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Hair Loss...
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S
Stew Meat
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e-man said:
Halo is a testosterone derivitive. It will convert to DHT via 5-AR.
-Stew
Anabolicum Mister
New member
I must disagree
Stew,
Those studies that you posted told me very little (if anything) about the metabolism of trenbolone. Other than the original post by E2, I have not seen one shred of evidence to prove your theory that trenbolone is 5-alpha reduced. You claim that it is because it is a structural analog of nandrolone. What does this have to do with anything? Many 3-keto-4 ene steroids are very similar structurally. Does this mean that they have the same binding affinities for the androgen receptor or the same efficacy when used in a cycle. No! Then why must they have the same affinity for 5-alpha reductase?
Let's first discuss how structurally similar these analogs are. In terms of the A-ring they are identical, since they are both 3-keto-4-ene steroids. Therefore, it is possible that trenbolone could be a substrate for the 5-alpha reductase enzyme. However, the B, C, and D rings differ considerably. You claim that trenbolone (17b-hydroxyestra-4,9,11-trien-3-one) converts to 5a-DHN (3a-hydroxy-5a-estran-17-one). For this to happen, the B ring would need to have the 9-10 double bond broken, the C ring would have to have the 11-12 double bond broken, and the D ring would need to have a ketone group replace the 17b-hydroxy group and the 17-a dihydro. What enzymes (or other method) do you propose catalyse these reactions? If these enzymes do exist, they are not common to the metabolism of other steroids and/or have not yet been discovered. In fact, in a study done on the urinary excretion of steroid metabolites, a 5-alpha reduced metabolite of trenbolone was not detected. In fact, the only trenbolone metabolite detected was 17-epitrenbolone. As such, I am very confident in saying that I highly doubt that trenbolone converts to DHN. Unless you can provide proof otherwise, I will stand by my conviction.
I believe what I have heard anecdotally that tren can be harsh on the hair in those susceptible. I very much would like to believe that this is not true, since I suffer from MPB myself. But I think that you are misinforming people when you claim that it is one of the best steroids in terms of hairloss effects. I believe (as do you) that for those truly afflicted with MPB, any steroid, deca included, can accelerate hairloss. While deca may be milder than most, I also believe that it is dose/individual dependent. I hate to burst anyone's bubble, but there is no 'safe' steroid when it comes to matters of hairloss.
A.M.
Stew,
Those studies that you posted told me very little (if anything) about the metabolism of trenbolone. Other than the original post by E2, I have not seen one shred of evidence to prove your theory that trenbolone is 5-alpha reduced. You claim that it is because it is a structural analog of nandrolone. What does this have to do with anything? Many 3-keto-4 ene steroids are very similar structurally. Does this mean that they have the same binding affinities for the androgen receptor or the same efficacy when used in a cycle. No! Then why must they have the same affinity for 5-alpha reductase?
Let's first discuss how structurally similar these analogs are. In terms of the A-ring they are identical, since they are both 3-keto-4-ene steroids. Therefore, it is possible that trenbolone could be a substrate for the 5-alpha reductase enzyme. However, the B, C, and D rings differ considerably. You claim that trenbolone (17b-hydroxyestra-4,9,11-trien-3-one) converts to 5a-DHN (3a-hydroxy-5a-estran-17-one). For this to happen, the B ring would need to have the 9-10 double bond broken, the C ring would have to have the 11-12 double bond broken, and the D ring would need to have a ketone group replace the 17b-hydroxy group and the 17-a dihydro. What enzymes (or other method) do you propose catalyse these reactions? If these enzymes do exist, they are not common to the metabolism of other steroids and/or have not yet been discovered. In fact, in a study done on the urinary excretion of steroid metabolites, a 5-alpha reduced metabolite of trenbolone was not detected. In fact, the only trenbolone metabolite detected was 17-epitrenbolone. As such, I am very confident in saying that I highly doubt that trenbolone converts to DHN. Unless you can provide proof otherwise, I will stand by my conviction.
