Needtogetaas does GW-501516 And loves it.
Posted by Needtogetaas | January 23rd, 2012

GW-501516 

 

 

GW-501516 is a PPARδ modulator compound is currently being investigated for drug use by GlaxoSmithKline. It activates the same pathways activated through exercise, including PPARδ and AMP-activated protein kinase. It is being trialed as a potential treatment for a few conditions consisting mainly of obesity, diabetes, dyslipidemia and heart disease. GW-501516 has a synergistic effect when combined with the AMP-K agonist AICAR: the combination has been shown to significantly increase exercise endurance in animal studies more than 40%. And from My own experience yes it works my friends.

GW-50156 regulates fat burning through a number of different pathways which includes exercise mimetic effects.  It increases glycogen retention in skeletal muscle tissue while increasing muscle gene expression. This shift changes the body’s metabolism to allow for more fat burning and for energy instead of carbohydrates or protein as the source of fuel. This is why the main reason why it’s being looked into as a treatment for diabetes.  As it will not allow the patients to endure and overly catabolic state, thus allowing energy levels and health to be stable at all times. GW-501516 clearly demonstrates that it increases muscle mass while keeping glucose from touching the adipose tissue sort of like Need2Slin but need2slin does much more then just this. Treatments with GW-501516 have been shown to increase HDL cholesterol by up to 79% and the compound is now undergoing Phase II trials to improve HDL cholesterol in humans. We dive into its attributes further later in the article But again let me speak from personal experience. I did a test with this drug and Winstrol. I know for my self when I take wonstrol it always kills my cholesterol levels. Last time I took it I ended up with an HDL of ten and a LDL over two hundred and it only took less then 2 weeks for this to happen. So knowing this I took wintrol for 4 weeks and also took GW-501516 along with it and I was amazed at the results. My cholesterol levels were BETTER at the end of the 4 week trial. So if cholesterol is of concern for you then you need to get some of this stuff my friend because trust me it works.

Concerns had been raised right before the 2008 Beijing Olympics that GW-501516 could be used by athletes as a performance enhancing drug which was not detectable nor tested for during the doping test. The main reason why athletes would use it is because of the increase in endurance through the increase of glycogen storage leading to increased muscular endurance, again ring a bell. Need2Slin does THE SAME THING! GW-501516 has yet to be label a controlled or banned substance by any national drug enforcement agency including Wada. Obviously no one will test positive for this drug, so if I were an Olympic athlete looking for a boost; this would be at the top of the list considering its much outweighed pros over cons. Any Athletes looking for a edge can use this drug and never have to worry about popping hot. They can not test for it my friends so you are golden. Some new testing is coming out in the next 3-5 years that will allow them to basically test your DNA to see if your bosy as been drug altered in anyway but this is years in the making. For now you are safe to take GW-501516 and not have to worry about popping hot.

Injecting GW501516 is like injecting a cardio session LOL

The benefits of endurance exercise on general health make it desirable to identify orally active agents that would mimic or potentiate the effects of exercise to treat metabolic diseases. Although certain natural compounds, such as reseveratrol, have endurance-enhancing activities, their exact metabolic targets remain elusive. We therefore tested the effect of pathway-specific drugs on endurance capacities of mice in a treadmill running test. Researchers found that PPARbeta/delta agonist and exercise training synergistically increase oxidative myofibers and running endurance in adult mice. Because training activates AMPK and PGC1alpha, they then tested whether the orally active AMPK agonist AICAR might be sufficient to overcome the exercise requirement. Unexpectedly, even in sedentary mice, 4 weeks of AICAR treatment alone induced metabolic genes and enhanced running endurance by 44%. These results demonstrate that AMPK-PPARdelta pathway can be targeted by orally active drugs to enhance training adaptation or even to increase endurance without exercise.  Now how does this peptide cause mice to lose weight without activity? Simple, the Activation of PPARβ/δ by GW501516 in skeletal muscle cells induces the expression of genes involved in preferential lipid utilization, β-oxidation, cholesterol efflux, and energy uncoupling. In addition, the treatment of muscle cells with GW501516 increases apolipoprotein-A1 specific efflux of intracellular cholesterol, thus identifying this tissue as an important target of PPARβ/δ agonists. Interestingly, fenofibrate induces genes involved in fructose uptake, and glycogen formation. In contrast, rosiglitazone-mediated activation of PPARγ induces gene expression associated with glucose uptake, fatty acid synthesis, and lipid storage. Furthermore, we show that the PPAR-dependent reporter in the muscle carnitine palmitoyl-transferase-1 promoter is directly regulated by PPARβ/δ, and not PPARα in skeletal muscle cells in a PPARγ coactivator-1-dependent manner. This study demonstrates that PPARs have distinct roles in skeletal muscle cells with respect to the regulation of lipid, carbohydrate, and energy homeostasis. Overall the peptide GW501516 (PPARβ/δ agonists) would increase fatty acid catabolism, cholesterol efflux, and energy expenditure in muscle, and speculate selective activators of PPARβ/δ may have therapeutic utility in the treatment of hyperlipidemia, atherosclerosis, and obesity.  (Dressel et al. 17 (12): 2477).. However I would advice only using this drug orally IMO..

 

Proof that GW5010516 increases insulin sensitivity

Elevated plasma free fatty acids cause insulin resistance in skeletal muscle through the activation of a constant chronic inflammatory process. This process involves nuclear factor (NF)-kappaB activation as a result of diacylglycerol (DAG) accumulation and following protein kinase Ctheta (PKCtheta) phosphorylation. At present, it is unknown whether peroxisome proliferator-activated receptor-delta (PPARdelta) activation prevents fatty acid-induced inflammation and insulin resistance in skeletal muscle cells. In C2C12 skeletal muscle cells, the PPARdelta agonist GW501516 prevented phosphorylation of insulin receptor substrate-1 at Ser(307) and the inhibition of insulin-stimulated Akt phosphorylation caused by exposure to the saturated fatty acid palmitate. This latter effect was reversed by the PPARdelta antagonist GSK0660. Treatment with the PPARdelta agonist enhanced the expression of two well known PPARdelta target genes involved in fatty acid oxidation, carnitine palmitoyltransferase-1 and pyruvate dehydrogenase kinase 4 and increased the phosphorylation of AMP-activated protein kinase, preventing the reduction in fatty acid oxidation caused by palmitate exposure. In agreement with these changes, GW501516 treatment reversed the increase in DAG and PKCtheta activation caused by palmitate. Consistent with these findings, PPARdelta activation by GW501516 blocked palmitate-induced NF-kappaB DNA-binding activity. These findings indicate that PPARdelta attenuates fatty acid-induced NF-kappaB activation and the subsequent development of insulin resistance in skeletal muscle cells by reducing DAG accumulation. The results of the study clearly demonstrate that PPARdelta activation is a pharmacological target to prevent insulin resistance. (Endocrinology 2010 Apr; 151(4) :1560-9.)

