Half Lives - PCT etc etc etc

[Mudge]

Not sure what brand you looked at but I can't find any HCG, and I have over a page long list of brands (HCG).

 

[Mudge]

There seems to be increasing evidence that progesterone may be valuable in restoring or maintaining HPTA functioning.
One study examined the effects of testosterone and estrogen on NPY receptors. Progesterone administration showed and increase in serum LH levels. The study demonstrated that Progesterone was an antagonist of the Y2 NPY receptor, which may account for a greater stimulation of the Y1 receptor, known to increase gnRH output.

Parker SL, Carroll BL, Kalra SP, St-Pierre S, Fournier A, Crowley WR.
Neuropeptide Y Y2 receptors in hypothalamic neuroendocrine areas are up-regulated by estradiol and decreased by progesterone cotreatment in the ovariectomized rat.
Endocrinology. 1996 Jul;137(7):2896-900

This would suggest that at least short-term controlled administration of progesterone may have an effect on HPTA restoration.

In females estrogen does exert a positive feedback effect on LH secretion immediately before ovulation. The LH surge is thought to actually induce ovulation. When progesterone synthesis is blocked with enzyme inhibitors, the LH surge is absent. So progesterone is clearly important for the preovulatory LH surge (1).

Males of any species, unlike females, are not supposed to exhibit any positive feedback effect of estrogen on LH production, or so the dogma goes. But your post got me searching medline to see if I could find any evidence of a positive effect of estrogen on LH in males when progesterone was administered. Remarkably, it seems to happen, at least in rats (2). I found that astonishing.

(1) Neuroendocrinology. 2003 Jul;78(1):29-35.

The luteinizing hormone surge is preceded by an estrogen-induced increase of hypothalamic progesterone in ovariectomized and adrenalectomized rats.

Micevych P, Sinchak K, Mills RH, Tao L, LaPolt P, Lu JK.

(2) Biol Reprod. 1982 Dec;27(5):1222-9.

Induction of luteinizing hormone, follicle-stimulating hormone surge in the estrogen-primed castrated male rat by progesterone.

McPherson JC 3rd, Mahesh VB.

1: Clin Endocrinol (Oxf). 2003 Apr;58(4):506-12.

Demonstration of progesterone receptor-mediated gonadotrophin suppression in the human male.

Brady BM, Anderson RA, Kinniburgh D, Baird DT.

Contraceptive Development Network and MRC Human Reproductive Science Unit, Centre for Reproductive Biology, University of Edinburgh, Edinburgh, UK.

OBJECTIVE: Synthetic gestogens in combination with testosterone have potential as a male hormonal contraceptive, predominantly acting by augmenting suppression of gonadotrophin secretion. Little is known, however, of the effects of gestogens in the male. Gestogens have affinity for both androgen and progesterone receptors but the relative contribution of action at these two receptors in gonadotrophin suppression remains unclear. In this study the effects of progesterone, with no significant androgen-receptor affinity are compared to desogestrel, a synthetic gestogen with relatively low affinity for the androgen receptor, on gonadotrophin secretion in normal men. DESIGN: Subjects received either 50 mg progesterone intramuscularly (i.m.) or 300 micro g desogestrel orally daily for 7 days. Frequent blood sampling over 12 h was undertaken before and after drug administration. GnRH [100 micro g intravenously (i.v.)] was administered 2 h before the end of the frequent sampling period. SUBJECTS: Twenty healthy men were randomly allocated to the two treatment groups. RESULTS: Both progesterone and desogestrel administration resulted in decreases in the concentration of both LH and FSH secretion, as well as testosterone. Analysis of the pulsatile nature of LH secretion indicated that both treatments reduced LH pulse amplitude, and that progesterone reduced LH pulse frequency. Progesterone, but not desogestrel, treatment also reduced the increase in LH secretion in response to GnRH. CONCLUSIONS: The effects of progesterone were at least as marked as those of a maximally effective dose of desogestrel. As progesterone has negligible affinity for the androgen receptor, these results are compatible with the suppressive effects of synthetic 19-norgestogens on gonadotrophin secretion in the male being mediated via the progesterone receptor, with its androgenicity contributing minimally to gonadotrophin suppression.

Publication Types:
Clinical Trial
Randomized Controlled Trial

PMID: 12641635 [PubMed - indexed for MEDLINE]

 

[Mudge]

Effect of test on LH/FSH:


Testosterone suppression of the HPT axis.

MacIndoe JH, Perry PJ, Yates WR, Holman TL, Ellingrod VL, Scott SD.

Department of Psychiatry, College of Medicine, University of Iowa, Iowa City, USA.

BACKGROUND: Although studies have demonstrated the suppression of normal gonadal function in the experimental setting, the specific mechanisms by which androgenic-anabolic steroids impact male gonadal function remain ill defined. Following 2 consecutive weekly injections of an identically appearing testosterone cypionate (TC) placebo, subjects were randomized to a TC dose of 100 mg/wk, 250 mg/wk, or 500 mg/wk. Following the last weekly injection of active agent the subjects received 12 consecutive weeks of TC placebo injections. RESULTS: Spermatogenesis was impaired by each of the doses of TC employed in this study, but the observed decreases in, sperm count were neither strictly dose dependent nor consistent between individuals treated with the same dose. Basal leuteinizing hormone (LH) and follicle stimulating hormone (FSH) became undetectable 2 weeks after the start of 250 and 500 mg/wk TC injections and were lost within 5 to 6 weeks of starting 100 mg doses. Pituitary gonadotropin responses to leutinizing hormone releasing hormone (LHRH) disappeared more slowly with FSH responses being lost 1 to 3 weeks after the loss of basal FSH activity. Leuteinizing hormone responses to LHRH appeared to be suppressed last, disappearing 4 to 6 weeks after FSH responses to LHRH. CONCLUSIONS: Exogenous testosterone-mediated inhibitory influences on the hypothalamic-pituitary-testicular axis were reversed following the cessation of drug treatment.

-----------------------------------

Evidence that follicle-stimulating hormone is necessary for the maintenance of quantitatively normal spermatogenesis in man:


J Clin Endocrinol Metab 1986 Jun;62(6):1184-92 Related Articles, Links


Chronic human chorionic gonadotropin administration in normal men: evidence that follicle-stimulating hormone is necessary for the maintenance of quantitatively normal spermatogenesis in man.

Matsumoto AM, Karpas AE, Bremner WJ.

