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#21

cockneyninja wrote:
http://www.xconomy.com/2008/01/04/gone-today-hair-tomorrow-follica-raises-funds-to-begin-human-trial-of-baldness-treatment/
Just scroll down to the comments.

Did you guys notice that the author of that comment - David Steinberg - is Foliica’s Chief Business Officer (http://www.puretechventures.com/content/team.asp?mainPage=team&subPage=all). In other words, his comments shouldn’t be taken lightly.

cockneyninja wrote:
Does anyone know what kind of devlopment period will they have? Do they still have to do the 3 Phase trials?.

well the last bit of the xconomy.com article stated the “trial has several phases, however, and Zohar cautions that final data won’t be in for at least a year”. So depending on the success of their formulation/ efficacy, we could see final result data in just over a year. Remember, unlike Aderans or Intercytex, Follica has the advantage to expedite testing on humans because their treatment process uses drugs already approved by the FDA.

This could get really interesting, really fast.

.


#22

interesting science…I’ve heard this myth a lot before that if you get your head shaved several times with a blade (not razor) it helps with hairloss. I never believed in it, but it could possibly be true!


#23

You mentioned:

I’ve personally gotten a couple of (terminal) hairs growing in my receded areas just from experimenting with needling & sandpapering a small spot a few months ago. And I didn’t make any effort to protect the abraded areas in any way whatsoever. I remember putting some salicylic acid on the spot once or twice, but nothing resembling the kind of perfect 9-day regimen & protections they’re talking about. Such a sloppy job, and yet I have a couple of legit dark hairs to show for this. One of them has grown 3-4cm long.

Thats the thing.
There seems to be three things happening.

  1. dermabrasion

  2. 9 days of blockage of WNT (green tea’s ecgc can do this)

  3. WNT protiens put on thereafter, apparently the more the better.

Mice dont shampoo or towel dry their little coats, so I imagine they’d want us to leave the area alone as much as possible also in order to not suture the wound in any concievable way or reaggravate it. Human hair was seen at day 25 or so (probably a hair just poking through the skin at that point and at day 50-something).

There first trial will be an exciting one to see if they can really get good density, etc. The way they put it, the more WNT they use, the thicker hair they could get based on the mouse results.

What is kind of exciting for me is that if someone is on finasteride when this new hair is made up front and stays on finasteride, they’d probably never lose it again. Ive seen Bryan Shelton mention that in his opinion if a man got on finasteride before he started going bald, he’d probably never have an androgenic stimulis in his follicles high enough to flip their response to androgens. Making this kind of hair might mean making hair that you will keep if you take finas. I take finas and have for many years so it would be no problemo for yours truly. Thats a reason Im interested in it. No donor hair loss either. It gives us another possible way to regain all our lost hair along with ICX and Aderans. Thats exciting in itself. Im for any method that works, even if it was standing on my head :slight_smile:


#24

In Between guys never tried that standing on head exercice ?

And for the DHT mice issue …Benji, even though the mouse is immunodeficient cosidering that the DHT hormone is a local one…cant you just think that the DHT is generated by the human grafted skin ?


#25

To tell you the truth, I’m not even all that worried about the DHT resistance of newly-formed hairs if the process is really as do-able as it sounds here.

We started getting major DHT in our system by our early teens, and yet most of us didn’t really begin to have visible hair loss trouble until at least a decade later. Our adult levels of DHT are still significant but they will probably never repeat the massive dose of DHT that our original hairs recieved during adolescence. And ICX and other companies are still hard at work on better ways to fight the DHT resistance.

If regenerating fresh hairs actually panned out as easily as it sounds on here (which is still a very big “IF”), I’d be willing to cut down on the Finasteride & topical regimens and just submit to redoing the process. Just get the dermabrasion/regrowth done a couple of times over the course of 10-15 years while the rest of the hair loss industry commercializes some better methods of preventing the DHT damage.


#26

Amilcar wrote:
And for the DHT mice issue …Benji, even though the mouse is immunodeficient cosidering that the DHT hormone is a local one…cant you just think that the DHT is generated by the human grafted skin ?”

