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| Since the Anabolic Steroids Control Act of 1990 became law on November 29, 1990, physicians have struggled with the ethics of becoming involved with patients using anabolic steroids. There are serious repercussions for doctors’ accused of prescribing anabolic steroids to patients for physique augmentation. In addition, most doctors know very little about anabolic steroids and tend to have an exaggerated view of their risks. This results in a reluctance of doctors to adequately care for patients who are suspected of or obviously using steroids. On the other side of this issue is the steroid-using patient. He or she is already hesitant to reveal to their doctor that they are in fact using steroids. They fear being judged by their physician, or even that their physician would try to report their illicit drug use to the authorities. In the end, it is the patient who loses out, not the physician. In an effort to empower and/or enable steroid using individuals to receive adequate care from their personal health care provider, this article will provide information that the patient can take to their physician to encourage a spirit of cooperation without forcing the physician to feel as if they are condoning illegal drug use. This doesn’t guarantee that your doc will cooperate, but it’s worth making the attempt. Communication Starting off on the right foot is a major step forward towards creating a working and mutually beneficial relationship with your physician. Keep in mind that your physician may only be familiar with rumored and overstated side effect associated with anabolic steroid use in the healthy population.1,2 With this in mind, it is important that you not be antagonistic towards your physician. You need him/her if you are to adequately monitor your health. So don’t try to convert or argue with your physician about the side effects. Graciously accept their words of warning or even criticism in exchange for their cooperation. Potential Health Problems Associated with Anabolic/Androgenic Steroid Use Cardiovascular Ask your physician what the greatest risk of using Anabolic/Androgenic steroids (AAS) is and he/she will probably tell you cardiovascular disease. In spite of this view there is no epidemiological data to support this belief. There are however alterations to both cholesterol homeostasis as well as structural changes to the heart muscle. Cholesterol Cholesterol makes up about 13% of the cell membranes. It plays an integral role in controlling the fluidity of the membrane. Acute muscle cell damage as experienced by strength athletes and bodybuilders increases the need for cholesterol and hence initiates cholesterol synthesis within the muscle cell to be used towards repairing the damaged membrane. Keep in mind that when the integrity of the cell membrane is compromised, the cell cannot carry out intracellular functions necessary for muscle growth. It is well known that some AASs can lower high density lipoprotein (HDL) levels . Because of the aromatization of testosterone to estradiol, lipid abnormalities usually do not develop with moderate amounts of the testosterone esters or suspensions, and the ratio of HDL to total cholesterol generally remains constant. However, those compounds that do not aromatize are known to lower HDL. Low HDL levels have been associated with increased cardiovascular risk. Recent research however shows that although some AAS can lower HDL, they may also create an anti-atherogenic environment. Testosterone, despite lowering HDL cholesterol, intensifies reverse cholesterol transport and thereby exerts an anti-atherogenic rather than a pro-atherogenic effect.3 Management Options for Hypercholesterolemia The first treatment option should be dietary. Try to avoid dietary cholesterol and keep saturated fat to 10% of total fat calories. If that doesn’t work, try switching to an aromatizable androgen such as Test enanthate or other ester. There are various drugs available to lower cholesterol. Of these certain ones should be avoided, namely, the "statins". Statins interfere with the cholesterol synthesis pathways, namely by inhibiting beta-hydroxy-beta-methylglutaryl CoA (HMG-CoA). HMG-CoA is used to make cholesterol within cells. The statins are notorious for causing myopathies such as myalgia, myositis and rhabdomyolysis. The drug of choice for the management of hypercholesterolemia in AAS using individuals should be the Fibrates, namely Tricor TM (Fenofibrate micronized/oral). Hematological AAS also change the properties of the blood. AASs increase hematocrit by increasing erythropoesis, or the synthesis of red blood cells. This can lead to increased blood viscosity (thickness). Some AAS using patients will also have an accelerated activation of their hemostatic system as evidence by increased generation of both thrombin and plasmin. On the other hand AAS may also cause suppression of clotting factors II, V, VII, and X, and an increase in prothrombin time. Anti-clotting drugs should never be combined with AAS, as there is a significant amplification of the anti-clotting effect. Treatment options Avoid use of oral anticoagulants while the patient is using AASs. Patients with an increased hematocrit may benefit from increasing they Omega-3 fatty acid intake to 2 grams per day. Also, proper hydration is very important. This may become an area of concern if a patient is preparing for a bodybuilding contest where diuretics are commonly used. Changes to Heart Muscle The changes to heart muscle caused by anabolic steroids are attributed to their anabolic properties in muscle tissue. Left ventricular hypertrophy is characterized by thickening of the left ventricular wall secondary to cardiac fiber enlargement. Left ventricular hypertrophy (LVH) is normally caused by a chronic increase in systemic blood pressure. It may also be seen with sudden or rapid weight gain. The thickening of the ventricular wall due to increased after-load from elevated vascular resistance can be viewed as adaptive protection up to a point. Beyond minor wall thickening, pathological LVH is a strong predictor of serious cardiovascular risk. It is important for physicians to realize that LVH can occur in strength athletes and bodybuilders even in the absence of anabolic steroids use. It was previously believed that the intermittent increase in blood pressure that is caused by heavy lifting was not sufficient to elicit concentric left ventricular hypertrophy (CLVH). Any evidence of CLVH in strength athletes or bodybuilders was seen as a sign of anabolic steroid use. During heavy lifting, systemic blood pressure is