Why Aren’t We All On Seti? Seems Better Than finasteride

[furrydome]

https://i.imgur.com/m8otWQI.png

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Keep in mind that everything on this chart is for maintenance/prevention including seti.

@alebaba If you want regrowth you need to add microneedling + a growth agent ( i.e minoxidil, PGE1, PGE2, Bimatoprost, Latanoprost etc.) on top of seti.

OT, but this post is quality... direct, informative, thorough. The info isn't new but we're painting a better picture of this Androgenetic Alopecia puzzle and more people are learning about it.

Congrats to the hair loss community. This is part of how we win.

 

[kawnshawn]

I've been on oral seti 2 grams split a day about over a month now. Itch is gone and I hardly shed, if I do shed its little hairs about 1-1.5 inch in total length. My hair is past my shoulders so they aren't thick terminal hairs. I'm thinking I might be getting some regrowth, so I'm gonna start dermarolling, adding oral minoxidil, and gonna look into growth factors so I can try to regrow much hair as possible.

 

[kawnshawn]

This. I'm not spending $400 per month on a completely unproven treatment with no long term safety data. Keep in mind this is a brand new class of medication. Maybe it will be fine. Maybe it won't.

How many times have you seen in the news some lawsuit over a drug because after 2-5 years they find out it has some unforeseen side effect?

No one has ever used a PGD2 inhibitor before. For all anyone knows these could cause dementia or anything else really in the long run. They're completely unknown both for effectiveness and safety.

Aren't you using darolutamide, a drug intended for castration resisted prostate cancer that's still in trials? You could argue the same that in 2-5 years you could have unforeseen side effects.

You should get into contact with SwissTemples, he is extremely knowledgeable in regards to the PGD2 angle.

 

[IdealForehead]

Aren't you using darolutamide, a drug intended for castration resisted prostate cancer that's still in trials? You could argue the same that in 2-5 years you could have unforeseen side effects.

Sort of. Daro is an androgen receptor antagonist. We've had androgen receptor antagonists for decades. We know what they generally as a class do and don't do. It's not a new drug class. If I want to read about the general risks of androgen receptor antagonism, there are many years of studies on flutamide, nilutamide, bicalutamide, topilutamide, and now enzalutamide and apalutamide.

Daro is the newest in the family, but the family is well known and they are all somewhat similar in their risks. The only thing particularly unique about daro is that it doesn't cross the blood brain barrier, which if anything should make it theoretically safer than the rest of its family members. It's possible some metabolic breakdown product of daro will turn out to be uniquely toxic, but I doubt it, and I am only using 1% of the doses that are used for prostate cancer (since I'm using it topically), so this doesn't worry me. It is stronger than other anti-androgens too and we have no long term data on it, so it's hard to say for sure.

These risks and unknowns are why I try not to encourage anyone else to use daro. While I'm happy that it has worked well for me without too many problems so far, I try to discourage too much enthusiasm about the drug in general and especially in people who aren't aware of the uncharted waters it might represent.

So I don't think I'm being selective or unfair in what I'm saying about seti/fevi. The reality is: no one really knows what PGD2 inhibition does throughout the body long term. We don't have long term PGD2 deprivation studies, like we have long term androgen deprivation studies.

Maybe it's nothing. Maybe it's no worse than taking an anti-histamine every day. That would be fantastic.

But sometimes the unknown turns out bad. eg. My dad takes pantoprazole for his heartburn. Everyone thought that was a great new type of drug when it came out. Now that we have some longer data, they say it increases your risk of stroke, so he's trying to stop.

I bet when finasteride hit the market in 1992 people thought it was a miracle. A drug that can cure hair loss! Amazing! Who could complain? I doubt anyone would have guessed that 26 years later people would be angrily complaining about its effects on neurosteroids etc. and trying to build a case that it is a permanently damaging drug.

Who knows what people will be saying about PGD2 inhibitors in 26 years? I don't know. I know some people have already noted sleep disruption on it. I am a poor sleeper to begin with. So that makes me personally nervous. Are people gonna say in 26 years PGD2 inhibition ruined their sleep centers so now they can't sleep at all?

Again, I truly don't know. I'm not trying to fear monger these drugs. If they are proven to work and be safe, it will be an incredible new class. Your results sound great. But when you're inhibiting a signal chain that's never been inhibited before, and we already know that it has effects on the brain, that makes me a little nervous.

I'd rather the devils I know than the devils I don't. I don't like unknown compounds. I prefer to only go that route when it's absolutely necessary. In my case it was necessary as finasteride and dutasteride don't work on me, so my choices were to try something different or go bald.