That is an interesting point that I didn’t even consider. DHT is made in the innermost portion of the outer-root sheath of hair follicles, and even though these were miniaturized hair follicles it stands to reason that some could be made. Most all DHT that gets to your hair is made right there at the follicle as globulin binds about 99-percent of cirulating DHT in the blood and 3 alphasteroid reductase quickly deactivates DHT in muscle tissue. The mice’s testosterone levels would be interesting to know ifthey had some hair on the rest of their backs. But when you really think about it, androgens probably would not have their deleterious effects until years after of daily damage, cellular injury, inflammation, etc. in the mice anyway. And…mice just dont live THAT long. Finasteride lowers DHT in mice and they make it, but I dont think it lowers their levels in serum quite as much as hours. In humans the type 2 created alpha five reductase enzyme is in the hair follicles, liver, seminal vesicles, prostate tissue, and I think some is in the kidneys (can’t remeber about the adrenal gland on whether its type one or two). The ONE enzyme is in the sebaceous glands, your brain, and some deeper tissues.

I read an experiment once that showed that mice given only black tea to drink had an averaga of 77 percent reduction in DHT, and found this very interesting-hoping that a natural type two inhibitor had been found. The researchers mentioned the possiblility in the comments section. In another experiment, it was claimed in rat liver microsomal assays a black tea component inhibited type one and not type two. I dont know what to believe there…

hmmmmmmmmmmmmm. lemme see…what else…

oh, the alpha five reductase enzyme gets more active as we age, even though our testosterone levels get lower. I dont know at what age the enzyme starts to slow down…but you probably have pretty high DHT stimulis in your late twenties and early thirties also. I know the testosterone levels get higher when you are younger, but the enzyme that converts it into dht supposedly gets more active a bit later than that.

Needless to say, Im going to be interested in what results their first pre-clinicals have in growing hair on men as there should really be no safety issue with this approach, and hope they try to abrate a good square inch or two of skin on some men. They have had no shortage of volunteers. If hair appears in a mere fifty days or so…we shouldn’t have to wait but perhaps three months or so after their first clinical for them to announce what growth they got


#27

Benji,

First, there is the scar issue that they need to address…After all it’s because of scars that HT is highly unpopular…and a 5mm wound is significant especially for the scalp.

Second, each day it’s getting more obvious that DHT is not the only player when it comes to MPB and hormonal balance , my proof is :
*the Huge number of people that just dont respond to Finasteride.
*In The Follica patent they are using prostaglandin inhibitors …why dont they just use a DHT inhibitor ??


#28

Im going to cut and paste someone else’s post on this in its entireity:

On the prostaglandin front - those same mice I mentioned earlier that overexpressed cox-2 andlosthair follicles and had sebaceous gland overddevelopment were looked at by Cotsarelis in his patent centred on PGD2 and compared to human balding areas.

Quote:
EXAMPLE 14: K14-COX2 MICE EXHIBIT PGD2 ELEVATION AND HAIR GROWTH

DEFECTS

[00530 ] K14-COX2 mice were examined for hair phenotype. The mice exhibited very low gross

10 hair coat volume, without significant change in hair follicle number and anagen percentage of mice at day 29, demonstrating an early defect in hair growth. Sebaceous hyperplasia was also detected at this age. By day 39, sebaceous glands had enlarged further and many hairs were miniaturized (Figure 1 I A).

[ 00531] To verify the contribution of L-PGDS to the phenotype of K14-COX2 mice, immunohistochemistry was performed with antibodies against L-PGDS. Adult mice expressed L-PGDS in an infiltrate of dermal cells, hair sheath fibroblasts, and melanocytes. Staining was detected in anagen dermal papilla in wild-type mice (Figure 1 IB).

[ 00532 ] PGD2 were measured in the Kl 4-COX2 mouse skin via mass spectrometry. PG D2 was 10- fold more abundant than PGE2 in K14-COX2 mice (820.4 ng/gram of tissue vs. 82.4 ng/gram). PGD2 levels were also significantly higher in K14-COX2 mice than in wild type mice in telogen (420.9 ng/gm of 20 tissue, p value=0.01). PGE2 was also elevated, although less so, compared to wild type mice (60.5 ng/gram of tissue). Slight elevations in PGJ-M, a metabolite of PGD2 were also detected (Figure 12).

[ 00533 ] These findings corroborate the above androgenetic alopecia findings in humans, by showing that elevations of PGD2 are associated with alopecia and sebaceous gland hyperplasia in mice as well.

The first part in bold shows these mice had not just hair loss but miniaturized hair follicles as well as sebaceous gland hyperplasia which sounds a hell of a lot like balding skin. You can see the same stuff reported in the studies where this line of mice were first developed.

I think the second part in bold is interesting because it shows that PGD2 seems to be a stronger growth inhibitor than PGE2 is a growth promoter. I think this is important because knocking out a whole bunch of prostaglandin production is probably a lot easier for us than selectively knocking out PGD2.

