280 replies to this topic

[noot_in_the_sky]

Great thread. Couple questions for Area1255 or anyone that can shed light on this:

 

1. Tribulus is recommended to increase DHT. From what I understand, trib contains phytosterols - including beta-sitosterol, which decreases DHT. Am I missing something here?

 

2. Does tongkat have any effect on DHT? I've read somewhere it might affect progesterone, which is the anti-DHT.

 

3. What's the final verdict on zinc? Good or bad for dht?

 

Thanks guys, very curious about this topic.

 

 

1.  We suggested for people to use the an extract with 80% or higher of Protodioscin, which is the compound that has been link to DHT increase. [Ref. 1]

 

2.  Perhaps it does by inhibiting the convertion of test to estrogen.[Ref. 2]

 

3. Zinc is good for DHT normal at normal and slightly high levels. [Ref. 4][Ref. 3]

 

 

[Ref. 1]

http://www.ncbi.nlm....rotodioscin dht

 

 

The hormonal effects of Tribulus terrestris and its role in the management of male erectile dysfunction--an evaluation using primates, rabbit and rat.

Gauthaman K1, Ganesan AP.

Abstract

Hormonal effects of Tribulus terrestris (TT) were evaluated in primates, rabbit and rat to identify its usefulness in the management of erectile dysfunction (ED). TT extract was administered intravenously, as a bolus dose of 7.5, 15 and 30 mg/kg, in primates for acute study. Rabbits and normal rats were treated with 2.5, 5 and 10mg/kg of TT extract orally for 8 weeks, for chronic study. In addition, castrated rats were treated either with testosterone cypionate (10mg/kg, subcutaneously; biweekly for 8 weeks) or TT orally (5mg/kg daily for 8 weeks). Blood samples were analyzed for testosterone (T), dihydrotestosterone (DHT) and dehydroepiandrosterone sulphate (DHEAS) levels using radioimmunoassay. In primates, the increases in T (52%), DHT (31%) and DHEAS (29%) at 7.5mg/kg were statistically significant. In rabbits, both T and DHT were increased compared to control, however, only the increases in DHT (by 30% and 32% at 5 and 10mg/kg) were statistically significant. In castrated rats, increases in T levels by 51% and 25% were observed with T and TT extract respectively that were statistically significant. TT increases some of the sex hormones, possibly due to the presence of protodioscin in the extract. TT may be useful in mild to moderate cases of ED.

 

 

[Ref. 2]

http://www.ncbi.nlm....pubmed/23810842

 

 

Eurycomanone, the major quassinoid in Eurycoma longifolia root extract increases spermatogenesis by inhibiting the activity of phosphodiesterase and aromatase in steroidogenesis.

Low BS1, Choi SB, Abdul Wahab H, Das PK, Chan KL.

Abstract

ETHNOPHARMACOLOGICAL RELEVANCE:

Eurycoma longifolia Jack (Simaroubaceae family), known locally as 'Tongkat Ali' by the ethnic population, is popularly taken as a traditional remedy to improve the male libido, sexual prowess and fertility. Presently, many tea, coffee and carbonated beverages, pre-mixed with the root extract are available commercially for the improvement of general health and labido. Eurycomanone, the highest concentrated quassinoid in the root extract of E. longifolia improved fertility by increasing testosteroneand spermatogenesis of rats through the hypothalamus-pituitary-gonadal axis, but the mechanisms underlying the effects are not totally clear.

AIM OF THE STUDY:

To provide evidences on the plant ethnopharmacological use and the involvement of eurycomanone, the major indigenous plant quassinoid in testosterone steroidogenesis and spermatogenesis increase.

MATERIAL AND METHODS:

The rat testicular Leydig cell-rich interstitial cells were isolated and incubated in the culture medium M199. The viability of the cells was determined with trypan blue staining and the concentration of the viable cells was counted with a haemocytometer. The 3β-hydroxysteroid dehydrogenase (HSD) staining method was used to measure the abundance of Leydig cells in the preparation. Eurycomanone and the standard steroidogenesis inhibitors were incubated with 1.0 × 10(5) cells, and after 2h, thetestosterone and the oestrogen concentrations were determined by the ELISA method. Computational molecular docking was performed to determine the binding affinity of the compound at the respective steroidogenesis enzymes.

RESULTS:

Eurycomanone (EN) significantly increased testosterone production dose-dependently at 0.1, 1.0 and 10.0 μM (P<0.05), but the two lower doses when combined with 3-isobutyl-1-methylxanthine (IBMX), the phosphodiesterase inhibitor were not significantly higher than EN or IBMX alone, except at a higher concentration. The molecular docking studies indicated EN and IBMX were binding at different sites of the enzyme. EN has no reversal of inhibition by aminoglutethimide, ketoconazole or nifedipine at the respective steroidogenesis enzyme. The quassinoid was also non-responsive to the inhibition of oestrogen receptor by tamoxifen, but displayed improved formestane inhibition of aromatase in reducing oestrogen production. The molecular docking studies further supported that EN and formestane bound to aromatase with similar orientations and free energy binding values.

CONCLUSION:

Eurycomanone enhanced testosterone steroidogenesis at the Leydig cells by inhibiting aromatase conversion oftestosterone to oestrogen, and at a high concentration may also involve phosphodiesterase inhibition. The quassinoid may be worthy for further development as a phytomedicine to treat testosterone-deficient idiopathic male infertility and sterility.

 

 

[Ref. 3]

     http://www.ncbi.nlm..../pubmed/8279712

 

 

Zinc arginine, a 5 alpha-reductase inhibitor, reduces rat ventral prostate weight and DNA without affecting testicular function.

Fahim MS1, Wang M, Sutcu MF, Fahim Z.

Abstract

Zinc has been implicated in steroid endocrinology of the prostate gland; and 5 alpha-dihydrotestosterone (DHT) is believed to express androgenic responses in the prostate. To note the effect of neutralized zinc (zinc gluconate + arginine) on the prostate, 50 sexually mature rats, weighing 325 +/- 20 g, were divided into five groups as follows: (1) control, (2) sham, (3) castrated, and injected intraprostatically with (4) 10 mg neutralized zinc, and (5) 20 mg neutralized zinc. Results indicated significant reduction (P < 0.05) of prostate weight, 5 alpha-reductase activity, and total protein and DNA concentrations in treated prostate tissue; no significant change in weight and histological structure of testes, epididymides, and seminal vesicles; and no significant effect on progeny and blood testosterone level of treated animals. These results suggest that direct application of neutralized zinc to the prostate offers a new modality for treatment of prostatitis without affecting spermatogenesis.

 

[Ref. 4]

http://www.ncbi.nlm..../pubmed/7271365

 

Effect of zinc administration on plasma testosterone, dihydrotestosterone, and sperm count.

Netter A, Hartoma R, Nahoul K.

Abstract

The effects of zinc therapy on plasma testosterone (T), dihydrotestosterone (DHT), and sperm count were studied in 37 patients with idiopathic infertility of more than five years duration. In the first group (T less than 4.8 ng/ml; 22 patients), T and DHT rose significantly after oral administration of zinc, as did the sperm count. Nine wives became pregnant, six within 3 months and three within 2 months of a second trial. In the second group (T greater than or equal to 4.8 ng/ml; 15 patients), T and sperm count were unaffected by zinc, while DHT increased significantly. There was no conception observed. The rationale of this treatment and the significance of the results are discussed.

