Testosterone increases soft plaque buildup?

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Fernando Almaguer

Well-Known Member
I was watching a video by Dr. Brad Stanfield on Youtube and he mentioned the benefits over risk for someone who truly is testosterone deficient. Saying that these individuals do need HRT but the majority of men do not. Ok, then he said that studies show soft plaque increases that cannot be seen on a calcium score test. Just curious about anyone on the forums thoughts on soft plaque and the dangers/management of said plaque.
 
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I was watching a video by Dr. Brad Stanfield on Youtube and he mentioned the benefits over risk for someone who truly is testosterone deficient. Saying that these individuals do need HRT but the majority of men do not. Ok, then he said that studies show soft plaque increases that cannot be seen on a calcium score test. Just curious about anyone on the forums thoughts on soft plaque and the dangers/management of said plaque.
I would like to see the "studies" that show soft plaque buildup from HRT (T).
 
I would like to see the "studies" that show soft plaque buildup from HRT (T).
It takes one year for soft plaque to become calcified plaque. When you have a CT heart scan is measuring the calcified plaque. It takes more than a year to know if you're slowing down the growth of plaque. That if someone does yearly heart CT scans. Which I wouldn't do because the heart CT scan uses radiation which contributes to cancer.
 
It takes one year for soft plaque to become calcified plaque. When you have a CT heart scan is measuring the calcified plaque. It takes more than a year to know if you're slowing down the growth of plaque. That if someone does yearly heart CT scans. Which I wouldn't do because the heart CT scan uses radiation which contributes to cancer.
Do we know why soft plaque increases substantially on TRT?
 
Do we know why soft plaque increases substantially on TRT?
I don't think it does. Many things contribute to plaque growth. All plaque that grows in the arteries starts as soft plaque. Then it's slowly becomes calcified plaque which is safe stable plaque. Uncontrol plaque growth can grow at 30% a year and that's where the issues come in. The unstable plaque can rupture and cause a blockage which can cause a heart attack or stroke.

Through exercise your arteries can open up and increase in size. Which will look normal with a catheterization. Through exercise you can also make shearing which is your body making natural bypasses.

A few years ago my dad had a stent put in his artery going to his kidney because it was blocked and when they looked at it they saw his body was already making a natural bypass.
 
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I don't think it does. Many things contribute to plaque growth. All plaque that grows in the arteries starts as soft plaque. Then it's slowly becomes calcified plaque which is safe stable plaque. Uncontrol plaque growth can grow at 30% a year and that's where the issues come in. The unstable plaque can rupture and cause a blockage which can cause a heart attack or stroke.

Through exercise your arteries can open up and increase in size. Which will look normal with a catheterization. Through exercise you can also make shearing which is your body making natural bypasses.

A few years ago my dad had a stent put in his artery going to his kidney because it was blocked and when they looked at it they saw his body was already making a natural bypass.
That is Amazing Vince.
 
I was watching a video by Dr. Brad Stanfield on Youtube and he mentioned the benefits over risk for someone who truly is testosterone deficient. Saying that these individuals do need HRT but the majority of men do not. Ok, then he said that studies show soft plaque increases that cannot be seen on a calcium score test. Just curious about anyone on the forums thoughts on soft plaque and the dangers/management of said plaque.


Testosterone Treatment and Coronary Artery Plaque Volume in Older Men With Low Testosterone (2017)
Matthew J. Budoff, MD, Susan S. Ellenberg, Ph.D., Cora E. Lewis, MD, MSPH, Emile R. Mohler, III, MD, Nanette K. Wenger, MD, Shalender Bhasin, MD, Elizabeth Barrett-Connor, MD, Ronald S. Swerdloff, MD, Alisa Stephens-Shields, Ph.D., Jane A. Cauley, DrPH, Jill P. Crandall, MD, Glenn R. Cunningham, MD, Kristine E. Ensrud, MD, MPH, Thomas M. Gill, MD, Alvin M. Matsumoto, MD, Mark E. Molitch, MD, Rine Nakanishi, MD, Negin Nezarat, MD, Suguru Matsumoto, MD, Xiaoling Hou, MS, Shehzad Basaria, MD, Susan J. Diem, MD, MPH, Christina Wang, MD, Denise Cifelli, MS, and Peter J. Snyder, MD



Screenshot (15078).png


 
 


Adverse cardiovascular events and mortality in men during testosterone treatment: an individual patient and aggregate data meta-analysis (2022)


