Steroids - Fact & Fiction
During the research for this article, the author could not find one definitive statistic that could categorically determine steroids as being the influential factor behind any single death yet, we are informed that smoking is the influential factor in 47,300 death’s, through various methods such as cancer, atherosclerosis and heart disease. Why is this linkage not possible with regard to AAS? The answer is simple. There is not enough research data available, as most governments will not allow such research to be carried out. Some research has been carried out regarding deaths from AAS use.
Darke, S. and Torok, M. (2014) researched the deaths of 24 males who all died at a mean age of 31.7 years. The characteristics, pathology and toxicology of the individuals were investigated. Characteristically the causes of death were accidental drug toxicity (62.5%), suicide (16.7%) and homicide (12.5%). In terms of drugs profiles, the following AAS profiles were found. Abnormal testosterone epitestosterone ratios were reported in 62.5%, followed by metabolites of nandrolone (58.3%), stanozolol (33.3%), and methandienone (20.8%). A key fact herein is that 23 of the 24 individuals tested positive for ‘other’ chemical substances including psychostimulants. In about 50% of the individuals there was also testicular shrinkage. Several of the individuals had increased left ventricle hypertrophy and narrowed coronary arteries.
The issue with this research is not the method or subsequent findings, it is the way in which other agencies or individuals such as the media, bloggers and anti-steroid proponents have represented this work. Headlines such as ‘Sudden or un-natural deaths involving anabolic androgenic steroids’ deviate the findings in a massive way and totally discount all of the evidence that has been represented. For example, nearly 30% of the individuals died as a result of homicide or suicide. In what way is the blood steroid profile relevant to this ‘fact’? The other individuals died as a result of drug toxicity which can include anything from an overdose, allergic reaction or ‘bad’ drugs. The fact that many of these subjects used stimulants has been totally discounted from the headline. This is a spurious representation of research findings when that research stated that ‘psycho-stimulant toxicity was the direct cause of death in eight of the 24 deaths and opioid overdose was the direct cause in seven’. The researchers have also not mentioned that stimulants can place a stress on the heart that can also increase left ventricle hypertrophy. Science is often misinterpreted to suit the agendas of individuals and not to divulge the truth.
Another study on adult male mice did provide some quite damning evidence to the proponents of steroid use. Bronson F.H., Matherne C.M. (1997) carried out a study on mice. The test group were exposed to four AAS for a period of 6 months. They were given the AAS at 5 or 20 times the normal levels that would be expected for mice. One year later the mice were around 20 months old. The following markers were found as a result of this experiment. 52% of the mice who were given the higher AAS dose had died. This was compared to 35% who had been given the lower dose. The control group had a far lower 12% deaths. When autopsied the mice who were given’ the AAS were typically found to have tumours in their livers and kidneys and some heart damage. Some mice had all of these conditions.
This study clearly identified that AAS do have some negative health implications and might certainly, in this instance, have resulted in premature death rates of the mice. However, it might be assumed that any significant overdose of any drug might have similar negative effects. Also, would the dosage being administered orally or intra-muscularly make a difference to these results? The death rate was dose dependant i.e. the greater the dose the more damaging the effect. This infringes on the premise of ‘use’ or ‘abuse’. Would a bodybuilder using smaller doses in a medically correct way, experience less physiological damage while reaping the muscular benefits? Finally, would the use of aromatase inhibitors such as Arimidex have reduced some of the negative health implications? Sometimes ‘answers’ require so many more questions. But this is the nature of science!
There are many more studies that are relevant to this specific area, but for now, we will move away from the morose study of drugs and death rates and move towards medical implications short of the individual demise.
Physiological Implications of AAS Utilisation
There are many physiological implications that are purportedly related to AAS utilisation. Some of the areas that might be of significance are:

There Are an Estimated 60,000 Recreational Steroid Users in the UK
As with all areas regarding science and the multi-dimensional human body, studies often show controversial or opposing findings. There is no doubt that anabolic steroids do have significant effects on the body. It is not in the remit of this article to cover each and every one. That would take an entire encyclopaedia of information. But as a conclusion to part two of this article, it must be realised that any drug has side effects and these may be beneficial or damaging. The actions they exhibit are based on a plethora of individual factors. We will discuss the physiological implications of steroid use in further articles.
References
Baggish, A. et al (2010). Long-Term Anabolic-Androgenic Steroid Use Is Associated With Left Ventricular Dysfunction. Circulation Heart Failure. 3: 472 - 476
Brower, K.J. (1997) Withdrawal from Anabolic Steroids. Current Therapy in Endocrinology and Metabolism 6: 338-343
Bronson, F.H., and Matherne, C.M. (1997). Exposure To Anabolic-Androgenic Steroids Shortens Life Span Of Male Mice. Medicine and Science in Sports and Exercise 29 (5): 615-619
Darke, S., Torok, M. and Duflou, J. (2014), Sudden or Unnatural Deaths Involving Anabolic-androgenic Steroids. Journal of Forensic Sciences.
