The Top Ten Testosterone Myths

The "dark side" dispelled

Testosterone is hot. It gets lead story status in big-name international newsmagazines like Time, and it's been making the rounds on both national and local news programs. Everybody, it seems, is suddenly intrigued by it. And moreover, everybody seems to want it.

It's quite a hormonal role reversal, considering that only a year ago, wearing a Testosterone T-shirt would grant you automatic pariah status on any street you happened to walk down. Likewise, asking the average physician about it would get you a raised eyebrow and a lecture – delivered in the requisite condescending tone – about the evils of steroids.

We're happy that the lay public "discovered" Testosterone and the concept of Testosterone replacement. It gives us delicious "I-told-you-so" status.

The trouble is, for every favorable report you hear about our favorite hormone, the news organization delivering it feels compelled to offer the "dark side," or "the bad news" about Testosterone.

Unfortunately, in almost 99% of the cases, they've got their heads up their collective asses.

The goal of this article is to help dispel most of the mythology concerning Testosterone, steroids, or prohormones, just in case you're considering getting your hands on some and your loved ones or peers have been eating up some or all of the media propaganda.

Myth #1. "Testosterone? Sure, that's fine, I guess. But steroids? That's a whole other subject!"

Most of the bobos in the news organizations think that Testosterone is somehow distinct from steroids. They think that Testosterone, while risky, is something worth looking at, but the very mention of the word steroid is enough to make them clamp shut their minds with the rapidity of a clam that just heard the seafood chef come into the kitchen.

The truth is, Testosterone is a steroid. It was first isolated in crystalline form by Laqueur in 1935 and was synthesized shortly thereafter. Once that happened, chemists around the world started synthesizing different versions of the drug.

Their hope was to somehow dissociate the masculinizing properties from the anabolic, or growth promoting, properties. No one is yet sure whether that's possible because it seems that the anabolic and androgenic (masculinizing) properties work through the same receptor complex.

Regardless, these synthetics, along with Testosterone, are all steroids.

Myth #2. Testosterone injections will give you liver cancer.

The truth is none of the Testosterone preparations currently used for Testosterone replacement in the United States have any negative effects on the liver.

Why then the age-old rumor? Most of the oral steroids (those that appear in pill form) have, in chemical terms, an alkyl group in the 17-alpha position. It doesn't matter if you know what this means. What does matter is that ordinarily, regular old Testosterone, taken orally, gets metabolized and inactivated by the liver before it reaches its target organs.

That means that you'd have to swallow a lot of it to have any noticeable effect at all. That's why all Testosterone esters are injectables.

However, in order to protect Testosterone from being broken down, chemists have put the aforementioned alkyl group in the 17-alpha position, thus making oral steroids a viable possibility.

Although this chemical juggling makes it an effective steroid, the liver suffers the consequences, sometimes leading to an increase in liver enzymes, cholestasis, and/or peliosis.

Whether or not these complications will lead to liver cancer is debatable. Although one study found an association between long-term treatment with methyltestosterone (a 17-alpha alkylated steroid) and liver tumors, another study found the association to be "incidental."(1,2)

Regardless, no doctors in the U.S. use any 17-alpha akylated steroids for T replacement. All use injectable versions.

Myth #3. Testosterone replacement will make your testicles shrink and you'll be sterile.

There's an element of truth to this "myth." If you introduce additional Testosterone into your body, your own supply is suppressed and the clearance rate increases. As a result, the testicles may take a vacation and actually shrink.

Simultaneously, the production of sperm cells will slow or stop. This is why the World Health Organization was thinking about recommending the use of steroids as a male contraceptive a few years back.

What the fear mongers don't tell you, however, is that these side effects are temporary and that the testicles almost always rebound within a few weeks. There are thousands of steroid users who have sired healthy babies.

One more point: this shutdown of the testes, however temporary, can usually be alleviated by the concurrent use of drugs like Clomid, HCG, and in some cases, a supplement like Tribex-500.

Myth #4. Testosterone replacement will make you grow lovely breasts.

Estrogen is the yin to Testosterone's yang. Let me explain. The body converts some of every male's Testosterone into the "female hormone" estrogen. Without this reaction, Testosterone wouldn't exert all its effects.

The trouble begins when the ratio of E to T is high. As a result, the excess estrogen binds to receptor sites on male breast tissue and initiates protein transcription; i.e. the male grows breasts.

Ironically, gynecomastia may also be a result of low T levels. Men who are hypogonadal (suffer from low levels of T) may, as a result, have high E/T ratios. Often, with the initiation of Testosterone replacement, the gyno can subside.

Most of the Testosterone preparations used for T replacement, with the exception of Testosterone Enanthate (and only in sensitive individuals), don't cause estrogen levels to increase too dramatically. In these "sensitive" patients, the solution is to either lower the dosage or switch to a different Testosterone preparation.

