Juicing + DHT blocker

Hey bro's

I'm starting my test. enth+deca+dboll cycle next week, but i have a few questions about androgenic side effects -> hairloss.

I am currently taking propecia and saw palmetto, it works well for me. Should i stop taking it when i start my cycle? Both products block DHT, and DHT is a X times stronger than testosteron. So DHT does play a role in gaining weight and strength. My cycle is week 1-10: 500 test enth, week 1-9: 400 deca, week 1-4: 30 dboll.
If i stop taking propecia and saw palmetto, will my gains be better? Or will it be the same?

Peace

anyone?

Haven't used deca but have heard proscar and deca are not good together. I believe dht does play a role in strength and size gains and you lose some of that when you use a dht blocker. How much do you lose? - not sure. I know one thing I take a DHT blocker while on and off cycle. I have not used deca because of the hairloss issues.

Another thing, if you are worried about hairloss and seems that you are if you are using things to prevent it, there is nothing on the market that will restore any hairline loss that you may have, once its gone its gone unless you are willing to do transplants at this time.

Why not drop the deca and run 1mg daily of proscar/propecia and see what happens. If you need another compound try EQ instead of deca.

With the deca, i'd be more worried about having fully functioning reproductive anatomy than hair loss. Anecdotaly, deca is easy on the hair, and I agree. I take proscar and saw palmetto on and off and I havent ever felt that it held me back in any way. That is the exact same cycle I plan on doing in about ten weeks btw, heard great things about it.

Yeah well.. There are some new breakthroughs in hairloss treatment. Ru58841, 6-benzyl aminopuride, t-flavanone. I am currently using inovate (6-BAP) and t-flavanone, there are new hairs growing on my temples. So i'm not afraid that the hairs won't come back. The roots are just minimized and not desolved.

Ever think of trying avodart? If proscar/propecia works for you (even keeping things from progressing) avodart might really turn things around for you and show a much greater degree of results than proscar.

Good article on DHT:

DHT and the Athlete: Is it the Enemy?

It is perhaps the most misunderstood steroid hormone, dihydrotestosterone (DHT). When the average bodybuilder hears those three letters, frantic thoughts of hair loss and exaggerated androgenic side effects usually come to mind. Questions like "does this steroid convert to DHT", or "is it DHT based" similarly arise often in steroid discussion. Although in some instances concerns about DHT conversion may be valid (in a technical sense only testosterone converts to DHT, although several testosterone and nandrolone derivatives do interact with the same enzyme to form new steroids), equating this steroid to a basic evil may in fact be a gross generalization. Indeed there is more to DHT than just side effects. And with the slated release of a DHT prohormone, the question arises: Is dihydrotestosterone the enemy to a happy and healthy cycle, or does it actually serve a purpose to the athlete?

The relation between DHT and Side Effects

Dihydrotestosterone is the most potent androgen found in the human body. It is roughly three to four times stronger an agonist of the androgen receptor than testosterone, and is produced from testosterone (via interaction with the 5-alpha reductase enzyme) in specific target tissues as a way to mediate androgen activity in the body where strong stimulation is needed. This includes areas of the skin, scalp, prostate and central nervous system. It is this process where one sees the obvious correlation between DHT and androgenic side effects; as such tissues are those that appear to be most sensitive in terms of producing such effects. The sebaceous glands responsible for secreting oils for instance are found in areas of the skin, which when over stimulated may cause acne to develop. Hair follicles in the scalp are also sensitive to androgens, and for those with a genetic predisposition, androgens will likely play a role at some point in promoting male pattern hair loss. Prostate tissues are also highly sensitive to androgens, and diseases such as benign prostatic hypertrophy (BPH) and prostate cancer are similarly responsive to androgens.

Clearly the local production of DHT in target tissues is relevant to the incidence of side effects with a drug such as testosterone. That however should not to mislead us into thinking that DHT is an isolated culprit, or that it serves no valuable purpose. Clearly all agonists of the androgen receptor share similar ability to promote androgenic activity in these tissues. If we block the 5-alpha reductase enzyme with an inhibitor for example, testosterone will still be able to activate the androgen receptor. Although testosterone is of course less active than DHT, in a sufficient dosage side effects will still result. A big misconception among athletes is that the use of finasteride, a 5-AR inhibitor, will block any chances for noticing hair loss with testosterone therapy. While it does offer help by means of lowered androgenic activity in the scalp, it is certainly not a cure-all for the balding steroid user.

