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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Basics & Questions
What is TRT and What is NOT TRT
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<blockquote data-quote="RobRoy" data-source="post: 259234" data-attributes="member: 42893"><p>So read a lot and Joseph Hernshaw maybe you should step away from your woke TRT movement and listen to what even the co-author had to say about the traverse study. The problem with you Joseph and read a lot is that you suffer from extreme confirmational bias. You cannot see the forest for the trees. Your writings will be used for some upcoming videos.</p><p></p><p></p><p>The Testosterone Replacement Therapy for Assessment of Long-term Vascular Events and Efficacy Response in Hypogonadal Men (TRAVERSE) trial was designed to determine the effects of testosterone-replacement therapy on the incidence of major adverse cardiac events among middle-aged and older men with hypogonadism and either preexisting or a high risk of cardio- vascular disease. </p><p></p><p></p><p></p><p></p><p></p><p>It enrolled 5,204 men, 45 to 80 years of age, with a mean treatment duration of 21.7 +-14.1 months </p><p></p><p></p><p></p><p></p><p></p><p>Inclusion criteria included meeting the study definition of clinical hypogonadism which was 2 serum testosterone levels less than 300 ng/dL collected between 5 AM and 11 AM </p><p></p><p></p><p>And, the presence of at least one sign or symptom that may be related to low testosterone such as:</p><p></p><p></p><p>Decreased libido, decreased morning erections, decreased energy or fatigue, depressed mood, loss of body hair or reduced shaving, or hot flashes</p><p></p><p></p><p></p><p></p><p></p><p>Participants also had to have pre-existing cardiovascular disease or at least three cardiovascular risk factors.</p><p></p><p></p><p></p><p></p><p></p><p>Pre-existing cardiovascular disease would be a diagnosis of coronary artery disease, cerebrovascular disease, or peripheral artery disease.</p><p></p><p></p><p></p><p></p><p></p><p>Cardiovascular risk factors included hypertension, dyslipidemia, current smoker, stage three kidney disease, diabetes, elevated CRP, or high coronary artery calcium score</p><p></p><p></p><p></p><p></p><p></p><p>Some baseline characteristics : average age was 63 , the average BMI was 35, and the median testosterone level was 227 ng/dL (188-258)</p><p></p><p></p><p></p><p></p><p></p><p>The patients were randomly assigned to either receive transdermal testosterone gel 1.62 % (40.5 mg)or placebo</p><p></p><p></p><p>The dose was adjusted to maintain testosterone levels between 350 and 750 ng/dL. The mean daily dose was 65 +-22mg. At 12 months the median increase in testosterone levels from baseline was 148 ng/dL (34-312)</p><p></p><p></p><p></p><p></p><p></p><p>The primary cardiovascular endpoint was a composite of cardiovascular mortality, nonfatal myocardial infarction or nonfatal stroke. The secondary cardiovascular endpoint was a composite of the primary endpoint plus coronary revascularization</p><p></p><p></p><p></p><p></p><p></p><p>The primary endpoint occurred in 182 patients (7.0%) in the testosterone group and 190 patients (7.3%) in the placebo group . Rates of the secondary endpoint and each of the components of the primary endpoint were similar between the groups.</p><p></p><p></p><p></p><p></p><p></p><p>The conclusion was that in men with hypogonadism and pre-existing or a high risk of cardiovascular disease testosterone replacement therapy was non-inferior to placebo with respect to the incidence of major adverse cardiac events</p><p></p><p></p><p></p><p></p><p></p><p>61% of patients in both groups dropped out ??? What does that tell us? </p><p></p><p></p><p>It tells us that if you only raise testosterone levels a little bit then the patients will notice minimal benefit and will discontinue treatment no different than discontinuing placebo. A little bit of testosterone is not much better than getting nothing at all and this is reflected in the identical dropout rate between the treatment group and the placebo group.</p><p></p><p></p><p></p><p></p><p></p><p>So here is what a couple of endocrinologist are saying about the study in the national media:</p><p></p><p></p><p>"It's important to emphasize that this is a study of men with bona fide testosterone deficiency and symptoms. It doesn't give carte blanche to prescribe to men with normal testosterone concentrations. It doesn't tell us about the safety of that"</p><p></p><p></p><p>“It is essential that the findings be interpreted appropriately and not applied to patient populations beyond middle-aged and older men with documented hypogonadism and established cardiovascular disease or high cardiovascular risk. “They don’t apply to athletes taking super-high doses or to people who don’t have low testosterone levels” </p><p></p><p></p><p></p><p></p><p></p><p>So are we to believe that we can give testosterone to very sick men and not have any major adverse cardiac events but yet we can give it to a relatively healthy man and somehow it will cause harm? Are we also to believe that we have to wait until someone develops cardiovascular disease or significant risk factors for cardiovascular disease along with hypogonadism until we are able to treat? Why do we not prevent cardiovascular disease and risk factors for cardiovascular disease before it occurs? Testosterone therapy has been shown in multiple studies to prevent these risk factors before they develop into actual cardiovascular disease.