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natty
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Heretic got banned for talking bad about steroids because this site is trying to sell books about steroids and how to get them so its a conflict of interest.
natty said:Heretic got banned for talking bad about steroids because this site is trying to sell books about steroids and how to get them so its a conflict of interest.
mrplunkey said:Doesn't the duration of your elevated BP have a massive effect on the risks associated with elevated BP? For example, aren't there a lot of studies that show breath-holding and the temporary elevation of BP during resistance overloading doesn't increase risk of anurism (one form of stroke)?
I know when I do an overloaded pull-over and grind out those last 2-3, I'll even breath hold and pressurize my entire body for the pull. I get up from the bench as red as a beet, light headed, seeing stars. I'm sure my BP is 220/150 or more -- but only for a few moments.
Isn't the effect with AAS similar? Even if you are on a regimen that is elevating your BP, it's a transient effect that may last 4, 6 or even 10 weeks -- not something you're going to live with for the next 10 years.
I know I made a jump from 2-3 minutes of elevated BP to 4-10 weeks, but wouldn't we see more lifters (particularly AAS users) dropping dead in weight rooms if elevated BP levels from lifting/steriods were that dangerous?
I agree, but wouldn't the jump from 3 minutes to 10 weeks be comparable to the jump from 10 weeks to 10 years? If a vessel popping were a simple issue of reaching a certain pressure, wouldn't a single breath-holding set do it well before you ever used any AAS? My only real point was that the duration of BP elevation seems to play some significant role -- whether it be minutes, weeks or years.poantrex said:Good grief man, having elevated BP for 10 weeks is far worse than having bad BP during a set of pullups.
And you're assuming that everyone does 8-10 week cycles....I know a ton of guys in the gym that are never off. I personally believe that 8-10 week cycles can still be damaging due to plaque buildup, too.
bigtbone said:I'm jumping in here late but there are several points I want to make such that I don't even know where to begin. But Ulter is right here.
First, the man stated he had a rare blood condition in which he is hypercoagulable. That IS the most likely cause of his stroke regardless of a lack of family history. Antiphospholipid antibodies, deficiencies of protein S or C, and presence of antithrombin 3 are the most common "rare" hypercoagulable conditions and all predispose to stroke. And, this would cause an ischemic stroke, not a hemorrhagic stroke which Heretic is referring to.
Yes Heretic, hemorrhagic stroke is the 3rd most common cause of stroke but that does not mean it is a common cause of stroke. Only 10% of strokes are hemorrhagic strokes. Yes, hypertension is a cause of hemorrhagic stroke, but one would have to have CHRONIC hypertension. The mechanism is that chronic hypertension causes intimal hyperplasia with hyalinosis in the vessel wall which predisposes to focal necrosis, causing breaks in the wall of the vessel. This can lead to subclinical leaks and massive hemorrhage can occur when the clotting system is unable to compensate for the disruption in the vessel wall.
The mild elevation in BP one may experience with AAS is not significant enough in value or, MORE IMPORTANTLY, in duration to cause such a process. Your average AAS cycle is only 8 weeks long!! And, unless they have pre-existing HTN or risk factors for such (like smoking, ongoing hyperlipidemia, familial HTN, etc), the large majority of AAS users will not have elevations in BP beyond the point of high-normal (130-139/85-89). The Framingham Heart Study (which is THE definitive study) found that the hazard ratio for a cardiovascular event after TEN YEARS for those with high-normal BP is 1.6 for men. This was for all forms of CVD. So that for stroke alone is even lower. This was TEN YEARS! Even if one does experience higher BP levels, eight weeks is not long enough in duration for the process described above to occur.
The same is true for altered lipid profiles and atherosclerosis. A temporary decrease in HDL is not significant enough to lead to stroke in a previously healthy person. Plaque formation and rupture requires time and chronicity.
To say that things cannot happen in medicine is crazy. Ulter is not saying it cannot happen. Hell anything CAN happen. He is saying it is highly unlikely and is being realistic; he is right. As far as Heretic's reference to the paper which states some athletes have had stroke with prolonged use, they say earlier in the paragraph that much of the evidence is anecdotal (at best) concerning the side effects of AAS. And, I've read the case report which that paper is referring to and, if I remember correctly, it was two athletes. You cannot show causality without a prospective cohort study. They cannot argue AAS is causative of stroke, only that those two athletes happen to be taking AAS and had a stroke. The number of people who have used AAS is enourmous. How many case reports are there of stroke in AAS users? Such a lower number that it is statistically insignificant and one could find a just as strong a correlation among such cases and the use of some benign substance they may all just happen to be taking (like water, to be extreme).
Next, proantrex, absolutey no correlation has been found between testosterone or DHT and the development of prostate cancer. I have given several presentations in endocrinology conferences regarding this. There is no elevation in PSA (a marker for prostate cancer) either. It isn't even debated anymore. Therapy with testosterone does, however, result in worse outcomes in those who have pre-existing prostate cancer. Also, your allegation that DHT is particularly bad is way off base and exactly the opposite. Studies have shown that DHT therapy results in less prostate stimulation than testosterone and can even cause regression. The theory is that ESTROGEN is the true culprit and that prostatic hypertrophy is actually a result of aromatization of testosterone to estrogen. DHT is not aromatizable and hence has less stimulation on the prostate. In fact, I am a member of a team currently conducting a clinical study involving this very issue.
bigtbone said:I'm jumping in here late but there are several points I want to make such that I don't even know where to begin. But Ulter is right here.
