Autor Tema: Terapija poslije ciklusa - PCT  (Pročitano 35950 puta)

0 članova i 2 gostiju pregledaju ovu temu.

Van mreže sele137

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« Odgovor #20 poslato: Septembar 26, 2009, 08:21:20 posle podne »
'Nitrom'
Isprazni sanduce ako zelis da ti posaljem PP  :rolleyes01:
http://www.healthdesigns.com/rewardsref/index/refer/id/53104/

5$ Discount Code:4089008

If I had it to do all over again, the only injectable I would ever use is Testosterone. I wouldn't waste one shot on anything else!!!
__________________________________
TESTOSTERONE IS THE SPINAL CORD OF THE BODYBUILDER,,NO SYNTETIC TESTOSTERONE = NO BODYBUILDER
__________________________________


Natural





The pros are using good old-fashioned Testosterone, Deca, Dianabol, insulin in the off-season, and GH pre-contest. Nothing fancy. But they're the pros because they're gifted, dedicated, and have been at it a long freaking time. Anybody that tells you different is either full of shit or trying to sell you garbage.



My goals are very simple:

1. Break The Law
2. Look Good Naked

Steroids will cause your kidneys to explode, your heart to blow a ventricle, and your liver to squirt out of your arse, fly across the room, and knock the cat off the futon.

The most obvious symptom is death which would hardly be missed by even the most focused and intensive bodybuilder.

Van mreže sele137

  • Ponosni vlasnik
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Odg: Terapija poslije ciklusa - PCT
« Odgovor #21 poslato: Septembar 26, 2009, 11:17:46 posle podne »
Anastrozole (1 mg ED for 10 weeks):

http://jcem.endojournals.org/cgi/content/full/85/7/2370

..eight males (aged 15–22 yr; four adults and four late pubertal) had isotopic infusions of [13C]leucine and 42Ca/44Ca, indirect calorimetry, dual energy x-ray absorptiometry, isokinetic dynamometry, and growth factors measurements performed before and after 10 weeks of daily doses of Arimidex (1 mg ED)
...Anastrozole treatment was well tolerated by all subjects. Glucose and insulin concentrations remained unchanged during these studies, as did plasma lipid concentrations, blood chemistries, and cell blood counts...


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2.5 mg of letrozole ED + 1 mg/kg of test once every 4 weeks for 12 MONTHS


http://jcem.endojournals.org/cgi/con...ull/86/10/4887

The boys in the T-treated group (12 boys) received T enanthate (1 mg/kg, im, every 4 wk, six times). The T- plus-letrozole-treated group (13 boys) received T enanthate (as above) and, in addition, an aromatase inhibitor, letrozole 2.5 mg, orally, once a day for 12 months

Safety

The concentrations of total cholesterol, low and high density lipoprotein cholesterol, triglycerides, transaminases, the leukocyte count, and the bone density were determined during the follow-up. In these safety parameters, no changes sufficient to indicate discontinuation of the treatment were observed in any of the boys. Letrozole was well tolerated; no side-effects were observed.


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http://jcem.endojournals.org/cgi/content/full/86/6/2869

Fifteen eugonadal men over 65 yr were treated for 9 weeks with 2.0 mg/day of anastrozole, an aromatase inhibitor
... After 9 weeks of aromatase inhibition, total cholesterol decreased significantly by 7 ± 10% (P = 0.016), and HDL cholesterol decreased by 7 ± 9% (P = 0.013). Calculated LDL showed a small decrease that was not statistically significant ...


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Effects of tamoxifen on lipid profile and coagulation parameters in male patients with pubertal gynecomastia.

Novoa FJ, Boronat M, Carrillo A, Tapia M, Diaz-Cremades J, Chirino R.

Department of Endocrinology, Hospital Universitario Insular, Las Palmas de Gran Canaria, Spain. jnovoa@cicei.ulpgc.es

BACKGROUND/AIM: The estrogenic actions of tamoxifen on lipid profiles and hemostasis have been extensively demonstrated in women. Due to limited experience with this drug in males, it is uncertain whether these effects are also present in men. The aim of our study was to assess the response of blood lipids, lipoproteins, and coagulation parameters in a group of men taking tamoxifen. METHODS: We studied 15 healthy boys with pubertal gynecomastia who were given 10 mg tamoxifen per day. Total testosterone, sex-hormone-binding globulin, estradiol, serum lipids, apolipoprotein B, apolipoprotein A-I, lipoprotein(a), fibrinogen, antithrombin III, von Willebrand factor, and markers of activated coagulation and fibrinolysis were determined at baseline and 1 and 3 months after beginning of the tamoxifen treatment. RESULTS: Total cholesterol and lipoprotein(a) showed moderate but significant decreases from baseline. Low-density lipoprotein and high-density lipoprotein cholesterol concentrations as well as triglyceride and apolipoprotein B levels became lower, but these changes were not statistically significant. Among clotting parameters, antithrombin III was reduced, and von Willebrand factor increased significantly. Markers of activated coagulation and fibrinolysis remained unchanged throughout the period of therapy. CONCLUSIONS: The effects of tamoxifen on blood lipids and hemostasis we found in this group of healthy young men were qualitatively similar, but lesser than those previously described in women. Copyright 2002 S. Karger AG, Basel


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from:
http://circ.ahajournals.org/cgi/con...ull/103/11/1497

..The decreases in LDL-C in the treated TVD and NCA groups did not reach significance compared with the untreated TVD group, whereas decreases in HDL-C were significant (P=0.05 and P=0.015, respectively; Figure 3A). Overall, there was no significant effect of tamoxifen on LDL:HDL ratio. Triglyceride levels showed substantial decreases in response to tamoxifen, reaching significance in the NCA group....



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Metabolism 1993 Apr;42(4):446-50 Related Articles, Links


The effect of testosterone aromatization on high-density lipoprotein cholesterol level and postheparin lipolytic activity.

Zmuda JM, Fahrenbach MC, Younkin BT, Bausserman LL, Terry RB, Catlin DH, Thompson PD.

Department of Medicine, Miriam Hospital, Providence, RI.

Stanozolol, an oral 17 alpha-alkylated androgen, increases hepatic triglyceride lipase activity (HTGLA) and decreases high-density lipoprotein cholesterol (HDL-C) levels, whereas intramuscular testosterone has comparatively little effect. In the present study, we tested the hypothesis that aromatization of androgen to estrogen blunts the lipid and lipase effects of exogenous testosterone. Fourteen male weightlifters received testosterone enanthate (200 mg/wk intramuscularly), the aromatase inhibitor testolactone (250 mg four times per day), or both drugs together in a randomized cross-over design. Serum testosterone level increased during all three drug treatments, whereas estradiol level increased only with testosterone alone (+47%, P < .05), demonstrating that testolactone effectively inhibited testosterone aromatization. Testosterone decreased HDL-C(-16%, P < .05), HDL2-C(-23%, NS), and apoprotein (apo) A-I (-12%, P < .05) levels, effects that were consistently but not significantly greater with simultaneous testosterone and testolactone administration (HDL-C, -20%; HDL2-C, -30%; apo A-I, -15%; P < .05 for all). In contrast, both testosterone regimens decreased HDL3-C levels by 13% (P < .05 for both). HTGLA increased 21% during testosterone treatment and 38% during combined testosterone and testolactone treatment (P < .01 for both). Lipoprotein lipase activity (LPLA) increased only during combined testosterone and testolactone treatment (+31%, P < .01), suggesting that estrogen production may counteract the effects of testosterone on LPLA. Testolactone alone had little effect on any lipid, lipoprotein, apoprotein, or lipase concentration.(ABSTRACT TRUNCATED AT 250 WORDS)


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Contrasting effects of testosterone and stanozolol on serum lipoprotein levels.

Thompson PD, Cullinane EM, Sady SP, Chenevert C, Saritelli AL, Sady MA, Herbert PN.

Department of Medicine, Miriam Hospital, Providence, RI 02906.

Oral anabolic steroids produce striking reductions in serum concentrations of high-density lipoprotein (HDL) cholesterol. We hypothesized that this effect related to their route of administration and was unrelated to their androgenic potency. We administered oral stanozolol (6 mg/d) or supraphysiological doses of intramuscular testosterone enanthate (200 mg/wk) to 11 male weight lifters for six weeks in a crossover design. Stanozolol reduced HDL-cholesterol and the HDL2 subfraction by 33% and 71%, respectively. In contrast, testosterone decreased HDL-cholesterol concentration by only 9% and the decrease was in the HDL3 subfraction. Apolipoprotein A-I level decreased 40% during stanozolol but only 8% during testosterone treatment. The low-density lipoprotein cholesterol concentration increased 29% with stanozolol and decreased 16% with testosterone treatment. Stanozolol, moreover, increased postheparin hepatic triglyceride lipase activity by 123%, whereas the maximum change during testosterone therapy (+25%) was not significant. Weight gain was similar with both drugs, but testosterone was more effective in suppressing gonadotropic hormones. We conclude that the undesirable lipoprotein effects of 17-alpha-alkylated steroids given orally are different from those of parenteral testosterone and that the latter may be preferable in many clinical situations.


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Metabolism 1997 Sep;46(9):992-6 Related Articles, Links


Effects of short-term stanozolol administration on serum lipoproteins in hepatic lipase deficiency.

Bausserman LL, Saritelli AL, Herbert PN.

Lipid Research Laboratory, Miriam Hospital, Brown University Medical School, Providence, RI, USA.

