[Lotus]

Hi Nexum, using topical progesterone builds glandular tissue and side branching, as does DHEA. 

Estrogel/Estradiol increases the breast size by way of elongation. I'm against cycling progesterone (P4) more than every other day. Essentially you lose progress by going from 2 weeks on P4 to 2 weeks off. As you can see by the amount of information being posted... I put a lot of time into gathering research to share why having a topical cream protocol. Even if you think you stalled, I uncovered research that states T.E.B.s (terminal end buds) have a reserve (15-20%) that has yet to be used. I believe in that statement because I saw an increase of 3-4 inches by using my program.

DHEA for Topical Application 

DHEA activates estrogen receptors. Further information identified how DHEA and its metabolites are synthesized by aromatase… That's a big discovery in my book, now I'm thinking that the combination(s) of DHEA may even stimulate tissue repair in the breast epithelial cells and T.E.B’s (aka- terminal end buds/terminal … or breast buds). 

The conversion of DHEA by aromatase to estriol and subsequently estradiol as an essential prerequisite for DHEA's impact upon in vivo healing and inflammation.

DHEA acts through the classical estrogen receptors (ER) to modulate repair.

DHEA modulates macrophage pro-inflammatory cytokine expression, and reducing inflammation helps better breast growth.

DHEA dampens the local inflammatory response and reduces the tissue levels of a number of pro-inflammatory cytokines. 

DHEA influenced the progressive dermal ischemia occurring following thermal injury to the skin, possible via a non-ER/AR mechanism. We show that DHEA can accelerate wound repair in an impaired model of healing secondary to estrogen-depletion, which mimics age-related healing (Ashcroft et al., 1997a, Ashcroft et al., 1997b

(Ischemia or ischaemia) is a restriction in blood supply to any tissue, muscle group, or organ of the body, causing a shortage of oxygen that is needed for cellular metabolism (to keep tissue alive).[3][4] Ischemia is generally caused by problems with blood vessels, with resultant damage to or dysfunction of tissue, i.e., hypoxia and microvascular dysfunction.)

Progressive ischemia and necrosis of the skin following thermal injury are reduced by postburn administration of the steroid hormone dehydroepiandrosterone (DHEA)

Findings showed that DHEA increased the antioxidant enzyme activity, decreased ROS generation, and inhibited apoptosis in H2O2-treated cells.

The protective effect of DHEA on BRL-3A cells was mainly associated with PI3K/Akt signaling pathways, rather than MAPK signaling pathways.

The decrease in circulating DHEA levels is associated with multiple metabolic consequences, including autoimmune diseases, aberrations in lipid metabolism, type 2 diabetes, and oxidative stress-related diseases. 

Recently, DHEA was reported to exhibit antioxidative effects under conditions of acute as well as chronic oxidative stress [10–12], and these antioxidant effects have been confirmed through in vivo [13, 14] and in vitro [15] experiments, including our recent study in which DHEA treatment was found to protect various types of cells against oxidative damage

PI3K/p-AKT pathways seem to be closely involved with these protective effects of DHEA on the liver cells.
https://www.hindawi.com/journals/omcl/2019/2985956/

The phosphatidylinositol 3 kinase (PI3K) pathway is one of the major pathways modulating cell growth, metabolism, survival, and angiogenesis. 
https://en.m.wikipedia.org/wiki/Angiogenesis

10 months ago I began reviewing my posts on DHEA and other research I had on it. I wanted to create a topical application program focusing on using HRT hormones and available products to assist in that breast growing program. I can report the combination of DHEA + P4 (micronized progesterone) added 3 inches in new growth in 3 months for myself. I'm listing 3 posts for discussion purposes… please note: it's a long post. Here's a few quotes I'd like to bring attention to. Bio-labs E1/E2, P4, and 17b applications. 

• application of DHEA that restored atrophy of the breasts and stimulates lobuloalveolar and ductal growth… "boob growth". 

• Supplemental DHEA raises estrogen in men and postmenopausal women

• breast size increase was similar to that observed in pregnancy/lactation, so it corresponds to a pretty significant increase of 1-3 digits in cup size. Finally, DHEA did not just increase breast size but it completely reversed the breast atrophy

• DHEA treatment was characterized by a marked stimulation of the ductal and mainly the lobular structures.

• DHEA stimulated lobuloalveolar and ductal growth, as well as the secretory activity of the acinar cells, thus resulting in a lobuloalveolar type of development of the mammary gland.

