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Cholesterol Conundrum with Dr Ross Walker

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Cholesterol Conundrum with Dr Ross Walker


One Australian dies every 12 minutes of a heart attack or some cardiovascular disorder. In the war on heart disease orthodox cardiologists often still view LDL and cholesterol as the crucial enemy and the end result is often a polypharmacy prescription to bring them to heel.

This is where Dr Ross Walker differs from his more conventional cardiology colleagues. He takes a more wholistic view and treats based on the best available evidence for cardiovascular disease.

In today's podcast, Dr Ross Walker reveals how to decisively treat heart disease using diet and lifestyle measures, with judicious use of nutraceuticals and warranted medications for demonstrated disease progression. 


Covered in this episode

[00:42] Welcoming back Dr Ross Walker
[01:39] Prevalence of heart issues in Australia?
[04:01] Five Keys to Ultimate Health
[06:57] Making the decision to "be healthy"
[08:34] LDL: Friend or foe?
[10:55] Don’t treat cholesterol, treat risk
[17:40] Stress is a very real factor of healthcare
[19:18] The LDL and saturated fat story
[22:37] Evidence-based interventions
[25:16] Ubiquinol and ubiquinone
[27:34] Watch the calcium score
[29:37] Plaques, inflammation and immunity
[38:12] Where are we at with Fish Oil?
[41:10] Understanding Lipoprotein(a)
[46:07] Utility of exercise
[50:12] Summary from today

Andrew: This is FX Medicine, I'm Andrew Whitfield-Cook. Joining me in the studio today is Doctor Ross Walker, an eminent practicing cardiologist with a passion for people and health and with over 35 years of experience as a clinician. For the past 20 years he's been focusing on preventative cardiology and is one of Australia's leading preventative health experts. 
Considered one of the world's best keynote speakers and life coaches, he's the author of seven bestselling books, a health presenter in the Australian media including regular appearances on the Nine Network’s Today Show, A Current Affair, Sky News, Switzer Business. He also has a weekly radio show on Sydney's 2UE, 4BC, and 2CC, and with other regular segments on, this is going to get tongue twisting, 2UE, 6PR, 4BC, and 3AW. Welcome Ross, do you have a rest? 
Ross: Typically not, Andrew, no.  
Andrew: Welcome warmly back to FX Medicine, How are you? 
Ross: Pleasure. 


Andrew: Now, we're going to be talking a little bit, certainly about cardiovascular disease, but partly about the cholesterol conundrum. What I'm interested in is residual risk with cardiovascular disease. But I guess first, can you take us through the prevalence of heart issues in Australia, why we're getting fatter, and where are we heading in the future? 
Ross: Sure. Well, firstly one Australian dies every 12 minutes of a heart attack or some cardiovascular disorder. It is seriously the commonest cause of death and disability around the world, and certainly Australia is part of that as well. And one of the big problems now is that everyone thinks heart disease is caused by cholesterol, and we've got to dismiss this nonsense. Seventy percent of heart disease is now directly related to the insulin resistant gene.  
And here's the problem with insulin resistance. 30% of Caucasians are insulin resistant, 50% of Asians and close to 100% of people with darker skin are insulin resistant. What does that do to you? It increases your risk for diabetes, blood pressure, cholesterol issues, maybe not a high cholesterol, but cholesterol issues, fat around the belly, so abdominal obesity, the dangerous fat, and then cardiovascular disease and even cancer. 
So 70% of arteriosclerotic cardiovascular disease is directly related to insulin resistance, 20%... And this is hardly even tested for in the Australian medical industry. Twenty percent is due to an elevated lipoprotein(a). So therefore you can explain 90% of cardiovascular disease when we haven't even mentioned high cholesterol. And here's the problem, because of this gene and because of the way we're living these days, 70% of Australians are now either overweight or obese, of males, and 50% of Australian females overweight or obese. 
And the reason is pretty damn obvious, food is freely available, all of our celebrations are based around food. We were designed to be hunter-gatherers, wondering around a jungle with a spear for 30, 40 years, having the acute feed of killing a beast and storing a bit of fat around the belly for a couple of days, till the next big feed a couple days later. And a bit of feast and famine in between time. What do we do now? Breakfast, lunch, dinner, sit in our bums all day, biggest meal at night time, sit and watch television. And we wonder why people are putting on weight, it is damn obvious. Sitting is the new smoking. So all of these things are happening. 
Andrew: So when we get into that Paleo lifestyle, we can't go back. 
Ross: No. 
Andrew: We've got to live in the 21st century. 
Ross: Of course we do. 


Andrew: I have a beautiful car and I like to drive it. So how do we manage this? What do we do to reduce the risk or negate these increasing risks of our genes? 
Ross: Okay, well, here's the problem. You see the medical profession have conned the public into believing that there's a pharmaceutical solution to every issue. If you can't fix it with a script pad or a scalpel then it doesn't work, and they don't believe in anything else. And this is the reality, if people practice what I call the five keys to ultimate health, we'd be seeing much less disease across the board. 


