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Study done on 600mg per week of deca

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  • Study done on 600mg per week of deca

    A study done with HIV and men which charted the lean mass building effecs of nandrolone decanoate. 30 people participated in this study/investigation, with each given the same weekly high dose. Haft did resistance training so that the two groups trained and untrained. The dose started with 200mg week one, 400 wk two, and 600mg for 10 wks of peak therapy. Dose was reduced from week 13 to 16 to withdraw patients slowly from the deca. Potential negative metabolic were looked at, including cholestrol and lipid levels, including subfractions of HDL and LDL, triglycerides, insulin sensitivty and fasting glucose levels. Even with high dose used no negative changes were noted in total LDL, triglycerides or insulin sensitivty. The group going under the resistance exercise showed improvement in LDL particle size distribution, lipoprotein (a) levels and triglyceride values, which all indicate improved cardiovascular diease risk. Carbohydrate metabolism was significantly improved in this group. Only negative thing was reduction in HDL vaules.

  • #2
    Wait a minute you mean to tell me the study was showing AAS in a good light?? Say it isn't so. This study had to have been conducted somewhere in Europe now way the United States would allow that lol

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    • #3
      Published in the american journal of Physiology Endocrinology and metabolism in july 2001. If use under doctor care and blood work, dose adjustment could make A/S somewhat safer.

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      • #4
        You are absolutely right, most scientific researchers, and I guess our common sence, prove that Testosterone is healthier then nandrolone (deca) a modified testosterone (nor19) this study proves deca 11 times more harmfull compared to testosterone.

        Toxicol Lett. 2007 Mar 8;169(2):129-36. Epub 2007 Jan 3.
        Detrimental effects of anabolic steroids on human endothelial cells.
        D'Ascenzo S, Millimaggi D, Di Massimo C, Saccani-Jotti G, Botr? F, Carta G, Tozzi-Ciancarelli MG, Pavan A, Dolo V.
        Department of Experimental Medicine, University of L'Aquila, Via Vetoio-Coppito 2, L'Aquila 67100, Italy.
        Abstract
        The aim of this study is to investigate the effects in vitro induced by androgenic anabolic steroids (AAS) (testosterone, nandrolone, androstenedione, norandrostenedione, and norandrostenediol) used illicitly in sport competitions, on the proliferation ability, apoptosis and the intracellular calcium concentration ([Ca2+]i) in human umbilical vein endothelial cells (HUVECs), selected as a prototype of a biological target system whose structure and function can be affected by steroids. For this purpose, we evaluated the proliferation inhibition by cytotoxic assay expressed as the concentration of drug inducing a 50% decrease in growth (IC50). The IC50 was reached for testosterone at 100 microM, androstenedione at 375 microM, nandrolone at 9 microM, norandrostenedione at 500 microM. The IC50 value for norandrostenediol was not reached until a concentration of 6000 microM. The apoptotic effect was evaluated by flow cytometry at IC50 for each drug. We observed that testosterone induced 31% of apoptotic cells, norandrostenedione 25%, androstenedione 15% and nandrolone 18%. We have analyzed the effects of these drugs on [Ca2+]i both in the immediate and long-term continuous presence of each compound. Our data show a statistically significant increase of [Ca2+]i in the acute condition and in long-term treated cultures, suggesting that androgen steroids modulate intracellular levels of calcium independent of incubation time or compound identity. As a whole, this study demonstrates that AAS might alter endothelial homeostasis, predisposing to the early endothelial cell activation that is responsible for vascular complications observed frequently in AAS users.
        PMID: 17267145 [PubMed - indexed for MEDLINE]

        In rodents the same goes for the heart
        E.M. Ammar, Shehta Said, Mohammed Hassan. Enhanced vasoconstriction and reduced vasorelaxation induced by testosterone and nandrolone in hypercholesterolemic rabbits. Pharmacological Research, doi:10.1016/j.phrs.2004.03.010.

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