• Estradiol treatment induced an increased number of ducts (d), accompanied by the presence of alveolar units (a) and small lobules.

• A marked increase in the amount of lobuloalveolar tissue (l) and in the secretory activity of the acinar cells accompanied by accumulation of secretory material (s) in the duct lumen (d) were observed after DHEA administration (F)

• DHEA (5%) in ethanol:olive oil (1:2) was topically applied to the buttock skin of volunteers 12 times over 4 weeks, and was found to significantly increase the expression of procollagen alpha1(I) mRNA and protein in both aged and young skin.

• To investigate the effects of topically applied 17beta-estradiol on the expression of extracellular matrix proteins in aged human skin, 17beta-estradiol (0.01%) and its vehicle (70% propylene glycol, 30% ethanol) were applied to aged (68-82 y, eight females and five males) human buttock skin under occlusion for 2 wk (three times per week). Topical 17beta-estradiol was found to increase the expression of type 1 procollagen mRNA and protein significantly in human aged skin in vivo.

• In conclusion, our results suggest that topical 17beta-estradiol treatment may improve the cutaneous function of aged human skin by improving the connective tissue and increasing epidermal thickness

Dehydroepiandrosterone (DHEA) is the principal human C-19 steroid. DHEA has very low androgenic potency, but serves as the major direct or indirect precursor for most sex steroids. DHEA is secreted by the adrenal gland and production is at least partly controlled by adrenocorticotropic hormone (ACTH). The bulk of DHEA is secreted as a 3-sulfo conjugate dehydroepiandrosterone sulfate (DHEAS). Both hormones are albumin bound, but DHEAS binding is much tighter. As a result, circulating concentrations of DHEAS are much higher (>100-fold) compared to DHEA. In most clinical situations, DHEA and DHEAS results can be used interchangeably. In gonads and several other tissues, most notably skin, steroid sulfatases can convert DHEAS back to DHEA, which can then be metabolized to stronger androgens and to estrogens.

DHEA is C-19 steroid (androgen) but has a very low potency Supplemental DHEA raises estrogen in men and postmenopausal women. (can also raise androgens (DHT) if some experienced users know how much to use. DHEA applied topically helps restore breast atrophy in an animal study (see below). I found this in another forum, and it describes an animal study using a topical application of DHEA that restored atrophy of the breasts and stimulates lobuloalveolar and ductal growth… boob growth. The author (haidut, smart fella btw) suggests a 15mg significantly increases all estrogens. 

The breast size increase was similar to that observed in pregnancy/lactation, so it corresponds to a pretty significant increase of 1-3 digits in cup size. Finally, DHEA did not just increase breast size, but it completely reversed the breast atrophy and other negative tissue changes seen in ovariectomized animals (a rodent model of menopause).

From the study,
DHEA treatment was characterized by a marked stimulation of the ductal and mainly the lobular structures. In addition, epithelial cell hypertrophy and a marked stimulation of secretory activity were seen, these effects being accompanied by the accumulation of clear and eosinophilic vacuoles in the cytoplasm of the acinar cells. - 

DHEA stimulated lobuloalveolar and ductal growth, as well as the secretory activity of the acinar cells, thus resulting in a lobuloalveolar type of development of the mammary gland. 
https://pubmed.ncbi.nlm.nih.gov/9449650/

Mammary gland histology in (A) intact control, (B) OVX control, and OVX rats treated with © MPA microspheres, (D) estradiol implants, (E) DHT implants, (F) DHEA, 30 mg, cutaneous application, twice daily, on an area of 3 × 3 cm of dorsal skin, (G) DHEA, 30 mg, cutaneous application, twice daily + FLU, 7.5 mg, sc, twice daily and (H) DHEA, 30 mg, cutaneous application, twice daily + EM-800, 250 μg, orally, once daily. An increase in the number of alveolar units (a) was observed in OVX animals treated with MPA © and DHT (E) with the formation of small primitive lobules (l) after DHT administration (E). Estradiol treatment induced an increased number of ducts (d), accompanied by the presence of alveolar units (a) and small lobules (l), without evidence of secretory activity (D). A marked increase in the amount of lobuloalveolar tissue (l) and in the secretory activity of the acinar cells accompanied by accumulation of secretory material (s) in the duct lumen (d) were observed after DHEA administration (F). The stimulatory effect of DHEA on the mammary gland was completely blocked by simultaneous treatment with FLU (G), whereas no significant histological change was seen after the addition of EM-800 to DHEA compared with DHEA alone (H). Compare with intact (A) and OVX (B) controls. Hematoxylin-eosin, magnification ×200(d, ducts; a, alveoli, l, lobules).