Those five keys, I'll go through them quickly very simple. You cannot be healthy and smoke, drink, too much grog or snort cocaine, so anyone who has any addictions to anything is sick. Number two... And we don't talk about this enough. Is every night of your life generate a good quality sleep habit. Seven to eight hours of good quality sleep every night is as good for your body as not smoking.  
Number three is nutrition. Nutrition is simple, it's called eat less and eat more naturally. Now it's very difficult in our modern world to eat naturally but if you can simulate the hunter-gatherer sort of diet as much as you can, and I'm not a great believer in paleo. I just think it's about sensible eating. The best diet with the proven health benefits is the Mediterranean diet. And it's not just the Mediterranean diet, it's the Mediterranean lifestyle. 
So they have their good sized breakfast of fresh fruits, and whole grains, then they burn off any extra carbs in the hot Mediterranean sun in the morning. Come home and have their biggest meal at lunch time. A bit of pasta, maybe a couple of glases of red, get a bit sleepy, have an afternoon sleep. Study of 23,000 Greeks those who had an afternoon sleep had a 40% reduction in cardiovascular disease. Then they wake up and they burn off any extra carbs in the hot Mediterranean sun in the afternoon, and don't have much for dinner. 
What do we do? Smallish breakfast, smallish lunch, snack between time because we're hungry. Have this huge evening meal, and sit in front of television. Now, the body is not like a car, you put fuel in a car use it when you like. But if you put fuel in this car if you don't burn it off within a few hours it gets laid down as fat.  
And so nutrition, straight forward. Eat less, eat more naturally, and what should we be eating? Well, of course basing our diets around fruits and vegetables, two to three pieces of fruit per day, three to five servings of vegetables per day. And people who do that have the lowest rates of heart disease and cancer, just by eating fruits and vegetables at that dose]. And here's the problem Andrew, only 10% of people in the modern world would have that amount of fruits and vegetables every day. 
And the rest of the Mediterranean diet is little bits of meat, eggs, dairy, chicken, fish, nuts and of course, the wonderful olive oil, with a couple of glasses of red wine. Now, I said little bits, but what we do is we over consume, we eat off big plates, big helpings…
Andrew: Sticking my hand up here Ross, sticking my hand up. 
Ross: Well, nobody's perfect mate. 
Andrew: I love good food... 
Ross: So do I. 
Andrew: But I have way too much of it. That drive of hunger is amazing, how do you get around that? How do you teach your patients to eat smaller portions? 
Ross: There are two great success principles on the planet, two, only two. Number one is discipline and perseverance. The more you eat the more you'll eat, the more you'll need to get the same hit. You've got to start disciplining yourself to eat off smaller plates, to eat smaller helpings, not to have second helpings. Don't graze between meals. We're not cows for God's sake, people say to me, "But doc I get hungry about 10:30." Get over it. There's nothing wrong with a bit of hunger. And finally, avoid desserts most of the time.  
Now, I have a thing called the cheesecake rule. So I think 19 meals out of 21 you should follow the program, the other two you can relax it a bit. But I love cheesecakes, it's one of my things I really get a strong urge for. So I would have a big piece of cheesecake maybe once every three months, and when I do, I reward myself and enjoy it and don't feel guilty. But some people think it's their right to have dessert every day, it's just outrageous. 
So I think what you've got to do is you just got to say okay, life isn't about making the big decision to be healthy, it's about making 30, 40, 50 small decisions every day. I won't eat that biscuit, I'll walk up the stairs rather than take the escalators. I won't yell at that fool who just cut in front of me in the traffic. Split second decisions that either take you towards good health and happiness or bad health and unhappiness. It's a moment by moment decision. It's not making that New Year's resolution which never works. You've got to wake up every morning press the reset button, and say I'm going to do it better... 
Andrew: Today.  
Ross: ..today. Every single day. 
Andrew: Now we've alluded to LDL as not being necessarily the bad player that we say. And you know some same say indeed it's our friend, but there seems to be this legion of research showing LDL reductions improving lifespan, what's going on here? What's the real story? 
Ross: Now, firstly, if you look at populations where they've had lifelong low LDLs, they don't get a lot of cardiovascular disease. There's no doubt about that. But here’s the issue that no one really has given any decent research to support. If you have someone who doesn't have cardiovascular disease doesn't, with a high LDL, and you then reduce their LDL with a pharmaceutical drug, are you doing them any good? So maybe they've gone 30, 40, 50 years with a high LDL, and they've got nothing in their arteries, what are we trying to achieve here? 
Because let me just quote a few studies on LDL cholesterol. So there's a place just north of Mexico called the US and they've done a study that was released in the November edition of "The Journal of the American College of Cardiology" 2015. They took five... it’s called MESA Study. They took 5000 people and they followed them for 10 years, 77% of the people in the MESA trial fitted the US criteria to be on a statin because of cholesterol abnormalities. But half of those people had a zero coronary calcium score.  
Now, coronary calcium scoring is the best predictor of heart disease risk. Now, I've got to make this very important point here. I'm not talking about intravenous CT coronary angiography, which should not be seen as a screening test for heart disease. It isn't. It has no prognostic value over the coronary calcium score. Coronary calcium score is about four or five chest X-rays of radiation, no dye, no injections. Intravenous CT coronary angiography... 
Andrew: Risk. 
Ross: Can be up to 300 chest X-rays of radiation. It makes your wallet at least $500 lighter, and you glow in the dark for a few days after the test. And it doesn't give you any extra prognostic information. 

So let's go back to the coronary calcium score, CT scan takes a snapshot of your arteries with no injections. If your coronary calcium score is zero... And half the people in this study had a zero calcium coronary score, half that's... Sorry half the 77% of the people with high cholesterol, zero calcium score. Their heart attack rate over the 10 years was so low, despite their high cholesterol, that at the conclusion of the trial, statins are worthless for people with zero calcium scores. 
Andrew: For primary prevention. 
Ross: So I don't treat cholesterol at all Andrew, I treat risk. And the best assessment of risk is a coronary calcium score. So all males at 50, all females at 60, should have that as a routine... Like you'd get your prostate checked, or your breasts checks, or your bowel checks, or whatever. But if, say for example, you said to me look Ross, I'm a 45 year old male, my dad had a heart attack at 50, I'd do a calcium score on you now.  
I've got a 42 year old woman whose mother had a heart attack at 48. Any calcium score above 400 is serious, her coronary calcium score is 550. So she needs aggressive risk factor modification, not just all the 5 keys of a being healthy. I haven't spoken about the last two, I'll get to that in a second. But she not only needs the no addictions, good sleep, good eating, we didn't mention three to five hours of exercise every week, and the best drug in the plant is a thing called happiness.  
So she needs all of those, and I think all of us need all us need all of those. They're not negotiable for anybody. But she also needs statin therapy to lower her cholesterol, she needs to keep her blood pressure well controlled, the 120, 130 range at the very most, low dose aspirin. All the stuff you would give anyone with proven vascular disease, because she's already at very high risk. But I don't care what... I've got to tell you another great story. 

Andrew: Yep
Ross: I've got a patient who came to see me when she was 58. Her lifelong cholesterol level was 9.5. She'd been on statins, they made her feel dreadful, she couldn't lift her leg, she had aches everywhere. And she said, "Look, I'm at my wits end my doctor's are all telling me I'm going to die if I don't take a statin, with a cholesterol of 9.5," And I said, "Well let's get a calcium score." Calcium score age 58 was? Zero. So I said, "Look, the statins have knocked your body around. You've got a zero calcium score. Clearly in your case, your LDL isn't causing you problems. You can get the sub fractions measured, you can do what you like, but you got zero score why bother?" You know it's not spilling into their artery. 

So anyhow for the next eight years she was told by every doctor she saw, "If you don't take Lipitor you're going to die," the nonsense I hear some GPs say. And anyhow, she came back to see me a year ago, having heard this but resisted going back on the statins. So now in her mid to late 60s, her calcium score had rocketed from zero with a lifelong cholesterol of 9.5 up to? Still zero. And so in her case, the statins were worthless. 

Now, in 2016, a big study came out of the UK published in the "British Medical Journal," 68,000 people over the age of 60, followed for 10 years. And showed that firstly, if you've made it to 60 without heart disease, there is no link between LDL cholesterol and heart disease, okay?  

Andrew: Right.
Ross: If you've made it to 60. Because what's that's saying is that in your case, your particular LDL isn't arthrogenic, so not always is the LDL bad. And it's not always small versus large, it's just some people have LDLs that aren't going to hurt them, some people do. But what it did show; the higher your LDL, over the age of 60 without treatment, without heart disease, the longer you live, the less cancer you have, the less gastrointestinal disease you have, the less infectious disease you have. Now the obvious question there is why? What is protecting you with a high LDL over the age of 60? 

