Pregnenolone, Progesterone, DHEA Increase Breast Size In Females

[milk_lover]

Girls either don't change your boobs' size or increase them. No going down.

 

[DaveFoster]

Oh, yeah, very much so, and even in females. Here are some things to consider.

Kinetics and effect of percutaneous administration of dihydrotestosterone in children. - PubMed - NCBI
"...BACKGROUND: Percutaneous administration of dihydrotestosterone (DHT) has been successful in promoting phallic growth in infants and children with 5 alpha-reductase deficiency raised as males. We investigated whether percutaneous administration of DHT is similarly effective in patients with micropenis due to alternative diagnoses.
METHODS: Six patients (age range 1.9-8.3 years) with micropenis of variable etiology were studied prospectively. 2.5% DHT gel was applied to the phallus once daily at a dose of 0.15-0.33 mg/kg body weight. Serum DHT concentrations were measured at 0, 2, 4, 8, 12 and 24 h following application of DHT gel.
RESULTS: Peak DHT concentrations were attained within 2-8 h after application of the gel and subsequently remained within the normal adult range in all but 1 patient, who had received the lowest dose of 0.15 mg/kg. An increase in phallic growth, ranging from 0.5-2.0 cm, was achieved after 3-4 months of treatment in all patients whose DHT concentrations were maintained within adult range.
CONCLUSION: Percutaneous administration of DHT in a dose of 0.2-0.3 mg/kg once daily for a period of 3-4 months may be useful in the management of patients with testosterone biosynthetic defects, who have sufficient masculinization to warrant male sex assignment, or in patients with micropenis prior to reconstructive surgery.


Masculinization of the distal tubular and external genitalia in female sheep with prenatal androgen exposure. - PubMed - NCBI
"...The reproductive tracts from 24 treated and 13 control postpubertal female offspring were examined at 10 months of age. The ovaries, oviducts, and uteri were grossly and histologically normal in both TP- and DHT-exposed sheep. However, in the DHT-treated sheep, the uterus connected to a misshapen, saccular vagina that opened into the urethra; in the TP-treated sheep, it ended in a blind sac. In both TP- and DHT-treated sheep, the urethra was approximately 5 times longer than that of control sheep, and it resembled a male urethra with bilateral male accessory genital glands. The urethra terminated in a fully developed penis in both TP- and DHT-treated sheep, and a scrotal sac was present (without testes). These results show that prenatal exposure of female sheep to exogenous androgens results in masculinization of the tubular and external genitalia."


The child with micropenis. - PubMed - NCBI
"...Transdermal DHT has also been reported to be effective in prepubertal children. Children with hypopituitarism and GH deficiency respond to appropriate hormonal therapy. Surgical correction is not indicated in the common endocrine types of micropenis. Many studies have shown that most testosterone treated children have satisfactory gain in length of penis and sexual function. Thus sexual reassignment is done very infrequently now."

Exposure of neonatal rats to anti-androgens induces penile mal-developments and infertility comparable to those induced by oestrogens. - PubMed - NCBI
"...Flutamide alone decreased penile length and weight significantly (p < 0.05), but it caused neither fat accumulation, nor affected fertility (80% vs. 87% in controls). Antide alone reduced penile length and weight significantly, and induced fat accumulation in 4/11 rats and infertility in 13/14 rats. Conversely, all 11 F + A-treated rats, similar to all nine DES-treated rats, had fat accumulation and loss of smooth muscle cells and cavernous spaces in the body of the penis and were infertile. In addition, reductions in penile length and weight were higher than in rats treated with F or A alone. DHT co-administration mitigated penile deformities in the DES group, but did not in the F + A group. Testicular testosterone was reduced by 70-95% at 7 or 12 days of age in all treated groups, except in the F group, which had threefold higher testosterone than controls. Collectively, data unequivocally show that reduced androgen production/action in the neonatal period, in the absence of oestrogen exposure, induces permanent infertility and malformed penis similar to that caused by oestrogen."

Testosterone, androstenedione, and 5alpha-dihydrotestosterone on male sexual behavior and penile spines in the hamster. - PubMed - NCBI
"...Gonadectomy completely suppressed MSB and induced a regression of penile spines. AD was more potent than T in restoring MSB, ejaculatory behavior being displayed by most castrated subjects with a lower dose of AD (50 microg/day) than of T (300 microg/day), and long intromissions being shown by all AD-treated castrated hamsters but only by 20% of T-treated ones, when doses of 1000 microg/day were given. DHT did not stimulate any copulatory response. The three androgens, even at the lowest dose, partially stimulated penis and penile epithelium growth, DHT showing the highest potency. Treatment of castrated hamsters with AD (50 microg/day), restored steroid levels to similar values as those of intact animals. These results show that AD and T restored MSB even with a partial stimulation of penile spines growth, AD being more potent than T. In contrast, DHT did not restore MSB in the hamster in spite of its peripheral androgenic potency."