[vrain]

Thanks for taking the time Noot. So a little more clarification just to make sure I have this right;

 

Are you saying tongkat increases dht? I've heard it may do the opposite because of an increase in progesterone. Any one have any insight to this? Sorry, no study, just a long ass thread I read years ago on Mind & Muscle when intelligent people used to post. Also mentions something along these lines on the herbal powers site (primary distributor of lj100). It is suggested the rise in progesterone may cause the decrease in estrogen. I could be right out to lunch on this, just wondering if anyone has any knowledges on this particular aspect of TA.

 

So normal or high doses of zinc increase dht? And so low doses do what....decrease it? What constitutes a low or high dose?

 

Thanks again, I'm reading so much conflicting info its making my head spin.

[noot_in_the_sky]

"Are you saying tongkat increases dht? I've heard it may do the opposite because of an increase in progesterone. Any one have any insight to this? "

If you want a definetly answer for this then you have to do blood test yourself, since it's rare for studies to directly measuer DHT

 

 

"So normal or high doses of zinc increase dht? And so low doses do what....decrease it? What constitutes a low or high dose?"

The upper tolerance is at 40 mg/day for someone 19years old and up.

 

 

https://ods.od.nih.g...rofessional/#h5

 

 

Zinc Deficiency

Zinc deficiency is characterized by growth retardation, loss of appetite, and impaired immune function. In more severe cases, zinc deficiency causes hair loss, diarrhea, delayed sexual maturation, impotence, hypogonadism in males, and eye and skin lesions [2,8,24,25]. Weight loss, delayed healing of wounds, taste abnormalities, and mental lethargy can also occur [5,8,26-30]. Many of these symptoms are non-specific and often associated with other health conditions; therefore, a medical examination is necessary to ascertain whether a zinc deficiency is present.

Zinc nutritional status is difficult to measure adequately using laboratory tests [2,31,32] due to its distribution throughout the body as a component of various proteins and nucleic acids [33]. Plasma or serum zinc levels are the most commonly used indices for evaluating zinc deficiency, but these levels do not necessarily reflect cellular zinc status due to tight homeostatic control mechanisms [8]. Clinical effects of zinc deficiency can be present in the absence of abnormal laboratory indices [8]. Clinicians consider risk factors (such as inadequate caloric intake, alcoholism, and digestive diseases) and symptoms of zinc deficiency (such as impaired growth in infants and children) when determining the need for zinc supplementation [2].

 

   https://ods.od.nih.g...rofessional/#h8

 

 

 

Zinc toxicity can occur in both acute and chronic forms. Acute adverse effects of high zinc intake include nausea, vomiting, loss of appetite, abdominal cramps, diarrhea, and headaches [2]. One case report cited severe nausea and vomiting within 30 minutes of ingesting 4 g of zinc gluconate (570 mg elemental zinc) [81]. Intakes of 150–450 mg of zinc per day have been associated with such chronic effects as low copper status, altered iron function, reduced immune function, and reduced levels of high-density lipoproteins [82]. Reductions in a copper-containing enzyme, a marker of copper status, have been reported with even moderately high zinc intakes of approximately 60 mg/day for up to 10 weeks [2]. The doses of zinc used in the AREDS study (80 mg per day of zinc in the form of zinc oxide for 6.3 years, on average) have been associated with a significant increase in hospitalizations for genitourinary causes, raising the possibility that chronically high intakes of zinc adversely affect some aspects of urinary physiology [83].

 

[noot_in_the_sky]

Soo what's the word, is there any reliable way to increase DHT besides creatine supplementation?
Should normal AI's be avoided at all costs?

 

 

This is a bit late of an answer, but I guess better late then never.

 

The answer is normal AI's are good to raise DHT -it will just depend a lot on each person.  Somethings that can affect your response to an AI are body fat, age, health, E levels, and if some form of HRT is been use either with SERM, Test, or Hcg.

 

 

Arimidex is that it's a reversible inhibitor with only  ~48h of half-life which is great to avoid lowering Estrogen too much.  It's also good for people who get a negative feedback fast. It also only lowers Estrogen 50% so that's to low to dry your joint up.  It also lowers IGF-1 for dose of you who want to keep that in check.  It has no change in SHBG and GH.

 

 Arimidex can be use .5mg every other day or so.  I have seen people using 1mg twice a week with Clomid and DAA.

 

 

Aromasin, base of indirect data, is the King of DHT when we talk about AIs.  Aromasin is a irreversible aromatase inhibitor so even though its half-life is less then 24 hours healthy male's don't return to base line until 4 to 5 days after one 25mg dose.  This is the one that gave made me loss hair (once more I'm in my 20s with my family not having a history of bold men).  If you look in forums users of Aromasin are more likely to report loosing hair the most.  Also Aromasin doesn't affect IGF-1, and decreases SHBG leaving more test to become DHT and allowing DHT to be free.  One of its metabolites can act as a weak androgen or increase the effects of androgen hormones -scientist aren't sure.

 

 A possible use which I haven't tested yet, is to take Aromasin once a week or perhaps use it twice with the second dose on the 3 or 4 day after the initial dose.  Perhaps I can also add some Arimidex just to keep the E low i

 

 

Letrozole has a long half-life, and it's been know to drop Estrogen too much.  However, in a study it was able to raise DHT enough that it completely negated the effect of finasteride. It also doesn't affect IGF-1. I haven't try this one yet.

 

 

 

Studies:

 

Arimidex

http://press.endocri.../jcem.85.7.6676

 

Estrogen Suppression in Males: Metabolic Effects

 

Abstract

We have shown that testosterone (T) deficiency per se is associated with marked catabolic effects on protein, calcium metabolism, and body composition in men independent of changes in GH or insulin-like growth factor I production. It is not clear, however, whether estrogens have a major role in whole body anabolism in males. We investigated the metabolic effects of selective estrogen suppression in the male using a potent aromatase inhibitor, Arimidex (Anastrozole). First, a dose-response study of 12 males (mean age, 16.1 ± 0.3 yr) was conducted, and blood withdrawn at baseline and after 10 days of oral Arimidex given as two different doses (either 0.5 or 1 mg) in random order with a 14-day washout in between. A sensitive estradiol (E2) assay showed an approximately 50% decrease in E2 concentrations with either of the two doses; hence, a 1-mg dose was selected for other studies. Subsequently, eight males (aged 15–22 yr; four adults and four late pubertal) had isotopic infusions of [13C]leucine and 42Ca/44Ca, indirect calorimetry, dual energy x-ray absorptiometry, isokinetic dynamometry, and growth factors measurements performed before and after 10 weeks of daily doses of Arimidex. Contrary to the effects of T withdrawal, there were no significant changes in body composition (body mass index, fat mass, and fat-free mass) after estrogen suppression or in rates of protein synthesis or degradation; carbohydrate, lipid, or protein oxidation; muscle strength; calcium kinetics; or bone growth factors concentrations. However, E2 concentrations decreased 48% (P = 0.006), with no significant change in mean and peak GH concentrations, but with an 18% decrease in plasma insulin-like growth factor I concentrations. There was a 58% increase in serum T (P = 0.0001), sex hormone-binding globulin did not change, whereas LH and FSH concentrations increased (P < 0.02, both). Serum bone markers, osteocalcin and bone alkaline phosphatase concentrations, and rates of bone calcium deposition and resorption did not change. In conclusion, these data suggest that in the male 1) estrogens do not contribute significantly to the changes in body composition and protein synthesis observed with changing androgen levels; 2) estrogen is a main regulator of the gonadal-pituitary feedback for the gonadotropin axis; and 3) this level of aromatase inhibition does not negatively impact either kinetically measured rates of bone calcium turnover or indirect markers of bone calcium turnover, at least in the short term. Further studies will provide valuable information on whether timed aromatase inhibition can be useful in increasing the height potential of pubertal boys with profound growth retardation without the confounding negative effects of gonadal androgen suppression.

