Steroids and Bodybuilding article in New York Times

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The New York Times highlights anabolic steroid use in pro bodybuilding today in an article that cites IFBB pro bodybuilders Flex Wheeler, King Kamali, and Bob Cicherillo; Iron Man Magazine's Jerry Brainum and mentions IFBB Pro Chariman Jim Manion and Chairman of IFBB medical commission Bob Goldman.

The study began 10 years ago when a kidney pathologist at Columbia University Medical Center in New York noticed that a bodybuilder had an advanced form of kidney disease. Curious, she started looking for similar cases and eventually studied 10 men with serious kidney damage who acknowledged using steroids. Nine were bodybuilders and one was a competitive powerlifter with a similar training routine.

All 10 men in the case series, published in November by the Journal of the American Society of Nephrology, showed damage to the filters of the kidney. Nine had an irreversible disease known as focal segmental glomerulosclerosis — the same disease contracted by Wheeler — even though the men in the study did not have other apparent risk factors. Their disease was worse than in obese patients with a higher body-mass index, suggesting that steroids — combined with the other practices — might be harming the kidneys.

http://www.nytimes.com/2009/12/10/sports/10steroids.html
 
The New York Times will certainly be denied press credentials next year for IFBB pro bodybuilding contests!
 
Note that this study was published as an abstract and presented at a conference. These data and conclusions should be considered preliminary until published in a peer-reviewed journal.

I'll be very interested to see if they publish what these 10 people were taking and the doses they were using

Medical News: ASN: Anabolic Steroid Abuse May Damage Kidneys - in Meeting Coverage, ASN from MedPage Today


She speculated that the damage results from a combination of the glomeruli being overworked because of the increased lean body mass and also, "a direct toxic effect of these androgens and these anabolic steroids on the glomeruli."

That combination likely explains the unusual severity of the disease in these bodybuilders, she said. A high-protein diet and exercise-induced hypertension were also likely contributors.
 
The authors of the article cited in the NYT piece have also published similar findings in the obese and nonobese with an increased muscle mass (abstracts below). While not discounting the possible role of AAS in the kidney pathology, I caution that often and without good evidence AAS are quickly grabbed on as the culprits for many pathologies only to later determine not to be the cause.

I will go and download the full article following and report back later. On first review, I am little impressed by the authors' attribution of AAS to the pathology. Admittedly, being a cynic I am more likely to take the position that the authors are looking for research dollars and the use of AAS as causation will help bring monies. Regardless, I hope that true independent third-party research confirms or refutes this hypothesis. One must be very careful though since others might grasp on this for their own research dollars (i.e., AAS addiction/dependency).


Herlitz LC, Markowitz GS, Farris AB, et al. Development of Focal Segmental Glomerulosclerosis after Anabolic Steroid Abuse. J Am Soc Nephrol 2009. Development of Focal Segmental Glomerulosclerosis after Anabolic Steroid Abuse

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.


Schwimmer JA, Markowitz GS, Valeri AM, Imbriano LJ, Alvis R, D'Agati VD. Secondary focal segmental glomerulosclerosis in non-obese patients with increased muscle mass. Clin Nephrol 2003;60(4):233-41.

BACKGROUND: Secondary focal segmental glomerulosclerosis (FSGS) is a pattern of glomerular injury mediated by hyperfiltration and other adaptive structural-functional responses. We describe 3 non-obese patients with elevated body mass index (BMI) owing to increased muscle mass who had renal biopsy findings favoring a form of secondary FSGS. METHODS: Clinical and pathologic data were obtained on 3 patients with 1) renal biopsy findings of focal segmental and/or global glomerulosclerosis with glomerulomegaly; 2) BMI > or = 30; 3) body fat percentage < 20%; 4) "highly muscular" appearance, and 5) proteinuria > or = 1 g/d without nephrotic syndrome. 24-hour urine creatinine excretion was used to estimate lean body mass and percentage body fat. RESULTS: The 3 patients were males (age 38 - 48 years) employed in jobs requiring strenuous physical activity. BMIs ranged from 30.4 - 32.1 kg/m2 with body fat percentages of 12.9 - 16.8%. Creatinine clearances at time of biopsy ranged from 113 - 208 ml/min. Renal biopsies showed focal segmental and/or global glomerulosclerosis affecting a minority of glomeruli with glomerular hypertrophy and minimal (mean 15%) foot process effacement. Treatments included angiotensin-converting enzyme inhibitor, angiotensin II receptor blocker, or weight loss. Over a mean follow-up time of 24.3 months, serum creatinine remained stable and proteinuria decreased in all patients. CONCLUSIONS: Non-obese patients with increased BMI due to elevated muscle mass are at risk of developing a secondary form of FSGS that resembles obesity-related glomerulopathy.


