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Nizoral IS a DHT blocker

Yeah the difference is when u say something is a DHT blocker like Propecia, is that propecia binds to the androgen hormone in your blood and systemically stops any of the DHT binding with anything else that is can attach to lik androgen receptors in your skin or brain, ie. it inactivates the DHT so it cannot bind to anyhing.

Whereas nizoral topical works topical by stopping the DHT from attaching to the androgen receptor locally. So it is blocking DHT but in a different and in my opinion better way by doing it at the receptor.

So i think its better if we clarify that and not confuse it with other DHT blockers like FIN and DUT.

Nizoral works by suppressing the androgen receptors in the scalp SKin/follicles.
And also has a non androgenetcic growth promoting ability that has yet to be scientifically understood.

When ketoconaozle is taken internally it will have DHT blocking like FIN and Dut

» » If you look at the recent Japan nizoral study they say it works by
» » » suppressing the androgen receptor and also by being a non androgen
» » related
» » » growth stimulator. So its not blocking DHT like propecia does.
» »
» » “suppressing the androgen receptor” = blocking DHT.
» »
» » DHT is an androgen. Supressing the receptor is stopping it from being
» » receptive to androgens (DHT), ie. blocking androgens (DHT).
»
» agreed that is whey they are called DHT blockers,

» Yeah the difference is when u say something is a DHT blocker like Propecia,
» is that propecia binds to the androgen hormone in your blood and
» systemically stops any of the DHT binding with anything else that is can
» attach to lik androgen receptors in your skin or brain, ie. it inactivates
» the DHT so it cannot bind to anyhing.
»
» Whereas nizoral topical works topical by stopping the DHT from attaching
» to the androgen receptor locally. So it is blocking DHT but in a different
» and in my opinion better way by doing it at the receptor.
»
» So i think its better if we clarify that and not confuse it with other DHT
» blockers like FIN and DUT.
»
» Nizoral works by suppressing the androgen receptors in the scalp
» SKin/follicles.
» And also has a non androgenetcic growth promoting ability that has yet to
» be scientifically understood.
»
» When ketoconaozle is taken internally it will have DHT blocking like FIN
» and Dut
»
»
» » » If you look at the recent Japan nizoral study they say it works by
» » » » suppressing the androgen receptor and also by being a non androgen
» » » related
» » » » growth stimulator. So its not blocking DHT like propecia does.
» » »
» » » “suppressing the androgen receptor” = blocking DHT.
» » »
» » » DHT is an androgen. Supressing the receptor is stopping it from
» being
» » » receptive to androgens (DHT), ie. blocking androgens (DHT).
» »
» » agreed that is whey they are called DHT blockers,

taking keto internally is not recommended
potentially fatal liver damage

» Whereas nizoral topical works topical by stopping the DHT from attaching
» to the androgen receptor locally. So it is blocking DHT but in a different
» and in my opinion better way by doing it at the receptor.

Saw palmetto works at the receptor site too. It binds to the receptor site so DHT can’t. If you say that mechanism is better, you are saying SP is better than propecia. Not knocking SP, cuz I’m using it, but I wouldn’t say it’s better than propecia.

» » Whereas nizoral topical works topical by stopping the DHT from attaching
» » to the androgen receptor locally. So it is blocking DHT but in a
» different
» » and in my opinion better way by doing it at the receptor.
»
» Saw palmetto works at the receptor site too. It binds to the receptor
» site so DHT can’t. If you say that mechanism is better, you are saying SP
» is better than propecia. Not knocking SP, cuz I’m using it, but I wouldn’t
» say it’s better than propecia.

I think Prop has a higher percentage of success but also comes with the side effects, however out of the dht blockers, it is one of the weakest, SP, that is
beta sis is 3000 times more powerful than SP

» » » Whereas nizoral topical works topical by stopping the DHT from
» attaching
» » » to the androgen receptor locally. So it is blocking DHT but in a
» » different
» » » and in my opinion better way by doing it at the receptor.
» »
» » Saw palmetto works at the receptor site too. It binds to the receptor
» » site so DHT can’t. If you say that mechanism is better, you are saying
» SP
» » is better than propecia. Not knocking SP, cuz I’m using it, but I
» wouldn’t
» » say it’s better than propecia.
»
» I think Prop has a higher percentage of success but also comes with the
» side effects, however out of the dht blockers, it is one of the weakest,
» SP, that is
» beta sis is 3000 times more powerful than SP

Guys,

I am sorry, but most of the posts in this thread are either wrong or have zero scientific support - Jesus I am sound like Brian (somebody shoot me).

