HDL Cholesterol with Dr. Mark Houston: Rational Wellness Podcast 203

Dr. Mark Houston discusses HDL Cholesterol with Dr. Ben Weitz.

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Podcast Highlights

4:28  What are LDL and HDL?  These are apolipoproteins that transport fats through the body and serve many functions, including immunological function. They help protect us against infections and parasites and they are part of our metabolic system for making steroids and vitamin D and sex hormones.  Today, the biggest threats to us are no longer infections, but more from environmental toxins, nutritional imbalances, obesity, and other risk factors that result in chronic diseases like heart disease and diabetes that kill us.  In order to protect us from environmental insults the LDL particle number may become elevated, which is the driving risk for heart disease and myocardial infarction.  LDL is considered the bad cholesterol and HDL is considered the good cholesterol.

7:24  The main job of HDL is to produce Reverse Cholesterol Transport (RCT), also termed Cholesterol Efflux Capacity (CEC), which are the primary functions of HDL that go into the cell and the artery walls and pick up the LDL like a garbage truck and take it back to the liver where it will be excreted with bile. HDL if it is functional can reduce atherosclerotic plaques and reduce rupture and it can improve plaque stability.  There is soft plaque that is composed of a very aggressive core of lipids and smooth muscle cells and inflammatory cells, and it’s surrounded by a sort of a firm top that is very thin. This protective top can rupture, resulting in the contents of the plaque spewing out into the artery and this can cause thrombosis and an acute myocardial infarction.  Such patients may present with an acute MI while doing intense training, such as interval training or a marathon, though they may not have much obstructive disease.  The other type is calcified plaque, which is more stable and less likely to rupture, but this type of plaque tends to become obstructive.  It may not result in any symptoms until you get to 95% stenosis.  Calcified plaques can be picked up by coronary calcium scans or by an exercise echo or by nuclear medicine scans, while soft plaques will often not be seen by such scans or tests. But soft plaques can often be seen on MRI imaging with contrast or by a PET scan or a CT angiogram.

12:36  HDL has a number of positive functions, including RCT, anti-inflammatory, antioxidant, and it reduces vascular immunologic damage in the arteries.  HDL is composed of over 100 different molecules, proteins, lipids, and other components and there are at least 25 different beneficial effects of HDL on atherosclerosis prevention.  We used to think that the HDL level and the HDL size determined the true risk, but the only thing that really gives you the true risk is the functionality of the HDL.

15:37  There are two labs that can measure HDL functionality, including Cleveland Heart Lab, which is owned by Quest Diagnostics, which offers the HDL Function Test.

18:35  There are some who feel that APOA is a better marker for assessing heart disease risk than HDL.  APOA, which is the carrier for HDL, may be a little better marker than HDL, but it still does not correlate as well with cardiovascular disease risk as HDL function does.  One study found that in a male if the HDL is over 50 or 55, and in a female if it is over 75 or 80, most of it is likely to be dysfunctional. 

20:28  Oxidized LDL and Myeloperoxidase (MPO). LDL is not atherogenic (will not cause vascular damage and create arterial plaque) until its oxidized or otherwise modified. MPO is a compound that is made by white blood cells and while it is antibacterial, it is a bad actor.  MPO increases coronary calcium and it can cause high blood pressure, coronary heart disease, atherosclerosis, and even plaque rupture. When you have high levels of oxidative stress and high MPO, it damages the HDL and makes it dysfunctional.

22:15  Dr. Houston has developed a nutraceutical that improves HDL functionality called CardioLux with Metagenics that contains quercetin, pomegranate, lycopene, and vitamin E.  These components reduce oxidative stress and inflammation, making the HDL more functional.

25:31  A lot of HDL functionality is related to the proteins in HDL. Essentially the reason why we have LDL and HDL particles is that fats don’t move readily through the bloodstream, which is water soluble, so they are surrounded with various proteins that coat the lipids.  One of the important proteins in HDL is PON1, peroxidase, which is very important for HDL function.  These nutritional compounds (quercetin, pomegranate, lycopene) protect and raise PON1 levels.

27:30  CoQ10 is a very important nutrient for heart health, but there is an issue with getting CoQ10 not only into the cell but into the mitochondria. There is a new form of CoQ10 that’s a thousand times more effective than regular CoQ10 at penetrating the mitochondrial membrane, called MitoQ.  Dr. Houston has a series of 10 patients who were on the cardiac transplant list who had end stage coronary heart disease. They couldn’t put stents in and they couldn’t do bypass surgery. He put them all on MitoQ and every one is now asymptomatic with no chest pain and their ejection fractions have gone up significantly and they’re off the transplant list.  Dr. Houston noted that he still uses the metabolic cardiology program, so he uses regular CoQ10 for the vasculature, MitoQ for the heart, and he also uses d-ribose, taurine, L-carnitine, magnesium and a few other supplements that improve the myocardial contractility and mitochondrial function.

29:44  The best diet for improving HDL functionality is a low refined carbohydrate intake and sugar intake should be less than 25 gms per day.  You should have at least 8 servings of organic multi-colored vegetables per day, which are rich in phytonutrients.  Wild game, a variety of berries, and pomegranates should be part of that diet.  Pomegranate raises HDL functionality through raising PON and it has been shown to reverse carotid atherosclerosis in one year.

