280 replies to this topic

[Area-1255]

Alright ladies and gentlemen - I have updated the DHT Article with a new bit of information!

 

 

   OTHER CENTRAL AND MOLECULAR CHANGES INDUCED BY DIHYDROTESTOSTERONE

 

 

1. Dihydrotestosterone appears to strongly increase MAPK; Mitogen-Activated-Protein-Kinase - this leads to a plethora of central and molecular changes as well as genomic/expressional changes(40)(41).
2. This action further reinforces and validates DHT's suppressive effects on serotonin systems (42) since activating MAPK leads to increased serotonin transporter (SERT)activity - an effect directly opposite of SSRI's (43) (44) (45)
3.  

• DHT increases Mitogen-Activated-Protein Kinase (MAPK) which leads to a variety of molecular changes and genomic changes as well as neural-changes; decreased serotonin activity in the brain and periphery. 

[noot_in_the_sky]

And that's what I don't like about DHT, perhaps I shall begin taking some Bacopa Monnieri or Lithium to increase serotonin. 

[Area-1255]

And that's what I don't like about DHT, perhaps I shall begin taking some Bacopa Monnieri or Lithium to increase serotonin. 

Decreasing serotonin is not necessarily a bad thing...unless you are uncomfortable being disinhibited and having high libido  / motivation....

Disinhibition is the only way people ever achieve success...or really get anything remarkable done.

Not saying serotonin is 100 % useless but certainly isn't a good thing even for mental states...look at how OCD is associated with ELEVATED serotonin.

Not only OCD , but schizophrenia is associated with elevated serotonin as well...now of course, this doesn't mean that you want high or low levels..it's just that the both physical and mental implications of serotonin are often shown in such a narrow-distorted-black and white picture that most don't understand it in a way that makes it applicable in the proper manner.

 

 

Eat Weight Disord. 2002 Sep;7(3):221-31.

Is there a common mechanism of serotonin dysregulation in anorexia nervosa and obsessive compulsive disorder?

Barbarich N1.

Author information

 

Abstract

Numerous studies have documented increased rates of comorbidity in patients with anorexia nervosa (AN) or obsessive compulsive disorder (OCD). The interaction of many possible factors influences this comorbidity, but one possible explanation involves the neurotransmitter serotonin, which is widely distributed in the brain and has been implicated in a number of psychological behaviours. Although low serotonin levels have been found in patients with impulsive and aggressive behaviour, high levels have been correlated with obsessive and compulsive behaviour. In an attempt to further our understanding of this relationship, a large number of studies have measured serotonin levels throughout different stages of illness in both AN and OCD; furthermore, serotonin challenge studies and drug treatment trials have provided further support for this theory. This paper discusses the evidence supporting the view that the obsessive behaviour characteristic of AN and OCD may be partially due to a dysregulation in the serotonergic system.

PMID:   12452254   [PubMed - indexed for MEDLINE]

[Area-1255]

The thing we have to remember is that increased uptake of serotonin often refers to increased uptake OUT of the synapse; depending on the context. 

If serotonin is moved out quicker - that means less serotonin binding to the receptors. 

Another thing that should be considered, besides proportions in volume or uptake - is that serotonin affects platelets and it's corresponding aggregating factors..high levels of serotonin are associated with increased bleeding and even bone loss - as demonstrated with SSRI's. At the same time, high levels of serotonin in coordination with other vascular factors can sometimes do the opposite - causing increased clotting. 

 

Antidepressant medications and osteoporosis

 

Drugs Aging. 2011 May 1;28(5):345-67. doi: 10.2165/11589340-000000000-00000.

Effects of selective serotonin reuptake inhibitors on platelet function: mechanisms, clinical outcomes and implications for use in elderly patients.

de Abajo FJ1.

