musclebeauty

You look incredible damn....your thick and nicely cut...love it

Thankyou very much

Hi there The primary purpose of use is treating androgen deficiencies, age being the most common culprit of the condition. It is, however, also used in pre-pubescent males as well. The hormone is also used as a fertility aid in men and this alone makes it a very unique anabolic steroid as most anabolic steroids tend to have the opposite effect. Proviron is not used to promote large buildups in mass, although it can serve an important purpose during such a phase of training. You will, however, find Proviron to be far more common in cutting cycles, but once again its purpose will be somewhat unique. Proviron will display very low anabolic traits. More importantly for the anabolic steroid user, it will make a larger percentage of the anabolic steroids used available in a free rather than bound state. A simple way to look at it is the anabolic steroids you’re taking become more powerful and potent. Adding in Proviron could possibly help the individual breakthrough a sticking point during his cycle. At some point and time in all cycles the progress begins to wane, and in some cases come to a complete halt. By the way Proviron enhances the total free state of the other steroids being used in a stack, it could possibly help the individual breakthrough this sticking point. Without question the best time to use Proviron will be during the cutting phase. This steroid has the ability to provide a bit of a hardening effect similar to Masteron, but more importantly the hardening effects of other steroids will be enhanced. There are possible side effects of Proviron use; however, this steroid carries one of the highest safety ratings among all anabolic steroids. Typical dosage for woman would be 10 to 20mg a day i would not recommend any higher than that....

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Had a cheat meal over the weekend my favorite pizza hut yum yum a much deserved one...since i am doing the omad fasting diet i dont eat all day till i eat my cheat meal so it was around 4pm when i ate and i love it cause i dont get any bloating whatsoever not like i used to when i ate 5 small meals a day...now gotta wait for another 2 weeks for my next cheat meal....

For Fat Loss, Do You Exercise First or Diet First? "Both!" you just answered, right? Yes, ideally you should start training and improving your diet simultaneously to lose fat. Why? Because... Diet without training just leads to a smaller, still-flabby body... and then the body fat boomerangs back.Training without a complementary diet often leads to zero fat loss, or maybe a little fat loss at first followed quickly by stagnation. "You can't out-train a bad diet," I wrote back in the 90s. For most people, that holds true. But as weird as it may sound to T Nation readers, most folks who want to lose fat say things like, "I need to diet and lose weight first, then I'll think about joining a gym." Maybe they assume every gym is filled with Amazons straight from Paradise Island and chiseled male specimens straight off the latest cover of Men's Health. They're "gymtimidated." But many just think that diet is the most important component of fat loss... and they're not wrong really. But a new study shows that if a newbie wants to lose fat, training first and worrying about diet later may be the smart way to go. The Study Researchers gathered up 2,680 sedentary people between the ages of 18 and 35. All were prescribed 30-minute aerobic workouts using stationary bikes, treadmills, or elliptical machines (their choice). They did these workouts three times a week for 15 weeks. And here's the interesting bit: they were ordered NOT to change their diets. The Results They changed their damn diets anyway! Defying instructions, most participants reduced or dropped the fried foods, sodas, and junk foods in favor of lean meats, fruits, and veggies. Why Did This Happen? In other studies, moderate exercise was shown to decrease preferences for high-calorie, higher-fat foods, probably via changes in dopamine levels. Note that with more intense training, hunger itself may increase, but the preferences for healthier fare could still occur. Or it could be more simple than that. After seeing their bodies begin to change, maybe they just got hooked on feeling good again. The next logical step is to add a diet component to complement their workouts and keep those good feels coming. Let's hope they added weight training to their cardio plans too. The researchers also observed that many of the participants previously believed that "their size was inevitable." No surprise really, since there are many health-at-any-size advocates out there preaching that exact message, which is known in scientific circles as "complete and utter monkey shit." As one researcher pointed out, one healthy habit can promote other healthy habits. In this case, working out first promoted better food choices later. How to Use This Info If you know someone who wants to get in shape and he or she is struggling with making diet changes, push them to get their butts to the gym. According to this study at least, once they're hooked on training the dietary changes will usually come along naturally.

Does Testosterone Cause Prostate Cancer? Back in the 1940's, doctors didn't know much about prostate cancer (or any cancer, for that matter). However, they noted that men with metastatic prostate cancer lived a bit longer when they were castrated. I should rephrase that. They noted that ONE man with metastatic prostate cancer lived longer when he was castrated (1). That's right, the effects of castration on one poor bastard's prostate cancer led several generations of doctors to assume that it was testosterone itself that promoted the disease. Mind boggling, isn't it? The Truth Men with low testosterone don't have anything to fear from TRT (testosterone replacement therapy). It won't increase their risk of developing prostate cancer. Consider the analysis of more than a quarter of a million records of men in Sweden that was released at the annual meeting of the American Urological Association in San Diego, California in 2016. The researchers found that men who'd been prescribed testosterone for longer than a year not only had no overall increased risk of prostate cancer, but their risk of aggressive disease had been reduced by 50 percent. And this is only the most recent of many studies that squelch the myth that TRT causes prostate cancer. Researchers in the United Kingdom looked at 1400 men who had received testosterone replacement therapy for up to 20 years and they found only 14 cases of prostate cancer over the course of the study (2). This prompted the co-author of the study, Dr. Malcolm Carruthers, medical director at the Center for Men's Health in London, to state: "This myth about testosterone replacement therapy being linked to prostate cancer has been rooted deep in medical consciousness for over 60 years, but this paper says no. Testosterone treatment is actually good for the prostate, not bad. References Morgentaler, A., "Testosterone and prostate cancer: an historical perspective on a modern myth," Eur Urol. 2006 Nov;50(5):935-9.Mark R. Feneley MD, FRCS (Urol), Malcolm Carruthers MD, "Is Testosterone Treatment Good for the Prostate? Study of Safety during Long-Term Treatment," The Journal of Sexual Medicine, 06 June 2012.

