r/tressless

You never smoked, no alcohol, no drugs.

Eat clean, no sugar, optimize nutrition and great sleep.

Work out, get lean, build muscle, great bloodwork. No wrinkles, no accepted* health issues.

Now look at your head: it is still balding.

Look at Michael Lustgarten, a great researcher by the way. He measures all his body parameters and tweaks each and every one of them. He has excellent body composition, a perfect vascular system. He still lost his hair.

And then I see other people who eat junk food all day, overweight, smoker, drinker, game through the night. But guess what: they look 10 years younger because they have full heads of hair.

What a cheap game this is. Nature marked us as old, aging. There is a clear delineation between youth and old age, the boring rest of ones life: pattern hair loss.

Oh and you notice that humans are extremely tuned to the hair loss pattern. It immediately evokes an impression of less vitality, even some kind of creepiness. Clowns shave the same pattern. There is a reason for this. I just need to paint the hair I got with some red or blue paint and I am ready as a clown. So you rather shave everything off instead. Interesting. Completely bald looks fine, that pattern is not.

Our bodies can grow lush hair, our bodies can grow new teeth, new limbs, even new cartilage. But our bodies simply do not want this. Scientists find new blocking mechanisms every day that simply prevent a perfect regeneration or health. Who or what added these blockages? The objectives of our bodies are different, a happy life is not one of them.

You can do everything right, your prostate will still continue growing until you suffer. Same dht mechanism as balding by the way.

But male pattern balding also shows us a truth about aging: We are all biological vehicles where under each trunk different parts were build to fail at different rates. That is it, that is aging. A biological machine that reproduces early and after that, the scary thing comes. Nobody cares anymore, nature does not care about you anymore. Pain, body horror, does not matter. Does not change the outcome. Without new science we are just there for the ride.

Now they found out now that 50 percent of aging is genetic. There are 110 year old people who smoke a pack of cigarettes each day.

You are on your own. Without artificial intervention there is nothing we can do about aging.

Solving male pattern baldness on a molecular level also solves aging.

*balding is a health issue, a loss of fitness, increases danger of skin cancer, makes one a more likely bullying target, less social competency can reduce healthspan and lifespan. That our looks biased, hypocritical society not accept balding as a disease means nothing in terms of science or reality.

https://en.kintor.com.cn/news_details/1803365125008502784.html
GT20029 has a real chance of replacing finasteride for many people if larger trials confirm the early data.

Unlike finasteride or dutasteride, it does not lower DHT systemically. It is a topical PROTAC designed to bind the androgen receptor, recruit an E3 ubiquitin ligase, and send that receptor to the proteasome for degradation. So instead of just lowering DHT, the goal is to reduce the receptor DHT uses inside the follicle environment.

This could make it a serious option for people who cannot tolerate finasteride, are worried about systemic hormone changes, or want a more targeted topical approach. And obviously it’s stackable with fin and dut.

https://en.kintor.com.cn/news_details/1803365151294205952.html
https://en.kintor.com.cn/news_details/1803365146143600640.html
The safety data is also promising. In both the China and U.S. Phase 1 studies, systemic exposure was extremely low, even after repeated dosing. That matters because the entire appeal of GT20029 is local scalp activity without meaningful systemic exposure. China phase 2 also showed low to zero systemic exposure.

https://pubmed.ncbi.nlm.nih.gov/41328006/

Where it comes to results, The China Phase 2 AGA data is promising.

The study tested 180 Chinese men across six groups: 0.5% once daily, 1.0% once daily, once-daily placebo, 0.5% twice weekly, 1.0% twice weekly, and twice-weekly placebo.

All GT20029 groups improved hair counts, but only 0.5% once daily and 1.0% twice weekly clearly beat their matching placebo groups. The 1.0% twice-weekly arm also improved hair width.

Now this could seem odd because you would expect 1.0% once daily to clearly outperform 0.5% once daily, but it did not. Instead, 1.0% twice weekly looked like one of the stronger arms. However the 1.0% once daily had started at a lower baseline hair count in the group than its placebo so perhaps that group has more severe AGA subjects which made GT underperform (especially with how small the groups are).

The mechanism of GT has a lot of promise. If larger and longer trials keep showing low systemic exposure and meaningful hair growth, then yes, I think it probably replaces finasteride for many people. It could also be stacked with finasteride or dutasteride because lowering DHT and degrading the androgen receptor are not the same mechanism.

https://pubmed.ncbi.nlm.nih.gov/39884271/
https://www.nature.com/articles/s41467-026-70153-4
Now, there is the recent GPR133 paper that’s making people think that outside of lowering scalp dht, there’s nothing effective enough to help slow or reverse hair loss like fin and dut.

