Mike Mutzel: Let’s put in to presentation mode, so we can kind of kick it off here and do a quick introduction. This is Mike Mutzel and Bettina Newman from Xymogen. Thanks for joining us. We’re going to get started here just very shortly, and we’re very excited to have Dr. Steve Parcell with us as we’re just talking here. I’ve known Dr. Parcell for quite some time actually. I saw him as a patient gets some IV therapy Dr. Steve back in the day, which is really nice.
Dr. Steve Parcell: I just forgot about that until now.
Mike Mutzel: That was cool. I looked bolder and I got a heavy metal test back from a practitioner friend of mine, and my arse, neck and cadmium levels roughed off the charts, and so we did some really great therapy at the clinic there, which was really awesome. So, thank you for that, and thank you for joining us. Dr. Steve is a graduate of Bastyr University in Kenmore, Washington, and has started NatureMed Clinic in Boulder, Colorado – a really successful clinic with multiple practitioners. You have a picture on the next slide there, Dr. Steve, right?
Dr. Steve Parcell: I do.
Mike Mutzel: Awesome. So, you have a rocking clinic, you have your book out. As we kick it off here, let’s talk about the evolution of how you got into really specializing in preventative cardiology and in advanced laboratory testing, and what really compelled you to write the book and tell us about that process a little bit.
Dr. Steve Parcell: That’s a great question, Mike. Thanks. The short version is that I had a heart scanned when I was doing my residency after graduation, and just as a perk; it was free. Back then, it was a $475 test. I was at the 91st percentile for my age, meaning only 9% of people my age in the rest of the world have a wall plaque than I did in my coronary artery. I kind of was shocked, “What the heck is this?” I kind of thought about it for a while and started becoming more interested checking more patients, started seeing reversals, and then I kind of blew it off a little bit because I have little kids and babies and everything, and then I got another scan and it showed that I’m going up like 38% in that period of time.
What just happened…. Here we go.
Mike Mutzell: If you’re on a Mac, this one happens.
Dr. Steve Parcell: Sorry. Here we go.
Mike Mutzel: Perfect.
Dr. Steve Parcell: So anyway, my score has gone up dramatically. At the same time, I have been getting arrhythmias, have visited my cardiologist and finally taking my cholesterol seriously, had seen a dramatic shift in my calcium score. In other words, plaque was decreased in one year by about 34%. I was really impressed. I was super excited because at that time the plaque’s just through; you didn’t reverse it. There was no discussion about it. I was almost very excited about that, so one of the things I tried to do is not just stabilize it, but actually get negative numbers on the page. So, one thing went to another, and then I wrote the book, and so on and so forth. There was a family tragedy that was somewhat related to this. An age 12, my dad did die of a heart attack, a massive heart attack. It’s only kind of now that I am bringing that out. It’s something that motivates me more because at that time, it was really just shocking.
Mike Mutzel: Sure. And so on the next slide you have a picture of your book and everything. I know you’re going to dive into the details, but if you can give everyone kind of an elevator speech – what’s the premise of the book and how can it help their patients out there on their health?
Dr. Steve Parcell: The goal of this book – it’s almost like a text book that’s written for someone with a college education. If a doctor reads it, they won’t be bored. It’s only referenced to mostly medical language, but I also, if it’s too technical, I explain it. The editors – I had four editors – and they drove me crazy. So, it’s kind of a cross between a textbook and a lay person’s book, which is just how I had to do it. It’s actually great for an ND to read or anybody or any kind of health practitioner. It’s not going to be boring. It’s loaded with data. Someone who’s interested to the lay person would buy it. So, I try to strike this balance. This next book will definitely be easier to read I think.
Mike Mutzel: Sure. That’s great.
Dr. Steve Parcell: The premise is kind of dig in to all the details and provide all the references for everything that has to do with detecting atherosclerosis both through imaging and blood biomarkers, and then interventions and the evidence behind these interventions, including statins by the way.
Mike Mutzel: Awesome.
Dr. Steve Parcell: Here’s our agenda if you want me to…
Mike Mutzel: Sure. Thanks for the introduction.
Dr. Steve Parcell: Yeah. Just you know, I live in Boulder, I’ve got two kids, I’m married, and I run this clinic with my wife. We have an MD there and we have another ND, so there are four practitioners. We see cancer; we see a lot of women’s health, and cardiology, and men’s health. So, I’m going to try to get through this in a reasonable amount of time and leave enough time for questions. I’ll quickly go through why the standard of care is inadequate. I will not discuss in detail advanced lipidology, but I will go through it because I could spend an hour and a half just on that. I will discuss the emerging biomarkers that are inexpensive and easy to run for the average clinician that’s so a lot of bang for the buck. I will discuss pathophysiology of plaque; it’s extremely important. You actually know what you’re talking about when you’re talking with patients, and then the Xymogen formulas that I’d like to use.
So, learning objectives. I will discuss the screening and how to read some of the advanced, and why they’re done. I won’t go into detail with the data, and then I will definitely go through the lipid disorders.
There is the disclaimer from Xymogen. I’m not a Xymogen employee, but I am a customer. If I do the job, maybe I’ll get compensation.
Let’s first talk about biomarkers. I want to just practice this with the fact that this whole slide presentation is taken from the thing I did in CNM, which was a CME event. They had me come over there and do a webinar on site. That was largely on biomarkers. We just have to understand that biomarker can be anything – it can be blood; it can be tissue; it can be a recording; it can be something on imaging. A lot of us think that biomarkers are something we find on blood work, but it can be an ultrasound or a CT scan.