</p><p></p><p></p><p>When we restrict care to only those with low testosterone levels then we are ignoring the medical literature that supports the fact that each man has his own so-called "normal level" below which he becomes symptomatic. This is based on genetic factors such as the length of the CAG repeat on the androgen receptor. We should focus more on symptoms and not numbers. If a man has symptoms suggestive of low testosterone then he should be given the opportunity to undergo a trial of testosterone replacement therapy. Now this is in the setting of this individual having already corrected all other potential causes of symptoms such as obesity or being overweight, inadequate sleep, stress, poor diet and nutrition, and lack of exercise. </p><p></p><p></p><p></p><p></p><p></p><p>Here are a couple of findings or better yet observations that are already causing some confusion and misinformation:</p><p></p><p></p><p></p><p></p><p></p><p>A higher incidence of atrial fibrillation (3.5% with testosterone vs. 2.4% with placebo), acute kidney injury (2.3% vs. 1.5%, respectively) and pulmonary embolism (0.9% vs. 0.5%, respectively) was OBSERVED in the testosterone group???</p><p></p><p></p><p></p><p></p><p></p><p>Primary endpoint(s) are typically efficacy measures that address the main research question and for which the trial was adequately powered . Secondary endpoints are additional events of interest but which the study is not specifically powered to assess. Tertiary endpoints typically capture outcomes that occur less frequently or which may be useful for exploring novel hypotheses. Tertiary endpoints can be interesting, thought-provoking, and hypothesis generating but cannot be utilized to establish causation. The traverse trial did not find that testosterone increased the incidence of atrial fibrillation, acute kidney injury, or pulmonary embolism. It was an observation only.</p><p></p><p></p><p></p><p></p><p></p><p>Dr. Abraham Morgentaler had the following to say:</p><p></p><p></p><p>“Those were TERTIARY endpoints.</p><p></p><p></p><p>Need to be REALLY careful</p><p></p><p></p><p>drawing conclusions. Difficult to</p><p></p><p></p><p>know if groups were similar at</p><p></p><p></p><p>baseline. Prior data re AF showed</p><p></p><p></p><p>T therapy reduced risk. Studies</p><p></p><p></p><p>have also previously shown no</p><p></p><p></p><p>increase in PE. Renal injury- never</p><p></p><p></p><p>heard this before.”</p><p></p><p></p><p></p><p></p><p></p><p>The co-author of the traverse study along with one of his colleagues had this to say :</p><p></p><p></p><p></p><p></p><p></p><p>“Bhasin said that the team plans to investigate those cases further to look for possible risk factors, including whether COVID-19 played a role in these outcomes because the trial took place during the pandemic and some participants in both study groups contracted the virus.</p><p></p><p></p><p></p><p></p><p></p><p>Regarding acute kidney injury, Anawalt said: "I don't know that I believe that...It's probably a statistical abnormality. It barely made...significance."</p><p></p><p></p><p></p><p></p><p></p><p>It is always a good idea to understand the prior literature on a topic in order to understand whether the conclusions of a new study make sense. So with regard to atrial fibrillation, acute kidney injury, and pulmonary embolism what does the previous literature show with testosterone therapy. Multiple studies revealed a reduction in atrial fibrillation as well as arrhythmias with testosterone therapy. Testosterone therapy has not been shown in any randomized controlled trial to increase the risk of venous thromboembolism and in fact multiple studies as well as systematic reviews and meta-analysis have not shown any association between testosterone use and VTE. Long-term testosterone therapy has also been shown to improve renal function and delay progression of chronic kidney disease.</p><p></p><p></p><p></p><p></p><p></p><p>When the weight of the previous literature favors the opposite result it raises the possibility that there was something about this particular study that confounded the results</p><p></p><p></p><p></p><p></p><p></p><p>This study was done during the pandemic and participants did develop Covid during the course of treatment. What do we know about Covid and the incidence of atrial fibrillation, pulmonary embolism, and acute kidney injury?</p><p></p><p></p><p>Covid infection significantly increases acute kidney injury, arterial and venous thromboembolic events, as well as cardiac arrhythmias and new onset atrial fibrillation.</p><p></p><p>So we cannot ignore 85 years of testosterone being utilize to treat men with hypogonadism and other disorders such as Klinefelter's syndrome. When testosterone was first used there were no labs for several decades (in high doses), and yet it did not cause an increase in atrial fibrillation, acute kidney injury, or pulmonary embolism. We cannot throw away decades of previous studies that also show no increase in these events. The traverse study was not powered for these events. Testosterone has been used and abused by literally hundreds of thousands of men over the last couple of decades and yet there has been no epidemic of arrhythmias, pulmonary embolism, or acute kidney injury.</p></blockquote><p></p>
