I hear people many times say “long term effects” but how to specify what range does the “long” mean ? 1 year,5,10 ?. I know few guys who have been on 500/week for like 3-4 years, no problems at all. But since every one is different, how fast things can go bad and how bad you can get things with 500test/week ? for a 3-4 month period, i think not realy bad, but lets say all years around with 500 ?
3-4 years… men live 78 years on average. I’ll look up some studies and report back on long term consequences of Supra physiological doses. Unless @readalot has some already.
Is this a question to help you feel better/rationalize about the use of supraphysiologic dosages of testosterone for years, or is the question a genuine interest in what the pathological consequences will be in 1, 5, 10, 20 years? Just curious.
It is a roll of the dice, as I am not aware of any genomic test to fully quantify an individual’s “fitness” for long term androgen abuse. Let’s call it abuse since that’s what it is. Here’s some studies to get you started. There is no answer such as, “abusing 500 mg/week of testosterone cypionate for XX weeks will reduce your lifespan YY years vs the control scenario.”
In general terms, the effect of supra test abuse is pretty well understood. At the individual level, I can’t answer. Just like someone’s Grandma can smoke two packs a day and live to 96 years young. Another question is on average does everyone who smokes two packs a day live to 96? What question is the critical one, how long you live or the average person or the rare exceptional person?
General comments but very hard to properly quantify what these people actually took in the case study examples…
Literature with rats…
Testosterone and androgenic anabolic steroids have been misused for enhancement of physical performance despite many reports on cardiac sudden death. Although physiological level of testosterone provided many regulatory benefits to human health, including the cardiovascular function, supra-physiological levels of the hormone induce hypertrophy of the heart with unclear contractile activation. In this study, dose- and time-dependent effects of high-testosterone treatment on cardiac structure and function were evaluated. Adult male rats were divided into four groups of testosterone treatment for 0, 5, 10, and 20 mg/kg BW for 4, 8, or 12 weeks. Increases in both percentage heart:body weight ratio and cardiomyocyte cross-sectional area in representing hypertrophy of the heart were significantly shown in all testosterone-treated groups to the same degree. In 4-week-treated rats, physiological cardiac hypertrophy was apparent with an upregulation of α-MHC without any change in myofilament contractile activation. In contrast, pathological cardiac hypertrophy was observed in 8- and 12-week testosterone-treated groups, as indicated by suppression of myofilament activation and myocardial collagen deposition without transition of MHC isoforms. Only in 12-week testosterone-treated group, eccentric cardiac hypertrophy was demonstrated with unaltered myocardial stiffness, but significant reductions in the phosphorylation signals of ERK1/2 and mTOR. Results of our study suggest that the outcome of testosterone-induced cardiac hypertrophy is not dose dependent but is rather relied on the factor of exposure to duration in inducing maladaptive responses of the heart.
Introduction: Anabolic-androgenic steroids are increasingly used in athletes and non-athletes elderly males. Several studies have suggested that synthetic testosterone have direct effects by causing cardiac hypertrophy and left ventricular contractile dysfunction. All of these factors contribute to an increased risk of ventricular arrhythmias and sudden cardiac death. However, limited data are available regarding interactions between anabolic hormones concentration and insulin-like growth factor I (IGF-I) expression in the heart in response to exercise training.
Therefore, we examined effects of supraphysiological testosterone administration on left ventricular remodeling and cardiac IGF-I concentrations in sedentary and exercise-trained rats.
Methods: Male Wistar rats (n=52) were randomly allocated to groups with a 6-week endurance training with or without testosterone, and sedentary animals with or without testosterone. The hormone (20mg/250 g BW) was administrated once a week for six weeks. After six weeks the animals were anesthetized and the heart was excised and weighted. The left ventricular was separated to biochemical analyses.
Results: Testosterone treated sedentary animals showed significant higher cardiac IGF-I concentrations compared to control group (p<0.001). In endurance-trained groups, cardiac IGF-I concentrations were significantly higher after testosterone administration (p<0.01). The administration of supraphysiological testosterone significantly increased left ventricular mass of sedentary rats and left ventricular mass to body weigh ratio in endurance trained animals compared to control group. However, this effect was relatively small in trained group with and without testosterone administration.
Conclusions: The data demonstrate that increased cardiac IGF-I concentration in response to higher serum testosterone might be responsible for heart hypertrophy observed in both sedentary and endurance- trained animals.
Androgen therapy provides cardiovascular benefits for hypogonadism. However, myocardial hypertrophy, fibrosis, and infarction have been reported in testosterone or androgenic anabolic steroid abuse. Therefore, better understanding of the factors leading to adverse results of androgen abuse is needed. The aim of the present study was to examine the impact of high dose of androgen treatment on cardiac biology, and whether exposure duration modulates this response. Male rats were treated with 10 mg/kg testosterone, three times a week, for either 4 or 12 weeks; vehicle injections served as controls. Four weeks of testosterone treatment induced an increase in ventricular wall thickness, indicative of concentric hypertrophy, as well as increased ejection fraction; in contrast, both parameters were blunted following 12 weeks of high‐dose testosterone treatment. Cardiac myocyte contractile parameters were assessed in isolated electrically stimulated myocytes (sarcomere and intracellular calcium dynamics), and in chemically permeabilized isolated myocardium (myofilament force development and tension‐cost). High‐dose testosterone treatment for 4 weeks was associated with increased myocyte contractile parameters, while 12 weeks treatment induced significant depression of these parameters, mirroring the cardiac pump function results. In conclusion, chronic administration of high‐dose testosterone initially induces increased cardiac function. However, this initial beneficial impact is followed by significant depression of cardiac pump function, myocyte contractility, and cardiac myofilament function. Our results indicate that chronic high‐testosterone usage is of limited use and may, instead, induce significant cardiac dysfunction.
@yeahbuddy27 I assume this information has given you pause to running supraphysiologic dosages of testosterone and value the long term health of your cardiovascular system. Is that the case?
I think this is another good study to look at to somewhat quantify the effects of long term high dose use.
The median dose and time was 675 mg of testosterone (all dosages of AAS were equated to an amount of testosterone), and 468 weeks of use. So this is pretty high levels of use.
Changes in heart were observed. Here is a graph of LV ejection fraction comparing users and non-users (all weight trainers though).