Myth #1
TESTOSTERONE (T) AND BEHAVIOR - “ROID RAGE”
It is a myth that T since being an anabolic steroid (naturally produced) then those who use it will automatically exhibit “roid rage” with aggressive and other undesirable behaviors. Major studies have now shown this to be incorrect. When 600 mg of T was given intramuscularly (I.M.) every week for 12 weeks or more. It showed that with these high T doses produced no significant behavioral changes in mentally normal old and younger men.
In my clinic in Santa Monica, California I have treated young (30 to 40 year old) insulin dependent diabetic men with doses of 1,000 mg of T or more per week to increase insulin sensitivity decrease their insulin needs and stabilize their glucose levels with such large T dosages. Sometimes their total T (TT) blood levels go up 7,000 ng/dl or more. I have seen improved and stabilized mood without abnormal behavior. However men with mental dysfunctions who use high T doses along with other legal and illegal steroids may exhibit “roid-rage” abnormal behaviors.
Those men who are low in T are not happy guys and often are most “grumpy”. After their T levels are balanced to normal they return to the clinic not in any stage of rage, anger or aggressiveness. When their free total T (TT) and free T (FT) “tanks” are balanced to high –normal levels they return smiling, confident and happy. FT is the unbound T that can enter cells and can therefore be used. Bound-up T cannot enter the cell and has no effect. When a man has empty or nearly empty T tanks (TT/FT) the opposite is seen.
Myth #2
The higher the T levels the higher or better libido, sex drive or function.
To have good libido and sex performance the “TT / FT tank” does not need to be 100 % full or “overflowing”. In most cases usually 1/3 to ¼ full tank of TT/FT is all you need.
However, when it comes to building muscle mass there is a much closer and tighter relationship of TT/FT and muscle mass. Those with higher T you can gain more muscle mass and faster than when at low – normal levels.
Myth #3
High T Levels Cause Prostate Cancer (PCA)
It has been believed by many for a long time that T is the only or main cause of prostate cancer (PCA). It is also believed that men who have had prostatectomies or other localized therapies for PCA should never ever be treated with T. There is now good evidence that a man who has successfully been treated for localized PCA and does not have detectable Prostate Specific Antigen (PSA) blood levels can be treated with T if they have low T levels.
When and how did the myth that T increases the risk of Prostate Cancer originate and that higher the T the greater the risk of Prostate Cancer (PCA)?
The origins of concern that T therapy increases the risk of PCA started with studies by Charles Huggins in the 1940’s. It was noted that castration (removal of testes) could successfully treat men with BPH (benign prostate hypertrophy or enlargement). Huggins and his coworkers went on to study men with prostate cancer that had spread outside the gland and into the bones (metastatic PCA). They castrated these men and noted that the marker for bone metastases called alkaline phosphatase (alk-phos) went down. Also when T was injected into these patients the levels of alk-phos went up. From then on PCA was treated either by castration or by estrogen therapy. Since estrogen increases clotting and heart attacks and men did not want their testes “cut off” drug therapy was started. Lutenizing hormone (LH) agonists were introduced in the 1980’s. The LH-like drugs produced brain signals (from hypothalamus) to be sent to the pituitary to stop lutenizing hormone (LH) release. Thereby leading to very little or no T production by the testes. The end result was “chemical castration”.
It is still is believed that T treatment or having high T levels would produce PCA. Therefore T replacement or raising T levels to high levels was like “pouring gasoline on a fire”. It was thought men with low T “should be therefore protected” against getting PCA by lowering T levels. Later it was determined that “more men with low T” levels had PCA upon biopsy of the prostate gland than those with higher T levels.
Does low T or high T cause PCA? What other than low T could increase PCA risk? Significant studies showed that T given to men with “prostatic intraepithelial neoplasia”, (a type of slow growing prostate cancer) for 1 year did not increase the cancer rate. It is important to note that other factors then T are involved with PCA such as DHT, estradiol (E) (both derived from T), growth factors and others. T is not the only “villain” as previously believed as it relates to PCA. There are other factors, which have not been studied well enough to come to definite conclusions.
Of importance is that PCA does not occur in men in there 20’s when most men have highest TT/FT, growth factors
(IGF-1 and others), DHT levels and also lower estrogen
(E) Levels. With aging T, IGF-1, and DHT decrease and E increases and the incidence of PCA also increases. Estrogen maybe a most important factor related to cause of PCA. More studies are needed.
Low T rather than high T may be a risk for PCA.