I believe what I have heard anecdotally that tren can be harsh on the hair in those susceptible. I very much would like to believe that this is not true, since I suffer from MPB myself. But I think that you are misinforming people when you claim that it is one of the best steroids in terms of hairloss effects. I believe (as do you) that for those truly afflicted with MPB, any steroid, deca included, can accelerate hairloss. While deca may be milder than most, I also believe that it is dose/individual dependent. I hate to burst anyone's bubble, but there is no 'safe' steroid when it comes to matters of hairloss.
A.M.
S
Stew Meat
Guest
Re: I must disagree
I NEVER claimed that it was 5-alpha reduced becasue it was an analog of nandralone. That has been an entirely different argument altogether.
I never said that the fact that it was structurally similar to nandralone that it reacted like nandralone. However, it does. The evidence is in the studies that I have already cited for you above. The fact that bolderone is 5-alpha reduced is not due to its structural similarity to testosterone, yet they behave they are both 5-alpha reduced. Likewise, trenbelone and methandrostenelone are 5-alpha reduced and are not structurally simillar.
I have already provided sufficient evidence.
-Stew
Anabolicum Mister said:
I NEVER claimed that it was 5-alpha reduced becasue it was an analog of nandralone. That has been an entirely different argument altogether.
I never said that the fact that it was structurally similar to nandralone that it reacted like nandralone. However, it does. The evidence is in the studies that I have already cited for you above. The fact that bolderone is 5-alpha reduced is not due to its structural similarity to testosterone, yet they behave they are both 5-alpha reduced. Likewise, trenbelone and methandrostenelone are 5-alpha reduced and are not structurally simillar.
As has already been stated several times by those who have not researched this, just becasue a hormone is structurally similar doesn't mean it has the same mode of action nor the same properties, i.e. testosterone and estrodiol are structurally similar, yet they have different properties that cause them to different actions.
I have already provided sufficient evidence.
-Stew
Anabolicum Mister
New member
You have provided no evidence. And by the way, Sherlock, boldenone is not 5-alpha reduced, it is 5-beta reduced.
S
Stew Meat
Guest
As if I haven't already provided sufficient refrences, check this one:
"Clinically significant drug interactions in dermatology"
Journal of the American Academy of Dermatology
April 1998 • Volume 38 • Number 4 • p599 to p612
If I find some more, I'll come back and add them here.
I'll try to find you a complete abstract or full text.
-Stew
"Clinically significant drug interactions in dermatology"
Journal of the American Academy of Dermatology
April 1998 • Volume 38 • Number 4 • p599 to p612
If I find some more, I'll come back and add them here.
I'll try to find you a complete abstract or full text.
-Stew
S
Stew Meat
Guest
Here's some great research on hairloss... It actually uses some of the same refrences that I've cited.
Hair loss is a particularly worrying occurrence for most men, especially in a society as image driven as ours. As unrelated as it may be, having a full head of hair is often equated to a self-sense of potency and masculinity among men. It is no wonder that the possibility of losing ones hair due to steroid use is one of the most common concerns of the steroid-using athlete. The release of the prescription medication Propecia® (finasteride) has given help to the multitude of men noticing the early signs of hair loss, and similarly has lent hope to many athletes that a medication could exist that would alleviate the worry regarding this particular steroid-related side effect. In order to assess the true usefulness of finasteride with athletes, it is likewise important to take a look at its action as well as the natural causes for hair loss.
It is technically termed androgenetic alopecia. As you might have assessed by the first word, this type of hair loss (the most common form) concerns the interplay of both androgenic hormones and a genetic predisposition. What happens for those genetically inclined is that androgen receptor stimulation in the scalp will slowly cause ones hair follicles to shrink. Hair loss will ultimately occur with its progression. Androgenic hormones are likewise the trigger for this activity, and often the target for hair loss medications. Here you can see the problem with steroid use, namely greatly enhanced androgen action in the body due to hormonal supplementation.