 

The peroxisome proliferator-activated receptor δ (PPARδ) regulates the expression of genes involved in cellular lipid and cell energy metabolism in many metabolically active tissues, such as liver, muscle, and fat, and plays a role in the cellular response to stress and environmental stimuli. The particular role of PPARδ in insulin-secreting β-cells, however, is not well understood; we recently identified the cell-specific role of PPARδ on mitochondrial energy metabolism and insulin secretion in lipotoxic β-cells. After treatment of HIT-T15 cells, a syrian hamster pancreatic β-cell line, with high concentrations of palmitate and/or the specific PPARδ agonist GW501516, we detected the gene expression changes for transcripts, such as peroxisome proliferator-activated receptor gamma co-activator 1 (PGC-1α), nuclear respiratory factor 1 (NRF-1), mitochondrial transcription factor A (mtTFA), the protein levels of the mitochondria uncoupling protein 2 (UCP2), mitochondrial morphology, the insulin secretion capacity and ATP/ADP ratio. Our results show that GW501516 treatment promoted generation of mitochondrial ATP, as well as expression levels of PGC-1α, NRF-1 and mtTFA, decreased basal insulin secretion, but had no effect on glucose-stimulated insulin secretion (GSIS), increased amounts of UCP2 and changed ATP-to-ADP ratio, improved mitochondrial morphology in palmitate-treated β-cells. GW501516-induced activation of PPARδ enhanced mitochondrial energy metabolism, but also promoted a concomitant mitochondrial uncoupling and resulted in decreased basal insulin secretion and restricted GSIS; this observation indicated the possible action of a protective mechanism responding to the alleviation of excessive lipid load and basal insulin secretion in lipotoxic β-cells. (Volume 343, Numbers 1-2, 249-256, DOI: 10.1007/s11010-010-0520-8) As you can see this peptide has a profound effect on the liver and pancreas resulting in lower blood sugar and controlled insulin output.

GW501516 prevents brain aging.

 

 

Brain inflammation plays a central role in numerous brain pathologies, including multiple sclerosis (MS). Microglial cells and astrocytes are the effector cells of neuroinflammation. They can be activated also by agents such as interferon-γ (IFN-γ) and lipopolysaccharide (LPS). Peroxisome proliferator-associated receptor (PPAR) pathways are involved in the control of the inflammatory processes, and PPAR-β seems to play an important role in the regulation of central inflammation. In addition, PPAR-β agonists were shown to have trophic effects on oligodendrocytes in vitro, and to give partial protection in experimental autoimmune encephalomyelitis (EAE), an animal model of MS. In the present work, a three-dimensional brain cell culture system was used as in vitro model to study antibody-induced demyelination and inflammatory responses. GW 501516 is a specific PPAR-β agonist that researchers chose to  examine for its capacity to protect from antibody-mediated demyelination and to prevent inflammatory responses induced by IFN-γ and LPS. GW 501516 decreased the IFN-γ-induced up-regulation of TNF-α and iNOS in accord with the proposed anti-inflammatory effects of this PPAR-β agonist. However, it increased IL-6 m-RNA expression. In demyelinating cultures, reactivity of both microglial cells and astrocytes was observed, while the expression of the inflammatory cytokines and iNOS remained unaffected. Furthermore, GW 501516 did not protect against the demyelination-induced changes in gene expression.  This suggests that the protective effects of PPAR-β agonists observed in vivo can be attributed to their anti-inflammatory properties rather than to a direct protective or trophic effect on oligodendrocytes.  We all know that both alzheimer’s and Dementia are caused by chronic inflammation within the brain. Further research is still needed but this peptide displays promise in preventing the aging of the brain. (Journal of Neuroinflammation 2009, 6:15 doi:10.1186/1742-2094-6-15)

GW501516 helps prevent the onset of Diabetes

In contrast to the well-established roles of PPARgamma and PPARalpha in lipid metabolism, little is known for PPARdelta in this process. We show here that targeted activation of PPARdelta in adipose tissue specifically induces expression of genes required for fatty acid oxidation and energy dissipation, which in turn leads to improved lipid profiles and reduced adiposity. Importantly, these animals are completely resistant to both high-fat diet-induced and genetically predisposed (Lepr(db/db)) obesity. As predicted, acute treatment of Lepr(db/db) mice with a PPARdelta agonist depletes lipid accumulation. In parallel, PPARdelta-deficient mice challenged with high-fat diet show reduced energy uncoupling and are prone to obesity. In vitro, activation of PPARdelta in adipocytes and skeletal muscle cells promotes fatty acid oxidation and utilization. Our findings suggest that PPARdelta serves as a widespread regulator of fat burning and identify PPARdelta as a potential target in treatment of obesity and its associated disorders. (Cell. 2003 Apr 18;113(2):159-70. PMID:12705865)

PPAR Agonist help prevent Dyslipidemia

In vitro and in vivo genetic and pharmacological studies have demonstrated PPARα regulates lipid catabolism. In contrast, PPARγ regulates the conflicting process of lipid storage. However, relatively little is known about PPARβ/δ in the context of target tissues, target genes, lipid homeostasis, and functional overlap with PPARα and -γ. PPARβ/δ, a very low-density lipoprotein sensor, is abundantly expressed in skeletal muscle, a major mass peripheral tissue that accounts for approximately 40% of total body weight. Skeletal muscle is a metabolically active tissue, and a primary site of glucose metabolism, fatty acid oxidation, and cholesterol efflux. Surprisingly, the role of PPARβ/δ in skeletal muscle has not been investigated. We utilize selective PPARα, -β/δ, -γ, and liver X receptor agonists in skeletal muscle cells to understand the functional role of PPARβ/δ, and the complementary and/or contrasting roles of PPARs in this major mass peripheral tissue. Activation of PPARβ/δ by GW501516 in skeletal muscle cells induces the expression of genes involved in preferential lipid utilization, β-oxidation, cholesterol efflux, and energy uncoupling. Furthermore, we show that treatment of muscle cells with GW501516 increases apolipoprotein-A1 specific efflux of intracellular cholesterol, thus identifying this tissue as an important target of PPARβ/δ agonists. Interestingly, fenofibrate induces genes involved in fructose uptake, and glycogen formation. In contrast, rosiglitazone-mediated activation of PPARγ induces gene expression associated with glucose uptake, fatty acid synthesis, and lipid storage. Furthermore, we show that the PPAR-dependent reporter in the muscle carnitine palmitoyl-transferase-1 promoter is directly regulated by PPARβ/δ, and not PPARα in skeletal muscle cells in a PPARγ coactivator-1-dependent manner. This study demonstrates that PPARs have distinct roles in skeletal muscle cells with respect to the regulation of lipid, carbohydrate, and energy homeostasis. Moreover, we surmise that PPARβ/δ agonists would increase fatty acid catabolism, cholesterol efflux, and energy expenditure in muscle, and speculate selective activators of PPARβ/δ may have therapeutic utility in the treatment of hyperlipidemia, atherosclerosis, and obesity.  (Dressel et al. 17 (12): 2477)

 

