AAS Research Mega Thread (not pro hormones)

[BeastFitness]

Short and Long esters are NOT the same. Long esters:
-cause higher levels of estrogen
-cause higher peak plasma levels
-
cause more suppression of the HPTA
-
cause more water retention
-
cause higher levels of nitrogen retention (muscle gain)

Androgen-stimulated pubertal growth: the effects of testosterone and dihydrotestosterone on growth hormone and insulin-like growth factor-I in the treatment of short stature and delayed puberty.

The purpose of this study was to investigate the roles of androgenic and estrogenic mechanisms in the stimulation of structural growth and plasma GH in male puberty. To resolve these two possible mechanisms, we compared the effect of two androgens in the treatment of constitutional delay in growth and adolescence: an aromatizable androgen, testosterone (T), and a nonaromatizable androgen, dihydrotestosterone (DHT). Nine adolescent males, Tanner stage 1 or 2, were studied before and during treatment with T enanthate (group A) or DHT heptanoate (group B). After 2.5 months of treatment, the height velocity (HV) was 12.6 +/- 2.8 cm/yr (n = 3) in group A and 8.9 +/- 1.7 cm/yr (n = 6) in group B, both within the range of peak HV for pubertal males. In group A, the integrated concentration of GH (ICGH) increased from 3.12 +/- 0.90 to 13.67 +/- 6.0 micrograms/L (P < 0.05), and plasma insulin-like growth factor-I (IGFI) increased from 126.7 +/- 2.5 to 350.3 +/- 20.3 micrograms/L (P < 0.01); plasma T increased from 0.8 +/- 0.5 to 33.8 +/- 11.0 nmol/L (P < 0.001), and the LH response to LHRH decreased from 27.6 +/- 10.7 to 5.9 +/- 2.5 IU/L (P = NS). In group B, ICGH decreased from 4.32 +/- 0.61 to 2.39 +/- 0.42 (P < 0.025), and IGF-I decreased from 218.3 +/- 39.2 to 184.0 +/- 15.8 (P = NS). Plasma T increased from 2.0 +/- 0.5 to 2.7 +/- 0.8 (P = NS), and the LH response to LHRH decreased from 45.7 +/- 14.5 to 10.7 +/- 5.8 (P < 0.05). To further evaluate the mechanism of the effect of DHT on plasma GH, seven male subjects with adolescent gynecomastia were treated with DHT heptanoate, and their responses were studied at 1 week and 3.5 months. ICGH decreased in conjunction with a decrease in the integrated T concentration (r = -0.77; P < 0.001) and to a slight degree with decreasing plasma estradiol (r = -0.39; P < 0.2). Plasma IGF-I did not show a significant change in the subjects with gynecomastia. Thus, the increase in GH at puberty in males appears to be due to an estrogen-dependent mechanism. The suppressive effect of DHT on GH secretion may be due to either suppression of estradiol production or a direct effect. Acceleration of HV into the peak pubertal range by DHT without an increase in plasma GH suggests that an increase in GH is not necessary for the pubertal growth spurt.


Pharmacokinetics and Pharmacodynamics of NandroloneEsters in Oil Vehicle: Effects of Ester, Injection Site and​ Injection Volume
​
We studied healthy men who underwent blood sampling for plasma nandrolone, testosterone and inhibin measurements
before and for 32 days after a single i.m. injection of 100 mg of nandrolone ester in arachis oil. Twenty-three men were randomized
into groups receiving nandrolone phenylpropionate (group 1, n 5 7) or nandrolone decanoate (group 2, n 5 6)​ injected into the gluteal muscle in 4 ml of arachis oil vehicle or nandrolone decanoate in 1 ml of arachis oil vehicle injected into either the gluteal (group 3, n 5 5) or deltoid (group 4, n 5 5) muscles. Plasma nandrolone, testosterone and inhibin concentrations​ were analyzed by a mixed-effects indirect response model. Plasma nandrolone concentrations were influenced (P, .001) by different esters and injection sites, with higher and earlier peaks with the phenylpropionate ester, compared with the decanoate ester. After nandrolone decanoate injection, the highest bioavailability and peak nandrolone levels were observed with the 1-ml gluteal injection. Plasma testosterone concentrations were also influenced (P , .001) by the ester and injection site, with the most rapid, but briefest, suppression being due to the phenylpropionate ester, whereas the most sustained suppression was achieved with the 1-ml gluteal injection. Plasma inhibin concentrations were also significantly influenced by injection volume and site, with the lowest nadir​ occurring after the nandrolone decanoate 1-ml gluteal injection. Thus, the bioavailability and physiological effects of a nandrolone ester in an oil vehicle are greatest when the ester is​ injected in a small (1 ml vs. 4 ml) volume and into the gluteal vs. deltoid muscle. We conclude that the side-chain ester and the injection site and volume influence the pharmacokinetics and​ pharmacodynamics of nandrolone esters in an oil vehicle in men.​

 

[Rodja]

Where are you gathering all of that info on long esters? Not only are these effects that depends on the compound, but some will completely contradict these statements (e.g. mast).

 

[BeastFitness]

Where are you gathering all of that info on long esters? Not only are these effects that depends on the compound, but some will completely contradict these statements (e.g. mast).

Reifenstein, et. al. Studies comparing the effects of certain testosterone esters in man.J Am Geriatr Soc. 1954 May;2(5):293-8.. PMID: 13162731

Journal of Andrology, Vol. 24, No. 5, September/October 2003 Copyright © American Society of Andrology Pharmacokinetics and Degree of Aromatization Rather Than Total Dose of Different Preparations Determine the Effects of Testosterone: A Nonhuman Primate Study in Macaca fascicularisGERHARD F. WEINBAUER*, CARL-JOACHIM PARTSCH, MICHAEL ZITZMANN, STEFAN SCHLATT AND EBERHARD NIESCHLAG

[Veldhuis JD, Metzger DL, Martha Jr PM, Mauras N, Kerrigan JR, Keenan B, Rogol AD, Pincus SM 1997 Estrogen and testosterone, but not a nonaromatizable androgen, direct network integration of the hypothalamo-somatotrope (growth hormone)-insulin-like growth factor I axis in the human: evidence from pubertal pathophysiology and sex-steroid hormone replacement. J Clin Endocrinol Metab 82:3414–3420

Keenan BS, Richards GE, Ponder SW, Dallas JS, Nagamani M, Smith ER 1993 Androgen-stimulated pubertal growth: the effects of testosterone and dihydrotestosterone on growth hormone and insulin-like growth factor-I in the treatment of short stature and delayed puberty. J Clin Endocrinol Metab 76:996–1001

Pharmacokinetics and Pharmacodynamics of Nandrolone Esters in Oil Vehicle: Effects of Ester, Injection Site and Injection VolumeCharles F. Minto, Christopher Howe, Susan Wishart, Ann J. Conway, and David J. HandelsmanJ. Pharmacol. Exp. Ther., Apr 1997; 281: 93.

Belkien, L., Schurmeyer, T., Hano, R., Gunnarson, P. O. and Nieschlag, E.: Pharmacokinetics of 19-nortestosterone esters in normal men. J. steroid Biochem. 5: 623-629, 1985


Obviously everything depends on the compound and the individual in question

 

[BeastFitness]

The effects of fluoxymesterone administration on testicular function.

Long term daily administration of fluoxymesterone (9alpha-fluoro-17alpha-methyl-11beta, 17beta-dihydroxyandrost-4-en-3-one) was associated with a modest suppression of sperm production and a profound suppression of testosterone levels in the absence of significant effects on plasma gonadotropin levels. Nine normal male volunteers took either 10, 20, or 30 mg of fluoxymesterone daily for twelve weeks. Plasma samples were obtained for testosterone, estrogen, LH and FSH levels at biweekly intervals before, during and for up to 12 weeks after fluoxymesterone treatment. Samples were obtained for dehydroepiandrosterone sulfate, testosterone binding globulin and free testosterone assays at representative times before, during and after treatment. Although lower sperm counts were observed at several points during both the treatment and follow up periods, significant consistent suppression of spermatogenesis could not be demonstrated. Reduced plasma testosterone levels were seen within 24 h after beginning fluoxymesterone, and further reductions were noted throughout the treatment period. Changes in plasma estrogen levels did not correlate with fluoxymesterone administration. Neither plasma LH nor plasma FSH levels were significantly altered by fluoxymesterone. A short term study utilizing a single dose of fluoxymesterone yielded similar findings. It is proposed that fluoxymesterone has a local effect on the Leydig cell which is not mediated by gonadotropins.

