβ.
The significant affinity of 8-prenylnaringenin (8-PN) for ERα can be attributed to its chemical structure, specifically the prenyl group attached to the flavonoid naringenin backbone. The prenyl group allows it to fit more snugly and conform the molecule to the binding pocket of ERα compared to ERβ, enhancing its binding affinity for ERα over ERβ in a more pronounced effect on ERα-mediated transactivation.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6062382/
The best characterized mode of phytoestrogen action is their ability to interact with estrogen receptors. The first receptor to bind estrogens was characterized in the 60s.
44 This receptor was called ER-alpha (ESR1) upon the discovery of a novel, homologous estrogen-binding receptor: ER-beta (ERS2) in the 90s.
45 ERα and ERβ are considered to exert opposite effects. ERα is considered to enhance estrogen-dependent cell proliferation,
46 while ERβ has been shown to counteract ERα-mediated proliferation, most likely
via alternative co-factor recruitment.
47 Generally, phytoestrogens are found to exert weak estrogenic activity
via both ERs, with 50% effect concentrations (EC50 values) that are 2 to 6 orders of magnitude lower compared to the endogenous ligand 17β-estradiol (E2).
48 Also, phytoestrogens display a higher affinity for ERβ than ERα, in contrast to E2.
49–
51 An exception here is the hop-derived phytoestrogen 8-prenylnaringenin (8-PN), which shows a more pronounced potency for ERα- than ERβ-mediated transactivation.
52 With only a 5-fold weaker potency for
in vitro ERα transactivation than 17β-estradiol, 8-PN is the most potent phytoestrogen known so far.
53
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8953904/
8-PN is one of the most potent phytoestrogens currently known. This has been confirmed by a variety of in vitro assays for estrogenic activity (
Table 2), including yeast-based screens expressing the human estrogen receptor (ER) and a reporter gene (usually luciferase, β-galactosidase or chloramphenicol acetyltransferase) under the control of estrogen-responsive sequences (ERE) [
5,
46,
58,
59], human cell lines responsive to estrogenic stimulation [
5,
7,
60,
61], and ER binding [
5,
7,
61,
62]. Compared with established phytoestrogens, such as coumestrol, genistein, and daidzein, the estrogenic activity of 8-PN has generally proven to be 0.6–150, 8–150, and 50–1500-fold stronger, respectively [
5,
7,
59,
62] (but see ERβ-specific data below), while concomitantly 5–250 times weaker than that of 17β-estradiol (E2) [
5,
7,
46,
59,
60,
61,
62,
63,
64]. The estrogenic activities of IX and 6-PN have been reported to be ~1% and <1% relative to 8-PN, respectively, while XN appears to be devoid of estrogenic properties [
7]. Likewise, the parent compound of 8-PN, naringenin, shows only very weak estrogenicity [
65,
66].
The studies cited above have primarily measured ERα-mediated responses. Initial studies suggested that the two enantiomers of 8-PN exhibit similar estrogenic activities in vitro and show no preferential affinity to the two forms of ERs—ERα and ERβ [
5]. However, this view was later contested by Schaefer et al. (2003) [
63], who reported that 2
S(−)8-PN shows moderately higher ER affinity and estrogenic activity in vitro and in vivo than 2
R(+) 8-PN. Furthermore, in their hands the affinity of 8-PN for ERα was >2-fold higher than for ERβ measured by in vitro competitive binding assay and the estrogenic activity at ERα was >3.6-fold higher than at ERβ in a transactivation analysis. In support of this, Overk et al. (2005) reported a 3-fold higher IC50 for ERβ vs. ERα binding [
61], and Helle et al. (2014) recorded a 3-fold greater relative affinity to ERα vs. ERβ for 8-PN relative to E2 [
66]. On the other hand, while using yeast cells expressing human ERs, Bovee et al. (2004) found quite the opposite: the affinity of 8-PN for ERβ was 3 times as high as for ERα [
67]. In any case, even the latter study confirmed that relative to E2, 8-PN shows higher potency at ERα vs. ERβ, and in this regard appears to conspicuously stand out from the bulk of other phytoestrogens, such as coumestrol, genistein, and daidzein, which are all clearly more potent at ERβ [
67]. In fact, genistein and daidzein may bind to ERβ with an affinity 85 or 1,4 times as great as that of 8-PN, respectively [
61]. They have also been reported to activate ERβ at lower concentrations than 8-PN [
68].