 

[washed_up]

There are people who took v**** and completely lost their sight. Inherent risk presides within every drug, no matter how seemingly benign, on earth.

Every drug commercial ends with a cavalcade of possible side effects and some of them include literal death. Everything is a calculated risk.

 

[IdealForehead]

There are people who took v**** and completely lost their sight. Inherent risk presides within every drug, no matter how seemingly benign, on earth.

Every drug commercial ends with a cavalcade of possible side effects and some of them include literal death. Everything is a calculated risk.

Absolutely agreed.

But when we're talking about these drugs, you can only do calculated risk if you have sufficient data. I'm a self-made guinea pig. I've tried to be an educated one, but that doesn't change what it is. All I'm saying is be wary of making yourself a guinea pig too.

If it's a binary choice between going bald and taking an unknown Russian Roulette drug, I would take the Russian Roulette every time. But I'm not gonna pretend that's not what it is.

The degree of risk you ought to take depends on your need and where you're coming from. If I was on finasteride and it was working perfect for me with no sides, I doubt I'd ever be playing with any experimental chemicals.

 

[Georgie]

Hi. Someone who tried 1.5g of seti here. Didn’t work. Sorry lads, hopefully you have better luck than me.

 

[INT]

I guess the answer to how expensive it is is also the answer why not everyone is on seti. A semester supply costs as much as a decent transplant.

 

[Georgie]

For how long did you take it?

A month.

 

[mowingdown]

A bit fast to conclude it doesn't work though.

But if fina or duta doesn't help, seti won't too I'm afraid.

How is your lyphar seti trial? Still shedding? I started taking it and have been experiencing some pretty serious brain fog. Any hints of that for you?

 

[IdealForehead]

How is your lyphar seti trial? Still shedding? I started taking it and have been experiencing some pretty serious brain fog. Any hints of that for you?

This is really probably not surprising. PGD2 has a massive amount of expression in the central nervous system (brain and spinal cord). The brain is the #1 area of the body PGD2 is made.

You can see here for more info.

I'm shocked more people aren't complaining of terrible cognitive side effects. Maybe people are noticing what they want to notice. Or maybe they haven't been using it long enough.

Also, unfortunately, from what i see both seti and fevi have terrible solubilities which makes them poor topical agents. So it's not even easy to limit their effect.

If you take them in massive oral doses long term, it is very likely you will affect your brain chemistry. We just don't what the consequences will be.

 

[westonci]

This is really probably not surprising. PGD2 has a massive amount of expression in the central nervous system (brain and spinal cord). The brain is the #1 area of the body PGD2 is made.

You can see here for more info.

I'm shocked more people aren't complaining of terrible cognitive side effects. Maybe people are noticing what they want to notice. Or maybe they haven't been using it long enough.

Also, unfortunately, from what i see both seti and fevi have terrible solubilities which makes them poor topical agents. So it's not even easy to limit their effect.

If you take them in massive oral doses long term, it is very likely you will affect your brain chemistry. We just don't what the consequences will be.

Here is a more recent study on CRTH2

https://www.docdroid.net/qAxmyM7/1-s20-s1098882317300151-main.pdf#page=5

Go to page 46 for a synopsis

It shows that blocking CRTH2 reduces "sickness behavior". It doesnt mention any negative brain CNS effects, although it mentions hypomyelination of the peripherral nervous system

Ive been on 2g/day seti for more than 6 months now and havent noticed any cognitive side effects.

I had sleep sides for 2 weeks when i started then it went away.

A small bonus us ive noticed a massive reduction in acne.

Also keep in mind that Seti doesnt block PGD2 but the CRTH2 receptor (see diagram below)

Sulfasalazine reduced PGD2 production and has a lot og negative cognitive sides.

 

[IdealForehead]

Here is a more recent study on CRTH2

https://www.docdroid.net/qAxmyM7/1-s20-s1098882317300151-main.pdf#page=5

Go to page 46 for a synopsis

It shows that blocking CRTH2 reduces "sickness behavior". It doesnt mention any negative brain CNS effects, although it mentions hypomyelination of the peripherral nervous system

Ive been on 2g/day seti for more than 6 months now and havent noticed any cognitive side effects.

A small bonus us ive noticed a massive reduction in acne.

Also keep in mind that Seti doesnt block PGD2 but the CRTH2 receptor

View attachment 85846

PGD2 works through two receptors. Seti blocks one of those two receptors, and the receptor it blocks has mood regulating effects on rats at least.