31:07  Dr. Houston has developed the Coronary Heart Disease Plaque Regression and Coronary Artery Calcium Regression Program, which includes about 15 different nutritional products, including Neo40 (a nitric oxide booster), Arterosil (which protects the glycocalyx), vitamin K2 MK-7 (a dosage of at least 360 mcg per day and K2 does not promote blood clotting or interfere with the blood thinner coumadin), omega 3 fatty acids (EFA-Sirt Supreme), VasculoSirt, curcumin, and quercetin.  Quercetin has anti-inflammatory, antioxidant, and anti-immune effects and it’s the only compound that reduces SASPs, which are senescent proteins.

35:30  Exercise.  Both resistance and aerobic exercise improve HDL functionality.  In Dr. Houston’s book, What Your Doctor May Not Tell You About Heart Disease, there’s 2 chapters on the best form of exercise that Dr. Houston wrote with Charles Poliquin, a great trainer who unfortunately died about a year ago with a heart attack.  Dr. Houston and Charles also wrote an exercise program that combines aerobics and resistance training with interval training to get the best cardiovascular benefits, which is published in a book titled, ABCT, Aerobics, Build, Contour, and Tone.

38:03  Most of the medications that have been developed to raise HDL levels have not been effective.  The exception is niacin, which actually improves total HDL, HDL particle number, HDL size, and HDL functionality.  There was an older lipid drug used in the VA-HIT trial, which raised HDL, but we don’t know if it improved functionality.


Dr. Mark Houston is an internal Medical Doctor and a hypertension and cardiovascular specialist. He is the director of the Hypertension Institute in Nashville, Tennessee. Dr. Houston is triple board certified in hypertension as an American Society of Hypertension specialist and Fellow of the American Society of Hypertension, Internal Medicine, and Anti-aging Medicine.  Dr. Houston teaches at the Institute of Functional Medicine and the A4M programs. He is a prolific writer and has written What Your Doctor May Not Tell You About Hypertension, What Your Doctor May Not Tell You About Heart Disease, Nutritional and Integrative Strategies in Cardiovascular Medicine, Nutritional and Integrative Strategies in Cardiovascular Medicine, and his two latest books, Vascular Biology for the Clinician, and Precision and Personalized Integrative Cardiovascular Medicine. You can contact Dr. Houston through The Hypertension Institute web site HypertensionInstitute.com.

Dr. Ben Weitz is available for nutrition consultations specializing in Functional Gastrointestinal Disorders like IBS/SIBO and Reflux and also specializing in Cardiometabolic Risk Factors like elevated lipids, high blood sugar, and high blood pressure and also weight loss and also athletic performance, as well as sports chiropractic work by calling his Santa Monica office 310-395-3111. Dr. Weitz is also available for video or phone consultations.


Podcast Transcript

Dr. Weitz:                            Hey, hey this is Dr. Ben Weitz, host of the Rational Wellness Podcast. I talk to the leading health and nutrition experts and researchers in the field to bring you the latest in cutting-edge health information. Subscribe to the Rational Wellness Podcast for weekly updates. And to learn more, check out my website drweitz.com. Thanks for joining me, and let’s jump into the podcast.

                                                Hello, Rational Wellness Podcasters. Today, our topic is HDL cholesterol, and we’ll be speaking with Dr. Mark Houston. The focus of HDL cholesterol which has been called the so-called good cholesterol is that this molecule could potentially help to prevent and reverse cardiovascular disease. Much of the research about heart disease has really been focused on the so-called bad cholesterol, the LDL, which is now generally seen as a significant player in the formation of atherosclerotic plaques in the artery walls that can lead to heart attacks, strokes, and heart failure over time.  of the cardiovascular medications are designed to lower LDL levels including statins, niacin, Zetia, bempedoic acid and the new PCSK9 inhibitors. And there are a number of nutraceuticals that are also effective at lowering LDL particles, including red yeast rice, fish oil, plant sterols, niacin, berberine among others.  We also know that the proper diet and exercise can also be very effective in reducing LDL cholesterol in our bodies especially the more atherogenic small dense LDL particles. But today, we’re going to be focused on the so-called good cholesterol, HDL. We’re going to go into how to understand it, how it works, and how we can improve HDL to improve our cardiovascular health.

                                                We first learned about the potential benefits of HDL cholesterol about 70 years ago. And in 1977, we learned through the Framingham Heart Study that low levels of HDL are generally associated with increased risk of coronary artery disease. And we thought at one time that simply the more HDL, the higher the levels, the better off we are.   But our thinking about this has changed as we have learned that the HDL story is much more complex than we thought it was. And drugs that were developed to raise HDL have really failed to be effective in reducing heart attacks or death. In fact, some people with very high levels of HDL may actually be more at risk for heart disease. And so, this is why we’ve asked the expert, Dr. Mark Houston, to join us to explain what current knowledge about HDL cholesterol is and how we can use this to prevent a reverse heart disease.