Author information

 

Abstract

Among the antidepressants, the selective serotonin reuptake inhibitors (SSRIs) are often preferred to other classes of antidepressants in the treatment of depression in the elderly because of their better safety profile. Most of the known effects of SSRIs, either beneficial or adverse, are linked to their inhibitory action on the serotonin reuptake transporter (5-HTT). This reuptake mechanism is present not only in neurons but also in other cells such as platelets. Serotoninergic mechanisms seem to play an important role in haemostasis, and their importance in this regard has long been underestimated. Abnormal activation may lead to a pro-thrombotic state, as may occur in patients with major depressive disorder, whilst downregulation, as occurs in patients treated with SSRIs, may have two clinical consequences, both of particular interest in the elderly. On the one hand, there may be an increased risk of bleeding; on the other hand, a reduction in thrombotic risk may be possible. Polymorphism in the promoter region of the gene that transcribes the 5-HTT has been shown to have a relevant impact on its function and, in turn, on the beneficial and adverse effects of SSRIs. Bleeding has been a concern since the introduction of SSRIs, with multiple case reports published and communicated to the pharmacovigilance systems. The first epidemiological study was published in 1999 and since then, 34 epidemiological studies from different areas, most of them including elderly patients in their study populations, have been published with a variety of results. Broadly, the epidemiological evidence supports a moderately increased risk of bleeding associated with the use of SSRIs, which may be critically dependent on patient susceptibility and the presence of risk factors. The impairment of primary haemostasis induced by SSRIs may result, as a beneficial counterpart, in a reduction in the thrombotic risk. A small number of clinical trials and an increasing number of epidemiological studies that include elderly patients have been conducted to clarify whether SSRIs reduce the risk of primary and secondary ischaemic disorders. However, the results have been inconclusive with some studies suggesting a preventive effect and others no effect or even an increased risk. Behind such contradictory results may be the role of depression itself as a cardiovascular risk factor and, therefore, a major confounding factor. How to disentangle its effect from that of the antidepressants is the methodological challenge to be overcome in future studies. In this complex scenario, the elderly seem to be at a crossroads, because they are the group in which both the risks and the benefits can be the greatest. Studies performed to date have provided us with some clues that can help orient clinicians in taking the most appropriate course of action. For instance, as the gastrointestinal bleeding risk appears to increase with age, prudent advice in patients with a previous history of upper-gastrointestinal bleeding or peptic ulcer, and in those who take NSAIDs, oral anticoagulants, antiplatelet drugs or corticosteroids, would be to suggest addition of an acid-suppressing agent to the drug regimen in those elderly patients in whom SSRIs are indicated.

PMID:   21542658   [PubMed - indexed for MEDLINE]

 

Edited by Area-1255, 12 September 2015 - 01:21 AM.

[Area-1255]

Also the other thing I would point out is DHT's effects are sort of dose-dependent...and it seems that most of the negative effects from super high doses of say, masteron can be negated simply by adding an alpha-1-blocker. 

[noot_in_the_sky]

I understand the purpose of serotonin, it's just that having my serotonin levels too low have cause a drop in the quality of my sleep.   

 

 

Although with all this said, I must point out that I may have arisen my DHT too much.  I was using an AI together with natural extracts.  It got to the point that I was loosing hair, and this is coming from someone whose not even close to been 30 & whose father has full hair.

 

 

 

Also the other thing I would point out is DHT's effects are sort of dose-dependent...and it seems that most of the negative effects from super high doses of say, masteron can be negated simply by adding an alpha-1-blocker. 

 

Do you know of any natural alternatives to alpha-1-blocker?

[Area-1255]

I understand the purpose of serotonin, it's just that having my serotonin levels too low have cause a drop in the quality of my sleep.   

 

 

Although with all this said, I must point out that I may have arisen my DHT too much.  I was using an AI together with natural extracts.  It got to the point that I was loosing hair, and this is coming from someone whose not even close to been 30 & whose father has full hair.

 

 

 

Also the other thing I would point out is DHT's effects are sort of dose-dependent...and it seems that most of the negative effects from super high doses of say, masteron can be negated simply by adding an alpha-1-blocker. 

 

Do you know of any natural alternatives to alpha-1-blocker?

Well alpha-1's sort of correlate with PKC; Protein Kinase C - so you can use stuff like Lemon Verbena extract to block adrenaline-induced-vasoconstriction and HBP which in turn will decrease hair loss by shuffling nutrients back into the follicle. 

May want to read these threads/studies. Even Arginine is shown to help with hair loss issues.

Although it depends on bodily utilization and genetics to an extent.

Yohimbe extract contains alpha-blockers but they have too short of a half-life to have any benefit for this purpose.

Pharmaceutical alpha-blockers are fairly easy to obtain , though...just stay away from Prazosin (MiniPress) if you want to avoid CNS-side-effects...some alpha-blockers have more affinity for the peripheral receptors and some do not cross the blood brain barrier very much.

