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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Basics & Questions
Dr Neal Rouzien's Position on Hematocrit and Estradiol Management
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<blockquote data-quote="Nelson Vergel" data-source="post: 27279" data-attributes="member: 3"><p>PART 2</p><p></p><p>That's triggering this increased risk of all cancers, not just breast cancer, but yet we associated with estrogen and say, "That's the estrogen that caused it." No, it's not. Interventional studies do not show that. Don't extrapolate an association to prove causation. You can't do that with testosterone and estrogen in women. Higher concentrations of estrogen, again, are associated with increased risk of breast cancer in postmenopausal women. Study after study shows baseline levels. These are not treatments, it's an association of a baseline level. Don't extrapolate it. If you're going to extrapolate it, you got to prove it. You got to do an interventional study and give estrogen to see if it causes it. So far we don't see that. </p><p> Now let's go to men. Men with higher estradiol levels had an increased risk of diabetes and heart disease. "Aha. See? It's that estrogen that causes that increase in belly fat." No, it's not. It's the increase in visceral fat that increases estrone production, which increases your estrogen levels. It's an association. It doesn't prove causation. How do you prove causation? You got to administer estrogen. Okay, let's see what happens. This is a study that's quoted by Life Extension and many other groups. "Aha. See? High level estrogen are associated with an increased risk of mortality and heart failure. Is that estrogen that's causing that problem." No, it's not. That's an observation. To prove causation you've got to intervene. </p><p> So far in interventional studies we don't see that. Participants with metabolic syndrome have high free and total estradiol, "which proves that estrogen causes that problem." No, that's an observation. It doesn't prove causation, but everyone will extrapolate the association proving causation. You can't do that. Mean body mass index is associated with high estrogen levels in men. "Maybe that estradiol that's causing that increase in heart disease." No, it's the increase in BMI and you always see this in men that how increased visceral fat, not in normal weight men. Obesity amongst aging men is associated with insulin resistance and hyperinsulinemia, as well as an increase in estrogen, but we've extrapolated and said that estrogen that's harmful, that's causing the belly fat. No, it's not. </p><p> It's the belly fat that's increasing the risk of high estrogen. It's just the opposite. Higher levels of estradiol are associated with lower risk of cardiovascular events in normal men. Oops. Now we're starting to see the opposite. Again that's an association. How do you prove causation? You have to intervene. Studies suggest that circulating sex hormones including estrogen have a beneficial effect on cardiovascular disease in men. All right. Now we see the opposite effect, but again it's an association. You got to prove it by administering estrogen. Okay, well let's look at this. In men that take LHRH agonists we wipe out the testosterone, we wipe out their estrogen, and when we do, we increase cardiovascular risk. </p><p> In every study so far, when we give LHRH agonists, there's an increased risk of death in these men. Thank god they didn't die from the prostate cancer, but they did die. We killed them. How do you then reverse that? In this study here they gave transnormal to improve the cardiovascular outcomes that are associated with poor outcomes with androgen deprivation therapy. Now we're intervening. Any study out there, where we give estrogen to men, that's harmful? No. "Yeah, but these studies ..." That's an association. These are interventional trials to prove whether there is harm or not. There's not. In this study transnormal estrogen was given and lowers the cholesterol. It raises the HDL and has a positive effect on all lipoproteins. It lowers the bad ones and raises the good ones, and it decreases mortality rates.