First, Nizoral (Ketoconazole) is a pretty non-specific inhibitor of steroid hormone synthesis. All steroid hormones originate with Cholesterol and thru numerous chemical steps end up as your favorite hormone. The CYP450 enymes enable many of these pathways and it is this action that Niz/Keto interferes with. Taken systemically you will really screw with you hormones. The World Health Organization wrote a pretty good paper on this.

This is the only scientific research I have seen on the mechanism for Niz/Keto.

Second, the one about something binding in the blood… that’s a hoot. Propecia/Finansteride is very specific in it’s mechanism; it inhibits 5AR and therefore blocks the production of DHT. Simple. The fact that DHT is not really the problem is a completely different story. Hormone-binding is an interesting and widely mis-understood area, e.g. the role of SHBG or cell-receptor binding.

Third, the SP mechanism remains unclear. It is also unclear that Betasitosterol is the active component of SP. I believe that there is enough evidence that SP works on some pathweays and is clearly independent of the Fin pathway and I do take it. But to be clear it’s mechanism is still unproven; and just because there are a bunch of websites that say it blocks cell receptors does not mean didly squat.

Four, cell receptors are very interesting, but very complex. There are many receptors active in hair cells; these vary by stage in the hair-cycle, location on the hair (bulb, etc), receptor-type (inside or edge of the cell) and location of hair on the body. The focus on the T-receptor in hair research is one reason that current approaches work for so few people. Our research in cell receptor chemisty is improving quickly, but there are soooooo many pathways and unknowns.

I do see so many people just repeating stuff that they have heard from others on this site; unfortunately this leads to threads like this one.

Brain (oops I mean GC)

» Yeah the difference is when u say something is a DHT blocker like Propecia,
» is that propecia binds to the androgen hormone in your blood and
» systemically stops any of the DHT binding with anything else that is can
» attach to lik androgen receptors in your skin or brain, ie. it inactivates
» the DHT so it cannot bind to anyhing.

Nope. Propecia was designed to prevent conversion of T to DHT by impacting the 5AR enzyme. There are 2 types of 5AR, both are genetically encoded. You may be thinking about Sex-Hormone-Binding-Globulin (SHBG), which is related to hairloss but in a very convoluted way.

»
» Whereas nizoral topical works topical by stopping the DHT from attaching
» to the androgen receptor locally. So it is blocking DHT but in a different
» and in my opinion better way by doing it at the receptor.
»
Nope. Nizoral (Ketoconazole) does what Propecia does, but it blocks more CYP450 enzymes (5AR is one/two) and therefore blocks many other hormones from developing, e.g. Estrogen also.

» So i think its better if we clarify that and not confuse it with other DHT
» blockers like FIN and DUT.
»
Here I agree. Clarity is good.

» Nizoral works by suppressing the androgen receptors in the scalp
» SKin/follicles.

I have not seen reserach that suggests this as a secondary mode of action for Nizoral but will read the Japanese study. I have research Nizoral/Keto extensively.

» And also has a non androgenetcic growth promoting ability that has yet to
» be scientifically understood.
»
Nope. Nizoral/Keto impact on androgens is very clearly understood. I have read many, many papers on this. It is simply a CYP450 inhibitor.

» When ketoconaozle is taken internally it will have DHT blocking like FIN
» and Dut
»
Nope. It’s gonna completely screw your hormone balance (HPTA-axis and also Thyroid) and you destroy your liver to the bargain.

»
» » » If you look at the recent Japan nizoral study they say it works by
» » » » suppressing the androgen receptor and also by being a non androgen
» » » related
» » » » growth stimulator. So its not blocking DHT like propecia does.
» » »
» » » “suppressing the androgen receptor” = blocking DHT.
» » »

Nope. For complete clarity suppressing the androgen receptor is not the same as blocking DHT. Close but not exact.

