Just wanted anyone who knows more than I do on als and aas thoughts (and other muscle wasting diseases)
Just curious here bros, not the least bit worried about any diseases
Here's a few studies I found
Drugs. 2004;64(7):725-50.
The anabolic androgenic steroid oxandrolone in the treatment of wasting and catabolic disorders: review of efficacy and safety.
Orr R1, Fiatarone Singh M.
Author information
Abstract
There has been increasing interest in the development of effective agents that can be safely used to promote anabolism in the clinical setting for patients with chronic wasting conditions as well as in the prevention and treatment of frailty associated with loss of muscle tissue in aging (sarcopenia). One such agent is the anabolic androgenic steroid (AAS) oxandrolone, which has been used in such clinical situations as HIV-related muscle wasting, severe burn injury, trauma following major surgery, neuromuscular disorders and alcoholic hepatitis for over 30 years. In the US, oxandrolone is the only AAS that is US FDA-approved for restitution of weight loss after severe trauma, major surgery or infections, malnutrition due to alcoholic cirrhosis, and Duchenne's or Becker's muscular dystrophy. Our review of the use of oxandrolone in the treatment of catabolic disorders, HIV and AIDS-related wasting, neuromuscular and other disorders provides strong evidence of its clinical efficacy. Improvements in body composition, muscle strength and function, status of underlying disease or recovery from acute catabolic injury and nutritional status are significant in the vast majority of well designed trials. However, oxandrolone has not yet been studied in sarcopenia.Unlike other orally administered C17alpha-alkylated AASs, the novel chemical configuration of oxandrolone confers a resistance to liver metabolism as well as marked anabolic activity. In addition, oxandrolone appears not to exhibit the serious hepatotoxic effects (jaundice, cholestatic hepatitis, peliosis hepatis, hyperplasias and neoplasms) attributed to the C17alpha-alkylated AASs. Oxandrolone is reported to be generally well tolerated and the most commonly documented adverse effects are transient elevations in transaminase levels and reductions in high density lipoprotein cholesterol level.However, optimal risk:benefit ratios for oxandrolone and other agents in its class will need to be refined before widespread clinical acceptance of AASs as a therapeutic option in sarcopenia and other chronic wasting conditions.
Amyotroph Lateral Scler Other Motor Neuron Disord. 2000 Dec;1 Suppl 4:21-5; discussion 25-6.
Oxandrolone in ALS: preliminary analysis.
Rosenfeld J1, King RM, Smith JE.
http://informahealthcare.com/doi/abs/10.1080/14660820050515674
PLoS One. 2012;7(5):e37258. doi: 10.1371/journal.pone.0037258. Epub 2012 May 14.
Dihydrotestosterone ameliorates degeneration in muscle, axons and motoneurons and improves motor function in amyotrophic lateral sclerosis model mice.
Yoo YE1, Ko CP.
Abstract
Amyotrophic lateral sclerosis (ALS) is a lethal disease characterized by a progressive loss of motoneurons. The clinical symptoms include skeletal muscle weakness and atrophy, which impairs motor performance and eventually leads to respiratory failure. We tested whether dihydrotestosterone (DHT), which has both anabolic effects on muscle and neuroprotective effects on axons and motoneurons, can ameliorate clinical symptoms in ALS. A silastic tube containing DHT crystals was implanted subcutaneously in SOD1-G93A mice at early symptomatic age when decreases in body weight and grip-strength were observed as compared to wild-type mice. DHT-treated SOD1-G93A mice demonstrated ameliorated muscle atrophy and increased body weight, which was associated with stronger grip-strength. DHT treatment increased the expression of insulin-like growth factor-1 in muscle, which can exert myotrophic as well as neurotrophic effects through retrograde transport. DHT treatment attenuated neuromuscular junction denervation, and axonal and motoneuron loss. DHT-treated SOD1-G93A mice demonstrated improvement in motor behavior as assessed by rota-rod and gait analyses, and an increased lifespan. Application of DHT is a relatively simple and non-invasive procedure, which may be translated into therapy to improve the quality of life for ALS patients.
