49 replies to this topic

[TheFountain]

Taking something like saw palmetto would prevent DHT binding in multiple receptor sites and in the prostate without causing infertility by blocking circulating estradiol concentrations at the same time.

First I've heard that S.P. blocks estradiol. Do you have a reference handy for that?

It reduces the effect of the aromatase enzyme which makes testosterone aromatizable to estradiol.

[seekonk]

Taking something like saw palmetto would prevent DHT binding in multiple receptor sites and in the prostate without causing infertility by blocking circulating estradiol concentrations at the same time.

First I've heard that S.P. blocks estradiol. Do you have a reference handy for that?

It reduces the effect of the aromatase enzyme which makes testosterone aromatizable to estradiol.

Maybe, but what I'm asking is whether you have a reliable reference handy for that. I have been unable to find a believable reference on S.P. as an AI. The fact that some guys get gynecomastia from S.P. makes me think that it cannot be a very good AI, if at all.

Edited by seekonk, 22 June 2009 - 05:07 PM.

[TheFountain]

Taking something like saw palmetto would prevent DHT binding in multiple receptor sites and in the prostate without causing infertility by blocking circulating estradiol concentrations at the same time.

First I've heard that S.P. blocks estradiol. Do you have a reference handy for that?

It reduces the effect of the aromatase enzyme which makes testosterone aromatizable to estradiol.

Maybe, but what I'm asking is whether you have a reliable reference handy for that. I have been unable to find a believable reference on S.P. as an AI. The fact that some guys get gynecomastia from S.P. makes me think that it cannot be a very good AI, if at all.

With the correlative effect of the following study, one can conclude that DHT production is successfully blocked while not incurring any other unwanted, major side effects, such as impotence probably by the mechanism I mentioned earlier.

A well-designed and conducted multicenter study" on the treatment of BPH was published in 1996. The 1098-patient study was conducted in nine European countries with the participation of an American biostastistician. In the study the subjects were given 320 mg Permixon (a preparation of saw palmetto berry extracts)/day or 5 mg finasteride/day for 6 months, under double-blind randomly assigned conditions. Both Permixon and finasteride caused substantial decrease in the International Prostate Symptom Score (-37% and -39%, respectively), improved quality of life (38% and 41%, respectively), and increased peak urinary flow rate (25% and 30%, , respectively). The researchers stated that "Permixon fared better than finasteride in a sexual function questionnaire and gave rise to less complaints of decreased libido and impotence" than fmasteride. However, finasteride differ from Permixon in that Permixon did not decrease prostate volume and serum prostate-specific antigen. Those conclusions are correct. These difference are important in that there is no possibility for saw palmetto berry or its extract to interfere with prostate cancer detection by lowering serum PSA level. The lack of effect on prostate volume does not necessarily indicate that saw palmetto berry or its extract is ineffective on treating LUTS. Two meta-analyses on the treatment of BPH with a preparation of saw palmetto berry extract were published in 1998. Wilt et al.6 reviewed 18 randomized controlled trials involving 2939 men, including the study mentioned above. The mean study duration was 9 weeks (range: 4 to 48 weeks). As compared with men receiving placebo, treatment with the saw palmetto berry extract caused a decrease in urinary tract symptom scores of 1.41 points (scale range: 0 to 19) and nocturia of 0.76 times, an increase in peak urine flow of 1.93 mL/second, and improvements in subjective self-rating of urinary tract symptoms. In many important aspects, Permixon yielded benefits that are practically not different from the benefits of finasteride, e.g., in International Prostate Symptom Score (the different being 0.37 out of 0 to 35 scale range). As compared to placebo, patients taking saw palmetto had decreased nocturia (weighted mean difference {WMD) -1.41 points {scale 0.76 times per evening) and increased peak urine flow (WMD, 1.93 ml/s). When compared to finasteride, men treated with saw palmetto had similar improvements in peak urine flow (WMD, 0.74 ml/s) and improvements in urinary tract symptom s cores (WMD 0.37 International Prostate Symptom Score points {scale range, 0-25}). These meta-analysts concluded that "the evidence suggests that S repens improves urological symptoms and flow measures. Compared with finasteride, S repens produces similar improvement in urinary tract symptoms and urinary flow and was associated with fewer adverse treatment events." This conclusion should be accepted with the following reservations: stating that the saw palmetto berry/its preparation is comparably as effective as fmasteride in treating BPH/LUTS may be an understatement (see, Bach, Schmitt and Ebeling'a (1996) a 3-year, 309 patient trial, saw palmetto was shown to improve objective urinary flow rate and subjective symptoms substantially, and a 50% in postvoid volume, whereas finasteride improved the flow rate only slightly and did not improved the post void volume. Wilt, et al., also stated that "further research is needed.. .to determine its long-term effectiveness and ability to prevent BPH complications." That statement is in error because one of the reviewed studies, Carraro et al.'s", was 6 months long, involving 87 urological centers in 9 European countries with 1098 patients. The patient base is greater than one-third of the total number of patients reviewed by the authors. In all senses, a study that lasted 6 months is a long term study. If a drug or nutrient does not show its effects in 6 months, it must be considered ineffective. On the other hand if efficacy is properly demonstrated within this period, as is the case of Carraro et al.'s study, (IPPS scores -37% and -39%, respectively; improved quality of life (by 38 and 41%, respectively); and increased urinary peak flow (+25% and +30%, p =0,035)) the efficacy must be accepted. . In Bach's 3-year study the patients enrolled in that multicenter study experienced increased urinary flow rate to 6.1 ml/s with a 50% decrease in residual urine volume (from 64 +2.3 ml to 32 + 2.0 ml; mean + SEM) while taking saw palmetto versus only a slight improvement in urine flow and no change in residual volume while taking finasteride.

