Ecklonia Cava as effective as Propecia? -- if I'm understanding this paper correctly, why is no one talking about this?

I'm talking about this particular(the only one actually) study:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3382810/?tool=pubmed

According to these charts, EC seems to be almost as effective as Propecia.





The question now is how much EC would we have to take? The units from the chart are quite vague. How much exactly is 2 nM? Would three pills of Fibroboost match the effectiveness of Propecia?
http://www.iherb.com/Nutricology-FibroBoost-75-Veggie-Caps/7777

This is topical extracts dude. Taking orally it might not be as strong.

I can get my hands on liquid extract to add to RejuvePlex, however, there is no precedent for me to use here...meaning, I have no idea what sort of directions I should give them as to how to extract it (ie. - how concentrated it ought to be) nor how much I should use in the formula...

2 things: It wasn't a topical application, it was actually done in vitro. Secondly, it blocks DHT in a dose dependent manner - the more you take, the more it blocks. The question now is HOW MUCH should we actually take? I'm not interested in topical applications.

Anyone with the knowledge of science can tell us how much is 2 Nm in mg? This is extremely important! Halt all the existing threads - the cure might just be here. This may be a reason why CS lists this as his NUMBER ONE supplement.

this is why unless clinical trials are done we grasp in the dark when we try to repeat in vitro trials on the human in vivio. There is no "formula" to translate in vitro to in vivio.

And note the inhibition at ten times the dose which gave the better response than minoxidil sulfate. You could well take the dose that is too high which ends up hurting your hair. AHK-Cu was the same in its dose dependence. There was a peak dose then it starts hurting your hair when you go higher.

What part don't you understand? Those are simple molecules. Both EC and Propecia inhibited the same number of 5AR. We don't need clinical studies to show us what would happen when you inhibit enough 5AR(Propecia levels).

This seems to be a natural and almost as effective alternative to Propecia. Can anyone confirm that?

I dont need a clinical study to tell you that when you inhibit enough 5ar to really be effective you will see the same sides as propecia either

I think the transition from in vitro to in vivo scenarios is the biggest wrench in the gears in making sense of all of these studies. And it doesn't help that a lot of scientists out there, especially a few with a big following here, are notorious for using in vitro evidence to make claims about in vivo circumstances. Enzymes are a miraculous thing, and unfortunately they don't behave in a beaker like they do in the body, just a miraculous aspect of human biology. Reactions often proceed completely differently in vivo, because the nature of competition between rxn. products is altogether different between the two contexts.

This has already been explained. Finasteride simply destroys 5AR that's already in the bloodstream. EC, through some mechanisms, tells the body - hey, there is no need to produce that much 5AR so don't, everything is working smoothly. 5AR is inversely correlated with oxidative stress so that may be the main method of action for EC. Do you get it now?

anthonyspencer54, but if EC blocks the same amount of 5AR in vitro as Propecia, wouldn't you think that vivo studies for both of those will have similar results as well? We have plenty of in-vivo studies for Propecia so we know it works fabulously. Why wouldn't EC work as well?

Why not learn what enzyme inhibition actually is. Maybe that would clear things up

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


EIs bind to enzymes.


The difference which is harped on at this site is the reversibility.

Whether the EK component is an irreversible inhibitor is an empirically testable question. I don't know if it is or not. Do they discuss that in the paper? It's probably reversible. I suppose sides are less on reversible, but accordingly results on the hair would be less as well. Does anyone want to explain why the effectiveness of a 5aR inhibitor would be worse if reversible

Why does propecia work so well if it's half life is only 6 or so hours?

Well I'm not going to argue with you about its side effects. I just want to know - if possible - how many mg/days of EC would I have to take to match 5AR levels of those using Propecia?

Try it and find out

I don't know. I'd imagine the assumptions and calculation are easier for topical. But still, I don't think there is a formula for this, for all the reasons anthony spencer stated. You just have to try it. This is exactly why drugs arent sold right after in vitro evidence pops up. Its why trials are used to determine how much is needed for an effect.

How would me taking it prove anything? I have absolutely no idea how much 5AR is one pill of fibroboost is blocking. All I know is that at SOME DOSAGE point, both Propecia and EC block the same amount of 5AR. What is that point? Does anyone know? Please tell me

The process of DHT inhibition is vastly different to finasteride. It's like comparing night and day. Finasteride destroys an enzyme, and ECE, uses oxidation reduction a completely natural process.

I began using it in 2006 because that is when it was available and there was literature already in existence that showed other promise for hair that occurs post DHT reaction.

It's best to combat hair loss from as many angles possible, since everyone is different.