 

 

Aromasin

http://press.endocri.../jc.2003-031279

 

Pharmacokinetics and Dose Finding of a Potent Aromatase Inhibitor, Aromasin (Exemestane), in Young Males

 

Suppression of estrogen, via estrogen receptor or aromatase blockade, is being investigated in the treatment of different conditions. Exemestane (Aromasin) is a potent and selective irreversible aromatase inhibitor. To characterize its suppression of estrogen and its pharmacokinetic (PK) properties in males, healthy eugonadal subjects (14–26 yr of age) were recruited. In a cross-over study, 12 were randomly assigned to 25 and 50 mg exemestane daily, orally, for 10 d with a 14-d washout period. Blood was withdrawn before and 24 h after the last dose of each treatment period. A PK study was performed (n = 10) using a 25-mg dose. Exemestane suppressed plasma estradiol comparably with either dose [25 mg, 38% (P ≤ 0.002); 50 mg, 32% (P ≤ 0.008)], with a reciprocal increase in testosterone concentrations (60% and 56%; P ≤ 0.003 for both). Plasma lipids and IGF-I concentrations were unaffected by treatment. The PK properties of the 25-mg dose showed the highest exemestane concentrations 1 h after administration, indicating rapid absorption. The terminal half-life was 8.9 h. Maximal estradiol suppression of 62 ± 14% was observed at 12 h. The drug was well tolerated. In conclusion, exemestane is a potent aromatase inhibitor in men and an alternative to the choice of available inhibitors. Long-term efficacy and safety will need further study.

 

Letro

http://www.sciencedi...197018615300516

 

Reduced estradiol synthesis by letrozole, an aromatase inhibitor, is protective against development of pentylenetetrazole-induced kindling in mice

 

Abstract

 

Neurosteroids, such as testosterone and their metabolites, are known to modulate neuronal excitability. The enzymes regulating the metabolism of these neurosteroids, thus, may be targeted as a noval strategy for the development of new antiepileptic drugs. The present work targeted two such enzymes i,e aromatase and 5α-reductase in order to explore the potential of letrozole (an aromatase inhibitor) on pentylenetetrazole (PTZ)-induced kindling in mice and the ability of finasteride (a 5α-reductase inhibitor) to modulate any such effects. PTZ (30 mg/kg, i.p.), when administered once every two days (for a total of 24 doses) induced kindling in Swiss albino mice. Letrozole (1 mg/kg, p.o.), administered prior to PTZ, significantly reduced the % incidence of kindling, delayed mean onset time of seizures and reduced seizure severity score. Letrozole reduced the levels of plasma 17β-estradiol after induction of kindling. The concurrent administration of finasteride and letrozole produced effects similar to letrozole on PTZ-kindling and on estradiol levels. This implies that the ability of letrozole to redirect the synthesis of dihydrotestosterone (DHT) and 5α-androstanediol from testosterone doesn't appear to play a significant role in the protective effects of letrozole against PTZ kindling. Letrozole, however, increased the levels of 5α-DHT in mice plasma. The aromatase inhibitors, thus, may be exploited for inhibiting the synthesis of proconvulsant (17β-estradiol) and/or redirecting the synthesis of anticonvulsant (DHT and 5α-androstanediol) neurosteroids.

 

The graph with the effect of letro in DHT

 1-s2.0-S0197018615300516-gr2.jpg   38.98KB   3 downloads

 

 

 

Some random study on DHT E2:

http://www.ncbi.nlm....pubmed/26483631

 

 

Neo-synthesis of estrogenic or androgenic neurosteroids determine whether long-term potentiation or depression is induced in hippocampus of male rat.

Di Mauro M1, Tozzi A2, Calabresi P3, Pettorossi VE1, Grassi S1.

Abstract

Estrogenic and androgenic steroids synthesized in the brain may rapidly modulate synaptic plasticity interacting with specific membrane receptors. We explored by electrophysiological recordings in hippocampal slices of male rat the influence of 17β-estradiol (E2) and 5α-dihydrotestosterone (DHT) neo-synthesis on the synaptic changes induced in the CA1 region. Induction of long-term depression (LTD) and depotentiation (DP) by low frequency stimulation (LFS, 15 min-1 Hz) and of long-term potentiation (LTP) by high frequency stimulation (HFS, 1 s-100 Hz), medium (MFS, 1 s-50 Hz), or weak (WFS, 1 s-25 Hz) frequency stimulation was assayed under inhibitors of enzymes converting testosterone (T) into DHT (5α-reductase) and T into E2 (P450-aromatase). We found that LFS-LTD depends on DHT synthesis, since it was fully prevented under finasteride, an inhibitor of DHT synthesis, and rescued by exogenous DHT, while the E2 synthesis was not involved. Conversely, the full development of HFS-LTP requires the synthesis of E2, as demonstrated by the LTP reduction observed under letrozole, an inhibitor of E2 synthesis, and its full rescue by exogenous E2. For intermediate stimulation protocols DHT, but not E2 synthesis, was involved in the production of a small LTP induced by WFS, while the E2 synthesis was required for the MFS-dependent LTP. Under the combined block of DHT and E2 synthesis all stimulation frequencies induced partial LTP. Overall, these results indicate that DHT is required for converting the partial LTP into LTD whereas E2 is needed for the full expression of LTP, evidencing a key role of the neo-synthesis of sex neurosteroids in determining the direction of synaptic long-term effects.

 

Edited by noot_in_the_sky, 26 December 2015 - 08:09 PM.

[Tubzy]

Also, IGF stimulates 5AR and the androgen receptor. So GH peptides could definitely help

[Tubzy]

Also, IGF stimulates 5AR and the androgen receptor. So GH peptides could definitely help

this da study?
http://www.ncbi.nlm....les/PMC3195902/
http://www.ncbi.nlm....pubmed/19251054

Yeah , plus it will repair the tissues/body faster in general bringing you to homeostatis quicker

[noot_in_the_sky]

 

 

Also, IGF stimulates 5AR and the androgen receptor. So GH peptides could definitely help

this da study?
http://www.ncbi.nlm....les/PMC3195902/
http://www.ncbi.nlm....pubmed/19251054

Yeah , plus it will repair the tissues/body faster in general bringing you to homeostatis quicker

 

 

 

Dam it guys, you beat me to the punch. 

 

I also found this info a few days ago and was going to share it.  Well at lease now I know that there are still people interested on this thread besides me.   

 

Anyhow,  I also found some interesting things while looking for information about IGF-1.

 

 

These things have a positive effect on IGF-1:

 

Cinnamon

A friend of mine has diabetes type 1, and neither cinnamon tea nor cinnamon pills seem to work for him.  However,  a family member has type 2 diabetes and they do have an improvement of glucose levels with cinnamon tea and pills.  This has made me wounder if the reason is the effect of Cinnamon on IGF-1, because people with type 1 diabetes have a IGF-1 deficiency.