</p><p> Estrogen administration to men has a positive effect on all lipo-parameters and decreases mortality rates in those that did not get estrogen. That's an interventional trial. Are there any interventional trials when we raise estrogen in men that's harmful? No. Are there any interventional trials where we raise estrogen in men are beneficial? Yes, every one. Then why do you lower estrogen? Because gynecomastia. Yeah, but what about the increase in heart disease? It's widely accepted that in women estrogen provide protection against the development of cardiovascular disease and we see the same thing now in men. It's the aromatization into estrogen that's protect them. That is protective. </p><p> Estrogen supplementation, this is an interventional trial, was done with estradiol. Blood pressure has decreased. HDL increased. There's a positive effect in all lipo-parameters. Their well-being improved. The side effects from the LHRH agonists were eliminated. This study demonstrates that the suppression of endogenous estrogen with aromatase inhibitor anastrozole results in impairment of flow-mediated dilatation of the blood vessels in men. Is there any study? Okay, we've done interventional. We've given estrogen. There was protective effects. It doesn't cause harm. Was there any studies showing that lowering estrogen in men is harmful? Yes. Was there any study showing that raising estrogen in men is beneficial? Yes. </p><p> Any study showing that lowering estrogen in men is beneficial? No. Then why do you lower it? We administer aromatase inhibitor Testlac to prevent the normal conversion of testosterone into estradiol, and then we studied to see what happened. In men that received the aromatase inhibitor, estradiol levels were profoundly suppressed, and as a result the HDL was suppressed. LDL went up. All of the lipoproteins has a negative effect. The bad apolipoprotein B increased. The good apolipoprotein A decreased. There's an adverse effect in all lipo-parameters when we block estrogen in men with aromatase inhibitor. Then why do you do it? </p><p> I gave this lecture a couple of years ago and there was a member of the audience that stood up and said, "We only want to lower it a little bit." Okay. We only want to lower HDL a little bit. We only want to raise LDL a little bit. We only want to adverse the effect lipoproteins a little bit. That makes no sense. It's physiologic levels of estradiol men that are important to maintain plasma levels of HDL. When you block it and lower it there's a harmful effect in all lipo-parameters. Then why do you do it? We only want to do it a little bit. The estrogen that's only produced in men has a cardio-protective effect. Different studies. In men with aromatase deficiencies, you see low levels of HDL. How do you get that up? You give them estrogen. </p><p> There're also adverse effects on libido and sexual function. How do you improve that? You give them estrogen. Estrogen acts along with testosterone to help maintain insulin sensitivity and when you block estrogen you increase insulin resistance. Why would you then do that? Elevated levels of estradiol reduce the risk of cardiovascular disease in men over 50 years of age. Why do you then block it? "We only want to block it a little bit." You only want to increase the risk of heart disease a little bit? In healthy men subjected to estrogen suppression what we saw is an adverse effect in cardiovascular disease in all lipo-parameters. In this study here they gave men aromatase inhibitors to increase testosterone levels. </p><p> What they found was the low levels appeared to decrease bone mineral density. You want to inhibit bone formation? Block estrogen. "We only want to block it a little bit." You only want to inhibit bones a little bit? In this study here they gave aromatase inhibitors to men and they looked at verbal memory and cognition. When you block the estrogen you significantly had an adverse effect on memory and cognition. In those that were not block, that the estrogen level was kept high, had improvement. Memory and verbal improvement depends on the level of estradiol. "We only want to block it a little bit." You only want to decrease memory and cognition a little bit? </p><p> This is a great article from JCEM. Despite the numerous publications from our group and others regarding the role of estrogen in bone metabolism in men, none of my colleagues inquire or seem to care one way or another about the estradiol levels. It's only the testosterone levels that they're concerned about, and estrogen is irrelevant. In this study here, bone mineral density decreased in those treated with anastrozole. There's a 50% increase in testosterone levels with anastrozole, but there's also a 20% reduction in estradiol and a significant adverse effect in bone. All recent studies show that same thing. When you block estrogen you have a harmful effect and fractures in bones. Relatively small reductions in estradiol appear to have a significant effect on bone mineral density and bone loss. </p><p> "We only want to block it a little bit." You only want to decrease bones significantly? Why would you do that. High estradiol levels are associated with maximum skeletal benefits. There's also evidence for estrogen in regulating body composition. In men, when