As a former Olympian and current Iron Man triathlete, (he qualified for the world championship in Hawaii this year!) Dr. Keith McCormick was diagnosed with severe osteoporosis at 45 years old. His own healing journey lead him to become a world expert on treating osteoporosis from a functional and integrative perspective. His 2008 book, The Whole Body Approach to Treating Osteoporosis, is useful for patient and clinician alike. This podcast is a goldmine of pearls for clinicians treating individuals with bone loss. Topics covered include underlying pathogenic mechanisms, laboratory evaluations and treatments-pharmaceutical and natural. Health savvy patients will find Dr. McCormick’s content useful.
Pearls from Dr. Keith McCormick
- Inflammatory mechanisms underlying osteoporosisa.
- Gut inflammation and osteoporosis
- Fatty bone marrow & osteoporosis. Think of it akin to non-alcoholic fatty liver in metabolic disease
- c. Similar drivers: IL-6, TNF-alpha, IL-1, NFKb, RANKL
- d. Associated CBC abnormalities that may suggest fatty bone marrow
- Essential natural and dietary interventions for osteoporosis
- Berberine, an essential phytochemical for osteoporosis treatment
- a. Increases osteoblastic activity while decreasing osteoclastic activity; improves blood sugar and treats dysbiosis
- Bone density scans: who’s at risk for fractures?
- Urine bone resorption assays: Essential for monitoring bone turnover/ how to interpret
- Which bisphosphonates to use and when
- Forteo-useful in these cases.
Dr. Fitzgerald: Hi everybody. Welcome to New Frontiers in Functional Medicine. I’m Dr. Kara Fitzgerald. Today, it’s my honor to be speaking with Dr. Keith McCormick who has been doing just really incredible work around osteoporosis. I think he really knows better than anybody in the world of integrative medicine on how to address this from a functional perspective.
So expect to get some really good, user-friendly Monday morning pearls today. If you’re an individual suffering with osteoporosis or osteopenia, today, you’ll have some great take homes as well you can either implement yourself or talk to your physician about.
Dr. McCormick is a board certified chiropractor in the state of Massachusetts, Colorado and California. He’s been in clinical practice since 1992. In addition to his general practice, Dr. McCormick is a board certified sports chiropractic physician and is a member of the University of Massachusetts Sports Medicine Department.
Dr. McCormick specializes in nutritional management of patients with bone fragility and is the author of The Whole-Body Approach to Osteoporosis. This is a great resource for clinicians and patients alike, this book, The Whole-Body Approach to Osteoporosis. I suggest that you check it out if you haven’t gotten it.
In 2011, Dr. McCormick founded Osteo Naturals, a company dedicated to providing information and quality nutrition products to individuals with bone loss. Again, this is a great company. His professional memberships include the American Society for Bone and Mineral Research, the International Bone and Mineral Society and the American Chiropractic Association.
Dr. McCormick earned his Bachelor’s in Human Biology at Stanford and his Doctorate at National College of Chiropractic. In addition to his chiropractic practice, Dr. McCormick is an avid athlete, competing in Iron Man Triathlons and was a member of 1976 US Olympic team in the sport of modern pentathlon.
Keith, it’s great to have you on the podcast today. Thank you so much for joining me.
Dr. McCormick: Thanks for inviting me, Kara. It’s good to be here.
Dr. Fitzgerald: And I know you’re recovering from your Iron Man last week. So again, I’m glad you’re here even in recovery mode.
Dr. McCormick: Oh, yes. I’m pretty good now.
Dr. Fitzgerald: Good. So give me a little bit of your background on how you came to focus in bone loss in your practice.
Dr. McCormick: Well, I have been an athlete all my life. Even when I was 45, I was training pretty hard. One day, I was joining a track workout and just had a lot of hip pain. One thing led to another. And within three or four days, I’ve had a couple of tests done. I found out that I had really severe osteoporosis and I had some microfractures in my hip. Over the next few months, I saw five endocrinologists. They all just wanted to put me on bisphosphonates and diuretics. I said, “That’s not what I wanted to do.”
At that point, I was 45 years old, I didn’t know anything about osteoporosis except that elderly women get it and that you’re supposed to drink milk. I didn’t want to just take bisphosphonates, so I immersed myself in the study of osteoporosis and tried to figure out what my problem was.
And then after I did that, I decided to write a book about it so I can have other people. Now, I do consults on patients with osteoporosis from all over the world really. So it has been a lot of fun. And hopefully I’ve been a help to people. That’s the story.
Dr. Fitzgerald: Thanks. Thanks for sharing it.
Dr. McCormick: I broke a lot of bones over the period of five years and now I don’t break anymore. I can do Iron Man again. It was actually a very good learning experience. It’s always good to have a little brush with your mortality and then come back from it.
Dr. Fitzgerald: Right. I know you’ve learned a lot. I’ve known you for years and we’ve dialogued extensively on this. I’ve learned so much from you. I know in addition to treating patients, you’re a great educator for professionals. I mean, we see people with bone loss to one degree or another in our practices all the time.
