Written by DR. GEORGE TOULIATOS
24 December 2019

 

 

 

Dr. Testosterone
By George Touliatos, MD

 

TESTOSTERONE

 

Testosterone is the main androgen, the hormone that separates children from men. It was manufactured right before World War II (1935) by the Germans, who received the Nobel Prize in 1939. Nazis used it extensively in order to sustain injuries and malnutrition, while aggressiveness was the main drawback of it.

 

Testosterone is produced during adolescence by the Leydig cells of the testicles, being responsible for the male secondary sexual characteristics. These include increase of the testicular size and scrotum (nut sack), hoarseness, hirsutism, alopecia (MPB), aggression and increase of libido and sex drive.

 

Testosterone’s effect on skeletal-striated contractile muscles is based on hypertrophy. This is something achieved by water and electrolyte retention, leading to edema. The swelling caused by sodium and water retention in the cytoplasm-sarcoplasm is most likely due to corticosteroids and their main representative, aldosterone. It enhances the ability of protein synthesis, through the assimilation of more animal protein (positive nitrogen balance).

 

Testosterone is not just anabolic, but androgenic as well. It oxidizes adipose tissue, thus making the body look harder. Testosterone becomes beneficial as an ergogenic agent during training through the aggression stimulus that it provides, especially in combination with other anabolic substances.

Testosterone has a balanced ratio between androgenic and anabolic index of 1:1.This is why it is used as a basis on each steroid cycle to provide a “pseudo HPTA.”

The administration of testosterone consists of 50% of an AAS cycle. It also reduces the abdominal fat (beta oxidation), as all androgens do anyway.

Testosterone’s concentration is proportional to that of somatomedin C, or insulin-like growth factor (IGF-1), released from liver. This practically translates into their synergistic action.

Testosterone has no benefits to connective tissue growth (cartilage, ligaments, tendons), unlike growth hormone. Abuse of testosterone results in tendons’ rupture, since there is no proportional development between muscles and connective tissue.

 

DRt2B

 

All AAS have an inverse relationship with glucocorticoids, of which the main representative is cortisol, thus they create an anabolic environment.

 

Steroids (i.e., stanozolol) also act as anti-inflammatory agents in certain diseases such as angioedema. However, the presence of glucocorticoids and cortisol has positive effect against inflammations of the musculoskeletal system.

 

Although the injection of cortisone in the tendon bears the risk of rupture, joint pains can be suppressed only by the presence of (hydro) cortisone. Furthermore, the suppression of inflammation is a phenomenon that acts negatively on the muscle development process, since it is based on the presence of inflammation in the muscle fiber.

The reduction of glucocorticoids during a steroid cycle lowers their anti-inflammatory effect in tendons and enhances the appearance of tendon ruptures.

In case excessive muscle development is not followed by proportional connective tissue development (something that GH-IGF-1 do), detachments and ruptures of tendons and ligaments occur.

Testosterone circulates in the blood in two forms: The total testosterone (TT), which is bound to a protein, the sex hormone-binding globulin (SHBG) and the free testosterone (FT), which is essentially the active form in tissues.

Total testosterone is not able to penetrate the cell membrane and join the androgen receptor. The majority of testosterone is bound to the SHGB protein, which transports it into the blood serum. A very small percentage (2%) remains free or detached from sex hormone-binding globulin.

The higher the rate of free testosterone, the better our libido and strength. Therefore, the values of free testosterone and SHBG are inversely proportional.

As we age, the value of SHGB increases and this is also one of the reasons of andropause. Also, the increase of beta-estradiol (E2) will increase the SHGB and reduce the FT. Obesity and the metabolic syndrome are diseases that elevate estrogens and beta-estradiol concentration.

 

One way to increase the value of free testosterone is to use a synthetic form of DHT (mesterolone, drostanolone) or even danazol (used for endometriosis). This way we improve the libido, since the SHGB is reduced.

Free testosterone enters the cytoplasm of cells and joins the androgen receptor (AR). The stronger the bonding between AAS-AR is, the greater the suppression of HPTA (flouoxymesterone). Moreover, the stronger the attachment between AAS-SHGB, the more FT circulated free, therefore libido increases.

 

Testosterone is one of the safest injectable AAS, since it is a natural hormone that is daily produced; unlike the plethora of synthetic derivatives (AAS). It is not hepatotoxic, but has a negative effect under chronic abuse (supraphysiological doses) on the atheromatic index and the HDL/LDL ratio. It also leads to left ventricular hypertrophy— LVH, or thickening of the left ventricular wall. This is something based on a variety of reasons:

 

a) Myocardium has androgen receptors

b) Heart muscle also consists of striated-skeletal fibers

Testosterone also increases production of sebum and skin becomes more elastic, with heavier odor. Sebum overproduction traps microbes and infection within the hair follicles results in the form of acne (inflammation).

Testosterone’s abuse results in testicular shrinkage, as a result of homeostatic cessation in endogenous testosterone production and Leydig cells. Testosterone’s chronic abuse, as with all androgens, may lead to psychosis and manic behavior. However, this is something that depends on the genetic predisposition of each individual.

