Testosterone and Anavar

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8 years 8 months ago #4916 by admin
thinksteroids.com/community/threads/pept...s-tendons.134295950/

Deca, equipoise, anavar, and Primobolan will ALL increase skeletal muscle while at the same time dramatically increase collagen syn and bone mass and density, leaving you with a substantially reduced chance of becoming injured than if you choose to use AAS like sus, cyp, or enth.

While testosterone will increase bone mass and density, even at supra-physiological levels, the result is weaker tendons due to inhibition of collagen syn.

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Testosterone thus opposes the benefits of Anavar for collagen synthesis, so I wouldn't use it even at low doses.

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8 years 8 months ago #4917 by repellent
Replied by repellent on topic Testosterone and Anavar
I can't seem to find any benefit of anavar specifically fopr cartilage but find things on testosterone levels being beneficial to cartilage

rheumatology.oxfordjournals.org/content/42/2/258.full.pdf

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8 years 8 months ago #4930 by admin
Replied by admin on topic Testosterone and Anavar
Here's a couple of good pieces of info I found (thanks to your private message):

First a patent:

Uses of oxandrolone

The subject invention additionally provides a method of promoting cartilage repair in a patient which comprises administering an oxandrolone to the patient.

EXAMPLE 1: The effect of oxandrolone on inflammation

The rat model of carrageenan-induced paw edema is used to assay the anti-inflammatory activity of oxandrolone. In this model, rats are given a sub-plantar injection of carrageenan into the left hind paw. The paw volume is measured by a Hg-displacement volumeter before and at hourly intervals after paw injection. Rats are divided into three groups. One group receives a subcutaneous injection of oxandrolone long before carrageenan administration. A second group receives a subcutaneous injection of oxandrolone closer to carrageenan administration. The other group does not receive any pretreatment and serves as a control.

The swelling response is reduced indicating efficacy of oxandrolone as an anti-inflammatory agent.

EXAMPLE 2 : The effect of oxandrolone on Synovial Inflammation

As a model for synovial inflammation and the ability of oxandrolone to inhibit such inflammation, the knee-joint (synovial) inflammation model in rats is utilized. (Ginsburg et al . , in "Bayer-Symposium VI: Experimental Models of Chronic Inflammatory Diseases", 256-299, 1977, Springer-Verlag) .

In this model, inflammation is induced by intraarticular injection of bacterial lipopolysaccharide endotoxin (LPS) . The degree of inflammation is reflected by the swelling of the synovial tissue and is measured as the increase in weight postadministration. The LPS toxin and oxandrolone are co-administered.

The LPS-induced synovial inflammation is inhibited which indicates efficacy of oxandrolone as an inhibitor of synovial inflammation.

EXAMPLE 3: The effect of Oxandrolone on Adjuvant-Induced Arthritis

The induction of joint inflammation in rats by administration of Freund's adjuvant is considered to be the model of choice for experimental rheumatoid arthritis (Newbould (1963), Brit. J. Pharmacol. 21: 127). An injection of the adjuvant (Freund's adjuvant with killed Mycobacterium Tuberculosis) into the foot pad results in an initial swelling of the paw, reaching a plateau after 3 days, followed after 14 days by a second increase in,paw and joint swelling, which persists for another 7-10 days. The second phase is regarded as the phase of immunologically- induced chronic arthritis. To examine the efficacy of oxandrolone as an anti-arthritic drug, oxandrolone is given subcutaneously (in doses expressed as mg per kg body weight) to adjuvant-treated rats during 14-21 days after adjuvant administration. Oxandrolone is given daily or on alternating days. As a negative control, saline is given subcutaneously to a second group of adjuvant-treated rats.

Joint inflammation is reduced which indicates efficacy of oxandrolone as an inhibitor of arthritis.


And if we wish to delve into the mechanisms of its action, there is the following:

Dynamics of Bone and Cartilage Metabolism: Principles and Clinical Applications

Androgens have been shown to inhibit IL-6 production by stromal and osteoblastic cells as well as stimulation of osteoclastogenesis by marrow osteoclast precursors [125, 126].


Interleukin-6 is a significant predictor of radiographic knee osteoarthritis: The Chingford Study.

CONCLUSION: This followup study showed that individuals were more likely to be diagnosed as having RKOA if they had a higher BMI and increased circulating levels of IL-6. These results should stimulate more work on IL-6 as a potential therapeutic target.


Also found this interesting piece:

The Role of IL-6 in Osteoarthritis and Cartilage Regeneration

DISCUSSION
This study demonstrates the increased presence of IL-6 in the synovial fluid of patients with symptomatic cartilage lesions and OA donors when compared to healthy donors. Furthermore, we demonstrated for the first time that chondrocytes produce high concentrations of IL-6 during regeneration, especially osteoarthritic chondrocytes. However, IL-6 does not seem to play a direct role in cartilage matrix turnover. Furthermore, only in OA chondrocytes, IL-6 does seem to play a role in proliferation, although the effect was
different in explants in the presence of synovial fluid compared to 3D differentiation by expanded chondrocytes.

SIGNIFICANCE
Soluble mediators, including IL-6, in the synovial fluid of knees with symptomatic cartilage defects are thought to cause progression to osteoarthritis and also hamper cartilage regeneration after cartilage surgeries such as autologous chondrocyte implantation. Identifying and targeting those soluble mediators will increase the success of cartilage
repair surgery and prevent the progression to early osteoarthritis.

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8 years 8 months ago #4936 by Bull Terrier
I'm calling BS on the article pulled from steroidology in opening post. Stanozolo has been shown to increase collagen synthesis ( www.ncbi.nlm.nih.gov/pubmed/9856839 ) but I can't find any credible information in scientific literature that testosterone inhibits collagen synthesis. Actually if anything it has a positive effect:

www.ncbi.nlm.nih.gov/pubmed/1529802
"Abstract
Testosterone and its metabolite 5 alpha-dihydrotestosterone (DHT) were compared with dexamethasone 21-acetate in two different animal models of arthritis and found to have effects on cartilage breakdown and inflammation. In the mouse air pouch, at the three dose levels used, significant effects were obtained with DHT and were more pronounced on cartilage breakdown than on inflammation. At the lowest dose of 0.3 mg kg-1 there was a 64% inhibition of collagen breakdown and 18% inhibition of glycosaminoglycans (GAGs) breakdown. In the antigen-induced arthritis mouse model testosterone had significant inhibitory effects on inflammation (synovial hyperplasia) and cartilage erosion."

www.ncbi.nlm.nih.gov/pmc/articles/PMC3975417/
"........The notion that testosterone decreases joint laxity is further supported by the reported increase in the collagen content of the prostate, breast and capsular tissue and an increase in knee ligament repair strength by testosterone "

Personally I would be surprised if there were to be any information in scientific literature investigating the effect of boldenone and collagen synthesis in humans, considering that it is a veterinary drug.

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