Should I add Minoxidil to my hair loss routine?

[CherryPopinski]

-9 Months on Fin (1mg Daily)
-Ketaconazole Shampoo 2x a week
-I need to try derma rolling/pens

I most certainly have noticed a regain in ground, but I wanna to address the areas of diffuse thinning. If I use Minoxidil there are a few caveats.

-There will be an initial shedding phase where my hair will look exponentially worse before I see true results which can take a minimum of 4-6 months

-There's no guarantee Minoxidil will work for me/potential for side effects

-There's a chance my hair will look worse than when I started if I use Minoxidil which is a lifetime commitment.

Current pic on RIGHT is wet after a shower, most people at this point can't tell I'm suffering from hair loss in some areas.

[Droopdx]

Text 50 year old tinder match and ask

[legbroke]

From my research, minoxidil seemed to be the safer of the big two. Less significant sides, and it's way more likely to help with varied types of baldness because it just brings more blood to your scalp (to my understanding, it really treats the symptoms - doesn't target specific causes like fin/DHT).

Shedding when using minox is also supposed to be a good sign. Seems a bit bro-sciencey, but hairworldmag agrees at least (lot of the "sources" out there are minoxidil sellers...) (https://www.hairworldmag.com/minoxidil-shedding/).

Gave up and am just laying down and baldrotting myself though so meh.

[CherryPopinski]

From my research, minoxidil seemed to be the safer of the big two. Less significant sides, and it's way more likely to help with varied types of baldness because it just brings more blood to your scalp (to my understanding, it really treats the symptoms - doesn't target specific causes like fin/DHT).

Shedding when using minox is also supposed to be a good sign. Seems a bit bro-sciencey, but hairworldmag agrees at least (lot of the "sources" out there are minoxidil sellers...) (https://www.hairworldmag.com/minoxidil-shedding/).

Gave up and am just laying down and baldrotting myself though so meh.

I’m more nervous about sides from Minoxidil than I am of Finasteride srs

Plus Minoxidil doesn’t treat the underlying cause of hair loss. If I only used it by itself I’d still be losing hair.

[Dirtymanjames]

I’m debating the same thing as you...in your case I say no because unless someone is taller than you no one will actually notice your thinning,

I have diffusé but it’s actually hitting my forelock and hairline as well, so I’m more tempted to start as it is noticeable..... but minoxidil is such a pain in the ass, especially if I want to go traveling

[meekmilli]

I just LOVE this addition to your hair loss routine for you. Its very prudent.

Cheers

[eatmycrackers]

lol @ haircels if you aren't stacking Min & Fin

I've been on that combo time for a few months now... did not notice the "exponentially worse" phase since starting Min its nbd really I do notice some new baby hairs at the hairline from Min alone.

Buy 3 month supply at Walmart for like $19 its cheap just dont have it drop all over your face some idiot here said he had hairs growing in the middle of his forehead because of that lmao.

[CherryPopinski]

lol @ haircels if you aren't stacking Min & Fin

I've been on that combo time for a few months now... did not notice the "exponentially worse" phase since starting Min its nbd really I do notice some new baby hairs at the hairline from Min alone.

Buy 3 month supply at Walmart for like $19 its cheap just dont have it drop all over your face some idiot here said he had hairs growing in the middle of his forehead because of that lmao.

I have a 3 month supply of Rogaine foam sitting unused in my bathroom.

I’m avoiding it cause I have anxiety issues, and side effects of Minoxidil can include heart palpitations and dizziness

[legbroke]

I’m more nervous about sides from Minoxidil than I am of Finasteride srs

Plus Minoxidil doesn’t treat the underlying cause of hair loss. If I only used it by itself I’d still be losing hair.

Re: not treating the underlying cause, it's not necessarily true that you'd have a net loss of hair if only using minox. Everybody is always losing hair regardless, just balding is when your rate of replacement is less than the amount you lose each day. Fin slows the rate of loss, and minox increases the growth rate.

I've also seen some stuff about taking creatine (not cell tech) that may be worth looking into - it's supposed to boost DHT (which fin is working against), so may be worth researching stopping creatine if you use.

[CherryPopinski]

Re: not treating the underlying cause, it's not necessarily true that you'd have a net loss of hair if only using minox. Everybody is always losing hair regardless, just balding is when your rate of replacement is less than the amount you lose each day. Fin slows the rate of loss, and minox increases the growth rate.

I've also seen some stuff about taking creatine (not cell tech) that may be worth looking into - it's supposed to boost DHT (which fin is working against), so may be worth researching stopping creatine if you use.

