Need a big favor. S Foote's theory in a nutshell?

[wookster]

Interesting...

http://www.pnas.org/cgi/content/full/99/11/7408

Vitamin E succinate inhibits the function of androgen receptor and the expression of prostate-specific antigen in prostate cancer cells

http://www.hairloss-research.org/vitamine.html

Out of prostate research comes some interesting findings about Vitamin E Succinate that could have possible implications for male pattern loss, which is largely mediated by the same hormonal factors implicated in prostate enlargement and prostate cancer. It was only the succinate version of vitamin E that produced these specific effects, which is inexpensive and widely available.

 

[wookster]

Some more info about the possible importance of DHT, even if it is not from PubMed :salut: nfire: :salut:

http://www.mesomorphosis.com/articles/arnold/dht.htm

I have heard several anecdotal reports of individuals who have stacked testosterone with proscar (a 5-AR inhibitor) and have noticed significantly reduced performance enhancement effects. What’s going on here? We know it couldn’t be due to the inhibition of the direct anabolic activity of testosterone on muscle anabolism. Most likely it is due to the reduction of androgenic effects in other parts of the body that contribute to the ergogenic effects, specifically the CNS, which is stimulated by androgens to increase neural output leading to greater strength and greater recoverability. Another possibility is a reduction in the production of androgen dependent liver growth factors (such as IGF-1), since DHT is an important androgen in the liver.

 

[wookster]

Dihydrotestosterone appears to have special importance and functions in adult humans?

http://circ.ahajournals.org/cgi/content/full/98/3/256

Androgen Receptors Mediate Hypertrophy in Cardiac Myocytes

[...]

A surprising, highly reproducible finding was that the testosterone metabolite dihydrotestosterone was able to increase ANP secretion, but testosterone was without effect. Although it is well established that various organs have differential responsiveness to testosterone and dihydrotestosterone, it is unusual for the markers of hypertrophy, amino acid incorporation into protein, and ANP secretion to be uncoupled. This finding suggests that distinct testosterone and dihydrotestosterone receptor isoforms may be present in myocytes that are identical in the region identified by PCR but have both shared and distinct effects on transcription of specific genes. There is precedent for differential tissue response to dihydrotestosterone but not to testosterone: prostate and perineum.

Clinical Implications
There are at least three pertinent areas in which these findings may have clinical implications. First, androgens have a direct growth-promoting effect on the heart, and as such, probably account at least in part for the difference in cardiac mass between men and women, even after other factors are controlled for. We demonstrate that androgen receptors are present in both infant and adult human heart of both sexes, conditions necessary for hypertrophic responses to androgens of children and adults.

[...]

In summary, we have demonstrated that mammalian cardiac myocytes from hearts of both sexes express the androgen receptor gene. Androgens are capable of mediating a hypertrophic response of cultured adult myocytes of a magnitude nearly that of the most efficacious hypertrophic stimuli identified for heart. Androgens must be considered among the neuroeffectors, paracrine factors, and hormones that act directly on the cardiac myocyte and regulate the cardiac hypertrophic response.

 

[Bryan]

Haven't you even been READING Stephen Foote's material for the last several months and years?? He doesn't deny the importance of androgens/androgen receptors in balding (and the value of antiandrogens), it's just that he thinks they affect balding by a different, more indirect route than what the rest of us normal, sane people think. He thinks that androgens (and antiandrogens) influence that "poor lymphatic drainage" that he blames for male pattern baldness. Did you really not understand that, even after THOUSANDS of posts on that subject from Stephen Foote?? :freaked:

Mr. Foote hardly ever talks about the molecular machinery invovled with the hair follicle itself. If my interpretation is correct, he doesn't deny the "importance" of androgen receptors but since his idea is one of lymphatic stagnation due to the hydraulic differrential existing in beard region and scalp region, the androgen receptors get upregulated as nature's way of maintaining DHT production. According to Foote, DHT has no direct effect on hair follicles with regards to the miniaturization process. DHT is a lymphatic-pump enhancer

Ahh...so I guess you HAVE been reading Mr. Foote's previous posts. If that's the case, then I'm asking you again: how does that information you posted previously about KD and androgen receptor polymorphisms supposedly "put another nail in the coffin" of Stephen Foote's theory?? Stephen would simply reply in his usual fashion by saying that the androgen receptor alteration in KD helps preserve hair by effectively reducing the androgenic stimulation, which in turn improves the lymphatic drainage from the scalp, etc.

 

[docj077]

Actually, DHT is not needed.

I don't trust doctors. Never have, never will

Fine by me. It will be shame one day when you're forced to trust someone that you thought you'd never have to trust, because you won't have a choice.

Everyone is humbled by their health one day.


Again, DHT is NOT needed.

