Full Transcript Introduction and Dr. McCormick's experience living with osteoporosis 0:02 Hey, Margie, here. What if osteoporosis 0:02 Hey, Margie, here. What if osteoporosis and heart disease are more connected 0:05 and heart disease are more connected 0:05 and heart disease are more connected than we realize? That's what today's 0:07 than we realize? That's what today's 0:07 than we realize? That's what today's episode is about. Osteoporosis expert 0:11 episode is about. Osteoporosis expert 0:11 episode is about. Osteoporosis expert Dr. Keith McCormick explains why bone 0:13 Dr. Keith McCormick explains why bone 0:13 Dr. Keith McCormick explains why bone loss and cardiovascular disease so often 0:16 loss and cardiovascular disease so often 0:16 loss and cardiovascular disease so often show up together, the shared factors 0:19 show up together, the shared factors 0:19 show up together, the shared factors that may be driving both, and what your 0:21 that may be driving both, and what your 0:21 that may be driving both, and what your blood work can reveal about your risk. 0:24 blood work can reveal about your risk. 0:24 blood work can reveal about your risk. You'll learn which test to ask your 0:26 You'll learn which test to ask your 0:26 You'll learn which test to ask your doctor for, what your routine blood work 0:29 doctor for, what your routine blood work 0:29 doctor for, what your routine blood work may already be telling you, and how 0:30 may already be telling you, and how 0:30 may already be telling you, and how inflammation, metabolic health affect 0:33 inflammation, metabolic health affect 0:33 inflammation, metabolic health affect both your bones and your blood vessels. 0:36 both your bones and your blood vessels. 0:36 both your bones and your blood vessels. Dr. Keith McCormick has been helping 0:37 Dr. Keith McCormick has been helping 0:37 Dr. Keith McCormick has been helping people with osteoporosis since 1982. 0:41 people with osteoporosis since 1982. 0:41 people with osteoporosis since 1982. He's the author of Great Bones, Taking 0:43 He's the author of Great Bones, Taking 0:43 He's the author of Great Bones, Taking Control of Your Osteoporosis, which I 0:46 Control of Your Osteoporosis, which I 0:46 Control of Your Osteoporosis, which I consider an encyclopedia on the subject 0:48 consider an encyclopedia on the subject 0:48 consider an encyclopedia on the subject and recommend all the time. He's also 0:50 and recommend all the time. He's also 0:50 and recommend all the time. He's also helped so many people in our community 0:52 helped so many people in our community 0:52 helped so many people in our community understand what may be contributing to 0:54 understand what may be contributing to 0:54 understand what may be contributing to their bone loss, and what they can do to 0:57 their bone loss, and what they can do to 0:57 their bone loss, and what they can do to improve their bone health. So, this 0:59 improve their bone health. So, this 0:59 improve their bone health. So, this episode goes deep, so let's get started. 1:06 >> [music] 1:06 >> [music] >> Welcome, Dr. McCormick. So happy to have 1:08 >> Welcome, Dr. McCormick. So happy to have 1:08 >> Welcome, Dr. McCormick. So happy to have you here on the podcast. This is such an 1:11 you here on the podcast. This is such an 1:11 you here on the podcast. This is such an important topic, and when I asked you 1:13 important topic, and when I asked you 1:13 important topic, and when I asked you what do you think you would like to talk 1:15 what do you think you would like to talk 1:15 what do you think you would like to talk about, you said, "We need to discuss 1:16 about, you said, "We need to discuss 1:16 about, you said, "We need to discuss this because this is missing." So, thank 1:19 this because this is missing." So, thank 1:19 this because this is missing." So, thank you so much for being here. 1:22 you so much for being here. 1:22 you so much for being here. >> Thanks for inviting me, Margie. Really 1:23 >> Thanks for inviting me, Margie. Really 1:23 >> Thanks for inviting me, Margie. Really appreciate it. 1:24 appreciate it. 1:25 appreciate it. >> Okay, so I know you have a lot of 1:26 >> Okay, so I know you have a lot of 1:26 >> Okay, so I know you have a lot of information, and everybody listening, 1:28 information, and everybody listening, 1:28 information, and everybody listening, don't worry if you don't get it all, but 1:31 don't worry if you don't get it all, but 1:31 don't worry if you don't get it all, but this is just really important. So, I'm 1:33 this is just really important. So, I'm 1:33 this is just really important. So, I'm going to turn it over to you, Dr. 1:36 going to turn it over to you, Dr. 1:36 going to turn it over to you, Dr. McCormick, and you can share your slides 1:38 McCormick, and you can share your slides 1:39 McCormick, and you can share your slides and get started. 1:40 and get started. 1:40 and get started. >> What I'm going to talk about today is 1:41 >> What I'm going to talk about today is 1:41 >> What I'm going to talk about today is the shared roots of osteoporosis and 1:44 the shared roots of osteoporosis and 1:44 the shared roots of osteoporosis and cardiovascular disease, and we're going 1:45 cardiovascular disease, and we're going 1:45 cardiovascular disease, and we're going to talk about lab testing and how to go 1:47 to talk about lab testing and how to go 1:47 to talk about lab testing and how to go about that to help us not only identify 1:50 about that to help us not only identify 1:50 about that to help us not only identify what's going on, but to understand what 1:53 what's going on, but to understand what 1:53 what's going on, but to understand what we're going to do for treatment, too. 1:54 we're going to do for treatment, too. 1:54 we're going to do for treatment, too. So, let me tell you a little bit about 1:56 So, let me tell you a little bit about 1:56 So, let me tell you a little bit about my background. I guess it's important 1:58 my background. I guess it's important 1:58 my background. I guess it's important because I have osteoporosis, which most 2:01 because I have osteoporosis, which most 2:01 because I have osteoporosis, which most people by now know if they know me at 2:04 people by now know if they know me at 2:04 people by now know if they know me at all. And that's how I got into working 2:07 all. And that's how I got into working 2:07 all. And that's how I got into working with people with osteoporosis. I ended 2:10 with people with osteoporosis. I ended 2:10 with people with osteoporosis. I ended up having a lot of fractures back when I 2:12 up having a lot of fractures back when I 2:12 up having a lot of fractures back when I was age 45. And I searched and searched 2:15 was age 45. And I searched and searched 2:15 was age 45. And I searched and searched for good doctor to work with. And after 2:18 for good doctor to work with. And after 2:18 for good doctor to work with. And after five endocrinologists, I finally found 2:21 five endocrinologists, I finally found 2:21 five endocrinologists, I finally found this man in the right lower hand corner, 2:23 this man in the right lower hand corner, 2:23 this man in the right lower hand corner, Dr. Royce, from University of 2:26 Dr. Royce, from University of 2:26 Dr. Royce, from University of Connecticut. And he was the actual 2:28 Connecticut. And he was the actual 2:28 Connecticut. And he was the actual godfather of osteoporosis in the United 2:31 godfather of osteoporosis in the United 2:31 godfather of osteoporosis in the United States. He was the number one guy. And 2:34 States. He was the number one guy. And 2:34 States. He was the number one guy. And he took me under his wing. He not only 2:37 he took me under his wing. He not only 2:37 he took me under his wing. He not only worked with me to help with my bone 2:39 worked with me to help with my bone 2:39 worked with me to help with my bone density, but also he taught me so much. 2:41 density, but also he taught me so much. 2:41 density, but also he taught me so much. And he was so open and such a kind man. 2:45 And he was so open and such a kind man. 2:45 And he was so open and such a kind man. And [clears throat] I owe a lot to him 2:46 And [clears throat] I owe a lot to him 2:47 And [clears throat] I owe a lot to him because he taught me an awful lot about 2:49 because he taught me an awful lot about 2:49 because he taught me an awful lot about osteoporosis. And one day he called me 2:51 osteoporosis. And one day he called me 2:51 osteoporosis. And one day he called me up and he said, "Hey Keith, you know, I 2:53 up and he said, "Hey Keith, you know, I 2:53 up and he said, "Hey Keith, you know, I can't go to NIH this weekend to meet 2:57 can't go to NIH this weekend to meet 2:57 can't go to NIH this weekend to meet with Camilla, the Duchess of Cornwall. 2:59 with Camilla, the Duchess of Cornwall. 2:59 with Camilla, the Duchess of Cornwall. She's the president of the Royal 3:00 She's the president of the Royal 3:00 She's the president of the Royal Osteoporosis Society. And And her 3:02 Osteoporosis Society. And And her 3:02 Osteoporosis Society. And And her sidekick, Prince Charles, I can't go to 3:05 sidekick, Prince Charles, I can't go to 3:05 sidekick, Prince Charles, I can't go to meet with them, but would you mind 3:06 meet with them, but would you mind 3:06 meet with them, but would you mind stepping in for me?" And so, I you know, 3:10 stepping in for me?" And so, I you know, 3:10 stepping in for me?" And so, I you know, even though osteoporosis was very, very 3:12 even though osteoporosis was very, very 3:12 even though osteoporosis was very, very devastating to me, it's also done an 3:15 devastating to me, it's also done an 3:15 devastating to me, it's also done an awful lot for me as far as 3:17 awful lot for me as far as 3:17 awful lot for me as far as allowing me to meet with different 3:19 allowing me to meet with different 3:19 allowing me to meet with different people. My world is so much bigger 3:21 people. My world is so much bigger 3:21 people. My world is so much bigger because of it. And then the biggest gift 3:23 because of it. And then the biggest gift 3:23 because of it. And then the biggest gift at all 3:24 at all 3:25 at all of all 3:25 of all 3:26 of all behind this is that I've gotten to work 3:27 behind this is that I've gotten to work 3:27 behind this is that I've gotten to work with so many patients and help them. I 3:31 with so many patients and help them. I 3:31 with so many patients and help them. I even got to meet with the Surgeon 3:32 even got to meet with the Surgeon 3:32 even got to meet with the Surgeon General back then when they wrote the 3:35 General back then when they wrote the 3:35 General back then when they wrote the Surgeon General's report on bone health 3:37 Surgeon General's report on bone health 3:37 Surgeon General's report on bone health and and osteoporosis. And 3:40 and and osteoporosis. And 3:40 and and osteoporosis. And this was way back in the late, you know, 3:42 this was way back in the late, you know, 3:42 this was way back in the late, you know, 1990s 3:44 1990s 3:44 1990s and early 2000s when people didn't 3:47 and early 2000s when people didn't 3:47 and early 2000s when people didn't really know anything about osteoporosis. 3:48 really know anything about osteoporosis. 3:48 really know anything about osteoporosis. There wasn't any major research. The The 3:51 There wasn't any major research. The The 3:51 There wasn't any major research. The The drug companies weren't didn't have a lot 3:53 drug companies weren't didn't have a lot 3:53 drug companies weren't didn't have a lot of medications for it. So, I feel 3:56 of medications for it. So, I feel 3:56 of medications for it. So, I feel honored and and fortunate that I was at 3:58 honored and and fortunate that I was at 3:58 honored and and fortunate that I was at the forefront of of much of this. 4:00 the forefront of of much of this. 4:00 the forefront of of much of this. >> Yeah, Dr. McCormick, it's so 4:02 >> Yeah, Dr. McCormick, it's so 4:02 >> Yeah, Dr. McCormick, it's so interesting, but I think even I really 4:04 interesting, but I think even I really 4:04 interesting, but I think even I really want this is to me the how long you've 4:06 want this is to me the how long you've 4:06 want this is to me the how long you've been involved and what's happened over 4:08 been involved and what's happened over 4:08 been involved and what's happened over the years and how many people's lives 4:10 the years and how many people's lives 4:10 the years and how many people's lives you've changed personally. But why don't 4:12 you've changed personally. But why don't 4:12 you've changed personally. But why don't you tell people, I think just very 4:14 you tell people, I think just very 4:14 you tell people, I think just very briefly, 4:15 briefly, 4:15 briefly, about your story so they know for those 4:17 about your story so they know for those 4:17 about your story so they know for those who don't know you why you are so 4:19 who don't know you why you are so 4:19 who don't know you why you are so passionate. You didn't just sort of into 4:21 passionate. You didn't just sort of into 4:21 passionate. You didn't just sort of into osteoporosis. So, why don't you just 4:23 osteoporosis. So, why don't you just 4:23 osteoporosis. So, why don't you just share real quickly where you you know, 4:25 share real quickly where you you know, 4:25 share real quickly where you you know, why you got into this and I think 4:28 why you got into this and I think 4:28 why you got into this and I think sometimes bad you know, sometimes when 4:30 sometimes bad you know, sometimes when 4:30 sometimes bad you know, sometimes when we struggle it turns into something 4:33 we struggle it turns into something 4:33 we struggle it turns into something wonderful and I think that's what 4:34 wonderful and I think that's what 4:34 wonderful and I think that's what happens in your case. 4:35 happens in your case. 4:35 happens in your case. >> It it certainly is. Yeah, I I didn't 4:39 >> It it certainly is. Yeah, I I didn't 4:39 >> It it certainly is. Yeah, I I didn't really know anything about osteoporosis 4:40 really know anything about osteoporosis 4:40 really know anything about osteoporosis back then. I'm a chiropractic physician. 4:42 back then. I'm a chiropractic physician. 4:42 back then. I'm a chiropractic physician. I knew a lot about, you know, 4:43 I knew a lot about, you know, 4:44 I knew a lot about, you know, kinesiology and biomechanics and you 4:46 kinesiology and biomechanics and you 4:46 kinesiology and biomechanics and you know, bone stuff, but not the metabolic 4:48 know, bone stuff, but not the metabolic 4:48 know, bone stuff, but not the metabolic nature of bone. And so when I you know, 4:51 nature of bone. And so when I you know, 4:51 nature of bone. And so when I you know, found out I had osteoporosis when I was 4:53 found out I had osteoporosis when I was 4:53 found out I had osteoporosis when I was starting to break a lot I had broken a 4:55 starting to break a lot I had broken a 4:55 starting to break a lot I had broken a lot of bones throughout my life. And I 4:58 lot of bones throughout my life. And I 4:58 lot of bones throughout my life. And I just knew I had to immerse myself in the 5:00 just knew I had to immerse myself in the 5:00 just knew I had to immerse myself in the study of it to figure things out. And so 5:02 study of it to figure things out. And so 5:02 study of it to figure things out. And so I've written two books on it, written a 5:04 I've written two books on it, written a 5:04 I've written two books on it, written a paper on it. I started a supplement 5:07 paper on it. I started a supplement 5:07 paper on it. I started a supplement company Osteo Naturals. I now, you know, 5:09 company Osteo Naturals. I now, you know, 5:09 company Osteo Naturals. I now, you know, have a my great bones education 5:11 have a my great bones education 5:11 have a my great bones education information services where I do consults 5:14 information services where I do consults 5:14 information services where I do consults with people with osteoporosis. So, it 5:16 with people with osteoporosis. So, it 5:16 with people with osteoporosis. So, it has totally transformed my life. So, 5:19 has totally transformed my life. So, 5:19 has totally transformed my life. So, yes, you're right. A bad thing certainly 5:21 yes, you're right. A bad thing certainly 5:21 yes, you're right. A bad thing certainly turned into a good thing and and and I 5:23 turned into a good thing and and and I 5:23 turned into a good thing and and and I said like I said, the biggest gift of 5:26 said like I said, the biggest gift of 5:26 said like I said, the biggest gift of all this is that I I feel like I can 5:28 all this is that I I feel like I can 5:28 all this is that I I feel like I can help a lot of people not just because I 5:31 help a lot of people not just because I 5:31 help a lot of people not just because I know a lot about the the disorder, but I 5:33 know a lot about the the disorder, but I 5:33 know a lot about the the disorder, but I think because I've been there and I have 5:35 think because I've been there and I have 5:35 think because I've been there and I have a lot more awareness to what people are 5:38 a lot more awareness to what people are 5:38 a lot more awareness to what people are going through when they when they find 5:40 going through when they when they find 5:40 going through when they when they find out they have 5:41 out they have 5:42 out they have fragile bones, you know. 5:43 fragile bones, you know. 5:43 fragile bones, you know. >> So, how many frac So, how many fractures 5:45 >> So, how many frac So, how many fractures 5:45 >> So, how many frac So, how many fractures did you have prior to dealing with this? 5:49 did you have prior to dealing with this? 5:49 did you have prior to dealing with this? >> Well, over my lifetime I've had 25. 5:51 >> Well, over my lifetime I've had 25. 5:51 >> Well, over my lifetime I've had 25. >> Okay, and then you went from 25 5:53 >> Okay, and then you went from 25 5:53 >> Okay, and then you went from 25 fractures to doing Iron Man, right? 5:56 fractures to doing Iron Man, right? 5:56 fractures to doing Iron Man, right? Which 5:57 Which 5:57 Which >> So, now I'm doing pretty good and I'll 6:00 >> So, now I'm doing pretty good and I'll 6:00 >> So, now I'm doing pretty good and I'll show you some slides later here at this 6:01 show you some slides later here at this 6:01 show you some slides later here at this morning today about of a bone biopsy 6:04 morning today about of a bone biopsy 6:04 morning today about of a bone biopsy that I had. So, you'll kind of see the 6:07 that I had. So, you'll kind of see the 6:07 that I had. So, you'll kind of see the the shape that my bones were in at one 6:09 the shape that my bones were in at one 6:09 the shape that my bones were in at one time. So, 6:10 time. So, 6:10 time. So, >> Okay, so let's continue but I just think 6:12 >> Okay, so let's continue but I just think 6:12 >> Okay, so let's continue but I just think that's important cuz you're a role model 6:14 that's important cuz you're a role model 6:14 that's important cuz you're a role model that this is possible. We can go from 6:17 that this is possible. We can go from 6:17 that this is possible. We can go from where you were to being strong, healthy, 6:20 where you were to being strong, healthy, 6:20 where you were to being strong, healthy, and really doing incredible exercise. 6:23 and really doing incredible exercise. 6:23 and really doing incredible exercise. Okay, so you let's let's move on. 6:26 Okay, so you let's let's move on. 6:26 Okay, so you let's let's move on. >> So, today we're going to look at the 6:28 >> So, today we're going to look at the 6:28 >> So, today we're going to look at the connections between osteoporosis and 6:30 connections between osteoporosis and 6:30 connections between osteoporosis and cardiovascular disease. 6:32 cardiovascular disease. 6:32 cardiovascular disease. And the more scientists learn about 6:34 And the more scientists learn about 6:34 And the more scientists learn about these two two diseases, the harder it 6:36 these two two diseases, the harder it 6:36 these two two diseases, the harder it becomes to think of them as completely 6:38 becomes to think of them as completely 6:38 becomes to think of them as completely separate entities. 6:40 separate entities. 6:40 separate entities. They share multiple signaling pathways 6:42 They share multiple signaling pathways 6:42 They share multiple signaling pathways and mechanisms that can simultaneously 6:46 and mechanisms that can simultaneously 6:46 and mechanisms that can simultaneously drive bone loss on one hand and vascular 6:48 drive bone loss on one hand and vascular 6:48 drive bone loss on one hand and vascular injury and calcification on the other. 6:50 injury and calcification on the other. 6:50 injury and calcification on the other. It's a phenomenon we call the calcium 6:52 It's a phenomenon we call the calcium 6:52 It's a phenomenon we call the calcium paradox. So, we're going to talk about 6:54 paradox. So, we're going to talk about 6:54 paradox. So, we're going to talk about things like that and then we're going to 6:55 things like that and then we're going to 6:55 things like that and then we're going to go look at a case. We'll call her Jane 6:57 go look at a case. We'll call her Jane 6:57 go look at a case. We'll call her Jane and she's a woman with both severe 6:59 and she's a woman with both severe 6:59 and she's a woman with both severe osteoporosis and cardiovascular disease. 7:03 osteoporosis and cardiovascular disease. 7:03 osteoporosis and cardiovascular disease. And we're going to see how laboratory 7:04 And we're going to see how laboratory 7:04 And we're going to see how laboratory biomarkers, lab tests, can tell us not 7:07 biomarkers, lab tests, can tell us not 7:07 biomarkers, lab tests, can tell us not just allow us to see what's happening 7:09 just allow us to see what's happening 7:09 just allow us to see what's happening physiologically, but why it's happening. 7:12 physiologically, but why it's happening. 7:13 physiologically, but why it's happening. And most important, come up with a good 7:14 And most important, come up with a good 7:14 And most important, come up with a good treatment program. Osteoporosis and 7:16 treatment program. Osteoporosis and 7:16 treatment program. Osteoporosis and cardiovascular disease frequently travel 7:18 cardiovascular disease frequently travel 7:19 cardiovascular disease frequently travel together. So, the next time you see your 7:21 together. So, the next time you see your 7:21 together. So, the next time you see your PCP or endocrinologist, I encourage you 7:24 PCP or endocrinologist, I encourage you 7:24 PCP or endocrinologist, I encourage you to ask them, "Hey, don't just look at my 7:26 to ask them, "Hey, don't just look at my 7:26 to ask them, "Hey, don't just look at my bone density. Look at my heart. Make 7:28 bone density. Look at my heart. Make 7:28 bone density. Look at my heart. Make sure I'm okay on that that front, too." 7:30 sure I'm okay on that that front, too." 7:30 sure I'm okay on that that front, too." So, 7:31 So, 7:31 So, more than 10 million Americans have
