AA's and irreversible cardio damage

[Montgomery]

As we all know, cholesterol, VLDL and LDL levels increase during and shortly after a cycle. I'm wondering if anybody has any knowledge of credible, academic research regarding the degree to which atherosclerosis is accelerated by juicing, and whether it's irreversible or not.

Thanks boys,

Montgomery

[Drake Hotel]

Excellent text on androgens as regards to CV health:

http://www.endotext.org/male/male16/maleframe16.htm

["Maximus"]

Try this:

don't know if it might ask you for some credentialing; I doubt but try:

http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum

I'm swamped w/tests at school but let me know what you make out of this.

Best,
max

["Maximus"]

Excellent text on androgens as regards to CV health:

http://www.endotext.org/male/male16/maleframe16.htm

I read this awhile back.. very interesting!

Nice find.

[LATS60]

As we all know, cholesterol, VLDL and LDL levels increase during and shortly after a cycle. I'm wondering if anybody has any knowledge of credible, academic research regarding the degree to which atherosclerosis is accelerated by juicing, and whether it's irreversible or not.

Thanks boys,

Montgomery

Iv'e not seen any, and is there any correlation.
All the studies iv'e read that relate to the deleterious effects of anabolic steroids on the cardiovascular system are in association with acute myocardial infarction.

[Montgomery]

Thanks boys. Good reading. Maximus, your first post required a subscription to read it. I typically do less than 700mg/ week and I do 2 cycles a year at the most, so most of those articles citing 'steroid abuse ' don't apply. I feel alright about it actually after reading some of that and some other things I found. Keep the cardio training up and should be ok.

Any other sources?

[Drake Hotel]

Thanks boys. Good reading. Maximus, your first post required a subscription to read it. I typically do less than 700mg/ week and I do 2 cycles a year at the most, so most of those articles citing 'steroid abuse ' don't apply. I feel alright about it actually after reading some of that and some other things I found. Keep the cardio training up and should be ok.

Any other sources?

Do note that in medical context "steroid abuse" refers to all use of steroids outside of a... well, medical context. It doesn't mean a 150-pounder who does 5g of roids, but everyone using AAS for cosmetic and not medical reasons.

[Montgomery]

Iv'e not seen any, and is there any correlation.
All the studies iv'e read that relate to the deleterious effects of anabolic steroids on the cardiovascular system are in association with acute myocardial infarction.

And even then only at high doses.

[Montgomery]

Do note that in medical context "steroid abuse" refers to all use of steroids outside of a... well, medical context. It doesn't mean a 150-pounder who does 5g of roids, but everyone using AAS for cosmetic and not medical reasons.

Good point - although most studies report that adverse affects (if any) are dose dependent.

[LATS60]

Free Testosterone Inversely Related to Carotid Atherosclerosis CME

Release Date: May 23, 2003; Valid for credit through May 23, 2004


May 23, 2003 — Serum free testosterone is inversely related to carotid intima-media thickness (IMT) and plaque score (PS), according to the results of a study published in the June issue of Diabetes Care. Prospective intervention trials are long overdue, the editorialist suggests.

"Male sex is an independent risk factor for cardiovascular disease (CVD)," write Michiaki Fukui, MD, from Osaka General Hospital in Japan, and colleagues. "There is evidence to suggest that low concentrations of testosterone are associated with an increased risk of CVD in men."

Of 253 consecutive men with type 2 diabetes, 154 underwent carotid ultrasound. Free testosterone was inversely correlated with IMT (r = -.206; P = .0103), with PS (r = - .334; P < .001), and with age (r = - .420; P < .0001), and it was positively correlated with total cholesterol (r = .145; P = .0238)

"Large prospective trials and intervention studies are needed to better assess the metabolic and cardiovascular benefits of testosterone," the authors write.