Tamulosin (Flomax) is one example; commonly prescribed for BPH-related issues and this has selectivity in blood vessels and is also uro-selective which means that it is rarely going to cause side-effects....although of interest, alpha-blockers are recently being investigated for PTSD and other stress disorders ... So it really depends on what the issue is, if you feel the DHT is affecting your anxiety level you can go with a non-selective-a1 blocker such as Prazosin but if you are concerned with the vascular effects or feel the DHT is causing peripheral effects then either Tamulosin or Doxasozin is best...lemon verbena extract and chuchuhuasi extract are two natural PKC inhibitors that can bypass the a1-adrenergic system and directly block vasoconstriction by secondary mediation blockade. They should be used together, though, as it is unlikely one or the other produces appreciable effects ALONE to counter system sympathetic vasoconstriction.

 

http://www.hairlossh...&threadid=76234

http://www.progressi...e-hair-loss.htm

http://www.livestron...nine-hair-loss/

[gamesguru]

Inhibition of the alpha 1 and alpha 2-adrenoceptor-mediated pressor response in pithed rats by raubasine [ajmalicine], tetrahydroalstonine and akuammigine.
The relative potencies of raubasine, tetrahydroalstonine (THA) and akuammigine on alpha 1- and alpha 2-adrenoceptors were assessed by comparing their effects on the rise in blood pressure induced by stimulation of the sympathetic outflow from the spinal cord or by injection of noradrenaline in pithed rats. Akuammigine was inactive in both cases. Raubasine preferentially antagonized the effects of electrical stimulation while THA antagonized the effects of injected noradrenaline. The results suggest that raubasine preferentially blocks alpha 1-adrenoceptors while THA is more selective for alpha 2-adrenoceptors.

Inhibitory effect of N(G)-nitro-L-arginine methyl ester on the anti-adrenergic response elicited by ayanin in the pithed rat.
In this study we evaluated the anti-adrenergic response elicited by ayanin, a flavonoid compound isolated from Croton schiedeanus Schlecht, in the pithed rat, and the inhibitory effect of NO synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME), and its acute toxicity profile in mice. In pithed rats ayanin (5 - 50 mg/kg i. v.) caused a dose-dependent decrease in the pressor and chronotropic responses induced by intravenous noradrenaline administration (0.25 microg/kg). This anti-adrenergic response was completely abolished by prior treatment with L-NAME (10 mg/kg i.v ) and the inhibitory effect of L-NAME was reversed after intravenous administration of L-arginine (100 mg/kg, i. v.). No lethal or major toxic effects were observed in mice receiving i. p. administration of ayanin up to a dose of 500 mg/kg. Our findings confirm that ayanin exerts protective cardiovascular effects against the increase in blood pressure and heart rate mainly through a mechanism that depends on the NO/cyclic guanosine monophosphate (cGMP) pathway without acute toxic effects. These results suggest that extracts of Croton schiedeanus, the native south American plant from which ayanin was isolated, might be beneficial in cardiovascular disease.

Indole alkaloid production by transformed and non-transformed root cultures of Catharanthus roseus
Ten transformed and two non-transformed root lines ofCatharanthus roseus were established. A systematic study of the growth kinetics and alkaloid content was performed over a culture cycle and showed significant differences between transformed and non-transformed cultures. Mean doubling times for transformed and normal root lines were 2.8 and 19.5 days, respectively. Alkaloid content in hairy roots was from two- to threefold higher than in the non-transformed tissues. The established transformed root lines produced a wide variety of indole alkaloids as can be observed from their complex thin layer chromatography patterns. A large quantity of serpentine was determined in two of the transformed root cultures. Alkaloid content, both quantitatively and qualitatively, has been stable in the hairy root cultures for more than 2 yr of subculturing.

 

ajmalicine, serpentine, and catharanthine, from Catharanthus roseus chemically similar to Rauwolscine from Rauwolfia, have activity [perhaps at α2 tho, not sure]

Attached Files

•  Untitled2.jpg   77.59KB   1 downloads

[Area-1255]

Eurycoma has selective anti-adrenergic effects; but mostly in regards to sexual function although it seems to lower blood pressure as well and can help combat malaria and general fever.
Modification of propranolol’s bioavailability by Eurycoma longifolia water-based extract
 

 

Effect of Tongkat Ali on stress hormones and psychological mood state in moderately stressed subjects

 

 

J Sex Med. 2012 Apr;9(4):1027-36. doi: 10.1111/j.1743-6109.2011.02296.x. Epub 2011 May 13.