                                                Dr. Mark Houston is a internal medical doctor and hypertension and cardiovascular specialist. He’s a go-to expert on cardiovascular disease in the functional medicine world. He’s the director of the Hypertension Institute in Nashville, Tennessee Dr. Houston is triple board certified in hypertension as an American Society of Hypertension Specialist and fellow of the American Society of Hypertension, Internal Medicine and Anti-Aging Medicine.  He also has a master’s degree in human nutrition and a master’s of science degree in functional and metabolic medicine from the University of South Florida. Dr. Houston teaches doctors around the world about cardiovascular medicine as part of the A4m programs. Dr. Houston is also a very prolific author, having written what your doctor may not tell you about hypertension, what your doctor may not tell you about heart disease, nutritional and integrative strategies, and cardiovascular medicine, nutritional and integrative strategies in cardiovascular medicine.  And his two latest books which are Vascular Biology for the Clinician And Precision and Personalized Integrative Cardiovascular Medicine. Dr. Houston, thank you so much for joining me.

Dr. Houston:                      Thank you, Ben. It’s a pleasure to be with you as always.

Dr. Weitz:                           So, maybe you can give us a little bit of a explanation in general what is HDL. In fact, what is LDL? Why do these molecules exist at all?

Dr. Houston:                      Well, let’s start with the LDL story first because I think people are most familiar with that one, explain why it exists and then we’ll merge into the HDL story a bit. These molecules are termed apolipoproteins in the medical world. And apolipoproteins exist for good reasons we have to have them for a lot of health benefits.   For example, one of the major benefits of all the types of cholesterol whether the LDL or HDL is immunological function. It actually protects you from any type of infection, whether it’s viral, bacterial, parasitic, fungal, or TB, and it’s also part of our metabolic system for making steroids and vitamin D and sex hormones. So, there’s a teleological explanation for why these lipids were important in the early time to protect people from getting serious infections and dying from them.   And so, over time, what has happened is the functionality, the levels of HDL and LDL, have changed because in our modern society, people don’t die so much of infections anymore. But they’re dying from other types of environmental toxins, nutritional problems, obesity, and a myriad of other risk factors like diabetes. And so, what has happened to our cholesterol levels, particularly LDL, and to a lesser extent HDL, they’re going in the wrong direction in an attempt perhaps to protect us from these various types of environmental insults.  So, LDL for example, if it’s protecting us from something, it tends to go to very high levels. The LDL level’s elevated. And then, what’s called LDL particle number becomes elevated which is the driving risk recording heart disease and MI. There’s also genetic forms of dyslipidemia. But most people who have dyslipidemia in this country, it’s environmental. It’s not genetic.  So, LDL has been considered, as you said, the bad cholesterol. And HDL is considered the good cholesterol. But it’s much more complicated obviously than that, and that’s what we’ll get into today. So, that’s sort of an introduction, and we can kind of banter back and forth with questions as you wish.

Dr. Weitz:                           So, we generally think of HDL, its main function is to produce reverse cholesterol transport, right?

Dr. Houston:                      Right.

Dr. Weitz:                           And so, what exactly happens during that process?

Dr. Houston:                      So, reverse cholesterol transport or RCT, also termed cholesterol efflux capacity or CEC, are the primary functions of HDL that go into the cell, attach to the cell wall through various receptors that pick up the LDL just like a garbage truck and then take it to the liver where it dumps the LDL and is excreted into the bile. That’s the normal process. However, if HDL, RCT and CEC are not working, our HDL becomes we say less functional, then that process does not occur.  LDL accumulates in the cell. And then, that starts the LDL process of particle size going up, LDL levels going up, LDL size being smaller. And then, you get atherosclerosis, coronary heart disease.

Dr. Weitz:                           And so, HDL can actually take the cholesterol from the artery walls, right?  And so, it can reduce plaques potentially.

Dr. Houston:                      That’s right. It can literally take them out of the cell. But also take them from the cholesterol wall itself, and it’s very important in reducing plaque rupture, and improving plaque stability in coronary heart disease.

Dr. Weitz:                           And what’s the significance of plaque stability?

Dr. Houston:                      So, there’s at least two, maybe three, major forms of plaque. There’s the vulnerable plaque which has a very aggressive core in the middle composed of lipids and smooth muscle cells and inflammatory cells, and it’s surrounded by a sort of a firm top that is very thin, and that protective top can rupture.  So, what happens is all this activity inside the plaque can eat through this protective coating or cap and rupture into the arterial wall once that spews out into the artery.  It causes acute thrombosis which is an acute myocardial infarction.  That’s the really bad type of plaque. It’s considered soft plaque. It’s usually not calcified as vulnerable.   The other plaque is one that has a much thicker cap and has less of a activity in the center with less lipids and inflammatory cells.  And because it’s more stable, it’s not as likely to rupture. But over time, it can become very obstructive and impede the blood flow through the artery.  The problem we have is those people who have stable plaque may not have any symptoms whatsoever until they get to a 95%-plus stenosis.  But the ones who have unstable plaque, the ones that have the really thin cap, those can be only a 50% blockage, but they tend to rupture.  And those are the ones that typically present with intense training, like they run a marathon, interval training, whatever, and the plaque ruptures, and they have an acute MI even without much obstructive disease.

Dr. Weitz:                           And those soft plaques wouldn’t be picked up, for example, by a coronary artery scan.

Dr. Houston:                      Those can be completely missed because they’re not necessarily calcified, and they can be missed by exercise echo and nuclear medicine scans and other non-invasive ways of looking at plaque because it’s only maybe 50%. So, it doesn’t obstruct the flow.

Dr. Weitz:                           So, what’s the best way to get a clue as to whether those exist or not?