Can you just walk us through basically the underlying mechanism of action with regard to osteoporosis?
Dr. McCormick: Yeah, sure.
Dr. Fitzgerald: And throw in any genetic thoughts you have around there.
Dr. McCormick: Yes. There are so many genetic inputs to this. The problem is there are so many. There are so many that they really can’t pinpoint as far as direct bone loss, but it’s related to bone loss. So yes, there are huge genetic components. And when you’re trying to figure out what’s going on with this person or that person for bone loss, you do have to have that in the back of your mind – you can do everything right and the person still has bone loss. It can be frustrating at times.
But the basic reason for bone loss is an uncoordinated bone remodeling process. So the osteoblasts have to form bones and they actually tell the osteoclasts through various signaling molecules, especially with one called RANKL, which is receptor activator for nuclear factor kappa-B ligand. That is a signaling mechanism to the osteoclasts to ramp up their activity.
You’ll think, “Why would the osteoblasts form bone and tell the osteoclasts to break down bones?”, the reason why is because the body is constantly trying to get rid of microfractures. If microfractures increase overtime, the whole skeleton gets weaker. So the body is always trying to remodel and renew the skeleton.
So the interaction between the osteoblasts and the osteoclasts is vital. That interaction breaks down and osteoclastic activity ramps up and osteoblastic activity naturally goes down as the person gets older.
And you think, “Why don’t osteoclasts naturally get tired and decrease overtime?” The reason why and the key to this whole thing is what happens if the person gets older? Well, they get less anabolic; they get more catabolic. They get more inflammatory problems, they get more inflammatory cytokines, interleukin-1, interleukin-6, tumor necrosis factor and things like that. That is what spurs on these osteoclasts.
And osteoclasts actually get to be almost like these burnt out light bulbs. When there’s background inflammation is happening, their life span might be shorter, but they become much more aggressive. The light bulb gets really, really bright before it gets burnt out and then it burns out. But in the meantime, it’s bright and then it burns out. It’s the same with these osteoclasts. They get very aggressive even though their life span might be shorter. They start breaking down bone more.
Dr. Fitzgerald: Wow! That’s okay. Thank you so much. That’s a great summary of what’s happening at the molecular level. I just wanted to reiterate that there are no genes that are really jumping out at you. It’s this fundamental mechanism that you’re thinking about.
Dr. McCormick: Well, there are genetic issues for vitamin D.
Dr. Fitzgerald: Right! Yeah, I got it.
Dr. McCormick: I mean, there are so many that are involved. And what are we going to do about it? I’m not sure. We can improve enzymatic activity and improve transcription activities as far as making sure we don’t have issues there. But really, there’s nothing to pinpoint that we can really change I think.
Dr. Fitzgerald: Okay. Okay. I hear you.
Dr. McCormick: But the whole body function can.
Dr. Fitzgerald: So just taking a full functional approach where you’re looking at the whole being and correcting the imbalances that you identify, that’s going to be a piece of the puzzle regardless of the underlying cause.
Dr. McCormick: The reason why is because everything is involved.
Dr. Fitzgerald: Yeah.
Dr. McCormick: I mean, every single organ is involved. You think of the bones as just being by themselves, but they’re not. The thyroid is involved, the pancreas is involved, the testicles, the ovaries. The gut is huge. I mean the gut, if you have gut dysfunctions, you’re going to have increased inflammation and you’re going to have production of pro-inflammatory cytokines, production of more kappa-B and the cells. I don’t think you could mention an organ that is not involved in this.
Dr. Fitzgerald: So RANKL is a fundamental player, this receptor activated NF kappa-B. This is the fundamental link to turning on the inflammatory cytokines that then really direct – or vice versa, the cytokines turn on RANKL and then RANKL cranks up the osteoclasts?
Dr. McCormick: Right. Yes, the osteoblasts naturally produce RANKL, but so do T cells. And when the immune system is offset and we have increased T cell production, we have increased RANKL production. What happens is they interfere with the transformation from the monocyte macrophages to the cytokines to the osteoclasts.
So we have hematopoietic stem cells and we have mesenchymal stem cells. There are actually three stem cells essentially, but those are the two main ones that we’re talking about. From the hematopoietic stem cells, we get the osteoclasts. The mesenchymal stem cells produce the osteoblasts. What happens is they’re talking to each other all the time within these stem cell [inaudible 00:11:44].
People don’t think of osteoclasts as being white blood cells, but essentially, they are. If you look at what a white blood cell does, it eats up bacteria and it eats up viruses and gets rid of them. And what do osteoclasts do? They eat up bone to get rid of microfractures. So they’re really essentially doing similar things and they are directed by similar signaling molecules.
And when the hematopoietic stem cells are interfered with, you have like the switch light mechanism that occurs. So what happens is you end up getting a switch that goes away from the monocyte macrophage production and more towards the osteoclastic production. That’s what happens when you have a huge amount of RANKL being produced by T cells. T cells as you know are the generals of the white blood cells or the immune system. So, they dictate what’s going on. So when there are chronic inflammatory issues from the gut or wherever, they’re going to keep producing more RANKL and that’s what flips the switch.