I don’t currently supplement with creatine

[andrew28]

I got a 3,168 graft FUT strip transplant by a top US doctor over a month ago.

Not touching that finasteride poison but I did one session of PRP at the end of my transplant procedure. Now I’m using minoxidil and a Low Level Laser Light Therapy Cap from iRestore every other day for 25 minutes. Cost $950.

I’m on TRT and no finasteride.....so yea I’m gonna probably need another transplant 5-10 years down the road. But I knew that. I won’t even take Saw Palmetto to reduce my DHT levels. That’s how scared I am of suppressing DHT.

[Harry815]

Yes OP I had asked my dermatologist about Fin, and he recommended stacking Fin and Min. Been on both for close to a year now and they worked to stop hair loss and rethicken/regrow hair too.

[mesobuild]

Taking something every day like this seems as bad as a system. It seems like a pain and does not do anything close to fin.

[elterrible987]

I have a 3 month supply of Rogaine foam sitting unused in my bathroom.

I’m avoiding it cause I have anxiety issues, and side effects of Minoxidil can include heart palpitations and dizziness

i use it and dont have any sides.

[CherryPopinski]

Taking something every day like this seems as bad as a system. It seems like a pain and does not do anything close to fin.

Fin is easy I don’t even think about it, but having to meticulously massage foam into my scalp every night seems very annoying

[elterrible987]

I got a 3,168 graft FUT strip transplant by a top US doctor over a month ago.

Not touching that finasteride poison but I did one session of PRP at the end of my transplant procedure. Now I’m using minoxidil and a Low Level Laser Light Therapy Cap from iRestore every other day for 25 minutes. Cost $950.

I’m on TRT and no finasteride.....so yea I’m gonna probably need another transplant 5-10 years down the road. But I knew that. I won’t even take Saw Palmetto to reduce my DHT levels. That’s how scared I am of suppressing DHT.

why not topical fin or topical ru?

you can even buy min with fin mixed in

[andrew28]

why not topical fin or topical ru?

you can even buy min with fin mixed in

I haven’t read up on topical fin or ru

enlighten me please

[elterrible987]

I haven’t read up on topical fin or ru

enlighten me please

im not an expert on either and havent used either but they both are used for the same purpose, lower dht at the scalp, not systemic ing the blood. RU applied on the scalp and you can buy min and fin premixed from online stores and have it on your scalp too.

the moreplatesmoredates youtube guy has like multiple 30 minute videos on these

also the dermarolling+min was shown to be better than min alone in official studies, though i would wait for dermarolling however long your doctor says post transplant.

[CanuckGame]

[gangaslayer]

ive just started with Min couple weeks ago, looks worse now but i expected the thinning stage. im just hoping after a while it comes back thicker and haven't done more damage. if it has i will just embrace the baldcel look.

[mesobuild]

im not an expert on either and havent used either but they both are used for the same purpose, lower dht at the scalp, not systemic ing the blood. RU applied on the scalp and you can buy min and fin premixed from online stores and have it on your scalp too.

the moreplatesmoredates youtube guy has like multiple 30 minute videos on these

also the dermarolling+min was shown to be better than min alone in official studies, though i would wait for dermarolling however long your doctor says post transplant.

Why would 5-AR locally do much for scalp DHT? This comes from the blood. Maybe a little less produced locally reduces local activity.

I think you would need to drop systemic production to stop DHT targetting scalp AR. Plus, I read something like <1/3 of local drugs like this stay local. You're still taking a strong systemic fin dose.

[Rixxen]

I don't have hair loss and have therefore never needed treatment, but:

I’m more nervous about sides from Minoxidil than I am of Finasteride srs

This is completely irrational. With Finasteride you're taking a drug that directly inhibits 5-alpha-reduction of Testosterone to DHT. So you're actually manipulating the metabolization of your hormones. With this come inherent risks of side effects like erectile dysfunction, depending on how heavily your DHT is reduced. You're rather lucky that you are not experiencing major side effects, which doesn't mean that you're not manipulating your hormones putting yourself at risk.

Minoxidil on the other hand does much less to you overall. Especially if you use it topically you most likely won't experience side effects, especially not systemic ones. The typical Minoxidil induced shedding that is always talked about is temporary, over the mid term the outcome should be a net positive one though. You could surely try and mitigate the temporary shedding by easing into it, using a smaller than recommended dose at first and working your way up.

Plus Minoxidil doesn’t treat the underlying cause of hair loss. If I only used it by itself I’d still be losing hair.

