Action Love and Dr. Lin

[md2002]

I cam upon this guys website and I have heard you guys mention him before. Is he for real or is he a quack??? Is anything he says true?

http://www.actionlove.com/extra/hailoss.htm#f

 

[The Gardener]

From his site:

"Finasteride tends to increase testosterone and estrogen( for breast growth!) but severely deplete DHT in the penile tissue, brain and bones after damaging the 5-alphase reductase gene and DNA in the liver, bone, testicles, penis, and of course, brain."

"When Finasteride kills the 5-alpha reductase gene expression in your pituitary glands and testicles and the liver..."

Sorry, but Finasteride does not "kill" any genes. That is not how it works, and genes are not "killed". I would consider his usage of this terminology to be potential medical quackery at worst, or scaremongering at best. Just my opinion.

Oh, and to complete the quote I started above:

"...When Finasteride kills the 5-alpha reductase gene expression in your pituitary glands and testicles and the liver 5-alpha reductase release, you will need a high dose of L-Arginine (1000 mg 3 times a day to work with ViaPal-hGH-J (or ViaPal-hGH-P if you are over age 30), 5-HTP, DeToxiA and Fish and Borage Oil(1000 mg each meal)..."

The products listed to help undo the damage being items sold on his website, naturally.

 

[drinkrum]

Dr. Lin is an idiot. Just read the name of his "center". I've talked about him and his retarded theories before. He's quite a laugh.

D.

 

[global]

He is a quack and a fake.

 

[Bryan]

He's a quack. There are factual errors in what he says.

Bryan

 

[Guest]

Just a minute ago I typed ''DHT nitric oxide'' on google and found this study.

OBJECTIVE: To examine the effects of androgens on erectile response and the expression of nitric oxide synthase (NOS) isoform mRNAs in the penile corpus cavernosum of castrated rats. MATERIALS AND METHODS: The study comprised 50 adult male Sprague-Dawley rats in five groups: sham controls; castrated; castrated and receiving testosterone; castrated and receiving dihydrotestosterone (DHT); castrated and receiving testosterone and 5alpha-reductase inhibitor (finasteride). Androgen replacements were administered via implants of silicone tubing. After 7 days, some animals underwent electrical stimulation of the cavernosal nerves and the remainder were used for further analysis. NOS activity was measured in the soluble fraction of the corpus cavernosum, using the Griess reaction. Total RNA was isolated and nNOS and eNOS mRNA expression examined using semiquantitative reverse-transcriptase polymerase chain reaction. RESULTS: Castration caused a marked decrease in erectile response and the ratio of maximal intracavernosal pressure (ICPmax) to systemic blood pressure (SBP), although both testosterone and DHT effectively restored the response to normal. NOS activity and the amount of nNOS mRNA were reduced in castrated rats but restored by androgen replacement. Although there was no significant difference in NOS activity between the androgens, nNOS mRNA expression was higher in rats treated with DHT. There were no effects of androgen in rats treated with finasteride, as the ICPmax/SBP ratio, NOS activity and amount of nNOS mRNA decreased. eNOS mRNA expression was independent of androgen. CONCLUSIONS: Androgens enhance nNOS gene expression in the penile corpus cavernosum of rats, suggesting that they play an important role in maintaining NOS activity. Of the two androgens, DHT was more potent.

So when finasteride lowers DHT, it ''lowers''(my english is not so good) nNOS gene expression in the penile corpus cavernosum. Does this mean lower DHT decreases nitric oxide production in the penis? That would explain why DHT is so important for erection.

This Dr. Lin suggests using arginine to overcome this problem. So this means by increasing nitric oxide production, you are trying to overcome the llowering of nNOs gene expression(what the hell does that mean!) due to finasteride.

For example if I would use a product which does not lower DHT, but prevents it from binding to ''the androgen receptor''(?), will this have the same lowering effect of nNOs gene expression as using finasteride/dutasteride which lower DHT?

Thanx in advance.

 

[Guest]

Gardener wrote:

"When Finasteride kills the 5-alpha reductase gene expression in your pituitary glands and testicles and the liver..."

Sorry, but Finasteride does not "kill" any genes. That is not how it works, and genes are not "killed". I would consider his usage of this terminology to be potential medical quackery at worst, or scaremongering at best. Just my opinion.