Why do we care about this? A lot of us get out of school and we think, “Oh well, we’ve got this cardiovascular thing figured out. What’s the big deal? We have it figured out.” Well, we don’t. It’s still the No. 1 killer. The reason it’s a big deal is preventive cardiology is not taught in naturopathic programs. It’s not taught in regular medical school, osteopathic school, chiropractic school, acupuncture school, and people who are listening to this webinar are prevention-minded practitioners, so they should cheer it’s the No. 1 cause of death. And here’s the thing – it’s actually preventable. That’s the thing; that’s the big thing. Cancer is No. 3; it’s pretty hard to prevent that. I’m sorry – cancer’s No. 2. Cancers are harder to prevent. There are way more genetics there. The other issue is it’s asymptomatic. The patients are not going to commend, usually with complaints, you find it fairly advanced without any symptoms. So, people who are prevention-minded should be all over this; it’s really not, by enlarge. We battle with cholesterol, but we’re really not digging in and actually preventing heart attacks as well as we could be.
Just some statistics – just to prove that it’s a big deal. 80 million adults and the cost is very high – 100 – it’s probably way more than $100 billion at this point. Average of one death in every 40 seconds. So, heart attacks happen all the time especially every after each 40 – don’t do well is stratify risk. We may run a lipid panel, look at someone’s BMI or their body fat percentage, their blood pressure – a lot more that can be done. A lot more can be done especially for those with cholesterol in intermediate ranges. We all know that someone who’s 22 years old with great cholesterol and their blood pressure is not a big deal, but what about someone who’s 38 with marginal cholesterol and marginal blood pressure. Where do they stand? We all know that someone who’s 88 with malignant hypertension and who smokes is at high risk, that the issue is the people in the intermediate risk. That’s the big issue, and these are most of our patients by the way. These people, “Well, you know – my dad – he did have a heart attack at age 68,” and this patient has a slightly elevated cholesterol. These are the people who could be at great risk; they won’t have symptoms.
We’ll just go through lipids here, just highlighting the most important points – particle size and number, the MPO issue with dysfunctional HDL, apolipoproteins (which are actually the particles – the cholesterol particles and cells that are more important than the actual cholesterol number), and triglycerides and oxidation.
So, we are not doing a good enough job, and that’s based on just the statistic we have. All of us who are – anyone who’s a frontline practitioner is in the perfect position to do the most work. Cardiologists are very busy doing interventions, and we are in a perfect position to do quite a bit.
So, probably half of the audience is familiar with some of these. This is just a nice pictorial view of what I talk about with patients all the time. If you’ve got a ball of cholesterol and it can be half-full, it can be really full, it can be partially full, and it’s just a ball and there’s a certain size – it can be big, medium, or small. You can have a lot of them; you can have a few of them. What this is showing here is the LDL level on the left is 125 and on the right is 125, but the patient on the right is at higher risk because they have more particles. Particle number is more important than the actual cholesterol number, and particle size after that is also important. In other way of saying this – this is two patients with an LDL level of 125; one could be at much lower risk than the other. Another way to show it here – LDL is 125 in both sides – big particles and small particles. So with that, we’ll get an A repeat pattern and some of the more sophisticated tests to stratify.
Large HDL is important, too, just like small LDL. Little, small HDLs aren’t as protective as large ones. The reason the large ones are good doesn’t mean they’re sucking up more cholesterol. So, it’s not the large ones are good in themselves. The large HDLs are a marker for excellent reverse cholesterol. HDL actually has a lot of functions that are very exciting, and that’s one of the reasons why the pharmaceutical industry’s been trying to develop drugs that mimic HDL. It’s not been successful yet, but vasodilation and antithrombotic antioxidant. We know all this, but we haven’t figured out a drug yet. The booster of this is nice.
MESA study – Basically, the only reason I put this slide up here is they looked at particle size and number, and what we found here is that particle number was actually more important than particle size. So, that’s actually right here on the conclusion. We talked a lot about particle size. In actuality, the latest data shows that particle number is more important than particle size. So, what I say in the next slide here is that… (Well, this isn’t after this one.) So, particle number predicts plaque more than size. See on here. And this is done with a Carotid IMT, so it’s basically how much plaque is in your carotid artery, and the more particles you have, the more plaque. That’s what this is saying here. So, particle number going up on the right here and the IMT on the left axis.
Still though, there was data and there was wrangling with this. There was data about the small particles, and this is just a picture I like to show patients. I’m not convinced. I do agree that particle numbers are important; that’s what the data shows, but I still think particle size may be important and data’s still forthcoming because the small particles can get through the endothelial layer and into the intima, which is shown here on the right. So, the large particles like tennis balls or the tennis court net – they can’t get through, but the small particles are like golf balls – they can go right through the tennis court. The tennis net can get into the endothelium – half the endothelium. I like to say additional work for practitioners who are listening like adding cheese to a sandwich. Every patient understands that. You’re adding fatty cholesterol in white blood cells and red blood cells and connected tissue in between the layers, in between the endothelium and the media.
Just a nice slide – just showing the different particle size and what’s going to happen happens here in the different… So, down here are these artery cleaners. HDL2b is actually the most effective at reverse-cholesterol transport. And what I like about the slide is that it has lipoproteins in little A’s, which you can see right here with little corkscrew tail off it, which is another unique type of cholesterol.
I have this slide in my office right above my computer that I show patients all the time. It helps them understand what I’m talking about. Same cholesterol, low or high risk. So, this is important.
If you’re in an area where maybe people don’t have a lot of insurance, you can do something called “Apolipoprotein B” – very inexpensive. It is basically particle number. It’s like $12 or something. It’s particle number, and it doesn’t have to be a fasting test because there are also patients whose fasting work is an issue. They maybe have to drive a long time before they get to the lab. You can do this test anytime of the day and get an accurate particle number for just a couple of bucks. It’s a big deal to lipid conferences because they’re always dealing with cost issues there.