GW5015016 decreases chances of Heart Disease

The peroxisome proliferator-activated receptors (PPARs) are dietary lipid sensors that regulate fatty acid and carbohydrate metabolism. The hypolipidemic effects of the fibrate drugs and the antidiabetic effects of the glitazone drugs in humans are due to activation of the alpha (NR1C1) and gamma (NR1C3) subtypes, respectively. In macrophages, fibroblasts, and intestinal cells, GW501516 increases expression of the reverse cholesterol transporter ATP-binding cassette A1 and induces apolipoprotein A1-specific cholesterol efflux. When dosed to insulin-resistant middle-aged obese rhesus monkeys, GW501516 causes a dramatic dose-dependent rise in serum high density lipoprotein cholesterol while lowering the levels of small-dense low density lipoprotein, fasting triglycerides, and fasting insulin. These results suggest that PPARdelta agonists may be effective drugs to increase reverse cholesterol transport and decrease cardiovascular disease which is typically associated with the metabolic syndrome X. (Proc Natl Acad Sci U S A. 2001 Apr 24;98(9):5306-11. Epub 2001 Apr 17. PMID:11309497)

 

As for as dosing is concerned, I recommend 5-20mgs once a day, and research on HUMANS has clearly shown that 5mg is sufficient to elicit its intended effects. I really don’t understand why this peptide is not as common as it should be. Its exercise in a vial LMAO.

Now onto the fun stuff guys. Dosing, stacking and uses for this drug. Many people would start out at a 5mg a day dose and I think this is fine but I would also add in another 5mg dose pre work out as well on work out days at the very least if not just run it 10mg every day IMO. IMO one could use this during pct allow you to keep calories high and not gain to much fat which is often what happens. I think its also great in combo with Sarms S4 as a bridge between cycles but I am against using S4 during pct. SO only use it after pct and you are sure you have recovered. Now here is the best part GW-501516 can be used with Drugs like winstrol, Beastdrol, and other orals that would cause problems with cholesterol and this would help keep the numbers to a minimum. High blood pressure, nose bleeds and high cholesterol is common with a lot of oral steroids and this drug will help in the sense that it will lower cholesterol levels..

 

That is all for now my friend. Always remember to Keep Killing that sh*t!!!!!

 

 

 

Posted in Body building, Endocrinology and Pharmacology., Professional Sports | Comments Off

Albuterol Better then Clen IMO
Posted by Needtogetaas | January 15th, 2012

Albuterol Albuterol sulfate is a selective fast butshort acting beta-2 adrenergic agonist,used for the relief of bronchospasm in conditions suchas asthma and chronic obstructivepulmonary disease. It is real similar in structure and mechanismto the well known cousin drug clenbuterol. Albuterol is readily available perprescription through a doctor within the United States. Clenbuterol is not FDAapproved which goes to show you it aint something to mess around with or takelightly. Albuterol is also sold under various brand names through a numberof other countries around the world. You will notice that Albuterol ismost commonly found in the form of a asthma inhaler, which is designed todisperse a measured amount of the drug immediately and directly to thebronchial tubes in a situation where one suffers a severe asthma attack. Theinhaler delivery of Albuterol provides the least amount of drug activitypossible, allowing the user to avoid unwanted cardiovascular side effects.Albuterol oral tablets are also available; however they do not provide the samecardio protective benefits that the inhalers are known to posses. Albuterol sulfate was introduced to the U.Sdrug market in 1968, sold under the brand name Ventolin. Albuterol sulfate has becomeone of the most popular drugs in recent history for its effectiveness and lackof side effects. This drug providesbenefits for athletes, bodybuilders, powerlifters and other individuals who areseeking to improve performance or their physical appearance. Albuterol is usuallyconsidered a fat burning agent in the bodybuilding community. Reason being isthat Albuterol has the ability to stimulate fat cells, increase lypolysis,decrease appetite, increase body temperature, as well as increasing basalmetabolic rate, increase cAMP, improve chlosterol while on cycle, and evenincrease strength. All of these factors, when combined with proper diet andtraining, would obviously help to increase the rate of fat loss in users.However the use of albuterol is not limited to simply fat loss. There isevidence that it can help to dramatically improve athletic performance as wellas helping to contribute to anabolism which well get into in a bit. However theperformance enhancing ability of albuterol is seemingly not limited to just strengthtraining. It was also shown that the times of users performing enduranceexercises significantly improved with the use of albuterol. It gets better; theseimprovements were completed without Albuterol negatively impacting the VO2respiratory breathing rate, heart rate or plasma free fatty acid and glycerolconcentration of users during the exercise conducted. Also the plasma lactateand potassium concentrations were altered constructively. This goes to showthat there is a reason why WADA banned Albuterol from athletic competition. Alittle bit about Beta-2 Receptors Beta receptors are found implantedin the cell’s outer phospholipid membrane. Beta receptors are stimulated by all the commonforms of stimulants such as ephedrine, DMMA and so on. The Beta receptors arebroken down into three subtypes: 1, 2, & 3, or more commonly seen as Beta-1, Beta-2, and Beta -3. Beta-1 is of no signifigance as Albuterol has noeffects on it. Beta-3 receptors tend not to really be biologically active inhumans as opposed to animals. So that leaves use with Beta-2 which is whereAlbuterol targets its stimulation of action upon. Stimulation of the Beta-2 receptors significantlystimulates the break down of fatty acids into the blood stream for use as fuel,thus causing a reduction in stored fat. When the blood flow increases so doesthe body’s temperature along heart rate. These actions in the body cause one tolose an appetite, which would explain why some people do not realize that theyhave gone the whole day without eating a stick of gum. I know some people wholiterally will have no urge to eat while on beta receptor agonists; they haveto literally force food down their mouth so that they receive sufficientdietary nutrient intake. Now we touch upon the anabolic aspects of Albuteroland other beta receptor agonists. Simply put is that Beta-agonists also stimulatea hormonal surge response that involves the activation of a compound calledcAMP aka cyclic-Adenosine Monophosphate. Once cAMP is stimulated, cAMPactivates calpistatin which is the inhibitor of calpain. Calpain is responsiblefor degrading protein within skeletal muscle. If you were to look at somestudies involving beta receptor agonists, especially Albuterol, you would seethat within an hour of ingesting a dose of it, testers bodily hormones roseincluding testosterone, thyroid hormones, cortisol, which is what also occurswhen you ingest forksolin. Forksolin is known to stimulate cAMP dramticallywhich is why for many years people who love supplements purchase Forksolin inbulk prior to their cutting and recomp cycles, reason being it provides greataid fat loss while aiding in maintaining muscle through the stimulation oftestosterone. cAMP also plays animportant role in controlling certain catecholamines secreted by the adrenalmedulla. Catecholamines have an inhibitory effect on muscle proteindegradation, Also crucial is that norepinephrine released from adrenergicterminals can in fact increase the rate of protein synthesis in oxidativemuscles, thereby leading to increased protein synthesis. As we all know greaterprotein synthesis leads to more anabolism which leads to more muscle gain.

Albuterol Outperforms Clen in the StrengthDepartment Clenbuterol does not match up withAlbuterol in the area of strength gains due to the fact that it dosedependently inhibits action potential firing within skeletal musclefibers. This is not directly stimulated byinnate Beta-2 stimulant activities. Reason being is that Clenbuterolblocked sodium currents in rat skeletal muscle fibers and in tsA201 cellstransfected with the human channel isoform, whereas Albuterol did not. Theeffects of clenbuterol were independent of beta-adrenoceptor stimulation.Instead, clenbuterol structure and physicochemical characteristics as well asblocking properties resembled those of local anesthetics, suggesting directbinding to the channels. (Mol Pharmacol. 2003Mar;63(3):659-70.)