Gardener, this Lin guy does not write that Finasteride kills any genes, he writes that finasteride kills the 5-alpha reductase gene expression. I think he means the ''conversion'' of Testosterone to DHT, which would normally happen because of the 5-alpha reductase gene expression, but because of finasteride is killed/blocked. That makes sense(for me, which does not mean it is correct :lol: )

Gene expression means the ability of a gene to produce a biologically active protein. So by writing ''finasteride kills the 5-alspha reductase gene expression'', he probably means that finasteride blocks gene/genes to produce the acive protein which makes it possible to convert testosterone to DHT.

Also found this study:

Testosterone down-regulates the levels of androgen receptor mRNA in smooth muscle cells from the rat corpora cavernosa via aromatization to estrogens.

Lin MC, Rajfer J, Swerdloff RS, Gonzalez-Cadavid NF.

Department of Surgery, UCLA School of Medicine, Torrance 90509.

Androgens down-regulate the levels of androgen receptors (AR) and AR mRNA in the penis and prostate of castrated rats, and are assumed to cause their decrease during sexual maturation in the penile smooth muscle of intact rats. In order to determine whether these effects occur directly at the target cell level, and to what extent they are due to testosterone (T) or to their metabolites, we have measured AR mRNA in cultures of smooth muscle cells from the adult rat corpora cavernosa treated in vitro with sex steroids. T at high concentrations (100 nM) acted like dihydrotestosterone (DHT) in increasing moderately the levels of AR mRNA in both proliferating and contact-inhibited cells. However, when conversion of T to DHT was blocked by the 5-alpha reductase inhibitor finasteride, the levels of AR mRNA were considerably down-regulated by T (10-500 nM), particularly in the contact-inhibited cells. Finasteride by itself was inactive. These effects in both types of cultures were inhibited by platelet derived growth factor (PDGF) (20 ng/ml), a growth factor that up-regulates AR mRNA levels, and by fadrozole (100 nM), an aromatase inhibitor of the T/estrogen conversion. Estradiol (50 nM) was even more potent than T in decreasing AR mRNA levels. With the exception of PDGF none of the treatments affected significantly cell growth, as measured by DNA synthesis and content. Our results indicate that it is possible to modulate in vitro AR mRNA levels in the penile smooth muscle cells, and that under normal conditions DHT and T act as moderate up-regulators. When DHT formation is inhibited, the aromatization pathway of T to estradiol will prevail and induce a pronounced down-regulation of AR mRNA levels. We assume that the in vivo AR down-regulation in the penile smooth muscle by androgens is an indirect effect mediated by a paracrine or endocrine mechanism elicited in another tissue.

PMID: 8499343 [PubMed - indexed for MEDLINE]

-Using finasteride will block conversion of testosterone to DHT
-Using finasteride will increase testosterone(temporary I believe) and
estradiol levels
-increase in Estradiol and Testosterone(?) down regulate AR mRNA
-the low DHT level caused by using finasteride, which blocks the
conversion of testosterone to DHT, will prevent the increase of AR mRNA
in both proliferating and contact-inhibited cells.

So there are some problems with finasteride:

1)low DHT which prevents the increase AR mRNA due to DHT. Does this
mean that androgen receptors can't increase, that DHT can't bind to AR?
2)high estradiol due to testosterone not being converted to DHT because
of finasteride, but being aromitized to estradiol which down regulates AR
mRNA. What does this mean exactly? Less androgen receptors?
3)finasteride blocks conversion of testosterone to DHT. DHT is important
for maintaining NOS(nitric oxide/vasodilation if I am correct) activity in
the penile corpus cavernosum.

Furthermore I remember reading somewhere that DHT is also antiestrogenic. DHT can compete with estrogen for the same receptor. Also that the ratio of androgens to estrogen is very important.

So by using finasteride which blocks conversion of T to DHT which makes estradiol levels increase we are changing the ratio of androgens to estrogen causing gynecomastia.

My opinion is to run as fast away as you can when you see finasteride/dutasteride!

 

[Bryan]

Gardener, this Lin guy does not write that Finasteride kills any genes, he writes that finasteride kills the 5-alpha reductase gene expression. I think he means the ''conversion'' of Testosterone to DHT, which would normally happen because of the 5-alpha reductase gene expression, but because of finasteride is killed/blocked. That makes sense(for me, which does not mean it is correct :lol: )

If Lin writes that the 5a-reductase gene expression is "killed", either he means that the 5a-reductase enzyme isn't being produced, or his writing skills are absolutely atrocious. If it's the former, he's WRONG about that. Finasteride doesn't stop the enzyme from being produced, it INHIBITS its function by binding to it irreversibly.