you blocked estrogen, there was an increase in body fat. These findings indicate that aromatization of testosterone and estrogen is critical not only for bone preservation, but also for body composition and body fat. I hear everyone else going around, "You got to block estrogen because you want to get rid of the belly fat." No, that's just opposite. When you block estrogen, you increase belly fat. "We want to block the estrogen because it causes heart disease." No, it doesn't. </p><p> In summary, whereas the concept of using aromatase blocker to enhance endogenous testosterone production was an attractive one, what we see is that there's an adverse effect on bone and an adverse effect on body composition by increasing visceral fat. These findings suggest that as males, we should perhaps be just as interested in our estradiol levels as we are in our testosterone levels. "We only want to block it a little bit." We only want to cause a little bit of harm. Patients that get LHRH agonists wipe out testosterone and estrogen. It causes an increased risk of dying. In all of these studies, when you give estrogen to men, it reverses that. </p><p> "I thought estrogen causes prostate cancer." No, it doesn't. It's been an armamentarium for treatment of prostate cancer for over 50 years. I used it as a resident way back when. I have several dozen men that I actively treat with estrogen that have prostate cancer spread beyond their capsule, and I have these men up to 50 years have been treated with estrogen without any progression of their disease. With LHRH agonists you get testosterone and independent tumors. Despite of the fact that you wipe out the testosterone, the tumor continues to grow and then they die. When you use estrogen it has a positive effect on cancers. It has a significant anti-angiogenic and a pro-apoptotic effect on prostate cancer cells. </p><p> It's a great treatment for prostate cancer, but I see everyone out there blocking estrogen because estrogen causes prostate cancer. No, it does. It's been a treatment for it for years, and if you say that you completely do not understand the medical literature. Estrogen have an added anti-cancer effect not otherwise seen with conventional LHRH agonists because of its androgen suppressive effect, but because of the pro-apoptotic and anti-angiogenic effect. In this study they gave 1 milligram of estradiol. When they gave LHRH agonists they lost bone. When they gave estrogen that bone loss, the [NTX 00:41:35] reversed. Moods improved, they were healthy, they got cardiovascular protection and they no longer had bone loss, and they no longer had the side effects of loss of estrogen.</p><p> Transdermal estradiol therapy effectively causes a tumor response. Transdermal estrogen improves androgen deprivation symptoms and improves quality of life scores, and improves bone density, and it protects against heart attacks and heart disease. It costs a tenth of the agonists, but I see everyone out there blocking estrogen because you fear it because someone said. Show me the evidence that it's harmful. "Someone said." No, I want evidence. I want to a study showing that raising it is harmful and causes cancer, and every study shows that it protects against cancer. The opposite. The risk of prostate cancer was 30% lower for a doubling of the concentration of estradiol. When you want to increase your risk of prostate cancer, lower your estrogen. </p><p> If you want to protect against that cancer, then raise your estrogen up as per study. High levels of testosterone and high levels of estrogen are associated with a reduced risk of prostate cancer and the aggressiveness of a cancer. Then why do you want to block? "We only want to block it a little bit." You only want to increase prostate cancer risk a little bit? Men with low levels of estrogen, estradiol are at risk for fractures in every study to date, and an increase in morbidity and mortality. Elderly men with low estradiol levels have an increased risk of mortality. Lowest levels of estrogen show the highest risk of mortality. Why would you block it? "We only want to block it a little bit." You only want to increase mortality a little bit? Yeah. </p><p> Then why do you block it? "Because someone said." Where's the evidence, where's the literature to support that someone says it's correct, when all the literature is just the opposite? This is a great study, if you haven't seen this study. This is something the New England Journal of Medicine 2014, last year. The article was on blocking estrogen in men. Androgen deficiency accounts for a decrease in lean muscle mass. Of course. But estrogen deficiency also has an adverse effect by an increase in body fat and a decrease in sexual function when you block it. Why