 

[michael barry]

"Everyone is humbled by their health one day. "


Brother ain't that the fuckin' truth. All of us older guys can relate to that.............................you dont believe it when you twenty, but even if you pump iron and eat right and all that shitt.............age hits you. Sore in the morning, joints popping on the way to the bathroom for your morning shower, aches and pains, back injuries, muscle pulls, eyesight weakening. Ageing is God's way of kicking us in the balls. Its second only to premature baldness in unfairness.

 

[michael barry]

Wook,


Here is some kind of "frizz control" spray product with tocopherol succinate in it, http://www.amazon.com/Fx-Shine-Weightle ... B000RYSSU8



Be interesting to buy some tocopherol succinate and see if it reduced some of YOUR body hair Wook. If it did (take about three months), you could report back to us that you found a winning receptor blocker that we could buy cheap.................

 

[michael barry]

Doctor,


Have to ask since you and Wook disagree a good deal about DHT........................are you back on finasteride? I remember you mentioned you got off of it for some reason the first time you were on it due to your response to it. Have you convictions changed towards it?

 

[michael barry]

Damn Wook, you left out the best parts:


"The University of Rochester researchers used an androgen-dependent human prostate cancer cell line to find out how vitamin E succinate prevents and combats cancer. In one experiment, vitamin E succinate was compared to the antiandrogen drug flutamide. While the addition of flutamide largely failed to combat growth stimulated by the addition of the androgen dihydrotestosterone (DHT), vitamin E succinate proved to be successful. However, when both compounds were added, a further repressing of DHT-mediated cell growth was observed. When tumor cells were replaced with cell cultures from normal prostate tissue, the same amount of vitamin E succinate only slightly inhibited cell growth, suggesting that the vitamin may selectively inhibit tumor cells that are androgen sensitive.
In another experiment that sought to determine the effect of vitamin E succinate on prostate specific antigen (PSA), a marker for prostate cancer, PSA expression was induced by the addition of DHT to the cell culture. When vitamin E was added, intracellular and secreted levels of PSA expression were repressed. This occurred together with down-regulation of androgen receptor protein levels. The androgen receptor is required for the initiation and progression of prostate cancer and Male Pattern Hair Loss. The authors write that vitamin E succinate may suppress the growth of prostate cancer and the expression of PSA "by inhibiting androgen receptor expression at both the transcription and translation levels." An oral dose of 800 i.u.'s would be appropriate to produce these effects"




Oral my ***...........................Im thinking topical. BRYAN?

It OUTDID FLUTAMIDE Bryan........................any remarks? Hell it wouldn't hurt to test it on a patch of body hair.





BTW-----gents I concluded my peppermint oil/distilled water experiment and my green tea topical extract experiment. Both reduced beard hair. Its hard to say, but I think the peppermint oil was a little more effective though. There is a guy on here putting peppermint oil on half his moustache. He has already noted the effect and sent me a picture of reduced growth there. In another month, he really might have some impressive pics. Like Ive said before, I'd be shocked if there wasn't a compound out there in nature that didn't bind with the human androgen receptor, be it a curcumoid, spearmint or peppermint sub-chemical, some fat sterol or plant extract.

 

[wookster]

Again, DHT is NOT needed.

:? eace: :?


Does Dihydrotestosterone have necessary functions in adult humans or not?

 

[wookster]

Be interesting to buy some tocopherol succinate and see if it reduced some of YOUR body hair Wook. If it did (take about three months), you could report back to us that you found a winning receptor blocker that we could buy cheap.................

How much topically applied vitamin E succinate would get to the hair follicle where it is needed? Vitamin C is supposed to help vitamin E in some way if I recall.

What is the optimal dose of vitamin E succinate as a supplement?

http://www.annals.org/cgi/content/full/ ... 40-00110v1

High-Dosage Vitamin E Supplementation May Increase All-Cause Mortality
Edgar R. Miller, III, MD, PhD; Roberto Pastor-Barriuso, PhD; Darshan Dalal, MD, MPH; Rudolph A. Riemersma, PhD, FRCPE; Lawrence J. Appel, MD, MPH; and Eliseo Guallar, MD, DrPH

4 January 2005 | Volume 142 Issue 1


Background: Experimental models and observational studies suggest that vitamin E supplementation may prevent cardiovascular disease and cancer. However, several trials of high-dosage vitamin E supplementation showed non–statistically significant increases in total mortality.