Well here it is. In healthy people the covering of the cell, the membrane, in a healthy person is 75% fat. I wrote about this in a book in 2002 called "The Cell Factor." And the cell factor was that 75% fatty membrane acts as a protective coating against outside toxins. So the sickest people on the planet are not fat Americans, which is what most people say. The sickest people on planet live in Africa, because they're malnourished. 
The worst thing for your body, is to not have enough fat in that membrane to protect you against outside toxins. So it's really easy for HIV, tuberculosis, malaria to cross those membranes and kill the person. That's why they have dreadful mortality rates, they die from serious infection. So if you've got a good LDL coating in that membrane, it's going to stop all the toxins getting in. Thus less cancer, less infectious disease, less gastrointestinal disease. And you don't get heart disease if you've made it to 60 with a high LDL. Well, you don't get heart disease from cholesterol. 
Andrew: Yeah, right. 
Ross: Okay, in fact, over the age of 60, the major cause of cardiovascular disease is hypertension. So hypertension is really the poorer cousin to cholesterol. Because we had the blockbuster drugs, the statins released 20, 30 years ago, and every man and his dog who’s cholesterol nudges up a bit is put on a statin. 

I had a phone call on my radio show... This is "Talking Lifestyle" on Sunday night that now goes all throughout Australia, 6 to 8, for anyone who's listening, 954 in your AM listening dial in Sydney, but anyway, sorry. So I had a phone call a couple of months ago, from a woman who said a general practitioner... Wait for this one, wanted to put her 95 year old father on a statin because his cholesterol had gotten to 5.2. Now, I've got to say to you, Andrew, there is not one shred of science that treating anyone's cholesterol who doesn't have heart disease... 
Andrew: Ridiculous waste of money.  
Ross: Over the age of about 70, has any benefits at all. There's no science at all, it's complete nonsense. It's throwing around these drugs like dish water. Another trial came out a few months ago showing that if you treat cholesterol in people who don't have heart disease over the age of 65, with a statin, you increase their death rate.  
So what I'm saying is that statins should be used, but not for people just because their cholesterol has gone up. So the only people I use statins in are people who have a high coronary calcium score. So a coronary calcium score that put you in the 25th percentile. So if I've got a 45 year old man with a strong family history and a coronary calcium score of 50, which is only in the middle of the mild range, he probably needs a statin, because he's already got muck in his arteries at the age of 45, and it's just going to get worse as he gets older. 
But if I've got a 70 year old man who's got a calcium score of 200, I congratulate him, it's not a big deal for a 70 year old to have that. And I certainly wouldn't give a statin to that person regardless of their cholesterol. But I give statins to everyone with a high percentile ranking coronary calcium score. Or if you've already had a heart attack, a stent, or a bypass, there is an evidence base that you will benefit from being on a statin. 
But the evidence base is nothing like those five keys of being healthy. So if I give you a statin in an average dose I'll reduce your risk for another cardiovascular event in the 20 to 30% range. If I get you to tighten up your lifestyle with those five keys of being healthy... A recent trial out of Holland called the "MORGEN Study" M-O-R-G-E-N- Study, showed if you do those five things well, you reduce your risk for cardiovascular disease 83% with no side effects. 
Andrew: So this is the thing that gets me, so for instance we talk about the French paradox, we talk about the Mediterranean diet, but as you mentioned it's the Mediterranean lifestyle, [so let's discuss] stress. 
Ross: Yeah, It's the whole package, stress...don't get me started. 
Andrew: I'll get you angry. 
Ross: No, the Walker rule number two of medicine is the patient is one with the disease it's not my problem. 

But look, stress is the big precipitant and we have so many people saying in the medical profession, "Oh, stress doesn't cause disease.” Give me a break. I would hardly ever see anybody who didn't present with some acute coronary syndrome who wasn't under stress at the time. And see the problem with stress in our society is that we live this 24 hour day, seven day a week lifestyle. We're on constant contact with those damn mobile phones, or electronics everywhere in our face you can't get away from it. And there are so many choices. 

Choice is a cause of stress as well, you can't just buy a car today, you have about 30 choices and about 30 different types within the choice. You can't just go and just get a cup of coffee, you got to, whether it’s decaf or a caffeinated or whether it's a cappuccino or a latte… there's just all these stresses from all the choices we've got. And the stress is from people wanting instant answers. You didn't reply to my email? I sent it five minutes ago, give me a break. 
But all of this sort of stuff, and I think that those are the situation… we’ve got these complex lifestyles, we got complex relationships, we got complex jobs, even complex travel, and people are just stressed out of their brain. And then they're not dividing their energy properly. And I think that body works well in about eight hours of active energy, eight hours of relaxation energy, and eight hours of sleep, but we're not doing that anymore. 
Andrew: I have to go back to LDL...  
Ross: Yeah, sure. 
Andrew: And the structure of LDL, of the molecule. The biggest mistake as I see it firstly, is that we say that cholesterol is the problem rather than lipoproteins. Is part of the problem what we're doing to the protein the glycation, the oxidation, is that a real issue? 
Ross: I think it's a huge issue. 
Andrew: Okay, so when somebody has a large pool of LDL, their levels are higher. They’re going to have more of...more numbers of, the small, the medium and the large. Some will be swayed towards one or the other. How real is that measurement? 
Ross: Let's now go to the LDL itself, the problem with LDL is that a lot of the data is being grubbied by the people that have familial hypercholesterolemia. They have a defect in their LDL receptor where they’re not incorporating cholesterol into the cells, so it spills outside. Now could it be that that LDL receptor defect is then allowing the fat to spill into the arteries? But skewing all this stuff about small versus large LDL. Because then you bring into the mix the whole discussion of saturated fat, which puts up your LDL cholesterol. 
Now, recently, a few months ago the "PURE Study" was released by Professor Salim Yusuf, one of the most respected epidemiologists in the world. Where he looked at 135,335 people in 18 countries over 7.4 years, and found that those who had the highest death rates, 28% increased death rates, were those who had the highest carbohydrate intake. The total fat intake, those who had the highest total fat intake, 23% reduction in death rates. Those who had the highest saturated fat intake... What we've been told for years by the brain-dead members of the medical profession who believe this nonsense, and nutritionists who believe that saturated fat causes... We've been told for years saturated fat causes heart disease. Show me the evidence? Because it's just not there. 
Those who had the highest intake of saturated fat in this particular study, had a 14% reduction in death and heart disease. A 19% reduction with those who had the highest intake of monounsaturated fats, things like olive oil. Those who had the highest intake of the omega-3 polyunsaturated fats, 20% reduction in death rate.  
So I'm over this whole saturated fat nonsense. But the problem is when you look at the LDL data large versus small, I think it's being grubbied by the fact that they're not dividing the large LDL people into the people with FH, familial hypercholesterolemia, as opposed to the people who just have a high-ish HDL cholesterol because they have a fair bit of saturated fat. 

