43 is my age
hey, thanks for being understanding and thank you for your input. i need time to learn about these disorders you mentioned. i have never heard of them. i have heard of epo, i think it something that is tested and stated on all my blood tests. i have to refer back.
yeah, facts for me, thanks for understanding.
i think now, (hey can i change my target, lol), maybe he is too small that movie. he looks a bit sickly now that i look at him again, strangely. i don’t know what to say as a good reference point. i need about 10 pounds more of muscle. and i am already beyond my genetic limits as a 43 year old. as a 22 year old i could probably have gotten to this level but not at 43, no way. i know myself and i have been lifiting off and on since about age 16 or 17.
yeah, if i got down to 7% body fat or less i would have my version of the fight club body.
again, a lot of this technical stuff, jargon, i am not familiar with. it seems to me that, yeah, any AAS can be nephrotoxic but not so directly (depends on the drug). they can be harmful or toxic to the kidneys indirectly if they are forcing the kidneys to work harder than normal to remove waste or metabolize whatever the body needs to metabolize.
need time to read you post carefully.
you and the other people like you put me in a bad mood and made me defensive. i am very appreciative of unreal and lord gains, iron yuppie, ben and a couple others who are offering their time and dropping that knowledge. make no mistake about this.
im also not interested in the shredded look. i dont know why i said my target is brad pitt fight club. i think it for a lack of a better reference point. i think the overly shredded look is sickly looking (outside of the sport of bodybuilding). when you are 43 and you look like that is pretty weird i think. and i am not going to starve myself that much or take fat burners. just cutting out refined sugar and honey and not eating bread, pasta and lower on my rice and quinoa intake will bring my BF% down to 10% if i stick to the diet long enough.
your opinion is important. thanks
so i am learning about this. here is what google says about why hypertension causes kidney damage:
The nephrons in the kidneys are supplied with a dense network of blood vessels, and high volumes of blood flow through them. Over time, uncontrolled high blood pressure can cause arteries around the kidneys to narrow , weaken or harden. These damaged arteries are not able to deliver enough blood to the kidney tissue.
further reading explains that the arteries “weaken, harden narrow” because:
“More than 90% of the time, renal artery stenosis is caused by atherosclerosis, a process in which plaque made up of fats, cholesterol, and other materials builds up on the walls of the blood vessels, including those leading to the kidneys.”
so can this be the same kind of plaque/situation that we have with coronary heart disease? is this an HDL, LDL, total cholseterol applicable situation? is vitamin K2 and omega 3 going to lower my risk? maybe BPC 157 during and post cycle would also be beneficial? also, cialis might be beneficial.
ps. so why does decreased blood flow into kidneys cause damage? maybe if blood cannot go in and out enough then urine formation is not efficient and stuff can build up inside the kidneys, and the kidneys cannot remove enough of this “stuff” and this buildup damages the kidneys.
pss. i feel this can be managed, controlled, monitored, with a BP monitor, with choosing the correct types of drugs and through preventive measures, such as certain types of sups and the like.
three of you guys on a way deeper level. lol. i cannot keep up. i cannot even read some of your short hand. 
i am taking your statements one paragraph at a time, or whatever seems to be the first step in understanding what you are writing. thank you
perhaps the common cause of kidney disease among body builders is the combination of: hypertenion, and high protein intake coupled with AAS chemicals. kidneys are overburdened.
10% of the population experiences kidney stones and it is not clear why some people are genetically at risk. and it has been said that these people are at a higher risk of developing kdiney damage which affects 10-15% of the population.
so some people have this genetic risk. their kidneys are in some way, weak, or unable to handle the same input as other people. then these people put additional burdens on their kidneys, such as with AAS, high protein consumption, and hypertension, and then they suffer kidney damage or renal failure.
so now i am still at the general question of which steroids are safer and how can safer steroids be taken to reduce risk.
and i have to continue to study your post and the other posts for this answer.
my question now is, why or how is binding affinity related to nephrotoxicity, exactly. sorry i am so slow
With stanozolol it’s probably secondary to cholastasis
notes:
“These unusual biopsy features suggest that, in addition to the expected metabolic strain that elevated lean body mass and high protein intake places on glomeruli, androgens may be exerting a toxic effect on podocytes.”
podocytes: terminally differentiated and highly specialized cells that are required for normal glomerular function.
glomeruli: blood vessels located in the kidneys
treatment: “hyperfiltration injury, such as renin-angiotensin system blockade along with lifestyle modification (including a reduction of strenuous exercise and weight loss), has been reported to help reduce proteinuria and stabilize renal function.”
renin-angiotensin system (RAAS): is a hormone system that regulates blood pressure and fluid and electrolyte balance, as well as systemic vascular resistance.