We have identified a kindred in Providence, RI, deficient in hepatic triglyceride lipase (HL). The two affected brothers have coronary heart disease and elevated levels of triglycerides, total cholesterol, high-density lipoprotein (HDL) cholesterol, and apolipoprotein [apo] A-I. The lipoprotein lipase (LPL) activity is normal. We and others have postulated that the effects of oral anabolic steroids on HDL metabolism are mediated by HL. To test this hypothesis, we treated these two men and two controls with the oral androgen stanozolol (6 mg/d) for 2 weeks. Consistent with other reports, HL activity increased a mean of 277% in controls with a concomitant decrease in HDL cholesterol (49%), HDL2 cholesterol (90%), HDL3 cholesterol (16%), and apo A-I (41%) and no change in apo A-II. Although stanozolol failed to induce HL activity in the HL-deficient man, HDL cholesterol, HDL2 cholesterol, and apo A-I were reduced a mean of 20%, 48%, and 32%, respectively. In contrast to controls, HDL3 cholesterol (46%) and apo A-II (14%) increased in HL-deficient subjects. Stanozolol treatment also increased LPL activity (124% +/- 86%, n = 4) and decreased lipoprotein(a) ([Lp(a)] 66% +/- 3%, n = 3) in the three men with detectable levels. The data indicate that in addition to stimulation of HL activity, stanozolol treatment changes HDL cholesterol concentration and subfraction distribution by other mechanisms.


http://www.healthdesigns.com/rewardsref/index/refer/id/53104/

5$ Discount Code:4089008

If I had it to do all over again, the only injectable I would ever use is Testosterone. I wouldn't waste one shot on anything else!!!
__________________________________
TESTOSTERONE IS THE SPINAL CORD OF THE BODYBUILDER,,NO SYNTETIC TESTOSTERONE = NO BODYBUILDER
__________________________________


Natural





The pros are using good old-fashioned Testosterone, Deca, Dianabol, insulin in the off-season, and GH pre-contest. Nothing fancy. But they're the pros because they're gifted, dedicated, and have been at it a long freaking time. Anybody that tells you different is either full of shit or trying to sell you garbage.



My goals are very simple:

1. Break The Law
2. Look Good Naked

Steroids will cause your kidneys to explode, your heart to blow a ventricle, and your liver to squirt out of your arse, fly across the room, and knock the cat off the futon.

The most obvious symptom is death which would hardly be missed by even the most focused and intensive bodybuilder.

Van mreže sele137

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  • Poruke: 1399
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Odg: Terapija poslije ciklusa - PCT
« Odgovor #22 poslato: Septembar 26, 2009, 11:54:12 posle podne »
New Theory on PCT!
Opioid Modulation & Potential for Preventing anabolic androgenic steroids Induced hpta Suppression
:
By: Eric M. Potratz
________________________________________


Post Cycle Therapy (PCT - post cycle therapy) is a key component in a steroid cycle, as suppression of the Hypothalamus, Pituitary, Testicular Axis (HPTA) is seemingly unavoidable to a steroid user. What I will be presenting in this article is a new idea to the world of anabolic androgenic steroids users. This exciting new concept addresses the possibility of limiting and possibly preventing suppression of the (HPTA) during cycle. More specifically, we will learn how we can actively modulate the hypothalamus & pituitary pulse generator during cycle and how this can prime our endocrine system for a quicker, smarter, and healthier recovery from anabolic androgenic steroids (anabolic androgenic steroids).

For a moment, let’s forget the concept of "post cycle therapy", and embrace the idea of "constant cycle therapy" – active therapy throughout a steroid cycle. The HPTA involves a constant biological interplay of responses and feedback loops that can ultimately become shutdown and degraded during exogenous hormone administration. However, research suggests suppression of the hypothalamus and pituitary may be preventable during steroid use. Before we delve into the details, lets first take a quick recap on the HTPA and how it responses to anabolic androgenic steroids.

HPTA – The basics
When the hypothalamus senses low hormone levels, it secretes gonandotropin releasing hormone (GnRH). This GnRH then travels a short distance to the nearby pituitary gland to stimulate gonadotrope receptors. These, in turn, secrete the gonadotrophins, luteinizing hormone (lh) and follicle stimulating hormone (FSH). These gonadotrophins travel all the way down to the testis, to activate their respective leydig and seritoli cells. LH initiates testosterone production via the leydig cell receptor (steroidogenesis), while FSH initiates sperm production via the sertoli cell receptor (spermatogenesis).

anabolic androgenic steroids’s inhibit hormone production just as endogenous hormones do. Testosterone interacts with the androgen receptor (AR) and estrogen interacts with the estrogen receptor (ER). When these hormones are in high concentration, they cause the hypothalamus to decrease its release of GnRH, which decreases LH and FSH production from the pituitary.1 This cuts off the signal to the testis and halts all hormone production. This process is a daily event for the rhythmic endocrine system. Spikes in LH & FSH are followed by spikes in testosterone, and spikes in testosterone result in a reduction of LH & FSH release until testosterone levels decline and LH & FSH is released again. The caveat with most steroids, is that hormone levels remain chronically high (24/7) and do not allow release of LH or FSH, thus leaving the pituitary and testis in a dormant state for as long as the steroids are administered.

While low-dose on-cycle HCG is a good protocol to mimic LH and keep the testis from atrophy, (to be covered in a future article) it does nothing to prevent pituitary atrophy. We forget that the pituitary is susceptible to the same degradation and atrophy as the testis. That is, when the GnRH secretion from the hypothalamus stops (during a steroid cycle), the pituitary reduces its number of GnRH receptors and becomes less and less responsive to GnRH stimulation as weeks pass.11 This is analogous to atrophy of the testis, during absence of an LH or FSH signal. On the same accord, both the pituitary and testis will decrease receptor concentration during over stimulation as well, as its been found from too much hCG use or too much GnRH stimulation.12,13 The point here, is that only minor stimulus is required for preservation of function and sensitivity. Perhaps a completely neglected and suppressed pituitary may explain the lack of full and prompt recovery for many steroid users, despite adherence to a "tried and true" hCG, Clomid + Nolvadex regimen. So the question is – How can we prevent suppression of the pituitary, and better yet, how can we prevent suppression of the hypothalamus?

A closer look –
In should be mentioned that another mechanism in which AAS inhibit LH and FSH release from the pituitary is by direct suppression upon the pituitary GnRH receptors and consequent quenching of LH & FSH secretion.35,38 However its appears that AAS which bind strictly to the AR, do not exert a direct negative effect on pituitary function or sensitivity.34,37,39 This agrees with the theory that non-aromatizing steroids such as Primobolan, Proviron or Masteron are not nearly as suppressive as an aromatizing AAS’s such as testosterone or Dianabol. Evidence suggests that estradiol is about 200x more suppressive than testosterone on a molar basis37, and that administration of Arimidex can greatly reduce testosterones suppression on GnRH and LH release.42 So, we know anti-estrogens can limit suppression of AAS, but this only solves half the problem.

When it comes to suppression of the hypothalamus, and what seems to be basic endocrinology, we find it is not so simple upon closer examination. There is more than a simple on-off switch for the hypothalamus control center, a lot more. Evidence suggests that there isn’t even a direct AR or ER action upon GnRH release.2-6 That is, steroid hormones do not directly influence GnRH release from the GnRH neurons.7

It was well summarized here by A.J Tilbrook et al,
"It follows, that the actions of testicular steroids on GnRH neurons must be mediated via neuronal systems that are responsive to steroids and influence the activity of GnRH neurons."

And again here by FJ Hayes et al
"It was thus postulated that estrogen-receptive neurons were acting as intermediaries in the non-genomic regulation of GnRH by estrogen"

There is a network of neurogenic intermediaries in the hypothalamus for GnRH release that communicate the inhibitory effects of steroid hormones. More specifically, it is the combined efforts of neuro-active peptides and catecholamines which send the message of "suppression" to the GnRH neurons once activated by steroid hormones.16 These primary messengers are known as a group of neuro-active peptides called endogenous opioid peptides (EOP’s).7,16 The EOP’s consist of the three main peptides -- b-endorphin, dynorphin, and enkephalins, which act upon their respective u-opioid, k-opioid, and s-opioid receptors. It appears that the most influential EOP in GnRH modulation is b-endorphin, acting upon the u-opioid receptor. 8-10 For this reason, b-endorphin will be the main focus of the article, although there are other intermediates involved.

When steroid hormones reach the hypophysial portal, they activate the EOP’s, which suppress GnRH. We know that steroid hormones must communicate with these opioid receptors in order for them to inhibit the release of GnRH from the GnRH neurons, since the GnRH neurons do not have AR or ER receptors. What’s most interesting here is that the suppression on GnRH neurons can actually be intercepted by a u-opioid receptor antagonist – such as naloxone, and the orally active congers naltrexone, and nalmefene.
This is accomplished by blocking the u-opioid receptor and preventing the inhibitory effects of b-endorphin upon the GnRH releasing neuron. It should be noted that this "antagonism" of suppression is not due to antagonism of the AR or ER itself, since u-opioid antagonists to not bind to these hormone receptors.15,32


Essentially, a u-opioid antagonist such as naloxone takes the brakes off of GnRH release and allows pulses of GnRH to occur as if no steroid hormones are present.17 Naloxone, and related u-opioid antagonists have consistently proven to block the suppressive effects of testosterone, dihydrotestosterone, and estrogen administration in both animals and humans.18-25 It also appears that these drugs have the ability to increase pituitary sensitivity to GnRH.26,27

U-opioid antagonists have long been used for treatment of opioid dependence; not only to control cravings of narcotics, but to restore a suppressed endocrine system.28,29 It’s well known that strong opioid based drugs such as methadone, blow, heroin and alcohol can suppress GnRH and therefore suppress LH & FSH. It seems that this decease of GnRH is due to the same EOP mechanisms seen with AAS induced suppression.33 In alcoholics, blow and heroin users, naltrexone and naloxone have been used to restore LH and testosterone levels.28,29 Naltrexone has even been proposed as a treatment for male impotence and erectile dysfunction.30,31

Naloxone, naltrexone and nalmefene seem progressively more powerful in their potency to dis-inhibit LH release, respectively14,18 Naloxone lacks oral bioavailability therefore injection is required. An injectable preparation could easily be made with BA water due to the water solubility of the compound. A 40mg subcutaneous injection would be a typical dose of naloxone. Naltrexone is orally active, with a safe and effective oral dose being about 100mg for a 220lb male.18 While a lower dose of about 25-50mg of nalmefene would seemingly have the same benefit.20,24 Increasing the dose with either of these drugs will surely increase the likelihood of side-effects without notably increasing the benefit. An every 3rd day protocol would seem appropriate with these drugs, as only to increase GnRH and LH release enough to prevent pituitary and testicular shrinkage – Just enough to keep them in the "ball game". Also, a twice a week dosing protocol would most likely limit the increased opioid sensitivity induced by the long-term use of the drugs.