Familial hypercholesterolemia is not a cholesterol of say eight and an HDL of two, and a triglyceride of 0.7, that's not FH. FH is an LDL or total cholesterol of eight, HDL maybe one, and a triglyceride that's pretty neutral that's FH. 
Andrew: I thought trigs was high in familial [hypercholesterolaemia]. 
Ross: No, no, no that's familial dyslipidemia. I'm talking about familial hypercholesterolemia. 
Andrew: High cholesterol... 
Ross: And the problem with familial hypercholesterolemia is that 50% of people have had a vascular event by age 50. But when you're an optimist, that means 50% of people haven't. So again even within that mix, there are some people whose LDL doesn't cause them a problem. 

So this one size fits all soon as your cholesterol nudges up we're working on a statin, there's no good science behind it, that's my concern. Now again, when I have anyone on a statin drug, I put everyone onto a few things to supplement that. I'll put them under a thing called BergaMet Pro Plus. And I was involved in a study where we gave people 20 milligrams of Rosuvastatin, the old Crestor… 
Andrew: Crestor... 
Ross: … which is the strongest of the four statins. We reduced their LDL down 56.5%. Then we cut it in half to 10 milligrams of Rosuvastatin, added the BergaMet Pro Plus twice a day, and got their LDL down 52.5%. But a much bigger rise in HDL, and a much bigger drop in triglycerides. Suggesting that we're affecting more the particle size with the BergaMet rather than just the statin alone. So it's actually better to be on a statin with BergaMet at a lower dose than just to be a bigger dose of statin by itself. 

Also all people on a statin... I believe all statins do affect your Coenzyme Q10, I put them all on ubiquinol not ubiquinone. Now, ubiquinone, the standard CoQ10, the problem with that is it has to be metabolized to ubiquinol. But here's the issue, when we hit 50, the diaphorase enzyme that converts you from ubiquinone to ubiquinol starts to drop. So you're not getting enough active ubiquinol in the mitochondria to protect you against the direct statin effect on the mitochondria that causes the muscle aches and pains, and also increased risk for diabetes. All works through what we call the GLUT4 pathway within the mitochondria.  
So therefore, I use ubiquinol in everyone who's on a statin. Now I personally take ubiquinol. I'm in my early 60s I'm not on a statin but I use ubiquinol just to give me energy. So I think it's terrific because it drives that mitochrondria. One of the major drivers to the mitochondria is ubiquinol. So I don't think there's any point using ubiquinone in anyone, use ubiquinol there's much data on that. 
Andrew: So I thought that ubiquinol... Sorry, forgive me, ubiquinone was okay particularly for younger group of patients, but once you start to age that enzyme dropped off so you couldn't recycle it? 
Ross: Yeah, but why bother using ubiquinone when you've got ubiquinol, you just use the active stuff. But the data is there. But mind you they did studies on young nurses, average age of about 20. And they found that even four weeks of being on ubiquinol improved their stress levels. In young athletes, 100 athletes out of Germany, same deal. That six weeks of being on ubiquinol actually improved their sports performance. So I think there's better data for ubiquinol, so I think ubiquinone is really probably dead as a supplement these days. 
Andrew: I know we're getting off the cholesterol issue but with regards to ejection fraction, does ubiquinol help ejection fraction? 
Ross: Oh yeah, there's quite a bit of very good data about ubiquinol improving endothelial function, improving ejection fraction, improving other parameters of cardiac performance as well. It's not just all about ejection fraction. Because when we talk about heart failure, we talk about heart failure with reduced ejection fraction, that's the systolic dysfunction, and then heart failure with preserved ejection fraction, that's diastolic dysfunction. 
So it's also having effects on all the different parameters of heart failure, and there's much better data with ubiquinol than there is with ubiquinone. But mind you, let's be scientific here, there was a study called "Q-Symbio" where they used ubiquinone. And that was in about 400 people, 200 milligrams a day of ubiquinone, and even doing that over two years reduced cardiac events by about 50%.  
Now, if there was a drug that did that the drug companies wouldn't leave us alone with the information. But that was just pushed aside and no-one's even really acknowledged that stuff. In the same way with my BergaMet data. I've got to admit I have an association with the company, I do all the research with my colleagues in Italy. I'm an honorary Calabrian citizen so be careful where….
Andrew: Watch out, don't cross you. 
Ross: I do know your address… What I'm saying is that we have science...evidenced-based data for ubiquinol, for BergaMet. And one of the things I also add in is magnesium orotate. And it's not the magnesium, it's the orotate... 
Andrew: Orotate. 
Ross: Which lifts up the ubiquinol in the mitochondria, so you're really giving that mitochondria the best bang for your buck, by using a combination of a high quality oratate product, with a high quality ubiquinol. Now another thing that I'm using these days as well, it's the new kid on the block really, is vitamin K2. Vitamin K2 is also... 
Andrew: Now this is really interesting. 
Ross: Well… but it's also affected by statin therapy so I give... And it must be 180 micrograms a day of K2, that's the dose. And it's got to be the MenaQ7 variety of K2, so I use that every day. And basically what I say to the patients... And this is very good science behind this. It takes the calcium out of your arteries and puts it back in the bones where it belongs. And I think that's a really, really good thing to do for people with cardiovascular disease, that combination of supplements. 
Andrew: So talking about the... Going back to the calcium score, I know this is going to be variable between every different person with a different lifestyle. 
Ross: Sure. 
Andrew: But as a generality if somebody let's say they come to your office at 50, and they have a coronary artery calcium of say eight, what would you say would be the likelihood of the progression of that to 60, i.e. would it.... 
Ross: Yeah, it's about 20% per year.  
Andrew: Twenty percent per year. 
Ross: So if you do the sums on that 20% per year... I mean I don't do anything but like from 8 to 60 over…
Andrew: So every 10 years you'll be really looking really dramatically increasing risk…
Ross: For people that have low calcium scores, I repeat the calcium score every five years.

Andrew: Right, ok. 