The same thing happens with the mesenchymal stem cells. The switch can happen there too. The same thing can occur there when we have more pro-inflammatory cytokines being produced instead of the mesenchymal stem cells producing osteoblasts. They end up producing more fat.
So if you look at a person’s CBC, you’d think, “What’s the CBC going to tell me on a person with osteoporosis?”, if you look at the CBC and look at their white blood cell count, you’re going to see red blood cell counts (with a person with severe osteoporosis), you’re almost always going to see it below 4.0.
The reason why is because these serially osteoporotic people have a lot of fat in their bone marrow. Why? Because the RANKL, the interleukin-1, interleukin-6, tumor necrosis factor, that all flip that switch from osteoblastic production to adipocyte production. And so, we have this huge amount of fat within the bone marrow. And then that fat crowds out the hematopoietic stem cells and that’s why the person ends up having less red blood cell production.
Dr. Fitzgerald: Thank you so much. That’s such a great outline of the underlying pathophysiology. I appreciate it. So really stoking inflammation from any part of the body, you’ve got the fundamental cytokines upregulated like interleukin-6, tumor necrosis factor alpha and interleukin-1 and then you turn on T cell production. T cells start cranking up the RANKL and just turning on the movement towards osteoclast activity as well as increased adiposity deposited in the bone marrow. Is that a good summary?
Dr. McCormick: Yes.
Dr. Fitzgerald: Okay.
Dr. McCormick: That’s perfect to me.
Dr. Fitzgerald: Okay, great. That’s extremely useful.
So I want to jump over to talking about what I’ve seen in my practice. Now, I do routinely quite well when osteoporosis is a co-morbidity.
In fact, in the case study book that I authored in 2011, I wrote about a rheumatoid arthritis patient who also had osteoporosis. We addressed the rheumatoid arthritis and we really just got her into balance and wellness, antibodies cleared, et cetera. And with little effort, her bone density improved really. We just quenched the inflammation, bone density bounced back and she was no longer osteoporotic as defined by T score. She was osteopenic at the point of the end of the case study.
So it was relatively straightforward. I introduced a few combinations, bone nutrients, but not a lot. In fact, this woman never exercised despite my repeated “please” with her and we were still able to improve her bone density by quenching inflammation.
On the other end of the spectrum though (and I think you fall into this category personally) are those people who present primarily with osteoporosis. Then it’s a different can of worms. It’s much more challenging to treat, these two pictures. Can you talk about that?
Dr. McCormick: I think you’re right. It goes back and forth. My book is called The Whole-Body Approach to Osteoporosis. You could say “The whole body approach to Alzheimer’s.” You could say “The whole body approach to heart disease… to diabetes.” I don’t think it really matters. Like you did with this patient, you approached that person by improving her body and her bone density happened to improve.
I think what we fall into is this old thing of “Oh, osteoporosis is bone loss. What are bones made of? Well, they’re made of calcium. Well, then the person needs some calcium.” That is so simplistic and wrong.
Like you said, you didn’t have this person exercise, they probably weren’t taking tons of calcium and they still got better in their bone density. And the reason why is because what’s more important than calcium is trying to improve that speaking between the osteoclasts and the osteoblasts. That was more important, much more important than giving the person calcium. So that addresses that.
Your other point in the osteoporosis as the primary is I think more difficult. The reason why is because we have all this genetic stuff going on. We have genetic markers for collagen, for vitamin D. There are so many things that are happening.
A person can have a – 2.5 and they’re falling apart and another person with – 2.5 is fine. The reason why is because we have bone quality and bone quantity and the only thing we can really measure at this point is bone quantity.
Bone quantity with the T scores is fine. But really, I think in 30 years or whenever we’re a lot smarter, we are going to be able to measure bone quality. That’s going to be so much more beneficial than measuring quantity.
The quantity is just minimally related to a person’s fracture risk. I mean, it’s a huge discrepancy. Like I said, one person, when they have 2.5, they will fracture and another person with -4.0 or -4.5 will not fracture (they’re going to fracture pretty soon, I’ll tell you that). It might get them to -5.0 before they fracture. But the quality, how do you measure that?
And when you have a person with just osteoporosis and they don’t have other diseases or issues yet, I do think it is harder. But I do think that you need to address them as though you may get Alzheimer’s, they may get diabetes, they may get these other things and then you treat it that way.
Dr. Fitzgerald: I got it. So you’re still going in with this foundational total body approach. We’re going to talk and we’re going to go back to that in just a second, but I wanted to just nail you down on the labs, quality versus quantity and the limitations of DEXA and T score.
So how are you getting an idea around quality? And talk to me about the bone resorption markers that you use routinely. So both things, how you get an idea around quality and your bone resorption markers, which I think are extremely useful tools.
