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What? Testosterone is androgenic lol
Oral Steroid Made My Hair Grow Back Thicker!
- Thread starter Davy Weir
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What? Testosterone is androgenic lol
Yes. Testosterone is androgenic. All androgens are androgenic, but not all androgens cause hair loss. Every steroid in your body causes a unique cascade of genes to be expressed. The genetic expression testosterone causes is different and unique from the expression that DHT causes. DHT will cause you to express genes that contribute to hair loss. Testosterone will not cause those same genes to be expressed.
I actually don't think that we need DHT for our skin.. at least not in any significant amount. I believe that DHT is almost like an inferior, but necessary, version of testosterone for when the body isn't functioning properly. I feel that it's the body's way of protecting itself from excessive estrogenism. When you see guys that have really good looking skin and hair... like godlike.. it's because they naturally don't express 5AR in the skin or hair. So, most of the androgens in their skin and hair are metabolized to estrogens and the rest are left for masculine features like facial hair growth. The guys that have very little testosterone in the skin probably don't end up having much facial hair or oil in their skin.
So, anyway, somewhere along the path of our geneology, our ancestors probably encountered some kind of chronic environmental stress over generations that caused us to express 5AR in places it didn't really belong in order to protect itself.
So, in the spirit of the original post, I've come across another person who has experienced thickening and cessation of hair loss with an anabolic steroid. Rather than anavar, this person experienced thickening while using nandrolone. After some time thinking and looking at the structure of nandrolone, I've determined that the mechanism for this is similar to anavar, except that nandrolone has the potential to actually work better. I will explain further in the next post.
So, I'm going to post here what I've explained to this other person with regard to how and why he experienced thickening of his hair while using nandrolone:
Nandrolone has a very high affinity for the androgen receptor.. much higher than testosterone and probably on par with or higher than DHT. So, in a competition with DHT, nandrolone will win at binding the androgen receptor at least 50% of the time (given equal concentration of both steroids) and possibly more. I’m unsure of the relative binding affinity of nandrolone with respect to DHT, so I can’t definitively say that it binds with significantly greater affinity, but it’s safe to assume that they’re both at least on par with one another.
Nandrolone also has relatively the same binding affinity for the 5AR enzyme that testosterone has.. possibly higher. So, it’s safe to assume that in competition with testosterone, nandrolone will win at binding 5AR at least 50% of the time (given equal concentration of both steroids).
Nandrolone is very similar to testosterone in structure. The only difference between the two is that nandrolone is missing a methyl group at the 10-carbon position shared by the A and B rings of the steroid. This is why it’s also called 10-Nortestosterone (or 19-Nortestosterone since that methyl group is actually classified as the 19th carbon of the cholesterol steroid backbone). The nor prefix simply means that the steroid is missing that methyl group at the specified position on the steroid backbone. So, this missing methyl group is actually pretty important because, without it, nandrolone cannot be aromatized to an estrogen. Normally, in testosterone, this methyl group is enzymatically hydroxylated, oxidized to a carboxyl group, and then made to leave as a formate ion with the help of an enzymatic peroxide. Since nandrolone is missing this methyl group, this doesn’t happen because it has no way to create a good leaving group.. it has a relatively stable proton instead.
Ok, so if you’re with me thus far, here’s why all three of those things are significant:
1. Nandrolone is not DHT. So, when nandrolone binds the androgen receptor, it does not cause the same gene transcription that DHT causes and so, very likely, does not cause the hair to shed and thin like DHT does. No two steroids that are unique cause the same gene expression. This is why it’s stupid when people talk about the androgenicity, or estrogenicity, or binding affinity, or strength of one steroid vs another while totally ignoring (or being unaware of) the fact that they cause unique genetic expressions. This is why testosterone does not contribute to hair loss and DHT does.
2. When nandrolone is in competition with testosterone for 5AR, it is going to bind at least half the 5AR enzyme present in tissue if both steroids are present in the same concentration. This means that at least 50% more testosterone will be available for aromatization than would normally be without the presence of nandrolone. If you can imagine 5AR as a destructive hungry monster, you’re essentially trying to feeding it something else instead of testosterone because it results in the synthesis of less DHT and an increase in available testosterone to be aromatized. Now, when nandrolone is reduced, it forms 5-alpha dihydronandrolone (DHN). Unlike DHT, DHN happens to have a weaker affinity for the androgen receptor than its non-reduced steroid. Remember, DHT and DHN are also two different steroids and do not cause the same genes to be expressed when they bind the androgen receptor. However, if DHN caused the expression of genetic code that led to hair loss, it would have a lesser effect than DHT due to its lower binding affinity to the androgen receptor. So, to recap, nandrolone will bind to 5AR and act as kind of a competitive inhibitor of the enzyme, freeing up a higher concentration of testosterone to be aromatized.