In this paper, the authors suggest DHT can activate GPR133 in the connective tissue sheath, causing sheath contraction, Piezo-type mechanosensitive ion channel component 1 activation, progenitor-cell stress, and reduced follicle growth. So in other words, DHT doesn’t need the Androgen Receptor to cause stress to the hair follicle. It may restrict its growth via GPR133 receptor. So this could mean drugs like GT are useless.

https://www.nature.com/articles/s41467-026-70153-4
However I have an issue with the paper as there are some inconsistencies that make me write off GPR being a major issue for Aga. Much of the work in the paper comes from isolated follicles, ex vivo systems, single-cell/spatial transcriptomics, and humanized mouse models. These are useful tools, but they do not prove that GPR133 inhibition restores AGA in a normal human scalp environment.

https://www.nature.com/articles/s41467-026-70153-4
The biggest issue is the dermal papilla data. The authors found that dermal papilla subcluster percentage and distribution were mostly comparable between healthy, non-balding, and balding follicles. That is strange because the dermal papilla is supposed to be one of the main structures disrupted in androgenetic alopecia. They typically reduce in number and size.

https://www.nature.com/articles/s41467-026-70153-4
https://pubmed.ncbi.nlm.nih.gov/35033537/
Even the authors acknowledge the issue. They note that AGA is usually understood through dermal papilla miniaturization, reduced dermal papilla volume, reduced cell number, and loss of inductive capacity. They also cite their own prior work showing androgen receptor upregulation in dermal papilla cells, reduction in size and density of these cells along with their signaling activity, and more comparable to their recent study they do note vascular regression around the dermal papilla. They admit their newer single-cell analysis did not show obvious dermal papilla changes beyond reduced angiogenesis signaling and that’s a major issue and contradiction of the literature and pathway of AGA.

https://pubmed.ncbi.nlm.nih.gov/35033537/
That is not a small detail. if the newer GPR133 paper finds balding and non-balding dermal papilla subclusters looking mostly similar, that discrepancy needs to be explained before we oversell the significance of GPR133 and DHT on the hair follicle.

https://www.nature.com/articles/s41467-026-70153-4
To me, this suggests the GPR133 paper is capturing one slice of AGA biology, not the whole disease. The study focused heavily on early miniaturizing anagen follicles from the frontal hairline edge, with a limited number of male samples. That is useful mechanistic data, but not enough to claim this pathway explains AGA broadly across the whole scalp.

That is why GT20029 still makes sense. If androgen receptor activity in the dermal papilla region is one of the main upstream problems, then locally degrading the androgen receptor remains a direct strategy. GPR133 may add another layer to DHT biology, but it does not replace the classic androgen receptor/dermal papilla pathway.

Hey guys

I have been using topical minoxidil for over a year now, but I’d like to try switching to oral minoxidil mostly for convenience and also better results.

I plan on taking 5mg daily.

I’ve looked into websites that sell it on Tressless, but I couldn’t figure out which product contains blister packs and which comes in a plastic bag (like the loxidil one from Thailand), as I’m looking only for blister packed pills to avoid humidity and oxidation

Does anybody know of a product? Also, would French Customs seize the product?

thank you very much

I have been on fin for almost 2.5 years now. Didn't get much regrowth only stabilization and no further loss. Which is not a bad thing as I had diffuse thinning, but could be better.

The thing I wanted to ask long-term fin uses is that do they still go through early sheds where their hair looks thinner? and then it grows back and looks a bit thicker, then it falls out again and so on?

It seems like I go through 2 sheds every year since I've been on fin, one in spring the other in Autumn.

My main hairline doesn't look proper receded from 4 years ago but I have noticed baby hairs I used to have around it miniaturized and are barely there now. I had a hairdresser in January tell me I looked like I was thinning on one of my temples and I dismissed it because I've always had thinner hair around there but now I'm taking it seriously and I think I've caught MPB at a early stage. I am taking TRT at the moment and have not dialed in levels properly yet (getting blood test in a couple days) but I want to get on this ASAP at a low dose. Does anyone here have experience taking 0.5 MWF as that is what I'm looking to start with. Also im 27

What are some famous celebrities/artists/politicians ect with full head of hair without transplant ?

Say someone is already Norwood 4–5 and has never used any hair loss meds before. They then get a 4K graft transplant — which realistically may not even be enough coverage for their level of loss. After the surgery, the clinic puts them on oral finasteride and minoxidil.

Now imagine that person turns out to be a really strong responder to the meds. Over the next year, they gain a lot more density and coverage from the medication itself, making the overall result look much better than the transplant alone would have achieved.

Then the clinic markets the case as proof of their transplant “mastery” and surgical skill.

Does anyone else feel like this probably happens a lot in the industry? Not saying every clinic does it, but I feel like meds can massively influence post-op results and sometimes the transplant gets all the credit.

Can we expect, that the results from redditors who take DHT Blockers as a monotherapy are the "average" results? Or do most people come here to post their 1 out of 1000 results like the so called hyper responders?

Same goes for people who don't see results at all and even say, that it gets worse. Very discouraging to be honest. I have the feeling, that they are a lot here on reddit.

I'm just asking because basically ALL studies say, that the majority of people get improvement but it takes time.