Albuterol GREAT For Cholesterol!!!!!! This is because Albuterol showssignificant benefits to cholesterol as it works to lower total cholesterol,specifically LDL (the bad stuff) while at the same time elevating HDL. A study evaluated theeffects of a beta(2)-agonist, albuterol, on serum lipids and carbohydratehomeostasis in eight healthy nonsmoking men aged 24 to 61 years. Collection offasting blood samples was completed in duplicate on separate days at baseline,during 14 days of oral albuterol administration (Proventil Repetabs, 8 mg twicedaily; Schering Pharmaceuticals, Kenilworth, NJ) and during a 7-day washoutperiod. Carbohydrate homeostasis was evaluated using the minimal modeltechnique at the end of the baseline and albuterol periods. Fasting glucose andinsulin, intravenous glucose tolerance, acute insulin response to intravenousglucose (AIRg), insulin sensitivity (Si), and glucose effectiveness (Sg) werenot significantly changed during albuterol administration. Significantalterations (P < or = .02) were observed in total cholesterol ([TC] 9.1%+/ 2.5%), low-density lipoprotein cholesterol ([LDL-C] 15.0% +/ 2.9%), andhigh-density lipoprotein cholesterol ([HDL-C] +10.4% +/- 3.2%) concentrations,as well as the TC/HDL-C (-17.4% +/- 2.6%) and LDL-C/HDL-C (-22.9% +/- 2.4%)ratios. During washout, TC and LDL-C returned to baseline levels, whereas HDL-Cremained elevated by 5.8% +/- 2.4% (P < .05). Thus, albuterol administrationwas associated with favorable changes in the serum lipid profile without markedimpairment of glucose tolerance or its physiologic determinants. (Metabolism.1996 Jun;45(6):712-7) Another study I came upon was done on thirteenpatients for a total of 3 months. All patients had bronchial asthma and weretreated with 2 mg salbutamol three times daily (one patient with 4 mg threetimes daily). The concentrations of serum total cholesterol and LDL-cholesterolwere slightly but not statistically significantly higher after 3 months withsalbutamol than before the medication. The serum HDL-cholesterol andtriglyceride concentrations remained constant during the therapy. Serum freefatty acid levels decreased slightly but not significantly during the therapy.Treatment with salbutamol did not elevate plasma free fatty acid levels, whichmay have arrhythmic effects. The results indicate that beta 2-adrenergicstimulation has no effect on basal serum lipid levels. So besides beinganabolic, its also good for cholesterol sounds like a winner to me. This makesit ideal to take on cycle because we all know the negative affects AAS can havecholesterol, you literally get the best of both worlds while on Albuterol.

Usual dosing should start at around 1-2 4mg tabletsper day and will up the dosage as their individual tolerance allows for. Somepeople get up to 24mgs a day because of a high tolerance to the drug. Veterans will often take their temperature anduse an increase in temperature as a measure to what effect the drug is having.It is important to note that after 2-3 weeks, the receptors will become burnout to stimulation. I recommend 25mgs of Benedryl to up regulate the receptorsback into full gear which should allow you to take just one week off as opposedto the normal 2 on and 2 off protocol. Sides The most commonly noted side effects are fine tremor,anxiety,headache,muscle cramps, dry mouth,and palpitation. Other symptoms may include tachycardia,arrhythmia,flushing, myocardial ischemia, shaking of hands orjitters, shortness of breath, insomnia and impulsive behaviour. Rarelyoccurring, but of importance, are allergic reactions of paradoxicalbronchospasm,urticaria,angioedema,hypotension,and collapse. High doses may cause hypokalaemiawhich are of concern in patients with renal failureand those on certain diuretics and xanthinederivatives. High doses can also cause fatal heart complications due tooverstimulation of the CNS. Detectiontime of AlbuterolAlbuterol has a half life of about 4 hours which iswhy bodybuilders will take 3 divided dosages. Only slow releasing tabs willallow 12 hour dosing intervals. Urinary salbutamol concentrations arefrequently measured in competitive athletic commissions, for which a levels exceedingthat of 1000 μg/L is considered to be a form of cheating aka performanceenhancement. The window of detection for urine testing is on the order of just24 hours, given the relatively short elimination half-life of the drug. Albuterolboosts athletic performanceThe present study examined whetheroral short-term administration of salbutamol (Sal) aka Albuterol modifiesperformance and selected hormonal and metabolic variables during submaximalexercise. Eight recreational male athletes completed two cycling trials at80-85% peak O(2) consumption until exhaustion after either gelatin placebo(Pla) or oral Sal (12 mg/day for 3 wk) treatment, according to a double-blindand randomized protocol. Blood samples were collected at rest, after 5, 10, and15 min, and at exhaustion to determine growth hormone (GH), cortisol, testosterone,triiodothyronine (T 3), C peptide, free fatty acid (FFA), blood glucose,lactate, and blood urea values. Time of cycling was significantly increasedafter chronic Sal intake (Sal: 30.5 +/- 3.1 vs. Pla: 23.7 +/- 1.6 min, P <0.05). No change in any variable was found before cycling except a decrease inblood urea concentration and an increase in T(3) after Sal that remainedsignificant throughout the exercise test (P < 0.05). Compared with rest,exercise resulted in a significant increase in GH, cortisol, testosterone,T(3), FFAs, and lactate and a decrease in C peptide after both treatments withhigher exercise FFA levels and exhaustion GH concentrations after Sal (P <0.05). Sal but not Pla significantly decreased exercise blood glucose levels.From these data, short-term Sal intake did appear to improve performance duringintense sub maximal exercise with concomitant increase in substrateavailability and utilization, but the exact mechanisms involved need furtherinvestigation. (J Appl Physiol. 2000Aug;89(2):430-6.) Soif you are looking for a replacement to Clen, Albuterol is your go to drug asit is shorter acting which should yield less overall sides. It also providesgreater strength than clen, while providing great fat loss and being morebeneficial to one’s lipids. Anyone on cycle should really consider Albuterolover a lot of fat burners and that is a fact. Also remember that this drug willprovide gains in endurance and increase breathing capacity during training,unlike what some notice with Clen. Albuterol may not be as known as Clen but it is definitely what I call agolden nugget trapped in a sealed mine. I would reconsider Albuterol for your next physique improving cycle.

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The Trenobolone Experience by Needtogetaas
Posted by Needtogetaas | January 15th, 2012

What is Trenobolone?

 

Trenbolone is a classified schedule III drug in the United States; which means that it is illegal. It is from the 19-nor family of anabolic steroids just as deca is. The 19-nor stands for the fact that the testosterone molecule was changed at the 19th position to make it into the new and more potent compound. It was originally an anabolic androgic steroid developed and used by veterinarians on livestock to increase muscle growth and appetite and later would make its way to the chemical athlete’s world.  The farmers clearly knew that these anabolics were the key to bigger and better breeds, allowing for faster income as well.  On the average farmers sell cattle that have less than 28% EBF, they will not exhibit enough finish to reach a USDA quality grade of low choice. The majority of cattle need to have at least 28.5-29.5% EBF in order to grade to their genetic potential.

 

Therefore, all these factors need to be taken into consideration when choosing an effective implant (Trennobolone acetate) strategy which include feed costs, animal costs, quality grade, genetics, economic advantages of weight (live & carcass), production goals, and carcass goals. There are trade-offs to all the above and implants can help you achieve your goals and benefit you economically in all circumstances.

 

The chart from this link (http://www.depts.ttu.edu/afs/implantdb/dbhome/Revalor%20Tech%20Bulletin%2012.pdf) displays that cattle had the fastest rate of growth while on Finaflex pellets with the least amount of money spent as well. Now if you are a farmer chances are you are going to tell yourself, I am going to take this option instead of the old fashion grass fed way. The study also noted that when taking Tren with estradiol, the weight gain was more proficient. Of course bodybuilders don’t want to take estradiol, but taking tesostosterone will allow for aromatization which in turn will increase the body’s estradiol production leading to more muscle gain. This one of the reasons why the Test-Tren stack is so popular besides the fact that testosterone helps the impaired libido from Tren.

 

 

Benefits of Tren

In many people’s eyes, tren is pound for pound the strongest compound for pure gains and stacks well with anything; although some may argue that it’s a No No while on nanodrolone aka deca however I have ran both successfully with no more or less problems than running them separate . Trenbolone significantly increases nutrient efficiency along mineral/vitamin absorption. Feed efficiency is the measurement of how much of an animal diet is converted into meat, and the more consumption of food it takes to finalize this meat, the lower the value. On the other hand, the less food consumed by the animal to finalize the meat; the higher the value/efficiency. As mentioned in the study above, Cattle given trenbolone gained high quality weight without having their diet changed; leading to improved feed efficiency. This is music to the ears of every bodybuilder because Tren guarentees that every calorie you eat will go to some value of nutrition. This allows for better utlilization of the nutrition you intake to go to the muscles and organs of the body. This would explain why the cattle grew so rapidly while on Finaflex pellets.

Trenbolone is one of the few anabolic androgenic steroids that can lead to fat loss without change in diet, and it also has scholarly literature stating so.  This makes it perfect on a recomp as you will lose all fat needed but pack on dense muscle at the same time, don’t get me wrong; you can still use it for other goals including bulking and cutting.

Like most all anabolic androgenic steroids the Trenbolone hormone greatly promotes nitrogen retention in the muscles, increases red blood cell count and dramatically reduces and blocks glucocorticoid steroids aka the stress hormone cortisol; this hormone destroys muscle and increases fat storing hormones. This also means that you can do all the cardio you need to lose fat without having to worry about losing your muscle gains. Dieting can also place major stress on the mind and body leading to more cortisol, but Tren can help cease the cortisol release. Tren sounds ideal on a cut if you ask me. Increased nitrogen retention also means increased nutrient deliver to the muscles allowing for more glycogen retention. More glycogen retention leads to better workouts and a fuller look.

As is with nearly all anabolic androgenic steroids the Trenbolone hormone can greatly promote cell repair and regeneration, which will speed up the healing process in the body. The main reason why you experience growth on anabolics is because your recovery times goes up allowing you to become faster stronger. The more weight with frequency you can lift, the more and faster you will grow. One of the reasons why Tren is so good at increasing recovery time is the fact that it significantly increases the body’s natural production of the potent anabolic hormone IGF-1. Tren also causes muscle satellite cells to be more responsive to IGF-1 and other growth factors. The amount of DNA per muscle cell will also experience a significant increase. For these reasons adding Igf-lr3 into a tren cycle is a no brainer.

Trenbolone severely binds to the androgen receptors therefore increasing growth of muscle mass and melting fat away. This is important, because the stronger a steroid binds to the androgen receptor the better that steroid works at activating androgen receptor’s dependant mechanisms of muscle growth. There is also strong supporting evidence that androgens which bind very firmly to the androgen receptor also help in shedding fat. The androgen receptors are like locks and the androgens are like different keys. Some keys open the locks much better than others. This is does not mean that AR-binding is the only way that steroids work. There are anabolics that barely have any considerable binding to the AR and yet display great capability to build muscle and strength. Trenbolone is also a highly androgenic hormone, when compared with testosterone; its 5 times more androgenic than it. Testosterone measures at 100 while Tren measures at 500. Potent androgenic anabolics offer dry gains which is great for limiting water retention but don’t think that Tren is water retention free; as it is derived from a progesterone after all. Again as stated due to its great feed efficiency properties, it has potent nutrient partritioning effects. This means more glycogen for the muscle, and less glucose in the adipose tissues. If the compound has higher androgen binding, it will cause the androgen receptors within the fat cells to burn fat more efficiently. This could be alsoe from the rise in leptin with the simulatenous rise in androgens. There is evidence that shows when leptin rises while androgens rise, the body will burn fat at a faster rate to try to lower leptin.  One thing to remember with Tren is that it does lower thyroid hormones. This is why you will notice lets of bodybuilders use T3 or T4 while on cycle. You can also use a product like Alpha t2 which IMO works great for this reason and combining this with Need2slin will give even greater results . Add T3-pct to the pct or a good thyroid stimulating ” natural product”.
Other perks of Tren are that it does not aromatize into estrogen/estradiol nor does it convert to 5a reductase hormone also known as DHT. The lack of conversions prevents early aggravation of the prostate, estradiol based gynecomastia but that does not mean its gyno free which we will dive into further later.

 

The Drawbacks to Tren

One of the most intriguing yet not fully understood issues with Tren is its ability to lower thyroid hormones. So not only does it dramatically raise prolactin but it undeniably cuts thyroid levels in half. Even though Tren does not aromatize it can aggrevate the glandular tissue of the breast tissue which can result in what many refer to as Progesterone/Prolactin gyno. At first the nipples get puffy, then they start to hurt, nipples start to poke out. My friend was on a 120mg of it and boy he looked like he was in the mood so to speak all the time LMAO. Women would giggle at him because they thought he had no self control. When he took off his shirt, the nipples looked more like women’s nipples which is not pleasant at all. He got it taken care of with the advice that I gave him but had he not done so, eventually his nipples would start to excrete a gooey puss that would like milk. After all the rise in prolactin in women during pregnancy is what allows them to feed their child. I always advice using Provirone or materon when using tren. This will lower estroben and progestirone and Provirone always adds more fat lose to any cycle.

The mood swings that come from Tren are brutal. I have seen and heard people blacking out and carrying out violent acts because of the fact that they became so irritable. I can tell you that training your ass off in the gym and lowering can easily subside this side effect that is obtained from tren. I like to think of being tren is like having a 24/7 menstraul cycle HAHAHA. I have gone crazy on tren a few times my self nearly getting my self in a lot of trouble.. You will be moody and annoyed rather easily but it’s manageable. It used to make me laugh because there was this bouncer near where I lived that was always cycling Tren ace. Every time someone said something he did not agree with, his temper would flare and he would get so red which is from the elevated blood pressure, this has to do with a sudden rise in a fight or flight response. Basically your brain through norepinedrine tells your body to either do something about the situation or run for preserving one’s life. It’s the same reaction people with high testosterone will tend to display. A study showed that when men with high testosterone so aggressive faces, their heart rate elevated due to the increase in their fight or flight response. Remember Tren acts as testosterone; it is an androgen with both anabolic and ANDROGENIC properties.