Right, but how effective is EC at inhibiting 5AR? If it inhibits as much 5AR as Propecia then EC by itself should be enough to halt hair loss(yes, I know low thyroid and heavy metals are still a main cause of MPB, but in the meantime I just want to halt my hair loss and then work on improving everything else which could potentially take years and that means more hair loss until then)
We all know that Propecia is able to halt hair loss purely by just reducing 5AR, the problem of course is eventual side effects and upregulation of AR sensitivity over time(5 years or so).

Would EC by itself be enough to halt hair loss? Can someone explain those charts? How much is 2 Nm converted to milligrams?

A major drawback to finding solutions for humans is that much of the research is done in vitro, or on rats. I was trained as a scientist, so maybe that's why I feel this way, but I believe we all should come together and test this EC out and put together our results. No use speculating and going back and forth. Not much to lose by using EC.. but if you win, you win big. I'm personally ready to take this approach, even though my hair loss has slowed down recently.

PS
moby,
If my math is right, 2nM of finasteride comes out to a very small number (0.00075 mg worth)

Not much to lose? Nothing except for major cash. EC is by far the most expensive supplement on the list.

>> If my math is right, 2nM of finasteride comes out to a very small number (0.00075 mg worth)

that can't be true. 2 nM blocks 90% 5AR in vitro. From what I know 1mg of Propecia blocks about 70% of 5AR. 2 nM has to be more than 1mg of Propecia.

CS once mentioned that if he was only allowed to use one product, he would use EC. I wonder if EC by itself is enough to halt hair loss?

in liquid form has no luck? (for topical application)

https://www.klonia.com/common/clientCustom.asp?UID=50362&guid=%5Bguid%5D§ionid=1

Also consider the studies were done on rat hair, which is similar to the human scalp hair but not the same. And if I'm not mistaken (please correct me if I'm wrong) there were no data indicating any type of regrowth or increase in density/thickness, just elongation of the hair shaft. And the problem with considering the in vitro studies is that more than likely there was competitive inhibition of the 5-ar enzyme, whereas in the body, enzymes tend to shuttle their products elsewhere or sequester them away in some molecular region that allows the enzyme to remain active. You would most definitely not see this type of 5-ar inhibiition in vivo. I'm not saying EC isn't totally worth the price, I think its a great antioxidant, anti-inflammatory, and an immuno-modulant, which the latter for me is probably why I'd take it for hair.

moby wrote:Not much to lose? Nothing except for major cash. EC is by far the most expensive supplement on the list..
CS once mentioned that if he was only allowed to use one product, he would use EC. I wonder if EC by itself is enough to halt hair loss?

That's a relatively small price to pay, given what's at stake here. You wonder if it's enough to halt hair loss, by your own admission. I recently ordered EC caps. After a few weeks, I'll report on how it works. Maybe someone else can give topical EC a shot. It's should be our goal to find out what works and what doesn't, and report findings.

moby wrote: that can't be true. 2 nM blocks 90% 5AR in vitro. From what I know 1mg of Propecia blocks about 70% of 5AR. 2 nM has to be more than 1mg of Propecia.

Okay but you're comparing apples to oranges here. Remember that 1mg finasteride is taken as an oral drug (IN VIVO), and the experiment you're referencing here uses 2 nM to refer to a solution's concentration IN VITRO (what happens in the body may very well be different from the results of a test tube experiment). Because 1mg refers to a solid weight, the 2nM figure can be composed of finasteride by ANY weight, provided that it's dissolved in enough solution to have 2 nano molars of the active ingredient (finasteride). It's like asking how much sugar you would put in making tea. Obviously, it depends on whether you're making just one cup.. or if you were making 500 liters.
Also, nM refers to concentration, so it would be 0.00075 mg PER 1 liter solution. I should have made this point more clear in my last post. So yes, the number I gave is true, but you can't compare both numbers head to head unfortunately, because they're used in different compositions, not to mention different settings.

A natural substance will never cause the body to inhibit 5AR to the extent that propecia does. I dont mean to be arrogrant but if people fail to understand this or why - they are still in the stone ages of understanding MPB.

This thread is money. Let's keep it rolling..

I love EC internally - better sleep, fast recovery from workouts, enhanced dream states and strong erections. The potential benefit to hair is a just a major bonus. Topical EC sounds like it could be very promising. But again, there is no concentration precedent set for topical application. We'd totally be the guinea pigs, which may not be worth the risk if we used too high EC concenctration and ended up being counter productive to hair growth..

Health science is awesome, but it really pisses me off sometimes..

cpio, I figured as much. But EC has gotta be up at the top right? I'm just curious, because I have seen lots of hype over EC, so I just ordered it yesterday.

TrueGround, how much benefit did EC have on your hair, honestly?