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Daz69

Some thoughts on AAS and Cardiovascular health

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There is much debate regarding AAS and cardiovascular health, and how that use may have negatively impacted major organs and tissue of the body.?

 

Several studies show that high doses of AAS such as nandrolone, may lead to growth-promoting effects on cardiac tissue, as seen in hypertrophic cardiomyopathy, followed by apoptotic cell death which is mediated by membrane-receptor second messenger cascades that increase intracellular Ca2+ influx..

 

AAS abuse associated with sudden cardiac death, myocardial infarction, ventricular remodelling and cardiomyopathy is related to apoptosis..

 

Several studies in isolated human myocytes have shown that AAS bind to androgen receptors and may directly cause hypertrophy, via tissue upregulation of the renin-angiotensin system..

 

AAS abuse causes decrease in high density lipoprotein cholesterol by 20% and increase in LDL cholesterol by 20% due to lipolytic degradation of lipoproteins and their removal by receptors through modification of apolipoprotein A-I and B synthesis. Apolipoprotein B has been experimentally linked to the development of atherosclerosis, mediating the interaction between LDL-C and the arterial wall...

 

These lipoprotein abnormalities increase the risk for coronary artery disease by three to sixfold and may occur within 9 weeks of AAS self-administration. Fortunately, lipid effects seem to be reversible after discontinuation..

 

AAS enhance platelet aggregation and thrombus formation by increasing platelet production of thromboxane A2, decreasing production of prostacyclin and increasing fibrinogen levels..

 

Ischaemic stroke can occur as a result of atherothrombosis or embolisation either in the carotids or the heart as AAS has been associated with changes in vascular reactivity, lipid profile, haemostasis and platelet aggregation. Accordingly, peripheral vascular disease can occur through the same mechanism..


 

I know I keep bringing up these cardiovascular issues on here periodically, but so few people consider them, and it really is worth having some awareness and an idea of how to ameliorate effects where possible...

 

However I think the take-home message is how all these vectors interact to cause serious health problems.

 

So, it's not just factors like lipids that cause clots - it's the platelet aggregation as the more acute factor. But furthermore, the AAS causing inflexibility of the vascular network (poor vasoreactivity) which promotes atherosclerotic plaque formation and makes the heart pump harder = the enlargement of the heart = inefficient pumping = reduced ejection fraction = relatively stagnant eddies of blood = increased risk of clotting.

 

And of course, is the likely increase in PCV (red blood cell concentration), which can be an equally important factor. It seems astonishing that most AAS users don't seem to be aware of the effect AAS have on RBCs and how that could aggravated their condition, but again that's part of the general lack of knowledge I keep referring to.


 

What can we do: fortunately, the lipid/thrombus issue is more of an acute concern that diminishes once the cycle is over, and for most people will pass unremarkably assuming they lead an otherwise healthy lifestyle and don't abuse high-dose AAS for prolonged periods..

 

Most guys on AAS should be using an angiotensin receptor blocker as standard in my opinion (eg Losartan, Olmesartan). Not only will it lower BP, it also prevents and reverses the accumulation of fibrotic tissue, both in the heart and across the cardiovascular system, which is the major concern from AAS use.

 

Cardio: The kind of adaptations we want in the heart are the kind that high intensity cardio bring. It can basically 'enlarge' the capacity of the heart (the chambers) and also improve the ejection fraction. So the heart becomes more efficient per beat, and hence the pulse rate tends to fall - very low in very fit athletes. It does cause a very mild form of hypertrophy, but it arranges the cardiac tissue structurally slightly differently to the type that forms from heavy weight lifting.

 

One of the other positives of HIIT is that it helps to stretch and (theoretically) break up the scarring/fibrotic tissue. We have to bear in mind that intense cardio pumps very large volumes of blood through the heart (unlike weights) which causes a nice eccentric stretch to the cardiac tissue, as opposed to more concentric-focus from weights...

 

Regular blood tests, and blood donation or venesection if hematocrit is too high..


 

[1] J. Payne, P.J. Kotwinski, H.E. Montgomery, Cardiac effects of anabolic steroids, Heart 90 (2004) 473?475.

 

[2] S. Nottin, L.-D. Nguyen, M. Terbah, P. Obert, Cardiovascular effects of androgenic anabolic steroids in male bodybuilders determined by tissue Doppler imaging, Am. J. Cardiol. (2006).