 

 

Capsaicin

http://www.sciencedi...096637407000639

It's cheap I'm getting myself some cayenne pepper.

 

 

Ursolic Acid

http://www.ncbi.nlm....pubmed/21641545

 The downside is that the extract is to expensive, and most options out there don't have a high level of concentration making the user have to take multiple capsules each serving.  The best option is  powder form which is Ursolic Acid 25% from a Loquat extract; loquat has been know to have anti-diabetic effects.  A positive effect is that ursolic acid is also an DBH inhibitor.  Perhaps the Holy Basil extract would be better since it also was able to increase testosterone in rabbits.

 

 

Pleurotus eryngii

http://dx.doi.org/10...ajas.2011.11329

Haven't try it but seems good.

 

 

Tribulus Terrestis 

http://suppversity.b...g-125-gday.html

They use 1,250mg

 

MK-677

It raises IGF-1 in a dose dependent manner, and the downside is that it causes raise in prolactin and glucose levels.  Which makes it a big no no for diabetics.  The prolactin side effect can be counter acted by using something such as pramipexole or l-dopa which will also raise HGH.   People can combine also mk-677  with cinnamon tea to help with the raise in glucose, and to of course enhance IGF-1 function.

 

 

Caffeine

It seems that caffeine does this by increasing cAMP, which  Forskolin also does.  It's also been know that Forskolin increases testosterone, therefore Forskolin could be a good alternative.

 

 

 

Things to avoid:

 

Quercitin,  potent inhibitors of the type 1 5α-reductase

 

Myricetin, potent inhibitors of the type 1 5α-reductase

 

baicalein, potent inhibitors of the type 1 5α-reductase

 

fisetin, potent inhibitors of the type 1 5α-reductase

 

Oleic Acid(18:1),   inhibitors of the type 1 5α-reductase

 

Linolenic Acid(18:2),   inhibitors of the type 1 5α-reductase

 

 

EGCG, if gallate ester is replace with a fatty acids it produce an even more potent 5alpha-reductase inhibitors

 

Lauric Acid (12:0), inhibits both more potent 5alpha-reductase inhibitors

 

Biochanin A, better inhibitors of the type 2 than the type 1 isozyme

 

Daidzein, better inhibitors of the type 2 than the type 1 isozyme

 

Genistein, better inhibitors of the type 2 than the type 1 isozyme

 

Kaempferol, better inhibitors of the type 2 than the type 1 isozyme

 

 

Myristic Acid (14:0),  inhibitors of the type 2.  It's effect on 5aR1 was not tested.

 

EPA/DHA

 

GLA

 

 

 

No effects on 5aR:

 

Palmitic  Acid (16:0) was inactive on both

 

Stearic Acid (18:0) was inactive on both

                             

 

 

SOME RANDOM THOUGHTS:

 

According to Wikipedia, 5ar type 1 may be responsible for some virilization of mice that lack the 5ar type 2 gene, and it's also associated with increase strength of limps. So perhaps someone who doesn't want DHT, while also keeping strength, like say women can use the type 2 inhibitors while also increasing strength.

 

 

DHT helps with verbal fluency, it comes as no surprise if one remembers that DHT has an effect on GABA-a receptors, and how pharmaceutical anti-androgens can cause seizures.  It would also explain what Isochroma said about feeling that nootropics work better with increase levels of androgens. 

 

 

Would taking an androgen antagonist, not to be confuse with a 5AR inhibitor,  help to counter act the negative feedback loop of say TRT or an AI?  I know that pharmaceutical anti-androgen can be too strong, but how about a natural one like pygeum.  It's taken multiple times a day which means it probably has a short half-life.  I know some men have reported taking it to increase their ejaculation volume, but perhaps it can also help does on TRT, steroid, and/or AI.  Does anyone have any experience with this herb?

 

L-carnitine also increase Androgen Receptors, by protecting the muscle during stress.

 

Also according to Patrick Arnold is good to use Cobalt to help slow down the clearance of androgens from the body.  It does this by inhibiting P450, such as grapefruit juice.  The P450 also breaks down estrogen.

 

Does anyone have any idea if using laser hair removal affect the levels of androgens in the body?  I have been wondering this.  If body hair production protects men from too much DHT been made by the prostate or if it has a damping effect by taking hormones that could be use by other parts of the body like muscles.   It would be interesting to know the effects of laser hair removal in men specially if it increases in popularity.

 

Electrical muscle stimulation increase androgen receptors, but it may be because it causes the same effects of stress in the muscle as strength training.

 

 

This is irrelevant, but I have been think that may be for men who want to grow a bear they can use some caprilyc acid on their face to help sensitize the androgen receptors.

 

 

Caprilyc Acid UPDATE:

 

I notice an improvement in muscle and strength when I went from 1 cap(600mg)/day to 2 caps (1200mg)/day.  I try going to 3 and 4, but I didn't notice anymore improvement and I was getting an upset stomach at those amounts.  There seem to be a staturation point and anything over it is just pointless.

 

Also keep in mind that it has an effect on both estrogen and androgen hormones so it may be more useful with an AI.

 

 

Studies no particulate order:

 

 

Rapid increase in the number of androgen receptors following electrical stimulation of the rat muscle

 

Summary

The changes in the number of androgen receptors in rat gastrocnemius muscle following muscle contraction caused by electrical stimulation were investigated. The gastrocnemius muscle of one leg, which was selected at random for each rat, was stimulated with needle type electrodes, e.g. for 2 s at 10 V and 100 Hz, with 5-s intervals. The contralateral leg was left unstimulated as a control. One set consisted of ten such stimuli, followed by 5-min rest. Three sets every 2 days caused a statistically significant increase in muscle mass, the increase being about 2.5% after the 3rd day of stimulation, 4.4% after the 5th day, 5.9% after the 13th day and 8.3% after the 27th day compared with each control muscle (P< 0.001 in each case). The protein content also increased but the water content did not change. Stimulation over 4 weeks induced an increase in the area of the cross-section of the muscle fibres to about 30076 more than that of the control muscles, though the total muscle fibre numbers were slightly, but significantly, reduced. Electromechanical properties supported the development of the muscle by stimulation, because the maximal isometric tetanic force and peak twitch force markedly increased in the stimulated muscle. The androgen receptors in the muscle cytosol fraction were determined by means of a binding assay involving [3H]methyltrieno-lone, which is an analogue of testosterone, the number having rapidly increased in the stimulated leg, when compared with that in the control leg, by about 25% after the 3rd day. The increase then slowed down, reaching a plateau after the 5th-day of stimulation. The receptor dissociation constants for [3H]methyltrienolone remained unchanged, i.e. approximately 0.3 to 0.4 nmol throughout the experimental period. These findings suggested that a rapid increase in the number of androgen receptors occurred as an early event for a practical increase in muscle mass and thus it may have contributed in part to the triggering of muscle hypertrophy by enhancing the muscle sensitivity to androgen.

 

 

 

Cinnamon extract promotes type I collagen biosynthesis via activation of IGF-I signaling in human dermal fibroblasts.

Takasao N1, Tsuji-Naito K, Ishikura S, Tamura A, Akagawa M.

