So who is wrong?

[orosco]

I was flamed on the last post saying i need to do more research. Well here is my conflicting point. I asked if taking clomid would be good while on a-var because a-var only supresses you and doe snot shut you down.. Well if you look at the a-review profile it will tell you that a-var doesnt aromatize at any dose and it doesnt shut down your natural test production. I copied and pasted the part im tlaking about..I only asked because i want to minimize acne PCT and thought a-var would be the best AAS for minimized post cycle acne. Im sick of taking EQ or prop ( which i love) and brekaing out horribly PCT.
Here the profile par im talking about....
" The third reason which speaks well for an intake of Oxandrolone is that even in a very high dosage this compound does not influence the body's own testosterone production. To make this clear: Oxandrolone does not suppress the body's own hormone production. The reason is that it does not have a negative feedback mechanism on the hypothalamohypophysial testicular axis, meaning that during the intake of Oxandrolone, unlike during the intake of most anabolic steroids, the testes signal the hypothalamus not to reduce or to stop the release of GnRH (gonadotropin releasing hormone) and LHRH Luteinizing hormone releasing hormone). This special feature of Oxandrolone can be explained by the fact that the substance is not converted into estrogen Oxandrolone (Anavar), when given to normal men in high doses does not reduce the seminal volume or count, nor can it be converted (aromatized) into estrogen. "

[Property of Steroid.com]

That profile is incorrect. Sorry. Anavar does influence testosterone production:

Clin Endocrinol (Oxf). 1993 Apr;38(4):393-8.
The effects of oxandrolone on the growth hormone and gonadal axes in boys with constitutional delay of growth and puberty.

Malhotra A, Poon E, Tse WY, Pringle PJ, Hindmarsh PC, Brook CG.

Endocrine Unit, Middlesex Hospital, London, UK.

OBJECTIVE: We studied the effects of oxandrolone on serum concentrations of LH, FSH, testosterone, GH, SHBG, DHEAS, IGF-I and insulin in boys with constitutional delay of growth and puberty. DESIGN: Ten boys with constitutional delay of growth and puberty, mean age 13.8 years (range 12.4-15.5) were studied. Twenty-four-hour serum concentration profiles of GH, LH and FSH were constructed by drawing blood samples at 20-minute intervals. Three study occasions over a period of 6 months were chosen to assess hormone concentrations before, during and 6 weeks after a 3-month course of oxandrolone (2.5 mg once daily) therapy. RESULTS: Growth velocity increased during oxandrolone treatment and stayed higher after therapy (pre 3.9 +/- 0.5; on 6.3 +/- 0.8; post 6.4 +/- 0.9 cm/year (mean +/- SEM) two way ANOVA, F = 5.3, P = 0.02). Oxandrolone had androgenic effects, suppressing mean serum LH concentrations from 1.7 +/- 0.3 to 1.1 +/- 0.2 U/I and serum testosterone concentrations from 1.9 +/- 0.6 to 0.8 +/- 0.1 nmol/l. SHBG concentrations were also reduced from 130.9 +/- 14.6 to 30.7 +/- 7.3 nmol/l. Serum GH concentration fell slightly from 5.9 +/- 0.6 to 4.8 +/- 0.5 mU/l. After cessation of treatment, there was a significant 'rebound' in mean 24-hour serum LH (2.6 U/l +/- 0.4) and testosterone concentrations (3.2 +/- 0.9 nmol/l) but no change in serum GH concentrations. SHBG values also rose but not to the same extent as those observed before therapy (82.0 +/- 8.4 nmol/l). There were no statistically significant differences in serum concentrations of FSH, DHEAS, IGF-I and insulin over the study period. In a stepwise multiple regression analysis of factors that might influence the growth rate observed, the 24-hour mean serum testosterone concentration and the treatment (on or off) with oxandrolone were the main influences. The relationship was described by the equation Height velocity = 0.69 (24-hour mean serum testosterone concentration)+1.70 (treatment regimen)+3.37 (adjusted R2 = 0.35, F = 8.39, P = 0.001). CONCLUSIONS: Oxandrolone has an androgenic action as shown by changes in serum LH, testosterone and SHBG concentrations and by the lack of effect on FSH. No effect of oxandrolone on the GH axis was documented. We suggest that the growth promoting effects of oxandrolone are related in part to the mild androgenic effects of the steroid and the growth acceleration following oxandrolone withdrawal may reflect increasing total serum testosterone concentrations and decreasing levels of SHBG and progress in puberty.



