Posted by JGUNS at CEM
How winny and proviron will make your cycle kick ass
Really, only a very small amount of Testosterone exists as “free” testosterone. Free test is testosterone that capable of binding to the Androgen Receptor, which is where all the rest of the magic happens, and allows for the following benefits:
-Enhanced growth factor activity (e.g. GH, IGF-1, etc.)
-Enhanced activation of myogenic stem cells (i.e. satellite cells)
-Enhanced myonuclear number (to maintain nuclear to cytoplasmic ratio)
-Enhanced protein synthesis
-New myofiber formation
Testosterone binds at around 45% to what is known as Sex Hormone Binding Globulin (SHBG), and about another 53% binds to proteins (albumin). The rest exists in a “free” state (about 2% if you did your math). Different variations of steroids also differ in the way in which they bind to proteins.
If one could unbind testosterone from SHBG by even a small percentage, it could make a big difference in the way that testosterone or other AAS exert their anabolic effects. Studies show that when testosterone is unbound from SHBG the “free” test does in fact exert greater effects than total T. As the following studies support:
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Demisch K, and Nickelsen T. Distribution of testosterone in plasma proteins during replacement therapy with testosterone enanthate in patients suffering from hypogonadism Andrologia 1983;15 Spec No:536-41.
Gandar R. Interpretation of the blood level of a steroid Rev Fr Gynecol Obstet 1985 Aug-Sep;80(8-9):635-40.
Legrand E., et al. Osteoporosis in men: a potential role for the sex hormone binding globulin Bone 2001 Jul;29(1):90-5.
Longcope C., et al. Diet and sex hormone-binding globulin. J Clin Endocrinol Metab 2000 Jan;85(1):293-296.
Valero-Politi J, and Fuentes-Arderiu X. Within- and between-subject biological variations of follitropin, lutropin, testosterone, and sex-hormone-binding globulin in men. Clin Chem 1993 Aug;39(8):1723-1725.
Proviron(1-Methyl Dihydrotestosterone) has been shown to bind with SHBG much more readily than test.
Relative binding affinity of anabolic-androgenic steroids: comparison of the binding to the androgen receptors in skeletal muscle and in prostate, as well as to sex hormone-binding globulin.
Saartok T, Dahlberg E, Gustafsson JA.
It is unclear whether anabolic steroids act on skeletal muscle via the androgen receptor (AR) in this tissue, or whether there is a separate anabolic receptor. When several anabolic steroids were tested as competitors for the binding of [3H]methyltrienolone (MT; 17 beta-hydroxy-17 alpha-methyl-4,9,11-estratrien-3-one) to the AR in rat and rabbit skeletal muscle and rat prostate, respectively, MT itself was the most efficient competitor. 1 alpha-Methyl-5 alpha-dihydrotestosterone (1 alpha-methyl-DHT; mesterolone) bound most avidly to sex hormone-binding globulin (SHBG) [relative binding affinity (RBA) about 4 times that of DHT]. Some anabolic-androgenic steroids bound strongly to the AR in skeletal muscle and prostate [ RBAs relative to that of MT: MT greater than 19-nortestosterone ( NorT ; nandrolone) greater than methenolone (17 beta-hydroxy-1-methyl-5 alpha-androst-1-en-3-one) greater than testosterone (T) greater than 1 alpha-methyl-DHT]. In other cases, AR binding was weak (RBA values less than 0.05): stanozolol (17 alpha-methyl-5 alpha- androstano [3,2-c]pyrazol-17 beta-ol), methanedienone (17 beta-hydroxy-17 alpha-methyl-1,4-androstadien-3-one), and fluoxymesterolone (9 alpha-fluoro-11 beta-hydroxy-17 alpha-methyl-T). Other compounds had RBAs too low to be determined (e.g. oxymetholone (17 beta-hydroxy-2-hydroxymethylene-17 alpha-methyl-5 alpha-androstan-3-one) and ethylestrenol (17 alpha-ethyl-4- estren -17 beta-ol). The competition pattern was similar in muscle and prostate, except for a higher RBA of DHT in the prostate. The low RBA of DHT in muscle was probably due to the previously reported rapid reduction of its 3-keto function to metabolites, which did not bind to the AR [5 alpha-androstane-3 alpha, 17 beta-diol and its 3 beta-isomer (3 alpha- and 3 beta-adiol, respectively)]. Some anabolic-androgenic steroids (only a few synthetic) bound to SHBG (1 alpha-methyl-DHT much greater than DHT greater than T greater than 3 beta-adiol greater than 3 alpha-adiol = 17 alpha-methyl-T greater than methenolone greater than methanedienone greater than stanozolol). The ratio of the RBA in rat muscle to that in the prostate (an estimate of the myotrophic potency of the compounds) was close to unity, varying only between about 0.4 and 1.7 in most cases.(ABSTRACT TRUNCATED AT 400 WORDS)
Skalba P, Korfanty A, Mroczka W, Wojtowicz M. Related Articles
[Changes of SHBG concentrations in postmenopausal women]
Ginekol Pol. 2001 Dec;72(12A):1388-92. Polish.