 

[Rodja]

Reifenstein, et. al. Studies comparing the effects of certain testosterone esters in man.J Am Geriatr Soc. 1954 May;2(5):293-8.. PMID: 13162731

Journal of Andrology, Vol. 24, No. 5, September/October 2003 Copyright American Society of Andrology Pharmacokinetics and Degree of Aromatization Rather Than Total Dose of Different Preparations Determine the Effects of Testosterone: A Nonhuman Primate Study in Macaca fascicularisGERHARD F. WEINBAUER*, CARL-JOACHIM PARTSCH, MICHAEL ZITZMANN, STEFAN SCHLATT AND EBERHARD NIESCHLAG

[Veldhuis JD, Metzger DL, Martha Jr PM, Mauras N, Kerrigan JR, Keenan B, Rogol AD, Pincus SM 1997 Estrogen and testosterone, but not a nonaromatizable androgen, direct network integration of the hypothalamo-somatotrope (growth hormone)-insulin-like growth factor I axis in the human: evidence from pubertal pathophysiology and sex-steroid hormone replacement. J Clin Endocrinol Metab 82:3414–3420

Keenan BS, Richards GE, Ponder SW, Dallas JS, Nagamani M, Smith ER 1993 Androgen-stimulated pubertal growth: the effects of testosterone and dihydrotestosterone on growth hormone and insulin-like growth factor-I in the treatment of short stature and delayed puberty. J Clin Endocrinol Metab 76:996–1001

Pharmacokinetics and Pharmacodynamics of Nandrolone Esters in Oil Vehicle: Effects of Ester, Injection Site and Injection VolumeCharles F. Minto, Christopher Howe, Susan Wishart, Ann J. Conway, and David J. HandelsmanJ. Pharmacol. Exp. Ther., Apr 1997; 281: 93.

Belkien, L., Schurmeyer, T., Hano, R., Gunnarson, P. O. and Nieschlag, E.: Pharmacokinetics of 19-nortestosterone esters in normal men. J. steroid Biochem. 5: 623-629, 1985


Obviously everything depends on the compound and the individual in question

Ok, so you skirted around my question, which was were are you getting this info regarding esters OR are you basing it off of just the ester effects of two compounds? I see the nandrolone study, which you've now posted twice, but that's for nandrolone and not the myriad of other steroids out there.

 

[BeastFitness]

Ok, so you skirted around my question, which was were are you getting this info regarding esters OR are you basing it off of just the ester effects of two compounds? I see the nandrolone study, which you've now posted twice, but that's for nandrolone and not the myriad of other steroids out there.

I haven't skirted around anything

I said "Obviously everything depends on the compound and the individual in question." You seem to not be able to keep things in context meaning, there will NEVER be an end all be all answer. Every smart person knows that. With what we're dealing with its so specific to the individual and the compound I would literally have to break down every specific variable of 1 single person to definitely say that "X compound will yield X result"

I copied in references that I'd advise you find the full text and read through thoroughly as it will help you get a better understanding of pharmacology in general

 

[Rodja]

I haven't skirted around anything

I said "Obviously everything depends on the compound and the individual in question." You seem to not be able to keep things in context meaning, there will NEVER be an end all be all answer. Every smart person knows that. With what we're dealing with its so specific to the individual and the compound I would literally have to break down every specific variable of 1 single person to definitely say that "X compound will yield X result"

I copied in references that I'd advise you find the full text and read through thoroughly as it will help you get a better understanding of pharmacology in general

You made the statements not me and that was my point. You don't see the contradiction in making a broad-brush statement yet saying it depends on the person?

I've been around, and used many, AAS over the years and here's the thing: most of these studies have hardly any applicability outside of testosterone. The doses are usually too small and it's even more rare to find healthy adult studies for these. While noble, this thread lacks one GIANT piece of information: cycle construction. That's the biggest confusion for most people and a data dump of articles that are mainly decades old doesn't help much on that end.

 

[BeastFitness]

You made the statements not me and that was my point. You don't see the contradiction in making a broad-brush statement yet saying it depends on the person?

I've been around, and used many, AAS over the years and here's the thing: most of these studies have hardly any applicability outside of testosterone. The doses are usually too small and it's even more rare to find healthy adult studies for these. While noble, this thread lacks one GIANT piece of information: cycle construction. That's the biggest confusion for most people and a data dump of articles that are mainly decades old doesn't help much on that end.

This thread isn't about cycle construction, its about PURE research.

Don't get me wrong, I agree that studies do not correlate to actual application but thats not the point of this thread.

 

[Rodja]

This thread isn't about cycle construction, its about PURE research.

Don't get me wrong, I agree that studies do not correlate to actual application but thats not the point of this thread.

Then what is the point?

 

[BeastFitness]

Then what is the point?

Seriously?

Its to learn WHAT the research says. Its the combination of RESEARCH AND ANECDOTAL EVIDENCE that is the best formula for success.

You seem to only comment on anything I post to try and derail them. I don't want this thread to be ruined by this so if you do not understand this reply or do not wish to contribute any research yourself, please don't clutter this thread. We want to keep it on topic. If you have a personal problem with me, shoot me a PM.

This is a research thread.

 

[Rodja]

Seriously?

Its to learn WHAT the research says. Its the combination of RESEARCH AND ANECDOTAL EVIDENCE that is the best formula for success.

You seem to only comment on anything I post to try and derail them. I don't want this thread to be ruined by this so if you do not understand this reply or do not wish to contribute any research yourself, please don't clutter this thread. We want to keep it on topic. If you have a personal problem with me, shoot me a PM.

This is a research thread.

I asked for some data to back up the points you made and you didn't present anything outside of a data dump. If there's any derail, it's to clarify your statement regarding esters. The only problem I have is that you answer by not answering. You give a statement, someone asks you about it, and then you always just circle back to individuality.

 

[Rodja]

Seriously?

Its to learn WHAT the research says. Its the combination of RESEARCH AND ANECDOTAL EVIDENCE that is the best formula for success.

You seem to only comment on anything I post to try and derail them. I don't want this thread to be ruined by this so if you do not understand this reply or do not wish to contribute any research yourself, please don't clutter this thread. We want to keep it on topic. If you have a personal problem with me, shoot me a PM.

This is a research thread.

I don't understand why you would even post research if it's either limited in application or irrelevant. Data is wonderful, but if it's irrelevant, then it might as well not exist for all intents and purposes. I asked about the ester info because it clashes with my anecdotal experience and the statements intrinsically contradict themselves. For those that are using this thread as a resource, everything should be clarified and open to question.

 

[KenTheEagle]

I don't understand why you would even post research if it's either limited in application or irrelevant. Data is wonderful, but if it's irrelevant, then it might as well not exist for all intents and purposes. I asked about the ester info because it clashes with my anecdotal experience and the statements intrinsically contradict themselves. For those that are using this thread as a resource, everything should be clarified and open to question.

I dont know why I feel like I missed you, Rodja. LOL Good to see you around!

 

[BeastFitness]

Mesterolone (Proviron) induces low sperm quality with reduction in sex hormone profile in adult male Sprague Dawley rats testis

Anabolic-androgenic steroid compounds are one of the most widely abused drugs by athletes and muscle builders with the goal of improving performance/muscle mass. However, increasing concern has been expressed because these compounds not only offer unappreciable benefits to infertile and subfertile males, but also might have deleterious effects on both human and animal physiology including sperm quality. In addition, there is the conflicting outcome of AAS usage in the clinical settings with its attendant reduced spermatogenesis and hypopituitarism in patient management. Hence, we aim to evaluate the effects of mestorolone, an anabolic-androgenic steroid, on the histomorphometry of seminiferous tubules with serum hormonal and seminal analyses in adult male Sprague-Dawley rat. Twenty adult male Sprague dawley rats divided into two groups of 10 each. The treated group received 0.06 mg/g body weight/ day of mesterolone (proviron) by oral gavage for six weeks while the control group received equal volume of 0.9% normal saline per day. SPSS analysis of data generated with P< 0.05 considered statistically significant. The result showed significant (P< 0.05) body weight gain in all the animals. However, both the raw testicular weight and relative testicular weight per 100 g bwt was significantly (P< 0.05) higher in control than treated. The mean sperm count significantly decreased by 28% (P< 0.05) and the motility reduced significantly by 56% (P< 0.05) in the treated compared to control. In addition, both FSH (follicle stimulating hormone) and T (testosterone) of the treated were significantly lowered by 73% (P< 0.05) and 63% (P< 0.05) respectively compared to the control. The use of mesterolone is with caution and short intermittent therapy is desirous for better semen quality and improved overall fertility.

 

[BeastFitness]

The anabolic androgenic steroid fluoxymesterone inhibits 11β-hydroxysteroid dehydrogenase 2-dependent glucocorticoid inactivation.

Anabolic androgenic steroids (AAS) are testosterone derivatives used either clinically, in elite sports, or for body shaping with the goal to increase muscle size and strength. Clinically developed compounds and nonclinically tested designer steroids often marketed as food supplements are widely used. Despite the considerable evidence for various adverse effects of AAS use, the underlying molecular mechanisms are insufficiently understood. Here, we investigated whether some AAS, as a result of a lack of target selectivity, might inhibit 11β-hydroxysteroid dehydrogenase 2 (11β-HSD2)-dependent inactivation of glucocorticoids. Using recombinant human 11β-HSD2, we observed inhibitory effects for several AAS. Whereas oxymetholone, oxymesterone, danazol, and testosterone showed medium inhibitory potential, fluoxymesterone was a potent inhibitor of human 11β-HSD2 (half-maximal inhibitory concentration [IC(50)] of 60-100nM in cell lysates; IC(50) of 160nM in intact SW-620, and 530nM in MCF-7 cells). Measurements with rat kidney microsomes and lysates of cells expressing recombinant mouse 11β-HSD2 revealed much weaker inhibition by the AAS tested, indicating that the adverse effects of AAS-dependent 11β-HSD2 inhibition cannot be investigated in rats and mice. Furthermore, we provide evidence that fluoxymesterone is metabolized to 11-oxofluoxymesterone by human 11β-HSD2. Structural modeling revealed similar binding modes for fluoxymesterone and cortisol, supporting a competitive mode of inhibition of 11β-HSD2-dependent cortisol oxidation by this AAS. No direct modulation of mineralocorticoid receptor (MR) function was observed. Thus, 11β-HSD2 inhibition by fluoxymesterone may cause cortisol-induced MR activation, thereby leading to electrolyte disturbances and contributing to the development of hypertension and cardiovascular disease.