Furthermore, the results of Bach's study demonstrate a sustained effect of saw palmetto which is posited for initial treatment of BPH with milder symptoms without complications. Saw palmetto is advised for mild to moderate BPH. In accordance with the United States Department of Health and Human Services Guidelines for Benign Prostatic Hyperplasia: Diagnosis and Treatment, patients with BPH complications (e.g., recurrent infection, urinary retention, renal failure, gross hematuria, bladder stones and bladder diverticuli) should always seed surgical consults (McConnell JD. Benign prostatic hyperplasia: treatment guidelines and patient classification. Br J Urol 1995;76 (Suppl) 29-46).

In clinical trials with therapeutic agents, the requirement of a trial duration greater than 6 months has hardly been required. Fitzpactrick and Lynch14 believe that in clinical trials it took 3 to 6 months to develop placebo effects. Carrarro's study demonstrated that a preparation of saw palmetto berry extracts (Permixon) is practically as effective as a "proven" and "approved" drug finasteride in treating BPH. If finasteride is acceptable as safe and effective, then this saw palmetto berry extract preparation must be accepted as safe and effective, even though a placebo group was not used in the study.

Published in the same year is the report of the Committee on Other Medical Therapies of the Fourth International Consultation.15 The 7 studies reviewed by this committee were also a part of the database that was reviewed by Wilt et al. The Committee stated that "the placebo-controlled studies are the ones being examined in this paper... Seven placebo-controlled studies with Permixon have been published, with the longest duration being 3 months... Only four of these included more than 50 patients in each study; in three of these trials, Permixon was statistically significant better than placebo in terms of effects on urinary frequency (nocturia and daytime) as well as peak flow rate. Peak flow rate improved by 26-50% in the Permixon patients, but only 2-35 % in the placebo-treated patients. The over-all symptom improvement demonstrated in the placebo-controlled trials was a reduction of baseline nocturia by 33-74% with Permixon compared to 13-39% with placebo."