 

dr TA

 

As with all androgens, testosterone has a positive effect on the bone marrow, and the production of erythropoietin (EPO) from kidneys. Erythrocytosis and polycytemia are extreme cases of red bone marrow overstimulation. This results in the rise of hemoglobin and hematocrit. The consequence of this is a greater blood viscosity and the risk of occlusive stroke and arterial hypertension.

Testosterone can improve insulin sensitivity (or decrease insulin resistance), by improving BMI and muscle mass. Therefore, diabetic patients who use testosterone should reduce their dosage of exogenous insulin.

Another issue with testosterone use is the hypertrophy of the prostate, known as benign prostatic hyperplasia (BPH), which occurs after the age of 40. As is well known, the main androgen is reduced to dihydrotestosterone (DHT) by the presence of 5-alpha reductase enzyme. Dihydrotestosterone is a powerful androgen, a metabolite of testosterone (x 5 in vivo). This reduction takes place in different tissues, as the prostatic gland, scalp and epidermis (skin).

It is advised to those who receive testosterone replacement therapy (TRT) after the age of 40 to measure the prostate-specific antigen (PSA) and undergo a digital rectal examination. It should be noticed that the gland is also getting enlarged, under the dominance of estrogens over androgens. Something that is mainly noticed in older people over 60.

The use of finasteride and dutasteride (inhibitors of the 5-alpha reductase enzyme) inhibit the activity of the enzyme in I and II receptors, which correspond to the prostate gland and the scalp respectively. Therefore, they deal with excessive hirsutism on the back as well as with androgenic alopecia (MPB).

 

5-alpha reductase inhibitors drugs are first choice medication against prostatic cancer. However, suppression of DHT will have a negative impact on a man’s libido, and may result in gynecomastia (anti-estrogenic action of DHT) and possible melancholia-moodiness (lack of DHT is associated with lower self-esteem).

DHT is an androgen with anti-estrogenic properties and five times (x5) more androgenic than testosterone (in vivo). However, there are no ergogenic benefits on muscle tissue. In local application on the nipples, it acts against gynecomastia.

Interruption during night sleep for urination (nocturia), difficulty during the start of urination and the leakage of a small amount of urine on the underwear, post urination, are signs of a potential growth of the prostate gland. This is something that could be the result of prostatitis (inflammation) and elevation of PSA. In older men, the theory of benign hypertrophy of the prostate gland was based on dihydrotestosterone.

 

Metabolites of DHT are those AAS that do not aromatize, like mesterolone, methenolone, stanozolol, oxandrolone, drostanolone and oxymetholone. Finasteride and dutasteride (5-alpha reductase inhibitors) have no effect on male pattern baldness (androgenic alopecia) and benign prostatic hyperplasia.

DHT derivatives have a less suppressive effect on HPTA, to a less extent than the metabolites of testosterone (equipoise, fluoxymesterone).

The administration of testosterone in men over 40 has been proven to be a major antidepressant, which contributes to anti-aging. Testosterone supports the muscular system, provides a more elastic skin, enhances libido and promotes self-confidence. The thoughts become more decisive, while women are attracted to men with high testosterone, through their skin odor.

Hormone replacement with testosterone (TRT) and DHEA has positive effects on reducing the abdominal fat and insulin resistance. The increase of abdominal fat promotes the creation of the metabolic syndrome, as well as insulin resistance, which promotes the creation of lipogenesis (a predisposing factor of diabetes mellitus type II, non-insulin dependent).

Because testosterone’s biosynthesis initiates from another steroid molecule, cholesterol, it is reasonable why diets low in saturated fats will have a negative impact on its endogenous production. Modern medication such as statins lower total cholesterol and low-density lipoprotein (LDL). The final result would be to lower total testosterone’s serum levels as well.

Biosynthesis of cholesterol is a process that takes place in the liver parenchyma. The Leydig cells of the testicles produce approximately between 7-10 mg of the hormone on a daily basis. This translates into approximately 50-70 mg on a weekly basis; roughly 10 to 20 times lower than the abuse of a competitive bodybuilder.

Just by this fact, we understand the degree of atrophy testicles undergo. It makes sense that after years of AAS abuse, the male ends up hypogonadic for life. A crushed libido and oligospermia, along with increased body fat, low self-confidence, poor muscularity and loss of muscle endurance-strength are present.

Not to neglect the negative consequences of a chronic overdose-abuse on the myocardium, the atheromatic index, the prostatic hypertrophy, polycytemia, androgenic alopecia.

 

Last but not least, the effects on mental health. This is the price every competitive or recreational bodybuilder has to pay eventually.

Slow esters of testosterone (enanthate, cypionate) are released gradually, reaching a peak around day four and remaining in the body for a prolonged timing (7-10 days).

 

Aromatization is easier to occur, as a result of this longer half-life. The clinical symptom of gynecomastia is an aesthetic issue, where the nipple is swollen and painful-touchy under palpation.