When the prenyl group was substituted with alkyl chains of varying lengths and branching patterns, the new 8-alkylnaringenins were found to span an activity spectrum ranging from full agonism all the way via partial agonism to antagonism. An intriguing example is 8-(2,2-dimethylpropyl)naringenin, which was a potent agonist of ERα, but pronounced antagonist of ERβ. Overall, the antagonist effect of the derivatives was more substantial on ERβ than ERα [
73].
Despite the similar affinity of the two well-established SERMs tamoxifen and endoxifen to both isoforms of ERs [
89], SERMs usually exhibit preference to one isoform of ER over the other one, which may explain the varying and tissue-specific responses to SERMs. As described earlier, the majority of phytoestrogens, inclusive of coumestrol, genistein, apigenin, naringenin, and kaempferol, have been reported to display higher affinity towards ERβ than to ERα [
90,
91,
92]. 8-PN is one of the very first known ERα-preferring phytoestrogens. Moreover, the ratio of ERα/ERβ abundances in target organs influences the overall action of SERMs in that tissue. In many tissues, ERβ receptors demonstrate antiproliferative actions, while ERα receptors mediate the opposite effect [
93]. Therefore, an increased ratio of ERα/ERβ correlates well with high levels of cellular proliferation [
94]. ERs and GPCR1 are abundantly expressed in central and peripheral tissues, reflecting the multifunctional nature of endo- and exogenous estrogens [
58]. Since 8-PN has preference for ERα, we will here focus on the tissue expression of ERα as well as the potential endocrine role of ERα–8-PN complex in the contexts of energy metabolism, pituitary function and bone physiology.
Even the tissue concentrations had been discovered:
As described above, many phytoestrogens can modulate the activity of a wide variety of enzymes involved in estrogen synthesis and metabolism
in vitro. But how relevant are these findings for women who use dietary supplements containing these phytoestrogens? One way to approach this question is to compare
in vitro effect concentrations with phytoestrogen concentrations in plasma or, even better, target tissues. However, only two studies were found that provided tissue concentrations upon phytoestrogen intake, namely breast tissue concentrations after soy intake (genistein and daidzein) and 8-PN supplement intake.
17,
31 For 8-PN, breast tissue levels between 0.8 and 4.8 nM
† were found after intake of low levels of 8-PN (0.1 mg, three times per day for 5 days). These breast tissue levels are lower than
in vitro concentrations where induction of CYP-mediated E2 metabolism in breast cells is observed (
Table 3). However, these breast tissue levels are in the same order of magnitude where 8-PN was found to inhibit aromatase activity
in vitro in ovarian KGN (IC50 8 nM)
107 and adrenal H295R cells (IC50 0.1 μM).
14 Also, a high single oral dose of 750 mg 8-PN can lead to higher plasma levels, up to 0.2 μM.
25 Considering that supplements can contain up to 1000 mg 8-PN
13 and are typically taken daily for a longer period of time, inhibition of aromatase activity potentially leading to decreased estrogen production in women taking these supplements is highly likely. High estrogen levels are associated with increased breast cancer risk in postmenopausal women
184 and aromatase inhibitors reduce the incidence of breast cancer.
185 Therefore, the aromatase inhibitory effects of 8-PN could reduce breast cancer risk in postmenopausal women. However, these favourable effects might be overcome by the potent ERα-mediated actions of 8-PN.
53 Genistein and daidzein concentrations attainable in breast tissue (0.09–0.5 μM genistein and 0.02–0.7 μM daidzein) and plasma (up to 2.8 μM, see
Table 2) are similar to concentrations at which modulation of the activity of several estrogen synthesizing/metabolising enzymes can occur (
Table 3).
It is possible that the phytoestrogen is an agonist, is a substitute in place of estrogen that reduces estrogen binding and activity. Therefore, this phytoestrogen can reduce estrogen based cancer propogation in cancer patients. However it also strongly affects ERα, which propogates cells. Not only does this show that it can increase growth, we also have a glimpse to the amounts that could enter the body. The amount of estradiol in the body from estradiol products was about 12.5 micrograms (µG or mcG).
