Prolactin "minitherapy" with SMI-1 (novel protocol for lowering prolactin locally)

[Will Be an Egg in 5 years]

Where did the Bayer thread go?

 

[Nsas]

We are dissolving it in PEG400 and in my case 10% DMSO also to dissolve 60mg/ml. Some people put that under the tongue. I put it in a gelatin capsule and swallow it.

Hi. Can you please direct me to where you’re ordering the 10% DMSO from? I’m only able to find pure or near pure DMSO. I know you mentioned in another post that you’re seeing decreased shedding. Are you experiencing regrowth yet?

 

[Chads don't bald]

Ok, but the study I just posted contradicts that. "NMN must first undergo extracellular degradation to nicotinamide, nicotinic acid, or nicotinamide riboside in order to be taken up into cells". I don't understand how you say you know that and then you go on to say the opposite. Perhaps you missed that part. Maybe this is not accurate, but if it is then NMN is not nearly as good as NR so you'd be taking a big risk taking NMN whereas you know NR works. Further studies have to be conducted on humans to determine which of these studies is correct. What we can say for sure is that NR works, so I see no reason to risk taking NMN instead. Even in best case scenario it won't work much better since NR is very good at converting to NAD. As of now there are more studies showing that NR works in humans than NMN. This could change, and NMN could be slightly better. I assume NMM popularity comes from David Sinclair, but even he admits that NR might be better, they need more study to find out. For now I will stick with the more stable molecule.

Yes I agree with you that for right now taking NR is the smart move.

I was just mentioning that there is another pathway for NMN to enter the cell where it doesn't have to convert to NR first.

So if that pathway is indeed present in humans, then it would be more efficient than NR. That's why there needs to be actual human studies comparing NR vs NMN head to head in humans.

Also there is the factor of bioavailibility, I believe NR has lower bioavailibility than NMN. That doesn't necessarily make it worse than NMN though if NMN has to convert to NR first.

All that being said though, I don't think NR or NMN have that much of an effect in humans as it does in mice. Are there any studies which show significant age reversal in humans with NAD+ boosters?

 

[Will Be an Egg in 5 years]

https://www.hairlosstalk.com/interact/threads/bayer-prolactin-receptor-antibody-for-male-and-female-pattern-hair-loss.127790/

thanks

 

[Will Be an Egg in 5 years]

Before I post my progress, I want to mention that I switched from finasteride to dutasteride, and from topical minoxidil to oral around 6 months ago. So any regrowth could be due to dutasteride and minoxidil, but personally I think it's SMI doing some of the work. Also, I have DUPA, most of the improvement I've seen has been on the top and back of my head, a little on the sides but there's a noticeable improvement imo.

Regimen:
Daily
Morning:
- Sulforaphane
- Vitamin D3
- Qualia (only weekdays)
- Pure Hyaluronic Acid
- Pure Apigenin
- Pure TMG
- Niacin
- Oral SMI 60mg
- Fisetin & Quercetin (only last week of the month)
- Oral minoxidil 2.5mg
- Krill Oil 1k mg

Night:
- Biotin
- ksm-66 Ashwagandha
- Oral SMI 60mg
- Oral minoxidil 2.5mg
- dutasteride 1mg
- Metformin 1kmg (3 times a week)

- Rapamycin 10 mg once a week
- Dermanator 2, 1.5mm every two weeks
- Keto shampoo, three times a week

View attachment 164863

View attachment 164864

SMI or not, this is amazing regrow in such a small period

 

[French]

So,
Take only pure SMI oraly Can be effectiv in hairloss ? Without doing other chemist thing for absortion ?

 

[bluesuedeshoes]

Curious to know how much the SMI cost. If any of you are in the discord group and have an invite please DM me. I need some hair for this supposed sl*t summer.

 

[thatguydrinksbeer]

Not sure if it's already been said in this thread, but it appears orgasms cause a prolactin rush. I always thought the anti-fap crowd was nutty, but maybe there's a nugget of truth to it.

 

[pegasus2]

Not sure if it's already been said in this thread, but it appears orgasms cause a prolactin rush. I always thought the anti-fap crowd was nutty, but maybe there's a nugget of truth to it.