would you block it? "We only want to block it a little bit." When testosterone levels falls so does estradiol levels. The potential role of concomitant decline in estrogen is typically ignored and estrogen deficiency is a responsible for the pathogenesis and consequence of male hypogonadism, but we fail to understand that and appreciate it. </p><p> Why did they publish a study in the New England Journal of Medicine? The effects of testosterone on aromatase inhibition on body composition were as follows. When you blocked estrogen in this group, there was significant increase in subcutaneous and visceral fat. Why would you do that? "We only want to block it a little bit." You only want to increase subcutaneous fat and visceral fat a little bit? Yeah. That makes no sense. Inhibition of estrogen synthesis also results in guess what? Significant decrease in sexual desire and erectile dysfunction. Why would you do that? "We only want to increase erectile dysfunction a little bit and we only want to decrease libido a little bit." That's why we block estrogen. Why would you do that? </p><p> "We only want to do it a little bit." Wow. Changes in body fat were associated with estradiol levels. The lower the level, the greater the body fat. Because increase in visceral fat reduces insulin sensitivity and is associated with diabetes, the metabolic syndrome, and mark an increase in intra-abdominal fat from aromatase inhibition, [pertains 00:45:40] an increase in cardiovascular risk and diabetes. Why would you do that? "We only want to do it a little bit." Our finding that estrogen has a fundamental role in the regulation of body fat and sexual function, coupled with the evidence from prior studies, show the same thing. A crucial role of estrogen in bone metabolism, a crucial role in body fat, increase in the risk of heart disease. </p><p> This suggests that measuring estradiol levels may be helpful in assessing the risk of sexual dysfunction and bone loss in men. Don't block it. My time is up. This next session you can look at in this slide presentation and it reviews polycythemia. We all know that testosterone causes polycythemia and it's harmful. No, it doesn't. It causes eritrocytosis. I recently presented this to my hematology group and they all sort of sat puzzled. They said, "High red blood cells cause an increased risk of clotting." Well, in this study, there's 200 million people that live in altitude that have eritrocytosis and some people with hemoglobin levels greater than 21. </p><p> Excessive eritrocytosis is what's it's called. Do [we lobotomize 00:46:53] those people. Do we tell all those people that live in altitude to rush to the beach, and live at the beach because they're going to get heart attacks and strokes? Because they have eritrocytosis? What we've done is we've extrapolated the harm of poly which is a blood cell dyscrasia that's easily diagnosed with a JAP2 gene test, to be harmful and it causes eritrocytosis. Polycythemia [varies 00:47:18] increased red cells, white cells and platelets, and platelet accounts is what's causing the clotting, not the high red blood cells. Nowhere in the world do we see in a increase risk of clotting in people that have eritrocytosis that live in altitude or that have COPD. </p><p> Yet I hear commentators lecture and say, "You got to lobotomize them every 3 months because you got to get that red blood cell down, because that causes clotting and clumping." No, it does not. I saw a patient recently from Cenegenics who's a physician, Cenegenics physician who had extreme fatigue. His iron level was 5 and his ferritin level was 5 ,and he couldn't figure out why he felt so bad. IV Venofer completely reversed that. He felt great within a week, but yet we're still taught you got to get that red blood cell count down. When I confronted one of my hematologist with this she said, "Giving testosterone is different than having high altitude eritrocytosis. It's completely different." </p><p> If you look at the studies that I showed here, the mechanism for eritrocytosis in people that live in altitude is? The testosterone levels go up significantly and that's what's causing the eritrocytosis, not an increased erythropoietin. Having said that, I hope that was fun. Doctor Morgentaler is going to speak after this. I will go outside and answer any questions that you may have. Contact me if you wish in order to get the slide presentation. This is the numbers that you want to copy down. You can email me and my email address is <a href="mailto:neal.rouzier@gmail.com">neal.rouzier@gmail.com</a>. If you're interested in the hormone courses that we teach, you can go to nealrouzier.com and look up the different courses. There's 4 different parts that we teach similar to the presentation that I've given today. I hope it was fun. Enjoy your stay. I'll answer any questions outside if you wish. Have a good day. Thank you.</p></blockquote><p></p>
