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Papain from papaya latex

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Originally Posted by westla90069
You don’t think the studies done by the makers of Propecia are true? The pill, which inhibits the enzyme type II 5 alpha-reductase to decrease serum and scalp DHT, stops hair loss and helps in regrowth. It’s worked for me for several years now.

Okay I’ll bite. First I’ll explain the MPB angle, then bring it back on topic towards the end.

As you know, Test converts to DHT via 5-AR Type I and Type II. With Propecia it has been found that the MPB condition is improved with a partial antagonism of the Type II which I don’t think anybody would disagree with.

That said, I think it would be foolish to assume that because of the above it means that DHT and nothing else is causing hairloss. After all, if that were true then not only would nobody be losing hair, but we’d all be re-growing a thick full head of hair.

DHT damages the mitochondria in susceptible cells, which causes it to produce cytochrome C, which in turn promotes Capase 9 (and further downstream Caspase 3). DHT also promotes TGF-beta2 which is known to activate the newly released Caspases, and it is Caspase 3 in particular which is thought to cause apoptosis, or cell death.

So to prevent MPB we need to break that cycle in one or more places, and DHT is way back up the chain. Preventing Caspase 3 would be the ideal point if possible.

Getting slowly back on topic; a side effect of MPB is the high degree of fibrosis on the scalp around the follicle, so even when you partially block DHT with via 5AR-TypeII, or more completely via Type I&II, we still do not get good regrowth unless the MPB is fairly recent. Some people have experienced better regrowth with skin peels (to the point of bleeding scalps!).

If DHT promotes TGF which causes fibrosis, then it may be the case that when we PE, we are causing the very thing that prevents growth. It’s like the body has its own direct negetive feedback - not via downregulation but by physically shoring up the affected area. This is very effective for healing cuts and wounds, but not for PE.

So, I propose that we do not want to reduce DHT as it serves for us a useful growth role. What we want to do instead is take off the brakes that short circuit growth. I believe one of those angles in lowering the TGF family to moderate levels.

As an aside, it it known that women (who have less testosterone!) have better healing capabilities than men. In castrated men there is no marked difference. It is thought that the reason for this is not the testosterone itself (which promotes growth), but the TGF that it also triggers after DHT conversion.

If (if) Papaya/Bromelain help MPB, then by the very same axis they will likely help in PE. A key question is whether the body determines fibrosis to be an injury site or normal tissue, as that will probably determine whether it is of any use or not.

Hope that helps to explain the reasoning behind my earlier post.


Last edited by Shiver : 08-17-2004 at .

That was out of my head from reading up on hair loss over the years so I can’t give specific references. A search on “Dr Sawaya” would be a good start though.

Re DHT: We should distinguish between prostate hyperplasia and cancer. I don’t want to spend too much time writing about this now, but will write a far more comprehensive post when I’ve got more facts together. Briefly; TGF-b1 is known to contain prostate size under growth conditions because it promotes collagen and inhibits smooth muscle formation. In a cancerous situation the TGF-b1 is often not effective in containing the cancer since it’s axis is different than that taken by the cancer.

There is a very real danger that creating conditions that help PE will also allow prostate growth (maybe not hyperplasia exactly but smooth muscle growth) - I’m not sure yet. I do know that it is a tissue specific response though. For example, although it has been shown to help CC growth, it did not affect the glans at all, so it depends whethere the prostate has the same TGF-b1 receptors as the CC.

Think of a tyre with radial wires inside. The wires are the collagen, the smooth muscle is the rubber. Without the collagen the tyre will blow up enourmously. The wires are needed for structure, but we need to deform and stretch them to modify the shape and allow the rubber to in-fill. If we inhibit rubber formation and add extra wires that are no longer radial but linked to each other, the potential to blow up the tyre to its maximal size is reduced. In extreme cases (such a peyronies), even a normal shape and size of tyre is unachievable. Conditions such as diabetes and age affect this. If you want a healthy pecker into a very mature age, then it’s worth looking at a lifestyle that maintains a moderate level of TGF production.


Last edited by Shiver : 08-18-2004 at .

Originally Posted by Hog6.5
Where can I get all that information?


http://hairsite2.com/waseda/amashiso/main.htm
http://www.morphollica.com/?newsid=26
http://www.emedicine.com/derm/topic21.htm
http://www-ermm.cbcu.cam.ac.uk/02005112h.htm

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If you can answer (you too Westla), are you a MD?


I am not a physician. I am a health care professional who has adequate research skills and nearly constant access to the Internet. If need be, I can get to a medical school library, but often I find what I need on the ‘net. I specifically have an interest in helping people understand human anatomy and physiology. A lot of the cellular level material being discussed here holds little interest for me, but I try to participate when I can.

Originally Posted by Shiver
I think it would be foolish to assume that… it means that DHT and nothing else is causing hairloss. …if that were true then not only would nobody be losing hair, but we’d all be re-growing a thick full head of hair.


If it were true that only DHT caused hair loss then nobody would be losing hair? That doesn’t make sense.