Kambham N, Markowitz GS, Valeri AM, Lin J, D'Agati VD. Obesity-related glomerulopathy: an emerging epidemic. Kidney Int 2001;59(4):1498-509.

BACKGROUND: We report the first large renal biopsy-based clinicopathologic study on obesity-related glomerulopathy. METHODS: Obesity was defined as body mass index (BMI)> 30 kg/m2. Obesity-related glomerulopathy (ORG) was defined morphologically as focal segmental glomerulosclerosis and glomerulomegaly (O-FSGS; N = 57) or glomerulomegaly alone (O-GM; N = 14). RESULTS: Review of 6818 native renal biopsies received from 1986 to 2000 revealed a progressive increase in biopsy incidence of ORG from 0.2% in 1986-1990 to 2.0% in 1996-2000 (P = 0.0001). Mean BMI in ORG was 41.7 (range 30.9 to 62.7). Indications for renal biopsy included proteinuria (N = 40) or proteinuria and renal insufficiency (N = 31). Seventy-one patients with ORG were compared to 50 patients with idiopathic FSGS (I-FSGS). Patients with ORG were older (mean 42.9 vs. 32.6 years, P < 0.001) and more often Caucasian (75% vs. 52%; P = 0.003). ORG patients had a lower incidence of nephrotic range proteinuria (48% vs. 66%; P = 0.007) and nephrotic syndrome (5.6% vs. 54%; P < 0.001), with higher serum albumin (3.9 vs. 2.9 g/dL; P < 0.001), lower serum cholesterol (229 vs. 335 mg/dL; P < 0.001), and less edema (35% vs. 68%; P = 0.003). On renal biopsy, patients with ORG had fewer lesions of segmental sclerosis (10 vs. 39%; P < 0.001), more glomerulomegaly (100% vs. 10%; P < 0.001), and less extensive foot process effacement (40 vs. 75%; P < 0.001). Glomerular diameter in ORG (mean 226 mu) was significantly larger than age- and sex-matched normal controls (mean 168 mu; P < 0.001). Follow-up was available in 56 ORG patients (mean 27 months) and 50 idiopathic FSGS controls (mean 38 months). A total of 75% of ORG patients received angiotensin-converting enzyme (ACE) inhibition or A2 blockade while 78% of the I-FSGS patients received immunosuppressive therapy. ORG patients had less frequent doubling of serum creatinine (14.3% vs. 50%; P < 0.001) and progression to ESRD (3.6% vs. 42%; P < 0.001). On multivariate analysis, presenting serum creatinine and severity of proteinuria were the only predictors of poor outcome in ORG. CONCLUSION: ORG is distinct from idiopathic FSGS, with a lower incidence of nephrotic syndrome, more indolent course, consistent presence of glomerulomegaly, and milder foot process fusion. The ten-fold increase in incidence over 15 years suggests a newly emerging epidemic. Heightened physician awareness of this entity is needed to ensure accurate diagnosis and appropriate therapy.
 
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the link didnt work, so i'm reprinting it here with obvious copyright attribution:

December 10, 2009

Bodybuilders See Kidney Damage With Steroids
By KATIE THOMAS


Many competitive bodybuilders take anabolic steroids to achieve their freakishly exaggerated physiques. That is no secret. But steroids can be only one part of an extreme regimen that can wreak havoc on the body.

Human growth hormone, supplements, painkillers and diuretics can also be used to create the ?shrink-wrapped? muscles so prized in the aesthetic. And the high concentration of muscle mass puts stress on the body, as if the lifter were obese.

Lifting weights in the gym is ?extremely healthy for you,? said Kenneth Wheeler, a former elite bodybuilder known as Flex. ?But if you want to be a bodybuilder and compete at the highest level, it has nothing to do with health.? A relatively rare form of kidney disease forced Wheeler to retire in 2003 at age 37, and he needed a kidney transplant later that year.