Pharmacol Res. 2012 Feb;65(2):221-30. doi: 10.1016/j.phrs.2011.12.001. Epub 2011 Dec 10.
The anabolic/androgenic steroid nandrolone exacerbates gene expression modifications induced by mutant SOD1 in muscles of mice models of amyotrophic lateral sclerosis.
Galbiati M1, Onesto E, Zito A, Crippa V, Rusmini P, Mariotti R, Bentivoglio M, Bendotti C, Poletti A.
Abstract
Anabolic/androgenic steroids (AAS) are drugs that enhance muscle mass, and are often illegally utilized in athletes to improve their performances. Recent data suggest that the increased risk for amyotrophic lateral sclerosis (ALS) in male soccer and football players could be linked to AAS abuse. ALS is a motor neuron disease mainly occurring in sporadic (sALS) forms, but some familial forms (fALS) exist and have been linked to mutations in different genes. Some of these, in their wild type (wt) form, have been proposed as risk factors for sALS, i.e. superoxide dismutase 1 (SOD1) gene, whose mutations are causative of about 20% of fALS. Notably, SOD1 toxicity might occur both in motor neurons and in muscle cells. Using gastrocnemius muscles of mice overexpressing human mutant SOD1 (mutSOD1) at different disease stages, we found that the expression of a selected set of genes associated to muscle atrophy, MyoD, myogenin, atrogin-1, and transforming growth factor (TGF)β1, is up-regulated already at the presymptomatic stage. Atrogin-1 gene expression was increased also in mice overexpressing human wtSOD1. Similar alterations were found in axotomized mouse muscles and in cultured ALS myoblast models. In these ALS models, we then evaluated the pharmacological effects of the synthetic AAS nandrolone on the expression of the genes modified in ALS muscle. Nandrolone administration had no effects on MyoD, myogenin, and atrogin-1 expression, but it significantly increased TGFβ1 expression at disease onset. Altogether, these data suggest that, in fALS, muscle gene expression is altered at early stages, and AAS may exacerbate some of the alterations induced by SOD1 possibly acting as a contributing factor also in sALS.
Just curious here bros, not the least bit worried about any diseases
Here's a few studies I found
Drugs. 2004;64(7):725-50.
The anabolic androgenic steroid oxandrolone in the treatment of wasting and catabolic disorders: review of efficacy and safety.
Orr R1, Fiatarone Singh M.
Author information
Abstract
There has been increasing interest in the development of effective agents that can be safely used to promote anabolism in the clinical setting for patients with chronic wasting conditions as well as in the prevention and treatment of frailty associated with loss of muscle tissue in aging (sarcopenia). One such agent is the anabolic androgenic steroid (AAS) oxandrolone, which has been used in such clinical situations as HIV-related muscle wasting, severe burn injury, trauma following major surgery, neuromuscular disorders and alcoholic hepatitis for over 30 years. In the US, oxandrolone is the only AAS that is US FDA-approved for restitution of weight loss after severe trauma, major surgery or infections, malnutrition due to alcoholic cirrhosis, and Duchenne's or Becker's muscular dystrophy. Our review of the use of oxandrolone in the treatment of catabolic disorders, HIV and AIDS-related wasting, neuromuscular and other disorders provides strong evidence of its clinical efficacy. Improvements in body composition, muscle strength and function, status of underlying disease or recovery from acute catabolic injury and nutritional status are significant in the vast majority of well designed trials. However, oxandrolone has not yet been studied in sarcopenia.Unlike other orally administered C17alpha-alkylated AASs, the novel chemical configuration of oxandrolone confers a resistance to liver metabolism as well as marked anabolic activity. In addition, oxandrolone appears not to exhibit the serious hepatotoxic effects (jaundice, cholestatic hepatitis, peliosis hepatis, hyperplasias and neoplasms) attributed to the C17alpha-alkylated AASs. Oxandrolone is reported to be generally well tolerated and the most commonly documented adverse effects are transient elevations in transaminase levels and reductions in high density lipoprotein cholesterol level.However, optimal risk:benefit ratios for oxandrolone and other agents in its class will need to be refined before widespread clinical acceptance of AASs as a therapeutic option in sarcopenia and other chronic wasting conditions.