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So to prevent MPB we need to break that cycle in one or more places, and DHT is way back up the chain. Preventing Caspase 3 would be the ideal point if possible.


Why? That’s pretty late in the series of events that destroys the follicle. Wouldn’t stopping it further “back up the chain” be a better place? And isn’t that what finasteride does?

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…a side effect of MPB is the high degree of fibrosis on the scalp around the follicle, so even when you partially block DHT with via 5AR-TypeII, or more completely via Type I&II, we still do not get good regrowth unless the MPB is fairly recent.


Not everyone agrees with that: link. Note that they place androgenetic alopecia, the kind of baldness we’re talking about, in the non-scarring category. In fact, a PubMed search for several combinations of DHT, follicular fibrosis, androgenetic alopecia, or other related terms brought up no links to studies showing fibrosis to be the end result of male pattern baldness (MPB). The only places that do show a link are web sites that propose a treatment of some sort (i.e. they want to sell you something). Besides, if the person did have follicular fibrosis it wouldn’t matter if he tried finasteride or whatever treatment you’re suggesting to stop caspace 3 from causing the follicle to self-destruct because it would be too late anyway.

Quote
If DHT promotes TGF which causes fibrosis, then it may be the case that when we PE, we are causing the very thing that prevents growth. It’s like the body has its own direct negetive feedback - not via downregulation but by physically shoring up the affected area. This is very effective for healing cuts and wounds, but not for PE.


Huh? What does PE have to do with this? What thing are we causing that prevents growth? Please elaborate.

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So, I propose that we do not want to reduce DHT as it serves for us a useful growth role. What we want to do instead is take off the brakes that short circuit growth. I believe one of those angles in lowering the TGF family to moderate levels.


How does DHT serve a role in growth? TGF (transforming growth factor) family? You’ve lost me. How does one (who is not a scientist working with rats) regulate TGF?

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As an aside, it it known that women (who have less testosterone!) have better healing capabilities than men. In castrated men there is no marked difference. It is thought that the reason for this is not the testosterone itself (which promotes growth), but the TGF that it also triggers after DHT conversion.


I think you’re trying to apply what happens to a hair follicle to the whole body or at least to the penis.

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If (if) Papaya/Bromelain help MPB, then by the very same axis they will likely help in PE. A key question is whether the body determines fibrosis to be an injury site or normal tissue, as that will probably determine whether it is of any use or not.


Bromelain doesn’t seem to be the thing usually recommended as a treatment for baldness by naturopaths.

I’m still not sure where you’re headed with this. Your original question, which didn’t get answered, was ‘do men who live in areas with high consumption of proteolytic enzymes have the same frequency of male pattern baldness as men in other areas.’ A quick Internet search suggests that race is the more likely determining factor than diet. Caucasians are the most susceptible, Asians about half as much, blacks and native peoples (such as American Indians) have a much lower incidence.


Last edited by westla90069 : 08-19-2004 at .

Hi Shiver,

no need to explain now the difference between hyperplasia and cancer. I just wanted to know your opinion on whether the increase in DHT could increase the risk factor for those ailments.

Good analogy that of the radial tire. It explains very well the rational behind the use of papain or bromelain to “soften” the connective tissue of the penis and Bu_do’s initial post, especially for those who come late. However, when you mention the fabric of collagen you’re referring to the connective tissue not the muscle tissue itself. What we want to do with the steel wires is to replace them with Kevlar ones to make the tire more ductile.

One issue to clear up is which enzyme works better for PE purposes, papain or bromelain. I have easy access to both. Are you sure papain isn’t available to you?


Take care,

Phew! Where to start?

Originally Posted by westla90069
Why? That’s pretty late in the series of events that destroys the follicle. Wouldn’t stopping it further “back up the chain” be a better place? And isn’t that what finasteride does?

Simply because DHT has many roles to play. If we could remove DHT from the body entirely then I think we’d have bigger problems than hair loss to worry about. If DHT is carpet bombing, then Caspase or TGF targeting in the follicle could be equated with a precision weapon.

Originally Posted by westla90069
Not everyone agrees with that: link.

Quote: “The division is arbitary and can often overlap” link and here link. I’m trying to avoid talking about MPB here since it’s off topic, but not to avoid your point, androgenic alopecia is just one form of MPB which largely involves the minaturisation of the follicle. The analagous effects I was instead referring to are the inflammation, itching, and fluid build up which are classic signs of the body defending itself which can in chronic cases result in fibrosis. Not to debate classifications here, but to generalise; fibrosis is one way the body takes care of things, whatever the cause of the event.

Originally Posted by westla90069
Huh? What does PE have to do with this? What thing are we causing that prevents growth? Please elaborate.

I don’t know how else to put it. Imho, Fibrosis is counterproductive to gains.

Originally Posted by westla90069
How does DHT serve a role in growth? TGF (transforming growth factor) family? You’ve lost me. How does one (who is not a scientist working with rats) regulate TGF?