Dr. Houston:                      You can do other testing. For example, the MRI imaging with contrast of the heart, which can pick up any kind of plaque, soft or hard. And there’s other types of metabolic testing called a PET scan which picks up activity of plaque in the arteries. You can do a CTA, CT angiogram, looking at plaque. And, of course, the gold standard is a coronary arteriogram where you actually inject dye into the coronary arteries.

Dr. Weitz:                           Is the MRI being used regularly?  I haven’t heard of it being used that often.

Dr. Houston:                      We use it routinely in the institute.  We have an MRI scanner, and it’s incredibly accurate for plaque but also for valve function, cardiac contractility, diastolic dysfunction.  It’s expensive.  But if you have a patient that needs it and get it pre-approved by the insurance, it’s extremely valuable when you don’t want to do an arteriogram.  But also, there’s no radiation exposure, usually not much and with a contrast or some.  But you can’t do it in people who have metal.  So, pacemakers and artificial joints, you can’t put them in an MRI.

Dr. Weitz:                           Right. So, we have a number of positive functions of HDL making plaques more stable, helping to reverse cholesterol transport. And in recent years, we’ve learned about the antioxidant and anti-inflammatory properties as well.

Dr. Houston:                      Right. HDL is composed of probably over 100 different molecules, proteins, lipids, and other components. And with that degree of composition being so complex, it has a very complex anti-atherosclerotic effect. You mentioned a few, anti-inflammatory, antioxidant, anti-immunologic which means it reduces vascular immunologic damage in the arteries, reverse cholesterol transport. I mean there’s probably 25 or 30 different beneficial effects of HDL on atherosclerosis prevention.   But the key point here is that no matter what your HDL level is and no matter what the size of HDL is, those used to be thought to be protective or good things.  But now, it turns out that those don’t actually tell you the true risk in an individual. The only thing that really gives you the true risk is the functionality of the HDL.   Now, in a population, if you look at statistically, is your HDL level this or is your HDL size this, there’s a correlation in a population.  But if you take an individual, and you measure their HDL total, you measure their HDL size, whether it’s big or small, and you measure the HDL map, and there’s five forms of HDL from pre-beta all the way up, those may look great on paper.  But that patient may still be at risk for coronary heart disease because you didn’t measure the true value and true risk which is functionality of the HDL.  Does it do all the things it’s supposed to do to protect you?

Dr. Weitz:                           Now, why is it that drugs that have been developed to raise HDL have all failed so far?

Dr. Houston:                      There’s a lot of reasons. Some of the studies were just bad studies. They didn’t have the right population. Another is they had other adverse effects, like one of the drugs raised blood pressure, and that counter balanced the effects of HDL. But what happened is all of the studies were done prior to the understanding really of what HDL function was all about. So, they may have raised HDL. But it wasn’t functional HDL. So, the HDL maybe went up 30 to 50%. But it didn’t work. So, there was no reduction, as you said, in MI or total mortality with it.

Dr. Weitz:                           Right. So, what is the best way to measure HDL and HDL functionality?

Dr. Houston:                      There are two labs that are presently available clinically to measure functionality of HDL, and that’s really the key to getting at the risk for a patient in their coronary heart disease and MI risk.  As I mentioned to you earlier, Ben, we’re in the process of completing a large clinical trial on HDL functionality looking at a nutraceutical compound that not only improves HDL function, but also can improve HDL size and also HDL particle number which is another thing I neglected to mention earlier.   And let me just maybe comment on that while we’re talking about it. HDL function is the most important thing to measure. So, we can do that now clinically. HDL particle number, how many particles of HDL do you have, is also very high correlated with HDL functionality. And you can measure this in traditional labs to do advanced lipid testing. So, when you look at those two, there’s a 90% correlation between HDL particle number and HDL functionality.  But what we’re trying to do is see which of those has the best overall predictability in a population and see if we can actually improve both of those numbers.

Dr. Weitz:                           And then, when it comes to particle size, you want larger HDL particles.

Dr. Houston:                      That’s what we used to think. But that now has not turned out to be correct either because there’s labs that do HDL mapping, and there’s five HDLs: pre-beta and alpha one, alpha two, and others that range from very small to the large ones. For example, the pre-beta which is a really small one is the one that actually picks up the HDL, excuse me, that picks up the LDL out of the cell.   So, if your pre-beta is not working well, you can’t do good transport out of the cell. But then as the HDL matures, it goes to different sizes, and that progress across there involves a lot of different enzymes, a lot of different complexities, but eventually gets to the form of HDL which takes it and dumps it into the liver through what’s called scavenger receptor SR1 receptor in the liver. So, you’ve got to have all five of these.   And we used to think, “Well, the big one’s like a big dump truck, and it can carry more LDL with it.” It turns out, the size turns out to be not a great predictor nor does the actual total HDL level for heart disease.

Dr. Weitz:                           Now, I’ve heard one prominent functional medicine doctor talk about measuring apoA, and that being maybe a better marker than HDL. What’s the relationship between apoA and HDL? And is there a value in measuring the apoA?

