Originally Posted by
Swifto
Right I have both full papers now.
To sum up...
It doesnt make comfortable reading at all. But dont bury your head in the sand and think AAS do NOT effect the heart, they do.
The study size is small (17 AAS user's, 9 non).
Mean age is 40 years old.
To quote:
...none of the participants had a history of hypertension,
atherosclerotic vascular disease, heart failure, or exercise
intolerance. AAS users reported taking median (quartile 1,
quartile 3) weekly doses of 675 (513, 950) mg of testosterone
equivalent for 468 (169, 520) lifetime weeks. The groups were
similar in age, prior duration of weightlifting, current number of
hours per week of weight training and other intense athletic
activity, body mass index, and body surface area, but as
expected, AAS users were significantly more muscular than
nonusers as measured by fat-free mass index (Table 1). In other
words, the AAS users had a similar body mass index to nonusers
because the former group had more muscle but less body fat.
Four of the 12 AAS users were currently taking supraphysiologic
doses of AAS at the time of evaluation; 3 were currently
taking only physiological doses of testosterone at 50 to 100
mg/week; 1 had discontinued a course of supraphysiologic AAS
3 weeks prior to evaluation; and the remaining 4 had not used
AAS for at least 6 months prior to the evaluation.
Six (50%) of the AAS users but none of the nonusers
reported a past history of opioid, cocaine, or alcohol dependence.
None of the participants reported amphetamine dependence.
Two (17%) AAS users but none of the nonusers
reported cannabis dependence, 1 past and 1 current. None of
the participants reported a history of cigarette use. Nine
(75%) AAS users but none of the nonusers reported at least
some use of human growth hormone, and 6 of these reported
human growth hormone use for 3 months
Discussion
Results from this study are consistent with previous findings
showing LV diastolic dysfunction10–12 and subclinical LV systolic
impairment10 in AAS users. However, our results suggest
that the cardiac impairment in long-term AAS users may be
more severe than previously reported. Specifically, long-term
AAS users were found to have significant LV systolic dysfunction
both by relative standards (compared to the AAS nonuser
cohort) and by absolute standards (as defined by current clinical
practice). To our knowledge, this study is the first to demonstrate
an association between long-term AAS use and a clinically
relevant reduction in LV ejection fraction.
There is a well-established relationship between LV dysfunction
and exposure both to certain medications29 and to
some drugs of abuse.30–32 Further, the prognostic importance
of toxin-induced cardiac dysfunction has been well documented.
33–36 Data from this study suggest that AAS, particularly
when used over long durations, may be another
important cause of toxin-mediated myocardial impairment.
Although confirmatory data are required, results from this
study suggest that AAS exposure should be a diagnostic
consideration among persons with asymptomatic LV dysfunction
or incident heart failure.
Although several previous studies have reported mild cardiac
dysfunction, LV dysfunction among our AAS users was more severe than previously reported. Several hypotheses might explain
this discrepancy. First, our AAS users were several years
older, on average, than those in 2 of the 3 most recent
studies.10,12 Second, these previous studies selected top-level
competitive bodybuilders,10 squad athletes,12 or individuals from
bodybuilding studios,12 thus possibly favoring healthier individuals
with better cardiac function than the largely noncompetitive
individuals21 in our study.
Finally, the specific AAS compounds
and dosages typically used by our American participants may
have differed from those of participants in previous studies,
which were largely conducted in Europe.
It is noteworthy that our analysis revealed no significant
relationship between cumulative AAS use and cardiac dysfunction.
This observation suggests that AAS-associated
cardiotoxicity might be only partially and unpredictably
related to lifetime dose in a manner similar to the cardiac
toxicity of alcohol.37 Further work is required to determine
whether cardiac function is influenced by factors such as the
recency of AAS use (eg, current versus long past), specific
AAS used (eg, possibly more toxic oral agents5,38 versus
injectable agents), duration of exposure to very high doses
(eg, 2000 mg/wk), or concomitant use of other drugs (eg,
human growth hormone39,40).
There are several important limitations to this study. First,
our sample might not be representative of the overall source
population of long-term AAS users or comparison weightlifters.
Although we used recruitment procedures designed to
generate a sample that is maximally representative,20,21 it is
possible that the group of AAS users in the present study is
not entirely representative of the overall population. Second,
our sample sizes were small and unequal. However, this
limitation would likely produce false-negative findings (ie,
type II errors) rather than false-positive results due to the
reduced statistical power afforded by small sample sizes.
Therefore, the highly statistically significant findings in the
present study, despite the small sample size, suggest that the
association between AAS use and cardiac pathology may be
particularly strong (ie, a very large effect size). Conversely,
the possibility of a type II error must be considered in
instances where group comparisons were not significant. For
example, the lack of association between AAS exposure and
cardiac dysfunction must be interpreted with caution. Future
study with adequate statistical power is warranted to examine
this issue. A third limitation is our reliance on participants’
self-reporting of AAS use. We recognize that errors based on
self-report could have arisen if actual AAS users denied use
and were misclassified as nonusers; individuals classified as
nonusers had unknowingly ingested supplements contaminated contaminated
with actual AAS; or individuals classified as users had
ingested only counterfeit black market AAS and, hence, had
not used genuine drugs.
However, each form of misclassification
would only narrow the differences between groups,
causing us to underestimate the true association of AAS use
with cardiac pathology. A fourth limitation is our use of
retrospective exercise exposure assessment and the possibility
that AAS-users differed from nonusers with respect to
exercise intensity. However, it is unlikely that this factor
contributed to our observations because no prior studies have
demonstrated LV dysfunction secondary to intense, sustained
exercise training. Finally, the cross-sectional nature of this
exploratory study does not permit definitive conclusions
about the long-term clinical implications of our findings and
represents an important area of future work.
In summary, data from the present study suggest that
AAS-induced LV dysfunction may be greater than previously
reported. The reductions in LV systolic function observed in
this group of AAS users are of a magnitude shown to increase
the risk of heart failure and sudden cardiac death in other
populations.41,42 Further work is needed to confirm our
findings and to determine the extent to which AAS-associated
cardiac dysfunction leads to adverse clinical outcomes.
Ouch!
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