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Polomac:
Anabolic Research Update

Why is my nose bleeding?

 

            I started getting nosebleeds during my last cycle of testosterone and trenbolone. It happened several times while training during the same week and took awhile to stop each time. I don’t normally get nosebleeds, so I know it is the steroids. My friends tell me it is normal. It freaked me out, so I stopped taking steroids for awhile. I want to start again, but I’m nervous. I know people are talking. Can you help me understand what caused this and if I can avoid it in the future?

            As you suspect, nosebleeds are a known possible side effect of steroid use. They occur at one time or another to a fair percentage of users. Physiologically, this problem is most directly caused by a combination of two factors. To begin with, when used at therapeutic and moderately supratherapeutic (above normally prescribed) dosages, anabolic steroids tend to decrease blood-clotting ability. If you want to know specifically what is happening, it appears the drugs increase plasmin, antithrombin III, and protein S levels, stimulate fibrinolysis (clot breakdown), and suppress clotting factors II, V, VII, and X.,[ii] If you look, you’ll see that the prescribing guidelines for anabolic/androgenic steroids in the U.S. warn of potential increases in prothrombin time, a measure of how long it takes for a blood clot to form.[iii] This ‘thinning’ of the blood also seems to make a full noticeable nosebleed more likely, and when it does occur, slower to stop.

            Before we move on to the next factor, you need know that steroids don’t always reduce blood clotting. In fact, when used at high supratherapeutic dosages, these drugs can actually have the exact opposite effect on the blood. It seems that anabolic steroids can also elevate levels of thrombin[iv] and C-reactive protein,[v] as well as thromboxane A2 receptor density,[vi] which support clotting. At a certain dosage level, which is yet to be determined and likely varying between individuals, the pro-clotting changes in the blood appear to overtake the anti-clotting effects discussed earlier. These changes have been well-documented in some steroid abusing subjects,[vii] as are reports of (sometimes fatal) blood clots, embolisms, and strokes.[viii],[ix],[x],[xi],[xii] I don’t mean to confuse you, but I do think this is important to know. And in a small regard, the nosebleeds you reported may be a positive sign that your blood does not have an increased clotting tendency that would increase the risk of stroke.

            The second big factor is probably very obvious: blood pressure. Although clinically consistently elevated blood pressure (hypertension) is not common in steroid users, it does occur with some frequency. I would first and foremost make sure I was not suffering from hypertension, as this is something that should never be ignored and can contribute to serious health issues. Often, elevated estrogen can be a key culprit in this side effect and slight changes in BP might be mitigated with a reduction in the estrogen level. Note, however, that hypertension is sometimes also reported with the use of non-aromatizing (purely anabolic/androgenic) compounds, so you can’t always rely on estrogen exclusively. Of course, during intense training, your blood pressure may become temporarily elevated as well. This likely explains why the nosebleeds were occurring during your training sessions. So increased blood pressure and reduced clotting could both be working hand in hand to support those nosebleeds.

            I am not a physician and can’t advise you on what you need to do. With that said, as you probably know by reading my column, I believe you should always put safety first. The first thing I think any logical person would tell you is that you should go to the doctor for a full checkup. This is always a good idea when you cycle, and really a necessity if you are noticing strong side effects. If you don’t want to do this, you need to at least rule out hypertension. Blood pressure is an especially easy thing to check. I’d call some local large-chain pharmacies, as many of them will have a blood pressure machine on site for free use. I would say that, provided hypertension or any other pathological condition is not the cause, an occasional nosebleed is probably not serious. Certainly it can be very uncomfortable, frightening, troubling and even embarrassing to endure— and as you now know, it may indicate a more serious underlying issue, so you don’t want to just ignore it.

 

Trenbolone Acetate or Enanthate?

 

            I want to use trenbolone and don’t know if I should get acetate or enanthate. I have access to both. What is the difference? What do you like better?