Not only after orgasm but during sexual activity as well. I believe edging to be very bad for hair, but the effect of moderate sexual activity to be negligible.

Prolactin concentrations increased (P < .05) immediately after SS[sexual stimulation] and SSE[sexual stimulation + ejaculation] and tended to rise during control bleedings in stallions previously exposed to SS or SSE. We conclude that 1) prolactin and Cortisol were secreted rapidly in response to SS and SSE, 2) the rise in Cortisol concentrations likely suppressed testosterone secretion within the next hour, and 3) stallions appeared to associate the distant sounds of other stallions with their own previous exposure to SS and SSE, resulting in a Cortisol response (and perhaps a prolactin response) even in the absence of direct stimulation.

Effects of Sexual Stimulation, with and without Ejaculation, on Serum Concentrations of LH, FSH, Testosterone, Cortisol and Prolactin in Stallions

Abstract. Six lighthorse stallions with previous sexual experience were used to determine the short-term effects of sexual stimulation (SS; 5 min exposure to an

academic.oup.com

 

[Photon]

So,
Take only pure SMI oraly Can be effectiv in hairloss ? Without doing other chemist thing for absortion ?

I had to mix it with 95% peg400 and 5% DMSO. But I think that's about it.

 

[FluxZ]

I found some evidence that extrapituitary prolactin is mediated by testosterone (maybe by dht?) in mice prostate.

Indeed it is an inference from the fact that in castrated mice there is no trace of ePRL in prostate tissue, while with the administration of exogenous testosterone we find ePRL.

If ePRL in follicles were mediated by androgens in humans, we would have found the connecting link of why antiandrogens work for Androgenetic Alopecia.

It must be said that there is also evidence that the expression of ePRL in the follicles appears to be increased by estrogen, but only with regard to the regulation of follicular cycles.

If this intuition were correct, obviously there would be no other way than silencing PRLR with antibody, or antagonizing it (I am referring to those who still believe that the chaste tree or other dopaminergics can help)

Minireview: Extrapituitary Prolactin: An Update on the Distribution, Regulation, and Functions

​

"Increasing evidence demonstrates the presence of ePRL, as well as its receptors, in male reproductive organs. ePRL mRNA was detected in the dorsal and lateral prostate of rats using Northern blotting and in situ hybridization. Immunostaining localized the protein to secretory granules of the apical cytoplasm of epithelial cells. Expression within the prostate was activated by testosterone, with castrated rats producing no ePRL whereas treatment with exogenous testosterone restored its production. This was confirmed in vitro using cultured prostatic cells, which express ePRL only in the presence of testosterone..."

 

[Roeysdomi]

I found some evidence that extrapituitary prolactin is mediated by testosterone (maybe by dht?) in mice prostate.

Indeed it is an inference from the fact that in castrated mice there is no trace of ePRL in prostate tissue, while with the administration of exogenous testosterone we find ePRL.

If ePRL in follicles were mediated by androgens in humans, we would have found the connecting link of why antiandrogens work for Androgenetic Alopecia.

It must be said that there is also evidence that the expression of ePRL in the follicles appears to be increased by estrogen, but only with regard to the regulation of follicular cycles.

If this intuition were correct, obviously there would be no other way than silencing PRLR with antibody, or antagonizing it (I am referring to those who still believe that the chaste tree or other dopaminergics can help)

Minireview: Extrapituitary Prolactin: An Update on the Distribution, Regulation, and Functions

​

"Increasing evidence demonstrates the presence of ePRL, as well as its receptors, in male reproductive organs. ePRL mRNA was detected in the dorsal and lateral prostate of rats using Northern blotting and in situ hybridization. Immunostaining localized the protein to secretory granules of the apical cytoplasm of epithelial cells. Expression within the prostate was activated by testosterone, with castrated rats producing no ePRL whereas treatment with exogenous testosterone restored its production. This was confirmed in vitro using cultured prostatic cells, which express ePRL only in the presence of testosterone..."

If I understood correctly the regrow that trans ppl get from estrogen is created by the same process that happend here?

 

[pegasus2]

I found some evidence that extrapituitary prolactin is mediated by testosterone (maybe by dht?) in mice prostate.

Indeed it is an inference from the fact that in castrated mice there is no trace of ePRL in prostate tissue, while with the administration of exogenous testosterone we find ePRL.