Dr. McCormick: Yeah. For example, that red blood cell thing, I look at a lot of different indices. I look at mean platelet volume. If that’s high, they’re have an inflammatory going on. I look at lots of little things like that.
And if they have probably -3.0 for the spine – it’s my tipping point where I get a little nervous about a person or something. I don’t get nervous at -2.5 usually. And usually -3.0, I am still not that nervous about them as far as saying, “Listen, we got to do a drug here.” But a -3.5, I start getting more nervous.
But I look at lots of other indices. And if this person is really unhealthy and they have a -3.0 and their MPV is high and their red blood cells are low and they have digestive issues and they have different things, then I start saying, “Okay, this person is really genuinely unhealthy.”
And it’s not just that they were born with lower density. A lot of women that are 110 lbs. and they have -3.5, they’re not going to fracture. They just have smaller bone volume. They may fracture. I shouldn’t say they’re not going to. But the chances of it are less I think.
Dr. Fitzgerald: Especially if the other parameters (obviously, you’re looking at those), they’re dialed in, they’re not an inflamed individual.
Dr. McCormick: That’s right.
Dr. Fitzgerald: Yeah.
Dr. McCormick: Yeah. They just have low bone density. And they get them all upset and say, “Oh, you have to go on a bisphosphonate.” That’s really criminal in my case. And they’ll do that with people with 2.0, which is osteopenia. I’ve seen a hundred pound woman with a -2.0 at age 50 being put on bisphosphonate. I [inaudible 00:22:25] when I see that.
Dr. Fitzgerald: Right.
Dr. McCormick: And speaking of bone resorption markers, a lot of these people – for example, that hundred pound woman who turns 50 – and that’s the people that I see in my practice mostly, they’re 50 year old women. When they turn menopausal, when they turn 50, their doctor says, “Okay, time to get your bone density.” And then what happens is the bone density comes back -2.0 or -2.5 (which is osteoporosis), then they pretty much oftentimes automatically put on a bisphosphonate.
And bone resorption markers aren’t done for a baseline. To me, it’s terrible. If you had given NTx (let’s look at N-telopeptide, it’s a urine marker for bone resorption), what happens on this –
There are three essentially basic bone resorption markers. There’s N-telopeptide, C-telopeptide and deoxypyridinoline. NTx is typically urine, CTx is typically blood (but they can actually get NTx now from blood). And then, there’s deoxypyridinoline, which is urine.
They’re all pretty good and all pretty bad at the same time. They fluctuate throughout the day, so it’s really important (especially the NTx and DPD) to do them at the same time each day.
Dr. Fitzgerald: And is there a time? Is there a time you recommend?
Dr. McCormick: Well, you should do it during the second morning urine because what happens is you’re having a lot of metabolic processes going on during the night, so it’s just good to look at it the same time. We don’t want that first urine; we want that second. So if a person gets up at 6:30 and they should pee and then 8:30 or so, they’d pee again. That’s the urine we want.
Let’s talk really quick about NTx because that’s what I use mostly. Sometimes I use CTx and once in a while, I use DPD, but I mostly use NTx. The best way to go is 24-hour urine NTx. That’s more stable and you don’t have to worry about the change throughout the day. But typically I use the second morning urine.
And I think the reference range is something like 15 to 65, which is totally ludicrous. You wouldn’t want somebody at 15 because that’s saying that they virtually have no osteoclastic activity. You don’t want them at 15.
When you take a bisphosphonate, it can get down to 20 or 15, which is, to me, dangerous. You would not want to keep a person on a bisphosphonate and get down to 15 because now, we’re not having any bone remodeling, they’re not having turnover bones. They are the people who I think have a chance of a typical [inaudible 00:25:49] fractures or osteonecrosis of the jaw development. So a person shouldn’t be on bisphosphonate if their NTx is down to 15.
And a lot of doctors don’t retest NTx’s. Before a person starts a bisphosphonate, starts a medication, they need to be tested to get a baseline. And while they’re being treated with bisphosphonate, they need to, every six months, have an NTx or CTx done again just to make sure they’re not getting too low.
Dr. Fitzgerald: Right.
Dr. McCormick: So the reference range is 15 to 65. You don’t want somebody at 60. If they’re at 65, that’s way too high. It should be below probably 45. So between 30 and 45 is the best for NTx.
What I do in my patients is I always get the NTx (sometimes CTx, whatever). I always get the bone resorption marker, I look at it and I say, “Okay, you have 100 for your NTx. We are going to get this down below 50 within four months. Depending on how ban your bone density is, if we don’t get it down below 50 within four months of just doing nutrition…” – and typically and almost always I do – “If we don’t, you’re going on a bisphosphonate.” That is especially if a person is a -3.5.
If they are at negative 4.0 and negative 4.2 and they fracture, I’m putting them on a bisphosphonate or Forteo right away. I’m going to still do all my nutrition with them, but I’m going to get them on a drug right away because I don’t want them fracturing anymore.
Nutrition works, but it’s a little slower and I want to get these people out of trouble as fast as we can. If you do a bisphosphonate short term, you’re not going to hurt them.