In an accompanying editorial, Shalender Bhasin, MD, and Karen Herbst, MD, PhD, from Charles R. Drew University of Medicine and Science in Los Angeles, California, review the effects of testosterone in animal models and in clinical studies of atherosclerosis, and they agree with the need for prospective, long-term, placebo-controlled, randomized clinical trials.

"The available data suggest that serum testosterone levels in the range that is mid-normal for healthy young men are consistent with an optimal cardiovascular risk profile at any age, and that testosterone concentrations either above or below the physiologic male range may increase the risk of atherosclerotic heart disease," they write. "Prescription sales of testosterone products have been increasing at an alarming rate.... These trends in testosterone sales are of great concern because the long-term risks and benefits of testosterone replacement in older men are largely unknown."

Clinical Context
According to editorialists Bhasin and Herbst, there is a widespread misperception that the sex differences in the prevalence of coronary artery disease (CAD) are due to higher testosterone concentrations in men and that testosterone supplementation in men would adversely affect the plasma lipoprotein profile, therefore increasing the risk of atherosclerotic heart disease.

Case reports of cardiovascular accidents among athletes who had abused androgenic steroids have strengthened this notion; however, there are no data substantiating a cause-and-effect relationship between androgens and cardiovascular disease.

Because there are currently no intervention studies on the effects of long-term testosterone administration on CAD, inferences about the risks of testosterone administration have been derived from studies assessing the effect of testosterone on lipoprotein metabolism, markers of inflammation, and insulin sensitivity.

Although larger than physiologic doses of testosterone and dihydrotestosterone (DHT) undoubtedly decrease plasma high-density lipoprotein (HDL) cholesterol levels, physiologic testosterone replacement in older men has been associated with only a modest decrease or no decrease in plasma HDL cholesterol. Cross-sectional studies of middle-aged men find a direct, rather than inverse, relationship between serum testosterone levels and plasma HDL cholesterol concentrations. Testosterone administration to men has very little effect on total cholesterol, triglyceride, and overall low-density lipoprotein (LDL) levels, but it does decrease LDL particle size.

As men age, their testosterone levels decline and fat mass increases. Serum testosterone levels are correlated inversely with fat mass, particularly visceral fat. Testosterone replacement in young and older hypogonadal men is associated with a reduction in overall fat mass and inhibition of uptake of labeled triglycerides and enhanced lipid mobilization in visceral fat.

Marin and colleagues, writing in the December 1992 issue of the International Journal of Obesity and Related Metabolic Disorders, reported that testosterone supplementation of middle-aged men with truncal obesity and low-normal testosterone levels is associated with a reduction in visceral fat volume, serum glucose concentration, blood pressure, and an improvement in insulin sensitivity, suggesting that testosterone is an important regulator of regional fat metabolism.

The available data suggest that serum testosterone levels in the range that is mid-normal for healthy young men are consistent with an optimal cardiovascular risk profile at any age, and that testosterone concentrations either above or below the physiologic male range may increase the risk of atherosclerotic heart disease. The effects of testosterone replacement on cardiovascular risk in humans have never been directly examined.

Testosterone tends to bind with sex hormone binding globulin (SHBG). But some testosterone remains freely circulating in the bloodstream. Total testosterone is a measure of both free and SHBG-bound forms of the hormone.

The aim of this study was to evaluate the relationship between serum testosterone concentration, and, in particular, free (unbound) testosterone concentration, and carotid atherosclerosis as well as major cardiovascular risk factors in men with type 2 diabetes.

Study Highlights
Serum free and total testosterone concentrations were measured in 253 consecutive men with type 2 diabetes. The relationship between serum testosterone concentration and carotid atherosclerosis, determined by ultrasonographically evaluated IMT and PS, in a subgroup of 154 diabetic patients was evaluated.
Inverse correlations were found between free testosterone concentrations and IMT and between free testosterone concentrations and PS.
The IMT and PS were significantly greater in patients with lower concentrations of free testosterone than in patients with higher concentrations of free testosterone. An inverse correlation was found between serum free testosterone concentration and age.
A positive correlation was found between serum free testosterone and total cholesterol concentrations.
Pearls for Practice
Serum total testosterone concentrations are not significantly different between patients with or without CVD. However, serum free testosterone concentrations were significantly inversely correlated with ultrasonographically evaluated mean IMT and PS, which are early preclinical markers of atherosclerosis.
Serum free testosterone concentration correlated with the severity of atherosclerosis, regardless of the presence of clinical manifestations.