A word of caution: The opioids antagonists mentioned in this article are recognized as safe and non-toxic at the given dosages, however they can cause severe withdrawal symptoms in opiate users (methadone, morphine, blow, and heroin addicts.) Caution is also advised when using opioid antagonists prior to sedation or surgery as they can reduce effectiveness of anesthetics. Temporary nausea, headache or fatigue, are occasional side-effects associated with the use of these drugs. Naltrexone has been reported to heighten liver enzymes, while naloxone and nalmefene do not appear to have this issue. At any rate, a twice a week protocol for 4-16 weeks is unlikely to cause any liver issues that may be associated with naltrexone.

A few point to consider -
For those who choose to embark on a every 3rd day protocol of an opioid antagonist several things should be considered. First, total prevention of HPTA suppression is unlikely in a cycle of 1gm or more per week of AAS. However, by following smart cycling guidelines, suppression will at least be minimized to the point where normal HPTA function could be regained within days of AAS clearance, rather than months. The protocol suggested in this article would at least allow steroid users to limit the usage of classic selective estrogen receptor modulator’s for PCT. Several things shall be considered when planning an AAS protocol designed to limit suppression.

It appears that progestin based AAS such as trenbolone and nandrolone which bind not only to the AR, but also to the progesterone receptor  also have a directly suppressive effect on pituitary sensitivity36 (similar to estrogens). It also appears that no opioid receptor antagonist or anti-aromatase can prevent suppression via the PR. Therefore, a multiple gram stack of testosterones and nandrolones is no doubtingly going to completely suppress HTPA function by causing suppression via the ER, AR and PR.40,41 If one hopes for a prompt and full recovery post cycle, perhaps nandrolones are better avoided, or at least not stacked with heavily aromatizing AAS without the concurrent use of a strong aromatase inhibitor.

As it was pointed out earlier in this article, estrogen has a markedly stronger effect on suppression of LH release compared to androgens since estrogens suppresses the hypothalamus and pituitary. Usage of an aromatase inhibitor such as anastrozole, letrozole, or exemestane (Aromasin) can reduce estrogen and greatly reduce suppression on GnRH, LH and FSH release by preventing excessive ER activation in the hypothalamus and desensitization of the pituitary gonadotropes. 35,37,38 Anastrozole has ~50% maximal total estrogen suppression at 1mg/day. Exemestane has ~50% maximal total estrogen suppression at 25mg/day. While letrozole has ~60% at 1mg/day. These are averages based on compiled data from several studies. Similar estrogen suppression can also been seen from only twice a week administration of these aromatase inhibitor’s.43-47