Ross: Ok, if you've got a high calcium score... So just say calcium score is getting 250, 300 plus, it's a waste of time doing it again. Because even if you have it done on the same machine five minutes later, you can’t absolutely guarantee you're in exactly the same position, they start the scanning from exactly the same spot at the suprasternal notch. You have the same breath hold, the same time your cardiac cycle. 
So even slight variations and that can take a score from 350 to 450 or 350 to... And you wouldn't believe how much… Just because of the brainwashing by the medical profession in patients, how much people are so fixated on numbers. I had a woman come in the other day "Oh doctor have you seen what's happened to my cholesterol?" It had gone from 5.2 to up to 5.4, I said “Yeah, so what? "But my triglycerides doctor have gone from 0.7 to 1?" I said so that could have been the Chinese meal the night you had before the test, cheat for the test next time. 
I'm just saying we get too obsessed with numbers, and this is what disturbs me. You’ve got this fat slob goes into the doctor, and, "Doctor, I've got a cholesterol problem." So the doctor says I can fix that, Lipitor – next! And the guy walks out going, "Oh phew, I didn't a lecture about being fat," and the doctor goes, "Oh, phew, I didn't have to talk to the patient." 
And then the perception is given to the public by the medical profession that the key to good health is lowering a number in your bloodstream. Not good. 
Andrew: Talk to us about plaques. When we're talking about calcification of a plaque, an unstable plaque or even a necrotic plaque. What are they? And can we actually regress them? 
Ross: The answer is yes, to maybe all of the above, but just let me explain to you what happens okay. What we're talking about here is the condition that everyone's heard of atherosclerosis. Now, atherosclerosis can even start in-utero, if the mother is a smoker, or has high cholesterol, or whatever. And little bits of what we call fatty streaks... 
Andrew: Streaks, yeah. 
Ross: Build up in the wall of the aorta, it's been shown in children who tragically were stillborn. I'm not saying that's the cause, but they’ve showed when they did an autopsy that there were streaks in the aorta already in that circumstance. 

But as soon as your mother gives you baby food which is full of synthetic muck, little droplets of fat start to increase in the wall of your arteries. So we're talking about a disease that occurs for decades in a pre-symptomatic phase. And here's where many people get it wrong, everyone thinks what happens is cholesterol slowly closes over the arteries. Complete nonsense. Imagine a doughnut hole in the middle, while the blood is going through the middle, the fat swelling outwards in the wall of the doughnut. And then what happens when that fat reaches a critical mass, it suddenly ruptures. That's what an acute coronary syndrome is. 
And this is really interesting, because I want to drill down on this quite a bit. The body uses calcium as a strengthening agent so it grows into the plaque to try and stabilize a fatty plaque. Now, the more fat you have in the plaque, the more dangerous it is, and the more it has a tendency to rupture. But here's the deal, if you have the standard risk factors for heart disease, so the sedentary guy in his 60’s, who smokes, and he's...maybe a bit of diabetes there, his blood pressure's up a bit, the cholesterol is not that good. And he suddenly has a heart attack that's a typical cardiac rupture. 
So I make the analogy to my patients that if you got a big juicy pimple and you squeeze it, all the pus comes out suddenly. That's what happens with a cardiac rupture. Of a big fatty plaque full of muck, ruptures into the channel, splits open into the channel, and a clot forms over where all the muck is and causes the heart attack. 
But here's the drum: you also have plaque erosion. Now if you imagine a red pimple, that doesn't have a lot of pus you squeeze that, not a lot of pus comes out. But it basically just splits open a bit of blood comes out. Now, that's what happens in younger people who don't have much of a cholesterol issue, don't have a lot of atherosclerosis, maybe a zero calcium score, and they still have a heart attack because they erode a plaque. Much more common with inflammation, and with thrombosis, whereas cholesterol is not a big issue there. It's inflammation and thrombosis.  
So when you hear about a 45 year old woman's had a heart attack, and their cholesterol wasn't that big a deal, and somebody might have done a calcium score, who knows why, and it was zero. But they still had a heart attack, so that calcium score stuff doesn't work? No, no it's a different problem it's plaque erosion, more caused by inflammation and tendency to thrombosis. 
So for example, when you hear a 25 year old woman took the pill for a month and has a stroke, they want to sue Bayer for making the pill. Or someone has a big clot in their legs traveling from here to over to Heathrow, and wants to sue Qantas because they got the economy syndrome. They should be suing their relatives for giving them the genes such as Factor V Leiden, prothrombin complex abnormality, antithrombin 3 deficiency, proteinase, protein C, MTHFR gene, LP, whatever it is, one of those things. 

That thickens your blood. So you take the pill and the pill was just the precipitant for your lousy genes. You have some inflammatory process going on, you get a bad dose of influenza. Study out of University of South Wales showed that people have a flu vaccine every year, have a 30% reduction in heart attack. Because they're reducing the inflammatory switch on by the influenza. A bad bout of pneumonia switches on your inflammatory system. I say it's like having a security guard on crack shoots before he asks questions. 
So the immune system's all fired up, sees a fatty plaque, erodes into it and causes erosion, not rupture. Because the activation of the immune system. So recently we've just seen the release of a thing called the "CANTOS Trial" where they used a monoclonal antibody called canakinumab, and this thing targets a thing called interleukin 1. Now, the results of that were pretty disappointing 
Andrew: Oh, really? 
Ross: Oh, yeah, yeah. 
Andrew: Because they were all throwing up their hands, I thought it was a cracker, because they thought “We now know that inflammation plays a part in heart disease.” 
Ross: I'll get to that in a second. But the "CANTOS Trial" showed that in the placebo group, the amount of heart attacks was something like 4.1 per 100 person years. The people who were treated with 150 milligrams of canakinumab which was the sweet spot dose. It was something like 3.86 per 100 person year. So it was at a 15% reduction in heart attack with the average… it was statistically significant, but it was pretty marginal. 
Andrew: But is that clinically relevant? 
Ross: …I don't know, well let me tell you, a mate of mine in Perth called Dr. Mark Nidorf has done a thing called the "LoDoCo Trial" in his own practice. This is just extraordinary work by a very, very good cardiologist. 

And what Mark did was gave his patients who had acute coronary syndromes that came in, over the next three years placebo controlled trial, gave them 500 micrograms of Colchicine. The drug you use for gout, because it also has very good anti-inflammatory properties. Now, the placebo group had a 16% recurrence rate of acute coronary syndrome, whereas the people given Colchicine had a 5% recurrence. That's huge. 
Andrew: Yeah, that's massive. So that's… Uric acid as a risk factor for coronary heart disease? 
Ross: Yeah, but also just the anti-inflammatory effects of the Colchicine. Much stronger than the very, very expensive canakinumab. 
Andrew: So hang on, not just working on uric acid, but as an anti-inflammatory in general? 
Ross: Yeah, in general. Anti-inflammatory, anti-fibrotic agent. It stabilises the plaque, you see we're talking about plaques... And that's where statins work. 

Statins, yes, of course they reduce cholesterol. Anyone who doesn't believe that is an idiot. Of course, statins block HMG-CoA reductase so have a significant prevention of reduction in LDL levels. There is no doubt about that. As do these new PCSK9 inhibitors. They pulverize LDL cholesterol. With again, a weak benefit on clinical events, a weak benefit. 