Gene expression means the ability of a gene to produce a biologically active protein. So by writing ''finasteride kills the 5-alspha reductase gene expression'', he probably means that finasteride blocks gene/genes to produce the acive protein which makes it possible to convert testosterone to DHT.

Like I said above, finasteride doesn't stop the production of the 5a-reductase enzyme. It inhibits it once it's formed. If Lin really did mean what you said, then he's wrong.

-Using finasteride will increase testosterone(temporary I believe) and estradiol levels

No, permanently. As long as you keep taking finasteride, of course.

-increase in Estradiol and Testosterone(?) down regulate AR mRNA

Not necessarily. According to Sawaya, the OPPOSITE of that happens in human hair follicles.

-the low DHT level caused by using finasteride, which blocks the conversion of testosterone to DHT, will prevent the increase of AR mRNA in both proliferating and contact-inhibited cells.

Again, not necessarily.

So there are some problems with finasteride:

1)low DHT which prevents the increase AR mRNA due to DHT. Does this mean that androgen receptors can't increase, that DHT can't bind to AR?
2)high estradiol due to testosterone not being converted to DHT because of finasteride, but being aromitized to estradiol which down regulates AR mRNA. What does this mean exactly? Less androgen receptors?

Sawaya found the OPPOSITE of that in one of her studies. She found an "intense upregulation" of androgen receptors in the hair follicle cells of finasteride users. The moral here is that what happens in a certain tissue in one particular species (rats) doesn't necessarily happen in a completely different tissue in a different species.

Bryan

 

[Guest]

Thnx for your respons Bryan.

About the Lin guy. Of course I can't look in his head to know what he exactly meant, but what he definitely did not mean was the using finasteride kills genes.

If Lin writes that the 5a-reductase gene expression is "killed", either he means that the 5a-reductase enzyme isn't being produced, or his writing skills are absolutely atrocious.

I think this Lin Guy has great knowledge, but have you checked his site? It really is a mess!

Music23 wrote:
-Using finasteride will increase testosterone(temporary I believe) and estradiol levels


No, permanently. As long as you keep taking finasteride, of course.

I thought many finasteride users reported a temporary rise in libido which I thought was due to a temporary testosterone rise. So basically finasteride will increase T and estradio levels so long you use it.

Music23 wrote:
-increase in Estradiol and Testosterone(?) down regulate AR mRNA

Not necessarily. According to Sawaya, the OPPOSITE of that happens in human hair follicles.

I was not completely accurate, sorry. My post is more about what it will do for the erection.

So according to Sawaya there is an increase AR mRNA in the human hair follicles. Isn't that bad news for finasteride users? Because that would mean I think that more AR would be made there so correct me if I am wrong more DHT can be binded.

Music23 wrote:
-the low DHT level caused by using finasteride, which blocks the conversion of testosterone to DHT, will prevent the increase of AR mRNA in both proliferating and contact-inhibited cells.


Again, not necessarily

For erection again. The low DHT will prevent an increase in androgen receptor mRNA in smooth muscle cells from the rat corpora cavernosa.

Music23 wrote:
So there are some problems with finasteride:

1)low DHT which prevents the increase AR mRNA due to DHT. Does this mean that androgen receptors can't increase, that DHT can't bind to AR?
2)high estradiol due to testosterone not being converted to DHT because of finasteride, but being aromitized to estradiol which down regulates AR mRNA. What does this mean exactly? Less androgen receptors?


Sawaya found the OPPOSITE of that in one of her studies. She found an "intense upregulation" of androgen receptors in the hair follicle cells of finasteride users. The moral here is that what happens in a certain tissue in one particular species (rats) doesn't necessarily happen in a completely different tissue in a different species.

Yes but it was again concerning the erection. You are correct that rats and humans are not the same. However I assume with the problems I have read certain people have with finasteride usage, I think the effect on humans and rats are the same. I could be wrong.

For erection
-Using finasteride will lower DHT, increase T and Estradiol.
-Using finasteride will decrease levels of AR mRNA in smooth muscle cells from the rat corpora cavernosa.
-Using finasteride lowers DHT. DHT is a potent androgen for enhancing NOS activity in the penis.

If this is correct, would Lin not be right when he writes that you need arginine? Arginine increases nitric oxide production which is lowered in the smooth muscle cells from the corpora cavernosa due to low DHT(finasteride).

