Check out this study Serious!

[Keepitreel]

Anabolic steroid abuse adversely affects the endocrine system, blood lipids, and the liver, but renal injury has not been described. We identified an association of focal segmental glomerulosclerosis (FSGS) and proteinuria in a cohort of 10 bodybuilders (six white and four Hispanic; mean body mass index 34.7) after long-term abuse of anabolic steroids. The clinical presentation included proteinuria (mean 10.1 g/d; range 1.3 to 26.3 g/d) and renal insufficiency (mean serum creatinine 3.0 mg/dl; range 1.3 to 7.8 mg/dl); three (30%) patients presented with nephrotic syndrome. Renal biopsy revealed FSGS in nine patients, four of whom also had glomerulomegaly, and glomerulomegaly alone in one patient. Three biopsies revealed collapsing lesions of FSGS, four had perihilar lesions, and seven showed ≥40% tubular atrophy and interstitial fibrosis. Among eight patients with mean follow-up of 2.2 yr, one progressed to ESRD, the other seven received renin-angiotensin system blockade, and one also received corticosteroids. All seven patients discontinued anabolic steroids, leading to weight loss, stabilization or improvement in serum creatinine, and a reduction in proteinuria. One patient resumed anabolic steroid abuse and suffered relapse of proteinuria and renal insufficiency. We hypothesize that secondary FSGS results from a combination of postadaptive glomerular changes driven by increased lean body mass and potential direct nephrotoxic effects of anabolic steroids. Because of the expected rise in serum creatinine as a result of increased muscle mass in bodybuilders, this complication is likely underrecognized

 

[Keepitreel]

The index case (patient 1) is a 30-yr-old white male professional bodybuilder who had no significant medical history and presented to a local hospital with lower extremity edema. The patient was on no prescription medications, but as part of his bodybuilding regimen, he regularly consumed a high-protein diet (>550 g/d) and dietary supplements including 10 g/d creatine monohydrate, 1000 mg/d branched-chain amino acids, 10 g/d glutamine, and multivitamins. For more than a decade, he regularly used anabolic androgenic steroids (AASs), including injectable testosterone, methyl-1-testosterone (taken orally), growth hormone, and insulin to augment his bodybuilding. At the time of biopsy, his steroid regimen consisted of growth hormone 4 IU 5 d/wk and testosterone 500 mg intramuscularly twice weekly. In addition, he took 75 mg of ephedrine and 600 mg of caffeine before each workout session.
Physical examination revealed a height of 71 inches (180 cm), a weight of 295 pounds (134 kg), and a body mass index (BMI) of 41.2 kg/m[SUP]2[/SUP] with an extremely muscular, highly toned physique. BP was 145/80 mmHg, and there was 2+ bilateral lower extremity edema. The patient was found to have a serum creatinine of 2.7 mg/dl, blood urea nitrogen of 24 mg/dl, serum albumin of 1.9 g/dl, total serum protein of 5.7 g/dl, serum cholesterol of 212 mg/dl, hematocrit of 45%, and white blood cell count of 10.3 × 10[SUP]9[/SUP]/L with a normal differential and platelet count of 254 × 10[SUP]9[/SUP]/L. Serum glucose and electrolytes including sodium, potassium, bicarbonate, chloride, and calcium were within normal limits. Serologic evaluation revealed a borderline positive ANA (titer 1:80 with a homogeneous pattern) with negative anti–double-stranded DNA antibody and negative viral serologies including HIV, hepatitis B surface and core antigens, and hepatitis C antibody. Serum complement levels including C3, C4, and CH50 were within normal limits. Urinalysis revealed 4+ protein, and microscopic examination showed fewer than five red blood cells per high-power field and no white blood cells or casts. Twenty-four-hour urine collection revealed proteinuria of 26.3 g/d and creatinine clearance (CrCl) of 91 ml/min. A renal biopsy was performed in August 2004 to determine the cause of the patient's nephrotic syndrome.

 

[rayjay]

Cliff notes??