 

[3] L. Fanton, D. Belhani, F. Vaillant, A. Tabib, L. Gomez, J. Descotes, et al., Heart lesions associated with anabolic steroid abuse: comparison of post-mortem findings in ath- letes and norethandrolone-induced lesions in rabbits, Exp. Toxicol. Pathol. (2009).

 

[4] P.D. Thompson, A. Sadaniantz, E. Cullinane, K. Bodziony, D. Catlin, G. Torek-Both, et al., Left ventricular function is not impaired in weight-lifters who use anabolic steroids, J. Am. Coll. Cardiol. (1992) 19.

 

[5] N.A. Hassan, M.F. Salem, M.A.E.L. Sayed, Doping and effects of anabolic androgenic steroids on the heart: histological, ultrastructural, and echocardiographic assessment in strength athletes, Hum. Exp. Toxicol. (2009).

 

[6] J. Marsh, M.H. Lehmann, R.H. Ritchie, J.K. Gwathmey, G.E. Green, R.J. Schiebinger, An- drogen receptors mediate hypertrophy in cardiac myocytes, Circulation 98 (1998) 256?261.

 

[7] P. Liu, A.K. Death, D.J. Handelsman, Androgens and cardiovascular disease, Endocr. Rev. 24 (2003) 313?340.

 

[8] A.D'Andrea,P.Caso,G.Salerno,R.Scarafile,G.DeCorato ,C.Mita,et al.,Left Ventricular early myocardial dysfunction after chronic misuse of anabolic androgenic steroids: a Doppler myocardial and strain imaging analysis, Br. J. Sports Med. 41 (3) (2007) 149?155.

 

[9] S. Sharma, Athlete's heart?effect of age, sex, ethnicity and sporting discipline, Exp. Physiol. 88 (2003) 665?669.

 

[10] M. Galderisi, N. Cardim, A. D'Andrea, O. Bruder, B. Cosyns, L. Davin, et al., The multi- modality cardiac imaging approach to the Athlete's heart: an expert consensus of the European Association of Cardiovascular Imaging, Eur. Heart J. Cardiovasc. Imaging 16 (4) (2015) 353.

 

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Something I've been made aware of only this morning, AAS make pacemaker cells of the heart hypersensitive, leading to conditions such as SVT (supra ventricular tachycardia), which is a super fast abnormal rhythm 100-300bpm.. 

Obviously avoid stimulants..

Symptoms usually subside on their own, but consider lowering your dose or switching compounds if you start to present with SVT..

 

 

 

 

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Hi Daz69,

 

I basically joined this forum because of how well-educated you are on the topic of AAS and health optimization. I have been a lurker for a while and am drawn to your posts. Love your posts about cardiovascular health as well as the mechanisms of trenbolone. I recently did my first cycle (test E at 600mg/wk for 12 weeks) and came off without issue.  I tried adding anavar in the beginning, but that gave me anxiety and insomnia so after trying to lower the doses without much help, I dropped it altogether. I did 500iu of hcg twice per week while on and this kept my nuts from "shutting down." It's been a couple months since cycle ended and my testosterone and other bloods are all back to pre-cycle levels. 

 

Anyways, my plan is to keep cycling, but only about twice per year, taking an equal amount of time off than on. I also have done a ton of research on various AAS and have decided that nandrolones (tren, deca, NPP) are just not for me. I don't even want to put that into my body. The potential for neurological issues, alteration in D2 receptors, and heart complications is enough to keep me far away from that stuff. I have gotten fantastic results from test only and have decided that just test and possibly masteron/proviron will be the only compounds I am going to run. Mast/proviron because they enhance the effects of testosterone and provide a nice hardening effect/boost in libido and erection function. I am basing my cycles off of these particular AAS due to the fact that these are relatively mild and testosterone has probably the most human research, and has been shown to be relatively safe in high doses, even for extended periods. My plan is to do two 3 month cylces per year and never do more than 1g of combined gear per week. 

 

Sorry for the long-winded introduction. My question to you is, do you think that staying away from nandrolones, sticking only to test/masteron/proviron is the safest route in preventing cardiovascular problems? 

 

I have several other bases covered as well, such as:

(1) Doing regular cardio

(2) Ensuring my BP stays <140/80, taking some losartan on cycle if it gets a little high, also if bloating is what's increasing BP, taking anastrazole as needed until BP comes back down

(3) Taking a baby aspirin every other day along with a little K2 to balance it out (K2 also prevents/reverses the calcification of arteries, which AAS promotes)

(4) Hcg a couple times per week (which helps utilize LDL cholesterol for conversion into pregnenolone in the P450 pathway, lowering total serum cholesterol). 