Effects of oral finasteride on erectile function in a rat model. - PubMed - NCBI
"...RESULTS: Serum T and DHT and intraprostatic DHT concentrations, erectile function, and mean weights of the corpus cavernosum and prostate were lowest in group 2. There was no significant difference in the serum T concentration and erectile function between groups 4 and 1. However, the serum and intraprostatic DHT concentrations were significantly lower in group 4 than in group 1 (both P < 0.001). The tissue weights of the corpus cavernosum and prostate were reduced by 25.9% and 92.3% in group 4 compared with group 1 (both P < 0.001). Histopathology revealed a significant atrophy of the prostate in groups 2 (castration) and 4 (finasterine). There was a significant decrease in the smooth muscle content in group 2, but not in groups 3 and 4.
CONCLUSIONS: In a rat model, finasteride treatment for 4 weeks reduces the weight of the corpus cavernosum but appears not to affect the erectile responses to electrical stimulation of the cavernous nerve. As erection is a complex process involving important signaling in the brain, further studies are necessary to demonstrate the long-term effects of finasteride on both central and peripheral neural pathways of erection.

Bottom line is this - if you are a male you better stay away from anything that is estrogenic or anti-adrogenic (especially the latter). Conversely, if you have a "size" problem down there things like DHT, DHEA, and androstenedione can help you look normal again. Finally, the rat study with androstenedione (AD), T and DHT showed that a human dose of as little as 3.5mg daily restored normal hormone levels of castrated male rats. Taking 5mg - 10mg DHEA daily will likely result in endogenous production of about 3mg AD (as a result of conversion) and thus be effective treatment for age- or disease-related hypogonadism.

Do you think topical Pansterone could increase penile growth to supraphysiological levels, as in increased girth and length?

Also, if not, do you know of any other ways to stimulate growth besides penis extenders? Topical 11-keto DHT maybe?

 

[haidut]

Do you think topical Pansterone could increase penile growth to supraphysiological levels, as in increased girth and length?

Also, if not, do you know of any other ways to stimulate growth besides penis extenders? Topical 11-keto DHT maybe?

I think topical 11-keto DHT would be the say to go to replicate this study properly. It has the same androgenic potency as DHT and this is what counts when it comes to penile length.

 

[DaveFoster]

@haidut

Thanks for the response; there's some worry with shutdown with 11-keto DHT if the forum posts are true.

I'll use Pansterone and report any wild anacondas spotted if expedient.

 

[Constatine]

Interesting thread...I think I'll chime in on this as well. It's not been too long but has anyone seen improvements yet?

 

[dreamcatcher]

Please keep in mind that this is a rodent study, and done on menopausal animals. However, I do not see a reason why these findings would not translate to other organisms as well, including healthy human females. The most notable finding IMHO is that DHEA achieved these effects by acting like a fully adrogenic compound and even DHT could not compete with its effects on breast size. This study underscores once again the androgenicity of DHEA when applied topically. 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). DHEA was applied topically on a portion of dorsal (back) skin of the animals. The DHEA dose used was high, it would correspond to a few hundred milligrams daily in humans. Given that topical application of 18mg (and above) DHEA daily produced statistically significant increases of all estrogens (estradiol, estrone, estriol) in humans I would advise keeping DHEA intake under 15mg daily. I think that if a smaller dose (15mg daily) of DHEA is applied directly on the breasts it would have similar effects to the much higher dose used by the study and applied to the back of the animals.
On a side note, Peat has written that development of cancer is almost always preceded by local tissue atrophy, and estrogenic activity in the local tissue. This is arguably especially true in the case of breast cancer. As you can see the authors agree with Peat and suggest that given the effects of DHEA on breast tissue atrophy and its mechanism of almost exclusive androgenicity it would be promising approach to implement for breast cancer treatment. Indirectly, they are also suggesting that other androgens like DHT would also be helpful. If prostate cancer is also estrogenically driven and the injections of testosterone into the prostate stopped terminal prostate cancer (as I posted in this thread: viewtopic.php?f=75&t=5579), then topical DHEA (in the pubic area or rectally) in small doses would also be a viable therapy for prostate cancer.

http://press.endocrine.org/doi/10.1210/ ... %3Dpubmed&

"...DHEA is a sex steroid precursor that is metabolized into active androgens and/or estrogens in peripheral intracrine tissues, depending upon the relative activities and types of steroidogenic enzymes expressed in each tissue and cell (31, 35). The mammary gland is likely to possess all the steroidogenic enzymatic systems necessary for the formation of androgens and estrogens from steroid precursors, such as DHEA (64, 65, 66, 67, 68, 69). The complete reversal of the ovariectomy-induced mammary gland atrophy seen after 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. As mentioned above, the above-indicated histological changes characterizing a rather lobuloalveolar type of development of the mammary gland, are analogous to those seen during pregnancy and lactation (14, 70)."