This is the conclusion that Canada has been talking about a lot. The latest consensus is that this apoB along with the regular lipid panel is far superior and a very good idea to do, so get your particle number.
Just to repeat what I said.
This is the key you can look at. It’s a new range. You’re like, “What is this apoB thing?” Here is the table of the ranges and what you’ll see is that it’s similar to LDL. It’s just “take ten off.” If you want LDL with a hundred or less, apoB is 90 or less, and you just remember that “take ten off.” If you want to be 70, apoB needs to be 60.
Mike Mutzel: Dr. Steve, really quick. I know you probably will talk about it in the end. Because apoB is really inexpensive and like you said, you don’t need it to be fasting – I mean, keeping healthcare cost and patient cost in mind – are you using apoB as like a prescreen if it comes back high, then you dig deeper with the expended panel?
Dr. Steve Parcell: Yes. I was just about to say that. Yes. That’s actually great. In fact, I say that in a couple of slides. Get the particle number first, get it down. So, you’ll do one of these things and the particle number won’t be ridiculous, like 140 or something. You’ve got to get that down. Forget about the sizes until later, especially if the patient’s paying cash. Get it down and then deal with the size. I don’t actually do that because currently, I’m using a lab that is riding off whatever insurance doesn’t cover so it’s free. I’m using a very sophisticated test. It’s free for all my insurance patients. So, I don’t do a lot of apoB, but I do especially free Obama care with cash patients.
Mike Mutzel: Sure.
Dr. Steve Parcell: This is an LDL particle, showing that the apoB is just a protein on the particle. They’re just identified with that tag.
Here we go. First, adjust the particle number down especially if LDL’s over 130, then you can do the lipoprotein subclasses. Most of these tests are $50 or so. And then more data is coming; they’re still kind of figuring this out.
Now, there are a lot of biomarkers here. I’m not going to go into all these. I’ll go into the juicier ones. These are considered noble. They’re called noble biomarkers, which are kind of – they’re not so noble anymore. Medicine, as we know, evolves very slowly, and these are “newer” less established. These are truly are newer and less established still. Even CoQ10 serum, which is actually – we can run that easier now in all the labs in the U.S. Cytokines are – I may present on something like that; cytokines are the new big thing.
MPO – we’ll talk about because it’s available now for a variety of different labs. Essentially, it’s the thing in white blood cells that generates the bleach-like substance that kills bacteria, and some people just have too much of it, and so what they get is they get these white blood cells and their plaques. They’re going crazy and causing all this oxidative stress. So, it’s great to have MPO to kill bacteria. It’s not great to have too much MPO in your white blood cells that are getting in your plaque. It basically accelerates the apostolic process by 10 fold. It contributes to plaque, causes endothelial dysfunction, puts you to high risk, and the other thing it does, it makes your HDL not work.
This is another nice test – inexpensive urine test. It’s the gold standard for oxidative stress markers in the urine. F2 – we just call it “F2.” Can I mention lab names, Mike?
Mike Mutzel: Yes. I was going to mention that earlier because I could sense by your voice. Go for it.
Dr. Steve Parcell: Cleveland HeartLab is the only one that does this for like 10 bucks or something or less. It’s a random urine. It’s an awesome test. You can do it, and then you can do it again. You can put people on stuff and then check it again. That data on it is fantastic. The papers are gone forever. So, you can intervene with the diet and you can do another F2. It does a lot of bad things; it’s a renal vasoconstrictor, good marker of oxidative stress. And you get to show the patient while you’re doing work. I like things that are inexpensive especially when I’m doing a presentation – things you can definitely crank out with the most minimalist patient.
PLA2 – another one – very solid – extremely solid. It’s more vascular-specific than CRP. I mean, high sensitivity or regular – they’re the same. It’s produced by macrophages and it’s found within atherosclerotic lesions, almost exclusively the liver can make it. That’s just one caveat. Someone live with high-liver enzymes with liver disease can have an elevated PLA2, but that’s the only other time you’ll see it. So if you see a patient with high PLA2 and you’re kind of unsure to figure out on what to do with their cholesterol – well, you need to do more. Conversely, if someone has maybe moderately elevated LDL, even as high as 140 and their PLA2 is normal – well, you know they have some kind of genetic protection against active plaque formation. You pretty much can prove this if you do a heart scan and someone would say you have someone with an elevated LDL, your PLA2 is normal. If you’re still not comfortable, send them for a heart scan, and it’s usually normal; they’re usually not big-plaque holders. I love this test. It also goes up and down with intervention, so we lower cholesterol and their PLA2 comes down because there’s less plaque formation. Great data and cheap. You can get it anywhere – Quest, LabCorp, Cleveland Berkeley – anybody can do it. I love this. I have this in my office to watch it with my patients. The thick fibrous cap on a stable plaque does not express PLA2 because it’s not leaky, so it’s a little bit like PSA and a prostate – an inflamed prostate that makes up the PSA, where you get a rupture-prone plaque. With the same ball, the PLA2 comes out. So, this is just one of the best tests. I think it’s even better than CRP – super awesome test. Anyone – everybody should get it – everyone over the age of 40, especially people with higher cholesterol.
CRP is not so noble anymore. It’s good. I like it because I’ve caught cancers; I’ve caught abscesses. I definitely want to run it because people that have these inflammatory conditions they’re not really aware of them, and when they do this thing, it would really pop up. And when you have the CRP with the PLA2, you know that you’ve got a double problem. Conversely, you can have a low PLA2 with a high CRP, and you start asking the patient one more question about the inflammatory process and things like that. Also, it relates to adipose tissue, and it’s another big thing. So, you know if you have someone with diabetes or metabolic syndrome and overweight issue, hsCRP is always a choice. It’s nice and it’s cheap test to have, and there’s lot of data on it. You know I like this last thing – In the Harvard Women’s Health Study, results of the CRP were more accurate than cholesterol levels in predicting heart problems – probably because they were overweight.