The connection between osteoporosis and cardiovascular health 7:35 more than 10 million Americans have 7:35 more than 10 million Americans have osteoporosis. And 50% of women, 16% of 7:38 osteoporosis. And 50% of women, 16% of 7:38 osteoporosis. And 50% of women, 16% of men will sustain a fracture because of 7:40 men will sustain a fracture because of 7:40 men will sustain a fracture because of it. And half of all adults in the United 7:42 it. And half of all adults in the United 7:43 it. And half of all adults in the United States have some level of cardiovascular 7:45 States have some level of cardiovascular 7:45 States have some level of cardiovascular disease, and almost a million die each 7:47 disease, and almost a million die each 7:47 disease, and almost a million die each year. That's one person every 34 7:50 year. That's one person every 34 7:50 year. That's one person every 34 seconds. And we always talk about LDL, 7:53 seconds. And we always talk about LDL, 7:53 seconds. And we always talk about LDL, the low-density lipoproteins, as being a 7:55 the low-density lipoproteins, as being a 7:55 the low-density lipoproteins, as being a problem, but half of those people that 7:57 problem, but half of those people that 7:57 problem, but half of those people that die have normal LDL cholesterol levels. 8:00 die have normal LDL cholesterol levels. 8:00 die have normal LDL cholesterol levels. So, if you have osteoporosis, your risk 8:02 So, if you have osteoporosis, your risk 8:02 So, if you have osteoporosis, your risk for cardiovascular disease is four times 8:04 for cardiovascular disease is four times 8:04 for cardiovascular disease is four times higher than someone with normal bone 8:06 higher than someone with normal bone 8:06 higher than someone with normal bone density. And this isn't just because the 8:08 density. And this isn't just because the 8:08 density. And this isn't just because the calcium 8:10 calcium 8:10 calcium from the breakdown of your bones 8:11 from the breakdown of your bones 8:11 from the breakdown of your bones sprinkles over passively and gets lodged 8:14 sprinkles over passively and gets lodged 8:14 sprinkles over passively and gets lodged into your arteries. It's an active 8:16 into your arteries. It's an active 8:16 into your arteries. It's an active cell-mediated process, similar to what 8:18 cell-mediated process, similar to what 8:18 cell-mediated process, similar to what we see in the skeleton when your 8:20 we see in the skeleton when your 8:20 we see in the skeleton when your osteoblasts are forming bone. So, when 8:21 osteoblasts are forming bone. So, when 8:22 osteoblasts are forming bone. So, when you osteoblasts form bone, there's a 8:24 you osteoblasts form bone, there's a 8:24 you osteoblasts form bone, there's a similar mechanism in your arteries that 8:27 similar mechanism in your arteries that 8:27 similar mechanism in your arteries that can make calcified plaque. So, we call 8:30 can make calcified plaque. So, we call 8:30 can make calcified plaque. So, we call the shared biological mechanisms of 8:32 the shared biological mechanisms of 8:32 the shared biological mechanisms of these two diseases the bone-vascular 8:35 these two diseases the bone-vascular 8:35 these two diseases the bone-vascular axis. This is the It's a unifying 8:37 axis. This is the It's a unifying 8:37 axis. This is the It's a unifying conceptual framework describing the 8:39 conceptual framework describing the 8:40 conceptual framework describing the network of communication between bone 8:42 network of communication between bone 8:42 network of communication between bone and the vascular system. It's a network 8:44 and the vascular system. It's a network 8:44 and the vascular system. It's a network that shares many of the same risk 8:46 that shares many of the same risk 8:46 that shares many of the same risk factors. 8:47 factors. 8:47 factors. I list the lot of list risk factors 8:49 I list the lot of list risk factors 8:49 I list the lot of list risk factors there, the aging, high lipids, sedentary 8:52 there, the aging, high lipids, sedentary 8:52 there, the aging, high lipids, sedentary lifestyle, stress, all those things. 8:54 lifestyle, stress, all those things. 8:54 lifestyle, stress, all those things. Same risk factors for both disorders. 8:56 Same risk factors for both disorders. 8:57 Same risk factors for both disorders. So, chronic systemic inflammation is 8:59 So, chronic systemic inflammation is 8:59 So, chronic systemic inflammation is probably the number one calling card of 9:01 probably the number one calling card of 9:01 probably the number one calling card of these comorbidities. And we're going to 9:03 these comorbidities. And we're going to 9:03 these comorbidities. And we're going to talk about this signaling pathway called 9:05 talk about this signaling pathway called 9:05 talk about this signaling pathway called the RANK-RANKL-OPG. 9:08 the RANK-RANKL-OPG. 9:08 the RANK-RANKL-OPG. And I apologize for getting a little bit 9:10 And I apologize for getting a little bit 9:10 And I apologize for getting a little bit too complex here maybe for some people, 9:13 too complex here maybe for some people, 9:13 too complex here maybe for some people, but I talk a lot about the 9:15 but I talk a lot about the 9:15 but I talk a lot about the RANK-RANKL-OPG system in my book. And 9:19 RANK-RANKL-OPG system in my book. And 9:19 RANK-RANKL-OPG system in my book. And so, if you miss what I'm going to say 9:20 so, if you miss what I'm going to say 9:20 so, if you miss what I'm going to say here, you can go there and look at that, 9:22 here, you can go there and look at that, 9:22 here, you can go there and look at that, but it's really important to understand 9:24 but it's really important to understand 9:24 but it's really important to understand this system. 9:26 this system. 9:26 this system. So, RANKL, or it's called receptor 9:28 So, RANKL, or it's called receptor 9:28 So, RANKL, or it's called receptor activator for nuclear factor kappa-B 9:30 activator for nuclear factor kappa-B 9:30 activator for nuclear factor kappa-B ligand. So, the ligand is just a 9:34 ligand. So, the ligand is just a 9:34 ligand. So, the ligand is just a molecule that signals are 9:36 molecule that signals are 9:36 molecule that signals are The RANKL is a protein, a chemical 9:39 The RANKL is a protein, a chemical 9:39 The RANKL is a protein, a chemical signal that activates osteoclasts to 9:41 signal that activates osteoclasts to 9:41 signal that activates osteoclasts to break down bone. It's also a trigger to 9:43 break down bone. It's also a trigger to 9:44 break down bone. It's also a trigger to for vascular calcification and and 9:46 for vascular calcification and and 9:46 for vascular calcification and and destabilizing existing plaque in your 9:48 destabilizing existing plaque in your 9:48 destabilizing existing plaque in your arteries. So, this RANKL really ties 9:51 arteries. So, this RANKL really ties 9:51 arteries. So, this RANKL really ties these two diseases together. 9:54 these two diseases together. 9:54 these two diseases together. And you can't have elevated RANKL 9:56 And you can't have elevated RANKL 9:56 And you can't have elevated RANKL without having bone loss and damage to 9:58 without having bone loss and damage to 9:58 without having bone loss and damage to your blood vessels in the heart. This 10:00 your blood vessels in the heart. This 10:00 your blood vessels in the heart. This next one here is nitric oxide and that's 10:03 next one here is nitric oxide and that's 10:03 next one here is nitric oxide and that's the [clears throat] smallest signaling 10:05 the [clears throat] smallest signaling 10:05 the [clears throat] smallest signaling molecule and plays an integral part in 10:07 molecule and plays an integral part in 10:08 molecule and plays an integral part in both diseases. And there's other other 10:10 both diseases. And there's other other 10:10 both diseases. And there's other other shared things that that go along with 10:12 shared things that that go along with 10:12 shared things that that go along with the two diseases. Hormones, vitamin D, 10:14 the two diseases. Hormones, vitamin D, 10:14 the two diseases. Hormones, vitamin D, vitamin K, sclerostin we're going to 10:16 vitamin K, sclerostin we're going to 10:16 vitamin K, sclerostin we're going to talk about later, kidney disease, and of 10:18 talk about later, kidney disease, and of 10:18 talk about later, kidney disease, and of course we have genetics. 50 to 70% of 10:21 course we have genetics. 50 to 70% of 10:21 course we have genetics. 50 to 70% of our density is probably governed by 10:23 our density is probably governed by 10:23 our density is probably governed by genetics. 10:24 genetics. 10:24 genetics. And thousands of genetic variants have 10:26 And thousands of genetic variants have 10:26 And thousands of genetic variants have been discovered that influence bone 10:28 been discovered that influence bone 10:28 been discovered that influence bone density. And for cardiovascular disease, 10:30 density. And for cardiovascular disease, 10:30 density. And for cardiovascular disease, 40 to 60% of your risk 10:32 40 to 60% of your risk 10:32 40 to 60% of your risk that was placed there by your parents' 10:34 that was placed there by your parents' 10:34 that was placed there by your parents' DNA. So, there's lots of genetic 10:36 DNA. So, there's lots of genetic 10:36 DNA. So, there's lots of genetic variants that have to do with the two 10:39 variants that have to do with the two 10:39 variants that have to do with the two disorders. And these variants, they're 10:42 disorders. And these variants, they're 10:42 disorders. And these variants, they're small changes in the DNA that can exert 10:46 small changes in the DNA that can exert 10:46 small changes in the DNA that can exert small incremental or what's called 10:47 small incremental or what's called 10:47 small incremental or what's called polygenic effects on bone and the 10:49 polygenic effects on bone and the 10:49 polygenic effects on bone and the cardiovascular system. So, this is a 10:51 cardiovascular system. So, this is a 10:51 cardiovascular system. So, this is a list of some of the most common variants 10:54 list of some of the most common variants 10:54 list of some of the most common variants and I'm not going to talk about all of 10:55 and I'm not going to talk about all of 10:55 and I'm not going to talk about all of them but but they include inflammatory 10:58 them but but they include inflammatory 10:58 them but but they include inflammatory genes, estrogen, bone morphogenetic 11:01 genes, estrogen, bone morphogenetic 11:01 genes, estrogen, bone morphogenetic protein, nitric oxide production. 11:04 protein, nitric oxide production. 11:04 protein, nitric oxide production. But if you go to that middle one, the 11:06 But if you go to that middle one, the 11:06 But if you go to that middle one, the APOE4, I'll just talk a little bit about 11:08 APOE4, I'll just talk a little bit about 11:08 APOE4, I'll just talk a little bit about that one specifically. And the reason 11:10 that one specifically. And the reason 11:10 that one specifically. And the reason why is because most of us think of the 11:12 why is because most of us think of the 11:12 why is because most of us think of the APOE4 11:14 APOE4 11:14 APOE4 gene variant is just giving us increased 11:16 gene variant is just giving us increased 11:16 gene variant is just giving us increased risk for Alzheimer's. But if you have 11:18 risk for Alzheimer's. But if you have 11:18 risk for Alzheimer's. But if you have the APOE variant and even if you only 11:20 the APOE variant and even if you only 11:21 the APOE variant and even if you only have one inherited copy, you can still 11:23 have one inherited copy, you can still 11:23 have one inherited copy, you can still have increased fracture risk. And this 11:25 have increased fracture risk. And this 11:25 have increased fracture risk. And this is due to its disruptive effect on 11:27 is due to its disruptive effect on 11:27 is due to its disruptive effect on osteocyte function. Remember, we have 11:29 osteocyte function. Remember, we have 11:29 osteocyte function. Remember, we have three 11:31 three 11:31 three bone cells. We have the osteoblast 11:33 bone cells. We have the osteoblast 11:33 bone cells. We have the osteoblast that form bone, the osteoclast that tear 11:36 that form bone, the osteoclast that tear 11:36 that form bone, the osteoclast that tear down bone, and then the osteocytes that 11:39 down bone, and then the osteocytes that 11:39 down bone, and then the osteocytes that they kind of govern the whole bone 11:41 they kind of govern the whole bone 11:41 they kind of govern the whole bone remodeling system as a whole. And when 11:44 remodeling system as a whole. And when 11:44 remodeling system as a whole. And when you have this APOE 11:46 you have this APOE 11:46 you have this APOE genetic variant, it disrupts the 11:49 genetic variant, it disrupts the 11:49 genetic variant, it disrupts the function of osteocytes. So, they can't 11:52 function of osteocytes. So, they can't 11:52 function of osteocytes. So, they can't really govern that bone remodeling 11:55 really govern that bone remodeling 11:55 really govern that bone remodeling system as well as they should. So, women 11:57 system as well as they should. So, women 11:57 system as well as they should. So, women with the APOE4 variant have a higher 12:01 with the APOE4 variant have a higher 12:01 with the APOE4 variant have a higher fracture risk even if their bone mineral 12:03 fracture risk even if their bone mineral 12:03 fracture risk even if their bone mineral density is not in the osteoporotic 12:05 density is not in the osteoporotic 12:05 density is not in the osteoporotic range. And then we're going to talk 12:06 range. And then we're going to talk 12:06 range. And then we're going to talk about these last three that MTHFR, 12:09 about these last three that MTHFR, 12:09 about these last three that MTHFR, sclerostin, and then finally this really 12:12 sclerostin, and then finally this really 12:12 sclerostin, and then finally this really neat gene variant called SMG6. So, the
MTHFR and homocysteine: why they matter 12:15 neat gene variant called SMG6. So, the 12:15 neat gene variant called SMG6. So, the MTHFR gene, it codes for an enzyme that 12:18 MTHFR gene, it codes for an enzyme that 12:18 MTHFR gene, it codes for an enzyme that activates the 12:20 activates the 12:20 activates the the vitamin folate. 12:22 the vitamin folate. 12:22 the vitamin folate. And folate's a key cofactor for helping 12:25 And folate's a key cofactor for helping 12:25 And folate's a key cofactor for helping us get rid of homocysteine. 12:27 us get rid of homocysteine. 12:27 us get rid of homocysteine. Homocysteine's a toxic metabolite 12:30 Homocysteine's a toxic metabolite 12:30 Homocysteine's a toxic metabolite produced when you eat protein, 12:31 produced when you eat protein, 12:31 produced when you eat protein, specifically the amino acid methionine. 12:34 specifically the amino acid methionine. 12:34 specifically the amino acid methionine. And if a person has this MTHFR gene 12:37 And if a person has this MTHFR gene 12:37 And if a person has this MTHFR gene variant, as many of us do, it's very 12:40 variant, as many of us do, it's very 12:40 variant, as many of us do, it's very common, then homocysteine levels 12:42 common, then homocysteine levels 12:42 common, then homocysteine levels increase in the blood. 12:44 increase in the blood. 12:45 increase in the blood. High homocysteine, especially when it 12:46 High homocysteine, especially when it 12:46 High homocysteine, especially when it gets above 15 micromoles per liter, can 12:49 gets above 15 micromoles per liter, can 12:49 gets above 15 micromoles per liter, can damage blood vessel walls, accelerate 12:51 damage blood vessel walls, accelerate 12:51 damage blood vessel walls, accelerate plaque formation, promote clotting, and 12:54 plaque formation, promote clotting, and 12:54 plaque formation, promote clotting, and bone it weakens the structural collagen 12:56 bone it weakens the structural collagen 12:56 bone it weakens the structural collagen crosslinks. It makes bones stiff, less 12:59 crosslinks. It makes bones stiff, less 12:59 crosslinks. It makes bones stiff, less flexible. And if it gets to 15 or 20 13:03 flexible. And if it gets to 15 or 20 13:03 flexible. And if it gets to 15 or 20 micromoles per liter, it can increase 13:06 micromoles per liter, it can increase 13:06 micromoles per liter, it can increase fracture risk two to three times. 13:09 fracture risk two to three times. 13:09 fracture risk two to three times. >> Hey Wajeeha. As a physical therapist, I 13:12 >> Hey Wajeeha. As a physical therapist, I 13:12 >> Hey Wajeeha. As a physical therapist, I know firsthand how important exercise is 13:15 know firsthand how important exercise is 13:15 know firsthand how important exercise is for our bones, overall health, and 13:17 for our bones, overall health, and 13:17 for our bones, overall health, and happiness. [music] 13:18 happiness. [music] 13:18 happiness. [music] And unfortunately, there's a lot of 13:20 And unfortunately, there's a lot of 13:20 And unfortunately, there's a lot of confusion on what exercises are safe and 13:23 confusion on what exercises are safe and 13:23 confusion on what exercises are safe and effective for people with osteoporosis. 13:25 effective for people with osteoporosis. 13:25 effective for people with osteoporosis. [music] 13:26 [music] 13:26 [music] That's why I created this handout that 13:29 That's why I created this handout that 13:29 That's why I created this handout that contains a 30-minute video [music] where 13:31 contains a 30-minute video [music] where 13:31 contains a 30-minute video [music] where I explain the concepts so you understand 13:34 I explain the concepts so you understand 13:34 I explain the concepts so you understand the do's and don'ts [music] when it 13:35 the do's and don'ts [music] when it 13:36 the do's and don'ts [music] when it comes to exercise. And this is important 13:38 comes to exercise. And this is important 13:38 comes to exercise. And this is important because this way you can go into any 13:40 because this way you can go into any 13:40 because this way you can go into any class and know what you should be doing 13:43 class and know what you should be doing 13:43 class and know what you should be doing and what [music] you should avoid 13:45 and what [music] you should avoid 13:45 and what [music] you should avoid because too many people are doing 13:47 because too many people are doing 13:47 because too many people are doing exercises that [music] actually increase 13:49 exercises that [music] actually increase 13:49 exercises that [music] actually increase their risk of spinal fractures. 13:52 their risk of spinal fractures. 13:52 their risk of spinal fractures. I also included videos of me 13:54 I also included videos of me 13:54 I also included videos of me demonstrating [music] 13:55 demonstrating [music] 13:55 demonstrating [music] effective balance, posture, and 13:57 effective balance, posture, and 13:57 effective balance, posture, and weight-bearing exercises [music] you can 13:59 weight-bearing exercises [music] you can 13:59 weight-bearing exercises [music] you can put into your day right away. So, all 14:02 put into your day right away. So, all 14:02 put into your day right away. So, all you need to do to access this [music] 14:04 you need to do to access this [music] 14:04 you need to do to access this [music] handout, it's free, is go to 14:07 handout, it's free, is go to 14:07 handout, it's free, is go to tinyurl.com/osteoporosisexercises. 