Dr Houston, first we'd like to get an idea of your history as a cardiologist. What peaked your interest to say there’s something more going on here than the normal things that you were taught in medical school?
Dr Houston: I realised that most of the people that were being treated for coronary heart disease, who’d had myocardial infarctions, bypass, grafting and stents, they were just having issues with recurrence of their disease even though they had really good numbers. I mean, normal LDL (Low-density lipoprotein) levels, good blood pressure, good blood sugars, they were losing weight, they were eating right, and I said, we’re missing something. Something’s not being measured. And, so I started looking into the literature and I realised that we were not addressing all of the risk factors that we even knew about correctly. And we weren’t even addressing another 395 that we didn’t even address at all.
So how has this field evolved?
Dr Houston: We’ve gone through an incredible transformation. The entire field of lipidology is in flux. And we’ve gone from (measuring) total cholesterol, then we went to LDL and HDL (high-denisty lipoproteins) and now we’ve gone to the subfractions of each of those. And, that’s gotten even more complicated looking at modifications of those, dysfuncitonality of HDL, so the entire field is in flux. And I think that we’re beginning to realise that we really don’t know much about lipidology compared to what we thought we knew. The whole field, with advanced lipid testing is evolving and that’s going to create another whole field. So, I think we’re just on the precipice of understanding, not just CVD, but understanding lipidology.
Are you’re saying it has now got to do with the dysfunctionality and modification of these particle sizes? Tell me more about this.
Dr Houston: The particle number never loses it’s predictability. It’s always number one no matter what you do. But within the LDL story, there’s the functionality of the LDL, by that I mean, it’s modified, it’s changed by inflammation and oxidative stress. So, the oxidised form, the acetylated form, the glycated form actually become the foreign type of LDL. In its native form, LDL is really not even atherogenic, whether big or small. It just turns out that the little ones are more likely to become modified than the big ones. Even the big ones can be atherogenic under certain circumstances, like inflammation.
So when you’re talking about particle number then is that the same as looking at just LDL?
Dr Houston: No, totally different. If you look at total LDL you cannot predict anything about risk, what the treatment is going to do and how far you need to drive the LDL down. So total levels, no matter whether you’re looking at, HDL or LDL, to my reading, are non useful information.
Well, the proponents of normal lipoprotein levels will say you have to drive these down even further. They’re calling for lower levels of LDL, as you’d be aware, so what do you say to your peers?
Dr Houston: Well the problem is, all of the studies are based on total LDL levels. What we’ve found is if you get the LDL particle number down, depending on the lab, we use one that gets it down about 700, that’s where the risk becomes pretty flat. But, that’s not the whole story. It’s what happens to the particles, how they change, and also the clean up crew, which is HDL - is it functional? It’s way more complicated than just looking at LDL. If you start saying we’re going to drive LDL down to these enormously low levels you’re going to start interfering with all sorts of biochemical pathways. And there are going to be long term problems with this! You’re going to have changes in vitamin D levels, steroid hormones, all these things that are downstream. We have LDL for a good reason.
One of the initial theories of the function of LDL was that it’s actually a healer, trying to get rid of inflammation. Can you explain this?
Dr Houston: Absolutely, its a very good point. LDL is actually a protective defence mechanism. It’s part of your innate immune system so, for example, if you’re infected with a virus or a bacteria one of the responses is LDL trying to contain the infection. It will take it, incorporate it so the polysaccharide coat of the bacteria is incorporated into the LDL, and the LDL then goes to the liver, and tries to get rid of the infection or whatever it is.
The problem is, while it’s doing all that, it becomes altered, it becomes oxidised or glycated. Then the body sees this particle as a foreign protein and so, unless it gets out of the system somehow, if it’s still floating around, it’s going to become a foreign antigen. The body is then going to start attacking the LDL or the LDL is going to create a secondary inflammatory response over and above the first one. So, LDL is not the bad guy. LDL is trying to protect you, but it becomes part of the damage, and your vascular system becomes the innocent bystander as part of the modification of LDL cholesterol.
Many around the world are calling for rethink of BMI as a measure of lean body mass. What simple tests do you advocate to look at your body composition?
Dr Houston: There are a lot of things you can do. BMI, as you know, misses people who have a lot of lean muscle. So, we typically use waist circumference, waist-to-hip ratio, but even that’s fraught with problems. The best is to do BIA (Body Impedance Analysis) which actually measure body fat percentage and visceral fat. That’s the most accurate.
Should we be doing more with regards to fasting glucose and looking at the acceptable levels? Can you tell me a little but more about where we’re going with that and what changes you see when you achieve those targets of a lower fasting glucose?
Dr Houston: We’ve really misdefined dysglycaemia in every lab. By the time your blood sugar is in the high-normal range you’ve already lost a lot of your insulin production. So you’ve gotta back it up and say ‘what’s really a normal fasting blood sugar’? It’s somewhere around 75-80 mg/dL (4.2-4.5 mmol/L).
In the US, our upper limit for fasting blood sugar is 99 mg/dL (5.5 mmol/L) so if you’re at 99 mg/dL you’re already at risk for CVD. And, it’s a 1:1 ratio, so if you’re at 100 mg/dL (5.5 mmol/L) you’re at almost 20-25% greater risk for having a heart attack. If you do a post prandial blood sugar or a 2 hour Glucose Tolerance Test it’s even worse and now becomes a 2:1 ratio.