 

[yoshi5674]

Can this be dumbed down some plz? My brain is oozing lol.

 

[Gerbil]

Basically their kidneys are in a bad way and their blood pressure is skewed. Atleast thats what I got from a quick read through.

 

[figdaddy]

Good post. It's a bit incomplete as they can never know what was caused by orals, Gh, slin, or other injectables. Good to know about kidney function tho. I would never mess w slin or Gh personally for those reasons. If people could Access data base studies free of charge I don't think anyone but those getting at least 7 figure salaries would use slin.

 

[Keepitreel]

I doubt it was the slin or gh most likely has to do with high protein diets and no high of a BMI for the body to handle also i feel the anabolics have a high impact on this kidney failures

 

[Gerbil]

I doubt it was the slin or gh most likely has to do with high protein diets and no high of a BMI for the body to handle also i feel the anabolics have a high impact on this kidney failures

Probably also the long term effects of creatine added in.

 

[Keepitreel]

this makes me wonder if there is a way to predict a "safe" BMI your body can handle like how much longer will guys like jay or ronnie live ive heard rumors saying ronnie is on dialysis from 700 g of prtoen a day

 

[tnubs]

this makes me wonder if there is a way to predict a "safe" BMI your body can handle like how much longer will guys like jay or ronnie live ive heard rumors saying ronnie is on dialysis from 700 g of prtoen a day

whatever you can get to naturally is probably a safe level. nobody needs those extreme level of protein. its one thing to give your life for bodybuilding and another to just look good naked to get girls. if you pick the first option, its an inherent risk that the BBer lifestyle will decrease your lifespan. it takes only a few months to start noticing ulceration on your heart from using steroids. theres no way you can lie to yourself and use it long term thinking its healthy.

 

[Keepitreel]

whatever you can get to naturally is probably a safe level. nobody needs those extreme level of protein. its one thing to give your life for bodybuilding and another to just look good naked to get girls. if you pick the first option, its an inherent risk that the BBer lifestyle will decrease your lifespan. it takes only a few months to start noticing ulceration on your heart from using steroids. theres no way you can lie to yourself and use it long term thinking its healthy.

can you show me a study with the ulceration to the heart issue

 

[tnubs]

can you show me a study with the ulceration to the heart issue

Cardiac Lesions Induced by Testosterone: Protective Effects of Dexrazoxane and Trimetazidine, Dalila Dalila Belhani,Cardiovascular Toxicology Published online: 12 May 2009


Abstract Further to our previous observation of post-mortem cardiac lesions after sudden death in several athletes with a history of anabolic steroid abuse, this study was intended to reproduce these lesions in rabbits administered testosterone oenanthate, a prototypic anabolic steroid abused by athletes, and to provide evidence for the protective effects of trimetazidine and dexrazoxane that are used as antianginal and cardioprotective drugs, respectively. Groups of six rabbits each were administered saline, testosterone, or a combination of testosterone and either trimetazidine or dexrazoxane for 3 months. Histologic cardiac lesions including necrosis, misshapen cell nuclei, interstitial and endocardial fibrosis, lymphocytic infiltrates, and vascular dystrophies were observed in testosterone-treated rabbits. In contrast, no significant lesions were observed in the animals treated withtestosterone combined with either trimetazidine or dexrazoxane. This is the first study providing evidence for testosterone cardiotoxicity following sub-chronic exposure in laboratory animals. In addition, these results suggest the protective role of trimetazidine and dexrazoxane.

Introduction

Not infrequently athletes tend to abuse anabolic steroids derived from testosterone, and a number of sudden cardiac deaths have been reported in relation to this abuse [1–4]. Indeed, sudden deaths may be 4–6 fold more frequent in athletes with a history of anabolic steroid abuse [5, 6]. Overall, the incidence of sudden deaths has been estimated to be 2–3/100,000/year in athletes versus 0.08/100,000/year in the general population [7, 8].