Forteo is a great drug. It gives them a cushion. It’s the only drug out there that actually builds bone and tissue. And then if you do Forteo with them, you always back it up with six months to a year of a bisphosphonate. Then you pull them off of the bisphosphonate and then you just give nutrition.
But you’re still constantly monitoring that bone resorption marker. Every six months, every four to six months, you’re doing NTx or CTx. If it gets up to a dangerous level, maybe you have to throw them back on a bisphosphonate for six months or something like that. But almost always, you should be able to bring that down.
For me personally, 15 years ago, my NTx was 125 or something. I brought it down to 48 or 50 (pretty consistently just below 50) with just nutrition. So you can do it. But then you have to monitor and make sure it stays down.
Dr. Fitzgerald: Great! That’s just incredibly useful information. Thank you so much, Keith.
Let’s see. Let’s start talking about what you’re doing nutritionally. Maybe there are some basic protocols for general bone health, a little bit of time on that. But really let’s dive into the nitty-gritty with somebody who’s got frank osteoporosis greater than -2.5, even some of the more severe folks you see.
Dr. McCormick: First thing, of course, is you make sure they’re good on their vitamin D. Minimal is 35 nanograms per ml, but I like them up to 50 or 60. A lot of people try to shoot for 80, but I don’t think you need to get 80 nanograms per ml. I think 60 is fine. I don’t think you’d get any more benefits from 80. But anyhow, you test.
One thing you don’t want to do is just say, “Oh, I’m going to give that person 2000 IUs of vitamin D” because many people don’t absorb that. They might have to be on 5000 IUs a day. But just test and check it out until you know that they’re always remaining throughout the winter months too.
Here in New England, we don’t have any good sun and D production in the wintertime. So the good time to test for vitamin D is in March or April because you want to make sure that what doesn’t happen is through the winter, they get down to 25 nanograms per ml and then they’re in the sun a little bit more in the summer, they get up to 45. You mistakenly test them in July and they’re 45 and you say, “Oh, they’re fine. I don’t need to test them again.”
No, you need to test them again in March and make sure that they’re holding that 45 throughout the year because sometimes people need to take 5000 to 7000 IUs a day during the winter and then they can drop it down to 2000 in the summer. Just make sure they always stay in probably around 40 to 50 at least through the winter months.
You can test for vitamin K. My metrics has the K test through the carboxylation of osteocalcin. So that’s not a bad test if you don’t know how their fat absorption is.
I think Vermeer did most of his studies on vitamin K and he found that the max you really need for full osteocalcin carboxylation is between 200 and 500 micrograms of K2. So I use some K2, MK4, MK7 (but mostly I think MK4 is the most important). In my OsteoStim product, I have 700 micrograms of a mixture of K2, MK4, plus 50 micrograms of the MK7. And that’s really all you need for good carboxylation of the osteocalcin.
Dr. Fitzgerald: Okay.
Dr. McCormick: One of the things that people don’t realize about osteocalcin – a lot of people have read the Japanese studies, they use 45 milligrams.
Dr. Fitzgerald: Yeah.
Dr. McCormick: I think that’s been refuted by a recent study. But to me, that’s a pharmacological dose. And where they came up with the 45 milligrams, I’m not sure as far as the testing. Why didn’t they pick 40? Why didn’t they pick 30? I don’t know. But they came up with the 45 and found out there was increased bone density, so now everybody got on the bandwagon and said, “Okay, let’s do 45 milligrams of K.”
But we don’t know that that K might over-carboxylate osteocalcin. And what is important for testosterone production is under-carboxylation of osteocalcin.
Dr. Fitzgerald: That was fascinating.
Dr. McCormick: And for pancreatic function, you also need a balance between osteocalcin being carboxylated and under-carboxylated
Dr. Fitzgerald: Wow!
Dr. McCormick: So when you start forcing the body to do things that maybe aren’t natural, i.e. 45 milligrams of K, you might be messing around with the energy balances for pancreatic function and insulin production and testosterone production.
So to me, let’s just do what Vermeer said when he did these studies. He found out that pretty good carboxylation is all you need for bone health and that’s at 500 micrograms.
Dr. Fitzgerald: Thank you.
Dr. McCormick: So that’s my vitamin K.
Dr. Fitzgerald: That’s great. That was a question on the list. I’m really glad you covered that because I know a lot of clinicians are familiar with the Japanese research and they are going with 45 milligrams –myself included. I love the rationale. If you know the citation for the study, the recent study you just mentioned, I’d like to get it.
Dr. McCormick: Yeah. I wanted to look that up and I forgot to. I’m almost positive within the last year or two years, something came out that showed 45 milligrams didn’t have – and I’m not sure how many people were in the study. I’m almost positive that it came up that it didn’t show increase in bone density.
Dr. Fitzgerald: Alright! But we can certainly…
Dr. McCormick: I don’t know how many people were in it.
Dr. Fitzgerald: We can definitely look at Vermeer’s work that you just mentioned, saturating osteocalcin at 500 micrograms with K2.