Heres some more stuff from humans. Cant remember if I already posted some of this stuff - its becoming a bit of a blur…

Quote:
[ 00517 ] In addition to the above genes, levels of the lipocalin (brain) isoform prostaglandin D2 synthase (PGD2S) were elevated in bald scalp relative to haired scalp (Figure 7A). To confirm this finding, PGD2 levels were tested in bald and haired tissue from 3 patients. PGD2 was elevated in all bald samples, at an average fold increase of 11.6 (Figure 7B). This increase in PGD2 was verified in 1 individual by mass spectrometry. PGD2 was detected as 17 pg/mg of tissue in haired scalp and 75.5 pg/mg in bald scalp, representing a 4.4 fold increase in bald tissue. PGF2a also was slightly elevated in bald scalp with 6.7 pg/mg in haired scalp and 15.9 pg/mg in bald scalp. PGE2, however, exhibited the reverse trend with PGE2 present at 22.7 pg/mg in the haired scalp and 12.0 pg/mg in the bald scalp (Figure 7C).

20 [ 00518 ] The RT-PCR results were further confirmed in 2 individuals not measured in the original array study by quantitative RT PCR, demonstrating a 5.23 and 10.7 fold increase of L-PGDS in bald scalp over haired scalp (Figure 7D). Immunohistochemical staining of L-PGDS revealed an increase in bald scalp, with L-PGDS appearing in the cells along the fibrous root sheath populated by dermal fibroblasts, as well as in scattered locations intrafollicularly. Given the lack of expression of L-PGDS in hematopoietic cells, increases in L-PGDS were not from the sparse inflammatory cell infiltrate occasionally present in AGA.

[ 00519 ] Thus, PGD2 synthase and PGD2 are targets for ameliorating common baldness, e.g. AGA.

EXAMPLE 11: PGD2S LEVELS ARE ELEVATED IN SKIN WITH SEBACEOUS GLAND
HYPERTROPHY

[ 00526 ] Sebaceous gland hypertrophy is induced in mice, using a nude mouse grafting model with an altered dermal component, using grafts with an unaltered dermal as a negative control, and PGD2 levels are measured in the both types of skin. PGD2 levels are elevated in the areas of the skin exhibiting sebaceous gland hyperplasia, indicating the role of PGD2 in sebaceous gland hyperplasia, acne, and rosacea.

EXAMPLE 12: PGD2S INHIBITION AMELIORATES SEBACEOUS GLAND
HYPERTROPHY

[ 00527 ] Mice with sebaceous gland hypertrophy are treated with inhibitors of PGD2, and extent of hypertrophy is determined. Sebaceous gland hypertrophy is ameliorated in skin treated with PGD2 inhibitors, but not in untreated areas of the same mice or untreated mice, confirming the role of PGD2 in sebaceous gland hyperplasia, acne, and rosacea.

EXAMPLE 13: APPLICATION OF PGD2S INDUCES ALOPECIA

25 MATERIALS AND EXPERIMENTAL METHODS

[ 00528 ] 25 day-old (corresponding to end of the first telogen stage) wild-type c57/black mice were treated with 200 ng of PGD2 (Cayman Chemicals) diluted in 200μl of acetone applied to the central back after shaving. Subsequent treatments were performed every 3 days, ending on day 40 for a total of 5 applications. Photographs were taken on day 46 of life, after the end of the 2nd anagen. In the second
experiment, mice were shaved and treated with 10 μg of PGD2 dissolved in 200 μl of acetone on days 66
and 69 of life, and then photographed on day #121.

RESULTS

[ 00529 ] The effect of PGD2 on hair growth was directly determined by applying PGD2 to the backs of mice. Application of PGD2 induced alopecia following the second anagen phase (Figure 10A). In another experiment, application of PGD2 was shown to prevent hair regrowth over 50 days after the last application (Figure 10B).

Wow - hair regrowth is still inhibited almost 2 months after the last application of PGd2 as Michael mentioned.
An average increase of PGD2 expression of 11.6 between balding and non-balding areas. And as Bryan will appreciate they controlled for the expression of genes elevated by UV light to make sure that the gene expression did not reflect the fact that balding areas get much more UV exposure


#29

After an area of the scalp sees its hair “become” sensitive to androgens at a certain age…then you’d pretty much have to stop all DHT 24/7 to keep them from slowly succumbing to it with anti-androgen therapy alone.

Most men in finasteride trials at year five had either SLIGHT REGROWTH or NO CHANGE.

Finasteride wont regrow a bunch of hair on most men. Dutasteride might regrow a little more.