Wheat, Dairy, Sugar, and Soy If you just focus on macros or calories, these foods don't seem like a big problem. Just consume them in the right amounts, right? Well, not so fast. Sure, their nutrition labels might tell you that whole grain pasta is a great source of fiber; that standard milk is a great source of calcium and a complete protein; that sugar can replenish your glycogen stores; and that soy is a complete source of protein. But their nutrition labels don't tell the whole story. These substances can be an issue – a big one – and possibly the reason you're not achieving the results you want or are suffering constant digestive issues. If these things prevent your gut from functioning properly, then you won't be able to completely digest and absorb what you're consuming. As a result, the food that enters our body can either be stored as fat or treated as an allergen, leading to low-grade inflammation and a host of metabolic issues (1). Here are the four biggest irritants and how your body may be reacting to them. 1. Wheat – The Zonulin Issue Gluten is a divisive issue. Many believe that unless you have celiac disease, it's nothing to worry about, and avoiding it is just a fad. But recent research has shown that most of us would be better off avoiding gluten and its wheat-protein cousin, gliadin. If you just look at the numbers, there isn't much of a difference between pasta and rice. Both have about 130 calories, 25 grams of carbohydrates, a gram of fat, and very little in the way of vitamins. However, wheat pasta contains gluten and gliadin. More and more studies are showing how both contribute to the release of something called "zonulin," a protein that modulates the permeability of tight junctions between cells of the wall of the digestive tract. (2, 3). Researchers are finding that zonulin opens up the spaces between the cells of the intestinal lining, a problem associated with autoimmune diseases and cancer (2, 4, 5, 6, 7). These spaces are indeed supposed to open up naturally, but zonulin basically causes them to open up too much. If you think about our intestinal lining as a pipeline, zonulin puts big holes in it, allowing substances into parts of our body they don't belong, causing hosts of problems such as allergic reactions. It doesn't matter if you're celiac or not. This is how our bodies are responding to the wheat we're eating today. Our bodies look at certain components of wheat as a harmful substances, like bad bacteria, and zonulin is released to open up the tight junctions in our intestinal lining (2). If we're able to keep a strong and intact intestinal lining then we can keep food where it's meant to be, optimizing digestion and limiting any adverse food reactions. This is likely a huge reason why so many people that are non-celiac are going gluten-free – because they feel and perform better without wheat and other gluten-containing foods (8). 2. Dairy – Sugar and Digestion Issues Unfermented dairy (regular milk for example) can also cause us a variety of problems due to the difficulty we have breaking down and digesting the sugar and protein, specifically lactose and casein (9,10). Research has linked excess dairy consumption to fat gain, insulin resistance, acne, osteoporosis, and diseases such as multiple sclerosis (11, 12, 13, 14, 15, 16). Most people don't think of milk as being high in sugar, but it is. In just one cup of milk there can be 13 grams of sugar, which is one reason you may have a better time tolerating yogurt and kefir – the fermentation process breaks down these sugars into beneficial bacteria, making dairy much easier to digest (17). Even though milk is a great source of whey and casein protein, if we aren't able to digest and absorb these proteins properly then they're of no use to us and can cause us more harm than good. You may be wondering, why were we brought up on human breast milk but now cow milk isn't agreeing with us? Well, they're composed of different percentages of whey and casein proteins. Human breast milk is 80 percent whey and 20 percent casein while cow milk is 20 percent whey and 80 percent casein, making cow milk more difficult for us to digest (18). And if the body isn't able to break down and assimilate what's ingested, then we can't put nutrients to work rebuilding our body after a great training session. Interestingly, the popular idea of post-workout chocolate milk was meant to promote muscle protein synthesis and replenish glycogen stores because it's a fast acting carbohydrate and a protein source, but because it's more difficult to digest, it's probably not the best idea. 3. Sugar – The Bacteria Problem Well, this one is obvious, unless you own a soft drink company. But there's more to the story. Overconsumption of sugar and other refined carbohydrates can lead to a whole host of issues from diabetes to bacterial overgrowth (19). A major epidemic right now is the prevalence of candidiasis, otherwise known as a yeast overgrowth (20). When we take antibiotics, they wipe out our entire microbiome, leaving no good or bad bacteria. If we don't replenish our microbiome with good bacteria from probiotics, then this leaves a breeding ground for yeast and other harmful bacteria to prosper (21, 22). This is why many people suffer from gastrointestinal issues after being prescribed antibiotics (23). The intake of sugar/refined carbohydrates feed these harmful bacteria (19), which, among other things, can lead to cravings for MORE sugar and refined carbs. We need an abundance of good bacteria in our large intestine, and when we have more bad bacteria than good, we'll have a difficult time using the food we eat. If this is the case, no matter how high of a quality of protein we eat, we won't get the benefits that we would if our digestion was functioning properly (24). 4. Soy – Impaired Thyroid Function (and More) Similar to these other foods, soy can wreak havoc on our gut lining, specifically resulting in impaired thyroid function (25). Phytoestrogens found in soy products can also disrupt sex hormones. This has been shown to affect ovulation, lower testosterone in men, and decrease fertility in animals (26, 27, 28). Even though it's a complete protein, soy has very low amounts of the essential amino acids tryptophan and methionine, making it a very low-level complete protein (29). If you have soy isolate in your protein shake, the way it's processed can make it even more of a problem. The heat damages the amino acids, further lessening the bioavailability of the protein (30). The amino acid, cysteine, is damaged during the heating process. Cysteine is responsible for supporting glutathione, an antioxidant which is found in high amounts in humans that live the longest (31, 32). In the United States many have turned soy into a primary source of protein, whereas in Asia it has always been more like a condiment, such as soy sauce or a small piece of tofu in a stir fry. On