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

Nsas

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This only works if your hair loss is caused by hyperprolactinemia causes hair loss, right? So if my prolactin level is 6, will this work still work for me? Is everyone getting their prolactin level checked before trying?
 

czecha

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This only works if your hair loss is caused by hyperprolactinemia causes hair loss, right? So if my prolactin level is 6, will this work still work for me? Is everyone getting their prolactin level checked before trying?
there is no way to check your intrafollicular prolactin. serum prolactin doesn't mean anything
 

temples_of_doom

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I'd be interested in trialling this too but im in Australia so it might complicate getting the stuff to me, regardless I wish you all the best of luck and thanks for the research your doing
 

Throwaway94

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I'd be interested in trialling this too but im in Australia so it might complicate getting the stuff to me, regardless I wish you all the best of luck and thanks for the research your doing
I'm trying from New Zealand but I guess your customs are even more strict
 

Zon Ama

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So Ray Peat was right saying prolactin causes male pattern baldness

Prolactin: The Most Likely Cause of Male Pattern Baldness

To summarize, Peat believes that prolactin, serotonin, estrogen, and
cortisol are the main culprits in hair loss. Peat spends most of the
interview talking about prolactin's relation to male pattern baldness.

Cortisol <> Prolactin <> Estrogen <> Serotonin

While I believe DHT has a hand in hair loss (if it didn't Propecia
would have zero effect), I believe it to be downstream from much more
important issues.

Overview:

It appears that prolactin along with other stress hormones are
elevated in those who are prematurely balding.

* There is conflicting information on the web, but prolactin may
increase the activity of the 5-alpha reductase enzyme.
* Prolactin has been found to modulate hair growth in mice, as
well as be a target for human hair follicles.
* Serotonin increases prolactin, which may increase hair loss
* Prolactin increaes Interleukin-6, an inflammatory marker that is
correlated with hair loss.
* Prolactin inhibits thyroid function (Kharrazian), and low
thyroid promotes prolactin, which can both cause hair loss.

What to do about it?

* Zinc seems to decrease prolactin
* Dietary tryptophan can increase prolactin levels. However, tryptophan is unavoidable if one is consuming animal products, so
assuring that tryptophan converts into niacin, and not serotonin, is
desirable. Obtaining an adequate intake of B6, B2, iron, and Vitamin A
can increase the conversion of tryptophan to niacin. Peat suggests
that the calcium to phosphate ratio is also important.
* An increase in parathyroid hormone (possible deficiencies of
vitamin D, vitamin K, vitamin A, zinc, magnesium or calcium) can cause
an increase in prolactin. Obtaining adequate calcium, as well as the
cofactors needed to absorb calcium is probably a smart idea. Sodium
and adequate protein may also increase calcium absorption.
* Estrogen increases prolactin secreation. This is a topic for another post, but you can maintain a healthy estrogen level by
providing the liver with enough sugar and avoiding dietary polyunsaturated fats.
* Alcohol consumption can increase prolactin.
* Salt restriction increases serotonin, which can increase prolactin.
 

hairDespair

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You say stress may be related to balding. Anecdotally, when I'm stressed on a problem, I'll often notice the "balding itch" exactly in places that I recede. I'm also hypothyroid and take meds for that. Most recent bloodwork had good cortisol level(12 mg/dL)
 

FollicleGuardian

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"While PRL promoted hair growth/hair shaft elongation in HFs derived from female frontotemporal scalp, PRL treatment of isolated male occipital scalp HFs resulted in premature catagen induction and thus the inhibition of hair growth.[77] This observation has been further substantiated on a molecular level, since PRL treatment resulted in sex‐ and site‐specific differences in gene expression.[77] Furthermore, analyses of plucked HFs from male frontal and occipital scalp revealed differential expression for several microRNAs (miRNAs) that target PRL signalling.[64] Together, these findings suggest that PRL action may contribute to the observed differences in Androgenetic Alopecia susceptibility between frontal and occipital HFs and the resulting characteristic hair loss pattern"

Cortisol is a known inducer of catagen. It's not causitive in male pattern baldness, but obviously anything that induces catagen will speed it up.
Ok this is getting scary now. Prolactin explaining the hair loss pattern. This is intriguing.
 