Dickerman R.D., Schaller F., McConathy W.J. (1998) Left ventricular wall thickening does occur in elite power athletes with or without anabolic steroid use. Cardiology. 90 (2):145-8
DrugScope (2014) Deaths: Statistics and Analysis. http://www.drugscope.org.uk/ (Date Accessed 2014)
Hartgens, F. Rietjens, G. Keizer, H., Kuipers, H. and Wolffenbuttel, B.(2004) Effects Of Androgenic-Anabolic Steroids On Apolipoproteins And Lipoprotein. British Journal of Sports Medicine. Jun, 38(3): 253–259.
Hartgens F., Kuipers H. (2004) Effects of Androgenic-Anabolic Steroids in Athletes. Sports Medicine. 34(8):513-54.
Hall, M. Ph.D.; Levant, S. and DeFrances, C. Ph.D. (2012) Hospitalization for Congestive Heart Failure in America. U.S. Department of Health and Human Services. United States America
Hoberman, J.M., and Yesalis, C.E. (1995) The history of synthetic testosterone. Scientific American 272(2): 76-81
Nilufer, A. (2012) 'Steroids killed our son': Teenager tried to bulk up his muscles. Within weeks he was dead’. http://www.mirror.co.uk/news/real-life-stories/teenager-used-steroids-to-bulk-up.
Sullivan, M.L., Martinez, C.M., Gennis, P. and Gallagher, E.J. (1998) The Cardiac Toxicity Of Anabolic Steroids. Progress in Cardiovascular Diseases. 41(1): 1-15
United Kingdom Office for National Statistics (2012) http://www.ons.gov.uk/ (Date Accessed 2012)
Vanberg, P. and Atar, D. (2010) Androgenic Anabolic Steroid Abuse and the Cardiovascular System. Handbook of Experimental Pharmacology Volume 195, pp 411-457
There are also some genitourinary issues such as reduced sperm count, menstrual irregularities and masculinization. But for this section, we will discuss cardiovascular based issues.
In terms of cardiovascular issues, there are many implications that are theorised to occur as a result of AAS use. Some of these include left ventricular hypertrophy, reduced left ventricular function, arterial thrombosis, pulmonary embolism, increased blood pressure and myocardial infarction.
Left ventricle hypertrophy is one of the theorised implications of AAS utilisation. Most studies that use echocardiographic methods of measuring heart size exemplify the fact that bodybuilders or powerlifters have significantly increased heart wall (myocardium) wall thickness. In post mortems, this physiological adaptation is also noted and is often attributed to the use of AAS which have been found in greater than normal amounts in the blood. Rather a clear-cut argument in the first instance but a study by Dickerman R.D., Schaller F., McConathy W.J. (1998) provided a significant counter-argument.
The researchers examined 4 elite resistance-trained athletes using two-dimensional echocardiography. They also examined data from the individual left ventricular dimensions of 13 bodybuilders from previous echocardiographic studies. All 4 elite resistance-trained athletes had left ventricular wall thicknesses beyond 13 mm. From the previous studies, 43% of the drug-free bodybuilders and 100% of the steroid users had left ventricular wall thickness beyond the normal range of 11 mm. In all of the subjects, there was no indication of diastolic dysfunction. The research demonstrated that left ventricular wall thicknesses were found routinely in elite resistance-trained athletes who have not used anabolic steroids.
However, in a study by Baggish et al (2010), 19 weightlifters of whom 12 were long-term AAS users and 7 whom were non-AAS users, were examined using echocardiography to assess left ventricle ejection fraction and left ventricular systolic strain. The research identified that left ventricle structural parameters were the same between the individuals. However, the AAS users had significantly lower left ventricular ejection fraction (50.6% - below normal). The AAS users also demonstrated decreased diastolic function. The researchers arrived at the conclusion that cardiac dysfunction was sufficiently higher in AAS users and might be sufficient enough to increase the risk of heart failure.
Now let us look at lipoproteins. Lipoproteins are special particles made up of droplets of fats surrounded by a single layer of phospholipid molecules. There are several types of lipoproteins, each with specific functions and profiles; for the purposes of this discussion, we will focus on Low-Density Lipoproteins (LDL) and High-Density Lipoproteins (HDL). LDL is considered to be the ‘bad’ lipoprotein as it is a carrier of cholesterol. The rationale behind this premise is that LDL Cholesterol is responsible for the build-up of plaque on arterial walls leading to conditions such as atherosclerosis. HDL’s are considered the good cholesterol and higher levels are desirable. HDL is believed to ‘scavenge’ and take LDL cholesterol away from the arteries. The question now arises is what is the relationship between steroid use and HDL/ LDL profiles.
Hartgens et al (2004) established that over a 14-week period AAS administration led to decreases in serum concentrations of HDL. This would be potentially detrimental. Hartgens and Kuipers (2004) also proposed in a further study that steroid use had profound effects on the cardiovascular system, mediated by the occurrence of AAS-induced atherosclerosis (due to unfavourable influence on serum lipids and lipoproteins). Many other studies concurred with similar findings regarding the LDL levels. However, it must also be pointed out that some studies are showing AAS interventions might have beneficial effects on LDL and HDL profiles.

