THE REVOLUTION IS HERE – HCGENERATE ES IS NOW ON SALE!
Limited quantity is available, get it while you can.
What is HCGenerate ES?
What is the Difference between HCGenerate and HCGenerate ES?
THE REVOLUTION IS HERE – HCGENERATE ES IS NOW ON SALE!
Limited quantity is available, get it while you can.
What is HCGenerate ES?
What is the Difference between HCGenerate and HCGenerate ES?
Skinny by Nature – the new hit series present by N2BM
Today, we are going to do is destroy the theory that anyone can get huge by eating right, working out right and using steroid cycles that would make Lee Preist and Ronnie Coleman call you crazy. The fact of the matter is it takes 3500 calories to gain a pound of muscle, which over the course of a day isn’t really that hard if you’re focused and ready for the huge challenge everyday.
You all have heard the line – “just up your calories but make sure to eat food , as protein shakes are a waste of money.” Yea the hell with that get your calories in the easiest way you can if you have to use shakes do it. Bad genes are indeed a real deciding factor sometimes, so your question is what are bad genes? Well, in short, it’s when no matter how hard you try you will never reach the genetic potential of say a Dennis Wolf because your body simply isn’t designed to reach those results. You yourself have a small body structure, small wrists, baby ankles and legs with no calves. Now this doesn’t mean you can’t look great, it just means you are never going to look like a walking refrigerator. Now I can hear the naysayers saying: well I was 109lbs my senior year of high school and now at 21 I’m huge and weight 175lbs. This means you have half way decent genes, so consider yourself very lucky. Men generally stop growing around the ages of 21 to 25, and, chances are, if you’re 25 years old or older and still 110lbs – you might just have bad genes.
While I throw all this negative information at you, I will now provide a light at the end of a dark tunnel. First off all, the guys out there that say it’s easy just eat more, fix your diet and train are normally guys that aren’t true ectomorphs and have no idea what a real ectomorph is. As I stated before, it takes 3500 calories to gain a pound of pure muscle mass. Thus, lets say you’re a newbie and want to go from 110lbs to a 130lbs; Easy, just eat junk food right?….wrong! If you’re a hardcore ectomorph you’re going to have to work as hard at eating as you do in the gym to get the results you want. You wanna get big and muscular not big and fat, so tune in your diet with chicken, milk, a great weight gainer etc., use N2BM Forums to get ideas on diets. Now, I’m going to tell you ectomorphs out there something that will change your life forever, so write this down, put it in your smartphone, get it tattooed on your arm – but wait a minute! before I tell you put down your drink and sit down I’ll wait……make sure you’re done drinking…….are you done drinking?…..good, now sit down, comfy - good…..ok good here we go. As an ectomorph your going to have to eat at least 3500 calories a day EVERYDAY pretty much FOREVER or as long you want to keep your muscle mass or until your body slows down, as, normally, ectomorphs have a fast metabolism.
As you put on mass, you’re going to need more calories. This is going to require dedication and money because food, supplements and protein prices aren’t cheap. So the next time someone gives you the old tired bulk up lines just tell them everyone is different and genes do play a role when it comes to bodybuilding. While you won’t look like Arnold, you can be the best you you can be, and, generally, 20lbs. of muscle over the course 3 to 6 months isn’t too shabby; remember, 20lbs is a hell of a lot of weight. Trust me, people will notice as you grow and will compliment you, which of course is always nice and those kind of muscle look great on anyone, so remember to enjoy your hard work as well.
Until next time! Stay hungry my friends.
Diet Suggestions for Ectomorphs
Ketotifen is a second-generation noncompetitive H1-antihistamine and mast cell stabilizer with a half life of around 12 hours. Due to its antihistiamine properties, it will bring down regulation of the beta receptors to a halt which we delve into more eventually. It is most commonly sold in as a salt of fumaric acid, ketotifen fumarate, and is available in two different deliveries. We as weekend warriors want to use its oral form, which is used to prevent asthma attacks. Side effects include drowsiness, weight gain, dry mouth, irritability, and increased nosebleeds, appetite, change, diarrhea, chills, increased sweating and insomnia. (http://www.pharma.us.novartis.com/product/pi/pdf/zaditor.pdf)
Individuals with wasting syndrome lose muscle aka lean body mass rather than body fat which is due to the lack of anabolic hormones in their body. Several possible alternatives to the approved drugs for AIDS-related wasting are discussed, one of them being Ketotifen. TNF inhibitors prevent inflammation from causing diseases such as Chron’s disease. As a reminder, inflammation is the biggest cause of all diseases. TNF-inhibitors also increase hunger as a decrease inflammation tends to lead in an increase in metabolic rate. This would make perfect sense since an elevated metabolic rate is associated with a healthy immune system. A study combining ketotifen and oxymetholone, the oral anabolic steroid, was presented at the Ninth International AIDS Conference. Preliminary data from a study combining ketotifen and oxymetholone showed that 18 out of 22 patients gained an average of 11.4 pounds after treatment of an average of 3.9 weeks. Sure it was not ketotifen alone, but considering their state of condition, it sure did not counter the effects of oxymetholone. (Smart T. GMHC Treat Issues. 1995 May;9(5):7-8, 12.)