DHT and the neuromuscular system

It has been suggested that inhibiting the reduction of testosterone to DHT may not always be a good thing in terms of performance enhancement. It seems clear that DHT plays a vital role in the organization and functioning of the central nervous system, effects mediated by androgen receptors in neural cells. The specific importance of DHT in this area is evidenced by studies showing this hormone has a profoundly greater impact in neural cells compared to testosterone. In one such study it was demonstrated that both testosterone and DHT would result in increased androgen receptor proliferation in neural cells at 3 hours and 7 hours post administration, however only DHT sustained this increase at 21 hours. This strong difference lends support to suggestions that DHT and testosterone effect neural cells differently, perhaps such that the dihydrotestosterone-receptor complex and testosterone-receptor complex might even activate the transcription of different target genes. Others maintain that such a difference in effect would only be due to DHT forming a more stable and lasting complex with the androgen receptor, but the vital importance of DHT still remains evident.

The strong interaction between the central nervous system and skeletal muscles may be of key importance to the athlete, as these two areas interact to form what is referred to as the neuromuscular system. Clearly the ability of the body to adapt to training and better call upon nerve endings in muscle tissue is reliant on the functioning of the central nervous/neuromuscular system. Inhibiting the formation of DHT during a testosterone cycle may therefore inadvertently cause less to be achieved in terms of strength and muscle mass gains. We might also take note of the fact that while the anabolic steroid nandrolone is a stronger agonist of the androgen receptor than testosterone, it is much less effective at promoting strength and muscle mass increases in comparison. It seems logical that the loss of DHT (nandrolone actually reduces to a weaker steroid upon interaction with the 5-alpha reductase enzyme) may have something to do with this outcome. What is obvious is that were androgen receptor stimulation in muscle tissue solely responsible for strength and muscle growth, nandrolone would be a more potent drug than testosterone. Yet testosterone compounds remain the primary mass and strength agents among bodybuilders.

DHT and Androgen/Estrogen action on body fat

Androgens and estrogens both play important roles in mediating the disposition of body fat and lean muscle mass. Their respective roles however appear to be very different. While androgens are the primary hormones responsible for muscle growth, they also seem to play a part in promoting fat loss. Results obtained during numerous androgen replacement studies for example strongly support a loss of body fat when androgen levels rise. The specific mechanism involved may be the support of catecholamine-induced lipolysis, caused by the androgen increasing the number of beta-adrenergic receptors (the primary triggers for fat mobilization) on the membrane surface of fat cells, an effect clearly demonstrated in animal models.

On the other hand we see that estrogens may act to promote the storage of body fat, an effect known to be particularly pronounced in men when given supraphysiological doses of estrogens. And as testosterone and several other anabolic steroids readily aromatize (convert to estrogens) in the body, such activity may be important to consider during a steroid cycle. The buildup of estrogens may likewise represent a counter balance during steroid use. In many instances an athlete will report increases in body fat when taking aromatizable compounds for example, presumably due to the buildup and activity of supraphysiological estrogen levels. While the androgenic activity may be promoting fat loss, the countering estrogenic activity may dominate the metabolism and new fat will be deposited.

It is for the purpose of fat loss that a non-aromatizable androgen such as DHT might prove most useful. Since DHT cannot be aromatized, its activity in the body is purely androgenic. As a result a notable shift in androgen/estrogen ratio would result with use, which can prove to be very beneficial in fostering a fat burning metabolism. As the ratio of androgenic to estrogenic action rises, so should the level of fat loss achieved. It is for this reason that many competitive bodybuilders will use non-aromatizable compounds such as stanozolol, methenolone, trenbolone, fluoxymesterone, Proviron (mesterolone; 1-methyl DHT) and Masteron (drostanolone; 2-methyl DHT) exclusively during contest season. Some will go so far as to avoid the milder anabolics nandrolone and boldenone at this point, as even the low amount of estrogen produced from these steroids could be unwanted if an extremely shredded look is desired.