The enzyme 5-alpha reductase plays a vital role in the development of androgenic alopecia in normal physiological situations. This enzyme is localized in androgen target tissues such as the skin, scalp, liver and prostate, and is responsible for the irreversible conversion of testosterone to dihydrotestosterone. Dihydrotestosterone is a more potent activator of the androgen receptor than testosterone, measured to have at least three to four times greater potency. With the local production of DHT taking place in the scalp, its strong action is most often linked to the onset of hair loss. 5-alpha reductase is likewise an excellent target to combat hair loss, as its inhibition can greatly lower the level of androgen stimulation in scalp by making the weaker hormone testosterone the dominant force in this area.
Finasteride is a potent inhibitor of the 5-alpha reductase enzyme, specifically 5AR type II localized in the scalp and prostate. 1mg and 5mg doses have been shown to lower scalp concentrations of DHT by 64.1% and 69.4% respectively (1). Serum DHT levels also drop significantly with use, declining by 71.4% and 72.2% with the same doses. Understanding the strong action of DHT this amounts to a considerable reduction in androgenic activity, allowing finasteride to be quite effective at combating hair loss. In trials the drug was shown to be effective at enhancing hair growth in 66% of long term (2 years) treated men with androgenetic alopecia (2). This figure rises to 83% when we measure the group noting a halt in the recession of scalp hair. But the question at hand is will this success port over to the steroid-using athlete.
Obviously testosterone is the principle target for 5AR, so finasteride does affect the dynamics of all testosterone preparations. The testosterone analogues methyltestosterone, fluoxymesterone (Halotestin®), methandrostenolone and boldenone also reduce to more potent steroids upon 5AR interaction (3,4). However this concludes the list of steroids that might call for the use of finasteride with hair-sensitive individuals. Methandrostenolone and boldenone in fact interact with 5-alpha reductase with extremely low affinity, so for all intents and purposed the benefit of finasteride with these drugs is likely insignificant.
Nandrolone and a few of its analogues also interact with 5-alpha reductase, however here this reduction is typically beneficial. Dihydronandrolone has a lower affinity for the androgen receptor than nandrolone; meaning here 5AR actually lowers the activity of this steroid in the scalp (5). The tendency is similar with ethylestrenol (Orabolin®), norethandrolone (Nilevar®) and trenbolone. What this basically means is that nandrolone and its analogues are typically slightly safer for hair loss than testosterone based drugs, in that they should exhibit greater activity in muscle tissue as compared to androgen target tissues such as the scalp due to this reduction. If we inhibit 5-alpha reductase with finasteride, we are inadvertently increasing scalp androgenicity.
Other synthetics including stanozolol (Winstrol®), oxandrolone (Oxandrin®), oxymetholone (Anadrol®) and methenolone (Primobolan®) lack the structural characteristics (c4-5 double bond) necessary for alteration by 5-alpha reductase (6,7). This trait helps to even out the muscle and androgenic target potencies of these drugs, as no 5AR caused enhancing or diminishing of its activity occurs as with testosterone and nandrolone. Obviously finasteride would be useless in such a situation. Some of the above drugs, most notably oxandrolone and methenolone, are usually though of as “mild” by athletes and favored when hair loss is a worry. However we can see that nandrolone and its analogues are better choices in this regard, due to the greater dissociation between muscle and scalp activity.
Androgen receptor stimulation is again the ultimate trigger of hair loss, so one should not be fooled by any choice stack or drug combination. All anabolic/androgenic steroids work by activating the androgen receptor, and those espousing that DHT is the only worry are way off the mark. The man noticing the early signs of hair loss should similarly consider no one drug safe. A performance-enhancing dose of any steroid usually comes with it a greatly enhanced level of androgen activity in the body; otherwise the drugs would not be working to enhance muscle growth. Even if we inhibit the specific reduction of testosterone or its analogues to more potent metabolites in the scalp, the parent steroids are still obviously capable of activating the androgen receptor. The much higher level of testosterone during steroid use for example can easily compensate for the loss of DHT production, and androgenetic alopecia can still progress. The same holds true for any steroid.