The aim of this study I came across was to identify the sites of the inhibitory action of TNF-alpha (tumor necrosis factor alpha) on LH/hCG injections-stimulated testosterone formation. By using cultured porcine Leydig cells as a model, TNF-alpha was shown to inhibit testosterone secretion when testicular cells were stimulated with hCG but not when incubated with 22R-hydroxycholesterol (a cholesterol substrate derivative that readily passes through cell and mitochondrial membranes). Such an observation suggested that the cytokine may affect cholesterol transport and even the availability to cytochrome P450scc in the mitochondria. Specifically, we report here that TNFalpha reduced in a dose- and time-dependent manner hCG-induced StAR (steroidogenic acute regulatory protein) levels. The maximal and half-maximal effects were obtained with 20 ng/ml and 1.6 ng/ml of TNFalpha, respectively. Maximal inhibitory effects of TNFalpha on StAR messenger RNA and protein levels were obtained after 48 h of treatment. Additionally, the presence of TNFalpha receptors P55 in terms of protein (identified through cross-linking experiments) and messenger RNA (identified through RT-PCR analysis) suggested that the effects of the cytokine are directly exerted on the testicular steroidogenic cell type. So in essence TNF alpha as it rises lowers levels of testosterone. Since, ketotifen is a TNF alpha inhibitor; it may indirectly increase testosterone levels quite substantially; especially if one may be at stake for waste syndrome. (Mauduit C, et.al Endocrinology 1998 Jun;139(6):2863-8)
I am going to take it one step further and show documentation of a study in which testosterone injections LOWERED levels of TNF alpha in hypogonadal men. Testosterone has immune-modulating properties, and current in vitro evidence suggests that testosterone may suppress the expression of the proinflammatory cytokines TNFalpha, IL-1beta, and IL-6 and potentiate the expression of the anti inflammatory cytokine IL-10. That is not to say that testosterone does not suppress the Immune system. When testosterone gets to high the body starts to produce less auto immune hormones to make more anabolic hormones. Back to the study; researchers reported a randomized, single-blind, placebo-controlled, crossover study of testosterone replacement in the form of Sustanon 100 vs. placebo in 27 men ranging in age from 53 to 71 years old with low levels of total and free testosterone. When the men were injected with testosterone, levels of TNF alpha and IL-1 beta dropped notably. Levels of cholesterol had also dropped significantly which shows the heart protective properties of keeping TNF-alpha under control. In conclusion, testosterone replacement shifts the cytokine balance to a state of reduced inflammation and lowers total cholesterol. Twenty of these men had established coronary disease, and because total cholesterol is a cardiovascular risk factor, and pro inflammatory cytokines mediate the development and complications associated with atheromatous plaque, these properties may have particular relevance in men with overt vascular disease. Another reason why a study in the future should be done on Ketotifen and its affects on sex hormones, I predict good things to come from a study of that kind. If you ask me, I will tell you it’s one heck of a drug and should be used in pct, not only because of its positive effects on testosterone but also IGF-1 which we will get into next. (Malkin CJ et.al. J Clin Endocrinol Metab. 2004 Jul;89(7):3313-8.)