The earliest marker for dysglycaemia is adiponectin (decreasing levels). The next thing that happens is your insulin levels start to go up, but your blood sugar remains fairly normal. It’s only once your insulin can’t keep up when blood sugar goes up. That’s when you’ve already progressed pretty far. By the time you have fasting dysglycaemia you’ve probably lost 20-25% of your insulin function.
Do you ever measure c-peptide?
Dr Houston: I do, I measure c-peptide, pro-insulin, insulin, adiponectin, fasting and post prandial glucose pretty routinely, depending on where they are on the curve. It gives you a very good idea of how bad they are and how far that it’s progressed.
Let’s move on to dietary intervention because this is really where, if you think about the causes, a lot of it comes from; that and sedentary lifestyle...
Now, in your book What your Dr may not tell you about heart disease you talk about the ABCT program and you also talk about a diet which you’ve developed which sort of blends 2 of the best diets together - the Mediterranean diet and the DASH II - it’s called the ICDPPD diet.
Can you explain what’s going on here?
Dr Houston: When you look at most of the diets that have been out there and studied, they have some issues.
For example, the old DASH diet was way too high in refined carbohydrates, so I modified that to a lower carbohydrate diet and made a few other twists. The Mediterranean diet has a few things that you want to modify as well. So by taking the two together you get the best of both of them.
Basically, what I did, I had very high quality protein that’s organic and no trans fats whatsoever. You limit the saturated fats, and you really load up with monounsaturated fats and omega-3 fatty acids. Then, carbohydrate is a very important issue.
Refined carbohydrate, in my opinion, are much more important in driving CHD risk than anything related to the fat story. If you look at saturated fats vs refined carbs, refined carbs are always worse than saturated fats. If you transport the calorie intake per day and you substitute refined carbohydrates for the saturated fats, you’re going to end up with more heart disease, no question about it. So I am really tough on patients when it comes to refined carbohydrates. I try to get them down to 75-100g a day, max; that’s really low.
Then we get a lot of vegetables, different colours. I minimise the fruit because that’s fructose and it gets converted right into glucose; berries are better. You’ve got to watch the GI (glycemic index) of the fruits, like bananas, grapes and so forth. Those things have to be modified. You don’t just say ‘well eat 10 servings of fruits and vegetables’, well 10 of which vegetables to eat? Ten of which fruits to eat? Tell me how many grams of refined carbohydrates not to go over.
You say do strength exercising before cardio exercising. Tell me more about the ABCT program.
Dr Houston: We recommend doing an hour at least 4 days a week. Forty minutes is resistance training, and that’s first, followed by twenty minutes of interval aerobics.
Now, the reason you do a 2:1 ratio and you do the resistance first, is there are some good studies that show if you do it that way, you increase your vascular endothelial production of NO (nitric oxide) and enhance arterial compliance and vascular health. If you do it the other way, you don’t get the same benefits.
So what other things do you do in ABCT program?
Dr Houston: In the resistance program, what you’re doing is heavy weights with low reps. Then you start to drop the weights and do higher reps. This is really a combined program and, the muscle fatigue that occurs where you get the lactic acid burn, is when you start increasing the beneficial hormones out of skeletal muscle, Growth Hormone, testosterone, IL-10 and other anti-inflammatory compounds. In women there is an increase in progesterone and oestrogen. There is also a drop the catabolic hormones, particularly cortisol and epinephrine. By doing so, the muscle becomes really a key endocrine organ in reducing CVD.
What nutraceutical supplements do you tend to use first in your patients?
Dr Houston: I routinely put people on omega-3 fatty acids. The reason I do this is because they have so many vast effects on lipids, BP, IR and other things.
Magnesium and coenzyme Q10 are also important. There are certain nutrients that I use that will rival drugs, if you know how to put them together.
Mark C. Houston, MD, MS, ABAARM, FACP, FAHA, FASH, is associate clinical professor of medicine at Vanderbilt University School of Medicine; director of the Hypertension Institute and Vascular Biology; and medical director of the Division of Human Nutrition at Saint Thomas Medical Group, Saint Thomas Hospital in Nashville, Tennessee. He is also on the faculty of the University of South Florida for the Functional and Metabolic Medicine Fellowship. He is chief medical officer for Destination Medical Centres in the United States, which is part of MVP Holdings, LLC. He is triple board certified by the American Board of Internal Medicine, the American Society of Hypertension (ASH), and the American Board of Anti-Aging and Regenerative Medicine (ABAARM). He also has a master of science degree in human nutrition.
Dr Houston has presented over 10,000 lectures nationally and internationally and has published more than 200 articles and scientific abstracts in peer reviewed medical journals. He is on the consulting editorial board for many medical journals and is editor-in-chief for JANA (Journal of the American Nutraceutical Association). He is an author and teacher and is active in clinical research.
Dr Houston specialises in hypertension, lipid disorders, prevention, and treatment of cardiovascular diseases, nutrition, clinical age management and general internal medicine with an active clinical and research practice as well as teaching responsibilities for Vanderbilt medical students, interns and residents.
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