Thread: Death count for AS?
02-01-2006, 08:58 PM #1
Death count for AS?
Anyone know an estimated/accurate total of people who have died from steroids ? I know its low. and most deaths are heart disease/heart failure/liver disease. I'm doing a midterm and wondering if anyone can give me a source where to find information. or if anyone has it on hand. thanks
02-01-2006, 09:00 PM #2
02-01-2006, 09:01 PM #3Originally Posted by USfighterFC
02-01-2006, 09:05 PM #4Originally Posted by 24labor
Thank you Collabulus
02-01-2006, 09:05 PM #5
yup zero. there's no scientific backing to prove steroids are respondsible for any death. I personally think that heavy year round or long term use can contribute to deaths in some cases, but isn't directly respondsible.
02-01-2006, 09:06 PM #6Originally Posted by USfighterFC
02-01-2006, 09:08 PM #7Originally Posted by onehundredk
02-01-2006, 09:10 PM #8Originally Posted by symatech
02-01-2006, 09:10 PM #9Originally Posted by onehundredk
02-01-2006, 09:11 PM #10Originally Posted by onehundredk
Like I said nothing has ever been factually proven to link steroids and death. Someone who may have died from heart diseases and steroid use also has other issues in it ranging from having a prior heart condition to high cholesterol to blocked artieries. If this person used steroids and died of a heart attack and had a healthy normal heart for a 20 something year old individual I think that it could make for a very solid case that steroids was indeed a direct cause of his death. But at the same time doctors have said there is no such tell tale calling card saying steroids was the cause of a persons death.
02-01-2006, 09:16 PM #11
What about someone injecting into a vein? Thought that could be fatal and if thats the case, i'm sure that someone out of all the users around has done that...
02-01-2006, 09:18 PM #12Originally Posted by Jakspro
02-01-2006, 09:20 PM #13Originally Posted by onehundredk
Receptor Down Regulation
There is as much misinformation about steroids as there is good information had among bodybuilding enthusiasts. Go to any gym and you will hear some kid spouting off to his buddies about how steroids do this, or how they do that, or whatever. This soon starts somewhat of a pissing contest (excuse the expression) as to who knows more about steroids. Itís the same kind of titillating and infectious banter that adolescent boys get into about girls and sex. With steroid banter you hear all the popular terms like Deca , Test, GH, gyno, zits, raisins, "h-u-u-u-ge", roid, freak, monster, roid-rage, "I knew this guy once", etc., etc.. If by some rare chance they are smart and have been reading this or some other high quality bodybuilding site on the net, they may actually get a few details right. More often than not they know just enough to be dangerous. Fortunately steroids havenít proven to be all that dangerous. Not only that, but most of these guys who are infatuated with steroids wonít ever use or even see them except in magazines.
This kind of ego driven gym talk doesnít really bother me until they begin giving advice to other clueless people who actually have access to them. Spewing out steroid lingo gives other less experienced kids the impression that these kids actually know what they are talking about. Thatís how all of the psuedo-science folklore about steroids perpetuates. This is also why most people who actually use steroids know little about them. This last fact should bother anyone who cares about bodybuilding and/or bodybuilders.
I started out with this article planning on giving some textbook style explanation as to why using steroids doesnít down regulate androgen receptors (AR). Then after considering some of my critics views that I tend to write articles that hardly anyone can read, I decided to write an easy to read, yet informative explanation about what androgens actually do and how this precludes androgen receptor down regulation. I still have a few references but not so many that it looks like a review paper.
Androgen receptors down-regulateÖ.Donít they?
One misunderstood principle of steroid physiology is the concept of androgen receptors (AR), sometimes called "steroid receptors", and the effects of steroid use on their regulation. It is commonly believed that taking androgens for extended periods of time will lead to what is called AR "down regulation". The premise for this argument is; when using steroids during an extended cycle, you eventually stop growing even though the dose has not decreased. This belief has persisted despite the fact that there is no scientific evidence to date that shows that increased levels of androgens down regulates the androgen receptor in muscle tissue.
The argument for AR down-regulation sounds pretty straightforward on the surface. After all, we know that receptor down-regulation happens with other messenger-mediated systems in the body such as adrenergic receptors. It has been shown that when taking a beta agonist such as Clenbuterol, the number of beta-receptors on target cells begins to decrease. (This is due to a decrease in the half-life of receptor proteins without a decrease in the rate that the cell is making new receptors.) This leads to a decrease in the potency of a given dose. Subsequently, with fewer receptors you get a smaller, or diminished, physiological response. This is a natural way for your body to maintain equilibrium in the face of an unusually high level of beta-agonism.