The role of FSH in the maintenance of spermatogenesis in man is poorly understood. To determine whether normal serum levels of FSH are necessary for the maintenance of quantitatively normal spermatogenesis, we first studied the effect on sperm production of selective FSH deficiency induced by chronic administration of hCG in normal men. Then, we determined the effect of FSH replacement in some of these men. After a 3-month control period, eight normal men (aged 30-39 yr) received 5000 IU hCG, im, twice weekly for 7 months. Then while continuing the same dosage of hCG, subjects simultaneously received 200 mg testosterone enanthate (T), im, weekly for an additional 6 months. hCG administration alone resulted in partial suppression of the mean sperm concentration from 88 +/- 24 (+/-SEM) million/ml during the control period to 22 +/- 7 million/ml during the last 4 months of hCG treatment (P less than 0.001 compared to control values). With the addition of T to hCG, sperm counts remained suppressed to the same degree. Except for one man who became azoospermic while receiving hCG plus T, sperm motilities and morphologies remained normal in all subjects throughout the entire study. During both the hCG alone and hCG plus T periods, serum FSH levels were undetectable (less than 25 ng/ml), and urinary FSH levels were comparable to those in prepubertal children and hypogonadotropic hypogonadal adults. We replaced FSH activity in four of the eight men in whom prolonged selective FSH deficiency and partial suppression of sperm production were induced by hCG administration. Immediately after the period of hCG plus T administration, T was stopped in four men who continued to receive hCG alone (5000 IU, im, twice weekly) for 3 months. Then, while continuing the same dosage of hCG, these men received 100 IU human FSH, sc, daily (n = 2) or 75 IU human menopausal gonadotropin, sc, daily (n = 2) for 5-8 months. During the second period of hCG administration alone, serum FSH levels were undetectable (less than 25 ng/ml), and sperm concentrations were suppressed (34 +/- 13 million/ml) compared to the control values for these four men (125 +/- 39 million/ml; P less than 0.001). With the addition of FSH to hCG, FSH levels increased (213 +/- 72 ng/ml) and sperm concentrations rose significantly, reaching a mean of 103 +/- 30 million/ml (P less than 0.03 compared to hCG alone...


---------------------------


Eur J Endocrinol 2002 Nov;147(5):617-24 Related Articles, Links


Maintenance of spermatogenesis in hypogonadotropic hypogonadal men with human chorionic gonadotropin alone.

Depenbusch M, von Eckardstein S, Simoni M, Nieschlag E.

Institute of Reproductive Medicine of the University, Domagkstr. 11, Munster D-48149, Germany.

OBJECTIVE: It is generally accepted that both gonadotropins LH and FSH are necessary for initiation and maintenance of spermatogenesis. We investigated the relative importance of FSH for the maintenance of spermatogenesis in hypogonadotropic men. SUBJECTS AND METHODS: 13 patients with gonadotropin deficiency due to idiopathic hypogonadotropic hypogonadism (IHH), Kallmann syndrome or pituitary insufficiency were analyzed retrospectively. They had been treated with gonadotropin-releasing hormone (GnRH) (n=1) or human chorionic gonadotropin/human menopausal gonadotropin (hCG/hMG) (n=12) for induction of spermatogenesis. After successful induction of spermatogenesis they were treated with hCG alone for maintenance of secondary sex characteristics and in order to check whether sperm production could be maintained by hCG alone. Serum LH, FSH and testosterone levels, semen parameters and testicular Volume were determined every three to six Months. RESULTS: After spermatogenesis had been successfully induced by treatment with GnRH or hCG/hMG, hCG treatment alone continued for 3-24 Months. After 12 Months under hCG alone, sperm counts decreased gradually but remained present in all patients except one who became azoospermic. Testicular Volume decreased only slightly and reached 87% of the Volume achieved with hCG/hMG. During treatment with hCG alone, FSH and LH levels were suppressed to below the detection limit of the assay. CONCLUSION: Once spermatogenesis is induced in patients with secondary hypogonadism by GnRH or hCG/hMG treatment, it can be maintained in most of the patients qualitatively by hCG alone, in the absence of FSH, for extended periods. However, the decreasing sperm counts indicate that FSH is essential for maintenance of quantitatively normal spermatogenesis.

 

[Mudge]

HCG - info and faq

Upon researching hcg and post cycle therapy i came across what i allready knew.........thus conflicting arguments on usage . certain gurus say at the start and during , while the opposite side of the spectrum some say post cycle....... the following is relative info in which i came across:

HCG: This does nothing with regard to inhibition of the hypothalamus and pituitary. Rather it acts like LH, and causes the testicles to produce testosterone just as if LH were present. It is useful then for avoiding testicular atrophy during the cycle. The best dosing method is to use small amounts frequently: 500 IU per day is sufficient, and 1000 IU may optionally be used. The amount may be given as a single daily dose or divided into two doses. Administration may be intramuscular or subcutaneous. More is not better: too much HCG can result in downregulation of the LH receptors in the testes, and is therefore counterproductive. Overdosing of HCG can also result in gynecomastia.

Steroids: The New Rules - Bringing The Science of steroid use into the 21st century....by Brock Strasser

I have some news for you that should change the way you look at and subsequently use and cycle anabolic steroids. For the longest time, we???ve developed and based our cycling theories on the limited pharmacodynamic and pharmacokinetic data that we???ve extrapolated from primarily murine (mice) and rat models. I don???t have to tell you that the effects a steroid has on a rodent probably aren???t homologous to the effects that a steroid will have on a human. Sure, they run around their cages flexing in the mirror all the time and tend to be more popular with all the lady mice, but despite this similarity with humans, there are differences.

After all, in rodents, steroids like Primobolan (methenolone esters) are better mass builders than Testosterone. Try telling any bodybuilder he should give up his DepoTest for Primobolan and at the very least, you???ll get laughed at. The rest of the "data" we???ve used comes from anecdotal reports overheard in the gym and on internet message boards. This isn???t exactly the most reliable data either, considering some people have hidden agendas (e.g. they???re selling a particular steroid) or they aren???t entirely forthcoming regarding what they used, when they used, and how much. And I haven???t even mentioned the "fudge factor" and imaginary gains claimed by some so they won???t appear to be slackers in the gym.

Because of this, perhaps more so than in any other therapeutic area in medicine, we don???t know a whole lot about steroids and how they interact with the human body. I???m going to change all that. I???ve located a mind-expanding study conducted on humans using two anabolic steroids, nandrolone phenylpropionate and nandrolone decanoate. My article here, based entirely on this study, is going to shatter some misconceptions regarding anabolic steroids. Sit back and prepare to be educated.


HPTA Suppression Is Imminent

Anyone who???s used anabolic steroids for any length of time will easily observe that when they discontinue using, they invariably "crash." That is to say, their body is producing next to zero endogenous androgens. This can lead to significant loss of muscle gain, loss of strength gains, lethargy, depression and a whole host of other disorders. Of course, drugs like HCG, HMG, clomiphene and similar gonadotrophics can help to ameliorate such symptoms, but these aren???t 100% cure-alls. The success or failure of such secondary drug use varies considerably between individuals.

In a quest to minimize HPTA insult, my friend and Biotest developmental team partner, Bill Roberts, came up with an innovative speculation: If you limit your use of anabolic steroids to short-acting compounds and don???t exceed two weeks of continual usage without a four week period of no usage, you might not depress endogenous androgen levels too much, if at all. This is the now famous "two on/four off" protocol.

I have the utmost respect for Bill and he possesses more knowledge about drugs than I ever will, but on this one topic, I don???t agree with him. The study I just reviewed utilized ten healthy male volunteers who were randomized to receive either the phenylpropionate or decanoate ester of nandrolone via intramuscular, oily depo injection. A single injection of only 100 mg of nandrolone phenylpropionate caused almost complete suppression of endogenous Testosterone by day three and lasted until around day eight.

Endogenous levels of Testosterone didn???t return to baseline levels for almost fifteen days, while the same type of injection with nandrolone decanoate caused almost complete inhibition of endogenous by day four. Endogenous levels of Testosterone didn???t return to baseline levels for greater than twenty days! All this from a single, 100-mg injection of nandrolone!

This tells me that no matter what you do, whether it???s a short lasting ester or a long lasting ester, you???ll end up totally shutting down your body???s ability to make androgens for at least two to three weeks. Since nobody (well, at least nobody male) uses only 100 mg of nandrolone per week, it???s reasonable to conclude that the suppression caused by 500mg of an esterified anabolic per week (an average dose) would be much greater than two to three weeks. This study didn???t deal with fast acting orals like stanozolol and oxandrolone, but there???s no reason to think that these won???t cause HPTA insult as well.