References
1. Hypothalamic Gonadotropin-Releasing Hormone: Basic and Clinical Aspects. Yen SSC. Raven Press, New York, pp 245–280 (1991)
2. Absence of androgen receptors in LHRH immunoreactive neurons. Huang X, Harlan RE. Brain Res 1993; 624:309–311
3. Augmented hypothalamic proopiomelanocortin gene expression with pubertal development in the male rat: evidence for an androgen receptor-independent action. Kerrigan JR, Martha PM, Krieg RJ, Queen TA, Monahan PE, Rogol AD. Endocrinology.128:1029-1035. (1991)
4. Distribution of estrogen receptorimmunoreactive cells in the preoptic area of the ewe: co-localisation with glutamic acid decarboxylase but not luteinizing hormone-releasing hormone. Herbison AE, Robinson JE, Skinner DC. Neuroendocrinology 1993; 57:751–759.
5. Unmasking the neural progesterone receptor in the preoptic area and hypothalamus of the ewe: no colocalization with gonadotropin-releasing neurons. Skinner DC, Caraty A, Allingham R. Endocrinology 2001; 142:573–579.
6. Multimodal influences of estrogen upon gonadotropin releasing hormone neurons. Herbison AE. Endocrine Reviews 1998; 19:302–330.
7. Negative Feedback Regulation of the Secretion and Actions of Gonadotropin-Releasing Hormone in Males. A.J. Tilbrook and I.J. Clarke. Biol Reprod, Mar 2001; 64: 735
8. Steroid Control of Gonadotropin-Releasing Hormone Secretion: Associated Changes in Pro-Opiomelanocortin and Preproenkephalin Messenger RNA Expression in the Ovine Hypothalamus
James A. Taylor, Marie-Laure Goubillon, Kevin D. Broad, and Jane E. Robinson. Biol Reprod, Mar 2007; 76: 524
9. Do gonadotropin-releasing hormone, tyrosine hydroxylase-, and ß-endorphin-immunoreactive neurons contain oestrogen receptors? A double-label immunocytochemical study in the Suffolk ewe. Lehman MN, Karsch FJ. Endocrinology 1993; 133:887–895
10. -Endorphin blocks luteinizing hormone-releasing hormone release by inhibiting the nitricoxidergic pathway controlling its release. Alicia G. Faletti, Claudio A. Mastronardi, Alejandro Lomniczi, Adriana Seilicovich, Martha Gimeno, Samuel M. McCann, and Valeria Rettori. PNAS, Feb 1999; 96: 1722.
11. The frequency of gonadotropin-releasing hormone stimulation determines the number of pituitary gonadotropin-releasing hormone receptors. Katt JA, Duncan JA, Herbon L, Barkan A, Marshall JC. Endocrinology. 116:2113–2115. (1985)
12. Exogenous gonadotrophin-releasing hormone (GnRH) stimulates LH secretion in male monkeys (Macaca fascicularis) treated chronically with high doses of a GnRH-antagonist. Weinbauer GF, Hankel P, Nieschlag E. J Endocrinol. 133:439–445. (1992)
13. Chronic administration of the luteinizing hormone-releasing hormone (LHRH) antagonist cetrorelix decreases gonadotrope responsiveness and pituitary LHRH receptor messenger ribonucleic acid levels in rats. Pinski J, Lamharzi N, Halmos G, et al. 1996. Endocrinology. 137:3430–3436.
14. Acute effects of testosterone infusion and naloxone on luteinizing hormone secretion in normal men.
GB Kletter, CM Foster, IZ Beitins, JC Marshall, and RP Kelch. J. Clin. Endocrinol. Metab., Nov 1992; 75: 1215 - 1219.
15. Naloxone-induced increases in serum luteinizing hormone in the male: mechanisms of action
TJ Cicero, CE Wilcox, RD Bell, and ER Meyer. J. Pharmacol. Exp. Ther., Mar 1980; 212: 573.
16. Endogenous opioids participate in the regulation of the hypothalamic-pituitary-luteinizing hormone axis and testosterone’s negative feedback control of luteinizing hormone. CICERO, T. J., SCHAINKER, B. A. AND MEYER, E. R. Endocrinology 104: 1286-1291, (1979)
17. Opiatergic control of LH secretion is eliminated by gonadectomy. BHANOT, R. AND WILKINSON, M.: Endocrinology 112: 399-401, (1983)
18. Role of endogenous opiates in the expression of negative feedback actions of androgens and estrogen on pulsatile properties of luteinizing-hormone secretion in man. Veldhuis JD, Rogol AD, Samojlik E, Ertel MH. J Clin Invest. 74:47–55 (1984)
19. Counteraction of gonadal steroid inhibition of luteinizing hormone release by naloxone. VAN VUGT, D. A., SYLVESTER, P. W., AYLSWOWRH, D. F. AND MNRRAS J. J. Chro- naloxone. Endocrinology 34: 274-278, 1982
20. Unexpected effects of nalmefene, a new opiate antagonist, on the hypothalamic-pituitary-gonadal axis in the male rat. P Limonta, CW Bardin, EF Hahn, and RB Thau. Steroids, Dec 1985; 46(6): 955-65.
21. In vivo evidence for a direct effect of naloxone on testicular steroidogenesis in the male rat. TJ Cicero, ML Adams, LH O'Connor, and B Nock. Endocrinology, Aug 1989; 125: 957
22. Endogenous opioids participate in the regulation of the hypothalamus- pituitary-luteinizing hormone axis and testosterone's negative feedback control of luteinizing hormone. TJ Cicero, BA Schainker, and ER Meyer. Endocrinology, May 1979; 104: 1286
23. Effect of naloxone on the plasma levels of LH, FSH, prolactin and testosterone in Beetal bucks.
Singh B, Dixit VD, Singh P, Georgie GC, Dixit VP. Department of Animal Production Physiology, CCS Haryana Agricultural University, 125004, Hisar, India
24. Endocrinology: The effect of nalmefene on pulsatile secretion of luteinizing hormone and prolactin in men. G.R. Graves, T.G. Kennedy, R.F. Weick, and R.F. Casper. Hum. Reprod., Oct 1993; 8: 1598 - 1603.
25. Effects of the novel opiate antagonist, SDZ 210-096, on luteinizing hormone secretion in the rat
RA Siegel and L Revesz. J. Pharmacol. Exp. Ther., Apr 1989; 249: 264.
26. Effect of antagonists of dopamine and opiates on the basal and GnRH-induced secretion of luteinizing hormone, follicle stimulating hormone and prolactin during lactational amenorrhoea in breastfeeding women. C.C.K. Tay, A.F. Glasier, and A.S. McNeilly. Hum. Reprod., Apr 1993; 8: 532 - 539.
27. Naltrexone administration modulates the neuroendocrine control of luteinizing hormone secretion in hypothalamic amenorrhoea. Alessandro D. Genazzani, Mario Gastaldi, Felice Petraglia, Cesare Battaglia, Nicola Surico, Annibale Volpe, and Andrea R. Genazzani. Hum. Reprod., Nov 1995; 10: 2868 - 2871.
Revives LH and testosterone in heroin users
28. Heroin and naltrexone effects on pituitary-gonadal hormones in man: interaction of steroid feedback effects, tolerance and supersensitivity. JH Mendelson, J Ellingboe, JC Kuehnle, and NK Mello. J. Pharmacol. Exp. Ther., Sep 1980; 214: 503.
29. Alcohol effects on luteinizing hormone and testosterone in male macaque monkeys. NK Mello, JH Mendelson, MP Bree, J Ellingboe, and AS Skupny. J. Pharmacol. Exp. Ther., Jun 1985; 233: 588.
Opioid antagonist enhances erectile function
30. Erectile function and naltrexone. Goldstein JA. Ann Intern Med 105:799 (1986)
31. Opiate antagonists in erectile dysfunction: a possible new treatment option? Results of a pilot study with naltrexone. van Ahlen H, Piechota HJ, Kias HJ, Brennemann W, Klingmuller D. Eur Urol 28:246–250 (1995)
32. The effects of opiates on androgen binding in the forebrain of the rat. PJ Sheridan and JM Buchanan
Int J Fertil, January 1, 1980; 25(1): 36-43. 33. Morphine exerts testosterone-like effects in the hypothalamus of the castrated male rat. CICERO, T. J., MEYER, E. R., GABRIEL, S. M., BELL, R. D. AND WILCOX, C. E. Brain Rae. 202: 151-164, (1980)
dihydrotestosterone and testosterone not suppressive to the pituitary like estrogens
34. Studies of gonadotropin-releasing hormone (GnRH) action using GnRH receptor-expressing pituitary cell lines. Kaiser UB, Conn PM, Chin WW. Endocr Rev. 18:46–70. (1997)
Estrogen decreases gonadotrope receptors for GrRH.
35. Patterns of LH secretion in castrated bulls during intravenous infusion of androgenic and estrogenic steroids: Pituitary response to exogenous luteinizing hormone-releasing hormone. M.J. D’occhio et al. Biology of reproduction 26, 249-257 (1982)
36. Demonstration of progesterone receptor mediated gonadotrophin suppression in men. Brady B, Anderson RA, Kinniburgh D, Baird DT 2002. J Endocrinol 3(Suppl):OC37
37. Bagatell CJ, Dahl KD, Bremner WJ. 1994 The direct pituitary effect of testosterone to inhibit gonadotropin secretion in men is partially mediated by aromatization to estradiol. J Androl. 15:15–21.
38. Sherins RJ, Loriaux DL. 1973 Studies on the role of sex steroids in the feedback control of FSH concentrations in men. J Clin Endocrinol Metab. 36:886–893
39. Santen RJ. 1975 Is aromatization of testosterone to estradiol required for inhibition of luteinizing hormone secretion in men? J Clin Invest. 56:1555–1563
40. Influence of nandrolondecanoate on the pituitary-gonadal axis in males. JW Bijlsma, SA Duursma, JH Thijssen, and O Huber. Acta Endocrinol (Copenh), September 1, 1982; 101(1): 108-12.
Both progestin (nandrolone) and testosterone more effective at reducing LH/FSH and causing azoospermia.
41. Endocrine approaches to male fertility control. UA Knuth and E Nieschlag; Baillieres Clin Endocrinol Metab, February 1, 1987; 1(1): 113-31.
42. Aromatization Mediates Testosterone's Short-Term Feedback Restraint of 24-Hour Endogenously Driven and Acute Exogenous Gonadotropin-Releasing Hormone-Stimulated Luteinizing Hormone and Follicle-Stimulating Hormone Secretion in Young Men. J. A. Schnorr, M. J. Bray, and J. D. Veldhuis
J. Clin. Endocrinol. Metab., June 1, 2001; 86(6): 2600 - 2606.
43. Short-Term Aromatase-Enzyme Blockade Unmasks Impaired Feedback Adaptations in Luteinizing Hormone and Testosterone Secretion in Older Men; Johannes D. Veldhuis and Ali Iranmanesh
J. Clin. Endocrinol. Metab., Jan 2005; 90: 211 – 218
44. Effects of Aromatase Inhibition in Elderly Men with Low or Borderline-Low Serum Testosterone Levels
Benjamin Z. Leder, Jacqueline L. Rohrer, Stephen D. Rubin, Jose Gallo, and Christopher Longcope
J. Clin. Endocrinol. Metab., Mar 2004; 89: 1174 - 1180.
45. Comparative Assessment in Young and Elderly Men of the Gonadotropin Response to Aromatase Inhibition. Guy G. T’Sjoen, Vito A. Giagulli, Hans Delva, Patricia Crabbe, Dirk De Bacquer, and Jean-Marc Kaufman. J. Clin. Endocrinol. Metab., Oct 2005; 90: 5717 - 5722.
46. Pharmacokinetics and Dose Finding of a Potent Aromatase Inhibitor, Aromasin (Exemestane), in Young Males. Nelly Mauras, John Lima, Deval Patel, Annie Rini, Enrico di Salle, Ambrose Kwok, and Barbara Lippe
J. Clin. Endocrinol. Metab., Dec 2003; 88: 5951 - 5956.
47. Differential Regulation of Gonadotropin Secretion by Testosterone in the Human Male: Absence of a Negative Feedback Effect of Testosterone on Follicle-Stimulating Hormone Secretion
Frances J. Hayes, Suzzunne DeCruz, Stephanie B. Seminara, Paul A. Boepple, and William F. Crowley, Jr.
J. Clin. Endocrinol. Metab., Jan 2001; 86: 53 - 58.
http://www.healthdesigns.com/rewardsref/index/refer/id/53104/

5$ Discount Code:4089008

If I had it to do all over again, the only injectable I would ever use is Testosterone. I wouldn't waste one shot on anything else!!!
__________________________________
TESTOSTERONE IS THE SPINAL CORD OF THE BODYBUILDER,,NO SYNTETIC TESTOSTERONE = NO BODYBUILDER
__________________________________


Natural





The pros are using good old-fashioned Testosterone, Deca, Dianabol, insulin in the off-season, and GH pre-contest. Nothing fancy. But they're the pros because they're gifted, dedicated, and have been at it a long freaking time. Anybody that tells you different is either full of shit or trying to sell you garbage.



My goals are very simple:

1. Break The Law
2. Look Good Naked

Steroids will cause your kidneys to explode, your heart to blow a ventricle, and your liver to squirt out of your arse, fly across the room, and knock the cat off the futon.

The most obvious symptom is death which would hardly be missed by even the most focused and intensive bodybuilder.

Van mreže Nitrom

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« Odgovor #23 poslato: Septembar 27, 2009, 12:45:08 pre podne »
Mislim da je dovoljno,ko nije svatio poentu posle ovolikih textova bolje da se ni ne upusta u ovu materiju :P  :clap:

imas pm inace  :rolleyes01:

Van mreže sele137

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« Odgovor #24 poslato: Oktobar 22, 2009, 11:06:30 posle podne »
MALE MEDICAL FERTILITY TREATMENT: HCG + PHARMACEUTICAL URINARY LH + FSH
TO INCREASE SPERM COUNT THROUGH SPERMATOGENESIS
 

National Medical Clinic, Inc. physicians provide a Male Medical Fertility Treatment consisting of the administration of Human Chorionic Gonadotropin (HCG), Luteinizing Hormone (LH) and Follicle-Stimulating Hormone (FSH) to increase male fertility (sperm count) or spermatogenesis in hypogonadotropic men when the pituitary gland is not secreting sufficient FSH, or is deficient in the production of both LH and FSH, such that spermatogenesis does not occur.

The purpose of HCG treatment with regard to male infertility is to increase spermatogenesis in hypogonadotropic men deficient in FSH, or is deficient in the production of both LH and FSH. The use of pharmaceutically manufactured gonadotropin LH combines with HCG to replace insufficient LH secretion by the pituitary. FSH is available mixed with LH in the form of Pergonal® or Menopur®, and other more purified forms of gonadotropins, as well as in a pure forms as recombinant FSH (Gonal F, Follistim). This treatment combines pharmacy compounded or manufactured HCG with pharmaceutically manufactured gonadotropin LH and FSH to induce spermatogenesis in hypogonadotropic men when the pituitary gland is not secreting sufficient LH, FSH or is deficient in the production of both LH and FSH such that spermatogenesis does not occur.

Hypogonadism is a medical term for a defect of the reproductive system that results in lack of function of the gonads (ovaries or testes). The gonads have two functions: to produce hormones (testosterone, estradiol, antimullerian hormone, progesterone, inhibin B), activin and to produce gametes (eggs or sperm). Deficiency of sex hormones can result in defective primary or secondary sexual development, or withdrawal effects (e.g., premature menopause) in adults. Defective egg or sperm development results in infertility.

Follicle-stimulating hormone (FSH) is a hormone synthesized and secreted by gonad tropes in the anterior pituitary gland. FSH regulates the development, growth, pubertal maturation, and reproductive processes of the human body. FSH and Luteinizing hormone (LH) act synergistically in reproduction. In males, FSH enhances the production of androgen-binding protein by the Sertoli cells of the testes, and is critical for spermatogenesis.

In males, FSH enhances the production of androgen-binding protein by the Sertoli cells of the testes, and is critical for spermatogenesis. FSH regulates the reproductive processes of the human body. Both LH (or HCG as a medication substitute for naturally produced LH) and FSH must be present for spermatogenesis.

Luteinizing hormone (LH) is a hormone produced by the anterior pituitary gland. LH is a glycoprotein. Each monomeric unit is a sugar-like protein molecule; two of these make the full, functional protein. Its structure is similar to the other glycoproteins, follicle-stimulating hormone (FSH), thyroid-stimulating hormone (TSH), and human chorionic gonadotropin (hCG). The protein dimer contains 2 polypeptide units, labeled alpha and beta subunits that are connected by two disulfide bridges:

In both males and females, LH is essential for reproduction. In the male, LH acts upon the Leydig cells of the testis and is responsible for the production of testosterone, an androgen that exerts both endocrine activity and intratesticular activity such as spermatogenesis.

The release of LH at the pituitary gland is controlled by pulses of gonadotropin-releasing hormone (GnRH) from the hypothalamus. Those pulses, in turn, are subject to the estrogen feedback from the gonads. LH levels are normally low in men during childhood. During the reproductive years typical male LH levels are between 5-20 mIU/ml. Physiologic high LH levels are seen during the LH surge. They typically they last 48 hours.

Persistently high LH levels are indicative of situations where the normal restricting feedback from the gonad is absent, leading to a higher pituitary production of both LH and FSH. High levels of LH and FSH in men may indicate gonadal dysgenesis, Turner Syndrome, castration testicular failure or CAH. Congenital adrenal hyperplasia (CAH) refers to any of several autosomal recessive diseases resulting from mutations of genes for enzymes mediating the biochemical steps of production of cortisol from cholesterol by the adrenal glands (steroidogenesis). Most of these conditions involve excessive or deficient production of sex steroids. Diminished secretion of LH can result in failure of gonadal function (hypogonadism), which is a medical condition that is typically manifested in males as failure in production of normal numbers of sperm.

LH is available mixed with FSH in the form of Pergonal or Menopur), and other forms of gonadotropins . More purified forms of gonadotropins may reduce the LH portion in relation to FSH. Recombinant LH is available as lutropin alfa (Luveris). All these medications have to be given parenterally. They are commonly in infertility therapy to stimulate follicular development, notably in IVF therapy. HCG medication is often used as a substitute for LH because it activates the same receptor. HCG medication is derived from urine of pregnant women, less costly, and has a longer half-life than LH.

Spermatogenesis is the process by which male spermatogonia develop into mature spermatozoa. Spermatozoa are the mature male gametes in many sexually reproducing organisms. Spermatogenesis produces mature male gametes, commonly called sperm but specifically known as spermatozoa, which are able to fertilize the counterpart female gamete, the oocyte, during conception to produce a single-celled individual known as a zygote. This is the cornerstone of sexual reproduction and involves the two gametes both contributing half the normal set of chromosomes (haploid) to result in a chromosomally normal (diploid) zygote.

Spermatogenesis takes place within several structures of the male reproductive system. The initial stages occur within the testes and progress to the epididymis where the developing gametes mature and are stored until ejaculation. The seminiferous tubules of the testes are the starting point for the process, where stem cells adjacent to the inner tubule wall divide in a centripetal direction-beginning at the walls and proceeding into the innermost part, or lumen-to produce immature sperm. Maturation occurs in the epididymis and involves the acquisition of a tail and hence motility.

Hormonal control of spermatogenesis varies among species. In humans the mechanism are not completely understood, however it is known that initiation of spermatogenesis occurs at puberty due to the interaction of the hypothalamus, pituitary gland and Leydig cells. If the pituitary gland is removed, spermatogenesis can still be initiated by follicle stimulating hormone and testosterone.

Follicle stimulating hormone (FSH) stimulates both the production of androgen binding protein by Sertoli cells, and the formation of the blood-testis barrier. Androgen binding protein is essential to concentrating testosterone in levels high enough to initiate and maintain spermatogenesis, which can be 20-50 times higher than the concentration found in blood. Follicle stimulating hormone (FSH) may initiate the sequestering of testosterone in the testes, but once developed only testosterone is required to maintain spermatogenesis. However, increasing the levels of follicle stimulating hormone will increase the production of spermatozoa by preventing the apoptosis of type A spermatogonia. The hormone inhibin acts to decrease the levels of follicle stimulating hormone.

The Sertoli cells themselves mediate parts of spermatogenesis though hormone production. They are capable of producing the hormones estradiol and inhibin. The Leydig cells are also capable of producing estradiol in addition to their main product testosterone.

In this male infertility treatment follicle stimulating hormone (FSH) is administered to treat male infertility by increasing the both the production of androgen binding protein by Sertoli cells, and the formation of the blood-testis barrier. After the androgen binding protein initiates the sequestering of testosterone in the testes and thereby causes testosterone concentration in levels high enough to initiate and maintain spermatogenesis, the LH and HCG stimulate the testes to increase the production of testosterone to maintain spermatogenesis. And spermatogenesis is the process of creating sperm. This treatment requires that a patient present with a insufficient levels of naturally produced LH or FSH or deficient in both LH and FSH. The gonadotropins FSH and LH in combination with HCG induces spermatogenesis in hypogonadotropic men.
This medical protocol does not include the administration of recombinant FSH to induce spermatogenesis. However, a medical treatment that includes the use of recombinant FSH may be indicated if the administration of the urinary FSH gonadotropin does not increase both the production of androgen binding protein by Sertoli cells, and the formation of the blood-testis barrier. The increase in testosterone production alone by LH or HCG is not sufficient to cause spermatogenesis in hypogonadotropic men. There must also be an FSH induced increase both the production of androgen binding protein by Sertoli cells, and the formation of the blood-testis barrier to increase the production of the androgen binding protein, which initiates the sequestering of testosterone in the testes and thereby causes testosterone concentration in levels high enough to initiate and maintain spermatogenesis. It is at this time that the increased production of testosterone resulting from the stimulation of the testes by administration of HCG and LH is essential to maintaining spermatogenesis

HCG is approved for use in cases of hypogonadotropic hypogonadism (hypogonadism secondary to a pituitary deficiency). It is used to stimulate the testes of men who are hypogonadal or lack sufficient testosterone production.

Diagnosis of Oligozoospermia

No single medical treatment has proven to be consistently reliable in increasing sperm count for patients diagnosed with Oligozoospermia or low sperm count. A diagnosis of Oligozoospermia is based on a symptom wherein a sample of semen contains less than 20 million spermozoa per ml of ejaculate.

Increasing Spermatogenesis in Hypogonadotropic Men

"Like urinary FSH, recombinant FSH in combination with HCG seems to induce spermatogenesis in hypogonadotropic men" See Drug Treatment of Male Fertility Disorders by Gerhard Haidl, et al. and specifically the discussion of HCG therapy therein. This article is located at URL: http://www.asiaandro.com/1008-682X/2/81.htm (Source: Wikipedia).

The Decline in Gonadal Stimulating Pituitary Hormone LH (Luteinizing hormone)

The natural decline in male testosterone production that occurs with aging is attributed to a decline in the gonadal stimulating pituitary hormone LH (Luteinizing hormone). As a result of the hypothalamus secreting less gonadoropin-releasing hormone (GhRH), which stimulates the pituitary gland to produce LH, the pituitary gland produces declining amounts of LH. This decrease in the pituitary secretion of LH reduces the stimulation of the gonads or male testes and results in declining testosterone and sperm production due to the decreased function of the gonads.

The decreased stimulation of the testes by the pituitary's diminished secretion of LH can also cause testicular atrophy. HCG stimulates the testis in the same manner as naturally produced. HCG Therapy is administered medically to increase male fertility by stimulating the testes to produce more sperm cells and thereby increase sperm count or Spermatogenesis.

How HCG Therapy Increases Plasma Testosterone Level in Hypogonadotropic Men

HCG therapy uses the body's own biochemical stimulating mechanisms to increase plasma testosterone level during HCG therapy. It is used to stimulate the testes of men who are hypogonadal or lack sufficient testosterone.

The male endocrine system is responsible for causing the testes to produce testosterone. The HPTA (hypothalamic-pituitary-testicular axis) regulates the level of testosterone in the bloodstream. and . The hypothalamus produces gonadotropin-releasing hormone (GnRH), which stimulates the pituitary gland to release Luteinizing hormone (LH).

LH released by the pituitary gland then travels from the pituitary via the blood stream to the testes where it triggers the production and release of testosterone. Without the continuing release of LH by the pituitary gland, the testes would shut down their production of testosterone, causing testicular atrophy and stopping natural testosterone produced by the testes.

As men age the volume of hypothalamus produced gonadotropin-releasing hormone (GnRH) declines and causes the pituitary gland to release less Luteinizing hormone (LH). The reduction if the volume of LH released by the Pituitary gland decreases the available LH in the blood stream to stimulate the testes to produce testosterone.

In males, HCG mimics LH and increases testosterone production in the testes. As such, HCG is administered to patients to increase endogenous (natural) testosterone production. The HCG medication administered combines with the patient's own naturally available LH released into the blood stream by the Pituitary gland and thereby increases the stimulation of the testes to produce more testosterone than that produced by the Pituitary released LH alone. The additional HCG added to the blood stream combined with the Pituitary gland's naturally produced LH triggers a greater volume of testosterone production by the testes, since HCG mimics LH and adds to the total stimulation of the testes.