Dr. Houston:                      There’s apoA1 and apoA2, and those are the carriers for HDL. So, that’s the apolipoprotein we mentioned earlier, and they are probably a little bit better than HDL total. But even those do not correlate well with risk because neither of those are functional tests. You’re again just measuring apolipoprotein as a carrier for HDL, and it can be again dysfunctional. So, for example, if you measured total HDL in a population, you could say, “Well, if it’s between…we’ll just throw out some numbers here, 30 to 100.  If you’re below 30, you’re probably in trouble, and if you’re over 100, you’re probably in trouble because those tend to be people who have more dysfunctional HDL. There’s actually a study that was done in men and women, and it suggested that if a male was over around 50 or 55 of their total HDL, most of it was likely to be dysfunctional.  And a female, if it was over 75 to 80, was more likely to be dysfunctional, and that’s because these tend to build up in the blood because they’re trying to cancel the bad effects of the LDL. So, you make more and more of it. But as you make more of it, it’s more dysfunctional. So, the levels keep going up. But less of it’s actually working.

Dr. Weitz:                           And what is the relationship between oxidized LDL and myeloperoxidase and HDL functionality?

Dr. Houston:                      So, all of those are inflammatory and oxidative stress measurements. Oxidized LDL is the form that is atherogenic. So, LDL and its circulating in the regular serum is not at atherogenic until it’s modified into a oxidized or some other form. There’s different forms of LDL that are called modified LDL, and that’s the one that go across the vascular endothelium and actually cause damage or plaque formation.  Myeloperoxidase or MPO is a compound that’s actually made by the white blood cell, and MPO causes all kinds of havoc. Well, it’s good that it kills bacteria. But if you keep making MPO due to other reasons, it causes high blood pressure, coronary heart disease, atherosclerosis, and even plaque rupture. It’s a bad actor and increases coronary calcium.  So, MPO has both inflammatory and oxidative stress implications. Now, once you develop those, they are the cause for atherosclerosis and myocardial infarction. So, your HDL has to be around to clean that up. What happens when you have a high oxidative stress and MPO level, it damages HDL, and it makes it dysfunctional. So, when your MPO is high, you can say, “Well, chances are, my HDL is not functioning well.”

Dr. Weitz:                           So, what’s the best way to improve HDL functionality?

Dr. Houston:                      What we’ve developed is a nutraceutical product that underwent initial study with 10 patients just to see if we could demonstrate effects, and that’s actually published as a white paper through… Can I mention the name of the company? Is that okay?

Dr. Weitz:                           Sure. Yeah.

Dr. Houston:                      Okay. So, the initial study with 10 patients with Metagenics. And then, they asked us to do a double blind placebo control trial which is really the way to get the true data. The initial trial showed that the nutraceutical proprietary compound that we’ve developed is called CardioLux, CardioLux, and it’s got pomegranate. It’s got quercetin, curcumin, vitamin E and few other things in it, looked positive in the initial pilot trial of 10 patients.    So, we’re in the process of finishing the double blind control trial now. We’ll be then done April 15th. I don’t know the results because I’m blinded, and we’ll do the statistical analysis. We will then publish the trial in a journal, and we’ll know the true efficacy of CardioLux in these patients.

Dr. Weitz:                           Now, why did you pick those particular nutritional compounds?

Dr. Houston:                      It’s based on all the scientific trials that are in the literature. Plus, what we’ve done in patients over the years trying to figure out which works the best. And when you take each one of those, it improves HDL function. Each one of those also has other good effects on reducing oxidative stress, inflammation, and immune dysfunction and although they actually had an effect on raising total HDL and improving the HDL mapping and the HDL particle number.  So, the only missing piece was can we put all this together into one product and take the best of each and make the entire picture better but specifically concentrating HDL functionality.

Dr. Weitz:                           Yeah. The interesting thing is those particular compounds, we generally think of a lot of them more as antioxidants than as cardiovascular-related compounds.

Dr. Houston:                      Yeah. And that’s exactly correct because it may be that what we’re doing when we reduce oxidative stress and inflammation is we’re making the HDL compound which has all these proteins and lipids in it work better. So, the functionality actually gets improvement. And the other thing we’ve seen then is when HDL becomes dysfunctional, it’s not all or none.  And so, think of it… We’ll just pick a number. Let’s say you’ve got 100 different components in HDL, and let’s say 20 of them become damaged, but the other 80 work well. So, that HDL still functions but just not at 100% whereas you can go all the way down to zero, everything gets wiped out. And you have no function whatsoever.   So, the two tests that we use actually give you the ability to measure the functionality of HDL with a number. So, you can see where you are on the scale from that 100% great to zero which is terrible.

Dr. Weitz:                          So, a lot of this functionality has to do with the proteins, and it’s my understanding that basically the reason why you have these LDL HDL particles is because fats don’t move readily through the bloodstream because that’s more water soluble. So, we surround them with these protein structures. So, you have all these various proteins that are coating the lipids and the HDL. And one of these proteins is PON1, I understand, which is an important one.

Dr. Houston:                      Yeah. What you said is exactly right, Ben. You have to package the lipids into a water-soluble form which is apolipoprotein. And so, one of the proteins you mentioned is called PON, peroxidase, and peroxidase is incredibly important to make HDL function. And if it’s damaged, HDL does not work well. And what we found in all the different compounds we were looking at, most of these raised PON, which helps to improve the functionality.

Dr. Weitz:                           It’s kind of interesting how in the body, if you want to get something into the bloodstream that’s a fat, you have to make it water soluble. And then in a lot of other areas, we’re taking things that are water soluble and surrounding them with lipids, so we can get them into the cell membranes.

Dr. Houston:                      Right. Yeah. It’s a conundrum of how to get it into the blood. But also get sure into the cell.