[QUOTE="Nelson Vergel, post: 27279, member: 3"] PART 2 That's triggering this increased risk of all cancers, not just breast cancer, but yet we associated with estrogen and say, "That's the estrogen that caused it." No, it's not. Interventional studies do not show that. Don't extrapolate an association to prove causation. You can't do that with testosterone and estrogen in women. Higher concentrations of estrogen, again, are associated with increased risk of breast cancer in postmenopausal women. Study after study shows baseline levels. These are not treatments, it's an association of a baseline level. Don't extrapolate it. If you're going to extrapolate it, you got to prove it. You got to do an interventional study and give estrogen to see if it causes it. So far we don't see that. Now let's go to men. Men with higher estradiol levels had an increased risk of diabetes and heart disease. "Aha. See? It's that estrogen that causes that increase in belly fat." No, it's not. It's the increase in visceral fat that increases estrone production, which increases your estrogen levels. It's an association. It doesn't prove causation. How do you prove causation? You got to administer estrogen. Okay, let's see what happens. This is a study that's quoted by Life Extension and many other groups. "Aha. See? High level estrogen are associated with an increased risk of mortality and heart failure. Is that estrogen that's causing that problem." No, it's not. That's an observation. To prove causation you've got to intervene. So far in interventional studies we don't see that. Participants with metabolic syndrome have high free and total estradiol, "which proves that estrogen causes that problem." No, that's an observation. It doesn't prove causation, but everyone will extrapolate the association proving causation. You can't do that. Mean body mass index is associated with high estrogen levels in men. "Maybe that estradiol that's causing that increase in heart disease." No, it's the increase in BMI and you always see this in men that how increased visceral fat, not in normal weight men. Obesity amongst aging men is associated with insulin resistance and hyperinsulinemia, as well as an increase in estrogen, but we've extrapolated and said that estrogen that's harmful, that's causing the belly fat. No, it's not. It's the belly fat that's increasing the risk of high estrogen. It's just the opposite. Higher levels of estradiol are associated with lower risk of cardiovascular events in normal men. Oops. Now we're starting to see the opposite. Again that's an association. How do you prove causation? You have to intervene. Studies suggest that circulating sex hormones including estrogen have a beneficial effect on cardiovascular disease in men. All right. Now we see the opposite effect, but again it's an association. You got to prove it by administering estrogen. Okay, well let's look at this. In men that take LHRH agonists we wipe out the testosterone, we wipe out their estrogen, and when we do, we increase cardiovascular risk. In every study so far, when we give LHRH agonists, there's an increased risk of death in these men. Thank god they didn't die from the prostate cancer, but they did die. We killed them. How do you then reverse that? In this study here they gave transnormal to improve the cardiovascular outcomes that are associated with poor outcomes with androgen deprivation therapy. Now we're intervening. Any study out there, where we give estrogen to men, that's harmful? No. "Yeah, but these studies ..." That's an association. These are interventional trials to prove whether there is harm or not. There's not. In this study transnormal estrogen was given and lowers the cholesterol. It raises the HDL and has a positive effect on all lipoproteins. It lowers the bad ones and raises the good ones, and it decreases mortality rates. Estrogen administration to men has a positive effect on all lipo-parameters and decreases mortality rates in those that did not get estrogen. That's an interventional trial. Are there any interventional trials when we raise estrogen in men that's harmful? No. Are there any interventional trials where we raise estrogen in men are beneficial? Yes, every one. Then why do you lower estrogen? Because gynecomastia. Yeah, but what about the increase in heart disease? It's widely accepted that in women estrogen provide protection against the development of cardiovascular disease and we see the same thing now in men. It's the aromatization into estrogen that's protect them. That is protective. Estrogen supplementation, this