 

[wookster]

...how does that information you posted previously about KD and androgen receptor polymorphisms supposedly "put another nail in the coffin" of Stephen Foote's theory?? Stephen would simply reply in his usual fashion by saying that the androgen receptor alteration in KD helps preserve hair by effectively reducing the androgenic stimulation, which in turn improves the lymphatic drainage from the scalp, etc.

http://www.mesomorphosis.com/articles/p ... lation.htm

"Regulation" of a receptor refers to control over the number of receptors per cell. "Sensitivity," in contrast, refers to the degree of activity each receptor has. It is a possible in many cases for the receptors of a cell to be sensitized or desensitized to a drug or hormone, independently of the number of receptors. Similarly, it is possible for the receptors to upregulate or downregulate, to increase or decrease in number, independently of any changes in sensitivity.

If sensitivity remains the same, then upregulation will yield higher response to the same amount of drug or hormone, and downregulation will result in less response.

Sensitivity and regulation are two different processes; regulation can be explained by Foote's theory but sensitivity cannot. There is less incidence of male pattern baldness in men with KD but some of them still have male pattern baldness.

That means that even the downregulated ARs are still sensitive to androgens. Sensitivity is caused by a direct effect of androgens. Mr. Foote says that male pattern baldness can only be caused by an indirect effect.

Not really a nail in the coffin of Foote's theory though... :ninja: aranoid: :alien:

 

[michael barry]

On this,
"Background: Experimental models and observational studies suggest that vitamin E supplementation may prevent cardiovascular disease and cancer. However, several trials of high-dosage vitamin E supplementation showed non–statistically significant increases in total mortality."




..................."non-statistically signifigant increases in mortality"...............


First, was it tocopherol succinate or another tocopherol like tocopherol acetate?


Tocopherol is in revivogen, tricomin shampoo and conditioner, crinagen, and I think its in folligen. Its an anti-oxidant. I believe just plain tocopherol has been associated with a lessening of receptor activity in some little critter or cell assay or another like B6, has but it really isn't concrete proven in humans to my knowledge. B6 is in both revivogen and crinagen.



Second, and most importantly in my opinion..................Bryan's recipie for topical spironolactone was for something like 3%. Minoxidil originally came in 2%. The topical melatonin experiment you cited was something like .1%. I dont know if tocopherol succinate would make it though the skin or not, that anti-frizz spray notwithstanding. If we can find a topical product meant to penetrate the dermis with tocopherol succinate in it, it might. It probably can be gotten through the skin with a vehicle almost surely though. If you bought some and mixed it at a one-to-twenty ratio with a purified water/alcohol mix or a cream mix and put it on the hair on your wrist for three months, and it reduced the hair......................but started to give you an odd ugly discoloration in the skin, something might be amiss. This would only be a five percent solution. Its hard to imagine that this would be harmful. We'd never know until we tried.

I DID find a nasal spray with tocopherol succinate in a google search.






Thirdly, I see you and Doctor just plain disagree about DHT. But do you consider the type two DHT made in hair follilces and the prostate utterly essential? I know type one alpha five reductase is in our brain, deeper tissues, and chest and back skin.........................but seeing that type 2 is only in hair and prostate tissue if I remember correctly, its hard to imagine that its absence would be just utterly disastorous. I mean we do have those men born without it and they supposedly live happy lives with less acne and no baldness and less body hair. We know DHT is almost not active at all in muscle tissue because of 3AR deactivating it. We know globulin binds DHT in the bloodstream all but roughly one percent of the time, and we know men on proscar for the most part seem Okey Dokey with it. If there is an effect, it must be subtle and take years to manifest itself. If you are worried about sex drive, let me put that to rest. Im as randy a rascal (still!) as I was in my late 20's. Im not what I was at 18 or anything, but that was ridiculous. Im glad I dont wake up pointing to the north star every morning anymore as that was a pain in the *** anyway. [/quote]

 

[Bryan]

...how does that information you posted previously about KD and androgen receptor polymorphisms supposedly "put another nail in the coffin" of Stephen Foote's theory?? Stephen would simply reply in his usual fashion by saying that the androgen receptor alteration in KD helps preserve hair by effectively reducing the androgenic stimulation, which in turn improves the lymphatic drainage from the scalp, etc.

Sensitivity and regulation are two different processes; regulation can be explained by Foote's theory but sensitivity cannot. There is less incidence of male pattern baldness in men with KD but some of them still have male pattern baldness.

That means that even the downregulated ARs are still sensitive to androgens. Sensitivity is caused by a direct effect of androgens. Mr. Foote says that male pattern baldness can only be caused by an indirect effect.

Not really a nail in the coffin of Foote's theory though...

I'm glad you finally admitted that.