Dr. Weitz:                          Right. Even a couple of the new vaccines for COVI actually take the RNA instructions and surround them with a lipophilic surrounding to get them into the cells.

Dr. Houston:                      Yeah. Exactly.

Dr. Weitz:                          And we do the same thing with glutathione and other ingredients that we’re trying to get incorporated into our cells.

Dr. Houston:                      Yeah. And actually, another compound that we use that everybody is familiar with is Coenzyme Q10. Well, the problem is it’s got to get into the mitochondria. So, it’s not only got to get into the cell, it’s got to get into the mitochondria to be affected. And a lot of the CoQ10s, they get in the serum fine. But they don’t even get into the cell. But if they get to the cell, they don’t penetrate the mitochondrial membrane.  So, there’s new forms of CoQ10 developed now, that get into the mitochondria in a concentration that’s like a thousand times greater than regular CoQ10. So we’ve able been able to reduce congestive heart failure, improve ejection fractions, reduce diastolic dysfunction using a very highly potent CoQ10 that gets into the mitochondria.

Dr. Weitz:                          Is that like the ubiquinol versus a ubiquinone?

Dr. Houston:                      No. It’s actually called MitoQ. MitoQ.

Dr. Weitz:                          Right, right, right.

Dr. Houston:                      It’s from New Zealand.

Dr. Weitz:                          I heard about that. I saw a study where it reversed… What was it? Like aortic stenosis or something like that.

Dr. Houston:                      Yeah. It’s amazing. Actually, I’ve got a series now of about 10 patients who were on the transplant list, a cardiac transplant list, and also a couple that were at end stage coronary heart disease. They couldn’t put stents in. They couldn’t do bypass. Every one of them that we put on CoQ10, has become asymptomatic with no chest pain for their coronary heart disease or their ejection fractions gone up significantly, and they’re off the transplant list. This stuff is a breakthrough, I think, in cardiology.

Dr. Weitz:                          Oh, interesting. Are you still using the combination of the CoQ10 and the ribose and the L-carnitine for the-

Dr. Houston:                      Yes, we still use the metabolic cardiology program. So, we use regular CoQ10 for the vasculature, CoQ10 MitoQ for the heart, and we use d-ribose, taurine, carnitine, magnesium and all these other wonderful supplements that improve the myocardial contractility and mitochondrial function.

Dr. Weitz:                          Interesting. So, what diet and lifestyle factors outside of these specific supplements?  What type of diet is beneficial for improving HDL functionality?

Dr. Houston:                      Well, you want to use a low refined carbohydrate intake. Sugar intake should be less than 25… excuse me 25 grams a day which is pretty strict, a lot of vegetables, at least probably eight servings of multi-colored vegetables per day. That’s got all your phytonutrients, high-quality protein that has no pesticides, organicized hormones in it.  So, you got to kind of go to wild game for that, and then a wide variety of berries particularly that are low glycemic index, blueberries, blackberry, strawberries, and always pomegranates.   So, pomegranate seeds, if you’re not prone to dysglycemia. You can use the juice. But any pomegranate whether it’s the seeds, the plant, or the juice has benefit in atherosclerosis and raising HDL in raising PON.

Dr. Weitz:                          Interesting. A pomegranate’s kind of an amazing compound seems to have a lot of efficacy and prostate issues as well.

Dr. Houston:                      Yeah, and it’s been shown to actually reverse carotid atherosclerosis in one year.

Dr. Weitz:                          Really?

Dr. Houston:                      Yeah.

Dr. Weitz:                          Wow. What’s your current protocol for patients who come in who have plaque who want to reverse it?

Dr. Houston:                      We have a very specific protocol. It’s called the Coronary Heart Disease Plaque Regression and Coronary Artery Calcium Regression Program. We’ve actually been able not only to stabilize plaque but actually to reverse it in patients. So, we use a whole host of things. It’s probably about 15 things we use. I’ll give you the name of some of them. We use Neo40 which is a nitric oxide booster. We use Arterosil which protects the glycocalyx, vitamins-

Dr. Weitz:                          Like a seaweed moss or something like that, sea moss.

Dr. Houston:                      Well, yeah. Sort of like that. It’s a glycocalyx with all kinds of glycoproteins in it. And you can get that from a company called Calroy. So, Arterosil. We use a vitamin K2 MK-7, omega-3 fatty acids.

Dr. Weitz:                          What’s the dosage of MK-7?

Dr. Houston:                      K2 MK-7 is a minimum of 360 micrograms minimum per day.

Dr. Weitz:                          So, how high might you go?

Dr. Houston:                      K2 MK-7 probably is very safe even up to 1000, 2000 micrograms. It’s really good for reducing coronary calcification and plaque formation.

Dr. Weitz:                          And unlike K1, there’s not a significant effect on blood thinning.

Dr. Houston:                      We’ve never seen any issues with Coumadin or warfarin with K2 MK-7. Now, if you got really high doses, it might. But at 360, there’s no issues like there is with K1 because that can interfere with the clotting. But it has no issues with the new antithrombotics, the factor X inhibitors like Eliquis. Those are not affected whatsoever by any form of vitamin K. So, they’re okay.   The other things we use are omega-3 fatty acids in high dose. We use one from biotics research called EFA-Sirt Supreme. Then, we have a compound called VasculoSirt which I developed about five years ago with Biotics, and it’s really good. It’s got 25 or 30 different compounds in it that improve endothelial function, reduce inflammation oxidative stress and so forth.   And then, we’ve got curcumin, use a very highly absorbable curcumin, quercetin, and then there’s a few other things you’re throwing. That’s the primary things that we use for plaque regression.