So when you give a statin, you actually do stabilize the plaque, if people have plaque in the first place. And that's my only concern. See I'm still…
Andrew: So find out if they have plaque? 
Ross: Yeah, I'm still a semi orthodox cardiologist, semi orthodox. But... And I treat people with heart disease, aggressively. I've had about four people in the last week, I've sent out for angiograms with a high grade lesions that need either stenting or bypass. I totally believe in all that stuff. 

But what I'm saying is the concern I have is that all the information of benefits of all of these drugs, come in the very high risk groups. And what the medical profession has done is extrapolate them down to people who are very low risk... 
Andrew: Low risk. 
Ross: Who have no evidence of significant plaques, and they're still filling them to the eyeballs with all these drugs.  
Andrew: So can you change a plaque? You can stabilize it, can you make it less necrotic, can you change the fatty acid composition? 
Ross: All of the above. Of course you can. 

But many, many years ago a mate of mine in the US called Dean Ornish did a study called the "Californian Lifestyle Study," and this had nothing to do with drugs. He basically put people in this really rigid, low fat diet, which I don't agree with. But a really rigid diet, that no one could stick to anyhow. Ten percent fat, pure vegetarian diet, five times a week supervise exercise program, with a little sitting defibrillator in the corner, these people had coronary disease. And here is the big deal, you mentioned stress before. Weekly encounter group, where they all sat around speaking about their life and their feelings and everything else. But daily, one hour of meditation. And these people had a significant regression, with no drugs, of their coronary artery disease.  
Now I believe there's quite a bit of work… Another mate of mine in California called Professor Matt Budoff, who works at the University of California in Los Angeles. He did a study on "Aged Garlic Extract," and found regression after 12 months of using a high potency aged garlic extract. So there are so many… so much evidence of high quality natural medicines combined with lifestyle, where you can regress plaque. Then again, if you've got quite severe disease, I'll bring in the statins as well, and I'll bring in whatever other trick there is to bring in, with some evidence based behind it. 
Andrew: Fish oil.

Ross: Yep.

Andrew: Can I have a comment? It was, you know, the GISSI P, the GISSI-HF, it was all, you know... Was it Roberto Marchioli was the proponent of this. And then Roberto Marchioli did a trial where he said no, doesn't work. Where are we at with fish oil?  
Ross: There's a little was known place in the U.S called The Mayo Clinic. One of the greatest institutions in the world. And the Mayo Clinic published in their "Mayo Clinic Proceedings" in January of 2017, this year. Published a meta-analysis of all the fish oil trials, okay? And they found that the randomized control stuff, which only went for a couple of years didn't do much.  
And here is the key point I'd like people to get, okay? But when they looked at the trials that were done beyond five years, there was an 18% reduction in cardiovascular disease. Fish oil, multi-vitamins, BergaMet, ubiquinol, vitamin K2, aged garlic, magnesium oratate, all these things work but they don't work as quickly like drugs. And here's the point, pharmaceutical drug is like a high performance motor car. Gets you from A to B very quickly, but with the potential of crashing and damaging yourself, possibly even killing yourself. So for a high performance motor car you’ve got to have seat belts, you’ve got to have all these safety requirements, you’ve got to have all these rules around driving. Whereas I see supplements like a bicycle, get you from A to B much slower, but you get some exercise along the way... 
Andrew: Probably enjoy yourself. 
Ross: Yeah, so a lot… much, much more contemplative. But it takes a lot longer to get there. So when you look at most of the studies of supplements, in the short term they don't do much. 

The Male Physicians Trial, the Nurses Health Study; they've been done in Harvard for the last 30 years. Multi-vitamins for example, up to 10 years, did absolutely nothing. I have patients take a multivitamin for a few months say, "I didn't feel any different doctor, so I stopped." But when you get to 10 years in the male, so this is randomized control stuff, we're not talking about just observational. Randomized control trial in the male, there was an 8% reduction in cataracts and common cancers

Now you’ll say 8% is not much Ross, but you’re only taking a multi-vitamin everyday.. and this is additive randomized control trial. When they got to the observational data in the nurses at 15 years, there was a 75% reduction in bowel cancer, 25% reduction in breast cancer, there's a 23% reduction cardiovascular disease. Now when you got to the… It just released couple of years ago, the 20 year data, randomized control data in the males. Those who took a multi-vitamin every day; a 44% reduction in cardiovascular disease. What you get with the statin, but it takes 20 years to do it. So you’ve got to be in it for the long haul.  
And here's the problem, whether we're talking about statin therapy, blood pressure treatment, multi-vitamins, or any sort of supplements. Only 50% of people are still taking the prescribed treatment after 12 months. Compliance is dreadful because human beings are human beings. They just give up, and they go, "I ran out, I forgot to reorder or whatever, or didn't go back to my doctor and get the script." And so that's why we're not seeing the great benefits we should be seeing with all of these things because people aren't in it for the long haul. 
Andrew: Back again to the LDL molecule. 
Ross: Ok. We keep coming back. 
Andrew: Lipoprotein(a), Apo-B to Apo-A, or Apo-A to Apo-B? Tell us about these, what are the risk factors, what's the importance and what do we need to do to control them? 
Ross: Right. Well, firstly, lipoprotein(a) is one of the major cardiovascular risk factors. One in five people wandering around the streets have a high level of LP(a) in their bloodstream. The problem is the randomized control trials have shown no difference treating it, because there is no real treatment. There's a new CETP inhibitor called Anacetrapib which does have an effect on LP(a), and has just been shown to have a reasonable benefit in cardiovascular mortality. Unlike the older ones, which have been shown to increase cardiovascular and mortality. 
So watch this space Anacetrapib may do something. But I still... Even though there isn't any strong evidence base in terms of a randomized control trial. I still routinely use in all of my patients a combination of vitamin E, vitamin C and lysine. So lysine, which is used for cold sores. 1000 milligrams of lysine I think blocks the lycile residues on the LP(a) molecule, and stops it getting into the wall of the arteries. And the vitamin C, vitamin E... Now, again, let's talk about that. Here’s another great story. 

