steroids and complications?

Badman22 said:
Name five bodybuilders or athletes who have died directly from steroid use. There's your answer
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I suspect the former is not a difficult proposition. Other athletes could be tough, since doping is obviously disallowed in pretty much all sports everywhere.

If you're on any bodybuilding forums, you will know of various members who drop out. You might request cause-specific mortality analysis for each case, but it doesn't take a rocket scientist to correlate sudden deaths and heart failures in young bodybuilders with steroid use...

There are reasons for regular blood work and diagnostic tests. Pay special attention to CRP and estradiol levels out of range - CRP is a good indicator for heart disease risk and does go up with steroid use, high estradiol marks a substantial increase in stroke risk (estradiol blood levels greater than 34.1 pg/mL resulted in this more than doubling of stroke incidence) (I've had levels over 120pg/mL, fwiw 8o). And it sure as hell doesn't hurt to have a BP monitor or two around for daily checks.
 
Right but is it the steroids or is it say bad diets. For example weve all heard stories of fifty year olds who's hearts go out. Some healthy guys or appear to be and others aren't healthy and often times obese and have poor diets. So are steroids really to blame?
 
Badman22 said:
Right but is it the steroids or is it say bad diets. For example weve all heard stories of fifty year olds who's hearts go out. Some healthy guys or appear to be and others aren't healthy and often times obese and have poor diets. So are steroids really to blame?
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[h=1]Androgenic anabolic steroid abuse and the cardiovascular system.[/h]Vanberg P1, Atar D.
[h=3]Author information[/h]
  • 1Chief Physician/Senior Cardiologist, Oslo University Hospital - Aker, Trondheimsveien 235, 0514-Oslo University Hospital, Oslo, Norway. [email protected]


[h=3]Abstract[/h]Abuse of anabolic androgenic steroids (AAS) has been linked to a variety of different cardiovascular side effects. In case reports, acute myocardial infarction is the most common event presented, but other adverse cardiovascular effects such as left ventricular hypertrophy, reduced left ventricular function, arterial thrombosis, pulmonary embolism and several cases of sudden cardiac death have also been reported. In this review we have studied the relevant literature regarding several risk factors for cardiovascular disease where the effects of AAS have been scrutinized:(1) Echocardiographic studies show that supraphysiologic doses of AAS lead to both morphologic and functional changes of the heart. These include a tendency to produce myocardial hypertrophy (Fig. 3), a possible increase of heart chamber diameters, unequivocal alterations of diastolic function and ventricular relaxation, and most likely a subclinically compromised left ventricular contractile function. (2) AAS induce a mild, but transient increase of blood pressure. However, the clinical significance of this effect remains modest. (3) Furthermore, AAS confer an enhanced pro-thrombotic state, most prominently through an activation of platelet aggregability. The concomitant effects on the humoral coagulation cascade are more complex and include activation of both pro-coagulatory and fibrinolytic pathways. (4) Users of AAS often demonstrate unfavorable measurements of vascular reactivity involving endothelial-dependent or endothelial-independent vasodilatation. A degree of reversibility seems to be consistent, though. (5) There is a comprehensive body of evidence documenting that AAS induce various alterations of lipid metabolism. The most prominent changes are concomitant elevations of LDL and decreases of HDL, effects that increase the risk of coronary artery disease. And finally, (6) the use of AAS appears to confer an increased risk of life-threatening arrhythmia leading to sudden death, although the underlying mechanisms are still far from being elucidated. Taken together, various lines of evidence involving a variety of pathophysiologic mechanisms suggest an increased risk for cardiovascular disease in users of anabolic androgenic steroids.
 
Badman22 said:
Right but is it the steroids or is it say bad diets. For example weve all heard stories of fifty year olds who's hearts go out. Some healthy guys or appear to be and others aren't healthy and often times obese and have poor diets. So are steroids really to blame?
Click to expand...