In this treatment HCG is administered to men to promote an increase in sperm production (spermatogenesis) by the testes. HCG combined FSH or both LH and FSH is also used to increase male spermatogenesis and medically treat male infertility.



http://www.healthdesigns.com/rewardsref/index/refer/id/53104/

5$ Discount Code:4089008

If I had it to do all over again, the only injectable I would ever use is Testosterone. I wouldn't waste one shot on anything else!!!
__________________________________
TESTOSTERONE IS THE SPINAL CORD OF THE BODYBUILDER,,NO SYNTETIC TESTOSTERONE = NO BODYBUILDER
__________________________________


Natural





The pros are using good old-fashioned Testosterone, Deca, Dianabol, insulin in the off-season, and GH pre-contest. Nothing fancy. But they're the pros because they're gifted, dedicated, and have been at it a long freaking time. Anybody that tells you different is either full of shit or trying to sell you garbage.



My goals are very simple:

1. Break The Law
2. Look Good Naked

Steroids will cause your kidneys to explode, your heart to blow a ventricle, and your liver to squirt out of your arse, fly across the room, and knock the cat off the futon.

The most obvious symptom is death which would hardly be missed by even the most focused and intensive bodybuilder.

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« Odgovor #25 poslato: Januar 27, 2010, 04:51:57 posle podne »
PCT” What is it and Why do we need it


Veterans’ Consensus Statement on Post-Cycle Recovery©

Anabolic/androgenic steroids are used widely in human and veterinary medicine, and are increasingly useful to the training methods of elite athletes. Benefits of the intelligent use of anabolic/androgenic steroids include enhanced quality of life and the promise of greater longevity, as well as marked improvements in body composition, strength, and stamina. However, anabolic/androgenic steroids produce their benefits by interfering with the endocrine system, a complex system of glands and brain structures that are normally kept in an homeostatic state of balance by the action of countless subtle, sensitive feedback mechanisms. The perturbation in normal endocrine function that is introduced by the use of anabolic/androgenic steroids can, through these feedback mechanisms, elicit compensatory endocrine responses, such as up- or down-regulation of essential enzyme stores or of receptor molecules, in order to maintain homeostasis. When these compensatory mechanisms persist into the post-cycle era after steroids have been withdrawn, unwanted effects can occur, such as fatigue, depression, loss of sex drive, loss of size and strength, and others. Fortunately, both prophylactic and restorative measures that the athlete can take in this situation are now fairly well known.

Many athletes have agreed that androgenic/anabolic steroids render appreciable gains for a limited time only. As said gain period differs between individuals, this CS will refrain from any recommendations to the optimum time of such therapy but discuss methods of restoring optimum normal endocrine function.

It should be noted that the longer a cycle lasts past the eight-week mark, the harder testosterone recovery becomes. The best way of gauging ones hormonal milieu and planning compensatory measures is to have blood tests done prior to and following cessation of AAS therapy. For the purpose of this Consensus Statement and the awareness of a lack of testing athletes, the following universally accepted post cycle hormone status is assumed:

a) Luteinizing Hormone (LH): low to none, Luteinizing Hormone Releasing Hormone (LHRH): low to none
b) Testosterone (T): low
c) Estrogen (E): high in relation to T
d) Cortisol (C): high
e) Red Blood Cell (RBC) count: falling

While all of these hormone measurements are assumed on the low end of the scale, biochemical individuality will ultimately determine where a person’s levels fall. So assumption of low to substandard levels will not always be true in everyone.

1. What are the goals of testosterone recovery?

The return of hormonal balance is but one goal of this program. To create a transitional period of minimized muscle loss and sustained and/or increased motivation is another.

2. Detailed Recommendations
If the athlete is ready to come off and is still taking long acting esters he shall switch to short acting drugs in order to have complete control of exogenous hormone levels. A “waiting period” for esters to clear is unacceptable and provides for a slow slide into the post cycle catabolic state. This period of short acting supplements shall last for a minimum of 2 weeks.

a) Luteinizing Hormone and shrunken testicles

H C G
If the testis have atrophied, the introduction of H C G at 1000iu x 14 days is necessary. To prevent this atrophy from happening, the use of H C G at 500-1000iu x 4-7 days every 2-3 weeks of the AAS cycle is recommended. This will provide exogenous LH and must only be used to restore/keep proper testicle size.
Week 1-2: H C G, 500-1000iu ed

C l o m i d
The practice of using Clomid at 50mg throughout the AAS cycle or 100mg a day for 3-5 days every 4th week has been used successfully to maintain proper testicle size.

b) Low testosterone and lack of motivation

The introduction of exogenous hormones to compensate for the low endogenous testosterone levels may help to keep loss of drive, strength and muscle at bay but may also slow the recovery process. The below drug and application was chosen for its limited impact on the HPTA

D i a n a b o l
Studies and empirical evidence have shown Dianabol to be beneficial to keep Cortisol in check and provide some intermediate relief from the symptoms of low testosterone via an increase of dopamine, IGF-1, and Central Nervous System stimulation. The heightened dopamine will combat Prolactin and help raise the levels of endogenous Human Growth Hormone. Other studies point to a lack of LH suppression when taken first thing in the morning. It shall be noted that only a low dose upon rising is recommended in order to avoid further disruption of the HPTA
Week 1-6: 10mg dbol am, ed

c) High Estrogen and suppressed Hypothalamus- Pituitary- Testicular- Axis (HPTA)

Estrogen acts as the primary messenger of testosterone production. Testosterone is aromatized into estrogen, which signals the Hypothalamus to stop producing the proper testosterone release hormones. Estrogen must be kept low.

A r i m i d e x
A powerful aromatize inhibitor shall be part of every cycle. For testosterone recovery it is used to keep the testosterone/ estrogen balance in favor of testosterone. It is also of help to keep any additionally occurring estrogen from dbol and Androgel low to none. Studies have shown a 54% increase of testosterone in eugonadal patients
Week 1-10: ½-1mg ed
C l o m i d
Universally accepted as THE testosterone recovery tool. It blocks estrogen from the HPTA and stimulates the production of LHRH. LHRH then initiates the production of LH, which in turn signals the testis (if not atrophied) to produce testosterone.
Week 3-5: 100mg ed
Week 6-8: 50mg ed
N o l v a d e x
A volume of research and empirical evidence suggest the usefulness of this estrogen blocker for recovery. Its action is very similar to Clomid but may be better suited for individuals who experience side effects from Clomid.
Week 1-8: 20mg ed

d) High Cortisol, suppressed HPTA and catabolism

Cortisol is catabolic. It is the enemy of all anabolism and must be kept in check. While it is blocked when under the influence of AAS, it is free to attach to the Anabolic Receptors (AR) once the steroids leave. Due to this blockage Cortisol tends to accumulate and increase when on. A low level is desirable however since it is important for other vital functions such as control of inflammation. Balance is the key.

V i t a m i n C
At 3-5g before heavy workouts, it keeps the exercise induced rise of Cortisol in check
Always: 3-5g before workouts

D H E A
A useless pro-hormone as far as anabolism is concerned, this substance is great to keep Cortisol within normal levels. There is a correlation between high Cortisol and low DHEA levels.
Week 1-6: 150mg am and pm

H u m a l o g
It is well known that insulin possesses powerful anti Cortisol/anabolic properties, specially when used at times when Cortisol is high, such as early morning and post workout.
It is of utmost importance to be educated about insulin and its proper use. However, this CS defers to other available research material for more detailed recommendations and cautionary measures.
A minimum of 10g of dextrose/Maltodextrin per iu with a high carb/mixed glycemic index meal 45 min after insulin injection is suggested as a rough guide line for Humalog use only.
Perfect with dextrose/malto and Creatine.
Week 1-5: 10iu am and 10iu post workout
Caution: DO NOT EXCEED THESE RECOMMENDATIONS

D e x t r o s e a n d M a l to d e x t r i n
It is neither a supplement nor a drug, but these carbohydrates have a very high glycemic index and keep Cortisol levels low by increasing endogenous insulin or keep blood sugar normal when used with exogenous insulin. They also provide excellent energy for heavy workouts. In order to not gain unwanted fat, dextrose and/or maltodextrin shall be ingested during your workout and with your post workout shake only.
Always: 100g with workout water and 100g with post workout shake

e) Red Blood Cell Count and Stamina

E P O
Causes the bone marrow to increase red blood cell production and may have anabolic, fat burning and rejuvenating benefits.
It is of utmost importance to be educate about EPO and its proper use. However, this CS defers to other available research material for more detailed recommendations and cautionary measures.
Week 8: 500-1,000iu ed for 7-10 days
Caution: DO NOT EXCEED THESE RECOMMENDATIONS

C r e a t i n e
The use of Creatine has shown to increase ATP metabolism and cellular water storage among many other things. This is very beneficial because it provides for heightened nutrient storage and a slight increase in anabolism as well as workout stamina. Perfect with dextrose/maltodextrin/.
Always: 5g with workout water and 10g with post workout shake

V i t a m i n B - 1 2 & I r o n
Prolongs the life of your RBC and may be beneficial for increased oxygen transport
Week1-8: 1,000mcg ed

Miscellaneous beneficial drugs, supplements and recommendations

H G H
Administration of exogenous HGH has been shown to help maintain an anabolic environment until natural testosterone levels have reached a satisfactory level.
Week 1-8: 2iu at mid morning and 2iu at mid afternoon

Z i n c
Assists with testosterone production and is always low in weight lifting subjects. Do not consume with calcium for ease of absorption
Week1-8: 50mg ed

M a g n e s i u m
Has too many benefits for weight lifters to list
Week 1-8: 800mg every evening

V i t a m i n B - 6
Assists with testosterone production, keeps Prolactin in check and is very relaxing
Week 1-8: 200mg every evening

M e l a t o n i n
May improve sleep pattern and help increase HGH. With this supplement, the less you take the more it works.
Always: 1.5mg at nite

D e p r e n y l
Known as one of the most favorite life extension drug this dopamine enhancer provides anti-depressant properties as well as possible IGF-1 increase. Do not take with Bromocriptine.
Week 7 & 8: 5mg eod in the morning

E p h e d r a
Ephedrine HCL and related products such as Clenbuteral or Nor-ephedrine (NYC) may offer limited anti catabolic and workout stimulating benefits.
Use as preferred, but do not combine with insulin due to similarities of hypoglycemic and Eph induced over stimulation episodes

N o o t r o p i c s
A course of these "smart drugs" may be beneficial to improve blood flow to the brain and HP. No specific drug, combination of drugs and/or drug course recommendations shall be made due to varying individual preferrences

W o r k o u t a n d c a l o r i c r e s t r i c t i o n
Workouts shall be brief and focus on retaining your newly gained strength after a week long layoff. A power lift routine may be advantages at this stage. Calorie intake shall match expenditure; a calorie-restricted diet shall commence only upon complete recovery of natural testosterone production.