Anti-androgens, unless they are so potent as to stop all androgenic uptake at the follicle whetehr it be DHT, androstenidione, DHEA, DHEAS, testosterone, etc. probably aren’t going to regrow a great deal of hair.

Alot of the “non-responders” to finas are older guys whose hair is already responding negatively to androgens over large areas. Finas just slows down the inevitable in such men. Finas would be best used in guys who around 20, but fear they will someday start losing hair as a preventative measure. To regrow hair, finas almost always needs help from trichotics like minox, ketoconazole, etc. Its not strong enough to regrow a bunch of hair.

EVEN CASTRATION doesnt really regrow hair, but merely halts its loss. Castrates still have adrenal testsoterone and their alpha five enzymes can make a small amount of DHT from that.

Dutasteride is probably as strong an anti-androgen internal that we will ever have for baldness.


#30

» After an area of the scalp sees its hair “become” sensitive to androgens at
» a certain age…then you’d pretty much have to stop all DHT
» 24/7 to keep them from slowly succumbing to it with anti-androgen therapy
» alone.
»
» Most men in finasteride trials at year five had either SLIGHT REGROWTH or
» NO CHANGE.
»
»
» Finasteride wont regrow a bunch of hair on most men. Dutasteride might
» regrow a little more.
»
» Anti-androgens, unless they are so potent as to stop all androgenic uptake
» at the follicle whetehr it be DHT, androstenidione, DHEA, DHEAS,
» testosterone, etc. probably aren’t going to regrow a great deal of hair.
»
»
» Alot of the “non-responders” to finas are older guys whose hair is already
» responding negatively to androgens over large areas. Finas just slows down
» the inevitable in such men. Finas would be best used in guys who around
» 20, but fear they will someday start losing hair as a preventative
» measure. To regrow hair, finas almost always needs help from trichotics
» like minox, ketoconazole, etc. Its not strong enough to regrow a bunch of
» hair.
»
»
»
» EVEN CASTRATION doesnt really regrow hair, but merely halts its loss.
» Castrates still have adrenal testsoterone and their alpha five enzymes can
» make a small amount of DHT from that.
»
»
» Dutasteride is probably as strong an anti-androgen internal that we will
» ever have for baldness.

Hi benji or anyone else…Any chance of giving me more details on Dutasteride.I’ve been on propecia for 18 months or so.It might of thickened up the top,not sure.I have had a bit of regrowth at the front,I lost a bit of hair at the front,when I had a motor accident,so I believe thats the reason for a little regrowth there.

What are side effects on dutasteride.

What other things could I use for regrowth that actually work,without side effects.

Thanks in advance


#31

» » After an area of the scalp sees its hair “become” sensitive to androgens
» at
» » a certain age…then you’d pretty much have to stop all
» DHT
» » 24/7 to keep them from slowly succumbing to it with anti-androgen
» therapy
» » alone.
» »
» » Most men in finasteride trials at year five had either SLIGHT REGROWTH
» or
» » NO CHANGE.
» »
» »
» » Finasteride wont regrow a bunch of hair on most men. Dutasteride might
» » regrow a little more.
» »
» » Anti-androgens, unless they are so potent as to stop all androgenic
» uptake
» » at the follicle whetehr it be DHT, androstenidione, DHEA, DHEAS,
» » testosterone, etc. probably aren’t going to regrow a great deal of hair.
»
» »
» »
» » Alot of the “non-responders” to finas are older guys whose hair is
» already
» » responding negatively to androgens over large areas. Finas just slows
» down
» » the inevitable in such men. Finas would be best used in guys who around
» » 20, but fear they will someday start losing hair as a preventative
» » measure. To regrow hair, finas almost always needs help from trichotics
» » like minox, ketoconazole, etc. Its not strong enough to regrow a bunch
» of
» » hair.
» »
» »
» »
» » EVEN CASTRATION doesnt really regrow hair, but merely halts its loss.
» » Castrates still have adrenal testsoterone and their alpha five enzymes
» can
» » make a small amount of DHT from that.
» »
» »
» » Dutasteride is probably as strong an anti-androgen internal that we
» will
» » ever have for baldness.
»
» Hi benji or anyone else…Any chance of giving me more details on
» Dutasteride.I’ve been on propecia for 18 months or so.It might of
» thickened up the top,not sure.I have had a bit of regrowth at the front,I
» lost a bit of hair at the front,when I had a motor accident,so I believe
» thats the reason for a little regrowth there.
»
» What are side effects on dutasteride.
»
» What other things could I use for regrowth that actually work,without side
» effects.
»
» Thanks in advance

how do you know if you have regrowth if you shave your head

does your girlfriend of NINETEEN YEARS mind


#32

Finas has been shown to decrease serum DHT levels by 65-70%

Dutasteride has been shown to decrease serum DHT levles by over 90%.