“Hyperfiltration injury is an important factor; patients with markedly elevated lean body mass require an increase in single-nephron glomerular filtration, similar to patients with obesity-related glomerulopathy”
hyperfiltration: the filtration of blood through kidneys (200l per day). removing waste from blood which is expelled from body in the form of urine.
“Numerous animal models have investigated the influence of sex hormones on the development of renal disease, and they generally show a protective role for estrogens, while androgens either are permissive or accelerate injury. Doublier and colleagues recently developed a mouse model of glomerulosclerosis associated with high testosterone levels. They demonstrated that podocytes express both androgen and estrogen receptors and that in vitro, testosterone can cause podocyte apoptosis, which is blocked by the addition of flutamide.”
in vitro: test tube studies on cells and microorganisms
glomerulosclerosis: refers to scarring or hardening of the glomeruli – blood vessels located in the kidneys.
podocyte apoptosis: the death of blood vessel cells in kidneys.
“Future studies aimed at improving understanding of the specific role of androgen signaling in these key podocyte processes are needed to better understand the mechanism of AAS-induced kidney disease.”
renin-angiotensin system (RAAS): is a hormone system that regulates blood pressure and fluid and electrolyte balance, as well as systemic vascular resistance.
First things first, you’re doing real good. Keep up the work, you’re on the right track! You surprise me, not many people get that far in a day.
Yes, that is essentially the same. LDL plays a role in plaque build-up. It gets incorporated into plaques.
No, vitamin K2 and Omega 3s are probably not going to lower your risk. The only thing shown there to better lipid parameters is DHA as Monotherapy not in combination. Omega 3s seem to lower cardiovascular incident risk though.
BPC 157 was studied mainly in tendon and ligament injuries IN MICE. It’s in my opinion a trial and error thing with that peptide. In my opinion it won’t lower CV risk.
Cialis is shown to improve symptoms of high pulmonary blood pressure. It is just a vasodilator with preference for some vessels. It does not protect from artherosclerosis.
That’s why I wrote the point about the RAAS inhibitor helping with lot of these problems.
I think you misinterpreted a sentence there. What’s meant here is the blood flow to the kidney CELLS. Every cell needs oxygen to live and oxygen is transported by the blood. So if blood flow to the kidney is low, the kidney will be ischemic and get damaged.
That is, at least, the opinion of the authors of the study. An important point is that AAS DIRECTLY damage the kidneys. It’s not because the kidneys have to get rid of substances and metabolites in the blood, it is because the steroids directly act on the kidney cells.
Glomeruli are not only the blood vessels, they are the filtration unit of the kidneys. They consist of very small blood vessels with little gaps like a filter and the bowman capsule which surrounds the vessels. The filtrate the flows as primary urine into the proximal and distal tube were it gets concentrated (electrolytes!) and important electrolytes and other stuff (glucose,…) get reabsorbed.
Your notes look good. Keep up the good work.
You see, which steroid is the least damaging is difficult to answer. One point is how well they bind to their receptor, the AR. That’s my post above. But as unreal pointed out there are many exceptions.
You’d also think compounds more prone to increasing red blood count would be more toxic to the kidney (direct action if more erythropoietin is theoretically being pumped out). Though I believe a direct effect on bone marrow also occurs (AR binding and bone marrow sensitisation regarding the effect of erythropoietin).
My hypothesis could be confirmed via the fact that boldenone is may be (sparse body of literature confirms) quite toxic. In which case drugs like fluoxymesterone (very high RBA, high affinity towards inducing hypertension, known to increase RBC count) would be particuarly toxic.
