[Lotus]

Hi Sweets… & Weezer, CM213, SensualTiffany and to the good people of BN. 

Sweets, I do remember both posts… LanaG? not so much I would consider the simultaneous administration of PC with Estradiol an experiment to try out sometime in the future. As when to begin the PC/E2 in a cis-females cycle would be after ovulation and ending prior to (or beginning) of menstruation. 

I think the topical program I introduced last year would benefit you (and others) more. Specifically, DHEA and E2… using the same as above (after ovulation and ending w/the start of menstruation). See, DHEA stimulates Estrogen Receptors (both ERα & ERβ), also… stimulates wound healing, helps to increase collagen, protein expression. I'll post more on the science of why using the two (DHEA & E2) makes sense. I see more programs getting more complex and adding too many unnecessary extra ingredients which has negative consequences in itself. 

Sticking with the usual sex-steriods (you know, estrogen, progesterone, some prolactin, IGF-1 etc, etc) is the best approach. I've tried many programs over the past 12 years of doing the thing (lol, growing boobs) only to realize the statement above. 

I'll say this about using DHEA cream, I'm sure most people know what's called a “Rescue Inhaler” (do a web search if you don't know) ... well, I consider DHEA to be a Rescue Boobhealer. DHEA is antioxidant, reduces ROS (reactive oxygen species), reduces inflammation, and about a f*ck ton more stuff I'll share later today. 

As for me?I'm still fighting the good fight with leukemia. We're also looking at secondary cancers, lol who's the lab rat now? 

Sorry, I'll get to answering others' queries asap. 

[LisaM]

I see DHEA capsules (Swansons) on iHerb, or is a cream preferable? Remembering again, UK based so US sources may not be possible.

[wee2er]

I'm UK to, and you can get DHEA cream from BIOVEA UK.
it's definitely on my list to try for helping feminisation and allergies, asthma, eczema, immune system, but like you, which way - capsules or cream?  
Hopefully our great saga Lotus will guide us

[SweetO]

Hi Sweets… & Weezer, CM213, SensualTiffany and to the good people of BN. 

Sweets, I do remember both posts… LanaG? not so much I would consider the simultaneous administration of PC with Estradiol an experiment to try out sometime in the future. As when to begin the PC/E2 in a cis-females cycle would be after ovulation and ending prior to (or beginning) of menstruation. 

I think the topical program I introduced last year would benefit you (and others) more. Specifically, DHEA and E2… using the same as above (after ovulation and ending w/the start of menstruation). See, DHEA stimulates Estrogen Receptors (both ERα & ERβ), also… stimulates wound healing, helps to increase collagen, protein expression. I'll post more on the science of why using the two (DHEA & E2) makes sense. I see more programs getting more complex and adding too many unnecessary extra ingredients which has negative consequences in itself. 

Sticking with the usual sex-steriods (you know, estrogen, progesterone, some prolactin, IGF-1 etc, etc) is the best approach. I've tried many programs over the past 12 years of doing the thing (lol, growing boobs) only to realize the statement above. 

I'll say this about using DHEA cream, I'm sure most people know what's called a “Rescue Inhaler” (do a web search if you don't know) ... well, I consider DHEA to be a Rescue Boobhealer. DHEA is antioxidant, reduces ROS (reactive oxygen species), reduces inflammation, and about a f*ck ton more stuff I'll share later today. 

As for me?I'm still fighting the good fight with leukemia. We're also looking at secondary cancers, lol who's the lab rat now? 

Sorry, I'll get to answering others' queries asap. 

Just to make sure, do you feel worse than usual or is it like a routine measure to rule out complications???

Sending you lots of hugs!!

[Lotus]

Hi BN Peoples, 

Below is new information on DHEA followed by what I posted last year on DHEA. The highlight(s) of the new information is how 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… or breast buds). I'll even go further and suggest B.O. (bovine ovary) supplement because I can explain how BO works scientifically, and it's not exactly the “like heals like '' version and other internet rumors and phenomena that's existed for ions. what I've compiled here on DHEA is a drop in the bucket lol, it's a good start. Happy reading if you dare

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, 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 ischaemia 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

Hi Breastnexum family, 3-4 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. I'll add additional info tomorrow about Bio-labs E1/E2, P4 and 17b applications. I'm tired.