The athlete noticing hair loss should likewise be cautious when considering steroid use. The best drug choice remains nandrolone, again due to its high ratio of anabolic to androgenic effect. With testosterone we should clearly consider finasteride as an aid in preventing hair loss, but drug dosage may be an equally important consideration. With 100mg weekly of an ester such as testosterone cypionate considered a typical replacement dose for example, one might not want to venture excessively higher if hair loss is a serious concern. Perhaps the most reasonable recommendation would be to use around 200mg weekly along with 1mg finasteride daily to inhibit DHT buildup, however this is just speculation and there may be more room for adjustment. I must stress again that with testosterone and finasteride, or even with nandrolone alone, a certain threshold can be reached where hair loss will progress. While the development of finasteride may equate to a milestone for men noticing hair loss under normal conditions, it is clearly not a cure-all for the steroid user.
1- The effect of finasteride on scalp skin and serum androgen levels. J Am Acad Dermatol 1999 Oct;41(4):550-4
2- Finasteride: a review of its use in male pattern hair loss. Drugs 1999 Jan;57(1):111-26
3- Relative importance of 5-alpha reduction for the androgenic inhibiting activities of delta-4-3-ketosteroids. Steroids. 1977 Mar;29(3):331-48
4- Testing for fluoxymesterone (Halotestin®) administration to man: Identification of urinary metabolites by gas chromatography-mass spectrometry. J Steroid Biochem 36(6):659-666
5- Relative binding affinities of testosterone, 19-nortestosterone and their 5-alpha reduced derivatives to the androgen receptor and to other androgen-binding proteins. J Steroid Biochem 1982 17:653-60
6- Classification of anabolic steroids using the method of competitive metabolism. Exp Clin Endocrinol 1986 Jul;87(2):125-32
7- Metabolism of anabolic androgenic steroids. Clin Chem. 1996 42:1001-20
Well, Mister, if this can't show you the light, nothing can
-Stew
Hair loss is a particularly worrying occurrence for most men, especially in a society as image driven as ours. As unrelated as it may be, having a full head of hair is often equated to a self-sense of potency and masculinity among men. It is no wonder that the possibility of losing ones hair due to steroid use is one of the most common concerns of the steroid-using athlete. The release of the prescription medication Propecia® (finasteride) has given help to the multitude of men noticing the early signs of hair loss, and similarly has lent hope to many athletes that a medication could exist that would alleviate the worry regarding this particular steroid-related side effect. In order to assess the true usefulness of finasteride with athletes, it is likewise important to take a look at its action as well as the natural causes for hair loss.
It is technically termed androgenetic alopecia. As you might have assessed by the first word, this type of hair loss (the most common form) concerns the interplay of both androgenic hormones and a genetic predisposition. What happens for those genetically inclined is that androgen receptor stimulation in the scalp will slowly cause ones hair follicles to shrink. Hair loss will ultimately occur with its progression. Androgenic hormones are likewise the trigger for this activity, and often the target for hair loss medications. Here you can see the problem with steroid use, namely greatly enhanced androgen action in the body due to hormonal supplementation.
The enzyme 5-alpha reductase plays a vital role in the development of androgenic alopecia in normal physiological situations. This enzyme is localized in androgen target tissues such as the skin, scalp, liver and prostate, and is responsible for the irreversible conversion of testosterone to dihydrotestosterone. Dihydrotestosterone is a more potent activator of the androgen receptor than testosterone, measured to have at least three to four times greater potency. With the local production of DHT taking place in the scalp, its strong action is most often linked to the onset of hair loss. 5-alpha reductase is likewise an excellent target to combat hair loss, as its inhibition can greatly lower the level of androgen stimulation in scalp by making the weaker hormone testosterone the dominant force in this area.