First, the man stated he had a rare blood condition in which he is hypercoagulable. That IS the most likely cause of his stroke regardless of a lack of family history. Antiphospholipid antibodies, deficiencies of protein S or C, and presence of antithrombin 3 are the most common "rare" hypercoagulable conditions and all predispose to stroke. And, this would cause an ischemic stroke, not a hemorrhagic stroke which Heretic is referring to.
Somewhere along the line I made it clear that even though this person had an "ischemic" stroke, I think that AAS could have had a hand in it. I have also stated that AAS can and does cause high BP and high BP can and does cause ICH. I realize this person did not siffer from this, but I figured I didn't have to spell everything out to you people.
Yes Heretic, hemorrhagic stroke is the 3rd most common cause of stroke but that does not mean it is a common cause of stroke. Only 10% of strokes are hemorrhagic strokes. Yes, hypertension is a cause of hemorrhagic stroke, but one would have to have CHRONIC hypertension. Not true at any level. I have treated people, young people, and have studied this very topic for years. All it takes is ONE episode of high BP to cause ICH. I've seen it, treated it and have studied it.The mechanism is that chronic hypertension causes intimal hyperplasia with hyalinosis in the vessel wall which predisposes to focal necrosis, causing breaks in the wall of the vessel. True, but have you read any cases where extreme high BP, one episode of extremely high BP which AAS is known to cause that has caused ICH? I have.This can lead to subclinical leaks and massive hemorrhage can occur when the clotting system is unable to compensate for the disruption in the vessel wall. LOL! I'm not sure where you are copying your stuff, but it sure sounds nice. I could sit here all day and explain things to you in Latin, but I'm not going to. I'm not as easily impressed as Ulter by big medical terms, especially when I'm trying to explain things to laymen with no medical training. So either you're copying from a book or you have some medical training but aren't going to tell us what type.
The mild elevation in BP one may experience with AAS is not significant enough in value or, MORE IMPORTANTLY, in duration to cause such a process. MILD elevation? I have personally had BP's of 220+/120+. That is CRITICALLLY elevated BP. All becasue of AAS use. My BP when off is never higher than 115/70 while at rest.Your average AAS cycle is only 8 weeks long!! So. It only takes one episode of high BP to cause stroke. And, unless they have pre-existing HTN or risk factors for such (like smoking, ongoing hyperlipidemia, familial HTN, etc), the large majority of AAS users will not have elevations in BP beyond the point of high-normal (130-139/85-89). I guess you're just going to thow out the minority then huh? They don't matter right? I'll tell you what. Do you know 20 people that use AAS? Wait until all are on cycle and take their BP. I bet you find one or two with extremely high BP. The Framingham Heart Study (which is THE definitive study) found that the hazard ratio for a cardiovascular event after TEN YEARS for those with high-normal BP is 1.6 for men. This was for all forms of CVD. So that for stroke alone is even lower. This was TEN YEARS! Even if one does experience higher BP levels, eight weeks is not long enough in duration for the process described above to occur. I'mnot sure where you are getting your info, but I am very familiar with the Fram Heart Study and it states that any BP over 140/90 for any period of time puts a person at risk. The ASA says the same.
The same is true for altered lipid profiles and atherosclerosis. A temporary decrease in HDL is not significant enough to lead to stroke in a previously healthy person. Plaque formation and rupture requires time and chronicity.Again you are talking apples and oranges. We are not talking about occlusive strokes. With that said though, certain AAS can and do raise your blood counts which can lead to occlusive strokes rather quickly.
To say that things cannot happen in medicine is crazy. Ulter is not saying it cannot happen. Hell anything CAN happen. He is saying it is highly unlikely and is being realistic; he is right. Being realistic? I think you're backwards here bro. I am being realistic. To bury your head in the sand and dismiss any dangers to any medication you are taking is foolish and ignorant.As far as Heretic's reference to the paper which states some athletes have had stroke with prolonged use, they say earlier in the paragraph that much of the evidence is anecdotal (at best) concerning the side effects of AAS.Almost ALL information on AAS when pertaining to athletic enhancement is ANECDOTAL at best. So what are you talking about? Are you just going to accept all the GOOD anecdotal evidence and ignore the bad? Smart. And, I've read the case report which that paper is referring to and, if I remember correctly, it was two athletes. You cannot show causality without a prospective cohort study. They cannot argue AAS is causative of stroke, No, how about high BP being causative of stroke and AAS being causative of high BP? only that those two athletes happen to be taking AAS and had a stroke. The number of people who have used AAS is enourmous. How many case reports are there of stroke in AAS users? About as many reports there are of the "enourmous" numbers you speak about. Show me where you get you facts? Your gym? and this board? I wouldn't say that 10,000 people is enourmous numbers. Such a lower number that it is statistically insignificant and one could find a just as strong a correlation among such cases and the use of some benign substance they may all just happen to be taking (like water, to be extreme).
Next, proantrex, absolutey no correlation has been found between testosterone or DHT and the development of prostate cancer. I have given several presentations in endocrinology conferences regarding this. There is no elevation in PSA (a marker for prostate cancer) either. It isn't even debated anymore. Therapy with testosterone does, however, result in worse outcomes in those who have pre-existing prostate cancer. Also, your allegation that DHT is particularly bad is way off base and exactly the opposite. Studies have shown that DHT therapy results in less prostate stimulation than testosterone and can even cause regression. The theory is that ESTROGEN is the true culprit and that prostatic hypertrophy is actually a result of aromatization of testosterone to estrogen. DHT is not aromatizable and hence has less stimulation on the prostate. In fact, I am a member of a team currently conducting a clinical study involving this very issue.
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