Clin Endocrinol (Oxf) 1997 Feb;46(2):209-16


Effect of low dose oxandrolone and testosterone treatment on the pituitary-testicular and GH axes in boys with constitutional delay of growth and puberty.

Crowne EC, Wallace WH, Moore C, Mitchell R, Robertson WH, Holly JM, Shalet SM.

Department of Endocrinology, Christie Hospital Trust, Manchester, UK.

OBJECTIVE: To investigate the effect of low dose oxandrolone and testosterone on the pituitary-testicular and GH-IGF-I axes. DESIGN: Prospective double-blind placebo-controlled trial. PATIENTS: Sixteen boys with constitutional delay of growth and puberty (CDGP) with testicular volumes 4-6 ml were randomized to 3 months treatment: Group 1 (n = 5), daily placebo: Group 2 (n = 5), 2.5 mg oxandrolone daily or Group 3 (n = 6), 50 mg testosterone monthly intramuscular injections with assessment (growth, pubertal development and overnight hormone profiles) at 0, 3, 6 and 12 months. MAIN OUTCOME MEASURES: LH and GH profiles (15-minute samples) were analysed by peak detection (Pulsar), Fourier transformation and autocorrelation. Testosterone levels were measured hourly and insulin, SHBG, IGF-I, and IGFBP-3 levels at 0800 h. Statistical analysis was by multivariate analysis of variance for repeated measures. RESULTS: LH and testosterone parameters increased significantly with time in all 16 (LH AUC, P < 0.001; peak amplitude, P = 0.02; number of peaks, P = 0.02; testosterone AUC, P = 0.02; morning testosterone, P = 0.002). In Group 2, however, LH and testosterone parameters decreased at 3 months followed by a rebound increase at 6 and 12 months. SHBG levels were markedly reduced at 3 months (P = 0.006) and a wider range of dominant GH frequencies was present although GH AUC was not increased until 6 months, with an increase in GH pulse frequency but not amplitude. IGF-I levels were increased at both 3 and 12 months. In Group 3, pituitary-testicular suppression was not apparent, but GH levels increased with an increase in GH amplitude at 3 and 12 months. CONCLUSION: Oxandrolone transiently suppressed the pituitary-testicular axis and altered GH pulsatility. Testosterone increased GH via amplitude modulation.

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http://jcem.endojournals.org/cgi/content/full/84/8/2705

Short-Term Oxandrolone Administration Stimulates Net Muscle Protein Synthesis in Young Men1

Melinda Sheffield-Moore, Randall J. Urban, Steven E. Wolf, J. Jiang, Don H. Catlin, David N. Herndon, Robert R. Wolfe and Arny A. Ferrando
Departments of Surgery (M.S.-M., S.E.W., D.N.H., R.R.W., A.A.F.), Anesthesiology (R.R.W.), and Internal Medicine (R.J.U., J.J.), University of Texas Medical Branch, and Shriners Burn Hospital for Children (D.N.H., R.R.W.), Galveston, Texas 77550; and the Department of Molecular and Medical Pharmacology, University of California, Olympic Analytical Laboratory (D.H.C.), Los Angeles, California 90025


Short term administration of testosterone stimulates net protein synthesis in healthy men. We investigated whether oxandrolone [Oxandrin (OX)], a synthetic analog of testosterone, would improve net muscle protein synthesis and transport of amino acids across the leg. Six healthy men [22 ± 1 (±SE) yr] were studied in the postabsorptive state before and after 5 days of oral OX (15 mg/day). Muscle protein synthesis and breakdown were determined by a three-compartment model using stable isotopic data obtained from femoral arterio-venous sampling and muscle biopsy. The precursor-product method was used to determine muscle protein fractional synthetic rates. Fractional breakdown rates were also directly calculated. Total messenger ribonucleic acid (mRNA) concentrations of skeletal muscle insulin-like growth factor I and androgen receptor (AR) were determined using RT-PCR. Model-derived muscle protein synthesis increased from 53.5 ± 3 to 68.3 ± 5 (mean ± SE) nmol/min·100 mL/leg (P < 0.05), whereas protein breakdown was unchanged. Inward transport of amino acids remained unchanged with OX, whereas outward transport decreased (P < 0.05). The fractional synthetic rate increased 44% (P < 0.05) after OX administration, with no change in fractional breakdown rate. Therefore, the net balance between synthesis and breakdown became more positive with both methodologies (P < 0.05) and was not different from zero. Further, RT-PCR showed that OX administration significantly increased mRNA concentrations of skeletal muscle AR without changing insulin-like growth factor I mRNA concentrations. We conclude that short term OX administration stimulated an increase in skeletal muscle protein synthesis and improved intracellular reutilization of amino acids. The mechanism for this stimulation may be related to an OX-induced increase in AR expression in skeletal muscle.