14:16 So, it's t i n y u r l .com 14:16 So, it's t i n y u r l .com >> [music] 14:16 >> [music] 14:16 >> [music] >> /osteoporosisexercises 14:21 or you can click the link in the show 14:21 or you can click the link in the show [music] notes. Now, back to the show. 14:25 [music] notes. Now, back to the show. 14:25 [music] notes. Now, back to the show. Yeah, we have to stop here for a second 14:27 Yeah, we have to stop here for a second 14:27 Yeah, we have to stop here for a second because this is so important. It's not 14:31 because this is so important. It's not 14:31 because this is so important. It's not an expensive test, but yet Dr. McCombs, 14:33 an expensive test, but yet Dr. McCombs, 14:33 an expensive test, but yet Dr. McCombs, most doctors are not ordering this as 14:35 most doctors are not ordering this as 14:35 most doctors are not ordering this as part of their routine. And a lot of 14:38 part of their routine. And a lot of 14:38 part of their routine. And a lot of people What number The thing is, if it's 14:40 people What number The thing is, if it's 14:40 people What number The thing is, if it's 14, it will show up as normal on a lot 14:43 14, it will show up as normal on a lot 14:43 14, it will show up as normal on a lot of 14:43 of 14:43 of >> Yeah. 14:44 >> Yeah. 14:44 >> Yeah. >> So, what what are the value What value 14:46 >> So, what what are the value What value 14:46 >> So, what what are the value What value do you like to see it below when you 14:48 do you like to see it below when you 14:48 do you like to see it below when you >> I like to keep it at eight or below or 14:50 >> I like to keep it at eight or below or 14:50 >> I like to keep it at eight or below or so. But, if it's a if it's a nine, it's 14:52 so. But, if it's a if it's a nine, it's 14:52 so. But, if it's a if it's a nine, it's not a big deal. But, yes, when you start 14:54 not a big deal. But, yes, when you start 14:54 not a big deal. But, yes, when you start getting to 12, 13, 14, that's of of 14:57 getting to 12, 13, 14, that's of of 14:57 getting to 12, 13, 14, that's of of concern. 14:58 concern. 14:58 concern. >> What I like about this is though, even 15:00 >> What I like about this is though, even 15:00 >> What I like about this is though, even if you don't test, you don't have to 15:02 if you don't test, you don't have to 15:02 if you don't test, you don't have to find You don't have to do the MTHFR the 15:05 find You don't have to do the MTHFR the 15:05 find You don't have to do the MTHFR the MTHFR test, but if you see your 15:07 MTHFR test, but if you see your 15:07 MTHFR test, but if you see your homocysteine is elevated, there's a 15:09 homocysteine is elevated, there's a 15:09 homocysteine is elevated, there's a really simple treatment. You want to 15:11 really simple treatment. You want to 15:11 really simple treatment. You want to just talk about what you do when you 15:13 just talk about what you do when you 15:13 just talk about what you do when you find someone has this elevated Yeah. 15:16 find someone has this elevated Yeah. 15:16 find someone has this elevated Yeah. >> Yeah, to get the MTHFR test, I don't 15:18 >> Yeah, to get the MTHFR test, I don't 15:18 >> Yeah, to get the MTHFR test, I don't know, it's a 100 bucks or 150 bucks or 15:20 know, it's a 100 bucks or 150 bucks or 15:20 know, it's a 100 bucks or 150 bucks or something like that. I I I don't ever 15:22 something like that. I I I don't ever 15:22 something like that. I I I don't ever test for it, so that's why I don't 15:23 test for it, so that's why I don't 15:23 test for it, so that's why I don't really know the number. But, a 15:25 really know the number. But, a 15:25 really know the number. But, a homocysteine test is is maybe like $20. 15:28 homocysteine test is is maybe like $20. 15:28 homocysteine test is is maybe like $20. So, it's it's much less expensive to 15:31 So, it's it's much less expensive to 15:31 So, it's it's much less expensive to get. Yes, as you said, everybody should 15:33 get. Yes, as you said, everybody should 15:33 get. Yes, as you said, everybody should get it. And I always There's a lot of 15:36 get it. And I always There's a lot of 15:36 get it. And I always There's a lot of companies that sell products that help 15:39 companies that sell products that help 15:39 companies that sell products that help cofactors for the enzyme that breaks the 15:42 cofactors for the enzyme that breaks the 15:42 cofactors for the enzyme that breaks the homocysteine down back in either to 15:44 homocysteine down back in either to 15:44 homocysteine down back in either to methionine or gets rid of it. But, the 15:47 methionine or gets rid of it. But, the 15:47 methionine or gets rid of it. But, the cofactors like vitamin B2, B6, B12, 15:51 cofactors like vitamin B2, B6, B12, 15:51 cofactors like vitamin B2, B6, B12, trimethylglycine. I I use a Designs for 15:54 trimethylglycine. I I use a Designs for 15:54 trimethylglycine. I I use a Designs for Health product called Homocysteine 15:56 Health product called Homocysteine 15:56 Health product called Homocysteine Supreme. Almost always, it'll take a 15:59 Supreme. Almost always, it'll take a 15:59 Supreme. Almost always, it'll take a homocysteine from a 15 and bring it 16:01 homocysteine from a 15 and bring it 16:01 homocysteine from a 15 and bring it right down to 10 or 8 or something like 16:03 right down to 10 or 8 or something like 16:03 right down to 10 or 8 or something like that. So, 16:04 that. So, 16:04 that. So, yes, it's a cheap test to get, 16:06 yes, it's a cheap test to get, 16:06 yes, it's a cheap test to get, inexpensive test to get, and it's easy 16:08 inexpensive test to get, and it's easy 16:08 inexpensive test to get, and it's easy to to fix. 16:10 to to fix. 16:10 to to fix. >> And has significant implications for 16:12 >> And has significant implications for 16:12 >> And has significant implications for both our bones and our cardiovascular 16:14 both our bones and our cardiovascular 16:14 both our bones and our cardiovascular and inflammation. So, I think it's 16:16 and inflammation. So, I think it's 16:16 and inflammation. So, I think it's something that everybody needs to 16:18 something that everybody needs to 16:18 something that everybody needs to >> Everybody should test for. 16:19 >> Everybody should test for. 16:19 >> Everybody should test for. >> Put on their radar. 16:20 >> Put on their radar. 16:20 >> Put on their radar. >> So, this is a a Everybody's probably 16:23 >> So, this is a a Everybody's probably 16:23 >> So, this is a a Everybody's probably familiar with with sclerostin. If you 16:25 familiar with with sclerostin. If you 16:25 familiar with with sclerostin. If you especially if you if you're familiar 16:27 especially if you if you're familiar 16:27 especially if you if you're familiar with the osteoporosis medication 16:29 with the osteoporosis medication 16:29 with the osteoporosis medication romosozumab, 16:31 romosozumab, 16:31 romosozumab, or what's called Evenity, then you've 16:33 or what's called Evenity, then you've 16:33 or what's called Evenity, then you've probably heard of sclerostin. It's a 16:35 probably heard of sclerostin. It's a 16:35 probably heard of sclerostin. It's a protein that your body produces to keep 16:37 protein that your body produces to keep 16:37 protein that your body produces to keep osteoblasts from producing too much 16:39 osteoblasts from producing too much 16:39 osteoblasts from producing too much bone. And I mean, you know, we always 16:41 bone. And I mean, you know, we always 16:41 bone. And I mean, you know, we always talk about osteoporosis as too little 16:43 talk about osteoporosis as too little 16:43 talk about osteoporosis as too little bone, but we also don't want to have too 16:45 bone, but we also don't want to have too 16:45 bone, but we also don't want to have too much bone, and that's where sclerostin 16:47 much bone, and that's where sclerostin 16:47 much bone, and that's where sclerostin comes in. It's also an important 16:49 comes in. It's also an important 16:49 comes in. It's also an important molecular link between bone and the 16:51 molecular link between bone and the 16:51 molecular link between bone and the vascular systems. Evenity is an antibody 16:53 vascular systems. Evenity is an antibody 16:54 vascular systems. Evenity is an antibody against sclerostin, so it it keeps it 16:57 against sclerostin, so it it keeps it 16:57 against sclerostin, so it it keeps it down since And since sclerostin prevents 16:59 down since And since sclerostin prevents 16:59 down since And since sclerostin prevents your osteoblasts from forming too much 17:01 your osteoblasts from forming too much 17:01 your osteoblasts from forming too much bone, taking it away taking that 17:03 bone, taking it away taking that 17:03 bone, taking it away taking that sclerostin away leads to increased bone 17:06 sclerostin away leads to increased bone 17:06 sclerostin away leads to increased bone density. 17:07 density. 17:07 density. And that's exactly what happens when we 17:09 And that's exactly what happens when we 17:09 And that's exactly what happens when we have a sclerostin gene variant. So, 17:12 have a sclerostin gene variant. So, 17:12 have a sclerostin gene variant. So, there's three basic types of variants 17:14 there's three basic types of variants 17:14 there's three basic types of variants for for this sclerostin gene, but only 17:18 for for this sclerostin gene, but only 17:18 for for this sclerostin gene, but only only going to be talking about one of 17:19 only going to be talking about one of 17:19 only going to be talking about one of them. It's the mildest form of all. It's 17:22 them. It's the mildest form of all. It's 17:22 them. It's the mildest form of all. It's relatively common. That's why I wanted 17:24 relatively common. That's why I wanted 17:24 relatively common. That's why I wanted to mention it. And it's a loss of 17:26 to mention it. And it's a loss of 17:26 to mention it. And it's a loss of function variant. So, in other words, it 17:28 function variant. So, in other words, it 17:28 function variant. So, in other words, it causes a slightly reduced sclerostin 17:30 causes a slightly reduced sclerostin 17:30 causes a slightly reduced sclerostin activity. If a person has this mild 17:33 activity. If a person has this mild 17:33 activity. If a person has this mild variant, it can result in like a 0.2, 17:36 variant, it can result in like a 0.2, 17:36 variant, it can result in like a 0.2, maybe 0.3 standard deviation higher bone 17:40 maybe 0.3 standard deviation higher bone 17:40 maybe 0.3 standard deviation higher bone density compared to somebody without the 17:42 density compared to somebody without the 17:42 density compared to somebody without the variant. So, it's not a a huge impact on 17:44 variant. So, it's not a a huge impact on 17:44 variant. So, it's not a a huge impact on density, but it's it's it's worth 17:46 density, but it's it's it's worth 17:46 density, but it's it's it's worth noting. So, let's say you have a bone 17:49 noting. So, let's say you have a bone 17:49 noting. So, let's say you have a bone density 17:50 density 17:50 density of a spine T-score of -2.7. 17:53 of a spine T-score of -2.7. 17:53 of a spine T-score of -2.7. And you have that's a fracture risk for 17:55 And you have that's a fracture risk for 17:55 And you have that's a fracture risk for sure, but it's not awful. But, you also 17:57 sure, but it's not awful. But, you also 17:57 sure, but it's not awful. But, you also happen to carry a mild loss of function 17:59 happen to carry a mild loss of function 17:59 happen to carry a mild loss of function sclerostin variant variant, which you 18:02 sclerostin variant variant, which you 18:02 sclerostin variant variant, which you don't know about cuz you haven't done 18:03 don't know about cuz you haven't done 18:03 don't know about cuz you haven't done genetic testing, which I'm not 18:05 genetic testing, which I'm not 18:05 genetic testing, which I'm not suggesting you should, but which makes 18:07 suggesting you should, but which makes 18:07 suggesting you should, but which makes your bone density not quite as low as it 18:10 your bone density not quite as low as it 18:10 your bone density not quite as low as it otherwise would be. In other words, the 18:12 otherwise would be. In other words, the 18:12 otherwise would be. In other words, the variant could partially mask the 18:14 variant could partially mask the 18:14 variant could partially mask the severity of your bone loss. Now, add a 18:17 severity of your bone loss. Now, add a 18:17 severity of your bone loss. Now, add a few other complications to this 18:18 few other complications to this 18:19 few other complications to this scenario. 18:20 scenario. 18:20 scenario. Your DEXA scan was performed 18:21 Your DEXA scan was performed 18:21 Your DEXA scan was performed incorrectly, not uncommon, and 18:23 incorrectly, not uncommon, and 18:23 incorrectly, not uncommon, and exaggerated the degree of your bone 18:25 exaggerated the degree of your bone 18:25 exaggerated the degree of your bone loss. 18:26 loss. 18:26 loss. You're also small, you're petite, you're 18:28 You're also small, you're petite, you're 18:28 You're also small, you're petite, you're less than 5 ft, you're only 98 lb. So, 18:32 less than 5 ft, you're only 98 lb. So, 18:32 less than 5 ft, you're only 98 lb. So, your bone density looks worse on paper 18:34 your bone density looks worse on paper 18:34 your bone density looks worse on paper than it really is because remember bone 18:36 than it really is because remember bone 18:36 than it really is because remember bone density scan is a two-dimensional 18:38 density scan is a two-dimensional 18:38 density scan is a two-dimensional picture of a three-dimensional object. 18:40 picture of a three-dimensional object. 18:40 picture of a three-dimensional object. So, so smaller people look a little bit 18:43 So, so smaller people look a little bit 18:43 So, so smaller people look a little bit worse on paper than they really are. 18:45 worse on paper than they really are. 18:45 worse on paper than they really are. Plus, your lipid panel is off. You have 18:49 Plus, your lipid panel is off. You have 18:49 Plus, your lipid panel is off. You have high LDL lipids, you have a high APOB, 18:54 high LDL lipids, you have a high APOB, 18:54 high LDL lipids, you have a high APOB, you have high LP little a, a genetic 18:57 you have high LP little a, a genetic 18:57 you have high LP little a, a genetic indicator that you have your LDLs are 18:59 indicator that you have your LDLs are 19:00 indicator that you have your LDLs are more sticky to they have a more chance 19:02 more sticky to they have a more chance 19:02 more sticky to they have a more chance of sticking to the side of the wall and 19:04 of sticking to the side of the wall and 19:04 of sticking to the side of the wall and causing plaque formation in your 19:06 causing plaque formation in your 19:06 causing plaque formation in your vessels. So, these things are elevated, 19:09 vessels. So, these things are elevated, 19:09 vessels. So, these things are elevated, so it does put you 19:10 so it does put you 19:10 so it does put you >> [clears throat] 19:11 >> [clears throat] 19:11 >> [clears throat] >> this person at a higher risk for 19:13 >> this person at a higher risk for 19:13 >> this person at a higher risk for cardiovascular disease. But, this 19:16 cardiovascular disease. But, this 19:16 cardiovascular disease. But, this person's 19:17 person's 19:17 person's doctor 19:18 doctor 19:18 doctor just got concerned about her T score, 19:21 just got concerned about her T score, 19:21 just got concerned about her T score, about her apparent fracture risk, just 19:24 about her apparent fracture risk, just 19:24 about her apparent fracture risk, just by looking at her T score, and 19:25 by looking at her T score, and 19:25 by looking at her T score, and prescribed Evenity. 19:26 prescribed Evenity. 19:27 prescribed Evenity. But, in reality, you didn't really need 19:28 But, in reality, you didn't really need 19:28 But, in reality, you didn't really need it because you not only had a sclerostin 19:31 it because you not only had a sclerostin 19:31 it because you not only had a sclerostin variant, but your DEXA was wrong. And 19:34 variant, but your DEXA was wrong. And 19:34 variant, but your DEXA was wrong. And you're petite. So, in this scenario, 19:36 you're petite. So, in this scenario, 19:36 you're petite. So, in this scenario, there's a possibility that 19:37 there's a possibility that 19:37 there's a possibility that cardiovascular risk associated with 19:39 cardiovascular risk associated with 19:39 cardiovascular risk associated with Evenity could be a tad bit higher in 19:41 Evenity could be a tad bit higher in 19:41 Evenity could be a tad bit higher in this setting. 19:43 this setting. 19:43 this setting. Proposed mechanism behind this 19:44 Proposed mechanism behind this 19:44 Proposed mechanism behind this cautionary tale is this. Genetic 19:47 cautionary tale is this. Genetic 19:47 cautionary tale is this. Genetic variants like this affect bone and can 19:49 variants like this affect bone and can 19:49 variants like this affect bone and can increase vascular inflammation and 19:51 increase vascular inflammation and 19:51 increase vascular inflammation and encourage arterial calcification. So, in 19:54 encourage arterial calcification. So, in 19:54 encourage arterial calcification. So, in other words, you become, at least 19:56 other words, you become, at least 19:56 other words, you become, at least theoretically, at more cardiovascular 19:58 theoretically, at more cardiovascular 19:58 theoretically, at more cardiovascular risk. And this risk is even greater if 20:01 risk. And this risk is even greater if 20:01 risk. And this risk is even greater if you have chronic kidney disease. So, the 20:03 you have chronic kidney disease. So, the 20:03 you have chronic kidney disease. So, the question is this. Is this a good idea to 20:05 question is this. Is this a good idea to 20:05 question is this. Is this a good idea to prescribe this woman Evenity? Well, the 20:07 prescribe this woman Evenity? Well, the 20:07 prescribe this woman Evenity? Well, the research on these effects are 20:09 research on these effects are 20:09 research on these effects are conflicting. And thankfully, any 20:11 conflicting. And thankfully, any 20:11 conflicting. And thankfully, any additional cardiovascular risk 20:13 additional cardiovascular risk 20:13 additional cardiovascular risk associated with this variant, with or 20:15 associated with this variant, with or 20:15 associated with this variant, with or without Evenity, is likely to be small 20:18 without Evenity, is likely to be small 20:18 without Evenity, is likely to be small if it exists at all. 20:19 if it exists at all. 20:19 if it exists at all. But, 20:20 But, 20:20 But, it's still something worth understanding 20:23 it's still something worth understanding 20:23 it's still something worth understanding because we do not have all the answers 20:25 because we do not have all the answers 20:25 because we do not have all the answers yet. And that's why prescribing 20:27 yet. And that's why prescribing 20:27 yet. And that's why prescribing physicians need to consider the 20:29 physicians need to consider the 20:29 physicians need to consider the patient's broader vascular 20:30 patient's broader vascular 20:30 patient's broader vascular cardiovascular risk. And that's by 20:32 cardiovascular risk. And that's by 20:33 cardiovascular risk. And that's by getting a more comprehensive lipid 20:35 getting a more comprehensive lipid 20:35 getting a more comprehensive lipid profile, not just triglycerides, you 20:38 profile, not just triglycerides, you 20:38 profile, not just triglycerides, you know, cholesterol, HDL. They need to 20:40 know, cholesterol, HDL. They need to 20:40 know, cholesterol, HDL. They need to look at APOB, at LP, need to look at the 20:44 look at APOB, at LP, need to look at the 20:44 look at APOB, at LP, need to look at the number and size of the LDL particles. 20:46 number and size of the LDL particles. 20:46 number and size of the LDL particles. And they often need to look at a 20:48 And they often need to look at a 20:48 And they often need to look at a person's metabolic health, what their 20:50 person's metabolic health, what their 20:50 person's metabolic health, what their glucose levels are is are, and their 20:52 glucose levels are is are, and their 20:52 glucose levels are is are, and their fasting insulin. And the reason why is 20:55 fasting insulin. And the reason why is 20:55 fasting insulin. And the reason why is because it's it's a lot of times it's 20:58 because it's it's a lot of times it's 20:58 because it's it's a lot of times it's it's a background of inflammation and 21:00 it's a background of inflammation and 21:00 it's a background of inflammation and possibly 21:01 possibly 21:01 possibly glucose handling, metabolic handling 21:03 glucose handling, metabolic handling 21:03 glucose handling, metabolic handling issues that actually cause injury to 21:05 issues that actually cause injury to 21:05 issues that actually cause injury to that wall, allowing the LDL particles to 21:09 that wall, allowing the LDL particles to 21:09 that wall, allowing the LDL particles to get in there and cause plaque. 