paper, soy looks great for us with its fiber and protein content. But it's extremely difficult to digest, which makes it more of an irritant than nourishment (33). References Cani, P. D., & Delzenne, N. M. (2009). Interplay between obesity and associated metabolic disorders: new insights into the gut microbiota. Current opinion in pharmacology, 9(6), 737-743. Fasano, A. (2012). Zonulin, regulation of tight junctions, and autoimmune diseases. Annals of the New York Academy of Sciences, 1258(1), 25-33. Simpson, M., Mojibian, M., Barriga, K., Scott, F.W., Fasano, A., Rewers, M., and Norris, J.M. (2009). An exploration of Glb1 homologue antibody levels in children at increased risk for type 1 diabetes mellitus. Pediatric Diabetes, 10(8), 563. Di Pierro, M., Lu, R., Uzzau, S., Wang, W., Margaretten, K., Pazzani, C., ... & Fasano, A. (2001). Zonula occludens toxin structure-function analysis: identification of the fragment biologically active on tight junctions and of the zonulin receptor binding domain. Journal of Biological Chemistry. Fasano, A., Fiorentini, C., Donelli, G., Uzzau, S., Kaper, J. B., Margaretten, K., ... & Goldblum, S. E. (1995). Zonula occludens toxin modulates tight junctions through protein kinase C-dependent actin reorganization, in vitro. The Journal of clinical investigation, 96(2), 710-720. Fasano, A. (2011). Zonulin and its regulation of intestinal barrier function: the biological door to inflammation, autoimmunity, and cancer. Physiological reviews, 91(1), 151-175.Wang, W., Uzzau, S., Goldblum, S. E., & Fasano, A. (2000). Human zonulin, a potential modulator of intestinal tight junctions. Journal of cell science, 113(24), 4435-4440. Bronski, P., & Jory, M. M. (2012). The Gluten-Free Edge: A Nutrition and Training Guide for Peak Athletic Performance and an Active Gluten-Free Life. The Experiment.Swallow, D. M. (2003). Genetics of lactase persistence and lactose intolerance. Annual review of genetics, 37(1), 197-219. Chabance, B., Marteau, P., Rambaud, J. C., Migliore-Samour, D., Boynard, M., Perrotin, P., ... & Fiat, A. M. (1998). Casein peptide release and passage to the blood in humans during digestion of milk or yogurt. Biochimie, 80(2), 155-165. Adebamowo, C. A., Spiegelman, D., Danby, F. W., Frazier, A. L., Willett, W. C., & Holmes, M. D. (2005). High school dietary dairy intake and teenage acne. Journal of the American Academy of Dermatology, 52(2), 207-214. Barr, S. I. (2003). Increased dairy product or calcium intake: is body weight or composition affected in humans?. The Journal of nutrition, 133(1), 245S-248S. Berkey, C. S., Rockett, H. R., Willett, W. C., & Colditz, G. A. (2005). Milk, dairy fat, dietary calcium, and weight gain: a longitudinal study of adolescents. Archives of pediatrics & adolescent medicine, 159(6), 543-550. Feskanich, D., Willett, W. C., Stampfer, M. J., & Colditz, G. A. (1997). Milk, dietary calcium, and bone fractures in women: a 12-year prospective study. American journal of public health, 87(6), 992-997. Malosse, D., Perron, H., Sasco, A., & Seigneurin, J. M. (1992). Correlation between milk and dairy product consumption and multiple sclerosis prevalence: a worldwide study. Neuroepidemiology, 11(4-6), 304-312. Turner, K. M., Keogh, J. B., & Clifton, P. M. (2015). Red meat, dairy, and insulin sensitivity: a randomized crossover intervention study–. The American journal of clinical nutrition, 101(6), 1173-1179. Gupta, S., & Abu-Ghannam, N. (2012). Probiotic fermentation of plant based products: possibilities and opportunities. Critical reviews in food science and nutrition, 52(2), 183-199. Martin, C. R., Ling, P. R., & Blackburn, G. L. (2016). Review of infant feeding: key features of breast milk and infant formula. Nutrients, 8(5), 279.Jackson, J. A., Riordan, H. D., Hunninghake, R., & Revard, C. (1999). Candida albicans: the hidden infection. J Orthomol Med, 14(4), 198-200. Sardi, J. C. O., Scorzoni, L., Bernardi, T., Fusco-Almeida, A. M., & Giannini, M. M. (2013). Candida species: current epidemiology, pathogenicity, biofilm formation, natural antifungal products and new therapeutic options. Journal of medical microbiology, 62(1), 10-24. Horn, D. L., Neofytos, D., Anaissie, E. J., Fishman, J. A., Steinbach, W. J., Olyaei, A. J., ... & Webster, K. M. (2009). Epidemiology and outcomes of candidemia in 2019 patients: data from the prospective antifungal therapy alliance registry. Clinical infectious diseases, 48(12), 1695-1703. Ortega, M., Marco, F., Soriano, A., Almela, M., Martínez, J. A., López, J., ... & Mensa, J. (2011). Candida species bloodstream infection: epidemiology and outcome in a single institution from 1991 to 2008. Journal of Hospital Infection, 77(2), 157-161. Jernberg, C., Löfmark, S., Edlund, C., & Jansson, J. K. (2010). Long-term impacts of antibiotic exposure on the human intestinal microbiota. Microbiology, 156(11), 3216-3223. Jandhyala, S. M., Talukdar, R., Subramanyam, C., Vuyyuru, H., Sasikala, M., & Reddy, D. N. (2015). Role of the normal gut microbiota. World journal of gastroenterology: WJG, 21(29), 8787. Doerge, D. R., & Chang, H. C. (2002). Inactivation of thyroid peroxidase by soy isoflavones, in vitro and in vivo. Journal of Chromatography B, 777(1-2), 269-279. Chavarro, J. E., Toth, T. L., Sadio, S. M., & Hauser, R. (2008). Soy food and isoflavone intake in relation to semen quality parameters among men from an infertility clinic. Human reproduction, 23(11), 2584-2590. Jefferson, W. N. (2010). Adult Ovarian Function Can Be Affected by High Levels of Soy, 2. The Journal of nutrition, 140(12), 2322S-2325S. Weber, K. S., Setchell, K. D., Stocco, D. M., & Lephart, E. D. (2001). Dietary soy-phytoestrogens decrease testosterone levels and prostate weight without altering LH, prostate 5alpha-reductase or testicular steroidogenic acute regulatory peptide levels in adult male Sprague-Dawley rats. Journal of Endocrinology, 170(3), 591-599. Kuiken, K. A., & Lyman, C. M. (1949). Essential amino acid composition of soy bean meals prepared from twenty strains of soy beans. J Biol Chem, 177, 29-36. Mariotti, F., Mahe, S., Benamouzig, R., Luengo, C., Dare, S., Gaudichon, C., & Tome_, D. (1999). Nutritional value of [15N]-soy protein isolate assessed from ileal digestibility and postprandial protein utilization in humans. The Journal of nutrition, 129(11), 1992-1997. Alhamdan, A. A., & Alsaif, A. A. (2011). The nutritional, glutathione and oxidant status of elderly subjects admitted to a university hospital. Saudi journal of gastroenterology: official journal of the Saudi Gastroenterology Association, 17(1), 58. Lokuruka, M. N. (2011). Effects of processing on soybean nutrients and potential impact on consumer health: an overview. African Journal of Food, Agriculture, Nutrition and Development, 11(4). D'Adamo, C. R., & Sahin, A. (2014). Soy foods and supplementation: a review of commonly perceived health benefits and risks. Alternative Therapies in Health & Medicine, 20.