Music23 wrote:
Gene expression means the ability of a gene to produce a biologically active protein. So by writing ''finasteride kills the 5-alspha reductase gene expression'', he probably means that finasteride blocks gene/genes to produce the acive protein which makes it possible to convert testosterone to DHT.


Like I said above, finasteride doesn't stop the production of the 5a-reductase enzyme. It inhibits it once it's formed. If Lin really did mean what you said, then he's wrong.

So finasteride binds with type 2 5alpha-reductase which stops the conversion of T to DHT. Correct?

Also found this from Lin:

The 5-alpha reductase inhibitor (Finasteride) globaly interferes with the entire liver (5-alpha reductase Type 1 gene) and testis/epididymis (5-alpha reductase Type 2 gene) gene expressions although it is assumed to block (target) the 5-alpha reductase gene expression. This gene interference causes the deficiency of acetylcholine, serotonin, dopamine and androgen hormones for penile and testicular shrinkage and semen production disorder (watery ejaculation like urethral female ejaculation, no semen!).

Found this on another site:

There has been no study performed on the effects of hepatic insufficiency for Finasteride pharmacokinetics. Also, a search of the medical literature did show a rise in liver enzymes in one of 14 subjects studied in healthy volunteers (Shimazaki and Nose). One case of hepatitis induced by Finasteride was reported in a patient with many organ problems including a high alcohol intake. The inability to find another cause for the hepatitis on this patient led the doctors to believe that this drug may have been the cause for the liver disease on this one patient.

Found this study about finasteride and it's effect on the brain sexual differentation.

5alpha-reductase 2 inhibition impairs brain defeminization of male rats: reproductive aspects.

Ribeiro CM, Pereira OC.

Department of Pharmacology, Institute of Biosciences, Sao Paulo State University- UNESP, 18618-000 Botucatu, SP, Brazil.

The present study was carried out to determine whether 5alpha-reductase 2 (5alpha-R2) metabolic pathway plays a key role in brain sexual differentiation. The inhibition of 5alpha-R2 by finasteride (20 mg/kg/day) from gestational day 19 to postnatal day 5 has long-term effects on sexual behavior and reproductive physiology detected only in adult life. Sexual maturation assessed by timing of preputial separation was unchanged. Finasteride-treated males were able to mate with untreated females which became pregnant but exhibited increased rate of pre-implantation loss. The subfertility observed was probably due to abnormally shaped sperm, since the sperm number was not altered. While plasma testosterone was enhanced, LH levels were not changed. The copulatory potential was not affected and all finasteride-treated rats presented male sexual behavior. Despite this, 53% of them showed homosexual behavior when pretreated with estradiol, suggesting an incomplete brain defeminization. These results indicate that 5alpha-R2 acts in brain sexual differentiation of male rats.Moreover, we suggest that 5alpha-R2 not only produces essential metabolites that act together with estradiol in brain sexual differentiation but also protects the brain from the damaging effects of estradiol excess.

I know many of these studies were not done on humans, but my opinion is that it really is not a smart thing to use finasteride for hair loss. Changing ratio's of androgens to estradiol, lowering DHT(penis, brain, liver). DANGEROUS! My advice to anyone using finasteride is stop using it!

Use a topical or something els which does not systematically change hormone levels. Use arginine for nitric oxide production and strong antioxidants and vitamin B complex, zinc, magnesium.

 

[Bryan]

I think this Lin Guy has great knowledge, but have you checked his site? It really is a mess!

There are factual errors in what he says. I don't trust him as far as I can throw him.

So according to Sawaya there is an increase AR mRNA in the human hair follicles. Isn't that bad news for finasteride users? Because that would mean I think that more AR would be made there so correct me if I am wrong more DHT can be binded.

It's not a particularly significant factor, in my opinion. If you reduce DHT sharply enough, it doesn't make much difference if there are more androgen receptors.

So finasteride binds with type 2 5alpha-reductase which stops the conversion of T to DHT. Correct?

Correct.

Bryan

 

[Guest]

I think these studies I provided are proof that the just ''2%'' of propecia users developed libido/erectile problem is BS.l It's a lie. Using finasteride for hair loss is really an unintelligent thing to do.

I know having nice hair is important, but it should not be so important for starting a medication which alters hormones systematically which cause side effects. Those who are considering to stop finasteride, DO IT RIGHT NOW!

I am 100% sure that in 20 years or so people will look back and say '' You knew back then we were really stupid using finasteride and changing stystematically our hormones''. Some people using finasteride simply are really damaging their body.

It's not that finasteride just alters hormones. It also has it effects on the liver, brain and penis.