 

Abstract

The breakdown of collagenous networks with aging results in hypoactive changes in the skin. Accordingly, reviving stagnant collagen synthesis can help protect dermal homeostasis against aging. We searched for type I collagen biosynthesis-inducing substances in various foods using human dermal fibroblasts and found that cinnamon extract facilitates collagen biosynthesis. Cinnamon extract potently up-regulated both mRNA and protein expression levels of type I collagen without cytotoxicity. We identified cinnamaldehyde as a major active component promoting the expression of collagen by HPLC and NMR analysis. Since insulin-like growth factor-I (IGF-I) is the most potent stimulator of collagen biosynthesis in fibroblasts, we examined the effect of cinnamaldehyde on IGF-I signaling. Treatment with cinnamaldehyde significantly increased the phosphorylation levels of the IGF-I receptor and its downstream signaling molecules such as insulin receptor substrate-1 and Erk1/2 in an IGF-I-independent manner. These results suggested that cinnamon extract is useful in antiaging treatment of skin.

 

 

 

Sex hormone-related variations of cognitive performance in !Kung San hunter-gatherers of Namibia.

Christiansen K1.

 

Abstract

The relation of circulating sex hormones and cognitive abilities was investigated in 114 healthy !Kung San men ('bushmen') of Namibia/Southern Africa who lived mainly as traditional hunter-gatherers. Blood and saliva samples were analysed by use of radioimmunoassays in order to determine the serum concentrations of total testosterone (Tser), 5 alpha-dihydrotestosterone (DHT), and estradiol (E2), as well as the level of bioavailable, non-SHBG-bound 'free' testosterone in the saliva. The cognitive ability was assessed with two verbal (verbal fluency) and three nonverbal tests (tactual-spatial functioning, field independence/field dependence). As to be expected from previous research on Western samples, all three androgens but not E2 are of significance to the !Kung San men's cognitive performance. Tser exhibits a positive relation to tactual-spatial abilities and to the degree of lateralization of this task; on the other hand, Tser is negatively correlated with verbal fluency. Testosterone in the saliva is also significantly positively correlated to tactual-spatial test scores and, in addition, to field independence. DHT and the ratio DHT/Tser are positively related to verbal fluency and negatively to the degree of lateralization of tactual-spatial performance.

 

 

Sex hormones metabolism in the brain: influence of central acting drugs on 5 alpha-reduction in rat diencephalon.

Kaneyuki T, Kohsaka M, Shohmori T.

Abstract

Rats after adrenalectomy-testectomy showed a gradual increase in diencephalon 3-oxo-5 alpha-steroid: (acceptor) delta4-oxidoreductase (5 alpha-reductase) activity for 3 days. The activity then returned near to the normal range on the 4th postoperative day. When rats were given testosterone propionate (TP) 3 days after adrenalectomy-testectomy, diencephalon 5 alpha-reductase activity returned to the preoperative range 2 hr after TP administration. Diencephalon 5 alpha-reductase activity showed a highly significant increase (p less than 0.01) after a single administration of carbamazepine, reserpine, diazepam, phenytoin, phenobarbital or disulfiram. A significant increase (p less than 0.05) was also found after a single administration of methylphenidate, caffeine or methamphetamine. Plasma testosterone decreased concurrently after administration of all these agents, except diazepam. Diencephalon enzyme activity decreased significantly after repeated disulfiram administrations (p less than 0.01) but increased significantly after methamphetamine administrations (p less than 0.05). Plasma testosterone showed a tendency to decrease after repeated methamphetamine administrations but tended to increase after repeated disulfiram administrations.

 

 

 

5α-Reductase-catalyzed conversion of testosterone to dihydrotestosterone is increased in prostatic adenocarcinoma cells: suppression by 15-lipoxygenase metabolites of gamma-linolenic and eicosapentaenoic acids

 

 

Abstract

Although the androgens, testosterone (T) and its highly active metabolite dihydrotestosterone (DHT) play a role in the development and progression of prostate cancer, the mechanism(s) are unclear. Furthermore, 5α-reductase which catalyze the conversion of T to DHT, has been a target of manipulation in the treatment of prostatic cancer, hence synthetic 5α-reductase activity inhibitors have shown therapeutic promise. To demonstrate that nutrients derived from dietary sources can exert similar therapeutic promise, this study was designed using benign hyperplastic cells (BHC) and malignant tumorigenic cells (MTC) derived from Lobund–Wistar (L–W) rat model of prostatic adenocarcinoma to test the effects of gamma-linolenic acid (GLA), eicosapentaenoic acid (EPA) and their 15-lipoxygenase metabolites on cellular 5α-reductase activity. Our data revealed: (i) that incubation of MTC with []-T resulted in marked conversion to []-DHT when compared to similar incubation with BHC; (ii) that DHT-enhanced activity of 5α-reductase was inhibited 80% by 15S-hydroxyeicosatrienoic acid, the 15-lipoxygenase metabolite of GLA, when compared to 55% by 15S-hydroxyeicosapentaenoic acid, the 15-lipoxygenase metabolite of EPA; and (iii) that their precursor fatty acids, respectively, exerted moderate inhibition. Taken together, the study underscores the biological importance of 15-lipoxygenase metabolites of polyunsaturated fatty acids (PUFAs) in androgen metabolism.

 

 

Inhibition of type 1 and type 2 5α-reductase activity by free fatty acids, active ingredients of Permixon

Abstract

In different cell systems, the lipido-sterolic extract of Serenoa repens (LSESr, Permixon®) inhibits both type 1 and type 2 5α-reductase activity (5αR1 and 5αR2). LSESr is mainly constituted of fatty acids (90±5%) essentially as free fatty acids (80%). Among these free fatty acids, the main components are oleic and lauric acids which represent 65% and linoleic and myristic acids 15%.

 

To evaluate the inhibitory effect of the different components of LSESr on 5αR1 or 5αR2 activity, the corresponding type 1 and type 2 human genes have been cloned and expressed in the baculovirus-directed insect cell expression system Sf9. The cells were incubated at pH 5.5 (5αR2) and pH 7.4 (5αR1) with 1 or 3 nM testosterone in presence or absence of various concentrations of LSESr or of its different components. Dihydrotestosterone formation was measured with an automatic system combining HPLC and an on-line radiodetector.

 

The inhibition of 5αR1 and 5αR2 activity was only observed with free fatty acids: esterified fatty acids, alcohols as well as sterols assayed were inactive. A specificity of the fatty acids in 5αR1 or 5αR2 inhibition has been found. Long unsaturated chains (oleic and linolenic) were active (IC50=4±2 and 13±3 μg/ml, respectively) on 5αR1 but to a much lesser extent (IC50>100 and 35±21 μg/ml, respectively) on 5αR2. Palmitic and stearic acids were inactive on the two isoforms. Lauric acid was active on 5αR1 (IC50=17±3 μg/ml) and 5αR2 (IC50=19±9 μg/ml). The inhibitory activity of myristic acid was evaluated on 5αR2 only and found active on this isoform (IC50=4±2 μg/ml).

 

The dual inhibitory activity of LSESr on 5α-reductase type 1 and type 2 can be attributed to its high content in free fatty acids.

 

 

 

Chronic caffeine intake increases androgenic stimuli, epithelial cell proliferation and hyperplasia in rat ventral prostate.

Sarobo C1, Lacorte LM, Martins M, Rinaldi JC, Moroz A, Scarano WR, Delella FK, Felisbino SL.