["Maximus"]

Free Testosterone Inversely Related to Carotid Atherosclerosis CME

Case reports of cardiovascular accidents among athletes who had abused androgenic steroids have strengthened this notion; however, there are no data substantiating a cause-and-effect relationship between androgens and cardiovascular disease.

Agreed!

Also,

1: Int J Sports Med. 2003 Jul;24(5):344-51.

Comment in:
Int J Sports Med. 2004 Apr;25(3):241-2; author reply 243-4.
Prospective echocardiographic assessment of androgenic -anabolic steroids effects on cardiac structure and function in strength athletes.Hartgens F, Cheriex EC, Kuipers H.
Netherlands Centre for Doping Affairs, Capelle aan den IJssel, The Netherlands. [email protected]

Since the abuse of androgenic-anabolic steroids (AAS) has been associated with the occurrence of serious cardiovascular disease in young athletes, we performed two studies to investigate the effects of short-term AAS administration on heart structure and function in experienced male strength athletes, with special reference to dose and duration of drug abuse. In Study 1 the effects of AAS were assessed in 17 experienced male strength athletes (age 31 +/- 7 y) who self-administered AAS for 8 or 12 - 16 weeks and in 15 non-using strength athletes (age 33 +/- 5 y) in a non-blinded design. In Study 2 the effects of administration of nandrolone decanoate (200 mg/wk i. m.) for eight weeks were investigated in 16 bodybuilders in a randomised double blind, placebo controlled design. In all subjects M-mode and two-dimensional Doppler-echocardiography were performed at baseline and after 8 weeks AAS administration. In the athletes of Study 1 who used AAS for 12 - 16 weeks a third echocardiogram was also made at the end of the AAS administration period. Echocardiographic examinations included the determination of the aortic diameter (AD), left atrium diameter (LA), left ventricular end diastolic diameter (LVEDD), interventricular septum thickness (IVS), posterior wall end diastolic wall thickness (PWEDWT), left ventricular mass (LVM), left ventricular mass index (LVMI), ejection fraction (EF) and right ventricular diameter (RVD). For assessment of the diastolic function measurements of E and A peak velocities and calculation of E/A ratio were used. In addition, acceleration and deceleration times of the E-top (ATM and DT, respectively) were determined. For evaluation of factors associated with stroke volume the aorta peak flow (AV) and left ventricular ejection times (LVET) were determined. In Study 1 eight weeks AAS self-administration did not result in changes of blood pressure or cardiac size and function. Additionally, duration of AAS self-administration did not have any impact on these parameters. Study 2 revealed that eight weeks administration of nandrolone decanoate did not induce significant alterations in blood pressure and heart morphology and function. Short-term administration of AAS for periods up to 16 weeks did not lead to detectable echocardiographic alterations of heart morphology and systolic and diastolic function in experienced strength athletes. The administration regimen used nor the length of AAS abuse did influence the results. Moreover, it is concluded that echocardiographic evaluation may provide incomplete assessment of the actual cardiac condition in AAS users since it is not sensitive enough to detect alterations at the cellular level. Nevertheless, from the present study no conclusions can be drawn of the cardiotoxic effects of long term AAS abuse.

PMID: 12868045 [PubMed - indexed for MEDLINE]

Now, this doesn't mean much... just says that the data/studies done so far are mixed and inconclusive about the subject of AAS and Heart/Cardiac atrophy. Nevertheless, it doesn't mean that you can "cycle forever" and won't get you screwed up at there's much more involved just than our cardiovascular system.