I decided to start this thread for anyone who would like to read about research done on anabolic steroids. I have access to many databases of medical research published in PEER REVIEWED JOURNALS so thats right....
NO BRO SCIENCE IN HERE PLEASE
I will update this thread as I come by new studies and if anyone would like to add to the collection of peer reviewed research please do so. So heres a few abstracts of some studies, if anyone could show me how to get a PDF up on here then let me know since all the studies are 200kb and up and the site only allows me up to 100kb...
Anabolic-androgenic steroids: a possible new risk factor of toxicant-associated fatty liver disease
Paulo Adriano Schwingel1,2, Helma P. Cotrim1, Bernardo Rios Salles1, Carlos Eduardo Almeida1,
Crim ´ erio Ribeiro dos Santos Jr2, Bruno Nachef1, Antonio Ricardo Andrade1 and Cl ´ audio C. Zoppi2
1 Programa de Po´ s-Graduac¸a˜o em Medicina e Sau´ de (PPgMS), Faculdade de Medicina da Bahia, Universidade Federal da Bahia (UFBA), Salvador, Bahia,
Brazil
2 Laborato´ rio de Pesquisa do Exerc´ıcio (LAPEX), Faculdade Social da Bahia (FSBA), Salvador, Bahia, Brazil
Keywords
anabolic agents – drug use – non-alcoholic
fatty liver disease – steatosis – toxicantassociated
fatty liver disease
Correspondence
Helma Pinchemel Cotrim, MD, Programa de
Po´ s-Graduac¸a˜ o em Medicina e Sau´ de (PPgMS),
Complexo Universita´ rio Professor Edgard
Santos, Rua Augusto Viana, s/n, 5o. andar,
Canela, Salvador, Bahia CEP 40110-060, Brazil
DOI:10.1111/j.1478-3231.2010.02346.x
Abstract
Background: Industrial toxin and drugs have been associated with nonalcoholic fatty liver disease (NAFLD); in these cases, the disease has been termed toxicant-associated steatohepatitis (TASH).
Aim: This study hypothesizes that the use of anabolic-androgenic steroids (AAS) could also be a risk factor to TASH or better toxicant-associated fatty liver disease (TAFLD) development.
Methodology: Case–control study including 180 non-competitive recreational male bodybuilders from August/2007 to March/2009. Ninetyfive had a history of intramuscular AAS use (cases; G1) and 85 were non-users (controls; G2). They underwent a clinical evaluation and abdominal ultrasound, and their blood levels of aminotransferases, creatine phosphokinase (CPK), lipids, glucose and insulin were measured.
TAFLD criteria: history of AAS use 42 years; presence of hepatic steatosis on ultrasound and/or aminotransferase alterations with normal CPK levels; exclusion of ethanol intake Z20 g/day or use of other drugs; and exclusion of obesity, dyslipidaemia, diabetes and other liver diseases. Homeostasis model assessment for insulin resistance Z3 was considered insulin resistant. Independent t-test, odds ratio (OR) and 95% confidence intervals (95% CI) were calculated.
Results: All cases were asymptomatic. Clinical and laboratorial data were similar in G1 and G2 (P40.05). TAFLD criteria were observed in 12.6% of the G1 cases and 2.4% of controls had criteria compliant with non-alcoholic fatty liver related to metabolic conditions. OR was 6.0 (95% CI: 1.3–27.6).
Conclusions: These results suggest that AAS could be a possible new risk factor for TAFLD. In this type of fatty liver disease, the individuals had a low body fat mass and they did not present insulin resistance.


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