 

[dustter]

Some good literature on Anavar

Oxandrolone enhances hepatic ketogenesis in adult men.

Abstract
BACKGROUND:
Immediate administration of oxandrolone markedly increases hepatic lipase activity and reduces levels of plasma high-density lipoprotein.
RATIONALE FOR THE STUDY:
We postulated that oxandrolone should increase hepatic lipase and that the nonesterified fatty acids generated would enhance hepatic ketogenesis during an extended fat tolerance test.
MAIN RESULTS:
Eighteen men participated in the study using short-term administration of oxandrolone (10 mg/d) over a week. Subjects had evaluation of hepatic ketogenesis at baseline and after 7 days of administration of oxandrolone. Ketogenesis was assessed by measuring plasma levels of 3-hydroxybutyrate during a fat tolerance test. Oxandrolone increased fasting levels of 3-hydroxybutyrate by 70%, and increased the area under the curve during an FFT by 53% above pretreatment levels without affecting the areas under the curve for nonesterified fatty acids, glycerol, or triglycerides. Fasting 3-hydroxybutyrate levels correlated with nonesterified fatty acids and with triglycerides; however, there were no significant correlations with any other parameter.
CONCLUSIONS:
This study shows that short-term administration of oxandrolone results in marked increases in hepatic ketogenesis. This finding is consistent with an increased influx of fatty acids into the liver secondary to lipoprotein lipolysis by increased hepatic lipase. However, the possibility cannot be ruled out that oxandrolone acts directly in the liver to stimulate fatty acid oxidation. Therefore, the observation of increased ketogenesis will require further studies to determine the molecular basis of the response.


The Effect of Oxandrolone on the Endocrinologic, Inflammatory, and Hypermetabolic Responses During the Acute Phase Postburn

Abstract
Objective and Summary Background Data:
Postburn long-term oxandrolone treatment improves hypermetabolism and body composition. The effects of oxandrolone on clinical outcome, body composition, endocrine system, and inflammation during the acute phase postburn in a large prospective randomized single-center trial have not been studied.

Methods:
Burned children (n = 235) with >40% total body surface area burn were randomized (block randomization 4:1) to receive standard burn care (control, n = 190) or standard burn care plus oxandrolone for at least 7 days (oxandrolone 0.1 mg/kg body weight q.12 hours p.o, n = 45). Clinical parameters, body composition, serum hormones, and cytokine expression profiles were measured throughout acute hospitalization. Statistical analysis was performed by Student t test, or ANOVA followed by Bonferroni correction with significance accepted at P < 0.05.

Results:
Demographics and clinical data were similar in both groups. Length of intensive care unit stay was significantly decreased in oxandrolone-treated patients (0.48 ± 0.02 days/% burn) compared with controls (0.56 ± 0.02 days/% burn), (P < 0.05). Control patients lost 8 ± 1% of their lean body mass (LBM), whereas oxandrolone-treated patients had preserved LBM (+9 ± 4%), P < 0.05. Oxandrolone significantly increased serum prealbumin, total protein, testosterone, and AST/ALT, whereas it significantly decreased α2-macroglobulin and complement C3, P < 0.05. Oxandrolone did not adversely affect the endocrine and inflammatory response as we found no significant differences in the hormone panels and cytokine expression profiles.

Conclusions:
In this large prospective, double-blinded, randomized single-center study, oxandrolone shortened length of acute hospital stay, maintained LBM, improved body composition and hepatic protein synthesis while having no adverse effects on the endocrine axis postburn, but was associated with an increase in AST and ALT.



Five-year outcomes after oxandrolone administration in severely burned children: a randomized clinical trial of safety and efficacy.

Abstract
BACKGROUND:
Oxandrolone, an anabolic agent, has been administered for 1 year post burn with beneficial effects in pediatric patients. However, the long-lasting effects of this treatment have not been studied. This single-center prospective trial determined the long-term effects of 1 year of oxandrolone administration in severely burned children; assessments were continued for up to 4 years post therapy.

STUDY DESIGN:
Patients 0 to 18 years old with burns covering >30% of the total body surface area were randomized to receive placebo (n = 152) or oxandrolone, 0.1 mg/kg twice daily for 12 months (n = 70). At hospital discharge, patients were randomized to a 12-week exercise program or to standard of care. Resting energy expenditure, standing height, weight, lean body mass, muscle strength, bone mineral content (BMC), cardiac work, rate pressure product, sexual maturation, and concentrations of serum inflammatory cytokines, hormones, and liver enzymes were monitored.

RESULTS:
Oxandrolone substantially decreased resting energy expenditure and rate pressure product, increased insulin-like growth factor-1 secretion during the first year after burn injury, and, in combination with exercise, increased lean body mass and muscle strength considerably. Oxandrolone-treated children exhibited improved height percentile and BMC content compared with controls. The maximal effect of oxandrolone was found in children aged 7 to 18 years. No deleterious side effects were attributed to long-term administration.

CONCLUSIONS:
Administration of oxandrolone improves long-term recovery of severely burned children in height, BMC, cardiac work, and muscle strength; the increase in BMC is likely to occur by means of insulin-like growth factor-1. These benefits persist for up to 5 years post burn.

In regards to this research and applying to bodybuilding how would one come to the math of what an average 6ft 200lb male would dose anavar at for like i said, bodybuilding purposes?

 

[BeastFitness]

In regards to this research and applying to bodybuilding how would one come to the math of what an average 6ft 200lb male would dose anavar at for like i said, bodybuilding purposes?

Honestly this is where real world application comes in. Typical dosages seen are

Therapeutic treatments: 5-10mgs per day

Male Bodybuilder looking to optimize its benefits: 20-80mgs per day

Female Bodybuilder looking to optimize its benefits: 5-20mgs per day


Obviously the ranges are very drastic due to everyone's individual response to it so typically beginning with the lowest dosage possible is a safe option so you can assess the side effects and make an informed decision to continue.

Here's some more literature on anavar for you!


Treatment with oxandrolone and the durability of effects in older men

We investigated the effects of the anabolic androgen, oxandrolone, on lean body mass (LBM), muscle size, fat, and maximum voluntary muscle strength, and we determined the durability of effects after treatment was stopped. Thirty-two healthy 60- to 87-yr-old men were randomized to receive 20 mg oxandrolone/day (n = 20) or placebo (n = 12) for 12 wk. Body composition [dual-energy X-ray absorptiometry (DEXA), magnetic resonance imaging, and 2H2O dilution] and muscle strength [1 repetition maximum (1 RM)] were evaluated at baseline and after 12 wk of treatment; body composition (DEXA) and 1-RM strength were then assessed 12 wk after treatment was discontinued (week 24). At week 12, oxandrolone increased LBM by 3.0 ± 1.5 kg (P < 0.001), total body water by 2.9 ± 3.7 kg (P = 0.002), and proximal thigh muscle area by 12.4 ± 8.4 cm2 (P < 0.001); these increases were greater (P < 0.003) than in the placebo group. Oxandrolone increased 1-RM strength for leg press by 6.7 ± 6.4% (P < 0.001), leg flexion by 7.0 ± 7.8% (P < 0.001), chest press by 9.3 ± 6.7% (P < 0.001), and latissimus pull-down exercises by 5.1 ± 9.1% (P = 0.02); these increases were greater than placebo. Oxandrolone reduced total (-1.9 ± 1.0 kg) and trunk fat (-1.3 ± 0.6 kg; P < 0.001), and these decreases were greater (P < 0.001) than placebo. Twelve weeks after oxandrolone was discontinued (week 24), the increments in LBM and muscle strength were no longer different from baseline (P > 0.15). However, the decreases in total and trunk fat were sustained (-1.5 ± 1.8, P = 0.001 and -1.0 ± 1.1 kg, P < 0.001, respectively). Thus oxandrolone induced short-term improvements in LBM, muscle area, and strength, while reducing whole body and trunk adiposity. Anabolic improvements were lost 12 wk after discontinuing oxandrolone, whereas improvements in fat mass were largely sustained.

 

[Rodja]

In regards to this research and applying to bodybuilding how would one come to the math of what an average 6ft 200lb male would dose anavar at for like i said, bodybuilding purposes?