The Committee drew heavily on Descotes' study16 and stated: "In the study of Descotes ... there was statistically significant improvement in frequency, nocturia, and flow rate. However, the same study showed that 'despite this evidence of symptomatic improvement, there was little difference between either the patients' or the physicians' global assessments of the efficacy of Permixon and placebo.' Patients satisfaction was 71% for Permixon and 68% for placebo (P> 0.05, NS), while the physicians' assessments were 57% for Permixon and 47% for placebo (P> 0.05, NS). Thus, the symptomatic improvement seen with Permixon after I month of treatment, although statistically significant, was felt to be of limited overall clinical significance by the patients with BPH in this study. Clearly, no definitive conclusions can be drawn from these aforementioned studies concerning Permixon since they were all short-term with a maximum duration of 3 months...." Those conclusions are not justified and the Committee have apparently overlooked some unique experimental procedures that might have contributed to the large improvements in the subjective scores of the placebo group. The extremely large placebo effects (68% and 47%) observed in the Descotes' study require careful examination of the study procedures to ascertain whether these data are acceptable. In most clinical trials, placebo effects range between 0% to 35 %. The Descotes et al.'s study is unique in that the researchers wanted to minimize placebo effect by having the patients to go through a base-line, placebo run-in period of 30 days. Only patients showing <30% improvement from base-line in peak urinary flow rate ("the nonresponding patient") were selected for the placebo-controlled study. Dr. Lin's experience as research scientist indicates that this type placebo run-in base-line period can cause exaggerated placebo effects in the subsequent actual study. This is probably due to the fact that patients in both treated and placebo groups somehow realized that they were entering a more important or more serious study period, and their mind subconsciously worked on the matter. Thus, the large placebo effect of the subjective assessment of the placebo group and treated group should be both discounted.

The more objective measurements of daytime and nocturnal urinary frequency and peak flow rate should be depended upon to make conclusions. In these cases, both objective parameters improved significantly with the saw palmetto berry preparation in comparison with the placebo group. (Although one can counter argue that frequency of urination and the urine flow rate are subject to the control of the mind to certain degrees and are thus not objective parameters, this argument cannot prevail because these functions, like most other bodily functions, are primarily physiologically controlled and not psychologically controlled. If one stretches psychosomatic interactions to the extreme, then all objective physiological measurements could be called subjective measurements. But such extremism is not the standard practice in biomedical sciences.) Thus, a definitive conclusion can be made that the saw palmetto berry preparation was at least effective for short term (30 days) treatment of BPH.

Critics of phytotherapy of BPH have relied heavily on the placebo effect to argue that the efficacy observed in open-label studies, which are often short term, should be discounted. Meta-analysts, including Fitzpactrick and Lynch12, and Schulze et al.'' are of the opinion that placebo effects of drug trials on BPH could occur as early as 3 to 6 months and last for at least 2 years. Such an argument has tow problems. Firstly, before the 4th month, placebo effects would be assumed to be nonexistence or small. The Descotes' data clearly do not support this contention. Secondly, had placebo effect be so long lasting and so powerful, then many placebos would be potent and long lasting drugs for BPH and patients of BPH would benefit from various placebos, This is certainly not the experience of patients of BPH and urologists. In reality, the placebo effect has sometimes been unscientifically used as a weapon to attack the results that are not consistent with the critics opinions.

Many other studies on the mitigating effects of saw palmetto berries or its preparations were not blinded and placebo-controlled and were not reviewed by these authors. Nevertheless, these studies can provide highly valuable information on the efficacy and safety of these substances and are discussed below.

http://www.sawpalmet...ttostudy02.html

[seekonk]

Taking something like saw palmetto would prevent DHT binding in multiple receptor sites and in the prostate without causing infertility by blocking circulating estradiol concentrations at the same time.

First I've heard that S.P. blocks estradiol. Do you have a reference handy for that?

It reduces the effect of the aromatase enzyme which makes testosterone aromatizable to estradiol.

Maybe, but what I'm asking is whether you have a reliable reference handy for that. I have been unable to find a believable reference on S.P. as an AI. The fact that some guys get gynecomastia from S.P. makes me think that it cannot be a very good AI, if at all.