Certain drugs can reduce/increase the number of androgen receptors, e.g. Rhetinoic Acid reduces the overall number of andgrogen receptors. This is receptor suppression in miy mind.

Receptor blocking is where the same number of receptors exist, but a substance is introduced that preferentially binds to the receptor and blocks the default compund from binding. In this case if we stop DHT binding to the T-receptor we stop the cascade of chemical reactions that follow; release of the Heat Shock Protein and local DNA modification.

There has been far less work on the T-receptor than the E-receptors (there are 2 in hair); this is because E-receptors are central to cancer research. Drugs named Specific-Estrogen-Receptor-Modulators (SERMs) are the output of this. Care needs to be taken as SERMs may have very different effects at different body locations. Tamoxifen is a SERM that blocks the E-receptor in breast cells.

» » » DHT is an androgen. Supressing the receptor is stopping it from
» being
» » » receptive to androgens (DHT), ie. blocking androgens (DHT).
» »
» » agreed that is whey they are called DHT blockers,

DHT blockers is a term used in hairloss discussions; scientific research is much more precise and the term is not used.

» » » » Whereas nizoral topical works topical by stopping the DHT from
» » attaching
» » » » to the androgen receptor locally. So it is blocking DHT but in a
» » » different
» » » » and in my opinion better way by doing it at the receptor.
» » »
» » » Saw palmetto works at the receptor site too. It binds to the
» receptor
» » » site so DHT can’t. If you say that mechanism is better, you are
» saying
» » SP
» » » is better than propecia. Not knocking SP, cuz I’m using it, but I
» » wouldn’t
» » » say it’s better than propecia.
» »
» » I think Prop has a higher percentage of success but also comes with the
» » side effects, however out of the dht blockers, it is one of the
» weakest,
» » SP, that is
» » beta sis is 3000 times more powerful than SP
»
» Guys,
»
» I am sorry, but most of the posts in this thread are either wrong or have
» zero scientific support - Jesus I am sound like Brian (somebody shoot
» me).
»
» First, Nizoral (Ketoconazole) is a pretty non-specific inhibitor of
» steroid hormone synthesis. All steroid hormones originate with Cholesterol
» and thru numerous chemical steps end up as your favorite hormone. The
» CYP450 enymes enable many of these pathways and it is this action that
» Niz/Keto interferes with. Taken systemically you will really screw with
» you hormones. The World Health Organization wrote a pretty good paper on
» this.
»
» This is the only scientific research I have seen on the mechanism for
» Niz/Keto.
»
» Second, the one about something binding in the blood… that’s a hoot.
» Propecia/Finansteride is very specific in it’s mechanism; it inhibits 5AR
» and therefore blocks the production of DHT. Simple. The fact that DHT is
» not really the problem is a completely different story. Hormone-binding is
» an interesting and widely mis-understood area, e.g. the role of SHBG or
» cell-receptor binding.
»
» Third, the SP mechanism remains unclear. It is also unclear that
» Betasitosterol is the active component of SP. I believe that there is
» enough evidence that SP works on some pathweays and is clearly independent
» of the Fin pathway and I do take it. But to be clear it’s mechanism is
» still unproven; and just because there are a bunch of websites that say it
» blocks cell receptors does not mean didly squat.
»
» Four, cell receptors are very interesting, but very complex. There are
» many receptors active in hair cells; these vary by stage in the
» hair-cycle, location on the hair (bulb, etc), receptor-type (inside or
» edge of the cell) and location of hair on the body. The focus on the
» T-receptor in hair research is one reason that current approaches work for
» so few people. Our research in cell receptor chemisty is improving quickly,
» but there are soooooo many pathways and unknowns.
»
» I do see so many people just repeating stuff that they have heard from
» others on this site; unfortunately this leads to threads like this one.
»
» Brain (oops I mean GC)

the mechanism of the natural “dht blockers” may not yet be defined , but in my case they work well and pygeum and nettles for example, seem to add to the benefit, as well as beta sitosterol

they do not seem capable of tremendous regrowth on bald areas, in fact none that I have noticed
but they have good abilities in halting excess fall out, and also thickening of thin areas…if the person is lucky enough to respond to them, as I was

Wow, you’re getting pretty technical, but thanks for clarifying things. You are right, there is a lot of misinformation on this thread.