3. Final word

This program is based on empirical evidence, research and experimentation and represents the maximum effort to recover one’s testosterone production. Some of the above supplements and drugs may not be required or may not agree with every individual and advances in medicine may provide newer and more useful drugs for the testosterone recovery following steroid therapy.
Furthermore, it must be noted that a period of 8 weeks of abstinence from all drugs (vitamins and supplements excluded) is the minimum time recommended and that a blood test to assess actual testosterone recovery act as the only gauge for the timing of the next hormone therapy.

Anabolic/androgenic steroids wisely used have many benefits, but they produce their benefits by perturbing the natural course of endocrine function, something that can have consequences for the athlete in terms of enduring dysregulation of said endocrine function upon the cessation of anabolic use. Fortunately, both prophylactic and restorative measures that the athlete can take to restore endocrine function and prepare the way for the next cycle of anabolics are fairly well known.

Ovdje ima dosta stvari sa kojim se ne bi slozio kao sto je doziranje i vrijeme na nekim stvarima ili uopste uzimanje nekih stvari kao sto je Dianabol za vrijeme PCT-a ali tekst je relativno interesantan za pocetnika...ako neko zeli da rabi nesto od ovoga neka prvo pita za doziranje i sl!!!
http://www.healthdesigns.com/rewardsref/index/refer/id/53104/

5$ Discount Code:4089008

If I had it to do all over again, the only injectable I would ever use is Testosterone. I wouldn't waste one shot on anything else!!!
__________________________________
TESTOSTERONE IS THE SPINAL CORD OF THE BODYBUILDER,,NO SYNTETIC TESTOSTERONE = NO BODYBUILDER
__________________________________


Natural





The pros are using good old-fashioned Testosterone, Deca, Dianabol, insulin in the off-season, and GH pre-contest. Nothing fancy. But they're the pros because they're gifted, dedicated, and have been at it a long freaking time. Anybody that tells you different is either full of shit or trying to sell you garbage.



My goals are very simple:

1. Break The Law
2. Look Good Naked

Steroids will cause your kidneys to explode, your heart to blow a ventricle, and your liver to squirt out of your arse, fly across the room, and knock the cat off the futon.

The most obvious symptom is death which would hardly be missed by even the most focused and intensive bodybuilder.

Van mreže zzz

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Odg: Terapija poslije ciklusa - PCT
« Odgovor #26 poslato: Januar 27, 2010, 05:17:57 posle podne »
vitamin c 3-5g pre treninga?
Budi svoj, sledi svoje instinkte!!!

Van mreže sele137

  • Ponosni vlasnik
  • *****
  • Poruke: 1399
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Odg: Terapija poslije ciklusa - PCT
« Odgovor #27 poslato: Januar 27, 2010, 09:55:22 posle podne »
vitamin c 3-5g pre treninga?

Ja bi to podjelio na ujutro, prije treninga!!!
http://www.healthdesigns.com/rewardsref/index/refer/id/53104/

5$ Discount Code:4089008

If I had it to do all over again, the only injectable I would ever use is Testosterone. I wouldn't waste one shot on anything else!!!
__________________________________
TESTOSTERONE IS THE SPINAL CORD OF THE BODYBUILDER,,NO SYNTETIC TESTOSTERONE = NO BODYBUILDER
__________________________________


Natural





The pros are using good old-fashioned Testosterone, Deca, Dianabol, insulin in the off-season, and GH pre-contest. Nothing fancy. But they're the pros because they're gifted, dedicated, and have been at it a long freaking time. Anybody that tells you different is either full of shit or trying to sell you garbage.



My goals are very simple:

1. Break The Law
2. Look Good Naked

Steroids will cause your kidneys to explode, your heart to blow a ventricle, and your liver to squirt out of your arse, fly across the room, and knock the cat off the futon.

The most obvious symptom is death which would hardly be missed by even the most focused and intensive bodybuilder.

Van mreže sele137

  • Ponosni vlasnik
  • *****
  • Poruke: 1399
  • Pol: Muškarac
  • ALPHA MALE
Odg: Terapija poslije ciklusa - PCT
« Odgovor #28 poslato: Januar 27, 2010, 09:58:30 posle podne »
CORTISOL BY CHRIS ACETO

Learning to control this muscle-eroding hormone will increase your muscle mass

Do you feel sore, tired, irritable or weak? Have you noticed that your gains have plateaued? These could be signs that your cortisol levels are out of whack.
Cortisol is a stress hormone that’s truly the antithesis of testosterone: whereas testosterone supports muscle building, excess cortisol kills it. Besides tearing down muscle tissue and preventing the body from storing carbs as muscle glycogen, cortisol actually lowers testosterone. It also interferes with testosterone’s ability to bind to its receptors within muscle cells and induce an anabolic effect. When testosterone levels drop, not only does it become harder to build muscle and recover, but oestrogen tends to have a stronger effect in the body. Oestrogen is correlated with water retention, and it also makes shedding bodyfat a lot more difficult.

Cortisol levels can be elevated for a variety of reasons — training itself can induce this rise. It’s important that bodybuilders learn how to control their cortisol levels to keep making the best gains. If you suffer from the symptoms mentioned earlier, institute the following suggestions to help get your cortisol levels under control.

1. Stay on top of your workout nutrition As mentioned, cortisol rises when you train — it’s a natural reaction. One of the best ways to avoid excessively elevated cortisol levels is to be disciplined with your postworkout nutrition. By supplying your body with exactly what it needs as soon as the work-out is done, you’ll jump-start your recovery and help blunt cortisol spikes.
After your workout, take in 30-50 grams (g) of whey Protein with 60 to 100 g of carbs. Maltodextrin is easy, but you can take in other fast-digesting carbs such as rice cakes, white bread or cold cereal. You can also add 5 g of branched-chain amino acids (BCAAs) to the mix, or take them before you work out — BCAAs before exercise help maintain testosterone levels and can be used to fuel muscles. Leucine, one of the BCAAs, also spikes insulin levels through a different mechanism than carbs, and insulin helps in the suppression of cortisol. Whey provides building blocks that help prevent catabolism — muscle breakdown — and preventing catabolism is directly related to lower cortisol levels. Finally, the carbs in this combo spike insulin to further offset Protein breakdown.

2. Control your workouts Training volume can have a direct impact on cortisol levels. If you’re overtraining, you’re taking your body past the point where you can make the best gains. Follow these rules to make the most of your muscle-building regime.
• Limit weight training to four sessions per week. Training more frequently prevents the body from attaining a full recovery.
• Keep sessions to about an hour. When you perform too many sets and exercises in a given session, you can break down your muscle tissue too much. Limiting the length of your training sessions helps avoid this.
• Emphasise multijoint movements. Exercises such as squats, deadlifts and bench presses are the most effective at stimulating muscle growth while helping to limit total training volume. They also best stimulate growth hormone (gh) and testosterone, which can help blunt cortisol.
• Avoid excessive pumping and finishing movements. When you perform numerous sets and reps of these types of exercises, you can raise your cortisol levels too high without stimulating as much muscle growth. Try to keep pumping and finishing movements to no more than three sets per bodypart at the end of the workout.

3. Be careful with your cardio If cardio exercise burned only bodyfat, then you could hop on a bike and cycle your way into the record books as the most ripped human ever. The problem is, though, that prolonged and excessive cardio causes an increase in cortisol, and this situation can begin to prioritise muscle tissue as an energy source, tearing it down instead of helping to build it.NO FUCKING CARDIO IN PCT  :nonono:


4. Eat six meals a day The benefits of eating multiple meals per day are numerous. Besides allowing you to stay lean, a diet strategy of smaller and more frequent meals has been shown to keep cortisol levels lower than less-frequent feedings. Multiple meals — at any calorie level — will result in greater cortisol control than less-frequent meals, and we know keeping cortisol in check yields less fat, more muscle, better recovery and more energy. Strive to take in six meals per day throughout all phases of your training programme.

5. Take vitamin C This water-soluble vitamin cushions the negative effects of free radicals, compounds that are released with training. Free radicals target tissues such as muscles, weakening them and increasing inflammation and breakdown. When this happens, cortisol levels spike. By providing your body with antioxidants, such as vitamin C, you can help control cortisol. One study showed that a daily dose of 1,000 milligrams (mg) helped weightlifters keep cortisol under control.

6. Supplement with vitamin E This fat-soluble vitamin offers many versatile benefits. Primarily, vitamin E helps combat the oxi-dative stress of training and dieting. Like vitamin C, vitamin E is also helpful at combating free radicals. Large amounts of vitamin E have been shown to decrease creatine kinase activity, a marker for muscle-fibre injury. That’s what happens when you train. It’s the irony of trying to get big: you tear down your muscles to rebuild them and make them grow bigger. Taking 800 international units of vitamin E daily may help to prevent severe breakdown, which, in theory, should allow you to recover more quickly from your training.