In this study, Conscious rats were injected intravenously with recombinant human TNFalpha or vehicle for 24 h. TNFalpha decreased the concentration of both total and free IGF-I in the plasma by 30-40%. This change was associated with a reduction in IGF-I mRNA expression in liver by 39%, gastrocnemius by 73%, soleus by 46% and the heart by 63%, but a 2.5-fold increase in the whole kidney. What I found interesting was that TNFalpha did not alter IGF-II mRNA expression in skeletal muscle. TNFalpha also increased IGFBP-1 in the blood (4times-fold) and this response was associated with an increase in IGFBP-1 mRNA expression in both liver (3times-fold) and kidney (9times-fold). However, IGFBP-3 levels in the blood were reduced 38% in response to the injection of TNFalpha. This change was accompanied by a 60-80% reduction of IGFBP-3 mRNA in the liver and kidney but no significant change in muscle. Hepatic mRNA levels of the acid-labile subunit were also reduced by TNFalpha by 46%. Finally, tissue expression of mac25 (also referred to IGFBP-related protein-1) mRNA was increased in gastrocnemius by 50% but remained unchanged in the liver and kidney. These results more fully characterize the changes in various elements of the IGF system and, thereby, provide potential mechanisms for the alterations in the circulating IGF system as well as for changes in tissue metabolism observed during catabolic insults associated with increased TNFalpha expression. As you see the same applies to IGF-1, the more the TNF alpha the less available IGF one will have. When a TNF inhibitor is presented, IGF levels will rise. (Lang CH et.al Growth Horm IGF Res 2001 Aug;11(4):250-60)
When individuals train hard, TNF alpha has been shown to rise. Of course we know that if you were to take ketotifen post training it would not be as great as prior to training but that is still fine. Caffeine in moderate doses is shown to increase performance yet keep cortisol lower compared to those who train without it. I simply suggesting that taking Ketotifen prior to training like most do will still provide the intended anti-catabolic effects that I theorize about. As I mentioned before, we need more studies done with ketotifen especially regarding its effects on the endocrine system. (Pedersen BK et. al. Exerc Immunol Rev 2001;7:18-31)
Mast cell activation is thought to be involved in visceral hypersensitivity, one of the main characteristics of the irritable bowel syndrome (IBS). A study was therefore undertaken to investigate the effect of the mast cell stabiliser ketotifen on rectal sensitivity and symptoms in patients with IBS. 60 patients with IBS underwent a barostat study to assess rectal sensitivity before and after 8 weeks of treatment. After the initial barostat, patients were randomized to receive ketotifen or placebo. IBS symptoms and health-related quality of life were scored. In addition, mast cells were quantified and spontaneous release of tryptase and histamine was determined in rectal biopsies and compared with biopsies from 22 age- and gender-matched healthy volunteers. Ketotifen but not placebo increased the threshold for discomfort in patients with IBS with visceral hypersensitivity. This effect was not observed in normosensitive patients with IBS. Ketotifen significantly decreased abdominal pain and other IBS symptoms and improved quality of life. The number of mast cells in rectal biopsies and spontaneous release of tryptase were lower in patients with IBS than in healthy volunteers. Spontaneous release of histamine was mostly undetectable but was slightly increased in patients with IBS compared with healthy volunteers. Histamine and tryptase release were not altered by ketotifen. This study shows that ketotifen increases the threshold for discomfort in patients with IBS with visceral hypersensitivity, reduces IBS symptoms and improves health-related quality of life. Whether this effect is secondary to the mast cell stabilising properties of ketotifen or H(1) receptor antagonism remains to be further investigated. (Gut. 2010 Sep;59(9):1213-21. Epub 2010 Jul 21.)
Combining Ketotifen with other agents
Due to ketotifen’s beta receptor upregulating properties, can be used as aid to one’s clenbuterol cycle. After a week or two on Clen, your beta 2 receptors will be saturated and down regulated. ketitofen will prevent this and even increases fat loss with its upregulating effect on the beta 3 receptors. You can take less of Clen while on ketotifen as well, since ketotifen will increase clen’s effectiveness by a third.
Taking ketotifen with ephedrine is pretty synergistic, as ephedrine works highly upon beta 3 receptors, ketotifen upregulates those beta receptors, thus making it more potent. Plus the fact that it reduces the amount you need for these agents, will in turn reduce the amount of side effects. IF you have the experience and tolerance, stacking all three of these agents would be a tremendous thermogenic fat burning stack.
I recommend taking 1mg of ketotifen 30 minutes prior to a meal twice a day. Remember take it while on clen or ECA to keep the receptors clean and maximize those cycles.
You can post comments about this Article here in this thread —————->>http://www.elitefitness.com/forum/anabolic-steroids/needtogetaas-my-take-ketotifen-980373.html
A phosphodiesterase type 5 inhibitor is a compound that blocks the degradation of phosphodiesterase type 5 on cyclic GMP in the smooth muscle cells lining of the blood vessels; which supplies the corpus cavernosum of the penis with blood flow. PDE-5 Ihibitiors such as Cialis are used in the treatment of erectile dysfunction, and were the first effective oral treatment available for this specific condition. PDE5 is also located in the arterial wall smooth muscle within the lungs, PDE5 inhibitors have also been used for the treatment of pulmonary hypertension, a disease in which blood vessels in the lungs become overflowed with fluid, usually due to the failure of the left ventricle of the heart. PDE5 inhibitors are clinically indicated for the treatment of erectile dysfunction. PDE5 inhibitors are primarily metabolized by the cytochrome P450 enzyme CYP3A4. The potential exists for adverse drug interactions with other drugs which inhibit or induce CYP3A4, including HIV protease inhibitors, ketoconazole, itraconazole, and other anti-hypertensive drugs such as Nitro-spray since it WILL lower blood pressure, which may result in a fatal drop of blood pressure. Taking PDE-5 Inhibitors with grapefruit juice or naringin will also prolong the effect of them, as grapefruit extract inhibits that enzyme from any other action but what is at state. (Adv. Cycl. Nucl. Res. 5:195-211, 1975.) Till this day, Sildenafil Citrate aka Viagra is the most popular PDE5 inhibitor, it was originally discovered during the search of a novel treatment for severe heart spasms. Studies in 2002 explored its potential for increasing the production of neurons after one has suffered as stroke. (Biochim. Biophys. Acta 284:220-226, 1972.)