            The first thing you need to keep in mind is that esters affect the release of the active steroid, in this case trenbolone. So either way, free trenbolone will be the drug actually doing the job. Provided both products were pharmaceutically pure and properly dosed, both would be acceptable choices if you wanted to use a trenbolone. But indeed there is a big difference between these two steroids, which is found in the rate in which trenbolone is released into the blood.

            Acetate is a very fast-acting ester and needs to be administered very frequently to maintain consistent blood levels. Usually it is given every other day, to every third day at the most. This can make for many repeat injections during a cycle. The short ester can also be painful for some people, caused by the inherent irritating properties of free short-chain fatty acids. Enanthate, on the other hand, is slow-acting (taken once per week usually) and more comfortable for most people to use.

            You might want to also consider that short-chain esters, such as acetate and propionate, are not widely used in human medicine at all. They were used regularly a long time (many decades) ago, but have since been brushed aside for longer esters, such as enanthate and cypionate. Enanthate actually dominates the global market for injectable testosterone right now. You won’t find testosterone acetate anywhere but in an obscure veterinary steroid these days. In general, if you do find a short-chain ester like an acetate or propionate, it is in a veterinary preparation. Obviously, the mental and physical comfort of an animal tends to be of a much lower priority. All things being equal, a long-chain ester like enanthate is preferable, as it would be more comfortable (if not necessarily more effective).

            There is another thing to consider, though. No registered drug company anywhere in the world is making a prescription trenbolone enanthate product. This material is used in the production of underground steroid products exclusively and while I’m sure there are many pure trenbolone enanthate products available, you should keep this in mind. Conversely, trenbolone acetate is still made by a number of U.S. and international drug companies. The U.S. Finaplix pellets, which have been sold in the U.S. without the same strict regulations, are also still available and almost guaranteed legitimate pharmaceutical quality. The chance of obtaining pharmaceutical-quality trenbolone acetate is, therefore, higher. So ultimately, there are some plusses and minuses whichever way you go— but either way, you are going trenbolone. If it were me, I’d make the choice based solely on my confidence in the sterility and purity of the preparation, regardless of the ester.

 

Liver Support?

 

            Do you think it is a good idea to take a natural liver supplement during oral cycles to help with liver stress? Is it necessary, or are all these products rip-offs?

            On the one hand, life-threatening liver toxicity is very rare with steroid use. Many steroid users take orals frequently and very few deaths are attributed to this. That is not to say they cannot cause liver failure— indeed, these drugs can and have. But I don’t want you to be too alarmed. If you use reasonable dosages and take the drugs for only periodic cycles, your odds of encountering a life-threatening issue are very low.

            On the other hand, serious issues like high elevations of hepatic enzymes and jaundice (bilirubin buildup caused by bile duct obstruction) are somewhat more common. Stories about yellowing of the skin or notable ‘sickness’ marked by nausea, vomiting, abdominal discomfort, or other ill feelings are quite common. I remember years ago my training partner telling me, “Dude, you’re turning yellow, man.” Sure enough, I was— so I’ve been there myself.

            While discontinuing the orals took care of the problem for me (and most people who have had these issues), I would have liked to have avoided getting there in the first place. In this regard, a good liver-support product can be a great thing to have. Indeed I don’t believe they are usually rip-offs, and in fact there are a lot of clinical data supporting the beneficial effects of certain natural ingredients. Products like Liv-52 (Himalaya Drug Co.) and Essentiale forte (Aventis) are well-known to reduce liver toxicity and are even prescribed in many countries to treat such things as hepatitis and cirrhosis of the liver. I also recently developed a product called Liver Stabil, under Molecular Nutrition, that incorporates a very wide range of proven hepatic support ingredients, and feel very comfortable recommending this to you as a first option as well. All of these products are very affordable. Regardless of which one you choose, I do think you should use one of them during all oral cycles. While nothing is for certain, a good liver supplement may very well help you avoid an unwelcome problem with liver toxicity.

 

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References:

            [1]. Anabolic steroids and fibrinolysis. Lowe GD. Wien Med Wochenschr, 1993;143(14-15):383-5.

