AAS side effects

[MastaDon]

Side effects of anabolic androgenic steroids abuse

Bonetti, A.a b , Tirelli, F.b , Catapano, A.c , Dazzi, D.d , Dei Cas, A.d , Solito, F.b , Ceda, C.d , Reverberi, C.e , Monica, C.f , Pipitone, S.f , Elia, G.g , Spattini, M.b , Magnati, G.d

a Department of Clinical Science, Curriculum of Sports Science and Physical Exercise, University of Parma, Via Gramsci, 43100 Parma, Italy
b Department of Clinical Science, Curriculum of Sports Science and Physical Exercise, University of Parma, Parma, Italy
c Department of Phamacologic Sciences, University of Milan, Milano, Italy
d Department of Internal Medicine and Biomedical Sciences, University of Parma, Parma, Italy
e Department of Heart and Cardiac Surgery, Azienda Ospedaliero-Universitaria Parma, Parma, Italy
f Central Laboratory, Azienda Ospedaliero-Universitaria Parma, Parma, Italy
g Infective Diseases Section, Azienda Ospedaliero-Universitaria Parma, Parma, Italy
Abstract

Long-term side effects of high doses of anabolic androgenic steroids self-administration were evaluated in this study. Twenty male bodybuilders, voluntarily starting steroid self-administration, were followed every 6 months over 2 years. Physical examination, haematological, metabolic and endocrine variables, semen analysis, hepatic and prostate ultrasound and echocardiographic evaluations were performed. LH values (baseline 3.43 ± 1.75) were suppressed at 18 (1.98 ± 1.99) (p = 0.026) and 24 (2.43 ± 2.17) (p = 0.026), and FSH (3.95 ± 2.01) at 6 (3.01 ± 2.16) (p = 0.031), 12 (2.45 ± 2.54) (p = 0.029), 18 (2.02 ± 2.29) (p = 0.032) and 24 (3.42 ± 2.64) (p = 0.032) months and SHBG (34.11 ± 10.88) values significantly lowered at 12 (24.81 ± 12.49) (p < 0.05), 18 (21.28 ± 11.15) (p < 0.01), 24 months (25.42 ± 11.16) (p < 0.01). A significant decrease in spermatozoa count (p < 0.01), and fertility index (p = 0.01) occurred. HDL-cholesterol (baseline 56.94 ± 13.54) was reduced at 18 (41.86 ± 14.17) (p < 0.01) and 24 (43.82 ± 18.67) (p < 0.05) months and Apo A-1 at 12 (p < 0.001), 18 (p = 0.05) and 24 (p = 0.05) months. The most important long-term adverse effects were lower fertility and the impairment of lipid profile associated with an increased cardiovascular risk. © Georg Thieme Verlag KG Stuttgart.

My notes:
This paper was published in 2008 in International Journal of Sports Medicine; volume 29, issue 8; pages 679-687.

This was a long-term observational study of 20 AAS users, mean age 27, height 175cm, weight 81kg, BMI 27kg/m2. 7 of the subjects withdrew from the study either b/c no explanation, emotional issues including aggression, sex problems, and family problems. BBers were examined every 6 months for 2 years. AAS was from UG, thus hazard of contamination was considered.

Plasma triglycerides, HDL and Apo A-1 values were significantly decreased with respect to (wrt) original values. LH, FSH, SBGH, and IGF1 values were significantly decreased by 24 months wrt to baseline. Authors reported no significant changes in GH, test, and estrogen levels during the study period.

16/20 subjects (which is all of them when you count the ones who dropped out) experienced hypogonadism associated with decrease sperm count and fertility index. 2 experienced azoospermia and another 2 “severe oligospermia”. It would have been good to point out which ancillaries were taken by subjects that led to azoo/oligospermia but this data was not included. It may have been the case that the 4 cases of severe sperm reduction may have been caused by improper PCT and/or HcG use, the use of other meds, and/or AAS type/dose. Prostate ultrasound examination showed normal size in all subjects, which was in contrast to earlier reports.

Hepatic profile included elevated ALT by 6 months, reduction of conjugated and total bilirubin by 12 months, increased LDH by 6 months, and hepatomegaly in 8 subjects. Echocardiogram showed normal cardiac morphology and function. 2 subjects showed pathological liver profile most likely due to AAS use (they used 17aa orals). Not all who used 17aa had pathological liver profile in the study. Furthermore, there was a significant inverse correlation between AAS dose and LH/FSH levels.




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In memory of our fallen soldiers.
You will never be forgotten.

[liftsiron]

It seems some of the subjects used orals for extended periods?

[JrMaFia]

i heard steroids shrink ur balls is that true?

[MastaDon]

It seems some of the subjects used orals for extended periods?

Lifts, the two cases with pathological liver profiles were profiled as the following:

case#1
42 weeks total AAS exposure (lifetime) done in 7 cycles
Cycle during study consisted of- 2.40g deca, 1.85g winni, 1.60g test, 0.800g androstenedione, 6.30g dhea, , 1.93g mestanolone, 0.630g oxandrolone (the latter 4 being orals)

case#2
36 weeks total AAS exposure in 8 cycles
0.200g methenolone IM, 2.27g deca, 0.600g winni, 3.7g test, 9.60g androstenedione, 2.00g dhea, 3.68g mestanolone, 0.150g methandrostenolone, 2.86g oxandrolone, 3.92g test (the latter 6 being orals)

It is indeed very confusing because the other user profiles indicate that there were people who:
1) had used more total weeks of AAS in more cycles, although these two cases were clearly at the higher end compared to the other subjects (mean values for total AAS use in weeks= 13, cycles=5)
2) had used what seems to be similar total dose of orals who did not have a pthological liver profile-- one subject use 2.8g each of 19-nor-androstenediol and 19-nor-androstenedione, 9.2g each of androstenediol, androstenedione, and norandrostenedione, and 5.3g each of dhea and mestanolone-- that's almost 45g of orals but no pathological liver

What is noteworthy is that case#2 used the most oxandrolone of any other subject in the study

That's why I think it would have been so useful to profile the use of ancillaries as the authors did for AAS... if they'd only let a BBer design these studies!!

EDIT: also some of the subjects were claimed to have used medicines (dumped in the ancillaries category and other agents like adrenergic agents, but this wasn't included in user profiles either. then there's issues with alcohol use that would be next to impossible to control and/or monitor, and the ubiquitous gene composition of the individual)

i heard steroids shrink ur balls is that true?

sorry to dissapoint you with the results here vet, truth is some members of forums claim to increase their size (who knows, it may be true and good for them) but this study CLEARLY demonstrated that regardless of HcG use indeed the boys shrunk.

perhaps it had to do with method of ancillary admin?? who knows, just trying to learn and share...

Also, it is a shame that this study in 2008 is one of a HANDFUL of studies on AAS use with the closest counterpart having been published well over 10 years ago

[liftsiron]

One thing that will skew any liver profile of oral steroid use, is if the person also uses tylonel for muscle soreness. Tylonel normally raises liver enzymes higher that most orals.