Updated Research and Knowledge - Cutting Edge

[Chemical]

hi Chemical
What is your diet?
How to apply with us?
thanks...

I eat junk food. And I take calcium + 10,000iu weekdays, L-theanine, and tryptophan supplements. Diets cant really fight androgenetic alopecia imo.

Great stuff man!

Few questions:

Where do you get your miconzole nitrate? And can I mix it into ru/neo.

Which brand of oleuropeim do you use on amazon?

I recently bought daktarin 2% which has miconazole nitrate, cant wait to start using it alongside keto.

I use swansons superior herbs 750mg oleuropein capsules

thats the highest dose I could find. And it was the most cost effective.

Mix the oleuropein and keto/mico wih ru/neo? I wouldnnt recommend it solely because I like to use creams by themselves and wait a few minutes before using the emu oil solution. It just appears to absorb better that way.

Hello,

I use miconazole once a day since 5 months...no result at all !
I use Nizoral (Ketoconazole) 2%, twice a week, and Stemoxydine, Adenosine, Zinc Sulphate.

All this since 5 month, no result !

I just added fin !

Using ketoconazole, even as a cream is not dangerous once a day???

I would scrap the stemoxydine, I've seen zero studies regarding it and I get the feeling its a snake oil marketed by a big brand which somehow makes it legit. Keep the adenosine, not sure bout the zinc.

You've probably got DHT and DKK1 preventing the WNTs from working, if you dont inhibit the antagonists the agonists will most probably have little effect.

I've no reason to believe ketoconazole is detrimental in cream form, the shampoo on the other hand may be an irritant hence why people recommend 3 days a week max.

Why 5 caps, and not say 10 into a bottle of minox? Would more capsules being dissolved into the mix yield greater effects or is there a point of diminishing return / maximum number of caps that can be dissolved into your standard minox bottle (60 ml)?

the caps I bought were 750mg, and I had 60ml of minoxidil. 0.4mg is what the study used, so 3750 seemed like alot. I was also curious to see if there really was a biphasic effect (little being more). And the oleuropein wasnt dissolving completely so I guessed it was saturated enough. I did however keep adding 2-3 capsules every week, with most of the powder just clumping up at the bottom.



I've noticed the most regrowth in the green regions, especially in the region circled because thats where I use the regimen the most. I use the emu oil solution mainly there and tilt my head to the otherside so it reaches the other areas. The dotted black regions are thickening up slowly although I've not been diligent in these areas for the past few weeks hence my slow progress.

For those of you that have missed the analysis, its at the bottom of page 1: here

[Chemical]

@Chemical

Thank you. See where I'm heading at though? Let's hypothetically assume that these factors are indeed deeply implicated in AGA. How does one work around that? Direct modulation of these factors for instance is something you can't really do I guess due to very serious safety concerns. I find it also interesting that 17b-estradiol can regrow hair to great extent sometimes but not always. I have seen pictures of people that have regrown a very big amount of hair due to being on anti-androgen therapy + estrogen. I think Cotsarelis puts this nicely again;

When you look at what estrogen actions are on the hair follicle it's quite broad; http://press.endocrine.org/doi/full/...0/er.2006-0020. Awesome study in relation to estrogen and the hair follicle. Some targets seem to be the likes of Cyclin D1, AP-1 (c-fos , c-jun proto-oncogenes), SHH, WNT's etc.

Does something stand out for you there? It does for me. All these targets of estrogen seem to be factors that control cell proliferation positively. And to no surprise estrogen is classified as a carcinogen and formulations of estrogen have a black box warning; http://www.cancer.org/cancer/cancerc...an-carcinogens.

When we look at AP1 for example induction of it can repress (antagonize) other factors like P53, P16 , P21 etc;

And all these factors P53, pRB, P21 etc. seem to act negatively on cell proliferation generally. Studies that I have shown that show these factors to be implicated in AGA.

Now there is way more to read upon these pathways how they interact with each other obviously. So this begs the question how do we fix this problem? Well I can only think that you can guinea pig yourself and start modulating these factors directly. But as one can imagine that would be incredibly dangerous due to obvious reasons.