Directly targeting the breasts: 0.8 and 4.8 nM times 7,500 (to equal a 750mg amount) is 6 micrometers (µM or mcM) to 36 micrometers (µM or mcM) in the breasts.
Plasma (from oral consumption): 0.2 μM is 0.016 times smaller than 12.5 micrograms (µG or mcG) because 12.5 micrograms (µG or mcG) is 62.5 times larger than 0.2 μM.
If we assume that on such a small scale, weight and distance are the same. The amount needed to be taken orally to reach 12.5 micrograms (µG or mcG) dose of 8-PN in the body would be 46,875 micrograms (µG or mcG) or 46.875 milligrams. This is a significantly high amount especially when 8-PN has lesser estrogenic effects. It is also concerning because all of this would be circulating the body and could still have relatively high estrogenic effects. It would make more sense to target the breasts. A 750mg amount would yield 6 micrometers (µM or mcM) to 36 micrometers (µM or mcM) in the breasts. 36 micrometers (µM or mcM) is approximately three times greater than 12.5 micrograms (µG or mcG). Assuming 5 times 12.5 micrograms (µG or mcG) is required for the minimum affect, 62.5 micrograms (µG or mcG) would be required to be absorbed in the body from a 3,750 micrograms (µG or mcG) amount. Even this 3,750 micrograms (µG or mcG) amount is 0.08 smaller than 46,875 micrograms (µG or mcG) because 46,875 micrograms (µG or mcG) is 12.5 times larger than 3,750 micrograms (µG or mcG). An amount of 3.75 milligram delivers a more direct and affect dosage than an amount of 46.875 milligrams. It is important to note that this is 8-PN extract and not hops extract, which would have a lower concentration of 8-PN.
EDIT: I found this newsletter from around the time that 8-Prenylnaringenin was discovered.
Prenylflavonoids are quite rare compounds in nature, but 8-prenylnaringenin is just one of a number of related prenylflavonoids in hops; others include xanthohumol, desmethylxanthohumol, isoxanthohumol, 6-prenylnaringen, 6,8-diprenylnaringenin, 3’-geranylchalconaringenin, 6-geranylnaringenin, 8-geranylnaringenin, and 4’-O-methyl-3’-prenylchalconaringenin.
Because hops contains so many compounds that can affect the endocrine system, hop baths had been used throughout Germany to treat gynecological disorders while Belgian women experienced menstrual disturbance while picking and working with hops. However, belief in the medicinal properties of hops has faded with time and hop picking is now done mechanically so the only widespread human exposure to 8-prenylnaringenin is likely to be via beer consumption. Usually, only a few grams of hops are used per liter of beer. Most beers use processed hops extracts and therefore usually contain less than 30 mcG/L of 8-prenylnaringenin, but when whole hops is used, as much as 240 mcG/L of 8-prenylnaringenin can be present. Despite the relatively high estrogenic activity of 8-prenylnaringenin, the total estrogenic activity of beer made using whole hops still is very low, and no detrimental health effects due to estrogens in beer have been reported or are to be expected.
Here, it states that a study on mice found that 100 mcg/mL levels of 8-prenylnaringenin was required to produce any sign of estrogenic activity. This is at least 400 times greater than what is found in any beer as even the most 8-prenylnaringenin concentrated beer has only 0.24 mcG/mL. Dry hops itself contains around 100 mg/Kg of 8-prenylnaringenin. Assuming ml and mg are the same, when 100 mg/Kg is reduced by a scale of 1000, it becomes 0.1 mg / g, while 0.24 mcG/mL is 0.00024 mg / g. That means that dry hops is 416.6667 times (0.1 g / 0.00024 mg) concentrated than a beer. So, not only is a concentration of 100 mcg/mL amount 400 times greater than the most concentrated beer, it is the minimum concertation required for any estrogenic effect. Dry hops would be needed to reach the 100 mcg/mL concentration. A standard beer in the US is 12 fluid ounces or 355 mL. A beer of this size concentrated at 100 mcg/mL of 8-prenylnaringenin would contain 35,500 mcg or 35.5 mg of 8-prenylnaringenin.