[QUOTE="RobRoy, post: 259234, member: 42893"] So read a lot and Joseph Hernshaw maybe you should step away from your woke TRT movement and listen to what even the co-author had to say about the traverse study. The problem with you Joseph and read a lot is that you suffer from extreme confirmational bias. You cannot see the forest for the trees. Your writings will be used for some upcoming videos. The Testosterone Replacement Therapy for Assessment of Long-term Vascular Events and Efficacy Response in Hypogonadal Men (TRAVERSE) trial was designed to determine the effects of testosterone-replacement therapy on the incidence of major adverse cardiac events among middle-aged and older men with hypogonadism and either preexisting or a high risk of cardio- vascular disease. It enrolled 5,204 men, 45 to 80 years of age, with a mean treatment duration of 21.7 +-14.1 months Inclusion criteria included meeting the study definition of clinical hypogonadism which was 2 serum testosterone levels less than 300 ng/dL collected between 5 AM and 11 AM And, the presence of at least one sign or symptom that may be related to low testosterone such as: Decreased libido, decreased morning erections, decreased energy or fatigue, depressed mood, loss of body hair or reduced shaving, or hot flashes Participants also had to have pre-existing cardiovascular disease or at least three cardiovascular risk factors. Pre-existing cardiovascular disease would be a diagnosis of coronary artery disease, cerebrovascular disease, or peripheral artery disease. Cardiovascular risk factors included hypertension, dyslipidemia, current smoker, stage three kidney disease, diabetes, elevated CRP, or high coronary artery calcium score Some baseline characteristics : average age was 63 , the average BMI was 35, and the median testosterone level was 227 ng/dL (188-258) The patients were randomly assigned to either receive transdermal testosterone gel 1.62 % (40.5 mg)or placebo The dose was adjusted to maintain testosterone levels between 350 and 750 ng/dL. The mean daily dose was 65 +-22mg. At 12 months the median increase in testosterone levels from baseline was 148 ng/dL (34-312) The primary cardiovascular endpoint was a composite of cardiovascular mortality, nonfatal myocardial infarction or nonfatal stroke. The secondary cardiovascular endpoint was a composite of the primary endpoint plus coronary revascularization The primary endpoint occurred in 182 patients (7.0%) in the testosterone group and 190 patients (7.3%) in the placebo group . Rates of the secondary endpoint and each of the components of the primary endpoint were similar between the groups. The conclusion was that in men with hypogonadism and pre-existing or a high risk of cardiovascular disease testosterone replacement therapy was non-inferior to placebo with respect to the incidence of major adverse cardiac events 61% of patients in both groups dropped out ??? What does that tell us? It tells us that if you only raise testosterone levels a little bit then the patients will notice minimal benefit and will discontinue treatment no different than discontinuing placebo. A little bit of testosterone is not much better than getting nothing at all and this is reflected in the identical dropout rate between the treatment group and the placebo group. So here is what a couple of endocrinologist are saying about the study in the national media: "It's important to emphasize that this is a study of men with bona fide testosterone deficiency and symptoms. It doesn't give carte blanche to prescribe to men with normal testosterone concentrations. It doesn't tell us about the safety of that" “It is essential that the findings be interpreted appropriately and not applied to patient populations beyond middle-aged and older men with documented hypogonadism and established cardiovascular disease or high cardiovascular risk. “They don’t apply to athletes taking super-high doses or to people who don’t have low testosterone levels” So are we to believe that we can give testosterone to very sick men and not have any major adverse cardiac events but yet we can give it to a relatively healthy man and somehow it will cause harm? Are we also to believe that we have to wait until someone develops cardiovascular disease or significant risk factors for cardiovascular disease along with hypogonadism