Another uncomfortable side effect that comes with most androgens is high blood pressure resulting in loss of breath, increase in body temperature, rapid heartbeat, tightness of the chest, headaches. Since Tren is derivative from a progesterone, it increases water retention within the body, thus leading to the increase of blood pressure. No matter what androgen you take, there is always a chance of needing to go the Emergency Room due to elevated pressure, so make sure to take good preventive measures while on cycle.

Acne is common with Tren, as with most androgens; more so with wetter compounds such as Deca or Testosterone cypionate. Oil based esters are always going to give bad acne because you are INJECTING OIL INTO YOUR SKIN. HAHAHAHA!!  On tren you will sweat a ton due to its thermogenic/fat loss properties so acne chances increase from that aspect alone. One method I know that works is to take a warm shower which opens up the pours allowing all the bacteria from the skin to come out, then dry off next to a fan so that the pours close up. If you ever wrestled in high school and/or college, you know what I am talking about.

Here is the most common side effect that you hear with all Tren users besides mood swings. The NIGHT SWEATS! How many times have you twisted and turned to see that you have only been sleeping for an hour, or have not even fully went into REM. It’s funny because you read on forums that people experience waking up in a puddle of sweat while on Tren. The main reason why people sweat on Tren is the body is trying to get back to homeostasis as it sense that there is abnormal rate of progesterones in the body, a man’s natural physiology does not have such high progersterone count, so the body tries to work its magic but of course comes short resulting in a slight fever. This is why some people will wake up the next day with a fever of over 100 and feel like crap. Sleepless nights on Tren can also be because of the fat burning properties that it has, let’s say at some point during the day you had a grapefruit. The grapefruit contains a flavonoid called naringin that extends the half life of drugs. It does this by inhibiting the C450 enzyme, the same enzyme that is responsible for aromatization within the liver. So if you want to increase the effectiveness of your androgen, taking it with grapefruit would do the job but it will also increase the side effects. In other words you are feeling the after affects of Tren because of the naringin. Something to consider as well, would be injecting yourself with an infected needle, this can also lead to night sweat/ fever and so on.

Increased Anxiety is also real COMMON with Tren usage. It has neuro stimulative properties it. This is also the reason why aggression goes up. As stated before when norepinedrine goes up, your brain will either tell you to be scared or to fight. Aggression means that your brain decided to tell you to fight but if you are scared it’s because your body told you to run. Anxiety is derived from fear and denial, so if you are not confident in yourself in the given premise, the sudden rise in norepinedrine will cause your anxiety to steadily rise. Symptoms could be tremors, increased heart rate, decreased cardio, uneasiness, constant thinking, and lack of focus/concentration. Of course further anxiety can lead to a panic attack. Boy let me tell you from experience; panic attacks suck big time. Your body feels like something is wrong when in reality you are totally fine. I had so bad that my heart kept palpitating, and after every palpitation I would lose breath. I also would have slight bouts of increase in heart rate. I could hear my heart beating at all times. I also was sweating a crap ton. The only thing that helped me was releasing endorphins whether it be from comedy or pleasure. Unfortunately, I went to the hospital at one point and found nothing wrong with me which included an AKG test, and you know that is not cheap. I learned to ignore the symptoms and control stress which led to me to never experiencing it again. Increased anxiety while on Tren will also cause insomnia which blows big time. So if you see yourself staring into the dark sky at night for hours, expect it to last for a while. The body usually gets accustomed to Tren so this side should subside. If not you may need to find something to help you ease yourself to sleep.

Hair loss is common with all androgens, in theory Tren would cause hair loss as it like testosterone, so when the 19-nor metabolites reaches the scalp, it has a negative effect on the follicles. Remember the only difference between testosterone and Tren is the altered position at the 19th position, so again hair loss is common even though Tren does not convert to DHT.

Also testicular atrophy is a GIVEN LMAO. This is stuff shuts you down harder than Test itself because of its potent androgen binding. Remember as explained before it’s 5 times more androgenic than Testosterone which means it binds 5 times stronger to the androgen receptors. The common belief is the harder the binding the harder the shutdown. It’s also a progesterone which means that it decreases dopamine which leads to an increase in prolactin. This leads a dramatic drop in testosterone and also a significant drop in libido. Dopamine is most responsible for your libido. Now keep in mind that the body knows that there is elevated androgens, so guess what happens, the body will also throw estradiol especially post cycle. Estrogen is the main inhibitor of testosterone. Your poor leydig cells take a double whammy from estrogen and prolactin. You will hear lot of guys laugh at the guy in the gym who has pea sized balls. Chances are he is on test and tren. I always advice running Aromasine 15mg every other day and Prami .5mg every 3 days with tren and combining this with Provirone or lasterone. This will help keep Prolactin and estrogen from getting to high as I said before. Add in Hcgenerate and Hcg alternated 4 weeks back and forth on both this will also help with shut down.

Forms of Tren

There are a couple of forms that Tren can be administered in order to gain the benefits of added muscle mass and strength.The two most common forms of Trenbolone are Trenbolone Acetate and Trenobolone  Ethanate. The way these esters work is that the plasma lipases cleave its ester group once it reaches the bloodstream leaving free trenbolone. Trenbolone and 17epi-trenbolone are both excreted through urine as conjugates that can be hydrolyzed with beta-glucuronidase. This would imply that trenbolone leaves the body as beta-glucuronides or as sulfates. Clearly the preffered form of Trenbolone is the acetate form as it only has a half of life 3 days meaning that it leaves the body fastest yet mg per mg it’s the strongest. Meaning you need less of it to get the intended benefits yet if side effects become too apparent, it would not take long for the sides to calm down after ceasing use.  Most people can be fine after 24 hours of ceasing use, but of course it also depends on dose and duration. Any form of Tren usually needs to be taken every other day to keep plasma blood levels concentrated.

 

Dosing

 

 

As for dosing Tren Ace, I recommend to start of with 60-90mg eod and see how it treats you. Honestly there is no point in exceeding 100mgs, you will notice that vets will use 120mgs every other day but its not needed to achieve those massive gains, only a slight difference. 8-12 weeks should be enough to gain mass and strength, Tren is rather toxic, for that reason I don’t recommend that one cycle it for longer periods of time. You can run tren Eth 200mg twice a week and Parapalon 300mg-400mg once a week.

