TRT Accelerates Artery Plaque Buildup

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I was surprised too because I had always read that TRT protected against heart disease. This was published in the Journal of the American Medical Association.

Testosterone Treatment and Coronary Artery Plaque Volume in Older Men With Low Testosterone (2017)

Design, Settings, and Participants

A double-blinded, placebo-controlled trial at 9 academic medical centers in the United States. The participants were 170 of 788 men aged 65 years or older with an average of 2 serum testosterone levels lower than 275 ng/dL (82 men assigned to placebo, 88 to testosterone) and symptoms suggestive of hypogonadism who were enrolled in the Testosterone Trials between June 24, 2010, and June 9, 2014.

Conclusions and Relevance

Among older men with symptomatic hypogonadism, treatment with testosterone gel for 1 year compared with placebo was associated with a significantly greater increase in coronary artery noncalcified plaque volume, as measured by coronary computed tomographic angiography. Larger studies are needed to understand the clinical implications of this finding.

*T Trials found a statistically significant 1-year increase in noncalcified plaque volume (estimated difference 41 mm3 [95% CI 14 to 67 mm3 ]) in hypogonadal elderly males receiving testosterone therapy compared to the placebo group. 29 no statistically significant difference was found in the number of cardiovascular events or calcified plaque progression between the intervention and control group.29


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Low Testosterone in Men: Recommendations on the diagnosis, treatment, and monitoring (2021)

post #9


*There is no evidence showing increased cardiovascular (CV) mortality or morbidity with TTh

*In conclusion, available data showed that when appropriately diagnosed and managed TTh in subjects with TD is not associated with increased CV mortality and morbidity. Possible preliminary positive results on CV outcomes should be confirmed through larger placebo-controlled RCT

*Men with significant erythrocytosis (hematocrit >52%), severe untreated obstructive sleep apnea, or untreated severe congestive heart failure should not be started on treatment with TTh without prior resolution of the co-morbid condition

post #13


*Some authors recommend that TTh be discontinued if hematocrit is >54%, which may be reasonable while baseline hematocrit level >50% is a relative contraindication for starting testosterone therapy. However, these recommendations are based on assumptions – the clinical significance of a hematocrit >54% is unknown

*The lack of increase in cardiovascular events with elevated hematocrit may be due to the fact that T acts as a vasodilator and has anti-atherosclerotic effects [223]. In addition, testosterone is able to decrease plasma concentrations of procoagulatory substances such as fibrinogen and PAI-1 as well as Factor XII [224] Isolated hematocrit elevations can be the result of insufficient fluid intake on a hot day. Only repeated measures of hematocrit >54% should be followed by concomitant administration of aspirin, bleeding, therapeutic phlebotomy, and/or discontinuation of TTh until hematocrit declines below 54%. After normalization of hematocrit levels, TTh can be continued with a reduced dosage

*Periodic hematological assessment is, however, indicated, i.e. before TTh, then 3–4 months and 12 months in the first year of treatment, and annually thereafter. Although it is not yet clear what upper limit of hematocrit level is clinically desirable, dose adjustments may be necessary to keep hematocrit below 52–54%

*Men with significant erythrocytosis (hematocrit >52%), severe untreated obstructive sleep apnea, or untreated severe congestive heart failure should not be started on treatment with TTh without prior resolution of the co-morbid condition


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Testosterone and cardiovascular diseases

Several meta-analyses were subsequently published pooling data from controlled trials, mostly reporting CV safety of TT, although no definitive conclusion could be drawn because of inhomogeneity of patient population, lack of adequate statistical power, and many low-medium quality studies involved.

*On this basis, in 2018 the TRAVERSE trial was implemented, aimed at evaluating the effect of TT on MACE and efficacy measures in hypogonadal men (NCT03518034). The adequate statistical power of the trial enrolling 6,000 men will hopefully provide next year (2022) a definitive answer to the outstanding issue of CV safety of TT.


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Daniel Kelly, Ph.D., Senior Lecturer of Biochemistry at Sheffield Hallam University, reviews data on testosterone’s complex impact on atherosclerosis. He outlines the key stages of atherosclerosis: monocyte activation, monocyte activation/adhesion, monocyte migration, and macrophage activation, and discusses how testosterone impacts each stage with supporting studies.
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