Leptin – let’s skip. It’s bad, but it’s extensive. It’s a tricky one.
Apolipoprotein E is nice to do. This is available through a number of different labs. It essentially indicates cholesterol, metabolism defects, and then when you get to a poor back, you can research. There are different diets and different things to do depending on it. The biggest thing here is the E. If you’re ApoE4, fish oil can actually make your LDL smaller, and increase your LDL. So if you actually give someone fish oil (I don’t know if anyone ever has this happen. It sure happened to me.), you check them six or eight weeks later, their cholesterol is worse. Here is why. Fish oil actually makes your LDL go up, and you get this charge – some things like this. So, alcohol is bad if you’re 4. Some of these things just really comes down to fat.
Like this test – it’s a hormone made by the heart when the heart – when you’re stressed out from too much exercise, not enough blood or not enough oxygen, or too much mechanical load and stretch. It’s traditionally a heart failure marker, but it’s also excellent for monitoring your patient – all your patient over 40 (definitely, it’s not 50). If this hormone is really good, it means that you don’t know they have plaque – they have excellent blood flow and they’re not overdoing it. It’s a great marker – excellent marker – and you can track it.
These – most of you guys know about.
I’m not going to talk about this because you know why? In three years, I’ve never seen a positive one, but it’s cool.
Uric acid – I love. A couple of bucks. We all know uric acid can leak out, but some of us may not remember that it irritates the kidney and also irritates the endothelium, and is related to cardiovascular disease, and a pro-inflammatory state, as well as hypertension. It irritates the kidney to the point where it can actually give you hypertension
This is another good one – GGT. It’s very inexpensive – not included by a lot of labs as part of the liver panel. We usually learn about it as a way of checking alcohol consumption, but it’s also – basically, the higher the GGT, the more glutathione depletion the body is experiencing. So, for a couple of bucks, you can check it, and someone might need more NAC or glutathione on board. Well, you might catch them if they’re actually drinking a lot. But it’s also directly involved with cardiovascular disease, atherosclerosis, as well as risk of cardiac death. There we go.
Vitamin D – I think most people are aware that it’s related to calcification as well as hypertension. You could spend your whole life studying vitamin D. It’s extremely important to check. I think most of us are up to speed on that.
Blood viscosity – I hope to discuss briefly. Essentially, if your blood has defect (this is how I explain it to patients), it’s extra hard for the heart to push around and it causes frictional damage to the walls of the vessels – makes sense, right? Blood viscosity – thickness of the blood – whether it be for red blood cells or fibrinogen or other cellular components. The thicker it is, the more damage it does to your vessels, and the harder it is to push around, the more damage, and the harder the work for the heart. It’s associated mostly with hematocrit and red blood cells. It can be done incidentally through regular labs at a very inexpensive price. Even Quest does it for… The last time I looked at it I was shocked – I think it’s $20 something. Now, I don’t do a lot of it, but in some more difficult patients where they’re still progressing with their plaque and I can’t figure out what’s wrong, I sometimes do it. It’s more significant for men, maybe why men get atherosclerosis before women. I think it’s definitely part of it. They have a higher red blood cell count. Super interesting stuff to study.
So, testosterone’s being used lately. Some studies say that it’s protective, and the higher your levels, the more protective. Others say, “No.” And I think we’re still looking at that. I can tell you from personal experience – with my patients, I’ve never seen anyone on testosterone replacement who’s had cardiovascular disease, who’s had bad cholesterol, who I have been monitoring with Carotid IMT, and heart scans do badly – not one person – so I do not think we should be worried. I just have never seen it. However, the caveat there is if you’re hematocrit is high because you’re on testosterone and your blood pressure is high, which is a side effect, and you’re not really dealing with some of the other issues, then it could be a problem. So if you’re going to do testosterone replacement therapy on patients, you’ve got to check on for their estrogen levels, and their hematocrit, and you’ve got to check their blood pressure. But it does a bunch of good things, too. There are receptors all over the body especially in the vasculature of the heart. Here are the things here. It can elevate your blood viscosity, increase your blood pressure, and I’ve never seen it, but it’s in the literature that it can lower HDL. And then just a couple of research – I’m just throwing these out there showing that I’m not just making this up.
So, what are you going to do with low testosterone as a risk factor, naturally high testosterone protects you – I mean, I think that what you’ve got to do is you’ve got to monitor the patient correctly if you know what you’re doing. We know that estrogen is bad for men. A lot of patients just keep putting on tea and the doctor never checks their estrogen. If they’re overweight and they’re not active, they can make a ton of estrogen out of testosterone that bad. So, this is really important. Stress test – they’re great if you want to go get surgery – they’re great if you have a doctor either who’s deciding whether to send you for an angiogram or not, but you can still pass the test and still have plaque and have a heart attack the next day. The fact George Bush Jr. and Tim Russert had both stress tests relatively recent to their cardiovascular events because plaque ruptures cause the heart attack. So, you can get oxygen like this one second from the right; that is a plaque rupture waiting to happen, and you can pass the stress test. Stress test – all that it means when a patient says, “Oh, I had a stress test.” Yeah, you’re getting enough blood to your heart right now. It doesn’t mean that one of these things is going to float.
Let’s not get into a whole thing with heart scans.
All I’ll say about calcium scoring is that it’s a fantastic thing to use to track your patients. The data is endless. They’re extremely accurate. They do get some radiation, but if you’re dealing with a patient who’s not sure what their risk is – they’re 58 years old and their dad had a heart attack, they have no symptoms and you just don’t know what to do – do a heart scan. If they have zero plaque, that’s fantastic; they get an A+. If they have plaque, you better watch it; you better track it. I do like this. I won’t talk about this. Just look at it later. The analogy is interesting how mammograms are done all the time covered by insurance, but heart attacks kill more women and they’re not covered by insurance.