"...Nevertheless, although it is reported that androgens can stimulate lobuloalveolar growth, our study demonstrates for the first time the stimulatory androgenic-like effect of DHEA on the mammary gland, which not only resulted in a complete reversal of the ovariectomy-induced atrophic changes of the mammary gland but also led to a profuse lobuloalveolar development. In addition, we have also demonstrated the potent stimulatory effect of DHT, a nonaromatizable androgen on the growth of the rat mammary gland, thus indicating that the above-described effects are mediated through the androgen receptor. Furthermore, in the present study, the absence of a significant increase in serum PRL levels in DHEA-treated animals appears to exclude the possibility of a role of PRL in the major DHEA-induced histological changes. Following the combined administration of DHEA and EM-800 to OVX rats, the same lobuloalveolar pattern of development of the mammary gland was seen as that observed after treatment with DHEA alone, thus practically eliminating the role of estrogens in the action of DHEA. It is also important to mention that EM-800 does not have any effect on the mammary gland histopathology when given to OVX rats, as reported for the mouse by Luo et al. (39). The 250-μg daily dose of EM-800 used in the one shown in a series of preclinical pharmacological and toxicological (our unpublished observations) studies (37, 38, 39, 73) to exert maximal antiestrogenic activity."

"...In conclusion, the present study shows the potent stimulatory effects of androgens on lobuloalveolar as well as ductal development in the rat mammary gland. Furthermore, the histological changes of the mammary gland induced by DHEA treatment provide evidence for its intracrine conversion into active sex steroids with predominant or even possibly exclusive androgenic activity in the mammary gland. Local formation of androgens and estrogens through intracrine activity plays a major role in the pathophysiology of both normal and tumoral hormone-sensitive mammary tissue in the human. Considering the predominant androgenic action of DHEA on normal mammary tissue as well as the well recognized and potent inhibitory action of DHEA on the development and growth of DMBA-induced mammary tumors, which is mainly considered an androgenic effect, we suggest that tissue DHEA metabolism plays an important role in the pathophysiology of the mammary gland and could be a useful preventive and therapeutic approach for breast cancer."

I wonder, for how long the DHEA was used to achieve these results reg breast growth?

 

[haidut]

I wonder, for how long the DHEA was used to achieve these results reg breast growth?

It said treatment was for 12 months. It was long, but it was needed to reverse complete atrophy of the mammary tissue. The equivalent would be to try and reverse complete atrophy of breasts in 75+ year old, postmenopausal female. So, for most women it probably does not apply and much shorter duration of treatment would be needed. I think some forum users reported breast growth after 1 month of oral DHEA but I can't seem to find that thread.

 

[dreamcatcher]

It said treatment was for 12 months. It was long, but it was needed to reverse complete atrophy of the mammary tissue. The equivalent would be to try and reverse complete atrophy of breasts in 75+ year old, postmenopausal female. So, for most women it probably does not apply and much shorter duration of treatment would be needed. I think some forum users reported breast growth after 1 month of oral DHEA but I can't seem to find that thread.

Thank you for your reply, it's very helpful! I understood that you initially recommended transdermal application of 15mg per day. Do you think oral supplementation is more effective? Do you remember what the internal dose was? Thank you.

 

[haidut]

Thank you for your reply, it's very helpful! I understood that you initially recommended transdermal application of 15mg per day. Do you think oral supplementation is more effective? Do you remember what the internal dose was? Thank you.

The study used subcutaneous method, which can be replicated pretty closely with DHEA dissolved in DMSO, as I mentioned in another thread. The dose they used was high, and it will have estrogenic effects in humans. In rodents, DHEA is like having the ability to eat 10 massive, juicy, fatty cakes a day and never getting an ounce of body fat. Rodents don't make much DHEA so when you give them the stuff, in any amount, their organism loves it and converts it massively in T and DHT and very little estrogen. But in humans, the studies show anything more than 18mg daily starts to raise estrogen, so I would say 15mg would be the cutoff and each dose should be no more than 5mg.

