Latest / Hardiness with Dr Paul Taylor / Preventive cardiology, exercise, nutrition, stress, and longevity with Dr. Ross Walker
Transcript
- 0:08Speaker 1: Dr. Ross Walker, welcome to the podcast.
- 0:11Speaker 2: Thank you, Paul.
- 0:13Speaker 3: So we met recently. Actually, before that, I met your daughter,
- 0:18Speaker 3: who's brilliant. She's a great speaker. She was actually emceeing
- 0:21Speaker 3: at a conference I was on. I was chatting to
- 0:23Speaker 3: her and she said who she was.
- 0:24Speaker 1: And I'm like, is your dad Ross Walker?
- 0:25Speaker 2: She's like, yeah.
- 0:26Speaker 3: And I'm like, Oh, I happen to be emceeing a
- 0:29Speaker 3: conference that he's talking at next month, which was really
- 0:33Speaker 3: quite funny. But you, I mean, I knew about you
- 0:37Speaker 3: before this thing because I'd heard you on the radio
- 0:40Speaker 3: lots of times and talk a lot of sense. I
- 0:43Speaker 3: think every Australian will probably have heard of you or
- 0:47Speaker 3: every Australian over a certain age because you're an extremely
- 0:51Speaker 3: famous preventative cardiologist in Australia, not many preventative.
- 0:55Speaker 2: Ones kicking around.
- 0:57Speaker 3: But for our international listeners, can you just give us
- 1:01Speaker 3: the quick, it has to be the quick summary of
- 1:03Speaker 3: your background because I know it's very, very extensive.
- 1:07Speaker 2: Right. Well, I've been a doctor for 47 years and cardiologist, obviously,
- 1:11Speaker 2: for most of that. And about 30 years ago, I
- 1:14Speaker 2: started focusing on prevention because this is going to shock you, Paul.
- 1:17Speaker 2: The best treatment of heart disease, cancer, Alzheimer's, osteoporosis, diabetes
- 1:23Speaker 2: is not to get them in the first place. Yeah.
- 1:25Speaker 2: My whole career is based on the concept of prevention.
- 1:29Speaker 2: And I believe over 90% of modern diseases are preventable.
- 1:32Speaker 2: I've written seven books. For the general public, my eighth
- 1:36Speaker 2: book's about to come out in the next six months
- 1:38Speaker 2: called Healthspan. Because again, I don't believe in lifespan. I
- 1:42Speaker 2: believe in being as healthy as you possibly can up
- 1:45Speaker 2: to the time you go into your death phase and
- 1:47Speaker 2: make your death phase as short as possible. So that's
- 1:50Speaker 2: a quick summary of my career.
- 1:52Speaker 1: I think you're very much like me.
- 1:53Speaker 3: I want to be out playing golf when I'm about 92,
- 1:57Speaker 3: come back, go to.
- 1:58Speaker 1: Bed and just not wake up.
- 2:00Speaker 2: Yeah, or 100.
- 2:01Speaker 1: Yeah, yeah, yeah. So that's clearly the way ahead. So
- 2:07Speaker 1: tell us this.
- 2:07Speaker 3: Why did you move from, I term it, the sick
- 2:12Speaker 3: care system into the health care system? Because I think
- 2:16Speaker 3: In Australia, and I think it's very similar, lots of
- 2:19Speaker 3: developed nations, about 98, 98.5% of all government spending on
- 2:24Speaker 3: healthcare is on tertiary treatment. And as we both know,
- 2:28Speaker 3: primary and secondary prevention are cheaper, they're more effective, and
- 2:31Speaker 3: they're less painful.
- 2:32Speaker 1: When did you, 30 years ago, I mean.
- 2:35Speaker 3: That's pretty progressive, 30 years ago. What was the driver
- 2:39Speaker 3: for you to make the jump?
- 2:41Speaker 2: But my interest started, back in the 1980s when I
- 2:44Speaker 2: was a cardiology registrar. And this is where I had
- 2:47Speaker 2: my light bulb moment. I was going down to the
- 2:50Speaker 2: post cardiac surgical ward and I saw people down there
- 2:55Speaker 2: having this mutilating operation on their chest. So having their
- 2:57Speaker 2: chest split open, not once, but sometimes two or three times.
- 3:02Speaker 2: And they were still fat and they were still smoking.
- 3:06Speaker 2: And as Albert Einstein said, there's nothing that's a more
- 3:08Speaker 2: certain sign of insanity than to do the same thing
- 3:10Speaker 2: over and over again, expect a different result. I thought
- 3:12Speaker 2: to myself back then in the 1980s, there's got to
- 3:15Speaker 2: be a better way of treating coronary artery disease, which
- 3:20Speaker 2: is obviously my main focus, than having your chest split
- 3:23Speaker 2: open on multiple occasions. And see, the problem is back then,
- 3:27Speaker 2: there's an old joke, Paul, what's the difference between God
- 3:30Speaker 2: and a cardiothoracic surgeon? God doesn't think he's a cardiothoracic surgeon.