is an interventional trial, was done with estradiol. Blood pressure has decreased. HDL increased. There's a positive effect in all lipo-parameters. Their well-being improved. The side effects from the LHRH agonists were eliminated. This study demonstrates that the suppression of endogenous estrogen with aromatase inhibitor anastrozole results in impairment of flow-mediated dilatation of the blood vessels in men. Is there any study? Okay, we've done interventional. We've given estrogen. There was protective effects. It doesn't cause harm. Was there any studies showing that lowering estrogen in men is harmful? Yes. Was there any study showing that raising estrogen in men is beneficial? Yes. Any study showing that lowering estrogen in men is beneficial? No. Then why do you lower it? We administer aromatase inhibitor Testlac to prevent the normal conversion of testosterone into estradiol, and then we studied to see what happened. In men that received the aromatase inhibitor, estradiol levels were profoundly suppressed, and as a result the HDL was suppressed. LDL went up. All of the lipoproteins has a negative effect. The bad apolipoprotein B increased. The good apolipoprotein A decreased. There's an adverse effect in all lipo-parameters when we block estrogen in men with aromatase inhibitor. Then why do you do it? I gave this lecture a couple of years ago and there was a member of the audience that stood up and said, "We only want to lower it a little bit." Okay. We only want to lower HDL a little bit. We only want to raise LDL a little bit. We only want to adverse the effect lipoproteins a little bit. That makes no sense. It's physiologic levels of estradiol men that are important to maintain plasma levels of HDL. When you block it and lower it there's a harmful effect in all lipo-parameters. Then why do you do it? We only want to do it a little bit. The estrogen that's only produced in men has a cardio-protective effect. Different studies. In men with aromatase deficiencies, you see low levels of HDL. How do you get that up? You give them estrogen. There're also adverse effects on libido and sexual function. How do you improve that? You give them estrogen. Estrogen acts along with testosterone to help maintain insulin sensitivity and when you block estrogen you increase insulin resistance. Why would you then do that? Elevated levels of estradiol reduce the risk of cardiovascular disease in men over 50 years of age. Why do you then block it? "We only want to block it a little bit." You only want to increase the risk of heart disease a little bit? In healthy men subjected to estrogen suppression what we saw is an adverse effect in cardiovascular disease in all lipo-parameters. In this study here they gave men aromatase inhibitors to increase testosterone levels. What they found was the low levels appeared to decrease bone mineral density. You want to inhibit bone formation? Block estrogen. "We only want to block it a little bit." You only want to inhibit bones a little bit? In this study here they gave aromatase inhibitors to men and they looked at verbal memory and cognition. When you block the estrogen you significantly had an adverse effect on memory and cognition. In those that were not block, that the estrogen level was kept high, had improvement. Memory and verbal improvement depends on the level of estradiol. "We only want to block it a little bit." You only want to decrease memory and cognition a little bit? This is a great article from JCEM. Despite the numerous publications from our group and others regarding the role of estrogen in bone metabolism in men, none of my colleagues inquire or seem to care one way or another about the estradiol levels. It's only the testosterone levels that they're concerned about, and estrogen is irrelevant. In this study here, bone mineral density decreased in those treated with anastrozole. There's a 50% increase in testosterone levels with anastrozole, but there's also a 20% reduction in estradiol and a significant adverse effect in bone. All recent studies show that same thing. When you block estrogen you have a harmful effect and fractures in bones. Relatively small reductions in estradiol appear to have a significant effect on bone mineral density and bone loss. "We only want to block it a little bit." You only want to decrease bones significantly? Why would you do that. High estradiol levels are associated with maximum skeletal benefits. There's also evidence for estrogen in regulating body composition. In men, when you blocked estrogen, there was an increase in body fat. These findings indicate that aromatization of testosterone and estrogen is critical not only for bone preservation, but also for body composition and body fat. I hear