Densiti - make yourself an equol producer :)

Hoppi

Senior Member
Reaction score
61
But surely erm, there are two points here I'd like to make.

First of all, as s-equol works by a completely different mechanism to finasteride, couldn't it be used as well as it to further enhance the androgen blockade?

Second, I believe I am right in saying that 5-alpha reductase type 2 performs other functions in the body, and inhibiting it too strongly creates side effects of it's own, regardless of the level of DHT reduction? I don't have any studies to hand to prove this but, I did feel that was the situation.

I just think it might be wise to at least experiment with such a curious chemical! :)


Like, check some of this

http://www.hair-loss-remedies.net/20014 ... ntion.html

In recent years, the pharmaceutical industry has developed drugs that inhibit a certain enzyme that converts testosterone to DHT. Unfortunately, these drugs have side effects. Equol, on the other hand, does not prevent DHT from being made but prevents it from functioning. It puts handcuffs on DHT, preventing it from binding to the androgen receptor and thereby preventing the prostate from growing. This may be particularly important for men who have been diagnosed with either an enlarged prostate (benign prostatic hyperplasia), or cancer of the prostate.

From a forum in 2006:

Hi Guys,

Thought I'd add my 2 scents worth...

The first thing is that this Equol business is no joke, it really does work as I've seen it, disables the DHT and given time a good proportion of the follicles on your head will revert to their former unshrunken state and voila thicker and stronger hair begins to grow, but remember keeping it up over time like he says in The Shawshank Redemption, that's all geology is, "pressure and time".

Second point I wanted to make is that our absorption propensity to any substance is much higher when that substance is part of a naturally digested foot item. E.g. The amount of vitamin A you absorb from a carrot and then store in fat in your liver will be far greater than the Vit A you ingest as a tablet (assuming equal quantities) and generally we seem to respond better to vits/minerals/chemicals taken within our natural diet rather then just pumping supplements into your body usually in hugely excessive amounts, most of which goes unused.

The same applies for Equol,you don't need huge amounts, you should be focussing on a diet (as I'm sure many are already) rich in Soya together with some natural Soya Isoflavones supplements if you wish and then trying to mirror the diet of the Japanese who have been doing this since time immemorial, that is rich in vegetables, green tea, sea weed foods etc. THAT is what will really adjust the bacterial composition in your intestine and give you the best chance to metabolise the Equol that will form part of your diet. BUT as will all these things, it's sustaining this diet over several weeks and months that counts before you start to really make a difference. Rome wasn't built overnight.


I agree with him but am inherently lazy, and would love to kill my hair loss and still eat pizza lol :)


http://www.stophairlossnow.co.uk/News/News185.htm

Two experiments demonstrated that injections of equol into male rats reduced the size of the prostate. In one study, the testes of male rats were removed, thereby eliminating all DHT production. When investigators injected DHT into rats, their prostates grew.

When they injected rats with both equol and DHT, the equol prevented the DHT from functioning as it normally would - as a stimulator of prostate growth.
 

Bryan

Senior Member
Staff member
Reaction score
42
Hoppi said:
But surely erm, there are two points here I'd like to make.

First of all, as s-equol works by a completely different mechanism to finasteride, couldn't it be used as well as it to further enhance the androgen blockade?

They work by different mechanisms, but the effect is the same: they reduce the amount of bioavailable DHT. If you want to "enhance the androgen blockade", I suggest you use an androgen receptor blocker like spironolactone or RU58841, along with whatever you're going to be using to suppress the effects of DHT (finasteride or equol).

Hoppi said:
Second, I believe I am right in saying that 5-alpha reductase type 2 performs other functions in the body, and inhibiting it too strongly creates side effects of it's own, regardless of the level of DHT reduction? I don't have any studies to hand to prove this but, I did feel that was the situation.