If ePRL in follicles were mediated by androgens in humans, we would have found the connecting link of why antiandrogens work for Androgenetic Alopecia.

It must be said that there is also evidence that the expression of ePRL in the follicles appears to be increased by estrogen, but only with regard to the regulation of follicular cycles.

If this intuition were correct, obviously there would be no other way than silencing PRLR with antibody, or antagonizing it (I am referring to those who still believe that the chaste tree or other dopaminergics can help)

Minireview: Extrapituitary Prolactin: An Update on the Distribution, Regulation, and Functions

​

"Increasing evidence demonstrates the presence of ePRL, as well as its receptors, in male reproductive organs. ePRL mRNA was detected in the dorsal and lateral prostate of rats using Northern blotting and in situ hybridization. Immunostaining localized the protein to secretory granules of the apical cytoplasm of epithelial cells. Expression within the prostate was activated by testosterone, with castrated rats producing no ePRL whereas treatment with exogenous testosterone restored its production. This was confirmed in vitro using cultured prostatic cells, which express ePRL only in the presence of testosterone..."

Interesting study, thanks for sharing. Just browsing it and here's some more interesting bits.

Similarly cleaved PRL fragments have been found in endothelial cells (discussed later in this review), raising the possibility that they also play a role in inhibiting endothelial cell proliferation...this 16-kDa fragment possessed binding sites on endothelial cells (54) and was a potent inhibitor of angiogenesis (55). In addition, it was found to induce apoptosis of endothelial cells through caspase activation

My theory has been that DHT increases binding of prolactin to its receptor by increasing oxygen, which increases intracellular pH. There is a 500-fold change in the dissociation rate of PRL to its receptor between pH 8.3 and pH 5.8. DHT>Oxygen/ROS>alkaline PH>increased PRLR binding>IL-6/STAT3/5/Twist1>Wnt shutdown>loss of progenitor cells>hair miniaturization>shiny dome. There's much more to it than this of course, but hair loss is caused by interruption of the Wnt pathway and this is triggered by the AR and PRLR. This study you found further supports this.

Dermal papilla cells under hypoxia do not react the same way to DHT. https://pubmed.ncbi.nlm.nih.gov/25647436/

AOS significantly ameliorated the DHT-induced alterations of regulatory factors in hHFDPCs and prolonged the anagen phase of hair follicle in mice. Although the fundamental mechanism of the antagonistic effects of AOS against Androgenetic Alopecia key features is unknown, we speculated that AOS likely exhibited its effects through its antioxidant activities.

Frontiers | Amelioration of Androgenetic Alopecia by Algal Oligosaccharides Prepared by Deep-Sea Bacterium Biodegradation

Androgenetic alopecia (Androgenetic Alopecia) is a dihydrotestosterone (DHT)-mediated hair loss disorder characterized by shortened anagen hair cycle. Oligosaccharides derived...

www.frontiersin.org

It seems more clear all the time that blocking the PRLR is more important than the AR.

 

[Dimitri001]

A little over three weeks.

Isn't that too short a period for it to have made any difference?

 

[Photon]

Isn't that too short a period for it to have made any difference?

Nyet

 

[FilthyFrancis]

Thousands. We are everywhere now. We're everyone you depend on. We're the people who do your laundry and cook your food and serve your dinner. We make your bed. We guard you while you're asleep. We drive the ambulances. We direct your call. We are cooks and taxi drivers and we know everything about you. We process your insurance claims and credit card charges. We control every part of your life.

@pegasus2 in a joking mood, that's pretty unusual. Good to know your spoofs are of great quality, just as the rest of your posts

As a buffoon myself, I can only invite you to pull more of these. Thanks for the good laugh

 

[FluxZ]

@pegasus2 how DHT would increase oxygen in scalp??

 

[Throwaway94]

We're doing a second round of the group buy for larger quantities. DM me if interested and you missed out the first time

 

[HairOnFire]

Have there been any dose-ranging studies with oral SMI-1? If known. how long is the half-life? I'm not interested in using it topically, just orally.

 

[French]

I wanted to try this product and expose my results week by week here .

I DM someone for the group buy and I'm waiting is answer.

We need to know clearly if this stuff Works or not