21:11 get in there and cause plaque. 21:11 get in there and cause plaque. So, 21:13 So, 21:13 So, we have to look at the metabolic health 21:15 we have to look at the metabolic health 21:15 we have to look at the metabolic health of the person also. 21:16 of the person also. 21:16 of the person also. >> Okay. Before we go on, this is such an 21:19 >> Okay. Before we go on, this is such an 21:19 >> Okay. Before we go on, this is such an important topic, actually, because we 21:21 important topic, actually, because we 21:21 important topic, actually, because we both know A vanities an incredible drug 21:24 both know A vanities an incredible drug 21:24 both know A vanities an incredible drug when it's used in the right person, and 21:26 when it's used in the right person, and 21:26 when it's used in the right person, and it's helped so many people. But, what 21:28 it's helped so many people. But, what 21:28 it's helped so many people. But, what I've been seeing in people in my 21:29 I've been seeing in people in my 21:29 I've been seeing in people in my community, and Dr. Millman and uh 21:33 community, and Dr. Millman and uh 21:33 community, and Dr. Millman and uh practitioners, people are seeing, Dr. 21:36 practitioners, people are seeing, Dr. 21:36 practitioners, people are seeing, Dr. McCormack, that they're not getting 21:38 McCormack, that they're not getting 21:38 McCormack, that they're not getting these complete, you know, they may they 21:40 these complete, you know, they may they 21:40 these complete, you know, they may they may send them, someone wants to put the 21:41 may send them, someone wants to put the 21:41 may send them, someone wants to put the endocrinologist wants to put the person 21:44 endocrinologist wants to put the person 21:44 endocrinologist wants to put the person on A vanity, so they send them to the 21:45 on A vanity, so they send them to the 21:46 on A vanity, so they send them to the cardiologist, but they're just doing 21:47 cardiologist, but they're just doing 21:47 cardiologist, but they're just doing very routine things. And so, they could 21:50 very routine things. And so, they could 21:50 very routine things. And so, they could be missing this. So, what you're saying, 21:51 be missing this. So, what you're saying, 21:51 be missing this. So, what you're saying, I just want to clarify, is they don't 21:54 I just want to clarify, is they don't 21:54 I just want to clarify, is they don't need to do the genetic testing, but they 21:56 need to do the genetic testing, but they 21:56 need to do the genetic testing, but they need to do this complete cardiovascular 21:59 need to do this complete cardiovascular 21:59 need to do this complete cardiovascular workup. And what do you find is 22:01 workup. And what do you find is 22:01 workup. And what do you find is typically missing? What test, 22:03 typically missing? What test, 22:03 typically missing? What test, specifically? 22:03 specifically? 22:03 specifically? >> Well, they the end 22:05 >> Well, they the end 22:05 >> Well, they the end >> Or the 22:06 >> Or the 22:06 >> Or the >> APOB, the LP little A, and what what's 22:09 >> APOB, the LP little A, and what what's 22:09 >> APOB, the LP little A, and what what's called an NMR, a nuclear magnetic 22:11 called an NMR, a nuclear magnetic 22:11 called an NMR, a nuclear magnetic resonance, where they can look at the 22:13 resonance, where they can look at the 22:13 resonance, where they can look at the the size and the and the number of those 22:15 the size and the and the number of those 22:16 the size and the and the number of those LDL particles, cuz if you have really 22:18 LDL particles, cuz if you have really 22:18 LDL particles, cuz if you have really small LDL particles, they have easier 22:22 small LDL particles, they have easier 22:22 small LDL particles, they have easier time to get in through that vessel wall 22:24 time to get in through that vessel wall 22:24 time to get in through that vessel wall and and cause plaque. So, yes, it's a 22:27 and and cause plaque. So, yes, it's a 22:27 and and cause plaque. So, yes, it's a more of a comprehensive lipid panel, but 22:29 more of a comprehensive lipid panel, but 22:29 more of a comprehensive lipid panel, but it's not terribly, terribly expensive 22:32 it's not terribly, terribly expensive 22:32 it's not terribly, terribly expensive either, and and should be done. And and 22:35 either, and and should be done. And and 22:35 either, and and should be done. And and the the message I'm trying to get across 22:37 the the message I'm trying to get across 22:37 the the message I'm trying to get across here is context is everything. You need 22:40 here is context is everything. You need 22:40 here is context is everything. You need to look at it more than just taking a 22:43 to look at it more than just taking a 22:43 to look at it more than just taking a quick glance at the DEXA T score and 22:45 quick glance at the DEXA T score and 22:45 quick glance at the DEXA T score and prescribing medication. And no, I'm not 22:48 prescribing medication. And no, I'm not 22:48 prescribing medication. And no, I'm not suggesting that everybody should 22:50 suggesting that everybody should 22:50 suggesting that everybody should get sclerostin gene testing. I'm not 22:52 get sclerostin gene testing. I'm not 22:52 get sclerostin gene testing. I'm not saying that at all. But, for most cases 22:54 saying that at all. But, for most cases 22:54 saying that at all. But, for most cases of osteoporosis and cardiovascular 22:56 of osteoporosis and cardiovascular 22:56 of osteoporosis and cardiovascular disease, genetic testing is not that 22:58 disease, genetic testing is not that 22:58 disease, genetic testing is not that helpful at at at least at this stage of 23:01 helpful at at at least at this stage of 23:01 helpful at at at least at this stage of of technology and our clinical 23:03 of technology and our clinical 23:03 of technology and our clinical understanding, genetic testing it can 23:05 understanding, genetic testing it can 23:05 understanding, genetic testing it can indicate possible risk polygenic nature 23:07 indicate possible risk polygenic nature 23:07 indicate possible risk polygenic nature of the two diseases, but it the reports 23:10 of the two diseases, but it the reports 23:10 of the two diseases, but it the reports usually don't really help us much at at 23:14 usually don't really help us much at at 23:14 usually don't really help us much at at all really in the clinic. It's different 23:16 all really in the clinic. It's different 23:16 all really in the clinic. It's different if we're trying to confirm, you know, 23:19 if we're trying to confirm, you know, 23:19 if we're trying to confirm, you know, specific genetic conditions such as 23:21 specific genetic conditions such as 23:21 specific genetic conditions such as osteogenesis imperfecta and things like 23:23 osteogenesis imperfecta and things like 23:23 osteogenesis imperfecta and things like that, but for for the typical 23:26 that, but for for the typical 23:26 that, but for for the typical osteoporosis patient, 23:28 osteoporosis patient, 23:28 osteoporosis patient, no, I don't I don't recommend going to 23:30 no, I don't I don't recommend going to 23:30 no, I don't I don't recommend going to that expense. 23:31 that expense. 23:31 that expense. >> Yeah, so I just wanted to say one more 23:32 >> Yeah, so I just wanted to say one more 23:32 >> Yeah, so I just wanted to say one more thing because this is a very popular 23:34 thing because this is a very popular 23:34 thing because this is a very popular medication and it is helping a lot of 23:36 medication and it is helping a lot of 23:36 medication and it is helping a lot of people and there is significant, you 23:38 people and there is significant, you 23:38 people and there is significant, you know, improvements that we see with this 23:40 know, improvements that we see with this 23:40 know, improvements that we see with this and so my question to you is what will 23:43 and so my question to you is what will 23:43 and so my question to you is what will happen? Like what would happen if this 23:45 happen? Like what would happen if this 23:45 happen? Like what would happen if this if this person or someone with these 23:47 if this person or someone with these 23:47 if this person or someone with these cardiovascular issues goes on, you know, 23:49 cardiovascular issues goes on, you know, 23:49 cardiovascular issues goes on, you know, what goes on and what are the possible 23:52 what goes on and what are the possible 23:52 what goes on and what are the possible side effects? 23:53 side effects? 23:53 side effects? >> I do think the cardiovascular risk can 23:55 >> I do think the cardiovascular risk can 23:55 >> I do think the cardiovascular risk can increase and I mean, that's my opinion, 23:58 increase and I mean, that's my opinion, 23:58 increase and I mean, that's my opinion, you know, we'll we'll know later on in 24:01 you know, we'll we'll know later on in 24:01 you know, we'll we'll know later on in 10 probably 10 years from now, 24:03 10 probably 10 years from now, 24:03 10 probably 10 years from now, but you know, and and as you said, I'm 24:05 but you know, and and as you said, I'm 24:05 but you know, and and as you said, I'm not against Evenity. I I've had many 24:07 not against Evenity. I I've had many 24:07 not against Evenity. I I've had many patients on Evenity that's helped 24:09 patients on Evenity that's helped 24:09 patients on Evenity that's helped tremendously, but I've also had doctors 24:11 tremendously, but I've also had doctors 24:11 tremendously, but I've also had doctors prescribe it when a person has a 24:12 prescribe it when a person has a 24:12 prescribe it when a person has a negative 2.6 or 2.7 and and they're not 24:16 negative 2.6 or 2.7 and and they're not 24:16 negative 2.6 or 2.7 and and they're not fracturing and then that doesn't make 24:18 fracturing and then that doesn't make 24:18 fracturing and then that doesn't make any sense to me. So, we need to do 24:22 any sense to me. So, we need to do 24:22 any sense to me. So, we need to do our homework and make sure we know the 24:26 our homework and make sure we know the 24:26 our homework and make sure we know the risk of that patient before we make 24:28 risk of that patient before we make 24:28 risk of that patient before we make decisions. 24:29 decisions. 24:29 decisions. >> Yeah, and we have seen in the community 24:31 >> Yeah, and we have seen in the community 24:31 >> Yeah, and we have seen in the community people that haven't gone to that and 24:33 people that haven't gone to that and 24:33 people that haven't gone to that and have had some issues. So, I think this 24:34 have had some issues. So, I think this 24:35 have had some issues. So, I think this is just such an important point. So, 24:37 is just such an important point. So, 24:37 is just such an important point. So, thank you so much for bringing this up. 24:38 thank you so much for bringing this up. 24:38 thank you so much for bringing this up. >> So, the other thing that you know, as I 24:40 >> So, the other thing that you know, as I 24:40 >> So, the other thing that you know, as I said, you know, 24:41 said, you know, 24:41 said, you know, regular genetic testing doesn't help us 24:44 regular genetic testing doesn't help us 24:44 regular genetic testing doesn't help us that much for these little variants, but 24:47 that much for these little variants, but 24:47 that much for these little variants, but now we're trying now we're trying to 24:49 now we're trying now we're trying to 24:49 now we're trying now we're trying to see which 24:51 see which 24:51 see which gene disorders, which gene variants can 24:54 gene disorders, which gene variants can 24:54 gene disorders, which gene variants can cause pleiotropic effect. In other 24:57 cause pleiotropic effect. In other 24:57 cause pleiotropic effect. In other words, one gene might affect 25:00 words, one gene might affect 25:00 words, one gene might affect two or three different disorders. 25:03 two or three different disorders. 25:03 two or three different disorders. And this next slide talks about this 25:06 And this next slide talks about this 25:06 And this next slide talks about this gene variant called SMG6. 25:09 gene variant called SMG6. 25:09 gene variant called SMG6. And I'm incredibly excited about it 25:11 And I'm incredibly excited about it 25:11 And I'm incredibly excited about it because so last year at Harvard, they 25:14 because so last year at Harvard, they 25:14 because so last year at Harvard, they identified 211 25:16 identified 211 25:16 identified 211 shared genes between bone density and 25:18 shared genes between bone density and 25:18 shared genes between bone density and coronary artery calcifications. And 25:20 coronary artery calcifications. And 25:20 coronary artery calcifications. And researchers revealed specific localized 25:22 researchers revealed specific localized 25:22 researchers revealed specific localized pathways, especially oxidative stress 25:25 pathways, especially oxidative stress 25:25 pathways, especially oxidative stress pathways and protein degradation 25:27 pathways and protein degradation 25:27 pathways and protein degradation pathways, that directly connected these 25:29 pathways, that directly connected these 25:29 pathways, that directly connected these two diseases. And that chromosome 17 was 25:33 two diseases. And that chromosome 17 was 25:34 two diseases. And that chromosome 17 was a major chromosome involved. It has 25:36 a major chromosome involved. It has 25:36 a major chromosome involved. It has about 1,200 protein coding genes and one 25:39 about 1,200 protein coding genes and one 25:39 about 1,200 protein coding genes and one of them is SMG6. So, what's SMG6 do? And 25:43 of them is SMG6. So, what's SMG6 do? And 25:43 of them is SMG6. So, what's SMG6 do? And the reason why I'm so excited about it 25:44 the reason why I'm so excited about it 25:45 the reason why I'm so excited about it is because it does have application, I 25:47 is because it does have application, I 25:47 is because it does have application, I think, to not most of us, but some of us 25:50 think, to not most of us, but some of us 25:50 think, to not most of us, but some of us might have both the comorbidity that of 25:54 might have both the comorbidity that of 25:54 might have both the comorbidity that of osteoporosis and cardiovascular disease. 25:57 osteoporosis and cardiovascular disease. 25:57 osteoporosis and cardiovascular disease. So, SMG6 makes an enzyme that cuts away 26:01 So, SMG6 makes an enzyme that cuts away 26:01 So, SMG6 makes an enzyme that cuts away faulty readings of mRNA. So, it's like a 26:04 faulty readings of mRNA. So, it's like a 26:04 faulty readings of mRNA. So, it's like a molecular scissors that cuts out protein 26:07 molecular scissors that cuts out protein 26:07 molecular scissors that cuts out protein defects and and it also has a disposal 26:10 defects and and it also has a disposal 26:10 defects and and it also has a disposal system or a shredder-like system that 26:12 system or a shredder-like system that 26:12 system or a shredder-like system that destroys worn-out proteins or proteins 26:15 destroys worn-out proteins or proteins 26:15 destroys worn-out proteins or proteins that have been misfolded or or damaged. 26:18 that have been misfolded or or damaged. 26:18 that have been misfolded or or damaged. And if SMG6 is impaired, damaged 26:21 And if SMG6 is impaired, damaged 26:21 And if SMG6 is impaired, damaged proteins pile up and we have increased 26:24 proteins pile up and we have increased 26:24 proteins pile up and we have increased oxidative stress and tissue 26:26 oxidative stress and tissue 26:27 oxidative stress and tissue dysregulation. It causes us to a feeling 26:30 dysregulation. It causes us to a feeling 26:30 dysregulation. It causes us to a feeling have feelings of really drained energy 26:33 have feelings of really drained energy 26:33 have feelings of really drained energy and and increase of the aging process. 26:36 and and increase of the aging process. 26:36 and and increase of the aging process. So, the reason why I bring this up is 26:38 So, the reason why I bring this up is 26:38 So, the reason why I bring this up is because genes can be dramatically 26:41 because genes can be dramatically 26:41 because genes can be dramatically involved in regulating our bone 26:43 involved in regulating our bone 26:43 involved in regulating our bone strength. And you know, completely 26:45 strength. And you know, completely 26:45 strength. And you know, completely diagnosing, completely figuring out 26:47 diagnosing, completely figuring out 26:47 diagnosing, completely figuring out what's going on, why a person has bone 26:49 what's going on, why a person has bone 26:49 what's going on, why a person has bone loss can be impossible because genetics 26:52 loss can be impossible because genetics 26:52 loss can be impossible because genetics like possibly a SMG6 variant, we can't 26:56 like possibly a SMG6 variant, we can't 26:57 like possibly a SMG6 variant, we can't you know, we don't know that. And even 26:58 you know, we don't know that. And even 26:58 you know, we don't know that. And even if you had the SMG6 tested, we still 27:01 if you had the SMG6 tested, we still 27:01 if you had the SMG6 tested, we still don't know if that's really causing any 27:03 don't know if that's really causing any 27:03 don't know if that's really causing any of your issues. So, at this point you 27:06 of your issues. So, at this point you 27:06 of your issues. So, at this point you know, testing I'm not advocating, but 27:09 know, testing I'm not advocating, but 27:09 know, testing I'm not advocating, but there are things like this that are 27:11 there are things like this that are 27:11 there are things like this that are important. And when I look at this SMG6 27:15 important. And when I look at this SMG6 27:15 important. And when I look at this SMG6 and then I look at a patient that you 27:17 and then I look at a patient that you 27:18 and then I look at a patient that you know, some of my patients that have 27:19 know, some of my patients that have 27:19 know, some of my patients that have extremely low P1NP, which is the lab 27:22 extremely low P1NP, which is the lab 27:22 extremely low P1NP, which is the lab marker for osteoblastic activity, and 27:25 marker for osteoblastic activity, and 27:25 marker for osteoblastic activity, and they have a crazy high C-terminal 27:27 they have a crazy high C-terminal 27:27 they have a crazy high C-terminal propeptide P1NP ratio. So, their CTX is 27:30 propeptide P1NP ratio. So, their CTX is 27:30 propeptide P1NP ratio. So, their CTX is high and their P1NP is doesn't match 27:34 high and their P1NP is doesn't match 27:34 high and their P1NP is doesn't match that CTX. And we can talk about that 27:36 that CTX. And we can talk about that 27:36 that CTX. And we can talk about that ratio business later, but when I see 27:38 ratio business later, but when I see 27:38 ratio business later, but when I see that kind of thing, when I see studies 27:40 that kind of thing, when I see studies 27:40 that kind of thing, when I see studies like this for the SMG6 as well, maybe 27:44 like this for the SMG6 as well, maybe 27:44 like this for the SMG6 as well, maybe we're we're starting to get closer to 27:46 we're we're starting to get closer to 27:46 we're we're starting to get closer to finding the answers to why somebody 27:48 finding the answers to why somebody 27:48 finding the answers to why somebody might have really, really low P1NP. 27:50 might have really, really low P1NP. 27:50 might have really, really low P1NP. Because their ability for their blast to 27:53 Because their ability for their blast to 27:53 Because their ability for their blast to function is less because of a gene a 27:56 function is less because of a gene a 27:56 function is less because of a gene a gene variant. Okay, we'll go on. So, 27:58 gene variant. Okay, we'll go on. So, 27:58 gene variant. Okay, we'll go on. So, where do we start? How do we look at a 27:59 where do we start? How do we look at a 28:00 where do we start? How do we look at a patient? What do we do? How do we figure 28:01 patient? What do we do? How do we figure 28:01 patient? What do we do? How do we figure out what's going on? The answer is 28:03 out what's going on? The answer is 28:03 out what's going on? The answer is everywhere. We just have to look under 28:05 everywhere. We just have to look under 28:05 everywhere. We just have to look under the rocks. And laboratory testing is