My point was that suppressing the androgen receptor reduces the likelyhood of androgens like DHT from binding. In essence, blocking DHT from binding because it has no receptor to bind to since it has been supressed, not that something else bound to the receptor.

» Wow, you’re getting pretty technical, but thanks for clarifying things.
» You are right, there is a lot of misinformation on this thread.
»
» My point was that suppressing the androgen receptor reduces the likelyhood
» of androgens like DHT from binding. In essence, blocking DHT from binding
» because it has no receptor to bind to since it has been supressed, not
» that something else bound to the receptor.

that is my question for years on this board that nobody seems to know the answer to
either saw palmetto and all the other naturals BLOCK the DHT at the androgen receptors on the prostate and at the base of the hair follicles…or they, being 5 AR inhibitors, prevent DHT from being manufactured in the first place, which would lower the blood levels of DHT , and cause all kinds of strange side effects

i was under the impression that propecia lowers blood levels of the male hormones, which makes sense but that Saw palmetto etc do NOT lower the blood levels of DHT etc, which in essence would mean that they are not 5AR inhibitors, or they are very weak 5 AR inhibitors, and they are more focused on blocked the DHT already in the blood

perhaps gc can clear this up

It WAS my understanding that saw palmetto just binds to the receptor site, but it seems there are studies that show it also inhibits 5AR, and has anti-inflammatory properties:

Studies have shown that Saw Palmetto extract reduced the uptake, in tissue specimens ,of both testosterone and dihydrotestosterone (DHT) by more than 40%. Other studies have shown that Saw Palmetto inhibits the conversion of the less active testosterone to the more active DHT by inhibiting the enzyme 5 alpha reductase. Hence Saw Palmetto, by blocking the binding of DHT to nuclear receptor sites and inhibiting the conversion of testosterone to DHT ,decreases the proliferative effects of DHT on prostate cells

Saw Palmetto also inhibits the cyclo-oxygenase and 5-lipoxygenase pathways, which results in prevention of biosynthesis of inflammation producing substances such as prostaglandin and leukotrienes. It also inhibits the arachidonic acid cascade, and all these account for the anti-inflammatory and anti-edematous properties of saw palmetto.

http://www.rxmed.com/b.main/b3.herb.monos/b3.1.monographs/saw.palmetto.html

» It WAS my understanding that saw palmetto just binds to the receptor site,
» but it seems there are studies that show it also inhibits 5AR, and has
» anti-inflammatory properties:
»
» Studies have shown that Saw Palmetto extract reduced the uptake, in
» tissue specimens ,of both testosterone and dihydrotestosterone (DHT) by
» more than 40%. Other studies have shown that Saw Palmetto inhibits the
» conversion of the less active testosterone to the more active DHT by
» inhibiting the enzyme 5 alpha reductase. Hence Saw Palmetto, by blocking
» the binding of DHT to nuclear receptor sites and inhibiting the conversion
» of testosterone to DHT ,decreases the proliferative effects of DHT on
» prostate cells

»
» Saw Palmetto also inhibits the cyclo-oxygenase and 5-lipoxygenase
» pathways, which results in prevention of biosynthesis of inflammation
» producing substances such as prostaglandin and leukotrienes. It also
» inhibits the arachidonic acid cascade, and all these account for the
» anti-inflammatory and anti-edematous properties of saw palmetto.

»
» http://www.rxmed.com/b.main/b3.herb.monos/b3.1.monographs/saw.palmetto.html

Chia, the site you reference is a little confusing since it says SP works the same way as Propecia and then it lists many other mechanisms.

I will go back and re-read my SP research and see if I can reach a conclusion; which I will share.

GC.