Author information

 

Abstract

Coffee intake has been associated with a low risk of developing cancer, including prostate cancer, which is one of the most commonly diagnosed cancer in men. However, few studies have evaluated the chronic effects of caffeine, which is the most abundant methylxanthine in coffee, on prostate morphology and physiology. In the present study, we investigated the effects of chronic, low-dose caffeine intake on rat prostate morphology from puberty to adulthood. Five-week-old male Wistar rats were randomized into two experimental groups: caffeine-treated (20 ppm in drinking water, n = 12) and control (n = 12). The ventral and dorsolateral prostates were dissected, weighted and submitted to morphological, morphometrical and immunohistochemical analysis of cellular proliferation, apoptosis and androgen receptor (AR) tissue expression. The testosterone (T) and dihydrotestosterone (DHT) concentrations were measured in the plasma. Our results show that caffeine intake increased the concentrations of T and DHT, organ weight, epithelial cell proliferation and AR tissue expression in the ventral prostatic lobe. All the ventral prostates from the caffeine-treated animals presented various degrees of epithelial and stromal hyperplasia. Our results suggest that chronic caffeine intake from puberty increases androgenic signalling and cell proliferation in the rat prostate gland and can be related to the development of benign prostatic hyperplasia.

 

 

 

Ursolic Acid-induced elevation of serum irisin augments muscle strength during resistance training in men.

Bang HS1, Seo DY2, Chung YM3, Oh KM4, Park JJ5, Arturo F6, Jeong SH2, Kim N2, Han J2.

Author information

 

Erratum in

Corrigendum to: Ursolic Acid-Induced Elevation of Serum Irisin Augments Muscle Strength During Resistance Training in Men. [Korean J Physiol Pharmacol. 2014]

Abstract

Ursolic acid (UA), a type of pentacyclic triterpenoid carboxylic acid purified from natural plants, can promote skeletal muscle development. We measured the effect of resistance training (RT) with/without UA on skeletal muscle development and related factors in men. Sixteen healthy male participants (age, 29.37±5.14 years; body mass index=27.13±2.16 kg/m(2)) were randomly assigned to RT (n=7) or RT with UA (RT+UA, n=9) groups. Both groups completed 8 weeks of intervention consisting of 5 sets of 26 exercises, with 10~15 repetitions at 60~80% of 1 repetition maximum and a 60~90-s rest interval between sets, performed 6 times/week. UA or placebo was orally ingested as 1 capsule 3 times/day for 8 weeks. The following factors were measured pre-and post-intervention: body composition, insulin, insulin-like growth factor-1 (IGF-1), irisin, and skeletal muscle strength. Body fat percentage was significantly decreased (p<0.001) in the RT+UA group, despite body weight, body mass index, lean body mass, glucose, and insulin levels remaining unchanged. IGF-1 and irisin were significantly increased compared with baseline levels in the RT+UA group (p<0.05). Maximal right and left extension (p<0.01), right flexion (p<0.05), and left flexion (p<0.001) were significantly increased compared with baseline levels in the RT+UA group. These findings suggest that UA-induced elevation of serum irisin may be useful as an agent for the enhancement of skeletal muscle strength during RT.

 

 

mRNA expression signatures of human skeletal muscle atrophy identify a natural compound that increases muscle mass.

Kunkel SD1, Suneja M, Ebert SM, Bongers KS, Fox DK, Malmberg SE, Alipour F, Shields RK, Adams CM.

Author information

 

Abstract

Skeletal muscle atrophy is a common and debilitating condition that lacks a pharmacologic therapy. To develop a potential therapy, we identified 63 mRNAs that were regulated by fasting in both human and mouse muscle, and 29 mRNAs that were regulated by both fasting and spinal cord injury in human muscle. We used these two unbiased mRNA expression signatures of muscle atrophy to query the Connectivity Map, which singled out ursolic acid as a compound whose signature was opposite to those of atrophy-inducing stresses. A natural compound enriched in apples, ursolic acid reduced muscle atrophy and stimulated muscle hypertrophy in mice. It did so by enhancing skeletal muscle insulin/IGF-I signaling and inhibiting atrophy-associated skeletal muscle mRNA expression. Importantly, ursolic acid's effects on muscle were accompanied by reductions in adiposity, fasting blood glucose, and plasma cholesterol and triglycerides. These findings identify a potential therapy for muscle atrophy and perhaps other metabolic diseases.

 

 

 

Structure–activity relationships for inhibition of human 5α-reductases by polyphenols

• Richard A. Hiipakka, 
• Han-Zhong Zhang, 
• Wei Dai, 
• Qing Dai, 
• Shutsung Liao^, 

 

Abstract

The enzyme steroid 5α-reductase (EC 1.3.99.5) catalyzes the NADPH-dependent reduction of the double bond of a variety of 3-oxo-Δ⁴ steroids including the conversion of testosterone to 5α-dihydrotestosterone. In humans, 5α-reductase activity is critical for certain aspects of male sexual differentiation, and may be involved in the development of benign prostatic hyperplasia, alopecia, hirsutism, and prostate cancer. Certain natural products contain components that are inhibitors of 5α-reductase, such as the green tea catechin (−)-epigallocatechin gallate (EGCG). EGCG shows potent inhibition in cell-free but not in whole-cell assays of 5α-reductase. Replacement of the gallate ester in EGCG with long-chain fatty acids produced potent 5α-reductase inhibitors that were active in both cell-free and whole-cell assay systems. Other flavonoids that were potent inhibitors of the type 1 5α-reductase include myricetin, quercitin, baicalein, and fisetin. Biochanin A, daidzein, genistein, and kaempferol were much better inhibitors of the type 2 than the type 1 isozyme. Several other natural and synthetic polyphenolic compounds were more effective inhibitors of the type 1 than the type 2 isozyme, including alizarin, anthrarobin, gossypol, nordihydroguaiaretic acid, caffeic acid phenethyl ester, and octyl and dodecyl gallates. The presence of a catechol group was characteristic of almost all inhibitors that showed selectivity for the type 1 isozyme of 5α-reductase. Since some of these compounds are consumed as part of the normal diet or in supplements, they have the potential to inhibit 5α-reductase activity, which may be useful for the prevention or treatment of androgen-dependent disorders. However, these compounds also may adversely affect male sexual differentiation.

[Tubzy]

Good stuff man. Yeah I actually read that cinnamon study a few months ago , it's good stuff. I add a big scoop of organic ceylon cinnamon into my post workout shake and also in my Greek yogurt.

While I'm on peptides I also use R-ALA along with cinnamon and fish oil for insulin resistance and blood sugar support.

Also a product called Quadracarn is good too if you are looking at ALCAR and glucose support.

For the peptides, I tried mk677 for a few months but it just made me so hungry all the time and hold water lol. I just switched to the mod grf 129 and ipamorelin stack and may add in epitalon. I read the shorter pules of GH are better than the longer acting pulse (like mk 677). So maybe mk677 should be avoided due to the cortisol and prolactin effects and stick with the cleaner short acting peptides. I seem to be leaning out better and skin has improved. Not water retention too. And yes I have noticed an increase in libido which I didn't notice on mk677 (possibly from the elevated prolactin?)

I'm pretty much recovered, just trying to get my consistent rock hard morning woods back. Get them and off just want them consistent again like prefin.