To finish it off here are some examples where estrogen has regrown hair;

And there are more cases. On another forum a transgender also is regrowing hair from NW5 to NW2. Doesn't happen always but it can happen. Estrogen is obviously no option though for any men . It's interesting nonetheless I guess. Perhaps you might find something.

Yes! I was planning to make another in depth post on estrogen receptor signalling and the effects on hair growth (specifically in males).

I'm so glad you found that article because it concisely sums up alot of the research that are scattered around the internet.

First of all, Estrogen acts through two receptors, ER alpha and ER beta. These receptors have different roles - sometimes even contradictory, depending on the tissue localisation and agonist binding affinity. Estrogen is not the only hormone that bind to these receptors, there can be other agents with much higher binding affinities and much much powerful activation. 3 Beta Diol can activate ER beta and it is way more potent than Estrogen itself. 3Beta Diol is actually a DHT derivative, in males, since we have less Estrogen floating around, the body has developed alternative ways of activating ER beta.

One clear frustration when analyzing the biochemichal pathways of Estrogen is the massive discrepancy f ER mediated pathways between genders and species. In females, ER beta in the hair follicles has a completely different distribution to males, and actually inhibits hair growth. The same in male mice. ER alpha inhibits hair growth and ER beta silences ER alpha.

The wide distribution of ERβ in human pilosebaceous unit suggests that estrogens play an important role in the maintenance and the regulation of the hair follicle and provides further evidence for estrogen action in nonclassic target tissues. Recently, it was reported that in cultured dermal papilla cells from nonbalding male donors, both ERα and ERβ showed a consistently higher expression, both at the RNA and protein levels, in occiput dermal papilla cells compared with vertex dermal papilla cells (258). With respect to ERβ immunoreactivity, we found that, in anagen VI follicles microdissected from frontotemporal skin, there was a remarkable distribution difference between male and female hair follicles from frontotemporal scalp skin: ERβ immunoreactivity was found in male scalp hair follicles predominantly in the matrix keratinocytes, whereas in female hair follicles, ERβ immunoreactivity was predominantly found in the dermal papilla fibroblasts (10). These data not only highlight substantial, previously underappreciated sex-dependent differences in ERβ expression of an important peripheral E2 target organ, but also underscore the importance of investigating whether E2 effects on the human hair follicle are location-dependent, as is well-recognized for the paradoxical hair growth effects of androgens (64, 259, 260).
Conflicting data have been presented concerning ER expression patterns in murine hair follicles. It has been reported that ERα was expressed only in the dermal papilla and outer root sheath of telogen and early anagen mouse hair follicles and that ERβ was undetectable (26, 250). Recently, however, we could show that both ERα and ERβ as well as the splice variant ERβ ins are expressed throughout the entire, depilation-induced murine hair cycle at both the protein and RNA levels (28). In addition, hair follicles in late anagen (anagen VI) were highly sensitive to regulation by topically applied E2, which rapidly induced premature catagen entry. Therefore, anagen VI mouse pelage hair follicles must express fully functional ERs (28).
ERα immunoreactivity peaks in murine telogen follicles within the dermal papilla and the sebaceous gland, whereas the inner root sheath and outer root sheath show weaker immunoreactivity. In anagen VI, ERα immunoreactivity (IR) is detectable in the outer root sheath and the dermal papilla, whereas in early catagen it is restricted to the dermal papilla and the secondary hair germ. In anagen VI follicles, ERβ is weakly positive in hair matrix and outer root sheath, whereas in catagen and telogen follicles, ERβ is expressed in the dermal papilla, inner root sheath, outer root sheath, and the sebaceous gland. By RT-PCR, ERα and ERβ transcripts can be detected in telogen, anagen V and VI, and late catagen skin mRNA extracts. Investigation of ERβ knockout mice showed an accelerated catagen development along with an increase in the number of apoptotic hair follicle keratinocytes (28). Taken together, this suggests that the catagen-promoting properties of E2 in murine skin are mediated by ERα and that ERβ mainly functions as a silencer of ERα action in murine hair biology. (An additional list on reported expression of estrogen signaling components is provided in Table 2).