3. Because nandrolone is non-aromatizable, nandrolone and dihydronandrolone will not cause the steroid regulatory systems in the body to downregulate aromatase or estrogen receptor expression. It will actually do the opposite. Binding of the androgen receptor will cause an increase in aromatase expression. This is important because hair loss sufferers likely have an aromatase and/or estrogen receptor insufficiency. I happen to think that most have an estrogen receptor insufficiency and, therefore, require higher levels of estrogens to provide sufficient estrogenic activity in the hair and skin compared to others. So, as a teenager, you have higher levels of androgens and maintain high aromatase expression and this results in oily skin and acne. As you age, steroid production decreases and less estrogens are created and there’s no longer enough estrogenic activity to keep your hair follicles healthy. For some this process happens more gradually and for others it’s aggressive and happens at a very young age. I believe it probably happens as a result of excessive aromatase expression in the brain and in other important tissues and when the body goes through puberty, this causes excessive estrogenism. The body’s only way to defend itself against this is to increase expression of 5AR to preserve androgens from being aromatized.
So, there’s a couple reasons why taking both deca [nandrolone] and testosterone on cycle contributed to hair thickness and cessation of loss. The deca [nandrolone] acted as a competitive 5AR inhibitor, but, at the same time, also bound the androgen receptor to increase [or at least maintain] aromatase expression without causing hair loss. (This is great compared to finasteride. Finasteride binds 5AR and you end up with less androgen receptor activation. This will ultimately cause aromatase expression to decrease and also leaves your entire body with excessive estrogenism due to testosterone being aromatizeable.)
Obviously, since you took the deca [nandrolone], your endogenous testosterone levels are going to decrease significantly. If you had not taken deca [nandrolone] with a base of testosterone, you very likely wouldn’t have experienced the benefits for the hair, but I will admit that it’s still possible.
Nandrolone has a very high affinity for the androgen receptor.. much higher than testosterone and probably on par with or higher than DHT. So, in a competition with DHT, nandrolone will win at binding the androgen receptor at least 50% of the time (given equal concentration of both steroids) and possibly more. I’m unsure of the relative binding affinity of nandrolone with respect to DHT, so I can’t definitively say that it binds with significantly greater affinity, but it’s safe to assume that they’re both at least on par with one another.
Nandrolone also has relatively the same binding affinity for the 5AR enzyme that testosterone has.. possibly higher. So, it’s safe to assume that in competition with testosterone, nandrolone will win at binding 5AR at least 50% of the time (given equal concentration of both steroids).
Nandrolone is very similar to testosterone in structure. The only difference between the two is that nandrolone is missing a methyl group at the 10-carbon position shared by the A and B rings of the steroid. This is why it’s also called 10-Nortestosterone (or 19-Nortestosterone since that methyl group is actually classified as the 19th carbon of the cholesterol steroid backbone). The nor prefix simply means that the steroid is missing that methyl group at the specified position on the steroid backbone. So, this missing methyl group is actually pretty important because, without it, nandrolone cannot be aromatized to an estrogen. Normally, in testosterone, this methyl group is enzymatically hydroxylated, oxidized to a carboxyl group, and then made to leave as a formate ion with the help of an enzymatic peroxide. Since nandrolone is missing this methyl group, this doesn’t happen because it has no way to create a good leaving group.. it has a relatively stable proton instead.
Ok, so if you’re with me thus far, here’s why all three of those things are significant:
1. Nandrolone is not DHT. So, when nandrolone binds the androgen receptor, it does not cause the same gene transcription that DHT causes and so, very likely, does not cause the hair to shed and thin like DHT does. No two steroids that are unique cause the same gene expression. This is why it’s stupid when people talk about the androgenicity, or estrogenicity, or binding affinity, or strength of one steroid vs another while totally ignoring (or being unaware of) the fact that they cause unique genetic expressions. This is why testosterone does not contribute to hair loss and DHT does.