Stable plaque doesn’t rupture. In other words, if someone – this is very important if their calcium score based on the heart scan is only up to less than 15% in one year, and I actually use 10%. That’s stable plaque. It’s hard to explain that to a patient. “What? That’s more than my credit card.” But it does mean that if you don’t treat a patient, it could be like a 150% a year just exponential growth of plaque, and we see that start to make sense when you start seeing it. So, I still like 15% or less. Most of my patients – it’s interesting. I see 7% and 9% growth per year and that’s been in the last 10 years. It was reasonable treatment, just reasonable naturopathic stuff – lipid control and blood pressure control. Not even chelation; I mean, if I add chelation to it, it’s really, really is good. So, I guess you can reverse plaque; that’s true. Don’t believe what they say.
This gets into too much path of physiology. That’ll wait for another time.
Arteries get stiff – a device is used to measure that.
This is interesting. The IMT is a great test. There’s no radiation. You can do it. You can buy a machine and rent a machine. You can lease a machine. You can send someone for one. It takes 10 minutes to put some ultrasound gel on the probe. The company trains you. I do this in my office. You can measure early atherosclerosis, asymptomatic atherosclerosis in one of the larger arteries of the body. This is a brilliant test. It’s less expensive than a heart scan. You can get so much information with this. The data’s good on it. It’s considered like an A1 test by the American Heart Association.
What’s we’re looking at is the distance between the intima and the media where the plaque builds up. Basically, the thicker it is, the more plaque you’ve got.
This is an important thing here. This is another reason why you can pass a stress test and have a heart attack the next day. What arteries do first is they remodel outward. The inner diameter stays the same most of the time, and the outer diameter remodels first. So, you can have a massive amount of plaque with no blood flow limitation. And this is the most common cause of heart attacks. It’s almost criminal that were not identified. This treadmill test is some kind of marker for heart health. It’s ridiculous. You better be doing an angiogram to see something, better yet a heart scan – way better. The heart scan’s going to pick up this plaque because after about two years old, there is going to be calcification.
This is a slide that is showing all the different types of lesions that an angiogram can’t even miss, because again, an angiogram’s looking for narrowing of the lumen. Most of the patients are asymptomatic.
What we’re dealing here is the intima and media. The intima right here – you can see it. The media – the plaque builds up between the intima and the media. And that is what the ultrasound machine checks for. That’s where it builds up.
And then consensus statements are abundant. It’s a great test. It’s just under-utilized. I just put this up here to show you I’m not making all this stuff up. So, the consensus on this thing was, “Ultrasonic detection of the carotid plaque and CIMT measurements can be useful for refining CVD risk assessment in some asymptomatic patients. This noninvasive approach can detect subclinical vascular disease and help identify patients at increased risk of CVD.” It’s perfect for typical patients mostly. I’ve seen amazing things, but it really has changed treatment a lot. Very important, though – you need a good new machine and you need to be properly trained. The new machines are automated so it takes the operator kind of out of the equation. And more and more on it.
That’s what I see when I look at one. We won’t get into that. I was showing with…
Here’s the internal and external carotid. And what they do and why they’re the most common cause of stroke.
If you have someone with bad carotids, you better get a heart scan, too, to make sure that you don’t have it there. A lot of patients ask, “If I have plaque in my heart, do I have it in my carotids?” And the answer is “Not always.” But the reverse is usually through more, so if your carotids are bad, you almost always have something going on in your coronary arteries, but sometimes, the carotids are spared. So, you really need to check both if you have a shot there.
We all know why it’s bad to have carotid stenosis. As you can track it, it’s bad that way. Once you get over about 1 millimeter, you’re getting into trouble.
Alright. We’ve been discussing cardiovascular disease in our scientific review. We will now turn our attention to generic nutrition. So, what do you do? Niacin has been proposed as an excellent first-line intervention. Vitamin B3 is best used to sustain release. You can do diet my style and run at it, but it just depends on the patient and what’s going on. If they’re loaded with plaque, it’s not really worth it; you’re wasting around too much. There are some patients who want to see what diet style they’ll do first. You can do it all. You’ve got to be careful with the diabetics. The perfect patient for niacin is a patient with low HDL, high triglycerides, and small dense LDLs. So, it gives you three things: increases your particle size, lowers LDLs similar to a statin, and it really cranks down the triglycerides. But you have to know what you’re doing. Interestingly, too – the niacin changes on HDL logarithmic. What this slide is saying here is you get bigger increases in HDL than LDL. In other way of saying – if you have a patient who has an LDL problem, don’t expect like massive or impressive results. But it is one of the best things for the lipoprotein A. It’s super great as a synergistic treatment with other thing, and occasionally on this. But I see practitioners sometimes only relying on niacin. You may not get the results you want and you can get elevated liver enzymes, elevated glucose, homocysteine, your gas, and lots of flushing and side effects, and the patient will eventually stop using it and not come back (if you wonder why). And so I wrote here, “Why?” Why does niacin decrease lipoprotein A by about 20%? Well, because lipoprotein A is a type of LDL. So whenever you lower LDL, you get rid of lipoprotein. How does it work? It inhibits the peripheral mobilization of free fatty acids, which decreases the substrate available for hepatic synthesis of triglycerides and very low-density lipoprotein. This in turn reduces hepatic conversion of VLDL particles to LDL particle. So, you’ll have less conversion to LDL and you have decreased triglyceride synthesis because it inhibits this enzyme – diacylglycerol acyltransferase 2. You want to titrate it for 500 every two weeks. There’s no reason to rush it. 500 for two weeks, then go to 1,000. Do it before bed because you get the flushing while you’re sleeping. Check the liver enzymes before and after just to make sure that you are improving the patient that this was what was then, this is what's now. You also want to make sure that they don’t have elevated liver enzymes before they start. And then they’re usually fine when you do it once or twice a year. The glucose can be elevated. It can go up, and so you also need to check it. Homocysteine can also go up so do a baseline and again, after a stable dose is achieved. You can give it to diabetics; you just got to make sure you’re handling everything.