No one actually knows what the PGD2 that our brain and spinal cord make does or how it works. I think it's interesting that these are the tissues of the rat that make the largest volume PGD2-producing enzymes, yet no one knows why or to what end.

I would be very curious to understand what PGD2's role is in the brain.

I'm happy you're doing well on it. I don't think you should stop if you're feeling fine. But I think people should be wary of this drug without knowing what it's actually doing to the nervous system.

To put it succinctly:

Prostaglandin D2 is the most abundant prostaglandin in the brain.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2386988/
​

But why?

 

[westonci]

PGD2 works through two receptors. Seti blocks one of those two receptors, and the receptor it blocks has mood regulating effects on rats at least.

No one actually knows whatthe PGD2 that our brain and spinal cord makes does or how it works. I think it's interesting that these are the tissues of the rat that make the largest volume PGD2-producing enzymes, yet no one knows why or to what end.

I would be very curious to understand what PGD2's role is in the brain.

I'm happy you're doing well on it. I don't think you should stop if you're feeling fine. But I think people should be wary of this drug without knowing what it's actually doing to the nervous system.

sulfasalazine reduces PGD2 and has host of sides which is why I avoid it.

 

[IdealForehead]

Here's what little I can find on CRTH2 (the receptor seti blocks) and the brain:

CRTH2, which is a second receptor for prostaglandin (PG) D2, is involved in inflammatory responses in peripheral tissue; however, its role in cognitive function remains unclear. Our study provides evidence that PGD2-CRTH2 signaling is involved in cognitive function and may represent a potential therapeutic target for cognitive dysfunction in patients with psychiatric disorders.

https://www.ncbi.nlm.nih.gov/pubmed/27481693


CRTH2 is a second prostaglandin D2 receptor involved in mediating the allergic response; however, its central function is not yet known. Here, we demonstrate that central CRTH2 mediates emotional impairment.

https://www.ncbi.nlm.nih.gov/pubmed/24523542
​

 

[westonci]

Our study provides evidence that PGD2-CRTH2 signaling is involved in cognitive function and may represent a potential therapeutic target for cognitive dysfunction in patients with psychiatric disorders.

https://www.ncbi.nlm.nih.gov/pubmed/27481693


CRTH2 is a second prostaglandin D2 receptor involved in mediating the allergic response; however, its central function is not yet known. Here, we demonstrate that central CRTH2 mediates emotional impairment.

https://www.ncbi.nlm.nih.gov/pubmed/24523542
​

Correct me if Im wrong but doesn't your post further validate that blocking CRTH2 reduces "sickness behavior" aka psyciatric disorders aka emotional impairment.

https://i.imgur.com/jIJ2I4B.png

 

[IdealForehead]

Correct me if Im wrong but doesn't your post further validate that blocking CRTH2 reduces "sickness behavior" aka psyciatric disorders aka emotional impairment.

Yeah, and that's the thing. None of what I'm saying is to suggest seti would necessarily have negative effects on the central nervous system. For all we know this could turn out to be all positive.

Maybe seti will one day be a preventative cure for dementia. Maybe everyone who takes seti will benefit from an incredible anti-inflammatory effect in the brain and improve their neural health well into their 90s.

Or maybe something else will happen.

Almost nothing is known about that massive amount of PGD2 made in the brain or what it's doing. So who knows? It will be quite an experiment to find out in a few decades.

 

[kiwi666]

I would personally say oral at 2g/day is better than topical. But if you are able to apply seti topically twice a day i dont see why it wouldnt be the same. Its very hard to do if you have an active social life.

Also do whatever growth promoting agents you can afford or have access to. The more the better.

• minoxidil
• PGE1
• PGE2
• Bimatoprost
• Latanoprost

And always add a microneedling regimen with these

Can you please share a link to the microneedling device you use

 

[westonci]

Can you please share a link to the microneedling device you use

http://shop.owndoc.com/product-info.php?dermastamp15-pid211.html

 

[allthegains]

Yeah, and that's the thing. None of what I'm saying is to suggest seti would necessarily have negative effects on the central nervous system. For all we know this could turn out to be all positive.

Maybe seti will one day be a preventative cure for dementia. Maybe everyone who takes seti will benefit from an incredible anti-inflammatory effect in the brain and improve their neural health well into their 90s.

Or maybe something else will happen.

Almost nothing is known about that massive amount of PGD2 made in the brain or what it's doing. So who knows? It will be quite an experiment to find out in a few decades.

meh I'll play labrat for a bit. My life can't get much worse anyways.

I'll try to perform cognitive self analysis every few days and I'll drop it at the first sign of malfunction