Determining the extent of the damage that bodybuilders inflict on themselves is difficult, in part because there is little interest in financing studies on such an extreme group, and because bodybuilders are not always honest about what they take. That is why a case study published last month by a top kidney journal is generating interest in the nephrology and bodybuilding communities. It is among the first to assert a direct link between long-term steroid use and kidney disease.

The study began 10 years ago when a kidney pathologist at Columbia University Medical Center in New York noticed that a bodybuilder had an advanced form of kidney disease. Curious, she started looking for similar cases and eventually studied 10 men with serious kidney damage who acknowledged using steroids. Nine were bodybuilders and one was a competitive powerlifter with a similar training routine.

All 10 men in the case series, published in November by the Journal of the American Society of Nephrology, showed damage to the filters of the kidney. Nine had an irreversible disease known as focal segmental glomerulosclerosis ? the same disease contracted by Wheeler ? even though the men in the study did not have other apparent risk factors. Their disease was worse than in obese patients with a higher body-mass index, suggesting that steroids ? combined with the other practices ? might be harming the kidneys.

Among the study?s most persuasive details is the story of a man, 30 years old at the time, who damaged his kidneys after more than a decade of bodybuilding. The patient?s condition improved after he stopped using the drugs, discontinued his regimen and lost 80 pounds. But it worsened after the man, who became depressed, returned to bodybuilding and steroids.

?These patients are likely the tip of the iceberg,? said Vivette D. D?Agati, the lead researcher. ?It?s a risk. A significant risk.?

Several experts not affiliated with the study said that while the claims were intriguing, the study?s value was limited because it focused only on intensive steroid users and because the bodybuilders? layered training practices had to be taken into account. ?I think it?s hard to be certain what?s causing their kidney disease,? said William Bremner, chairman of the Department of Medicine at the University of Washington and an endocrinologist who studies steroids.

D?Agati said, ?It?s probably multiple factors that are converging in these patients, but the common entity in all of them is anabolic steroids.?

One participant in the study, Patrick Antonecchia, 46, competed in powerlifting and strong man events for more than 25 years and said he used steroids, supplements and a high-protein diet to attain feats such as pulling a 40,000-pound truck. He ended his career and stopped using steroids about a year ago, and in February received a diagnosis of serious kidney damage. His doctors warned him not to use the drugs again. ?They said: ?Pat. Don?t. Because it comes back,? ? he said.

Antonecchia has lost about 50 pounds and said he misses the attention his 290-pound frame attracted: ?The toughest thing now is it was my identity for 25 years. Now, when people see me, they say, ?What happened to you?? ?

Jerry Brainum writes a column for Iron Man Magazine called Bodybuilding Pharmacology and said he welcomes more research on the subject. ?I found it very alarming, quite frankly,? Brainum said.

Since the 1990s, at least eight accomplished bodybuilders have died at a young age, and in addition to Wheeler, another six were forced to stop competing because of serious illness, often involving kidney disease.

The main source of information for bodybuilders is word of mouth and experimentation, Brainum said. ?These guys have no guidance, they talk among themselves, and they don?t even tell the truth to each other,? he said.

The risk-taking has been made worse by a trend toward ever larger physiques among the sport?s top competitors, some said. Jay Cutler, who won the 2009 Mr. Olympia contest, weighs almost 40 pounds more than Arnold Schwarzenegger did when he won the title in 1974, even though Cutler is five inches shorter.

?Each decade you have a guy that comes along that sets new standards and you say O.K., now I?m going to have to take it to the next level,? said Shahriar Kamali, a professional bodybuilder known as King.

The International Federation of Body Building and Fitness reserves the right to test for steroids and human growth hormone at the professional level, and testing is done on a random basis, said Bob Cicherillo, athlete representative for the federation, which is the main governing body for bodybuilding.

But several bodybuilders said the testing was nearly nonexistent, and Cicherillo said he could not provide specific figures on competitors who tested positive. In addition, the chairman of the organization?s medical commission, Robert M. Goldman, is a leading champion of the anti-aging effects of human growth hormone, a drug that is banned by most sports governing bodies.

James Manion, who runs the professional division of the federation, did not return several calls seeking comment.

Some bodybuilders expressed doubt that their practices were dangerous, pointing to former competitors who are still healthy in their 70s. They attributed the deaths of elite bodybuilders to the abuse of over-the-counter painkillers and diuretics, not steroids. The bodybuilding federation tests for diuretics at professional events, although competitors said they are still used.