- 3:35Speaker 2: And back then, the cardiac surgeons, I'm not saying they
- 3:37Speaker 2: are now, but they were a tad arrogant. So they
- 3:41Speaker 2: thought that once they did the operation on you, you
- 3:43Speaker 2: were cured. So people would go home from the hospital
- 3:46Speaker 2: with no medications, no lifestyle advice, just go home, I've
- 3:50Speaker 2: cured you. And it was just complete nonsense. So back six, seven,
- 3:54Speaker 2: eight years later, this is when we're doing vein grafts
- 3:56Speaker 2: rather than the mammary grafts. But then I just progressively
- 4:00Speaker 2: got more interested in the concept of prevention because it
- 4:02Speaker 2: was just logical to me. Why put up with the
- 4:05Speaker 2: misery of chronic disease, of being on buckets of medications?
- 4:09Speaker 2: And I'm not saying you can walk away from medications
- 4:12Speaker 2: if you've got a chronic disease, but I now have
- 4:14Speaker 2: developed what I call my 80-10-10 protocol. 80% is lifestyle.
- 4:20Speaker 2: So how you look after yourself, what I call the
- 4:22Speaker 2: five keys of being healthy, which I'll go through, is
- 4:25Speaker 2: four times more powerful than anything a damn doctor can suggest.
- 4:29Speaker 2: So what are the five keys? From the least important
- 4:32Speaker 2: to the most important. Number one, you cannot be healthy
- 4:35Speaker 2: and have any addictions. You cannot be healthy and smoke
- 4:38Speaker 2: or vape, smoke marijuana. You cannot be healthy and drink
- 4:41Speaker 2: too much grog. You cannot be healthy and use any
- 4:44Speaker 2: illegal drugs. Number two, good quality sleep. Seven to eight
- 4:47Speaker 2: hours of good quality sleep is as good for your
- 4:49Speaker 2: body as not smoking. Number three, third best drug on
- 4:53Speaker 2: the planet is good nutrition. And nutrition's simple. Eat less food,
- 4:58Speaker 2: eat more natural food. That's all you need to know.
- 5:01Speaker 2: It's a tragedy, Paul. that only five percent of the
- 5:04Speaker 2: modern world has two or three pieces of fruit per day,
- 5:08Speaker 2: three to five servings of vegetables per day, only five percent.
- 5:11Speaker 2: And those who do have the lowest rates of heart disease, cancer, Alzheimer's,
- 5:15Speaker 2: et cetera, doesn't do zip to your cholesterol. It keeps
- 5:18Speaker 2: your immune system healthy. Number four is the second best
- 5:22Speaker 2: drug in the planet that you and I are very
- 5:24Speaker 2: strong proponents of. It's called exercise. Yeah. Three to five
- 5:28Speaker 2: hours a week of exercise, two thirds cardio, a third
- 5:31Speaker 2: resistance training. And again, tragically, only 25% of adults do that.
- 5:35Speaker 2: And even worse, only 10% of people over the age
- 5:39Speaker 2: of 65 have a three to five hour a week
- 5:42Speaker 2: exercise habit. And just by doing that, you reduce your
- 5:44Speaker 2: risk by 30%. Heart disease, cancer, Alzheimer's, diabetes, 50% reduction
- 5:50Speaker 2: in osteoporosis and depression. You drop your blood pressure and
- 5:53Speaker 2: you sleep better. There's no pharmaceutical preparation known to man
- 5:57Speaker 2: that comes anywhere near the strength of exercise. And I
- 6:00Speaker 2: say all the time in my professional talks, There is
- 6:03Speaker 2: no such thing as healthy aging without exercise. Then finally,
- 6:07Speaker 2: number five, which is easily the most important drug on
- 6:10Speaker 2: the planet, it's a thing called happiness. And there's this
- 6:13Speaker 2: little known university in America called Harvard. Harvard have been
- 6:18Speaker 2: doing for the last 85 years the grant study, which
- 6:21Speaker 2: shows beyond a doubt the one key to health and
- 6:24Speaker 2: happiness is to have someone else in your life who
- 6:26Speaker 2: loves and cares for you, who you love and care for.