2. When nandrolone is in competition with testosterone for 5AR, it is going to bind at least half the 5AR enzyme present in tissue if both steroids are present in the same concentration. This means that at least 50% more testosterone will be available for aromatization than would normally be without the presence of nandrolone. If you can imagine 5AR as a destructive hungry monster, you’re essentially trying to feeding it something else instead of testosterone because it results in the synthesis of less DHT and an increase in available testosterone to be aromatized. Now, when nandrolone is reduced, it forms 5-alpha dihydronandrolone (DHN). Unlike DHT, DHN happens to have a weaker affinity for the androgen receptor than its non-reduced steroid. Remember, DHT and DHN are also two different steroids and do not cause the same genes to be expressed when they bind the androgen receptor. However, if DHN caused the expression of genetic code that led to hair loss, it would have a lesser effect than DHT due to its lower binding affinity to the androgen receptor. So, to recap, nandrolone will bind to 5AR and act as kind of a competitive inhibitor of the enzyme, freeing up a higher concentration of testosterone to be aromatized.
3. Because nandrolone is non-aromatizable, nandrolone and dihydronandrolone will not cause the steroid regulatory systems in the body to downregulate aromatase or estrogen receptor expression. It will actually do the opposite. Binding of the androgen receptor will cause an increase in aromatase expression. This is important because hair loss sufferers likely have an aromatase and/or estrogen receptor insufficiency. I happen to think that most have an estrogen receptor insufficiency and, therefore, require higher levels of estrogens to provide sufficient estrogenic activity in the hair and skin compared to others. So, as a teenager, you have higher levels of androgens and maintain high aromatase expression and this results in oily skin and acne. As you age, steroid production decreases and less estrogens are created and there’s no longer enough estrogenic activity to keep your hair follicles healthy. For some this process happens more gradually and for others it’s aggressive and happens at a very young age. I believe it probably happens as a result of excessive aromatase expression in the brain and in other important tissues and when the body goes through puberty, this causes excessive estrogenism. The body’s only way to defend itself against this is to increase expression of 5AR to preserve androgens from being aromatized.
So, there’s a couple reasons why taking both deca [nandrolone] and testosterone on cycle contributed to hair thickness and cessation of loss. The deca [nandrolone] acted as a competitive 5AR inhibitor, but, at the same time, also bound the androgen receptor to increase [or at least maintain] aromatase expression without causing hair loss. (This is great compared to finasteride. Finasteride binds 5AR and you end up with less androgen receptor activation. This will ultimately cause aromatase expression to decrease and also leaves your entire body with excessive estrogenism due to testosterone being aromatizeable.)
Obviously, since you took the deca [nandrolone], your endogenous testosterone levels are going to decrease significantly. If you had not taken deca [nandrolone] with a base of testosterone, you very likely wouldn’t have experienced the benefits for the hair, but I will admit that it’s still possible.
In case I wasn't very clear, when you look at the conformational structures (basically 3D structural orientation) of those 4 steroids, testosterone, anavar, and nandrolone have very similar conformations in the A ring.. they're kind of flattened into what's called a half-chair conformation. DHT, on the other hand has more of a chair conformation. This difference in conformation between DHT and the other 3 steroids is responsible for the difference in genetic expression when bound to the androgen receptor. The steroid will bind the androgen receptor and lock the androgen receptor complex into a particular conformation. This unique conformation that the androgen receptor takes on is what is responsible for it causing different genes to be expressed depending on its shape.
The two anabolic steroids, nandrolone and anavar, would be more likely to cause the expression of genes similar to testosterone, rather than DHT, when binding the androgen receptor. So, rather than contributing to hair loss, like DHT, they act more like testosterone while still having the benefit of binding the androgen receptor (and 5AR, in the case of nandrolone). This is unlike finasteride, which binds 5AR and turns it into a permanently denatured dud, causing the body to be deprived of much needed androgenic activity (which turns out, you NEED in order to have higher aromatase expression).
The two anabolic steroids, nandrolone and anavar, would be more likely to cause the expression of genes similar to testosterone, rather than DHT, when binding the androgen receptor. So, rather than contributing to hair loss, like DHT, they act more like testosterone while still having the benefit of binding the androgen receptor (and 5AR, in the case of nandrolone). This is unlike finasteride, which binds 5AR and turns it into a permanently denatured dud, causing the body to be deprived of much needed androgenic activity (which turns out, you NEED in order to have higher aromatase expression).
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Looks like there's a little darkening of vellous hairs. I'm interested to see how things look after a week or two.
Keep in mind that anyone attempting this without dealing with the DHT problem will likely not see any results. Hair loss is a double-ended problem... it's the presence of DHT and the lack of presence of estrogenic activity in the hair follicle. Both must be addressed for hair to grow normally. The further you push each of these problems in the opposite direction, the better things get.