everyone else going around, "You got to block estrogen because you want to get rid of the belly fat." No, that's just opposite. When you block estrogen, you increase belly fat. "We want to block the estrogen because it causes heart disease." No, it doesn't. In summary, whereas the concept of using aromatase blocker to enhance endogenous testosterone production was an attractive one, what we see is that there's an adverse effect on bone and an adverse effect on body composition by increasing visceral fat. These findings suggest that as males, we should perhaps be just as interested in our estradiol levels as we are in our testosterone levels. "We only want to block it a little bit." We only want to cause a little bit of harm. Patients that get LHRH agonists wipe out testosterone and estrogen. It causes an increased risk of dying. In all of these studies, when you give estrogen to men, it reverses that. "I thought estrogen causes prostate cancer." No, it doesn't. It's been an armamentarium for treatment of prostate cancer for over 50 years. I used it as a resident way back when. I have several dozen men that I actively treat with estrogen that have prostate cancer spread beyond their capsule, and I have these men up to 50 years have been treated with estrogen without any progression of their disease. With LHRH agonists you get testosterone and independent tumors. Despite of the fact that you wipe out the testosterone, the tumor continues to grow and then they die. When you use estrogen it has a positive effect on cancers. It has a significant anti-angiogenic and a pro-apoptotic effect on prostate cancer cells. It's a great treatment for prostate cancer, but I see everyone out there blocking estrogen because estrogen causes prostate cancer. No, it does. It's been a treatment for it for years, and if you say that you completely do not understand the medical literature. Estrogen have an added anti-cancer effect not otherwise seen with conventional LHRH agonists because of its androgen suppressive effect, but because of the pro-apoptotic and anti-angiogenic effect. In this study they gave 1 milligram of estradiol. When they gave LHRH agonists they lost bone. When they gave estrogen that bone loss, the [NTX 00:41:35] reversed. Moods improved, they were healthy, they got cardiovascular protection and they no longer had bone loss, and they no longer had the side effects of loss of estrogen. Transdermal estradiol therapy effectively causes a tumor response. Transdermal estrogen improves androgen deprivation symptoms and improves quality of life scores, and improves bone density, and it protects against heart attacks and heart disease. It costs a tenth of the agonists, but I see everyone out there blocking estrogen because you fear it because someone said. Show me the evidence that it's harmful. "Someone said." No, I want evidence. I want to a study showing that raising it is harmful and causes cancer, and every study shows that it protects against cancer. The opposite. The risk of prostate cancer was 30% lower for a doubling of the concentration of estradiol. When you want to increase your risk of prostate cancer, lower your estrogen. If you want to protect against that cancer, then raise your estrogen up as per study. High levels of testosterone and high levels of estrogen are associated with a reduced risk of prostate cancer and the aggressiveness of a cancer. Then why do you want to block? "We only want to block it a little bit." You only want to increase prostate cancer risk a little bit? Men with low levels of estrogen, estradiol are at risk for fractures in every study to date, and an increase in morbidity and mortality. Elderly men with low estradiol levels have an increased risk of mortality. Lowest levels of estrogen show the highest risk of mortality. Why would you block it? "We only want to block it a little bit." You only want to increase mortality a little bit? Yeah. Then why do you block it? "Because someone said." Where's the evidence, where's the literature to support that someone says it's correct, when all the literature is just the opposite? This is a great study, if you haven't seen this study. This is something the New England Journal of Medicine 2014, last year. The article was on blocking estrogen in men. Androgen deficiency accounts for a decrease in lean muscle mass. Of course. But estrogen deficiency also has an adverse effect by an increase in body fat and a decrease in sexual function when you block it. Why would you block it? "We only want to block it a little bit." When testosterone levels falls so does estradiol levels. The potential role of concomitant decline in estrogen is typically ignored and estrogen deficiency is a responsible for the pathogenesis and consequence