This is very classic. Oh, boy… You know you’ve got to tell every single patient about the flushing. I even had people go to the ER to urgent care. It’s not dangerous. They just need to know about it. If it’s really bothersome, they can take even baby aspirin or normal aspirin. They can ramp up slowly. They can take less. They can eat it with more food. But some people will not be able to handle it, so you need to try something else. Don’t feel that you’re not doing something right. Women, in particular – postmenopausal times – cannot even handle 500 mg. They never get used to it, and it makes them crazy. Be careful with gout patients. You can give it to them, but make sure you’re monitoring their uric acid. And obviously, you can handle homocysteine – you can give Methyl Protect.
So, niacin’s been in the news. What I’m saying here is… When you add a niacin to some statins, obviously you get better lipids, but then one exciting study that I like is that they saw an actual reversal in plaque when they had it.
This is an important study – ARBITER study – showing that yes, it worked – in the statin and in the placebo group. The IMT in the carotid increased. When they added the niacin, they saw the decrease in plaque in the carotid. By the way, the CIMT test is the gold standard for evaluating lipid medications. So, when you’re going to prove you’re in statin or anything of that, they use CIMT test to actually demonstrate that it does anything. They don’t use heart scans; they use the CIMT. It’s what they use, so I get to prove.
Now, unfortunately, niacin’s being slammed in the literature lately showing that it doesn’t do the work we thought. I just don’t agree. I just have to tell you. Clinically, what I’ve seen – this is not true. Let’s just keep waiting and look, and waiting and watching. I just don’t see it. What I see is when you add niacin, you get better lipids and you get better plaque progression.
Red yeast rice lowers LDL mostly, raises HDL slightly, and may lower triglycerides modestly. Just like a statin is a statin; it’s just a natural one. It contains menacolins. It’s extremely important to stick with the good quality brand. The strength differs extremely wildly between brands. The last thing you ever want to do is send someone out to the health food store or wherever just to get one or unwind. It’s absolutely not acceptable at all. If there’s anything they should be getting, they should be from you, it’s definitely a red yeast rice. I’m just stringent about that, especially if you’re monitoring someone’s cholesterol, you can’t have them taking all these different brands. That’s ridiculous.
Brands – this is actually from that company that does independent passé – found that the cholesterol-lowing compounds there is as much as 10-fold. It best should come as no surprise. The citrinin is toxic to the kidney; it’s a mycotoxin. The Xymogen product is citrinin-free. I’m also stringent about that. I tell every patient about that. It’s pretty toxic stuff, and it’s been found in a lot of over the counters. It’s been found in cereals. It’s kind of like an aspergillus – it’s a mold that grows in cereals.
So, there is data to suggest that red yeast rice is better tolerated the synthetic statins, and it clearly will modulate lipids. It still depletes CoQ10. As far as the Xymogen product, which I think is 600 or 900 mg (I think it’s 600) – two to four days usually is the zone you need to be in. Some patients will need six or even more unfortunately if they have familial hypercholesterolemia. If they do have that, sometimes a lot has a dose of statin too, just because taking eight red yeast rice a day is won’t be as much. So, that’s another thing you can do. It’s really important. You can get someone generic Simvastatin or Lipitor like 10 mg, and then give them two to four with red yeast rice on top of it. So, that kind of you’re finding a compromise and you’re getting the lipid lowering that you need. You can do it all with red yeast rice. What happens to patients is they’re not compliant all the time; they just won’t take that much for that that long. It works very nice. When they feel bad, they don’t want to come back to you and say they couldn’t continue with it.
This is a nice study in the Annals of Internal Medicine concluding that the red yeast rice was better tolerated. It didn’t increase CPK levels or pain levels in patients, and worked in patients who are already statin-intolerant. So, hello? The cardiologists still don’t know this and actually, I can’t blame them for not knowing this even though they wanted to know about this because they don’t have access to a good-quality red yeast rice. People – who knows what they’re getting? But if you have it in your office and you know it works, that would different. This is actually funded by the Commonwealth of Pennsylvania. That was great.
Nattokinase is something I also like because I check fibrinogen levels and I also check blood viscosity in high-blood patients and hypertension. It’s anticlotting enzyme. It does decrease fibrinogen factor VII and factor VIII, and that’s been proven in human studies. It has four times the fibrinolytic activity of plasmin. It will and can lower blood pressure, and it has been shown to lower blood viscosity in humans. It does not change INR. Despite what some people have heard – I did some research on this recently on blogs and places like that on the web –there are doctors are saying it’s a farce and you can’t absorb it. I just prefer the human studies that actually showed that it works. When you have a human study that shows that it lowers fibrinogen – well, how could that be possible if you couldn’t absorb it? So, it actually escapes the action of digestive enzymes and is absorbed from the small intestines. I have this couple of studies here – Nutrition Research 2009 – showing that it does this. And then again in Hypertension Research 2008 on the blood pressure, and this is a randomized control. The reason I’m doing this is it’s lowering blood viscosity. When you have thinner blood – it’s kind of like summer oil versus winter oil. When you’re running less viscous blood, the pressure in the system is lower just by default.