 

[Felk]

Those who are considering to stop finasteride, DO IT RIGHT NOW! It's not that finasteride just alters hormones. It also has it effects on the liver, brain and penis.

I think that is a tad on the scaremongering side. Also, doesn't finasteride have no effect on the brain, since it only effects type 2 5AR, and only type 1 5AR is found in the brain?

 

[H/B]

I think these studies I provided are proof that the just ''2%'' of propecia users developed libido/erectile problem is BS.l It's a lie. Using finasteride for hair loss is really an unintelligent thing to do.

I know having nice hair is important, but it should not be so important for starting a medication which alters hormones systematically which cause side effects. Those who are considering to stop finasteride, DO IT RIGHT NOW!

I am 100% sure that in 20 years or so people will look back and say '' You knew back then we were really stupid using finasteride and changing stystematically our hormones''. Some people using finasteride simply are really damaging their body.

It's not that finasteride just alters hormones. It also has it effects on the liver, brain and penis.

You did not provide anything useful. In rats at what dosage?
Useless.

The safety, efficiency and effectiveness of finasteride has been proven in human double blind with placebo and has been followed up over and over since the drug was developed over a decade ago.
You are 100% sure?... You are 100% full ofshit.

 

[Guest]

You are 100% sure?... You are 100% full ofshit.

Yes and those guys having difficulty having erection/libido issues were not using 100 grams of finasteride a day were they? All of them were using 1 mg or so, maybe little bit more, maybe little bit less.

finasteride alters certain hormone levels systematically:
DHT lowered
T increased
Estradiol increased

''Moreover, we suggest that 5alpha-R2 not only produces essential metabolites that act together with estradiol in brain sexual differentiation
but also protects the brain from the damaging effects of estradiol excess.''

DHT protects brain from estradiol. When you lower DHT, estradiol can do more damage. They are talking about 5alpha-R2 not type 1!

One study shows DHT changes NOS activity in the smooth muscle of the

The safety, efficiency and effectiveness of finasteride has been proven in human double blind with placebo and has been followed up over and over since the drug was developed over a decade ago.

What is a decade? You know a lot of people get older then 60! Furthermore there have been quite some people experiencing ED, which is caused by lowering NOS activity in the penis with the downregulation of AR and AR mRNA. Merck tells us 2% experienced these sort of problems. That is just huge lie, to keep earning the bucks of those who are desperate in maintaining their hair! Merck owners and scientists should be put into jail!

When you have a head ache, you don't cut your head of. DHT is important for men.

 

[powersam]

''Moreover, we suggest that 5alpha-R2 not only produces essential metabolites that act together with estradiol in brain sexual differentiation
but also protects the brain from the damaging effects of estradiol excess.''

DHT protects brain from estradiol. When you lower DHT, estradiol can do more damage. They are talking about 5alpha-R2 not type 1! "

there are men born without the ability to produce 5ar2 and they live completely healthy and normal lives. so i'm afraid that the above simply has no leg to stand on. not to mention the fact that this drug has been out for 14 odd years now and if it were to cause the kinds of problems mentioned here they would most definately have been documented by now.

 

[Guest]

Keeping your hair with a little bit of regrowth by using finasteride which lowers DHT, increases T and Estradiol. Changing the ratio of androgens, decreasing NOS activity in penis, lower libido etc... You must be very desperate to use finasteride!

 

[H/B]

Keeping your hair with a little bit of regrowth by using finasteride which lowers DHT, increases T and Estradiol. Changing the ratio of androgens, decreasing NOS activity in penis, lower libido etc... You must be very desperate to use finasteride!

My penis, libido and liver is fine. Go spread your bullshit over at propecia side-effects.com with the rest of the mentalcases you delusional twisted f***. This is a place to help people, not to frighten them with unfounded bullshit.

 

[random32]

More than 2 years of using finasteride and no negative side effects at all

I think personal experience counts a lot more than vague 'studies'

 

[Felk]

Keeping your hair with a little bit of regrowth by using finasteride which lowers DHT, increases T and Estradiol. Changing the ratio of androgens, decreasing NOS activity in penis, lower libido etc... You must be very desperate to use finasteride!

Kindly reply to PowerSam's point, if you would be so kind...

 

[Thinning]

BTW Using Arginine for ED may be a good short term solution, but it causes a prolactin release, which will kill your libido. Over time, you may still get rock hard erections, but will have litle desire for sex.

Do searches on Arginine and Prolactin and see for yourself.