until we are able to treat? Why do we not prevent cardiovascular disease and risk factors for cardiovascular disease before it occurs? Testosterone therapy has been shown in multiple studies to prevent these risk factors before they develop into actual cardiovascular disease. When we restrict care to only those with low testosterone levels then we are ignoring the medical literature that supports the fact that each man has his own so-called "normal level" below which he becomes symptomatic. This is based on genetic factors such as the length of the CAG repeat on the androgen receptor. We should focus more on symptoms and not numbers. If a man has symptoms suggestive of low testosterone then he should be given the opportunity to undergo a trial of testosterone replacement therapy. Now this is in the setting of this individual having already corrected all other potential causes of symptoms such as obesity or being overweight, inadequate sleep, stress, poor diet and nutrition, and lack of exercise. Here are a couple of findings or better yet observations that are already causing some confusion and misinformation: A higher incidence of atrial fibrillation (3.5% with testosterone vs. 2.4% with placebo), acute kidney injury (2.3% vs. 1.5%, respectively) and pulmonary embolism (0.9% vs. 0.5%, respectively) was OBSERVED in the testosterone group??? Primary endpoint(s) are typically efficacy measures that address the main research question and for which the trial was adequately powered . Secondary endpoints are additional events of interest but which the study is not specifically powered to assess. Tertiary endpoints typically capture outcomes that occur less frequently or which may be useful for exploring novel hypotheses. Tertiary endpoints can be interesting, thought-provoking, and hypothesis generating but cannot be utilized to establish causation. The traverse trial did not find that testosterone increased the incidence of atrial fibrillation, acute kidney injury, or pulmonary embolism. It was an observation only. Dr. Abraham Morgentaler had the following to say: “Those were TERTIARY endpoints. Need to be REALLY careful drawing conclusions. Difficult to know if groups were similar at baseline. Prior data re AF showed T therapy reduced risk. Studies have also previously shown no increase in PE. Renal injury- never heard this before.” The co-author of the traverse study along with one of his colleagues had this to say : “Bhasin said that the team plans to investigate those cases further to look for possible risk factors, including whether COVID-19 played a role in these outcomes because the trial took place during the pandemic and some participants in both study groups contracted the virus. Regarding acute kidney injury, Anawalt said: "I don't know that I believe that...It's probably a statistical abnormality. It barely made...significance." It is always a good idea to understand the prior literature on a topic in order to understand whether the conclusions of a new study make sense. So with regard to atrial fibrillation, acute kidney injury, and pulmonary embolism what does the previous literature show with testosterone therapy. Multiple studies revealed a reduction in atrial fibrillation as well as arrhythmias with testosterone therapy. Testosterone therapy has not been shown in any randomized controlled trial to increase the risk of venous thromboembolism and in fact multiple studies as well as systematic reviews and meta-analysis have not shown any association between testosterone use and VTE. Long-term testosterone therapy has also been shown to improve renal function and delay progression of chronic kidney disease. When the weight of the previous literature favors the opposite result it raises the possibility that there was something about this particular study that confounded the results This study was done during the pandemic and participants did develop Covid during the course of treatment. What do we know about Covid and the incidence of atrial fibrillation, pulmonary embolism, and acute kidney injury? Covid infection significantly increases acute kidney injury, arterial and venous thromboembolic events, as well as cardiac arrhythmias and new onset atrial fibrillation. So we cannot ignore 85 years of testosterone being utilize to treat men with hypogonadism and other disorders such as Klinefelter's syndrome. When testosterone was first used there were no labs for several decades (in high doses), and yet it did not cause an increase in atrial fibrillation, acute kidney injury, or pulmonary embolism. We cannot throw away decades of previous studies that also show no increase in these events. The traverse study was not powered for these events. Testosterone has been used and abused by literally hundreds of thousands of men over the last couple of decades and yet there has been no epidemic of arrhythmias, pulmonary embolism, or acute kidney injury. [/QUOTE]
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What is TRT and What is NOT TRT
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