Tadalafil Citrate is a PDE5 inhibitor, currently marketed in pill form for treating erectile dysfunction under the name Cialis; and also under the brand name of Adcirca for the treatment of pulmonary arterial hypertension. It initially was developed by the ICOS, and then again refined and marketed world-wide by Lilly ICOS, LLC, the joint partnership company of ICOS Corporation and Eli Lilly & Company. Cialis tablets, in 5 mg, 10 mg, and 20 mg doses, are yellow, film-coated, and almond-shaped. The approved dose for pulmonary arterial hypertension is 40 mg once daily which would have me walking around the house with a hard on all day long for 3 days. LOLOLOL. The US approved Cialis for erectile Dysfunction treatment on November 21, 2003. Recently in May of 2009, Adcirca aka Cialis was passed as an official treatment for pulmonary arterial hypertension. Since it has the ability to stay potent for 3 days, people started to call it the Weekend Pill. For those who don’t get it, basically the dude would take Cialis Friday, and would be screwing from Friday Night to Sunday; to then get ready for the next work week. I personally feel its start to lose its potency after 48 hours from my personal experience. Since it lasts long, dosing is easier than with other PDE-5’s, which also means it acts smoother than the other PDE-5’s as well. I know from experience this holds true, 30 minutes after ingesting Viagra I have to be careful if I go out to public places, as anything could trigger the loyal soldier LOL. With Cialis I do not have that problem; on top of that I never get headaches with Cialis. With Viagra, there are times I have to keep drinking water and not strain so hard, or it will cause me to pass out within the 3 hours of taking it.
Seventy-four consecutive patients were treated on demand with sildenafil 50 mg and tadalafil 20 mg. The success in obtaining sexual intercourse was recorded and total (tT) and free testosterone (fT) levels were studied before and after 3 months of treatment. Basal level of tT and fT were at the bottom of the normal range and LH levels were at the top of the high normal range. After treatments, this endocrine pattern was reversed in both groups. However, the T increase in Sild-treated patients was significantly lower than in those treated with Tad (4·7 ± 2·7 vs. 5·1 ± 0·9, P < 0·001). fT levels followed a directly proportional pattern, while the inverse was found when LH production was studied. The average free testosterone levels increased from 59.9 pmol/L before treatment to 80.4 pmol/L after 3 months of treatment, the authors report. Total testosterone levels also rose (from 11.9 nmol/L to 16.3 nmol/L), while luteinizing hormone (LH) levels declined (from 4.7 IU/L to 2.7 IU/L). The intercourse rate reflected this effect: in fact, the Sild group showed a 4·9 ± 2·9/month full sexual intercourse rate while in the Tad group a significantly higher rate of sexual intercourse was found (6·9 ± 4·6/month, P = 0·04). However, drug consumption was comparable between the groups. (Clin Endocrinol, (Oxf) 2004;61:382–6.)
Researchers had participants perform three 30-second maximum output sprints to exhaustion and measured testosterone and cortisol responses to exercise. They found that only after Cialis and exercise did testosterone increase, however Cialis also increased cortisol levels which lets us know that you are going to want up your VitaminC intake to combat catabolism. The increase in cortisol also led to lowered levels of DHEA, a drop in DHEA will increase stress and drop immune system capabilities. The study demonstrates that Cialis increases the “stress” response to the body, just as caffeine does. Caffeine will also temporarily boost testosterone. Caffeine at high doses can cause NON SPECIFIC PDE inhibition. Remember also, an increase in dopamine from the testosterone should result in by product conversion to norepinepherine which would be responsible for the increase in alertness. (Int J Sport Nutr Exerc Metab, 2008 Apr;18(2):131-41.)
