Testosterone replacement is an issue that concerns most men over the age of 35 or 40. Although these men may feel great, they know, deep down, that they feel differently than when they were in their twenties. Granted, a lot of it has to do with general wear and tear and a host of age-related declines, but some of it has to do with the steady decline in testosterone production.
Few men take advantage of testosterone replacement, though. Either they accept all of the propaganda perpetuated by the media and the various health-care practitioners who haven’t bothered to bone up on the subject, or they just don’t know enough about it.
This article may give you the info that you need to pursue this avenue. True, most of the research on the subject concerns men who need total testosterone replacement. But the information still applies to those who are clinically deficient and need only a little boost to regain the sexual staying power and the muscle-building ability that they had in their twenties.
Hey, you with the bulge in your pants…yeah, you. Been feeling a little hornier than usual lately? Have you found yourself passing trees and musing about how like a young girl’s legs the limbs are, and how inviting that knothole in the crotch is, if only that woodpecker would fly the hell away? Does everything with a hole in it, whether it be a doughnut or a soap-on-a-rope, conjure up amorous fantasies?
C’mon, you can level with ol’ TC. You’ve even been eyeing that pumpkin on the stoop, haven’t you? That eye socket looks so moist, so inviting and, come Monday, the day after Halloween, that bitch is gonna’ be yours…
Ahh, but who can blame you? It’s October, and the testosterone levels of the North American male are up — way up — this time of year. Like other animals, homo sapiens have circannual variations in testosterone production — as much as 25%, depending on the time of year. October, at least according to one group of researchers (Smals, et al., 1976), is the month, while other researchers (Dabbs, 1990) think that we get a little hornier in December.
Regardless of the exact month, most of us seem to be having a lot of trouble focusing on things lately. But some of us aren’t having any trouble focusing at all. Some men, because of advancing age or assorted medical problems, have low testosterone. It may not be an issue for you…yet. But sooner or later, your T levels will begin to drop, as surely as the value of my stock portfolio dropped when I invested in Ian King’s new signature line of industrial-strength panty shields.
Being able to focus on things a little better is probably a plus. But when you weigh that small advantage against all the other side effects of low testosterone, lack of concentration seems to be an appealing alternative. Consider the following symptoms of low T:
• Decreased bone mass
• Skin atrophy, along with paleness and fine wrinkles
• Muscle atrophy
• Erectile dysfunction
• Decrease in sperm count
• Decrease in volume of ejaculate
• Decrease in libido
• Shrinkage and softening of the testes
• Disappearance of spontaneous erections
• Prostate shrinkage (below normal)
Now, I really think that Tribex-500 can boost T levels and help stave off that age-related decline, but it’s probably never going to take the place of various pharmaceutical testosterone preparations.
As far as the medical community is concerned, the goal of T replacement is to get levels as close to physiologic concentrations as possible. We at T pretty much agree with that, but we’d like to see docs push the envelope a bit and get all of us close to high normal, but no matter.
In the beginning…
In the beginning of the whole science of T replacement, only the basic esters of testosterone were all based on the real thing. Then, scientists started to tinker with testosterone, trying to make it better. Basically, there were three roads that they could take: work on different routes of administration, chemical modification of the molecule itself, or esterification in the 17-beta position of the T molecule.
Ever wonder why you can’t just drink T down instead of shooting it into a butt cheek? Contrary to popular belief, you can actually drink most injectable steroids. Testosterone is absorbed pretty well from the gut, but the liver grabs a hold of the stuff, metabolizes it, and inactivates it before it gets to the target organs. This phenomenon is known as the “first pass effect.”
Only when the dosage exceeds 200 mg — which is about 30 times the amount produced daily in normal, healthy man — is the liver outgunned. Of course, if you were suffering from total testicular shutdown, you’d have to suck down 400-600 mg a day to see any positive effects. That, of course, aside from causing some potential health problems, would force you to hock your Beemer.