We have completed our scientific review of various aspects of cardiovascular disease. We will now turn attention to specific dietary supplements. So, these are just the Xymogen versions. This is the slow-release niacin. I like to supplement this a lot. I really like that because some patients actually get away with just one of those a day.
Mike Mutzel: If I may just jump here really quick here as we go through this, Dr. Steve. One thing I see a lot of practitioners make a mistake of purchasing a inositol hexanicotinate because it’s marketed even by a professional brand as “time-release niacin.” I’m sure you have comments on that, but it’s really not the same. Any comments for…
Dr. Steve Parcell: Yes, super important. Thanks for bringing that up. I’m embarrassed to say I had it in my office when I first started. It just didn’t work, and then I realized it really doesn’t work. The reason it doesn’t work is there’s less niacin. It’s inositol hexanicotinate. I guess actually what that means is there are six inositol molecules around this one niacin molecule, and the amount in there is just less. It’s like the reason it doesn’t work is because instead of 500 mg, you’re getting like 10. So, I think that stuff shouldn’t be taken. Patients have never-ending questions about because there’s immediate-released niacin, there’s slow- or sustained-release niacin, and then there’s this flush-free stuff – and the whole thing makes everyone crazy. So, just get used to it. Instant release is a bad idea. Slow and sustained are the same thing. The other thing is – the other problem is that the slow-release by default gives you less flushing. It’s kind of like flush-free and then there’s the true flush-free, and the reason why it’s flush-free is because there isn’t much in there.
Any other… let’s do questions.
Mike Mutzel: Yes, let’s do questions. There are quite a few questions here. I’m going to highlight this special. That was a great webinar there, Dr. Steve. I’m going to take over the presenter here really quick. Some of the products that we were just discussing, we have a great special on those so we’ll highlight that. So, some of the questions that came up here –
If homocysteine elevates with niacin therapy, what’s the mechanism? What do you suggest – doing additional MTHFR testing? Any thoughts there?
Dr. Steve Parcell: Good question. I actually never looked into the mechanism because it just does it so frequently. You know what I do is I just give – the thing is it really doesn’t matter about the MTHFR. I mean, it’s nice to do so you can prove to someone that their hormones and I guess that they need to take higher doses of folic acid or the like. But if you got to, you just need to give B12, B6, folic acid and TMG, and it will just come down. I never really deal with it because if you have to, you have to give the… And basically, it will always work. Sometimes, you have to give more. I’ve had a couple of patients where I need to give two or three Methyl Protect to get it down.
Mike Mutzel: Sure. When you referred to really thick blood and everything else, we’re looking at for the diagnostic or the biomarker fibrinogen. Was that right? Blood viscosity?
Dr. Steve Parcell: Yes. Fibrinogen and white blood cell count, but hematocrits are the largest determinant of blood viscosity. There are other ones even just – any cellular components of white blood cells. By enlarge, 90% of the people will see it from their hematocrit, and that’s men – men on testosterone, men living on high altitude. And then secondly will be fibrinogen – high fibrinogen gives elevated blood viscosity.
Mike Mutzel: I’ve seen that very commonly with some practitioner friends or just myself, even where my RBC, hematocrit – all that is running really high. Is that where you’d like to run the Nattokinase and different things or donating blood? What do you typically recommend in that situation?
Dr. Steve Parcell: I have to say donating blood is definitely the better way to go. It treats cause, so you have to take so much nattokinase. Another point, you can get blood for free. And clearly, the data shows – actually, the data really shows – if you have hematocrit anything over 47, it increases blood viscosity and the risk goes up. But 50 is definitely my absolute cut-off. I’m also altitude so I need to get a little more reasonable. But if I see a level of over 47, it’s just kind of a hard thing to talk to about patients. It’s really kind of complex, but they also get it when you say, “You have thick blood.” They get that right away. They kind of make sense. But lot of times they don’t take – I actually have to bug them. I’ll say, “You really need to get blood four times a year,” and I’ll put little ticklers on my computer to remind me to call them. They kind of forget. They don’t really understand. It’s actually hematology. It’s rheology, the whole science of blood flow and full mechanics. It’s hard to get them across the patient.
Mike Mutzel: Sure. What about just like preventative health measure donating blood? I mean, is there some therapeutic value in that?
Dr. Steve Parcell: And patients love this, “Hey, you’ve got blood living,” “Hey, I love this.” They think it’s a riot. It’s funny because I feel like I’m the only one talking about it, but it’s actually normal. Therapeutic blood isn’t a thing that people have to get all the time, but often it’s missed in primary care. I could tell you how many times a guy would come in with hematocrit of like 54 or 55, and the primary care doctor doesn’t say anything. They don’t care. They just could care less. Now, when they get off to 60, they’re going to start. They just don’t say it. It’s actually polycythemia; it’s important to treat, and it damages your vessels. You’re going to age faster; you’re going to have higher blood pressure. So interestingly, too, people will feel better. Your blood flow’s better, and there’s even studies, and this is kind of very interesting for me. So, the whole thing with blood doping and EPO… There are actually studies that above 50, your actual oxygen delivery is less, and it’s because your blood is so thick. It’s fascinating science. Something’s going on there. It clearly puts you in an elevated risk. They’re running these high hematocrits. That’s definitely dangerous.
Mike Mutzel: Wow. Some questions came in on the ApoE-4 genotype and negative response to fish oil potentially. Any comments there?