Now we come to what separates Cialis from other PDE in inhibitors. In this study, researchers discovered that the increase in testosterone from taking Cialis is mediated by a reduction in estrogen demonstration that Cialis may have anti-estrogenic properties. Research has shown consistently that T/estradiol ratio was associated with LONG TERM Cialis treatment. in LH levels did not rise from Cialis, indicating that Cialis did not directly stimulate testosterone production, but indirectly by lowering estrogen. This could explain why I noticed that I lose water retention while on Cialis, I also get a dry mouth which also is due to the rise Nitric Oxide. I also tend to urinate more often on it, I may have to do some blood work while on Cialis. (Greco EA, Pili M, Bruzziches R, Corona G, Spera G, Aversa A. Testosterone: Estradiol ratio changes associated with long-term tadalafil administration: A pilot study. J Sex Med, 2006;3:716–22.)
I came upon a study that involved three maximum power sprints to determine if Cialis could increase anaerobic threshold. The study found no significant differences in peak power, average power or fatigue differences compared to the placebo, but it was noted was that Cialis decreased the time to reach peak power. The researchers concluded, “Cialis did not have an effect on peak power, but time to peak power output was reduced. Only to sports that need to reach maximum power output in a few seconds could Cialis administration be beneficial.” So those who want faster recovery in between sets will notice a difference while on Cialis, which is probably why guys get so pumped on it. If you are not taking long breaks like before due to the increase endurance, you will notice that you are pushing your limits, causing your muscles to be engorged with blood flow. (Br J Sports Med, 2008 Feb;42(2):130-3.)
Nitric Oxide is one of the main signals for satellite cell activation. Nitric Oxide is an important regulator of hepatocyte growth factor (HGF), which is a cytokine with various cellular functions on muscle. A research study showed that stretched muscle-induced hypertrophy via release of HGF found that the release of HGF was dependent on NO concentrations. Researchers then measured HGF levels in serum after an intense bout of eccentric exercise. They found that the liver-derived HGF rose 19 percent approximately 4 hours post exercise, which resulted in an activation of satellite cells! It is possible that the observed rise in serum HGF showed that HGF could have been carried to the site of injury by immune cells rushing to the site of injury, which are increased in number during the inflammatory response to muscle damage. As we all know when muscle damage occurs, the overall amount of cytokines present in the body multiplies. The amount of HGF will be much more available while on Cialis, which in essence should increase muscle tissue. (Mol Biol Cell, 2000;11:1859 –1174.)
Another interesting study reported in the Journal of Muscle and Nerve was that Nitric Oxide actually was able to reverse the damaging effects of cortisol-induced satellite cell depletion. They found that Nitric Oxide had a dose-dependent effect on increasing satellite cell levels as well. If you use the citation you can see the graph, as too much will cause muscle damage and buch of other problems. This brings me to my next point, if you add creatine with Cialis you get a super increase of Satelite cells, this in turn will definitely aid in recovery while improving muscular endurance. A great cocktail conjuction would be N2KTS, 10-20mg of Cialis and 5 grams of creatine monohydrate/ Ancient Strength. (Muscle Nerve, 2008 Feb;37(2):203-9.)
I just want to remind you guys that when taking Cialis, be sure to start gradual. Start with 5mg, then work your way up by 5mg increments. THERE IS NO NEED TO INGEST MORE THAN 20MG’s within a 3 day period. Other things to take with it to spice up your love life include HCGenerate, iPT 141, Pramipexole, D-aspartic Acid, Unleashed/PostCycle and forma-stanzol.
The one thing that people forget about this drug is the fact that it does NOT stimulate libido. Yes we know that it will increase blood flow to the penis but it no way shape of form stimulates to get it on. In fact, in order for the penis to work, a hydrogen sulfide signal must be sent from the brain to the penis to allow the nitric oxide flow to begin, on top of that, androgens must be present so that the body can begin the mating process. The body works all in one motion, not in separate terms as you can see. If you stimulate one part, the rest IS affected by it in some way. I tell you what if you combine something like iPT 141 and Cialis, you will be going for rounds and rounds of sex.
It would seem these days everyone has there own version of how a steroid cycle should be run and how pct should go. Every single board guru and internet commando swears he is right and has the studies to prove it. WOW HOW CAN SO MANY PEOPLE BE RIGHT ALL AT ONCE? Well its simple my friends. Many of them are right. But they are only right for them and maybe not you. This is why I have never written a “this is the only way to do it” Article about steroid cycles or pct and I never will.
However every day I am asked to at the very least address the issue and write something. So here I sit wondering HMMM where to start? The main factors to think about when setting up a cycle and pct is “keeping your gains, Recovery of the HPTA, and of course as little side effects as possible”. So Rather then slam you with a cookie cutter program I will Just share what I have learned and what I have seen work for hundreds of thousands of others out there.