Pleased clarify. Are you asking about DHT growth, TGF growth/inhibition, or the relationship between the two? As for the last part I haven’t suggested any way of controlling TGF yet (other than Bromleain, which nill not stop TGF but merely moderate excess). I stated ealier that I am exploring the area to try to understand what may be going on, and only then to look at ways of influencing it.

Originally Posted by westla90069
I think you’re trying to apply what happens to a hair follicle to the whole body or at least to the penis.

In a certain context, Yes.

Originally Posted by westla90069
Bromelain doesn’t seem to be the thing usually recommended as a treatment for baldness by naturopaths.

You’re right about that.

Originally Posted by westla90069
I’m still not sure where you’re headed with this. Your original question, which didn’t get answered, was ‘do men who live in areas with high consumption of proteolytic enzymes have the same frequency of male pattern baldness as men in other areas.’ A quick Internet search suggests that race is the more likely determining factor than diet. Caucasians are the most susceptible, Asians about half as much, blacks and native peoples (such as American Indians) have a much lower incidence.

I don’t know where I’m headed with it either. It was just a simple one-liner question that I asked out of curiosity on a whim.

The bottom line for me is that nobody has found a consistantly successful method with PE that works for everyone all the time. I know in my own case that if something isn’t working then the answer is probably not to keep doing it. I’m looking for the elegant solution - the way the body does it.

Originally Posted by Hog6.5
Hi Shiver,

no need to explain now the difference between hyperplasia and cancer. I just wanted to know your opinion on whether the increase in DHT could increase the risk factor for those ailments.

I don’t thing DHT (alone) will cause hyperplasia or cancer. I do think it would exacerbate either condition though if already present.

Originally Posted by Hog6.5

Good analogy that of the radial tire. It explains very well the rational behind the use of papain or bromelain to “soften” the connective tissue of the penis and Bu_do’s initial post, especially for those who come late. However, when you mention the fabric of collagen you’re referring to the connective tissue not the muscle tissue itself. What we want to do with the steel wires is to replace them with Kevlar ones to make the tire more ductile.

One issue to clear up is which enzyme works better for PE purposes, papain or bromelain. I have easy access to both. Are you sure papain isn’t available to you?


Take care,

Also I don’t think papain or bromleain would soften tissue. I believe it may have a role to play in limiting the rate that it ‘toughens’ (by that I mean fibrosis). For that I would look to the crosslink breaker drugs such as ALT-711 coupled with N-Acetyl-Carnosine. But then again it’s early days yet, lets keep learning :)

As for which is more effective, I saw a PPT file recently that had tables showing which enzymes acted on what. There was some overlap between the two, but my feeling was that bromelain was more suited to our puposes. If in doubt though use both as they probably won’t fight.

Hello,
I hope you guys don’t mind my linking my thread here. They are very similar and had I seen this one, I would not have starte mine but added to this.

We are mostly talking about the same problem.

Why gains slow!

Cheers,
PS

Hog6.5 and Shiver

I have little/no faith in unregulated homeopathic products in the USA. Attached is a link to a website in U.K. that I use to obtain prescriptin drugs w/o a prescription. Would appreciate knowing which product/products contain bromelian as the main component. Also papain. Thanks. www.mastersmarketing.com

Bud,

I don’t have papain, but got my bromelain from www.beyond-a-century.com (made by the company ‘Now’)

I got the caps as it said not to breathe the powder, which sounded iffy, but the powder is cheaper if you’re thinking of using it as a transdermal. It has a MW of 28,000 Daltons though, so I’m not sure it would be a good candidate for transdermal. That said, it does of course depend on the carrier. At least as important also is the hydration level of the skin it is applied to.

Shiver,

Any update on how the old fella is doing with the addition of the bromelain?

I’ve not done any PE for a couple of days as I was away in the mountains this weekend. I also wasn’t taking any supplements.

I think I’ve seen all that I’m going to see with this stuff (quicker healing, minimal edema even when pumping with excessive Hg). All of these effects manifested themselves within the first day. I’ll keep taking it for as long as I have a supply since that can only be helpful, but I don’t believe it has any magical properties.

Originally Posted by Shiver

I’m noticing some changes in a very short space of time that I wasn’t expecting (with bromelain that is). My unit is looking very healthy, but it’s as if it’s turning back into a grower rather than a shower. In one way this is great since it looks very healthy and uniform in colour, but in another way I am getting concerned that it’s shrinking. A quick ruler test of Flaccid stretch and BPEL reassures that all is well though.

Perhaps, because bromelain is a diuretic it causes reduced flaccid. Drinking extra water can increase flaccid hang, thus losing it could potentially reduce it.


:flame: "If you build it, they will cum."

Redwood\'s Progress Report/Routines Thread.

I was using bromelain last year. It made my flaccid longer and recovery was faster, by it’s effects on reducing inflammation.


Starting stats: 6.4" / 5.6" Current Stats: 7.4" / 5.8" Short term goal: 7" / 6" Long term goal: 8" / 6.5"

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