• 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

Here we go, any test subjects?.......another find. I hope ya'll like it. I did try this!, and tbh, it perked my boobs up lol.  

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 (note to missB). Supplemental DHEA raises estrogen in men and postmenopausal women. But it can also raise androgens (DHT) in 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. Used daily?, I'd be inclined to say a few times per week to start. 

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. - See more at: http://press.endocrine.org/doi/10.1210/endo.139.2.5762?url_ver=Z39.88-2003&rfr_id=ori%3Arid%3Acrossref.org&rfr_dat=cr_pub%3Dpubmed&#sthash.0mwEgt3M.dpuf

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).

Shutting off gonadal function is much easier than you think. The technology is present (in the testes, via Sertoli cells). There is a back door function through 3 beta diol and FSH (follicle stimulating hormone) synthesis. In other words you can turn the testes into an estrogen producing factory.

Here's another example: say you have a situation of testicular failure, giving a supra-physical (massive) dose of testosterone cypionate will result in a cascade conversion to E2.

Hi Lotus,

Ah, so maybe it has happened in humans.

I've posted a couple articles on research I found in this thread:
http://www.breastnexus.com/showthread.php?tid=24439

Grew_some, 

I think it happens IRL but less documented. Picture this hypothetical, if we can modulate a cycle of T to a low point of testicular function, (test result of 50 ng/dl), then add DHEA at a 50 mg dose, add to this a fast of 12-14 hours (which promotes GH), next... the aromatase conversion of DHEA will promote E1/E2 synthesis, 3 beta diol is in this result too. Many other possibilities here.

This scenario is done a few times a week btw, add other products of NBE for synthesis of burning fat and adding adipocytes (thermogenesis).

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.

2 studies, similar effect. In any event DHEA looks like it can build a bigger butt, and....,the way it looks, mr. happy can benefit from a topical DHEA solution, oops!  

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.
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.

(Source-, ray peat forum)

[LisaM]

Thanks Lotus that's rather a lot to digest, can you expand on your Bovine Ovary comment, and perhaps a simplified suggested daily usage amount for DHEA and best method (topically, orally) You may have had this info in your post, but it's hard to filter through all the scientific stuff. Clearly in your case it worked wonders.

[Heaven's Night]

That's a lot of cool info, saved for later. Did you just suggest between the lines to try 50mg DHEA orally along with 12-14 hour fast? Because I happen to have 50mg DHEA pills lying around, a whole lot of them and I'm already fasting overnight as part of the GH + IGF-1 routine.

And what's the BO thing? So far I've only heard of one study done on mice, I never saw that text and everything else has been internet rumours and personal anecdotes. Would be neat if there were some light shed on this.

[wee2er]

Wow, thanks Lotus you are an absolute star  
Lots of info to go through slowly to digest, but think the gist of it is that we can use DHEA cream with olive oil (1:2?) and slap in on boobs and butts 3(ish) times a week = boob & butt growth  
Intrigued about how DHEA can help wound healing, wonder it that includes eczema?
Either way, roll on being paid for the next job I'm lining up as I reckon its worth a try for 3-months  
Like Lara has asked, what's this about BO, we are all very intrigued!!!!

[Lotus]

Hi BN, after many hours, days and years of research on BO I've found some key pieces of information on how using BO could have better results growing breasts. My approach to finding this information looked at the bovine ovary and granulosa cells. So, bovine ovary promotes aromatase (via the CYP19 enzyme & cAMP dependent signaling pathway. It also stimulates IGF-1, and probably the biggest discovery on BO is how it stimulates Sirtuins, and its family (see study below). Sirtuins are powerful, it's been reported how they extend lifespans. 

So how I'd use BO is with the topicals, meaning with DHEA, E2 (cream or gel) and Progesterone cream. I'd also recommend using a Nipple Pump to facilitate lactation. I've tried all of the above and can say it works. I've used some of the best electric breast pumps out there, and the one I'll share tomorrow works the best for me. I will say I've converted breast pumps to nipple pumps and get some of the best overall lactation results. 

There's other information to share about BO but I've run out of time (or gas). 

Granulosa cells (GC) are critical regulators of ovarian function and fertility. 