Finasteride is a potent inhibitor of the 5-alpha reductase enzyme, specifically 5AR type II localized in the scalp and prostate. 1mg and 5mg doses have been shown to lower scalp concentrations of DHT by 64.1% and 69.4% respectively (1). Serum DHT levels also drop significantly with use, declining by 71.4% and 72.2% with the same doses. Understanding the strong action of DHT this amounts to a considerable reduction in androgenic activity, allowing finasteride to be quite effective at combating hair loss. In trials the drug was shown to be effective at enhancing hair growth in 66% of long term (2 years) treated men with androgenetic alopecia (2). This figure rises to 83% when we measure the group noting a halt in the recession of scalp hair. But the question at hand is will this success port over to the steroid-using athlete.
Obviously testosterone is the principle target for 5AR, so finasteride does affect the dynamics of all testosterone preparations. The testosterone analogues methyltestosterone, fluoxymesterone (Halotestin®), methandrostenolone and boldenone also reduce to more potent steroids upon 5AR interaction (3,4). However this concludes the list of steroids that might call for the use of finasteride with hair-sensitive individuals. Methandrostenolone and boldenone in fact interact with 5-alpha reductase with extremely low affinity, so for all intents and purposed the benefit of finasteride with these drugs is likely insignificant.
Nandrolone and a few of its analogues also interact with 5-alpha reductase, however here this reduction is typically beneficial. Dihydronandrolone has a lower affinity for the androgen receptor than nandrolone; meaning here 5AR actually lowers the activity of this steroid in the scalp (5). The tendency is similar with ethylestrenol (Orabolin®), norethandrolone (Nilevar®) and trenbolone. What this basically means is that nandrolone and its analogues are typically slightly safer for hair loss than testosterone based drugs, in that they should exhibit greater activity in muscle tissue as compared to androgen target tissues such as the scalp due to this reduction. If we inhibit 5-alpha reductase with finasteride, we are inadvertently increasing scalp androgenicity.
Other synthetics including stanozolol (Winstrol®), oxandrolone (Oxandrin®), oxymetholone (Anadrol®) and methenolone (Primobolan®) lack the structural characteristics (c4-5 double bond) necessary for alteration by 5-alpha reductase (6,7). This trait helps to even out the muscle and androgenic target potencies of these drugs, as no 5AR caused enhancing or diminishing of its activity occurs as with testosterone and nandrolone. Obviously finasteride would be useless in such a situation. Some of the above drugs, most notably oxandrolone and methenolone, are usually though of as “mild” by athletes and favored when hair loss is a worry. However we can see that nandrolone and its analogues are better choices in this regard, due to the greater dissociation between muscle and scalp activity.
Androgen receptor stimulation is again the ultimate trigger of hair loss, so one should not be fooled by any choice stack or drug combination. All anabolic/androgenic steroids work by activating the androgen receptor, and those espousing that DHT is the only worry are way off the mark. The man noticing the early signs of hair loss should similarly consider no one drug safe. A performance-enhancing dose of any steroid usually comes with it a greatly enhanced level of androgen activity in the body; otherwise the drugs would not be working to enhance muscle growth. Even if we inhibit the specific reduction of testosterone or its analogues to more potent metabolites in the scalp, the parent steroids are still obviously capable of activating the androgen receptor. The much higher level of testosterone during steroid use for example can easily compensate for the loss of DHT production, and androgenetic alopecia can still progress. The same holds true for any steroid.
The athlete noticing hair loss should likewise be cautious when considering steroid use. The best drug choice remains nandrolone, again due to its high ratio of anabolic to androgenic effect. With testosterone we should clearly consider finasteride as an aid in preventing hair loss, but drug dosage may be an equally important consideration. With 100mg weekly of an ester such as testosterone cypionate considered a typical replacement dose for example, one might not want to venture excessively higher if hair loss is a serious concern. Perhaps the most reasonable recommendation would be to use around 200mg weekly along with 1mg finasteride daily to inhibit DHT buildup, however this is just speculation and there may be more room for adjustment. I must stress again that with testosterone and finasteride, or even with nandrolone alone, a certain threshold can be reached where hair loss will progress. While the development of finasteride may equate to a milestone for men noticing hair loss under normal conditions, it is clearly not a cure-all for the steroid user.