- 6:30Speaker 2: And so it's really important to do those five keys. Now,
- 6:32Speaker 2: there are two studies, two major studies, one called the
- 6:35Speaker 2: Morgan Trial, M-O-R-G-E-N, out of Holland, showed that if you
- 6:40Speaker 2: practice those five keys to being healthy compared with the
- 6:42Speaker 2: people who do it the worst, so the highest quintile
- 6:45Speaker 2: versus the lowest quintile, you reduce your risk for cardiovascular
- 6:49Speaker 2: disease by 83%. Whereas something like a standard statin drug
- 6:55Speaker 2: in standard doses is probably about a 20% to 30% reduction,
- 6:58Speaker 2: with the potential for side effects, but we can talk
- 7:00Speaker 2: about that later. Now, that's 80% of your management. 10%
- 7:04Speaker 2: of your management is the appropriate use of orthodox medicine
- 7:07Speaker 2: and all of the techniques that go where, the pharmaceutical drugs,
- 7:10Speaker 2: the procedures, whatever. And the final 10%, which most doctors
- 7:14Speaker 2: don't even believe in, is the use of evidence-based supplements.
- 7:18Speaker 2: Supplements have to have an evidence base, not just because
- 7:22Speaker 2: you're in a health food store and it's claiming something.
- 7:24Speaker 2: That's often nonsense. And we should probably at some stage
- 7:28Speaker 2: talk about one of my favorite topics, which is the
- 7:30Speaker 2: MTHFR gene. But anyway, we can talk about that later.
- 7:33Speaker 2: But that's 80-10-10, and that's how I practice medicine. And
- 7:37Speaker 2: those principles are there for all my patients. And I've
- 7:40Speaker 2: got to tell you, tragically, only 10% of my patients
- 7:43Speaker 2: follow it to the letter, and they're the ones long-term
- 7:46Speaker 2: who do the best. Brilliant.
- 7:49Speaker 3: There's so much in that. I think there's five different
- 7:51Speaker 3: podcasts there. There's a podcast on each one of the keys.
- 7:54Speaker 2: Sure.
- 7:55Speaker 3: But let's double click on a couple of them as
- 7:58Speaker 3: we go through this. I want to talk about exercise first.
- 8:02Speaker 3: Do you know the thing for me? Actually, let me
- 8:04Speaker 3: take a step back. The world's biggest killer, everybody knows,
- 8:08Speaker 3: is cardiovascular disease. I think in Australia now, for females,
- 8:12Speaker 3: it's dementia. But overall, it's cardiovascular disease. But I actually
- 8:18Speaker 3: think that the biggest driver of it is sarcopenia.
- 8:23Speaker 1: And I want to get your opinion on it, right?
- 8:25Speaker 3: Because we know that falls are the fifth biggest killer
- 8:29Speaker 3: of people in their 70s, and that comes from muscle wasting.
- 8:32Speaker 1: But if you.
- 8:32Speaker 3: Have poor levels of muscle, and therefore you're not getting
- 8:37Speaker 3: all the myokines that come from the muscle contraction, poor
- 8:41Speaker 3: muscle and poor exercise, as you said, dramatically increases your
- 8:44Speaker 3: risk of cardiovascular disease. If you're sedentary, it dramatically increases
- 8:49Speaker 3: your risk of neurodegenerative diseases, which I think are the
- 8:51Speaker 3: second biggest killer. If you're sedentary, it dramatically increases your
- 8:55Speaker 3: risk of metabolic diseases and significantly increases your risk of cancer.
- 9:00Speaker 3: So I think here we have the fifth one directly
- 9:02Speaker 3: and then all four pulling the levers massively. And I
- 9:08Speaker 3: don't think there's anything else that does that.
- 9:11Speaker 2: No, no, no. I totally agree with you. I think
- 9:14Speaker 2: that everyone talks about osteoporosis, but what they don't realize
- 9:18Speaker 2: is one of the major drivers of osteoporosis is exactly
- 9:21Speaker 2: what you said, which is sarcopenia. If you don't have
- 9:23Speaker 2: strong muscles to support your bones, your bones are in
- 9:27Speaker 2: big trouble. And if you don't have strong muscles that
- 9:29Speaker 2: allow you to get out of a chair. So we
- 9:31Speaker 2: know things like grip strength and your ability to get
- 9:34Speaker 2: up from a chair without any issues is a great
- 9:38Speaker 2: marker for sarcopenia frailty. And all of these things are
- 9:41Speaker 2: so bad for you. And Now we're getting people in there,
- 9:44Speaker 2: and I've just turned 70, but we're getting people in
- 9:47Speaker 2: their 70s and 80s who are on multiple medications and
- 9:51Speaker 2: they're incredibly frail and they're not doing anything to support
- 9:55Speaker 2: their muscles. And so that's why I say, people say, oh, doctor,
- 9:57Speaker 2: I go for a walk every day. Yeah, but do you...