Right, it doesn't treat the underlying cause of hair loss - that's what you're already using Finasteride for. Minoxidil does actively promote growth though, while Finasteride simply blocks 5-alpha-reduction. The reason why Minoxidil itself wouldn't stop you from losing your hair over the long run is simply because while it promotes growth, it can't stop the process of follicle miniaturization. When you have (DHT induced) androgenic alopecia a drug like Minoxidil promoting growth just isn't going to be enough to offset the rate of shedding caused by miniaturization - which is why commonly Finasteride is seen as what stops the process of hair loss (and at least partly reverses it) while Minoxidil is seen as the drug that helps regrowth.

[Autumnal]

Just lmao at misc haircels. Brb taking a fckin daily stack to regrow 5% more hair. What’s the point? Do you brahs think any part of your life is going to improve from having a slightly fuller head of hair? Your virgin dream unicorn girl will finally fall into your arms since this was the one thing keeping you apart? My hair is thinning but JFL at the thought of taking multiple medications with bad side effects to accomplish almost nothing. May as well start using penis pumps and wearing makeup to hide your wrinkles.

[andrew28]

Just lmao at misc haircels. Brb taking a fckin daily stack to regrow 5% more hair. What’s the point? Do you brahs think any part of your life is going to improve from having a slightly fuller head of hair? Your virgin dream unicorn girl will finally fall into your arms since this was the one thing keeping you apart? My hair is thinning but JFL at the thought of taking multiple medications with bad side effects to accomplish almost nothing. May as well start using penis pumps and wearing makeup to hide your wrinkles.

I can’t speak for people taking that finasteride/propecia poison but I dished out 14k on a hair transplant by a very good US doctor and couldn’t be happier. Having hair makes an enormous difference in your appearance.

[MaiGainsbrough]

You should absolutely take minoxidil. And you should Microneedle (1.5 mm, weekly) to increase its efficacy.

If you get dry skin or dandruff, switch to the foam.

I'm currently re-growing hair on cell-tech (500 scoops) with the following stack:

RU58841 150 mg per day (It's cheap when you buy direct from the source: "Lyphar" on Alibaba)
Dutasteride 1 mg per day
Minoxidil 1 ml per day (I get unbearable brain-fog on 2 ml per day)
Micro-needle 1.5 mm once per week (Dr.Pen A6)

It was the minoxidil and micro-needling that caused the regrowth.

[ziggurat]

Shave it and embrace your destiny.
There is no use obsessing about hair.


lmao @ the cope

[syrk]

-9 Months on Fin (1mg Daily)
-Ketaconazole Shampoo 2x a week
-I need to try derma rolling/pens

I most certainly have noticed a regain in ground, but I wanna to address the areas of diffuse thinning. If I use Minoxidil there are a few caveats.

-There will be an initial shedding phase where my hair will look exponentially worse before I see true results which can take a minimum of 4-6 months

-There's no guarantee Minoxidil will work for me/potential for side effects

-There's a chance my hair will look worse than when I started if I use Minoxidil which is a lifetime commitment.

Current pic on RIGHT is wet after a shower, most people at this point can't tell I'm suffering from hair loss in some areas.

Pm me I have HT before and after pics including using fin and minox

[MyBaddBrah]

General word is minoxidil will age the **** out of you because it seeps down onto your face, even if you don't realize it.

[rootcon]

I haven't read this all but seems like it has good info

https://www.frontiersin.org/articles...019.01528/full

Many hormones participate in the regulation of hair follicle (HF) growth and cycling, of which androgens are the most representative(Al-Nuaimi et al., 2010; Inui and Itami, 2013). Androgens have a profound effect on the growth of human scalp and body hair, such as promoting beard growth but leading to hair loss in androgenetic alopecia (AGA) in males (Randall et al., 2000; Randall, 2007). AGA results from an abnormal sensitivity of balding scalp HFs to circulating testosterone (T). In 1996, Itami showed that a higher level of 5a-reductase type 2 (5aR2) was found in balding scalp HFs than in occipital scalp HFs, which can convert T to the more potent DHT (Itami et al., 1996). This finding indicates that balding scalp HFs have a higher level DHT than nonbalding scalp HFs, which is consistent with the results of a double-blind study showing that DHT levels were significantly higher in a bald scalp than in a hair-containing scalp (Dallob et al., 1994). Once 5aR2 is inhibited by finasteride, an oral drug that can decrease both serum and scalp skin DHT levels, AGA progression is delayed (Drake et al., 1999; Price, 1999). These findings suggest that androgens are required to maintain AGA balding.