DHEA, 30 mg, cutaneous application, twice daily + FLU, 7.5 mg, sc, twice daily and (E) DHEA, 30 mg, cutaneous application, twice daily + EM-800, 250 μg, orally, once daily.

Two studies, similar effects. In any event, DHEA looks like it can build a bigger butt, and… 
Topical application of 17beta-estradiol increases extracellular matrix protein synthesis by stimulating tgf-Beta signaling in aged human skin in vivo.
Son ED1, Lee JY, Lee S, Kim MS, Lee BG, Chang IS, Chung JH.
Author information

* 1 Amorepacific Corp/R&D Center, Gyeonggi-do, Korea.
Abstract
To investigate the effects of topically applied 17beta-estradiol on the expression of extracellular matrix proteins in aged human skin, 17beta-estradiol (0.01%) and its vehicle (70% propylene glycol, 30% ethanol) were applied to aged (68-82 y, eight females and five males) human buttock skin under occlusion for 2 wk (three times per week). Topical 17beta-estradiol was found to increase the expression of type 1 procollagen mRNA and protein significantly in human aged skin in vivo. In addition, metalloproteinase (MMP-1 protein levels were reduced by topical 17beta-estradiol. The expressions of TGF-beta1, TGF-beta type II receptor, and Sma and Mad related (Smad)3 were increased by topical 17 beta-estradiol in aged human skin, and TGF-beta1 neutralizing antibody inhibited 17beta-estradiol-induced procollagen synthesis in cultured fibroblasts. We also found that the expressions of tropoelastin and fibrillin-1 mRNA and protein and elastic fibers in aged skin were also increased by topical 17beta-estradiol Topical 17beta-estradiol also increased keratinocyte proliferation and the epidermal thickness in aged human skin. We also observed the same effects of topical 17beta-estradiol in young skin. In conclusion, our results suggest that topical 17beta-estradiol treatment may improve the cutaneous function of aged human skin by improving the connective tissue and increasing epidermal thickness.
PMID: 15955089 [PubMed - indexed for MEDLINE]

Modulation of collagen metabolism by the topical application of dehydroepiandrosterone to human skin.[/b]
Shin MH1, Rhie GE, Park CH, Kim KH, Cho KH, Eun HC, Chung JH.
Author information

* 1Department of Dermatology, Seoul National University College of Medicine and Laboratory of Cutaneous Aging Research, Clinical Research Institute, Seoul National University Hospital, 28 Yungon-dong, Chongno-Gu, Seoul 110-744, Korea.
Abstract
Dehydroepiandrosterone (DHEA) and its sulfate conjugate (DHEA-S) are the most abundantly produced human adrenal steroids to be reduced with age. DHEA may be related to the process of skin aging through the regulation and degradation of extracellular matrix protein. In this study, we demonstrate that DHEA can increase procollagen synthesis and inhibit collagen degradation by decreasing matrix metalloproteinases (MMP)-1 synthesis and increasing tissue inhibitor of matrix metalloprotease (TIMP-1) production in cultured dermal fibroblasts. DHEA was found to inhibit ultraviolet (UV)-induced MMP-1 production and the UV-induced decrease of procollagen synthesis, probably due to the inhibition of UV-induced AP-1 activity. DHEA (5%) in ethanol:olive oil (1:2) was topically applied to buttock skin of volunteers 12 times over 4 weeks, and was found to significantly increase the expression of procollagen alpha1(I) mRNA and protein in both aged and young skin. On the other hand, topical DHEA significantly decreased the basal expression of MMP-1 mRNA and protein, but increased the expression of TIMP-1 protein in aged skin. We also found that DHEA induced the expressions of transforming growth factor-beta1 and connective tissue growth factor mRNA in cultured fibroblasts and aged skin, which may play a role in the DHEA-induced changes of procollagen and MMP-1 expression. Our results suggest the possibility of using DHEA as an anti-skin aging agent.

[Stevenator_]

Lotus, thank you for creating this thread!

[Heaven's Night]

Thanks for posting it all in one, I remembered to save the entire post. No need to memorise all DHEA + P4 info from now on. This stuff is well worth saving for later as my memory leaks like 486 running Windows 95.