That's a rather theoretical issue, and there _may_ be some validity to it. It does seem to be the case, though, that most side effects from finasteride are of a sexual nature (low libido, erection problems, etc.), which would seem to be related just to the suppression of DHT.

Hoppi said:
I just think it might be wise to at least experiment with such a curious chemical! :)

Go ahead and knock yourself out, but don't say you haven't been warned! :)
 

Hoppi

Senior Member
Reaction score
61
haha fair enough :)

I'll let you know how I get on!
 

Old Baldy

Senior Member
Reaction score
1
Haven't been here in a while but I thought this thread might be where all of you might want a little more info on finasteride. (It is not male pattern baldness related, it speaks to the ability of finasteride to reduce the chances of contracting prostate cancer.)

It can help in preventing prostate cancer and, as all of you have noted, can have some effect on libido. (I fail to see how equol, in sufficient doses, would do otherwise but I really haven't spent time on that "drug".)

I would think Bryan is, as usual, correct in his conclusions on equol but I really don't' know much about that specific drug. However, ANYTIME you adjust your hormones, there will be an effect IMHO. Unless, the drug is a purely topical one and doesn't get into your bloodstream.

Prostate cancer runs in my family, so I take 1/4 tablet of finasteride on Monday, Wednesday and Friday. I have had 3 transplants, totaling 7,600 grafts, so male pattern baldness is not a big concern for me any longer. (But I do use minoxidil, spironolactone/phenytoin cream, etc., fairly regularly just in case. I never quite kicked my habit of using other stuff. :) )

Anyway, here is the current thinking among some medical professionals on finasteride and prostate cancer:

Finasteride Reduces Prostate Cancer Risk, but Which Men Should Receive It?
Roxanne Nelson

Authors and Disclosures

Print This
processing....


Information from Industry
Metastatic GIST: New Case Study Program
Dr. Joaquina Baranda and three colleagues present the case of a 53-year-old female with unresectable GIST to help you gain insight into diagnosing and treating gastrointestinal stromal tumors.
Click here February 11, 2010 — Finasteride (Proscar) reduced the risk for prostate cancer by nearly 25% in the large Prostate Cancer Prevention Trial (PCPT), which was conducted in men 55 years and older.

But this finding begs the question of who to recommend the drug to, say the authors of a new analysis published online February 1 in the Journal of Clinical Oncology.

Despite the encouraging findings of the PCPT, the use of finasteride to prevent cancer in the community remains low and is not widely used, explained lead author Andrew Vickers, PhD, associate attending research methodologist at Memorial Sloan-Kettering Cancer Center in New York City.

"This suggests that, for the average man, the benefits of finasteride, in terms of reduced risk, do not outweigh the harms," he told Medscape Oncology.

The analysis conducted by Dr. Vickers and colleagues found that risk-group stratification for treatment with finasteride is "unlikely to be beneficial for preventing all prostate cancers detectable at biopsy." But if cancers found as a result of routine clinical care are used as an end point, then the optimal strategy would be to treat a subgroup of men at high risk rather than the whole at-risk population, they write.

The interpretation of these results, in relation to whether finasteride should be used as chemopreventive therapy for all men or for only for those at higher risk, depends on the relative clinical significance of cancers found during the end-of-study biopsy, the authors explain.

Basically, clinicians should recommend finasteride to all men if they want to reduce the risk for any biopsy-detectable prostate cancer.

However, "clinicians who believe that it is unnecessary to prevent all cancers, but that preventing those readily detectable by screening is desirable, would be best off recommending finasteride only to a high-risk subgroup," they write.

Balancing Benefit and Harms

The primary adverse effect associated with finasteride is decreased sexual function, the authors explain. Even though this effect is generally mild, the reduction in libido can be experienced immediately. Conversely, men at higher risk have a greater potential benefit from finasteride. Therefore, note the authors, a strategy that focuses on high-risk men might tip the balance between the benefits and harms of finasteride in favor of treatment.

