The shit, jice, guear, whatever you want to call them, let’s talk about steroids. The abuse of anabolic-androgenic steroids (AAS) has become an increasingly popular topic in the lay media, whether it is discussion of abuse by athletes or the proceedings in congress. It’s an always-popular topic on internet bodybuilding websites with varying outlooks and advice being offered. Generally, even amongst self proclaimed expert users or users that have “done the research” there is an attitude that the medical literature does not delineate any significant risks that might be associated with AAS abuse, or that it would be impossible to draw a conclusion from what literature exists on the subject. This just isn’t true.
This article is not supposed to go into issues of morality or judge behaviors. I’m not even going to tell you “don’t do drugs!” This article is supposed to be a no-nonsense look at selected published and peer-reviewed articles related to the use of AAS in the fashion that bodybuilders and other athletes use them—which in the medical literature is considered abuse. It is an attempt to make sure people that insist on taking risks at least have a better idea of the risks they are potentially taking and the possible ramifications of said risks.
So what does the medical literature say? Are there double-blind placebo controlled case studies evaluating the efficacy and safety of various AAS compounds for packing on tons of lean mass and getting yoked? Of course not. No researcher would ever find funding or approval from a research board for a study like that.
So what does the medical literature say? More accurately, what can be inferred from the literature without making quantum leaps of faith regarding the safety of steroid use (I feel AAS efficacy is unquestionable and irrelevant at this point)? Volumes. To try and cover it all would be extremely difficult. With that in mind I have selected a specific risk that might be associated with AAS abuse—a risk I consider to be both the most significant and researched supported. Let’s look at the potential risk of cardiovascular complications.
This is going to be sort of a crash course in cardiovascular pathology, specifically atherosclerosis, and then we will tie it all back to AAS use. I’m going to spare you my vast knowledge of things like VCAM-1, the various cytokines and chemokines, and all that junk and just try and give you a clear picture of what’s going on.
So basically, blood vessels are made of three layers. From outside in they are the Adventitia, the Media, and the Intima. The Intima is lined by a single continuous layer of epithelial cells that normally just sit around minding their own business while blood flows in a nice laminar column over them. When these cells are disturbed they become “activated.” That means they start expressing certain molecules on their surface that make them extra sticky and attract cells of inflammation that are designed to help remove and repair the damaging stimulus. The Media contains smooth muscle cells (SMCs) that will migrate to the Intima, proliferate and elaborate collagen under circumstances of chronic injury. This is a bad sign—it is a key marker of a mature atherosclerotic lesion. Don’t worry about the Adventitia for this discussion.
So, let’s discuss things that damage endothelial cells and why this is important. The current model of the pathogenesis of atherosclerosis involves something called the “response-to-injury” hypothesis. That is, chronic injury to the endothelium is seen as the initiating event in the cascade of atherosclerosis.
Time out number two. Let’s talk statistics real quick. Currently, about 40% of US deaths are due to cardiovascular disease (CVD). That means this is relevant information to everyone, because if you don’t die from it, statistically speaking, your best friend will.
Great. So what are sources of chronic endothelial injury? Smoking is a huge one. Cytokines probably have a role as well as virus and other microbes. But the most important are hemodynamic disturbances and hypercholesterolemia.
Here’s a scary thought. The nearly half of you reading this right now, statistically doomed to die of CVD, are already dying and have been since your first decade of life. No joke. Autopsies of kids that have died from unrelated causes (like trauma) almost always have atherosclerotic change or precursor lesions. That’s why what you do as a teenager or young adult can have a drastic impact on speeding you up on the road to death.
Back to atherosclerosis. LDL is made in the liver and its function is essentially to transport cholesterol to the tissues. HDL does the reverse; it brings cholesterol back to the liver (that’s why it’s called good cholesterol) and higher levels are associated with lower risk of developing CVD. So now say your LDL skyrockets and your HDL tanks. The endothelium is damaged and LDL starts to accumulate in the Intima with a decreased transporter back to the liver. This is bad, it doesn’t belong there, so cells called macrophages (think of them as cellular vacuums) come in and start sucking up the LDL trying diligently to digest it, all the while releasing chemicals that attract more help.
Lymphocytes show up and start releasing chemicals that make the macrophages kick into overdrive. Before long they are spilling toxic free radicals all over the Intima causing more damage and oxidizing LDL. Oxidized LDL is bad business. It causes more inflammatory cells to move in to try and help clean up. It eventually begins to accumulate in the phages and SMCs as undigested material in large vacuoles (called foam cells). It also accumulates in the tissue where it is cytotoxic (that means it kills cells). Necrosis (tissue death) begins to occur. By now SMCs have moved in and are dividing and laying down excessive collagen over this big ball of dead cell debris and oxidized LDL and you’ve got a fully matured atherosclerotic lesion. A self-perpetuating cycle. A chink in the armor, a time bomb planted and ready to kill you—be it by occlusion, aneurysm, or acting as a site for generating an embolism.