Not much considering this dose would come out to 10mg/day for a 220lb male. Obviously, dosing for anavar for men is well above this number and is closer to female dosing. Fun fact about the drug, but not too applicable, which is my point.

 

[dustter]

Not much considering this dose would come out to 10mg/day for a 220lb male. Obviously, dosing for anavar for men is well above this number and is closer to female dosing. Fun fact about the drug, but not too applicable, which is my point.

I think because i did random math in my head compared to the average weighing male child then coordinated to myself, (6ft 200lbs) and i got like a weird 42mg number. sorry i dont remember exactly did math this morning at work, but im on it now just from all other reviews, logs, basically anything concerning var is to run 50-100mgs after knowing what your sides are, but like i said 50mgs being the lowest dose to see any bodybuilding attributes.. Have you had any experience?

 

[Rodja]

I think because i did random math in my head compared to the average weighing male child then coordinated to myself, (6ft 200lbs) and i got like a weird 42mg number. sorry i dont remember exactly did math this morning at work, but im on it now just from all other reviews, logs, basically anything concerning var is to run 50-100mgs after knowing what your sides are, but like i said 50mgs being the lowest dose to see any bodybuilding attributes.. Have you had any experience?

I don't have much experience with anavar, but my cycle was a 4 week run at 50mg/day. Strength went up, lost some BF, and I was drier.

 

[BeastFitness]

Prospective study of topical testosterone gel (AndroGel) versus intramuscular testosterone in testosterone-deficient HIV-infected men.

PURPOSE:
Testosterone replacement therapy via deep intramuscular injections causes extraphysiologic variations in serum testosterone concentrations. A topical transdermal testosterone gel formulation (AndroGel(R)) provides sustained physiologic concentrations of serum testosterone. The objective of this open-label switch study was to compare pharmacokinetics, safety, tolerability, and efficacy of delivery of daily testosterone gel versus intramuscular testosterone injection every 1 or 2 weeks in hypogonadal human immunodeficiency virus (HIV)-infected men.
METHOD:
Patients received intramuscular testosterone (100-200 mg/wk) for 8 weeks, then switched to daily topical testosterone gel (5-10 g gel/day) for 8 weeks. Study endpoints included free serum testosterone concentrations and quality-of-life scores.
RESULTS:
Thirty patients (average age, 45 years) were recruited; 24 completed the study. Mean peak free testosterone concentrations with intramuscular testosterone and testosterone gel were 42 pg/mL and 23 pg/mL, respectively, and mean peaktrough fluctuations in free testosterone were 26.7 +/- 12.8 pg/mL and 2.7 +/- 10.7 pg/mL, respectively (p < .001). Quality-of-life scores indicated more improved physical and emotional well-being with gel versus intramuscular testosterone. No significant changes in laboratory parameters or lean body mass were noted.
CONCLUSION:
Daily testosterone gel produced stable testosterone concentrations and improved quality of life compared with intermittent intramuscular testosterone injections.

 

[Driven2lift]

^Verified anecdotally.

Transdermal > inject for TRT

This thread is still going great

 

[dustter]

^Verified anecdotally.

Transdermal > inject for TRT

This thread is still going great

So only for TRT or for lets say test on cycle?

 

[Hyde]

So only for TRT or for lets say test on cycle?

Just using the study (never mind anecdote) we can see blood levels are considerably higher with IM testosterone. You want to blast the amount of work applying would become a chore.

No reason someone on prescribed gel couldn't add their own IM test on top of their gel to blast, of course.

 

[BeastFitness]

^Verified anecdotally.

Transdermal > inject for TRT

This thread is still going great

Trying to post a few studies a week!

So only for TRT or for lets say test on cycle?

Just using the study (never mind anecdote) we can see blood levels are considerably higher with IM testosterone. You want to blast the amount of work applying would become a chore.

No reason someone on prescribed gel couldn't add their own IM test on top of their gel to blast, of course.

^^Yep

 

[BeastFitness]

The Role of Anabolic Hormones for Wound Healing in Catabolic States

Objective: The purpose of this paper is to present an overview of the interrelationship between hormones, nutrition, and wound healing.
Methods: The data on various hormones and their effects on specific elements of nutrition and wound healing are reviewed.
Results: The key anabolic hormones are human growth hormone, insulin-like growth factor-1, insulin, and testosterone and its analogs. Although each has specific metabolic actions, there is also a very important hormone-hormone interaction. A deficiency of these hormones occurs in acute and chronic catabolic states, resulting in lean mass loss and impairing the healing process.
Conclusion: There is a well-recognized interrelationship between hormones, nutrition, and wound healing. The anabolic process of protein synthesis, with new tissue formation, requires the action of anabolic hormones. Exogenous administration of these agents has been shown to maintain or increase lean body mass as well as directly stimulate the healing process through their anabolic and anticatabolic actions.

Invalid Link Removed

 

[Driven2lift]

Shame that was a data review and not a study. That looks like a few paragraphs of just speculation TBH.

Wound healing is an interesting topic with AAS, as are all potential medicinal uses

 

[Hyde]

Shame that was a data review and not a study. That looks like a few paragraphs of just speculation TBH.

Wound healing is an interesting topic with AAS, as are all potential medicinal uses

Old board member Detroit Hammer had some interesting things to say about his opinion of anadrol and its perceived effect on healing his shattered femur (combined w test and localized peps as I recall). This kind of anecdote doesn't belong in here but it would be really neat if there were some studies supporting/refuting this notion.

He said he healed so much faster than the doc expected he was speechless when he was ready to ditch the crutches.

 

[dustter]

Old board member Detroit Hammer had some interesting things to say about his opinion of anadrol and its perceived effect on healing his shattered femur (combined w test and localized peps as I recall). This kind of anecdote doesn't belong in here but it would be really neat if there were some studies supporting/refuting this notion.

He said he healed so much faster than the doc expected he was speechless when he was ready to ditch the crutches.

i have seen this as well with anavar used for torn muscles/ligaments..

 

[BeastFitness]

Shame that was a data review and not a study. That looks like a few paragraphs of just speculation TBH.

Wound healing is an interesting topic with AAS, as are all potential medicinal uses

Old board member Detroit Hammer had some interesting things to say about his opinion of anadrol and its perceived effect on healing his shattered femur (combined w test and localized peps as I recall). This kind of anecdote doesn't belong in here but it would be really neat if there were some studies supporting/refuting this notion.

He said he healed so much faster than the doc expected he was speechless when he was ready to ditch the crutches.

i have seen this as well with anavar used for torn muscles/ligaments..

Completely agree! I'm honestly trying to do my thesis on the wound healing effects of AAS…not sure how effectively I can do this though given the limited research on the topic

 

[BeastFitness]

Sex Hormones and Wound Healing

Animal Studies
Few studies have examined androgens and wound healing. In contrast to the beneficial effects of estrogen, most of the recent evidence suggests that androgens have a negative effect on wound repair. Ashcroft and Mills[41] castrated male mice to render them hypogonadal and created full-thickness incisional wounds on their bodies 1-month post-castration. Wound healing of the castrated mice was then compared to similarly injured sham-castrated and intact control groups. Results indicated that wound healing was significantly accelerated in the castrated mice compared with the intact animals. The castrated group exhibited smaller wounds than the control group on Day 5 macroscopically and histologically. Cross-sectional wound areas were also significantly decreased in the castrated animals versus the control on Days 3 and 7 (P < 0.05) after wounding (Figure 3). Wounds of the castrated group were approximately 75% smaller than the intact group on Day 3 and approximately 60% smaller on Day 7. Sham-operated mice and intact mice healed at similar rates.

Human Studies
As part of a wound-healing study on humans, Ashcroft and Mills determined wound healing rates in 18 health status-defined elderly men by creating punch biopsy wounds and measuring wound size by planimetry on Day 7 post-wounding. The authors then correlated healing to systemic testosterone levels. Their results showed a significant wound repair delay that correlated with increasing testosterone levels (P = 0.001) in the healthy elderly men (Figure 4).[41]
Increased testosterone levels are associated with delayed wound healing in elderly men.[42] Elderly men also heal more slowly than elderly women.[19] Results of a retrospective cohort study on 325 patients indicate that male gender was one of the predisposing factors to poor healing of venous ulcers.[43]

However, patients in catabolic states (eg, as a result of severe burn injury) may experience beneficial effects from anabolic steroids, such as testosterone. In a randomized, double-blinded, placebo-controlled study on the effects of the testosterone analog oxandrolone on wound healing, the drug was administered to 11 patients at a dose of 20 mg/day starting between Days 2 and 3 after severe burn injury. Wound healing time of standardized donor sites was measured. The oxandrolone-treated patients took a significantly shorter time to heal compared to the placebo group (9 ± 2 days versus 13 ± 3 days).[44] A similarly designed study comparing placebo, oxandrolone, and another anabolic agent, human growth hormone (HGH), yielded similar results. The complete healing time of a standardized donor site decreased from the control value of 14 ± 2 days to 10 ± 3 days for HGH and 10 ± 2 days for oxandrolone.[45] It is postulated that since oxandrolone is an anabolic steroid, it might have different effects on wound healing in comparison to classic androgens, such as testosterone and dihydrotestosterone.[45] In a study on rats, Demling suggested that the positive effect of oxandrolone on wound repair might be linked to an increase in the hydroxyproline content of the healing wound, unrelated to any generalized increase in mass and weight.46 Full-thickness linear wounds created on the back of the rats closed completely in 12 ± 3 days in the group given oral oxandrolone compared to 18 ± 3 days in the placebo group. Hydroxyproline content of the healed incision site was 23 ± 4 mg/g tissue versus 17 ± 3 mg/g in the oxandrolone and placebo groups, respectively. Both parameters were significantly affected by oxandrolone. The rate of body weight gain was identical in both groups, indicating that it was not a factor.[46]