The deeper lab testing approach 28:07 the rocks. And laboratory testing is 28:07 the rocks. And laboratory testing is what helps us look under those rocks. 28:09 what helps us look under those rocks. 28:09 what helps us look under those rocks. And so, for osteoporosis, we don't just 28:12 And so, for osteoporosis, we don't just 28:12 And so, for osteoporosis, we don't just look for vitamin low vitamin D or just 28:16 look for vitamin low vitamin D or just 28:16 look for vitamin low vitamin D or just you know, elevated calcium or 28:17 you know, elevated calcium or 28:17 you know, elevated calcium or parathyroid hormone that indicates 28:19 parathyroid hormone that indicates 28:19 parathyroid hormone that indicates hyperparathyroidism 28:21 hyperparathyroidism 28:21 hyperparathyroidism or low TSH for an overactive thyroid. 28:24 or low TSH for an overactive thyroid. 28:24 or low TSH for an overactive thyroid. Yes, those are important, but they are 28:26 Yes, those are important, but they are 28:27 Yes, those are important, but they are very easy to spot. And that's usually 28:30 very easy to spot. And that's usually 28:30 very easy to spot. And that's usually not finding out the cause of somebody's 28:32 not finding out the cause of somebody's 28:32 not finding out the cause of somebody's bone loss is is usually not that easy. 28:35 bone loss is is usually not that easy. 28:35 bone loss is is usually not that easy. We have to look at 28:37 We have to look at 28:37 We have to look at all the labs. We look for abnormal 28:39 all the labs. We look for abnormal 28:39 all the labs. We look for abnormal patterns, trends, red flags, and hidden 28:42 patterns, trends, red flags, and hidden 28:42 patterns, trends, red flags, and hidden clinical correlations. So, we're going 28:44 clinical correlations. So, we're going 28:44 clinical correlations. So, we're going to go through some of those right now. 28:47 to go through some of those right now. 28:47 to go through some of those right now. For cardiovascular disease, as we talked 28:49 For cardiovascular disease, as we talked 28:49 For cardiovascular disease, as we talked about earlier just now, you have to get 28:51 about earlier just now, you have to get 28:51 about earlier just now, you have to get more than just a basic lipid panel. 28:54 more than just a basic lipid panel. 28:54 more than just a basic lipid panel. So, for example, LP little A, APOB, this 28:57 So, for example, LP little A, APOB, this 28:57 So, for example, LP little A, APOB, this NMR testing for the LDL size and 28:59 NMR testing for the LDL size and 28:59 NMR testing for the LDL size and particle number, and so I mentioned 29:01 particle number, and so I mentioned 29:01 particle number, and so I mentioned metabolic health, the hemoglobin A1C, 29:04 metabolic health, the hemoglobin A1C, 29:04 metabolic health, the hemoglobin A1C, fasting insulin, those things are 29:07 fasting insulin, those things are 29:07 fasting insulin, those things are important to get. So, let's go to Jane
Janeu2019s case: severe osteoporosis and cardiovascular disease 29:09 important to get. So, let's go to Jane 29:09 important to get. So, let's go to Jane and we'll and we'll see how lab testing 29:12 and we'll and we'll see how lab testing 29:12 and we'll and we'll see how lab testing helped us here. So, Jane is 52, 29:15 helped us here. So, Jane is 52, 29:15 helped us here. So, Jane is 52, post menopause. Uh she was a marathon 29:17 post menopause. Uh she was a marathon 29:17 post menopause. Uh she was a marathon runner. She had a heavy use of NSAIDs 29:19 runner. She had a heavy use of NSAIDs 29:19 runner. She had a heavy use of NSAIDs because of that, which I knew right away 29:21 because of that, which I knew right away 29:21 because of that, which I knew right away to look for a gut issues possibly with 29:23 to look for a gut issues possibly with 29:23 to look for a gut issues possibly with her. Uh she was on rosuvastatin 10 mg 29:27 her. Uh she was on rosuvastatin 10 mg 29:27 her. Uh she was on rosuvastatin 10 mg because she had cardiovascular disease. 29:29 because she had cardiovascular disease. 29:29 because she had cardiovascular disease. So, her mom had osteoporosis, her dad 29:31 So, her mom had osteoporosis, her dad 29:31 So, her mom had osteoporosis, her dad died of heart failure or a heart attack. 29:34 died of heart failure or a heart attack. 29:34 died of heart failure or a heart attack. Jane herself had several fractures, a T8 29:37 Jane herself had several fractures, a T8 29:37 Jane herself had several fractures, a T8 compression fracture, forearm, multiple 29:40 compression fracture, forearm, multiple 29:40 compression fracture, forearm, multiple lower extremity uh stress fractures. Her 29:43 lower extremity uh stress fractures. Her 29:43 lower extremity uh stress fractures. Her T-score was a -4.3 in her spine, and she 29:46 T-score was a -4.3 in her spine, and she 29:46 T-score was a -4.3 in her spine, and she had several 50% blockages in the 29:49 had several 50% blockages in the 29:49 had several 50% blockages in the arteries around her heart. So, she 29:51 arteries around her heart. So, she 29:51 arteries around her heart. So, she definitely had a cardiovascular issue, 29:54 definitely had a cardiovascular issue, 29:54 definitely had a cardiovascular issue, and it was a good thing she was on the 29:56 and it was a good thing she was on the 29:56 and it was a good thing she was on the rosuvastatin. 29:58 rosuvastatin. 29:58 rosuvastatin. So, when Jane went to see her 30:00 So, when Jane went to see her 30:00 So, when Jane went to see her cardiologist at the beginning of this 30:02 cardiologist at the beginning of this 30:02 cardiologist at the beginning of this whole thing, she asked, "What can I do, 30:05 whole thing, she asked, "What can I do, 30:05 whole thing, she asked, "What can I do, you know, to help my cardiovascular 30:07 you know, to help my cardiovascular 30:07 you know, to help my cardiovascular issue, you know, all this plaque in my 30:09 issue, you know, all this plaque in my 30:09 issue, you know, all this plaque in my in my arteries and stuff?" And and her 30:11 in my arteries and stuff?" And and her 30:11 in my arteries and stuff?" And and her doctor just said, "Take your 30:13 doctor just said, "Take your 30:13 doctor just said, "Take your rosuvastatin. That's all you can do." 30:15 rosuvastatin. That's all you can do." 30:15 rosuvastatin. That's all you can do." The doctor didn't even know that she had 30:17 The doctor didn't even know that she had 30:17 The doctor didn't even know that she had osteoporosis. It might have been in her 30:18 osteoporosis. It might have been in her 30:18 osteoporosis. It might have been in her chart, but did she care about it? I 30:21 chart, but did she care about it? I 30:21 chart, but did she care about it? I don't know. And I think that's the 30:23 don't know. And I think that's the 30:23 don't know. And I think that's the failing of the system. You we are in a 30:25 failing of the system. You we are in a 30:25 failing of the system. You we are in a population-based industrialized medicine 30:28 population-based industrialized medicine 30:28 population-based industrialized medicine system, and doctors 30:30 system, and doctors 30:30 system, and doctors are in a bad situation. They're pushed 30:33 are in a bad situation. They're pushed 30:33 are in a bad situation. They're pushed beyond their ability to give good care 30:37 beyond their ability to give good care 30:37 beyond their ability to give good care sometimes by the whole industry. And so, 30:40 sometimes by the whole industry. And so, 30:40 sometimes by the whole industry. And so, we as patients have a difficult time, I 30:44 we as patients have a difficult time, I 30:44 we as patients have a difficult time, I think, getting good health care 30:45 think, getting good health care 30:45 think, getting good health care sometimes. So, I don't fault doctors, I 30:49 sometimes. So, I don't fault doctors, I 30:49 sometimes. So, I don't fault doctors, I fault the system. And I think your 30:51 fault the system. And I think your 30:51 fault the system. And I think your doctor, in general, is incredibly 30:54 doctor, in general, is incredibly 30:54 doctor, in general, is incredibly interested in helping you out, but they 30:56 interested in helping you out, but they 30:56 interested in helping you out, but they have time constraints. So, you have to 30:58 have time constraints. So, you have to 30:58 have time constraints. So, you have to fight for your own health here and try 31:01 fight for your own health here and try 31:01 fight for your own health here and try to encourage your doctor to look and see 31:03 to encourage your doctor to look and see 31:03 to encourage your doctor to look and see if you do have osteoporosis, just have 31:06 if you do have osteoporosis, just have 31:06 if you do have osteoporosis, just have them check take a look at your 31:08 them check take a look at your 31:08 them check take a look at your cardiovascular health, too. Okay. So, 31:11 cardiovascular health, too. Okay. So, 31:11 cardiovascular health, too. Okay. So, when Jane came to me, 31:13 when Jane came to me, 31:13 when Jane came to me, these are the lab tests that I got. I I 31:16 these are the lab tests that I got. I I 31:16 these are the lab tests that I got. I I separate them here. There There's 31:17 separate them here. There There's 31:17 separate them here. There There's overlap, of course, but 31:19 overlap, of course, but 31:19 overlap, of course, but I The typical osteoporosis labs are on 31:22 I The typical osteoporosis labs are on 31:22 I The typical osteoporosis labs are on the left. The typical ones are 31:24 the left. The typical ones are 31:24 the left. The typical ones are cardiovascular system are on the right. 31:26 cardiovascular system are on the right. 31:26 cardiovascular system are on the right. Like I said, there's overlap, but And I 31:29 Like I said, there's overlap, but And I 31:29 Like I said, there's overlap, but And I And you don't have to get all these 31:30 And you don't have to get all these 31:30 And you don't have to get all these tests, and that's not what I'm saying. I 31:31 tests, and that's not what I'm saying. I 31:32 tests, and that's not what I'm saying. I bolded the ones that I think are the 31:33 bolded the ones that I think are the 31:33 bolded the ones that I think are the most important. So, we're going to go 31:35 most important. So, we're going to go 31:35 most important. So, we're going to go through this for a couple minutes here 31:37 through this for a couple minutes here 31:37 through this for a couple minutes here and see how to work with some of these 31:39 and see how to work with some of these 31:39 and see how to work with some of these labs. For 31:40 labs. For 31:41 labs. For the your bone health and how it's either 31:44 the your bone health and how it's either 31:44 the your bone health and how it's either building up or tearing down, the 31:46 building up or tearing down, the 31:46 building up or tearing down, the C-telopeptide and the P1NP are probably 31:49 C-telopeptide and the P1NP are probably 31:49 C-telopeptide and the P1NP are probably the most important to get. So, CTX or 31:52 the most important to get. So, CTX or 31:52 the most important to get. So, CTX or C-telopeptide 31:54 C-telopeptide 31:54 C-telopeptide is the bone resorption marker. It 31:56 is the bone resorption marker. It 31:56 is the bone resorption marker. It measures osteoclastic activity. And for 31:59 measures osteoclastic activity. And for 31:59 measures osteoclastic activity. And for every 32:01 every 32:01 every increased standard deviation increase of 32:04 increased standard deviation increase of 32:04 increased standard deviation increase of CTX, your fracture risk will increase 32:07 CTX, your fracture risk will increase 32:07 CTX, your fracture risk will increase 27%. 32:09 27%. 32:09 27%. So, 32:10 So, 32:10 So, we say, "What's a standard deviation?" 32:12 we say, "What's a standard deviation?" 32:12 we say, "What's a standard deviation?" Well, 32:13 Well, 32:13 Well, that's hard to really explain and and 32:17 that's hard to really explain and and 32:17 that's hard to really explain and and but for an example, if you had a 400 CTX 32:21 but for an example, if you had a 400 CTX 32:21 but for an example, if you had a 400 CTX versus a 600 CTX, that would be about 32:24 versus a 600 CTX, that would be about 32:24 versus a 600 CTX, that would be about one standard deviation. So, going from a 32:27 one standard deviation. So, going from a 32:27 one standard deviation. So, going from a 400 to 600 really does increase fracture 32:30 400 to 600 really does increase fracture 32:30 400 to 600 really does increase fracture risk. And we want to keep CTX 32:33 risk. And we want to keep CTX 32:33 risk. And we want to keep CTX 400 or below, about. P1NP, that's the 32:37 400 or below, about. P1NP, that's the 32:37 400 or below, about. P1NP, that's the bone formation or osteoblastic activity. 32:40 bone formation or osteoblastic activity. 32:40 bone formation or osteoblastic activity. And it's nice to try to keep these two 32:42 And it's nice to try to keep these two 32:42 And it's nice to try to keep these two within a ratio of 10:1, 9:1, some ratio, 32:45 within a ratio of 10:1, 9:1, some ratio, 32:45 within a ratio of 10:1, 9:1, some ratio, something like that. Jane had a ratio of 32:47 something like that. Jane had a ratio of 32:47 something like that. Jane had a ratio of 14:1. So, so either way too much clastic 32:51 14:1. So, so either way too much clastic 32:51 14:1. So, so either way too much clastic activity or not nearly enough blastic 32:53 activity or not nearly enough blastic 32:53 activity or not nearly enough blastic activity, but her ratio was very poor. 32:55 activity, but her ratio was very poor. 32:55 activity, but her ratio was very poor. Celiac testing. So, we want to make sure 32:57 Celiac testing. So, we want to make sure 32:58 Celiac testing. So, we want to make sure that a person doesn't have celiac 32:59 that a person doesn't have celiac 32:59 that a person doesn't have celiac disease or even to have a sensitivity to 33:03 disease or even to have a sensitivity to 33:03 disease or even to have a sensitivity to gluten because that can increase 33:06 gluten because that can increase 33:06 gluten because that can increase antibodies which increase osteoclastic 33:10 antibodies which increase osteoclastic 33:10 antibodies which increase osteoclastic activity. I always tell patients one of 33:13 activity. I always tell patients one of 33:13 activity. I always tell patients one of the most important things I tell them is 33:15 the most important things I tell them is 33:15 the most important things I tell them is your osteoclast is a form of a white 33:17 your osteoclast is a form of a white 33:17 your osteoclast is a form of a white blood cell. In other words, anything 33:19 blood cell. In other words, anything 33:19 blood cell. In other words, anything that ramps up your immune system and 33:22 that ramps up your immune system and 33:22 that ramps up your immune system and spews out more either if you have more 33:25 spews out more either if you have more 33:25 spews out more either if you have more oxidative stress, free radicals, you 33:27 oxidative stress, free radicals, you 33:27 oxidative stress, free radicals, you have more pro-inflammatory cytokines, 33:29 have more pro-inflammatory cytokines, 33:29 have more pro-inflammatory cytokines, anything that riles up that immune 33:31 anything that riles up that immune 33:31 anything that riles up that immune system will probably talk to the 33:33 system will probably talk to the 33:33 system will probably talk to the osteoclast and then they have one action 33:38 osteoclast and then they have one action 33:38 osteoclast and then they have one action and that is to tear down bone. So, 33:40 and that is to tear down bone. So, 33:40 and that is to tear down bone. So, things like having a celiac test to make 33:44 things like having a celiac test to make 33:44 things like having a celiac test to make sure you're not not just that there's 33:46 sure you're not not just that there's 33:46 sure you're not not just that there's not damage to the endocytes in them in 33:48 not damage to the endocytes in them in 33:48 not damage to the endocytes in them in the vessel in the intestinal wall, but 33:51 the vessel in the intestinal wall, but 33:51 the vessel in the intestinal wall, but that you're not even having a antibody 33:53 that you're not even having a antibody 33:53 that you're not even having a antibody reaction to gluten. That's important. 33:56 reaction to gluten. That's important. 33:56 reaction to gluten. That's important. Just the same as it's important to look 33:58 Just the same as it's important to look 33:58 Just the same as it's important to look at the gut. Well, I have a slide later 34:00 at the gut. Well, I have a slide later 34:00 at the gut. Well, I have a slide later on about where we'll look at the gut and 34:01 on about where we'll look at the gut and 34:01 on about where we'll look at the gut and how important that is because 70% of 34:03 how important that is because 70% of 34:03 how important that is because 70% of your immune system is in your digestive 34:06 your immune system is in your digestive 34:06 your immune system is in your digestive tract, is in your gut. So, when you have 34:08 tract, is in your gut. So, when you have 34:08 tract, is in your gut. So, when you have digestive issues, gut issues, bacterial 34:11 digestive issues, gut issues, bacterial 34:11 digestive issues, gut issues, bacterial overgrowth, you often will affect those 34:14 overgrowth, you often will affect those 34:14 overgrowth, you often will affect those osteoclasts. Vitamin D, PTH, CBC, CMP, 34:18 osteoclasts. Vitamin D, PTH, CBC, CMP, 34:18 osteoclasts. Vitamin D, PTH, CBC, CMP, the comprehensive metabolic profile, 34:20 the comprehensive metabolic profile, 34:20 the comprehensive metabolic profile, these are all really important tests to 34:22 these are all really important tests to 34:22 these are all really important tests to get. And on the cardiovascular side, as 34:25 get. And on the cardiovascular side, as 34:25 get. And on the cardiovascular side, as I mentioned earlier, we need to do 34:27 I mentioned earlier, we need to do 34:27 I mentioned earlier, we need to do a much better job at getting a more 34:30 a much better job at getting a more 34:30 a much better job at getting a more comprehensive profile on people. APOB, 34:33 comprehensive profile on people. APOB, 34:33 comprehensive profile on people. APOB, LP little A, the high sensitivity 34:36 LP little A, the high sensitivity 34:36 LP little A, the high sensitivity C-reactive protein. That's a It's a 34:38 C-reactive protein. That's a It's a 34:38 C-reactive protein. That's a It's a generalized inflammatory marker. It's 34:40 generalized inflammatory marker. It's 34:40 generalized inflammatory marker. It's not specific, but it can help look out 34:42 not specific, but it can help look out 34:42 not specific, but it can help look out for for chronic systemic inflammation. 34:45 for for chronic systemic inflammation. 34:45 for for chronic systemic inflammation. Homocysteine, we already talked about 34:47 Homocysteine, we already talked about 34:47 Homocysteine, we already talked about that. And these numbers after that, I 34:49 that. And these numbers after that, I 34:49 that. And these numbers after that, I didn't mention those are Jean Jane's 34:51 didn't mention those are Jean Jane's 34:51 didn't mention those are Jean Jane's values. So, like what APOB, you know, 34:56 values. So, like what APOB, you know, 34:56 values. So, like what APOB, you know, you really need to keep that below 80. 34:57 you really need to keep that below 80. 34:57 you really need to keep that below 80. She was in 83. Homocysteine was way up 35:00 She was in 83. Homocysteine was way up 35:00 She was in 83. Homocysteine was way up at 14.8. Hemoglobin A1C was right at 35:03 at 14.8. Hemoglobin A1C was right at 35:03 at 14.8. Hemoglobin A1C was right at borderline of pre-diabetes. So, you 35:06 borderline of pre-diabetes. So, you 35:06 borderline of pre-diabetes. So, you know, she did have a a terrible diet, 35:08 know, she did have a a terrible diet, 35:08 know, she did have a a terrible diet, and so we had to work with that. Then 35:11 and so we had to work with that. Then 35:11 and so we had to work with that. Then there's some other ones here, the LDH. 35:13 there's some other ones here, the LDH. 35:13 there's some other ones here, the LDH. We're going to talk about the TMAO and 35:15 We're going to talk about the TMAO and 35:15 We're going to talk about the TMAO and ADMA. 35:17 ADMA. 35:17 ADMA. But, you know, you everybody doesn't 35:18 But, you know, you everybody doesn't 35:19 But, you know, you everybody doesn't have to get those. That's not what I'm 35:20 have to get those. That's not what I'm 35:20 have to get those. That's not what I'm saying. I'm saying that there is a whole 35:23 saying. I'm saying that there is a whole 35:23 saying. I'm saying that there is a whole battery of tests for osteoporosis, for 35:26 battery of tests for osteoporosis, for 35:26 battery of tests for osteoporosis, for cardiovascular disease, that can really 35:28 cardiovascular disease, that can really 35:28 cardiovascular disease, that can really paint 35:30 paint 35:30 paint the picture, a very nice picture of 35:32 the picture, a very nice picture of 35:32 the picture, a very nice picture of what's going on in a patient's 35:34 what's going on in a patient's 35:34 what's going on in a patient's physiology. Okay, so let's go to the 35:36 physiology. Okay, so let's go to the 35:36 physiology. Okay, so let's go to the next slide. So, as I promised earlier,