Finas targets the type 2 enzyme of alpha five reductase present in your hair follicle’s outer root sheaths, liver, seminal vesicles, prostate tissue, adrenal

The type one enzyme exists in the sebaceous glands, brain, some of the body’s deeper tissues.

Dutasteride gets about 98% of type two alpha five reducatse blocked and about 52 percent of type one. It has a longer half life in the body and is present in the body a few months at low levels after you get off of it. Its stronger, hence it has more side effects in men. It will lessen sebum production. I take finas personally because I think dutas is a tad strong.

I wish that finas inhibited type two alpha five as well as dutasteride without affecting the type one enzyme in my brain, etc. Finas is quite good though, the charts say that.


#33

» Finas has been shown to decrease serum DHT levels by 65-70%
»
» Dutasteride has been shown to decrease serum DHT levles by over 90%.
»
»
»
» Finas targets the type 2 enzyme of alpha five reductase present in your
» hair follicle’s outer root sheaths, liver, seminal vesicles, prostate
» tissue, adrenal
»
» The type one enzyme exists in the sebaceous glands, brain, some of the
» body’s deeper tissues.
»
»
» Dutasteride gets about 98% of type two alpha five reducatse blocked and
» about 52 percent of type one. It has a longer half life in the body and is
» present in the body a few months at low levels after you get off of it. Its
» stronger, hence it has more side effects in men. It will lessen sebum
» production. I take finas personally because I think dutas is a tad strong.
»
»
» I wish that finas inhibited type two alpha five as well as dutasteride
» without affecting the type one enzyme in my brain, etc. Finas is quite
» good though, the charts say that.

Thanks benji


#34

» Finas has been shown to decrease serum DHT levels by 65-70%
»
» Dutasteride has been shown to decrease serum DHT levles by over 90%.
»
»
»
» Finas targets the type 2 enzyme of alpha five reductase present in your
» hair follicle’s outer root sheaths, liver, seminal vesicles, prostate
» tissue, adrenal
»
» The type one enzyme exists in the sebaceous glands, brain, some of the
» body’s deeper tissues.
»
»
» Dutasteride gets about 98% of type two alpha five reducatse blocked and
» about 52 percent of type one. It has a longer half life in the body and is
» present in the body a few months at low levels after you get off of it. Its
» stronger, hence it has more side effects in men. It will lessen sebum
» production. I take finas personally because I think dutas is a tad strong.
»
»
» I wish that finas inhibited type two alpha five as well as dutasteride
» without affecting the type one enzyme in my brain, etc. Finas is quite
» good though, the charts say that.

Saw Palmetto inhibits both type 1 and type 2


#35

Study: Human prostatic steroid 5 alpha-reductase isoforms–a comparative study of selective inhibitors.

This study suggests that Fenistride (active ingredient of Propecia) only inhibited the Type 2 form of 5 alpha reductase where Saw Palmetto extract inhibited both type 1 and 2 forms of 5 alpha-reductase and was more potent than Fenistride.

AUTHOR
Iehlé C; Délos S; Guirou O; Tate R; Raynaud JP; Martin PM

JOURNAL
J Steroid Biochem Mol Biol, 54: 5-6, 1995 Sep, 273-9

ABSTRACT
The present study describes the independent expression of the type 1 and 2 isoforms of human 5 alpha-reductase in the baculovirus-directed insect cell expression system and the selectivity of their inhibition. The catalytic properties and kinetic parameters of the recombinant isozymes were consistent with published data. The type 1 isoform displayed a neutral (range 6-8) pH optimum and the type 2 isoform an acidic (5-6) pH optimum. The type 2 isoform had higher affinity for testosterone than did the type 1 isoform (Km = 0.5 and 2.9 microM, respectively). Finasteride and turosteride were selective inhibitors of the type 2 isoform (Ki (type 2) = 7.3 and 21.7 nM compared to Ki (type 1) = 108 and 330 nM, respectively). 4-MA and the lipido-sterol extract of Serenoa repens (LSESr) markedly inhibited both isozymes (Ki (type 1) = 8.4 nM and 7.2 micrograms/ml, respectively; Ki (type 2) = 7.4 nM and 4.9 micrograms/ml, respectively). The three azasteroids were competitive inhibitors vs substrate, whereas LSESr displayed non-competitive inhibition of the type 1 isozyme and uncompetitive inhibition of the type 2 isozyme. These observations suggest that the lipid component of LSESr might be responsible for its inhibitory effect by modulating the membrane environment of 5 alpha-reductase. Partially purified recombinant 5 alpha-reductase type 1 activity was preserved by the presence of lipids indicating that lipids can exert either stimulatory or inhibitory effects on human 5 alpha-reductase.