The amount needed to be taken orally to reach a 12.5 micrograms (µG or mcG) dose of 8-PN in the body would be 46,875 micrograms (µG or mcG) or 46.875 milligrams. 35.5 out of 46.875 milligrams is 0.7573. This is 75.73%, which is still a decent amount and apparently this lesser amount is required to have any sign of estrogenic effect whatsoever. 0.7573 of 12.5 micrograms (µG or mcG) is 9.467 micrograms (µG or mcG). From 35,500 mcg or 35.5 mg of 8-prenylnaringenin, 9.467 micrograms (µG or mcG) would be absorbed, only providing around 75% of of the 12.5 micrograms (µG or mcG) that I identified for any estrogenic effect. To reach this concentration, the concentration would have to be not 416.6667, but 501.1251 times stronger than a beer.
Assuming the dry weight of hops cones ranges from 75.7 mg or 0.0757 g to 260.8 mg or 0.2608 g, on average (0.16825 g per hops cone), it would take 1000 g / 0.16825 g = 5,944 flowers to reach 1 kilogram of hops cones. Assuming 5 times 12.5 micrograms (µG or mcG) is required for the minimum affect (because 8-PN is 5 to 250 times weaker than estradiol), 62.5 micrograms (µG or mcG) of 8-prenylnaringenin would be required to be absorbed in the body from a 3,750 micrograms (µG or mcG) topically administered amount. Therefore a kilogram of hops flowers could provide at least 26 doses (100 mg / 3.75 mg = 26.66666666666667) and only 37.5 g of dry hops would be required for each dose as 3.75 mg / 100 mg x 1,000 g = 37.5 g.
Bust-Enhancing Products by Adriane Fugh-Berman, MD (Pages 41-43)
Hops and Women’s Health by Stuart Milligan, MA, DPhil (Pages 44-48)
American Health Consultants, Volume 4, Number 6, June 1, 2002, Pages 41-48, Alternative Therapies in Women's Health, AHCPub,
http://www.newslettersonline.com/us...TWH062002.pdf?T=open_article,453708&P=article.
https://www.reliasmedia.com/ext/resources/pdfs/articles/45/453/4537/45370/453708.pdf?1421780593
https://web.archive.org/web/20021210081027/http://www.ahcpub.com/ahc_online/atwh.html
2002:
https://web.archive.org/web/2002110...=3?T=open_non_issue,70000171125,5&P=non_issue
June 1, 2002:
https://web.archive.org/web/2003063...as/s=6/fp=3/tp=3?T=open_issue,58721,Y&P=issue
June 1, 2002 Issue PDF:
http://www.newslettersonline.com/us...TWH062002.pdf?T=open_article,453708&P=article
https://www.reliasmedia.com/articles/120079-bust-enhancing-products
https://www.reliasmedia.com/articles/120078-hops-and-women-8217-s-health
UPDATE: I discovered that 8-Prenylnaringenin has two other names, 8-isopentenylnaringenin and sophoraflavanone B. This means that there are more plant sources other than Hops for 8-Prenylnaringenin such as Ku Shen, Wu Zhu Yu, and Batino (Anaxagorea Luzonensis). It's interesting that many of these (and some other plants I looked into) are from Asia.
8-Prenylnaringenin
Chemical name or synonym: 5,7,4’-trihydroxy-8-prenyl-flavanone, 8-isopentenylnaringenin
Chemical family: prenylflavonoids, flavanones
Molecular weight: 339,4 g/mol
Molecular formula: C20H20O5
Natural sources:
• Female hop cones, Humulus lupulus, Cannabinaceae (Milligan et al. 1999)
• Heartwood of Anaxagorea luzonensis, Annonaceae (Kitaoka et al. 1998)
PLANTS - Annonaceae (Anaxagorea luzonensis); Cannabaceae (Humulus lupulus); Fabaceae (Sophora flavescens); Rutaceae (Evodia daniellii)
A group of recently described relatively potent phytoestrogens are of the naringenin type (Milligan et al., 1999; Milligan et al., 2002; Zierau et al., 2002 ). Especially 8- prenylnaringenin (8-PN) from hops, Humulus lupulus (L.) and beer, initially described as 8-isopentenylnaringenin (Kitaoka et al., 1998) has been characterized as an extremely potent phytoestrogen (Kitaoka et al., 1998; Milligan et al., 1999; Schaefer et al., 2003). The estrogenic activity of 8-PN in vitro is the highest of all plant derived estrogens known so far (Matsumura et al., 2005).