In reality this example using Clenbuterol is not an appropriate one. Androgen receptors and adrenergic receptors are quite different. Nevertheless, this is the argument for androgen receptor down-regulation and the reasoning behind it. The differences in the regulation of ARs and adrenergic receptors in part show the error in the view that AR down-regulate when you take steroids. Where adrenergic receptor half-life is decreased in most target cells with increased catecholamines, AR receptors half-liveís are actually increased in many tissues in the presence of androgens.1
Let me present a different argument against AR down-regulation in muscle tissue. I feel that once you consider all of the effects of testosterone on muscle cells you come to realize that when you eventually stop growing (or grow more slowly) it is not because there is a reduction in the number of androgen receptors.
Testosterone : A multifaceted anabolic
Consider the question, "How do anabolic steroids produce muscle growth?" If you were to ask the average bodybuilding enthusiast I think you would hear, "steroids increase protein synthesis." This is true, however there is more to it than simple increases in protein synthesis. In fact, the answer to the question of how steroids work must include virtually every mechanism involved in skeletal muscle hypertrophy. These mechanisms include:
∑ Enhanced protein synthesis
∑ Enhanced growth factor activity (e.g. GH, IGF-1, etc.)
∑ Enhanced activation of myogenic stem cells (i.e. satellite cells)
∑ Enhanced myonuclear number (to maintain nuclear to cytoplasmic ratio)
∑ New myofiber formation
Starting with enhanced growth factor activity, we know that testosterone increases GH and IGF-1 levels. In a study by Fryburg the effects of testosterone and stanozolol were compared for their effects on stimulating GH release.2 Testosterone enanthate (only 3 mg per kg per week) increased GH levels by 22% and IGF-1 levels by 21% whereas oral stanozolol (0.1mg per kg per day) had no effect whatsoever on GH or IGF-1 levels. This study was only 2-3 weeks long, and although stanozolol did not effect GH or IGF-1 levels, it had a similar effect on urinary nitrogen levels.
What does this difference in the effects of testosterone and stanozolol mean? It means that stanozolol may increase protein synthesis by binding to AR receptors in existing myonuclei, however, because it does not increase growth factor levels it is much less effective at activating satellite cells and therefore may not increase satellite cell activity nor myonuclear number directly when compared to testosterone esters. I will explain the importance of increasing myonuclear number in a moment, first lets look at how increases in GH and IGF-1 subsequent to testosterone use effects satellite cellsÖ
In part 2 we will discuss the role of satellite cells and myonuclei and how testosterone (androgens) activates these systems to create muscle growth far beyond what simple activation of the androgen receptor can produce.
In part 1 of this article we discussed the mistake of thinking about androgen receptors (testosterone receptors) in the same way we think of other receptors such as beta-receptors. Beta-receptors down regulate in response to beta-adrenergic stimulation whereas there is good evidence that androgen receptors increase in numbers in response to androgens. We also discussed the various affects of testosterone on muscle growth. Testosterone does far more than simply increase the rate of protein synthesis!
Now in part 2 we will finish our discussion of androgen receptor regulation as it pertains to the way muscle cells grow. The very mechanism of real muscle growth opens the door for increased androgen receptor number in response to testosterone treatment.
Donít forget Satellite cells!
Satellite cells are myogenic stem cells, or pre-muscle cells, that serve to assist regeneration of adult skeletal muscle. Following proliferation (reproduction) and subsequent differentiation (to become a specific type of cell), satellite cells will fuse with one another or with the adjacent damaged muscle fiber, thereby increasing the number of myonuclei for fiber growth and repair. Proliferation of satellite cells is necessary in order to meet the needs of thousands of muscle cells all potentially requiring additional nuclei. Differentiation is necessary in order for the new nucleus to behave as a nucleus of muscle origin. The number of myonuclei directly determines the capacity of a muscle cell to manufacture proteins, including androgen receptors.
In order to better understand what is physically happening between satellite cells and muscle cells, try to picture 2 oil droplets floating on water. The two droplets represent a muscle cell and a satellite cell. Because the lipid bilayer of cells are hydrophobic just like common oil droplets, when brought into proximity to one another in an aqueous environment, they will come into contact for a moment and then fuse together to form one larger oil droplet. Now whatever was dissolved within one droplet (i.e. nuclei) will then mix with the contents of the other droplet. This is a simplified model of how satellite cells donate nuclei, and thus protein-synthesizing capacity, to existing muscle cells.