Dr. Weitz:                          Right. How does quercetin have activity in this regard?

Dr. Houston:                      Quercetin is an amazing nutraceutical. It has anti-inflammatory effects, antioxidant effects, anti-immune effects, and it’s the only compound I know that actually reduces SASPS. SASPS were like the garbage in the cells. If a cell gets sick, for example, it starts to die, and it makes saps. So, it’s senescence proteins.

Dr. Weitz:                          Oh okay.

Dr. Houston:                      Senescence proteins. And so, these senescent proteins leak out, and they kill all the cells around it. So, you start to get a fast aging process in the blood vessel or you get a fast aging process in general. So, quercetin reduces SASP formation. So, it actually can slow down vascular aging and aging in general.

Dr. Weitz:                          Interesting. interesting. So, you’re talking about cleaning out the garbage from cells.  Do you think intermittent fasting or fasting can play a role as well?

Dr. Houston:                      Absolutely.  Intermittent fasting of any type, we’ve used the prolonged trial.  We published it.  It’s going to be published pretty soon, we hope. But the initial data with fasting, in general, is you can slow down aging.  You can actually reduce some of the SASPS.  You can improve stem cell production, increase nitric oxide, and actually maybe even stabilize reverse type 2 diabetics.

Dr. Weitz:                            Really? Wow. Cool. And what about the benefits of exercise? Can exercise play a role in HDL functionality and then reversing cardiovascular disease?

Dr. Houston:                      Absolutely. HDL is generally improved in all the parameters we’ve talked about with resistance and aerobic exercise. In one of the books you mentioned, what your doctor may not tell you about heart disease, there’s two chapters in there on the best form of exercise that we developed with one of the great strength trainers, Charles Poliquin, who unfortunately died about a year ago with a heart attack. But Charles and I did some clinical trials.   And then, we wrote together an exercise program which is published in this book called ABCT, Aerobics, Build, Contour and Tone. And it’s combining aerobics and resistance training with interval training to get the best cardiovascular benefits, protection for coronary heart disease but also improve your lipid profile and your blood pressure.

Dr. Weitz:                          Interesting. What about hormones? I know some of the men that I’ve seen who had the lowest HDL levels were guys who were taking testosterone.

Dr. Houston:                      Yeah. That’s a really tricky topic. In my practice, I have really not done hormones. I’m not trained in hormones, and I’m really probably not qualified to even prescribe them and really talk intelligently about them, and then source in. So, I would just say this. When I review the data hormones and heart disease and hormones and lipids, it’s very confusing. It’s very controversial and you can kind of find whatever you want to out there to support your opinion. So, I’ll leave it at that and let the hormone specialist get into the intricacies of that topic.

Dr. Weitz:                          Yeah. Did you see that paper, that Felish Gersh published recently on the benefits of estrogen for reversing cardiovascular disease?

Dr. Houston:                      Yeah.  There’s a lot of good articles out there that you can read.  Absolutely.

Dr. Weitz:                          Yeah.  I mean you know it makes some sense since we know women have much lower rates of heart disease than men until menopause. So, it makes sense that estrogen has somewhat of a protective role.

Dr. Houston:                      Right.  Exactly.

Dr. Weitz:                          Cool.  And what about any of the medications for HDL?

Dr. Houston:                      None of them work. There’s a whole list of things out there. Probably niacin’s been sort of the primary nutraceutical that’s been looked at. And niacin actually does work. But it’s not really a medication per se. I mean, obviously, you can get it as a prescription. You consider it that way. But we don’t think [crosstalk 00:38:29]. Niacin improves total HDL, HDL particle number, HDL size, and HDL functionality. They’re one of the few supplement/drugs that does that.   Most of the other drugs that have been attempted really don’t work well. There was an older lipid drug that was used in the VA-HIT trial, and it raised HDL. But they didn’t even measure the functionality in that study. So, we don’t really know whether that change in HDL had anything to do with the outcomes.

Dr. Weitz:                          I mean when you look at all the benefits of niacin, it’s pretty amazing. It’s one of the few compounds that will increase LDL particle size. It’s one of the few compounds that can have measurable effect on Lp(a). It’s one of the few things that can improve HDL, and yet it’s not generally considered something that should be recommended by most cardiologists today.

Dr. Houston:                      Yeah, and that’s a shame, Ben, because it’s based on three clinical trials that came out that said that niacin didn’t work to reduce coronary heart disease and all these other things. But if you go back and look at all those studies as you’ve read them as I have. They’re flawed. They have an incredibly bad methodology. I mean you can take them apart literally, just massacre those trials if you really know about what they looked at.   And I’ve written several editorials with a lot of folks that that tear up the studies and say, “Look. Niacin is still a good supplement. It’s a good drug, [inaudible 00:40:13] you want to classify it.” You should use it. But you have to know how to use it. You’ve got to know what dose to give. You got to know what side effects it has, and what to monitor.   If you know how to do that, you can be a very wise clinician and use niacin to improve your lipidology and your coronary heart disease risk and a lot of other factors.