Androgen abuse has been linked to several serious adverse cardiovascular events. Cardiac arrhythmias, QT dispersion, atrial fibrillation, myocardial infarction, heart failure and atherogenesis have all been linked to androgen abuse by athletes [14]. Melchert and Welder proposed 4 hypothetical models of anabolic-induced adverse cardiovascular effects [21,22]:

an ‘atherogenic’ model involving the effects of androgen-anabolic steroids (AASs) on lipoprotein concentrations;
a ‘thrombogenic’ model involving the effects of AASs on clotting factors and platelets;
a ‘vasospasm’ model involving the effects of AASs on the vascular nitric oxide system;
a ‘direct myocardial injury’ model involving the effects of AASs on myocardial cells.
Our study shows that the administration of testosterone in high doses exerts toxic effects on the myocardial cells. This probably correlates with the direct myocardial injury model of the effects of androgen-anabolic steroids on the myocardial cells. The mitochondria are particularly damaged and appeared edematous, with diminished cristae. The morphometric approach showed that the mitochondria of the experimental group were larger and more rounded.

The contractile apparatus showed signs of deterioration, with disorganization of the sarcomeres and the Z discus. These observations have been reported earlier and have been characterized as typical for early heart failure [23,24].

Another interesting finding of this study, using the Masson’s trichrome staining, was the presence of collagen fibrils inside the myocardium and particularly between the capillaries and the myocardium cells. This perivascular myocardial fibrosis, together with the hypertrophy that was also induced, may be the cause of myocardial ischemia [25,26] as well as a substrate for arrhythmias [27,28]. The presence of collagen was not noted in the hearts of the control rats. The collagen may increase the stiffness of the myocardium and reduce its compliance. Crisostomo et al. [3] reported that acute exposure of hearts to testosterone significantly reduces the −dP/dt (a measure of cardiac compliance).

The myocardial hypertrophy observed in the present study and also in our previous experiments [29], as well as by other researchers [30,31], has a significant role in the testosterone-induced reduction of myocardial compliance. The hypertrophy of the myocardium correlates with the enhanced expression of the androgen receptor after testosterone administration [29]. Myocardial hypertrophy is also associated with myocardial dysfunction due to abnormal intracellular calcium cycling [32]. Abnormalities of the circulating levels of other hormones may induce adverse cardiovascular effects. Increased levels of the protein hormone leptin have been found to induce cardiac hypertrophy although diastolic dysfunction was not associated with leptin levels [33]. Another set of hormones, the thyroid hormones, do have an impact on the myocardial diastolic properties among other various cardiovascular effects [34].

An unusually large number of micropinocytic vesicles was observed in the cytoplasm of the endothelial cells. Although it is common for these vesicles to occur in capillary endothelial cells, especially in the striated muscles, the abundance of such vesicles is a sign of heightened pinocytic activity that permits the cell to receive substances through the cell membrane [35].

Apoptosis is the programmed cell death and is mediated by 2 pathways: the extrinsic death receptor signaling pathway and the intrinsic mitochondrial control pathway [36,37]. Caspases exert significant action in both pathways. Caspase-3 (CPP 32) is a member of the interleukin-1 beta-converting enzyme (ICE) family of mammalian proteases that specifically cleaves substrates at the C-terminal side of aspartic residues. Members of this family have been implicated in apoptosis, and caspase-3 acts as a control mediator of programmed cell death in mammalian cells. Caspase-3 is synthesized as an inactive 32kD proenzyme and is processed during apoptosis to its active form, which is responsible for the cleavage of poly (ADP-ribose) polymerase (PARP), actin and sterol regulatory element binding protein (SREDP) [38–40]. In the present study, testosterone overdosing significantly activated apoptosis, as was clearly seen by immunohistochemistry. The staining for caspase-3 was negative in the control rats. Although it has been reported that apoptosis activated by testosterone enanthate is due to the ester [21], experimental exposure of myocardial cells to enanthate alone did not activate apoptosis [14]. Apoptosis causes the loss of myocardial cells and ultimately the depression of myocardial performance. The abuse of androgen anabolic substances has been causally linked with sudden cardiac death, myocardial infarction, ventricular remodeling and cardiomyopathy. These events are related to the activation of apoptosis due to AASs abuse. Myocardial death without coronary vessel disease or atherosclerosis has also been attributed to the activation of apoptosis by AASs [41,42].

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3560513/
 
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