So what does this mean? To me, it means that HPTA insult is inevitable and should be planned for accordingly in your cycle. That is to say, you should plan on crashing for a few weeks post-cycle no matter what. Because of this, you???re going to want to extend and "beef up" your cycle so that you overshoot your final goal.

Remember, you???re going to crash and lose some of your gains. So if you want to gain "X" pounds of muscle, shoot for "X+Y" pounds of muscle and accept that within two to six weeks after the cycle, you???ll end up losing most of the "Y" portion.


Volume and Concentration

Steroids come in all shapes and sizes. In other words, you can find nandrolone (or Testosterone or boldenone) esters in 25 mg/ml, 50 mg/ml, 100 mg/ml, 200 mg/ml and so forth. Is a 400 mg injection using two milliliters of a 200 mg/ml oily solution the same as using four milliliters of a 100 mg/ml solution? After all, the net amount is still 400 mg, right? Unfortunately, this isn???t the case.

Steroid concentration in the solution greatly affects the dynamics and kinetics. In this study, some of the men received a 100 mg/ml injection of nandrolone decanoate and other men received a 100 mg injection using a 25 mg/ml solution (which means they received four milliliters, of course). Those that received the 100 mg/ml injection reached significantly higher (between 30% and 50%) plasma levels of nandrolone than those who got 100 mg via the 25 mg/ml solution. To top it off, the 100 mg/ml group???s plasma nandrolone level stayed elevated for a little bit longer; however, the length of suppression of endogenous Testosterone was almost identical.

What does this tell us? It tells us that if we want to maximize plasma levels of hormone (and thereby, maximize gains in lean muscle) we want to opt for the most concentrated version of whatever steroid(s) we decide we???re going to use. If we???re using Testosterone, we surely want to use a 200mg/ml enanthate over something like 100mg enanthate. If we???re using nandrolone, we want to use Ttokkyo???s 300mg/ml stuff over 50mg/ml or 100mg/ml nandrolone decanoate made by others.


Injections Sites

Another thing that superficially seems trivial but makes a huge difference in plasma steroid concentrations is where you inject. That???s right, this seems utterly trivial but this study concluded that gluteal injections yielded far superior plasma levels as opposed to injections in the deltoid.

Of all the locations that nandrolone injections were given in this study (100 mg/ml x 1 ml in the glutes, 25 mg/ml x 4 ml in the glutes and 100 mg/ml x 1 ml in the deltoid), the deltoid injections yielded the lowest plasma levels of nandrolone by a huge factor, with peak concentrations being 50% lower than the 100 mg/ml gluteal injection and around 10% lower than the 100 mg/ml x 4ml gluteal injection. Lesson learned here: Only inject in the glutes for maximal steroidal efficacy.


Short Esters Are Better Esters

Perhaps the most important thing I learned in reviewing this study is that short-chain esters (steroids of shorter half life) yield a much higher plasma concentration of steroid than steroids of longer side chain esters. In this study, a single 100 mg/ml x 1 ml intragluteal injection of nandrolone phenylpropionate caused a peak plasma concentration of almost double that of the 100 mg/ml x 1 ml intragluteal injection of nandrolone decanoate. This level remained increased for almost seven days, too. By fourteen days, even though the nandrolone decanoate ester demonstrated a much higher plasma level than the nandrolone phenylpropionate level, the net amount of both was so low as to be ineffective.

This tells me that the effects I can see from using 500 mg of Testosterone enanthate per week probably won???t be the same as using 500 mg of Testosterone propionate or even Testosterone suspension per week. I???m going to see better results with the propionate and even better results with the suspension. Sure, I may need to inject the propionate and suspension more often, but in the long run it???ll pay off for me. (Not that I???d use steroids, of course. No sir, not me. They???re illegal!)


Conclusions

To recap everything mentioned here in this article, remember the following:

1) HPTA suppression is virtually inevitable. Even a single 100mg injection of nandrolone will cause full suppression for almost a week and you won???t return to a normal HPTA for at least two weeks. Plan your cycle accordingly and overshoot your goals knowing you???ll lose something.

2) Injection volume and concentration are important. When available, opt for the highest concentration on a mg/ml basis.

3) Injection site is important. The best place for maximal plasma levels seems to be the glutes.

4) Side chain ester length is probably the single most important factor in influencing plasma levels. The shorter the ester (and the half life) the better. You may have to inject more often, but in the long run it???ll be worth it.

There you go, the new "rules" of steroid use. Put them to use wisely!


Reference

The Journal of Pharmacology And Experimental Therapeutics, Vol 281, No. 1; 93-102, 1997.

 

[Mudge]

Lipid profiles

Worst side of AAS use and how to counter
Why is it that users don't realize that the worst side of steroid use is a VERY shitty lipid profile. Well I think it's because one cannot SEE a shitty lipid profile and you don't feel bad with it.

I would venture to say that it is universal with men that are taking even half decent doses of gear.

Total cholesterol usually doesn't go up that much with roids, although it can climb, and triglycerides sometimes go down but usually stay about the same. What makes steroid use so scarry is the TERRIBLE affect it have on hdl. Hdl(good cholesterol) really takes a dive. Hdl to total cholesterol ratio's are OFTEN as bad as 15 or 20 to 1 and that is very significant indeed. The last time I had my lipid profile checked my doc had a COW!! I don't know if I will ever do test and tren again for a long eight week cycle.
People with a low hdl have a significantly higher risk for heart disease.
There is plenty of evidence to suggest that heart disease doesn't happen in a few years in old or middle age. It is most often though to be the result of a slow build up of aterial plaque over many many years and perhaps starting in childhood!

So with all this in mind it makes sence to limit androgen use as much as possible and to take plenty of time off between cycles.

SUGGESTIONS
Bill Llewellyn suggests moderate doses of non 17aa mild aromatizing androgens like EQ and perhaps a liitle nandrolone. Low doses of test are not that bad either. Seems that a little estrogen may be helpful here. Nothing hammers my hdl more than tren and we know it is the most powerful androgen and doesn't aromatize.
Bill also suggests the use of an estrogen blocker throughout the cycle , such as clomid or nolva. He reports that Nolva has helped his hdl. There are a couple studies that suggest that nolva can be helpful for men with heart disease but these men are not on AAS. Nolva has not helped me BTW but perhaps it's worth a try.

Short two week cycles may be an option for some as even if the lipid profile is hammered the short time would reduce risks associated with this change.
I have posted a good deal on two weekers over at Elite. They can work IF done properly. Huge gains cannot be expected of course but decent gains can be made.

DRUG THERAPY.
Niacin increases hdl more than any drug. Lipidor and the like are better at reducing ldl.
Niacin needs to be taken in high dose in order to be effective. 1500mg to 3000 mg per day. Do NOT use the old time released niacins as they are very hard on the liver. Even regular niacin can have some impact so be sure to be followed by your doc.
I take non fluch niacin at about 1800mg per day and it does seem to help. BEWARE..the flush from regular niacin is UNREAL but some poeple actually grow to enjoy it he he he . Start slow and build up.

FOODS
Omega 3 and 6 oils help so get some flax seed and grind it up in a coffee grinder and throw it into your protein drinks...a few table spoons is good. Flax is a great source of Omega three's. You can also buy flax oil or combo oils like Udo's select oil.