#36

» » Finas has been shown to decrease serum DHT levels by 65-70%
» »
» » Dutasteride has been shown to decrease serum DHT levles by over 90%.
» »
» »
» »
» » Finas targets the type 2 enzyme of alpha five reductase present in your
» » hair follicle’s outer root sheaths, liver, seminal vesicles, prostate
» » tissue, adrenal
» »
» » The type one enzyme exists in the sebaceous glands, brain, some of the
» » body’s deeper tissues.
» »
» »
» » Dutasteride gets about 98% of type two alpha five reducatse blocked and
» » about 52 percent of type one. It has a longer half life in the body and
» is
» » present in the body a few months at low levels after you get off of it.
» Its
» » stronger, hence it has more side effects in men. It will lessen sebum
» » production. I take finas personally because I think dutas is a tad
» strong.
» »
» »
» » I wish that finas inhibited type two alpha five as well as dutasteride
» » without affecting the type one enzyme in my brain, etc. Finas is quite
» » good though, the charts say that.
»
» Saw Palmetto inhibits both type 1 and type 2

HanginInThere thanks


#37

» » » Finas has been shown to decrease serum DHT levels by 65-70%
» » »
» » » Dutasteride has been shown to decrease serum DHT levles by over 90%.
» » »
» » »
» » »
» » » Finas targets the type 2 enzyme of alpha five reductase present in
» your
» » » hair follicle’s outer root sheaths, liver, seminal vesicles, prostate
» » » tissue, adrenal
» » »
» » » The type one enzyme exists in the sebaceous glands, brain, some of
» the
» » » body’s deeper tissues.
» » »
» » »
» » » Dutasteride gets about 98% of type two alpha five reducatse blocked
» and
» » » about 52 percent of type one. It has a longer half life in the body
» and
» » is
» » » present in the body a few months at low levels after you get off of
» it.
» » Its
» » » stronger, hence it has more side effects in men. It will lessen sebum
» » » production. I take finas personally because I think dutas is a tad
» » strong.
» » »
» » »
» » » I wish that finas inhibited type two alpha five as well as
» dutasteride
» » » without affecting the type one enzyme in my brain, etc. Finas is
» quite
» » » good though, the charts say that.
» »
» » Saw Palmetto inhibits both type 1 and type 2
»
» HanginInThere thanks

Saw Palmetto is , even though a weak 5 AR inhibitor, very effective for some guys, and it has very few cases of side effects. However some guys do not respond at all to it. If you are a lucky responder, however, you will increase your results by adding other natural 5 AR inhibitors, pygeum nettles, green teas, pumpkin seed oil, beta sitosterol, well at least that was my experience


#38

saw palmetto has been tried in humans, but serum levels of DHT were unchanged when it was given to actual people. DHT in prostate tissue was reduced by 32%.

Here are some studies confirming this:

Saw Palmetto, DHT, Hair Loss and the Prostate
Comparison of finasteride (Proscar), a 5 alpha reductase inhibitor, and various commercial plant extracts in in vitro and in vivo 5 alpha reductase inhibition.
Rhodes L,
Primka RL,
Berman C,
Vergult G,
Gabriel M,
Pierre-Malice M,
Gibelin B.
Department of Biochemistry, Merck Research Laboratories, Rahway, New Jersey 07065.

Human prostate was used as a source of 5 alpha reductase. Compounds were incubated with an enzyme preparation and [3H]testosterone. [3H]-dihydrotestosterone production was measured to calculate 5 alpha reductase activity. IC50 values (ng/ml) were finasteride = 1; Permixon = 5,600; Talso = 7,000; Strogen Forte = 31,000; Prostagutt = 40,000; and Tadenan = 63,000. Bazoton and Harzol had no activity at concentrations up to 500,000 ng/ml. In castrate rats stimulated with testosterone (T) or dihydrotestosterone (DHT), finasteride, but not Permixon or Bazoton, inhibited T stimulated prostate growth, while none of the three compounds inhibited DHT stimulated growth. These results demonstrate that finasteride inhibits 5 alpha reductase, while Permixon and Bazoton have neither anti-androgen nor 5 alpha reductase inhibitory activity. In addition, in a 7 day human clinical trial, finasteride, but not Permixon or placebo, decreased serum DHT in men, further confirming the lack of 5 alpha reductase inhibition by Permixon. Finasteride and the plant extracts listed above do not inhibit the binding of DHT to the rat prostatic androgen receptor (concentrations to 100 micrograms/ml). Based on these results, it is unlikely that these plant extracts would shrink the prostate by inhibiting androgen action or 5 alpha reductase.