[OphelieBoots]

Just a question regarding DHEA. In many countries, such as mine, Switzerland, DHEA is a forbidden substance which can cost heavy fines if caught at the border. As a steroid, it is considered as a doping substance...


Do you suggest any alternative? I understand PG creams could be the answer, but any other opinion on that? I don't want to end up in jail for that... :-)

[Lotus]

Thank you Stevenator and Lara. 

Just a question regarding DHEA. In many countries, such as mine, Switzerland, DHEA is a forbidden substance which can cost heavy fines if caught at the border. As a steroid, it is considered as a doping substance...


Do you suggest any alternative? I understand PG creams could be the answer, but any other opinion on that? I don't want to end up in jail for that... :-)

Hi OphelieBoots, you could try Wild Yam or Maca to support DHEA. Check for the information the Breast Growing Guide. 

[Lotus]

Hi Nexum, I think we can't overlook what Red Clover can do in a topical application. We know what RC (information to follow) when taken orally. RC induces Lipogenesis, which is another name for feminizing fat (fat redistribution) by breaking down lipoproteins… and adipocytes (fat cells). So, when you do things that activate PPAR (peroxisome proliferator-activated receptor) , think of it as a means to feminize your body fat and help to LOSE weight. In the next post I'll be following up with ways to use Red Clover for skin application. 

Hi BN, 

Red Clover is beneficial for NBE. If you don't know what PPAR (peroxisome proliferator-activated receptor), you should. (Info supplied below). 
red clover extract: a putative source for simultaneous treatment of menopausal disorders and the metabolic syndrome.
Mueller M1, Jungbauer A.
Author information
Abstract
OBJECTIVE:
Currently, red clover extract is used to treat menopausal disorders as an alternative to classic hormone therapy. Several human and animal studies have attributed hypolipidemic, hypoglycemic, or antiatherosclerotic effects to red clover extract or isoflavones. This study was designed to determine the peroxisome proliferator-activated receptor (PPAR) gamma activation by red clover extract.
DESIGN:
The PPARgamma binding affinities and the transactivation activities of red clover extracts, isoflavones, and their metabolites were analyzed. The presence of specific substances in the extracts was proved by high-performance liquid chromatography/electrospray ionization/mass spectrometry.
RESULTS:
The red clover extracts and the compounds genistein and biochanin A were potent PPARgamma ligands and activators. Several metabolites exerted higher binding affinities or transactivational activities than their precursor molecules. 6-Hydroxydaidzein exerted a more than 100-fold higher binding affinity than its precursor daidzein. The maximal transactivational activity of 6-hydroxydaidzein and 3'-hydroxygenistein exceeded even that of rosiglitazone, a known PPARgamma agonist. Equol and O-desmethylangolensin showed an approximately fivefold higher binding affinity and, in the case of O-desmethylangolensin, a four fold higher PPARgamma agonistic activity than the precursor. The daily dose of Menoflavon forte, a widely used red clover extract for treatment of menopausal disorders, provides theoretically 15% to 30% of the daily recommended dose of rosiglitazone. Considering the more active metabolites formed, activity must be higher in vivo.

CONCLUSIONS:
This study shows that red clover extracts, the major compounds, and especially several main metabolites exert significant PPARgamma binding and transactivation activity. Red clover extract, which is currently used for treating menopausal disorders, could be simultaneously used for ameliorating the metabolic syndrome.
http://www.ncbi.nlm.nih.gov/pubmed/18724264