"Along with many other groups, we have shown that the risk of getting prostate cancer over the course of next 5 to 10 years is strongly dependent on your PSA [prostate-specific antigen] level," said Dr. Vickers. "If you have a high PSA level, you are naturally a candidate for immediate biopsy. But even among those who are not candidates for biopsy, higher PSA means higher risk."

As an example, few clinicians would consider biopsying a man with a PSA of 0.8 ng/mL or one with a PSA of 1.6 ng/mL. "However, the man with the PSA of 1.6 ng/mL has a much higher risk of being diagnosed with prostate cancer over the next 5 to 10 years," he said.

Dr. Vickers explained that, in this study, he and his colleagues demonstrate that not only is the risk higher with increasing PSA, but the effects of finasteride are larger for men with a higher PSA level. "For example, the risk of cancer goes down by about 1% for the man with a PSA of 0.8 ng/mL but nearly 3% for the man with a PSA of 1.6 ng/mL," he said.

"We go on to show, using decision analysis, that it makes the most sense to offer finasteride not to all men at risk for prostate cancer, but only to men with a PSA above 1.3 ng/mL or those with a PSA above 2 ng/mL," Dr. Vickers continued. "Whether you choose 2 or 1.3 ng/mL for your cut-point depends on your views about the relative benefits and harms of taking finasteride."

A patient who is anxious about prostate cancer might be advised to take finasteride for a PSA of 1.5 ng/mL, for example, whereas one who prefers not to take drugs unless needed might be advised to take finasteride if his PSA is above 2 ng/mL, he added.

Study Details

In the current study, Dr. Vickers and colleagues used raw data from the PCPT to model chemopreventive treatment strategies to determine whether PSA levels can identify a high-risk subgroup in which the benefits of finasteride treatment outweigh the potential harm.

For their analysis, they weighed the benefits and harms for each strategy using number-needed-to-treat (NNT) thresholds, or the maximum number of patients that a clinician would need to treat with finasteride to prevent 1 cancer.

Their analysis consisted of 9058 men, 1957 of whom were diagnosed with prostate cancer during the 7-year study period: 798 (18.3%) men were in the finasteride group and 1159 (24.7%) were in the placebo group. Demographic characteristics such as baseline PSA, age, race, and family history were similar in both groups.

The overall risk of being diagnosed with cancer was 21.6% and, in both groups, approximately half of all cancers were detected by a biopsy that followed an elevated PSA level and/or an abnormal digital rectal exam result.

The authors observed that PSA levels were significantly associated with the outcome of all cancers and for-cause cancers (P < .001 for both). The data were divided into approximate quintiles according to baseline PSA, and then the clinical net benefit of treating by each of these cut points was determined.

They note that for the outcome of detecting all cancers, it is difficult to justify stratifying the population into risk groups and treating only men who are at high risk. For an extremely conservative clinician, such as one who would treat no more than 10 men to prevent 1 cancer, the highest clinical net benefit would be obtained from treating only the highest quintile of the population. But for the other NNT threshold, they write, the optimal strategy would be to treat either all men at risk or all but the lowest-risk quintile.

If only cancers that are detected by a for-cause biopsy are considered, "there is a clear case for recommending finasteride to some, but not all, men," they write. The optimal strategy, across all NNT thresholds, is to treat either 20% or 40% of those with the highest PSA levels. If only men with a PSA of 1.3 ng/mL or greater are given finasteride, the treatment rate would be reduced by 62%, with only a small increase in the event rate (from 9.6% to 9.9%).

Restricting the use of finasteride to men with a PSA of greater than 2 ng/mL would reduce the treatment rate by 83% and result in a cancer rate only 1.1% higher than treating all men, they note.

The study was supported in part by funds from David H. Koch provided through the Prostate Cancer Foundation, the Sidney Kimmel Center for Prostate and Urologic Cancers, and a SPORE grant from the National Cancer Institute. Dr. Vickers and coauthor Hans Lilja, MD, PhD, also from Memorial Sloan-Kettering Cancer Center, report receiving honoraria from GlaxoSmithKline. Hans Lilja also reports owning stock in Arctic Partners Oy.