Bodybuilders said that they were unfairly singled out as drug abusers when athletes in most other sports were also using performance-enhancing drugs. ?Like anything else, it?s use and abuse,? Cicherillo said. ?We?re the ones who are visual. We?re the ones who walk around, and you see us with the big muscles.?

Wheeler said he was convinced steroid use did not cause his kidney disease, although it might have made it worse.

The patient whose case was the centerpiece of the kidney study said he was most likely predisposed to develop the condition. ?The drugs weren?t the reason I got sick,? said the man, who declined to be identified because his steroid use was illegal. After taking a year off from steroids and bodybuilding because of the kidney disease, the man, age 34, is returning to competition. His symptoms have worsened, a sacrifice he said he is willing to accept.

?It?s just really hard to walk away from it,? he said. ?I know I can only do this until my early 40s, so I really want to give it my all now.?

Copyright 2009 The New York Times Company
 
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You also have to take into account the absurdly high amounts of calories and protein that a professional bb will injest on a daily basis - that may be a contributing cause to the kidney problems noted in the article

However - there is this

Dtsch Med Wochenschr. 1999 Sep 10;124(36):1029-32.

[Severe cholestasis with kidney failure from anabolic steroids in a body builder]
[Article in German]

Habscheid W, Abele U, Dahm HH.

Medizinische Klinik, Paracelsus-Krankenhaus Ruit, Esslingen.

HISTORY AND ADMISSION FINDINGS: A 28-year-old body builder was admitted because of jaundice. For 80 days, until 3 weeks before hospitalization, he had been taking moderately high doses of anabolic steroids: metandienone (methandienone), 10-50 mg daily by mouth, and stanozolol, 50 mg intramuscularly every other day. Physical examination was unremarkable except for yellow discoloration of the skin and sclerae. INVESTIGATIONS: Bilirubin concentration was raised to 4.5 mg/dl, cholestasis enzymes were normal, while transaminase activities were raised. Liver biopsy was compatible with cholestasis induced by anabolic steroids. TREATMENT AND COURSE: Although the steroids had been discontinued, the patient's general condition deteriorated over 7 weeks. Serum bilirubin rose up to a maximum of 77.9 mg/dl. In addition renal failure developed with a creatinine concentration of 4.2 mg/dl. The patient's state improved simultaneously with the administration of ursodeoxycholic acid and the biochemical values gradually reached normal levels after several weeks. CONCLUSION: Anabolic steroids can cause severe cholestasis and acute renal failure. In this case there was a notable temporal coincidence between the administration of ursodeoxycholic acid and the marked clinical improvement.

PMID: 10506840 [PubMed - indexed for MEDLINE]


Also - look at the amount of steoids used by pro bb's - that could be a factor - are all steroids taken excreted by the body?

MLB Baseball Player Steroid Cycles Relatively Safe Compared to Pro Bodybuilders
 
I agree with Dr Scally. More than one factor is involved, but for reasons having -- in my opinion -- to do with the muscle-hating psychology of many individuals, these findings may be considered by them to be a useful weapon against anabolic steroids.

It is actually a reasonable argument that supraphysiological androgen levels may aggravate glomerulosclerosis where it is already developing, or perhaps be "the last straw" if other factors contribute. Or perhaps even with some forms of use being sufficient as a sole factor. There is considerable evidence that testosterone, even at physiological levels, can be an aggravating factor.

However, whether this is due to anything but hypertension, I don't know.

Certainly hypertension is strongly linked to this disease state, and is prevalent among those with high BMI, whether from extreme muscle mass or from obesity. Androgens also can raise blood pressure, but of course the individual can monitor this and so by no means is this an inevitable side effect.

I have never had anyone I consulted with on steroid use -- which is certainly more than a thousand individuals -- come back and report to me that they suffered kidney problems from following my advice, whether at the time or years later. It certainly is not an inevitable outcome when reasonable care is taken.

As an example reference on the link between hypertension and glomerulosclerosis, which could well be the best explanation for the reported result or a possibly-necessary factor (first part of the abstract only):


Med Clin North Am. 2009 May;93(3):733-51.
Obesity and hypertension: mechanisms, cardio-renal consequences, and therapeutic approaches.
Reisin E, Jack AV.