Mr. Freeze For those of you unfamiliar with what goes on in a whole-body cryotherapy center, you strip naked except for your underpants, a pair of gloves, and a pair of socks, kind of what you wear to a swinger's party in Oslo. You then walk into a kind of upended tanning bed, but unlike a tanning bed, your head sticks out of the top of it so you look like some super villain who was fatally injured in an industrial accident and then reanimated when they attached his head to a bulky super computer. Then some sprite of a girl, usually in her late teens or early twenties, stops texting long enough to clomp the door behind you and turn the temperature knob to minus 200 degrees Fahrenheit, or somewhere thereabouts. You emerge about three minutes later, well on your way to reduced muscle pain, weight loss, firmer skin, improved sleep, and a heartier immune system, or so the brochures say. Sure, your testicles took receding to a whole new level by catching the next red-eye to Miami, but they'll be back by next Tuesday after they've warmed up a bit. Any Evidence Cryotherapy Works? A just-released study compared the effects of whole body cryotherapy against both cold-water immersion (sitting in ice water) and placebo on athletes who'd done a high-volume, heavy-load workout that resulted in increased soreness, "disturbances of muscle function," and increased inflammation. The authors wrote, "With the exception of CRP (C-reactive protein) at 24 hours, neither cryotherapy intervention attenuated the inflammatory response compared to placebo." As far as accelerating recovery, neither of the cold treatments proved to be more effective than placebo. So yes, applying cold, either through whole body cryotherapy or whole body immersion, appears to quell at least one marker of inflammation. Other studies have found that whole body cryotherapy reduces other inflammatory markers as well, namely TNF-alpha, MMP-9, NF-kappaB, and TGF-beta, although these were done over multiple sessions and mostly in patients with inflammatory diseases as opposed to workout-related soreness. It really doesn't look like cryotherapy does much to speed up recovery – let alone any of that other aspirational stuff – but even if it did, lifters should look at inflammation, or at least acute inflammation, as their friend and nobody wants to drive away a friend. All Fired Up Chronic inflammation is bad. It's the response to any injury or infection that sticks around a long time. Acute inflammation, however, is essential to healing. Without it, knife wounds would never close. Paper cuts would bleed forever. Hickeys would last a lifetime. You get the idea. Acute inflammation is also what leads to muscle growth. When you damage your muscle cells through exercise, non-phagocytic macrophages come surging in like Aquaman and his gilled allies to bathe the injured muscle fiber in the growth hormone IGF-1, which significantly increases the rate of muscle regeneration. Exercise-damaged muscle cells also release cytokines, which results in decreased levels of myostatin, the protein that tells the body to stop growing muscle (less myostatin equals more muscle). Low-level inflammation also brings about a rise in cyclooxygenase (COX) enzymes, which play a big part in initiating satellite cell proliferation, differentiation, and fusion. (Satellite cells are dormant cells that spring to life after injury to form new muscle cells.) Clearly, you need acute inflammation in order to make muscles grow, and whole body cryotherapy, even if it works a little, would work contrary to your goal. (The same is true of NSAIDS – non-steroidal anti-inflammatory drugs.) It is true, however, that cryotherapy or NSAIDS could make aches and pains go away a bit faster, but this seems like a strategy more suited to people who play some sport where they're required to perform at a high level day in and day out – not weight lifters who need to come back bigger and better each time they train. What Should You Use Instead of Cryotherapy? If you're really uncomfortable after a workout and you want some relief, go ahead and try a session at a cryotherapy center, but if freezing yourself seems like too damn much trouble, you could probably get away with using some acetaminophen, which is more of an analgesic than an anti-inflammatory. Curcumin would be a better choice, though, as it blocks a host of inflammatory responses by a reasonable percentage rather than stopping any one particular response by 100 percent.