 

 

 

 

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Needtogetaas does IGF-LR3
Posted by Needtogetaas | June 21st, 2011

Lr3IGF-1 (Long R3 Insulin-like Growth Factor-I or Long R3IGF-I) is an 83 amino acid analog of human IGF-I that comprises the complete human IGF-1 sequence but with the replacement of an Arg for the Glu at position 3, as well as a 13 amino acid chain peptide at the N-terminus. This makes Long R3IGF-I two to three more potent than IGF-I in studies, because it has a lower affinity to be made inactive by IGF binding proteins, and as a result more possible activity in the body. The enhanced potency of Lr3IGF-1 over IGF-1 is due to the decreased binding of Long R3 IGF-1 to all known IGF binding proteins. These binding proteins normally inhibit the biological actions of IGF’s. This also will allow the peptide to have a longer half life of around 20-30 hours. Increasing the activity of biological IGF results in positive are increased amino acid transport to cells, increased glucose transport, increased Protein synthesis, decreased Protein degradation, and increased RNA synthesis.

In another investigation, injection of LR3-IGF-1 in various amounts to investigate the effects on the somatotropic axis (plasma levels of IGF-1 and 2, IGFBPs) was done. They have reported that plasma Long-R3 increased when administered subcutaneously but with no such activity when administered orally. Additionally, LR3 lowered the levels of native IGF-1 in rbGH-injected in calves, but L-R3 increased the amounts of IGF-II concentrations when administered with L-R3 subcutaneously. The parenteral administration of the Long R3 IGF-1 decreased the growth hormone concentration but did not affect the secretion of GH. It was also reported that the somatotrophic acis is essentially functioning in neonatal calves and can be influenced by nutrition, growth hormone and Long-R3-IGF-1 (IGF1-LR3). (Hammon and Blum 1997). Furthermore, it has been shown that in mycocytes, IGF-1 R3 stimulates the cardiomyocyte splitting in vivo (Sundgren et al. 2003).

IGF-1LR3 Mechanisms of function

First primary action is to bind to the IGF1R, a receptor tyrosine kinase, which initiates intracellular signaling. IGF-1 is one of the most powerful endogenous activators of the AKT signaling pathway, a stimulator of cell growth and production, and a strong inhibitor of involuntary cell death. IGF-1 LR3 actions have been blocked by the ERK and P13K which completely abolished the BrdU uptake. This causes IGF-1 to produce GH which is crucial for health of maintenance of bodily organ functions. Even though it does bind to insulin receptors, its binding frequency to insulin is not as strong as compared to IGF-1 but noted.

IGF-1

IGF-1 also known as somatomedin C is a polypeptide of 70 amino acids (7650 daltons), and is one of the number of associated insulin-like growth factors present in the flow. This polypeptide hormone about the same size as insulin and mimics insulin as well. So if one decides to stack the two, be careful because IGF-1 will make the effects of insulin much more potent. It is produced mostly in the Liver in response to growth hormone (GH) release from the pituitary gland. The molecule shows approximately 50% sequence homology with pro insulin and has a number of biological activities comparable to insulin. IGF-1 is a moderator of longitudinal growth in humans which translates to how tall you are capable of becoming. Total Serum IGF-1 concentrations are altered by age, nutritional state, body composition, and of course growth hormone secretion. A single basal IGF-1 level is useful in the assessment of short stature in children and in nutritional support studies of acutely ill patients. For diagnosing the condition acromegaly, a single IGF-1 concentration is much more reliable than a random GH measurement (Oppizi, et al., 1986). IGF-1 can be used for the evaluation of disease activity in acromegaly (Barkan, et al., 198.

IGF-1’s effects are not limited to building new muscle, however. It has a strong effect on lipid/ cholesterol metabolism, and helps the body shed fat at a drastically prominent rate. Also to be noted, IGF-1 is both a neuroprotector and neuro regenerator (nerve reproduction), which improves cognitive functions such as reflexes, memory, and learning ability.IGF is also important for production of connective tissue and insuring proper bone mineral density. In other words IGF Be it LR3 or DES is the golden EGG of the feel good peptides. 

One study displayed rats that were given IGF-1 and did nothing were bigger and stronger than rats that weren’t given IGF-1 but exercised. Logically the group of rats that were given IGF-1 and exercised were the most muscular, and strongest rats in the house. The positive effects of IGF-1 on the rats continued for months even after the rats stopped getting the supply of the peptide hormone, while the exercising rats immediately lost size and strength as soon as they stopped exercising.

In another study, the muscle fibers of 27 month old rats (considered old age for rats) were given IGF-1 during middle age, exhibited no weakening of muscle fibers that indicate the usual and foreseeable signs of aging. These rats did not lose any fast twitch muscle fibers during or post treatment. These fibers are responsible for power and speed which are found in abundance among athletes. Also interesting to note, they had the same speed and power output that they had when they were six months of age.

IGF-1 Deficiency and Diseases

Lacking the ability to produce sufficient amounts of IGF and GH can result in conditions, diseases and even cancer. One such disorder, termed Laron dwarfism does not respond at all to growth hormone treatment due to a lack of GH receptors. The IGF signaling pathway appears to play a crucial role in cancer. Several studies have shown that increased levels of IGF lead to an increased risk of cancer. Especially in the prevention of lung cancer, here is an abstract from study that shows the potential of IGF-1 treatment with patients suffering from lunger cancer in conjunction with their chemotreatment:

“Lung cancer is the leading cause of cancer-related death in the United States. Despite the availability of several cytotoxic and a few molecularly targeted agents, the outlook for patients with advanced non-small cell lung cancer continues to be dismal. Novel approaches are desperately needed. The insulin-like growth factor (IGF) pathway plays an important role in a number of human malignancies contributing to unregulated cell proliferation. The IGF pathway has several targets for therapeutic intervention. Preclinical studies of IGF inhibitors have demonstrated synergism when combined with chemotherapy agents and radiation. Clinical studies are currently ongoing to investigate the safety and efficacy of IGF inhibitors in combination with chemotherapy agents. In this review, we discuss the biology of the IGF pathway and various potential targets for therapy.

Transfection of IGFBP-3 into lung cancer cell lines seemed to have profound antitumor effect to the tumor cells in vitro and in vivo.45,46 Similar results have been found using recombinant human IGFBP-3 in lung carcinoma models using 3LL Lewis lung carcinoma allograft, suggesting a potential therapeutic role of IGFBP-3.47,48 Thus, IGBP-3 may also represent a potential target.

In summary, the IGF pathway seems to play a critical role in human neoplasia in general and in lung cancer in particular. Clinical trials with IGF inhibitors just begun in NSCLC hopefully will show promising results.” (Journal of Thoracic Oncology:

September 2006 – Volume 1 – Issue 7 – pp 607-610)

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needtogetaas does Clomiphene, Clomid when he has to lol.
Posted by Needtogetaas | June 21st, 2011

I am not the biggest fan of clomid however it is a drug that has been around for years and it has its uses and its place among us. With the invention and discovery of newer herbs,supplements natural compounds and synergistic blend. Clomid is fast become a thing of the past and rarely used by anyone other then old school hard heads. Still My job has always been to educated the masses and who am I to leave out information one mite need. Besides what works best for one may not work at all for another and if you love clomid then all the power to you.  In this text I will give you the blah blah blah run down of clomid. But I think you would be wise to also read this thread http://www.elitefitness.com/forum/anabolic-steroids/taking-anabolic-steroids-101-a-642856.html Post 5-6-7 .