Additionally, there are various prescription estrogen "blockers" on the market. One of the newest and best is called Arimidex. Some innovative doctors might be persuaded to prescribe the drug concurrently with Testosterone replacement.

So yes, it's possible for Testosterone replacement to make you grow lovely breasts, but it isn't likely.

Myth #5.
A high level of Testosterone automatically makes you a sex machine.

Taking additional T doesn't always result in automatic horniness. There's often a latency period between T administration and increase in sexual desire (at least in hypogonadal men) that takes from days to several weeks.

Besides, just how much T you need to sexually function as a male is debatable. The normal physiologic range is a lot higher than you need to maintain normal sexual functions.

Additionally, while extra T will presumably, sooner or later, lead to increased sexual desire, increased sexual frequency, and possibly stiffer erections, it won't cure premature ejaculation or necessarily make you a better lover. If you're currently a dud in bed, extra T will make you a hornier dud.

Myth #6. Testosterone replacement will automatically turn you into a behemoth.

Not necessarily true. The effect of steroids on muscles varies tremendously from individual to individual. It has a lot to do with the age of the patient, existing T levels (primarily existing levels of free Testosterone), exercise stimulus, nutritional factors, growth hormone, and various muscle growth factors.

However, taking amounts of Testosterone above and beyond that which a man might need for the purposes of T replacement will generally lead to additional muscle mass, even without exercising. The landmark study of 1996 by Bashin and associates found that 600 mg of Test, given weekly over a course of several weeks, resulted in muscle mass gains that generally exceeded those of an average weight trainer who was working out regularly but who wasn't taking steroids.(3)

Even so, having high levels of T generally makes it easier to put on muscle mass than for individuals with lower T. Still, even that's uncertain because men differ on how their bodies process the stuff. Some men may have more testosterone receptors, which would probably improve responsiveness. Others might have a higher clearance rate of Testosterone, which would probably decrease responsiveness. And, another group might have very high levels of bound T, but very low levels of free T (the stuff that's biologically available for growing muscle and the rest of the stuff associated with T).

Myth #7.
Testosterone replacement will automatically cause your hair to fall out in tufts.

Take a look at almost any young boy or any woman – you'll notice that their hairlines go straight across their foreheads. However, once these boys start to produce T, their hairlines start to recede at the temples. And, if the genetic predisposition exists, they'll eventually go bald.

Therefore, it is true that T replacement – taken to normal or slightly supra-normal levels – can lead to hair loss, if the patient has a genetic predisposition to androgen-related hair loss.

Looking at case histories of castrates easily proves this. They don't suffer from baldness, but once you start giving them T, they can develop male pattern baldness.

Why does Testosterone sometimes cause varying degrees of baldness? Well, when a portion of the testosterone produced or introduced into the body gets converted into another form of T known as Dihydrotestostesterone, or DHT. Some of this DHT binds to intracellular androgen receptors – cellular parking spots, really – and prevents hair from developing normally.

DHT-bound follicles gradually produce thinner and thinner hair, along with the shortening of the anagen phase (the hair's life span) and lengthening of the telogen phase (the dormant, or rest phase). This can then culminate in the connective tissue sheath of the hair becoming chronically inflamed and long-term baldness is the result.

Still, the hair-loss phenomenon varies from individual to individual. As mentioned above, the genetic predisposition for hair loss must be present. Additionally, some men may convert Testosterone to DHT at a higher rate.

In any event, raising T levels to mid-range normal or high normal in itself won't necessarily cause your hair to fall out. And, if it is a potential problem, the drug finasteride will block DHT from binding to the hair follicle, thus usually preventing further hair loss.

Now, some steroids don't convert to DHT (or estrogen), but because of this, they won't exhibit the full spectrum of activities associated with T, so that makes them an undesirable candidate for T replacement.

As we learn more and more about steroids, scientists might soon be able to develop drugs for specific purposes. So we might eventually have steroids that don't cause hair loss. As an example the steroid 7-alpha-methyl-19-nortestosterone is experiencing a kind of renaissance because its highly androgenic but has little effect on the prostate, which brings us to Myth #8.

Myth #8.
Testosterone replacement causes prostate cancer.

Your average physician is convinced that the main problem associated with Testosterone replacement (or steroid or prohormone use in general) is prostate growth.

It is true that the prostate is a haven for DHT receptors, and elevated T generally leads to elevated DHT levels. Consequently, the DHT parks on the prostate receptor, eventually initiates protein transcription, and presumably causes the prostate to grow.

Why does mere growth potentially lead to cancer? Who knows, maybe the additional cell divisions prompted by the DHT are especially prone to mutations that lead to cancer.