The RANK/RANKL/OPG pathway connecting bones and blood vessels 35:39 next slide. So, as I promised earlier, 35:39 next slide. So, as I promised earlier, I'm going to talk about this rank rankle 35:41 I'm going to talk about this rank rankle 35:41 I'm going to talk about this rank rankle OPG system. And the reason why is 35:43 OPG system. And the reason why is 35:43 OPG system. And the reason why is because it's involved in bone. It's 35:45 because it's involved in bone. It's 35:45 because it's involved in bone. It's involved in the immune system. It's 35:46 involved in the immune system. It's 35:46 involved in the immune system. It's involved in skeletal muscle, cardiac 35:48 involved in skeletal muscle, cardiac 35:48 involved in skeletal muscle, cardiac muscle, smooth muscle. It's the most 35:51 muscle, smooth muscle. It's the most 35:51 muscle, smooth muscle. It's the most prominent molecular pathway that links 35:54 prominent molecular pathway that links 35:54 prominent molecular pathway that links osteoporosis and cardiovascular disease. 35:56 osteoporosis and cardiovascular disease. 35:56 osteoporosis and cardiovascular disease. And it involves that protein rankle. And 35:59 And it involves that protein rankle. And 35:59 And it involves that protein rankle. And that signals osteoclastic activity. And 36:03 that signals osteoclastic activity. And 36:03 that signals osteoclastic activity. And it also causes inflammation in blood 36:05 it also causes inflammation in blood 36:05 it also causes inflammation in blood vessels and converts 36:07 vessels and converts 36:08 vessels and converts vascular smooth muscle cells in those 36:10 vascular smooth muscle cells in those 36:10 vascular smooth muscle cells in those blood vessels to turn into, and this is 36:14 blood vessels to turn into, and this is 36:14 blood vessels to turn into, and this is amazing, it's called 36:15 amazing, it's called 36:15 amazing, it's called transdifferentiation. 36:16 transdifferentiation. 36:16 transdifferentiation. The process is called that. And what it 36:19 The process is called that. And what it 36:19 The process is called that. And what it does is it when you have high rankle, it 36:22 does is it when you have high rankle, it 36:22 does is it when you have high rankle, it actually changes those 36:25 actually changes those 36:25 actually changes those vascular smooth muscle cells and makes 36:27 vascular smooth muscle cells and makes 36:27 vascular smooth muscle cells and makes them turn into osteoblast-like cells, 36:30 them turn into osteoblast-like cells, 36:30 them turn into osteoblast-like cells, causing them to calcify plaque within 36:33 causing them to calcify plaque within 36:33 causing them to calcify plaque within the arterial walls. 36:35 the arterial walls. 36:35 the arterial walls. >> Okay. 36:35 >> Okay. 36:35 >> Okay. >> Now, the next slide's going to show us 36:37 >> Now, the next slide's going to show us 36:37 >> Now, the next slide's going to show us that little how it works. So, in 36:39 that little how it works. So, in 36:39 that little how it works. So, in osteoporosis on the left here, we have 36:42 osteoporosis on the left here, we have 36:42 osteoporosis on the left here, we have the big cell on the left is is a 36:45 the big cell on the left is is a 36:45 the big cell on the left is is a osteoblast. And then the in the upper 36:47 osteoblast. And then the in the upper 36:47 osteoblast. And then the in the upper left, that's a a pre-osteoclast. 36:50 left, that's a a pre-osteoclast. 36:50 left, that's a a pre-osteoclast. So, the the blast have that RANKL, 36:53 So, the the blast have that RANKL, 36:53 So, the the blast have that RANKL, that's the the ligand RANKL, and it will 36:57 that's the the ligand RANKL, and it will 36:57 that's the the ligand RANKL, and it will then 36:58 then 36:58 then deform into that RANK receptor, 37:00 deform into that RANK receptor, 37:01 deform into that RANK receptor, deforming it, stimulating those 37:03 deforming it, stimulating those 37:03 deforming it, stimulating those osteoclast, those pre-osteoclast, to 37:06 osteoclast, those pre-osteoclast, to 37:06 osteoclast, those pre-osteoclast, to differentiate into a mature osteoclast, 37:10 differentiate into a mature osteoclast, 37:10 differentiate into a mature osteoclast, and then they form they break down bone. 37:12 and then they form they break down bone. 37:12 and then they form they break down bone. That OPG is really important. That See 37:14 That OPG is really important. That See 37:14 That OPG is really important. That See that OPG? That's called osteoprotegerin, 37:18 that OPG? That's called osteoprotegerin, 37:18 that OPG? That's called osteoprotegerin, and that's a soluble decoy receptor that 37:21 and that's a soluble decoy receptor that 37:21 and that's a soluble decoy receptor that shields the RANKL ligand from 37:26 shields the RANKL ligand from 37:26 shields the RANKL ligand from activating that RANK receptor. So, the 37:28 activating that RANK receptor. So, the 37:28 activating that RANK receptor. So, the more OPG you have, the less osteoclastic 37:32 more OPG you have, the less osteoclastic 37:32 more OPG you have, the less osteoclastic activity you're going to have. 37:34 activity you're going to have. 37:34 activity you're going to have. And on the right side, in a blood 37:36 And on the right side, in a blood 37:36 And on the right side, in a blood vessel, damaged blood vessels start 37:39 vessel, damaged blood vessels start 37:39 vessel, damaged blood vessels start producing too much RANKL. Normally, the 37:41 producing too much RANKL. Normally, the 37:41 producing too much RANKL. Normally, the blood vessel produces a lot of OPG, a 37:43 blood vessel produces a lot of OPG, a 37:43 blood vessel produces a lot of OPG, a lot of osteoprotegerin, which helps 37:45 lot of osteoprotegerin, which helps 37:45 lot of osteoprotegerin, which helps prevent calcification. But when blood 37:47 prevent calcification. But when blood 37:47 prevent calcification. But when blood vessels are stressed and damaged by 37:49 vessels are stressed and damaged by 37:49 vessels are stressed and damaged by inflammation, oxidative stress, the high 37:52 inflammation, oxidative stress, the high 37:52 inflammation, oxidative stress, the high blood sugars we talked about earlier, 37:54 blood sugars we talked about earlier, 37:54 blood sugars we talked about earlier, metabolic health, that blood sugar is is 37:57 metabolic health, that blood sugar is is 37:57 metabolic health, that blood sugar is is is deadly to vessel walls. Both the 38:00 is deadly to vessel walls. Both the 38:00 is deadly to vessel walls. Both the endothelial cell walls cells lining that 38:02 endothelial cell walls cells lining that 38:02 endothelial cell walls cells lining that blood vessel, and the vascular smooth 38:04 blood vessel, and the vascular smooth 38:04 blood vessel, and the vascular smooth muscle cells, they start producing less 38:07 muscle cells, they start producing less 38:07 muscle cells, they start producing less osteoprotegerin and more RANKL. So, when 38:11 osteoprotegerin and more RANKL. So, when 38:11 osteoprotegerin and more RANKL. So, when a woman goes through menopause, or a man 38:14 a woman goes through menopause, or a man 38:14 a woman goes through menopause, or a man has low testosterone, or a person is 38:16 has low testosterone, or a person is 38:16 has low testosterone, or a person is under high stress and increased 38:18 under high stress and increased 38:18 under high stress and increased cortisol, or they're taking prednisone, 38:21 cortisol, or they're taking prednisone, 38:21 cortisol, or they're taking prednisone, or they have elevated levels of 38:23 or they have elevated levels of 38:23 or they have elevated levels of parathyroid hormone cuz they have a a 38:25 parathyroid hormone cuz they have a a 38:25 parathyroid hormone cuz they have a a para- a benign parathyroid adenoma in 38:28 para- a benign parathyroid adenoma in 38:28 para- a benign parathyroid adenoma in their in their throat in their 38:29 their in their throat in their 38:30 their in their throat in their parathyroid glands. All these lower 38:32 parathyroid glands. All these lower 38:32 parathyroid glands. All these lower osteoprotegerin. So, all of these allow 38:35 osteoprotegerin. So, all of these allow 38:36 osteoprotegerin. So, all of these allow more RANKL to stimulate RANK through 38:38 more RANKL to stimulate RANK through 38:38 more RANKL to stimulate RANK through which 38:40 which 38:40 which turns into osteoclast, which breaks down 38:43 turns into osteoclast, which breaks down 38:43 turns into osteoclast, which breaks down bone, which also causes a 38:45 bone, which also causes a 38:45 bone, which also causes a transdifferentiation of those vessel 38:48 transdifferentiation of those vessel 38:48 transdifferentiation of those vessel smooth 38:49 smooth 38:49 smooth uh muscle cells and converting them into 38:52 uh muscle cells and converting them into 38:52 uh muscle cells and converting them into osteoblast-like cells that calcify the 38:55 osteoblast-like cells that calcify the 38:55 osteoblast-like cells that calcify the plaque that's there. 38:57 plaque that's there. 38:57 plaque that's there. It's an amazing system. So, the next 38:59 It's an amazing system. So, the next 38:59 It's an amazing system. So, the next slide, please. So, this is one of my 39:02 slide, please. So, this is one of my 39:02 slide, please. So, this is one of my favorite $5, $6 tests. This is CBC. I'm
Other labs to look at for bone and cardiovascular health 39:05 favorite $5, $6 tests. This is CBC. I'm 39:05 favorite $5, $6 tests. This is CBC. I'm I'm not going to talk about all these. 39:07 I'm not going to talk about all these. 39:07 I'm not going to talk about all these. In my book, I I talk about the RBCs, the 39:09 In my book, I I talk about the RBCs, the 39:09 In my book, I I talk about the RBCs, the mean platelet volume, the 39:11 mean platelet volume, the 39:11 mean platelet volume, the uh the neutrophil-lymphocyte ratio, and 39:13 uh the neutrophil-lymphocyte ratio, and 39:13 uh the neutrophil-lymphocyte ratio, and all that. So, I'm not going to I don't 39:14 all that. So, I'm not going to I don't 39:14 all that. So, I'm not going to I don't have time to go through that, but you 39:16 have time to go through that, but you 39:16 have time to go through that, but you can go to the book and and read about 39:18 can go to the book and and read about 39:18 can go to the book and and read about them and how important they are in in 39:21 them and how important they are in in 39:21 them and how important they are in in giving us an insight into what's going 39:23 giving us an insight into what's going 39:23 giving us an insight into what's going on. But, I want to talk about the red 39:25 on. But, I want to talk about the red 39:25 on. But, I want to talk about the red blood cells because that's one of the 39:26 blood cells because that's one of the 39:26 blood cells because that's one of the most important. And a low count, yes, 39:29 most important. And a low count, yes, 39:29 most important. And a low count, yes, might be from anemia, but also might be 39:32 might be from anemia, but also might be 39:32 might be from anemia, but also might be from a buildup of fat in the bone 39:34 from a buildup of fat in the bone 39:34 from a buildup of fat in the bone marrow. Even if a person's skinny, they 39:37 marrow. Even if a person's skinny, they 39:37 marrow. Even if a person's skinny, they might have fat in their bone marrow. 39:39 might have fat in their bone marrow. 39:39 might have fat in their bone marrow. So, aging, systemic inflammation, 39:41 So, aging, systemic inflammation, 39:41 So, aging, systemic inflammation, oxidized LDLs, loss of estrogen, as I 39:44 oxidized LDLs, loss of estrogen, as I 39:44 oxidized LDLs, loss of estrogen, as I said before, that can derail the 39:47 said before, that can derail the 39:47 said before, that can derail the development of the stem cells in bone 39:50 development of the stem cells in bone 39:50 development of the stem cells in bone marrow away from forming into 39:51 marrow away from forming into 39:51 marrow away from forming into osteoblasts and towards develop into fat 39:55 osteoblasts and towards develop into fat 39:55 osteoblasts and towards develop into fat cells. And the fat cells then crowd out 39:57 cells. And the fat cells then crowd out 39:57 cells. And the fat cells then crowd out another stem cell 39:59 another stem cell 39:59 another stem cell that should be producing red blood 40:01 that should be producing red blood 40:01 that should be producing red blood cells, but because the fat is there, 40:04 cells, but because the fat is there, 40:04 cells, but because the fat is there, then we don't have this red blood cell 40:06 then we don't have this red blood cell 40:06 then we don't have this red blood cell connect formation. So, the fat is in the 40:08 connect formation. So, the fat is in the 40:08 connect formation. So, the fat is in the form much of it is in the form of 40:10 form much of it is in the form of 40:10 form much of it is in the form of saturated palmitic acid, which is 40:13 saturated palmitic acid, which is 40:13 saturated palmitic acid, which is poisonous to stem cells, 40:15 poisonous to stem cells, 40:15 poisonous to stem cells, and causes even more inflammation and 40:17 and causes even more inflammation and 40:17 and causes even more inflammation and cell damage. So, 40:19 cell damage. So, 40:19 cell damage. So, how do you get rid of that palmitic 40:21 how do you get rid of that palmitic 40:21 how do you get rid of that palmitic acid? Vitamin D, eating like avocados 40:24 acid? Vitamin D, eating like avocados 40:24 acid? Vitamin D, eating like avocados and olive oil for the oleic acid and the 40:27 and olive oil for the oleic acid and the 40:27 and olive oil for the oleic acid and the phenolitic compounds, fish oil. I know a 40:29 phenolitic compounds, fish oil. I know a 40:29 phenolitic compounds, fish oil. I know a lot of people now are taking gamma and 40:31 lot of people now are taking gamma and 40:31 lot of people now are taking gamma and delta tocotrienols, which is a great 40:33 delta tocotrienols, which is a great 40:33 delta tocotrienols, which is a great product. And then for women, going on 40:37 product. And then for women, going on 40:37 product. And then for women, going on HRT, re- keeping that estradiol level 40:40 HRT, re- keeping that estradiol level 40:40 HRT, re- keeping that estradiol level high, that will help decrease the 40:43 high, that will help decrease the 40:43 high, that will help decrease the toxicity, decrease the the fat in their 40:46 toxicity, decrease the the fat in their 40:46 toxicity, decrease the the fat in their in their bone marrow, reduce this 40:48 in their bone marrow, reduce this 40:48 in their bone marrow, reduce this inflammation, and improves red blood 40:50 inflammation, and improves red blood 40:50 inflammation, and improves red blood cell count. So, 40:52 cell count. So, 40:52 cell count. So, when I was first diagnosed with 40:54 when I was first diagnosed with 40:54 when I was first diagnosed with osteoporosis, 40:56 osteoporosis, 40:56 osteoporosis, if you go to the next slide, you're 40:57 if you go to the next slide, you're 40:57 if you go to the next slide, you're going to see the bone biopsy of me on 40:59 going to see the bone biopsy of me on 41:00 going to see the bone biopsy of me on the right and a normal bone biopsy on 41:02 the right and a normal bone biopsy on 41:02 the right and a normal bone biopsy on the left. So, the at the top of the 41:05 the left. So, the at the top of the 41:05 the left. So, the at the top of the slide on the right is the outer part of 41:08 slide on the right is the outer part of 41:08 slide on the right is the outer part of my iliac crest and the the bottom part 41:10 my iliac crest and the the bottom part 41:10 my iliac crest and the the bottom part there is the inner inner cortex. You can 41:14 there is the inner inner cortex. You can 41:14 there is the inner inner cortex. You can see how thin thin that is and how few 41:17 see how thin thin that is and how few 41:17 see how thin thin that is and how few trabeculae there are in there compared 41:19 trabeculae there are in there compared 41:19 trabeculae there are in there compared to the the normal bone biopsy on the 41:21 to the the normal bone biopsy on the 41:21 to the the normal bone biopsy on the left. And what I want to show here is 41:24 left. And what I want to show here is 41:24 left. And what I want to show here is not just that there's not many 41:26 not just that there's not many 41:26 not just that there's not many trabeculae, so not much strength there. 41:29 trabeculae, so not much strength there. 41:29 trabeculae, so not much strength there. Trabeculae are those little squiggly 41:31 Trabeculae are those little squiggly 41:31 Trabeculae are those little squiggly lines in the in the inside of the bone. 41:34 lines in the in the inside of the bone. 41:34 lines in the in the inside of the bone. But, if you go to the next slide, you're 41:36 But, if you go to the next slide, you're 41:36 But, if you go to the next slide, you're going to see on the left of that slide 41:39 going to see on the left of that slide 41:39 going to see on the left of that slide all those white round circles, that's 41:41 all those white round circles, that's 41:41 all those white round circles, that's fat. So, I'm pretty skinny. I'm 150 lb, 41:44 fat. So, I'm pretty skinny. I'm 150 lb, 41:44 fat. So, I'm pretty skinny. I'm 150 lb, almost 6 ft, and I don't have much fat 41:47 almost 6 ft, and I don't have much fat 41:47 almost 6 ft, and I don't have much fat on me, about 6 and 1/2 7% fat. But, my 41:50 on me, about 6 and 1/2 7% fat. But, my 41:50 on me, about 6 and 1/2 7% fat. But, my bone marrow was completely not 41:53 bone marrow was completely not 41:53 bone marrow was completely not completely, but it was very filled with 41:54 completely, but it was very filled with 41:54 completely, but it was very filled with fat. 41:55 fat. 41:55 fat. And my red blood cell count was a 3.9 to 41:58 And my red blood cell count was a 3.9 to 41:58 And my red blood cell count was a 3.9 to 4.0, or a 3.9 to 4.0. So, I had a lot of 42:01 4.0, or a 3.9 to 4.0. So, I had a lot of 42:02 4.0, or a 3.9 to 4.0. So, I had a lot of fat in my bone marrow. The next couple 42:03 fat in my bone marrow. The next couple 42:03 fat in my bone marrow. The next couple slides is just showing that I also had 42:05 slides is just showing that I also had 42:05 slides is just showing that I also had this what's called intermittent 42:07 this what's called intermittent 42:07 this what's called intermittent deposition of bone. I would lay down 42:09 deposition of bone. I would lay down 42:09 deposition of bone. I would lay down bone matrix and calcify it, and then I 42:11 bone matrix and calcify it, and then I 42:11 bone matrix and calcify it, and then I then the next layer of bone did not 42:14 then the next layer of bone did not 42:14 then the next layer of bone did not calcify. So, those are just closer views 42:16 calcify. So, those are just closer views 42:16 calcify. So, those are just closer views of that. Probably genetic issue. Okay, 42:18 of that. Probably genetic issue. Okay, 42:18 of that. Probably genetic issue. Okay, go to the next slide of inflammation