9-hydroxycanthin-6-one induces penile erection and delays ejaculation.

Chiou WF1, Wu TS.

Author information

 

Abstract

INTRODUCTION:

Eurycoma longifolia Jack (Simaroubaceae) has the reputation as a male aphrodisiac because it is claimed to increase virility and sexual prowess. Nevertheless, whether or not E. longifolia regulates directly the muscle tone of corpus cavernosa and/or seminal vesicle (SV) remains unclear. Even until now, the compositions that could account for its aphrodisiac property are still unknown

AIM:

We examined the effect of 9-hydroxycanthin-6-one (9-HC-6-one), a β-carboline alkaloid isolated from E. longifolia, on penile erection and ejaculation, and further elucidated the mechanism of action.

MAIN OUTCOME MEASURES:

9-HC-6-one induces penile erection and delays ejaculation.

METHODS:

Drug's effect was studied on rat corpus cavernosum (CC) and SV in vitro, and on the changes in intracavernosal pressure (ICP) after IC injection and intraluminal pressure (ILP) of the SV after hypogastric nerve stimulation (HNS), respectively.

RESULTS:

9-HC-6-one relaxed significantly phenylephrine (PE)-precontracted CC. Such response was not attenuated by endothelium disruption, N(G) -nitro-L-arginine methyl ester, or 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one treatment, suggesting that a nitric oxide/cyclic guanosine monophosphate-dependent pathway was precluded. 9-HC-6-one attenuated PE-induced contraction by blocking cell surface and internal calcium channels with a higher potency for internal calcium release. This compound also antagonized calcium-evoked contraction in Ca2+ -free, high K+ -depolarizing condition, suggesting that interfering with the entry of calcium through voltage-dependent channels also contributed to 9-HC-6-one-induced corporal relaxation. After IC application of 9-HC-6-one, a significant rise in ICP was observed as compared with the application of normal saline. 9-HC-6-one relaxed significantly norepinephrine (NE)- and KCl-precontracted SV, and antagonized NE-induced oscillatory contraction as potent as clomipramine. Finally, the HNS-evoked increase in ILP was dose-dependently repressed after challenge by 9-HC-6-one.

CONCLUSION:

9-HC-6-one might be the active component that contributed to the aphrodisiac effect of E. longifolia by antagonizing the smooth muscle tone of CC as well as SV probably through interfering with Ca2+ mobilization.

© 2011 International Society for Sexual Medicine.

PMID:   21569213   [PubMed - indexed for MEDLINE]

 

Edited by Area-1255, 19 September 2015 - 08:23 PM.

[Area-1255]

 

Endocrinology. 2005 Apr;146(4):2091-7. Epub 2005 Jan 20.

Dihydrotestosterone increases hippocampal N-methyl-D-aspartate binding but does not affect choline acetyltransferase cell number in the forebrain or choline transporter levels in the CA1 region of adult male rats.

Romeo RD1, Staub D, Jasnow AM, Karatsoreos IN, Thornton JE, McEwen BS.

Author information

 

Abstract

Testosterone, acting through its androgenic metabolite 5alpha-dihydrotestosterone (DHT), can increase dendritic spine density in the CA1 region of the male rat hippocampus. The mechanisms mediating this increase in spines are presently unknown. In female rats, estrogen (E) has been shown to increase spine density, which is in part mediated by increases in N-methyl-d-aspartate (NMDA) receptors in the CA1 region and cholinergic forebrain inputs to the hippocampus. Whether similar mechanisms are responsible for the DHT-induced increase in spines in the male remains to be determined. In the first experiment, we used [(3)H]glutamate NMDA receptor binding autoradiography to assess whether DHT-treated males had higher NMDA receptor levels in the CA1 region of the hippocampus, compared with oil-treated males. In the second set of experiments, we used choline acetyltransferase (ChAT) in situ hybridization and immunohistochemistry to assess whether DHT could affect ChAT cell number in the forebrain. We also investigated the effect of DHT on hemicholinium-3-sensitive choline transporter levels in the CA1 region of the male hippocampus. We found that DHT significantly increased NMDA receptor binding in the CA1 region of males but had no effect on ChAT cell number in the forebrain or hemicholinium-3-sensitive choline transporter protein levels in the CA1 region. These data indicate that, similar to E-induced spinogenesis in females, DHT-induced increases in spine formation in males may require increases in NMDA receptors. However, unlike E-treated females, these data suggest that DHT does not influence cholinergic inputs to the hippocampus.