J Clin Oncol. Published online February 1, 2010. Abstract


I thought all of you might be interested in how finasteride can sometimes help men reduce their chances of contracting prostate cancer later in life.
 

Hoppi

Senior Member
Reaction score
61
There are some fascinating studies on the www.naturalequol.com site. A whole page of brilliant studies and research, with tests on men, analysis of the SE5-OH supplement, fermentation process, pretty much everything you could ever want to know and more (except of course the effects on serum DHT, as far as I can tell lol)

Point is... it's all pretty cool and DOES suggest the pure substance is bioavailable orally.
 

Hoppi

Senior Member
Reaction score
61
Erm, aren't the properties of soy as a whole relatively unconnected to those of one of it's metabolites? o_O
 

Jacob

Senior Member
Reaction score
44
Hoppi..I posted this in the Densiti thread..where soy is mandatory for it to supposedly work.
 

Hoppi

Senior Member
Reaction score
61
Sorry, perhaps it's my fault for digressing! Perhaps I should have posted that in the normal Equol thread :)

It's just this was active a bit more recently so I stuck it here! :)
 

grove12345

Member
Reaction score
0
I think the lack of Japanese men going bald has less to do with the diet and more of the fact on genes. The mere fact that Japanese pretty much all have brown eyes and black hair means a lack of diversity in jeans.

I got some densiti in the mail long long ago for free as part of a trial. But didnt go through because you basically need soy to go with it. Why not just include it?
 

Hoppi

Senior Member
Reaction score
61
Possibly true about the genes, I can't say either way. But it's always best to keep an open, informed and analytical mind, rather than risk jumping to conclusions which can miss huge things out. There is a reason why scientists favour real studies over assumptions or assumed "logic". Anyway, that's what I think :)
 

abcdefg

Senior Member
Reaction score
782
Yes I think some areas like japan are just many people with same common gene pool with common traits so hair loss seems less common because less people have the male pattern baldness genes so it gets passed around less. I will say this I see some koreans that are old like 30+ years old that look like they could be 15. What do they all have in common that I see? None of them have any facial hair at all coincidence I dont think so. The more I see the more I think its just solely androgens not really anything else but propecia is just not good enough. I think testosterone is involved too.
With equol I am with Bryan on this one its silly to think removing DHT directly as this claims to do would have any less sides than how finasteride disables DHT by stopping the conversion of T to DHT especially if equol removes enough DHT to equal the strength of finasteride. I think CB or ascj 9 have the right idea by trying to destroy receptors or disable them so androgens can not bind to them. That sounds like a much safer way of doing things if they can actually pull it off.
 

LawOfThelema

Experienced Member
Reaction score
18
are their studies which show the distribution of the gene polymorphisms associated with androgenetic alopecia in asian populations?

it is not silly to think removing dht would have different effects from an inhibition of the 5 alpha reductase enzymes themselves.
 

Jasperdje

Established Member
Reaction score
0
hey Hoppi so what happened with this experiment?

http://www.ergogenics.org/trinovin.html
Use google translate please.

If you search his posts you will find that he started in august 2010, trying to produce equol. In september he is on finasteride. So he never gave it a chance. This is not something you'll do in 4 weeks :S.. Anyway
Here's a study about soy. The test was 360 days long on rats. Soy increases DHT and doesn't touch Testosteron. This is because; Equol binds with DHT, and then DHT doesn't fit the receptors anymore and goes back into the blood.
So in the blood test they find a higher DHT level.

Other study's showned that; male pattern baldness in Thailand is higher than suspected, they think this is because the western diet has take a place there. Mac donalds, KFC, Burgerking are examples. So if it only genes decided
the male pattern baldness, the western diet has no impact on it, right?