Dr. McCormick: Right.
Dr. Fitzgerald: Alright! So keep going with your protocol.
Dr. McCormick: So we did the D and the K either way. I make sure they’re taking calcium, magnesium. I think people really should try to get a lot of their calcium from their diet. I think if you have a good diet high in vegetables, even if you don’t have dairy, you can get 500, 600 or 700 milligrams of calcium. So then, you should supplement them between 500 and 800 milligrams of calcium, a good form of calcium – calcium malate, chelate, calcium glycinate, something like that.
Just try to stay away from I think calcium carbonate. For younger people, calcium carbonate is okay I think. But as you get older and you get less hydrochloric acid production, you get less ability to utilize that carbonate.
Dr. Fitzgerald: Okay.
Dr. McCormick: Magnesium, as you know, everybody’s deficient in magnesium. Magnesium isn’t just good for bones. It’s good for decreasing inflammation. And what’s the problem with a lot of these people is inflammation. Magnesium helps bring down key factor in other inflammatory molecules. I don’t know, 400 to 500 milligrams of magnesium.
Make sure you have trace minerals. Trace minerals are so important to get. In my products, I put in trace minerals in them. So the minerals are important.
So those are the basics I guess. I think what’s really, really important is that remodeling system. To do that, what I use is alpha lipoic acid and N-acetyl cysteine. Alpha lipoic acid gets in all of the nooks and crannies of your body. It’s both fat-soluble and water-soluble, it gets in all those areas. So, it really helps decrease that inflammation.
I typically use between 300 and 600 milligrams of that. Oftentimes, I see that is the one thing that really helps drop NTx, the alpha lipoic acid.
Dr. Fitzgerald: Lipoic?
Dr. McCormick: Yeah. And then I use Berberine because there’s a fair amount of study that show that Berberine decreases osteoclastic and increases osteoblastic activity. It does both of them, which is really cool because there’s not many things do that. There are not many things that affect both the osteoclasts and the osteoblasts.
Dr. Fitzgerald: How do you dose the Berberine?
Dr. McCormick: I think I normally do 250 to 300 milligrams or something like that. In my product, I do the Berberine HCl. But I think there’s another form of Berberine that’s okay. I use the HCl. I’m looking at my product, OsteoStim right now. I think I use 250 milligrams to 300 milligrams.
Dr. Fitzgerald: Okay. It’s not that much. I mean, that’s a pretty modest Berberine.
Dr. McCormick: That’s true. Yeah.
Dr. Fitzgerald: Okay.
Dr. McCormick: Yeah. For gut issues, you’re going to use a heck lot more, but for Berberine, that’s what I use and it seems to work.
You can obviously increase any of these amounts. On the NAC, I guess I wouldn’t go too much higher than 1500, but I just use 500 or 600 of the NAC. As for alpha lipoic acid, I guess I wouldn’t do more than 600. But I use between 300 and 500 of alpha lipoic acid.
Taurine is really good for stimulating osteoblasts. I use milk-basic protein, which has been shown to improve osteoblastic activity. Green tea, everyone knows that that’s really good for decreasing pro-inflammatory cytokines and decreasing osteoclastic activity.
I used to give people 10 bottles of all these stuff and I thought, “This is crazy!” So that’s why I stock it all in my OsteoStim product. This makes everybody’s life a lot easier.
Dr. Fitzgerald: Yeah.
Dr. McCormick: And if I had one thing to give my patients, it would be my OsteoStim product because that has all the balancing and remodeling process factors. I would have them eat better, I would have them decrease inflammatory issues, fix their gut and I would have them take Osteostim. I would have them do that way before I would have them take calcium and magnesium and everything else.
If they eat a really good diet, I’m hoping they’re going to get the minerals they’re going to want. And hopefully they’re going to get outside and exercise and get some sun. They’re going to get their vitamin K from vegetables. But what they’re not going to get is the whole package as far as remodeling that.
Dr. Fitzgerald: Right, the lipoic acid.
Dr. McCormick: Yeah, all the remodeling…
Dr. Fitzgerald: Yeah.
Dr. McCormick: Yeah.
Dr. Fitzgerald: Any issue with milk-basic protein in sensitive individuals. I imagine you’d just avoid it in those [inaudible 00:40:09].
Dr. McCormick: No. Great question! I don’t know. I always tell people, “I don’t think you’re going to have a problem with it.” It’s not casein, it’s not lactose. It’s more immunoglobulins. I don’t think they’re going to have a problem. So actually more people…
Dr. Fitzgerald: And you haven’t seen it?
Dr. McCormick: Yeah, I haven’t seen it. So I say try it. If you’re really, really, really sensitive to milk, then don’t. But if you don’t have milk sensitivity, try it. If you have a problem, I’ll just give your money back. I don’t think I’ve given anybody’s money back. But like I said, if they are really extremely sensitive to milk, then I would say don’t take it. I don’t think it’s going to be an issue.