As mentioned before, androgens stimulate hair growth in many areas and have paradoxical effects on human HFs. They cause males to have more hair on the face and promote pubic and axillary hair development in both sexes, while often causing balding in the same individual (Hamilton, 2010; Ceruti et al., 2017; Miranda et al., 2018). However, androgens are essential for hair growth. Male pseudohermaphroditism patients show nearly no beard growth or AGA hair loss because of a lack of 5aR2, which suggests that DHT is necessary for beard growth (Andersson et al., 1991; Adachi et al., 2000; Jakubiczka, 2015). Moreover, androgens regulate hair growth in both males and females. There are a number of female subjects with abnormal hair growth, such as hirsutism in polycystic ovary syndrome (PCOS) patients, hair loss in females affected by AGA and female pattern hair loss, and these conditions are closely related to androgens (Blumepeytavi and Hahn, 2008; Lizneva et al., 2016). However, the mechanisms by which androgens have simultaneous but different effects on one organ, the HF, in different areas of the body in the same individual have not been well studied.

The Wnt/β-catenin pathway is known to positively affect mammalian HF growth and cycling (Andl et al., 2002; Ito et al., 2007). After activation, β-catenin accumulates in the cytoplasm and then translocates to the nucleus, where it interacts with Lef/Tcf transcription factors to regulate the expression of genes responsible for HF growth. The activity of β-catenin, the key molecule in the Wnt/β-catenin pathway, can be suppressed by glycogen synthase kinase-3β (GSK-3β), which is inhibited by phosphorylation. DHT abrogates the ability of dermal papilla cells (DPCs) from patients with AGA to induce HF stem cell differentiation via inhibition of the Wnt/β-catenin pathway in DPCs, which involves inhibiting GSK-3β activity (Mulholland et al., 2005). Therefore, we hypothesized that the Wnt/β-catenin pathway is essential to HF growth regulation by DHT.

The present study shows that the impact of DHT on HF growth and cycling varies at different concentrations by interacting with the Wnt/β-catenin signaling pathway. We provide evidence that activation of the Wnt/β-catenin pathway can weaken the negative influence of high-dose DHT on HFs.

Discussion

Studies have found that 5αR2 is more highly expressed in the AGA balding scalp and beard HFs in males than in nonbalding AGA scalps (Price, 1999), so we speculated that the region-specific expression of 5αR2 induces the distinct effects of androgens on HF growth. However, it is difficult to assess the influence of 5αR2 on HF growth because 5αR cannot be maintained in culture systems in vitro. Therefore, we used DHT in our study. We found that DHT at concentrations of 10-5 mol/L and 10-6 mol/L significantly inhibited HF growth, while 10-7 mol/L DHT promoted HF growth compared with 10-8 mol/L DHT. Moreover, the effect of DHT on hair growth in C57BL/6 mice is similar to that on in vitro HFs. These results suggest that different concentrations of DHT greatly contribute to androgen-induced HF development. Many scholars have demonstrated that the scalp skin DHT concentration in AGA is significantly higher than that in hair-containing scalp (Price, 1999), which is consistent with the results of our experiments showing that high-dose DHT inhibits HF growth. However, after treatment with finasteride, the scalp skin DHT levels decreased, and AGA progression was delayed (Bang et al., 2004; Buchanan and Robaire, 2010; Prahalada et al., 2015). In our study, we found a similar phenomenon: when the DHT concentration decreased from 10-6 mol/L to 10-7 mol/L, the HFs grew much better than in the presence of higher DHT concentrations. In fact, the results suggest that an appropriate level of DHT is required for normal androgen-sensitive HF growth. Once the DHT concentration decreased from 10-7 mol/L to 10-8 mol/L, the HF growth rate showed no significant difference from that in the control group, which explains why beard growth is weaker in castrated males.