increased from what is called the valsalva maneuver. It is simply the act of forceful expiration with the mouth and nose closed producing a "bearing down" on the abdomen. Most people do this during heavy lifts such as squats or deadlifts. Pressure also increases due to blood vessels being occluded by contracting muscles. It should be noted that the LVH seen in bodybuilders and power lifters is called "concentric left ventricular hypertrophy", meaning that it is the result of contracting against acute increased systemic pressure, and is not considered pathological (i.e. unhealthy). "Eccentric" LVH is caused by constant increases of blood pressure, not as a result of the valsalva maneuver but instead due to clinical hypertension that forces the ventricle to expand against resistance. AAS further exacerbate the effects of lifting on the heart. AASs cause anabolism in heart muscle, at times increasing left ventricular wall thickness to 16mm (11mm is considered normal).4 However, LVH caused by resistance training either alone or in conjunction with AAS has yet to result in diastolic dysfunction, or in other words, there is yet no evidence that this thickening of the ventricular wall is pathologic. Treatment options Upon cessation of high intensity resistance exercise and obviously AAS use, ventricular wall thickness returns to within normal ranges as long as hypertension unrelated to lifting is not present. There are no treatment suggestions for LVH caused by resistance training with or without the use of AAS. Hepatic Abnormal liver function tests are another common reported side effect of AAS use. However the main concern, or danger, is the appearance of peliosis hepatitis (An abnormal condition characterized by the occurrence of small blood-filled cystic lesions throughout the liver) or liver tumors. The occurrence of these serious problems is rare. Almost all reported cases are associated with heavy 17alpha-alkylated anabolic steroid use and occur in patients with pre-existing medical conditions.5 As with left ventricular hypertrophy, physicians unfamiliar with the effects of resistance training often misdiagnose abnormal liver function tests. A recent study from the Department of Medicine, University of North Texas Health Science Center had this to say: Numerous reports have noted "hepatic" dysfunction secondary to anabolic steroid use based on elevated serum aminotransferase levels. The authors' objective was to assess whether primary care physicians accurately distinguish between anabolic steroid-induced hepatotoxicity and serum aminotransferase elevations that are secondary to acute rhabdomyolysis resulting from intense resistance training. Surveys were sent to physicians listed as practicing family medicine or sports medicine in the yellow pages of seven metropolitan areas. Physicians were asked to provide a differential diagnosis for a 28-year-old, anabolic steroid-using male bodybuilder with an abnormal serum chemistry profile. The blood chemistries showed elevated aspartate aminotransferase (AST), alanine aminotransferase (ALT), and creatine kinase (CK) levels, and normal gamma-glutamyltransferase (GGT) levels. In the physician survey (n = 84 responses), 56% failed to mention muscle damage or muscle disease as a potential diagnosis, despite the markedly elevated CK level of the patient. 63% percent indicated liver disease as their primary diagnosis despite normal GGT levels. Prior reports of anabolic steroid-induced hepatotoxicity that were based on aminotransferase elevations may have overstated the role of anabolic steroids. Correspondingly, the medical community may have been led to emphasize anabolic steroid-induced hepatotoxicity and disregard muscle damage when interpreting elevated aminotransferase levels. Therefore, when evaluating enzyme elevations in patients who use anabolic steroids, physicians should consider the CK and GGT levels as essential elements in distinguishing muscle damage from liver damage.6 High intensity resistance training will often lead to elevated AST, ALT, and CK while GGT remains in the normal range. This is simply a result of normal acute muscle damage caused by training and is not pathological. Treatment options for signs of liver stress In such cases where 17-alkylated steroids have been abused, there are several treatment options. First and foremost, the individual should be advised of the risks and pathology associated with such drugs and alternatives should be suggested. Because hepatitis associated with AAS use is not due to infection, treatment options are limited. There are some herbal supplement that have shown promise in the treatment of liver disease, namely Milk Thistle and Picrorhiza.7 Silybum marianum (milk thistle) has been shown to have clinical applications in the treatment of toxic hepatitis, fatty liver, cirrhosis, ischemic injury, radiation toxicity, and viral hepatitis via its antioxidative, anti-lipid peroxidative, antifibrotic, anti-inflammatory, immuno-modulating, and liver regenerating effects. Picrorhiza kurroa, though less well researched than Silybum, appears to have similar applications and mechanisms of action. When compared with Silybum, the hepatoprotective effect of Picrorhiza was found to be similar, or in many cases superior, to the effect of Silybum.7 References 1. Windsor RE & Dumitru D 1988 Anabolic steroid use by athletes – how serious are the health hazards? Postgraduate Medicine 84 37–38, 41–43, 47–49. 2. Friedl KE 1993 Effects of anabolic steroids on physical health; anabolic steroids in sport and health. In Human Kinetics, pp 107–150. Ed. CE Yesalis. Champaign, IL, USA: Human Kinetics. 3. Langer C, Gansz B, Goepfert C, Engel T, Uehara Y, von Dehn G, Jansen H, Assmann G, von Eckardstein A. Testosterone up-regulates scavenger receptor BI and stimulates cholesterol efflux from macrophages. Biochem Biophys Res Commun. 2002 Sep 6;296(5):1051. 4. Dickerman RD, Schaller F, McConathy WJ Left ventricular wall thickening does occur in elite power athletes with or without anabolic steroid use. Cardiology 1998 Oct;90(2):145-8 5. Haupt HA & Rovere GD 1984 Anabolic steroids: a review of the literature. American Journal of Sports Medicine 12 69–484. 6. Pertusi R, Dickerman RD, McConathy WJ Evaluation of aminotransferase elevations in a bodybuilder using anabolic steroids: hepatitis or rhabdomyolysis? J Am Osteopath Assoc 2001 Jul;101(7):391-4 7. Luper S. A review of plants used in the treatment of liver disease: part 1. Altern Med Rev. 1998 Dec;3(6):410-21.<!-- google_ad_section_end --> <!-- / message --> <!-- Postbit Legacy changes by DataHero --> | |
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