Oxymetholone is also known to shoot up red cell count.
haven’t gotten to your post yet. going to get to it soon. thanks a lot
yes, i see there are maybe four major risks to the kidneys as an AAS user. next is to look into what you say about RAAS inhibitor or whatever. and the correlation to AR binding affinity and kidney damage.
hope to put it all together in a slightly dumbed down easy read summary soon enough.
WORK IN PROGRESS (last update: september 19, 2020.
This summary is intended as a suggestive guide for someone who wants to take AAS at the lowest risk possible for kidney damage.
OVERVIEW OF MAJOR RISKS TO KIDNEYS FROM AAS:
1.increase in red blood cells can damage the kidneys in this manner: rbc induces hypertension.
2.hypertension (high blood pressure) can damage kidneys in this manner: blood vessels leading to kidneys can become blocked with plaque like the plaque that can block other arteries in the body. Less blood supply to kidneys means less oxygen supply to kidney cells with results in kidney cell death (kidney damage).
3.AAS are directly toxic to the kidneys in this manner: “anabolic steroids are directly toxic to glomeruli and that segmental sclerosis is the result of podocyte loss mediated by apoptosis through a podocyte androgen receptor” (
4.increased lean body mass: being larger than your natural size means that your kidneys have to filter more waste and more blood. If the kidneys are overburdened they might be unable to remove waste. Hence protein showing up in your urine as well as other waste elements.
notes: people with kidney stones (1 in 10 people) have an increased risk for developing kidney damage (10-15% of people develop kidney damage).
Correlation between androgen receptors and toxicity by AAS:
SPECULATIVE OVERVIEW OF AAS AND SUPPLEMENTS
Oral steroids: such as Dbol should be avoided. They are reportedly directly highly toxic to kidneys.
Anavar (oxandralone): there was a study done on children with growth problems as well as on burn victims. the study indicated that there were no ill side effects to the kidneys. though anavar “metabolizes” in the kidneys, instead of in the liver, it is not proved to be toxic to the renal system.
Sarms: regarding LGD, RAD 140, and many others, there is not much literature or studies on these drugs. the studies that do exist appear dubious. there are some anecdotal reports of kidney damage from taking these drugs. even the half life of these drugs is uncertain. at least the oral forms of these drugs should probably be avoided by those who have weak kidneys. there are safer PEDs than sarms.
HGH Injections: might be harmless to kidneys.
IGF-1 peptide: probably more safe than MK 677. might be harmless to kidneys.
MK 677: seems relatively safe. but there are no studies to confirm if it is or not.
Trenbolone: not safe. Many anecdotal resports of kidney damage from trenbolone.
Metandienone (dianabol, ment, dbol): is very unsafe for kidneys.
turinabol (tbol): this is an oral steroid and can be harmful to kidneys.
Boldenone (e.q., quipoise): many reports of it having a high risk for kidney damage.
Testosterone: risk is probably less in comparison most other steroids. But testosterone can increase red blood cell count. It can raise blood pressure. The direct toxicity is probably less than most steroids but if taken in unconventional doses (above 200) the toxicity and all other side effects are likely to be compounded.
Stanozolol (winstrol): there is case of a young man who developed life threatening kidney damage as a result of taking testosterone, stanozolol and creatine. he also consumed large amounts of protein.
Nandrolone (decadurabolin): is given to people who are suffering from anemia which is a symptom of chronic kidney disease. therefore, it is safe to assume that this drug is relatively harmless to the kidneys. also keep a careful eye on things such as blood pressure and proteinuria which is protein in the urine (a sign that the kidneys are not functioning correctly).
Masteron: there are some reports of kidney damage occurring as a result of this drug.
Metenelone (primobolan): i cannot find any reports strongly linking primobolan use to kidney damage.
Creatine: it has been reported that creatine can be harmful to kidneys, epsecially in large doses for a long period of time. for those with kidney problems, this supplement should be probably be avoided seeing the benefits are probably offset by the risks.
Protein shakes: can cause kidney stones.