Anyhow, the association between T and prostate cancer isn't clear at all. For the most part, T therapy hasn't caused any prostate-related problems.

For instance, Testosterone therapy has been shown to increase the prostate size of hypogonadal men, but only to the size of age-matched controls. That means that low T had caused their prostates to shrink while replacement caused the prostate to "catch up" to normal.

A recent study at the University of Iowa showed that men who had received T therapy for four years showed only mild increases in prostate specific antigen (PSA).(4) (PSA is generally regarded as a good indicator of prostate health.)

Another study done in Poland tracked 30 men who had all received T therapy for between 1.5 and 6 years, with the average duration being 3.35 years.(5) Although the average PSA doubled from 0.65 ng/dl to 1.35 ng/dl, this level was well within desired ranges (anything under 4.0 is considered acceptable).

It is true, however, that patients with existing prostate cancer should not get T replacement as it could make matters worse. (Medically speaking, this is practically the one pre-existing medical condition, along with breast cancer, where the use of steroids is contraindicated.)

Interestingly enough, scientists are beginning to think that estrogen also plays a role in the hormonal regulation of the prostate.(6) If that's true, it could explain a lot. Prostate cancer is almost epidemic in this country, but so are levels of environmental and dietary estrogens.

Given that the relationship – as shown by the many studies – between T therapy and prostate cancer is unclear, it makes the supposition of estrogen involvement especially interesting.

Myth #9. Testosterone replacement will cause your heart to stop.

Out of 30 studies looking at the relationship between coronary disease and T, 18 found an inverse relationship (meaning that low T positively correlated with heart disease), 11 found no association, and only 1 found a positive association.

Another case-control study of 50 men who were matched up by age and ethnic background – but differed only by T levels – found that low levels of Testosterone were associated with a higher BMI (body mass index, i.e., they were fatter), higher waist-to-hip ratio, higher systolic blood pressure, higher fasting and 2-hour glucose and insulin levels, higher levels of cholesterol and triglycerides, in addition to a lower HDL-C (good cholesterol).(7)

In other words, although these men hadn't suffered heart attacks yet, low T made them ideal candidates for coronary problems.

Now, it is true that supplemental T can lead to supraphysiological levels of hemoglobin, erythrocytes, and hematocrit, which can possibly lead to stroke or a coronary event, but any conscientious doctor will monitor such parameters through routine blood tests.

If indeed there's evidence of the aforementioned problems, he may actually drain some of the "excess" blood. An adjustment of dosage may also be in order.

It's this reporter's humble opinion that many of the cardiac problems associated with T or steroids in general results from using either extremely high doses, or in lousy dietary habits that often come part-and-parcel with steroid use.

The user, despite eating "bad" foods, sees his body fat continue to drop. With this perception of body fat invulnerability playing a role in his decision making, he begins to eat all the foods he shouldn't be eating, including those that contain large amounts of saturated fat or trans fatty acids. The end result is poor coronary health.

Myth #10. Testosterone replacement will cause you to kill your parents, or any man, woman, flower or bug that gets in your way.

Generally speaking, hormones don't cause personality changes per se; they only alter the probability that a particular behavior will pop up in the presence of a particular stimulus.

Now it is true that violent offenders often have higher T levels, but there's some evidence to suggest that, at least in animals, previous experiences in aggression can sometimes be more important than T levels in determining aggressiveness. That means that if a kid was beaten and abused, he might well grow up to be a felon, regardless of T levels.

Dr. Christina Wang of UCLA found that men with low T were more likely to be aggressive and ill humored than men who had high T. However, once these aggressive men received T replacement, their anger disappeared.(8)

Another study conducted in 1992, found that high T levels correlated with emotional well being.(x)

How then, do we explain the "roid rage" behavior that's part of bodybuilding legend? One explanation is that these men take enormous amounts of steroids and once a certain threshold is passed, all bets are off. Another explanation might be that the same impulses that caused them to be risk takers and aggressive might play a part in their decision to abuse steroids. Thus, the steroids only increase the probability that they're going to act aggressively.


There is no evidence that the judicious, sane use of Testosterone or steroids in general is life shortening. Of course, there's not a whole lot of evidence (yet) that T will lengthen life. There is, however, plenty of evidence that they can improve the quality of life.


1. Lancet 1975; (I):430-2
2. JAMA 1986; (255):906
3. J Clin Endocrinol Metab 1997;(82):407-13
4. Pharmacotherapy, 1999 Aug;19(8):951-6
5. Pol Arch Med 1998 Sep;100(3):212-21
6. J Androl 1994;(15):97-99
7. J Clin Endocrinol Metab 1997;(82):682-85
8. Time Magazine, 2000 April 24: p. 64
9. J Androl 1992 (13):297-304