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Trained legs today....now lets see this is what my leg routine looks like.... -10 sets of walking lunges deep -5 sets of leg extensions light weight so i go upto about 50 to 75 reps per set. -Inner and outer thigh machine 5 sets each again light weight reps upto 150 -lying down leg curl light weight 5 sets of 100 reps per set. Than usually i cant walk so i go and do cardio on the bike for about 40 mins to help loosen my legs a bit....

We've long speculated that certain steroids and prohormones (like 4-AD or the new 4-AD-EC) might be okay to use for extended periods of time with little or no side effects. Although we've seen evidence of this in the real world, we decided to ask Cy Willson to delve into the pharmacology behind this type of usage and report back to us on its feasibility. This article will sum up his findings and provide guidelines to those who want to give long term usage a shot. Anabolic steroids. You gotta love 'em. After all, what other substances allow you to achieve so much in such a short time frame? Steroids improve the two aspects of living often referred to as the "spice of life": more muscle and less fat. And on top of that, you'll feel pretty damned good about the world when on them, at least in most cases. (Okay, maybe that's just my version of the "spice of life," but I digress.) The results you get when "on" are so remarkable that you may be tempted to stay on for extended periods. Not a good idea. But there may be a way to do this while minimizing or even avoiding most side effects. The same may also be true for legal steroids like prohormones or prosteroids. What I'm going to do is let you in on a way to continually stay on a few select androgens while causing a minimal amount of inhibition when it comes to your endogenous Testosterone production. I'm going to explain what the two main determinants are that essentially cause inhibition of endogenous Testosterone production, explain how to minimize this, and list which drugs or supplements are best to use. Essentially, the fate of Testosterone production depends on both the AR and ER. The AR (Androgen Receptor) The first determinant of how well any given androgen will inhibit endogenous Testosterone production is the degree to which it binds to the androgen receptor. Hence, the stronger or more avidly it binds to the AR, the more it will inhibit Testosterone production. How do I know? Glad you asked! Get ready for my usual flood of studies. First, in one study using normal men, they found that "blocking" the androgen receptor (using a nonsteroidal androgen receptor antagonist called flutamide)and hence preventing androgens from binding to the AR, caused an increase in LH (luteinizing hormone). As you might know, LH signals the testicles to produce Testosterone. (1) In short, no binding of androgens, no decrease in Testosterone. In another study, dihydrotestosterone (DHT), which binds to the AR even better than Testosterone, was given to twelve normal men for a period of ten days. What did they find? Testosterone, both free and unbound, as well as LH, were significantly reduced. (2) Binding of androgens? A decrease in Testosterone. In yet another study, researchers gave normal men either Testosterone by itself or Testosterone along with testolactone (Teslac), an aromatase inhibitor which prevents Testosterone from converting to estrogen, and evaluated the effects on LH. In the group that only received Testosterone, they found a 50% reduction of LH and a 50% increase of estradiol. However, in those receiving both Testosterone and testolactone there was no increase in estradiol, but there was still a significant reduction of LH. This means there's definitely another way in which androgens inhibit endogenous Testosterone production, aside from conversion to estrogen. The degree to which they bind to the AR is surely that other mechanism. (3) DHT was also found to suppress LH even greater than Testosterone alone. (4) This idea is also supported in other ways. Take a look at trenbolone acetate (TA), which is far more androgenic. TA binds to the AR much more avidly than Testosterone and as such it's nearly three times as antigonadotropic. (5) Nandrolone also binds well and is extremely effective at binding to the AR, although the fact that it promotes progesterone may contribute to its potent effects in terms of reducing LH and Testosterone. (6,7) In short, it's pretty conclusive that the tighter a steroid binds to the androgen receptor, the more it ends up inhibiting your own production of Testosterone. The ER (Estrogen Receptor) Okay, now this portion shouldn't be much of a surprise to most of you. When an androgen is converted (aromatized) to an estrogen, that estrogen will then bind to estrogen receptors in the hypothalamus and pituitary and thus cause suppression of LH secretion. After all, this is the mechanism through which anti-estrogens such as clomiphene exert their "Testosterone-boosting" effects. By simply acting as estrogen antagonists at the ER, they increase LH levels and in turn increase Testosterone production. This is the same reason why anastrozole (Arimidex) is effective at increasing LH and Testosterone, since it inhibits estrogen formation all together. (8,9) So, with this in mind, using an anti-estrogen along with an androgen that aromatizes should at the very least reduce the severity of LH and consequently, Testosterone secretion. A study that supports this notion consisted of 47 healthy young men either receiving KTCZ (a drug that inhibits Testosterone formation) alone, KTCZ along with estradiol, KTCZ and Testosterone, or KTCZ, anastrozole (Arimidex) and Testosterone. Of course, there was also a placebo group. What did they find? When administering estrogen or Testosterone without the aromatase inhibitor, LH was decreased significantly. However, when Testosterone was given along with anastrozole, no effect was seen on LH. In other words, there was no suppression. (10) Awesome right? Well, yes, but the only problem is that they were using ten milligrams per day and that's just a bit excessive. I think one milligram would be sufficient for our intended purposes. The take home message is that if estrogen binds to the estrogen receptor, it ends up causing a decrease in your own production of Testosterone. Putting It All Together Now that I've provided this info you're probably wondering how it will apply to you. Well, with the two mechanisms above in mind, we can conclude that an androgen that doesn't bind very avidly to the AR and doesn't aromatize to estrogen would be the best in terms of preventing an excessive reduction of endogenous Testosterone production. So, with