Effects of Follicle-Stimulating Hormone, Insulin-Like Growth Factor 1, Fibroblast Growth 
Factor 2, and Fibroblast Growth Factor 9 on Sirtuins Expression and Activity in Bovine Granulosa Cells

Abstract
Granulosa cells (GC) are critical regulators of fertility. During the process of ovarian folliculogenesis, these cells undergo profound changes while producing steroid hormones that are important to control follicular growth, oocyte maturation, and ovulation. Sirtuins are enzymes that regulate several biological processes and have been associated with control of GC function. However, how sirtuins are regulated in GC during ovarian folliculogenesis remains to be unveiled. The present study was designed to investigate effects of hormones that control GC proliferation, differentiation, and steroidogenesis on expression of the seven members of the mammalian sirtuins family (SIRT1-7) and on histone deacetylase activity of nuclear sirtuins (SIRT1, 6, and 7) in GC. Bovine granulosa cells were isolated from small antral follicles (1-5 mm) and were treated with or without follicle-stimulating hormone (FSH), insulin-like growth factor 1 (IGF-1), and fibroblast growth factors 2 (FGF2) and 9 (FGF9). Following treatments, cell proliferation was determined via a cell analyzer, estradiol synthesis and histone deacetylase activity were determined via ELISA, and sirtuins mRNA expression was determined via qPCR. Treatments with FSH and IGF-1 stimulated cell proliferation while addition of FGF2 or FGF9 suppressed estradiol production stimulated by FSH plus IGF-1. In terms of treatments that regulated sirtuins expression in GC, fibroblast growth factors were the most impactful: FGF2 alone increased SIRT1 mRNA expression in comparison to several treatments and increased mRNA abundance of SIRT2 and SIRT7 when added to the combination of FSH and IGF-1; the addition of FGF9 to the combination of FSH and IGF-1 increased mRNA expression of SIRT2, SIRT3, SIRT4, SIRT6, and SIRT7 and increased mRNA expression of SIRT5 in comparison to the negative control group that received no treatment. Also, FGF2 alone increased histone deacetylase activity of sirtuins in comparison to all treatments that contained FSH and/or IGF-1. Furthermore, several correlations were observed between treatments and sirtuins expression and activity, between estradiol or GC numbers and sirtuins expression, and between expression of sirtuins. As FGF2 and FGF9 are considered anti-differentiation factors of GC that stimulate GC proliferation while suppressing estradiol production in combination with FSH and IGF-1, data of this study suggest that sirtuins are associated with control of differentiation of bovine GC.

High Levels of SIRT1 Expression as a Protective Mechanism Against Disease-Related Conditions
In literature, it was shown that sirtuins' hyperactivity could reduce these negative outcomes both in vivo and in vitro due to its neuroprotective role (68–71)
https://www.frontiersin.org/journals/end...00614/full

The 5′-Flanking Region of the Ovarian Promoter of the Bovine CYP19 Gene Contains a Deletion in a Cyclic Adenosine 3′,5′-Monophosphate-Like Responsive Sequence
https://academic.oup.com/endo/article/13...ogin=false

Effects of IL-11/IL-11 Receptor Alpha on Proliferation and Steroidogenesis in Ovarian Granulosa Cells of Dairy Cows
Taken together, these data indicate that the effects of IL-11/IL-11Rα on the proliferation and steroidogenesis in bovine GCs is mediated by the JAK1-STAT3, PKA-CREB, p38 MAPK, and ERK1/2 signaling pathways. Our findings provide important insights into the local action of the IL-11 system in regulating ovarian function.

Weezer, thank you for your kind words. As for the skin healing with DHEA, you can find additional research at the bottom of each research link. 

Hi Lara, yes… 50 mg of DHEA taken orally produces more aromatase, but not to DHEA's metabolites: 
androst-5-ene-3beta,17beta-diol (ADIOL), androst-5-ene-3,17-dione, and androst-4-ene-3,17-dione were activators of PXR and (PPAR) subfamily.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2423429/

Sweets, apologies, I'll share (hopefully tomorrow) why more tests are being run.

[DruLactin]

praying that every test says you'll be fine~

also, new fountain of youth just dropped XD.... sirtuins, fascinating stuff. by "use BO with topicals" do you mean use BO topically like Tanya Marie Squirrel did(And Miss Mad Scientist on the other forum...), and use it topically alongside the DHEA, PG, and E2 topicals?
Or do you just mean take BO orally at the same as you apply the topical regimen?

thx for the lovely nuggets of information, stay safe~

Aria