Activation of the Wnt/β-catenin pathway is important for HF regeneration and hair shaft growth. It has been reported that HFs cannot form when β-catenin, a key signaling molecule in this pathway, is mutated in the hair substrate of mice. When the mutant is induced in normal mice, the HFs do not enter the next hair growth cycle (Huelsken et al., 2001). Moreover, the loss of β-catenin activity directly leads to a block in the differentiation of HFSCs into HF cells (Povelones and Nusse, 2002; Furlong, 2005). Thus, we concluded that DHT affects HF growth differently by regulating the translocation of β-catenin, which is mediated by GSK3β. GSK3β activity is determined by several factors, and it has been demonstrated that phosphorylation at ser-9 is essential for decreasing GSK3β activity (Shimizu and Morgan, 2004; Mulholland et al., 2005). As expected, the Wnt/β-catenin pathway is negatively influenced by high levels of DHT (10-5 and 10-6 mol/L) in cultured HFs. Our results are in agreement with those of Leirós GJ et al., who found that DHT can downregulate the expression of p-GSK3β (ser9) and β-catenin in HFs from AGA patients (Leirós et al., 2012). Notably, HFs treated with 10-7 mol/L DHT showed an obvious increase in the nuclear expression of β-catenin in the hair matrix. Therefore, we hypothesized that 10-7 mol/L DHT promotes HF growth by activating the Wnt/β-catenin signaling pathway, while high levels of DHT have the opposite effect. In the normal hair follicle cycle, immunofluorescence staining indicated that AR is expressed in the dermal papilla cells and hair matrix cells, so we speculate that DHT might regulate Wnt/β-catenin signaling pathway by binding with AR in these two types of cells. However, the exact mechanism needs to be further confirmed.

To further demonstrate the role of the Wnt signaling pathway in HF growth, we used IM12 and 21H7 to mimic the effects of activating and inhibiting the Wnt signaling pathway (Schm?Le et al., 2010; Tsai et al., 2014). In the presence of IM12, a β-catenin-specific activator that impacts GSK3β, the growth rate of HFs in vitro was significantly accelerated. Overwhelming evidence has shown that the activation of β-catenin is necessary to induce HFs (Celso et al., 2004). However, the addition of the β-catenin inhibitor 21H7 markedly inhibited the growth of HFs. David Enshell-Seijffers et al. also found that ablation of β-catenin in HFs results in dramatic hair shortening and thinning (Enshell-Seijffers et al., 2010). A similar positive effect of IM12 on HFs was observed upon cotreatment with 10-6 mol/L DHT. Considering both of these results, it is conceivable that DHT is involved in regulating HF growth by modulating the translocation of β-catenin to the nucleus. From our results, we conclude that the effects of DHT are closely related to its concentration; actually, DHT can activate the Wnt pathway at an appropriate concentration.

Functional cross-talk between the androgen and Wnt/β-catenin signaling pathways has been described in this study. Our results indicate that DHT can regulate the expression of molecules necessary for HF development, and some of these factors involved in androgen-induced hair growth are encoded by target genes of the Wnt/β-catenin pathway. We found that an appropriate concentration of DHT resulted in an increase in p-GSK3β (ser-9) levels in cultured HFs, followed by β-catenin translocation into the nucleus and activation of the transcription of downstream target genes (here means activate Wnt/β-catenin pathway), which prompted faster HF growth. As shown in our study, high-dose DHT had a negative effect on HFs that was diminished by cotreatment with a β-catenin activator.

Previous studies have found that androgen has different effects on hair follicles in different regions, and appropriate concentrations of androgens can promote hair growth, while excessive concentrations of androgens can inhibit hair growth (Itami and Inui, 2005). Dermal papilla cells (DPC) can induce hair follicle stem cells (HFSC) to differentiate into hair follicles, while DHT inhibits HFSC differentiation by interfering with Wnt pathway in a coculture model with human DPC and HFSC (Leirós et al., 2012; Leirós et al., 2017). Of course, these studies have given us a much clearer understanding of the growth of hair follicles, but we also have found that these studies have not been fully verified from the organ level. Therefore, this study verified the effects of different concentrations DHT on the hair follicle, and found that the expression levels of Wnt pathway protein (β-catenin) changed significantly in DHT cultured hair follicles, and the activator of Wnt pathway (IM12) antagonized the inhibition of high concentration DHT on hair follicle growth in vitro, and further confirmed that the growth of hair follicles was indeed regulated by androgen and Wnt/β-catenin pathway at the organ level.

Unfortunately, our experiments have not found the cause of the regional effects of DHT on HFs. As mentioned above, the concentration of DHT explains these differences, and AR is also involved in the development of AGA, so there may be some unknown mechanisms which regulate the growth of HF. Therefore, in the coming studies, it’s necessary to elucidate the mechanism by which DHT regulates GSK3β activity, and which type of DHT target cells in the hair follicle will be, and what pathway of DHT could activate or inhibit the Wnt pathway. Until now, according to previous studies and our findings, we infer that the kinases that participate in phosphorylating GSK3β at ser-9 may be target genes of DHT.

[carcano67]

I knew a guy who used to gel his hair everyday and is now bald