In a recent study conducted with Lyon Institute of Forensic Medicine, we observed various cardiac lesions during the post-mortem examination of several athletes with a history of anabolic steroid abuse [9]. Concomitantly, we evidenced focalized as well as disseminated cardiac lesions in rabbits treated with norethandrolone, a potent anabolic steroid. These lesions were reminiscent of those observed in toxic myocarditis, e.g., myocarditis due to anthracyclines. They mostly consisted of myolysis, fibrosis, disorganized myocardial fibers, and misshapen cell nuclei, and were characterized by the presence of lymphocytic infiltrates. Moreover, arteriolar lesions suggested the possible involvement of myocardial ischemia.

The present study was undertaken to demonstrate whether the sub-chronic administration of testosterone to rabbits could induce similar cardiac lesions as testosteronecardiotoxicity has seldom been investigated in laboratory animals. In addition, the possible protective effects of trimetazidine, which exerts anti-ischemic and anti-anginal effects [10], and of dexrazoxane, which is used to prevent the cardiotoxicity of anthracycline derivatives in human cancer patients [11], were investigated in rabbits concomitantly treated with testosterone.
</br>
Materials and Methods

...

Treatment

The rabbits were randomly assigned to four groups of six animals each. All subsequent treatments were administered by the intraperitoneal route. Group I (control) animals were given saline once a day using the same volume as in treated animals. Group II animals were given 8 mg/kg of testosterone (Bayer Santé, Puteaux, France) once a month for 3 months and saline daily on the other days. Group III animals were given 8 mg/kg of testosterone once a month plus 5 mg/kg of trimetazidine (Servier laboratories, Courbevoie, France) daily for 3 months. Group IV animals were given 8 mg/kg of testosterone once a month plus 60 mg/kg of dexrazoxane (Novartis Pharma, Rueil-Malmaison, France) once a week, and saline daily on the other days for 3 months.

Discussion

In this study, the administration of testosterone was found to induce various histologic cardiac lesions in rabbits including misshapen cell nuclei, necrosis, interstitial, and endocardial fibrosis. Similar lesions of the myocardium have been previously reported in athletes with a history of anabolic steroid abuse [3, 6, 12]. We also observed dysplasia of the precapillary arterioles, which can cause ischemia leading to morphologic changes including contraction bands, acidophilia, and undulation of myocardial fibers. At a later stage, liquefaction necrosis is a common finding. Finally, we found that testosterone can induce acute inflammatory lesions of cardiomyocytes as previously reported [13–15]. Testosterone has been reported to exert pro-inflammatory effects with the release of TNF-a and IL-1ß, and this in turn resulted in apoptosis of cardiac cells [16]. Interestingly, as compared to non-castrated males, castrated rats had lesser cytokine release and reduced apoptotic response measured from caspase-1, caspase-3, and caspase-11 activation, and Bcl-2 expression. That no evidence of apoptosis was found in the present study may be explained by the sensitivity of the method used, or more probably by the conditions of exposure, i.e., sub-chronic versus acute.

No cardiac hypertrophy was observed in animals treated with testosterone alone in this study. This may be due to the rather short duration of treatment (3 months) as the development of cardiac hypertrophy in athletes has been suggested to require chronic testosterone exposure [17]. Following prolonged exposure, testosterone can induce hypertrophic cardiac lesions [2, 6] leading to sudden death via a reduction of ventricular compliance [2] and/or the induction of disorders of diastolic relaxation [18]. The sudden death of a 32-year-old transsexual woman treated with intramuscular testosterone 125 mg/kg once or twice monthly for 2 years has been reported [19]. Her post-mortem examination revealed hypertrophic cardiopathy and atheromatous plaques on the left and right coronary arteries that resulted in over 90% coronary stenosis in the proximal end of the anterior interventricular artery.