Androgens and the Immune Response
Androgens undoubtedly play an important role in regulating the immune response. Androgens have been documented to have suppressive effects on B-cell function in autoimmune diseases, which may partly account for the predominance of autoimmune diseases, such as rheumatoid arthritis, lupus erythematosus, and Hashimoto's thyroiditis, in women.[42] Cell-mediated immunosuppression by androgens was likewise documented in female rats who were pretreated with dihydrotestosterone (DHT) for 20 days prior to induced soft-tissue trauma and hemorrhagic shock. The ability of macrophages to release IL-1 and IL-6 was significantly reduced in the DHT pretreated female mice compared to the vehicle-treated female mice. Female mice pretreated with DHT displayed macrophage activity comparable with male mice that had likewise been subjected to trauma and hemorrhage.[47] Another study[48] that supports the immunosuppressive properties of androgens involves the use of flutamide, a testosterone receptor antagonist, on burn-injured mice. Flutamide/anti-androgen treatment was shown to improve cellular immunity by partially restoring IL-2 production and IL-2 receptors on splenocytes. A study on human gingival fibroblasts[49] has illustrated significant (P < 0.05) inhibition of IL-6 production in the presence of testosterone and DHT at concentrations of 5 x 10-8 to 10-7 M. This inhibitory effect was so strong that it could not be reversed by concentrations of even up to 2 x 10-5 M of the anti-androgen flutamide.

Androgens and Inflammation
Androgens, just like estrogens, are thought to exert their influence on the phases of wound repair. Their effects on the inflammatory phase are the most elucidated. Inflammation can contribute to delayed wound healing by leading to increased proteolytic destruction of collagen and fibronectin. Androgens are associated with an enhanced inflammatory response.

Smad3 is an intracellular mediator of TGF-β function. It inhibits wound healing by slowing epithelization and enhancing inflammatory responses.[13] It plays a role in androgen-mediated inhibition of wound healing.[2,13] Castration was shown to accelerate wound healing in wild-type male mice, which was reversible by exogenous androgen treatment. In contrast, in the Smad3-null mice, administration of exogenous androgens did not have a significant effect on the wound healing response.[13]

Ashcroft and Mills[41] investigated tumor necrosis factor (TNF)-α levels in wounds of castrated and intact male mice. TNF-α is a mediator whose downstream effect is the up-regulation of proinflammatory cytokines. Reduced expression of TNF-α was observed on Days 5 and 21 after wounding in castrated mice compared to intact mice. The authors further established that testosterone acted to up-regulate TNF-α expression through androgen receptors. Systemic blockage of androgen action via oral administration of the androgen receptor antagonist flutamide accelerated healing rates, dampened inflammatory responses, and decreased levels of TNF-α similar to that observed in castrated mice.[41]

By way of its effects on TNF-α, testosterone co-treatment with beta-estradiol has been shown to increase E-selectin and vascular cell adhesion molecule-1 (VCAM-1) expression on endothelial cells.[50] This may be of importance in the inflammatory response, since E-selectin and VCAM-1 potentially enhance inflammation by facilitating leukocyte migration and adhesion to the endothelium. McCrohon et al.[51] documented that exposure of human umbilical vein endothelial cells to DHT in the absence of estrogen resulted in increased expression of VCAM-1. Compared with the vehicle control, monocyte adhesion was increased in the androgen-treated endothelial cells in a dose-dependent fashion (116 ± 6% for DHT 40 nmol/L and 128 ± 3% for 400 nmol/L).

Androgens and Wound Remodeling
Androgen administration also influences the remodeling phase of wound healing by increasing collagen deposition. An intricate balance between the synthesis and degradation of collagen characterizes the remodeling phase. Matrix metalloproteinases play a role in this androgenic effect. Androgen receptors have been demonstrated to negatively regulate MMP-1 expression,[52] possibly reducing proteolytic action on the forming matrix and tipping the balance toward increased collagen deposition of the wound. This may increase the tendency for keloid formation and hypertrophic scarring.




References

Hardman MJ, Ashcroft GS. Hormonal influences on wound healing: a review of current experimental data. WOUNDS. 2005;17(11):313-320.

Williams CL, Stancel GM. Estrogens and progestins. In: Hardman JG, Limbird LE, Molinoff PB, Rudden RW, eds. Goodman and Gilman's the Pharmacological Basis for Therapeutics. New York, NY: McGraw-Hill; 1996:1411-1440.

Thornton MJ. The biological actions of estrogens on skin. Exp Dermatol. 2002;11(6):487-502.

Dunn LB, Damesyn M, Moore AA, Reuben DB, Greendale GA. Does estrogen prevent skin aging? Results from the First National and Health Nutrition Examination Survey (NHANES I). Arch Dermatol. 1997;133(3):339-342.

Denda M, Koyama J, Hori J, et al. Age- and sex-dependent change in stratum corneum sphingolipids. Arch Dermatol Res. 1993;285(7):415-417.

Brincat M, Versi E, Moniz CF, Magos A, de Trafford J, Studd JW. Skin collagen changes in postmenopausal women receiving different regimens of estrogen therapy. Obstet Gynecol. 1987;70(1):123-127.

Brincat M, Versi E, O'Dowd T, et al. Skin collagen changes in post-menopausal women receiving oestradiol gel. Maturitas. 1987;9(1):1-5.

Schmidt JB, Binder M, Macheiner W, Kainz C, Gitsch G, Bieglmayer C. Treatment of skin ageing symptoms in perimenopausal females with estrogen compounds. A pilot study. Maturitas. 1994;20(1):25-30.

Pierard GE, Letawe C, Dowlati A, Pierard-Franchimont C. Effect of hormone replacement therapy for menopause on the mechanical properties of the skin. J Am Geriatr Soc. 1995;43(6):662-665.

Punnonen R, Vaajalahti P, Teisala K. Local oestriol treatment improves the structure of elastic fibers in the skin of postmenopausal women. Ann Chir Gynaecol Suppl. 1987;202:39-41.

Varila E, Rantala I, Oikarinen A, et al. The effect of topical oestradiol on skin collagen of postmenopausal women. Br J Obstet Gynaecol. 1995;102(12):985-989.

Ashcroft GS, Dodsworth J, van Boxtel E, et al. Estrogen accelerates cutaneous wound healing associated with an increase in TGF-beta1 levels. Nat Med. 1997;3(11):1209-1215.

Ashcroft GS, Mills SJ, Flanders KC, et al. Role of Smad3 in the hormonal modulation of in vivo wound healing responses. Wound Repair Regen. 2003;11(6):468-473.

Ashcroft GS, Yang X, Glick AB, et al. Mice lacking Smad3 show accelerated wound healing and an impaired local inflammatory response. Nat Cell Biol. 1999;1(5):260-266.

Abe R, Shimizu T, Ohkawara A, Nishihira J. Enhancement of macrophage migration inhibitory factor (MIF) expression in injured epidermis and cultured fibroblasts. Biochim Biophys Acta. 2000;1500(1):1-9.

Ashcroft GS, Mills SJ, Lei K, et al. Estrogen modulates cutaneous wound healing by downregulating macrophage migration inhibitory factor. J Clin Invest. 2003;111(9):1309-1318.

Pirila E, Parikka M, Ramamurthy NS, et al. Chemically modified tetracycline (CMT-8) and estrogen promote wound healing in ovariectomized rats: effects on matrix metalloproteinase-2, membrane type 1 matrix metalloproteinase, and laminin-5 gamma2-chain. Wound Repair Regen. 2002;10(1):38-51.

Shapiro SD. Matrix metalloproteinase degradation of extracellular matrix: biological consequences. Curr Opin Cell Biol. 1998;10(5):602-608.

Pirila E, Ramamurthy N, Maisi P, et al. Wound healing in ovariectomized rats: effects of chemically modified tetracycline (CMT-8) and estrogen on matrix metalloproteinases -8, -13 and type 1 collagen expression. Curr Med Chem. 2001;8(3):281-294.

Ashcroft GS, Greenwell-Wild T, Horan MA, Wahl SM, Ferguson MW. Topical estrogen accelerates cutaneous wound healing in aged humans associated with an altered inflammatory response. Am J Pathol. 1999;155(4):1137-1146.

Margolis DJ, Knauss J, Bilker W. Hormone replacement therapy and prevention of pressure ulcers and venous leg ulcers. Lancet. 2002;359(9307):675-677.