Inflammation, metabolism, and cardiovascular risk 42:20 go to the next slide of inflammation 42:20 go to the next slide of inflammation oxidative stress markers. We always talk 42:22 oxidative stress markers. We always talk 42:22 oxidative stress markers. We always talk about 42:24 about 42:24 about inflammation. How do you tell a person 42:25 inflammation. How do you tell a person 42:25 inflammation. How do you tell a person has a chronic systemic inflammation? 42:27 has a chronic systemic inflammation? 42:27 has a chronic systemic inflammation? It's very difficult. There's no way 42:30 It's very difficult. There's no way 42:30 It's very difficult. There's no way anybody can just look at a person and 42:32 anybody can just look at a person and 42:32 anybody can just look at a person and say, "You have chronic systemic 42:33 say, "You have chronic systemic 42:33 say, "You have chronic systemic inflammation." We have some tests, but 42:36 inflammation." We have some tests, but 42:36 inflammation." We have some tests, but they help, but they're not definitive. 42:38 they help, but they're not definitive. 42:38 they help, but they're not definitive. You would think that if you have 42:39 You would think that if you have 42:39 You would think that if you have systemic inflammation, everybody's high 42:42 systemic inflammation, everybody's high 42:42 systemic inflammation, everybody's high sensitivity C-reactive protein would be 42:44 sensitivity C-reactive protein would be 42:44 sensitivity C-reactive protein would be elevated, but that's not true. But, 42:46 elevated, but that's not true. But, 42:46 elevated, but that's not true. But, these markers do help. As you can see 42:48 these markers do help. As you can see 42:48 these markers do help. As you can see under that HS-CRP, 42:51 under that HS-CRP, 42:51 under that HS-CRP, greater than 2.4, you have a 30% to 60% 42:54 greater than 2.4, you have a 30% to 60% 42:54 greater than 2.4, you have a 30% to 60% greater risk of cardiovascular disease. 42:57 greater risk of cardiovascular disease. 42:57 greater risk of cardiovascular disease. And it's above two, you have a 23% 43:01 And it's above two, you have a 23% 43:01 And it's above two, you have a 23% increase increased risk of low bone 43:03 increase increased risk of low bone 43:03 increase increased risk of low bone mineral density. So, all these things 43:05 mineral density. So, all these things 43:05 mineral density. So, all these things can help us look at cardiovascular and 43:09 can help us look at cardiovascular and 43:09 can help us look at cardiovascular and skeletal health risk. Okay, next slide. 43:11 skeletal health risk. Okay, next slide. 43:11 skeletal health risk. Okay, next slide. Estrogen, as I said before, is so 43:13 Estrogen, as I said before, is so 43:13 Estrogen, as I said before, is so important. So, when a woman goes through 43:16 important. So, when a woman goes through 43:16 important. So, when a woman goes through menopause, they lose that estrogen, it 43:18 menopause, they lose that estrogen, it 43:18 menopause, they lose that estrogen, it can really disrupt the whole immune 43:20 can really disrupt the whole immune 43:20 can really disrupt the whole immune system and the whole bone remodeling 43:22 system and the whole bone remodeling 43:22 system and the whole bone remodeling system. Estrogen helps us decrease 43:26 system. Estrogen helps us decrease 43:26 system. Estrogen helps us decrease osteoclastic activity. It decreases 43:28 osteoclastic activity. It decreases 43:28 osteoclastic activity. It decreases oxidative stress. It protects our 43:31 oxidative stress. It protects our 43:31 oxidative stress. It protects our endothelial glycocalyx, and we're going 43:33 endothelial glycocalyx, and we're going 43:33 endothelial glycocalyx, and we're going to see what the endothelial glycocalyx 43:35 to see what the endothelial glycocalyx 43:35 to see what the endothelial glycocalyx does and why, and it's really cool. So, 43:39 does and why, and it's really cool. So, 43:39 does and why, and it's really cool. So, if you haven't heard of endothelial 43:40 if you haven't heard of endothelial 43:40 if you haven't heard of endothelial glycocalyx, look it up on the internet 43:42 glycocalyx, look it up on the internet 43:42 glycocalyx, look it up on the internet cuz it's really fascinating. 43:44 cuz it's really fascinating. 43:44 cuz it's really fascinating. Estrogen also helps us lower LDL 43:47 Estrogen also helps us lower LDL 43:47 Estrogen also helps us lower LDL cholesterol, relaxes blood vessels, so 43:49 cholesterol, relaxes blood vessels, so 43:49 cholesterol, relaxes blood vessels, so it increases nitric oxide. Nitric 43:51 it increases nitric oxide. Nitric 43:51 it increases nitric oxide. Nitric oxide's produced by that endothelial 43:54 oxide's produced by that endothelial 43:54 oxide's produced by that endothelial glycocalyx. Okay, metabolic evaluation, 43:57 glycocalyx. Okay, metabolic evaluation, 43:57 glycocalyx. Okay, metabolic evaluation, I've already talked about that, how 43:58 I've already talked about that, how 43:58 I've already talked about that, how important that is, that we don't just 44:01 important that is, that we don't just 44:01 important that is, that we don't just look at the person's lipids, but we look 44:03 look at the person's lipids, but we look 44:03 look at the person's lipids, but we look at their how their body deals with 44:07 at their how their body deals with 44:07 at their how their body deals with glucose. Okay, this next slide is about
Gut-bone-cardiovascular axis 44:10 glucose. Okay, this next slide is about 44:10 glucose. Okay, this next slide is about the gut bone cardiovascular axis. 44:13 the gut bone cardiovascular axis. 44:13 the gut bone cardiovascular axis. And as I mentioned before, everybody 44:15 And as I mentioned before, everybody 44:15 And as I mentioned before, everybody should really if you have a gut issue, 44:18 should really if you have a gut issue, 44:18 should really if you have a gut issue, bloating, constipation, diarrhea, I use 44:20 bloating, constipation, diarrhea, I use 44:20 bloating, constipation, diarrhea, I use a lab test called from diagnostic 44:23 a lab test called from diagnostic 44:23 a lab test called from diagnostic solutions called the GI map which I like 44:27 solutions called the GI map which I like 44:27 solutions called the GI map which I like a lot but there's a lot of companies 44:28 a lot but there's a lot of companies 44:28 a lot but there's a lot of companies that have other stool tests that are 44:30 that have other stool tests that are 44:30 that have other stool tests that are very very good and can help physicians 44:33 very very good and can help physicians 44:33 very very good and can help physicians look at the health or ill health of a 44:36 look at the health or ill health of a 44:36 look at the health or ill health of a person's gut 44:38 person's gut 44:38 person's gut and it's really important to assess that 44:41 and it's really important to assess that 44:41 and it's really important to assess that if a person has gut involvement, they 44:45 if a person has gut involvement, they 44:45 if a person has gut involvement, they can easily increase their risk for 44:48 can easily increase their risk for 44:48 can easily increase their risk for osteoporosis and cardiovascular issues. 44:50 osteoporosis and cardiovascular issues. 44:50 osteoporosis and cardiovascular issues. Okay, just want to talk about this one 44:52 Okay, just want to talk about this one 44:53 Okay, just want to talk about this one thing is called TMAO. It's a byproduct 44:56 thing is called TMAO. It's a byproduct 44:56 thing is called TMAO. It's a byproduct of your gut bacteria and if you know, 44:59 of your gut bacteria and if you know, 44:59 of your gut bacteria and if you know, I'm not saying everybody should be 45:00 I'm not saying everybody should be 45:00 I'm not saying everybody should be tested for this but with change hers was 45:03 tested for this but with change hers was 45:04 tested for this but with change hers was high so I'm putting it here. It 45:05 high so I'm putting it here. It 45:05 high so I'm putting it here. It increases inflammation, it increases 45:08 increases inflammation, it increases 45:08 increases inflammation, it increases osteoclastic activity, decreases blastic 45:10 osteoclastic activity, decreases blastic 45:10 osteoclastic activity, decreases blastic activity. It damages that endothelial 45:13 activity. It damages that endothelial 45:14 activity. It damages that endothelial glycocalyx so has lowered nitric oxide 45:17 glycocalyx so has lowered nitric oxide 45:17 glycocalyx so has lowered nitric oxide production. So all those things are 45:19 production. So all those things are 45:19 production. So all those things are important so we looked at that. We also 45:21 important so we looked at that. We also 45:21 important so we looked at that. We also looked at her ADMA. 45:23 looked at her ADMA. 45:23 looked at her ADMA. This is a really cool little simple test 45:26 This is a really cool little simple test 45:26 This is a really cool little simple test blood test to get and it's a 45:29 blood test to get and it's a 45:29 blood test to get and it's a it's a 45:30 it's a 45:30 it's a nice blood test for preclinical 45:32 nice blood test for preclinical 45:32 nice blood test for preclinical cardiovascular disease. 45:34 cardiovascular disease. 45:34 cardiovascular disease. We'll go through that quickly but but 45:36 We'll go through that quickly but but 45:36 We'll go through that quickly but but the reason why that's important is 45:38 the reason why that's important is 45:38 the reason why that's important is because if that's high, it can indicate 45:42 because if that's high, it can indicate 45:42 because if that's high, it can indicate that yeah 45:43 that yeah 45:43 that yeah this person has cardiovascular risk and 45:47 this person has cardiovascular risk and 45:47 this person has cardiovascular risk and then we have to look closer and see 45:49 then we have to look closer and see 45:49 then we have to look closer and see what's going on. Here's that endothelial 45:51 what's going on. Here's that endothelial 45:51 what's going on. Here's that endothelial glycocalyx that I talked about. It's a 45:54 glycocalyx that I talked about. It's a 45:54 glycocalyx that I talked about. It's a thin carbohydrate rich layer that lines 45:57 thin carbohydrate rich layer that lines 45:57 thin carbohydrate rich layer that lines the inside of your blood vessels. It 45:58 the inside of your blood vessels. It 45:58 the inside of your blood vessels. It senses the blood flow. So as that 46:01 senses the blood flow. So as that 46:01 senses the blood flow. So as that blood's pulsing through your arteries, 46:03 blood's pulsing through your arteries, 46:03 blood's pulsing through your arteries, your your arterioles, it it senses that 46:06 your your arterioles, it it senses that 46:06 your your arterioles, it it senses that blood flow and then it stimulates the 46:09 blood flow and then it stimulates the 46:09 blood flow and then it stimulates the cells that line that vessel to produce 46:11 cells that line that vessel to produce 46:11 cells that line that vessel to produce nitric oxide. And nitric oxide is what 46:14 nitric oxide. And nitric oxide is what 46:14 nitric oxide. And nitric oxide is what allows vessels to contract and relax and 46:18 allows vessels to contract and relax and 46:18 allows vessels to contract and relax and and uh maintains the health of that 46:21 and uh maintains the health of that 46:21 and uh maintains the health of that vessel wall. If you have damaged 46:24 vessel wall. If you have damaged 46:24 vessel wall. If you have damaged endothelial glycocalyx, 46:26 endothelial glycocalyx, 46:26 endothelial glycocalyx, it allows for an increase in 46:28 it allows for an increase in 46:28 it allows for an increase in inflammation, oxidative stress, and 46:30 inflammation, oxidative stress, and 46:30 inflammation, oxidative stress, and allows adhesion molecules to form, and 46:33 allows adhesion molecules to form, and 46:33 allows adhesion molecules to form, and so white blood cells can attach that 46:35 so white blood cells can attach that 46:35 so white blood cells can attach that wall and then increase plaque formation 46:38 wall and then increase plaque formation 46:38 wall and then increase plaque formation in the wall itself. And the interesting 46:40 in the wall itself. And the interesting 46:41 in the wall itself. And the interesting thing is people know a lot about the 46:43 thing is people know a lot about the 46:43 thing is people know a lot about the endothelial glycocalyx now. A lot of 46:45 endothelial glycocalyx now. A lot of 46:45 endothelial glycocalyx now. A lot of people have heard about it, 46:46 people have heard about it, 46:46 people have heard about it, but they haven't heard of the next 46:48 but they haven't heard of the next 46:48 but they haven't heard of the next slide. And that is in bone. There's this 46:52 slide. And that is in bone. There's this 46:52 slide. And that is in bone. There's this exactly Well, not exactly, but a very 46:55 exactly Well, not exactly, but a very 46:55 exactly Well, not exactly, but a very similar system there. We have a 46:57 similar system there. We have a 46:57 similar system there. We have a glycocalyx in the osteocyte dendrites. 47:01 glycocalyx in the osteocyte dendrites. 47:01 glycocalyx in the osteocyte dendrites. So, we have as I mentioned before, the 47:03 So, we have as I mentioned before, the 47:03 So, we have as I mentioned before, the osteocyte is the cell that monitors the 47:07 osteocyte is the cell that monitors the 47:07 osteocyte is the cell that monitors the actions of and regulates the actions of 47:10 actions of and regulates the actions of 47:10 actions of and regulates the actions of blasts and class, and they have little 47:12 blasts and class, and they have little 47:12 blasts and class, and they have little dendrites that go between them, and 47:14 dendrites that go between them, and 47:15 dendrites that go between them, and there is a glycocalyx in that 47:18 there is a glycocalyx in that 47:18 there is a glycocalyx in that dendrite. 47:19 dendrite. 47:19 dendrite. So, if you have endothelial glycocalyx 47:22 So, if you have endothelial glycocalyx 47:22 So, if you have endothelial glycocalyx damage, you're probably going to have 47:25 damage, you're probably going to have 47:25 damage, you're probably going to have osteocyte glycocalyx damage, too. 47:28 osteocyte glycocalyx damage, too. 47:28 osteocyte glycocalyx damage, too. Osteoclasts aren't going to be able to 47:29 Osteoclasts aren't going to be able to 47:29 Osteoclasts aren't going to be able to talk to each other well, and now you're 47:31 talk to each other well, and now you're 47:31 talk to each other well, and now you're going to have a disruption of bone 47:33 going to have a disruption of bone 47:34 going to have a disruption of bone remodeling. Okay, so Jane, let's look at 47:36 remodeling. Okay, so Jane, let's look at 47:36 remodeling. Okay, so Jane, let's look at the Let's quickly at her picture. She 47:38 the Let's quickly at her picture. She 47:38 the Let's quickly at her picture. She had a high carb diet, and that was one 47:41 had a high carb diet, and that was one 47:41 had a high carb diet, and that was one of her major downfalls. It 47:44 of her major downfalls. It 47:44 of her major downfalls. It promoted arterial wall injury and made 47:47 promoted arterial wall injury and made 47:47 promoted arterial wall injury and made her high lipids now get into those walls 47:51 her high lipids now get into those walls 47:51 her high lipids now get into those walls causing plaque. There's no doubt about 47:53 causing plaque. There's no doubt about 47:53 causing plaque. There's no doubt about it, she had endothelial glycocalyx 47:55 it, she had endothelial glycocalyx 47:55 it, she had endothelial glycocalyx dysfunction. She had exercise-induced 47:59 dysfunction. She had exercise-induced 47:59 dysfunction. She had exercise-induced high blood pressure and her ADMA was 48:02 high blood pressure and her ADMA was 48:02 high blood pressure and her ADMA was high. So, she had inflammatory markers 48:05 high. So, she had inflammatory markers 48:05 high. So, she had inflammatory markers that were high. Her blood glucose was on 48:07 that were high. Her blood glucose was on 48:07 that were high. Her blood glucose was on the verge of pre-diabetes. 48:10 the verge of pre-diabetes. 48:10 the verge of pre-diabetes. So, she clearly had issues. So, these 48:12 So, she clearly had issues. So, these 48:13 So, she clearly had issues. So, these are some of the things we did. She was
Sample treatment plan to support bone and cardiovascular health 48:14 are some of the things we did. She was 48:14 are some of the things we did. She was put on a statin, as you know, 48:16 put on a statin, as you know, 48:16 put on a statin, as you know, rosuvastatin. And that has 48:17 rosuvastatin. And that has 48:17 rosuvastatin. And that has [clears throat] pleiotropic effects. It 48:18 [clears throat] pleiotropic effects. It 48:18 [clears throat] pleiotropic effects. It does a lot of things. It doesn't just 48:20 does a lot of things. It doesn't just 48:20 does a lot of things. It doesn't just Statins don't just lower LDLs. They help 48:22 Statins don't just lower LDLs. They help 48:22 Statins don't just lower LDLs. They help increase a little bit HDLs. They lower 48:25 increase a little bit HDLs. They lower 48:25 increase a little bit HDLs. They lower interleukin 6. They increase actually 48:28 interleukin 6. They increase actually 48:28 interleukin 6. They increase actually bone morphogenetic protein for for more 48:30 bone morphogenetic protein for for more 48:30 bone morphogenetic protein for for more more bone formation. Not all the statins 48:32 more bone formation. Not all the statins 48:32 more bone formation. Not all the statins do, but at least the lipophilic ones do, 48:36 do, but at least the lipophilic ones do, 48:36 do, but at least the lipophilic ones do, the the ones like atorvastatin and 48:38 the the ones like atorvastatin and 48:38 the the ones like atorvastatin and simvastatin. Not that I think that 48:40 simvastatin. Not that I think that 48:40 simvastatin. Not that I think that they're better. I actually like 48:42 they're better. I actually like 48:42 they're better. I actually like rosuvastatin better, but that's a 48:44 rosuvastatin better, but that's a 48:44 rosuvastatin better, but that's a different story. 48:45 different story. 48:46 different story. We can talk about later. But, she was 48:48 We can talk about later. But, she was 48:48 We can talk about later. But, she was put on a statin and I suggested other 48:51 put on a statin and I suggested other 48:51 put on a statin and I suggested other things such as TUDCA and selenium. The 48:54 things such as TUDCA and selenium. The 48:54 things such as TUDCA and selenium. The that they can help reduce mitochondrial 48:57 that they can help reduce mitochondrial 48:57 that they can help reduce mitochondrial reactive oxygen species and reduce 49:00 reactive oxygen species and reduce 49:00 reactive oxygen species and reduce endoplasmic 49:02 endoplasmic 49:02 endoplasmic reticulum stress, which is Remember that 49:04 reticulum stress, which is Remember that 49:04 reticulum stress, which is Remember that endopla- plasmic reticulum helps you 49:07 endopla- plasmic reticulum helps you 49:07 endopla- plasmic reticulum helps you make proteins. And when there's stress, 49:10 make proteins. And when there's stress, 49:10 make proteins. And when there's stress, you're going to have misfolded proteins 49:13 you're going to have misfolded proteins 49:13 you're going to have misfolded proteins and that's not good. So, we want to 49:15 and that's not good. So, we want to 49:15 and that's not good. So, we want to decrease the the you know, any stress 49:19 decrease the the you know, any stress 49:19 decrease the the you know, any stress reactive oxygen species stress, any 49:22 reactive oxygen species stress, any 49:22 reactive oxygen species stress, any inflammation in your body that is going 49:25 inflammation in your body that is going 49:25 inflammation in your body that is going to help improve a person's health. 49:27 to help improve a person's health. 49:27 to help improve a person's health. Taking CoQ10 and atom E, those are all 49:30 Taking CoQ10 and atom E, those are all 49:30 Taking CoQ10 and atom E, those are all important. I I suggested to her 49:32 important. I I suggested to her 49:32 important. I I suggested to her nattokinase and berberine. Those things 49:34 nattokinase and berberine. Those things 49:34 nattokinase and berberine. Those things can help with the vessel walls. She also 49:37 can help with the vessel walls. She also 49:37 can help with the vessel walls. She also went on timolol and then a year of 49:39 went on timolol and then a year of 49:39 went on timolol and then a year of bisphosphonates. She also went on 49:41 bisphosphonates. She also went on 49:41 bisphosphonates. She also went on transdermal HRT. Remember that helped 49:45 transdermal HRT. Remember that helped 49:45 transdermal HRT. Remember that helped lower the RANKL. It helped increase 49:48 lower the RANKL. It helped increase 49:48 lower the RANKL. It helped increase osteoprotegerin. 49:49 osteoprotegerin. 49:49 osteoprotegerin. It lowered her interleukin 6 or 49:52 It lowered her interleukin 6 or 49:52 It lowered her interleukin 6 or inflammatory markers, so her transdermal 49:56 inflammatory markers, so her transdermal 49:56 inflammatory markers, so her transdermal HRT was a vital part of her treatment 49:59 HRT was a vital part of her treatment 49:59 HRT was a vital part of her treatment plan. We changed her diet, for sure. We 50:01 plan. We changed her diet, for sure. We 50:01 plan. We changed her diet, for sure. We decreased her sugar. We did things to 50:03 decreased her sugar. We did things to 50:03 decreased her sugar. We did things to improve her gut health and increase her 50:05 improve her gut health and increase her 50:05 improve her gut health and increase her nitric oxide production. Beets and, you 50:08 nitric oxide production. Beets and, you 50:08 nitric oxide production. Beets and, you know, taking the TUDCA, doing things 50:11 know, taking the TUDCA, doing things 50:11 know, taking the TUDCA, doing things like urolithin A, which is I'm a big 50:13 like urolithin A, which is I'm a big 50:13 like urolithin A, which is I'm a big proponent of urolithin A. So, and like I 50:15 proponent of urolithin A. So, and like I 50:15 proponent of urolithin A. So, and like I said, we tried to do things to help 50:17 said, we tried to do things to help 50:17 said, we tried to do things to help improve her gut health. And these are 50:19 improve her gut health. And these are 50:19 improve her gut health. And these are just some of the specifics. Vitamin D 50:22 just some of the specifics. Vitamin D 50:22 just some of the specifics. Vitamin D and K. We did the V's and the 50:24 and K. We did the V's and the 50:24 and K. We did the V's and the trimethylglycine to lower homocysteine. 