Studies also suggest that DHT acts as an anti-aromatase in the body, further combating estrogenic action and supporting the desired state of metabolism. It is believed that this occurs by DHT having some affinity to interact with the aromatase enzyme, yet due to its structure is incapable of being altered by it (no estrogen is produced). As the enzyme's binding site is temporarily occupied by DHT, other substrates such as testosterone will not be able to bind to it, and an anti-aromatase effect is achieved. It is to this end in which Proviron (mesterolone; 1-methyldihydrotestosterone) is typically utilized by the athlete, although again, this oral DHT preparation is also popular as a non-aromatizable cutting steroid. Some studies suggest that DHT may even interfere with aromatase activity through other, non-competitive means as well.

DHT and free testosterone

In the human body only a very small percentage of testosterone (our primary anabolic hormone) is free at any given time to interact with cellular receptor sites. This is because the vast majority (98%) will form temporary complexes with the plasma binding proteins Sex Hormone Binding Globulin (SHBG) and albumin (the distribution between the two is roughly equal), which prevent the hormone from exerting activity in the body. It is here that dihydrotestosterone differs from testosterone in another important way, in that it binds several times more avidly to SHBG in comparison. In terms of bodybuilding, administration of these two compounds could likewise produce a synergistic effect. As the level of DHT rises in the body, so would the amount of free testosterone, as the former hormone will be out competing the latter for binding to SHGB. This would occur in a dose dependent manner, the greater the ratio of DHT to testosterone the better the effect achieved. This is an excellent, though previously not suggested, use for our oral DHT preparation Proviron, as due to its slightly altered structure it binds even more avidly to SHBG than dihydrotestosterone.

BPH and DHT as an androgen replacement

A common worry among males, particular as we age, is the possible development of prostate diseases. Prostate cancer and benign prostatic hypertrophy for example, are partially androgen dependent conditions that clearly respond to the high presence of DHT in prostate tissues. Initially the reduction of testosterone to DHT was targeted with the drug finasteride in such cases, the intention to minimize androgen action in the prostate and interfere with the progress of the disease. However we find this therapy less that ideal because on one hand testosterone is still capable of maintaining androgen action in the absence of DHT, and on the other we have come to find that both androgens and estrogens play synergistic roles in the induction of BPH. Today estrogen is often targeted in conjunction with the testosterone to DHT reduction when treating this condition. In terms of androgen replacement for an aging male at possible risk for BPH, we find that DHT may even make a better drug of choice over testosterone. Although no form of androgen replacement can be considered safe with a disease responsive to these hormones, due to the non-aromatizable nature, as well as anti-aromatase and estrogen suppressing action of DHT, it may represent a safer alternative to testosterone when such therapy is indicated.

Clearly we should realize that there is a lot more to dihydrotestosterone than just side effects. The formation of this hormone in the human body plays a crucial role in several areas, including sexual functioning, the maintenance and functioning of the central nervous system, and support of bone density and muscle mass. Admittedly DHT is a poor anabolic itself, as it seems to be much more rapidly metabolized to inactive form in muscle tissues compared to testosterone. This is not to say however that its presence in the body serves the athlete no purpose, or that it does not support muscle growth. Indeed inhibiting its formation may have strong consequences in terms of muscle mass and strength gains when undergoing therapy with a testosterone. Unmistakably there are two sides to this androgen, and as users of the oral DHT preparation Proviron typically report, one of them appears to be that of a useful compound in terms of performance enhancement.

Bibliography

Alterations in granulosa cell aromatase activity accompanying preovulatory follicular development in the rat ovary with evidence that 5alpha-reduced C19 steroids inhibit the aromatase reaction in vitro. Hillier SG, van den Boogaard AM, Reichert LE Jr, van Hall EV. J Endocrinol 1980 Mar;84(3):409-19

Androgen and estrogen metabolism: relationship to obesity. Longcope C, Baker R, Johnston CC Jr. Metabolism 1986 Mar;35(3):235-7

Effects of testosterone and estrogens on deltoid and trochanter adipocytes in two cases of transsexualism. Vague J, Meignen J.M. and Negrin J.F. Horm. Metabol. Res. 16 (1984) 380-381