PMID: 8381228 [PubMed - indexed for MEDLINE]

1: Eur Urol. 1994;26(3):247-52. Links

Comparison of finasteride (Proscar) and Serenoa repens (Permixon) in the inhibition of 5-alpha reductase in healthy male volunteers.
Strauch G,
Perles P,
Vergult G,
Gabriel M,
Gibelin B,
Cummings S,
Malbecq W,
Malice MP.
Eclimed Pharmacologie Clinique, Hopital Universitaire Cochin, Paris, France.

A total of 32 healthy male volunteers (age range 20-30 years) were enrolled in a 1-week open, randomized, placebo-controlled study comparing finasteride (Proscar), a 5 alpha-reductase inhibitor, with Permixon, the plant extract of Serenoa repens. The objective of the study was to evaluate the effect of single and multiple doses of the drugs on the inhibition of 5 alpha-reductase as assessed by serum dihydrotestosterone level determination. Following baseline measurements on day 1, the subjects were randomized to finasteride 5 mg once a day (n = 10), Permixon 80 mg x 2 twice a day (n = 11), or to placebo once a day (n = 11) for 7 days. Serum testosterone and dihydrotestosterone levels, were determined on day 1 (baseline and 12 h) and on days 2 (24 h), 3 (48 h), 4 (72 h), 6 (120 h), and 8 (168 h). After 12 h, a single dose of finasteride 5 mg reduced the serum dihydrotestosterone level by 65% (p < or = 0.01). The decreases ranged from -52 to -60% with multiple doses of finasteride 5 mg once a day (p < or = 0.01). As in the placebo group, there was no effect of Permixon on the serum dihydrotestosterone level. No significant difference was detected between finasteride and Permixon or between finasteride and placebo with respect to serum testosterone, except on days 3 and 6, respectively (p < or = 0.05). However, the corresponding serum testosterone levels remained within the normal ranges. These data confirm the efficacy of finasteride as inhibitor of 5 alpha-reductase.(ABSTRACT TRUNCATED AT 250 WORDS)

PMID: 7805711 [PubMed - indexed for MEDLINE]

1: Prostate. 2006 Feb 1;66(2):115-23. Links

Saw palmetto is an indirectly acting sympathomimetic in the rat-isolated prostate gland.
Cao N,
Haynes JM,
Ventura S.
Prostate Research Co-Operative, Faculty of Pharmacy, Monash University, Parkville, Victoria, Australia.

BACKGROUND: To investigate whether saw palmetto that inhibits alpha1-adrenoceptor binding in vitro affects contractility of the rat prostate gland. METHODS: The effects of a commercially available saw palmetto extract were examined on the contractility of rat-isolated prostate glands. The extract was tested in the presence and absence of phentolamine, prazosin, yohimbine, propranolol, hexamethonium, cocaine, desipramine, nifedipine, guanethidine, atropine, and alpha,beta-methylene ATP to evaluate the mechanism of action. Isolated preparations of rat vas deferens and bladder were used for comparison. RESULTS: Unexpectedly, saw palmetto extract caused contractions of the rat prostate gland that could be attenuated by prazosin, phentolamine, nifedipine, guanethidine, cocaine, and desipramine but not by any of the other pharmacological tools. Similar contractile effects were observed in rat-isolated vas deferens preparations but not in rat-isolated bladder preparations. CONCLUSIONS: In the rat prostate gland, saw palmetto extract causes indirect alpha1-adrenoceptor-mediated contractions via the release of noradrenaline from sympathetic neurons. Copyright 2005 Wiley-Liss, Inc.