            2. Effect of anabolic steroids on plasma antithrombin III. alpha2 macroglobulin and alpha1 antitrypsin levels. Walker ID, Davidson JF, Young P, Conkie JA. Thromb Diath Haemorrh, 1975 Sep 30;34(1):106-14.

            3. Depo-Testosterone. Pharmacia. U.S. Prescribing Information, Revised August 2002.

            4. Anabolic-androgenic steroid abuse in weight lifters: evidence for activation of the hemostatic system. Am J Hematol, Ferenchick GS, Hirokawa S, Mammen EF, Schwartz KA, 1995 Aug;49(4):282-8.

            5. Raised concentrations of C reactive protein in anabolic steroid using bodybuilders. F M Grace, B Davies et al. Br J Sports Med, 2004;38:97-98.

            6. Testosterone increases human platelet thromboxane A2 receptor density and aggregation responses. Ajayi AA, Mathur R, Halushka PV. Circulation, 1995 Jun 1;91(11):2742-7.

            7. Androgenic-anabolic steroid abuse and platelet aggregation: a pilot study in weight lifters. Ferenchick G, Schwartz D, Ball M, Schwartz K. Am J Med Sci, 1992 Feb;303(2):78-82.

            8. Pulmonary embolism associated with the use of anabolic steroids. Liljeqvist S, Helldén A, Bergman U, Söderberg M. Eur J Intern Med, 2008 May;19(3):214-5. Epub 2007 Sep 19.

            9. Coronary thrombosis and ectasia of coronary arteries after long-term use of anabolic steroids. Tischer KH, Heyny-von Haussen R, Mall G, Doenecke P. Z Kardiol, 2003 Apr;92(4):326-31.

            [1]0. Massive pulmonary embolus and anabolic steroid abuse. Gaede JT, Montine TJ. JAMA, 1992 May 6;267(17):2328-9.

            1[1]. Steroid anabolic drugs and arterial complications in an athlete— a case history. Laroche GP.  Angiology, 1990 Nov;41(11):964-9.

            [1]2. Death caused by pulmonary embolism in a body builder taking anabolic steroids (metanabol). Siekierzyńska-Czarnecka A, Polowiec Z, Kulawińska M, Rowinska-Zakrzewska E. Wiad Lek, 1990 Oct 1-15;43(19-20):972-5.

 http://www.musculardevelopment.com/articles/chemical-enhancement/2032-anabolic-research-update.html

Polomac:
Using Anabolic Steroids: New Study Says Watch for Kidney Damage

The physiology of man evolved such that he maintains optimum health and performance in conditions that are commonly encountered. Over time, man deviated from nature as he established the ability to create shelter against the changing climate; developed trans-geographic commerce to provide a more diverse and stable food supply; and discovered substances that affect the mind and body, such as alcohol and opium.

People in developed countries who enjoy the luxuries of personal vehicles, labor-saving devices, and calorie-laden diets suffer from an epidemic of chronic diseases. Ironically, societies that have achieved the pinnacle of progress through financial and political stability, in addition to scientific advances, appear to erode the physical health of citizens through the promotion of gluttony. Truly, it appears that moderation is the best policy.

Bodybuilders, athletes and fitness extremists pursue not just health, but maximal performance. These individuals are often viewed as the healthiest by the [superficial] general public, but they also experience chronic injury if their training, diet or drug use becomes extreme— tendonitis is a daily experience for many; eating disorders develop; and adverse effects from performance-enhancing drug use/abuse or weight-loss products are unfortunately common.

The most commonly-used class of drugs for sports and physique enhancement is anabolic-androgenic steroids (AAS). From junior high school on, most boys and men become familiar with the multicolor diagram showing a variety of side effects that are implied to be inevitable consequences of AAS use. Of the many organs and systems harmed or damaged by AAS, one paired set of vital organs is easily overlooked— the kidneys.

In the poster "The Harmful Effects of Steroids," a muscular figure is shown hitting a front double biceps pose, while his multicolored innards are penetrated by lines connecting them to a litany of harm caused by AAS. The kidneys are listed with the vague comments of "kidney disease" and "kidney stones," but as they are not visible when the body is viewed from the front, there are no DayGlo-colored organs to go with the statement, not even a connecting line.

Kidney disease and kidney stones are serious matters. The kidneys are vital organs that are taken for granted because most people do not consider their kidneys as long as they are able to urinate— able to pee, worry-free. Yet, when the kidneys begin to fail, serious consequences follow. If the kidneys fail completely, a person will die in days unless he is placed on dialysis.1 Tumors of the kidneys occur, although there is no reported increased risk of cancer in the kidneys in recreational AAS users. One rare cancer of the kidney (Wilms' tumor) has been reported in an AAS user.2

Kidney stones arise in the tiny filtering ducts of the kidney, starting as small crystals, but grow as crystals do until they become lodged and prevent the passage of urine. As spiky, jagged masses, when these crystalline stones dislodge, pray that you are not driving— the pain is equated to the labor pains a mother goes through as she delivers a baby. On a scale of 1 to 10, the pain is often rated as a 10. There are several types and causes of kidney stones; again, no causal association is reported in the medical literature linking AAS use to kidney stones.
AAS Use and Kidney Disease

A possible relationship between recreational AAS use and kidney disease received recent press due to a poster presentation at the American Society of Nephrology.3,4 Pathologist Leal Herlitz, M.D. and colleagues reported their findings relating to the development and progression of a specific form of kidney disease in adult men. Their study compared two groups of men who were diagnosed as having the condition of focal segmental glomerulosclerosis (FSGS). The disorder is characterized by scarring in the cells that filter and secrete waste products into the urine, as well as retaining or reabsorbing essential biomolecules that the body does not want to waste or lose.

FSGS is suspected when kidney function diminishes (as determined by lab tests) and protein is 'spilled' into the urine. Normally, the urine is protein free, but as the filtering units begin to fail, levels of urinary protein increase. When urine protein levels become elevated, the urine will become foamy. Final diagnosis is usually obtained through a kidney biopsy.5

The study groups were composed of 10 men who had admitted to many years of anabolic steroid use (and other performance-enhancing drugs), and 10 men with the condition who were morbidly obese. The initial lab tests demonstrated greater strain and signs of impaired kidney function among the AAS users. Serum (blood) creatinine, the metabolic waste product generated from creatine (yes, the same molecule as the supplement) and cleared from the body by the kidneys, was markedly higher in AAS users (3.0 vs. 1.47 mg/dL— normal serum creatinine range is 0.8 to 1.4 mg/dL). As creatinine can only be secreted by the kidneys, serum concentration rises when the kidneys begin to fail. Urinary protein was also elevated to a significantly greater degree in the AAS-using group as protein 'leaked' into the urine.

When kidney tissue obtained by biopsy was examined under the microscope, the extent of tissue damage was greater in the AAS-users as well, represented by scarring of the glomerular and tubulointerstitial fields (areas involved in filtering urine).

Among the AAS-using men, eight were followed for an average of slightly longer than two years. All eight discontinued AAS use, reduced exercise, and were placed on drug therapy. One rapidly progressed to a dialysis-dependent condition called end stage renal disease. The others showed signs of improvement, with serum creatinine approaching the upper limit of normal, and urinary protein decreasing significantly— although it remained above the normal range seen in healthy people in several of the subjects.

One of the AAS-using subjects became dissatisfied with his body image, claiming he would rather be dialysis-dependent than live without a muscular body. [This would almost certainly qualify the subject for body dysmorphic syndrome. For those nodding in agreement with sacrificing your kidneys to fill an XXXL shirt— trust me, you do not want to become dialysis-dependent.] He went back to using AAS again, despite a history of AAS-related damage. His serum creatinine doubled from near-normal to again being indicative of FSGS. His urinary protein, which had happily cleared down to zero, became elevated to 14 within three and one-half years. At that rate, Dr. Herlitz predicted that he (the AAS-user) could progress to end stage renal disease in another four to five years.

This comparison suggested to Dr. Herlitz that AAS contribute to kidney damage. She proposed that in addition to supporting a greater body mass and placing greater stress on the kidneys, AAS may also have a direct toxic effect on the cells. Dr. Herlitz noted that creatinine is primarily produced in skeletal muscle, so logically a person with greater muscle mass will have elevated serum creatinine compared to a sedentary person, even if they are of similar weight. Furthermore, the higher dietary protein intake common to athletes and bodybuilders, as well as exercise-related hypertension (high blood pressure during physical exertion), can promote injury to the glomerular units of the kidney.

Other Factors Affect Your Kidneys

From the presentation, one might conclude that AAS are at least associated with a greater risk of kidney damage, and potentially may play both a direct and indirect role in harming that vital, paired set of organs. Further, the damage being done appears to be particularly virulent when compared to the control group used in this study, the morbidly obese (average BMI >40). However, FSGS is a non-specific finding present in a variety of conditions, and secondary to a number of known causes. The control group may or may not have been appropriately matched to the AAS-using group, as BMI cannot be used as an approximation for lean body mass, sometimes referred to as fat-free mass index.

Other known agents or conditions that may affect kidney status were not accounted for, so far as the press reports of this study revealed. Among the many factors that are associated with this form of kidney damage (i.e., use of opiate drugs, hypertension, hepatitis B, HIV, etc.), several have been reported in AAS users.6-9 Ibuprofen (e.g., Advil) has been associated with kidney damage, but a different form than FSGS.

Among the many drugs commonly used in conjunction with AAS, FSGS has been reported in a woman being treated for breast cancer with anastrozole.10 This drug, known by the brand name Arimidex, is often used in conjunction with AAS as it inhibits the enzyme aromatase. Using anastrozole, or related drugs, is common in AAS users wishing to self-treat or avoid estrogen-related side effects (many AAS are converted into estrogens by the enzyme aromatase). It is possible that the use of aromatase inhibitors or non-aromatizing AAS may be a significant factor in FSGS, or it may not be an issue at all. It is just too early to discern the factors related to AAS-associated kidney damage.

What is revealed by this study is that at least one type of kidney damage (FSGS) is related to AAS use. The presence of FSGS in AAS users is not proof of the drugs' causing or worsening the disease. The concentration of the disease in such a small geographic area, among a limited population, appears to be greater than one might suspect. The news release did not clarify the period when these cases appeared. The fact that the condition was resolved, at least partially when the men ceased using AAS, supports the possible involvement of AAS in the development or progression of FSGS. Another convincing observation was the case of the gentleman who returned to AAS use after his lab tests returned to normal, only to see the condition return and worsen with continued AAS use.

What does this report mean in terms of recreational AAS use? It should serve as a reminder that these are powerful drugs, and along with the benefits of greater strength and muscle mass, one also is exposed to the risk of any number of side effects. Few people take the time (and expense) of being screened for pre-existing conditions prior to using AAS. Few monitor the function of vital organs during and following AAS use to ensure that adverse side effects are not developing.
In addition to liver damage, psychological/mood disorders, changes in blood lipids, etc., AAS users should consider the potential for damaging their kidneys. Those who use AAS recreationally should have their kidney function checked prior to starting a cycle (preferably before the first cycle) by measuring serum (blood) levels of BUN and creatinine, as well as urine protein, including the sensitive microalbuminuria test.

AAS users should monitor their urine, looking for the development of foamy urine; purchasing urine dipsticks that will detect the presence of protein in the urine is even better. These urine dipsticks can be purchased online, but the use is no substitute for professional medical supervision and is no guarantee of safety.

Individuals who use AAS never want to hear of risks, dangers, injury, etc. There are many. AAS can be used safely but not indiscriminately. Placing these drugs in the hands of untrained and risk-seeking individuals is tantamount to harm. It is the cavalier attitude of many users that supports AAS legislation and restrictions on medical professionals.

Choosing to use AAS for performance enhancement or physique augmentation is viewed by many as a personal liberty, despite the legal disincentives. Regardless of one's philosophical stance, those choosing to use any drug, diet or technology need to do so in an informed manner. The revelation of kidney strain/damage in a representative group of AAS users needs to be considered during the decision process. Those who eventually use AAS need to be aware of the need to monitor the health and function of the kidneys, in addition to other potential risks.

References:

1. Hsu CY, Ordonez JD, et al. The risk of acute renal failure in patients with chronic kidney disease. Kidney Int, 2008 July;74(1):101-107.

2. Prat J, Gray GF, et al. Wilms tumor in an adult associated with androgen abuse. JAMA, 1977 May 23;237(21):2322-3.

3. Herlitz L, et al. "Development of FSGS following anabolic steroid use in bodybuilders." ASN, 2009; Abstract TH-PO163.

4. Neale T. ASN: Anabolic Steroid Abuse May Damage Kidneys. Medpage Today, 2009 Oct 30. Available at http://www.medpagetoday.com/tbindex.cfm?tbid=16705, accessed November 9, 2009.

5. Thomas DB. Focal segmental glomerulosclerosis: a morphologic diagnosis in evolution. Arch Pathol Lab Med, 2009 Feb;133(2):217-23.

6. Wines JD Jr, Gruber AJ, et al. Nalbuphine hydrochloride dependence in anabolic steroid users. Am J Addict, 1999 Spring;8(2):161-4.

7. Grace F, Sculthorpe N, et al. Blood pressure and rate pressure product response in males using high-dose anabolic androgenic steroids (AAS). J Sci Med Sport, 2003 Sep;6(3):307-12.

8. Crampin AC, Lamagni TL, et al. The risk of infection with HIV and hepatitis B in individuals who inject steroids in England and Wales. Epidemiol Infect, 1998 Oct;121(2):381-6.

9. Bolding G, Sherr L, et al. Use of anabolic steroids and associated health risks among gay men attending London gyms. Addiction, 2002 Feb;97(2):195-203.

10. Kalender ME, Sevinc A, et al. Anastrozole-associated sclerosing glomerulonephritis in a patient with breast cancer. Oncology, 2007;73(5-6):415-8.

http://www.musculardevelopment.com/articles/chemical-enhancement/1983-robbie-durand.html

The_Bulldog:
Great idea for post, Poloms...

Polomac:

--- Citat: The_Bulldog  Februar 14, 2010, 10:16:30 posle podne ---Great idea for post, Poloms...

--- Kraj citata ---
Kao i brdo tvojih..tnx..

Polomac:
IGF-1 and Mortality

Most of the anabolic effects that occur with human growth hormone release result from the production of insulinlike growth factor 1 by HGH, which largely occurs in the liver. IGF-1, however, is produced in muscle due to intense exercise, even without any HGH stimulus. IGF-1 helps repair damaged muscle fibers by triggering the activity of satellite cells, which are special immature muscle cells. The result is muscle growth.

Insulinlike growth factor 1 has a number of other benefits, including prevention of cardiovascular disease. Having lower levels of IGF-1 is linked to increased artery plaque, ischemic heart disease and stroke. In addition, IGF-1 helps preserve neurons in the brain and prevent brain degeneration. The more IGF-1 older people have, the better their overall heath, brain function and vigor.

While it appears that having more IGF-1 benefits both brain and body, the substance is nonetheless shrouded in controversy, mostly in connection with longevity and cancer. In recent years scientists have observed several animal species born without IGF-1 or with defective IGF-1 systems that live longer than their normal counterparts. A recent study explained the common observation that smaller dogs live longer than larger dogs because they carry around less IGF-1.

The picture in humans, however, is less clear. While many scientists suggest that smaller amounts of IGF-1 extend human life, their reasoning is hardly definitive.

IGF-1 is linked with accelerated human mortality chiefly because of its association with cancer. Some patients with breast, prostate and colon cancers do indeed have abnormally high IGF-1. Some researchers reason that because it aids cellular replication and because cancer involves out-of-control cellular replication, IGF-1 stimulates cancer. IGF-1 also inhibits a process known as apoptosis, whereby a cell detects its abnormalities and destroys itself. Cancer cells resist that process.

One problem with linking IGF-1 to cancer is that no one has yet proved which comes first, the cancer or the IGF-1. Since IGF-1 would facilitate the spread of cancer—most cancers prove fatal only when they begin to spread, or metastasize—some suspect that tumors themselves produce the hormone.

Like other hormones, IGF-1 is carried in the blood mostly bound to proteins. Of the six known protein carriers, the most potent is IGFBP-3. IGF-1 is active only when it isn’t bound to proteins, and only unbound, or free, IGF-1 causes hormone-induced activity.

Why that’s important to all who engage in exercise, especially weight training, is that all types of exercise, particularly lifting weights, stimulate increased IGF-1. If IGF-1 were indeed a carcinogen, as some researchers suggest, you’d have to conclude that exercise itself is the source of cancer. In fact, though, countless studies show the opposite: that exercise, through various mechanisms such as bodyfat reduction, decreases overall cancer risk.

What about those who use human growth hormone? They fall into two broad categories. The first consists of patients with HGH deficiency—some children and some aging adults—who get hormone-replacement therapy. The second consists of athletes, including bodybuilders, whose doses far exceed the therapeutic limits. Because no research predicts the future health effects of using high doses of HGH for extended periods, athletes are in uncharted territory. Studies examining the far more conservative replacement-therapy doses, however, often lasted 10 years and reveal no significant side effects—including no increased rates of cancer.

A recent study involving 6,226 adults over age 20 across the United States examined the connection between IGF-1 and mortality risk.1 It found no link whatever between the hormone and death from cardiovascular disease or cancer. In fact, it revealed that having lesser amounts of both IGF-1 and IGFBP-3 was linked to higher death rates.

Anabolic Steroids and Brain-Cell Destruction

Last year, I reported the results of a study by a Yale University researcher who concluded that testosterone in amounts comparable to what’s prescribed for testosterone-replacement therapy destroyed neurons, the working cells of the brain. It was an in-vitro, or isolated-cell, study, although the author claimed to have used a replacement-therapy dose. I pointed out then that the method in which the isolated brain cells were exposed to testosterone was unlikely to occur in the human body. Indeed, numerous other studies showed that, if anything, testosterone seemed to help protect the brain. Older males who have such brain-degenerative diseases as Alzheimer’s are usually abnormally low in testosterone.

A new in-vitro study treads the same territory, featuring isolated cells derived from the cortical area of the brain—of a mouse.2 What makes it intriguing is that it focused not only on the effects of testosterone but also on what happens when brain cells are exposed to three different anabolic steroid drugs that are popular with athletes and bodybuilders.

The experiment centered on a process called excitotoxicity, which results in the death of brain cells. The proposed question was whether testosterone and anabolic steroid drugs prevented or contributed to the death of brain cells under excitotoxic conditions.

To get a good picture of the research and why it’s relevant to bodybuilders, let’s bring forward some deep background. Excitotoxicity involves the heightened activity of the amino acid glutamate. Normal levels of glutamate stimulate brain-cell activity, which makes for improved alertness and learning ability. Abnormally high production of glutamate, however, overexcites neurons, causing them to die.

Glutamate interacts with two particular brain cell receptors, called NMDA and AMPA, but too much of it overstimulates them. When that happens, they open the brain cells to an overdose of calcium ions. The calcium in turn stimulates enzymes that basically kill the neuron.

Excitoxicity occurs under several conditions that result in the destruction of various portions of the brain: strokes; traumatic brain injury, such as being knocked out or suffering a concussion; and Alzheimer’s and other neurodegenerative diseases, such as Parkinson’s and ALS, or Lou Gehrig disease. Anything from a brain seizure to hypoglycemia can pump up brain glutamate and lead to excitotoxicity. Patients who suffer from excitotoxicity are often put in induced comas to slow brain activity and prevent further destruction of neurons.