PMID:   15661864   [PubMed - indexed for MEDLINE]

 

[Area-1255]

Also these should probably be linked for those who haven't seen it yet. 

LC - LongeCity - Andractim Review and Information

 

Independent Andractim/Andractrim DHT Gel Review & Information

Edited by Area-1255, 23 September 2015 - 10:26 PM.

[Area-1255]

Progesterone  EQUIVALENT just published for all to see!

 

http://area1255.blog...aining-how.html

[Tubzy]

Also these should probably be linked for those who haven't seen it yet. 

LC - LongeCity - Andractim Review and Information

 

Independent Andractim/Andractrim DHT Gel Review & Information

 

I have been on Andractim for almost a week now and can confirm it definitely works.  I apply it directly to my dick before bed every night.  You also could use DMSO beforehand to increase absorption, but not manadatory.

 

 

Few things I noticed:

 

-bigger/thicker flaccid hang

-increase morning wood and strength 

-loads are like pure white (not watery at all like when I was on fin)

-minor amount of hair growth in my dick area

 

Masteron/proviron I believe is stronger, but in the dick area andractim definitely improves erections and size.  I would suggest trying it if you are suffering from PFS and try it with DMSO too.  Topical DMSO will also help too since it breaks up fibrosis.  Lack of androgens (like from taking fin for longer periods of time) in the penis could cause venous leak.  So they could work in synergy.

 

This study was interesting as well

http://www.ncbi.nlm....pubmed/26352087

[Tubzy]

Also, for everyone still struggling with MPB related hair loss, my buddy has been doing some research and has had promising results by addressing the downstream effects of DHT but not DHT itself (e.g not using finasteride/dutasteride).  

 

I just wanted to share some of my buddy's awesome regrowth. I am member of a private hair loss forum that has been researching the prostaglandin approach to MPB hair loss. Here is the link of my buddy (Swiss) who has had extremely awesome results and regrew hair on SLICK bald temples. Please clink the link below.

http://swisstemples....y-progress.html

I would suggest reading through the blog.

Instead of addressing DHT, we are simply inhibiting the downstream effect of DHT. For example,

Testosterone-->DHT--->PGD2--->Miniaturizes follice and dies

We are simply inhibiting the PGD2 (prostaglandin) that causes the follicle to shrink instead of lowering/blocking DHT. A compound that does this is called Setipiprant which is currently in FDA trials now.

http://www.kythera.c...05-setipiprant/

How we know this is b/c there was a study done that PGD2 levels are 12 times higher in the scalp compared to non-balding males and DHT levels remain the same.

 

I'm very sensitive to anti androgens (i love my DHT =]) so this is very exciting for me.  I will not touch fin every again.
 

Edited by Tubzy, 27 September 2015 - 01:52 AM.

[Area-1255]

 

Also these should probably be linked for those who haven't seen it yet. 

LC - LongeCity - Andractim Review and Information

 

Independent Andractim/Andractrim DHT Gel Review & Information

 

I have been on Andractim for almost a week now and can confirm it definitely works.  I apply it directly to my dick before bed every night.  You also could use DMSO beforehand to increase absorption, but not manadatory.

 

 

Few things I noticed:

 

-bigger/thicker flaccid hang

-increase morning wood and strength 

-loads are like pure white (not watery at all like when I was on fin)

-minor amount of hair growth in my dick area

 

Masteron/proviron I believe is stronger, but in the dick area andractim definitely improves erections and size.  I would suggest trying it if you are suffering from PFS and try it with DMSO too.  Topical DMSO will also help too since it breaks up fibrosis.  Lack of androgens (like from taking fin for longer periods of time) in the penis could cause venous leak.  So they could work in synergy.

 

This study was interesting as well

http://www.ncbi.nlm....pubmed/26352087

 

Excellent to hear of your progress my friend. 

[Area-1255]

Progesterone and the Brain and Interactions with DHT

[Flex]

wow really nice and well researched thread

Edited by Flex, 11 October 2015 - 11:45 PM.

