Do you ever worry about...
Do you ever worry about...
Do you ever worry about Cardiacmyoapthy or CardiacMeglia?
How could you test for these potential conditions before starting AAS?
Could you have gene tests done, or would a simple Cardiologist do?
This way you know you can be safe starting a cycle and won't run have these problems.
Originally Posted by kbm8795
Originally Posted by BigDyl
Let's all join together and SPEAK ENGLISH IN AMERICA.
My Scottish great aunt was diagnosed wtih an enlarged heart at age 58. She died at age 87 from diabetic complications (type II). She was not overweight. She did not damage her heart by working hard at her bakers job, as was supposed for years. She did rise at 2am, and this disturbed sleep cycle. When combined with her traditional British diet and the stress of early widowhood and a lack of regular exercise, plus a Scots-Irish genetic disposition towards cardiovascular disease - the stage was set for cardiovascular disease progression. Her enlarged heart was due to liver lipid problems associated with adult onset diabetes. Insulin a potent anabolic.
Now why do you think I caution so many here to watch their insulin spiking, eh?
Tight glucose tolerance and avoidance of undue insulin release (the goddamned bulking bullshit), will do wonders for avoiding this unhappy side effect of steroid use, when ad nauseum use of steroids is avoided as well.
Not all who use steroids will have cardiomyopathy or ventricular disease. Not all who use steroids and have shitty glucose tolerance will develop heart problems - but, when these factors are combined with a fatty, high carb diet to gain mass and a lack of cardiovascular conditioning - watch you, you are treading on thin ice.
Its not possible to accurately predict who will have cardiac complications from use of steroids. Its possible to inteliigently conject who might be predisposed, based on lifestyle/diet/sleep/CV fitness and family health history.
Once again, how well you have prepared yourself for steroid use is key to avoiding many of the more serious side effects.
- Rep Points
Originally Posted by Trouble
- Rep Points
How does one formulate whether or not your in good CV health? Does being able to run a mile in under seven minutes mean anything? A resting heart rate of 50? I mean, at what point can somebody say they have a healthy CV system?
To start with you would need to have some blood work done. And even with that, I don't think you would ever know for sure what risk factors you face. My GF just had a male friend die. He had a heart attack. He was 39.
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Thats really ashame. Was there anything wrong with him physically, i.e. overweight?
Originally Posted by dg806
The management of conditioned nutritional requirements in heart failure. Allard ML, Jeejeebhoy KN, Sole MJ.. Division of Cardiology, University Health Network, Toronto. Heart Fail Rev. 2006 Mar;11(1):75-82.
Patients suffering from congestive heart failure exhibit impaired myocardial energy production, myocyte calcium overload and increased oxidative stress. Nutritional factors known to be important for myocardial energy production, calcium homeostasis and the reduction of oxidative stress, such as thiamine, riboflavin, pyridoxine, L-carnitine, coenzyme Q10, creatine and taurine are reduced in this patient population. Furthermore, deficiencies of taurine, carnitine, and thiamine are established primary causes of dilated cardiomyopathy. Studies in animals and limited trials in humans have shown that dietary replacement of some of these compounds in heart failure can significantly restore depleted levels and may result in improvement in myocardial structure and function as well as exercise capacity. Larger scale studies examining micronutrient depletion in heart failure patients, and the benefits of dietary replacement need to be performed. At the present time, it is our belief that these conditioned nutritional requirements, if unsatisfied, contribute to myocyte dysfunction and loss; thus, restoration of nutritional deficiencies should be part of the overall therapeutic strategy for patients with congestive heart failure.
Conditioned nutritional requirements: therapeutic relevance to heart failure.
Sole MJ, Jeejeebhoy KN. Heart 2002 Mar; 27(2): 174-8.
BACKGROUND: The advent of disease, genetic predisposition or certain drug therapies may significantly alter the nutritional demands of specific organs. Several specific metabolic deficiencies have been found in the failing myocardium: (1) a reduction in L-carnitine, coenzyme Q10, creatine, and thiamine--nutrient cofactors important for myocardial energy production; (2) a relative deficiency of taurine, an amino acid integral to intracellular calcium homeostasis; (3) increased myocardial oxidative stress and a reduction of antioxidant defenses. Deficiencies of carnitine or taurine alone are well documented to result in dilated cardiomyopathy in animals and humans. Each of these deficiencies is amenable to restoration through dietary supplementation. A variety of nutrients have been investigated as single therapeutic agents in pharmacologic fashion, but there has been no broad-based approach to nutritional supplementation in congestive heart failure to correct this complex of metabolic abnormalities.
METHOD AND RESULTS: We have demonstrated deficiencies in carnitine, taurine and coenzyme Q10 in cardiomyopathic hamster hearts during the late stage of the cardiomyopathy. In another study, we randomized placebo diet against a supplement containing taurine, coenzyme Q10, carnitine, thiamine, creatine, vitamin E, vitamin C, and selenium to cardiomyopathic hamsters during the late stages of the disease. Supplementation for 3 months markedly improved myocyte sarcomeric structure, developed pressure, +dp/dt, and -dp/dt. We also documented carnitine, taurine and coenzyme Q10 in biopsies taken from human failing hearts, the levels correlating with ventricular function. A double-blind, randomized, placebo-controlled trial of a supplement containing these nutrients, given for 30 days, restored myocardial levels and resulted in a significant decrease in left ventricular end-diastolic volume.
CONCLUSION: These experiments suggest that a comprehensive restoration of adequate myocyte nutrition may be important to any therapeutic strategy designed to benefit patients suffering from congestive heart failure.
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