Hi Marinera,
When you compare transdermal application with oral, or injections, the question does come down to how effective one is in hitting the targeted area. If one was to compare transdermal to oral, depending upon the location of the targeted tissue, the amount of hormone that could be presented to the target tissue is much higher. A good analogy to this is in the treatment of gynecomastia (unwanted breast growth in men), where the protocol is for transdermal DHT, and concurrent estrogen suppression. Indeed, one of the causes of gynecomastia, is when the enzymes that convert T into DHT are suppressed. With reduced levels of DHT, and elevated levels of estrogen, the estrogen’s cause an increase in breast size. This also tends to show that there is not such a clear area between a receptor being turned off, or turned on.
Comparing transdermal to injection can be a difficult comparison. Targeting the point of injection, knowing how far the injection will flow, how fast the reaction takes place, etc,are part of the variables. When injecting into the CC, it is an easy target, with a fairly large volume (at least for an injection) so the variables are reduced. Also,since the CC is full of blood, dispersion throughout the CC is easy, although in the case of IGF-1 I do suggest that one alternates his injection site from one side to the other. This is why injecting with PGE-1 works well, and why injecting IGF-1 seems to work well. Injecting into the tunica would be challenging due to poor blood flow in connective tissue, radius of effective dispersal of the injectate, etc. Basically, injecting into the tunica is not at all practical.
To be sure, transdermal application has its challenges. Blood flow taking away the hormone from the targeted tissue is the big one. And interesting test in that regard is to apply DMSO to the penis liberally, and see how long it takes to taste the DMSO. The deeper the target tissue is, the more difficult transdermal application becomes. On the other hand, if blood is to be the dispersant, the penis has the advantage of being able to restrict blood flow somewhat and thereby keep the hormome available to the target tissue longer. Transdermal is also quite effective in bringing hormones into the body without having to go through the stomach or liver, which de activate to a considerable degree what has been swallowed.
As to the effectiveness of DHT on the adult male, there is evidence on both sides, but not much comes along that is on point for PE. Certainly DHT is one of the prime hormones in penis growth in puberty, and after puberty, those receptors are turned off, more or less. Once again, we get to a point where the devil is in the details. How does one quantify a response in these cases? How much growth can be attributed to the response of the body to tension? How effective are the DHT receptors? What growth factors can be utilized? The bottom line is that there is no definitive answer.
The statement that a hormone has no effect because the receptor is “turned off” is not an absolute, it is a relative. The relationship is how the interpretation of the signal is received. Hormones work by being at a target, or by not being at a target, or in opposition at the target with other hormones. Probably the best known of later, is the menstrual cycle. In that cycle, the estrogen’s start it off by telling the uterus to increase the endometrium. This continues until just before ovulation, when progesterone increases significantly. Progesterone has quite a number of uses, but in the uterus it acts as the opposition to the estrogen’s, telling it to no longer add to the endometrium. It is also the “glue” that keeps the blood and tissue in the endometrium attached (and it is what keeps the fetus from falling out of the uterus). The estrogen’s cause water retention, progesterone is a mild diuretic. Women that “spot” in the early part of their menstrual cycle do so because they lack progesterone, which is a fat soluble hormone, and if there are no fat stores, there is none to be had early in the menstrual cycle.’
When it comes to relating with other hormones, there are a number of variables. For instance, one synthetic progesterone (a progestin) is Depo Provera. Depo works by being very difficult for the body to expel, since it is not a natural hormone at all, the body has a very hard time metabolizing it. Therefore, when a woman takes it, her body reads it as progesterone, and since her progesterone levels appear to be high, she cannot have a period, hence, it is a birth control method. However, when Depo is given to males, it completely overpowers testosterone, and is referred to as “chemical castration”
Relative strengths of the hormones is also interesting when one considers PE. As an example, a healthy woman may make 300 mcg of estradiol at her high point in her menstrual cycle. She will also make about 20 to 25 mg of Progesterone at the high point in Progesterone production. The point being that ounce for ounce, the estrogen’s are some 60-100 times stronger in result that progesterone is.
When it comes to males, it is the same problem. A typical 18 year old may have a total testosterone level of 1,000, with maybe as much as 400-500 free testosterone. He will be able to have a number of ejaculations during a 24 hour period. However, if you supplement him with a 1 mg pill of estradiol (an estrogen) he will most likely be impotent in a day or so. The estrogen is perhaps 10 to 20 times stronger than testosterone on an ounce for ounce basis. As males age, testosterone declines, and the estrogen’s increase. This results in a loss of libido, poor erections, potential for gynecomastia, and reduced muscle mass. Adding DHT to the mix, makes a significant improvement to the aging male. Unfortunately, the body builders have abused this so much in the US that it is banned here. Sigh.
DHT is a very powerful hormone, and it is made in small amounts, which is kind of like the estrogen’s. Adding DHT will raise male libido significantly. As to PE, it will do nothing all by itself to the adult male, but to the adult male with a PE program, it comes into the “maybe helpful” category. Certainly the “tension over time” is required for growth factors to be released, but with them, if DHT is present, well, again, it is a maybe. Defining hormonal response to a “turned off” receptor, is difficult to quantify. This is one reason that I maintain an interest in the Chem PE side. I remain hopeful for more documentation to see what can happen. Sadly, it is hard to find, one way or the other.
Kind of a long response to a simple question. Sorry