8-Isopentenylnaringenin [8-Prenylnaringenin] ALX-385-025-M005 5 mg Isolated from hops (Humulus lupulus L.) Prenyl flavonoid. Phytoestrogen. Selective, nonsteroidal estrogen receptor α (ERα) ligand. Potent inhibitor of angiogenesis in vitro and in vivo. Chemopreventive agent against cancer induced by heterocyclic amines. LIT: Prenylflavonoids: a new class of non-steroidal phytoestrogen (Part 2). Estrogenic effects of 8-isopentenylnaringenin on bone metabolism: M. Miyamoto, et al.; Planta Med. 64, 516 (1998) Identification of a potent phytoestrogen in hops (Humulus lupulus L.) and beer: S.R. Milligan, et al.; J. Clin. Endocrinol. Metab. 84, 2249 (1999) The endocrine activities of 8-prenylnaringenin and related hop (Humulus lupulus L.) flavonoids: S.R. Milligan, et al.; J. Clin. Endocrinol. Metab. 85, 4912 (2000) 8-prenylnaringenin, a novel phytoestrogen, inhibits angiogenesis in vitro and in vivo: M.S. Pepper, et al.; J. Cell Physiol. 199, 98 (2004) 8-Prenylnaringenin, inhibits estrogen receptor-alpha mediated cell growth and induces apoptosis in MCF-7 breast cancer cells: E. Brunelli, et al.; J. Steroid Biochem. Mol. Biol. 107, 140 (2007) For a comprehensive bibliography please visit our website.
A natural product that could properly be called 8-prenylnaringenin is known to exist, for example from the Fabaceous shrub native to Asia, Sophora flavescens Ait. This compound is known in the literature as 8-isopentenylnaringenin (Kitaoka et al., 1998) or “sophoraflavanone B” (Mizobuchi and Sato, 1994). Because it is less cumbersome than “(±)-8-prenylnaringenin”, it may be preferable that investigators use the name “hopein” coined by Professor De Keukeleire, when referring to the estrogen from hops. By using the name hopein, it should then be understood that the compound in question is the estrogenic racemate from hops, rather than the chiral estrogen from Asian shrubs.
A natural product that could properly be called 8- prenylnaringenin is known to exist, and is produced by a Fabaceous shrub native to Asia, Sophora flavescens Ait. Interestingly, this compound has never been referred to in the literature as 8-prenylnaringenin, but is known rather as “sophoraflavanone B”. In order to keep in line with existing literature, however, the estrogen from hops was called “8-prenylnaringenin” throughout the present work.
The lavandulyl group is not directly transferred to the flavanone skeleton, but it was shown to be formed by two dimethylallylations between which the 2'-hydroxylation occurred: the biosynthetic pathway goes thus from naringenin (78) to 77, via 8-prenylnaringenin (sophoraflavanone B, 78a) and leachianone G (78b) [42b].
Bioassay-guided fractionation of a methanolic extract of a Thai crude drug, derived from heartwood of ANAXAGOREA LUZONENSIS A. Gray (Annonaceae), resulted in the isolation of 8-isopentenylnaringenin (1) as an estrogen agonist with an activity of about an order of magnitude greater than genistein. Various flavonoids possessing isopentenyl side chains in the A-ring have been prepared and evaluated for their ability to bind estrogen receptor. In addition, enantiomers of 1 were separated and the respective enantiomers were assayed. These studies have demonstrated that the presence of an 8-isopentenyl group is an important factor for binding. Flavones, flavanones and flavonols having an isopentenyl substituent at C-8 exhibited an appreciable affinity for estrogen receptor. Conversely, isoflavones possessing an 8-isopentenyl substituent at C-8 did not show this activity. Movement of the isopentenyl group from position 8 to 6 resulted in loss of the activity. No significant difference was observed between 2(S)- and 2(R)-enantiomers of 1 in their binding affinity. Prenylflavonoids are reported to possess a wide range of biological activities; however, estrogenic activity has not been described.