of male hypogonadism, but we fail to understand that and appreciate it. Why did they publish a study in the New England Journal of Medicine? The effects of testosterone on aromatase inhibition on body composition were as follows. When you blocked estrogen in this group, there was significant increase in subcutaneous and visceral fat. Why would you do that? "We only want to block it a little bit." You only want to increase subcutaneous fat and visceral fat a little bit? Yeah. That makes no sense. Inhibition of estrogen synthesis also results in guess what? Significant decrease in sexual desire and erectile dysfunction. Why would you do that? "We only want to increase erectile dysfunction a little bit and we only want to decrease libido a little bit." That's why we block estrogen. Why would you do that? "We only want to do it a little bit." Wow. Changes in body fat were associated with estradiol levels. The lower the level, the greater the body fat. Because increase in visceral fat reduces insulin sensitivity and is associated with diabetes, the metabolic syndrome, and mark an increase in intra-abdominal fat from aromatase inhibition, [pertains 00:45:40] an increase in cardiovascular risk and diabetes. Why would you do that? "We only want to do it a little bit." Our finding that estrogen has a fundamental role in the regulation of body fat and sexual function, coupled with the evidence from prior studies, show the same thing. A crucial role of estrogen in bone metabolism, a crucial role in body fat, increase in the risk of heart disease. This suggests that measuring estradiol levels may be helpful in assessing the risk of sexual dysfunction and bone loss in men. Don't block it. My time is up. This next session you can look at in this slide presentation and it reviews polycythemia. We all know that testosterone causes polycythemia and it's harmful. No, it doesn't. It causes eritrocytosis. I recently presented this to my hematology group and they all sort of sat puzzled. They said, "High red blood cells cause an increased risk of clotting." Well, in this study, there's 200 million people that live in altitude that have eritrocytosis and some people with hemoglobin levels greater than 21. Excessive eritrocytosis is what's it's called. Do [we lobotomize 00:46:53] those people. Do we tell all those people that live in altitude to rush to the beach, and live at the beach because they're going to get heart attacks and strokes? Because they have eritrocytosis? What we've done is we've extrapolated the harm of poly which is a blood cell dyscrasia that's easily diagnosed with a JAP2 gene test, to be harmful and it causes eritrocytosis. Polycythemia [varies 00:47:18] increased red cells, white cells and platelets, and platelet accounts is what's causing the clotting, not the high red blood cells. Nowhere in the world do we see in a increase risk of clotting in people that have eritrocytosis that live in altitude or that have COPD. Yet I hear commentators lecture and say, "You got to lobotomize them every 3 months because you got to get that red blood cell down, because that causes clotting and clumping." No, it does not. I saw a patient recently from Cenegenics who's a physician, Cenegenics physician who had extreme fatigue. His iron level was 5 and his ferritin level was 5 ,and he couldn't figure out why he felt so bad. IV Venofer completely reversed that. He felt great within a week, but yet we're still taught you got to get that red blood cell count down. When I confronted one of my hematologist with this she said, "Giving testosterone is different than having high altitude eritrocytosis. It's completely different." If you look at the studies that I showed here, the mechanism for eritrocytosis in people that live in altitude is? The testosterone levels go up significantly and that's what's causing the eritrocytosis, not an increased erythropoietin. Having said that, I hope that was fun. Doctor Morgentaler is going to speak after this. I will go outside and answer any questions that you may have. Contact me if you wish in order to get the slide presentation. This is the numbers that you want to copy down. You can email me and my email address is [email]neal.rouzier@gmail.com[/email]. If you're interested in the hormone courses that we teach, you can go to nealrouzier.com and look up the different courses. There's 4 different parts that we teach similar to the presentation that I've given today. I hope it was fun. Enjoy your stay. I'll answer any questions outside if you wish. Have a good day. Thank you. [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Basics & Questions
Dr Neal Rouzien's Position on Hematocrit and Estradiol Management
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