The increasing prevalence of obesity in the industrialized world is causing an alarming epidemic. Almost 70% of American adults are overweight or obese. The link between increasing body weight and hypertension is well established. Obesity hypertension through metabolic, endocrinic, and systemic hemodynamic alteration causes structural vascular and cardiac adaptations that trigger concentric, eccentric left ventricular hypertrophy and electrophysiological changes, which may increase the risk for congestive heart failure and sudden cardiac death as a result of arrhythmias. The increased renal blood flow in conjunction with a decreased renal vascular resistance causes renal hyperperfusion and hyperfiltration. Such changes lead to glomerulomegaly, focal segmental glomerulosclerosis, tubulointerstitial inflammation, and fibrosis that characterize the renal damage in obese hypertensive subjects.
 

yea but i recall Steve Michalik's Village Voice interview from years back, suggesting that some UGL contaminants may not. i know he's gotten hysterical on the issue, but black market products can be very toxic by definition. Conversely, such contamination is a good argument for decriminalization and legalization...same with street drugs.

i liken it to many of the health effects of heroin injection actually coming from adulterants. black-market status is a way for government to was its hands of AAS users. When Great Britain was giving junkies government heroin, their health was better and their likelihood to commit crimes to support their habit was far lower.
 
You also have to take into account the absurdly high amounts of calories and protein that a professional bb will injest on a daily basis - that may be a contributing cause to the kidney problems noted in the article

However - there is this...

HISTORY AND ADMISSION FINDINGS: A 28-year-old body builder was admitted because of jaundice. For 80 days, until 3 weeks before hospitalization, he had been taking moderately high doses of anabolic steroids: metandienone (methandienone), 10-50 mg daily by mouth, and stanozolol, 50 mg intramuscularly every other day. Physical examination was unremarkable except for yellow discoloration of the skin and sclerae. INVESTIGATIONS: Bilirubin concentration was raised to 4.5 mg/dl, cholestasis enzymes were normal, while transaminase activities were raised. Liver biopsy was compatible with cholestasis induced by anabolic steroids. TREATMENT AND COURSE: Although the steroids had been discontinued, the patient's general condition deteriorated over 7 weeks. Serum bilirubin rose up to a maximum of 77.9 mg/dl. In addition renal failure developed with a creatinine concentration of 4.2 mg/dl. The patient's state improved simultaneously with the administration of ursodeoxycholic acid and the biochemical values gradually reached normal levels after several weeks. CONCLUSION: Anabolic steroids can cause severe cholestasis and acute renal failure. In this case there was a notable temporal coincidence between the administration of ursodeoxycholic acid and the marked clinical improvement.

11 weeks of running Winnie--even IM EOD--and Dbol is stupidity, plain and simple.

I'll readily concede that running TWO methylated compounds for DOUBLE the time that they should be run will cause liver and kidney problems.

I'll also say that some people have no business taking anything stronger than aspirin. This person is undoubtedly one of them.
 
I agree with Dr Scally. More than one factor is involved, but for reasons having -- in my opinion -- to do with the muscle-hating psychology of many individuals, these findings may be considered by them to be a useful weapon against anabolic steroids.

It is actually a reasonable argument that supraphysiological androgen levels may aggravate glomerulosclerosis where it is already developing, or perhaps be "the last straw" if other factors contribute. Or perhaps even with some forms of use being sufficient as a sole factor. There is considerable evidence that testosterone, even at physiological levels, can be an aggravating factor.

However, whether this is due to anything but hypertension, I don't know.

Certainly hypertension is strongly linked to this disease state, and is prevalent among those with high BMI, whether from extreme muscle mass or from obesity. Androgens also can raise blood pressure, but of course the individual can monitor this and so by no means is this an inevitable side effect.

I have never had anyone I consulted with on steroid use -- which is certainly more than a thousand individuals -- come back and report to me that they suffered kidney problems from following my advice, whether at the time or years later. It certainly is not an inevitable outcome when reasonable care is taken.

As an example reference on the link between hypertension and glomerulosclerosis, which could well be the best explanation for the reported result or a possibly-necessary factor (first part of the abstract only):


Med Clin North Am. 2009 May;93(3):733-51.
Obesity and hypertension: mechanisms, cardio-renal consequences, and therapeutic approaches.
Reisin E, Jack AV.