In 2004, a guy called Edgar Miller, did an editorial in the "Annals of Internal Medicine" saying vitamin E not only doesn't work, but may even increase mortality. Now that was done from an analysis of high dose vitamin E. He looked at 11 trials, eight the 11 were mono-therapy, and most of those trials were, as you say, dl-alpha-tocopheryl. Which is synthetic rubbish, which should not be used, okay?
The only three trials where they combined vitamin E with vitamin C... Because in my view vitamin E doesn't work without vitamin C. So the only three trials where they combined vitamin E with vitamin C, they used synthetic vitamin E. So they're using the rubbish vitamin E, and they showed a slightly higher trend towards mortality in people in these trials, these 11 trials. But they completely ignored the only two trials in the history of evidence based medicine, where they've taken natural vitamin E with vitamin C. Both of those trials the I-V-U-S trial the "IVUS Trial," and the "ASAP Trial," both showed a 25% reduction in the progression of atherosclerosis, when you combine the two things together. 
So I use C, E and lysine for LP(a). And people who have a very high risk, they've either had a very high calcium score, or they've already had clinical heart disease, I try to encourage them to take short-acting nicotinic acid. And see there's been a huge.... 
Andrew: Good old flushing nicotinic acid yeah. 
Ross: Good old flushing and look... 
Andrew: It works better than the long term right?
Ross: The long term stuff doesn't work. Two major trials showed that long acting nicotinic acid doesn't work. But the older trials of nicotinic acid, the immediate release stuff, the stuff that gives you flush, have shown regression and improvement in cardiac events.  
So what I do with my patients? 250 milligram nicotinic acid. Get them to cut into quarters, and then they just gradually build up the dose of nicotinic acid over a few months to whatever they can tolerate. Two pills twice a day, half a pill twice a day. I don't care as long as they get a bit of flushing for about five minutes twice a day. Because the flushing is telling them that the stuff's opening up their microvasculature. But I don't want them to walk around with a red face all day, that's ridiculous... 
Andrew: And it's a horrible itch, it's a really an interesting itch. 
Ross: Yeah, an itch as well. And so, if you just give them a little bit of flushing twice a day. It reminds them the stuff's working, and that has been shown to reduce LP(a) by around 25% 30%. So I use nicotinic acid in that situation or in people who've got pretty vicious vascular disease, anyhow, so that's a good drug.  
And I've got to say vitamin B3 has been getting a really good press lately, it's been getting a great press. The seminal work from the Garvan Institute at St. Vincent's where they showed that B3, a good old fashioned niacin, actually reduced birth defects and miscarriages. There's been a lot of work by the wonderful Australian researcher is now at Harvard, David Sinclair, the anti-aging guy. Which is not a topic for today's discussion but he's been... 
Andrew: Next week… 
Ross: But he has shown in his work, that nicotinamide added to a riboside ring, so nicotinamide riboside, actually improves longevity by about 20% in experimental animals. So they're now doing human trials in this as well. 

So I think B3 is been often the forgotten supplement, and we need to really be focusing on different aspects of B3. Whether it's nicotinic acid, nicotinamide riboside, or just straight nicotinamide. Because there’s a very good study using a product called Insolar. Where if you have 500 milligrams twice nicotinamide, it reduces skin cancer risk.
Andrew: Yeah, yeah, for 28% or something? 
Ross: Yeah, 28% reduction.
Andrew: Over 12 months, not 6 or something. That to me is really interesting. Topic for another day. 

But I have to ask you about exercise. We talk about cardio exercise, then there's HIT training. I think it was Mark Houston said, "Do the strength before the cardio." Does this have a real effect on how your cardiac health is affected? 
Ross: Yeah, look... Can I say, I'm not an exercise physiologist, and I'm not really sure about the Mickey Mouse aspects of whether you're better off doing strength training before your cardio whatever. 

I think the important thing... And this is the real message here, is you got to exercise. I mean that's the point. Whether you're doing one or the other, I don't really think it matters. I think the important thing is that we get what I call the ‘Walker suggested dose of exercise’, which is three to five hours every week of some form of exercise. 
And I think exercise should be about two thirds cardio, a third resistance training. So whether that resistance training is lifting light weights… and I think certainly for people over the age of 50, going crazy with this stuff is ridiculous. I say the only joint you blow over the age of 50 is your hip or your knee, and I think it's important not to go overboard with exercise when you get to that age, I think exercise can be dangerous. 
I'll give you a couple of quick examples. I had a 65 year old man who wanted to walk the Kokoda trail. His daughter... Now this is Twilight Zone stuff. His daughter had a dream before he went away that he died in the Kokoda trail. So she insisted he come in to see me for a cardiac check up before he did the Kokoda trail. No symptoms, no history, no major risk factors. 

Put him on the treadmill do a stress echocardiogram; takes a picture of the heart, with ultrasound, before and after exercise. He had no symptoms during the stress test, he had no ECG changes whatsoever, but his echo at the end of exercise almost slowed down to nothing. And I said, "Let's forget about the Kokoda trail." Put him in the local hospital, severe triple-vessel disease, coronary artery bypass grafting. 

My message there is that I think exercise is the second best drug on the planet. But, if you're listening to this and want to start an exercise program, or want to get your patients on to exercise. I think it's important they... 
Andrew: Get a checkup. 
Ross: They should have a cardiovascular check before they do so. I also was one of those stupid old farts that played soccer until I was 52. I've completely destroyed my right knee and that's a topic for another day. 

But a month before I stopped playing soccer, I was playing over 45 old fart soccer. And a 61 year old man in the opposition, drops dead in front of me. Again, people running around a field with...without a proper cardiovascular check up, go and play the sport. Now, because he was a fullback I resuscitated him. If he was a forward, I would have let him die of course, he had bypass surgery within two hours and he's now one of my faithful patients. 
But the point I'm making here is firstly, if you're going to do exercise, make sure you're well enough to do exercise. Secondly, two thirds cardio, a third resistance, and the resistance can be the light weights, or can be the yoga, it can be Pilates, and the cardio can be whatever cardio you would do. 

So when you get into the Mickey Mouse aspects, whether it should be the high intensity interval training or the... Look, we just want to get people out there exercising, not to make it too complicated for people. A brisk half an hour walk every day is three and a half hours a week of exercise. Just from doing that, it's better than sitting on your bum. 

Now here's the issue, is more better? And the answer is no. The evidence doesn't show that any more than five hours a week is better for you than three to five hours which is the sweet spot. It's like red wine, maybe having no red wine a week doesn't help you, a couple of glasses is good, but once you get above that you get problems. 
So again there are some people who do perform high performance exercise. I saw one of my patients who's an ultra marathon runner. He's already had a heart attack. He came to see me the other day, he was doing a run from Newcastle to Sydney. I told him there was a perfectly good bus service, just absolutely ridiculous.  
But look exercise, what does it do for you? If you have a three to five hour a week exercise habit you reduce your risk for cardiovascular disease, 30%, cancer, 30%, Alzheimer's, 30%, diabetes, 30%. Reduce depression, 50% reduction osteoporosis, drops your blood pressure, and you sleep better. There is no pharmaceutical preparation known to man that is stronger than exercise, there's only one drug on the planet that's better and that's a thing called happiness.  
Andrew: Ahh, now there's a whole podcast, happiness. 
Ross: Sure is. 
Andrew: Mindfulness. 
Ross: Happy to do that one as well. 
Andrew: Dr Ross Walker, I can't thank you enough. By goodness we've traveled a lot today.  
Ross: Well, it's typical of my bizarre brain... 
Andrew: You got the speed of freight train I tell you. Thank you, so much for joining us and taking us through the important issues, the undiscovered or the unlooked-for issues, that are evading so many practitioners. Particularly medicos, with regards to cardiovascular disease. Number one, coronary artery calcium score... 