With the correlative effect of the following study, one can conclude that DHT production is successfully blocked while not incurring any other unwanted, major side effects, such as impotence probably by the mechanism I mentioned earlier.

No, it does not follow at all from this study that S.P. is an A.I. Did you just invent that hypothesis yourself?

Edited by seekonk, 22 June 2009 - 05:52 PM.

[TheFountain]

Taking something like saw palmetto would prevent DHT binding in multiple receptor sites and in the prostate without causing infertility by blocking circulating estradiol concentrations at the same time.

First I've heard that S.P. blocks estradiol. Do you have a reference handy for that?

It reduces the effect of the aromatase enzyme which makes testosterone aromatizable to estradiol.

Maybe, but what I'm asking is whether you have a reliable reference handy for that. I have been unable to find a believable reference on S.P. as an AI. The fact that some guys get gynecomastia from S.P. makes me think that it cannot be a very good AI, if at all.

With the correlative effect of the following study, one can conclude that DHT production is successfully blocked while not incurring any other unwanted, major side effects, such as impotence probably by the mechanism I mentioned earlier.

No, it does not follow at all from this study that S.P. is an A.I. Did you just invent that hypothesis yourself?

I agree that more studies are needed, but from the studies indicated thus far one can extrapolate a conclusion that saw palmetto is a possible androgen and DHT inhibitor.

I can't believe you are arguing on the basis of incomplete studies when so many people on this web site base half their supplement and dietary regimen on incomplete data.

Edited by TheFountain, 22 June 2009 - 06:50 PM.

[seekonk]

Taking something like saw palmetto would prevent DHT binding in multiple receptor sites and in the prostate without causing infertility by blocking circulating estradiol concentrations at the same time.

First I've heard that S.P. blocks estradiol. Do you have a reference handy for that?

It reduces the effect of the aromatase enzyme which makes testosterone aromatizable to estradiol.

Maybe, but what I'm asking is whether you have a reliable reference handy for that. I have been unable to find a believable reference on S.P. as an AI. The fact that some guys get gynecomastia from S.P. makes me think that it cannot be a very good AI, if at all.

With the correlative effect of the following study, one can conclude that DHT production is successfully blocked while not incurring any other unwanted, major side effects, such as impotence probably by the mechanism I mentioned earlier.

No, it does not follow at all from this study that S.P. is an A.I. Did you just invent that hypothesis yourself?

I agree that more studies are needed, but from the studies indicated thus far one can extrapolate a conclusion that saw palmetto is a possible androgen and DHT inhibitor.

I agree with you that it is quite likely based on the evidence that S.P. inhibits DHT formation and/or androgens. However, being a DHT/androgen inhibitor is a far cry from being an aromatase inhibitor - for the latter claim, I have seen no evidence at all, and you are the first person I have ever seen suggesting it.

I can't believe you are arguing on the basis of incomplete studies when so many people on this web site base half their supplement and dietary regimen on incomplete data.

Your hypothesis that S.P. is an AI is not supported by incomplete data. It is, as far as I can tell, supported by no data.

Edited by seekonk, 22 June 2009 - 07:03 PM.

[TheFountain]

Taking something like saw palmetto would prevent DHT binding in multiple receptor sites and in the prostate without causing infertility by blocking circulating estradiol concentrations at the same time.

First I've heard that S.P. blocks estradiol. Do you have a reference handy for that?

It reduces the effect of the aromatase enzyme which makes testosterone aromatizable to estradiol.

Maybe, but what I'm asking is whether you have a reliable reference handy for that. I have been unable to find a believable reference on S.P. as an AI. The fact that some guys get gynecomastia from S.P. makes me think that it cannot be a very good AI, if at all.

With the correlative effect of the following study, one can conclude that DHT production is successfully blocked while not incurring any other unwanted, major side effects, such as impotence probably by the mechanism I mentioned earlier.