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True that. Ya still early. Applying once a day. I get headaches after application for a a minute or two.
I ordered forskolin and dmso gonna make a topical. Apparently it’s excellent for increasing camp.
And increases aromatase in endolethial cells.
I think we need to focus on increasing aromatase in the skin. Only. Not in the body which fucks things up
That's interesting. I also experience a headache from using prostaglandin E2, but it lasts for probably at least 30 minutes. So, that indicates that both prostaglandin E2 and dexamethasone are inducing an increase in aromatase expression. And they should... it's not really a surprise. There are studies that support this quite strongly.
Figure 1 in this study shows the effects of 5 different compounds which affect aromatase expression compared to control. A compound called tetradecanoyl phorbol acetate (TPA) most strongly increased aromatase expression with prostaglandin E2 (PGE2) falling shortly behind and dexamethasone falling shortly behind PGE2.
https://academic.oup.com/jcem/article/88/6/2810/2845614
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And yes, this is true. Certain compounds we can use due to their short acting behavior in the body.. they are quickly used and/or broken down before they are able to get too far in the body. Obviously with PGE2 and dexamethasone, it's clear that they make it into the vasculature and are able to go so far as to cause a temporary headache. One the other hand, you have finasteride and dutasteride which can cause lost lasting suppression of 5AR activity throughout the entire body. This is primarily due to the fact that they permanently denature the 5AR enzyme and not so much due to the half-lives of the drugs.
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Makes absolute sense!
My concern is dexa can’t be used long term. And studies I read said it had the best effects pulsed with minimal side effects.
However they weren’t in regards to hair
Studies on any compound relevant to our interests should be focused on endolethial cells and Dp cells.
But the point is I gotta becareful with dexa. Studies on murine models showed it induced caravan but it could be only for murine or only for normal growing human hair not prone to balding.
Too much dexa can destroy my skin. So I think it will have a biphasic response curve. If it helps with hair.
To me when I look at all the posts people have showed about their hair success. The more powerful ones have been ones that included estradiol. Not necessarily spironolactone. Just estradiol and a dht inhibitor.
The results are amazing if there is still hair their they tend to grow it all back. As long as the vellus hair are like the ones in my pics. Not the ones u can’t capture on a photo easily.
It’s clear that many women suffer from male pattern baldness but are protected by it due to aromatase expression in scalp and outer root sheath.
Or everyone has male pattern baldness and men without male pattern baldness jus the have high aromatase in their scalp. I am surprised their are not studies examinimg this. The study on the scalp only compared men to women aromatase expression. We need one between balding and non balding men
It's really all about the degree to which a person expresses 5AR and aromatase. Someone who expresses high 5AR and low aromatase is going to experience severe hair loss. Someone who expresses high aromatase and moderate 5AR will generally have a thicker hair shaft diameter, but they will also lose a moderate amount of hair (their hair won't be as dense as it could be... there are a lot of women with this issue, but most would look at them and not think that they're suffering from any type of hair loss, despite the moderate loss they experience). Someone who expresses low to moderate 5AR and moderate aromatase will generally have a full head of hair, but maybe a moderate to fine hair shaft diameter. Someone with low 5AR expression and high aromatase expression will have a full head of hair and their hair shaft diameter will be pretty much as thick as it's capable of being for their ethnicity.
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Interesting take on this. Man this thread is full of great info.
I will say when I took aromatase inhibitors for gyno once. My hair started falling out like no other. Nothing has made my hair fallout like exmestane. Not even superdrol.
Exemestane is what triggered my hairloss from the beginning. Not a steroid cycle. But a freaking aromatase inhibitor.
I was trying to nuke gyno. So I was taking massive doses that dried out my bones and joints
Yeah, I've taken letrazole and it definitely will cause you to shed. The pain in the joints isn't cool either, but for me it was relatively mild. Anything that alters estrogen synthesis or binding of estrogens with their receptors (SERMs like clomiphene and tamoxifen) will generally make someone who is already low in aromatase or estrogen receptor expression lose hair.
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Omg Letro probably would’ve made me nw7 in a week.
Hey do u know anyone with Addison’s disease? I was trying to see if baldness was a trait they expressed and I can’t seem to find enough images of people who have. Kennedy has addisons and he had insane hairline for his. Age.
My nan has Addison's. She's lost loads of hair and has to wear a wig. Pretty sure Bin Laden had it too.