 

[dreamcatcher]

The study used subcutaneous method, which can be replicated pretty closely with DHEA dissolved in DMSO, as I mentioned in another thread. The dose they used was high, and it will have estrogenic effects in humans. In rodents, DHEA is like having the ability to eat 10 massive, juicy, fatty cakes a day and never getting an ounce of body fat. Rodents don't make much DHEA so when you give them the stuff, in any amount, their organism loves it and converts it massively in T and DHT and very little estrogen. But in humans, the studies show anything more than 18mg daily starts to raise estrogen, so I would say 15mg would be the cutoff and each dose should be no more than 5mg.

That's very interesting, thank you. I have Biomatrix DHEA and1.2 mg (1 drop) of BioMatrix DHEA is equivalent to 3 mg of micronized oral DHEA. The other ingredients are glycerin and alcohol. I've only started using it 4 days ago by applying it to the skin so I can't report any change just yet.

 

[Kray]

That's very interesting, thank you. I have Biomatrix DHEA and1.2 mg (1 drop) of BioMatrix DHEA is equivalent to 3 mg of micronized oral DHEA. The other ingredients are glycerin and alcohol. I've only started using it 4 days ago by applying it to the skin so I can't report any change just yet.

I've just started this brand supplement as well. Would appreciate your report on how you're doing with it.

 

[dreamcatcher]

I've just started this brand supplement as well. Would appreciate your report on how you're doing with it.

I've given it away after using it for a week, I had bad side effects from it such as eye bags, abdominal cramps and fatigue.

 

[Momado965]

Some forum members have already experienced penis enlargement from using pregnenolone and DHEA. See this thread for more info, and make sure you read all of it as the discussion continues until the end:
viewtopic.php?f=75&t=6019#p71414

What about progesterone + dhea (cortinon) for penile growth?

 

[Yggr]

I was just thinking, female bodybuilders who ab/use androgen derivatives like oxandrolone don’t seem to get breast enlargement but quite the opposite. @haidut could I trouble you for some insight into this matter?

 

[TheBeard]

I was just thinking, female bodybuilders who ab/use androgen derivatives like oxandrolone don’t seem to get breast enlargement but quite the opposite. @haidut could I trouble you for some insight into this matter?

Oxandrolone is purely androgenic.
The hormones mentioned on this thread as responsible for breast enlargement are not.

 

[Yggr]

Hi @TheBeard thank you for responding. I was under the impression the effect was caused by their topical conversion into androgenic substances like DHT.

 

[Ji.]

Excellent! :-D
And the study I posted found that DHEA causes the same magnitude of breast enlargement as pregnancy. So, it could be a good alternative to menopausal women willing to reverse mammary atrophy or just firm up the breasts in general.

Would the same treatment work for young female affected by birth control during puberty?

 

[Weslemkoon1969]

Please keep in mind that this is a rodent study, and done on menopausal animals. However, I do not see a reason why these findings would not translate to other organisms as well, including healthy human females. The most notable finding IMHO is that DHEA achieved these effects by acting like a fully adrogenic compound and even DHT could not compete with its effects on breast size. This study underscores once again the androgenicity of DHEA when applied topically. 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). DHEA was applied topically on a portion of dorsal (back) skin of the animals. The DHEA dose used was high, it would correspond to a few hundred milligrams daily in humans. Given that topical application of 18mg (and above) DHEA daily produced statistically significant increases of all estrogens (estradiol, estrone, estriol) in humans I would advise keeping DHEA intake under 15mg daily. I think that if a smaller dose (15mg daily) of DHEA is applied directly on the breasts it would have similar effects to the much higher dose used by the study and applied to the back of the animals.
On a side note, Peat has written that development of cancer is almost always preceded by local tissue atrophy, and estrogenic activity in the local tissue. This is arguably especially true in the case of breast cancer. As you can see the authors agree with Peat and suggest that given the effects of DHEA on breast tissue atrophy and its mechanism of almost exclusive androgenicity it would be promising approach to implement for breast cancer treatment. Indirectly, they are also suggesting that other androgens like DHT would also be helpful. If prostate cancer is also estrogenically driven and the injections of testosterone into the prostate stopped terminal prostate cancer (as I posted in this thread: viewtopic.php?f=75&t=5579), then topical DHEA (in the pubic area or rectally) in small doses would also be a viable therapy for prostate cancer.

http://press.endocrine.org/doi/10.1210/ ... %3Dpubmed&

"...DHEA is a sex steroid precursor that is metabolized into active androgens and/or estrogens in peripheral intracrine tissues, depending upon the relative activities and types of steroidogenic enzymes expressed in each tissue and cell (31, 35). The mammary gland is likely to possess all the steroidogenic enzymatic systems necessary for the formation of androgens and estrogens from steroid precursors, such as DHEA (64, 65, 66, 67, 68, 69). The complete reversal of the ovariectomy-induced mammary gland atrophy seen after 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. As mentioned above, the above-indicated histological changes characterizing a rather lobuloalveolar type of development of the mammary gland, are analogous to those seen during pregnancy and lactation (14, 70)."