Unfortunately, you still see stuff in health food stores that contains dried up animal testis. Now, eating these things like popcorn kernels could theoretically work, but there’s another problem: unlike other endocrine glands, the testes don’t contain a lot of stored up hormone, so eating hundreds of them wouldn’t do any good anyhow. Makes you wonder how they can still sell these extracts, doesn’t it?
In an effort to thwart this first pass effect and produce “edible” steroids, scientists started making synthetic forms that were alkylated at the 17-alpha position of the molecule. In essence, that protected them from the metabolizing effects of the liver. The trouble is that these are the steroids that give steroids a bad rap. They cause toxic side effects such as elevated liver enzymes, cholestasis (a stoppage of bile flow), and peliosis (the presence of blood-filled cysts in the liver). These drugs have also been implicated in liver tumors.
Synthetic forms had other problems, too. Trouble was, these synthetic forms didn’t duplicate all the actions of T. For instance, some of them didn’t convert to 5-alpha DHT or estrogen — and, despite the bad press that both of these compounds get, they’re vital to normal human function.
That’s why doctors don’t typically prescribe anything else other than “natural” forms of T. After all, the stuff’s been used for over six decades and has one of the highest safety records of any drug. There will probably be exceptions in the future, though. For instance, 7 alpha-methyl-19-nortestosterone (MENT) is experiencing a kind of renaissance, since it has high androgenecity and low growth-promoting effects on the prostate. Likewise, researchers continue to look at testosterone undeconoate. Unlike other “designer” steroids, this drug was esterified in the 17-beta position. It has virtually none of the side effects of the 17-alpha drugs, but it has such a short half-life that it ought to be prescribed in a Donald Duck Pez dispenser.
Delivery systems…mouth, nose, butt, or needle?
After pretty much settling on natural testosterone as the best hormonal thing since the invention of sliced hormonal bread, researchers started monkeying around with delivery systems. One relatively new delivery system involves incorporating T into cyclodextrins. When they’re administered orally, you get a T spike that lasts about the length of an average feature-length movie. In order for it to do any good, you’d have to remember to pop some in your mouth several times a day. Consequently, this type of delivery system’s pretty much been tossed out with yesterday’s chicken salad. Interestingly, a lot of supplement companies have adopted this delivery system for use with their androstenedione products. A nice idea but, again, the spike is very short-lived and very uneven.
Another delivery system that never achieved widespread popularity (outside of San Francisco) is rectal administration, via suppository. Too bad, too, because it works pretty well. You avoid the first pass effect, and a dose of only 40 mg can cause a boost in serum T that lasts about four hours. Nasal application has also been investigated. You can avoid the first pass effect this way, too, but the effects are unreliable and short-lived. Besides, one sneeze, and you’ve got snot and steroids on your sleeve.
There was recently some work done with microspheres in which tiny, time-release chemical nuggets were injected directly into the bloodstream. A dosage of just 315 mg raised T levels gradually to a peak over the course of eight weeks, then gradually reaching sub-clinical levels after eleven weeks. Again, the method had its problems. The spheres lacked stability and were hard to make. No one’s really done any work with them since ’96 (Bhasin and Swerdloff).
Rod-shaped implants, similar to the Norplant birth-control implants used by some women, are experiencing renewed interest. These things exert their effects for several weeks or months. Along the same lines, actual testes-shaped implants are available, too. They consist of about 10 grams of vinyl and about 6.4 grams of T. Once implanted in the scrotal sac, they keep T levels normal for about a year. Obviously, the use of these is problematic, unless you’re missing a nut or don’ t mind having a third. Maybe an alternative would be to put them just under the skin over the biceps so that the patient can have instant Robbie Robinson-like biceps peaks.
One method that’s in widespread use is the patch. Even though putting one on in the morning and taking it off the next morning produces a great pharmokinetic profile (with fairly natural rises and falls in T), the patch has its problems. For one thing, it’s hard to control absorption rates. Scrotal skin is the thinnest and easiest to permeate and has an absorption rate that’s about 40 times higher than the forearm. Other areas work, but you have to use an alcoholic enhancer, which makes skin reactions more probable.