Dr. Steve Parcell: Yes. It’s clearly on the data. I’ll just tell you – Berkeley HeartLab’s the first to come out with great information online, and lot of them you can just get off for free. Quest just bought Berkeley, and now you have to go to Quest to get that, but you can get all these charts and things. Patients are really impressed. It’s really been great clinically. I’ve had people come in, they’re like, “I don’t know what’s going on. I take fish oil, and this goes up and that goes up. I go on a low-carb diet, and my LDL went up and my triglycerides go up.” When you run these tests, it explains why. Just briefly that the ApoE-4’s – they need a low-carb diet. The 3’s can have more Mediterranean. The 2’s need a low-carb diet. So, it’s about 20% of the population that’s actually forced. It’s not super uncommon; you see it all the time. The other cool thing is, “Oh, you’re homozygous 44.” That’s why you got high cholesterol. These people – these patients are beating themselves over the head with their cholesterol thinking they’re doing something wrong in their lives. It’s just genetic. And then they just kind of feel better about it. “Now, you have to take these things.” These patients – they’re on for like 12 different diets; they’re trying everything in the world, but it’s still high. They’re going crazy and no one can figure out why, and then you just tell them, “Here’s why.” They should look good – I got to say.
Mike Mutzel: Right.
Dr. Steve Parcell: And Berkeley again – they were the first ones to really get out with that, and now it’s available. HDL Labs has it, so you can get it anywhere. Quest has it.
Mike Mutzel: So that’s pretty standard then what you’re saying. Do the high prevalence – 20% – this is something that you’d like to run in pretty much every patient?
Dr. Steve Parcell: Definitely.
Mike Mutzel: Okay.
Dr. Steve Parcell: Yes, probably 90% of the patients.
Mike Mutzel: Great. And that’s on the standard HDL test that you do, right?
Dr. Steve Parcell: Well, the HDL Labs – they have it. Because that’s a super lab – they run everything. But Quest still does it for sure.
Mike Mutzel: Some questions came in here on elevated Lp-PLA2 in individuals that do a lot of high-intense exercise and also have high HDL. Do you have anything along those lines?
Dr. Steve Parcell: No, nothing that comes to my… What a surprise, though. Usually, it’s found in the lesion itself. You shouldn’t see it. That would be odd. If I had an anaphylactic patient who’s high HDL and PLA2, I would be scratching my hood, honestly. Well, what I would do – I’ll scratch my head and then I’ll send him for a heart scan and/or do carotid just to see if they have any plaque. If they don’t have plaque, I’d turn at most and say it’s an aberration because it doesn’t fit. I mean, you shouldn’t see that.
Mike Mutzel: Right. So, there’s really no reason for it to be elevated unless there is some plaque going on?
Dr. Steve Parcell: Yes, there’s should be plaque, and you certainly wouldn’t think that in anaphylactic and high HDL patient. There are these genetic admiralities with HDL. We can have a subtype of HDL that’s really, really small that’s actually can almost – they’re starting to think it’s a pathogenic now. This is kind of new. I think I blogged on it once, but there are some data now that suggests the finally, we’re to the point where not all HDLs is protected. That’s one of those zebra things.
Mike Mutzel: Interesting. What about things like plant sterols and fiber?
Dr. Steve Parcell: Yes, they work, and actually, what’s interesting is they work differently depending on your ApoE genotype. So, fiber tends to work for all of them, and sterols work – I think it’s for the 2’s more than the 4’s. I have to look at the chart again. They actually provide a chart that gives you the treatment options. But I still use the sterols. They are effective, but you have to give a fair amount – 4 to 6 capsules – and some people absorb too much of the sterols and improve their cholesterols. That’s one thing to remember, too, is that some of the cholesterol machines that check it get confused by sterols in the blood and cholesterol, so it can kind of make you a little crazy there, which is one reason why I do like – I love the fact that I can mention labs. I can’t do this the last time. The HD (Health Diagnostics) Lab actually offers a full-sterol panel, which is really cool to do. You can see if they’re hyper absorbers of sterols. Because imagine if you gave plant sterols to someone who’s a hyper-absorber. That’s a nightmare. And this happened to me, actually. It happened in a patient who can’t tolerate anything, and I gave her the sterols and the cholesterol – one of them. I think she just left the practice, and then later or years later, I figured out why.
Mike Mutzel: Wow. That’s wild.
Dr. Steve Parcell: Yeah.
Mike Mutzel: That’s really good to know.
Dr. Steve Parcell: She put machine off, and the machine thinks it’s cholesterol.
Mike Mutzel: Right. Same kind of biochemistry, huh?
Dr. Steve Parcell: Yeah.
Mike Mutzel: Okay, fantastic. That was some great information. Some people want to ask, Dr. Steve, about the access to your slides. What’s your comfort level there? We obviously will send out this video. This has been recorded. We’ll send that out. But what’s your comfort level in the slides? I mean, you obviously have this information in the book. I think if you want more information, just go on Amazon and check out your book.
Dr. Steve Parcell: Yes, really good detail and information with the references. The book is the best because I did present this in CNM. It’s part of the webinar, which is still for sale. I should probably be careful about just popping those out there. I maybe want to check on them because they are still kind of selling the webinar, although I don’t know if they really care. I basically have no problem with it as long as CNM doesn’t mind.
Mike Mutzel: Well, just to avoid any complexity, we won’t go there. I was just looking at the price of your book. It looks like $115 on Amazon, 300+ pages and all kinds of references. So, if you guys want more information here and you can use it in your practice, have it on your desk right there in the clinical setting, I think that it will be a great asset for all of you. So, thanks again Dr. Steve. This was amazing. For all the practitioners on the line, we do have the wholesale discount up to 25% off on some of the formulas that we discussed tonight – the omega-3 fats and Nattokinase, Red Yeast Rice, and Cardio Essential. You can take advantage of that, and hope you all had a great evening. Dr. Parcell, thanks again, and I hope you stay warm there in the cold weather.
Dr. Steve Parcell: Thank you. That’s great.
Mike Mutzel: Okay, talk to you soon.
Dr. Steve Parcell: Bye Mike.