Clomiphene Citrate (Clomid)

Clomiphene citrate is an anti estrogenic drug that is prescribed to women to treat an ovulation infertility which is an incapability to ovulate. It started to come about extensively during the early 1970s, and still used to induce fertility in women with this specific medical condition. In clinical medicine it is specifically referred to as a non steroidal ovulating inducing stimulant. The drug works by interacting with estrogen receptors, often in an antagonistic manner, in various tissues of the body including the hypothalamus, pituitary, ovary, endometrial, vagina, and cervix. One main focus is that the drug will oppose the negative feedback of estrogens on the hypothalamic pituitary ovarian axis, enhancing the release of gonadotropins (LH and FSH). This surge in gonadotropins may cause egg release, ideally leading to conception. Clomiphene shares the triphenylethylene structure with tamoxifen and toermiphene, while raloxifene is a benzothiophene derived substance. Clomid carries the trans isomers of clomiphene and tamoxifen have more antiestrogenic activity than do the cis isomers. This plays a role as tamoxifen tends to be marketed as ONLY the trans isomer, whereas clomiphene is available as the combination mixture of both cis and trans isomers. Due to structure differences, there tends to be an increased required daily dose of clomiphene compared to tamoxifen for the same effectiveness.  Clomiphene works as a weak estrogen agonist and a moderate estrogen antagonist. It is believed to act through antagonizing estrogen receptors in the HPTA (or HPTO in the female). To be more specific; it’s an agonist at the alpha receptors and an antagonist at the beta receptors.  By blocking estrogen’s negative feedback inhibition of gonadotropin secretion, clomiphene increases FSH and LH secretion and thereby induces ovulation in the female and spermatogenesis in the male. Most researchers suggest that Clomid can restore natural testosterone within 2 weeks. I never suugest taking more than 100mgs of Clomid even for jumpstarting the HPTA, since a study conducted displayed that 150-300mgs desensitized LH as opposed 25-100mgs of Clomid which sensitized LH. Obviously one would want their LH to work be sensitized so that it has the ability to continue to trigger leydig cells in producing testosterone, a crucial aspect to HPTA restoration. IMO though if you have to/must use clomid one should never have to run it above 25mg every day. You can combine other products with clomid to enhance its effectiveness and lesson see here (http://www.elitefitness.com/forum/pct-post-steroid-cycle-therapy/why-you-should-use-hcgenerate-if-you-take-nolva-clomid-pct-682879.html)

Clomid has also been touted by many physicians as an HRT jumpstart or alternative to testosterone. Here is a well known study which engages on Clomid given to patients suffering from hypogonadism.

One study had consisted of 36 Caucasian males with hypogonadism defined as serum testosterone level less than 240 ng/dL. Each patient was treated with a single daily dose of 25 mg clomiphene citrate and followed throughout the entire trial.  The average age was 39 years old, and the average pre treatment testosterone and estrogen levels were 247.6 ± 39.8 ng/dL and 32.3 ± 10.9, respectively. By the first follow-up visit of 4 to 6 weeks; the average testosterone level rose to 610.0 ± 178.6 ng/dL (P < 0.00001). In addition, the Testosterone to estrogen  ratio improved from 8.7 to 14.2 (P < 0.001). There were no apparent side effects reported by the patients. Low doses of  clomiphene citrate is effective in increasing serum total testosterone levels and improving the testosterone to estadiol ratio in males with hypogonadism. This therapy displays an alternative to testosterone therapy by stimulating the endogenous androgen production passageway. (J Sex Med 2005;2:716–721.)

The constant toll of endurance sports and over training on the body causes serious problems for sex hormone production; especially androgens. One of the main reasons for this is that over training causes the HPTA in the brain to stop producing the crucial hormone gondatropin releasing hormone. GnRH stimulates the production of LH and FSH in the pituitary gland. These are two hormones that are responsible stimulating the Leydig cells to produce more testosterone. The researchers of a recent study decided to apply this knowledge to a 29 year old man who showed signs of severe over training. The man was 1.70 metres tall and weighed a measly 52 kg, but as a result of over training he had developed stress fractures in his pelvis bone. He had been running between 80 and 140 km a week since he was fifteen years of age. For most people running is good for their bones, but too much of anything becomes a problem which is why running in moderation is key. He was suffering from osteoporosis. He’d also had encountered sexual performance issues since the age of twenty: he’d had increasing difficulty getting an erection. When the doctors tested his blood, they discovered that the man’s testes were producing too little testosterone. His total testosterone level was 4.5 nmol/L. A normal level for men is between 12.5 and 34.3 nmol/L. The man’s free testosterone level was 9.0 pmol/L. The normal level for this is 45.0 to 138.7 pmol/L. The man’s LH and FSH levels were just within the boundary of normal limits, but were on the real low side. The doctors gave the individual 50 mgs clomid daily. Within 20 weeks his testosterone had rose by a factor of four or 400%. In week 24 the doctors stopped giving the individual clomid because of the success in the treatment. When the complaints returned as a result, and had not disappeared after three months, the doctors put the guy on 25 mg clomid per day. The man apparently was not prepared to change his lifestyle in a way that would normalize his testosterone levels naturally. (Fertil Steril. 1997 Apr;67(4):783-5.)

Proof for HPTA Restoration

A discovery came about in 1995 when a second-year medical student scored a scientific first in the medical field. Carol Bickelman, still studying at the University of New Mexico School of Medicine, published in the Western Journal of Medicine the first medical study that described how a chemical using  bodybuilder restored his testosterone levels that had dropped after a serious cycle of androgenic anabolic steroids,by using the anti-estrogenic fertility inducing drug Clomiphene Citrate. The competitive bodybuilder in Bickelman’s study was 29 and had just finished an 8 month cycle of anabolic androgenic steroids. He had used 1500-1800 mgs of testosterone cypionate per week and 80 mg oxyandrolone per day. After his steroids cycle the bodybuilder became impotent, and treated his erectile dysfunction by taking a four-week cycle of hCG injections  with no results. After about a year the bodybuilder was still tormented by impotence, and he went to see a doctor. The doctor noted that the man was very muscular, also noted that his testicles were small [volume: 10 ml] and that he had 2 cm gynos around both his nipples. The man’s LH and FSH production was very low, as was his concentration of free testosterone. When the bodybuilder doubled the dose to 100 mg clomid/day was he capable of daily sex after a month. His hormone levels improved significantly especially testosterone.  They researchers proposed that Clomid had this effect because the HPTA realized the lack of estrogen so produced testosterone in order to cause aromatization which you get a continuous pattern of estrogen blocking while testosterone steadily rises through the negative feedback loop mechanism. (West J Med. 1995 February; 162(2): 158–160.)

Clomid is also pro-estrogenic in bone, which is a good thing, as it increases bone density. It can also improve your lipid profile by acting as an estrogenic agonist in the liver. The attributes makes it quite the catch when coming off a cycle that brutalized your lipids, tendons and liver.

Remember clomid is not something to take lightly my friend. Use it sparingly and when possible use Natural products. If you have any experence with clomid you are no str anger to how it can make you feel some times

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