Testosterone Cypionate (Common / slang name: ‘CYP’)
Seen under the names: CYPIOBOLIC, CYPIOJECT, CYPIOLIC, CYPIONAX™, CYPIONEX 250, CYPIOTEST 250, CYTEX 250, DEPO-CYP 250, DEPO-TESTOSTERONE™, TEST-C 200, TESTABOL DEPOT™, TESTACYP, TESTAN 100, TESTAPLEX 250, TESTEX PROLONGATUM™, TESTOCYP, TESTOSTERONA C, TESTOXYL, VK TEST C 300.
Found in dosages: 50, 100, 125, 200, 250 and 300mg per 1 or 2ml single ampoules, also in 5 and 10ml multidose vials at all strengths.
Presentation: 1, 5, 10 and 20 single 1ml vials per box. 10ml vials; vet use and UG only.
First off to avoid any confusion, let me state that CYCLOPENTYLPROPIONATE is the same ester as the standard cypionate ester as exemplified in the photo above, it has just been shortened to save on the tongue-twisting…CLOPENTYLPRO .
Testosterone cypionate (hereafter referred to as ‘cyp’), was introduced to the U.S. drug market in the mid 1950’s under the brand name of DEPOT-TESTOSTERONE (a brand still being produced today), developed by UPJOHN (now PHARMACIA and UPJOHN). On the legal market, cyp is limited mainly to the U.S., so is a favourite of the American bodybuilding and strength fraternity. It does show up in this country (both pharma and UG), and was very popular a couple of decades ago, but it is mostly the ENANTHATE version (pharma/UG), which we see over here these days.
We can see that cyp and enanthate esters of testosterone are more or less interchangeable with regard to half-life, physical effect and pharmacokinetics…so don’t expect much of a write up for enanthate . The only viable difference of note between the two is the PIP (POST INJECTION PAIN), where CYPIONOLIC ACID(cypionate) is slightly LESS irritating at the injection site than ENANTHOLIC ACID (enanthate), for a small number of users…but that’s about it.
Test’ cypionate in school medicine has historically been used for the treatment of low androgen levels in men, but other uses have been noted. For example, during the 1960’s prescribing recommendations included the support of bone structure maturity, MENORRHAGIA (heavy periods in women), excessive lactation (females only), increase of muscle mass and prevention of OSTEOPOROSIS (brittle bone syndrome). It was recommended as a male fertility booster by SUPPRESSING testosterone/spermatogenesis during its use (200mg per week for 6-10 week periods), then rebounding to higher levels of both AFTER its cessation (weird back-asswards I know).
Obviously the FDA got stronger powers in the 70’s, and the broad uses for cyp were narrowed drastically. The ‘rebound therapy’ as stated above was removed as a treatment (no shit). Treatment of menstrual irregularities and lactation were removed also due to female virilising side effects. The elderly were also taken care of by removing osteoporotic treatment too, since the high androgens left most of the old folk burnt out…our ageing metabolisms don’t hold well with high androgen levels after they have been low for many years: all the side effects without the gains perhaps from permanent age-related androgen receptor shutdown. This left only use for androgen deficiency in males as a standalone treatment from its use.
So today, CYP in the U.S. is approved for hormone replacement therapy in men with endogenous androgen deficiency and as a secondary treatment for inoperable metastatic breast cancer in women (although rarely used these days in the latter).
Structurally, this compound is ‘simply’ the base testosterone molecule with a carboxylic acid ester (cyclopentylpropionic acid), attached at the 17-beta hydroxyl group. Since esterified forms of testosterone are less ‘polar’ than free test’, they are absorbed much more slowly from the injection site. When in the circulatory system, the ester is removed via ESTERASE enzymes in the blood to yield free testosterone (i.e. no ester attached; the base molecule), which can then attach to various receptors within the body. Esterified versions of drugs are manufactured to prolong the active effect of the drug in the body to allow for less frequent administration than would be needed with the base drug itself. As mentioned previously, the half-life of the enanthate ester is around 8 days, yielding and active life of anywhere from 10-14 days (as seen in the diagram above), depending on the patients metabolic efficiency.