The artificial sweetener aspartame, some think, induces excitotoxicity by virtue of its 40 percent content of aspartic acid. The theory is that while aspartic acid is found in most protein, it must compete with other amino acids in foods for entry into the brain. Normally, only small amounts of aspartic acid enter the brain—not enough to do any damage. Yet as a dipeptide made up of only two amino acids, aspartic acid and phenylalanine, it enters the brain far more rapidly, thus raising the risk of excitotoxicity. Critics of the theory say you’d need to take in vast amounts of aspartame for that to happen.

Okay, so much for background. Now back to our new study. Mouse brain cells were first exposed to the excitotoxic NMDA, then selectively exposed to testosterone and anabolic steroids. Testosterone amplified the effects of NMDA only when the brain cells were exposed to very high amounts of the hormone. Lesser amounts resulted in either protective or no activity. When aromatase-inhibiting drugs were added to the brew, however, even small amounts of testosterone promoted brain-cell destruction through excitotoxicity.

Time out for another bit of background. As most bodybuilders—especially those who stack steroids—have long known, aromatase is the ubiquitous enzyme that converts androgens, such as testosterone, into estrogen. Excess estrogen in men is linked to increased subcutaneous fat, water retention and gynecomastia. Since many anabolic steroids besides Big T are also vulnerable to aromatase, aromatase-blocking drugs are a featured player in the competition scene.

The anti-aromatase drugs used in the mouse-brain-cell study were aminoglutethimide and anastrozole, which are sold under the trade names Cytadren and Arimidex, respectively. Adding them to testosterone converted a normally benign amount of testosterone into a toxic spike. Whereas normal amounts of testosterone in the brain are partially converted to estrogen, which protects the neurons, blocking the estrogen conversion meant that testosterone could move in on the neurons for the kill by amplifying the effects of excitoxicity.

The three anabolic steroid drugs used in the study were nandrolone (trade names Durabolin and Deca Durabolin), stanozolol (trade name Winstrol) and gestrinone. The last-named is a principal ingredient in the notorious designer steroid tetrahydrogestrinone—a.k.a. THG and The Clear. Its widespread use resulted in a major sports scandal.

All three drugs have one thing in common: None are subject to conversion into estrogen by aromatase. When exposed to the brain cells in nanomolar concentrations (billionth of a gram!), they aggressively amplified the excitoxic effects of NMDA, and anti-aromatase drugs had no effect. Another drug, flutamide, which interferes with androgen-cell-receptor activity, did block the toxic effects of these drugs. Importantly, none of the steroids were toxic in the absence of NMDA, which meant that unless excitoxicity was previously induced by something else, the drugs didn’t harm the brain in any way.

DHEA, a popular adrenal steroid that is a precursor of other steroid hormones, including testosterone and estrogen, protects the brain under excitotoxic conditions. Much of the damage caused by excitoxicity results from the diminished presence of an antioxidant called glutathione (not to be confused with the amino acid glutamate). That implies that taking in nutrient precursors of glutathione, such as whey, acetylcysteine and lipoic acid, guards against the destructive effects of excitoxicity because the brain will have plenty of glutathione onboard.

The authors suggest that athletes who use anabolic steroids not subject to aromatization or who use aromatase-blocking drugs could be placing their future brain health at considerable risk. They cite the high potency of these drugs in accelerating the brain damage induced by excitotoxicity. Bottom line: You want to do everything possible to keep your brain healthy so you can avoid adventures in any kind of toxicity. Using even over-the-counter aromatase-blocking supplements without a break could be dangerous under some conditions. Purveyors of such products usually warn users to get off the supplements after a number of weeks, which is a word to the wise.

References

1 Saydah, S., et al. (2007). Insulinlike growth factors and subsequent risk of mortality in the United States. Amer J Epid. 166:518-526.

2 Orlando, R., et al. (2007). Nanomolar concentrations of anabolic-androgenic steroids amplify excitotoxic neuronal death in mixed mouse cortical cultures. Brain Res. In press.  IM

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