[Tubzy]

 

 

Also these should probably be linked for those who haven't seen it yet. 

LC - LongeCity - Andractim Review and Information

 

Independent Andractim/Andractrim DHT Gel Review & Information

 

I have been on Andractim for almost a week now and can confirm it definitely works.  I apply it directly to my dick before bed every night.  You also could use DMSO beforehand to increase absorption, but not manadatory.

 

 

Few things I noticed:

 

-bigger/thicker flaccid hang

-increase morning wood and strength 

-loads are like pure white (not watery at all like when I was on fin)

-minor amount of hair growth in my dick area

 

Masteron/proviron I believe is stronger, but in the dick area andractim definitely improves erections and size.  I would suggest trying it if you are suffering from PFS and try it with DMSO too.  Topical DMSO will also help too since it breaks up fibrosis.  Lack of androgens (like from taking fin for longer periods of time) in the penis could cause venous leak.  So they could work in synergy.

 

This study was interesting as well

http://www.ncbi.nlm....pubmed/26352087

 

Excellent to hear of your progress my friend. 

 

 

Yeah man, high DHT is the shit.  I suggest someone else trying this out too lol

[lourdaud]

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?

[gamesguru]

The effect of Ginger on serum testosterone of infertile men

sperm count up 16.2% ... sperm motility up 47.3% ... sperm viability up 40.7% ... ejaculate volume up 36.1% ... serum testosterone up 17.7%

 

 

3beta-hydroxysteroid dehydrogenase type II (degradatory enzyme)  inhibitors could take over a week to exert their full increase.

Genistein^[1]

N-(4-chlorobenzoyl)-melatonin^[2]

 

Try aromatase inhibitors, which will reduce estrogen and increase test (and perhaps therefore DHT).

Numerous natural product extracts, from plant, fungal, and microbial terrestrial and marine sources, have been evaluated for aromatase inhibition using various noncellular, cell-based, and in vivo assays. Some of the more active extracts included those of Agaricus bisporus (Lange) Imbach (white button mushrooms) [115] and Vitis L. sp. (grape seed extract and/or wine) [86, 106, 107]

 

Limit intake of 17beta-hydroxysteroid dehydrogenase (synthesizing enzyme) inhibitors

Green tea^[1]

Bacopa^[2]

 

Limit intake of 5-alpha-reductase (synthesizing enzyme) inhibitors

• Rice (source)
• Fenugreek (source)
• Saw palmetto (source)
• Astaxanthin (source)
• Safflower (source)
• Finasteride (source)
• Reishi (source)

 

[lourdaud]

Thanks! Think I'll give GSE a go. But will an AI really raise DHT? I'm not that interested in rasing testosterone as my levels are very high already.

I have yet to get a full hormonal panel done but I suspect I may have high estrogen and possibly low DHT (several symptoms and four different estrogen related genetic mutations!)

How about 5-alpha-reductase activators?
 

[gamesguru]

I'm not sure one can naturally have excessive test, like 800-1000 ng/dL is perfectly desirable.  Maybe even 1200, idk.

 

In theory less test → estrogen, means more test →DHT.   If you have high estrogen, GSE/button shrooms are definitely worth trying. 

DHT also regulates itself by stimulating aromatase^[1], thereby adjusting the estrogen:DHT ratio.  This is especially concerning for ppl already with high estrogen, because increasing DHT will further increase estrogen, hence AI.

 

IGF1 promotors: Androgen induction of steroid 5 alpha-reductase may be mediated via insulin-like growth factor-I.

Sorghum: http://www.longecity...ts/#entry527119

[lourdaud]

Ahaa I see. That was helpful, thanks.
Well my T levels were at 850 ng/dL after years of prolonged stress, sleep deprivation, low carb diets and excessive alcohol and now that I'm taking better care of myself they should be even higher. I'm not worried about excessive test but I don't think I'd see that many benefits from raising testosterone.
IGF-1.. I don't know, already taking cerebrolysing.. And I don't want to shorten my lifespan..

Guess I'll try sorghum!

[BasicBiO]

Well, the TLR DHT compound didn't seem to do much for libido or physique and with their reputation being questioned, I've opted to get some Andractim per 1255's advice. 