peroxisome proliferator-activated receptor (PPAR) in mediating the effects of fibrates and fatty acids on gene expression.
Schoonjans K1, Staels B, Auwerx J.
Author information
Abstract
The three types of peroxisome proliferator-activated receptors (PPAR), termed alpha, delta (or beta), and gamma, belong to the nuclear receptor superfamily. Although peroxisome proliferators, including fibrates and fatty acids, activate the transcriptional activity of these receptors, only prostaglandin J2 derivatives have been identified as natural ligands of the PPAR gamma subtype that also binds thiazolidinedione antidiabetic agents with high affinity. PPARs heterodimerize with retinoic X receptor (RXR) and alter the transcription of target genes after binding to response elements or PPREs, consisting of a direct repeat of the nuclear receptor hexameric DNA recognition motif (PuGGTCA) spaced by 1 nucleotide (DR-1). Upon activation by fatty acids (FAs) and drugs that affect lipid metabolism, PPARs control the expression of genes implicated in intra- and extracellular lipid metabolism, most notably those involved in peroxisomal beta-oxidation. PPARs partially mediate the inductive effects of fibrates and fatty acids on high density lipoprotein (HDL) cholesterol levels by regulating the transcription of the major HDL apolipoproteins, apoA-I and apoA-II. The hypotriglyceridemic action of fibrates and certain fatty acids also involves PPAR and is constituted of: 1) increased hydrolysis of plasma triglycerides due to induction of LPL and reduction of apoC-III expression; 2) stimulation of cellular fatty acid uptake and conversion to acyl-CoA derivatives due to increased expression of genes for fatty acid transport protein and acyl-CoA synthetase; 3) increased peroxisomal and mitochondrial beta-oxidation; and 4) decreased synthesis of fatty acids and triglycerides and decreased production of very low density lipoprotein (VLDL). Hence, both enhanced catabolism of triglyceride-rich particles and reduced secretion of VLDL particles contribute to the hypolipidemic effect of fibrates and fatty acids. Finally, PPARs appear to be involved in differentiation processes because activation of PPAR gamma 2 triggers adipocyte differentiation and stimulates expression of several genes critical to adipogenesis. It is suggested that PPARs are key messengers responsible for the translation of nutritional and pharmacological stimuli into changes in gene expression and differentiation pathways.
PMID: 8725145 [PubMed - indexed for MEDLINE] Free full text

Increase In Visceral Fat During Menopause Linked With Testosterone
http://www.sciencedaily.com/releases/200...161144.htm
In middle-aged women, visceral fat, more commonly called belly fat, is known to be a significant risk factor for cardiovascular disease, but what causes visceral fat to accumulate?
The culprit is likely not age, as is commonly believed, but the change in hormone balance that occurs during the menopause transition, according to researchers at Rush University Medical Center.
"Of all the factors we analyzed that could possibly account for the increase in visceral fat during this period in a woman's lifetime, levels of active testosterone proved to be the one most closely linked with abdominal fat," said Imke Janssen, PhD, assistant professor of preventive medicine and the study's lead investigator.
The study, which has been published early online in the medical journal Obesity, included 359 women in menopausal transition, ages 42 to 60, about half black and half white. Fat in the abdominal cavity was measured with CT scans, a more precise measurement than waist size. Blood tests were used to assess levels of testosterone and estradiol (the main form of estrogen). Medical histories covered other health factors possibly linked with an increase in visceral fat.

___________________________________________

Screening of herbal extracts for activation of the human peroxisome proliferator-activated receptor
http://www.ncbi.nlm.nih.gov/pubmed/17152989
The peroxisome proliferator-activated receptors play a pivotal role in metazoan lipid and glucose homeostasis. Synthetic activators of PPARalpha (fibrates) and PPARgamma (glitazones) are therefore widely used for treatment of dislipidemia and diabetes, respectively. There is growing evidence for herbal compounds to influence nuclear receptor signalling e.g. the PPARs. We recently reported carnosic acid and carnosol, both being diterpenes found in the labiate herbs sage and rosemary, to be activators of PPARgamma. The subsequent screening of a variety of ethanolic extracts, obtained from traditionally used herbs, for PPAR activation, led to an exceptionally high hit rate. Among 52 extracts nearly half significantly activated PPARgamma and 14 activated PPARalpha in addition, whereas three of them were pan-PPAR activators, which also activated PPARdelta. The most active extracts, for which a concentration dependent effect could be shown, were the extracts of Alisma plantago aquatica (ze xie/european waterplantain), Catharanthus roseus (madagascar periwinkle), Acorus calamus (sweet calamus), Euphorbia balsamifera (balsam spurge), Jatropha curcas (barbados nut), Origanum majorana (marjoram), Zea mays (corn silk), Capsicum frutescens (chilli) and Urtica dioica (stinging nettle). The results of the present study provide a possible rationale for the traditional use of many herbs as antidiabetics.