No, it does not follow at all from this study that S.P. is an A.I. Did you just invent that hypothesis yourself?

I agree that more studies are needed, but from the studies indicated thus far one can extrapolate a conclusion that saw palmetto is a possible androgen and DHT inhibitor.

I agree with you that it is quite likely based on the evidence that S.P. inhibits DHT formation and/or androgens. However, being a DHT/androgen inhibitor is a far cry from being an aromatase inhibitor - for the latter claim, I have seen no evidence at all, and you are the first person I have ever seen suggesting it.

I can't believe you are arguing on the basis of incomplete studies when so many people on this web site base half their supplement and dietary regimen on incomplete data.

Your hypothesis that S.P. is an AI is not supported by incomplete data. It is, as far as I can tell, supported by no data.

Well the incomplete data tells us two things, that possibly through some type of androgen manipulation DHT production is stopped, but the mechanism of this androgen manipulation is unknown, since aromatase converts androgen to estrogen it is definitely possible that this is the root mechanism involved, hence why saw palmetto is often recommended for infertility. You are correct in that I did 'suggest' this. It would be amazing if it were true that this herb can both block DHT and the production of estradiol at the same time. The studies thus far conducted as well as anecdotal evidence suggests that maybe it can. Exactly how is a matter of more studies.

Edited by TheFountain, 22 June 2009 - 08:24 PM.

[seekonk]

Well the incomplete data tells us two things, that possibly through some type of androgen manipulation DHT production is stopped, but the mechanism of this androgen manipulation is unknown, since aromatase converts androgen to estrogen it is definitely possible that this is the root mechanism involved, ...

I think you are confusing your enzymes. Aromatase does not produce DHT. The enzyme that produces DHT from testosterone is 5α-reductase, and it is possible, indeed likely, that this enzyme is blocked by S.P. But this enzyme is different from the aromatase enzyme that produces estrogens from testosterone.

[TheFountain]

Well the incomplete data tells us two things, that possibly through some type of androgen manipulation DHT production is stopped, but the mechanism of this androgen manipulation is unknown, since aromatase converts androgen to estrogen it is definitely possible that this is the root mechanism involved, ...

I think you are confusing your enzymes. Aromatase does not produce DHT. The enzyme that produces DHT from testosterone is 5α-reductase, and it is possible, indeed likely, that this enzyme is blocked by S.P. But this enzyme is different from the aromatase enzyme that produces estrogens from testosterone.

I did not say aromatase produced DHT I said it converted Androgen to estrogen. I was just contemplating whether or not there was a link between this and the reason saw palmetto blocks both androgen and DHT. Maybe it is possible it blocks, or at least in some way manipulates, both 5A-reductase and aromatase.

[seekonk]

Well the incomplete data tells us two things, that possibly through some type of androgen manipulation DHT production is stopped, but the mechanism of this androgen manipulation is unknown, since aromatase converts androgen to estrogen it is definitely possible that this is the root mechanism involved, ...

I think you are confusing your enzymes. Aromatase does not produce DHT. The enzyme that produces DHT from testosterone is 5α-reductase, and it is possible, indeed likely, that this enzyme is blocked by S.P. But this enzyme is different from the aromatase enzyme that produces estrogens from testosterone.

I did not say aromatase produced DHT I said it converted Androgen to estrogen. I was just contemplating whether or not there was a link between this and the reason saw palmetto blocks both androgen and DHT. Maybe it is possible it blocks, or at least in some way manipulates, both 5A-reductase and aromatase.

You are just digging yourself in deeper. Are you sure this

saw palmetto blocks both androgen and DHT

is what you want to say?

[TheFountain]

Well the incomplete data tells us two things, that possibly through some type of androgen manipulation DHT production is stopped, but the mechanism of this androgen manipulation is unknown, since aromatase converts androgen to estrogen it is definitely possible that this is the root mechanism involved, ...