Oxymetholone (anadrol): high risk to kidneys.
fluoxymesterone (Halo): high risk to kidneys
TREATMENTS
disuse of steroids is the only sure way to possibly stave off increased kdiney damage once the process has begun. Do not exercise too much. Stop eating high amounts of protein. Lower blood pressure.
Note: there are many reports that kidney stones can form as a result of high protein intake from animal protein as well as protein shakes or drinks commonly used by bodybuilders.
PREVENTIVE MEDS AND METHODS
ACE inhibitor: can dialate your blood vessels and arteries and thereby help lower blood pressure. (this is a drug that probably requires professional oversight.)
BPC 157 reported to increase blood vessel growth but studies on mice cannot should not be relied on as you cannot be sure you are getting real BPC and you cannot be sure that what works for mice works for people.
vitamin K2: studies show it lowers plaque buildup in arteries leading to kidneys.
omega 3: studies show it lowers cholesterol…
Cialis: is shown to improve symptoms of high pulmonary blood pressure. It is just a vasodilator with preference for some vessels. It does not protect from artherosclerosis (clogging of arteries).
DHA: suggested to be used as a monotherapy (not to be taken at the same time as other drugs). can reduce plaque build up in blood vessels feeding kidneys.
Cycles: it seems that a lower dose cycle of longer duration would be safer than a shorter cycle with larger doses. keeping BP and RBC low as well as cholesterol is easier to manage at a lower dose. gradual increases or decreases might also help stave off negative effects on kidneys.
FINAL SUGGESTION
try a longer cycle at lowest dosage possible.
Some AASs seem to be “less” directly toxic to kidneys. blood pressure must be kept low, as it too can cause damage to kidneys. check urine for presence of protein which, if found, would indicate that kidneys are not functioning correct.
It is not necessary to eat massive amounts of protein in order to build muscle. it is easier that way, but not necessary. alternate forms of protein might be beneficial, such as rice and legumes, dairy, quinoa, etc.
Testosterone: seems relatively safe for those who wish to take above normal doses. But be careful of blood pressure rising. probably it would be best to stay in the range of 250mg to 600mg if you are looking for supraphysiological dosing. everyone’s body is different–what one body can tolerate, another body cannot. check your blood and urine monthly and get an ultrasound at least once every 6 months.
Primobolan: i cannot find any reports strongly linking primobolan use to kidney damage.
Decadurabolin: is actually given to people who are suffering from anemia as a result of chronic kidney disease. so it stands to reason that nadralone is relatively harmless to kidneys within a normal dosing range.
Anavar (oxandralone): there was a study done on children with growth problems as well as on burn victims. the study indicated that there were no ill side effects to the kidneys. though anavar “metabolizes” in the kidneys, instead of in the liver, it is not proved to be toxic to the renal system. in one research report, anavar is said to increase ldl and decrease hdl, though perhaps this is dose dependent. in the same report it is said to cause gynocomastia which is very unlikely for this drug. therefore, we must understand that this report might be erring on the side of caution.
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im a bit confused, does hypertension increase rbc or does rbc contribute to hypsertension. or does it go both ways?
Increase in RBC usually raises BP. Think of a mechanical pump set up in a loop. If you increase the viscosity (what happens when RBC increases), the pump works harder (has to generate more pressure). The pump generating more pressure is the same as your heart and an increase in BP.
that’s what i thought. thanks for clarifying it
please elaborate: 1. it is popularly reported that k2 and omega three decrease bad cholesterol so why would the not be a benefit to the kidneys in the prevention of plaque build up in the blood vessels that feed the kidney?
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if calias works to vasodialate then would it not be beneficial at least temporarily in the dialation of blood vessels feeding the kidneys? or do you know that the preference to vessels excludes those connected to kidneys?
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why DHA as a monotherapy? you are saying there will be or could be drug interaction that could reduce or elimination it’s potential? so for example (dha and a dht steroid taken at the same time woudl not be as effective or the effectiveness is unsure)? or are you saying DHA in combo with omega 3 and k2?
Yes, I thought about that, thanks for bringing it up. Until now I could not quantify how toxic it would be for the kidney if it gets overstimulated for EPO production. Seems like a similar mechanism only on other cells of the kidney. I’ll look into that.