Edited by Tubzy, 07 February 2016 - 08:52 PM.

[noot_in_the_sky]

I also was avoiding MK-677 because of its effect on cortisone and prolactin, but I have been trying it the last few weeks.  I got some from someone who didn't wanted it, because it raise there sugar levels to high.  I had already finish my previous bash, and my previous supplier isn't selling anymore  so I figure I was going to give MK-677 a shot.

 

I'm using 5mg/day of MK-677 with some pramipexole, and I did notice an effect in libido without the hunger.  At does doses MK-677 feels like a bit stronger then 80mcg x 2/day ipamorelin.  Anyhow, as I said it's just a trial of MK-677, and I'm also worry about the effect on fasting glucose, so I may just leave it after I'm done with this bottle or use it from a few times a year to let my body rest from the injections.

 

Btw, where are you getting your ipamorelin from?  Can you pm your source?

[Tubzy]

I also was avoiding MK-677 because of its effect on cortisone and prolactin, but I have been trying it the last few weeks. I got some from someone who didn't wanted it, because it raise there sugar levels to high. I had already finish my previous bash, and my previous supplier isn't selling anymore so I figure I was going to give MK-677 a shot.

I'm using 5mg/day of MK-677 with some pramipexole, and I did notice an effect in libido without the hunger. At does doses MK-677 feels like a bit stronger then 80mcg x 2/day ipamorelin. Anyhow, as I said it's just a trial of MK-677, and I'm also worry about the effect on fasting glucose, so I may just leave it after I'm done with this bottle or use it from a few times a year to let my body rest from the injections.

Btw, where are you getting your ipamorelin from? Can you pm your source?

MK seemed like an oral version of GHRP 6 for me. I was taking 25mg a day when I started then cut the dose in half. I was still holding some water though. IPA and mod grf way way better in terms of leaness and NO water weight.

I'm starting epitalon too only downside is the price but it can help normalize FSH/LH/prolactin along with other multiple benefits.

Yeah I'll send you a PM.

[Tubzy]

any update on this?

[noot_in_the_sky]

any update on this?

 

 

I try 2mg IGF-1 LR3 follow by Ipamoreline + CJC with Dac  from peptide science, and I wasn't very impress with IGF-1.  My felling was that it may have been under dose.

 

My experience with IGF-1:

1. I didn't loose fat.

 

2. I didn't seem to gain much muslce.

 

3. After 40 min of my first dose @ 60mcg I check my glucose level & it was 83.  Some people say that IGF-1 should lower your blood glucose levels a lot and make you feel hungry.  This didn't happen.  I did feel a bit depress, but don't know if it was because it lower my blood glucose.  I try eating something sweat, and it help most of the time, but don't know.

 

4. It did gave me an increase pump.   I know that the LR3 form should have 20 - 30hr half-life, so I use it early in the morning and exercise later in the day.  So at have the proper half-life.

 

5. It seem to increase my testicle size just a bit, an other know effect of IGF-1.

 

6. My body temperature felt higher.

 

 

Overall:

 I'm not going to use Peptide Science IGF-1 LR3 again.  It's too expensive and didn't really give me my moneys worth.  Even at .1mg /day I didn't saw the muscle building, fat shredding effect.  Too bad since I was really had high expectations from this.  Especially after reading a paper about IGF-1 causing virilization on women with IGF-1 deficiency.  I'll be trying an other web site and see how their stuff compares.

 

 

My experience with Ipamoreline + CJC with DAC from peptide science:

1.  A few minutes after injecting myself my hand got numb. I read this can be a side of increase GH.

 

2. My body temperature felt higher.

 

3. I seem to have lost some fat.

 

4. No visible gains of muscle.

 

5. My sleep improve a bit.

 

6. I got very ichy at the site of the injection as if I had an allergic reaction.

 

Overall:

I like this one more then the IGF-1 LR3, and it's cheaper.  I only use it after the IGF-1 LR3, since I read about using Ipa+CJC w/ DAC after an IGF-1 cycle.  Similar to running a SERM+HCG after an steroid cycle.  All I'm going to say is that this one is here to stay, perhaps I'll cycle it with MK 677 to let my body rest from the injections.

 

 

I'll recommend to get Epitalon from Ceretropics, and get the N-Acetyl Epitalon Amidate form.  I have use it before and it does help.  One thing I notice with N-Acetyl Epitalon Amidate  vs  Epitalon, is that I got more vivid dreams of people in my past.  I hear Ed Park on youtube mention this as a side effect he got from telemarse activation.  I don't attribute it to placebo, because I heard this after been on Epitalon for several weeks and already experiencing that effect.

 

 

I'll be posting some very good info I found about DHT and IGF-1 this week, but I still need to get it all together.

 

Here is the video I'm referring to, it's a talk with Liz Parrish the gene therapy lady:

 

Edited by noot_in_the_sky, 06 April 2016 - 02:48 PM.

[BasicBiO]

Your IGF-1 experiences are pretty much par for the course with most users and myself.  It won't put mass on you and is really for those advanced physique competitors hoping to activate a few more satellite cells to "hopefully" make hypertrophic in the future. IMO, it's best use is for us mortals is healing injuries. Healed a class 3-4 sprained ankle for me in a week or so.

[Nero]

Hair loss causes more psychological problems then dht blockers.   The younger generation isn't going through hair loss like the generation before them  look at guys like Justin Bieber , Zac Efron , Zayn Malik.  These guys went through puberty and haven't lost a single hair.  They don't have dht resistant scalps but were smart enough to get on propecia before puberty.   Justin Bieber even hinted he was on anti-androgen propecia by  making fun of prince William about his hair loss.

Edited by Nero, 14 April 2016 - 10:44 PM.

[gamesguru]

prolactin too...

Transcriptional regulation of the mouse steroid 5α-reductase type II gene by progesterone in brain

from a patent that might be BS:
"An isolated DNA molecule capable of acting as a promoter for the type II 5α-reductase gene derived from human beings, the DNA molecule being selected from the group consisting of:
(a) a polynucleotide comprising the DNA sequence represented by SEQ ID NO:1, the polynucleotide comprising a continuous DNA sequence extending from position 1 to 6022;"

[EhrenM]

DHT and Androgens may protect against Amyotrophic Lateral Sclerosis (Lou Gehrig's Disease).

Androgen Exposure May Put the Finger on ALS Risk

 

Arch Neurol. 1980 Mar;37(3):129-31.

Possible role of androgen receptors in amyotrophic lateral sclerosis. A hypothesis.

Weiner LP.

Abstract

Androgen receptors have been demonstrated in both cranial nerve and spinal motor neurons. This article proposes that amyotrophic lateral sclerosis (ALS) may be a disease in which androgen receptors in motor neurons are lost or not functioning. This is suggested by the male-to-female ratio of the disease, the age of onset, and the sparing of neurons of cranial nerves III, IV, and VI that coincidentally lack androgen receptors. The hypothesis is that ALS may be due to a loss of androgen receptors that results in an inability to respond to a variety of insults including axonal damage.

PMID:   7356416   [PubMed - indexed for MEDLINE]

 

[EhrenM]

(Dihydrotestosterone) Ameliorates Degeneration in Muscle, Axons and Motoneurons and Improves Motor Function in Amyotrophic Lateral Sclerosis 

Edited by EhrenM, 25 May 2016 - 06:36 PM.