Dr. Fitzgerald: Any other nutrients? I want to just move on to some diet pearls.
Dr. McCormick: Boron is really good for stimulating that estrogen and you really want estrogen. You really want estrogen production to be optimal, the adrenal gland, just the adrenal glands. When a person goes through a menopause, who’s going to take up the slack for estrogen? That’s fat cells and the adrenals.
So many of these osteoporotic women just don’t have any fats about them, so I try to beef them up, I make sure they’re eating well. I do things. I have them take fat from the triglyceride, the…
Dr. Fitzgerald: The EPA and DHAs.
Dr. McCormick: No, from coconut oil.
Dr. Fitzgerald: Oh, coconut oil.
Dr. McCormick: Yes.
Dr. Fitzgerald: Okay, the medium chains?
Dr. McCormick: Yeah, the medium chain fats. I think of that as like this rocket fuel for people. I know it’s used for weight loss. But for really thin people, I think it’s good for weight gain. So I have them take that and I just have them eat as much as they can. If we can get in 5 lbs. on a person that’s 100 lbs. and 5”6 inches, I want to do it to get a little bit of meat on them, a little bit of fat on them and then address your adrenals, making sure that they’re not tanked on that.
Dr. Fitzgerald: In protein?
Dr. McCormick: Sixty to seventy grams a day. I do think that’s really important for another reason. So many people have read that protein is bad for us to process. So I have people coming in and saying, “I read that the more protein you eat, the worse your osteoporosis get.” So they weight in at 40 grams of protein or something. They’re not eating and they’re avoiding protein.
Protein is the basis for bone and collagen. So if you don’t have the protein in there, you’re not going to have bones. And the more muscles you have, the more active muscles you have, the more myokines you’re going to produce and myokines stimulate the osteoblasts to form bone. So you need to have good muscle tone and a really healthy protein intake. And that’s not red meat. You don’t want to do really acidic stuff.
Dr. Fitzgerald: Okay.
Dr. McCormick: For my vegetarians, you can get a lot of good proteins from rice.
Dr. Fitzgerald: Okay. Listen, we were coming to the end. What about strontium?
Dr. McCormick: I think strontium has only been shown to improve bone density. I shouldn’t say that. It will improve bone density in pretty much everybody. But does it decrease fracture risk? That’s the major question. And it has really only been shown to decrease fracture risk in 80 year olds.
So to me, to take a 60 year old and put them on strontium, I don’t think we should do it most of the time. There are times when I put people on strontium. I’m not against strontium. I just use it when I think it has the best chance of helping out.
I would much really put a person on a bisphosphonate for one year and really try and make sure that they’re getting the calcium that they need than to allow a person to have a high N-telopeptide, have a 60 or so for a bone resorption marker and put them on strontium and have a false increase in bone density two years later because the strontium molecule is twice as dense as the calcium. So it will look as though we have higher density, but we actually probably have the same density or we may even have less density and we probably have increased risk for fracture.
So you have to be really careful with strontium. Like I said, I’m not against it. I use it sometimes, but I really look at that person and what our options are with that person.
Dr. Fitzgerald: Okay.
Dr. McCormick: Like I said, you have to really realize that that density is going to come back better, but their fracture risk may not be lower.
Dr. Fitzgerald: Right. So what you’re saying is that it hasn’t been – I don’t know that it’s been confirmed that the fracture risk doesn’t change with strontium. It just hasn’t been demonstrated in a younger population that it actually decreases.
Dr. McCormick: Yes, it has not been demonstrated.
Dr. Fitzgerald: Okay.
Dr. McCormick: And the ones that it has been demonstrated with, that’s strontium ranelate. That isn’t legal here in the United States. So the strontium carbonate…
Dr. Fitzgerald: Citrate.
Dr. McCormick: …glycinate. What else? What forms…
Dr. Fitzgerald: Citrate is the most common.
Dr. McCormick: Citrate, yeah, I don’t think there have been any studies that have shown decreased fracture risk with citrate or carbonate.
Dr. Fitzgerald: Okay, alright. Alright, I got it. As far as your bisphosphonates, what are you recommending?
Dr. McCormick: Each generation of bisphosphonates has gotten stronger and stronger and more problems. You have the alendronate and risedronate. They are the two basic ones that came out. For alendronate, that’s Fosamax. For risedronate, that was Actonel. They’re now at 70 milligrams once a week. I think they’re pretty good. Alendronate is a little bit better than risedronate. You take it once a week.
If the person doesn’t have any esophageal issues, then that’s what they should stay on. If they have esophageal issues, then they have to go through an infusion. You can get ibandronate, which is Boniva. And that seems like it causes a lot of problems with people as far as muscle aches and pains, joint aches and pains. So I’d say stay away from Boniva.
Then there’s the year-long infusion of zoledronic acid, Reclast and that is pretty good. I can’t remember exactly, but it’s something like a thousand times more potent than Fosamax. And so you really got to make sure that that’s what you want them on because if they have a bad reaction to it, then they can be pretty miserable for three months.
