3rd BioCeuticals Research Symposium: Meet Dr Mark Houston

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3rd BioCeuticals Research Symposium: Meet Dr Mark Houston

3rd BioCeuticals Research Symposium: Meet Dr Mark Houston

Published: Jan 12, 2015
Author: BioCeuticals - Editor

Meet the speaker: Dr Mark Houston, MD MS ABAARM FACP FAHA FASH
With the 3rd BioCeuticals Research Symposium program evolving, Senior Educator Andrew Whitfield-Cook has the opportunity to interview Keynote Speaker Dr Mark Houston. Here he shares his thoughts on cardiovascular disease.

Dr Houston, first I’d like to get an idea of your history as a cardiologist. What peaked your interest in aspects of health other than the standard things you learn in medical school?

MH: I realised that most of the people that were being treated for coronary heart disease – who had myocardial infarctions, bypass, grafting and stents – were just having issues with recurrence of their disease even though they had really good numbers. I mean: normal LDL levels, good blood pressure, good blood sugars, they were losing weight, they were eating right. I said, “we’re missing something. Something’s not being measured.” And so I started looking into the literature and  realised that we were not correctly addressing all of the risk factors that we knew about. And we weren’t even addressing another 395 that existed.

So how has the field of cardiovascular health evolved?

MH: We've gone through an incredible transformation. The entire field of lipidology is in flux. And we've gone from (measuring) total cholesterol, to then measuring LDL and HDL and now we've gone to the subfractions of each of those. And, that's gotten even more complicated looking at modifications of those, dysfunctionality of HDL; so the entire field is in flux. 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.

Tell me more about the dysfunctionality and modification of these particle sizes.

MH: The particle number never loses its 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.

When you're talking about particle number, is that the same as looking at just LDL?

MH: 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 not 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. What do you say to your peers?

MH: 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 and 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?

MH: Absolutely, it's 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 part of 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 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 the rethink of BMI as a measure of lean body mass. What simple tests do you advocate to look at body composition?

MH: 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:hip ratio; but even that's fraught with problems. The best is to do body impedance analysis (BIA), which actually measures 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? What changes do you see when you achieve targets of a lower fasting glucose?

MH: 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 got to back it up and say "what's a normal fasting blood sugar?" It's somewhere around 75-80mg/dL (4.2-4.5mmol/L). In the US, our upper limit for fasting blood sugar is 99mg/dL (5.5mmol/L), so if you're at 99mg/dL, you're already at risk for CVD. And, it's a 1:1 ratio, so if you're at 100mg/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 two 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 after your insulin can't keep up that 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?

MH: 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 it's progressed.

Let's move on to dietary intervention. In your book "What your doctor may not tell you about heart disease" you talk about a diet you've developed which blends two of the best diets – the Mediterranean and the DASH II. Can you explain the benefits?

MH: 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 of the fruits, like bananas and grapes. Those have to be modified. You don't just say "well eat 10 servings of fruits and vegetables" – well which 10 vegetables or fruit do you eat? Tell me how many grams of refined carbohydrates not to go over.

You say to do strength exercise before cardio exercise. Tell me more about the aerobics, build, contour and tone (ABCT) program.

MH: We recommend doing an hour, at least 4 days a week. Forty minutes of resistance training, and that's first, followed by 20 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 nitric oxide and enhance arterial compliance and vascular health. If you do it the other way, you don't get the same benefits.

What other things do you recommend in the ABCT program?

MH: 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, IL10 and other anti-inflammatory compounds. In women there is an increase in progesterone and oestrogen. There is also a drop in catabolic hormones, particularly cortisol and epinephrine. By doing so, the muscle becomes a key endocrine organ in reducing CVD.

What nutraceutical supplements do you tend to use first in your patients?

MH: I routinely put people on omega-3 fatty acids. The reason I do this is because they have so many vast effects on lipids, blood pressure, insulin resistance (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.

Dr Houston it's been an absolute pleasure. Thank you so much for joining us today.

To see Dr Mark Houston at the 3rd BioCeuticals Research Symposium, we encourage you to take advantage of the Early-Bird rate. Click here to register today!

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