Lets first take a look at the old old school ways pct. This is basic and anyone can follow the crowed of lemmings that have been running down the same road for decades. Never stopping once to learn anything new. This train of that is that Clomid,nolvadex,and hcg is all one could ever need. Toss in a few ai’s and what is there to worry about right? Man they could not be more wrong.
Some recovery ideas involve the use of orals to ‘bridge’. A bridge is the time period between cycles. The notion here being that one oral dose per day is metabolized quick enough to not be detected by the hypothalamic pituitary testicular axis (HPTA) and cause suppression of natural hormones (testosterone). Its a huge load of crap.
Then there are other compounds that can be used to enhance recovery, such as GH, IGF, insulin, PGF, GHRP,CJC and some natural compounds with merit like creatine, phosphatidylserine, forme-stanzol, Hcgenerate,bulbine, protodiocin and perhaps the branch chain amino acids (BCAA’s) like the ones found in Gear.
Cycling what products to use and for how long and at what dosage, is complex. Many factors influence what the user determines is best for them. These are: goals, level of experience, access, years of training, knowledge, etc. I think it is important that one start of light and short when it comes to cycles. Personally I feel there is nothing wrong with running a all oral cycle first or a short injection cycle.
Length Of Cycle
Probably the biggest factor to affect recovery is the length of a cycle. Longer cycles increase the chance that recovery will be delayed and possibly not 100%. This is why many people advocate the short blast cycles. However the traditional cycle is usually 8-10 weeks, which is still relatively safe for recovering normal testicular function. The longer the cycle, the higher the chance of impaired recovery.
A critical factor in cycle length often overlooked is the steroid ester one is using. With prohormones it’s also the affect that particular prohormone has on HPTA function. Doing an 8 week cycle of Deca Durabolin for example, is in actuality perhaps a 10-11 week cycle due to the long acting ester Deca Durabolin.
For the last 2-3 weeks that the user is trying to recover, perhaps using Clomid and HCG for example, nothing is happening because the deca metabolites are still active and shutting down the HPTA. So that’s 2-3 weeks of little anabolic activity and no endogenous testosterone. Bad idea.
Worse, with deca in particular, Nerve Growth Factor(NGF) is inhibited, further affecting quick recovery. Deca, as you can see, is best used at the beginning of a cycle, not the end. Other long acting esters, such as Testosterone Cyp or Enanthate, also delay recovery, as their metabolites remain active.
With prohormones like 4-hydroxy-testosterone (4OHT), little or no HPTA down regulation occurs. This is because a metabolite of 4OHT is Formestane, which up regulates HPTA function. So a cycle of 4OHT with other mild agents like methyl-4-hydroxy-nandrolone (MOHN), or Ergomax would present little concern with post cycle recovery.
Switching To A Bridge?
For steroid users, compounding this problem is the notion that switching to safer anabolic steroids like Anavar will enable a ‘bridge’, is erroneous. Any exogenous steroid is going to down regulate endogenous testosterone levels and inhibit recovery. Even clomid inhibits HPTA recovery.
The idea of a once per day dose of orals as a bridge will also delay recovery. Orals are metabolized in hours by the body, but the binding of the androgen receptor is much longer. So even a once daily dose of 10 mg of D’bol will inhibit HPTA recovery.
In general, for faster recovery, it is advised to switch the last 4 weeks of a cycle to fast acting esters and orals. Fast acting esters include hormones attached to nothing (suspension), or an acetate or propionate ester. Winstrol, Testosterone Propionate and PH’s suspended in MCT oil are examples.
Fast acting esters and orals clear the body faster and as such allow recovery to begin faster. A chemist once told me that ideally the last injectable used should be metenolone.
The first carbon atom has a ‘beta-methyl’ group on the a-ring. This structure of metenolone supposedly makes it harder for the HPTA to ‘see’ it. He recommended using either 30-50 mg of the oral, or 100 to 200 mg of the depot.
Mesterolone would be even harder for the HPTA to recognize, since it has an alpha, instead of beta, methyl group. Here, up to 200 mg/day can be used. Since it’s basically DHT, side effects like hair loss could be an issue.
Consider the 4/2 cycle theory, and/or switch to fast acting Esters and orals for the last 4 weeks of a traditional 8-10 week cycle. Know the compounds you are using in a cycle so that you can plan a proper recovery cycle.
The recovery phase should ideally be considered a part of any cycle. Although it typically begins during the last 2 weeks of a cycle and lasts from 2-4 weeks after (perhaps more), it really is a process that should be used during the entire cycle.
Measures should be taken to prevent excessive testicular atrophy during a cycle and not just at the end.