And, a slightly bizarre problem — one that few people even considered a few years ago — was person-to-person transfer. Just hugging a spouse or child is enough to androgenize them, leading to masculine traits in the female or premature sexual development in children.
Unfortunately for needle-phobics everywhere, it seems that needles are around to stay — at least for the time being — as intramuscular delivery elicits the fewest number of side effects or problems. Currently, there are three common testosterone esters used in T replacement therapy:
• Testosterone propionate
• Testosterone cypionate
• Testosterone enanthate
For complete T replacement, testosterone propionate must be injected every two to three days, while enanthate requires a shot of 200-250 mg every two weeks. This dosage is, of course, for total T replacement, and partial T replacement would require much less. One other testosterone ester, testosterone cyclohexanecarboxyate, has similar properties but is less widely used that the other three.
Given the shortcomings of intramuscular T therapy (a big spike in the beginning, followed by a gradual decline) and all of the shortcomings of the various preparations and delivery systems, the World Health Organization initiated a steroid synthesis program in 1980 to develop different types of steroids. As far as I can tell, they didn’t make too much headway. But they did develop testosterone buciclate, a single shot (600 mg) of which produced normal T levels in hypogonadal men for 12 weeks. This stuff will probably be made available in a year or two.
And the Chinese found that testosterone undeconoate, when dissolved in teaseed oil and used intramuscularly (instead of swallowed as a capsule), produced pharmacological effects similar to testosterone enanthate. Later studies used castor oil instead of teaseed oil and found that a 1,000-mg shot had effects lasting as long as eight weeks. Whether or not this will catch on as the testosterone replacement drug of choice remains to be seen.
What happens after T therapy begins?
Generally, good things happen after T therapy begins. Abdominal fat generally goes down, muscle mass goes up, and all of the “bad” symptoms of low T go bye-bye. Other inconsequential things happen, too. For instance, beard growth and frequency of shaving goes up. Interestingly, giving total T replacement to a hypogonadal man will affect his hairline, too. Now, I’m not talking about baldness necessarily, but the actual front hairline which, in women or children or men with virtually no T, stretches straight across the forehead. Once T levels rise, though, recession around the temples occurs.
Baldness, of course, is a possibility in those genetically predisposed to the condition.
Sebum production goes up, too, so you can go through that whole adolescent acne thing all over again. Gynecomastia may also become a problem, but that can usually be handled just by adjusting dosages or switching preparations. Additionally, there are several prescription-type aromatase inhibitors that may be used to fight the problem (interestingly, these aromatase inhibitors themselves might be used to raise T production — we’ll have an article on nonprescription forms of aromatase inhibitors in the next week or two).
What bad things happen after T therapy begins?
This may surprise you, but virtually nothing bad happens after T replacement therapy begins, at least not in the vast majority of patients. No negative side effects occur to the liver (remember, all the bad things took place as a result of using the 17-alpha alkylated stuff you generally get from dealers or overseas markets). No definite negative cardiovascular effects have been noted. Even the prostate, long regarded as the first organ to take the plunge after using “evil” steroids, is relatively safe. The truth is that it’s pretty much accepted now that prostate growth occurs through the action of 5-alpha DHT and that these effects are related to things that happen exclusively within the prostate and are not influenced by serum concentrations of T or 5-alpha DHT. Furthermore, estrogens are believed to be the true culprit by some. T therapy increases the prostate size slightly, but only to the point of normalcy. If any doubt of this remains, a recent study (Hajjar, 1997) tracked men in their seventies who had been receiving T replacement therapy for two years. The treatment group experienced less prostate growth than the control group.
In fact, the only possible problem seen with T therapy is an occasional rise in red blood cell count (hematocrit) which, if unchecked, could contribute to stroke or cardiovascular episodes of some kind. In those cases, either the dosage was adjusted or the patient was asked to donate an occasional pint of blood.
In fact, it was the conclusion of one pair of authors (Nieschlag and Behre, 1999) that “…there is no proof that testosterone is a life-shortening agent. The risks inherent to testosterone, be it of endogenous or exogenous origin, would then appear to be the tribute men have to pay for being men.”
Couldn’t have said it better myself.