In males, Estrogen - I'm struggling to find any evidence of which receptor specifically - actually stimulates significant hairshaft elongation in a time dependant manner:

Estrogens and Human Scalp Hair Growth—Still More Questions than Answers

This study found further discrepancies in In-Vitro and In-Vivo effects of ER Beta:

We found only two corresponding reports in the published literature, one using human anagen hair follicles from an unspecified scalp skin location of what appears to be two male individuals aged 17 and 35 y (Kondo et al, 1990), and one recent meeting abstract based on the use of female occipital scalp skin follicles (Nelson et al, 2003). Both studies report that E2 (Kondo et al: 18 nM; Nelson et al: 10 nM), significantly inhibits human scalp hair shaft elongation in vitro.

Here theyre saying E2 inhibted hair in-vitro. This only adds to the confusion. They also did a study themselves on female hair:

Recently, we have also studied the effects of E2 (1 nM–1 muM, Sigma St. Louis, MO) on female occipital scalp hair follicles, and have essentially confirmed hair shaft elongation-inhibitory properties of E2, which were maximal at 1 muM

In females, Estrogen inhibits hair growth.

Then theres this:

Therefore, we have investigated in a single, large, frontotemporal scalp skin sample (healthy male individual, no medications, 46 y; how E2 addition to the medium (1–100 nM, Sigma, diluted in serum-free William's E medium, supplemented with l-glutamine, penicillin, streptomycin, insulin, and hydrocortisone) affected hair shaft elongation, anagen duration, hair follicle pigmentation and hair matrix keratinocyte proliferation in microdissected, organ-cultured male anagen VI hair follicles from the frontotemporal scalp skin region.

Surprisingly, compared to the vehicle control, the hair shaft elongation of male frontotemporal scalp hair follicles was significantly stimulated by 1–100 nM E2 already as early as 1 d after the start of organ culture, and this stimulation became even more pronounced at the end of organ culture (days 7 and 9) Figure 1. This stimulation of hair shaft formation (which is the result of stringently coordinated proliferation and differentiation of hair matrix keratinocytes (Stenn and Paus, 2001) corresponded to a significant stimulation of hair matrix keratinocyte proliferation by 10 nM E2 at day 9 (average number of Ki-positive-cells: in the control group 14 cells (SEM 3.21) and 26 cells in the E2-treated (10 nM) group (SEM 4.38); level of significance: pless than or equal to0.05, Mann–Whitney test). While no evident differences were noted by H&E or Fontana–Masson histochemistry between E2- and vehicle-treated hair follicles in the hair follicle pigmentary unit or in the degree of hair follicle degeneration during organ culture (data not shown), a slight, though not statistically significant, anagen-prolonging effect of E2 was seen in E2-treated test hair follicles as compared to vehicle controls (data not shown).

There was a time dependant increase in hair follicle growth in frontotemporal hair follicles in 46 year old male, I presume with a full head of hair.

The question is, how does estrogen do this? Since there are no clear studies outlining which receptor mediates the hair growth promoting effects of Estrogen in males, nor are there any consistent animal studies with similar receptor actions, we are left to deduce.

ER beta is known to inhibit Hif-1 and VEGF as a means of counteracting the pro-carcinogenic effects of androgens on the prostate, which Ivee covered in more detail in my first post. And the prostate is more closely related to the scalp than female scalp tissue or mice skin. furthermore, this study shows how ER alpha enhances prostate cancer cell proliferation:

ABSTRACT

While high doses of estrogen, in combination with androgens, can initiate prostate cancer (PCa) via activation of the estrogen receptor α (ERα), the role of ERα in PCa cells within established tumors is largely unknown. Here we show that expression of ERα is increased in high grade human PCa. Similarly, ERα is elevated in mouse models of aggressive PCa driven by MYC overexpression or deletion of PTEN. Within the prostate of PTEN-deficient mice, there is a progressive pattern of ERα expression: low in benign glands, moderate in tumors within the dorsal, lateral and ventral lobes, and high in tumors within the anterior prostate. This expression significantly correlates with the proliferation marker Ki67. Furthermore, in vitro knockdown of ERα in cells derived from PTEN-deficient tumors causes a significant and sustained decrease in proliferation. Depletion of ERα also reduces the activity of the PI3K and MAPK pathways, both downstream targets of non-genomic ERα action. Finally, ERα knockdown reduces the levels of the MYC protein and lowers the sensitivity of cellular proliferation to glucose withdrawal, which correlates with decreased expression of the glucose transporter GLUT1. Collectively, these results demonstrate that ERα orchestrates proliferation and metabolism to promote the neoplastic growth of PCa cells.

There are studies talking briefly about the interaction between ER alpha and IGF-1R including upregulation, which the anabolic steroid stanozolol activates to increase muscle IGF1 levels.

This brings me back to the theory of using topical tamoxifen, which is a ER alpha agonist and ER beta antagonist. DHT seems to activate ER beta in the prostate via the 3Beta Diol metabolite and 3beta Diol is elevated in balding scalp as a result of increased 3 Beta HSD (which ketoconazole inhibits).

Topical tamoxifen has been shown to have minimal systematic absorbtion if used in doses up to 1mg with similar efficiency in blocking ER beta and activating ER alpha as higher doses.

There is also the theory that Estrogen receptors interact with Androgen metabolism (suppressing their activity), but I havent seen any significant links.

[Trouse5858]

I find the bit about estrogen receptors to be particularly interesting. I'm currently taking a SERM to reduce the effects of gyno I got after taking RU for several months. It's 30 mg of Raloxifene, said to be stronger than tamoxifen, that I am taking now every other day. It's not topical but I'll certainly try to keep my eye on any noticeable results, as unlikely as they are.

[baldybald]

This guy knows what he is talking about,won't be surprised if he got a cure for baldness!

[Medium]

Do you think that it's possible to mix the oleuropein capsules into castor oil instead of minox?

[Chemical]

I find the bit about estrogen receptors to be particularly interesting. I'm currently taking a SERM to reduce the effects of gyno I got after taking RU for several months. It's 30 mg of Raloxifene, said to be stronger than tamoxifen, that I am taking now every other day. It's not topical but I'll certainly try to keep my eye on any noticeable results, as unlikely as they are.

You probably wont notice any hair growth since any agonistic activity of raloxifene on ERa will be negated by DKK1 that is strongly induced by DHT. I'm more interested in seeing you use oleuropein with raloxifene since that'll address both ends of spectrum, and I plan to mix tamoxifen with a separate minox bottle to test out this theory in the next two weeks or so.

This guy knows what he is talking about,won't be surprised if he got a cure for baldness!

Why thank you baldybald, but I believe a cure can be found if we work together, combining our knowledge and trying novel approaches instead of just waiting for these big drug companies to give us false hope. These companies are just people motivated by money, with their time and resources they should be trying to figure out how the complex biomechanics work (like DKK1 and how it' actually induced or that there are might be other factors like 3Beta-Diol inhibiting hair follicle blood vessel formation) instead of blindly trying to create single compounds that will miraculously cure baldness in a vaccuum. The human body isn't black and white, its not just a few simple interactions either, its ridiculously complex with feedback loops designed to adapt and requires an approach that will tackle all the factors. "Igf-1 increases hair growth - lets spend millions trying to create compound that can deliver igf-1 to hair follicles, it worked in-vivo and in-vitro, so it will definitely work if we put in the necessary R&D". Its a system that can be exploited if you're brave enough to take calculated risks. Just my 2 cents that I'd wanted to share.

Do you think that it's possible to mix the oleuropein capsules into castor oil instead of minox?