Avoiding Testicular Atrophy
The best way to prevent testicular atrophy is to regularly use compounds that can stimulate the testes. For example, every 4 weeks a one week dose of recovery items would be included in the cycle. This recovery week would include arimidex, clomid, bromocriptine and HCG perhaps.
Bromocriptine acts to decrease the amount of prolactin that the pituitary releases. It keeps prolactin in check while stimulating sperm production and erectile function. If used too frequently or for too long, it can lead to poor appetite and decreased receptor sensitivity.
Clomid and arimidex work on various aspects of the HPTA, and help stimulate the testes, preventing excessive atrophy.
Ideally we want to keep estrogen low during the entire cycle. Contrary to popular belief, estrogen suppression does not inhibit protein synthesis(1) as was believed, and in addition, excess estrogen will make you fat2.
In rats3 and humans4 estrogen supplementation increases GH levels, but reduces skeletal growth by decreasing somatomedin levels.’ The idea of bulking agents, like hard androgens, adding more weight is due to the intramuscular and organ fat deposition the excess estrogen causes!
You don’t need this fat. Worse, estrogen deposits fat cells with higher estrogen sensitivity, like around the waist. This may contributes to the bloated gut current bodybuilders have. Research indicates this fat location also increases risk of heart disease.
In addition, estrogen also causes an increase of sex hormone binding globulin (SHBG). As SHBG increases, anabolics cease to work. In fact this could be the main reason that after a while anabolics don’t work as they used to; a rise in SHBG. Yet another reason keeping estrogen low may help.
Which Anti-Estrogen Is Best for you?
Therefore, using arimidex (anastrozole) or aromasin (exemestane)during the entire cycle is a good idea if one can afford to. There are cheaper, generic versions of arimidex available now from overseas that work great. Arimidex is better than clomid due to its mechanism of action; it blocks conversion of testosterone to estrogen. Clomid is a weak estrogen that only acts to block estrogen receptors (as well as stimulate gonadotropin releasing hormone (GnRh) release).
If you can’t access arimidex, then clomid could be used. Novaldex can also be used and some have reported it may be more effective at GnRH stimulation than clomid. 5 This is because clomid is a weak estrogen and can act to suppress HPTA function.
The choice of clomid over novaldex is an area that appears to be hotly debated currently. Novaldex has some reported toxicity issues, so this is an area of concern. However, novaldex is the choice for gyno (versus say arimidex) since it blocks estrogen that has already formed in the body.
In addition, reports that anti-estrogens, like Novaldex, lower IGF levels could be due to the fact that the acute pharmacokinetics of these compounds may increase clearance rates of IGF from the blood, not an inhibition of IGF release itself. Clearing IGF from the blood does not mean it is lowered on a consistent basis.
Natural supplements that work to lower estrogen are the aromatase suicide inhibitors that contain 4-androstene-3, 6, 17-trione. Examples are 6OXO and the more cost effective Aromax by ALRI. Another unique natural product that enables recovery is Impact by ALRI. This is a sterile, oil based matrix of 7-Keto DHEA, phosphatidylserine and formestane the noted aromatase inhibitor.
Impact is the most underrated product on the market. The science behind its development is impeccable. Formestane not only blocks estrogen and stimulates HPTA function, resulting in increased testosterone levels; it also increases IGF levels by over 25 percent.
No other anti-estrogen does this. 7-keto-DHEA increases thyroid function, enabling more fat burning, and along with phosphatidylserine block cortisol, the catabolic hormone. Higher doses are required for the proper effect and to note the slight anabolic effect of formestane.
Consider rotating different anti-estrogens (ex. arimidex during cycle and formestane post-cycle) to keep low estrogen levels consistently.
Testosterone Levels & Shrinkage
Although penis size is unaffected, hormones can make your testicles shrink – sometimes permanently. However teste size and function are not necessarily correlated. Most of testes size comes from sertoli cells (sperm production) with small leydig cells (testosterone production) spaced between.
So yes, one can have adequate T with smaller testes. If one chooses to get a blood test, 280 to 1400 ng/dL is “normal” but I’d say it ‘should’ be above 600 ng/dL at least.
Don’t measure testosterone in the morning; it can be 20 to 30 percent higher then. Be careful; the doc’s might like to avoid prescriptions for testosterone. To do so they will schedule tests in the morning.
This may leave you a bit hypogonadal (and non-functional) the rest of the day and the Docs may just simply tell you ‘it’s-in-your-head’. Testosterone levels can also be higher in later afternoon just before dinner.
A high morning measurement might give you a false sense of security. You’d like it high all day long, and really high early in the morning. Any endogenous Testosterone level above 700 ng/dL is good and healthy. High is above 900 ng/dL.