"...Nevertheless, although it is reported that androgens can stimulate lobuloalveolar growth, our study demonstrates for the first time the stimulatory androgenic-like effect of DHEA on the mammary gland, which not only resulted in a complete reversal of the ovariectomy-induced atrophic changes of the mammary gland but also led to a profuse lobuloalveolar development. In addition, we have also demonstrated the potent stimulatory effect of DHT, a nonaromatizable androgen on the growth of the rat mammary gland, thus indicating that the above-described effects are mediated through the androgen receptor. Furthermore, in the present study, the absence of a significant increase in serum PRL levels in DHEA-treated animals appears to exclude the possibility of a role of PRL in the major DHEA-induced histological changes. Following the combined administration of DHEA and EM-800 to OVX rats, the same lobuloalveolar pattern of development of the mammary gland was seen as that observed after treatment with DHEA alone, thus practically eliminating the role of estrogens in the action of DHEA. It is also important to mention that EM-800 does not have any effect on the mammary gland histopathology when given to OVX rats, as reported for the mouse by Luo et al. (39). The 250-μg daily dose of EM-800 used in the one shown in a series of preclinical pharmacological and toxicological (our unpublished observations) studies (37, 38, 39, 73) to exert maximal antiestrogenic activity."

"...In conclusion, the present study shows the potent stimulatory effects of androgens on lobuloalveolar as well as ductal development in the rat mammary gland. Furthermore, the histological changes of the mammary gland induced by DHEA treatment provide evidence for its intracrine conversion into active sex steroids with predominant or even possibly exclusive androgenic activity in the mammary gland. Local formation of androgens and estrogens through intracrine activity plays a major role in the pathophysiology of both normal and tumoral hormone-sensitive mammary tissue in the human. Considering the predominant androgenic action of DHEA on normal mammary tissue as well as the well recognized and potent inhibitory action of DHEA on the development and growth of DMBA-induced mammary tumors, which is mainly considered an androgenic effect, we suggest that tissue DHEA metabolism plays an important role in the pathophysiology of the mammary gland and could be a useful preventive and therapeutic approach for breast cancer."

https://mospace.umsystem.edu/xmlui/bitstream/handle/10355/53165/age000977.pdf?sequence=1&isAllowed=y
"...Since 1 ug EB plus 3 mg of P stimulated DNA, these compounds were each injected at the 3 mg level (Table 27). These compounds increased the DNA over that produced by EB alone as follows: Pregnenolone 29.0 percent, 17ahydroxyprogesterone 26.5 percent, androstenedione 35.8 percent, and testosterone 33.0 percent."

I am fascinated by this conversation and these studies you've shared. I am a responding a little late here but wanted to ask a question. I am presently using your CortiNon. I'm wondering if applying, topically, DHEA (on it's own) to the breast tissue would add too much DHEA along with the oral dosing of CortiNon? Is there a way to administer it both orally and topically if one wants to see if it will increase breast size?

 

[CuriousKay]

I am fascinated by this conversation and these studies you've shared. I am a responding a little late here but wanted to ask a question. I am presently using your CortiNon. I'm wondering if applying, topically, DHEA (on it's own) to the breast tissue would add too much DHEA along with the oral dosing of CortiNon? Is there a way to administer it both orally and topically if one wants to see if it will increase breast size?

I am also intrigued by this thread.

I have a couple of skin conditions that seem to be related to hormones, and when I took CortiNon internally, it triggered one of them. I have been taking progesterone for 5 years with amazing benefits. I am curious if applying CortiNon topically to the breast tissue would be okay.

I've lost maybe 15-20lbs in the last 5 years, and have good muscle tone, but loose skin from stretch marks on thighs, butt and belly, and I've gone down 1.5 bra sizes. I had a breast reduction 21 years ago when I was young and plump, so now I'm down to almost nothing.

I'd love to see if CortiNon would help my breast tissues, and I wonder if there would be any benefit to applying it topically to any other parts of my body.

I'd love to hear anyone's thoughts on what I've mentioned here :)

 

[Ras]

Did any women here try this?