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Non-Genomic Actions of Anabolic Steroid Hormones

Mr. Haycock,

I consider myself well versed on steroids and how they work, but one thing that continually has me puzzled is this; if there is only one androgen receptor that all steroids bind to in order to induce growth, how come there are so many diverse effects of different synthetic steroids. Some make you bloat, others don’t. Some give you insomnia, other don’t. Some give you hiccups and make you snore, while yet again, others don’t. No one has been able to offer me an explanation for this. Any insight you might shed on this would be really appreciated.

Thanks in advance.

Answer:Much of the confusion about the wide range of side effects of steroids comes from their various non-genomic actions. As the term “non-genomic” doesn’t seem to come up very often in locker room steroid conversations let me explain.

Most people know that there is only one typical, or sometimes called “classical”, androgen receptor (AR). The AR is an intracellular receptor, meaning that it resides within cells (as apposed to the membrane surface) and once bound to an androgen, travels to the nucleus of the cell and binds to the DNA where it initiates the expression of various proteins.

The AR exerts a wide range of effects even though there is only one typical AR. Testosterone (Test) is able to exert different effects in different tissues by virtue of it acting “as is” in some tissues, and acting as its 5-alpha reduced counterpart dihydrotestosterone (DHT) in the same and/or other tissues.

DHT has different binding properties than Test. DHT binds stronger, and stays bound longer than Test. This subtle difference in the strength and duration of binding is able to produce a tremendous range of different actions in the body from the time you’re a fetus to a full grown adult.

Some synthetic steroids are more like Test, and others are more like DHT. But this still doesn’t explain all the differences seen among synthetic androgens. The differences beyond binding properties can then be explained by these “non-genomic” properties mentioned earlier.

Within the last 5 years or so, more attention has been drawn to the non-genomic effects of steroids and trying to understand them. They are called “non-genomic” because they don’t directly involve the steroid bound to the AR acting directly on the cells DNA.

It is now understood that steroids can act on the cell membrane to bring about various second messenger effects. These second messenger pathways involve kinase pathways driven by classical receptors (MAPk, ERK, MEK, etc), as well as cyclic AMP, lipase and other kinase pathways (PI3K, PKA, PKC, etc), including ion fluxes (Ca), which are driven by atypical receptors. All in all, steroids affect cells through several different pathways and at least one atypical steroid receptor, none of which involve what most people consider the true “intracellular” mechanism of steroid action.

Most all of these non-genomic affects of steroids are acute, or immediate. Meaning, they occur within seconds or minutes of the steroid interacting with the cell. This helps to explain why so many different organs have androgen receptors or are sensitive to androgen levels. For example, in tissues taken from rats, (in order of sensitivity):

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Anabolicum Vister (Quinbolone)

Anabolicum Vister (quinbolone) is a prodrug of boldenone. It is the exact same molecule but with a cyclopentenyl ether modification at the 17beta hydroxy position. Unlike the ester modifications at the 17 position commonly used for injectable anabolic steroids, this modification provides enhanced oral bioavailability.

As with esterified compounds, the Anabolicum Vister molecule is not active in its modified form, and becomes effective only when the cyclopentenyl ether group is metabolically removed, yielding boldenone. At this point, properties are the same as boldenone delivered via de-esterification of injected boldenone undecylenate or other boldenone ester. The duration of action of this oral form is almost undoubtedly much shorter, however.

Quinbolone is not very potent (effective per milligram) compared to injected boldenone undecylenate (Equipoise) or any injected anabolic steroids, or to most oral anabolic steroids. I know of no athletes who use this product.

Quinbolone is the chemical name of active ingredient in Anabolicum Vister. Anabolicum Vister was a registered trademark of Parke Davis (Italy) in the United States and/or other countries prior to cancellation.

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Prostaglandin PGF2a

Prostaglandins are part of a class of substances called eicosanoids. Eicosanoids are a group of substances derived from fatty acids and include prostaglandins, thromboxanes, and leukotrienes, all of which are formed from precursor fatty acids by the incorporation of oxygen atoms into the fatty acid chains. This reaction is called oxygenation and is carried out by cyclo-oxygenase enzymes. Prostaglandins and their metabolites have been found in virtually every tissue in the body.