Enanthate and cypionate esters release a smaller amount of active testosterone, around 70%. In contrast, fast esters (propionate, suspension) have very immediate results, with the disadvantage that they have to be administered more often – three times a week for the propionate and on a daily basis for the water-soluble-suspension, ester-free form. They provide a greater amount of testosterone (80% and 100% respectively). Therefore, testosterone suspension is the most powerful type among injectable testosterones.

 

Fast-acting esters have a lesser chance for aromatization, as a result of their short half-life into the body. They are preferably used during pre-contest preparation. However, it should be noticed that the more estrogenic an AAS is, the greater anabolic properties it has. After all, aromatization and water retention is a fundamental biochemical environment that supports muscle growth and strength. Testosterone is converted into estrogen by the enzyme aromatase in the mammary gland, adipose-fat tissue, liver and brain. Obese individuals have elevated levels of (E2) beta-estradiol, as a result of greater body fat percentage.

Testosterone applied in the form of a gel increases the serum levels of dihydrotestosterone (DHT), since the skin has increased concentration of 5-alpha reductase enzyme. The transdermal absorption of testosterone has only 10% absorbency, but the advantage of sustained release and stable blood levels, compared to the intramuscular (IM) use.

Parenteral (intramuscular) type of administration acts acute into the circulation. The subcutaneous (SC) use has a delayed absorption and this is why insulin is usually administrated under the skin.

Somatropin (HGH) is administrated subcutaneously because of its lipolytic (fat burning) ability, that also provides a delayed absorption time. During a steroid cycle, the ratio between androgens and anabolics should be (2:1). This will ensure there is no crush on libido and sexual drive.

Testosterone has the ability to suppress the production of catabolic cortisol (the main corticosteroid). This is the reason why after the end of a cycle, both cortisol and estrogens rebound and rise dramatically. As a result of it, the physique gets smooth and muscle wasting occurs (catabolism).

The use of anti-estrogenic compounds (SERMs, tamoxifen) has a negative impact on testosterone’s benefits, regarding muscle growth. Tamoxifen citrate is known to suppress IGF1 in liver. On the other hand, the significance of the estrogenic environment to muscle growth is fundamental.

Estrogens enhance muscle glycogen synthesis through water retention. Therefore, muscle strength and stamina is enhanced. Estrogens are known to improve steroid receptors’ affinity to the steroid molecules. Estrogens improve joint lubrication, by retaining water into the synovial cavity. This is something critical under off-season, heavy-duty training.

Proof that women produce testosterone, but a lesser amount than men, is the fact that older women have increased facial hair, known as hirsutism. This practically occurs after menopause when estrogens are no longer produced. Androgens produced by the adrenal glands and ovaries continue their action, and therefore manifest their androgenic secondary characteristics. Androgens can act therapeutically, though, for a woman in the case of breast cancer. The estrogens are in exacerbation, so androgens (fluoxymesterone, drostanolone) act as an alternative treatment.

 

Nowadays, under the new generation of anti-estrogens (anastrozole, letrozole, exemestane), the use of 17-alkylated hepatotoxic AAS is no longer necessary.

As a doctor who has followed TRT for the past five years, my belief is that TRT is ruining big pharma sales. You see, testosterone is a cheaper drug compared to other medications that treat some of the symptoms testosterone does: insulin resistance and DM2, as well as anemia, arthritis, osteopenia, depression, erectile dysfunction, dyslipidemia, obesity and metabolic syndrome.

Certainly each medical treatment faces potential side effects, but in every treatment we always should balance pro and cons. The point is that hypogonadic men can’t live without testosterone. However, they surely can live without growth hormone during andropause and GHRH deficiency. But nothing can replace the main androgen (as women are suffering in the absence of estrogens during menopause).

It’s a fact that the plethora of benefits TRT provides in different tissues means that it should be considered a wonder medicine, and apparently this is not accepted by the big pharmaceutical industries.

Testosterone was given a bad name throughout its abuse from bodybuilders. This is how the medical world became skeptical and deals with suspicion the main androgen. Testosterone, however, is a familiar hormone and not a synthetic derivative like the rest of AAS. It has no side effects in liver and lipids, unlike anabolic steroids.

George Touliatos, MD is an author, lecturer, champion competitive bodybuilder and expert in medical prevention regarding PED use in sports. Dr. Touliatos specializes in medical biopathology and is the medical associate of Orthobiotiki.gr and Medihall.gr, Age Management and Preventive Clinics in Athens, Greece. Heis the author of four Greek books on bodybuilding, has extensively developed articles for www.anabolic.org and is the medical associate for the book Anabolics, 11th Edition (2017). Dr. Touliatos has been a columnist for the Greek editions of MuscleMag and Muscular Development magazines, and has participated in several seminars across Greece and Cyprus, making numerous TV and radio appearances, doing interviews in print and online. His personal website is https://gtoul.com/

 

 

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WATCH EPISODE 42 OF ASK DR. TESTOSTERONE