FSH-induced aromatase activity in porcine granulosa cells: non-competitive inhibition by non-aromatizable androgens. Chan WK, Tan CH. J Endocrinol 1986 Mar;108(3):335-41

Neural androgen receptor regulation: effects of androgen and antiandrogen. Lu S, Simon NG, Wang Y, Hu S. J Neurobiol 1999 Dec;41(4):505-12

Testosterone increases lipolysis and the number of beta-adrenoceptors in male rat adipocytes. Xu XF, De Pergola G, Bjorntorp P. Endocrinology 1991 Jan;128(1):379-82

Transdermal Dihydrotestosterone Treatment of "Andropause". Bruno De Lignieres. Annals of Medicine 1993 25: 235-241

I do remember hearing that Deca and maybe Finasteride will make all your hair fall out if taken together. I would do a search and do some more research just to make sure. Better safe than sorry.

I'm taking Test and D-bol right now, as well as Finasteride (propecia)...I dont find it is hindering me at all.

D

I train natural, but take avodart and I haven't noticed any loss in power, but everyone is different. It could have been that I was holding more water with the avodart and thus saw some power gains. On a different note, the Avodart has been working great for me!! My hair looks so much better and I am seeing growth at the hairline and temples. You'd never think by looking at me that my hair was falling out. I love science!! ;) BTW I take .5mg's EOD and have been on for 1 year.

Peace,

CC

Ok bro's i won't take finasteride, saw palmetto or dutasteride while i'm on cycle.
But i will take 2% spironolactone cream, so that my hair won't fall out, 2% is only effective on the scalp. I'll also use innovate ( + MSM + Biotin + l-arginine + ALA as one topical) and flavacyte to stimulate the hair growth.

Quote:

Originally Posted by bbwannabe

Ok bro's i won't take finasteride, saw palmetto or dutasteride while i'm on cycle.
But i will take 2% spironolactone cream, so that my hair won't fall out, 2% is only effective on the scalp. I'll also use innovate ( + MSM + Biotin + l-arginine + ALA as one topical) and flavacyte to stimulate the hair growth.

Throw in some 5% rogain too! Good luck!

CC

2% rogaine doesn't work for me. and 5% ****s my skin, i get some white stuff my hair. Innovate (6-benzyl aminopurine) works much better for me than rogaine does.

Yea I get that white stuff in my hair... What is this Innovate stuff? I'm currently using Nisim shampoo and rogaine 2% my head is always very itchy. I'd like to try somthing else.

go to minoxidil.com - dr. lee makes a 5% version that is light in what irritates you scalp. Works great.

If you're going to take a reductase inhibitor (finasteride, dutasteride), it is very important not to take it with nandrolone. The reductase enzyme is the only efficient pathway to break down nadrolone. When nandrolone is used in conjunction with a reductase inhibitor, nandrolone will bind to the same sites that DHT would.

Scott, - thanks for the info

Proscar ques?

Quote:

Originally Posted by chrisAdams

If you're going to take a reductase inhibitor (finasteride, dutasteride), it is very important not to take it with nandrolone. The reductase enzyme is the only efficient pathway to break down nadrolone. When nandrolone is used in conjunction with a reductase inhibitor, nandrolone will bind to the same sites that DHT would.

Hey chris, do you know if proscar and Tren will fix ok? Trenbolone is a deriavitive of nandrolone so Im afraid it may be a bad mix with the proscar. Anyways if you know anythting please let me know.

Thanks,

FD

Quote:

Originally Posted by Fartdaemon

Hey chris, do you know if proscar and Tren will fix ok? Trenbolone is a deriavitive of nandrolone so Im afraid it may be a bad mix with the proscar. Anyways if you know anythting please let me know.

Thanks,

FD

I'll check out got fina, i'm sure they have the answer. brb.

Although tren is a nandrolone derivative, it is not reduced by alpha reductase, and thus propecia will not amplify its effects on hairloss. However, it won't help either. Propecia is basically only useful (or should i say most useful) when used in conjunction with testosterone.. as it can prevent all dht formed from test.

So, saw palmeto and finasteride are out of question because nandrolone can not convert if one of those products is used? nandrolone is more androgenic than DHT, so more hair will fall out?
That sucks :(
Well let's see what spironolactone 2% cream and nizoral 2% can do for me.