ATHERSCLEROSIS AND AAS ABUSE
AAS abuse can negatively affect your lipid profile in the worst way. AAS can jack up LDL while decreasing HDL. AAS also cause vessels to over-respond to vasoconstrictors and under-respond to certain vasodilators. So there you are. Two major causes for endothelial injury can be induced by AAS abuse: hemodynamic change and hypercholesterolemia. This is well documented in various animal models (which are the norm for the study of atherosclerosis).
Many will argue that most abusers of AAS are on a short cycle. As I mentioned, atherosclerotic disease is a response to chronic injury that begins very early in life so a short cycle might not be sufficient to induce injury; however, consider the following. By the time most users are doing their first cycle (for 2/3 of users this is age 16) they likely already have some atherosclerotic change, and the 4-16 week increase is just adding fuel to an already burning fire. Add to that the average AAS abuser has 5 cycles under their belt and they are experiencing a significant amount of time with an altered lipid profile. And, although this is purely speculative, possibly ample time to cause serious damage.
About now most people are asking “where are the bodies?” Where’s the proof that this actually happens? There are several published case reports of young AAS abusers that died of cardiac sudden death; however, at autopsy there were no abnormalities of their coronary arteries. So while this doesn’t help with making a connection between AAS use and atherogenesis, it does create at least a casual relationship between AAS use and rare cardiac complications.
There are other case reports that seem to indicate AAS abuse is an independent risk factor for atherogenic and cardiac events. For example, there was a report of a young AAS abusing bodybuilder with no other risk factors for atherogenesis that was diagnosed with extensive and multiple coronary artery lesions after experiencing an arrhythmia. There are at least three other reports of young AAS abusing bodybuilders who suffered an acute cardiovascular event (myocardial infarction or stroke) with no other risk factors. There is additional information fingering AAS abuse as causes of cardiac hypertrophy and associations with other cardiac disorders such as dilated cardiomyopathy. This information, when taken as a collection, becomes quite relevant and alarming.
The people I believe to be most frequently experiencing premature death are much older—in their mid 30s to late 40s. These are people that likely would have died from CVD anyway, but much later in life. They won’t test positive for steroids and have likely long forgotten the moments of indiscretion in their youth and thus slip through the net of the epidemiologist.
So you can see the problem. It would certainly be prudent to consider AAS abuse completely contraindicated in those that already have elevated risk factors for CVD, most notably a family history, genetic abnormalities, hyperlipidemia, hypertension, smokers, and diabetics.
The only way to determine if you are in this category is to get blood work before your cycle. Things to check are triglycerides, total cholesterol, LDL, and HDL. You can get this done for free by donating blood. If any of these values are elevated or borderline, AAS use isn’t for you. If these values do come back elevated, you should consider having homocysteine and C-reactive protein levels measured. While their exact mechanisms in atherosclerosis aren’t completely understood, they are generally accepted as good predictors of prognosis and how aggressively you should be treated.
Monitor your blood pressure. If it is consistently over 130 systolic or 90 diastolic (considered borderline hypertensive under the JNC7) you need to abstain from AAS use. Hypertension is intimately associated with CVD. The same goes for athletes with diabetes and smokers. I know I promised not to say, “don’t use drugs” but I am going to say don’t smoke. It does nothing good. I can’t stress enough, if you already have risk factors for CVD, adding an additional risk factor is a terrible, and probably deadly, idea.
If you decide AAS abuse is for you, despite the potential risks, I highly recommend you take action to counter their lipid altering effects. If you are using an alkylated steroid you need to forget about alcohol. These compounds are already significantly hepatotoxic, and adding liquor is just adding insult to injury. Also, quit smoking. I’m serious. Niacin and statins are of course an option, but are not without side effects of their own. An alternative is phosphatidyl inositol. Research shows it to be equally effective in raising HDL as niacin. A good source is lecithin.
Fish oil and SesaThin are also two compounds that have been shown to be beneficial in lipid control. Antioxidants are also very important—especially vitamin C. Inflammation and oxidation are key steps in the progression of atherosclerosis and this might be a cheap means of putting the breaks on the cycle. The cornerstone of any lipid control protocol should be a healthy diet, with an emphasis on avoiding transfatty acids and saturated animal fats. Please keep in mind these countermeasures will all be a bit like pissing in the wind. The only real way to normalize the changes will be cessation of drug abuse and return of hormones to normal levels.
