Hair loss at 21 what stuff to use

Tike wrote:
So yes i am proud of my looks, i have a nice 8 pack and 15 inch biceps, i work hard for it to. Now my hair is thinning and it there is a small line forming. How bad is propecia and rogaine for running? Do any of you use it?
I like the long cuts, with hair going to near my eyes, so i figured i better move quick now that i still have it.
What do you do about this stuff?
What price should i look in to? What is reasonable? So that i don't get ripped off?

Choices:

1) Accept it, shave head or cut hair very short, lose no money, experience no side effects.

2) Fight it. If you choose to fight it, you have options--

A) Drugs such as finasteride and dutasteride which work very well, but can nuke your libido and cause limp noodle syndrome among other things.

B) Topical products such as Nizoral shampoo, 5-10% minoxidil, etc. which won't cause sides but don't work as well, or

C) Both.

Personally, I suggest you avoid the anti-DHT drugs. DHT is your friend, if you are a guy.

------------------------------------------

DHT - Is It All Bad?

by Patrick Arnold

A considerable chunk of my work day is always spent answering people’s

questions about prohormones and steroids. Of course, one of the

biggest concerns people have is about estrogen and estrogen related

side effects. Right behind that however are questions about DHT. It

seems that people have the misconception that DHT is some evil

androgen by product that serves no purpose in the body but to make our

prostates blow up and our hair fall out.

The real situation is of course much more complex. DHT is one of those

good guy / bad guy hormones that is sorely misunderstood. For many

people, it is NOT something that you want to reduce or eliminate in

the body. For some others though, keeping DHT levels under control is

probably a prudent course of action. Knowing the facts about DHT will

help you decide just which group you belong to.

Testosterone is a prohormone?

The main androgen secreted by the testes is of course testosterone.

However, in most of the body, the androgenic signal is not carried

through by testosterone. In these tissues, which include the brain

(CNS), skin, genitals – practically everything but muscle – the active

androgen is actually DHT. Testosterone in this case simply acts as a

prohormone that is converted to the active androgen DHT by the action

of the enzyme 5alpha reductase (5-AR).

5-AR is concentrated heavily in practically every androgen dependent

area of the body except for skeletal muscle. This results in very

little testosterone actually getting through to these parts of the

body to bind to androgen receptors. Instead, it is quickly transformed

into DHT, which then interacts with receptors.

This transformation serves a very important biological function in

these tissues. You see, DHT is a much stronger androgen than

testosterone – it binds about 3-5 times more strongly to the androgen

receptor. If you took away 5-AR from these tissues and blocked the

formation of DHT, then you would see some dramatic changes in

physiology.

A good case in point is demonstrated in male pseudohermaphroditism due

to congenital 5-AR deficiency. This is a relatively rare disorder,

however it is actually quite common in the Dominican Republic. In this

disorder, males are born with little or no 5-AR enzyme. They have

ambiguous genitalia and are often raised as girls. When puberty

occurs, their testosterone levels elevate normally although their DHT

levels remain very low. Their musculature develops normally like that

of other adults, however, they end up with little or no pubic / body

hair and underdeveloped prostate and penis. Their libido and sexual

function is often disrupted also.

Testosterone is the active androgen in muscle

Skeletal muscle is unique from other androgen dependent tissues in the

body. It actually contains little or no 5-AR, so little or no DHT is

actually formed in the muscle. In addition to this, any DHT that is

formed, or that is already present in the blood and travels to the

muscle, is quickly deactivated by an enzyme called 3alpha-

hydroxysteroid reductase (3a-HSD).

So at least as far as muscle is concerned, testosterone is the primary

active androgen. This is not to say that administering exogenous DHT

is not without any anabolic effect. It actually does have some

anabolic activity in the muscle, albeit significantly weaker than that

of an equal amount of testosterone. This is due to its quick breakdown

by 3a-HSD into the weak metabolite 5alpha-androstan-3a,17b-diol. If

this enzyme were somehow blocked, it is likely that DHT would exhibit

very potent anabolic effects on muscle.

It is important to understand that even though testosterone is the

active androgen in muscle, and DHT exhibits relatively little direct

anabolic effects on muscle in men, DHT is still very important for the

full performance enhancement effects from testosterone. What I

specifically mean here are the effects of DHT on the central nervous

system, which lead to increased neurological efficiency (strength),

and increased resistance to psychological and physical stress - not to

mention optimal sexual function and libido.

I have heard several anecdotal reports of individuals who have stacked

testosterone with proscar (a 5-AR inhibitor) and have noticed

significantly reduced performance enhancement effects. What’s going on

here? We know it couldn’t be due to the inhibition of the direct

anabolic activity of testosterone on muscle anabolism. Most likely it

is due to the reduction of androgenic effects in other parts of the

body that contribute to the ergogenic effects, specifically the CNS,

which is stimulated by androgens to increase neural output leading to

greater strength and greater recoverability. Another possibility is a

reduction in the production of androgen dependent liver growth factors

(such as IGF-1), since DHT is an important androgen in the liver.