I tried that, it did not go well. You end up with oleuropein still in its powder form and when the oil dries up it leaves a hard residue of oleuropein that is a nightmare, especially since I recommend applying the solution as often as possible to keep tissue concentrations high. You want the oleuropein to dissolve as much as possible so it can be carried through the skin layers by emu oil. Emu oil also helps with imflammation allowing you to use keto/mico and minox without irritation. I also dissolved saw palmetto, not sure if that actually did anything.

And here are some more recent pictures of my hairline. I've noticed alot less stubble since I stopped using it everyday (I'm just waiting for minoxidil to come through to make a new 3 month batch).

2 weeks ago:



You can see my most recent pictures here: http://imgur.com/a/g6TdQ

[Medium]

Great,
Thanks for the response.
My only concern is that I don't want to get on minox, so would dissolving the oleuropein capsules in emu oil still be effective?

[tiktok]

I plan on trying to use http://www.nowfoods.com/Olive-Leaf-G...tarian-2oz.htm with emu oil.

[Swooping]

Chemical thanks . I’ll get in on this discussion on a later point (busy atm). But here is what I think about androgenetic alopecia (AGA) as a whole. Hopefully it can help you.

First of all AGA is androgen and AR dependent right (Androgens > AR)? This begs the question; Why does AR activation lead to hair loss?
Well we don’t know, but to simplify it I would just like to call that AR activation causes cellular stress in AGA.

We can already maintain hair simply by castration. So we know that castration removes the “stress” right? So is it really beneficial for us to search for other “stress” factors beside the AR? One could argue it is because of possible better therapies that could give someone maintenance of their hair state. For instance let’s assume hypothetically that pathway “X” is implicated after AR activation in AGA. This would make the pathway chain; Androgens > AR > X. So if that was the case we could modulate X too and provide someone with maintenance of hair just like removing the AR would provide or castration does. Perhaps modulation of X would be something better because of a better side effect profile. This is exactly what Kythera (Cotsarelis) their hypothesis is made of. Instead of X however they argue that PGD2 functions highly upstream after AR activation and this leads to hair loss. So in their hypothesis modulation of PGD2 should work too (I don't think that is even the case but we will see.).

However will that bring back our hair? No right? I mean castration doesn't do it either. That is why I think in terms of reversal of AGA it’s less important to understand what causes the damage but rather what happens because of the damage. So let’s assume it is Androgens > AR > X. That causes the damage or “stress”. But what happens in response to that ? I have showed you the studies that points out to rather major pathways that seem to be implicated in AGA. And the thing is they seem to be implicated in stress responses like ROS and DNA damage. In this sense we can perhaps broaden the damage factor to DNA damage or ROS. So because of what happens in AGA these pathways react to the damage and this can be for example DNA damage or ROS. To make a example one might argue that Androgens > AR causes DNA damage and because of the DNA damage pathways come into action that react to this cellular stress.

Really I believe it all originates from the dermal papilla cells too. They are the master cells of the hair follicle. Dermal papilla numbers correlate with hair follicle size. A decline of dermal papilla is seen in AGA as the hair follicle continues to miniaturize. Several studies have pointed this out. Not only that we know that in bald scalp we lack progenitor cells. Well guess what? The dermal papilla regulates these progenitor cells. So if the dermal papilla cells get stressed and altered it could easily lead to a lack of progenitors. Studies have pointed out that the dermal papilla regulates progenitors as recently confirmed again by a abstract on the hair congress;

Getting It Right: Coordinating Progenitors and Their Niche to Specify Hair Size and Structure

ABSTRACT: The size and shape of the hair shaft is dependent on the number and activity of hair progenitor cells, which is in turn dependent on the number and activity of the dermal papilla cells that comprise their niche

Anyway back to the original point again. I have shown you the papers that point out the evidence of the pathways that seem to be implicated in AGA . And as you can see it is these pathways, exactly these pathways that react to cellular stress. I would like to simply call AGA cellular stress. Then they decide what action to take with a cell. Is it apoptosis? Is it senescence? Is it cell cycle arrest? Is it repair? What action is taken in AGA that leads to a miniaturized hair follicle? It might be even a combination for instance there might be a wave of apoptosis first before cell cycle arrest or senescence. For instance as seen here in a animal model;

http://s22.postimg.org/iojfxcpu9/senescne6.jpg

“Activation of P14, but not of P16, also caused a rapid but transient wave of apoptosis prior to the generation of senescent cells”.