Josefsson E, Tarkowski A, Carlsten H. Anti-inflammatory properties of estrogen. I. In vivo suppression of leukocyte production in bone marrow and redistribution of peripheral blood neutrophils. Cell Immunol. 1992;142(1):67-78.

Ito I, Hayashi T, Yamada K, Kuzuya M, Naito M, Iguchi A. Physiological concentration of estradiol inhibits polymorphonuclear leukocyte chemotaxis via a receptor mediated system. Life Sci. 1995;56(25):2247-2253.

Miyagi M, Aoyama H, Mori****a M, Iwamoto Y. Effects of sex hormones on chemotaxis of human peripheral polymorphonuclear leukocytes and monocytes. J Periodontol. 1992;63(1):28-32.

Kafienah W, Buttle DJ, Burnett D, Hollander AP. Cleavage of native type 1 collagen by human neutrophil elastase. Biochem J. 1998;330(Pt 2):897-902.

McDonald JA, Kelley DG. Degradation of fibronectin by human leukocyte elastase. Release of biologically active fragments. J Biol Chem. 1980;255(18):8848-8858.

Clark RAF. Overview and general considerations of wound repair. In: Clark RAF, Henson CP, eds. The Molecular and Cellular Biology of Wound Repair. London, UK: Plenum Press; 1988:3-10.

Herrick S, Ashcroft G, Ireland G, Horan M, McCollum C, Ferguson M. Up-regulation of elastase in acute wounds of healthy aged humans and chronic venous leg ulcers are associated with matrix degradation. Lab Invest. 1997;77(3):281-288.

Ashcroft GS, Horan MA, Herrick SE, Tarnuzzer RW, Schultz GS, Ferguson MW. Age-related differences in the temporal and spatial regulation of matrix metalloproteinases (MMPs) in normal skin and acute cutaneous wounds of healthy humans. Cell Tissue Res. 1997;290(3):581-591.

Montesano R, Orci L. Transforming growth factor beta stimulates collagen-matrix contraction by fibroblasts: implications for wound healing. Proc Natl Acad Sci USA. 1988;85(13):4894-4897.

Falanga V, Shen J. Growth factors, signal transduction and cellular responses. In: Falanga V, ed. Cutaneous Wound Healing. London, UK: Martin Dunitz, Ltd, 2001.

Brincat M, Moniz CF, Studd JW, Darby AJ, Magos A, Cooper D. Sex hormones and skin collagen content in postmenopausal women. Br Med J (Clin Res Ed). 1983;287(6402):1337-1338.

Stampfer MJ, Colditz GA, Willett WC, et al. Postmenopausal estrogen therapy and cardiovascular disease. Ten-year follow-up from the nurses' health study. N Engl J Med. 1991;325(11):756-762.

Lindsay R, Hart DM, MacLean A, Clark AC, Kraszewski A, Garwood J. Bone response to termination of oestrogen treatment. Lancet. 1978;1(8078):1325-1327.

Hodis HN, Mack WJ, Azen SP, et al. Hormone therapy and the progression of coronary-artery atherosclerosis in postmenopausal women. N Engl J Med. 2003;349(6):535-545.

Manson JE, Hsia J, Johnson KC, Rossouw JE, et al. Estrogen plus progestin and the risk of coronary heart disease. N Engl J Med. 2003;349(6):523-534.

Herrington DM, Howard TD. From presumed benefit to potential harm—hormone therapy and heart disease. N Engl J Med. 2003;349(6):519-522.

Rossouw JE, Anderson GL, Prentice RL, et al. Risks and benefits of estrogen plus progestin in healthy postmenopausal women: principal results from the Women's Health Initiative randomized controlled trial. JAMA. 2002;288(3):321-333.

Rivera-Woll LM, Davis SR. Postmenopausal hormone therapy: the pros and cons. Intern Med J. 2004;34(3):109-114.

Gilliver SC, Wu F, Ashcroft GS. Regulatory roles of androgens in cutaneous wound healing. Thromb Haemost. 2003;90(6):978-985.

Ashcroft GS, Mills SJ. Androgen receptor-mediated inhibition of cutaneous wound healing. J Clin Invest. 2002;110(5):615-624.

Olsen NJ, Kovacs WJ. Gonadal steroids and immunity. Endocr Rev. 1996;17(4):369-384.

Taylor RJ, Taylor AD, Smyth JV. Using an artificial neural network to predict healing times and risk factors for venous leg ulcers. J Wound Care. 2002;11(3):101-105.

Demling RH, Orgill DP. The anticatabolic and wound healing effects of the testosterone analog oxandrolone after severe burn injury. J Crit Care. 2000;15(1):12-17.

Demling RH. Comparison of the anabolic effects and complications of human growth hormone and the testosterone analog, oxandrolone, after severe burn injury. Burns. 1999;25(3):215-221.

Demling RH. Oxandrolone, an anabolic steroid, enhances the healing of a cutaneous wound in the rat. Wound Repair Regen. 2000;8(2):97-102.

Angele MK, Ayala A, Monfils BA, Cioffi WG, Bland KI, Chaudry IH. Testosterone and/or low estradiol: normally required but harmful immunologically for males after trauma-hemorrhage. J Trauma. 1998;44(1):78-85.

Messingham KA, Shirazi M, Duffner LA, et al. Testosterone receptor blockade restores cellular immunity in male mice after burn injury. J Endrocrinol. 2001;169(2):299-308.

Gornstein RA, Lapp CA, Bustos-Valdes SM, Zamorano P. Androgens modulate interleukin-6 production by gingival fibroblasts in vitro. J Periodontol. 1999;70(6):604-609.

Zhang X, Wang LY, Jiang TY, et al. Effects of testosterone and 17-beta-estradiol on TNF-alpha-induced E-selectin and VCAM-1 expression in endothelial cells. Analysis of the underlying receptor pathways. Life Sci. 2002;71(1):15-29.

McCrohon JA, Jessup W, Handelsman DJ, Celermajer DS. Androgen exposure increases human monocyte adhesion to vascular endothelium and endothelial cell expression of vascular cell adhesion molecule-1. Circulation. 1999;99(17):2317-2322.

Schneikert J, Peterziel H, Defossez PA, Klocker H, de Launoit Y, Cato ACB. Androgen receptor-Ets protein interaction is a novel mechanism for steroid hormone-mediated down-modulation of matrix metalloproteinase expression. J Biol Chem. 1996;271(39):23907-23913.

 

[Hyde]

So HGH and anavar, and perhaps other more anabolic compounds (as well as estrogen) will speed healing typically but it points to androgens inhibiting recovery if anything?

 

[dustter]

So HGH and anavar, and perhaps other more anabolic compounds (as well as estrogen) will speed healing typically but it points to androgens inhibiting recovery if anything?

sorry, im confused. What exactly is your question? That AAS supports healing or reduces healing?

 

[Rodja]

sorry, im confused. What exactly is your question? That AAS supports healing or reduces healing?

He's saying that anabolics and oestrogens help, but highly androgenic steroids don't help. You don't hear anything about tren or halo helping out.

 

[Driven2lift]

Another young guy on TRT....So many youngsters here needlessly on hormone replacement. Makes no sense.

I wouldn't say it was needless, it was 2 years with an endo before i got back to normal.

Pituitary damage isn't a common type of case they see either.
I am not even sure alternatives are capable of working, on me.

I was with one of the best endo's in Ontario through this and needless to say I also researched every suggestion myself.



It does suck though.
To be young and take that hit.
Not many know just how hard it can be, it hit my life with magnificently bad timing too.

Make sure anyone considering hormonals knows how it can backfire. (No I did not use any AAS, wasn't even supplementing anything at the time as I was on a trip)

 

[Driven2lift]

Are you saying you now make your own test?

No, still quite below range, but if you have questions for me pm > here.

 

[BeastFitness]

On the case of TRT, just a quick mini-rant…

I've had a lot of clients come to me after prepping for a natural show, getting to striated glute (truly stage ready) status, and then hormone levels NEVER bouncing back…I honestly haven't found a clear indication as to why they never have because some people have horrible preps and levels bounce right back and others have easier/smarter preps and they levels just never return.

It sucks but when someone comes to you who's 20ish years old, cannot get an erection, has zero energy, and is f'ed hormonally, they really only have 2 options (if its at that extreme point.)

1. Put up with it and have a miserable life and risk the possibility of loosing your significant other
OR
2. See a Dr. and begin some form of hormone replacement therapy

At the end of the day I'd chose quality of life and health > anything else

/end rant

haha

More research time! Something I haven't really posted about…I'll be trying to get more full texts for you guys.


Growth hormone and insulin combine to improve whole-body and skeletal muscle protein kinetics.

BACKGROUND:
A cooperative effect of exogenous insulin and recombinant human growth hormone (r-hGH) with respect to whole-body and skeletal muscle protein metabolism has not been demonstrated previously. This study examined the effect of r-hGH and insulin administration during euglycemic clamping and concurrent amino acid supplementation.