In contrast to testosterone alone, the combination of testosterone with trimetazidine was not associated with the development of any consistent cardiac lesions in rabbits after 3 months of treatment. Although the mechanism of the cardioprotection achieved by trimetazidine in this study is not clearly elucidated, several mechanisms can be proposed. Trimetazidine can decrease intracellular acidosis and alterations in transmembrane ion movements caused by ischemia, and thus reduce the migration and infiltration of neutrophils and lymphocytes to the cardiac tissue during ischemia/reperfusion [20]. Thus, trimetazidine could reduce the release of pro-inflammatory cytokines induced by testosterone. Second, trimetazidine exerts protective effects during ischemia in inhibiting the opening of mitochondrial permeability transition pores during ischemia/reperfusion [21]. Kajstura et al. [22] showed that the extent of cardiac lesions, such as myocardial necrosis and apoptosis during myocardial ischemia is significantly reduced by trimetazidine. Thirdly, Ruixing et al. [23] found that capase-3 activation and mitochondrial cytochrome C release were decreased in rabbits treated with trimetazidine as compared to untreated animals. In addition, the apoptotic index was negatively correlated to serum superoxide dismutase activity, and positively correlated to malondialdehyde levels, which suggests that trimetazidine could prevent myocardial lesions during ischemia-reperfusion. Based on these data, it is suggested that the anti-apoptotic effects of trimetazidine could inhibit apoptosis induction by testosterone, and thus prevent the development of cardiac lesions in rabbits treated with testosterone alone.

Similarly to rabbits treated with trimetazidine, rabbits treated with dexrazoxane did not develop any consistent cardiac lesions despite concomitant testosterone exposure. Dexrazoxane plays an important role in the cardioprotection of patients treated with anthracycline derivatives [11, 24]. It is indeed well recognized that these derivatives can induce various histological lesions of the heart, such as myocardial necrosis, cellular infiltrates, myofibrillar loss, and cytoplasmic vacuolization. The mechanism of this protective effect of dexrazoxane is not fully understood. It is at least in part related to the prevention of apoptotic and necrotic lesions involving the reduced formation of Fe3+-anthracycline complexes that generate the production of free radicals that induce alterations of mitochondria [25]. Therefore, the cardioprotection evidenced during the present study following treatment with either trimetazidine or dexrazoxane in testosterone-treated rabbits could result from similar mechanisms involving decreased mitochondrial alterations.

In conclusion, this study provides confirmative evidence that anabolic steroids, and in particular testosterone, induce cardiotoxic effects resulting in heart lesions similar to those seen in toxic myocarditis. The lack of cardiac lesions in testosterone-treated rabbits when given trimetazidine or dexrazoxane concomitantly suggests that either drug can have a cardioprotective effect, which warrants further investigation.

 

[JD261985]

Obviously steroids aren't healthy. Bodybuilding is the most unhealthy sport by far.

 

[Gerbil]

Obviously steroids aren't healthy. Bodybuilding is the most unhealthy sport by far.

I would go with wrestling as the most unhealthy but for different reasons.

 

[AwhYeah]

Well this is discouraging...I just want my 18inch arms, 405lbs 1RM bench, 495lbs squat and a 600lbs 1RM deadlift...then I'm doing cycling (famous last words)

 

[Gerbil]

Well this is discouraging...I just want my 18inch arms, 405lbs 1RM bench, 495lbs squat and a 600lbs 1RM deadlift...then I'm doing cycling (famous last words)

I like how the only part of that which is truly difficult is the arms, atleast in my eyes at least. I will hit all of those things before I get the 18 inch arms.

 

[AwhYeah]

I like how the only part of that which is truly difficult is the arms, atleast in my eyes at least. I will hit all of those things before I get the 18 inch arms.

Really? Damnit. Well I guess I need to keep going then re-evaluate. I'm hoping either steroids get less toxic or medicine advances enough that I don't need to worry about it. *donating to research*

 

[Gerbil]

Really? Damnit. Well I guess I need to keep going then re-evaluate. I'm hoping either steroids get less toxic or medicine advances enough that I don't need to worry about it. *donating to research*

Follow a strength program and most of those are doable, either natural or close to natural.

 

[AwhYeah]

Follow a strength program and most of those are doable, either natural or close to natural.