In summary, our findings indicate that testosterone treatment did not increase the risks of any subtype of a cardiovascular event in men with hypogonadism and did not identify any patient characteristics that were associated with a significantly increased risk of cardiovascular events during testosterone treatment.
Furthermore, we observed a similar mortality rate during testosterone treatment when compared with placebo, which was reassuring. A meta-analysis of several observational studies63 reported an association between low endogenous testosterone concentrations and increased risk of cardiovascular events, suggesting, notwithstanding the possibility of reverse causality, that testosterone therapy might result in some beneficial effects on the cardiovascular system. According to the results of our analysis, the overall short to the medium-term effect of testosterone seems neutral.

In view of the lack of consistent cardiovascular event classification, adjudication, or reporting within trials, we did a masked analysis of each individual adverse event by two independent clinicians to classify cardiovascular events from all IPD studies objectively. We successfully obtained data from 3431 (61·3%) of the 5601 participants included in eligible published trials, but IPD from some studies could not be included due to data loss, retirement or death of lead investigators or unwillingness of two pharmaceutical sponsors (Bayer AG, Kyowa Kirin) to disclose them. To assess the effect of studies for which IPD were not available, we extracted appropriate aggregate study-level data and incorporated them alongside the IPD using two-stage IPD random-effect meta-analyses.64 Our aggregate meta-analysis suggested that outcome data were not significantly discrepant between our IPD and non-IPD studies. Nevertheless, we cannot exclude that a high number of unreported cardiovascular events in the nonIPD studies could ultimately change the conclusions of our analysis. The very small total number of deaths recorded during testosterone trials limits our ability to analyze why they occurred. The mean follow-up of included randomized controlled trials was 9·5 months, which might be too short for atherosclerotic plaque progression to accrue. This is important since the Testosterone Trials observed that a 12-month duration of testosterone treatment was associated with a significantly greater increase in coronary artery non-calcified plaque volume versus placebo, in older men.65 This finding has led some to advocate coronary artery calcium scoring before treatment of high-risk individuals with underlying cardiovascular disease, due to the remaining possibility that testosterone might be riskier in such individuals.

*However, we observed no significant associations between existing (baseline) cardiovascular or cerebrovascular events and risks of future events during the first 9·5 months after initiation of testosterone treatment
 


The data remain inconclusive, and many men with hypogonadism who might benefit from testosterone replacement therapy could be unnecessarily deterred from this potentially helpful therapy.

To help shed light on this clinical dilemma, in this issue of The Lancet Healthy Longevity, Jemma Hudson and colleagues10 did a meta-analysis of 35 placebo-controlled trials of testosterone replacement therapy that included 5601 men with low baseline testosterone concentrations (≤12 nmol/L [350 ng/dL]) and 17 of these trials had individual patient-level data available. The mean duration of treatment was 9·5 months. However, during this short-term follow-up, reassuringly, there was no significantly increased risk of cardiovascular events between the testosterone replacement therapy group and placebo groups (odds ratio 1·07 [95% CI 0·81–1·42]; p=0·62). Furthermore, there was no particular subgroup identified at significantly increased risk for cardiovascular events with testosterone replacement therapy. The average age of participants in the trials was 65 years (SD 11), and about 8% of participants had a history of myocardial infarction. However, there was no evidence for treatment interaction by baseline cardiovascular status or age.

First, congratulations to the authors for performing the largest individual-level analysis of testosterone trials to date. The authors were able to investigate the relationship of testosterone replacement therapy with multiple subtypes of cardiovascular disease and non-cardiovascular outcomes, as well as changes in several physiological markers (ie, glycemia, blood pressure, hematocrit, and lipids).
Although the authors report significant reductions in total cholesterol, high-density lipoprotein cholesterol, and triglycerides with testosterone replacement therapy, it should be acknowledged that these changes were rather modest— for example, only a 3% difference in low-density lipoprotein cholesterol concentrations was observed.

Although their analysis is reassuring for safety, meta-analyses are only as good as the underlying data available. Unfortunately, the data are still too insufficient to make conclusions on outcomes because the follow-up period was too short. The duration ranged from 3 months to 3 years in the trials and results were not changed by including follow-up time in the models, but there was little evidence to support cardiovascular safety beyond a 12-month duration. Future trials will require longer follow-ups.