METHODS:
Twenty-three normal volunteers in the postabsorptive state were either treated with r-hGH for 3 consecutive days before a metabolic study (GH group; n = 10) or not treated (CTRL group; n = 13). The r-hGH dose was 0.2 mg/kg/day (n = 5) or 0.1 mg/kg/day (n = 5). All subjects then received an infusion of 14C-labeled leucine and tritiated phenylalanine, followed by measurement of baseline protein kinetics (GH and CTRL). Subsequently a euglycemic insulin infusion (1 mU/kg/min) with concurrent amino acid infusion was administered, and protein kinetic measurements were repeated at steady state.

RESULTS:
GH and insulin separately produced an increase in whole-body and skeletal muscle protein net balance. GH plus insulin was associated with a higher net balance of protein than was insulin alone.

CONCLUSIONS:
r-hGH and insulin in the presence of amino acids and glucose combine to improve whole-body and skeletal muscle protein kinetics

 

[BeastFitness]

Augmentation by Propranolol of Growth Hormone-Releasing Hormone-(l-44)-NH2-Induced Growth Hormone Release in Normal Short and Normal Children

The effect of a 90-min iv infusion of propranolol, a β-adrenergic antagonist (0.2 mg/kg BW), on basal plasma GH levels and the GH responses to an iv bolus injection of GHreleasing hormone-(l-44)-NH2 (GHRH; 1 μg/kg BW) was examined in 10 prepubertal children (6 short but otherwise normal and 4 normal). The iv injection of GHRH resulted in significant increases in plasma GH, comparable to those after either insulininduced hypoglycemia or arginine infusion. Only a small and inconsistent increase in plasma GH levels occurred during the iv infusion of propranolol, whereas simultaneous administration of propranolol with GHRH caused marked enhancement of GHRH-induced GH release in all subjects. The difference between the plasma GH response to GHRH given with propranolol and the response to GHRH given with 0.9% saline was significantly greater than that between the plasma GH level after propranolol and that after 0.9% saline infusion without GHRH injections. There was no difference in plasma GH responses to GHRH, propranolol, or both in the normal short children or normal children.
These findings indicate thatβ-adrenergic blockade potentiates GHRH-induced GH secretion in prepubertal children.
- See more at: Invalid Link Removed

 

[dustter]

So, i am not very smart in the science/availability part of things but, when dosing your AAS/PH/DS based on your metabolicrate, age, height, etc.... does it matter when you time your doses of your AAS and cycle supports? Such as, we all know BMR is usually slower upon waking and right before you enter phase 3 of sleep, so would that effect if you were to take your doses earlier such as on waking or dosing before sleep? Or would it be better for absorption to dose maybe 3-4hrs after waking with say a small meal?

P.S. i am working on my dietary nutritionist/athletic training degree so all this info is phenomenal for me.

 

[BamBam0319]

So, i am not very smart in the science/availability part of things but, when dosing your AAS/PH/DS based on your metabolicrate, age, height, etc.... does it matter when you time your doses of your AAS and cycle supports? Such as, we all know BMR is usually slower upon waking and right before you enter phase 3 of sleep, so would that effect if you were to take your doses earlier such as on waking or dosing before sleep? Or would it be better for absorption to dose maybe 3-4hrs after waking with say a small meal?

P.S. i am working on my dietary nutritionist/athletic training degree so all this info is phenomenal for me.

Are you talking oral steroids? Because I don't think meals or anything would really impact absorption of injections

 

[dustter]

Are you talking oral steroids? Because I don't think meals or anything would really impact absorption of injections

Yes orals of course. I should have specified that. So we know the half life of things like anavar is 8-9 hrs, but with a full stomach your true metabolism would actually slow the absorption of the anavar or maybe dbol? So does timing your dose at certain times of the day effect the absorption of the oral steroid if taken with or without a meal? I also know its reccommended by some to not take a protein shake with an oral because it reduces the availability/absorption of the steroid... Or am I mistaken?

 

[Driven2lift]

Yes orals of course. I should have specified that. So we know the half life of things like anavar is 8-9 hrs, but with a full stomach your true metabolism would actually slow the absorption of the anavar or maybe dbol? So does timing your dose at certain times of the day effect the absorption of the oral steroid if taken with or without a meal? I also know its reccommended by some to not take a protein shake with an oral because it reduces the availability/absorption of the steroid... Or am I mistaken?

I don't think this is the thread for this, but know:

Digestion will slow, half-life and anything else will be unaffected.

With a heavy enough meal with lots of calcium for example may slow digestion, definitely in the stomach where you want an acidic environment to cleave your oral compounds.

I wouldn't ever worry myself over taking it with a meal but given the choice I would take it with smaller meals possibly.

 

[BeastFitness]

So, i am not very smart in the science/availability part of things but, when dosing your AAS/PH/DS based on your metabolicrate, age, height, etc.... does it matter when you time your doses of your AAS and cycle supports? Such as, we all know BMR is usually slower upon waking and right before you enter phase 3 of sleep, so would that effect if you were to take your doses earlier such as on waking or dosing before sleep? Or would it be better for absorption to dose maybe 3-4hrs after waking with say a small meal?

P.S. i am working on my dietary nutritionist/athletic training degree so all this info is phenomenal for me.

Are you talking oral steroids? Because I don't think meals or anything would really impact absorption of injections

Yes orals of course. I should have specified that. So we know the half life of things like anavar is 8-9 hrs, but with a full stomach your true metabolism would actually slow the absorption of the anavar or maybe dbol? So does timing your dose at certain times of the day effect the absorption of the oral steroid if taken with or without a meal? I also know its reccommended by some to not take a protein shake with an oral because it reduces the availability/absorption of the steroid... Or am I mistaken?

I don't think this is the thread for this, but know:

Digestion will slow, half-life and anything else will be unaffected.

With a heavy enough meal with lots of calcium for example may slow digestion, definitely in the stomach where you want an acidic environment to cleave your oral compounds.

I wouldn't ever worry myself over taking it with a meal but given the choice I would take it with smaller meals possibly.

^^^This

I honestly don't feel the difference is going to be extremely apparent BUT obviously a smaller meal would be digested faster. I wouldn't worry about that to be completely honest though Dustter

 

[BeastFitness]

Since you brought up methandrostenolone


[Severe cholestasis with kidney failure from anabolic steroids in a body builder].

A 28-year-old body builder was admitted because of jaundice. For 80 days, until 3 weeks before hospitalization, he had been taking moderately high doses of anabolic steroids: metandienone (methandienone), 10-50 mg daily by mouth, and stanozolol, 50 mg intramuscularly every other day. Physical examination was unremarkable except for yellow discoloration of the skin and sclerae. Bilirubin concentration was raised to 4.5 mg/dl, cholestasis enzymes were normal, while transaminase activities were raised. Liver biopsy was compatible with cholestasis induced by anabolic steroids. Although the steroids had been discontinued, the patient's general condition deteriorated over 7 weeks. Serum bilirubin rose up to a maximum of 77.9 mg/dl. In addition renal failure developed with a creatinine concentration of 4.2 mg/dl. The patient's state improved simultaneously with the administration of ursodeoxycholic acid and the biochemical values gradually reached normal levels after several weeks. Anabolic steroids can cause severe cholestasis and acute renal failure. In this case there was a notable temporal coincidence between the administration of ursodeoxycholic acid and the marked clinical improvement.


Benign liver-cell adenoma associated with long-term administration of an androgenic-anabolic steroid (methandienone).

A 19-year-old man with paroxysmal nocturnal hemoglobinuria treated for 3 years with methandienone was admitted to the hospital with hemoperitoneum due to the rupture of an hepatic tumor. Histology revealed that it was a benign liver cell adenoma, with a pathologic appearance and mode of clinical presentation closely resembling those of cases observed to develop in association to contraceptive steroids.



[Virilization caused by methandrostenolone-containing cream in 2 prepubertal girls].

Two prepubertal girls were treated with Dianabol cream by their family physicians during 6 and 8 months because of an anal exzema. In both of them, growth velocity and bone maturation were accelerated, and there was hypertrophy of the clitoris and deepening of the voice. In one girl, all symptoms with the exception of the deep voice had disappeared six years after the discontinuation of treatment. In the other girl, final evaluation is not yet possible. The two observations show that androgens and anabolic steroids may have a marked systemic action if applied percutaneously. Treatment with these compounds is indicated very rarely in children and should be restricted to pediatric endocrinologists.

 

[BeastFitness]

Sorry for the delay in posts! I was at the Arnold all weekend and got to meet up with clients and friends and DAMN was it fun!!! Time to get back to it

Effects of nandrolone phenylpropionate in the horse: (2) general effects in animals undergoing training.

The effect of 11 weekly injections of nandrolone phenylpropionate (400 mg) was investigated by a crossover trial (2 training periods) in 6 Thoroughbred geldings undergoing training. A decrease in body weight and flank measurement occurred only during the first training period and was not modified by the anabolic steroid. Urinary nitrogen excretion was lower in the anabolic treated animals only in the first training period. Neither training nor training plus nandrolone phenylpropionate administration caused any marked alteration in blood biochemistry or haematology. A significant decrease in plasma chloride and increase in haematocrit occurred independent of treatment in the latter, more extensive anaerobic training of both parts of the crossover. No change in urinary pH or specific gravity was found throughout the study. No evidence of improved racing performance due to nandrolone phenylpropionate administration was observed. Behavioural changes attributed to the drug could be detected for at least 6 weeks after the cessation of treatment.