PMID: 16114061 [PubMed - indexed for MEDLINE]

: Prostate. 1999 Feb 15;38(3):208-15. Links

Saw palmetto extracts potently and noncompetitively inhibit human alpha1-adrenoceptors in vitro.
Goepel M,
Hecker U,
Krege S,
Rubben H,
Michel MC.
Department of Urology, University of Essen, Germany. mark.goepel@uni-essen.de

BACKGROUND: We wanted to test whether phytotherapeutic agents used in the treatment of lower urinary tract symptoms have alpha1-adrenoceptor antagonistic properties in vitro. METHODS: Preparations of beta-sitosterol and extracts of stinging nettle, medicinal pumpkin, and saw palmetto were obtained from several pharmaceutical companies. They were tested for their ability to inhibit [3H]tamsulosin binding to human prostatic alpha1-adrenoceptors and [3H]prazosin binding to cloned human alpha1A- and alpha1B-adrenoceptors. Inhibition of phenylephrine-stimulated [3H]inositol phosphate formation by cloned receptors was also investigated. RESULTS: Up to the highest concentration which could be tested, preparations of beta-sitosterol, stinging nettle, and medicinal pumpkin were without consistent inhibitory effect in all assays. In contrast, all tested saw palmetto extracts inhibited radioligand binding to human alpha1-adrenoceptors and agonist-induced [3H]inositol phosphate formation. Saturation binding experiments in the presence of a single saw palmetto extract concentration indicated a noncompetitive antagonism. The relationship between active concentrations in vitro and recommended therapeutic doses for the saw palmetto extracts was slightly lower than that for several chemically defined alpha1-adrenoceptor antagonists. CONCLUSIONS: Saw palmetto extracts have alpha1-adrenoceptor-inhibitory properties. If bioavailability and other pharmacokinetic properties of these ingredients are similar to those of the chemically defined alpha1-adrenoceptor antagonists, alpha1-adrenoceptor antagonism might be involved in the therapeutic effects of these extracts in patients with lower urinary tract symptoms suggestive of benign prostatic obstruction.

PMID: 10068345 [PubMed - indexed for MEDLINE]


#39

the fact that Saw Palmetto does not reduce serum DHT levels is a good thing
you do not want to change blood hormone levels, if you do, you get all the nasty side effects sexually

You DO WANT, do prevent the DHT in the blood from BINDING to the prostate, or the base of the hair follicle, which is what Saw palmetto does do

propecia does this but it reduces SERUM dht levels in the blood, that is the reason for all the nasty side effects


#40

» the fact that Saw Palmetto does not reduce serum DHT levels is a good
» thing
» you do not want to change blood hormone levels, if you do, you get all the
» nasty side effects sexually
»
» You DO WANT, do prevent the DHT in the blood from BINDING to the prostate,
» or the base of the hair follicle, which is what Saw palmetto does do
»
» propecia does this but it reduces SERUM dht levels in the blood, that is
» the reason for all the nasty side effects

Hangin’,
an androgen receptor is an androgen receptor is an androgen receptor

There is NOT/b]a “dht” receptor, but an androgen receptor that any male hormone (DHT, Testesoterone, androstenidione, Dehydroespiandrosterone, Dehydroepdiandrosterone Sulfate, etc) can bind to.

If saw palmetto is an androgen receptor blocker, then one might as well take flutamide. Likely, saw palmetto reduces cholesterol and it gives the body less cholesterol to synthesize testosterone with, and it likely increases globulin which binds free testosterone, and its an anti-inflammatory, and may have a specific effect on certain negative growth inhibitors or even a prostaglandin or two. 

WE KNOW FOR A FACT that the “free form” NOT TRIGLYCERIDE, fatty acids like palmitic and linolenic that are in saw palmetto oil do indeed inhibit alpha five reductase enzymes in test tubes. However, after they pass throgh the human digestive system and make their way to the scalp, seem to not be able to do this. Its been speculated for a long while that saw palmetto would be an effective TOPICAL anti-androgen, and hence why its included in alot of topicals and was found to reduce sebum secretions in an italian study, but internally…it should effect internal DHT. If it was blocking androgen receptors internally the side effects would be the same as flutamide (tits, no libido, some stomach upset, nausea, etc.). These things dont seem to be in evidence unless extremely large doses (over 1000 milligrams a day) are taken.

The one study (6 out of 10 men reporting improvement) is rather small, and was funded by a source that apparently stood to gain from it, and it was based on the men’s reportage. No photographs or hair weights were taken. I think it would be better to use some saw palmetto oil in a man’s shampoo along with its internal usage to be safe.

I will say this…You’d think that growers of saw palmetto would be all to happy to fund a big study that measured hair weights in the same area, and their circumferences, along with global photographic assessment to release to the public. But they’ve had many years to have done this and have not. That kinda rings a bell for me.

Ive taken finasteride for over a decade and have had no problems personally.

Just my opinion though. If people are happy on S.P., then its their business.