Salmon Tuna Macheral and Sarines are pretty good sources of Omegas three, especially sardines..so start making your Grampa's sardines sandwiches.

Avoid saturated fat like the plague(land animal fat and egg yolks)
Okay some is okay but be careful as a high saturated fat diet WILL mess with your lipid profile.

Limit cholesterol a little, although saturated fat is FAR WORSE...just don't be eating a half dozen egg yolks per day.

Avoid trans fats. Trans fatty acids are man made fats and are found in large doses in PARTIALLY hydrogenated oils(margerine).
Another way of saying partially hydrogenated is "Vegetable oil shortening."
Avoid all store bought oils except extra virgin olive oil. All oils, except for cold pressed olive oil, have been super heated to over 400 degree's and as a result their chemical composition changes and they become toxic as hell and really mess with your lipid profile!
Butter is a neutral fat and is far better than margerine or corn oil etc, even though its saturated.

NEVER fry with any oil above 250 degree's ..get an electric frying pan. The safest oils to fry with are olive oil and butter. NEVER EVER fry with oils high in Omega 3 or 6 as they become very unstable.

Buy the book "Fats that Heal Fats that Kill" by Udo Erasmus. EXTREMELY EXCELLENT BOOK!

CARDIO
Do 30 minutes of cardio at a decent intensity three time per week as this help increase hdl.

 

[Mudge]

Looks like when you can't get HMG, HCG/Nolva/Clomid is going to be the arsenal of choice.

"An Uncontrolled Clinical Trial for Treatment of
Androgen Induced Hypogonadism" by Michael C. Scally, M.D. And Andrew L. Hodge, M.S. :

"It was discovered that although both clomiphene citrate and tamoxifen met with some success, when combined together they achieved a more significant increase in gonadotropin production."

 

[Mudge]

Blood test reference ranges from Quest Diagnostics (biggest lab network in the US):

CBC with Differential and Platelet
White Blood Cell count: 3.8 - 10.8 Thous/mcL
Red Blood Cell count: 4.2 - 5.8 Mill/mcl
Hemoglobin: 13.2 - 17.1 g/dL
Hematocrit: 38.5 - 50.0%
MCV: 80 - 100 fL
MCH: 27 - 33 pg
MCHC: 32 - 36 g/dL
RDW: 11 - 15%
Platelet Count: 140 - 400 Thous/mcL
MPV: 7.5 - 11.5 fL
Neutrophils, Absolute: 1500 - 7800 Cells/mcL
Lymphocytes, Absolute: 850 - 3900 Cells/mcL
Monocytes, Absolute: 200 - 950 Cells/mcL
Eosinophils, Absolute: 15 - 500 Cells/mcL
Basophils, Absolute: 0 - 200 Cells/mcL

Glucose, non-fasting: 65 - 125 mg/dL
Glucose, fasting: 65 - 109 mg/dL

Automated Chemistries
Urea Nitrogen: 7 -25 mg/dL
Creatinine: 0.5 - 1.4 mg/dL
BUN/Creatinine: 6 - 25
Sodium: 135 - 146 mmol/L
Potassium: 3.5 - 5.3 mmol/L
Chloride: 98 - 110 mmol/L
Carbon Dioxide: 21 - 33 mmol/L
Calcium: 8.5 - 10.4 mg/dL
Phosphorus: 2.5 - 4.5 mg/dL
Alkaline Phosphatase: 20 -125 U/L
Liver enzyme, AST: 2 - 50 U/L
Liver enzyme, ALT: 2 - 60 U/L
Bilirubin, Total: 0.2 - 1.5 mg/dL
Bilirubin, Direct: 0.0 - 0.3 mg/dL
Protein, Total: 6.9 - 8.3 g/dL
Albumin: 3.7 - 5.1 g/dL
Globulin, Calculated: 2.2 - 4.2 g/dL
A/G ratio: 0.8 - 2.0
LD: 100 - 250 U/L
Uric Acid: 2.7 - 8.2 mg/dL
GGT: 2 - 80 U/L
Cholesterol, Total: < 200 mg/dL
Triglycerides: < 150 mg/dL
Iron: 40 - 190 ug/dL

Thyroid Panel
T3, Total: 60 - 181 ng/dL
T4, Free: 0.8 - 1.8 ng/dL
T4, Total: 4.5 - 12.8 ug/dL
TSH: 0.4 - 5.5 mIU/L

Homocysteine (Cardio) , FPIA
Homocysteine: < 11.4 MICROmol/L

PSA - Prostate Specific Antigen
PSA, Total: < 4.1 ng/mL
PSA, Free and Free %: See ref. scale below
Reference scale:
PSA, 0 - 2 ng/mL = approx. 1% Probability of Cancer
PSA, 2 - 4 ng/mL = approx. 15% Probability of Cancer
PSA, 4.1 - 10 ng/mL & Free 0-10% = approx. 56% Probability of Cancer
PSA, 4.1 - 10 ng/mL & Free 11-15% = approx. 28% Probability of Cancer
PSA, 4.1 - 10 ng/mL & Free 16-20% = approx. 20% Probability of Cancer
PSA, 4.1 - 10 ng/mL & Free 21-25% = approx. 16% Probability of Cancer
PSA, 4.1 - 10 ng/mL & Free > 26% = approx. 8% Probability of Cancer
PSA > 10 = > 50% Probability of Cancer

Testosterone, LH & Estradiol
Testosterone, Total: 260 - 1000 ng/dL
Testosterone, Free: 50 - 210 pg/mL
Testosterone, Free %: 1.0 - 2.7%
Estradiol: < 32 pg/mL
LH: 1.5 - 9.3 mIU/mL

 

[Mudge]

1. Use a superior antiestrogen and/or a superior antiprolactin/antiprogestronic DURING the cycle. Aromasin is the superior antiestrogen and Dostinex is the superior antiprolactin med. dostinex is useful when using DECA, Tren/FINA, etc.

2. Keep your AAS cycles eight weeks or so long.

3. Keep your dosing moderate.

This advise applies to those with average genetics (the majority). There are a small number of you who can successfully exceed or ignore these guidelines (the true mesomorphs).

4. Begin your recovery cycle the same week or the next week after the AAS cycle.
Weeks one thru three of recovery:
2,000U of HCG, IM, Mon, Wed, Fri
20mg Nolvadex daily.
Weeks four thru six:
20mg Nolvadex daily.

Clomid 50mg daily should be added, paralleling Nolvadex, if you are coming off a prolonged, heavy cycle. This cycle may need to be repeated once or even twice. If you do not recover, then you need to see an endocrinologist for exam to check for other physiological problems and possible lifelong HRT. Most young, healthy people recover, assuming they have something to recover. How do you know if you have something to recover? Baseline Testos blood levels.

After reading the boards for over four years, I am still amazed at the number of people not using ancillaries, not doing a recovery cycle, not doing blood testing, and not doing adequate recovery cycles.

 

[Mudge]

LH=LUTEINIZING HORMONE. RESPONSIBLE FOR STIMULATING TESTOS PRODUCTION IN TESTES.
FSH=FOLLICLE STIMULATING HORMONE. RESPONSIBLE FOR STIMULATING SPERM PRODUCTION IN TESTES.

 

[Mudge]

High bodyfat = gyno risk because, it is the aromatase enzyme in adipose tissue that does most of the conversion of testos to estrogen.

 

[BigMike]

clenbuterol and "clem"

Is clenbuterol and "clem" the same thing? And are they better to take for a male than Deca Durabolin?

Anyone?Anyone?

 

[Mudge]

Clenbuterol is the correct spelling, clem is not but clen is used for shorthand.

They are not even closely related, clen is anti-catabolic but it is not massively anabolic either, it is not an injectable steroid, so dont expect a clen cycle to be magical like test + deca. Personally I would not do deca by itself.
Clen
http://www.anabolicreview.com/drugprofiles.php?steroid=89

Deca-Durabolin
http://www.anabolicreview.com/drugprofiles.php?steroid=32

 

[Mudge]

Clomid
Pharmaceutical Name: Clomiphene (as citrate)
Molecular weight of base: 405.9663
Molecular weight of ester: 192.125 (citric acid, 6 carbons)
Effective dose: 100-150 mg/day orally
______________
Nolvadex
Pharmaceutical Name: Tamoxifen (as citrate)
Molecular weight of base: 371.5212
Molecular weight of ester: 192.125 (citric acid, 6 carbons)
Effective dose: 20-40 mg / day orally

Info:
While practically similar compounds in structure, few people ever really consider Clomid and Nolva to be similar. Its not just a common myth in steroid circles, but even in the medical community. This misconception originates from their completely different uses. Nolvadex is most commonly used for the treatment of breast cancer in women, while clomid is generally considered a fertility aid. In bodybuilding circles, from day one, clomid has generally been used as post-cycle therapy and Nolvadex as an anti-estrogen.
But as I intend to demonstrate this is in essence the same. I believe the myth to have originated because Nolva is clearly a more powerful anti-estrogen, and the people selling clomid needed another angle to sell the stuff, so it was mostly used as a post-cycle aid. But few users really understand how clomid (and also Nolvadex, logically) works to bring back natural testosterone in the body after the conclusion of a cycle of androgenic anabolic steroids. After a cycle is over, the level of androgens in the body drop drastically. The body compensates with an overproduction of estrogen to keep steroid levels up. Estrogen as well inhibits the production of natural testosterone, and in the period between the return of natural testosterone and the end of a cycle, a lot of mass is lost. So its in everybody's best interest to bring back natural test as soon as humanly possible. Clomid and Nolvadex will reduce the post-cycle estrogen, so that a steroid deficiency is constated and the hypothalamus is stimulated to regenerate natural testosterone production in the body. That's basically how the mechanism works, nothing more, nothing less.
Both compounds are structurally alike, classified as triphenylethylenes. Nolvadex is clearly the stronger component of the two as it can achieve better results in decreasing overall estrogen with 20-40 mg a day, than clomid can in doses of 100-150 mg a day. A noteworthy difference. Triphenylethylenes are very mild estrogens that do not exert a lot, if any activity at the estrogen receptor, but are still highly attracted to it. As such they will occupy the receptor and keep it from binding estrogens. This means they do not actively work to reduce estrogen in the body like Proviron, Viratase or arimidex would (by competing for the aromatase enzyme), but that it blocks the receptor so that any estrogen in the body is basically inert, because it has no receptor to bind to.
This has advantages and disadvantages. The disadvantage is that when use is discontinued, the estrogen level is still the same and new problems will develop much sooner. The advantage is that it works much faster and has results sooner than with an aromatase blocker like Proviron or arimidex. Therefor, when problems such as gynocomastia occur during a cycle of steroids one will usually start 20 mg/day of Nolva or 100 mg/day of clomid straight away, in conjunction with some Proviron or arimidex. The proviron or arimidex will actively reduce estrogen while the clomid or Nolvadex will solve your ongoing problem straight away. This way, when use is discontinued there is no immediate rebound.
So which one should you use? Well personally, I'd have to say Nolvadex. Both as an on-cycle anti-estrogen and a post-cycle therapy. As an anti-estrogen its simply much stronger, demonstrated by the fact that better results are obtained with 20-40 mg than with 100-150 mg of clomid. For post-cycle, this plays a key role as well. It deactivates rebound estrogen much faster and more effective. But most importantly, Nolvadex has a direct influence on bringing back natural testosterone, where as clomid may actually have a slight negative influence. The reason being that Tamoxifen (as in Nolvadex) seems to increase the responsiveness of LH (luteinizing hormone) to GnRH (gonadtropin releasing hormone), whereas clomid seems to decrease the responsiveness a bit1.
Another noteworthy fact about Nolvadex is that it acts more potently as an estrogen in the liver. As you remember, I mentioned that clomiphene and tamoxifen are basically weak estrogens. Well, tamoxifen is apparently still quite potent in the liver. This offers us the positive benefits of this hormone in the liver, while avoiding its negative effects elsewhere in the body. As such Nolvadex can have a very positive impact on negative cholesterol levels2 in the body, and therefore too should be considered a better choice than clomid. It will not solve the problem of bad cholesterol levels during Steroid use, but will help to contain the problem to a larger degree.
Another reason why I promote the use of Nolvadex over Clomid post-cycle (as if being 3-4 times stronger and having more of a direct effect on restoring natural test wasn't enough) is because it's a lot safer. Not just because it improves lipid profiles, but also because it simply doesn't have the intrinsic side-effects that Clomid has. Clomid causes more acne for sure, but that's mainly because you need to use a 3-4 times higher dose. But Clomid seems to also affect the eyesight. Long-term clomid therapy causes irreversible changes in eyesight3 in users. Irreversible. For me that alone is reason enough to prefer Nolvadex.
Lastly, one should be aware that use of these compounds can reduce the gains made on steroids. Nolvadex more so than clomid, simply because it is stronger. Estrogen is responsible for a number of anabolic factors such as increasing growth hormone output, upgrading the androgen receptor and improving glucose utilization. This is why aromatizing steroids like testosterone are still best suited for maximum muscle gain. When reducing the estrogen levels, we therefore reduce the potential gains being made. For this reason one may opt to try clomid during a cycle instead of Nolvadex. Although I would imagine that the problem that needed solved would be of more concern, in which case Nolva remains the weapon of choice. It's a plain fact that there is a high correlation between gains and side-effects. Either you go for maximum gains and tolerate the side-effects, or you reduce the side-effects, and with it the gains. That's life, nothing is free.
Stacking and Use:
If problems of Gynocomastia or other estrogen related symptoms tend to pop up during a cycle the use of 20-30 mg of Nolvadex or 100 mg of Clomid daily should easily contain the problem, and be used until a few days after the problem subsides. For best results and the least amount of problems upon cessation it is best stacked with Proviron (50 mg) or arimidex (0.5 mg) for this duration as well. Its not advised that these products be ran concomitantly with the steroid for the entire duration of the stack, as this will reduce your gains. Instead cease the usage of anti-estrogens once the problem is contained, and should the problem resurface, simply recommence the use of the products in the same manner as described above.
Once a cycle of steroids is concluded one should always initiate a post-cycle therapy to help bring back natural testosterone as soon as possible. This will help you to retain the mass you gained. How this is done depends highly on the type of steroid used. If only orals were used, therapy should start immediately, even the last day of the stack. If short-acting esters or water-based injectables were used, therapy should commence within 4-7 days after last injection, and if long-acting esters were used then it should commence 1.5 to 2 weeks after the last injection was given. The length of the therapy will vary as well, from 3-5 weeks. The longer acting the product was, the longer therapy should be continued to make sure all suppressive factors are cleared before use of Clomid/Nolvadex is discontinued.
For best results, it is best stacked with HCG (Human Chorionic gonadotrophin), which functions as an LH analog and can help bring testicle size back up. HCG use starts the last week of a cycle, and on from there every 5-6 days (usually 1500-3000 IU) and discontinued 1.5 to weeks prior to the cessation of Nolvadex/clomid. The reason being that HCG itself is also suppressive of natural testosterone and should be out of the body before therapy is over, or it will inhibit natural testicle function. But I can not stress enough that HCG possibly plays a more important role in post-cycle therapy than clomid/Nolvadex. For Clomid and Nolvadex, doses are usually tapered down. Its best to start with 40-50 mg of Nolvadex or 150 mg of Clomid for the first week or the first two weeks, and then finish the program with 20-25 mg of Nolvadex or 100 mg of Clomid for an additional two weeks.
*************************************

-BigCat

 

[Mudge]

Clomid and HCG
By Nick and Bigfella - MuscleTalk.co.uk moderators
Nick can be contacted through the Muscletalk forum for any questions or comments.