 

Currently using toremifene, creatine, L-Dopa, P-5-P, ashwagandha, and Forskohlin 95% in an attempt to reboot. I feel better mentally and have had some erectile and libido improvements, but nothing stellar.

[Tubzy]

Well, the TLR DHT compound didn't seem to do much for libido or physique and with their reputation being questioned, I've opted to get some Andractim per 1255's advice.

Currently using toremifene, creatine, L-Dopa, P-5-P, ashwagandha, and Forskohlin 95% in an attempt to reboot. I feel better mentally and have had some erectile and libido improvements, but nothing stellar.

What is your torem dosage ? I had to at least take 60-90mg to get any effect. It made my nuts hang really low and big (which was good). I'm trying out RS transdermal now which is neurosteroid (which finasteride lowers) based test booster with natural AI's. I just started my second week and I def have a higher libido and wake up with strong morning wood. Planning to stay on for a while though so will continue to evaluate.

Edited by Tubzy, 27 November 2015 - 08:01 PM.

[BasicBiO]

I did 3 days of 120mg, and am now on 60mg. Planning to run that dose until supply runs out by which time my Andractim should be here..hopefully.

 

[Tubzy]

I posted this on another forum, figure I post it here too.

 

I'm on this now (rs transdermal) and this is the greatest I have felt. I know a few people have tried dermacrine but this is way stronger. I didn't start to really notice anything about 2 to 3 weeks in. Like I don't feel stimulated or weird , I feel normal like prefin. I tried masteron and had a pretty crazy libido, but I was also very aggressive and didn't feel normal like prefin.

Read this article and it makes perfect sense.

http://bodybuilding....stosterone-gel/

DHEA is absorbed through the skin about 10x better than it is absorbed orally. Most fascinating is that DHEA actually converts to other anabolic hormones as it passes through your skin. Since the skin is extremely concentrated in the steroidogenic enzymes required to convert DHEA to other hormones such as 7alpha-DHEA, androstenediol, androstenetriol and testosterone, it is these hormones that are responsible for the muscle building, fat burning and sexual stimulating effects of RS Transaderm.

Now, you may be thinking that a bunch of pro-hormones are not going to help with post steroid cycle recovery therapy or PCT, however, the pro-hormones DHEA and pregnenolone have some interesting properties. You see, if you were to inject pure testosterone it would degrade the steroidogenic enzymes responsible for its own creation.1 Meaning, if you take injectable testosterone, over time it becomes harder for you to produce your own natural testosterone. However when you administer DHEA and pregnenolone, they will actually increase the enzymes required for their own production, making your natural testosterone production increase and making output more efficient. (DHEA helps move cholesterol into the mitochondria for further hormone production.2 Pregnenolone has been shown to have a positive effect on the gonadotropin release of Luteinizing hormone (LH) and follicle-stimulating hormone (FSH) .3 Gonadotropin release is a fancy way of saying that Pregnenolone stimulates your gonads or testes to synthesize and secrete more testosterone.

The part in bold is very important as it's stimulating my body to produce the proper enzymes again the propecia has deactivated or lowered.

[BasicBiO]

http://www.philly.co...mer_s_Risk.html

[noot_in_the_sky]

Here ares some studies I found about DHT:

 

 

 

http://www.ncbi.nlm....pubmed/20228125

Increased intratumoral androgens in human breast carcinoma following aromatase inhibitor exemestane treatment.

Takagi K1, Miki Y, Nagasaki S, Hirakawa H, Onodera Y, Akahira J, Ishida T, Watanabe M, Kimijima I, Hayashi S, Sasano H, Suzuki T.

 

Abstract

Sex steroids play important roles in the development of many human breast carcinomas, and aromatase inhibitors are used for the anti-estrogen therapy. Recent studies have demonstrated that aromatase suppressed 5alpha-dihydrotestosterone (DHT) synthesis in breast carcinoma cells, but intratumoral concentration of androgens and its significance have not been reported in the breast carcinoma patients treated with aromatase inhibitors. Therefore, we examined androgen concentrations in breast carcinoma tissues treated with exemestane, and further performed in vitro studies to characterize the significance of androgen actions. Intratumoral DHT concentration was significantly higher in breast carcinoma tissues following exemestane treatment (n=9) than those without the therapy (n=7), and 17beta-hydroxysteroid dehydrogenase type 2 (17betaHSD2) status was significantly altered to be positive after the treatment. Following in vitro studies showed that 17betaHSD2 expression was dose dependently induced by both DHT and exemestane in T-47D breast carcinoma cells, but these inductions were not additive. DHT-mediated induction of 17betaHSD2 expression was markedly suppressed by estradiol (E(2)) in T-47D cells. E(2)-mediated cell proliferation was significantly inhibited by DHT in T-47D cells, associated with an increment of 17betaHSD2 expression level. These findings suggest that intratumoral androgen actions are increased during exemestane treatment. 17betaHSD2 is a potent DHT-induced gene in human breast carcinoma, and may not only be involved in anti-proliferative effects of DHT on breast carcinoma cells but also serve as a potential marker for response to aromatase inhibitor in the breast carcinoma patients.