7. Try phosphatidylserine Phosphatidylserine (PS) is a phospholipid, a quasi fat that is derived from soya beans. PS has been shown to help control cortisol levels. When you take 800 mg immediately after training, it saves muscles by blunting the total amount of cortisol released by your body. In theory, you can train like a madman and rapidly recover if you follow up the hard training with this anticortisol supplement. Another benefit is that when you keep cortisol levels under control, it’s easier for your muscles to “carb up”. With escalating cortisol levels, muscles experience a downgrade in their ability to take up carbs and deposit them as stored muscle glycogen.

8. Eat (or supplement with) garlic This bulbous flavourful herb common to Asian, Mediterranean and Middle Eastern cooking has a long-deserved retion as a health food. Recent research has shown that garlic along with a high-casein diet altered the body’s hormonal status, yielding lower levels of stress hormones such as cortisol. Other studies have shown that garlic may help increase testosterone levels. In general, the higher your testosterone levels, the lower your cortisol levels. So supplement with garlic powder — 450 mg twice daily with meals — or with a garlic supplement that provides about 4 mg of allicin with casein Protein shakes. This may help keep cortisol to a minimum.

9. Get your glutamine You knew it had to show up here, right? Recent studies have pooh-poohed glutamine’s beneficial effects on cortisol levels, but I disagree. There are many other studies that take a pro-glutamine view in muscle building. Glutamine works to spare BCAAs, and keeping BCAAs high helps keep cortisol levels from rising. In addition, glutamine pushes water into muscles, and hydrated muscles remain anabolic. Several studies show that supplemental glutamine can help keep cortisol levels in check.
Glutamine can help suppress the amount of cortisol circulating in blood. Glutamine also increases gh levels, combating cortisol’s catabolic effects. For a beneficial effect on cortisol levels, athletes may need a lot more glutamine than amounts that are often suggested. I recommend taking 5 to 10 g before and another 5 to 10 g after training to help reduce cortisol levels.

10. Add arginine to your supplement regime Arginine is now touted as a nitric oxide inducer; yet, it remains an effective gh releaser. Arginine may also have effects on cortisol levels. When gh levels rise, which naturally occurs with sleep, cortisol levels fall. As you get older, the sleep-induced gh boost just isn’t what it used to be, which allows cortisol levels to rise. Rising cortisol makes it harder for your body to grow, to hold mass and to get lean. Take 9 to 12 g of arginine before bed without carbs to increase gh levels and to blunt cortisol.
http://www.healthdesigns.com/rewardsref/index/refer/id/53104/

5$ Discount Code:4089008

If I had it to do all over again, the only injectable I would ever use is Testosterone. I wouldn't waste one shot on anything else!!!
__________________________________
TESTOSTERONE IS THE SPINAL CORD OF THE BODYBUILDER,,NO SYNTETIC TESTOSTERONE = NO BODYBUILDER
__________________________________


Natural





The pros are using good old-fashioned Testosterone, Deca, Dianabol, insulin in the off-season, and GH pre-contest. Nothing fancy. But they're the pros because they're gifted, dedicated, and have been at it a long freaking time. Anybody that tells you different is either full of shit or trying to sell you garbage.



My goals are very simple:

1. Break The Law
2. Look Good Naked

Steroids will cause your kidneys to explode, your heart to blow a ventricle, and your liver to squirt out of your arse, fly across the room, and knock the cat off the futon.

The most obvious symptom is death which would hardly be missed by even the most focused and intensive bodybuilder.

Van mreže sele137

  • Ponosni vlasnik
  • *****
  • Poruke: 1399
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  • ALPHA MALE
Odg: Terapija poslije ciklusa - PCT
« Odgovor #29 poslato: Januar 27, 2010, 10:18:38 posle podne »
Regular bloodwork being done by the AS using bodybuilder is an indispensable part of our routine.

It is not wise to leave these type of things to chance and just hoping that "everything will return to normal for me". Even if you continue to cycle after seeing some problem areas in your bloodtest results, you will at least be able to work on clearing these up before you do so.

Also, as I have mentioned before, High Cholesterol can be the silent killer that catches up with us later when we don't keep an eye on it. Most guys worry a lot about their nads coming back, or proper testosterone levels, or even their sperm count if they want children someday.

We don't see nearly as much concern for our cholesterol levels though.

Below is a brief discussion of the components of a blood profile and what the indicators reveal in terms of bodily functions.

Such information may help you to see at a glance what is going on in your body when you get a copy of your results. At the least you will be able to more intelligently discuss your situation with your doctor.

I am not a Physician but this information is generic in nature regarding the functions of the liver and kidneys as seen in bloodwork profiles.

It is not meant to be used for self-diagnosis and is only for personal interest.

Too many factors come in to play with bodybuilding to attribute elevated levels to impaired function of a particular organ without precise and qualified investigation by a Physician

> Blood Glucose

Steroids can change our sensitivity to insuline and especially certain ones such as Human Growth Hormone, the direct use of Insuline, as well as others. Checking this level will help monitor your insuline sensitivity.

> Blood Urea Nitrogen (BUN)

This reading will help a physician to determine the function of the kidneys in terms of urea filtration in the kidneys. Steroids have the potential of damaging the filtration system of your kidneys.

> Creatinine

This again checks the function of the kidney's by way of its ability to clear the by-product creatinine from the system. These levels could also be high due to creatine usage as the by-product of creatine usage is creatinine. It is important to have a doctor who you trust and whom you can reveal all the particulars to.

> BUN/Creatinine Ratio


Again, this is a predictor of kidney problems whether they be temporary or permanent.

> Total Protein

Blood excesses MAY indicate kidney damage. It is important to note that in some of these areas of indicators bodybuilders may have levels that are higher in a transient way rather than a permanent way. Also, whenever I have used creatine, my levels of creatinine were higher but their was no indication otherwise of kidney damage. It was just a by- product of the creatine usage. This is one reason that I advocate that bodybuilders use Physicians that are familiar with Sports Medicine and the various peculiarities that go with supplementation but which may only be fleeting changes in blood chemistry.

> Albumin

Can indicate Kidney damage.

> Globulin

Again can indicate the possibility of Kidney damage.

> Albumin/Globulin Ratio

Aspects pertinent to kidney function.

> Total Bilirubin


Liver damage is sometimes indicated by high levels of bilirubin.

> Alkaline Phosphatase

High levels of this can be a marker for liver damage.

> GGTP

This is the most reliable and specific marker for liver damage and can be stubborn in bringing down if total recovery is even possible. In some cases such as chemical induced hepatitis and other instances of damage it may remain elevated indefinitely. The liver is a very resilient organ but it does have its limitations.

> AST(SGOT)

A marker for muscle/liver damage.

> ALT(SGPT)

Also a marker for liver damage.

> LDH

An indicator for muscle/liver/coronary problems. I keep a close eye on this one as I think that it is more indicative of real problems than the changing nature of my cholesterol levels which are only temporary.

> Cholesterol


This helps your doctor to decide if you are in the realm of coronary risk. The elevation of cholesterol even if temporary is a pretty inescapable aspect of AS usage. I eat very clean with respect to saturated fats at all times. Also, I do a lot of cardio off cycle and on cycle, unless gains are crucial. Additionally, I use a niacin supplement, guggul, and Chinese rice yeast to spike my healthy cholesterol which in turn "fights" the unhealthy cholesterol.

> HDL and LDL Cholesterol Levels

It is important to have a proper balance of these two. The HDL(good cholesterol) helps keep the LDL in balance but the HDL is often driven down with AS usage. HDL less than 35 is not good and can have serious implications in terms of health consequences.

> Cholesterol/High Density Lipoprotein (HDL)

The HDL level is looked at here to assess the risk of coronary artery damage in conjunction with any other relevant findings that would confirm that.

> Triglycerides

If these levels are high it could also be an indicator of coronary damage. Other factors such as high sugar consumption and alcohol could also be the culprit.

> Total Testosterone

Helps to assess the function of our natural testosterone production and depending on how long one has been off the cycle it may indicate whether your levels are functioning normally again or not. Long term usage without proper cycling or long durations of excessively high dosages of AS can permanently alter these levels in a negative way.

> Cortisol

Much can be said about how cortisol levels change in the athlete as he/she trains, but generically these levels are watched to look for adrenal problems or to indicate over- training.

Again remember that diet, heavy training and subsequent muscle breakdown, deep tissue massage, prolonged levels of mental stress, overtraining, creatine usage, recent antibiotic usage, tylenol, and other factors can also temporarily alter blood levels of various these indicators.
http://www.healthdesigns.com/rewardsref/index/refer/id/53104/

5$ Discount Code:4089008

If I had it to do all over again, the only injectable I would ever use is Testosterone. I wouldn't waste one shot on anything else!!!
__________________________________
TESTOSTERONE IS THE SPINAL CORD OF THE BODYBUILDER,,NO SYNTETIC TESTOSTERONE = NO BODYBUILDER
__________________________________


Natural





The pros are using good old-fashioned Testosterone, Deca, Dianabol, insulin in the off-season, and GH pre-contest. Nothing fancy. But they're the pros because they're gifted, dedicated, and have been at it a long freaking time. Anybody that tells you different is either full of shit or trying to sell you garbage.



My goals are very simple:

1. Break The Law
2. Look Good Naked

Steroids will cause your kidneys to explode, your heart to blow a ventricle, and your liver to squirt out of your arse, fly across the room, and knock the cat off the futon.

The most obvious symptom is death which would hardly be missed by even the most focused and intensive bodybuilder.