One of the most frequently asked questions on MuscleTalk is how to use Clomid and HCG correctly.

(A note to Americans - when I say 'oestrogen' I mean 'estrogen' - we spell it correctly in the UK!)

Why Bodybuilders Use Clomid
Clomid is a generic name for Clomiphene Citrate and is a synthetic oestrogen. It is prescribed medically to aid ovulation in low fertility females. Another generic name is Serophene.

Most anabolic steroids, especially the androgens, cause inhibition of the body's own testosterone production. When a bodybuilder comes off a steroid cycle, natural testosterone production is zero and the levels of the steroids taken in the blood are diminishing. This leaves the ratios of catabolic : anabolic hormones in the blood high, hence the body is in a state of catabolism, and, as a result, much of the muscle tissue that was gained on the cycle is now going to be lost.

Clomid stimulates the hypothalamus to, in turn stimulant the anterior pituitary gland (aka hypophysis) to release gonadotrophic hormones. The gonadotrophic hormones are follicle stimulating hormone (FSH) and luteinizing hormone (LH - aka interstitial cell stimulating hormone (ICSH)). FSH stimulates the testes to produce more testosterone, and LH stimulates them to secrete more testosterone. This feedback mechanism is known as the hypothalamic-pituitary-testes axis (HPTA), and results in an increase of the body's own testosterone production and blood levels rise, to, in part, compensate for the diminishing levels of exogenous steroids. This is vital to minimise post cycle muscle losses.

Not all steroids do cause shut down of the feedback mechanism. Everyone is different and you must also take into account how long you have been using a certain steroid and at what dose in order to determine if you need Clomid or not.

Clomid also works as an anti-oestrogen. As it's a weak synthetic oestrogen, it binds to oestrogen receptors on cells blocking them to oestrogen in the blood. This minimises the negative effects like gynecomastia and water retention that may be a result of oestrogen that has aromatised from testosterone.

It's effect as an anti-oestrogen are quite weak though, and it should not be relied upon if you are going to be using androgenic steroids that aromatise at a rapid rate, or if you are pre-disposed to gynecomastia. Arimidex and Nolvadex (Tamoxifen) are far more effective anti-oestrogens.

Important note: Clomid does not, as is often thought, stimulate the release of natural testosterone, but rather works at reducing the oestrogenic inhibition caused by the steroid cycle. It does this in a similar manner to the way it and Nolvadex block oestrogen receptors in nipples to combat gyno development, i.e. by blocking the oestrogen receptors in the hypothalamus and pituitary thus reducing the inhibition from the elevated oestrogen. This allows LH levels to return to normal, or even above normal levels, and in turn, natural testosterone levels to also normalise.

Inhibition of the HPTA is caused by either elevated androgen, oestrogen or progesterone levels. On cessation of the steroid cycle, androgen levels begin to fall and Clomid dosing is normally commenced according to the half-life of the longest acting drug in the system (see below).

This may also explain the reason individuals often find post-deca recovery more difficult, as the progesterone presence is untouched by the Clomid. We know that Clomid and Nolvadex (being very similar chemically) are both ineffective with regard to reducing progesterone related gyno, so it is reasonable to assume that Clomid has little effect against progesterone levels.

Clomid During A Cycle
When we use anabolic steroids, the level of androgens in the body rises causing the androgen receptors to become more highly activated, and through the HPTA, a signal tells our testes to stop producing testosterone. During a cycle the body has far higher than normal levels of androgens and, as long as this level is high enough, Clomid will not help to keep natural testosterone production up. It will be almost all but completely shut off, in theory.

Some heavy androgen users, however, do advocate a small burst of Clomid mid-cycle, though it must be hard for them to say if it really of any benefit, due to the amount of gear they are using. Therefore, the only purpose of Clomid during a cycle is as an anti-estrogen.


When To Start Clomid
The correct time to commence Clomid depends on the type and cycle of steroids you have been using. Different steroids have different half-lifes (indicates the time a substance diminishes in blood), and Clomid administration should be taken accordingly.

As we have seen above, Clomid taken when androgen levels in our blood are still high will be a waste. It is crucial to wait for androgen levels to fall before implementing our Clomid therapy. However, if taken too late we could possibly lose gains.

The list below determines when you should start Clomid. Select from the list any steroids you've used in your cycle and whichever one has the latest starting point is the time to commence Clomid. For example, if Dianabol, Sustanon and Winstrol were cycled, the time for administering Clomid should be 3 weeks post cycle, as Sustanon remains active in the body for the longest period of time.

Steroid Time after
last administration Length of
Clomid Cycle
Anadrol50/Anapolan50: 8 - 12 hours 3 weeks
Deca durabolan: 3 weeks 4 weeks
Dianabol: 4 - 8 hours 3 weeks
Equipoise: 17 - 21 days 3 weeks
Finajet/Trenbolone: 3 days 3 weeks
Primabolan depot: 10 - 14 days 2 weeks
Sustanon: 3 weeks 3 weeks
Testosterone Cypionate: 2 weeks 3 weeks
Testosterone Enanthate/Testaviron: 2 weeks 3 weeks
Testosterone Propionate: 3 days 3 weeks
Testosterone Suspension: 4 - 8 hours 2-3 weeks
Winstrol 8 - 12 hours 2-3 weeks


How To Take Clomid
Clomid has a long half-life (possibly 5 days), so there is no need to split up doses throughout the day. If Sustanon has been used and Clomid is commenced 3 weeks after the last injection, I would estimate that androgen levels are low enough to start sending the correct signals. If androgen levels are still a little high, we need to start at a high enough amount that will work or help, even if androgen levels are still a little high. Try 300mg on day 1; then use 100mg for the next 10 days; followed by 50mg for 10 days.

Using HCG
It is our opinion that HCG is probably one of the most misunderstood and misused compounds in bodybuilding. Hopefully this information will go some way towards rectifying that for the members of MuscleTalk. HCG stands for Human Chorionic Gonadotrophin and is not a steroid, but a natural peptide hormone which develops in the placenta of pregnant women during pregnancy to controls the mother's hormones. (Incidentally, this is the reason you may hear of people testing for growth hormone (HGH) with a pregnancy testing kit - If their HGH shows 'pregnant', they've been ripped-off with cheaper HCG - but we digress slightly).