50:27 trimethylglycine to lower homocysteine. 50:27 trimethylglycine to lower homocysteine. We gave her NMN and the urolithin A and 50:30 We gave her NMN and the urolithin A and 50:30 We gave her NMN and the urolithin A and alpha lipoic acid to help with her 50:32 alpha lipoic acid to help with her 50:32 alpha lipoic acid to help with her mitochondria support. I'm a big 50:35 mitochondria support. I'm a big 50:35 mitochondria support. I'm a big proponent of resveratrol and quercetin. 50:38 proponent of resveratrol and quercetin. 50:38 proponent of resveratrol and quercetin. Those were important to reduce 50:39 Those were important to reduce 50:39 Those were important to reduce inflammation. There's two products that 50:42 inflammation. There's two products that 50:42 inflammation. There's two products that I really like from Designs for Health 50:43 I really like from Designs for Health 50:43 I really like from Designs for Health called Vasculonox and Arterosil that 50:46 called Vasculonox and Arterosil that 50:46 called Vasculonox and Arterosil that help with that nitric oxide production 50:49 help with that nitric oxide production 50:49 help with that nitric oxide production and improvement of that endothelial 50:51 and improvement of that endothelial 50:51 and improvement of that endothelial glycocalyx. Fish oil, of course, or 50:53 glycocalyx. Fish oil, of course, or 50:54 glycocalyx. Fish oil, of course, or I 50:54 I 50:54 I have most people on. And just eating 50:57 have most people on. And just eating 50:57 have most people on. And just eating better, you know, we needed to get rid 50:59 better, you know, we needed to get rid 50:59 better, you know, we needed to get rid of her meat and potato diet. You know, 51:01 of her meat and potato diet. You know, 51:01 of her meat and potato diet. You know, we had her increase her her veggies, her 51:03 we had her increase her her veggies, her 51:03 we had her increase her her veggies, her berries, her beets, garlic, pomegranate. 51:06 berries, her beets, garlic, pomegranate. 51:06 berries, her beets, garlic, pomegranate. And I had her on collagen because 51:08 And I had her on collagen because 51:08 And I had her on collagen because collagen helps 51:10 collagen helps 51:10 collagen helps stimulate 51:11 stimulate 51:11 stimulate the osteoblasts to form bone. So, 51:15 the osteoblasts to form bone. So, 51:15 the osteoblasts to form bone. So, collagen is not taken for the amino 51:18 collagen is not taken for the amino 51:18 collagen is not taken for the amino acids. It's taken for the polypeptide 51:21 acids. It's taken for the polypeptide 51:21 acids. It's taken for the polypeptide chains that some of them can actually be 51:23 chains that some of them can actually be 51:23 chains that some of them can actually be absorbed intact that directly stimulate 51:25 absorbed intact that directly stimulate 51:25 absorbed intact that directly stimulate the blast to 51:28 the blast to 51:28 the blast to form bone. And when a person's P1NP is 51:30 form bone. And when a person's P1NP is 51:30 form bone. And when a person's P1NP is low, that's her blastic activity, 51:32 low, that's her blastic activity, 51:33 low, that's her blastic activity, remember. So, if the P1NP is low, 51:35 remember. So, if the P1NP is low, 51:35 remember. So, if the P1NP is low, collagen can help that. And, of course, 51:37 collagen can help that. And, of course, 51:37 collagen can help that. And, of course, probiotics because uh her gut was not 51:40 probiotics because uh her gut was not 51:40 probiotics because uh her gut was not doing well. 51:41 doing well. 51:41 doing well. So, I know I went through those last few 51:44 So, I know I went through those last few 51:44 So, I know I went through those last few slides quickly, but at least I hope that 51:46 slides quickly, but at least I hope that 51:47 slides quickly, but at least I hope that I gave you lots and lots to think about. 51:49 I gave you lots and lots to think about. 51:49 I gave you lots and lots to think about. >> Two quick questions on these slides. I 51:51 >> Two quick questions on these slides. I 51:51 >> Two quick questions on these slides. I the company, I think it's Calroy, right, 51:54 the company, I think it's Calroy, right, 51:54 the company, I think it's Calroy, right, who does the vast 51:55 who does the vast 51:55 who does the vast and answers. All right, right, right. 51:57 and answers. All right, right, right. 51:57 and answers. All right, right, right. So, it's not 51:57 So, it's not 51:57 So, it's not >> Oh, sorry about that. Yeah, yeah, yeah. 51:58 >> Oh, sorry about that. Yeah, yeah, yeah. 51:58 >> Oh, sorry about that. Yeah, yeah, yeah. >> Sorry, that's okay. And the second thing 52:00 >> Sorry, that's okay. And the second thing 52:00 >> Sorry, that's okay. And the second thing was did you want to mention about her 52:02 was did you want to mention about her 52:02 was did you want to mention about her iron cuz that was an issue as well? 52:04 iron cuz that was an issue as well? 52:04 iron cuz that was an issue as well? >> Yeah, she if you know it, well, probably 52:07 >> Yeah, she if you know it, well, probably 52:07 >> Yeah, she if you know it, well, probably people don't remember, but at the very 52:08 people don't remember, but at the very 52:08 people don't remember, but at the very beginning I showed what supplements she 52:10 beginning I showed what supplements she 52:10 beginning I showed what supplements she was taking and she was taking iron. And 52:14 was taking and she was taking iron. And 52:14 was taking and she was taking iron. And there's this 52:15 there's this 52:15 there's this condition called ferroptosis. 52:18 condition called ferroptosis. 52:18 condition called ferroptosis. And ferroptosis is this iron-dependent 52:21 And ferroptosis is this iron-dependent 52:21 And ferroptosis is this iron-dependent form of regulated cell death. 52:23 form of regulated cell death. 52:23 form of regulated cell death. So, it involves lipid peroxidation and 52:27 So, it involves lipid peroxidation and 52:27 So, it involves lipid peroxidation and dysregulation of causing an iron 52:29 dysregulation of causing an iron 52:29 dysregulation of causing an iron overload. So, her ferritin was high, she 52:31 overload. So, her ferritin was high, she 52:31 overload. So, her ferritin was high, she had all these inflammatory issues, and 52:34 had all these inflammatory issues, and 52:34 had all these inflammatory issues, and so when a person has this ferroptosis, 52:38 so when a person has this ferroptosis, 52:38 so when a person has this ferroptosis, this like I said, high iron and lipid 52:41 this like I said, high iron and lipid 52:41 this like I said, high iron and lipid peroxidation situation, it causes cell 52:44 peroxidation situation, it causes cell 52:44 peroxidation situation, it causes cell structure instability. And so, if the if 52:48 structure instability. And so, if the if 52:48 structure instability. And so, if the if the cell membrane is irritated, is is 52:52 the cell membrane is irritated, is is 52:52 the cell membrane is irritated, is is dysfunctional, is damaged, good stuff 52:56 dysfunctional, is damaged, good stuff 52:56 dysfunctional, is damaged, good stuff leaks out and bad stuff leaks in. The 52:58 leaks out and bad stuff leaks in. The 52:58 leaks out and bad stuff leaks in. The person's energy production suffers and 53:01 person's energy production suffers and 53:01 person's energy production suffers and she certainly was feeling that and the 53:03 she certainly was feeling that and the 53:03 she certainly was feeling that and the cell receptors don't work as well. I you 53:06 cell receptors don't work as well. I you 53:06 cell receptors don't work as well. I you know, the OPG Y OPG, the rank rank local 53:10 know, the OPG Y OPG, the rank rank local 53:10 know, the OPG Y OPG, the rank rank local system and other systems that were not 53:13 system and other systems that were not 53:13 system and other systems that were not working well in her. And it leads to the 53:15 working well in her. And it leads to the 53:15 working well in her. And it leads to the increased osteoclastic activity, 53:16 increased osteoclastic activity, 53:16 increased osteoclastic activity, decreased osteoblastic activity, 53:19 decreased osteoblastic activity, 53:19 decreased osteoblastic activity, dysregulation of the of the lipids and 53:21 dysregulation of the of the lipids and 53:21 dysregulation of the of the lipids and damage to heart cells. So, ferroptosis 53:24 damage to heart cells. So, ferroptosis 53:24 damage to heart cells. So, ferroptosis is not something that we should have 53:26 is not something that we should have 53:26 is not something that we should have going on, so I asked her to stop the 53:29 going on, so I asked her to stop the 53:29 going on, so I asked her to stop the iron supplements, at least to get that 53:31 iron supplements, at least to get that 53:31 iron supplements, at least to get that started. 53:31 started. 53:31 started. >> Okay. So, wow, Dr. McCormick, this was 53:35 >> Okay. So, wow, Dr. McCormick, this was 53:35 >> Okay. So, wow, Dr. McCormick, this was just fantastic and everybody listening, 53:38 just fantastic and everybody listening, 53:38 just fantastic and everybody listening, don't worry if you don't get all of 53:39 don't worry if you don't get all of 53:39 don't worry if you don't get all of this. You can watch this. That's the 53:40 this. You can watch this. That's the 53:41 this. You can watch this. That's the beautiful thing about podcast, It stays 53:43 beautiful thing about podcast, It stays 53:43 beautiful thing about podcast, It stays up there, so you can review this. But I 53:45 up there, so you can review this. But I 53:45 up there, so you can review this. But I think what's your your main point? I I 53:48 think what's your your main point? I I 53:48 think what's your your main point? I I think you're me you have a few main 53:50 think you're me you have a few main 53:50 think you're me you have a few main points that you really feel so 53:51 points that you really feel so 53:51 points that you really feel so passionate to tell everybody about. 53:54 passionate to tell everybody about. 53:54 passionate to tell everybody about. >> I guess just number one, the awareness
Advocating for your health and asking for the right tests 53:56 >> I guess just number one, the awareness 53:56 >> I guess just number one, the awareness that these two disorders, these two 53:58 that these two disorders, these two 53:58 that these two disorders, these two diseases are can be comorbidities. They 54:01 diseases are can be comorbidities. They 54:02 diseases are can be comorbidities. They are not unusual to travel together. 54:05 are not unusual to travel together. 54:05 are not unusual to travel together. And that you need to stand up for your 54:07 And that you need to stand up for your 54:07 And that you need to stand up for your health 54:08 health 54:08 health and speak with your doctor about these 54:11 and speak with your doctor about these 54:11 and speak with your doctor about these things and and ask for good testing. It 54:14 things and and ask for good testing. It 54:14 things and and ask for good testing. It is amazing how resistant some doctors 54:17 is amazing how resistant some doctors 54:17 is amazing how resistant some doctors are to getting a simply getting a CTX 54:20 are to getting a simply getting a CTX 54:20 are to getting a simply getting a CTX and P1NP or simply getting the LP little 54:24 and P1NP or simply getting the LP little 54:24 and P1NP or simply getting the LP little A and APOB. These tests do not cost a 54:27 A and APOB. These tests do not cost a 54:27 A and APOB. These tests do not cost a lot and I'm not and I'm totally confused 54:31 lot and I'm not and I'm totally confused 54:31 lot and I'm not and I'm totally confused of why a doctor would want to save an 54:32 of why a doctor would want to save an 54:32 of why a doctor would want to save an insurance company, you know, $200 for 54:36 insurance company, you know, $200 for 54:36 insurance company, you know, $200 for not doing these tests when they're so 54:38 not doing these tests when they're so 54:38 not doing these tests when they're so important to look at. So, I guess that's 54:42 important to look at. So, I guess that's 54:42 important to look at. So, I guess that's my 54:43 my 54:43 my >> It's an important message because we 54:45 >> It's an important message because we 54:45 >> It's an important message because we believe in digging deep and when you dig 54:47 believe in digging deep and when you dig 54:47 believe in digging deep and when you dig deep, that's when you get the results 54:49 deep, that's when you get the results 54:49 deep, that's when you get the results and things come up. So, share with 54:52 and things come up. So, share with 54:52 and things come up. So, share with everybody, but you you see patients and 54:54 everybody, but you you see patients and 54:54 everybody, but you you see patients and you do a lot of consults and you've 54:55 you do a lot of consults and you've 54:55 you do a lot of consults and you've helped so many people in the community. 54:57 helped so many people in the community. 54:57 helped so many people in the community. So, tell people how they can get in 54:59 So, tell people how they can get in 54:59 So, tell people how they can get in touch with you if they want if they do 55:00 touch with you if they want if they do 55:00 touch with you if they want if they do want to work with you. 55:02 want to work with you. 55:02 want to work with you. >> Well, my office is the called Great 55:04 >> Well, my office is the called Great 55:04 >> Well, my office is the called Great Bones and Education and Consulting and I 55:08 Bones and Education and Consulting and I 55:08 Bones and Education and Consulting and I do Yeah, I do 55:09 do Yeah, I do 55:10 do Yeah, I do consults with with people on their bone 55:12 consults with with people on their bone 55:12 consults with with people on their bone density. 55:13 density. 55:13 density. >> Now, you've been so helpful because you 55:14 >> Now, you've been so helpful because you 55:14 >> Now, you've been so helpful because you work with where people are at and you 55:16 work with where people are at and you 55:16 work with where people are at and you work with their So, a lot of when people 55:19 work with their So, a lot of when people 55:19 work with their So, a lot of when people are confused, oh gosh, I just don't know 55:21 are confused, oh gosh, I just don't know 55:21 are confused, oh gosh, I just don't know what to do. Do I go on medication? Do I 55:23 what to do. Do I go on medication? Do I 55:23 what to do. Do I go on medication? Do I not? So, I always like Dr. McCormick and 55:26 not? So, I always like Dr. McCormick and 55:26 not? So, I always like Dr. McCormick and you've helped them. You've really shown 55:28 you've helped them. You've really shown 55:28 you've helped them. You've really shown them what the path is. Are they missing 55:30 them what the path is. Are they missing 55:30 them what the path is. Are they missing any root causes? And that's what that's 55:32 any root causes? And that's what that's 55:32 any root causes? And that's what that's what we believe in. We believe in this 55:34 what we believe in. We believe in this 55:34 what we believe in. We believe in this type of approach and it's so effective. 55:36 type of approach and it's so effective. 55:36 type of approach and it's so effective. That's the beautiful thing. 55:37 That's the beautiful thing. 55:37 That's the beautiful thing. >> Well, what I try to do is just help a 55:39 >> Well, what I try to do is just help a 55:39 >> Well, what I try to do is just help a person understand and navigate, you 55:42 person understand and navigate, you 55:42 person understand and navigate, you know, what's going on with their system 55:43 know, what's going on with their system 55:43 know, what's going on with their system so that they then can go back to their 55:45 so that they then can go back to their 55:45 so that they then can go back to their doctor cuz I can't act as their doctor 55:48 doctor cuz I can't act as their doctor 55:48 doctor cuz I can't act as their doctor here. So, I am just helping them 55:51 here. So, I am just helping them 55:51 here. So, I am just helping them navigate not the system, not the medical 55:54 navigate not the system, not the medical 55:54 navigate not the system, not the medical system, but navigate their health and 55:56 system, but navigate their health and 55:56 system, but navigate their health and see what's important to see how they can 55:59 see what's important to see how they can 55:59 see what's important to see how they can interact with their doctor to encourage 56:01 interact with their doctor to encourage 56:01 interact with their doctor to encourage them to 56:02 them to 56:02 them to get the right test, to ask the right 56:04 get the right test, to ask the right 56:04 get the right test, to ask the right questions, to make sure that, you know, 56:07 questions, to make sure that, you know, 56:08 questions, to make sure that, you know, they are getting the optimal health that 56:10 they are getting the optimal health that 56:10 they are getting the optimal health that they if they need. 56:12 they if they need. 56:12 they if they need. >> Well, you're doing an incredible job and 56:14 >> Well, you're doing an incredible job and 56:14 >> Well, you're doing an incredible job and I always believe and I've said this a 56:16 I always believe and I've said this a 56:16 I always believe and I've said this a million times, knowledge is power. And 56:18 million times, knowledge is power. And 56:18 million times, knowledge is power. And the people listening, they want to learn 56:20 the people listening, they want to learn 56:20 the people listening, they want to learn as much as they can and it really does 56:21 as much as they can and it really does 56:21 as much as they can and it really does pay off. So, thank you so much for 56:24 pay off. So, thank you so much for 56:24 pay off. So, thank you so much for joining me here today and sharing this 56:26 joining me here today and sharing this 56:26 joining me here today and sharing this really, really important information. 56:29 really, really important information. 56:29 really, really important information. >> Thanks for having me, Marci, and and I 56:30 >> Thanks for having me, Marci, and and I 56:30 >> Thanks for having me, Marci, and and I really appreciate being invited on to 56:33 really appreciate being invited on to 56:33 really appreciate being invited on to talk about this really important 56:34 talk about this really important 56:34 talk about this really important subject. 56:35 subject. 56:35 subject. >> Thanks so much. 56:37 >> Thanks so much. 56:37 >> Thanks so much. Wow, this was filled with so much great 56:39 Wow, this was filled with so much great 56:39 Wow, this was filled with so much great information and I hope you have a better 56:41 information and I hope you have a better 56:41 information and I hope you have a better understanding now of the relationship 56:43 understanding now of the relationship 56:43 understanding now of the relationship between bone health and heart health and 56:46 between bone health and heart health and 56:46 between bone health and heart health and what tests you should order. All the 56:48 what tests you should order. All the 56:48 what tests you should order. All the links will be in the show notes and I 56:49 links will be in the show notes and I 56:50 links will be in the show notes and I also wanted to mention that on September 56:52 also wanted to mention that on September 56:52 also wanted to mention that on September 8th, I'll be having a free webinar on 56:55 8th, I'll be having a free webinar on 56:55 8th, I'll be having a free webinar on strong bones for life. We'll I'll go 56:57 strong bones for life. We'll I'll go 56:57 strong bones for life. We'll I'll go over testing, nutrition, exercise, and 57:00 over testing, nutrition, exercise, and 57:00 over testing, nutrition, exercise, and all the things you need to do for to 57:02 all the things you need to do for to 57:02 all the things you need to do for to really be successful in an integrative 57:04 really be successful in an integrative 57:04 really be successful in an integrative approach. 57:06 approach. 57:06 approach. So, that's going to be at noon on 57:07 So, that's going to be at noon on 57:07 So, that's going to be at noon on September 8th and if it's past the day, 57:09 September 8th and if it's past the day, 57:09 September 8th and if it's past the day, I'll be having them on a continual 57:11 I'll be having them on a continual 57:11 I'll be having them on a continual basis. So, just check the show notes for 57:13 basis. So, just check the show notes for 57:13 basis. So, just check the show notes for that. So, thank you so much for tuning 57:16 that. So, thank you so much for tuning 57:16 that. So, thank you so much for tuning in and I look [music] forward to seeing 57:17 in and I look [music] forward to seeing 57:17 in and I look [music] forward to seeing you on the next episode.
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