There is an ongoing cardiovascular outcome trial for testosterone replacement therapy—the TRAVERSE trial (NCT03518034). This trial enrolled 5246 men between the ages of 45–80 years with low serum testosterone concentrations (<300 ng/dL) who have at least one sign or symptom of hypogonadism and either have established cardiovascular risk or are at high risk for cardiovascular disease. Participants were randomly assigned to receive testosterone gel or placebo, and the primary outcome is a major adverse cardiovascular event (nonfatal myocardial infarction, non-fatal stroke, or cardiovascular death) at 60 months. The trial began in 2018 and is anticipated to finish in late 2022.

In summary, we should wait for the results of TRAVERSE to be published before the widespread use of testosterone replacement therapy is considered. Certainly, great caution is advised regarding the use of testosterone replacement therapy in people with established atherosclerosis due to the findings of plaque progression in the Testosterone Trials7 and the excess cardiovascular events observed in the TOM trial.6 At this time, hormone therapy should still be used selectively, paying attention to the cardiovascular risk profile in individuals.
 
I was watching a video by Dr. Brad Stanfield on Youtube and he mentioned the benefits over risk for someone who truly is testosterone deficient. Saying that these individuals do need HRT but the majority of men do not. Ok, then he said that studies show soft plaque increases that cannot be seen on a calcium score test. Just curious about anyone on the forums thoughts on soft plaque and the dangers/management of said plaque.
I have a heart doctor and around 2004 i felt a little off. In 2009 he did a heart catheterization procedure were he found minimal plaque build up in 2 areas and he said nothing to worry about just come see me once a year. In 2014 he did a follow-up heart catheterization and no changes. I started TRT , i believe 2016 which my heart doctor was ok with it and mentioned to keep an eye on my hematocrit. In 2021 i was feeling off so he did a follow up heart cath and the 2 areas where he had found plaque build up were clean with no plaque.(I also change the way I was eating, cut most of my sugars out, no corn, flower... mainly eating good carbs and keeping up with protein intake. I eat lots of salmon, chicken, turkey meat.....)My problem was a small progression of my COD. He found a small area in one of my arteries that was a little wider than normal causing sluggish flow. Nothing to do with TRT and also recommend to stay on TRT. From my research TRT levels below 500 can cause heart disease an many otther problems . Besides my trt levels being low and dealing with COD this is why I decided to get on trt. At times i have my moments dealing with sluggish flow but thats when im extremely exorting myself while exercising. My mind wants to keep going but my body cant keep up. I guess its part of getting old. Besides that i feel strong and healthy. Keep strong and keep doing your research. Hope this helps.
 


4. Conclusion

The therapeutic approach for TT for symptomatic hypogonadism and low testosterone levels associated with aging, obesity, and systemic illness presents challenges. These conditions are intricately linked with CVD outcomes and may confound the relationship between low testosterone and CVD. Although observational studies suggest an association between low testosterone and increased risk of CVD, results from testosterone supplementation are inconsistent. RCTs indicate that short-term TT at standard replacement is not associated with increased CVD risk. Nevertheless, the cardiovascular sub-study of T Trials observed increases in NCP and CAC, signaling the need for further investigation into potential long-term implications of TT.

The TRAVERSE trial, a landmark study unique in its capacity to evaluate CVD events, contributes valuable insights into the short-term safety of TT at lower physiological levels. However, the long-term effects and implications of mid to high physiological testosterone levels are not yet fully understood. The trials’ limitations — achievement of only low-normal testosterone levels, high discontinuation rates, brief follow-up period, and high loss to follow-up rate — suggest that the findings should be interpreted with caution. It is important to avoid generalizing the safety of TT based on these results alone and to approach the extrapolation of TRAVERSE’s conclusions to higher dosages or longer-term therapy with caution.

The decision to initiate TT requires a nuanced approach, which must account for current gaps in evidence regarding CV safety. A personalized assessment and management of CVD risk factors is essential for older men with known CVD. The CV effects of exogenous testosterone, when given to maintain physiological levels, remain to be fully explored. In this regard, an important question remains the identification of male patients with symptomatic hypogonadism who may benefit from TT. This topic continues to be the subject of ongoing debate. Hopefully, future trials will provide clarity on whether TT confers beneficial, neutral, or adverse cardiovascular effects in middle-aged and older men. Until definitive evidence surfaces, clinical practice should exercise caution and prioritize individualized care with informed discussions regarding the potential CV implications of TT.
 
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