Greetings.

- - - Updated - - -

Densiti itself is a combination of only 2 things - Bacillus Coagulans and green tea extract. Along with that you must ensure around 20 billion CFUs or above of lactobacillus acidophilus (I use Florajen for this), and consume at least 8-10 ounces of soymilk twice daily.


Hoppipolla! ^_^

I don't get it. Bacillus Coagulans and Lactobacillus are the same?? 8-10 ounces of soymilk is too low. You must get at least 400mg isoflavones, and with 8-10 onces you'll not get this. Btw you'll need more things than this to (try) produce equol.
 

LawOfThelema

Experienced Member
Reaction score
18
just ignore hoppi. he's off eating beef livers, coconut oil, and gallons of OJ daily in hopes they will cure his male pattern baldness
 

ABJac

Member
Reaction score
2
In a 2004 study from the University of Minnesota, isoflavone supplementation plus Lactobacillus acidophilusDDS+1 and Bifidobacterium longum did not generally increase S-equol production among a group of 20 women compared to controls (isoflavones alone). However, S-equol production went up significantly amongst a few of the women. The researchers concluded that, “the large differences between plasma and urinary equol in some subjects suggest that equol producer status may be modifiable in some individuals.”
However, in a 2011 study from Italy with twelve menopausal women, Lactobacillus sporogenes supplementation resulted in a 24% increase in genistein-related equol, while diadzein metabolite equol production only went up for some of the women but not all.
Another 2011 laboratory study indicated that Lactobacillus rhamnosus may increase diadzein S-equol production.
But a more recent study from Germany’s Institute of Human Nutrition published in January’s issue of the Journal of Nutrition has found that the intestinal probiotic bacteria (conveniently) named Slackia isoflavoniconvertenswill convert both genistein and diadzein to 5-hydroxy-equol.

-

http://li123-4.members.linode.com/f...toestrogen Metabolism and Plasma Hormones.pdf

-

A Spanish Research Centre has patented three Lactobacillus strains capable of growing in soy milk and improving the bioavailability of isoflavones through their a-galactosidase and ß-glucosidase activity. Moreover, due to their tolerance to low pH and bile salts (up to pH=3.5 and 2%, respectively) they can survive and colonize the gastrointestinal tract, thus being suitable for manufacturing probiotic foods derived from soymilk.
Partners are sought for license and development agreements.

Description:
Phytoestrogens included in the diet must be activated by intestinal bacteria to become highly biologically active, since most of them are conjugated to glucosides. Isoflavones are conjugated to glucosides forming daidcine, genistine and glicitine, and must be hydrolysed by the ß-glucosidase of the gut microflora. In addition, gut microorganisms produce dehydroxylation, reduction and breach of the isoflavones ring, and demethylation, generating compounds with high estrogenic and antioxidant activity (equol) as well as inactive compounds (such as O-DMA). The proportion among active or inactive compounds depends on the gut microbiota species and strains, and therefore only 30-50% population is able to produce Equol and up to 90% generate inactive compounds from daidzein (the first product generated from the hydrolisis of daidzin).
Three strains with high ß-glycosidase have been isolated from human intestinal tract (Lactobacillus plantarum E112, L. casei BA3 y L. rhamnosus G92), being capable to release isoflavone from the isoflavone-glycoside conjugates with up to 95% efficiency for the two last strains. This high ß-glycosidase activity has been found when the strains were cultured in media or in commercial soymilk (up to 75 U / ml).
The strains are resistant to acids and bile salts, so they could be used as probiotics. Furthermore, they acidify and ferment the soymilk producing a product with viscosity similar to that of yogurt.



why does Densiti say you must get 20 million IUs of Acidophillus?
 

Jasperdje

Established Member
Reaction score
0
because they just don't know. Some people produce equol with just eating soy, fatty fish, probiotine food and drinking green tea.
 
Top