Really high is anything above 1200 ng/dL. 280 to 450 ng/dL is for those 50 to 60yr olds- stressed-out semi-impotent businessmen who complain about ‘male-menopause’ -too low for good health but high enough that an MD won’t get off his or her butt to help out. Don’t stay in this range if you’re inadvertently still in it as a consequence of that last cycle.
Restoring HPTA With Anti-Estrogens?
Another writer claims anti-estrogens alone will do little to restore HPTA function since the testes have become smaller and lost mass, rendering them insensitive to even heightened levels of LH.
According to him, Clomid and Novaldex alone will increase LH levels but not enough to shock the testes back into production mode.5 Therefore this theory involves using HCG post cycle in a high dose to ‘shock’ the testes into recovering is the best route.
The levels of LH provided by anti-estrogens alone supposedly will not do this according to him. However, use of HCG post-cycle can lead to such an increase in testosterone that estrogen will also rise, leading to further HPTA inhibition.
HCG use post cycle, on a low dose (250-500 iu/day) and short time frame, can work to enhance recovery, provided anti-estrogens are also used to prevent excess estrogen inhibiting recovery.
Also Clomid and Novaldex can bypass the HPTA and stimulate the testes directly, acting as exogenous FSH and LH. Since they don’t risk causing a rise in estrogen levels, they may be a better choice.
Nootropics: Smart Drugs Anyone?
Another facet of recovery is increasing NGF in the HPTA. NGF increases the recovery rate of the glands in the brain, specifically the hypothalamus and pituitary. The class of compounds known as ‘smart drugs’ or nootropics because of their life and brain enhancing qualities are specifically successful at raising NGF levels.
They include Hydergine, Piracetem, and Selegiline among others. Growth hormone can also increase NGF, and acts to increase testosterone through this mechanism. Some natural compounds will also increase NGF, such as Acetyl- L-Carnitine (ALC) and Ginko Biloba. Selegiline will also act to increase dopamine levels, which is also critical for recovery as dopamine drives the male brain.
While serotonin is the primary neurotransmitter in women’s brains, men are oriented around dopamine. Dopamine is responsible for aggression (or assertiveness), and is critical in the sex drive also. If you can get your hands on them, nootropics could be beneficial for recovery. Even Ginkgo and ALC (1500 mg/day) could be used post cycle to aid recovery.
Conclusion: The Kitchen Sink
The best route to ensure recovery is to use as many non-hormone items you can get your hands on. First off the best route is to make your last four weeks of a cycle fast acting injectables like Trenbolone, Test Prop and Winstrol and orals like D’bol.
Ideally you would be using a small amount of arimidex or formestane during the entire cycle to keep estrogen down, unless you are using non-aromatizable steroids like trenbolone and winstrol. Clomid and/or novaldex can also be used during the cycle. At a minimum, during the cycle, every 4 weeks you should use a one-week recovery of arimidex and clomid. This keeps the testes primed to bounce back faster post-cycle.
The critical time for recovery is the last two weeks of the cycle until about 4 weeks out. During the last two weeks of a cycle, use clomid (50-100 mg/day) with arimidex (even when using non-aromatizing steroids this should be used as it stimulates FSH).
This would be followed by at least 2 more weeks of arimidex only (tapering down to 0.25 mg/day at the end). Don’t use clomid post cycle as it down regulates the HPTA. If you still need to use an anti-estrogen for some reason, use Novaldex post-cycle. If you have access to Bromocriptine, use that as well for a short period of time (3 weeks).
Know when the drugs you are using have cleared your system. For example, with trenbolone, about 3 days after your last shot you can assume most of the drug has been cleared from the blood. So technically its 3 days after your last shot of trenbolone that your cycle is ended. That’s when you would also stop using clomid.
If you can access HCG, use it. Best application is to use during a cycle in small amounts, every fourth week during your mini-recovery protocol of clomid and arimidex, for several days to keep the testes from shrinking. At the end of a cycle, best use is the last week or two of the cycle to restore teste size.
Other compounds like GH, and nootropics are also useful adjuvants to assisting the recovery phase. Use them if you can. A lower cost and legal option is to use products like Impact and Aromax by ALRI. Training should also be modified – post cycle where catabolism is a real threat, short, intense workouts are best.
High intensity training (HIT) like that espoused by Yates and Mentzer is best for a post-cycle training regimen.
In addition, save the creatine for post cycle also – anabolics already enhance creatine uptake, so better to use it post cycle for whatever little edge it may give you in the down phase of recovery. Glutamine and BCAA’s are also effective post-cycle supplements.