» » Wow, you’re getting pretty technical, but thanks for clarifying things.
» » You are right, there is a lot of misinformation on this thread.
» »
» » My point was that suppressing the androgen receptor reduces the
» likelyhood
» » of androgens like DHT from binding. In essence, blocking DHT from
» binding
» » because it has no receptor to bind to since it has been supressed, not
» » that something else bound to the receptor.
»
» that is my question for years on this board that nobody seems to know the
» answer to
» either saw palmetto and all the other naturals BLOCK the DHT at the
» androgen receptors on the prostate and at the base of the hair
» follicles…or they, being 5 AR inhibitors, prevent DHT from being
» manufactured in the first place, which would lower the blood levels of DHT
» , and cause all kinds of strange side effects
»
» i was under the impression that propecia lowers blood levels of the male
» hormones, which makes sense but that Saw palmetto etc do NOT lower the
» blood levels of DHT etc, which in essence would mean that they are not 5AR
» inhibitors, or they are very weak 5 AR inhibitors, and they are more
» focused on blocked the DHT already in the blood
»
» perhaps gc can clear this up

I have seen no conclusive research on how SP works; yet like others I continue to use it (which may be a mistake).

Propecia systemically reduces DHT by inhibiting 1-type of 5AR; it does nothing by direct action to reduce systemic T levels.

Blocking T-to-DHT may result in an increase in Estrogen; there is some research that supports this.

The DHT-5AR is an unusual hormone-enzyme combo in that it has a feed-forward mechanism; the more DHT that is produced the more 5AR that is produced, producing more DHT. Most hormone systems in the body have a feedback mechanism.

There is also significant evidence that DHT mutations may be the cause of some significant diseases.

I think of the problem as follows;

  1. MPB is triggered by hormones; but probably not exclusively
  2. What types of hormones are there?
  3. Where are hormones made?
  4. How do they get to the hair cells; i.e. mode of transportation?
  5. What is the mechanism for impacting the cell; cell-receptor binding?
  6. On binding, what is the sequence of biochemical processes that occur?
  7. How does all this relate to a normal hair-cycle?

Once I completed my research on this I then started to focus on what is normal body process and what are the things that happen unusually for people with hairloss.

I believe that many people and much of the research is focused on trying to prevent processes that are not the root problem.

Most of the good research relates to cancer treatments.

I have observed in myself that the “dht blockers” such as saw Palmetto, Nettles, Pygeum, etc can have a powerful effect on halting excess fallout, and also on
regrowth , thickening in thinning areas,

why they do not have this same effect on all men, to me is a mystery, why they can have zero effect on some guys, is perplexing

However, for example, my regimen, if guys try to copy it, they pick and choose a few items, and ignore the vitamins and minerals. I have always stressed the importance of the super hair vitamins and minerals. Most guys pooh pooh this and say they cannot regrow hair. Possibly true, but I was on only Super hair vitamins and minerals for 20 yrs, not even Saw Palmetto Pygeum etc, and I think it had a noticeable delaying effect on my MPB. Why guys dismiss this notion is beyond me, Perhaps it is too simplistic for them, and not supported by enough studies.

I do think hair loss is a complicated problem that must be addressed by many supplements interally as well as many topicals. to really get a handle on it.

I would be curious to see if the rest of your hair fills in also. If in fact the hair follicles do not die, I am curious as to why after four years, that some of the follicles in your crown seem so resistant to the same treatment that the other hairs have so vigorously responded to

Your progress has convinced me that the hair follicles do not die, which is certainly a good thing. Sure raises your spirits to see some new growth, does mine

I will keep the board updated on my niz cream results,

» Nizoral is a DHT blocker. Seems to be some debate on this.

I’ve read this entire thread with great amusement, because of all the confusion it contains over TERMINOLOGY!:slight_smile: For the love of God, people need to start using the same terminology that doctors and scientists use. Why? SO THAT PEOPLE CAN UNDERSTAND WHAT THE HELL YOU’RE TALKING ABOUT!:angry:

Case in point: what does the expression “DHT blocker” mean (see quoted sentence above)?? Does it mean something that blocks androgen receptors (like flutamide, spironolactone, or RU58841), thereby keeping DHT from binding to them? Or does it mean something that stops testosterone from being converted into DHT (like finasteride, dutasteride, or turosteride)?

For the first case above, use either “androgen receptor blocker”, or simply “antiandrogen”. For the second case, use “5a-reductase inhibitor”. THERE! Problem solved!

Whenever I see somebody say “DHT blocker” on a hairloss forum, it makes me wanna just THROTTLE the guy!!:frowning:

Bryan

» Interestingly Nizoral impacts Adrenal as well as HPTA
» endocrinology;

Not when it’s used TOPICALLY, which is what we’re talking about in this thread. Topical ketoconazole isn’t absorbed systemically to any significant extent.