Variations of sex hormone-binding globulin in thyroid dysfunction.
Brenta G, Schnitman M, Gurfinkiel M, Damilano S, Pierini A, Sinay I, Pisarev MA.
Department of Endocrinology and Metabolism, French Hospital, Buenos Aires, Argentina.
[email protected]
With the aim of understanding the variations of the levels of sex hormone-binding globulin (SHBG) in thyroid dysfunction, we studied the influence of factors that also modify SHBG, such as menopausal status, age, and body mass index (BMI) in women with hypothyroidism and hyperthyroidism, both overt and subclinical. Statistical analysis was performed by means of analysis of variance (ANOVA), stepwise multiple regression, and partial correlation. The ANOVA showed a significant statistical difference among the means of SHBG of all groups (p<0.01). The difference was due to the group that included hyperthyroid women. Multiple regression analysis showed that the main factors influencing SHBG were BMI and age, except for the hyperthyroid group, where the most important independent variables were triiodothyronine (T3) and thyroxine (T4). Partial correlation controlling the effect of BMI and age showed no association between SHBG and the other variables in all groups except for the subclinical hyperthyroid and hyperthyroid, where we found a significant association between SHBG and T4 and T3. The premenopausal or postmenopausal status did not modify SHBG levels. When the patients are taken as a whole, BMI, age, T4, and T3 all have an association with SHBG levels according to the multiple regression analysis.
Determinants of sex hormone-binding globulin blood concentrations in premenopausal and postmenopausal women with different estrogen status. Virgilio-Menopause-Health Group.
Pasquali R, Vicennati V, Bertazzo D, Casimirri F, Pascal G, Tortelli O, Labate AM.
Department of Internal Medicine and Gastroenterology, University of Bologna, Italy
Just a quote: 2) SHBG values are correlated positively with estradiol and negatively with insulin and testosterone concentrations, but the predictive value of these variabiles on SHBG appears to be different in premenopause and postmenopause;
Here is a fun little fact: the level of SHBG can also be influenced by other factors. There is a direct relationship between the level of estrogen and thyroid hormones and the level of SHBG. Estrogen goes up, SHBG goes up. Estrogen goes down SHBG goes down. Same for Thyroid hormones triiodothyronine (T3) and thyroxine (T4). Also, there is a relationship with diet and insulin, but that is something I will save for later. Higher androgen levels due to AS administration has been shown to considerably lower levels of SHBG as well. The AS Winstrol (stanozolol) was shown in a 1989 study to lower levels of SHBG by 50% after oral administration.
Sex hormone-binding globulin response to the anabolic steroid stanozolol: evidence for its suitability as a biological androgen sensitivity test.
Sinnecker G, Kohler S.
Department of Pediatrics, University of Hamburg, West Germany.
Both the androgen-induced decline in serum sex hormone-binding globulin (SHBG) levels during puberty and the anabolic effect of exogenous testosterone are absent in patients with androgen insensitivity (testicular feminization). To determine whether the androgen-induced decline in serum SHBG could be used as a test of androgen sensitivity, we studied the effect of the anabolic-androgenic steroid stanozolol (17 beta-hydroxy-17 alpha-methyl-5 alpha-androstano-[3,2-c]pyrazol) on serum SHBG in 25 control subjects, 3 patients with complete androgen insensitivity, and 4 patients with partial androgen insensitivity. Stanozolol was administered orally for 3 days (0.2 mg/kg.day); blood samples were taken before and 5, 6, 7, and 8 days after the beginning of the test for measurements of serum SHBG. The lowest value (i.e. the peak response) in each subject was used as the measure of the response to stanozolol. In the control subjects the mean nadir serum SHBG level was 51.6 +/- 5.9% (+/- SD) of the initial value (P less than 0.001). In the 4 patients with partial androgen insensitivity the nadir serum SHBG ranged from 73-89%, and in the 3 patients with complete androgen insensitivity it ranged from 93-97% of the initial value. Thus, the decrease in serum SHBG after short term administration of stanozolol reflects androgen responsiveness and, thus, may be used to differentiate patients with androgen insensitivity syndromes from those with other causes of male pseudohermaphroditism.
Here’s the thing: This was after oral administration, so I am not sure that I can extrapolate the data to injectable as well. SHBG is made in the liver so even an injectable winny would have to be processed there, albeit slower, due to the slower release of injectable winny and it’s direct release into the bloodstream. That could possibly make it a little less effective in this regard.
In a nutshell: Proviron and Winny could provide the mechanisms to increase the value of other AS. Proviron would work because by binding to SHBG, it leaves hormone in a free state to bind to the AR. Proviron is a terrible Anabolic, but its affinity for SHBG would essentially “displace”other steroids from binding to SHBG. Winstrol would work to reduce the overall amount of SHBG, thereby having the effect of freeing up hormone to bind to the AR. What a stack!
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