Pharmacokinetics and pharmacodynamics of nandrolone esters in oil vehicle: effects of ester, injection site and injection volume.

We studied healthy men who underwent blood sampling for plasma nandrolone, testosterone and inhibin measurements before and for 32 days after a single i.m. injection of 100 mg of nandrolone ester in arachis oil. Twenty-three men were randomized into groups receiving nandrolone phenylpropionate (group 1, n = 7) or nandrolone decanoate (group 2, n = 6) injected into the gluteal muscle in 4 ml of arachis oil vehicle or nandrolone decanoate in 1 ml of arachis oil vehicle injected into either the gluteal (group 3, n = 5) or deltoid (group 4, n = 5) muscles. Plasma nandrolone, testosterone and inhibin concentrations were analyzed by a mixed-effects indirect response model. Plasma nandrolone concentrations were influenced (P < .001) by different esters and injection sites, with higher and earlier peaks with the phenylpropionate ester, compared with the decanoate ester. After nandrolone decanoate injection, the highest bioavailability and peak nandrolone levels were observed with the 1-ml gluteal injection. Plasma testosterone concentrations were also influenced (P < .001) by the ester and injection site, with the most rapid, but briefest, suppression being due to the phenylpropionate ester, whereas the most sustained suppression was achieved with the 1-ml gluteal injection. Plasma inhibin concentrations were also significantly influenced by injection volume and site, with the lowest nadir occurring after the nandrolone decanoate 1-ml gluteal injection. Thus, the bioavailability and physiological effects of a nandrolone ester in an oil vehicle are greatest when the ester is injected in a small (1 ml vs. 4 ml) volume and into the gluteal vs. deltoid muscle. We conclude that the side-chain ester and the injection site and volume influence the pharmacokinetics and pharmacodynamics of nandrolone esters in an oil vehicle in men.

 

[dustter]

Sorry for the delay in posts! I was at the Arnold all weekend and got to meet up with clients and friends and DAMN was it fun!!! Time to get back to it

Effects of nandrolone phenylpropionate in the horse: (2) general effects in animals undergoing training.

The effect of 11 weekly injections of nandrolone phenylpropionate (400 mg) was investigated by a crossover trial (2 training periods) in 6 Thoroughbred geldings undergoing training. A decrease in body weight and flank measurement occurred only during the first training period and was not modified by the anabolic steroid. Urinary nitrogen excretion was lower in the anabolic treated animals only in the first training period. Neither training nor training plus nandrolone phenylpropionate administration caused any marked alteration in blood biochemistry or haematology. A significant decrease in plasma chloride and increase in haematocrit occurred independent of treatment in the latter, more extensive anaerobic training of both parts of the crossover. No change in urinary pH or specific gravity was found throughout the study. No evidence of improved racing performance due to nandrolone phenylpropionate administration was observed. Behavioural changes attributed to the drug could be detected for at least 6 weeks after the cessation of treatment.


Pharmacokinetics and pharmacodynamics of nandrolone esters in oil vehicle: effects of ester, injection site and injection volume.

We studied healthy men who underwent blood sampling for plasma nandrolone, testosterone and inhibin measurements before and for 32 days after a single i.m. injection of 100 mg of nandrolone ester in arachis oil. Twenty-three men were randomized into groups receiving nandrolone phenylpropionate (group 1, n = 7) or nandrolone decanoate (group 2, n = 6) injected into the gluteal muscle in 4 ml of arachis oil vehicle or nandrolone decanoate in 1 ml of arachis oil vehicle injected into either the gluteal (group 3, n = 5) or deltoid (group 4, n = 5) muscles. Plasma nandrolone, testosterone and inhibin concentrations were analyzed by a mixed-effects indirect response model. Plasma nandrolone concentrations were influenced (P < .001) by different esters and injection sites, with higher and earlier peaks with the phenylpropionate ester, compared with the decanoate ester. After nandrolone decanoate injection, the highest bioavailability and peak nandrolone levels were observed with the 1-ml gluteal injection. Plasma testosterone concentrations were also influenced (P < .001) by the ester and injection site, with the most rapid, but briefest, suppression being due to the phenylpropionate ester, whereas the most sustained suppression was achieved with the 1-ml gluteal injection. Plasma inhibin concentrations were also significantly influenced by injection volume and site, with the lowest nadir occurring after the nandrolone decanoate 1-ml gluteal injection. Thus, the bioavailability and physiological effects of a nandrolone ester in an oil vehicle are greatest when the ester is injected in a small (1 ml vs. 4 ml) volume and into the gluteal vs. deltoid muscle. We conclude that the side-chain ester and the injection site and volume influence the pharmacokinetics and pharmacodynamics of nandrolone esters in an oil vehicle in men.

could post your sources for this info please?

 

[BeastFitness]

could post your sources for this info please?

Sure can! Full PDFs available there..good reads!

Invalid Link Removed

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[BeastFitness]

The effect of a low-calorie diet alone and in combination with triiodothyronine therapy on weight loss and hypophyseal thyroid function in obesity.

The effect of a low-calorie diet (200 kcal) composed of about 50 per cent glucose and 50 per cent protein on body weight, thyroid hormone levels and pituitary thyrotrophin response was studied in 18 grossly obese subjects (relative weight 131-205 per cent) for 28 d; during the last 14 d eight subjects (Gp B) served as controls, while in the other ten subjects (Gp A) the low T3-high rT3 state was treated by T3 supplementation (150 micrograms daily). During the first 14 d (period 1) weight loss (corrected for the sodium diuresis) appeared to be constant and to be equal for both groups. The thyroid hormone concentration and the basal and TRH stimulated TSH concentrations were similar to the results from previous total starvation studies. Despite marked changes in serum T3 levels a normal pituitary TSH response was maintained and no delayed response of TSH to TRH occurred. During T3 supplementation the serum T3 levels increased to high values, the rT3 concentration declined to below initial values, the T4 and TSH concentrations were depressed and the response of the TSH concentration to TRH disappeared; apparently these 'high normal' levels of serum T3 must be considered inappropriate for this condition of severe calorie restriction. In the controls the serum T3 levels remained constant after the end of the first period; the serum rT3 concentration declined from day 14 to day 28, but remained above the initial values. The serum T4 concentration remained almost constant during the whole study; basal and TRH stimulated TSH concentrations did not change during the whole study. During period 2 weight loss diminished in the control group, but remained constant in Gp A (T3 supplemented); the correlation between the weight loss and the increase of the serum T3 concentration during triiodothyronine supplementation was significantly negative (r = -0.64; P less than 0.05). The well-being of the subjects did not change during T3 administration and no signs of hyperthyroidism developed. One could speculate this reflects a decrease in number or sensitivity of intracellular receptor sites. It is concluded that at the peripheral level no complete resistance develops against T3 administration; in the low T3 state the hypothalamic-pituitary axis reacts as if euthyroidism exists

 

[rtmilburn]

The effect of a low-calorie diet alone and in combination with triiodothyronine therapy on weight loss and hypophyseal thyroid function in obesity.

The effect of a low-calorie diet (200 kcal) composed of about 50 per cent glucose and 50 per cent protein on body weight, thyroid hormone levels and pituitary thyrotrophin response was studied in 18 grossly obese subjects (relative weight 131-205 per cent) for 28 d; during the last 14 d eight subjects (Gp B) served as controls, while in the other ten subjects (Gp A) the low T3-high rT3 state was treated by T3 supplementation (150 micrograms daily). During the first 14 d (period 1) weight loss (corrected for the sodium diuresis) appeared to be constant and to be equal for both groups. The thyroid hormone concentration and the basal and TRH stimulated TSH concentrations were similar to the results from previous total starvation studies. Despite marked changes in serum T3 levels a normal pituitary TSH response was maintained and no delayed response of TSH to TRH occurred. During T3 supplementation the serum T3 levels increased to high values, the rT3 concentration declined to below initial values, the T4 and TSH concentrations were depressed and the response of the TSH concentration to TRH disappeared; apparently these 'high normal' levels of serum T3 must be considered inappropriate for this condition of severe calorie restriction. In the controls the serum T3 levels remained constant after the end of the first period; the serum rT3 concentration declined from day 14 to day 28, but remained above the initial values. The serum T4 concentration remained almost constant during the whole study; basal and TRH stimulated TSH concentrations did not change during the whole study. During period 2 weight loss diminished in the control group, but remained constant in Gp A (T3 supplemented); the correlation between the weight loss and the increase of the serum T3 concentration during triiodothyronine supplementation was significantly negative (r = -0.64; P less than 0.05). The well-being of the subjects did not change during T3 administration and no signs of hyperthyroidism developed. One could speculate this reflects a decrease in number or sensitivity of intracellular receptor sites. It is concluded that at the peripheral level no complete resistance develops against T3 administration; in the low T3 state the hypothalamic-pituitary axis reacts as if euthyroidism exists

Got any research on eq or masteron?

 

[BeastFitness]

Got any research on eq or masteron?

Yep! I'll try and post some up later today/tomorrow