Bryan

» » DHT is an androgen. Supressing the receptor is stopping it from being
» » receptive to androgens (DHT), ie. blocking androgens (DHT).
»
» agreed that is whey they are called DHT blockers,

Don’t use the term “DHT blocker”. It’s ambiguous and unscientific. You don’t see it used in medical studies or textbooks. Use “androgen receptor blocker” or simply “antiandrogen”.

Bryan

» » Nizoral is a DHT blocker. Seems to be some debate on this.
»
» I’ve read this entire thread with great amusement, because of all the
» confusion it contains over TERMINOLOGY!:slight_smile: For the love of God, people
» need to start using the same terminology that doctors and scientists use.
» Why? SO THAT PEOPLE CAN UNDERSTAND WHAT THE HELL YOU’RE TALKING
» ABOUT!:angry:
»
» Case in point: what does the expression “DHT blocker” mean (see quoted
» sentence above)?? Does it mean something that blocks androgen receptors
» (like flutamide, spironolactone, or RU58841), thereby keeping DHT from
» binding to them? Or does it mean something that stops testosterone from
» being converted into DHT (like finasteride, dutasteride, or turosteride)?
»
» For the first case above, use either “androgen receptor blocker”, or
» simply “antiandrogen”. For the second case, use “5a-reductase inhibitor”.
» THERE! Problem solved!
»
» Whenever I see somebody say “DHT blocker” on a hairloss forum, it makes me
» wanna just THROTTLE the guy!!:frowning:
»
» Bryan

there seems to be some debate as to whether the naturals such as Saw Palmetto, are 5 AR inhibitors, and actually block conversion of testosterone to DHT, or whehter they block the DHT and other male hormones from binding to the androgen receptors at the base of the hair follicles and on the prostate

it seems to me they are weak 5 AR inhibitors and more likely to be blocking the androgen receptors, although even when this happens it is not a total block, Saw Palmetto is documented to bind 40 percent less to the prostate, with use of Saw Palmetto

» there seems to be some debate as to whether the naturals such as Saw
» Palmetto, are 5 AR inhibitors, and actually block conversion of
» testosterone to DHT, or whehter they block the DHT and other male
» hormones from binding to the androgen receptors at the base of the hair
» follicles and on the prostate
»
» it seems to me they are weak 5 AR inhibitors and more likely to be
» blocking the androgen receptors, although even when this happens it is not
» a total block, Saw Palmetto is documented to bind 40 percent less to the
» prostate, with use of Saw Palmetto

Yep. I’ve seen claims that saw palmetto has BOTH of those abilities: it’s (supposedly) both a 5a-reductase inhibitor AND an androgen receptor blocker. I believe I have studies right here in my own Study Stack attesting to those separate functions. Not sure just how effective it is at either one, though. That’s anybody’s guess.

Bryan

» » there seems to be some debate as to whether the naturals such as Saw
» » Palmetto, are 5 AR inhibitors, and actually block conversion of
» » testosterone to DHT, or whehter they block the DHT and other male
» » hormones from binding to the androgen receptors at the base of the hair
» » follicles and on the prostate
» »
» » it seems to me they are weak 5 AR inhibitors and more likely to be
» » blocking the androgen receptors, although even when this happens it is
» not
» » a total block, Saw Palmetto is documented to bind 40 percent less to
» the
» » prostate, with use of Saw Palmetto
»
» Yep. I’ve seen claims that saw palmetto has BOTH of those abilities:
» it’s (supposedly) both a 5a-reductase inhibitor AND an androgen receptor
» blocker. I believe I have studies right here in my own Study Stack
» attesting to those separate functions. Not sure just how effective it is
» at either one, though. That’s anybody’s guess.
»
» Bryan

it is a weak 5 AR inhibitor however I responded well to it, and the other naturals such as Pygeum nettles beta sitosterol seem to work in different pathways, since after addding them they enhanced my results

» Whenever I see somebody say “DHT blocker” on a hairloss forum, it makes me
» wanna just THROTTLE the guy!!:frowning:

DHT blocker :stuck_out_tongue:

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