As depicted in Table 1, arterial steady state was achieved during the sampling hour (240–300 min) of both the control period and after 5 days of OX administration. However, arterial enrichments were significantly higher after OX treatment (Table 1; P < 0.05). Due to noncompliance with medications by one subject, all data presented include only the results from five subjects.


Serum OX concentrations on day 3 (1.9 ± 0.4 ng/dL) and day 5 (2.2 ± 0.3 ng/dL) of OX administration, measured 10 h after each evening’s oral dose (2100 h), remained steady. However, by 18 h posttreatment on day 5, serum OX levels were markedly reduced (0.48 ± 0.06 ng/dL; P < 0.01) compared to day 3 or day 5 10-h values. Total serum T concentrations were within normal physiological range on day 0 (449 ± 35 ng/dL) and day 3 (441 ± 44 ng/dL) of OX treatment. However, by day 5, total serum T concentrations were significantly reduced (282 ± 45 ng/dL; P < 0.05) below day 0 and day 3 values (Fig. 3). Serum free T concentrations were within normal physiological range on days 0, 3, and 5. However, by day 5, serum free T concentrations were significantly reduced (98 ± 10 pg/mL; P < 0.001) below day 0 (121 ± 12 pg/mL) and day 3 (126 ± 9 pg/mL) values. Hence, the total androgen concentration (T + OX) was reduced in parallel to the reduction in T (Fig. 3)

We examined the response of muscle protein kinetics to OX administration in normal young men. We demonstrated that a moderate dose of OX, given over 5 days, stimulated muscle protein anabolism in young men. Further, we demonstrated for the first time in humans an increase in skeletal muscle ARs after anabolic intervention. Muscle anabolism during OX treatment occurred by stimulation of protein synthesis, as protein breakdown was unchanged. Moreover, a significant decrease in model-derived outward transport (FV,M) along with the calculated increase in protein synthetic efficiency indicate increased intracellular reutilization of amino acids. Taken together, these results demonstrate the mechanism of OX’s anabolic properties in fasted skeletal muscle.

A recent study from our laboratory (7) demonstrated that 5 days after a single im injection of TE (200 mg), FSR and model-derived protein synthesis increased 2-fold, with no change in FBR. Further, in agreement with the present findings, Ferrando et al. (7) demonstrated an increased utilization of intracellular amino acids by showing a strong relationship between protein breakdown and protein synthesis. Although our kinetic data strongly support these findings, the magnitude of the synthetic response with OX was not as great as that with TE. With OX, we found 44% and 28% increases in FSR and model-derived protein synthesis (FO,M), respectively. Several important factors may account for these differences.

In our previous study, the total T concentration increased to twice the physiological norm 2 days after TE injection (2094 ± 561 ng/dL). Further, T was still in the upper physiological range (953 ± 283 ng/dL) by day 5 and was statistically different from preinjection T concentration (425 ± 99 ng/dL) (7). In contrast, the magnitude of response we found in serum OX concentration was much less than that reported with TE. For example, total serum OX, as measured in the morning 10 h after oral ingestion, was consistent on days 3 and 5, whereas total serum and free T concentrations declined significantly from days 0 and 3 to day 5. Viewed in combination, total serum androgen levels with OX treatment were far below those obtained with TE. Although the total androgen exposure to the skeletal muscle with OX may have been considerably less than that we found previously with TE, an increase in protein synthesis was nonetheless observed. This suggests that OX may exert a greater anabolic influence on skeletal muscle than TE, thereby overcoming the decrease in the T concentration.

[jucinator]

Hooker knows everything and yeah im kissin ass!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!Get BIG!!!!!!!!!!!!!!!!!!!!

[Property of Steroid.com]

Nah. These are old studies Billy Bathgate posted. I used them because I didn't need to go in and highlight all the important parts, since he already did it.

[jucinator]

yeah but you and Money Boss Hustla still know your shit and everyone on this board whos been here for more than a week knowes that. Hell i almost blindly follow what you guys say when it comes to gear .you know your shit!!!!!!!!!!!!