If a person gets irritated, gets muscle/joint pains from Fosamax or Actonel, alendronate or risedronate, you take them off and they’re fine within three weeks.
Dr. Fitzgerald: Okay.
Dr. McCormick: That’s why I like the less potent ones. You’re not going to get in trouble with osteonecrosis of the jaw or anything like that if you do it a year or so, even two years of these things. It’s when you get to three years or four years or five years with using these drugs. That’s crazy. That can lead to problems.
Okay. Then we have SERMs, the selective estrogen receptor modulators. I think those are totally crazy because they do improve density and they do maybe decrease spine fractures, but they really haven’t been shown to decrease hip fractures and they’re less effective. And hey increase risk of thromboembolisms quite actually at a high rate I think. So why would you use that over bisphosphonate? I’m not sure.
So I don’t recommend SERMs. If you’re going to do that, then just use estrogen, a low dose of estrogen, which definitely helps bone density. I wouldn’t start estrogen on somebody who’s five to seven years past menopause. But if they’re three years to five years past menopause, I think it’s a good choice to do an estrogen with somebody, low dose estrogen, especially if their estrogen level, their estrodiol level is at five micrograms per ml or something like that. If they’re at 15 micrograms per ml, I wouldn’t do an estrogen.
I know I’m going a little faster, but I’m trying to wrap up on the medications.
And then you have the RANKL inhibitor, which is new. It’s called Prolia. I don’t recommend that either because once you’re on it, you have to stay on it. There’s a rebound effect when you get off of it. So if a person gets off of it after a year, their bone density goes back to where it was, if not worse.
So to me, it’s a great drug for the drug companies because once you’re on it, you’re really stuck on it and the drug companies will like that.
Dr. Fitzgerald: Do you…
Dr. McCormick: It’s called Prolia. Alright, go ahead.
Dr. Fitzgerald: And then Forteo? I know you mentioned it.
Dr. McCormick: Forteo is great. There’s a two year box warning on it. You can’t take it after two years because it causes osteosarcoma in rats during the testing phase. But it’s the only thing out there that builds bone.
The only thing is it loses its effectiveness after about 18 months. It’s in daily injections, so I think people should probably just take it for 18 months or so. But two years is typical.
When it comes to personal gain, you get 7% or 8% or 9% of bone density for the first year and only 2% or 3% increase in density on the second year. It really peters out towards the end.
Dr. Fitzgerald: Okay.
Dr. McCormick: Eighteen months is great. And then, you have to back it up with a bisphosphonate because you not only stimulate osteoblastic activity, but you also stimulate osteoclastic activity with Forteo. And those osteoclasts are like a RoundUp hornet’s nest. You have to kill them off to succeed and maintain the benefits from Forteo after use.
Dr. Fitzgerald: So you transition them over to a bisphosphonate and you go for the oral ones if possible. Are there any supportive nutrients that might help them tolerate? Would you use DGL or anything to reduce the potential for esophageal irritation that you’re aware of?
Dr. McCormick: I don’t know that. I think it’s pretty caustic stuff.
Dr. Fitzgerald: Yeah, I know.
Dr. McCormick: I’m not sure you’d be able to.
Dr. Fitzgerald: Okay, alright. I just thought I’d throw it out.
Dr. McCormick: Yeah. And then there is a new one out on the block again. It was a cathepsin K inhibitor. It’s either coming out this year or it is out, I’m not sure.
So, that’s about it. That’s for the drug course. That’s about all we got.
Dr. Fitzgerald: Alright! This has been an amazing podcast, just a really amazing ride. I am certain that folks listening to this will be influenced by your expertise and have some good Monday morning take-homes.
Again Keith, I really appreciate you being here. Your next Iron Man is when?
Dr. McCormick: Well, I just finished one four days ago and then I qualified for the World Championships in Hawaii on October 10th. So I could go there for the [inaudible 00:53:25].
Dr. Fitzgerald: That’s great. Congratulations! And good luck to you.
Dr. McCormick: Thanks, Kara.
Dr. Fitzgerald: You’re welcome.
Dr. R. Keith McCormick is a Board Certified Chiropractor in the states of Massachusetts, Colorado, and California. He has been in clinical practice since 1982. In addition to a general practice, Dr. McCormick is a Board Certified Sports Chiropractic Physician and a member of the University of Massachusetts Sports Medicine Department. Dr. McCormick specializes in the nutritional management of patients with bone fragility and is the author of The Whole Body Approach to Osteoporosis. In 2011 he founded Osteo Naturals, LLC, a company dedicated to providing information and quality nutrition products to individuals with bone loss. His professional memberships include the American Society for Bone and Mineral Research, the International Bone and Mineral Society, and the American Chiropractic Association. Dr. McCormick earned his bachelor’s degree in Human Biology at Stanford University and his doctorate at the National College of Chiropractic. In addition to his chiropractic practice, Dr. McCormick is an avid athlete competing in Ironman triathlons and was a member of the 1976 U.S. Olympic Team in the sport of Modern Pentathlon.