(5) Eating a healthy diet, low in total fat

(6) Ensuring that my BMI does not get too high, which can be a stress to the heart (will never allow it to get >30)

 

If you know of any other ways to prevent cardiovascular complications from AAS, please tell.  What is the best way to keep our hearts health, cycling AAS?

 

I know this is a lot, but I really appreciate your knowledge on these topics. I believe that we all should be investigating how to cycle safely so that we can continue to be doing this into old age if we so choose. That's my goal anyways.  We need to be kind to our organs. Thank you in advance for any input!

 

 

 

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Obviously the best cardio protective method would be to abstain from AAS..

Tissues of the cardiovascular system are AR-positive, with I believe greater receptor density than skeletal muscle, so expect some form of deleterious changes whatever your dosing schedule.. 

 

HIIT cardio is optimal..

 

Losartan is prescription only in NZ, but prudent to include on-cycle if hypertensive for its effects on reducing/reversing myocardial stiffening/fibrosis..

 

Bloating is not your enemy,  embrace it..

 

Anastrozole might be an option (very low dose) to combat effects of oxidative damage from estrogen metabolites...

 

Aspirin, K2 good idea.. (someone's being doing their research)..

 

Cholesterol/fats should be included in all healthy food options, refined sugars/fructose are the issue, not fats.. (I have a post somewhere discussing atherogenic dyslipidemia, dietary fats, cholesterol) its worth a read... What we thought we knew about dietary fats for the last 50 years has been totally reversed, fats are good and always have been.. (if combined with healthy fresh food options, no processed, no refined fructose etc..)....

 

BMI doesn't take into account waist size so totally worthless, muscle is roughly 3 times heavier than fat, height/weight ratio means nothing without taking into account bf%...

 

 

Some of the known harms from AAS cycles include direct oxidative damage to various cells in the testes and brain. And there is some experimental evidence that various free radical scavengers can attenuate these oxidative harms or balance natural recuperative systems. So in terms of cost/benefit it's likely very worthwhile to take some additional supplements on cycle that may help, like taurine, NAC, astragalus, raw cacao, royal jelly, bioavailable curcumin, etc...

 

There has been much advancement in our knowledge regards the importance of mitochondrial health, and their contribution towards oxidative stress within the cellular environment... We have already discussed means of reducing or negating oxidative stress, but that is only one mechanism.. Overworking mitochondria without sufficient time to rest on a daily basis can trigger a negative cascade of mitochondrial stress response and/or death.. Overworking sertoli/leydig cell mitochondria via the use of exogenous hormones or LH mimetics (hCG), without the advantage of pulsatile release, plus off time present with natural hormones, might induce mitochondrial and subsequent cell dysfunction or death...

 

Regards hCG: hCG can cause active Leydig cells to release test in a dose-dependent fashion, and rather like a bleed, unlike the pulsatile way the body does. Which means even if you only have, say, 30% functional Leydig cells left, enough LH can still cause them to release above average levels of test. Which gives the outward appearance of having maintained testicular function, but doesn't protect the cells from on-cycle damage. So it's like squeezing more juice out of fewer active 'testosterone factories' (it also doesn't protect Sertoli cells).

It's only when you cut off that artificial LH tap and hormonal bleed, that you get to see what damage you've actually caused.

 

Low dose hCG does anecdotally seem to help guys on cycle from a number of perspectives like mood, libido etc. It may keep cells more sensitised so that when you come off cycle and natural LH/FSH comes on tap, there's a chance test might start at a slightly higher level. But tbh the idea of 'sensitisation' seems pretty bunk.

In this study, for example: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2360778 all hCG did is inhibit genuine recovery. It caused a transient increase in test output back to normal physiological levels while using hCG, then as soon as that was stopped test dropped back lower than where they started and only slowly recovered naturally thereafter. Which implies hCG didn't sensitise in any way, and if anything caused the opposite.

That could be down to the dose of hCG used, or a number of other factors.

 

hope this is of help..

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On 10/19/2018 at 7:06 PM, Daz69 said:

Some of the known harms from AAS cycles include direct oxidative damage to various cells in the testes and brain

 

Kinda scary the more I read it, starting to put me off cycling.

I always take the taurine and royal jelly, but god knows what damage has been done.

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