this reasoning, if you were to use something like methandrostenolone (D-bol), along with anastrozole or an estrogen antagonist of some sort, you could prevent most of the suppression of LH and endogenous Testosterone. (D-bol alone, however, causes around a 50% reduction of LH and a 69% reduction of Testosterone in normal men). Stanozolol (Winstrol) would be a good candidate for a long-term drug but one study showed it to decrease Testosterone by 55%. True, it isn't as much of a reduction as D-bol, but I think the fact that it works by binding to androgen receptors is the reason for the reduction. Fluoxymesterone (Halotestin/Stenox) is probably the closest thing to an illegal steroid that we could use long-term, aside from D-bol used in combo with an anti-estrogen. The drug was shown to have no effect on LH in normal men. (11,12,13) As far as legal steroids, we need to take a long hard look at 4-AD. This is probably the best option aside from D-bol along with anastrozole (Arimidex) or an estrogen antagonist (clomiphene). First, 4-AD doesn't bind well to the AR so it must work via some non-AR mediated mechanism. Secondly, it doesn't aromatize so this makes it a perfect candidate for long term usage. Essentially, that's why I've written this article. With a few select androgens, you can stay on for a longer period of time without having to worry about suppression of your endogenous Testosterone production. This will also help to alleviate some of the "crash" most guys experience after coming off of a cycle. Of course, when you include the fact that the two androgens I did mention are 17 alpha-alkylated, this limits the amount of time you should be using them because of liver toxicity issues. The only other option that leaves us with would be low dosages of Testosterone (<200 mg per week) taken concurrently with anastrozole or 4-AD. Even so, the overall winner in each case is 4-AD. If you look at 4-AD, it isn't 17-AA, doesn't aromatize, and doesn't bind well to the AR. Now, there's still one problem you need to consider and this is inherent of most androgens: a potentially negative effect on blood lipids. Well, considering that 4-AD actually increasesendogenous Testosterone production to a high normal range, this will actually decrease LDL and increase HDL. In other words, it may actually be good for your blood lipids. (14-17) But then again, we still have to remember that this is an androgen so I suppose we should still be somewhat cautious here. Even so, negatives effects seen with changes in blood lipids don't occur immediately and take years to develop. With that being said, I'm going to take a middle of the road approach and recommend 100 to 200 mg of 4-AD per day for 12 to 16 weeks without taking a break. After 16 weeks, you'll only need to take two weeks off and then you may repeat for another 12 to 16 weeks and so on. The best version of 4-AD in terms of bioavailability and duration of action would be 4-AD-EC. If you decide to go with D-bol and anastrozole, try 50 to 75 mg per day along with 1 mg of anastrozole. Remember though, it's a 17-AA androgen so there's the risk for liver toxicity with prolonged usage. With fluoxymesterone, you can try 15 to 40 mg per day, but once again it's 17-AA so the same reasoning applies. Again, the 4-AD-EC route is the best in terms of safety. The fact that it's legal makes it a nice choice, too. Armed with all this info, I wish you luck on your "never ending" cycle! Highlights for Long-Term Usage: • D-bol in combo with anastrozole might be the safest, although liver problems are a risk. • Halotestin is also an option, but it possesses the same potential for liver damage as the D-bol. • 4-AD, or 4-AD-EC, definitely seems to be the safest for long-term usage (possibly up to 16 weeks at a time). References Cited 1) Urban RJ, et al. "Acute androgen receptor blockade increases luteinizing hormone secretory activity in men." J Clin Endocrinol Metab 1988 Dec;67(6):1149-55 2) Kuhn JM, et al. "Effects of 10 days administration of percutaneous dihydrotestosterone on the pituitary-testicular axis in normal men." J Clin Endocrinol Metab 1984 Feb;58(2):231-5 3) Marynick SP, et al. "Evidence that testosterone can suppress pituitary gonadotropin secretion independently of peripheral aromatization." J Clin Endocrinol Metab 1979 Sep;49(3):396-8 4) Santen RJ. "Is aromatization of testosterone to estradiol required for inhibition of luteinizing hormone secretion in men?" J Clin Invest Dec;56(6):1555-63 5) Neumann F. "Pharmacological and endocrinological studies on anabolic agents." Environ Qual Saf Suppl 1976;(5):253-64 6) Knuth UA, et al. "Clinical trial of 19-nortestosterone-hexoxyphenylpropionate (Anadur) for male fertility regulation." Fertil Steril 1985 Dec;44(6):814-21 7) Tafurt CA, et al. "Effects of progestin-estrogen combination and progestational contraceptives on pituitary gonadotropins, gonadal steroids and sex hormone-binding globulin." Fertil Steril 1980 Mar;33(3):261-6 Hayes FJ, et al. "Aromatase inhibition in the human male reveals a hypothalamic site of estrogen feedback." J Clin Endocrinol Metab 2000 Sep;85(9):3024-6 9) Mauras N, et al. "Estrogen suppression in males: metabolic effects." J Clin Endocrinol Metab. 2001 Apr;86(4):1836-8 10) Schnorr JA, et al. "Aromatization mediates testosterone's short-term feedback restraint of 24-hour endogenously driven and acute exogenous gonadotropin-releasing hormone-stimulated luteinizing hormone and follicle stimulating hormone secretion in young men." J Clin Endocrinol Metab 2001 Jun;86(6):2600-6 11) Holma P, Adlercreutz H. "Effect of an anabolic steroid (metandienon) on plasma LH-FSH, and testosterone and on the response to intravenous administration of LRH." Acta Endocrinol (Copenh) 1976 Dec;83(4):856-64 12) Small M, et al. "Alteration of hormone levels in normal males given the anabolic steroid stanozolol." Clin Endocrinol (Oxf) 1984 Jul;21(1):49-55 13) Jones TM, et al. "The effects of fluoxymesterone administration on testicular function." J Clin Endocrinol Metab 1977 Jan;44(1):121-9 14) Zhao S, et al. "Plasma levels of lipids, lipoproteins and apolipoproteins affected by endogenous testosterone." Hunan Yi Ke Da Xue Xue Bao 1998;23(3):299-301 15) Shapiro J, et al. "Testosterone and other anabolic steroids as cardiovascular drugs." Am J Ther 1999 May;6(3):167-74 16) Zmuda JM, et al. "Longitudinal relation between endogenous testosterone and cardiovascular disease risk factors in middle-aged men. A 13-year follow-up of former Multiple Risk Factor Intervention Trial participants." Am J Epidemiol 1997 Oct 15;146(8):609-17 17) Barret-Connor EL. "Testosterone and risk factors for cardiovascular disease in men." Diabete Metab 1995 Jun;21(3):156-61