The increasing prevalence of obesity in the industrialized world is causing an alarming epidemic. Almost 70% of American adults are overweight or obese. The link between increasing body weight and hypertension is well established. Obesity hypertension through metabolic, endocrinic, and systemic hemodynamic alteration causes structural vascular and cardiac adaptations that trigger concentric, eccentric left ventricular hypertrophy and electrophysiological changes, which may increase the risk for congestive heart failure and sudden cardiac death as a result of arrhythmias. The increased renal blood flow in conjunction with a decreased renal vascular resistance causes renal hyperperfusion and hyperfiltration. Such changes lead to glomerulomegaly, focal segmental glomerulosclerosis, tubulointerstitial inflammation, and fibrosis that characterize the renal damage in obese hypertensive subjects.

Based on these 2 studies

http://content.nejm.org/cgi/reprint/335/1/1.pdf

Effects of Pharmacological Doses of Nandrolone Decanoate and Progressive Resistance Training in Immunodeficient Patients Infected with Human Immunodeficiency Virus -- Sattler et al. 84 (4): 1268 -- Journal of Clinical Endocrinology & Metabolism

would 600mgs Testosterone Enanthate and 200mgs Nandrolone Decanoate per wek be a relatively safe cycle with regard to blood lipids and would 8-10 weeks be long enough?
 
I agree with Dr Scally. More than one factor is involved, but for reasons having -- in my opinion -- to do with the muscle-hating psychology of many individuals, these findings may be considered by them to be a useful weapon against anabolic steroids.

It is actually a reasonable argument that supraphysiological androgen levels may aggravate glomerulosclerosis where it is already developing, or perhaps be "the last straw" if other factors contribute. Or perhaps even with some forms of use being sufficient as a sole factor. There is considerable evidence that testosterone, even at physiological levels, can be an aggravating factor.

However, whether this is due to anything but hypertension, I don't know.

Certainly hypertension is strongly linked to this disease state, and is prevalent among those with high BMI, whether from extreme muscle mass or from obesity. Androgens also can raise blood pressure, but of course the individual can monitor this and so by no means is this an inevitable side effect.

I have never had anyone I consulted with on steroid use -- which is certainly more than a thousand individuals -- come back and report to me that they suffered kidney problems from following my advice, whether at the time or years later. It certainly is not an inevitable outcome when reasonable care is taken.

As an example reference on the link between hypertension and glomerulosclerosis, which could well be the best explanation for the reported result or a possibly-necessary factor (first part of the abstract only):


Med Clin North Am. 2009 May;93(3):733-51.
Obesity and hypertension: mechanisms, cardio-renal consequences, and therapeutic approaches.
Reisin E, Jack AV.

The increasing prevalence of obesity in the industrialized world is causing an alarming epidemic. Almost 70% of American adults are overweight or obese. The link between increasing body weight and hypertension is well established. Obesity hypertension through metabolic, endocrinic, and systemic hemodynamic alteration causes structural vascular and cardiac adaptations that trigger concentric, eccentric left ventricular hypertrophy and electrophysiological changes, which may increase the risk for congestive heart failure and sudden cardiac death as a result of arrhythmias. The increased renal blood flow in conjunction with a decreased renal vascular resistance causes renal hyperperfusion and hyperfiltration. Such changes lead to glomerulomegaly, focal segmental glomerulosclerosis, tubulointerstitial inflammation, and fibrosis that characterize the renal damage in obese hypertensive subjects.

Based on these 2 studies

http://content.nejm.org/cgi/reprint/335/1/1.pdf

Effects of Pharmacological Doses of Nandrolone Decanoate and Progressive Resistance Training in Immunodeficient Patients Infected with Human Immunodeficiency Virus -- Sattler et al. 84 (4): 1268 -- Journal of Clinical Endocrinology & Metabolism

would a weekly cycle of 600 mg of Testosterone Enanthate and 200mgs of Nandrolone Decanoate be relatively safe with regard to blood lipids?

Also - would 10 weeks be long enough?
 
Not based on those studies, but practical experience, cycling on and off of a protocol such as that can be safe and ordinarily is.

An example of where it could be a health risk would be in a person who is driven into very high blood pressure with it. Or if it were observed that blood lipid profile was just awful while on-cycle, then it would be advisable to use such a protocol only rather few weeks per year. Being "on" for example half the time if personally having a large adverse effect on blood lipid profile might well add to health risk. It probably would, I would think, just as an opinion.

The studies you mentioned don't look at that combination. The testosterone study found little change in blood lipid profile; in the nandrolone study, they didn't bother measuring LDL and HDL separately for some reason, so not much can be said there on outcome.

it isn't unusual in practice thought for blood lipid profile to be worse during a steroid cycle.