Anti – Estrogen effects of DHT

One important function of DHT in the body that does not get much

discussion is its antagonism of estrogen. Some men that take Proscar

learn this the hard way – by developing a case of gynecomastia. By

reducing DHT’s protection against estrogen in the body, these men have

fallen victim to its most dreaded ramification – bitch tits!

How does DHT protect against estrogen? There are at least three ways

that this likely occurs. First of all, DHT directly inhibits estrogens

activity on tissues. It either does this by acting as a competitive

antagonist to the estrogen receptor or by decreasing estrogen-induced

RNA transcription at a point subsequent to estrogen receptor binding.

Second of all, DHT and its metabolites have been shown to directly

block the production of estrogens from androgens by inhibiting the

activity of the aromatase enzyme. The studies done in breast tissue

showed that DHT, androsterone, and 5alpha-androstandione are potent

inhibitors of the formation of estrone from androstenedione. 5alpha-

androstandione was shown to be the most potent, while androsterone was

the least.

Lastly, DHT acts on the hypothalamus / pituitary to decrease the

secretion of gonadotropins. By decreasing the secretion of

gonadotropins you decrease the production of the raw materials for

estrogen production – testosterone and androstenedione (DHT itself

cannot aromatize into estrogens). This property of DHT comes into

particular utility when it is administered exogenously, and this is to

be discussed in further detail in the next section.

DHT, estrogen, and the prostate

When it comes to sex hormones, few things are as misunderstood by the

general consumer as the relationship of the prostate to DHT. The

inaccurate and overly simplistic attitude that DHT is responsible for

prostate hypertrophy, and even prostate cancer predominates amongst

most people.

The real situation is, of course, much more complex. One must

understand that there are marked differences between healthy prostate

growth (developmental growth), prostate growth due to BPH, and

cancerous prostate growth.

The first period of prostate growth, deemed developmental growth, is

connected to puberty and the testicular secretion of androgens. This

takes the prostate from its prepubertal dormancy to the normal sized,

healthy, and functional prostate gland of an adult. During the early

and mid adult years the prostate stays at this stage, despite the

constant high levels of androgens in the body. However, if androgens

are blocked in the body then the adult prostate will shrink in size.

This can occur by castration, or even by blockade of 5-AR (recall that

DHT is the active androgen in the prostate).

Later in life, there is often a second stage of growth. This growth is

deemed benign prostate hypertrophy (BPH) and this growth occurs in a

wholly different hormonal environment than that of developmental

growth. Evidence is mounting that the existence of a high estrogen /

androgen ratio – a condition common in older men – is highly

correlated to the development of BPH.

Experimental studies have shown the inability of androgens with

saturated A rings (DHT related) to induce an initial condition of

prostate hypertrophy. These compounds are non-aromatizable.

Aromatizable androgens on the other hand, such as testosterone or

androstenedione can induce hyperplasic modifications of the prostate

of monkeys, but these effects are reversed by the addition of an

aromatase inhibitor.

So apparently, estrogen is a causative factor in BPH or, probably more

accurately, estrogen in the presence of a minimum, permissive amount

of androgen.

None of this may come as news to many of you, but I bet that very few

of you know that DHT can actually be used to treat BPH!! How can it do

that? It basically does this by replacing the testosterone in the

body, which then has the effect of reducing the amount of estrogen in

the body. As I started to explain before, DHT is a strong androgen

that will signal the pituitary to decrease the production of

gonadotropins. The decrease in gonadotropins will then cause less

testosterone to be produced which will in turn cause the estrogen

levels to drop. The resulting change in the hormonal milieu (high DHT,

low estrogen) then apparently results in a regression of BPH.

The clinical application of this theory is discussed in US patent

5,648,350 "Dihydrotestosterone for use in androgenotherapy". The

following illustrates the results:

"In 27 subjects in which the plasma DHT level was controlled, so as to

modulate the administered doses, said levels have been increased to

2.5 to 6 ng/ml. There resulted a decrease in gonadotrophy as well as

in the plasma levels of testosterone which exceeded at least 1.5 ng/ml

(from 0.5 to 1.4 according to the case); as to the estradiol plasma

levels, these decreased by 50%.

Among this group of subjects, the volume of the prostate diminished

significantly, as was evaluated by ultrasound and by PSA (Prostate

Specific Antigen). The mean volume of the prostates was from 31.09.+-.

16.31 grams before treatment and from 26.34.+-.12.72 grams after

treatment, for a mean reduction of 15.4%, the treatment having a mean

duration of 1.8 years with DHT (P=0.01)."

This kind of flies in the face of the traditional thinking concerning

BPH now doesn’t it?

Conclusion

People have a natural tendency to classify things as either good or

bad, with no gray areas. DHT (like estrogen) has recently been on

everyone’s bad list, and is often considered to be a hormone that

serves no function in the body except to cause harm. As you can see,

this view is far from the truth. In my opinion, the widespread use of

5-AR inhibitors such as Proscar as a prophylactic agent for people

that really don’t need it should be reconsidered. So give DHT a break.

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