Have you ever been promised something that sounded so great you almost wet your pants? Well, then you know a little about how Ponce de Leon felt. He, while on a conquest of the New World (Columbus's second trip to the Americas), was promised a "fountain of youth." After many years of searching, he never did find that fabled fountain. Now, five hundred years later, we're still searching for it, and Ponce looks every bit his age. The idea of eternal youth resurfaced big time in mainstream America in the late 1980's. Judging by all those plasticized, liposucked, and Botoxed women in South Beach and on Rodeo Drive, I'd say the quest for eternal youth is still going strong. But what if I told you that you could take a simple little injection that would help you slash body fat, restore your skin to its tautness of yesteryear, and perhaps even add years to your life? Wouldn't you also want to dive headfirst into this potential fountain of youth? A Little Background As most of you probably guessed, today's fountain of youth (and perhaps what Ponce was looking for) is growth hormone. Human Growth Hormone (hGH or GH), is one of several endocrine hormones. "Endocrine" means that the hormone is produced in one place (in this case, the anterior pituitary), but its action occurs elsewhere (throughout the body). Some of the other endocrine hormones are estrogen, progesterone, Testosterone and DHEA. GH is also known as somatotropin. It's made up of 191 amino acids (a polypeptide) and its release can be stimulated by growth hormone releasing hormone (GHRH). In other words, the anterior pituitary will release GH if GHRH is secreted from the hypothalamus. Increase GHRH and you'll increase GH. You'd expect that if you administered exogenous GHRH, the body would respond by overproduction of GH, but sorry, it doesn't. So forget trying to use GHRH in this manner. The natural overproduction of GH results in acromegaly (think Andre the Giant), while underproduction results in dwarfism (think Hank, the Angry Dwarf). How are "normal" GH levels determined? Normally, the body produces about 500 micrograms of GH daily from a total of six to eight pulse secretions. This "normal" number decreases as we age. GH levels decline by about 14% per decade after the age of 30. Obviously, the time period in our lives when our GH levels are at their peaks is during the adolescent years. Doctors can normally determine if your body is producing enough GH by a few different means. The most utilized test for GH – the gold standard – is the insulin tolerance test (ITT). Other reliable tests include employing arginine infusions (500 mg/kg infused over a 30-minute period), oral L-dopa (500 mg for an adult), clonidine (4 mcg/kg orally), or even sleep or twenty minutes of vigorous exercise. Depending on the test employed, the determination of your GH level can be at the twenty-minute mark or as much as 120 minutes after you started the test. If you have any of these tests done and your GH is determined to be less than 10 nanograms per deciliter (<10 ng/dl), you're more than likely GH deficient. Currently, the FDA has approved GH for Adult GH Deficiency. Therefore, it's legal and ethical for a physician to prescribe GH therapy. For methods of testing your GH at home, see the article Hormone Testing at Home published a while back in T-mag. As an aside, several medications are known to increase GH levels. Most of these medications are neuroendocrine (by extension used in psychiatry). These medications include Zolmitriptan, Clonidine, Apomorphine, Baclofen, Bromocriptine, Pergolide mesylate, L-692,429 and L-163,255 (compounds in development by Merck), ghrelin (a developmental drug) and other dopamine and GABA agonists. Please note that the duration of elevated GH from any of these medications isn't yet defined. Why do athletes use GH? The short answer is because they can. However, the real question should be, is it beneficial for the athlete to take GH? Besides wanting to look like Arnold, the answer is yes. And in fact, that benefit stretches all the way to those people who are looking to lose weight and cut body fat. Most high-level bodybuilders use GH in order to gain muscle, which is a mistake. While it's true that GH enhances protein synthesis rates (as does exercise and the ingestion of amino acids), it doesn't directly translate into new muscle growth. Unfortunately, bodybuilders hear about the increased protein synthesis and think that it means an easy path to larger muscles. It's interesting to note that the greatest abundance of GH receptors is along the intestinal tract. So, it's not surprising that most GH-using pro-bodybuilders look pregnant! Medically, GH is used for people with intestinal disorders such as short bowel syndrome. The incorporation of GH into their therapy aids in absorption of protein and other nutrients in order to sustain life, much different than that bloated guy onstage doing his best not to lay tracks while going through a posing routine. What about GH as an "Anti-Aging" medicine? Those who sell GH cite several reasons as to why GH levels decline as we age. For starters, while the body has a hormone that enhances the secretion of GH, it also has a counter-regulatory hormone known as somatostatin. It's thought that as we age (past the age of 40) somatostatin activity increases, thus GH production falls. So some anti-aging docs pharmaceutically look to alter somatostatin activity as a means to bolster GH levels back to those of the younger years. Another thought is that GHRH (the releasing hormone) becomes less sensitive to signals from the hypothalamus, thus less GHRH is produced and even worse yet, your GH levels fall. Another theory is that the cell receptors for GH throughout the body become less responsive to GH and don't let it bind, so the GH never totally reaches its target tissue. The proponents of GH therapy as an anti-aging medicine claim that they can help you gain muscle without exercising, improve sexual function, reduce wrinkles, enhance