 

 

http://link.springer...3-4-13#/page-1 

 

 

 

Effects of eight weeks of an alleged aromatase inhibiting nutritional supplement 6-OXO (androst-4-ene-3,6,17-trione) on serum hormone profiles and clinical safety markers in resistance-trained, eugonadal males

•  
• Abstract

The purpose of this study was to determine the effects of 6-OXO, a purported nutritional aromatase inhibitor, in a dose dependent manner on body composition, serum hormone levels, and clinical safety markers in resistance trained males. Sixteen males were supplemented with either 300 mg or 600 mg of 6-OXO in a double-blind manner for eight weeks. Blood and urine samples were obtained at weeks 0, 1, 3, 8, and 11 (after a 3-week washout period). Blood samples were analyzed for total testosterone (TT), free testosterone (FT), dihydrotestosterone (DHT), estradiol, estriol, estrone, SHBG, leutinizing hormone (LH), follicle stimulating hormone (FSH), growth hormone (GH), cortisol, FT/estradiol (T/E). Blood and urine were also analyzed for clinical chemistry markers. Data were analyzed with two-way MANOVA. For all of the serum hormones, there were no significant differences between groups (p > 0.05). Compared to baseline, free testosterone underwent overall increases of 90% for 300 mg 6-OXO and 84% for 600 mg, respectively (p < 0.05). DHT underwent significant overall increases (p < 0.05) of 192% and 265% with 300 mg and 600 mg, respectively. T/E increased 53% and 67% for 300 mg and 600 mg 6-OXO, respectively. For estrone, 300 mg produced an overall increase of 22%, whereas 600 mg caused a 52% increase (p < 0.05). Body composition did not change with supplementation (p > 0.05) and clinical safety markers were not adversely affected with ingestion of either supplement dose (p > 0.05). While neither of the 6-OXO dosages appears to have any negative effects on clinical chemistry markers, supplementation at a daily dosage of 300 mg and 600 mg for eight weeks did not completely inhibit aromatase activity, yet significantly increased FT, DHT, and T/E.

 

 

http://onlinelibrary...1674.x/abstract

 

 

The Direct Pituitary Effect of Testosterone to Inhibit Gonadotropin Secretion in Men Is Partially Mediated by Aromatization to Estradiol

 

ABSTRACT: In men, administration of exogenous testosterone (T) exerts direct negative feedback effects at the pituitary as well as at the hypothalamic level. This study was undertaken to determine whether T itself causes the inhibitory effects on the pituitary, or whether conversion to estradiol (E₂) or dihydrotestosterone (DHT) is required. We assessed the biological activity of serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH), as well as immunoactivity. Blood samples were drawn before, during, and after a continuous, 72-hour i.v. infusion of T (15 mg/day), E₂ (90 μg/day), or DHT (500 μg/day). Each of these doses is twice the daily production rate of the steroid. Each man received each of the three steroid infusions. We studied four men, ages 23–35, with idiopathic hypothalamic hypogonadism (IHH), who were treated with pulsatile gonadotropin releasing hormone (GnRH) until their gonadotropins reached the normal range. Serum levels of T, E₂, DHT, and levels of immunologically active and biologically active LH and FSH were measured. We found that administration of each steroid increased serum levels of the infused steroid to the upper physiologic range. Administration of T or E₂ resulted in decreased mean levels of biologically and immunologically active LH and FSH; administration of DHT did not alter gonadotropin secretion. These data suggest that some of the direct effect of T at the pituitary level in men is mediated by E₂, whereas peripherally formed DHT may not play an important role in this process.

 

 

 

 

[vrain]

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.