As you can see it displays the multi-facetted role these pathways can take upon this stress and the several actions they can take."

What sort of stress or damage is it furthermore in AGA? Is it ROS or DNA damage? Maybe something else. I guess we don’t understand the specifics details yet. In my opinion the picture is becoming clear though. To no wonder, more and more researchers and studies are starting to point out in the same direction.

Finally here are some related pictures that go with this all.

Senescence (note how they mention that it causes SASP (inflammatory response, would explain the inflammation in AGA and also how they mention that it may not only affect differentiated cells but also stem and progenitor and limit the regenerative capacity of tissues):




Cell cycle (arrest):

[Swooping]

Forgot this one. Shows some pathways that are implicated in senescence due to different stress causes (DNA damage, ROS etc.);

[Chemical]

Great,
Thanks for the response.
My only concern is that I don't want to get on minox, so would dissolving the oleuropein capsules in emu oil still be effective?

I'm terribly sorry, I had a feeling you wanted to avoid minoxidil altogether, in which case you can make vehicle to dissolve the oleuropein with the following:

50% (v/v) ethanol, 30% water, and 20% propylene glycol.

You really need to dissolve the oleuropein so that it gets absorbed effectively.

I plan on trying to use http://www.nowfoods.com/Olive-Leaf-G...tarian-2oz.htm with emu oil.

The oleuropein extract would be ideal, and I wouldnt encourage anything else. You need the extract, not the leaf. Theres not a whole lot of brands out there that make oleuropein in extract form. Its a pain but it's worth it imo.

You probably wont notice any hair growth since any agonistic activity of raloxifene on ERa will be negated by DKK1 that is strongly induced by DHT. I'm more interested in seeing you use oleuropein with raloxifene since that'll address both ends of spectrum, and I plan to mix tamoxifen with a separate minox bottle to test out this theory in the next two weeks or so.

I'd also like to add that SERMs are especially useful for increasing testosterone by negating the negative feedback loop of estrogen on the pituitary, thus increasing LH and subsequently testosterone. More testosterone = more DHT and more DKK1. This is why its also important to have a serm that acts locally vith little systematic absorbtion, and raloxifene is very very potent stuff, along with tamox.

@Swooping

It seems you're a better researcher than me. This community needs more people like yourself.

Those diagrams are excellent. And I like your philosophy of targeting the root cause instead of damage control.

I'll keep this brief and to the point but I'll expand later.

Like you've pointed out, the DPC control the Mesenchymal stem cells, possibly by HGF/c-met, WNTs, and IGF1 which acts as a pro-survival cytokine. In short, if the DPC need to grow hair, they will signal to the progenitor cells to maintain their pluripotency. They stop growing, the progenitor no longer needs to be kept pluripotent and they may start to differentiate. This could explain why its hard for nw5s to grow back hair without aggressive treatment. However, these stem cells can be reactivated with consistent agonist activity and stimulation from IGF-1, EGF, or HGF/KGF. The AR is the cause of all of this. But I've given on this avenue because its notoriously difficult to inhibit AR locally and feasibly.

The pathways that induce senescence are not exactly a switch, they're actually on all the time. Its when they start winning the tug of war that bad stuff happens, like aging and hair loss. I'm also aware that ROS activates P53 and from the diagram it appears p16 and p21 too. I posted a study on my first post about L-threonate an Ascorbic Acid derivative abolishing the inhibitory effect of DHT-induced DKK1, where L-threonate completely prevented the growth inhibition. DHT is known to increase P53, and this study I found after a quick search does confirm the hypothesis that Androgens do increase reactive oxygen species generation (mitochondria dependant pathway in that study). ROS is a clear mediator of cellular apoptosis and senescence.