Can you achieve strength and hypertrophy with the same routine? I've heard it's all nutrition, really, in respect to growth.

I've been doing pyramids 10, 8, 6, 4 or 12, 10, 8, 6. I want to try and hit all the rep ranges. I'll look into some strength routines too. I've read good things about PHAT and 5x5

 

[Gerbil]

Can you achieve strength and hypertrophy with the same routine? I've heard it's all nutrition, really, in respect to growth.

I've been doing pyramids 10, 8, 6, 4 or 12, 10, 8, 6. I want to try and hit all the rep ranges. I'll look into some strength routines too. I've read good things about PHAT and 5x5

PM me so we can stop thread jacking

 

[heavylifter33]

Did i seriously see mention of "high protein diet" and "creatine" being issues...? Wut lol?

 

[Gerbil]

Did i seriously see mention of "high protein diet" and "creatine" being issues...? Wut lol?

Too much of anything can kill you.

 

[Keepitreel]

Can you achieve strength and hypertrophy with the same routine? I've heard it's all nutrition, really, in respect to growth.

I've been doing pyramids 10, 8, 6, 4 or 12, 10, 8, 6. I want to try and hit all the rep ranges. I'll look into some strength routines too. I've read good things about PHAT and 5x5

you could stimulate hypertrophy and all that but nothing increases protein synthesis like some anabolics

 

[heavylifter33]

Too much of anything can kill you.

Sure, but you can't mention AAS abuse, and then talk about creatine and protein intake. C'mon lol....

 

[Gerbil]

Sure, but you can't mention AAS abuse, and then talk about creatine and protein intake. C'mon lol....

True but it is rather hard to find articles that only have on extraneous factor on steroid abuse. It comes with many other factors.

 

[heavylifter33]

True but it is rather hard to find articles that only have on extraneous factor on steroid abuse. It comes with many other factors.

Completely agree, however i doubt the severity of creatine and protein use. Especially protein. Heck, creatine has been around for a long time and we have plenty of empirical data proving its safety.

 

[Keepitreel]

The main issue is that protein was found in they urine which means its not being reabsorbed into the body like its supposed to, This could be from two things: 1) creatine which some people say damages kidney function ( i doubt this is causing it). 2) could be the fact that a high protein diet pared with the body synthesizing all of them at a higher speed (do to AAS) is causing stress on the kidneys and the protein cant be reabosorbed into a normal size glomerolus so the golomerolus has to increase size which into turn makes it collapse and die

 

[heavylifter33]

The main issue is that protein was found in they urine which means its not being reabsorbed into the body like its supposed to, This could be from two things: 1) creatine which some people say damages kidney function ( i doubt this is causing it). 2) could be the fact that a high protein diet pared with the body synthesizing all of them at a higher speed (do to AAS) is causing stress on the kidneys and the protein cant be reabosorbed into a normal size glomerolus so the golomerolus has to increase size which into turn makes it collapse and die

Well, with AAS elevating protein absorption above baseline, and the body being able to absorb plenty of protein naturally to begin with... that adds up to kidney damage from orals (to me at least). Protein isn't the issue, it's the AAS abuse.

 

[Keepitreel]

Well, with AAS elevating protein absorption above baseline, and the body being able to absorb plenty of protein naturally to begin with... that adds up to kidney damage from orals (to me at least). Protein isn't the issue, it's the AAS abuse.

Thats what im trying to say its not a protein issue but rather a drug issue

 

[heavylifter33]

I doubt it was the slin or gh most likely has to do with high protein diets and no high of a BMI for the body to handle also i feel the anabolics have a high impact on this kidney failures

Thats what im trying to say its not a protein issue but rather a drug issue

^^ But yes, we are somewhat in agreement.

 

[tnubs]

I dont think excess protein will mess up healthy kidneys, but im pretty sure excess protein combined with damaged kidneys is a no no... or at least thats what dieticians are taught in school.

 

[Keepitreel]

^^ But yes, we are somewhat in agreement.

I dont consider HGH and slin steroid hormones they are anabolic but different