10 weeks is certainly long enough for a cycle to be effective.

Comparisons should be as equal as possible. Rather than saying "Well a 14 week cycle will obviously do more than a 7 week cycle," which is kind of brain-dead, a better comparison is "I'm thinking of being 'on' half the weeks of the year and using this particular total amount of drugs per year. Which is going to do better for me: two 14 week cycles per year, or four 7 week cycles?"

The answer is the latter.

This is not to say that something such as a 12 week cycle never makes sense. For example, if there's a specific date to be met such as a contest, it makes sense to use the longer cycle timed to peak at that date.
 
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Not based on those studies, but practical experience, cycling on and off of a protocol such as that can be safe and ordinarily is.

An example of where it could be a health risk would be in a person who is driven into very high blood pressure with it. Or if it were observed that blood lipid profile was just awful while on-cycle, then it would be advisable to use such a protocol only rather few weeks per year. Being "on" for example half the time if personally having a large adverse effect on blood lipid profile might well add to health risk. It probably would, I would think, just as an opinion.

The studies you mentioned don't look at that combination. The testosterone study found little change in blood lipid profile; in the nandrolone study, they didn't bother measuring LDL and HDL separately for some reason, so not much can be said there on outcome.

it isn't unusual in practice thought for blood lipid profile to be worse during a steroid cycle.

10 weeks is certainly long enough for a cycle to be effective.

Comparisons should be as equal as possible. Rather than saying "Well a 14 week cycle will obviously do more than a 7 week cycle," which is kind of brain-dead, a better comparison is "I'm thinking of being 'on' half the weeks of the year and using this particular total amount of drugs per year. Which is going to do better for me: two 14 week cycles per year, or four 7 week cycles?"

The answer is the latter.

This is not to say that something such as a 12 week cycle never makes sense. For example, if there's a specific date to be met such as a contest, it makes sense to use the longer cycle timed to peak at that date.

Assume four 7 week cycles per year - how long would pct be run between cycles?
 
There's never a need to run it past the point where good testosterone production is restored. Depending on the individual and the cycle, this is typically but not always 2-4 weeks, assuming the PCT is started at the point where levels from injectables have fallen sufficiently to allow recovery to begin.
 
There's never a need to run it past the point where good testosterone production is restored. Depending on the individual and the cycle, this is typically but not always 2-4 weeks, assuming the PCT is started at the point where levels from injectables have fallen sufficiently to allow recovery to begin.

Look at this study

Effects of Pharmacological Doses of Nandrolone Decanoate and Progressive Resistance Training in Immunodeficient Patients Infected with Human Immunodeficiency Virus -- Sattler et al. 84 (4): 1268 -- Journal of Clinical Endocrinology & Metabolism

Subjects were randomized to nandrolone alone or nandrolone plus PRT. The study design did not include a no treatment or placebo control group. The first dose of nandrolone was 200 mg, and the second dose was 400 mg. The dose was 600 mg for weeks 312. This dose was based on discussions with a number of body builders and our goal to study a relatively "high end" dose (but not maximum) commonly used for large anabolic effects and expected to be well tolerated in 60- to 70-kg men. Doses were reduced gradually during weeks 1316 (400, 200, 100, and 50 mg, respectively) to withdraw patients from pharmacological doses.

Is tapering of the steroids up and down a good idea or not?
 
Not for bb'ing purposes.

It is more efficient to be at the most-desired level for gains versus side effects or cost considerations, or at a level allowing natural LH production, rather than spending needless time at intermediate levels that aren't much if any good for either gains or recovery.
 
OFF Topic Radio had show tonight featuring another bodybuilder with kidney problems: retired IFBB pro Luke Wood.

http://www.rxmuscle.com/radio/OT-12162009.mp3

I was reading through this old thread about steroids and kidney problems. It's well worth (re)reading.

I also wanted to follow up on Luke Wood. A couple years after he did this interview with OFF Topic Radio, he died of complications from a kidney transplant. This was last year - August 31, 2011.

http://www.dailytelegraph.com.au/news/bodybuilder-luke-wood-dies-after-kidney-transplant/story-e6freuy9-1226129243854
 
If anyone has any questions about this I can try to answer them or get them answered. I am currently going through treatment of FSGS. Or if anyone has any input on going through treatment it would be much appreciated.
 
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