bone density, improve your memory, enhance wound healing time, bolster the immune system and improve heart function. Some people claim that GH can also promote the regrowth of heart, liver, spleen, kidneys and other internal organs that "shrink" with age. I'm not sure whether that would work or not, but the claims exist nonetheless. Research with GH in the older population has generally yielded positive results. In fact, Dr. Jeffrey Blumberg of Tufts University recently stated, "Aging is a disease! We could save billions of dollars if we could delay the onset of chronic diseases by as little as ten years. There are more anti-aging agents than you can imagine and probably more that science can discover in the next century. But many of these barriers to aging are here now, right in front of our faces in the form of vitamins, minerals, natural enzymes, amino acids and other natural substances. Evidence is piling up, showing how they can fight aging. Prestigious medical journals are full of reports, unimaginable ten years ago, documenting the awesome powers of such natural substances to prevent, halt and reverse the deterioration that comes with advancing years." In the paper from where this quote was taken, direct reference to the studies on GH replacement were made. These studies demonstrated that GH replacement might, as Cher would sing, "turn back time." Furthermore, according to Steven Grinspoon, M.D. of Harvard Medical School, GH replacement therapy can have a positive effect on body composition and blood lipids (reducing the bad cholesterol, LDL), in addition to enhancing bone density (good for fighting osteoporosis) and cardiac function. These are the real benefits; the ones that aren't usually marketed. What are the downsides of using GH? Downsides, besides having the guts of today's professional bodybuilders? There are a few, but it's important to understand that the downsides are usually related to GH abuse or overuse. The first concern is that overdoing it with GH can cause fluid retention and high blood pressure as well as carpal tunnel syndrome. Minor muscle aches can also occur. The major side effects can be lengthening of bone plates (often visually observed as changes in the jawbone, forehead and feet) and insulin resistance (which can turn into diabetes). It may also turn on cancer "on and off" switches known as oncogenes, which may progress to various forms of cancer. What are the upsides of using GH? The positives, like the negatives, are dose related. Think of it this way, the higher the dose you take, the greater the chance you'll experience a negative side effect. However, strong research is accumulating that low dose GH is the way to go for body-fat reduction or reducing the risks of diabetes and heart disease. Eight good clinical trials have been published recently in top tier medical journals indicating the low-dose GH therapy is the way to go for altering body composition. One study examined seven years of low dose GH replacement. The scientists found that an average daily dose of 1.83 IU (or 0.61 mg/day) per day significantly reduced body fat while actually improving insulin sensitivity! In yet another study of 595 adults, low-dose GH treatment resulted in a 4.38% increase in lean body mass and a body fat reduction of 6.35%. Interestingly enough, it appears that gender makes a difference as men had more favorable results than females. In all of the "low dose" studies, the only side effect noted was arthralgia (muscle aches) and that occurred in the conventional treatment group (they received the normal GH replacement dose (0.0125 mg/d). What is a "low-dose"? Low dose treatment or usage of GH is typically in a range of 0.05 mg to 1.0 mg/day. Most people start high and reduce their GH dose as time marches on. (Note: To understand the milligram (mg) and International Units (IU's) equivalence thing, the rule of thumb is that one milligram equals three IU.) Most therapeutic long term treatments geared toward fat loss and enhanced lean-body mass are safely engaged with lower than normal doses. (The goal is maximum long term benefit with little to no downside, thus no need for conventional dosing). Bodybuilders, on the other hand, will take ten or more IU's daily, thus not really reaping the benefits of Ponce de Leon's dream. Remember that all good clinical trials have used lower doses than what bodybuilders tend to use and have yielded great results. If you want life extension and/or a greater quality of life, then listen to the research. Where do people get GH? Believe it or not, you can get GH from your physician. Good luck, though. Many doctors don't understand why someone would want to use GH to lose weight or increase their vitality. The sad fact is that many physicians aren't well read in this arena, thus they'll give you a hard time. However, there are many good physicians and centers that will help you if you wish to have your GH levels tested. It's very easy to get GH if you're found to be GH deficient as an adult. Some places to contact if you're interested in learning more about GH for fat loss are: • Clinical Research for Human Growth Hormone. Their website is GrowthHormoneTherapy.net, phone number 800-815-7443. • American Academy of Anti-Aging Medicine. Their website is HumanGrowth-Hormone.org, phone number 1-866-DIAL-GH. • AA & T Clinics in Atlanta, Georgia. Their websites are RenewMan.comand RenewWoman.com. Phone number 800- 859-7511.

Thankyou yeah i found it very interesting

Keep up the great work guys obviously it's paying off for both of you as for myself I do the omad fasting diet and I freaking love it same as you guys I have tons of energy and sometimes don't know what to do with it so the odd time I actually end up going back to the gym after I'm done even work

No problem funlog let me know how they turn out for u

Please let me know for sure....

Welcome aboard

Welcome aboard

Welcome aboard

Welcome aboard good to have another canadian....

Welcome aboard

Welcome aboard