Testosterone and its esters are readily converted to estrogens (mostly ESTRADIOL), in the body via the aromatase enzyme. Elevation of estrogens in the body causes side effects such as increased water retention (with possible increases in blood pressure), abnormal breast tissue growth (gynaecomastia), and body fat gain (if the estrogen levels overpower the androgen levels). Even with this, testosterone is still only classed as MODERATELY estrogenic. Sometimes, minimal estrogenic action can be ‘blocked’ using SERM’s (SELECTIVE ESTROGEN RECEPTOR MODULATORS), such as TAMOXIFEN or CLOMIPHENE CITRATE, but if the estrogens get out of control stronger anti aromatase drugs like ANASTROZOLE or LETROZOLE may be warranted, which block the actual estrogenic conversion process itself. Bear in mind however, that aromatase inhibitors have side effects in their own right, such as a negative influence on blood fats (HDL/LDL).
Bear in mind that estrogenic side effects will increase relative to the amount of estrogens present in the blood, which in turn are dose related to the amount of testosterone one is administering, i.e. the more test’ you take, the worse the intensity of estrogenic side effects. Since lower doses of cyp are only generally applied for androgen replacement therapy in ANDROPAUSE (natural, age related testosterone diminution), it is normally a given that bodybuilders WILL be using higher doses which will have accompanying high estrogenic conversion rates…so please have those estrogen blockers or anti aromatase drugs on hand tom combat this. Many bodybuilders have only thought of cyp as a bulking drug, since the water retention from high estrogens covers any fat loss that may be occurring from a sub-maintenance caloric intake and/or cardio, but I disagree with this. Remember, the water held subcutaneously is only water, and not fat. Yes, it is proven that fat loss will be slowed by higher estrogen levels in the blood, but if these are limited by anti aromatase drugs like anastrozole and letrozole (NOT blockers like tamoxifen, as the estrogen is still present in the blood), then there is absolutely no reason that you cannot get lean on cyp, as long as you are taking the relevant estrogenic treatment compounds at the same time. The notion that you must swap to test’ propionate and the like to ‘get rid of the water’ is kinda right, but not entirely correct an assumption. The lower dosages typically employed with the application of these ‘dieting’ drugs (most test’ prop’ esters are 100mg/ml, whereas cyp is mostly 200-250mg/ml), may be responsible for a lot of the muscle mass losses we typically see in the neophyte competitor, rather than the employment of a strict diet. Taking an overall lower mg dosage of testosterone per week WILL cause a concommitment loss of muscle if all other variables remain constant…LESS mg’s = LESS MUSCLE.
Testosterone is obviously the chief male androgen responsible for the maintenance (and development) of secondary male sexual characteristics. Taking the cypionate ester of testosterone will glean the usual androgenic side effects of oily skin, acne, body/facial hair growth, and an increase in hair loss in those with a genetic predisposition. These side effects go for women too but will show up much quicker and be much stronger even at low mg dosages.
Testosterone can convert to DHT (DIHYDROTESTOSTERONE) by ‘reduction’ via the 5α reductase enzyme, which is a ‘super’ androgenic hormone in itself. The body has DHT receptors everywhere, but particularly high concentrations are found in the scalp, the prostate, and the sebaceous glands in the skin. We can fugure that it is not the test’ itself which causes accelerated hair loss, excessive skin oil production giving acne, and prostate enlargement…it is the DHT. These side effects can be reduced greatly however by accompanying exogenous testosterone use with a 5α reductase inhibitor such as FINASTERIDE (PROSCAR™), or DUTASTERIDE (AVODART™). But remember, muscles grow best with some DHT present, so don’t overdo these inhibitors dosage-wise and avoid them completely when the test’ dosage employed is only low. I would say add in small doses of the DHT treatment drugs only at testosterone dosages of 500mg/week+, and increase their micro-dosages incrementally only as the test’ dose increases.