 

[wookster]

Thirdly, I see you and Doctor just plain disagree about DHT. But do you consider the type two DHT made in hair follilces and the prostate utterly essential?

http://www.mesomorphosis.com/articles/arnold/dht.htm

I have heard several anecdotal reports of individuals who have stacked testosterone with proscar (a 5-AR inhibitor) and have noticed significantly reduced performance enhancement effects. What’s going on here? We know it couldn’t be due to the inhibition of the direct anabolic activity of testosterone on muscle anabolism. Most likely it is due to the reduction of androgenic effects in other parts of the body that contribute to the ergogenic effects, specifically the CNS, which is stimulated by androgens to increase neural output leading to greater strength and greater recoverability. Another possibility is a reduction in the production of androgen dependent liver growth factors (such as IGF-1), since DHT is an important androgen in the liver.

http://en.wikipedia.org/wiki/Finasteride

In the Prostate Cancer Prevention Trial (PCPT), 25 percent fewer men taking the drug finasteride developed prostate cancer than men not taking the drug. However, men who developed prostate cancer while taking finasteride were more likely to have high-grade cancers, which can spread quickly even if the tumors are small.

Two different people can have the equally high levels of DHT. One develops prostate cancer and goes cue-ball bald. The other keeps a full head of hair and has no prostate problems.

Too much androgen sensitivity must be in the genes :wink:

 

[wookster]

Nano-technology ...interesting

http://www.news.cornell.edu/stories/Feb ... ys.kr.html

Cornell University researchers have fabricated a set of "nano-keys" on the same scale as molecules to interact with receptors on cell membranes and trigger larger-scale responses within cells, such as the release of histamines in an allergic response.

How cell membranes control cellular function has long been studied but with few results. However, nanotechnology now gives researchers new tools to better understand the role of cell membranes in activating responses within cells.

http://www.morphollica.com/research/mal ... opecia.pdf

A moderate perifollicular, lymphohistiocytic
infiltrate, perhaps with concentric layers of
perifollicular collagen deposition, is present
in 40% of cases of androgenetic alopecia, but
only 10% of normal control subjects.
Occasional eosinophils and mast cells can be seen.
The cellular inflammatory changes also occur
around lower follicles in some cases and occa-
sionally involve follicular stellae. The diagnos-
tic and prognostic significance of the degree of
the inflammation is not known.

Androgen "sensitivity" almost seems like an allergic reaction :freaked:

 

[Old Baldy]

Wook: Isn't it more like the immune system response to receptor sensitivity, and the resulting cascade of events after DHT exposure, is somewhat similar to an allergic reaction?

Except cells are killed off in male pattern baldness?

 

[wookster]

Wook: Isn't it more like the immune system response to receptor sensitivity, and the resulting cascade of events after DHT exposure, is somewhat similar to an allergic reaction?

Except cells are killed off in male pattern baldness?

http://ajp.amjpathol.org/cgi/content/full/165/1/259


quote:

Neurogenic Inflammation in Stress-Induced Termination of Murine Hair Growth Is Promoted by Nerve Growth Factor

Recently, we have revealed the existence of a "brain-hair follicle axis" in murine skin and have identified the neuropeptide substance P (SP) as a key mediator of stress-induced hair growth inhibition in vivo. Published evidence suggests that increased numbers of SP-immunoreactive sensory fibers, as seen in the dermis of stressed mice in anagen-catagen transition, are a result of transient high levels of nerve growth factor (NGF). Thus, we now aimed at dissecting the role of NGF in stress-triggered hair growth termination in our murine model. By real time PCR and immunohistochemistry, stress-exposed mice showed an up-regulation of NGF and its low-affinity receptor p75NTR; the NGF high-affinity receptor TrkA was moderately down-regulated. On neutralization of NGF, premature onset of catagen, apoptosis, and increased number/activation of perifollicular mast cells and antigen-presenting cells, which reflects the skin response to stress, was significantly abrogated. Stress or subcutaneous injection of recombinant NGF (to mimic stress) resulted in an increased percentage of SP+ neurons in dorsal root ganglia, as measured by retrograde tracing. Taken together, these data suggest that NGF is a central element in the perifollicular neurogenic inflammation that develops during the murine skin response to stress and antagonizing NGF may be a promising therapeutic approach to counter the negative effect of stress on hair growth.


:scratch: :alien: :scratch:

 

[wookster]

http://www.hairlosstalk.com/discussions ... hair transplant=#242700

I'm pretty much convinced that DHT is needed in the male body and lowering it in any way is not beneficial.

:freaked: :freaked: :freaked:

 

[docj077]

http://www.hairlosstalk.com/discussions/viewtopic.php?p=242700&highlight=#242700

I'm pretty much convinced that DHT is needed in the male body and lowering it in any way is not beneficial.

:freaked: :freaked: :freaked:

Oops, you caught me. Too bad human beings are quite capable of changing their opinions. Especially, as they become more informed. That was almost a year ago. But, nice try.

By the way, you have way too much time on your hands if you're able to look back that far through someone's posting history. Time to get out and do something with your day.

:roll: :roll: :roll: