got em from meso
Growth Hormone (gh - growth hormone (somatropin) - ) for Post Cycle Therapy (PCT - post cycle therapy - )?
Q: What are your thoughts of using growth hormone during PCT?
A: I think it is certainly a viable option, though the main focus is preserving lean body mass and not increasing the return to homeostasis with androgen production. The main support for this use of GH came from a study published in 2001, in the Journal of Clinical Endocrinology and Metabolism (volume 86 number 5, pp 2211-19). It was a study done to examine if growth hormone or IGF-1 could counter the catabolic effects of hypogonadism (low testosterone levels). The investigation involved a group of 13 healthy subjects with a mean age of 22 years. The subjects were given a GnRH (Gonadotropin Releasing Hormone) analog, which caused their bodies to shut down the normal production of testosterone. After 6 weeks from reaching baseline levels they were given either GH or IGF-1, to see if the drugs would prevent the catabolism normally associated with low testosterone levels. Final measures were taken 10 weeks from the start of the study.
The study demonstrated that both IGF-1 and growth hormone were able to preserve protein synthesis rates, even during a period of severe androgen deprivation. The subjects, likewise, did not lose a statistically significant amount of fat free mass/muscle tissue, in contrary to what is documented with hypogonadism alone. While it is far from conclusive evidence GH or IGF-1 should become integral to every steroid user’s PCT program, it certainly lends a lot of support for the idea of using one of these drugs in this manner. Note, however, that the study did show that androgens were required for the full anabolic effects of Growth Hormone and IGF-1. In other words, GH/IGF-1 may help you maintain muscle mass when coming off steroids, but you will get your most growth from the drugs if they are taken when androgen levels are normal or even elevated.
No More Spot Injections?
Q: I listened to your lecture at the Lord’s Cricket Ground in London. In it you said that you do not recommend spot injections. How come? I’ve injected in my biceps, triceps, and calves without problems. Are you going soft on us?
A: No, I don’t think I am. Maybe it could be said I am getting softer to some degree. I have been thinking more of health than I did in my 20’s. At that time in your life you tend to feel indestructible. I’m in my 30’s now, and more in touch with the fragility of life I guess. I’d never do today some of the things I did when I was 24 (2000mg of testosterone in one week, what the hell was I thinking?) So I guess I am trying to preach a message of steroid conservatism a bit more than I used to. But my recommendation in the London Lord’s lecture was not really based solely on that. It was more a function of my role in the conference. To give you some background, I was invited to speak with many of the great people that run and work in the needle exchange clinics throughout the UK. My goal was to not only educate the group, but to provide a strategy for what they term “harm reduction”.
Harm reduction is a concept that addresses the fact the people are using illegal drugs, and tries to minimize the negative impact of their use instead of simply judging the user. That is the function of these clinics. Some may say they facilitate drug use (often IV narcotics) by supplying free needles and syringes to users. Others, and I am one of them, believe this is far outweighed by the health protecting benefits of clean needles and free counseling. As far as steroids are concerned, I tried to provide some simple guidelines for reducing the health risks associated with their use for the average person. The cornerstone of this was the use of reasonable doses, limited administration of toxic oral steroids, regular checkups of health during and post cycle, and finding legitimate (as opposed to underground or counterfeit) drugs.
My recommendation for avoiding spot injections was simply another part of “harm reduction”. After all, I think few people will deny that there is a greater chance for injection error when trying to navigate the smaller muscle groups as opposed to the glutes and thighs, the recognized universal injection points for slow acting oil-based (depot) injections. Health issues due to local (small muscle) injections are not extremely uncommon. You hear them all the time. At the same time, many people have the experience and skill to run numerous cycles with many repeat injections into small muscles with no issue. My advice was to be applied to everyone that comes through the doors. Those that know what they are doing and have every intention of spot injecting will probably just ignore it. For those that are inexperienced, however, I definitely still believe that “spot” injections should be left for a much later time.
Long-term Oral Steroid Cycles?
Q: I’ve been on and off steroids for years. I respond well to them even at pretty low doses (300-600mg/week), but always crash afterwards no matter what I do. Lately I’ve been trying something different. For the past 12 weeks I’ve been taking 100mg of orals (Winstrol, Dianabol, Anadrol) per week, and have slowly been gaining size (about 5 pounds of lean mass) and strength. I am hoping this will produce more permanent gains; less estrogen conversion to worry about and it shouldn’t suppress my natural testosterone. Do you have any knowledge of the efficacy of low-dose long-term use of anabolics?
A: Given that most of the oral anabolics have less estrogenicity than the standard of reference (testosterone), you should find that size is better maintained at the conclusion of a cycle compared to injectable testosterones, as you are holding, and as a result will be excreting, less water weight. When all is said and done, you’ll seem to hold more of the weight you gained on oral anabolics simply because more of what you gained was quality muscle (not water bulk) in the first place. Anadrol is an exception among your list as it is highly estrogenic. Given the doses you are using, however, I suspect you will not notice this trait much, and (in line with what you stated) should be noticing some modest but measurable gains in strength and lean muscle mass. In the end you’ll probably gain more lean mass on a formidable dose of testosterone, but again, the difference between your on-cycle bulk weight and your off-cycle retained mass weight will be more noticeable on a cycle like this too.
If my math is correct, you are taking about 15 milligrams of oral anabolics per day. I don’t want you to be mistaken into thinking this is a “very low” dose. O.K., by some of the standards of excess today it may be considered low, but in a clinical sense it most certainly is not. Winstrol is given at a dose of 6 milligrams per day or less most commonly. When Dianabol was widely prescribed in the U.S., the common application was 5 milligrams per day. Aside from Anadrol, the doses you are taking are outside of the therapeutic range, and enough to present significant gains in lean tissue, as you have noticed. In fact, during the 1960’s and ‘70s fifteen milligrams per day was a common dose for athletes and bodybuilders. This level of use is also more than sufficient to suppress natural testosterone production, so you still going to have to deal with some type of crash at the conclusion of this cycle, even if it is less pronounced due to less water retention. As such, a proper PCT (Post-Cycle Therapy) program is probably a good idea to look at.
The main concern I have with this practice is the fact that you are applying a sufficient dose of c-17 alpha alkylated oral steroids each day, and it is continuing for a significant amount of time. The usual cutoff point is 6-8 weeks. Immediately, I would question what your serum lipids are doing. How are you HDL (good) and LDL (bad) cholesterol levels responding to this cycle? As you may know, oral c-17 alpha alkylated steroids present much more toxicity to the body than injectable testosterones (and related non-alkylated steroids). They tend to greatly shift the HDL:LDL balance in an unfavorable direction (increasing the risk of cardiovascular disease), and place some strain on the liver. While I wouldn’t be go so far as to say this type of practice is outright dangerous to your immediate health, I would most certainly recommend that you take caution. With any oral cycle, especially one going on for a prolonged period of time, you should be getting periodic checks on your lipids, liver enzymes, blood pressure, and general markers of health. If you find the drugs are placing too much strain on your body, they probably aren’t worth it. If you find such is true in your situation, you’d likely be much better off looking back at the old standby injectables like testosterone and nandrolone, which present no significant liver stress and have a much lower negative effect on serum lipids – crash and water retention be damned.
Sore from Enanthate
Q: I’ve been getting very sore from testosterone enanthate injections. I’ve also had a fever two times for a couple of days after my shot. It is the first time I have used the drug. I’ve only tried Deca-Durabolin - nandrolone decanoate - and oral steroids before. Is it normal? I am actually planning to stop my cycle short because of it. It is just too uncomfortable.
A: Soreness, fever, and tissue sensitivity are possible reactions to some steroid injections, and may be caused by a number of things. You never made any reference to the exact kind of testosterone enanthate you are using, so it does limit my ability to answer you to some degree. Were it a product from an underground lab, for example, I might suggest that the sterility or cleanliness of the product may be in question. Your body could be reacting to the presence of some irritant or toxin with a normal immune response, which could include the symptoms you described. The underground product may also be unusually high in benzyl alcohol, perhaps to facilitate a greater steroid concentration per milliliter or as a way of trying to assure the sterility of the solution. This is a common issue with “homegrown’ steroids, which are not carefully assembled under conditions that would ensure the proper amounts (and sterility) of all ingredients (carriers, anti-microbial agents, steroids, etc.). More fundamentally, you may be reacting to the use of enanthoic acid (enanthate) as the ester for testosterone. Carboxylic acid esters like this can be irritating to the body, especially the shorter chain ones. Enanthate is fairly long and well tolerated by most users, but even so a small percentage of patients do react to injections with the symptoms you described.
In a clinical setting, the type of reaction you are experiencing would be cause to change the method of therapy. It is clearly an unwanted adverse effect, and not something you should have to endure. You want the benefits of the drug without discomfort or adverse effects, the central focus in clinical medicine when it comes to the development of new androgen replacement therapies. If it is the enanthate ester itself that is causing the problem, an easy solution is to switch to a more comfortable ester. Testosterone cypionate is a common substitute for testosterone enanthate when this occurs, and in fact appears to be more popularly used in U.S. medicine. If you are using an underground or counterfeit product, the problem may be the same, or it may be something of greater concern. I always advise against the use of underground gear, and would certainly tell you to stop using it if that is the case. There would be no way to know for sure what is going on, of course, unless you had access to an American prescription testosterone enanthate product, which would eliminate the factors associated with underground manufacturing. Either way, I wish you luck, and hope you have a more comfortable cycle in the future should you decide to try again.
Dianabol Taste Test
Q: I’ve had two different dbols before, and both pills tasted very bitter. I have a new one that tastes very different, kind of bland. Did I get a fake? Does Dianabol taste bitter?
A: I’ve heard different “taste testing” strategies for identifying steroids before. I must confess that I’ve never given the concept a great deal of time. That is to say, I have never made any systematic examination of the different tastes of pure steroid chemicals, so I’d have little reference point to start from when it comes to evaluating their tastes as part of a blended compound. I can give you this little bit of information, however, which will hopefully put the whole thing into perspective. Dianabol usually comes as a 5mg tablet, meaning there are 5 milligrams of active drug in it. A typical tablet contains a whole lot more material than 5 milligrams. In fact, it is likely to contain 20 times that amount or more in the form if different binders, fillers, and perhaps coloring agents. Any combination of these materials may have different properties when it comes to taste. It is highly unlikely that even the most trained taste buds will be able to notice such a tiny amount of Dianabol next to an abundance (and variety) of other materials. In my opinion, this just isn’t a viable option for determining if you have a real drug or not. You are much better off examining the packaging of the product very closely, and comparing it to known legitimate products. You should make much more progress here. If you are buying an underground item, however, you are kind of on your own without some type of lab analysis.
Traveling with Gear
Q: I have a script for testosterone cypionate from my doctor. I need to fly next week to LA and will be away when my injection is scheduled. Do you know if I can I take syringes and steroids with me on the plane?
A: First, I am not an expert on the policies of the FAA, so I suggest you don’t do anything without checking with the airline you plan to travel with first. I wouldn’t want to misdirect you just to get a letter next week about your nightmare in the airport and my crappy advice. I am sure you can find all the policies online or with a quick phone call. I will tell you what I know, however, but please take the previous disclaimer to heart. You mentioned you had a valid prescription for the drug, so there should logically be no issues traveling with it. You have every right to travel with your medication so long as it is properly labeled as such, especially within U.S. borders where your prescription will always be recognized. It is perfectly legal to travel on a plane with syringes as well so long as they are accompanied by injectable medication. Depending on the airline, you can likely even take them on the plane in a carry-on bag. Some, however, may require that they be stored with your checked baggage, as the equipment is not essential to your health during travel. Again, check with your carrier first. At the very least, it should be no issue to put them together with the labeled vial of prescription testosterone and tuck them in a safe spot in the middle of your clothes. Remember, your bags might not be gingerly handled the entire time they are out of your sight. That is probably the issue you should be worrying about more. Good luck and travel safe.
Prostate Specific Antigen (PSA), TRT, and Finasteride
Q: I have watched my PSA rise and have had some urological problems recently. I have seen 3 urologists. One said discontinue TRT now and the other two were not quick to discontinue anything. Should older guys be thinking about a 5AR while on exo test?
A: Brief discussion below. Also, have you considered the use of finasteride, etc.? A thought after any pathology has been ruled out.
Benign Prostatic Hyperplasia - The development of BPH requires the presence of androgens and that the marked reduction in serum testosterone caused by chemical or surgical castration causes reduced prostate volume. Studies have failed to demonstrate exacerbation of voiding symptoms attributable to BPH during testosterone supplementation.
Prostate volume, as determined by ultrasonography, does increase significantly during testosterone-replacement therapy.Urine flow rates, postvoiding residual urine volumes, and prostate voiding symptoms did not change significantly in these studies. This is explained by the poor correlation between prostate volume and urinary symptoms. Individual men with hypogonadism may occasionally have increased voiding symptoms with TRT.
Prostate Cancer - There is no scientific peer-reviewed literature that definitely establishes a link between the administration of testosterone and the increasing the risk or development of prostate cancer. There is no compelling evidence that testosterone has a causative role in prostate cancer or to suggest men with higher testosterone levels are at greater risk of prostate cancer or that treating hypogonadism with exogenous androgens increases this risk. Just remember the incidence of prostate cancer rises with aging which is associated with declining testosterone levels. Prostate cancer becomes more prevalent exactly at the time of a man's life when testosterone levels decline.
Over 200,000 men are given a diagnosis of prostate cancer each year and most are first detected by a rise in the PSA level unrelated to testosterone therapy.
Interestingly the underlying prevalence of occult prostate cancer in men with low testosterone levels appears to be substantial. A history of prostate cancer has been considered an absolute contraindication to testosterone-replacement therapy which is now under active debate for men who are deemed cured.
PSA – The 2002 U.S. Preventative Services Task Force recommendations on the screening for prostatic cancer concludes that the evidence is insufficient to recommend for or against routine screening for prostate cancer using prostate-specific androgens (PSA) testing or digital rectal examination (DRE), "Screening is associated with important harms including frequent false-positive results and unnecessary anxiety, biopsies, and potential complications of treatment of some cases of cancer that have never affected a patient's health. The USPSTF concludes that evidence is insufficient to determine whether the benefits outweigh the harms for a screened population."
PSA values used to trigger prostate biopsy include an increase of 1.5 ng per milliliter within two years or a total increase of 2.0 ng per milliliter over any period. These recommendations have been based on observational population studies in untreated men. I would use 0.75 ng over 12 months.
These are free downloadable files.
Rhoden EL, Morgentaler A., Risks of testosterone-replacement therapy and recommendations for monitoring, N Engl J Med. 2004 Jan 29;350(5):482-92.
Screening for prostate cancer: recommendation and rationale. (2002). Ann Intern Med, 137(11), 915-916.
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Recommendations if PSA is high BUT Prostate Biopsy is Negative
Q: if a man tests high on a single PSA or shows some acceleration in PSA with numbers as you suggest AND evaluation by biopsy proves negative, should continued high scores on PSA be ignored? Should avadart or something similar be used to lower the score?
A: I had a number of patients with an elevated PSA. Each was checked out by a urologist with periodic monitoring. The acceleration is something I would particularly careful for. It is pretty unusual to have sexual dysfunction while on T and an alpha –reductase blocker. I usually suggested to patients. One could use Dutasteride (forgot the brand name) instead of Finasteride but it is probably not worth the cost. Overall, dutasteride is a more efficient steroid 5 -reductase inhibitor than finasteride. They have been shown to be protective for prostate cancer. But, as I said previously there are no studies linking TRT to PrCa. Testosterone replacement therapy in men with erectile dysfunction and hypogonadism is associated with a minor PSA elevation.
In a study in hypogonadal men with and without high grade prostatic intraepithelial neoplasia (PIN), which is considered a prostatic precancerous lesion, after 1 year of TRT men with PIN did not have a greater increase in PSA or a significantly increased risk of cancer than men without PIN. These results indicate that TRT is not contraindicated in men with a history of PIN.
Dihydrotestosterone (dihydrotestosterone) is the primary metabolite of testosterone in the prostate and skin. Testosterone is converted to DHT by 5alpha-reductase, which exists in two iso-enzyme forms (types 1 and 2). DHTis associated with development of benign prostatic hyperplasia (BPH), and reduction in its level with 5 alpha-reductase inhibitors improves the symptoms associated with BPH and reduces the risk of acute urinary retention and prostate surgery. A selective inhibitor of the type 2 iso-enzyme (finasteride) has been shown to decrease serum DHT by about 70%.
We hypothesized that inhibition of both iso-enzymes with the dual inhibitor Dutasteride would more effectively suppress serum DHT levels than selective inhibition of only the type 2 iso-enzyme.
DIHYDROTESTOSTERONE (DHT), A STEROID hormone produced from testosterone by the enzyme 5alpha- reductase is the primary active metabolite of testosterone. In male fetal development and puberty, it is essential for normal masculinization of the external genitalia and normal development of the prostate gland. In later life, DHT is associated with the development of benign prostatic hyperplasia (BPH) and androgenetic alopecia. The enzyme 5 alpha-reductase is present throughout the body in two forms, type 1 and type 2. Type 1 has been reported to be located predominantly in the skin, both in hair follicles and sebaceous glands, as well as in the liver, prostate, and kidney. Type 2 is found in the male genitalia and the prostate; recent research has also identified type 1 mRNA and enzyme activity in the prostate.
The first available 5-alpha reductase inhibitor (finasteride) is selective for the type 2 iso-enzyme. Its clinical utility in reducing enlarged prostates, relieving symptoms associated with BPH, and reducing the risk of associated complications has been documented in several clinical trials. More recently, 5 alpha-reductase inhibition has been proven effective in treating androgenetic alopecia. Finasteride suppresses serum DHT by about 70%. Dutasteride is a 6-azasteroid, which inhibits both type 1 and type 2 5_-reductase iso-enzymes. The IC50 for type 1 5 alpha-reductase is 0.7 and 81.0 nm for dutasteride and finasteride, respectively, and for type 2 5 alpha-reductase, 0.05 and 0.16 nm, respectively.
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New Markers for Prostate Cancer
Q: have you used the AMACR in lieu of the PSA? Is AMACR ready to replace PSA as a PC indicator?
A: I have no personal experience with AMCAR. I do not think it is even commercially available. For others a brief background follows with some links to downloadable articles.
Prostate specific antigen (PSA) is a sensitive serum marker for pathology in the prostate (cancer, infection, benign hyperplasia). The level of PSA, however, is poorly correlated with grade and stage of prostate cancer. Genomic and proteomic methodology has recently been used to discover more then 200 putative new markers for prostate cancer like alpha-methylacyl CoA racemase (AMACR), hepsin, glutathione S-transferase ?, EZH2 and DD3(PCA3). To date, none of these markers have been adequately validated for clinical use.
Prostate cancer is the second-leading cause of cancer-related death in American men (1). Although the use of prostate-specific antigen (PSA) screening has led to the earlier detection of prostate cancer, the impact of PSA screening on cancer-specific mortality is still unknown, pending the results of prospective randomized screening trials. Interpretation of the serum PSA test is made on the basis of PSA levels, with levels of 0–4 ng/mL being considered normal and levels of greater than 4 ng/mL being considered clinically significant for prostate cancer screening. A major limitation of the serum PSA test is its lack of specificity for prostate cancer, especially in the intermediate range of PSA levels (4–10 ng/mL). In this range, the specificity of the PSA test to detect prostate cancer has been reported to be only 20% at a sensitivity of 80%. This poor specificity is, in part, associated with the fact that serum PSA levels can be increased in patients with nonmalignant conditions such as benign prostatic hyperplasia or prostatitis and that PSA is highly expressed in both benign prostatic epithelia and prostate cancer cells.
One such prostate cancer biomarker is -methylacyl-CoA racemase (AMACR), an enzyme that catalyzes the racemization of R-stereoisomers of branched-chain fatty acids to S-stereoisomers and plays an important role in peroxisomal -oxidation of branched-chain fatty acids. Differential display and expression array analyses have identified the AMACR gene as a gene whose expression is higher specifically in prostate cancer epithelia relative to benign prostatic epithelia. AMACR
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