Due to media attention, most people will say steroids are bad for your liver. Well, testosterone ISN’T (or at least, VERY unlikely). One study looked at potential for liver stress of testosterone administration by giving a group of male subjects 400mg per day (2,800mg per week!); the androgen was administered orally to ensure maximum stress concentrations in the liver reached a peak as quickly as possible. After 20 days, there was no significant change in liver enzyme values, which would have indicated a reaction to stress/poison. As a rule of thumb, all testosterone esters are good to go as far as NOT causing any liver distress (5 grams a week here I come!).
With relevance to cardiovascular risk, testosterone has dramatically less impact than synthetic and/or oral steroids. Since testosterone is a ‘natural’ endocrine hormone, the liver can metabolise it easily (unlike synthetic and most oral steroids), so does not stress itself unduly, so leaving it to do its job of cholesterol management efficiently. And strangely, because testosterone normally converts to estradiol, this in itself has a protective effect over any negative effects from androgens on serum lipids (cholesterol). An example of this is from a study of 280mg testosterone (enanthate ester), weekly given to test subjects where only slight changes occurred with regard to HDL. However, in the same study, when subjects did concomitant ingestion of an aromatase inhibitor as well, a strong 25% decrease of HDL was seen. So, think twice when adding in anastrozole or letrozole willy-nilly…it could mess your blood fats up. TAMOXIFEN or CLOMIPHENE as blockers, are a much better choice as an anti-estrogen treatment (gynaecomastia only, as the estrogens are still there, but blocked at the mammary gland site). Another study showed a 13% decrease in HDL using 300mg testosterone weekly, which increased to 21% when the dosage was increased to 600mg weekly. Indicating that negative HDL changes are also dose related; the more you take the more your cholesterol ratios change for the worse. A take home rule of thumb here is that doses lower than 600mg per week of ‘long’ test’ esters have shown to be relatively safe with regard to negative changes in HDL, VHDL/LDL, triglycerides, apolipoprotein B/C-III, C-reactive protein and insulin sensitivity; all listed cardiovascular risk factors. Also, if you can do without them at these lower test’ doses, stay away from anti-aromatase drugs, and at worst take only estrogen blockers, as these do act like estrogens in the liver, so do not short circuit the body’s cholesterol management systems.
So, we see that ‘evil’ testosterone isn’t actually all that bad for us, but what about natural androgen suppression? This is where the good stuff comes unstuck. I’ll treat you to one of my steroid commandments here. Ahem,
‘IF THOU TAKEST ENOUGH GEAR TO GET GAINS, THOU WILST SUPPRESS NATURAL TESTOSTERONE PRODUCTION’
It matters not whether it’s the weakest girly-girl steroid on the market, if you get some muscular gains from taking a high enough dose of it, there will exist a negative feedback loop that causes the body to shut down its own natural testosterone production, verbatim. The same is exactly true of any testosterone ester, but probably more so as it has not been modified in any way to avoid these negative HPTA effects as might be the case with other synthetic steroids. Without the intervention of natural testosterone stimulating substance (HCG, clomiphene, mesterolone and the like), it is almost certain that testicular shrinkage will occur as there is no ‘need’ for them to stay big and produce testosterone, the body is monitored has having enough and in most cases usually too much from the exogenous use. These drugs are sometimes taken during a cycle to prevent testicular tissue shrinkage, and even though the tissue is not particularly active, it makes the job of kick-starting these big gonads into life come androgen cessation much easier. Even if these drugs are NOT employed during the cycle, the typical post cycle therapy of drugs (see elsewhere in the book), will get them up and running to avoid the usual post cycle crash. Not using them after a cycle? Then wave goodbye to most if not all of the gains you made on the steroids, and say hello to accelerated fat loss, loss of sex-drive, and depression. Some ‘clever’ users of strong androgens kind of ‘step-down’ to milder drugs like METHENOLONE (PRIMOBOLAN™) or DROSTANOLONE (MASTERON™), as a preparation phase for coming off totally, but in reality it is doing nothing except removing some of the water retained during test’ use, so the crash isn’t as soul destroying at the ‘real’ cycles end. Just do the post-cycle therapy as listed elsewhere in the book to limit your losses (other options are open, but I’ll save these for later :).