Its action in the male body is like that of LH, stimulating the Leydig cells in the testes to produce testosterone even in the absence of endogenous LH. HCG is therefore used during longer or heavier steroid cycles to maintain testicular size and condition, or to bring atrophied (shrunken) testicles back up to their original condition in preparation for post-cycle Clomid therapy. This process is necessary because atrophied testicles produce reduced levels of natural testosterone, this situation should be rectified prior to post-cycle Clomid therapy.

HCG administration post-cycle is common practice among bodybuilders in the belief that it will aid the natural testosterone recovery, but this theory is unfounded and also counterproductive. The rapid rise in both testosterone, and thus oestrogen due to aromatisation, from the administration of HCG causes further inhibition of the HPTA (Hypothalamic/Pituitary/Testicular Axis - feedback loop discussed above); this actually worsens the recovery situation. HCG does not restore the natural testosterone production.

The typically observed dosing of 2000 to 5000IU every 4 to 5 days causes such an increase in oestrogen levels via aromatisation of the natural testosterone that this has been responsible for many cases of gynecomastia.

From the above discussion it is clear that HCG is best used during a cycle, either to:

1) Avoid testicular atrophy, or
2) Rectify the problem of an existing testicular atrophy.

Doses of HCG
Smaller doses, more frequently during a cycle will give best overall results with least unwanted side effects. Somewhere between 500iu and 1000iu per day would be best over about a two-week period. These doses are sufficient to avoid/rectify testicular atrophy without increasing oestrogen levels too dramatically and risking gynecomastia. This dosing schedule also avoids the risk of permanently down-regulating the LH receptors in the testes.

Presentation and Administration of HCG
Synthetic HCG is often known as Pregnyl (generic name) and is available in 2500iu and 5000iu (not ideal for the above doses!). Administration of the compound is either by intra-muscular or subcutaneous injection. It comes as a powder which needs to be mixed with the sterile water. The powder is temperature-sensitive prior to mixing and should not be exposed to direct heat. After mixing, it should be kept refrigerated and used within a few weeks - though there are sterility issues which need to be considered after mixing.

 

[Mudge]

I just finished reading ALR's book, Building the Perfect Beast. I highly recommend your reading this book. There was a line in this book that got me thinking about Nolvadex vs. Clomid.

I still believe that HCG use--either throughout the cycle or during a distinct PCT cycle--is required. It is imperative to rapidly increase testicular mass. Now, previously, I was touting Nolvadex as the antiestrogen of choice to use along with the HCG. Nolvadex acts as an antiestrogen here to block new estrogen formation as a result of recovery and it stimulates the pituitary to begin releasing LH again. The only pitfall with using Nolvadex is that it does, in fact, reduce IGF-1 levels. This is important--we do not want to reduce IGF-1 levels..EVER. So, let's substitute Clomid in place of Nolvadex. I believe that, despite the debate of Clomid vs Nolvadex (effectiveness, sides, etc), lowering IGF-1 levels is taboo. Clomid does everything that Nolvadex does. Clomid has not been proven to lower IGF-1 levels, as far as I know. Thanks to ALR and his great book, Building the Perfect Beast.

 

[Mudge]

Interactions of the Hypothalamus, Pituitary, and Testes (HPTA)

During a cycle of AAS, natural production of testosterone decreases, often times to zero. In many cases, the diminished natural testosterone production causes a cessation of sperm production (spermatogenesis), and the male becomes sterile. After the cycle, the body's ability to make testosterone may take months to start again. Aside from the undesirable sterility and loss of strength, other hormone levels get out of whack because of the low testosterone, and cause other problems such as increased body fat and depression. The body produces many hormones, and the levels of most hormones are interrelated. This article will examine the factors involved in regulating the production of certain hormones in the body, particularly by the Hypothalamic-Pituitary-Testicular Axis. As always, the author does not condone the use of steroids by persons not under the care and guidance of a qualified physician.

Endogenous Testosterone
Where is testosterone made in the body? Well, about 95% is produced in the testicles, in special cells called "interstitial cells" or Leydig cells. These cells surround cells in the seminiferous tubules, called Sertoli cells, whose function is to produce sperm. Spermatogenesis in the Sertoli cells requires testosterone, and when endogenous testosterone diminishes, then sperm production stops (and you end up with raisins). Bear in mind that Leydig cells and Sertoli cells are in close proximity to each other. Therefore, the testosterone concentration is high, relative to the concentration in the bloodstream. Sertoli cells require high testosterone concentration for the sperm cells to begin the maturation process. So, even though you might have "a lot" of exogenous testosterone when on-cycle, the concentration is not high enough at the Sertoli cells to promote spermatogenesis because the Leydig cells have shut down. This, combined with a lack of Follicle Stimulating Hormone (FSH), renders many men sterile during a cycle.

The "Axis"
Hang on a minute, the Leydig cells shut down? Why? How?

Well, the short answer is, "hormones". Hormones are the body's way of sending signals, or information from one part of the body to another. In a computer, electrons (electricity) act as the signal; in the body (which doesn't have wires!), the signals must be sent with chemicals, and that is the role of hormones. The term "HPT Axis" refers to the interaction of the hypothalamus, pituitary, and testes (there are other axes as well). For the Leydig cells, Luteinizing hormone (LH) is released from the pituitary and it signals the Leydig cells to produce testosterone. Similarly, the pituitary releases FSH, and it tells the Sertoli cells to make sperm (as well as androgen-binding-protein). The pituitary is a gland that produces and stores a number of hormones, under the control of the hypothalamus. The hypothalamus might be considered to be the General (as in military), and the pituitary would be a Colonel under the General's command. The hypothalamus decides how the body's organs should operate, and the pituitary gives the actual "orders" to the target organs. Some of the "signaling" hormones made or stored in the pituitary are:

Growth Hormone
IGF-I and IGF-II
Thyroid Stimulating Hormone (TSH)
Vasopressin (or Antidiuretic hormone)
Luteininzing Hormone (LH)
Follicle Stimulating Hormone (FSH)
Adrenocorticotropic Hormone (ACTH)

The hypothalamus and the pituitary are very close together, and are located at the base of the brain. Just as the pituitary uses hormones to signal the target organ (testes, thyroid, etc) to do something, the hypothalamus uses other hormones to signal the pituitary to do its job. Some of these "Hypothalamic Releasing Factors" are (along with the pituitary hormones affected):

Hypothalamic Hormone: Regulates:
Gonadotropin Releasing Hormone LH, FSH
Growth Hormone Releasing Hormone GH
Thyrotropin Releasing Hormone TSH
Corticotropin Releasing Hormone ACTH

But how does the hypothalamus know when its commands have been carried out? By what's called a "feedback loop". Just as a General relies on reports from the field, the hypothalamus must monitor the results of its commands. The hypothalamus has sensors (receptors) to determine the levels of the chemicals (hormones) produced by the target organs. For our purposes, we will examine only one feedback loop, the one involving the testes.

The hypothalamus has both androgen receptors and estrogen receptors. When the level of either hormone gets too high, the receptors become more highly activated, and the hypothalamus stops sending Gonadotropin Releasing Hormone to the pituitary. The pituitary, in turn, stops sending LH and FSH to the testes. Thus, the signal is, "stop producing testosterone (and sperm)". We know that androgens (and NOT just estrogen) stop the action of the testes because exogenous DHT by itself (which cannot convert to estrogen) is very effective at shutting down the testes. A schematic of the HPTA (and other glands) is shown below. Note that the other glands are involved in feedback mechanism also.