I think you are confusing your enzymes. Aromatase does not produce DHT. The enzyme that produces DHT from testosterone is 5α-reductase, and it is possible, indeed likely, that this enzyme is blocked by S.P. But this enzyme is different from the aromatase enzyme that produces estrogens from testosterone.

I did not say aromatase produced DHT I said it converted Androgen to estrogen. I was just contemplating whether or not there was a link between this and the reason saw palmetto blocks both androgen and DHT. Maybe it is possible it blocks, or at least in some way manipulates, both 5A-reductase and aromatase.

You are just digging yourself in deeper. Are you sure this

saw palmetto blocks both androgen and DHT

is what you want to say?

What I was trying to articulate earlier is the possibility that it blocks both enzymes. I admit I am still learning about this stuff ( and thus my terminology suffers a little as a result), but instead of coming off as combative just try to entertain the 'what if' principle. What if the effects of both enzymes are blocked by this supplement through different mechanisms?

Also, I know I have the virtue of thinking outside the box on this subject since I have not dedicated my life to it, I am not sure if that's a good or a bad thing. I think you know all this and are being a little condescending therefor, thinking I know nothing, which is not the case.

Edited by TheFountain, 23 June 2009 - 01:35 PM.

[TheFountain]

Well the incomplete data tells us two things, that possibly through some type of androgen manipulation DHT production is stopped, but the mechanism of this androgen manipulation is unknown, since aromatase converts androgen to estrogen it is definitely possible that this is the root mechanism involved, ...

I think you are confusing your enzymes. Aromatase does not produce DHT. The enzyme that produces DHT from testosterone is 5α-reductase, and it is possible, indeed likely, that this enzyme is blocked by S.P. But this enzyme is different from the aromatase enzyme that produces estrogens from testosterone.

I did not say aromatase produced DHT I said it converted Androgen to estrogen. I was just contemplating whether or not there was a link between this and the reason saw palmetto blocks both androgen and DHT. Maybe it is possible it blocks, or at least in some way manipulates, both 5A-reductase and aromatase.

You are just digging yourself in deeper. Are you sure this

saw palmetto blocks both androgen and DHT

is what you want to say?

On another note here is a quote from you earlier:

'I agree with you that it is quite likely based on the evidence that S.P. inhibits DHT formation and/or androgens.'

So why would I not have meant to say that? I openly admit I am not as versed on this subject as some other people here, but I think I have a minor grasp on some of the principles. I am still learning. Playing mind games with me is not going to move this forward.

Edited by TheFountain, 23 June 2009 - 01:32 PM.

[seekonk]

Well the incomplete data tells us two things, that possibly through some type of androgen manipulation DHT production is stopped, but the mechanism of this androgen manipulation is unknown, since aromatase converts androgen to estrogen it is definitely possible that this is the root mechanism involved, ...

I think you are confusing your enzymes. Aromatase does not produce DHT. The enzyme that produces DHT from testosterone is 5α-reductase, and it is possible, indeed likely, that this enzyme is blocked by S.P. But this enzyme is different from the aromatase enzyme that produces estrogens from testosterone.

I did not say aromatase produced DHT I said it converted Androgen to estrogen. I was just contemplating whether or not there was a link between this and the reason saw palmetto blocks both androgen and DHT. Maybe it is possible it blocks, or at least in some way manipulates, both 5A-reductase and aromatase.

You are just digging yourself in deeper. Are you sure this

saw palmetto blocks both androgen and DHT

is what you want to say?

So why would I not have meant to say that?

Because you say it as if it has something to do with aromatase. Aromatase blocks neither androgens or DHT.

[TheFountain]

Well the incomplete data tells us two things, that possibly through some type of androgen manipulation DHT production is stopped, but the mechanism of this androgen manipulation is unknown, since aromatase converts androgen to estrogen it is definitely possible that this is the root mechanism involved, ...

I think you are confusing your enzymes. Aromatase does not produce DHT. The enzyme that produces DHT from testosterone is 5α-reductase, and it is possible, indeed likely, that this enzyme is blocked by S.P. But this enzyme is different from the aromatase enzyme that produces estrogens from testosterone.