1- The effect of finasteride on scalp skin and serum androgen levels. J Am Acad Dermatol 1999 Oct;41(4):550-4
2- Finasteride: a review of its use in male pattern hair loss. Drugs 1999 Jan;57(1):111-26
3- Relative importance of 5-alpha reduction for the androgenic inhibiting activities of delta-4-3-ketosteroids. Steroids. 1977 Mar;29(3):331-48
4- Testing for fluoxymesterone (Halotestin®) administration to man: Identification of urinary metabolites by gas chromatography-mass spectrometry. J Steroid Biochem 36(6):659-666
5- Relative binding affinities of testosterone, 19-nortestosterone and their 5-alpha reduced derivatives to the androgen receptor and to other androgen-binding proteins. J Steroid Biochem 1982 17:653-60
6- Classification of anabolic steroids using the method of competitive metabolism. Exp Clin Endocrinol 1986 Jul;87(2):125-32
7- Metabolism of anabolic androgenic steroids. Clin Chem. 1996 42:1001-20
Well, Mister, if this can't show you the light, nothing can
-Stew
Anabolicum Mister
New member
O.K. Stew, now at least I know you didn't pull this out of your ass...lol. The tone of the article is very much in line with my own feelings regarding steroids and hairloss.
However, that is an article, not a research paper. Also, nowhere in the article does it state that trenbolone is 5-alpha reduced to DHN, which is what you are claiming. The closest the article comes to this is stating that similar to nandrolone, trenbolone is 5-alpha reduced to a less potent androgen. You will notice that, while the nandrolone conversion to the less harmful DHN is referenced, there is no reference to back up the statement about trenbolone. This is because it is purely speculation on the part of the author. In fact, nowhere in any of the references does it show the 5-alpha reduction of trenbolone to DHN. Ironically, if you take a close look at the study in reference (7), you will see that no 5-alpha reduced metabolite of trenbolone was detected at all, let alone DHN. This is the study that I eluded to earlier. Again, no evidence exists to back up your statement.
So, Stew, I guess Anabolicum Mister will be left alone in the dark while you enlighten the masses with this misinformation. I only wish you could look at my posts objectively and with an open mind and consider, just for a minute, that someone else could be right. If you do find some shred of evidence that proves me wrong, I would welcome the opportunity to admit my mistake. In any case, the brothers on the board can take a look at both of our arguments and come to their own conclusions. I only hope that most can think for themselves, rather than attaching a stigma to a name and following your advice blindly.
A.M.
However, that is an article, not a research paper. Also, nowhere in the article does it state that trenbolone is 5-alpha reduced to DHN, which is what you are claiming. The closest the article comes to this is stating that similar to nandrolone, trenbolone is 5-alpha reduced to a less potent androgen. You will notice that, while the nandrolone conversion to the less harmful DHN is referenced, there is no reference to back up the statement about trenbolone. This is because it is purely speculation on the part of the author. In fact, nowhere in any of the references does it show the 5-alpha reduction of trenbolone to DHN. Ironically, if you take a close look at the study in reference (7), you will see that no 5-alpha reduced metabolite of trenbolone was detected at all, let alone DHN. This is the study that I eluded to earlier. Again, no evidence exists to back up your statement.
So, Stew, I guess Anabolicum Mister will be left alone in the dark while you enlighten the masses with this misinformation. I only wish you could look at my posts objectively and with an open mind and consider, just for a minute, that someone else could be right. If you do find some shred of evidence that proves me wrong, I would welcome the opportunity to admit my mistake. In any case, the brothers on the board can take a look at both of our arguments and come to their own conclusions. I only hope that most can think for themselves, rather than attaching a stigma to a name and following your advice blindly.
A.M.
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