What does the estrogen/androgen feedback loop mean to bodybuilders? It means that, when using exogenous androgens, the hypothalamus is very effectively signaled (by binding to the AR's on the hypothalamus) that there is plenty of androgen, and that the testes should be shut down. As long as the level of exogenous androgen is high enough, no reasonable amount of Clomid (or other estrogen-blocker) will be able to keep the testes functioning. So, the only reason to take Clomid during a cycle is if you are susceptible to gyno, or want to try to reduce the bloating associated with elevated estrogens. Both of these actions take place at sites other than at the hypothalamus.

How does hCG work and what does it do? This hormone (produced by pregnant females) acts very much like LH, and it even closely resembles LH (and FSH) in chemical structure. So, administration of hCG sends a signal to the testes to start production of testosterone (thus, hCG can help prevent testicular atrophy during a long cycle). However, remember that the testosterone produced can signal the hypothalamus to stop sending the signals to turn on the testes. So, hCG can be somewhat inhibiting to the natural process of hormone release. That is why many believe that hCG should not be used at the end of a cycle, when the desire is to stimulate natural production of hormones.

It has become standard practice to use Clomid at the end of a cycle; because it is felt that blockage of the estrogen receptors on the hypothalamus will cause it to start signalling for the production of testosterone by releasing Gonadotropin-releasing hormone. While this sounds very good in theory and works in many cases, it does not always work, particularly in older men. For some, the use of clomid does not help "jump-start" the gonads at the end of a cycle, and some believe that only time will allow the hypothalamus to begin action again. Doctors still rely on the combination of clomid and hCG (yes, even after a cycle), and there appear to be indications that this combination therapy is a little more successful than clomid by itself. To be absolutely sure, a man who uses exogenous steroids should have blood work done after being off-cycle for a while, in order to ensure that the hormone levels have come into normal ranges.

Finally, many men who use steroids get high blood pressure very early in a cycle. While many have attributed this to erythropoiesis (production of too many red blood cells and thickening of the blood), I believe that the increase in BP is due to a direct action of androgens on the hypothalamus, altering the release of Vasopressin. Doctors who prescribe hormone-replacement therapy often monitor the hematocrit (% of red blood cells), and recommend that the patient donate blood if the hematocrit exceeds 50.
Credit: Sanjac

 

[alexvega]

Hey MUdGEbro respect to you from me . i´m a little boys in this topic, i have to much to learn, but i started to learn, my firt topic to review is PCT. thanks

 

[alexvega]

Hi MUDGE. i had a problem i started a cycle on deca and equipose 3 weeks ago for just 2 weeks because i got a disease in my lung, i took antibiotics by 7 days ,and stoppped the cycle.
now i´m start to take novaldex 20mg/day. that´s correct.

what do you recomen to me.
thanks

 

[GFR]

Ok I cant open this for some reason......I was told that it is the site for Upjohn or pfiezer or pharmacia ????

http://wwwsearch.pfizer.com/search?...ife+of+testosterone&ip=70.162.85.126&filter=p

http://www.pfizer.com/pfizer/downloa...stosterone.pdf



saying the half life of test Cypo is 8 days???????????

 

[rhouser30]

got a question alittle off topic but is most of this stuff gotten from overseas that is what i have seen, how legit is it?

 

[GFR]

got a question alittle off topic but is most of this stuff gotten from overseas that is what i have seen, how legit is it?

It depends.....we need more details to give you any kind of an answer

 

[rhouser30]

like to get tren or test without homebrew

 

[ironfreak2]

very good info

 

[alexvega]

Hey MUdGEbro respect to you from me . i´m a little boys in this topic, i have to much to learn, but i started to learn, my firt topic to review is PCT. thanks

Hello everyone, longtime since i wrotte the firts time in this forum.
givenu alot of thanks for the great inf that i can learn about the gears o roids whetever u can call it.

by the way in three time along 8 yeas reading this topic i had did 3 cycles all of them with test enanthato plus nandro o EQ, the results were amanzing, i want to be honest i falldown in some depresion in the firts 5 days. i could be part of the hormone brain imbalace.

but after a one year off the roids iwoul like to star one moretime a short cycle.

but i dont have test enanthate available this time,what other roid can a use instead .

againg thanks alot u all.

 

[8Ball]

Oral steroids Drug Active half-life
Anadrol / Anapolan50 (oxymetholone) 8 to 9 hours
Anavar (oxandrolone) 9 hours
Dianabol (methandrostenolone, methandienone) 4.5 to 6 hours
Methyltestosterone 4 days
Winstrol (stanozolol)
(tablets or depot taken orally) 9 hours



Depot steroids Drug Active half-life
Deca-durabolin (Nandrolone decanate) 15 days
Equipoise 14 days
Finaject (trenbolone acetate) 3 days
Primobolan (methenolone enanthate) 10.5 days
Sustanon or Omnadren 15 to 18 days
(I have now seen data from a lab tech 'proving' that EOD is neccessary for good blood levels with sust)
Testosterone Cypionate 12 days
Testosterone Enanthate 10.5 days
Testosterone Propionate 4.5 days
Testosterone Suspension 1 day
* Winstrol (stanozolol) 1 day


*Winstrol depot does not actually possess a classical half-life because it is un-esterified. Instead, the microcrystals dissolve slowly. Once they have all dissolved levels of the drug fall very rapidly. It is still an important consideration, and we have included it with a half-life of one day.


Steroid esters Drug Active half-life
Formate 1.5 days
Acetate 3 days
Propionate 4.5 days
Phenylpropionate 4.5 days (dont believe this is correct)
Butyrate 6 days
Valerate 7.5 days
Hexanoate 9 days
Caproate 9 days
Isocaproate 9 days
Heptanoate 10.5 days
Enanthate 10.5 days
Octanoate 12 days
Cypionate 12 days
Nonanoate 13.5 days
Decanoate 15 days
Undecanoate 16.5 days



Ancillaries Drug Active half-life
Arimidex 3 days
Clenbuterol 1.5 days
Clomid 5 days
Cytadren 6 hours
Ephedrine 6 hours
T3 10 hours


A practical example is if one was to inject 100mg of testosterone propionate and allow blood levels to peak. In 4.5 days time (half-life duration from the above tables) and providing no other injections had taken place, the level would be reduced to 50mg. Again, a further 4.5 days down the line and levels would have dropped to 25mg, and the value keeps halving every 4.5 days.

Active Half-life of Steroids and Esters

Detection times for AAS

Boldenone Undecyclenate 4-5 months
Clen 4-5 Days
Ephedrin 6-10 Days
Halo 2 months
Proviron 5 weeks
D-Bol 5 weeks
Methamphetamin 6-10 Days
Primo Depot 4-5 weeks
Deca 18 months
Nandrolon Phenylprop 12 months
Anavar 3 weeks
Anadrol 2 months
Winny oral 3 weeks
Winny inj 2 months
Test cyp 3 months
Test enat 3 months
Sustanon 3 months
Test Prop 2-3 weeks
Andriol 1 week
Tremolon Acet 4-5 weeks
Test supspenison No metabolites. t/e should
be back to normal in days.

Factors which influence the detection times


Metabolism
Fluid intake
Tolerance to the drug
Frequency of intake
Duration of intake
Body fat
Potency of drug
Dosage

Ester actual mg/100mg dose
test no ester 100
tren acetate 87
test prop 83
test enanth 72
test cyp 70
test undecan 63

This style info is why I joined this forum. Thanks