In over 20 studies showed that total T (TT) levels were not higher in PCA group compared to men without PCA. Men with higher T had “less risk “to develop PCA that men with lower T. Therefore raising one’s T to a high level does not increase the risk of PCA. Treating men with very low T levels (hypogonadal) does not increase PCA risk.
CONCLUSIONS
1.Low T blood levels “do not protect against PCA” and may even increase risk.
2.High T levels do not increase PCA risk.
3.T “might” increase PCA in those men who have already had “metastatic PCA” and have been noted to have low T.
Ironically, Huggins was awarded a Nobel Prize in 1966 for his work showing PCA cells grew or shrunk depending on what the T levels were.
New T Products:
1.Nebido: In Europe a long acting intramuscular (I.M.) form of T called testosterone undecanoate was approved in 2005. A 1000 mg injection is given every 3 months (12 weeks). In the U.S.A it is called Nebido and is awaiting FDA approval. Some using Nebido from Europe report that supplementing with T cypionate intramuscular 3 to 4 weeks before the next Nebido injection is helpful to keep T levels at a better range and feel better. Some men feel better getting Nebido injections every 9 weeks instead of 12 weeks.
2.Testopel, (subcutaneous T Pellet) has been approved in the U.S.A. It is implanted under the skin and can maintain good T levels for 3 to 6 months. Usually 6 to 8 pellets are put into the buttocks (6 to 8 pellets about size of rice grains). Some men prefer this treatment done a few times a year rather than daily gel applications or injections every 1 to 2 weeks. Dosage: Usual starting doses are 150-450 mg (2-8 pellets) implanted under the skin every 3 to 6 months. If your Testosterone I.M. dose is about 100 mg per week then about 6 to 8 pellets may be needed. Once put under the skin the pellets cannot be removed.
3.ANDROXAL is the most exciting product in late stage drug development. Androxal is a small molecule single isomer of clomophine citrate taken as an oral tablet, (Repros Therapeutics, U.S.A.) Some may know that Clomophine Citrate (Clomid), which is widely used for infertility especially in women and men who may have finished a “steroid cycle”. It causes release of LH. Clomophine acts as an estrogen receptor blocker. Thereby it “fools the brain” into believing that estrogen levels are low and that causes the pituitary to increase the release of LH, which stimulates the testes to make more T. The evolutionary reason being that estrogen can only be derived from T. and adequate estrogen levels are necessary for species survival. Androxal also has a most interesting effect of also lowering blood glucose. With the explosion of the cardio-metabolic syndrome (diabetes, abnormal lipids, weight gain, high blood pressure along with low T and other problems). Androxal if approved will be one of the biggest “breakthroughs” in T therapy and will help treat the diabetes-obesity epidemic. Head to head trials of Androxal (25 mg orally taken for 6 months) against a T gel (AndroGel, Solvay) showed that Androxal produced as good of if not better T levels and enhanced fertility in “secondary hypogonadal” men - hypogonadism from failure of the brain - pituitary gland to release sufficient LH. Androxal would not work in those with primary testicular failure. Also called primary hypogonadism - the testes cannot produce sufficient T and sperm. Androxal increased testicular size more than AngroGel. A trial was recently started looking at Androxal effects against the more potent T gel called Testim (Auxillium corp.) for 6 months or more. Androxal may prove to be valuable in the treatment of AIH – androgen induced hypogonadism from use or abuse of steroids often seen in men who have overdone various steroid cycles. I have many such men in my practice who often doing some “steroid cycles” in their 20’s later wish to regain their fertility and produce naturally normal T levels in their 40’s.
4.Selective Androgen Receptor Modulator’s (SARM’s) are in early stages of development. They are a novel class of androgen receptor modulators. One such is 7 alpha-methyl-19 nortesterone. There are about 5 SARM’s in various stages of development. The SARM concept is similar to SERM’s (selective estrogen receptor modulators like Raloxifine, (Evista or Tamoxifen). They are meant to have the same effect as androgen drugs (T and other anabolic steroids), but are more highly selective in their tissue effects. This would allow them to be used for many more clinical applications. Oral SARM’s are being developed, which can have positive effects in muscle and bone but not other tissues. Some of the SARM’s in development have much greater favorable anabolic to androgen ratios from 3:1 or up to even 10:1. Testosterone has an anabolic: androgen ratio of 1:1. SARM’s are being developed to target androgen receptors in specific tissues such as stimulating the androgen-receptors in the brain, bone, heart, and skeletal muscle while avoiding stimulation of the androgen-receptors in the prostate, hair follicles and other undesirable tissues.