1919

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Yes it really does look like it comes down to AR/PRLR. Neutralize them both and throw in a potent Wnt agonist, and this could get really good. I can't wait for SMI and KY to get here. I feel like a kid waiting for Christmas lol
You got your hands on KY ? Do you know if any company trying to bring it to market or did it fizz out?
 

Armando Jose

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"While PRL promoted hair growth/hair shaft elongation in HFs derived from female frontotemporal scalp, PRL treatment of isolated male occipital scalp HFs resulted in premature catagen induction and thus the inhibition of hair growth.[77] This observation has been further substantiated on a molecular level, since PRL treatment resulted in sex‐ and site‐specific differences in gene expression.[77] Furthermore, analyses of plucked HFs from male frontal and occipital scalp revealed differential expression for several microRNAs (miRNAs) that target PRL signalling.[64] Together, these findings suggest that PRL action may contribute to the observed differences in Androgenetic Alopecia susceptibility between frontal and occipital HFs and the resulting characteristic hair loss pattern"

Cortisol is a known inducer of catagen. It's not causitive in male pattern baldness, but obviously anything that induces catagen will speed it up.
Confligting results,
"The seemingly conflicting effects reported in the literature (Table 1) may well be reconciled if one interprets them as representations of site- and/or gender-dependent HF responses to PRL. If confirmed, these differences will add a fascinating new dimension to our understanding of sexual dimorphism in HF responses to hormonal stimulation, and highlight the need for a systematic exploration of gender- and/or location-specific PRL-mediated signaling in the physiology and pathology of peripheral PRL target tissues in the human system."

And:
Moreover, we cannot entirely exclude
the possibility that differences in cell
composition, or cell number, between
frontal and occipital pHFs, for example,
due to the onset of miniaturization in frontal HFs, may have confounded our
results. To substantiate the present findings
and to elucidate the complex biological
processes leading to Androgenetic Alopecia, future
investigations should involve the analysis
of paired HF samples from males across
different age groups (prepubertal boys,
elderly men); alternative sampling approaches;
and refined analysis strategies,
for example, single-cell transcriptomics
and immune histochemical staining.
Insights into Male Androgenetic Alopecia:
Differential Gene Expression Profiling of
Plucked Hair Follicles and Integration with
Genetic Data
Journal of Investigative Dermatology (2019) 139, 235e238; doi:10.1016/j.jid.2018.06.182
 
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1919

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CK biotech, it's not even in phase 1 yet. Thought this was common knowledge on here.
Sorry, joined not long ago and havent seen any KY threads yet. Only saw it in passing at Follicle Thought. Hearing phase 1 always hurts :(((
 

Tom4362

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Yes it really does look like it comes down to AR/PRLR. Neutralize them both and throw in a potent Wnt agonist, and this could get really good. I can't wait for SMI and KY to get here. I feel like a kid waiting for Christmas lol
By Christmas you can be Johnny Deps' stand-in for the new Pirates of the Caribbean movie
 
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Dimitri001

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What are the best sources to research potential sides of suppressing PRL activity?

Are there studies of other antagonists or other means of suppression? Disorders where it's lowered? Anything else I could look for?

Yes it really does look like it comes down to AR/PRLR. Neutralize them both and throw in a potent Wnt agonist, and this could get really good. I can't wait for SMI and KY to get here. I feel like a kid waiting for Christmas lol

You think addressing PRL alone or PRL + androgens wouldn't do the whole trick without wnt?
 

Dimitri001

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Is there an easier-to-reach prlr antagonist for us

IDK, but this paper from 2010 says SMIs are not yet available. It mentions the possibility of blocking it with a modified version of the PRL molecule, tho. It's an 11 year old paper, tho, maybe things have changed.
 
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