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Van mreže Polomac

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Anabolic Research Update
« poslato: Februar 14, 2010, 08:28:43 posle podne »
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],
  • ,[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.


Know Your Gear! William Llewellyn’s ANABOLICS 9th Edition (2009) is out NOW. Order your copy of this monster steroid reference guide today, by calling 888-828-8008 or visiting www.AnabolicsBook.com.



            [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.


Van mreže Polomac

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Odg: Anabolic Research Update
« Odgovor #1 poslato: Februar 14, 2010, 08:31:45 posle podne »
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.


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.


Van mreže The_Bulldog

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Odg: Anabolic Research Update
« Odgovor #2 poslato: Februar 14, 2010, 10:16:30 posle podne »
Great idea for post, Poloms...

Van mreže Polomac

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Odg: Anabolic Research Update
« Odgovor #3 poslato: Februar 14, 2010, 10:20:33 posle podne »
Great idea for post, Poloms...
Kao i brdo tvojih..tnx..

Van mreže Polomac

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Odg: Anabolic Research Update
« Odgovor #4 poslato: Februar 14, 2010, 11:51:54 posle podne »
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.


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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Odg: Anabolic Research Update
« Odgovor #5 poslato: Februar 14, 2010, 11:53:29 posle podne »
IGF-1: Killer or Savior?

Insulinlike growth factor 1 is so named because of its resemblance to insulin. IGF-1 is synthesized both in the liver and in muscle. There are two variants of the hormone in muscle, and each is a potent stimulator of satellite cells, which are muscle stem cells and are required for muscle repair and growth. Most scientists say that IGF-1 is the primary anabolic effector of growth hormone, and GH stimulates IGF-1 synthesis in the liver. Scientists are looking at IGF-1 therapy with great interest, as it appears to reverse many of the effects of aging. As with GH, IGF-1 concentration drops with age, and many older people have 50 percent less than younger people do.

Numerous studies show that maintaining an optimal count of IGF-1 forestalls many of the typical signs of aging. For example, a lack of IGF-1 is linked to heart failure, which affects more than half of those over age 60. IGF-1 is also required to maintain brain cells, or neurons. Without a sufficient amount in the brain, neurons undergo a cellular suicidal process called apoptosis. Insufficient IGF-1 also makes muscles and connective tissue break down, resulting in the weakness and stiffness that older adults often experience.

With all these benefits, you’d think that just about every person over age 40 who’s low in the hormone would be supplementing it in some way. Thus far, however, commercial forms of IGF-1—which must be injected, as the hormone is protein based and composed of 79 amino acids in a particular sequence—are prescribed only to treat certain forms of childhood growth problems.

Because IGF-1 spurs cellular growth, some scientists voice concern that at high concentrations it could stimulate cancer. Indeed, higher amounts of IGF-1 are associated with certain forms of cancer, such as those of the prostate, breast and colon. The big debate among researchers is a chicken-and-egg argument: Does IGF-1 promote tumor growth and spread, or do tumors themselves increase IGF-1? IGF-1 is useful to tumors because it prevents their apoptosis.

Complicating the cancer connection is the fact that teenagers, still in a growth stage and thus producing large amounts of IGF-1, have low rates of cancer. By contrast, older adults have the highest rates of various cancers yet also have the lowest blood IGF-1 counts. A more rational scenario is that while IGF-1 doesn’t cause cancer, taking it in large doses may result in tumor activity. One recent study found that higher levels of IGF-1 are inversely associated with testicular cancer.1

Also confusing IGF-1 as a health issue is the way some animals react to the hormone. Studies with worms and other invertebrates show that a lack of IGF-1 helps extend life. Mice and rats deficient in IGF-1 live longer than rodents not deficient in it. Female mice having defects in IGF-1 cellular signaling appear to age more slowly than other rodents. Animal studies, however,  usually involve lifelong exposure, which isn’t the case with human studies. The hormone may also act differently in relatively short-lived animals, such as mice and rats, than in longer-lived humans.

Preliminary studies of IGF-1 with human subjects have shown beneficial effects. For example, researchers recently examined the effects of IGF-1 on human mortality.2 Critics of IGF-1 and GH therapy often say that rather than offering a fountain of youth, the hormones may hasten death, citing the longevity of some animals that are hormone deficient. In the eight-year human mortality investigation of IGF-1, which involved 376 healthy subjects aged 73 to 94, higher amounts of IGF-1 were associated with longer life and reduced cardiovascular risk. Those with the least IGF-1 in their bodies showed nearly twice the risk of death of those who had more. Those who had a lot of age-related overall body inflammation were particularly at risk; IGF-1 appears to douse the flames of out-of-control inflammation. Inflammation plays a major role in nearly all causes of premature death, including cardiovascular disease, cancer and such degenerative brain diseases as Alzheimer’s and Parkinson’s.

One major theory of why we age relates to cellular structures called mitochondria, the site of energy production and fat oxidation. Because mitochondria are the cell’s power supply, when they die or cease to function, so does the whole cell. The main cause of mitochondrial death is oxidation. The high rate of energy production in mitochondria also generates the highest rate of free-radical production in the body. By-products of oxygen metabolism, free radicals attack cell membranes. Mitochondria have extensive fat-based membranes, making them particularly prone to oxidation.

If you can maintain mitochondria as you age, the process of aging should slow down, as should the incidence of age-related degenerative disease. A new study shows that one way that IGF-1 may retard aging is by protecting mitochondria.3 Loss of mitochondria isn’t usually an issue in young people because of their higher IGF-1 counts. In the study, giving IGF-1 to aging rats normalized mitochondrial oxidative damage and function while reducing free-radical generation.

Another study done by the same researchers also provided low doses of IGF-1 to aging rats.4 Old rats deficient in IGF-1 have a lack of serum antioxidants, which were restored with IGF-1. Older rats also have more glucose, insulin, fat and cholesterol in their blood. All those metabolic abnormalities were corrected when the rodents got low doses of IGF-1. What happened in the study is important because insulin resistance increases with age and is often linked to a loss of lean mass, mainly muscle. Insulin resistance results in insulin spikes in the blood, which are linked to premature aging and diabetes, itself a cause of premature death.

The study also showed that old rats suffer brain and liver damage because of inadequate antioxidant defenses, but the low IGF-1 dose normalized antioxidant protection as well as mitochondrial dysfunction. Low-dose IGF-1 also increased testosterone, not a minor effect for anyone who wants to maintain muscle size and strength with the passing years.

Does that mean you should consider taking IGF-1 injections as a means of slowing the aging process?  If you’re deficient in the hormone, you will more likely be given GH itself. Since GH increases IGF-1, the benefits will be similar. Also, most physicians have more experience in providing GH than IGF-1, so the optimal doses of GH are better established. Drug forms of IGF-1 were approved by the United States Food and Drug Administration in 2005, but one form was removed from the market in 2007, leaving only one (Increlex) available. Athletes and bodybuilders have used a form called long R3 IGF-1 for years. It’s structured to last longer in the blood, thus extending its active time.

Taking too much IGF-1, as some bodybuilders and athletes do, could lead to problems. The primary side effect of large doses of IGF-1 is hypoglycemia, or low blood sugar, which points up similarities between insulin and IGF-1. In other words, large doses of IGF-1 could start to act like insulin. That isn’t likely to happen with IGF-1 drug forms that also include IGF-binding proteins, which extend and delay the activity of the hormone. Unlike insulin, IGF-1 doesn’t stimulate bodyfat synthesis, although it does stimulate internal organ growth, resulting in the bloated abdomens you see on some athletes. That occurs only with doses far bigger than you’d ever use for antiaging purposes. The same holds true for GH: Small doses are beneficial, but large doses place you in unknown biophysical territory.

In the near future gene therapy will be available for placing IGF-1-producing genes directly in muscle. Preliminary studies with rodents show startling gains in muscle size and a 35 percent increase in strength with the technique. The idea is that the therapy will eliminate the extensive weakness and loss of muscle that come with age, turning 70-year-old muscle back into 19-year-old muscle. Even so, the technique is experimental with humans and needs refining. Attempting to try it now could lead to catastrophe, such as turning on cancer-friendly genes.

For now, take solace in the fact that regular exercise is the most potent method of maintaining an optimal measure of IGF-1; weight training is the best form of exercise for that. A high-protein diet is also directly related to IGF-1, with lower protein intake linked to less total IGF-1 in the body. Some studies suggest that taking DHEA, an adrenal steroid, can normalize low IGF-1 and may be the reason that DHEA is often called an antiaging hormone.

How to Live to 90 or More

A study published last February in the Archives of Internal Medicine included some tips on how to live to 90 or more.5 Twin studies found that one-fourth of the variation in human life span is attributed to genetic factors, which means that 75 percent of life span is linked to modifiable risk factors. The research involved 2,357 men who participated in an ongoing project called the Physicians’ Health Study. At the beginning of the study in 1981, the men, average age 72, provided such information as height, weight, how often they exercised, blood pressure, cholesterol counts and so on. Twice during the first year and then once a year through 2006, they completed a questionnaire about changes in their habits, health status and ability to complete daily tasks.

A total of 870 men, or 41 percent, lived to age 90 or older. Those who made it to that age had a negative relation to several preventive risk factors—most related to common sense—such as not smoking, not having diabetes, not being fat and not having high blood pressure. Their positive relation to exercise, meanwhile, was particularly effective. The authors suggest that a 70-year-old man who doesn’t smoke, has normal weight and blood pressure and no diabetes and works out two to four times a week has a 54 percent probability of living to age 90. With the presence of adverse factors in his profile, his probability of living to 90 was reduced by the following amounts:

• Sedentary lifestyle, 44 percent

• Hypertension, 36 percent

• Obesity, 26 percent

• Smoking, 22 percent

• Three factors—such as no exercise, being fat and having diabetes—14 percent

• Five other factors, 4 percent

The primary point of the study is that if you adhere to a healthful lifestyle as you age, your chances of living longer are enhanced. Conversely, having favorable genetics but living an unhealthful lifestyle can shorten your life. One example of that was the former king of late night TV, Johnny Carson, who came from a family of long-lived adults, with both his father and grandfather living past 90. Carson, however, was a heavy smoker most of his life and also drank too much alcohol. Such behavior took its toll, overruling Carson’s favorable genetics. He died at age 79 from the effects of emphysema related to his cigarette smoking.


1 Chia, V.M., et al. (2008). Insulin-like growth factor-1, insulin-like growth factor-binding protein 3, and testicular germ-cell tumor risk. Am J Epidemol. 167:1438-1445.

2 Brugts, M.P., et al. (2008). Low circulating IGF-1 bioactivity in elderly men is associated with increased mortality. J Clin Endocrin Metab. 93(7):2515-2522.

3 Puche, J.E., et al. (2008). Low doses of insulin-like growth factor-1 induce mitochondrial protection in aging rats. Endocrinol. 149(5):2620-2627.

4 Garcia-Fernandez, M.G., et al. (2008). Low doses of insulin-like growth factor-1 improve insulin resistance, lipid metabolism, and oxidative damage in aging rats. Endocrinol. 149(5):2433-2442.

5 Yates, L.B. (2008). Exceptional longevity in men: Modifiable factors associated with survival and function to age 90 years. Arch Intern Med. 168:284-290.  IM

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« Odgovor #6 poslato: Februar 14, 2010, 11:54:33 posle podne »
IGF-1: Is It the Real Deal?
February 3, 2010 by Jerry Brainum

Insulinlike growth factor-1 is so named because of its resemblance to insulin. It consists of 70 bonded amino acids, which makes it a protein-peptide hormone. That means that like growth hormone, IGF-1 must be injected. Otherwise it degrades in the gut, rendering it useless.

IGF-1 is considered the key to growth hormone’s anabolic effects, and GH release promotes its synthesis in the liver. The liver also synthesizes six binding proteins that work with IGF-1, with one, IGFBP-3, being the primary IGF-1-bonding protein in the blood. A substance called the acid-labile subunit prevents the premature degradation of IGF-1. The complex of IGF-1, binding protein and the acid-labile subunit extend the time that IGF-1 lasts in the blood to 15 hours or more—compared to the 10 minutes that unbound IGF-1 lasts.

Because IGF-1 is so similar to insulin, it can interact with insulin cell receptors and produce some of the same effects as insulin. In fact, the primary side effect of both excess insulin and IGF-1 is hypoglycemia, or low blood glucose, although insulin is 10 times more potent than IGF-1 in that effect. When you train for an extended time—more than one hour—the liver upgrades its release of IGF-binding protein 3 to prevent the onset of hypoglycemia that would otherwise ensue because of the increased release of IGF-1. IGF-1 also amplifies the action of insulin, even at low doses. Insulin helps maintain blood IGF-1 by boosting the synthesis of IGFBP-3.

The primary role of IGF-1, though, isn’t to transport glucose into cells, as in the case of insulin. Instead, it fosters cellular division and growth. It’s also involved in cell repair, particularly in brain, heart and muscle. Its function in cell division has led many scientists to suggest that IGF-1 has a role in several types of cancer. That makes sense, since cancer is a process of uncontrolled cellular division; however, the evidence for that is not yet definitive by any means. True enough, IGF-1 inhibits apoptosis, or cellular suicide. Out of that you get the theory that tumors would upgrade synthesis of local IGF-1 to keep themselves alive and thereby encourage the spread of cancer throughout the body. Yet some researchers suggest that it’s a classic chicken-and-egg scenario, in that IGF-1 doesn’t cause cancer but is instead produced by tumors.

Meanwhile, studies show that people low on IGF-1 have a greater chance of dying from a heart attack. That’s because IGF-1 prevents the death of heart cells and offers protection when the cells are highly stressed, as occurs during a heart attack.

While the liver synthesizes IGF-1 and packages it with the binding proteins for transport into the blood, two variants of IGF-1 that are produced in muscle, one of which is called mechano growth factor, play a major role in muscle gains. They spur the activity of other proteins that are involved in muscle protein synthesis and encourage the activity of muscle stem cells, called satellite cells, which repair damaged muscle—and training does damage muscle. In fact, intense weight training is a primary stimulus of the release of IGF-1 in muscle. (Another protein, myostatin, prevents muscle growth by interfering with satellite-cell proliferation.)

A recent study used specially bred mice that produced only tiny amounts of IGF-1 in their livers, 75 to 85 percent lower than normal mice.1 Despite that, they show normal growth patterns and development. Their bodies compensate by secreting a lot of GH.

The IGF-1-deficient mice have low bodyfat and tend to stay lean as they age. The reason they make so much GH is that IGF-1 is the primary feedback inhibitor of GH release from the pituitary gland. Less IGF-1 in the blood equals more GH release from the brain. Interestingly, human studies show that testosterone also blunts the IGF-1 signal to the brain, thus helping maximize the effects of GH. That’s likely one reason why GH is considered synergistic with testosterone and anabolic steroids, which are synthetic forms of testosterone.

But back to the mice. The lack of systemic release of IGF-1 doesn’t affect its local production in muscle. Researchers showed that by having the mice engage in resistance exercise. No, the mice didn’t do any barbell curls or squats. They climbed a ladder with tiny weights attached to their bodies—a 16-week rodent weight-training routine. Another group of mice not deficient in IGF-1 did the same exercise. The groups produced equivalent muscle gains. The researchers concluded that systemic IGF-1 produced in the liver isn’t required for muscle hypertrophy. The IGF-1 forms produced in muscle following exercise are the important ones.

Bodybuilders and other athletes have been using IGF-1 injections for years. The drug is often used along with GH, anabolic steroids and insulin. One popular formulation is Long R3IGF-1, which is thought to be more potent than IGF-1 produced in the body. The hormones can interact with cellular receptors only when they’re free, or unbound from their plasma-binding proteins. Because the Long R3 IGF-1 lasts longer in the blood than natural IGF-1, it could present a serious threat to health. The free IGF-1 can interact with tumors, causing cancer progression. It could also convert a benign or inactive tumor into an active one. Another experimental form of IGF-1 said to be used by athletes is des(1-3) IGF-1. It’s a short form of IGF-1 that is not protein-bound and is often directly injected into muscles, and it’s rumored to lead to hyperplasia, or the splitting of muscle fibers to form new fibers. It’s strictly conjecture, as there is thus far zero proof of the effect in healthy athletes.

The prescription form of IGF-1 is mecasermin, trade name Increlex. Manufactured using recombinant DNA technology, it’s used to treat IGF-1 deficiency and growth problems. Increlex is also prescribed for patients who have developed antibody resistance to GH therapy. Unlike Long R3 IGF-1, Increlex is identical to natural IGF-1, retaining the 70 amino acid sequence of IGF-1 that the body produces.

Although it appears that only the version of IGF-1 produced in muscle has any true anabolic effects, many bodybuilders and athletes who’ve used IGF-1 claim to have benefited from the drug. There is no scientific evidence for that, but there is some evidence of benefits for people deficient in IGF-1.
Hormone-deficient patients who get IGF-1 experience increased rates of fat loss and fat oxidation. What causes that isn’t known, but one theory is that the IGF-1 may suppress circulating insulin. In addition, fat cells contain IGF-1 receptors, so the hormone can interact with fat cells.

From the standpoint of protein synthesis, IGF-1 injections provide the anticatabolic effects of insulin combined with the increased protein synthesis induced by GH. Like insulin, IGF-1 encourages amino acid uptake into muscle cells. It stimulates peripheral tissue uptake of glucose, which lowers blood glucose levels. It also suppresses liver glucose production, which is actually good for those who are insulin resistant, since the liver under that circumstance tends to produce too much glucose, which perpetuates the insulin insensitivity and can eventually result in diabetes. Indeed, IGF-1 is being considered as a diabetes-prevention drug.

From an athletic point of view, IGF-1 may share insulin’s role in increasing glycogen synthesis, which powers intense training. Possible side effects of IGF-1 injections include jaw pain, facial and hand swelling and heart-rhythm disturbances. The last-named effect is more likely if doses of more than 100 micrograms are injected. That can cause the heart to stop beating (yikes!) and blood pressure to drop dramatically. The effect is caused by an IGF-1-induced drop in blood phosphate and can be prevented by administering phosphate with the IGF-1. An increase in IGF-1 caused by either GH or IGF-1 injections is thought to play a major role in producing the repulsive bloated abdomen seen on some competitive bodybuilders. Adding insulin to the stack exponentially increases the chance of that particular side effect showing up. Note that all internal organs have an extensive supply of both insulin and IGF-1 cell receptors. Providing an abundance of either or both hormones will lead to organ growth, contributing to the abdominal bloat.

Several factors affect IGF-1 production in the body. Insufficient protein or calories cause it to plummet, and excess calories may cause it to increase. One study of normal-weight women who overate found a 19 percent increase in IGF-1 after two weeks of gorging, with 46 percent of the bodyweight gain attributed to lean mass and 54 percent to bodyfat. Fasting insulin doubled in the women, and testosterone levels rose significantly. Thus the lean mass gain produced by overeating could be the result of an increase in IGF-1, insulin or testosterone—or all three. I would quickly add that overeating is not a good method of adding muscle mass, as most of the weight gain consisted of bodyfat. It does, however, explain why bulking up was a popular technique for gaining mass among bodybuilders of the past and, to a certain extent, those of today. Other nutrients necessary to maintain IGF-1 in the body include the minerals magnesium and zinc and thiamine, a.k.a. vitamin B1. Zinc is particularly important.
Exercise boosts IGF-1. Some studies suggest that the antiaging effects of DHEA use come from an increase in IGF-1 in the body. IGF-1 maintains both muscle and connective tissue, as well as brain and heart cells, so it’s not a stretch to think that having more IGF-1 will make you feel and possibly look younger. Recent human studies confirm the antiaging effects of IGF-1 and GH. Yet animals deficient in IGF-1 live longer and show no cancer whatsoever. Clearly, that’s an example of how animal physiology may differ from that of humans. On the other hand, countless people who’ve used GH therapy say that they feel younger, but that’s rarely evident in their appearance. Excess bodyfat is associated with lower IGF-1 and GH. One recent study examined lifestyle factors that affect IGF-1 in college-age women and found a positive correlation with soy protein and the mineral selenium.2 Drinking alcohol blunted the effects of IGF-1 in the women.

The greatest future use of IGF-1 will without doubt involve gene therapy, which directly places genes that produce IGF-1 in muscle, usually by attaching them to an inactive virus or vector that penetrates the muscle cells. Studies with young mice show that the procedure results in a 15 percent increase in muscle mass, along with a 14 percent increase in strength. Gene therapy in old mice led to a 27 percent increase in strength, along with a total regeneration of aged muscle. In another mouse study, the IGF-1 gene was placed in the animals’ glutes and calves, which resulted in a 17 to 115 percent increase in muscle-cross-sectional area. One hopes the growth occurred mainly in the calves rather than the glutes!
Studies with the muscle-specific form of IGF-1 have yielded similar or better results. Some scientists speculate that once the procedure is perfected for humans, it will spell the end of age-related muscle weakness and frailty. They foresee an 80-year-old man who can produce the same muscle gains as a 19-year-old. Older people don’t gain as much muscle as younger people because satellite cell activity either doesn’t occur or is ineffective. That defect is completely repaired with IGF-1 gene therapy.

Some predict that gene therapy will replace drugs as the main form of doping in the future. No one has any idea of how to detect gene therapy doping yet. The only possible way would be a muscle biopsy, but even that would prove problematic because complete uptake of the IGF-1 gene may not occur, and the biopsy may reveal just normal muscle tissue.

Rumors abound that some athletes have already subjected themselves to IGF-1 gene therapy. That isn’t hard to believe when you consider that one of the therapy’s developers, H. Lee Sweeney, Ph.D., of the University of Pennsylvania School of Medicine, says he’s besieged by athletes and coaches from around the world who offer to be his guinea pigs. In truth, however, the technique is not ready for prime time, for some earlier gene-therapy experiments resulted in patient deaths. Future subjects could experience fatal immune reactions to the vectors used to place the gene in the body. Another danger is an inability to control the expression of the gene, which could translate into a rapidly spreading cancer. Or the expression of the gene could extend from skeletal muscle into heart muscle, resulting in excessive heart muscle growth that portends premature heart failure.

Last and perhaps not least, while IGF-1 injections work great on paper, real-world results are mixed. Most athletes suggest that using IGF-1 alone does little or nothing to boost muscle gains, which makes sense in light of the mouse study that linked only local muscle IGF-1 to mass gains. Many steroid manuals suggest that IGF-1 injections are best used with other anabolic agents, such as GH, testosterone and insulin. In that case, how do you ascertain just how well IGF-1 is working? The gains attributed to IGF-1 may in fact result from the other drugs in the combo. Nor can you discount the placebo effect. If you think something will work and truly believe that it will, it often does. Perhaps those who tout the “massive muscle gains” they’ve allegedly made from IGF-1 injections made those gains because they trained harder and believed from their head down to their diamond-shaped calves that the drug would work.

And for them, it did. Or did it?


1 Matheny, W., et al. (2009). Serum IGF-1-deficiency does not prevent compensatory skeletal muscle hypertrophy in resistance exercise. Exp Biol Med. 234:164-170.
2 Karl, J.P., et al. (2009). Diet, body composition, and physical fitness influences on IGF-1 bioactivity in women. Growth Hor IGF-1 Res. In press.


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Odg: Anabolic Research Update
« Odgovor #7 poslato: Februar 22, 2010, 06:50:44 posle podne »
Anabolic Research Update: The New Anti-Estrogens
One of the areas of medicine in particular that has seen a lot of progress is the field of breast cancer treatment. Researchers here focus heavily on the reduction of estrogenic activity in the body, as estrogen inhibition can help the disease by starving breast cancer cells that are responsive to this hormone. Their work has spawned several new commercial drug products that are very effective in this regard. Since anti-estrogenic drugs are also widely used by bodybuilders for side-effect mitigation and as hardening/cutting aids, I thought it would be of interest to take a look at a few of the new drugs that have hit the market in recent years. In think you’ll find that the agents discussed here not only hold a great deal of promise, but may even bring us to places that the old-standard anti-estrogens simply could not.


Fareston (toremifene citrate)

Fareston is an estrogen receptor antagonist with mixed agonist/antagonist properties. It’s classified as a “SERM,” which is short for Selective Estrogen-Receptor Modulator. It is specifically a nonsteroidal triphenylethylene derivative, similar in structure and action to both Nolvadex (tamoxifen citrate) and Clomid (clomiphene citrate). Fareston is used for the treatment of breast cancer in postmenopausal women with estrogen-receptor positive or estrogen-receptor unknown (unsure if the cancer is estrogen responsive) tumors. It works by attaching to the estrogen receptor in various tissues, blocking endogenous estrogen from exerting biological activity. This agent in the newest mixed estrogen receptor agonist/antagonist to get our attention in the bodybuilding world, and was approved by the FDA in 1997.

Like Nolvadex, Fareston has an added benefit of being somewhat intrinsically estrogenic in the liver. This allows it to support positive changes in serum cholesterol values, an effect tied to estrogenic activity. It may turn out, however, that Fareston is the measurably better agent of the two in this regard. One study, for example, compared the lipid altering effects of tamoxifen and toremifene in a group of 49 postmenopausal women. Standard oral doses of either tamoxifen (20 milligrams) or toremifene (60 milligrams) were given to the patients for a period of three years.

Both antiestrogens caused a significant reduction in serum total and LDL (bad) cholesterol levels, however the change in HDL/LDL ratio (the more important measure) was much more favorable with the Fareston group. This drug caused an increase in HDL cholesterol levels by 14 percent, whereas tamoxifen use in this case actually decreased HDL values by five percent. In the end, the toremifene group noted much more favorable changes in serum lipid profiles and cardiovascular disease risk. It may turn out to be that Fareston is the antiestrogen of choice for the heart-conscious athlete.


Faslodex (fulvestrant)

Faslodex is one of the newest weapons in the war on estrogen, approved by the FDA in 2002 for the treatment of estrogen receptor positive breast cancer. It’s a highly selective estrogen receptor antagonist (it’s also classified as an estrogen receptor downregulator). This means it does not target the production of estrogen, but like Nolvadex and Clomid, prevents this hormone from being able to exert activity in the body by blocking available receptors. Faslodex seems well equipped to compete with even some of the newer aromatase inhibitors. One study, for example, shows Faslodex to be as effective in Arimidex in treating breast cancer patients who have already failed with first line endocrine treatments.[ii] Another shows the drug to prevent tumor cell turnover and growth significantly more effectively than tamoxifen citrate.[iii] Studies investigating the physiological response to Faslodex made note that its strong actions allow it to downregulate estrogen receptor concentrations, and progesterone receptor concentrations as well.[iv] Clearly, when it comes to anti-estrogens, Faslodex is far more advanced than the “standard-issue” agents we have been using in the bodybuilding world for years.

There are only two real drawbacks to Faslodex. For one, it’s a pure estrogen receptor antagonist, not a mixed agonist/antagonist. This makes is quite different from Nolvadex or Clomid, drugs that actually tend to improve serum cholesterol values because they act as estrogens in certain tissues like the liver. Although I have been unable to find studies looking at cholesterol levels in response to Faslodex, knowing how closely tied estrogen is to the synthesis of HDL cholesterol, I can only assume it will have as strong an influence (negative) here as do aromatase inhibitors.

The other major problem is price. A single five milliliter injection runs over $900 at the pharmacy. I guess when you make a medicine that people are only going to need once per month, you aren’t going to make millions on it if you sell it for $50. Mind you, I have no knowledge of how costly this drug is to manufacture, but if I had to guess I would think the price has much more to do with how much the company thinks they should get from a patient on a monthly basis. Since it’s expensive, of course, there is little chance this drug will catch on with the bodybuilding public.


Aromasin (exemestane)

Aromasin is a steroidal suicide aromatase inhibitor, extremely similar in structure and action to formestane. It works to lower estrogen production in the body by blocking the aromatase enzyme, which is responsible for synthesizing estrogens. The FDA approved Aromasin in late 1999 for the treatment of advanced breast cancer, specifically in post-menopausal women whose disease has progressed following therapy with a first line agent such as tamoxifen. It’s given only to post-menopausal women because before menopause most of a woman’s estrogen comes directly from the ovaries, not aromatization (aromatase is the principle source of estrogen after menopause). Aromasin is being advertised as the only “aromatase inactivator” available, which ignores the fact that formestane is sold as an over-the-counter nutritional supplement in the U.S. right now. Although both these agents essentially do the same thing in the body, Aromasin does the job far more effectively.

Aromasin may be the most effective aromatase inhibitor available to date, in fact. While Arimidex boasts of estrogen suppression around 78 percent in its packaging insert, Aromasin reports it can lower estrogen as much as 85 percent on average.[v] Feedback from bodybuilders tends to support the preference for Aromasin over other aromatase inhibitors, so this may very well be the case. Regardless of which one is the true “king,” all of the newer aromatase inhibitors— Arimidex, Femara, Aromasin— should be looked at as extremely effective for reducing estrogen synthesis in the body. A possible 10 percent difference in inhibition between the weakest and the strongest of the three is really not going to amount to all that much during your next cycle. If you are looking at one of these agents to prevent gynecomastia and help you lose fat and water on your next cycle, they are all going to do a good job for you. If you absolutely need the best agent, my money would be on this one.





Antiatherogenic effects of adjuvant antiestrogens: a randomized trial comparing the effects of tamoxifen and toremifene on plasma lipid levels in postmenopausal women with node-positive breast cancer. Saarto T, Blomqvist C, Ehnholm C, Taskinen MR, Elomaa I. J Clin Oncol 1996 Feb;14(2):429-33


[ii] Fulvestrant, Formerly ICI 182,780, Is as Effective as Anastrozole in Postmenopausal Women With Advanced Breast Cancer Progressing After Prior Endocrine Treatment. Howell A, Robertson JFR, Quaresma Albano J, Aschermannova A, et al. J Clin Oncol. 2002; 1:57.


[iii] Fulvestrant, an estrogen receptor downregulator, reduces cell turnover index more effectively than tamoxifen. Anticancer Res. 2002 Jul-Aug;22(4):2317-9.


[iv] Fulvestrant. Cheung KL, Robertson JF. Expert Opin Investig Drugs 2002 Feb;11(2):303-308

[v] High activity and tolerability demonstrated for exemestane in postmenopausal women with metastatic breast cancer who had previously failed on tamoxifen treatment. Kvinnsland S, Anker G et al. Eur J Cancer 2000 May;36(8):976-82

Black Market Update

Weratestone 250. This particular product contains testosterone enanthate, in a concentration of 250mg/ml. Weratestone is made by the French pharmaceuticals manufacturer Weimer Pharma, however it is not available for sale on the domestic prescription drug market in France. Instead, it is exported to French-speaking countries in Africa, such as Algeria, Zimbabwe and Mozambique. This steroid very rarely circulates in the United States, however it’s found from time to time in Western Europe. Testosterone enanthate is, of course, one of the most abundantly manufactured steroids worldwide. It’s also one of the most frequently counterfeited, and indeed many of the more popular brands in Europe, such as Testoviron, Primoteston and Testosteron Depot, are copied with alarming frequency. Although glass ampules such as the one Weratestone 250 comes in are by no means difficult to duplicate, the less than popular nature of this particular brand has kept it pretty low on the counterfeiters’ radar. So long as your source is otherwise reliable, you can probably trust this item when located.

Shown also this month is a counterfeit vial of nandrolone decanoate that’s supposed to originate in Russia. It is listed to contain the steroid in a concentration of 200mg/ml, and holds a nicely sized 10ml volume of oil. Farmadon, who is labeled to have made the drug, was a real company operating in the steroid business at one time. It has been closed for a couple of years, however, and definitely did not make this product. When it did make anabolic steroids, it packaged them in very odd, tall and thin glass ampules, not 10ml multi-dosed (American-style) vials like this. It appears that an underground manufacturer, who is believed to be in Russia, has simply taken up the abandoned name and started producing a number of different products including this Deca, nandrolone phenylpropionate, testosterone enanthate, testosterone propionate, and a Sustanon clone. The contents of these products have not yet been verified, but judging by the positive feedback, they probably do contain some amount of real steroid. –WL



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« Odgovor #8 poslato: April 10, 2010, 11:29:56 posle podne »
 Important  “Medical Mistakes” to Avoid During Your Next Cycle!


Anabolic Doc

By Thomas O’Connor, M.D.                 


Important “Medical Mistakes” to Avoid During Your Next Cycle!

Part 1


            Hey folks, it’s the Anabolic Doc coming at you for another information-filled article. Even though I have been with Muscular Development for only a few months, all I can say is that it has been super exciting. I would first like to thank Steve Blechman for giving me the opportunity to lead the “Anabolic Community” with true medical direction and guidance. For years our “Brothers and Sisters in Iron” have had to deal with a lot of their medical problems on their own. Getting valid information from a doctor even willing to monitor your anabolic steroid and performance-enhancing drug regimen and do their best to keep you healthy, has been nonexistent. This is where I come in, because I am willing to put it all on the line to make sure that you get the best medical care in the world when you are one of my patients.

            I always get e-mails asking what kind of things should be avoided during a cycle from a medical perspective. We have all read these boring articles on basic ideas of what to do and not do during a cycle to help improve your results. But this series is going to take it over the top and won’t be like anything you have ever read before. I am going to discuss with you the most important medical mistakes to avoid during your next cycle. I am going to touch on some very basic ideas first off, because many of our readers here at MD may be planning their very first cycle.

            You may be familiar with some ideas that I present in this series, and many of them will not be so familiar. A lot of powerlifters and bodybuilders avoid these issues out of ignorance, or sheer laziness. Next, I will discuss some advanced information as well, to help those who may be doing more intricate stacks that even a top pro bodybuilder could relate to. I am going to cover the most important mistakes that I see in my clinical practice that athletes who do use performance-enhancing drugs are guilty of committing. I am going to give you the real deal here, people. I am not just going to sprout off some textbook info at you, hoping you can decipher heads or tails of what I am about to explain.

            Remember, I want to be scientific in my explanations, but I know that the majority of the readership at MD is not doctors or scientists but hardcore bodybuilders who want to know as much about the “Anabolic Science” and its medical application and health prevention. With this, you can expect me to help you understand the science of medicine in relation to anabolic steroid use and their side effects. I will be presenting things in layman’s terms as well, so everyone can truly take advantage of all the information that I have to offer.


Time to Be Responsible

            Now before I get to discussing the medical mistakes that I want cover with this issue, it is imperative to know that as a strength athlete who has decided to go to the dark side and incorporate performance-enhancing drugs into their program, I want you to be responsible. Now when I say responsible, I don’t mean to be responsible to pay your cable bill on time or to make sure you take out the garbage. I am also not talking about being responsible about making sure you fork over half your paycheck every week for child support, due to that one-night-stand you had with that exotic dancer named Bambi, while you were blitzed into a Jager Bomb coma. I just hate those fucking DNA tests; oops sorry— I fell off track there for a minute.

            No, I am talking about being responsible for taking care of your health. When I say health here I am not talking about today or tomorrow, I am talking about thinking about the next 20-plus years of your life. Oh, I know the scene and what happens in the shadows of anabolic enhancement, so you should know that I am not one of those uptight asshole doctors who wears his smock around his office with his nose turned up at you. No, I am nothing of that sort. In fact, I detest that arrogant type of attitude and when you deal with me, you are guaranteed a warm smile and a true sincere doctor who wants the best for your competitive career and your long-term health.

            The problem with many strength athletes, both bodybuilders and powerlifters, is the fact that they do not think about the long-term consequences of their actions. They only think of what is happening right now— today. Like I mentioned earlier, this is the wrong attitude to have because remember, you reap what you sow. The decisions you take today may come and bite you on the ass like a rabid pit bull tomorrow, so you have to make sure that you always think of the possible repercussions of choices.

            Now, I don’t want to sound like one of those guys who harps on things, but the reality is, as a patient of mine or even one who reads my columns, I want you to take responsibility for your health. With this said, let’s now take a look at what the ‘Anabolic Doc’ has to offer!


Not Getting Blood Work Done

            This right here is the most important piece of information that I am going to give you, bar none. This is the first and most critical thing you are going to do to keep yourself healthy. No, I am not saying this so you come and see me so I can bill you— not at all. This is not my intention in the least. No matter who your doctor is, you must get this done at least twice per year as a minimum. This includes a full panel of things like your cholesterol, both HDL and LDL. Your blood pressure, triglycerides, homocysteine levels, liver values, and kidney function should also be monitored regularly, among others.

            This is the bare minimum that you should do to know how your organs are functioning. How do you know what is going on with your body and your organ health if you don’t get checked at least a couple times per year? Now I know some bodybuilders who are more responsible do this, but I still know that it is not more than 20 percent of those who use steroids. The biggest offenders in this arena are powerlifters. I know you are my “Brothers in Iron,” but the fact remains that way too many of you are lazy asses and don’t get this done at all. Hell, I have had world-class powerlifters come into my office and they have been using steroids close to 14 years and not once have they ever got their blood work done. What the hell is that!? This, in my opinion, is the most irresponsible thing you could do. Now not only is this irresponsible for you— but what about your wife and kids? Don’t you owe it to them to at least try and take care of your health?

            Like I mentioned earlier, if you decide to tread down the “Anabolic Path,” then you have to be responsible for your actions. You can’t do something like go on 30 cycles over a decade of use and abuse and then think, “Hey maybe I should get some blood work done to see if my liver isn’t bloated like a fucking dead horse.” I hate to say this, but if this is you or your current mental state, then you are going to pay the fucking piper and pay him with your ass if you don’t step up to the plate and be a true man about taking care of your health.

            Now you may be thinking that the Anabolic Doc is some type of arrogant prude, but no, I am not. I truly care for your health and want you to be the best competitive athlete you can be— but at the same time, I want you to realize that you are taking prescription-strength drugs to enhance your performance. That 50 mg of Thai Dbol that you chugged down this morning with your oatmeal were not “Hot Tamales” (I just loved that candy as a kid), so you cannot take this lightly. These are serious medications, (some more than others, and you will see this when we start discussing insulin and thyroid drugs) so you cannot just think that you can just do whatever you want and get away with it for years on end. This is not the case.

            You may think you are a bad-ass because you weigh 260 pounds with 8 percent body fat, but listen to me closely here for a minute. When one of your organs fails, or another major health ailment takes you down, then you will see right away that you are not made of molten steel, but flesh and bones. Even the biggest bad-ass can be brought to his knees when even a simple medical ailment hinders his body from functioning the way it should. So please, no matter if you can bench press 600 pounds or if your arms are 23 inches, don’t let this make you think that you are indestructible. Because when reality hits you in the face like a bitch slap from a pimp on 125th and Highland Avenue, you will wish you listened to the Anabolic Doc and the important message he tried to convey!


Using Underground Steroids

            Now I can see all of the cyber experts reading this now and saying, “This guy doesn’t know the reality of the scene, man— he’s out of his environment.” No actually, I am not out of the scene, you 21-year-old ass-clown, because I have been in the underground trenches longer than you have been alive. I knew the ins and outs of anabolic pharmacology and the underground street scene when your mother was wiping your ass. So don’t give me any of your ignorant rhetoric. Now you may be thinking how he can say that in a time like this, being the fact that most readers live in the United States. OK, let me explain.

            I fully understand what is going on in the scene at the underground hardcore level. I know what happened with Operation Gear Grinder back in 2005; they put a major halt on much of the veterinary-grade gear coming out of Mexico that supplied 90 percent of the black market in this country. Quality Vet, Denkall, Animal Power, Brovel, Tornel, SYD Group and others were the major players in the U.S. steroid black market. This major bust ultimately caused the massive increase of clandestine labs to be set up and hence the underground craze that started in this country.

            But first you have to look at the medical perspective. Do you really know where your stuff is being made? No you don’t! You could have some guy making this stuff in his garage with an environment that resembles a slum in Calcutta. This is what you want to inject into your body? No wonder so many guys are getting abscesses like it is going out of style. Cleanliness is of utmost importance— not only so you don’t get an abscess that erupts like Mount Vesuvius but also for you organ health. If you think you are doing your kidneys any favors by injecting dirty gear, think again, my friend.

            Didn’t you ever wonder what years of injecting dirty shit could do to your organs? Sterile prep conditions are only one of the problems you could run into. What about metals, carcinogens and contaminants? We all know that the majority of raw powders that these underground labs use come from China. Now, if you have watched the news over the last couple years, you know that they don’t have the best reputation for quality control.

            OK, let me see— the lead paint used in children’s toys or the melamine in the baby milk formulas? Close to 300,000 Chinese babies were affected and became ill over this whole melamine scam that took place in the baby formula scandal. Six of these babies died with still several hundred in critical condition because of major kidney shutdown. If they are willing to cut corners to save money and risk a major health crisis like this in their own country, what is their compassion toward bodybuilders living in the U.S.?

            MMM… if they don’t give a rat’s ass about all these contaminants that even go out to their own people, including babies, then are they going to care if they send Bob Smith living in “Butt-Fuck Idaho” some Test Enanthate powder laced with mercury, lead or PCBs? The answer is a big FUCK NO! Think about this for one minute here and take note, as this is a serious matter. PCBs, which are known as polychlorinated biphenyls, consist of close to 210 different chemicals that have similar structures. They were developed in 1929 and used for many different industrial purposes. The problem with this stuff is that it is super-resilient; it takes forever to break down. 

            Now this is where it gets juicy. The International Agency for Research on Cancer has stated several times that being exposed to PCBs can increase your chances for cancer and listen up here folks, specifically liver and kidney cancer! If this doesn’t make you sit up and take notice, I don’t know what will. From tests done that I have seen, many of the underground labs do contain an abundance of heavy metals and other contaminants and this was confirmed by our own Team MD writer William Llewelyn.           Think about that for a minute, my friends. Not only do you not know the conditions in which your underground gear is made, you also don’t even know the company the powder is coming from in China or the conditions in which it is manufactured. Maybe the same company that is pumping hormone powders on the black market is making a chemical that is carcinogenic in the same manufacturing equipment. How do you know? Then you are getting trace remnants of that carcinogen in your gear powder and then you guys back home in the heart of America are injecting this into your bloodstream. Scary, isn’t it!? I bet you didn’t think of that scenario the last time you bought a bottle of underground Deca from your boy “Big Mike” in the change room of your local gym.

            Now I know you are going to break my balls and tell me that it’s hard to get real pharmaceutical gear and all that. I know the reality of the scene and the product that was available in the ’80s and ’90s that was American-made and all the goodies from Europe are no longer a viable option. So I understand that those who use steroids in America are between a rock and a hard place. But in the end, that doesn’t change the fact that you could be introducing potent carcinogens into your system via injection because Mao Lee in Shanghai doesn’t give a “flying Commie fuck” if your raw hormone powder contains impurities that will give you cancer in 10 years. Nothing replaces real pharmaceutical gear for performance and health, and that is the bottom line!


Take My Words to Heart

Now with this installment, I covered some basic but very important mistakes that are critical for maintaining your health during your next cycle. Even though they are very elementary in nature, how many of you reading this who do use anabolic steroids avoid them? I know many of you and I am not talking about just the beginners, but also the veterans in the sport have fallen prey to these anabolic blunders. I hope that I have opened up some eyes with this issue and have actually made you think about what you are doing in your path to build that ultimate physique. Like I said from the beginning, if you take this path in life, you have to be fully aware of the consequences and you must do all that you can to prevent health conditions down the road.


Anabolic Doc 411

            Now one of the additions to my regular column is the Anabolic Doc 411. This will be a nice little segment about me and my personal practice. Here you can take a glimpse inside what I am currently up to with my clients and personal life. Here I will give you some insight on what is going on with my training program to break yet another record in the bench press. You can look forward to my opinions on some different topics and what is currently going on in the media with the “War on Steroids” propaganda that is launched day in and day out in this country. So starting next month, get ready for some interesting hardcore snippets into the life and times of the Anabolic Doc!



            www.usdoj.gov,DEA Leads Largest Steroid Bust in History.

            Buckley C, More than 54,000 Affected by Milk Scandal, National Post.

            Polychlorinated biphenyls (PCBs) [CAS Number 1336-36-3]. Integrated Risk Information System (IRIS), 1997.

            Llewellyn W, Counterfeit Analysis Report, Muscular Development.

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« Odgovor #9 poslato: April 10, 2010, 11:33:07 posle podne »
 Anabolic  Pharmacology: Equipoise - Anabolic Androgenic Steroid


Anabolic Pharmacology

By Seth Roberts



Pharmacology is the study of drugs and their effects. Anabolic pharmacology is the study of drugs that have a growth-promoting effect in muscle. This column will explore anabolic pharmacology by profiling a different anabolic drug and its effects each month. The focus of discussion this month will be the anabolic androgenic steroid, Equipoise.

Boldenone is a 1-dehydro derivative of testosterone that has been sold as a veterinary preparation under the name Equipoise, and is largely known by this name. The formation of a double-bond in the 1,2 position changes the shape of the molecule slightly. This also changes the potency and characteristics of the molecule. Boldenone has a lower affinity than testosterone for the androgen receptor, making it less potent on a milligram-for-milligram basis.1 This steroid can be converted to estrogen, but less so than testosterone. In addition, boldenone is metabolized to 1,4 dienedione, which is a potent aromatase inhibitor.

Boldenone is converted by 5-alpha reductase to 1-testosterone, a more potent steroid, as well as to the 5-beta isomer— which is thought to be an inactive metabolite.2,3 Binding to sex hormone-binding globulin (SHBG) is much lower with boldenone than with testosterone, meaning a larger free plasma concentration but a shorter half-life in plasma.4 There is little-to-no binding to progesterone or glucocorticoid receptors, and no real data on the interaction of boldenone with the different enzyme systems.1

The undecyclenate ester of boldenone was the ester marketed under the original trade name. In recent years, the free base and other esters have become available as underground preparations. On the street, Equipoise is erroneously considered to have the same activity as Deca and is often substituted for Deca in a stack. Dan Duchaine, if not the originator of this myth, at the very least propagated it in his book Underground Steroid Handbook II. If you look at the structure, you can see that boldenone is structurally identical to dianabol without the C-17 alkylation.

Most people experience much less side effects with boldenone, compared to methandrostenolone. This is because boldenone converts to estradiol, while methandrostenolone converts to methylestradiol. Methylestradiol is a much more potent and long-lasting estrogen than plain estradiol. Since there is no C-17 alkylation, there is no liver toxicity associated with boldenone. Boldenone is rumored to be very good at increasing red blood cell production. While all androgens stimulate erythropoiesis, there is no evidence in the scientific literature that boldenone is superior in producing this effect.5,6,7,8

Boldenone undecyclenate is generally injected every four or five days, but some people will inject every day while others will inject once per week. The longer half-life of the undecyclenate ester would dictate an injection frequency of every 10-14 days, but there has been a trend toward more frequent dosing by anabolic-androgenic steroid (AAS) users, even with drugs known to have long half-lives. Dosing is generally kept pretty low (300-500 milligrams per week), but the low binding affinity would argue for twice that dosage, taken with testosterone.

The anabolic-to-androgenic ratios are favorable for boldenone, but people do not consider boldenone a particularly potent steroid— possibly due to the low doses that are utilized. Also, boldenone does not cause much water retention— so many people assume it is not working if they do not put on 10 pounds in one week. Boldenone is said to cause an increase in vascularity, although there is no mechanism to explain why boldenone would do this more than any other AAS.

Seth Roberts is a former pharmaceutical research scientist with over 10 years of pharmacological research in the discovery and development of novel therapeutics. If you want to learn more about Anabolic Steroids, pick up Seth’s new book Anabolic Pharmacology at www.Ergogens.com. [© Seth Roberts, 2009. All rights reserved. For informational purposes only, not to be considered as medical advice or an endorsement of the use of illegal substances.]



1. Ojasoo T, Delettre J, Mornon JP, Turpin-VanDycke C, Raynaud JP: Towards the mapping of the progesterone and androgen receptors. J Steroid Biochem, 27(1-3):255-69, 1987.

2. Schanzer W, Donike M: Metabolism of boldenone in man: gas chromatographic/mass spectrometric identification of urinary excreted metabolites and determination of excretion rates. Biol Mass Spectrom, Jan;21(1):3-16, 1992.

3. Schanzer W: Metabolism of anabolic androgenic steroids. Clin Chem, Jul;42(7):1001-20, 1996.

4. Saartok T, Dahlberg E, Gustafsson JA: Relative binding affinity of anabolic-androgenic steroids: comparison of the binding to the androgen receptors in skeletal muscle and in prostate, as well as to sex hormone-binding globulin. Endocrinology, Jun;114(6):2100-6, 1984.

5. Gorshein D, Murphy S, Gardner FH. Comparative study on the erythropoietic effects of androgens and their mode of action. J Appl Physiol, 35(3):276-8, 1973.

6. Paulo LG, Fink GD, Roh BL, Fisher JW. Effects of several androgens and steroid metabolites on erythropoietin production in the isolated perfused dog kidney. Blood, 43(1):39-47, 1974.

7. Sanchez-Medal L, Gomez-Leal A, Duarte L, Guadalupe Rico M. Anabolic androgenic steroids in the treatment of acquired aplastic anemia. Blood, 34(3):283-300, 1969.

8. Alexanian R. Erythropoietin and erythropoiesis in anemic man following androgens. Blood, 33(4):564-72, 1969.


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Odg: Anabolic Research Update
« Odgovor #10 poslato: April 10, 2010, 11:35:56 posle podne »
Growth Hormone Therapy Cuts Fat and Builds Muscle

            Many bodybuilders and older adults take growth hormones to decrease body fat, build muscle mass and increase energy levels and joie de vivre (the joy of living). Synthetic growth hormone has been widely used for more than 10 years, so we have many studies to help evaluate its effectiveness. Kavya Mekala from the Lahey Medical Center in Burlington, Massachusetts and Nicholas Tritos from Tufts University School of Medicine in Boston combined the results of 27 studies on growth hormone, using a statistical technique called meta-analysis. Growth hormone decreased fat mass by an average of 2 pounds, fat by 1 percent, visceral fat by 9 inches, low density lipoprotein (bad cholesterol) by 9 mg/dl and total cholesterol by 7 mg/dl. Lean body mass increased by 4 pounds. Five to 7 percent of people experienced side effects such as joint pain, swelling and numbness to the hands and feet. There were small increases in blood sugar and insulin, but these effects were short-term and temporary. Growth hormone decreases abdominal fat and increases muscle mass, without causing changes in bodyweight. The authors cautioned that we need long-term studies to assess the effectiveness of growth hormone supplements and their effects on the heart and longevity. (Journal Clinical Endocrinology Metabolism, 94:130-137, 2009)

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« Odgovor #11 poslato: April 18, 2010, 12:56:19 posle podne »
Testosterone Makes You Not So Giving


            Does your wife or girlfriend ever accuse you of being an insensitive, selfish, self-absorbed and uncaring S.O.B.? Well, you can blame it on testosterone. That’s right, fellas. You have a hormonal excuse. Testosterone gives men more skeletal muscle mass than women, but on the flip side, it can make men behave badly— very badly. According to a recent news report, “testosterone makes tough muscular men much less generous than weedier peers.” Shouldn’t that be weanier? Aw heck.

            First of all, we know that exercise itself can cause transient elevations in testosterone. What happens, though, if you give a guy a testosterone boost with a little bit of cream? Accordingly, a testosterone cream caused a 27 percent reduction in the generosity of cash offers during a money sharing game.

            A new study has found those with high testosterone levels are less generous than men with lower levels of the hormone. Scientists tested the generosity of 25 male students at Claremont Graduate University. The volunteers were given a testosterone-containing gel, which doubled the amount of the big T in their bloodstream and compared it to a placebo cream. The students then played a simple economic game with another participant via a computer. Mmm… sounds innocuous, right? Then they asked one volunteer to split $10 with another volunteer in any way he likes.

            The other volunteer either accepted the offer or rejected it as unfair, in which case no one received any money. And each volunteer played this game in both roles, on and off the testosterone gel. And guess what? Overall, the testosterone cream caused a 27 percent reduction in the generosity of the offers, from averages of $2.15 to $1.57.

            Also, men with the most DHT in their bloodstream offered their partners a paltry $0.55 of the $10, while men with the least amount of DHT tendered $3.65, on average. So there you have it. Evidence that your selfishness is in fact due to your gonads secreting the big T. I guess if your wife or girlfriend complains, tell her you just can’t help it. (This research was presented at the Society for Neuroscience in Chicago IL). Read more: http://www.dailymail.co.uk/sciencetech/article-1223293/Testosterone-makes-tough-muscular-men-generous-weedier-peers.html#ixzz0VEA06gTt.


Elevates Erections and Testosterone

            We already know that exercise-related stress activates hypothalamus-pituitary-adrenal (HPA) axis; and that NO or nitric oxide is one of the mediators of the HPA axis response to stress. And we also know that phosphodiesterase type 5 inhibitors influences nitric oxide, too. Thus, this study determined whether a single oral long half-life phosphodiesterase type 5 inhibitor (tadalafil aka Cialis [remember if your erection lasts 4 hours or more, go to your doctor; or just lock yourself in a hotel room with your girlfriend) administration influences the HPA axis response to exercise-related stress.

            This study involved nine healthy male athletes. All subjects performed a maximal exercise test, then they received a single oral administration of tadalafil or placebo. After a two-week washout period, they were crossed over and repeated the exercise test. The average salivary cortisol concentration increased immediately after exercise after both tadalafil and placebo; however, the cortisol increase was significantly higher after tadalafil administration.

            On the other hand, an increased salivary testosterone after exercise was observed only after tadalafil administration. Tadalafil administration amplified the salivary cortisol and testosterone responses to a maximal exercise-related stress in healthy trained humans.1 So what does this mean? Not sure. Though it does seem that tadalafil elevates the stress response. Which is odd in that the primary use of the drug requires that you aren’t stressed. Perhaps a different exercise protocol would produce elevations in T which could override the effects of cortisol?


Nandrolone a Great Recovery Steroid

            This study determined if anabolic steroid administration, specifically nandrolone decanoate or ND, improves skeletal muscle regeneration from bupivacaine-induced injury. Male mice were castrated 2 weeks prior to muscle injury induced by an intramuscular bupivacaine injection into the tibialis anterior (TA) muscle. Dang. You’d think castration itself was enough. Anabolic steroid (nandrolone decanoate (ND), 6 mg/kg) or sesame seed oil was administered at the time of initial injury and continued every 7 days for the study's duration. And they found indeed that nandrolone decanoate administration can enhance muscle regeneration during the recovery from bupivacaine-induced injury.2 This points to the fact that one of the reasons that androgens work so well is because of the dramatic effects on recovery. No wonder elite athletes love this stuff.


Amino Acid and Testosterone

            Aspartic acid (D-Aspartic acid [D-Asp]) is a nonessential amino acid in humans. But just because it is nonessential, doesn’t mean it isn’t important. The carboxylate anion of aspartic acid is known as aspartate. D-Asp is involved in the steroidogenesis, specifically the synthesis of the big T, testosterone.3,4 A recent study investigated the role of D-aspartate in both rats and humans. In humans, a group of 23 men were given a daily dose of D-aspartate for 12 days, whereas another group of 20 men were given a placebo.

            In rats, a group of 10 rats drank a solution of either 20 mM D-aspartate or a placebo for 12 days. Then LH and testosterone accumulation was determined in the serum and D-aspartate accumulation in tissues. The effects of D-aspartate on the synthesis of LH and testosterone were gauged on isolated rat pituitary and Leydig cells. Sorry, can’t do that in humans. 

            What did they discover? In humans and rats, sodium D-aspartate induces an enhancement of LH and testosterone release. Amen to that! Bottom line is: this amino acid, though technically non-essential, is very essential for making testosterone!


Ca++ and Testosterone

            The effects of four weeks of calcium supplementation were determined in 30 healthy male athletes who were equally divided into three study groups, as follows: Group 1 non-exercising subjects receiving 35 mg calcium per kg bodyweight; Group 2 subjects receiving 35 mg calcium per kg bodyweight undergoing training routines for 90 minutes per day, 5 days a week and Group 3 subjects undergoing training routines for 90 minutes per day, 5 days a week. They found that training results in increased testosterone levels in athletes and that the increase is greater if accompanied by calcium supplementation.5 The dose used is about 3,200 milligrams, give or take.


            Jose Antonio, Ph.D., is vice president of the National Strength and Conditioning Association. He has a Ph.D. in muscle physiology and is chief executive of the International Society of Sports Nutrition.


            1. Di Luigi L, Baldari C, Sgro P, Emerenziani GP, Gallotta MC, Bianchini S, Romanelli F, Pigozzi F, Lenzi A, Guidetti L: The type 5 phosphodiesterase inhibitor tadalafil influences salivary cortisol, testosterone, and dehydroepiandrosterone sulphate responses to maximal exercise in healthy men. J Clin Endocrinol Metab, 2008, 93(9):3510-3514.

            2. White JP, Baltgalvis KA, Sato S, Wilson LB, Carson JA: The Effect of Nandrolone Decanoate Administration on Recovery from Bupivacaine-induced Muscle Injury. J Appl Physiol, 2009.

            3. D'Aniello A, Di Cosmo A, Di Cristo C, Annunziato L, Petrucelli L, Fisher G: Involvement of D-aspartic acid in the synthesis of testosterone in rat testes. Life Sci, 1996, 59(2):97-104.

            4. Lamanna C, Assisi L, Vittoria A, Botte V, Di Fiore MM: D-Aspartic acid and nitric oxide as regulators of androgen production in boar testis. Theriogenology, 2007, 67(2):249-254.

            5. Cinar V, Baltaci AK, Mogulkoc R, Kilic M: Testosterone levels in athletes at rest and exhaustion: effects of calcium supplementation. Biol Trace Elem Res, 2009, 129(1-3):65-69.


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« Odgovor #12 poslato: April 18, 2010, 12:57:35 posle podne »
The Best and Worst Foods for Altering Testosterone



By Dan Gwartney, M.D.

The Best and Worst Foods for Altering Testosterone
            Dietary strategies to promote natural testosterone production may seem meaningless to a person using anabolic steroids. As a matter of fact, they pretty much are, since androgen levels are controlled via syringe, rather than by the innate feedback system. The body monitors testosterone levels and adjusts production of the hormone within the testes by altering output of stimulatory hormones released from the hypothalamus and pituitary (glands in the brain). If the circulating (blood) testosterone concentration is low, the hypothalamus detects this and signals the pituitary gland to release a hormone that stimulates the testes called LH.

            LH travels through the blood to the testes and drives testosterone production to increase output. As testosterone concentration rises in the blood, the hypothalamus detects the elevation and reduces the pituitary’s demand.1 In the case of a person using anabolic steroids, androgen levels are kept higher than the cut-off chronically, so the testes do not need to function (relative to producing testosterone) and atrophy (shrivel) as they do not receive a LH signal from the pituitary. However, when the cycle is finished, close attention needs to be paid to promoting the restoration of natural testosterone production.
            Of course, the system is not as simple as one switch that is either ‘off’ or ‘on.’ In an anabolic, steroid-free environment, a person’s testosterone concentration is affected by conditions such as: sleep, physical demand, available rest, amount and quality of food, and presence of certain nutrients.2,3 While there is no scientific evidence that any one food or even the most selective diet will make a difference in regard to testosterone level and subsequent muscle growth over time (since no one has ever studied the demographics of strength and muscularity), the discriminating bodybuilder or fitness enthusiast will pay close attention to what he/she consumes. After all, it does no good to struggle to build muscle in the gym if a fad-diet lifestyle is sabotaging the anabolic response. Also, informal observations are fairly convincing in suggesting that vegans have a difficult time putting on muscle and the chronically undernourished live on the threshold of catabolism.
            Before plunging into the buffet of knowledge ahead, this does not imply that other hormones that are modulated by the diet are not equally important. For the sake of clarity and brevity, this article will focus solely on the testosterone-diet associations.

Testosterone is a cholesterol-based chemical and many industrial sources (pharmaceutical companies) synthesize testosterone using steroid-ring precursors. However, testosterone is not created from dietary cholesterol in the body to a great degree. The starting chemical for endogenous production (natural testosterone production) appears to be acetyl-CoA, which is produced as sugar (glucose) and burned for calories. The body produces sugar in times of need, so even if one is on a strict ketogenic diet, acetyl-CoA should still be available. Acetyl-CoA goes through a series of reactions to become a molecule called hydroxymethylglutary-CoA, or HMG-CoA.4 Fortunately for the ketogenic dieters, HMG-CoA is also produced during ketogenesis, so the starting blocks for steroid production are well-provided.
            HMG-CoA is then shuttled into another series of reactions to form squalene. A key reaction responsible for changing HMG-CoA is called the rate-limiting step. It is like the slowest walker on a prison chain gang. No matter how fast the rest of the crew is, they cannot move faster than the slowest moving prisoner. The top-selling cholesterol-lowering drugs, called statins (e.g., Lipitor®), work by making the slowest, rate-limiting reaction move even slower.5 Ironically, dieticians and drug companies worked for years on limiting dietary cholesterol, but it is the body’s own cholesterol-making machinery that is the cause of most cholesterol-related health problems.
            Squalene is converted to a primitive steroid called lanosterol; this is the steroid equivalent of a cave man. Lanosterol is finally processed to form cholesterol; cholesterol can be processed to the more readily-recognized steroid hormones, such as: testosterone, androstenedione, DHEA, estradiol, progesterone, cotisol, etc.6 It is difficult to keep track of the number of chemical reactions involved, but it is a complicated process. This very brief introduction into steroidogenesis is provided to illustrate that the body doesn’t make testosterone simply and there really is no way to directly consume something that will directly convert into testosterone— at least not a food product. This revelation will likely disappoint fans of Rocky Mountain oysters and participants at Testicle Festival eating contests. Certainly, several products have been introduced into the sports nutrition market that are steroid precursors, or prohormones. However, these are not chemicals that are common in the food chain and some are thinly-veiled drugs.   
            The reactions in creating a steroid backbone (let alone the specific androgens, estrogens, glucocorticoids, etc.) require a great deal of energy. Additionally, the processes are predominantly oxidizing reactions. The pressure in Western society has long been to promote antioxidant consumption. Antioxidants suppress oxidizing reactions; this is beneficial in many situations, as free radicals can damage structural proteins in the cell or the DNA. However, the body burns calories and generates bio-molecules through oxidizing reactions as well, so the question must be asked, “Can you have too much of a good thing (antioxidants)?” In exploring this many, many years ago, I learned of reductive stress, but it appears to be a neglected area of research.
            The foods that promote testosterone production primarily offer certain minerals which help form the metalloproteins and metalloenzymes involved in the chemical reactions to create cholesterol and eventually testosterone.7,8 Additionally, B vitamins are important co-factors (helpers); total calories and protein quality is also important.8 The most commonly referred foods that promote testosterone production are: oysters, eggs, beef, garlic, and broccoli. These foods are high in zinc, cholesterol, B vitamins, and arachidonic acid (AA).
            Arachidonic acid is a fatty acid that sits in the membrane of cells lining the Leydig cells of the testes (the actual site of testosterone production from cholesterol). Under the influence of LH from the pituitary, released when testosterone levels are registered as being low, enzymes pull AA from the membrane and form messenger chemicals that go to the nucleus (the control center of the cell where the DNA is located) and turn on the production of StAR (steroidogenic acute regulatory protein).9 Interestingly, AA can go down three pathways in the Leydig cell; two promote StAR production, but the third suppresses it. This third pathway is the cyclo-oxygenase pathway and research into promoting testosterone production via cyclo-oxygenase 2 inhibition is underway.10 Many people are familiar with Celebrex®, a drug used to treat the symptoms of arthritis, this is a cyclo-oxygenase 2 inhibitor. At this time, only animal studies have been performed to investigate the effect of Celebrex® on testicular function. Some protection of steroidogenesis during inflammatory challenge has been recorded, but no real increase in baseline testosterone production.11
            Another common drug class, the statins (e.g. Lipitor®), may reduce testosterone by reducing the available pool of cholesterol to use in steroidogenesis. Data are conflicting at this time, but it appears that while total testosterone may be reduced, bioavailable testosterone is not affected.12,13 Men started on statins who experience symptoms of androgen deficiency may wish to be more diligent in monitoring testosterone concentrations through their physicians.
            The dietary attention really needs to be paid to foods that may lower testosterone production— either through antioxidant suppression of the oxidizing reactions, promoting the conversion of testosterone to estrogen, or by acting as an estrogen directly. Research has shown that several foods, many of which are increasing in popularity in the U.S., suppress testosterone production. Some of this data is based on test-tube experiments, others from animal studies and the majority of the remainder from epidemiologic studies (observing trends in large groups).

Green tea— a beverage so healthy that the only worries are about the water added to the tea bags— or is there more to consider? Green tea is full of antioxidants, leading to the health claims about promoting health and prolonging life. Yet, recall that testosterone production is dependent upon oxidizing reactions. Recently studies looking at the effect of green tea, specifically the polyphenol compounds (antioxidant), on testosterone levels have reveal a dark side to green tea— at least for the muscle-building athlete.
            Green tea has been shown in the lab to inhibit certain effects of testosterones, apparently by inhibiting the conversion of testosterone to the more potent androgen, DHT.14,15 Green tea, specifically EGCG, may also affect aromatase— the enzyme that converts testosterone to estrogen; in some studies aromatase is suppressed, in others it is increased.16,17 Animal studies and epidemiologic studies have shown that green tea consumption is associated with lower androgen and estrogen levels in Asians.18 Green tea appears to be protective against cancers that respond to sex hormones (prostate, breast).19
            Yet, what about testosterone? If estrogen and DHT are lower because testosterone is not being converted into those metabolites, then testosterone levels should be higher. However, tissue studies suggest otherwise. Rats treated with green tea had a much lower response to hCG, the hormone used to stimulate testosterone at the end of an anabolic steroid cycle.20 Interestingly, when the tissue cultures were provided with androstenedione, the steroid that immediately precedes testosterone in the natural production sequence, normal testosterone response to hCG was seen. This suggests that the inhibition of green tea occurs earlier in the steroid production sequence and may affect other steroid classes.
            Another Asian staple that has entered Western diets is soy. Soy is a protein-rich vegetable that also contains other bioactive components. Among these are genistein and isoflavones. Soy intake has also been shown to decrease testosterone, making the use of it as the primary protein source of questionable value for male athletes— but this has been challenged.21,22 Available soy products include protein powders and ready-to-drink shakes. A number of products contain soy protein to attract female members of the gym, as the isoflavones have estrogenic-support properties.
            Another diet trend, also supported by observations of Asian societies, is food restriction. Certain communities in Japan are known for their longevity; often attributed to green tea, low saturated fat, soy and other habits, the basis for much of this longevity is life-long caloric restriction.23,24 These people consume less than the maintenance calories daily, much less than the average American. Caloric restriction has been shown to prolong life in lab rats. Yet, this same life-extending diet also suppresses testes function, resulting in lower testosterone. Remember, the body does not want to support any more muscle than it uses because muscle uses energy, and the body is designed to preserve calories to survive winters/famine/etc.
Even short-term fasting suppresses testosterone levels. Men fasting for 3½ days saw a 30-50 percent decrease in testosterone, which was due to changes in the pituitary signal, rather than the testes function.25 It is important to realize that supporting testosterone function is more than offering the building blocks used by the testes.
            A final example of the need for a suitable diet was demonstrated in a study looking at wrestlers who lost weight rapidly to meet the weight restrictions of their class. During a two- to three-week training regimen, wrestlers’ average testosterone concentration dropped approximately 30 percent.26 An earlier study even demonstrated that during a two-day tournament, resting testosterone concentration dropped.27
            The body needs to know that the environment is safe for adding on metabolically demanding tissue, such as muscle. This includes consuming sufficient calories to avoid muscle wasting, eating a quality diet including animal-based protein, focusing on foods that are high in zinc and B vitamins. Men striving to lose weight, consuming soy-based foods and drinking green tea should be aware that one consequence is a probable reduction in testosterone concentration that will make building and maintaining muscle much more difficult. Of course, it is unwise to overdo any diet, as obesity is not the goal of most readers and the increase in adipose tissue will lead to elevations in estrogens. Further, the health benefits of green tea and soy, possibly flaxseed as well, need to be weighed against sports or physique goals.

            1. Nehra A. Treatment of endocrinologic male sexual dysfunction. Mayo Clin Proc, 2000 Jan;75 Suppl:S40-5.
            2. Alemany JA, Nindl BC, et al. Effects of dietary protein content on IGF-I, testosterone, and body composition during 8 days of severe energy deficit and arduous physical activity. J Appl Physiol, 2008 Jul;105(1):58-64.
            3. Penev PD. Association between sleep and morning testosterone levels in older men. Sleep, 2007 Apr 1;30(4):427-32.
            4. Päivä H, Thelen KM, et al. High-dose statins and skeletal muscle metabolism in humans: a randomized, controlled trial. Clin Pharmacol Ther, 2005 Jul;78(1):60-8.
            5. Rosenson RS. Pluripotential mechanisms of cardioprotection with HMG-CoA reductase inhibitor therapy. Am J Cardiovasc Drugs, 2001;1(6):411-20.
            6. Payne AH, Hales DB. Overview of steroidogenic enzymes in the pathway from cholesterol to active steroid hormones. Endocr Rev, 2004 Dec;25(6):947-70.
            7. Ebisch IM, Thomas CM, et al. The importance of folate, zinc and antioxidants in the pathogenesis and prevention of subfertility. Hum Reprod Update, 2007 Mar-Apr;13(2):163-74.
            8. Jana K, Samanta PK, et al. Protective effect of sodium selenite and zinc sulfate on intensive swimming-induced testicular gamatogenic and steroidogenic disorders in mature male rats. Appl Physiol Nutr Metab, 2008 Oct;33(5):903-14.
            9. Castilla R, Maloberti P, et al. Arachidonic acid regulation of steroid synthesis: new partners in the signaling pathway of steroidogenic hormones. Endocr Res, 2004 Nov;30(4):599-606.
            10. Wang X, Shen CL, et al. Cyclooxygenase-2 regulation of the age-related decline in testosterone biosynthesis. Endocrinology, 2005 Oct;146(10):4202-8.
            11. Winnall WR, Muir JA, et al. Effects of chronic celecoxib on testicular function in normal and lipopolysaccharide-treated rats. Int J Androl, 2008 Jun 2. [Epub ahead of print].
            12. Stanworth RD, Kapoor D, et al. Statin therapy is associated with lower total but not bioavailable or free testosterone in men with type 2 diabetes. Diabetes Care, 2009 Apr;32(4):541-6.
            13. Kocum TH, Ozcan TI, et al. Does atorvastatin affect androgen levels in men in the era of very-low LDL targeting therapy? Exp Clin Endocrinol Diabetes, 2009 Feb;117(2):60-3.
            14. Liao S, Hiipakka RA. Selective inhibition of steroid 5 alpha-reductase isozymes by tea epicatechin-3-gallate and epigallocatechin-3-gallate. Biochem Biophys Res Commun, 1995 Sep 25;214(3):833-8.
            15. Hiipakka RA, Zhang HZ, et al. Structure-activity relationships for inhibition of human 5alpha-reductases by polyphenols. Biochem Pharmacol, 2002 Mar 15;63(6):1165-76.
            16. Satoh K, Sakamoto Y, et al. Inhibition of aromatase activity by green tea extract catechins and their endocrinological effects of oral administration in rats. Food Chem Toxicol, 2002 Jul;40(7):925-33.
            17. Monteiro R, Assunção M, et al. Chronic green tea consumption decreases body mass, induces aromatase expression, and changes proliferation and apoptosis in adult male rat adipose tissue. J Nutr, 2008 Nov;138(11):2156-63.
            18. Goh VH, Tong TY, et al. Interactions among age, adiposity, bodyweight, lifestyle factors and sex steroid hormones in healthy Singaporean Chinese men. Asian J Androl, 2007 Sep;9(5):611-21.
            19. Zhou JR, Li L, et al. Dietary soy and tea combinations for prevention of breast and prostate cancers by targeting metabolic syndrome elements in mice. Am J Clin Nutr, 2007 Sep;86(3):s882-8.
            20. Figueiroa MS, César Vieira JS, et al. Green tea polyphenols inhibit testosterone production in rat Leydig cells. Asian J Androl, 2009 May;11(3):362-70.
            21. Goodin S, Shen F, et al. Clinical and biological activity of soy protein powder supplementation in healthy male volunteers. Cancer Epidemiol Biomarkers Prev, 2007;16:829-33.
            22. Kalman D, Feldman S, et al. Effect of protein source and resistance training on body composition and sex hormones. J Int Soc Sports Nutr, 2007 Jul 23;4:4.
            23. Rehm S, White TE, et al. Effects of food restriction on testis and accessory sex glands in maturing rats. Toxicol Pathol, 2008;36(5):687-94.
            24. Chen H, Luo L, et al. Aging and caloric restriction: effects on Leydig cell steroidogenesis. Exp Gerontol, 2005 Jun;40(6):498-505.
            25. Aloi JA, Bergendahl M, et al. Pulsatile intravenous gonadotropin-releasing hormone administration averts fasting-induced hypogonadotropism and hypoandrogenemia in healthy, normal weight men. J Clin Endocrinol Metab, 1997 May;82(5):1543-8.
            26. Karila TA, Sarkkinen P, et al. Rapid weight loss decreases serum testosterone. Int J Sports Med, 2008 Nov;29(11):872-7.
            27. Kraemer WJ, Fry AC, et al. Physiological and performance responses to tournament wrestling. Med Sci Sports Exerc, 2001 Aug;33(8):1367-78.

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« Odgovor #13 poslato: April 26, 2010, 10:25:21 posle podne »
Nandrolone Promotes Recovery From Muscle Injury

Many bodybuilders take testosterone supplements to increase muscle mass and strength. Medically, the drug is often used to treat physical deterioration that accompanies aging and prevents muscle wasting in patients with degenerative diseases or undergoing cancer treatment. Its role in muscle injury repair has been controversial. Anabolic steroids increase the release of corticosteroids, which have been implicated in strains and sprains in athletes.

James Wright and colleagues from the University of South Carolina found that mice injected with a drug designed to create muscle injury recovered faster after treatment with the anabolic steroid nandrolone decanoate (Deca). After 42 days of treatment, animals given nandrolone showed larger fiber diameter and enhanced muscle regeneration compared to those treated with a placebo (fake nandrolone). The study showed that nandrolone decanoate promoted recovery from muscle injury. (Journal of Applied Physiology, 107: 1420-1430, 2009)

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« Odgovor #14 poslato: April 26, 2010, 10:26:28 posle podne »
 Growth  Hormone and IGF-I: Two Might Be Better than One for Muscle Growth


Growth Hormone and IGF-I: Two Might Be Better than One for Muscle Growth

Growth hormone (GH) and insulin-like growth factor (IGF-I) are powerful anabolic hormones that promote muscle growth and fat use. During the 1980s, as part of the space program, Dr. John Linderman from the University of Toledo in Ohio showed that the combination of GH and IGF-I promoted muscle hypertrophy better than either hormone alone.

Michael Graham and co-workers from Newman University in Great Britain, in a review of literature, speculated that the combination of hormones would be effective for preventing muscle loss with aging (sarcopenia). Sarcopenia is a devastating aspect of aging. Reduced muscle mass in the lower body and low levels of muscle strength are linked to premature death and an increased risk of diabetes. We need well-controlled scientific studies to determine the effectiveness of supplementing both hormones on muscle hypertrophy and preventing muscle wasting during aging. (Journal of Exercise Physiology, online December 2009)