Enhanced activation of satellite cells by testosterone requires IGF-1. Those androgens that aromatize are effective at not only increasing IGF-1 levels but also the sensitivity of satellite cells to growth factors.3 This action has no direct effect on protein synthesis, but it does lead to a greater capacity for protein synthesis by increasing fusion of satellite cells to existing fibers. This increases the number of myonuclei and therefore the capacity of the cell to produce proteins. That is why large bodybuilders will benefit significantly more from high levels of androgens compared to a relatively new user.
Testosterone would be much less effective if it were not able to increase myonucleation. There is finite limit placed on the cytoplasmic/nuclear ratio, or the size of a muscle cell in relation to the number of nuclei it contains.4 Whenever a muscle grows in response to training there is a coordinated increase in the number of myonuclei and the increase in fiber cross sectional area (CSA). When satellite cells are prohibited from donating viable nuclei, overloaded muscle will not grow.5,6 Clearly, satellite cell activity is a required step, or prerequisite, in compensatory muscle hypertrophy, for without it, a muscle simply cannot significantly increase total protein content or CSA.
More myonuclei mean more receptors
So it is not only true that testosterone increases protein synthesis by activating genetic expression, it also increases the capacity of the muscle to grow in the future by leading to the accumulation of myonuclei which are required for protein synthesis. There is good reason to believe that testosterone in high enough doses may even encourage new fiber formation. To quote the authors of a recent study on the effects of steroids on muscle cells:
"Intake of anabolic steroids and strength-training induce an increase in muscle size by both hypertrophy and the formation of new muscle fibers. We propose that activation of satellite cells is a key process and is enhanced by the steroid use."7
Simply stated, supraphysiological levels of testosterone give rise to increased numbers of myonuclei and thereby an increase in the number of total androgen receptors per muscle fiber. Keep in mind that I am referring to testosterone and testosterone esters. Not the neutered designer androgens that people take to avoid side effects.
Another group of researchers are quoted as saying:
"Öit is intriguing to speculate that the upregulation of AR levels via the administration of pharmacological amounts of androgens might convert some muscles that normally have a minor or no response to muscles with enhanced androgen responsiveness"(8)
This is not an argument to rapidly increase the dosages you use. It takes time for these changes to occur and the benefits of higher testosterone levels will not be immediately realized. It does shed some light however on the proportional differences between natural and androgen assisted bodybuilders physiques.
Maintenance of the kind of muscle mass seen in top-level bodybuilders today requires a given level of androgens in the body. That level will vary from individual to individual depending on their genetics. Nevertheless, if the androgen level drops, or if they were to "cycle off" the absolute level of lean mass will also drop. Likewise, as the level of androgens goes up, so will the level of lean mass that individual will be able to maintain. All of this happens without any evidence of AR down regulation. More accurately it demonstrates a relationship between the amount of androgens in the blood stream and the amount of lean mass that you can maintain. This does not mean that all you need is massive doses to get huge. Recruitment of satellite cells and increased myonucleation requires consistent "effective" training, massive amounts of food, and most importantly, time. Start out with reasonable doses. Then, as you get bigger you can adjust your doses upwards.
1. Kemppainen JA, Lane MV, Sar M, Wilson EM. Androgen receptor phosphorylation, turnover, nuclear transport, and transcriptional activation. Specificity for steroids and antihormones. J Biol Chem 1992 Jan 15;267(2):968-74
2. Fryburg DA., Weltman A., Jahn LA., et al: Short-term modulation of the androgen milieu alters pulsatile, but not exercise- or growth hormone releasing hormone-stimulated GH secretion in healthy men: Impact of gonadal steroid and GH secretory changes on metabolic outcomes. J Clin Endocrinol. Metab. 82(11):3710-37-19, 1997
3. Thompson SH., Boxhorn LK., Kong W., and Allen RE. Trenbolone alters the responsiveness of skeletal muscle satellite cells to fibroblast growth factor and insulin -like growth factor-I. Endocrinology. 124:2110-2117, 1989
4. Rosenblatt JD, Yong D, Parry DJ., Satellite cell activity is required for hypertrophy of overloaded adult rat muscle. Muscle Nerve 17:608-613, 1994
5. Rosenblatt JD, Parry DJ., Gamma irradiation prevents compensatory hypertrophy of overloaded extensor digitorum longus muscle. J. Appl. Physiol. 73:2538-2543, 1992
6. Phelan JN, Gonyea WJ. Effect of radiation on satellite cell activity and protein expression in overloaded mammalian skeletal muscle. Anat. Rec. 247:179-188, 1997
7. Kadi F, Eriksson A, Holmner S, Thornell LE. Effects of anabolic steroids on the muscle cells of strength-trained athletes. Med Sci Sports Exerc 1999 Nov;31(11):1528-34
8. Antonio J, Wilson JD, George FW. Effects of castration and androgen treatment on androgen-receptor levels in rat skeletal muscles. J Appl Physiol. 1999 Dec;87(6):2016-9.