What about dosages of cyp? In school medicine, androgen deficiency is treated with a 50-400mg shot every 2-4 weeks to keep the patient in a normal physiological range. Bodybuilders and strength athletes however are doing weekly doses of anywhere from 400-1000mg (I have seen well over 2 GRAMS weekly in more than a few though). Lower doses of 200mg weekly will only have the effect of replacing your natural testosterone (if you indeed have any), and shutting you down, which will not aid in physique enhancement any, so makes no sense at all.
As testosterone is THE male androgen, users witness excellent gains in muscle size and strength with sufficient dosages, and normally employ longer cycles with the long esters of 8, 12, 16+ weeks in length. Some stay on test’ year round with intermittent HRT phases of 200mg weekly between their higher dose phases, especially in the older (40+) athlete where natural androgens are at a low ebb as a matter of natural course, courtesy of good old Father Time.
Due to the osmotic effects of cyp, many use it in off season cycles when water retention and a little fat gain are of minimal concern, but maximum mass and strength are. It can be used in cutting cycles as previously mentioned, but timing of shots, diet and ancillary drug use will need much more thought and application. It is rare to see ‘testosterone-only’ use, with many stacking the drug with other, more anabolic injectables and/or orals, but it has been done by those in the know who don’t need to spend a fortune on flamboyant compounds to get results. Remember, testosterone is the Daddy of muscle/strength gain, so no matter how fancy you get, no other drug will put it on as well (see cycle design chapter later).
Stacking with other compounds however, can let you use a lower dose of test’ with similar results since the anabolic drugs may have a synergistic effect with test’. 400-600mg/week of a NANDROLONE ester goes well with any test’ ester, as does 500-800mg/week of BOLDENONE…both boosting size and strength to new heights while needing not much more than 400-600mg cyp’ per week. For less bulkier results, some will combine it with injectable drostanolone (300-500mg/week), to temper some of the estrogens produced making for a much drier cycle. Sometimes methenolone (400-500mg/week), can be added to enable lower test’ dosage use, whilst still giving appreciable gains of better quality. For better strength and mass, TRENBOLONES (150-400mg/week depending on ester type), are a great addition too but temper and blood pressure must be watched closely for sharp rises in both. Orals can be added too; OXYMETHELONE (ANADROL™) or METANDIENONE (dbol), for out and out mass and power at 50-100mg/day, OXANDROLONE (ANAVAR™) for strength at 40-80mg/day, and STANOZOLOL (WINSTROL™) at 30-50mg/day, for its SHBG binding properties to increase test’s unbound state in the blood.
Yes, more experienced (bigger) women do use testosterones in their gaining phases, but seldom the cypionate ester, more likely the faster esters like propionate or suspension to cease use if over-aggressive virilising symptoms show up, to ensure they are out of the system within days rather than weeks. Cyp is used in school medicine sometimes as a treatment for inoperable breast cancer, but this is a very rare occurrence these days due to the availability of other more effective drugs with less harmful and disturbing side effects.
MENS DOSAGE: 400-1000mg/week injected weekly or split twice weekly.
WOMENS DOSAGE: Rarely used by females.
PRICE: £4-6 per single amp box Pharma grade. Black Market, £25-40 per 10ml multiple use vial or 10 x 1ml amps, depending on dose per ml (200-350mg/ml).
Comparison of Testosterone, dihydrotestosterone, luteinizing hormone, and follicle-stimulating hormone in serum after injection of Testosterone enanthate or Testosterone … Schulte-Beerbohm, Nieschlag E. Fertility and Sterility 33 (1980) 201-3.
Enzyme induction by oral testosterone. Johnson SG et al. Clinical Pharmacology and Therapeutics, 1976, 20(2):233-7.
High-density lipoprotein cholesterol is not decreased if an aromatizable androgen is administered. Friedl et al. Metabolism, Vol 39, Issue 1, January 1990, Pages 69–74.
Testosterone dose-response relationships in healthy young men. Bhasin et al. Am J Physiol Endocrinol Metab. 2001 Dec;281(6):E1172-81.
Please note that this excerpt is only a small sample of the book chapter it is taken from. A great deal more content is available on this and many other topics in the Break the Code book.
Excerpts from Break The Code
© 2015—2016 Asgard Publications Inc.