Ross: Yep.

Andrew: Lipoprotein(a)…
Ross: Yeah… Insulin resistance, we spoke about the place of LDL cholesterol whether it is or isn't important. It is in some people, it isn't for other people. 
We spoke... The most important message I’d like to give anyone are those five keys of being healthy. You cannot be healthy if you have addictions, you want good quality sleep, good quality eating and less of it, three to five hours of exercise and happiness. 

If everyone cultivated those things well in the society, we'd see a marked reduction in all diseases, so that's the major point for today. And also there is very good evidence base around supplementation. And the supplements that I encourage all my patients to have a good multi-vitamin every day, some form of omega 3 whether it's fish or krill whatever suits the patient. I'm a great believer in the BergaMet Pro Plus, I'm a great believer in ubiquinol. I think ubiquinol is great for energy, but certainly statins and heart failure, it's great there. And if you want to make it even more powerful use the magnesium oratate, vitamin K2 to take the calcium out of the arteries, put it back in the bones. And the aged garlic extracts also very good with studies on reversal and blood pressure control. 
Andrew: The only negative thing I can see coming out of this podcast is I'm going to be hungrier. Dr Ross Walker, thanks, so much. 
Ross: Good on you, Andrew. 
Andrew: This is FX Medicine, I'm Andrew Whitfield-Cook.

Additional Resources

Dr Ross Walker
Book: The Cell Factor by Dr Ross Walker
Dr Mark Nidorf
Dr Dean Ornish
Prof Matthew Budoff
The Mayo Clinic

Research Covered in this episode

*In order by mention in podcast

Ravnskov U, Diamond DM, Hama R, et al. Lack of an association or an inverse association between low-density lipoprotein cholesterol and mortality in the elderly: a systematic review. BMJ Open. 2016;6:e010401.

Hoevenaar-Blom MP, Spijkerman AMW, Kromhout D, et al. Sleep Duration and SLeep Quality in Relation to 12-Year Cardiovascular Disease Incidence: The MORGEN Study. SLEEP. 2011;34(11):1487-1492.

Dehghan M, Mente A, Zhang X, et al. Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study. Lancet 2017; 390: 2050–62.

The Nutrition Source. PURE study makes headlines, but the conclusions are misleading. Harvard University School of Public Health. 2017 Sep 8.

Gliozzi M, Walker R, Muscoli S, et al. Bergamot polyphenolic fraction enhances rosuvastatin0-induced effect on LDL-cholesterol, LOX-1 expression and Protein Kinase B phosphorylation in patients with hyperlipidemia. Int J Cardiol. 2013 Dec 10;170(2):140-5.

What is Q-Symbio. Q-Symbio Study site. (Accessed 29/1/2018)

MacIntyre CR, Heywood AE, Kovoor P, et al. Ischaemic heart disease, influenza and influenza vaccination: a prospective case control study. Heart 2013;99: 1843–1848.

Ridker PM, Everett BM, Thuren T, et al. Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease. N Eng J Med. 2017 Sep 21;377(12):1119-1131.

Nidorf M. Colchicine for 2(ndary) Prevention of Cardiovascular Disease LoDoCo2 - An Australian-Dutch Collaboration. [Presentation]. ACRA 27th Annual Scientific Meeting, 2017.

Nidorf M, Verma S. Is There a Role for Colchicine in Acute Coronary Syndromes? J Am Heart Ass. 2015 Aug;4:e002372.

Ornish D, Scherwitz LW, Billings JH, et al. Intensive Lifestyle Changes for Reversal of Coronary Heart Disease. JAMA. 1998;280:2001-2007.

Budoff MJ, Takasu J, Flores FR, et al. Inhibiting progression of coronary calcification using Aged Garlic Extract in patients receiving statin therapy: a preliminary study. Prev Med. 2004 Nov;39(5):985-91.

Ages Garlic Extract Reduces Low Attenuation Plaque in Coronary Arteries of Patients with Metabolic Syndrome in a Prospective Randomized Double-Blind Study. J Nutr. 2016 Feb 1;1S-6S.

Marchioli R, Barzi F, Bomba E, GISSI-Prevenzione Investigators, et al. Early protection against sudden death by n-3 polyunsaturated fatty acids after myocardial infarction: time-course analysis of the results of the Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardico (GISSI)-Prevenzione. Circulation. 2002 Apr 23;105(16):1897-903.

O'Keefe JA, Jacob D, Lavie CJ. Omega-3 Fatty Acid Therapy: The Tide Turns for a Fish Story. Mayo Clin Proc. 2017 Jan;92(1):1-3.

Alexander DD, Miller PE, Van Elswyk ME, et al. A Meta-Analysis of Randomized Controlled Trials and Prospective Cohort Studies of Eicosapentaenoic and Docosahexaenoic Long-Chain Omega-3 Fatty Acids and Coronary Heart Disease Risk. Mayo Clin Proc. 2017 Jan;92(1):15-29.

Sesso HD, Christen WG, Bubes V, et al. Multivitamins in the Prevention of Cardiovascular Disease in Men. The Physicians' Health Study II Randomized Controlled Trial. JAMA. 2012;308(17):1751-1760.

Christen WG, Glynn RJ, Manson JE, et al. Effects of multivitamin supplement on cataract and age-related macular degeneration in a randomized trial of male physicians. Ophthalmology. 2014 Feb;121(2):525-34.

Gaziano JM, Sesso HD, Christen WG, et al. Multivitamins in the Prevention of Cancer in Men: The Physicians’ Health Study II Randomized Controlled Trial. JAMA. 2012 Nov 14; 308(18):1871–1880.

Miller ER, Pastor-Barriuso R, Dalal D, et al. Meta-Analysis: High-Dosage Vitamin E Supplementation May Increase All-Cause Mortality. Ann Internal Med. 2005 Jan 4;142(1):37-46.

Salonen JT. Clinical trials testing cardiovascular benefits of antioxidant supplementation. Free Radic Res. 2002 Dec;36(12):1299-306.

Shi H, Enriquez A, Rapadas M, et al. NAD Deficiency, Congenital Malformations, and Niacin Supplementation. N Engl J Med. 2017 Aug 10;377(6):544-552.

Chen AC, Martin AJ, Choy B, et al. A Phase 3 Randomized Trial of Nicotinamide for Skin-Cancer Chemoprevention. N Engl J Med. 2015 Oct 22;373(17):1618-26.

Other episodes with Ross include:


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