The discovery of prostaglandins and determination of their structure began in 1930, when Raphael Kurzrok and Charles Lieb, both new York gynecologists, observed that human seminal fluid stimulates contraction of isolated uterine muscle. A few years later in Sweden, Ulf von Euler confirmed this report and noted that human seminal fluid also produces contraction in intestinal smooth muscle and lowers blood pressure when injected into the blood stream. It was Von Euler who came up with the name prostaglandin for this mysterious substance. The name prostaglandin seemed appropriate because he thought it originated in the prostate gland. Today, we know that prostaglandin production is not limited to the prostate, in fact, there is virtually no soft tissue in the body that doesn’t produce them. The name, however, has stuck with us through the years. If Von Euler had known his name for prostaglandins would still be with us into the next millennia, I’m sure he would have chosen to name them “Von Eulers” or “UVEs” instead of prostaglandins. By 1960, several specific prostaglandins had been isolated in pure crystalline form and their structures determined. Because our concern with prostaglandins involves primarily PGF2a, and perhaps PGE2, we will not go into detail about the myriad of other prostaglandins. Just know that prostaglandins are abbreviated “PG”. The additional letter and numerical script indicate the type and series. The various types differ in the functional group present in the five-membered ring.

While scientists were studying the structure of these new compounds, other research was being done to determine their role in human physiology and their potential as drugs. Initially these compounds were extremely expensive to synthesize and/or isolate in sufficient quantities for research. In 1969, the price of prostaglandins dropped dramatically with the discovery that the gorgonian sea whip, or sea fan, is a rich source of prostaglandin-like materials. Now however, there is no need to rely on natural sources because chemists have developed highly effective laboratory methods for the synthesis of almost any prostaglandin or prostaglandin analog.

Endogenous production from Arachidonic Acid

Prostaglandins (PGs) are not stored in the tissues of your body. PGs are produced in response to some physiological trigger. The starting material for PG synthesis are unsaturated fatty acids that have 20 carbon structures. The fatty acid that is used to make PGF2a is arachidonic acid.

Functions of prostaglandins in the body

Prostaglandins are classified as autocrine (effecting the same cell that produced it), as well as paracrine (effecting adjacent cells), regulators. They do not really fit into the category of hormones, nor are they neurotransmitters, instead they are simply considered as a corollary of the endocrine system.

The following are some of the regulatory functions of prostaglandins in various organs and systems of the body:

Inflammation & Pain – PGs promote many aspects of the inflammatory response. They are involved in the sensation of pain associated with inflammation and vasoconstriction and/or dilation, and the development of fever. PGs, when injected directly into the hypothalamus, induce fever. Anecdotally, the use of PGF2a also induces a rise in body temperature presumably by interacting with the hypothalamus as well.

Reproductive systems. PGs may play a role in ovulation and corpus luteum function in the ovaries and in contraction of the uterus. Excessive PG production may be involved in premature labor, endometriosis, dysmenorrhea (menstrual cramps), and other gynecological disorders. PGs are often given to induce labor.

Gastrointestinal tract – The stomach and intestine produce PGs. PGs are believed to inhibit gastric secretions and influence gastric motility as well as fluid absorption. Drugs such as aspirin that inhibit prostaglandin production can lead to overproduction of gastric secretion. This predisposes the person to gastric ulcers.

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Testosterone – The Good, the Bad, the Ugly

One of the most infamous hormones around is Testosterone. You hear Clueless news anchors about it on the evening news. You hear about it in the gym. You even read about it in the “growing older with style” magazines. Depending on who you talk to, it is both the good, the bad, and the ugly of hormones.

In bodybuilding it is hailed as the king of muscle builders. Among forward-thinking baby boomers it is considered the fountain of youth. In other circles it is pointed to as the cause of all men’s shortcomings including violence and sexual promiscuity. Finally, it has even been associated with potentially lethal diseases that threaten the lives of thousands of men each year. So how can one hormone be so many different things to so many different people? Taking a closer look at this complex hormone may shed some light on this question.

First, what exactly is testosterone? Testosterone is the principle male hormone and belongs to a class of steroid chemicals called androgens (andro = man, gen = to make). It is produced primarily in the testes but can also be made by enzymatically converting other androgens (e.g. androstenediol) secreted from the adrenal gland into testosterone. Testosterone plays a role in everything from growth and maintenance of the male sexual organs during puberty, to male pattern baldness in the later years. It also plays an important role in bone growth, sexual behavior, male fertility, muscle protein synthesis, as well as inducing the appearance of secondary male sexual characteristics such as facial hair, body hair, and deepening of the voice.