[gamesguru]

The promoter of the rat 5alpha-reductase type 1 gene is bidirectional and Sp1-dependent.

Method and compositions for regulation of 5-alpha reductase activity US 6696484 B2

[Brazzo]

To all the guys how tried masteron/proviron, doesn't your prostata swell up on it?

[PeaceAndProsperity]

I have been using masteron now, 300 MG E3D from this source, geneza : https://www.napsgear.org/product_info.php?ref=2522&products_id=6717
for 3 months now. I've noticed the following and am very impressed, this isn't a spam message.

• extreme drying, all my veins are suddenly poking out!
• massive libido increase, and increase in motivational drive.
• holy supreme strength for workouts, and my lifts have went up 50 lbs!
• i can run an extra 10 miles without getting worn out!
• i put 6 lbs on of pure muscle. (have been using black ant extract too though)

What about your voice? Has your voice deepened? What about body hair growth?
It seems that estrogen crashes are a problem with masteron.

Edited by YOLF, 14 July 2016 - 09:38 AM.

[JayZin]

This awesome post needs to be bumped, just unearthed it!

[PeaceAndProsperity]

You can order anabolics and male hormones online but you're eventually going to get caught, unless you live in the UK.

[Wagner83]

I'd like to increase DHT, I've tried sorghum which, sure enough, leads to increased hair loss. I have had nice benefits from sorghum a few times but it seems to become inefficient afterwards.

I also have highish shbg, since dht has very high binding affinity with shbg wouldn't it make sense to think over time shbg will increase if we try to increase dht?

The only herbs that I see I could benefit from are the famous nettle root extract (divanil) and tongkat ali if it ever does what it is supposed to do. Although I'd bet the body would be smart enough to adapt to those fairly quickly as well (even if used 5 on 2 off).

[PeaceAndProsperity]

since dht has very high binding affinity with shbg wouldn't it make sense to think over time shbg will increase if we try to increase dht?

 

Fortunately that's not how it works. SHBG is almost entirely dependent upon estrogen levels. That's what the body checks for when it raises SHBG.

Dht may extremely poorly reduce lh levels but that's so small a change that it doesn't matter.

[Wagner83]

Ok is that backed by science , personal experience or personal belief? (just curious)

I don't understand why I'd get good effects from sorghum for a few days and then none. 

 

Coffee and sorghum seem to work to increase dht, however wouldn't the body become immune to whatever process increases 5AR in those foods? 

 

I also remember using white button mushrooms in large quantities for days/ weeks, I would get a lot of hair loss from it, more facial and body hair growth, weird symptoms in the spine and joints, wet dreams (had none for the past decade ) and yet I wouldn't feel that much better overall (libido wise, erection wise, mood wise). Does it make sense if I say wbm may lower estrogen too low if one has average E2 levels and eats copious amount of them over a decent period of time?

These two threads are what got me into eating wbm in the first place:

 

http://www.propeciah....php?f=6&t=7770

http://forums.steroi...elp-please.html

 

WBM have also been reported as being 5AR inhibitors, so I don't know what to make of them when it comes to boosting DHT.

 

 

 

 

Edited by Wagner83, 14 August 2016 - 03:22 PM.

[PeaceAndProsperity]

Ok is that backed by science , personal experience or personal belief? (just curious)

I don't understand why I'd get good effects from sorghum for a few days and then none. 

 

Coffee and sorghum seem to work to increase dht, however wouldn't the body become immune to whatever process increases 5AR in those foods? 

 

I also remember using white button mushrooms in large quantities for days/ weeks, I would get a lot of hair loss from it, more facial and body hair growth, weird symptoms in the spine and joints, wet dreams (had none for the past decade ) and yet I wouldn't feel that much better overall (libido wise, erection wise, mood wise). Does it make sense if I say wbm may lower estrogen too low if one has average E2 levels and eats copious amount of them over a decent period of time?

These two threads are what got me into eating wbm in the first place:

 

http://www.propeciah....php?f=6&t=7770

http://forums.steroi...elp-please.html

 

WBM have also been reported as being 5AR inhibitors, so I don't know what to make of them when it comes to boosting DHT.

That's based upon science. If you lower estrogen, shbg goes down. If you lower dht, shbg doesn't move a bit. And if you take andractim (dht gel), or inject yourself with dht, shbg might actually go down and this might actually increase testosterone (happened to me) due to one of dht's (and testosterone's) metabolites blocking estrogen receptors. You can actually get an estrogen crash from dht.

 

To simplify things, estrogen receptor activation increases shbg and lowers gonadotropins, which consequently leads to lower free test. and lower total test.

Among the things shbg bind to, they are dht, test. and estrogen.

 

Estrogen is actually what, in conjunction with androgens, give the "male feeling" and dominance. I've tested this on myself, applying dht alone and then dht with an estrogen receptor activator. And to my surprise, dht alone does not produce the male feeling, but in conjunction with estrogen it does.

However, estrogen alone does not produce the male feeling either. 

And thus, it's been stated that estrogen sensitizes androgen receptors. It's also been said that test. to est. conversion in specific parts of the brain cause the territorialness in at least apes. Both are probably true.

So, in conclusion, you need both test. and est. to "feel masculine". 

And no, "feeling masculine" has NOTHING to do with "confidence" or "low self-esteem" or any of those estrogen-brained poppsychology slogans.

[Wagner83]

Ok what made sense to me was if 5AR is increased, then less testosterone is converted to estrogen , therefore estrogen is lower , shbg decreases. This in turn increases bio available t and dht. However I thought that overtime shbg could increase if dht is too high, looks like it's not the case, how long did you use dht compounds for? Wouldn't there be a difference between artificial dht and increasing 5AR?

 

As for the rest , I'm not sure about the estrogen part, crushing estrogens completely does not sound healthy anyway (osteoporosis? joints? libido?), optimized but balanced hormones sound better , and then what balanced hormones are may vary between individuals, but I ain't a pro. 

Edited by Wagner83, 14 August 2016 - 04:34 PM.

[Wagner83]

Interesting, a rep for napgear recommends me to inject a steroid and buy it off his site, of course I ordered 10 right away I can't wait .

Edited by Wagner83, 14 August 2016 - 08:15 PM.

[noot_in_the_sky]

If you're looking for something natural then you can give Epiandrosterone a chance.  It's some natural steroid, which is found in Pine Pollen among other things.

Edited by noot_in_the_sky, 20 August 2016 - 01:49 PM.

[Wagner83]

Thanks do you have a good source for that? I heard pine pollen needs to be cycled is that true?

Did you give a try to sorghum and if so have you noticed the body develops a tolerance to it?

Proviron looks quite interesting to boost dht, it seems a low dose may not be dangerous for natural production of hormones. Has anyone good information on it?

I'm going to give a try to lj100 (olympus labs) , world abs TT is interesting too. Of course all of these supplements need to be cycled a lot which makes using them a pain in the arse.

 

 

Lauric Acid (12:0), inhibits both more potent 5alpha-reductase inhibitors

So coconut oil could be bad for dht.

I wonder how much tomatoes (rich in lycopene) affect dht (if at all).

 

Edit: Nevermind I read that pine pollen, as any pro hormone could be hard on organs and had to be cycled anyway.

 

It would be interesting to have more info on wbm, and whether the anti aromatase properties are superior enough to its anti dht properties.

Edited by Wagner83, 21 August 2016 - 10:18 AM.