In aerobic organisms the energy needed to fuel biological functions is produced in the mitochondria via the electron transport chain. In addition to energy, reactive oxygen species (ROS) with the potential to cause cellular damage are produced. ROS can damage DNA, RNA, and proteins, which, in theory, contributes to the physiology of ageing.

ROS are produced as a normal product of cellular metabolism. In particular, one major contributor to oxidative damage is hydrogen peroxide (H2O2), which is converted from superoxide that leaks from the mitochondria. Catalase and superoxide dismutase ameliorate the damaging effects of hydrogen peroxide and superoxide, respectively, by converting these compounds into oxygen and hydrogen peroxide (which is later converted to water), resulting in the production of benign molecules. However, this conversion is not 100% efficient, and residual peroxides persist in the cell. While ROS are produced as a product of normal cellular functioning, excessive amounts can cause deleterious effects.[14] Memory capabilities decline with age, evident in human degenerative diseases such as Alzheimer's disease, which is accompanied by an accumulation of oxidative damage. Current studies demonstrate that the accumulation of ROS can decrease an organism's fitness because oxidative damage is a contributor to senescence.

And guess what, Ascorbic Acid and its derivates are known to be powerful ROS scavengers. So perhaps we need an effective ROS scavenger. The other tumor suppressor proteins could be ignored since we cannot and shouldnt trying to eliminate them, but preventing ROS generation will most definitely reduce the amount of DNA damage cause by androgens.

I'd like to hear your thoughts on this too.

[Trouse5858]

@ Chemical you're obviously very well informed on a lot of these topics. I was wondering if I could get your opinion on taking Raloxifene. I read somewhere that it can have a detrimental effect on libido, even though at the same time it is raising testosterone production. I was wondering if you could shed any light on this whatsoever. I may be feeling this side effect right now but it could also be a placebo..any insight on safe dosages or long term implications for men? Thanks

[Chemical]

@ Chemical you're obviously very well informed on a lot of these topics. I was wondering if I could get your opinion on taking Raloxifene. I read somewhere that it can have a detrimental effect on libido, even though at the same time it is raising testosterone production. I was wondering if you could shed any light on this whatsoever. I may be feeling this side effect right now but it could also be a placebo..any insight on safe dosages or long term implications for men? Thanks

Libido actually heavily depends on estrogen converted from testosterone via aromatase. The brain is quite sensitive to estrogen receptor changes, and among the steroid users who use ralox or tamox or even letro like I did, some notice a sharp decline in libido/sex drive, and a select few not so much. Its not a placebo effect if you're feeling it, but its short term so as soon as you stop you'll be fine. It also reduces sperm count temporarily. As for dosages, Ralox has a 27 hr half life, you're better off taking it everyday to reduce the gyno quicker, and you'll be able to come off it sooner. Its good for your HDL levels and unlike letro it wont **** up your bone mineral density so you dont have to be extra cautious when using it for more than 2 months, and I'd say its the best SERM out there to treat gyno.

[TheKingofFighters]

Libido actually heavily depends on estrogen converted from testosterone via aromatase. The brain is quite sensitive to estrogen receptor changes, and among the steroid users who use ralox or tamox or even letro like I did, some notice a sharp decline in libido/sex drive, and a select few not so much. Its not a placebo effect if you're feeling it, but its short term so as soon as you stop you'll be fine. It also reduces sperm count temporarily. As for dosages, Ralox has a 27 hr half life, you're better off taking it everyday to reduce the gyno quicker, and you'll be able to come off it sooner. Its good for your HDL levels and unlike letro it wont **** up your bone mineral density so you dont have to be extra cautious when using it for more than 2 months, and I'd say its the best SERM out there to treat gyno.

Wow thx for ur hard work! Can u check profile? Would oleupein help me in activating stem cells? Im using minoxidil but it has only grown some tiny baby hairs thst nv seem to terminal. Would oleupein turn them terminal?

[Trouse5858]

Yeah that was an even more in depth answer than I was anticipating, I appreciate the information.