The recent increase in media attention to AAS abuse is actually a good thing. It will make it more difficult for young people to obtain them; additionally, it has already sparked a significant amount of research in the area. Just this month a multitude of studies have been published including a cohort study indicating AAS users are more likely to experience certain illnesses than non-using parts of the population.
This research will ultimately bring up the same question any potential AAS abusers must consider: do the ends justify the means? For instance, say that you decide not to abuse AAS based on my theory and the theory later turns out to be completely wrong. You’ve essentially lost nothing. You can still build a great body without chemical modification; it’s just a little tougher. On the other hand, if I’m correct and you choose to not head my warning you could be putting yourself in an early grave. Be warned. Be safe.
Kumar V, Abbas AK, Fausto N: Robbins and Cotran Pathologic Basis of Disease 7th Edition. Elsevier, 2005.
Glass CK, Witzum JL: Atherosclerosis: the road ahead. Cell 104:503, 2001
American Heart Association (AHA). Heart Disease and Stroke Statistics – update 2005.
Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7)
Hall R, Hall R: Abuse of Supraphysiologic Doses of Anabolic Steroids. Southern Medical Association, 2005.
National Institute on Drug Abuse (NIDA). Research report. Anabolic steroid abuse; 2000.
Ammar EM, Said SA, Hassan MS. Enhanced vasoconstriction and reduced vasorelaxation induced by testosterone and nandrolone in hypercholesterolemic rabbits. Pharmacol Res. 2004 Sep;50(3):253-9.
Merkel LA, Rivera LM, Bilder GE, Perrone MH. Differential alteration of vascular reactivity in rabbit aorta with modest elevation of serum cholesterol. Circ Res. 1990 Sep;67(3):550-5.
Sanz M, Ganado P, Ruiz E, Tejerina T. Effect of trandolapril on vascular responsiveness in cholesterol-fed rabbit-isolated arteries. Eur J Pharmacol. 2000 Jun 2;397(2-3):359-65.
Ferrer M, Encabo A, Marin J, Balfagon G. Chronic treatment with the anabolic steroid, nandrolone, inhibits vasodilator responses in rabbit aorta. Eur J Pharmacol. 1994 Feb 3;252(2):233-41.
Mudaliar JH, Freischlag JA, Johnson D, Coe DA, Kelly H, Hanson L, Cambria RA, Seabrook GR, Towne JB. Combined exposure to cigarette smoke and hypercholesterolemia decreases vasorelaxation of the aorta. J Vasc Surg. 1997 May;25(5):884-9.
Huie MJ, An acute myocardial infarction occurring in an anabolic steroid user. Med. Sci. Sports Exerc. 26 (1994), pp. 408–413.
Fischer M, Appleby M, Rittoo D and Cotter L, Myocardial infarction with extensive intracoronary thrombus induced by anabolic steroids. Br. J. Clin. Pract. 50 (1996), pp. 222–223.
Meuis C, Spyridopoulos I, Kühlkamp V and Seipel L, Manifestation of severe coronary heart disease after anabolic drug abuse. Clin. Cardiol. 19 (1996), pp. 153–155.
Frankle MA, Eichberg R and Zachariah SB, Anabolic androgenic steroids and a stroke in an athlete: a case report. Arch. Phys. Med. Rehabil. 69 (1988), pp. 632–633.
Glazer G, Atherogenic effects of anabolic steroids on serum lipids levels. Arch. Intern. Med. 151 (1991), pp. 1925–1933.
Kantor MA, Bianchini A, Bernier D, Sady SP and Thompson PD, Androgens reduce HDL2-cholesterol and increase hepatic triglyceride lipase activity. Med. Sci. Sports Exerc. 17 (1985), pp. 462–465.
Schänzer W, Metabolism of anabolic androgenic steroids. Clin. Chem. 42 (1996), pp. 1001–1020.
Fineschi V, Baroldi G, Monciotti F, Paglicci RL and Turillazzi E, Anabolic steroid abuse and cardiac sudden death. Arch. Pathol. Lab. Med. 125 (2001), pp. 253–255.
Kennedy MC and Lawrence C, Anabolic steroid abuse and cardiac death. Med. J. Aust. 158 (1993), pp. 346–348.
Dickerman RD, Schaller F, Prather I and McConathy WJ, Sudden cardiac death in a 20-year-old body builder using anabolic steroids. Cardiology 86 (1995), pp. 172–173.
Petersson A, Garle M, Granath F, Thiblin I. Morbidity and mortality in patients testing positively for the presence of anabolic androgenic steroids in connection with receiving medical care A controlled retrospective cohort study.
Drug Alcohol Depend. 2005 Aug 23