Glitazones for type 2 diabetes
http://www.nps.org.au/conditions/hormone...glitazones
____________________________________
Anti-diabetic medication
Drugs used in diabetes treat diabetes mellitus by lowering glucose levels in the blood. With the exceptions of insulin, exenatide, liraglutide and pramlintide, all are administered orally and are thus also called oral hypoglycemic agents or oral antihyperglycemic agents. There are different classes of anti-diabetic drugs, and their selection depends on the nature of the diabetes, age and situation of the person, as well as other factors.
Diabetes mellitus type 1 is a disease caused by the lack of insulin. Insulin must be used in Type I, which must be injected.
Diabetes mellitus type 2 is a disease of insulin resistance by cells. Type 2 diabetes mellitus is the most common type of diabetes. Treatments include (1) agents that increase the amount of insulin secreted by the pancreas, (2) agents that increase the sensitivity of target organs to insulin, and (3) agents that decrease the rate at which glucose is absorbed from the gastrointestinal tract.
Several groups of drugs, mostly given by mouth, are effective in Type II, often in combination. The therapeutic combination in Type II may include insulin, not necessarily because oral agents have failed completely, but in search of a desired combination of effects. The great advantage of injected insulin in Type II is that a well-educated patient can adjust the dose, or even take additional doses, when blood glucose levels are measured by the patient, usually with a simple meter, as needed by the measured amount of sugar in the blood.
http://wikipedia.org/wiki/Anti-diabetic_drug

Thanks for reading 

[Heaven's Night]

Very cool about Red Clover. The text talks about extract, I wonder if that's in which form it would work the best used topically? Likely it would be many times more potent than a cream. I'm interpreting the text as it could do the same thing Volufiline does and perhaps be even better at it. Worth a try maybe.

[Lotus]

Red clover induces progesterone, (activates ER-a & b receptors) 

Biological characterization of non-steroidal progestins from botanicals used for women’s health

Progesterone plays a central role in women’s reproductive health. Synthetic progestins, such as medroxyprogesterone acetate (MPA) are often used in hormone replacement therapy (HRT), oral contraceptives, and for the treatment of endometriosis and infertility. Although MPA is clinically effective, it also promiscuously binds to androgen and glucocorticoid receptors (AR/GR) leading to many undesirable side effects including cardiovascular diseases and breast cancers. Therefore, identifying alternative progestins is clinically significant. The purpose of this study was to biologically characterize non-steroidal progestins from botanicals by investigating their interaction and activation of progesterone receptor (PR). Eight botanicals commonly used to alleviate menopausal symptoms were investigated to determine if they contain progestins using a progesterone responsive element (PRE) luciferase reporter assay and a PR polarization competitive binding assay. Red clover extract stimulated PRE-luciferase and bound to PR. A library of purified compounds previously isolated from red clover was screened using the luciferase reporter assay. Kaempferol identified in red clover and a structurally similar flavonoid, apigenin, bound to PR and induced progestogenic activity and P4 regulated genes in breast epithelial cells and human endometrial stromal cells (HESC). Kaempferol and apigenin demonstrated higher  potency in the HESC compared to breast epithelial cells. Furthermore, phytoprogestins were able to activate P4 signaling in breast epithelial cells without downregulating PR expression. This data suggest that botanical extracts used for women’s health may contain compounds capable of activating progesterone receptor signaling.


Only red clover (20 μg/ml) significantly activated PRE-luciferase induction.

Red clover and a structurally similar flavonoid, apigenin, bound to PR and induced progestogenic activity and P4 regulated genes in breast epithelial cells and human endometrial stromal cells.

Hi BN, 
Red Clover is beneficial for NBE. If you don't know what PPAR (peroxisome proliferator-activated receptor), you should. (Info supplied below). 
red clover extract: a putative source for simultaneous treatment of menopausal disorders and the metabolic syndrome.
Mueller M1, Jungbauer A.
Author information
Abstract
OBJECTIVE:
Currently, red clover extract is used to treat menopausal disorders as an alternative to classic hormone therapy. Several human and animal studies have attributed hypolipidemic, hypoglycemic, or antiatherosclerotic effects to red clover extract or isoflavones. This study was designed to determine the peroxisome proliferator-activated receptor (PPAR) gamma activation by red clover extract.
DESIGN:
The PPARgamma binding affinities and the transactivation activities of red clover extracts, isoflavones, and their metabolites were analyzed. The presence of specific substances in the extracts was proved by high-performance liquid chromatography/electrospray ionization/mass spectrometry.
RESULTS:
The red clover extracts and the compounds genistein and biochanin A were potent PPARgamma ligands and activators. Several metabolites exerted higher binding affinities or transactivational activities than their precursor molecules. 6-Hydroxydaidzein exerted a more than 100-fold higher binding affinity than its precursor daidzein. The maximal transactivational activity of 6-hydroxydaidzein and 3'-hydroxygenistein exceeded even that of rosiglitazone, a known PPARgamma agonist. Equol and O-desmethylangolensin showed an approximately fivefold higher binding affinity and, in the case of O-desmethylangolensin, a fourfold higher PPARgamma agonistic activity than the precursor. The daily dose of Menoflavon forte, a widely used red clover extract for treatment of menopausal disorders, provides theoretically 15% to 30% of the daily recommended dose of rosiglitazone. Considering the more active metabolites formed, activity must be higher in vivo.