Dr. Weitz:                          Yeah. I think if you use niacin as part of the package rather than just rely on a super high dosage of niacin, you can avoid some of the blood sugar, liver stress that can occur.

Dr. Houston:                      Yeah. And you’re exactly. If you keep it in kind of a low dose and you use it as a combination agent, I mean I don’t usually go much over 500 milligrams of niacin in one day with one exception in Lp(a), that’s about the only time, and that’s about the only thing that really works. You’ve got to go to higher doses to get Lp(a)down. But for the other things we’ve talked about, 500 milligrams used with other compounds is very effective, and you don’t get the hyperhomocysteinemia, the hyperglycemia, the liver dysfunction, the itching, the pruritus, all that stuff is not very, very bad.

Dr. Weitz:                          Yeah. Lp(a) is a tough one. Anything new on the horizon for that?

Dr. Houston:                      Well, it’s interesting you should ask me that because our next clinical trial product development will be with Lp(a), and we’ll be working again with Metagenics on that one. [crosstalk 00:41:40] the HDL trial. I hope that we’ll be starting the Lp(a) study.

Dr. Weitz:                          Let me guess.

Dr. Houston:                      There is a drug being developed in fast track as you know that could be out within one to two years if everything goes well.

Dr. Weitz:                          Right. Then, all of a sudden, all the conventional MDs will want to measure Lp(a). But right now, you try to get it measured [inaudible 00:42:06] What are you doing that for? It’s a [crosstalk 00:42:07].

Dr. Houston:                      Once you get the drug for, people will start measuring kind of backwards thinking.

Dr. Weitz:                          Well, let me guess. Niacin, L-carnitine, let’s see, vitamin C, lysine.

Dr. Houston:                      But what we’ve got right now, we’ve got niacin [inaudible 00:42:29] aronia berry which is chokeberry. Yeah.  It doesn’t work all the time. It works pretty good. And you mentioned the others. There’s a Linus Pauling Protocol, vitamin C, lysine, proline, carnitine, CoQ… I mean there’s a lot of things that may work. The number consistent is the problem.

Dr. Weitz:                          All right. Okay. Cool. Okay. I think that’s the things I really wanted to talk about here. Any final thoughts you want to leave our listeners and viewers?

Dr. Houston:                      I think you’ve covered the topic incredibly well, Ben. You’ve asked all the pertinent questions, and I think that’s kind of the state of the art right now. Now, you and I both know it could change in a month. But at least after today, we’re up to date.

Dr. Weitz:                          So, are there any conferences that are going to occur this year or is that going to be-

Dr. Houston:                      Yeah. We’re getting back online. We’re going to probably have A4M in Las Vegas in December.

Dr. Weitz:                          Oh really?

Dr. Houston:                      I think that’s going to happen. They actually have something even in the fall if this pandemic ends. But I think the virtual meetings are going to phase out, and we’re finally get back to live ones pretty soon.

Dr. Weitz:                          By the way, I don’t say we’re going to wrap this up. But have you had any long COVID patients with cardiovascular issues, and do you have any insights on that?

Dr. Houston:                      I will give you my insight. I have had not very many patients in Tennessee. I live in Nashville. So, at least in my practice. I haven’t had a lot of patients who’ve had COVID. I’ve had a few. But just give me just a second. I think the reason I haven’t had a lot of people in my practice with it is because we had a lot of patients on high dose vitamin D plus a lot of nutraceuticals. They were healthy people in that respect.   And so, that was a protective thing. But the ones who did get COVID, none of them got very stick with it. Very few of them even ended up having more than like a seven-day period. They quarantined, but they stayed at home. Almost none of them ended up in the hospital. But I’ve had a few that have ended up in the hospital.

Dr. Weitz:                          Have you had any that had the long-term-

Dr. Houston:                      We’ve had a few people had had, I would say, more short-term stuff with shorts of breath. But I haven’t really seen any long-term in my practice like long-term effects with cardiac dysfunction or pulmonary dysfunction.

Dr. Weitz:                          Okay. Cool. What’s the best way to get a hold of you?

Dr. Houston:                      Oh, probably go to my website. We’ve got everything on there. It’s hypertensioninstitute.com. Our website’s very user-friendly. You can find our emails, phone numbers, all our protocols, books and so forth thrown there.

Dr. Weitz:                          And once again, the product from Metagenics for HDL is-

Dr. Houston:                      CardioLux, C-A-R-D-I-O-L-U-X, CardioLux.

Dr. Weitz:                          And that’s currently available.

Dr. Houston:                      Available through Metagenics presently.

Dr. Weitz:                          And the dosage that you recommend for that.

Dr. Houston:                      It’s two twice a day with food.

Dr. Weitz:                          Okay. Excellent thank you so much, Mark.

Dr. Houston:                      My pleasure, Ben.

Dr. Weitz:                            Well, thank you, listeners, for making it all the way through this episode of the Rational Wellness Podcast. Please, take a few minutes and go to Apple Podcast and give us a five star ratings and review. That would really help us, so, more people can find us in their listing of Health Podcast.  I’d also like to let everybody know that I now have a few openings for new clients for nutritional consultations. If you’re interested, please, call my office in Santa Monica at 310-395-3111. That’s 310-395-3111, and take one of the few openings we have now for a individual consultation for nutrition with Dr. Ben Weitz. Thank you and see you next week.


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