Amyotroph Lateral Scler Other Motor Neuron Disord. 2000 Dec;1 Suppl 4:21-5; discussion 25-6.
Oxandrolone in ALS: preliminary analysis.
Rosenfeld J1, King RM, Smith JE.
http://informahealthcare.com/doi/abs/10.1080/14660820050515674
PLoS One. 2012;7(5):e37258. doi: 10.1371/journal.pone.0037258. Epub 2012 May 14.
Dihydrotestosterone ameliorates degeneration in muscle, axons and motoneurons and improves motor function in amyotrophic lateral sclerosis model mice.
Yoo YE1, Ko CP.
Abstract
Amyotrophic lateral sclerosis (ALS) is a lethal disease characterized by a progressive loss of motoneurons. The clinical symptoms include skeletal muscle weakness and atrophy, which impairs motor performance and eventually leads to respiratory failure. We tested whether dihydrotestosterone (DHT), which has both anabolic effects on muscle and neuroprotective effects on axons and motoneurons, can ameliorate clinical symptoms in ALS. A silastic tube containing DHT crystals was implanted subcutaneously in SOD1-G93A mice at early symptomatic age when decreases in body weight and grip-strength were observed as compared to wild-type mice. DHT-treated SOD1-G93A mice demonstrated ameliorated muscle atrophy and increased body weight, which was associated with stronger grip-strength. DHT treatment increased the expression of insulin-like growth factor-1 in muscle, which can exert myotrophic as well as neurotrophic effects through retrograde transport. DHT treatment attenuated neuromuscular junction denervation, and axonal and motoneuron loss. DHT-treated SOD1-G93A mice demonstrated improvement in motor behavior as assessed by rota-rod and gait analyses, and an increased lifespan. Application of DHT is a relatively simple and non-invasive procedure, which may be translated into therapy to improve the quality of life for ALS patients.
Pharmacol Res. 2012 Feb;65(2):221-30. doi: 10.1016/j.phrs.2011.12.001. Epub 2011 Dec 10.
The anabolic/androgenic steroid nandrolone exacerbates gene expression modifications induced by mutant SOD1 in muscles of mice models of amyotrophic lateral sclerosis.
Galbiati M1, Onesto E, Zito A, Crippa V, Rusmini P, Mariotti R, Bentivoglio M, Bendotti C, Poletti A.
Abstract
Anabolic/androgenic steroids (AAS) are drugs that enhance muscle mass, and are often illegally utilized in athletes to improve their performances. Recent data suggest that the increased risk for amyotrophic lateral sclerosis (ALS) in male soccer and football players could be linked to AAS abuse. ALS is a motor neuron disease mainly occurring in sporadic (sALS) forms, but some familial forms (fALS) exist and have been linked to mutations in different genes. Some of these, in their wild type (wt) form, have been proposed as risk factors for sALS, i.e. superoxide dismutase 1 (SOD1) gene, whose mutations are causative of about 20% of fALS. Notably, SOD1 toxicity might occur both in motor neurons and in muscle cells. Using gastrocnemius muscles of mice overexpressing human mutant SOD1 (mutSOD1) at different disease stages, we found that the expression of a selected set of genes associated to muscle atrophy, MyoD, myogenin, atrogin-1, and transforming growth factor (TGF)β1, is up-regulated already at the presymptomatic stage. Atrogin-1 gene expression was increased also in mice overexpressing human wtSOD1. Similar alterations were found in axotomized mouse muscles and in cultured ALS myoblast models. In these ALS models, we then evaluated the pharmacological effects of the synthetic AAS nandrolone on the expression of the genes modified in ALS muscle. Nandrolone administration had no effects on MyoD, myogenin, and atrogin-1 expression, but it significantly increased TGFβ1 expression at disease onset. Altogether, these data suggest that, in fALS, muscle gene expression is altered at early stages, and AAS may exacerbate some of the alterations induced by SOD1 possibly acting as a contributing factor also in sALS.