02-01-2006, 10:48 PM #14
although there is no case of steroid OD
look how many cardiovascular related deaths there are people who were known users or on at the time..it seems every so months someone popular in the game dies..and whats sad is the age is around 30-40
something to think about
be smart...you need bloodwork and DAILY blood pressure monitoring. a bp cuff and steth can be had under 20 bux. no excuse. and do cardio, even if your bulking..burning 400 cals is no big deal, you can eat that in a snack to make it up
02-01-2006, 10:48 PM #15
oh ya...and the ultimate warrior's heart exploded from juice
so death count = 1
02-01-2006, 11:03 PM #16Anabolic Member
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02-02-2006, 01:03 AM #17Junior Member
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02-02-2006, 01:42 AM #18
ive never heard of anyone dying from gear, but i plan on doing as many cycles as i can possibly afford to do, so maybe il be the first
02-02-2006, 07:51 AM #19Originally Posted by Billy_Bathgate
death count = 2
02-02-2006, 06:06 PM #20
if youve ever injected aas, you will die... its a fact... a fact the white man forces upon us...
02-02-2006, 06:45 PM #21Originally Posted by decadbal
02-02-2006, 10:17 PM #22Originally Posted by Keyser Sozey
you must be a young guy and not remeber the rumors from like 85-87 era...the word was that his heart exploded from steroids and thats why he retired while he was in his prime
02-04-2006, 06:24 PM #23New Member
Originally Posted by symatech
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- Jan 2006
I thought this was very interesting, but perhaps, symatech, you can tell me how you interpret this. Basically what I am concluding from your the article is that there is no AR down-regulation from continuing low testosterone doses (e.g., 3 mg/kg/wk...say for a 70kg person would be around 200mg / wk). So you could continue this dose forever, reap the benefits, and never really have to cycle.
I ask this because I'm taking around 100mg/wk of TE with 2iu/day (1 off) of HGH, and plan to keep this up indefinitely. If I wanted to up the TE, could I do it without problems to 200mg/wk ... or 300 mg/wk?
These are smaller doses than a lot of people on this site use, but I have different (life extension/enhancement vs. bodybuilding) objectives than a lot of the posters
02-04-2006, 07:05 PM #24Originally Posted by ipso facto
I think you would experience bad side affects if you ran an indefinite dose of testosterone -albeit a low one- for life. I mean it affects us all differently, and I can tell you that at around 500mg/week long acting test makes me uncomfortable at about 3 months time. you may be different. I don't think that it would be wise to run test indefinitely unless you really needed it ie. you are on HRT.
Can I ask how old you are?
02-05-2006, 12:23 AM #25New Member
Originally Posted by symatech
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- Jan 2006
I have to agree about the misgivings of running anything forever. But look at it this way. In your late 50s your hormones are already out of balance. As long as you don't initiate any negative feedback loops (which is really what my question was about) I feel the results can only be positive.
Now on the HGH, the 2IU 6/1 days forever seems to be supported by a good bit of data. The testosterone on the other hand I have mixed knowledge of. Dosage for HRT seems to be 50-200mg/wk, and I'm guessing at the low end you can do this forever at my age, and not exacerbate any feedback loops. In fact, with tamoxifin, you could reverse the aromatase feedback loop that you tend to develop in your late 50s.
But your post seems to indicate that at higher levels, I could be safe as well.
Because a lot of the feedback from this site is empirical, and subjective based on individual users perceptions of their gains, well-being and so forth, I think it is easier to get reliable feedback on larger doses (e.g., regular BB cycles) than it is on HRT, where the effects may be highly subjective, and not really captured in blood tests.
Since I am my own lab subject (treatment) I am always interested in expanding my knowledge on HRT. This let's me experiment in safety, and monitor my own subjective assessments that much better. This site has been great for that.
When you say you can feel the 500mg/wk dosages of testosterone, can you elaborate? I'm presuming that the effect is not particularly comfortable.
Last edited by ipso facto; 02-05-2006 at 12:26 AM.
02-05-2006, 02:14 AM #26Banned
Originally Posted by Billy_Bathgate
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once again the abuse of any subtance could/will lead to some sort of medical condition
02-05-2006, 02:17 AM #27Banned
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