I did not say aromatase produced DHT I said it converted Androgen to estrogen. I was just contemplating whether or not there was a link between this and the reason saw palmetto blocks both androgen and DHT. Maybe it is possible it blocks, or at least in some way manipulates, both 5A-reductase and aromatase.

You are just digging yourself in deeper. Are you sure this

saw palmetto blocks both androgen and DHT

is what you want to say?

So why would I not have meant to say that?

Because you say it as if it has something to do with aromatase. Aromatase blocks neither androgens or DHT.

I was referring to the possibility that estradiol production was slowed down somehow through an androstenedione-estrone-testosterone-estradiol deficit effect and that the result was a lack of estradiol and change in overall DHT volume, and that perhaps this is the mechanism that allows the herb to block DHT while also not promoting impotance as a side effect (sorry if that was confusing, I 'think' I know what I am talking about, let me know if this makes any sense to you! Me=Still a student). Maybe 'block' was not the right term, if I did use it to connect the dots earlier.

Edited by TheFountain, 23 June 2009 - 09:10 PM.

[hamishm00]

On the resveratrol & testosterone point: trans-Resveratrol relaxes the corpus cavernosum ex vivo and enhances testosterone levels and sperm quality in vivo

1: Arch Pharm Res. 2008 Jan;31(1):83-7.Links
trans-Resveratrol relaxes the corpus cavernosum ex vivo and enhances testosterone levels and sperm quality in vivo.Shin S, Jeon JH, Park D, Jang MJ, Choi JH, Choi BH, Joo SS, Nahm SS, Kim JC, Kim YB.
College of Veterinary Medicine, Chungbuk National University, Heungdeok-gu, Cheongju, Chungbuk 361-763, Korea.

We examined the effects of trans-resveratrol on male reproductive functions; ex-vivo penile erection and in-vivo sperm counts and quality. For the ex-vivo study, the relaxation effects of resveratrol on isolated New Zealand white rabbit corpus cavernosum, precontracted by phenylephrine (5x10(-5) M) were measured. The in-vivo study measured reproductive organ weights, blood testosterone levels, testicular histopathology, sperm counts, as well as the epididymal sperm motility and deformity of male ICR mice given an oral dose of resveratrol (50 mg/ kg) for 28 days. Resveratrol elicited a concentration-dependent relaxing effect on corpus cavernosum, leading to a median effective concentration (EC50) of 0.29 mg/mL. Repeated treatment with resveratrol (50 mg/kg) did not cause an increase in body weight, reproductive organ weight or testicular microscopic findings; however, resveratrol did elicit an increase in blood testosterone concentration, testicular sperm counts and epididymal sperm motility by 51.6%, 15.8% and 23.3%, respectively, without influence on sperm deformity. In conclusion, we propose that resveratrol has a positive effect on male reproductive function by triggering a penile erection, as well as enhancing blood testosterone levels, testicular sperm counts, and epididymal sperm motility.

PMID: 18277612 [PubMed - in process]

[Johann]

The shampoo Nizoral works great. It has been proven to affect hair growth. Google it.

[1kgcoffee]

What do you guys think about the safety and efficacy of saw palmetto and beta sitosterol for hair loss? I'm starting to notice some thinning and I think finasteride is a little too hardcore.

[hamishm00]

I think it's worth a shot.

I also use nisim shampoo and extract, and I add additional saw palmetto extract to the nisim extract for topical application - twice a day.

I also take saw palmetto caps twice daily.

Anecdotally, it's very very effective.

[JLL]

I think it's worth a shot.

I also use nisim shampoo and extract, and I add additional saw palmetto extract to the nisim extract for topical application - twice a day.

I also take saw palmetto caps twice daily.

Anecdotally, it's very very effective.

Before/after pics?

[osris]

I wish this thread hadn't gone off topic. I'd like the OP's original post to be answered. What supplements cause hair loss, rather than what supplements stop hair loss?