Research has shown that resistance exercise can significantly raise testosterone levels. (1) This is good news if you’re looking to build a more muscular body. When in comes to muscle growth, testosterone production is the key to success. Testosterone literally turns on the genetic machinery leading to bigger and stronger muscles. It works like this. Testosterone binds to receptors inside your muscle cells. These receptors then transport the testosterone molecule to the nucleus. The nucleus is where your DNA is located. Your DNA contains blue prints for every protein found in your body. This androgen receptor, once bound to testosterone, acts as a messenger that tells the DNA which proteins to make from the blue prints. In muscle tissue the whole process results in the production of contractile proteins, which are used to make your muscle contract more forcefully, as well as structural proteins that are used to make the cell larger to accommodate the new contractile proteins. In plain and simple terms, testosterone is a messenger that tells your muscles to grow! Still, this barely touches the surface of the many secondary roles testosterone plays in muscle tissue as well as in the brain.

Clearly, testosterone is important to both mind and body. Among the anti-aging crowd, testosterone stands as a symbol of youth and vitality. One of the signs of aging is a reduction in the circulating levels of testosterone. This in turn has been associated with a decrease in muscle mass and strength as the years go by. Doctors are now calling this “andropause”. (2) Through testosterone replacement therapy, many older patients express a sense of psychological well-being and vitality they haven’t experienced since they were 30 years younger. (3,4) If men desire it, in the near future hormone replacement for men will be just as common as it is for women today.

Unfortunately, testosterone is not free from negative effects on the body. One common undesirable effect of testosterone, which could be considered minor, is alopecia or male pattern baldness. The drug Propecia, a 5-alpha reductase inhibitor, prevents the conversion of testosterone into a more potent androgen called dihydrotestosterone (DHT). DHT, and a set of your parent’s genes, is responsible for male pattern baldness. In many men Propecia is effective at preventing further hair loss and even allowing some to grow back. (5) On a more serious note, DHT may also be a serious risk factor for some cancers such as prostate cancer. (6) Treatment of prostate cancer often involves a total elimination of circulating testosterone. Although this helps to reduce the growth rate of tumors, removing a man’s testosterone leaves him feeling emotionally disoriented, there is a complete loss of sex drive and sexual function, muscle is lost and fat patterning takes on a feminine characteristic, even hot flashes, usually associated with female menopause, are experienced.

All in all testosterone plays a very important role in a man’s sense of health and well-being. It is the major muscle-building hormone; it increases the strength of both muscles and bones, and even affects our brains. Certainly a man’s interest in keeping his testosterone levels optimized is justified despite the unavoidable risks and negative effects it may impart. A healthy lifestyle including proper diet and regular resistance exercise will ensure that you are getting all the benefits testosterone has to offer.

Don’t think for a minute that testosterone is only important for men. For more information on how testosterone effects women, check out Contrarian Endocrinology Part I: Testosterone for Women by Karlis Ullis and Josh Shackman .

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Are Steroids Your Key to Preventing Andropause?

Division of Reproductive Biology, Department of Biochemistry and Molecular Biology, Johns Hopkins University, School of Hygiene and Public Health, 615 North Wolfe Street, Baltimore, MD 21205, USA.

Source: Proc Natl Acad Sci U S A 1999 Dec 21;96(26):14877-81


Based on the observations that reactive oxygen is capable of damaging components of the steroidogenic pathway and that reactive oxygen is produced during steroidogenesis itself, we hypothesized that long-term suppression of steroidogenesis might inhibit or prevent age-related deficits in Leydig cell testosterone production. To test this, we administered contraceptive doses of testosterone to groups of young (3 months old) and middle-aged (13 months old) Brown Norway rats via Silastic implants to suppress endogenous Leydig cell testosterone production. After 8 months, the implants were removed, which rapidly (days) restores the ability of the previously suppressed Leydig cells to produce testosterone. Two months after removing the implants, when the rats of the two groups were 13 and 23 months of age, respectively, the Leydig cells in both cases were found to produce testosterone at the high levels of young Leydig cells, whereas significantly lower levels were produced by the 23-month-old controls. Thus, by placing the Leydig cells in a state of steroidogenic “hibernation,” the reductions in Leydig cell testosterone production that invariably accompany aging did not occur. If hormonal contraception in the human functions the same way, the adverse consequences of reduced testosterone in later life (osteoporosis, reduced muscle mass, reduced libido, mood swings, etc.) might be delayed or prevented.


OK, I will admit that I am biased about the use of androgens. Frankly, I think politicians and the popular press have unjustly vilified them. This being the case I tend to take notice to studies involving androgens. This particular study was a real surprise.

Male aging is accompanied by reduced testosterone production by the Leydig cells, the testosterone-producing cells of the testis. The mechanism by which this occurs is unknown. In the above study they suppressed testosterone production with androgen implants in male rats for eight months. The researchers called this behavior of the testes as “steroidogenic hibernation”.

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