CONCLUSIONS:
This study shows that red clover extracts, the major compounds, and especially several main metabolites exert significant PPARgamma binding and transactivation activity. Red clover extract, which is currently used for treating menopausal disorders, could be simultaneously used for ameliorating the metabolic syndrome.
http://www.ncbi.nlm.nih.gov/pubmed/18724264

peroxisome proliferator-activated receptor (PPAR) in mediating the effects of fibrates and fatty acids on gene expression.
Schoonjans K1, Staels B, Auwerx J.
Author information
Abstract
The three types of peroxisome proliferator-activated receptors (PPAR), termed alpha, delta (or beta), and gamma, belong to the nuclear receptor superfamily. Although peroxisome proliferators, including fibrates and fatty acids, activate the transcriptional activity of these receptors, only prostaglandin J2 derivatives have been identified as natural ligands of the PPAR gamma subtype that also binds thiazolidinedione antidiabetic agents with high affinity. PPARs heterodimerize with retinoic X receptor (RXR) and alter the transcription of target genes after binding to response elements or PPREs, consisting of a direct repeat of the nuclear receptor hexameric DNA recognition motif (PuGGTCA) spaced by 1 nucleotide (DR-1). Upon activation by fatty acids (FAs) and drugs that affect lipid metabolism, PPARs control the expression of genes implicated in intra- and extracellular lipid metabolism, most notably those involved in peroxisomal beta-oxidation. PPARs partially mediate the inductive effects of fibrates and fatty acids on high density lipoprotein (HDL) cholesterol levels by regulating the transcription of the major HDL apolipoproteins, apoA-I and apoA-II. The hypotriglyceridemic action of fibrates and certain fatty acids also involves PPAR and is constituted of: 1) increased hydrolysis of plasma triglycerides due to induction of LPL and reduction of apoC-III expression; 2) stimulation of cellular fatty acid uptake and conversion to acyl-CoA derivatives due to increased expression of genes for fatty acid transport protein and acyl-CoA synthetase; 3) increased peroxisomal and mitochondrial beta-oxidation; and 4) decreased synthesis of fatty acids and triglycerides and decreased production of very low density lipoprotein (VLDL). Hence, both enhanced catabolism of triglyceride-rich particles and reduced secretion of VLDL particles contribute to the hypolipidemic effect of fibrates and fatty acids. Finally, PPARs appear to be involved in differentiation processes because activation of PPAR gamma 2 triggers adipocyte differentiation and stimulates expression of several genes critical to adipogenesis. It is suggested that PPARs are key messengers responsible for the translation of nutritional and pharmacological stimuli into changes in gene expression and differentiation pathways.
PMID: 8725145 [PubMed - indexed for MEDLINE] Free full text

[Lotus]

Very cool about Red Clover. The text talks about extract, I wonder if that's in which form it would work the best used topically? Likely it would be many times more potent than a cream. I'm interpreting the text as it could do the same thing Volufiline does and perhaps be even better at it. Worth a try maybe.

I've tried red clover w/organic vegetable oil and in alcohol. In organic vegetable oil I think we'd want to use isopropyl alcohol for faster absorption. And in alcohol I'd use a carrier oil, like almond oil, olive oil or coconut oil. Either way, red clover seems likely to feminize fat. Building fat however calls for using progesterone and dhea. The whole idea of the Topical Cream Protocol is building glandular tissue in breasts. . 

Good luck 

[Heaven's Night]

This definitely sounds interesting. Maybe I'll put it to a test when I can afford it. I'm already doing great on absobrtion enhancing stuffs so likely wouldn't even need to add anything for that. I thought maybe I could find Red Clover extract of some kind which is pure without extra ingredients, that might work out well mixed with the creams rather than RC cream as likely those would have way lower concentration anyway. I have to see what I can get. 

I read quickly through the study quote about the effects and saved the entire text. I'm compiling this thead into easy to read text file, I should arrange it so it fits the screen easily.