- 10:00Speaker 2: do any resistance training do you do pilates or yoga
- 10:03Speaker 2: or have some weights and i i do half an
- 10:06Speaker 2: hour on my bike every day that sort of thing
- 10:08Speaker 2: over my shoulder there's my exercise bike i've broken four
- 10:11Speaker 2: since i gave up soccer at 52. um and from
- 10:15Speaker 2: over years i'll do a half an hour when we
- 10:16Speaker 2: finish this podcast on that and i do that every
- 10:18Speaker 2: day but i also do 15 minutes of weights and
- 10:21Speaker 2: stretching every morning to keep the muscles strong and i
- 10:23Speaker 2: think that's so important because it there's no doubt that
- 10:28Speaker 2: that exercise habit reduces your risk for the four horsemen
- 10:31Speaker 2: that you just mentioned.
- 10:32Speaker 3: Yeah yeah absolutely and mental health like the impact on
- 10:36Speaker 3: mental health is massive as well.
- 10:37Speaker 2: Well again just on that studies have shown i mentioned
- 10:41Speaker 2: the reduction in depression but The studies have shown beyond
- 10:44Speaker 2: a doubt that having a regular exercise habit is probably
- 10:47Speaker 2: good as an antidepressant.
- 10:49Speaker 3: The British Medical Journal, 218 studies, looking at, importantly, they
- 10:55Speaker 3: were looking at the clinical outcome. I can't remember what
- 10:59Speaker 3: it's called. Geez, I'm forgetting now. Where the individual feels better, right?
- 11:02Speaker 3: Not statistical significance, but whatever it was. But they found
- 11:06Speaker 3: that every exercise intervention was, absolutely trumped an SSRI, right?
- 11:12Speaker 3: But let's, I want to talk about actually something that
- 11:15Speaker 3: just came to mind. Like this is the.
- 11:17Speaker 1: Slam dunk for heart health and exercise.
- 11:20Speaker 3: I'm not sure if you're familiar, I'm sure you are,
- 11:22Speaker 3: the Dallas Bedrest and Retraining Study by Ben Levine, where
- 11:26Speaker 3: they took these people, it was in the 60s, I believe,
- 11:31Speaker 3: four or five, I think it was, young men, put
- 11:34Speaker 3: them in complete bedrest for two weeks, imaged their hearts
- 11:37Speaker 3: at the start, and then imaged them at the end.
- 11:40Speaker 3: And at the end of three weeks, their hearts had
- 11:42Speaker 3: aged for 30 years. And then they trained them and
- 11:47Speaker 3: they got all their VO2 max back and actually had improvements.
- 11:51Speaker 3: But then they found them again in their 50s, brought
- 11:55Speaker 3: them into the lab and found that in their 50s,
- 11:58Speaker 3: their hearts were in better shape than they were after
- 12:00Speaker 3: three weeks of bed rest in their 20s, right? And
- 12:03Speaker 3: then they trained these guys again. And they improved on
- 12:08Speaker 3: all measures of heart function, whatever they may be. But
- 12:12Speaker 3: then the same group did another bunch of people in
- 12:15Speaker 3: their sixties who were recently sedentary. And they find that
- 12:18Speaker 3: they didn't get anywhere near the benefits of doing it
- 12:22Speaker 3: in their fifties. So I think for me, you know,
- 12:25Speaker 3: as you will know, early doing this stuff early, not,
- 12:29Speaker 3: not thinking to yourself, my career is a priority. I'm
- 12:33Speaker 3: going to leave fitness until I retire. because then it's
- 12:37Speaker 3: nowhere near as effective.
- 12:38Speaker 2: As it is. And the reason being, and let me
- 12:41Speaker 2: be brutal to most people listening to this podcast, our
- 12:44Speaker 2: body evolutionary-wise was only designed to work well for 30,
- 12:48Speaker 2: 40 years running around a jungle with a spear, and
- 12:50Speaker 2: then you died from either trauma or infection. So old
- 12:54Speaker 2: age is actually a disease process. And part of the
- 12:57Speaker 2: old age process is fibrosis and scarring of all the tissues.
- 13:02Speaker 2: And if you throw on top of that metabolic syndrome
- 13:04Speaker 2: with fat buildup in the heart and the brain. So
- 13:06Speaker 2: the reason these GLP receptor agonists have gone nuts is
- 13:09Speaker 2: because they also take the fat out of the organs
- 13:11Speaker 2: as well. So you've got aging organs. So every decade,
- 13:16Speaker 2: the heart gets stiffer, the arteries get stiffer. So for
- 13:19Speaker 2: all us men over 50, everything stiffens up apart from
- 13:21Speaker 2: the bit you want to. Sorry, I have to throw
- 13:27Speaker 2: in the jokes every now and then. But everything gets
- 13:30Speaker 2: stiffer apart from that bit. And so therefore, that's why
- 13:33Speaker 2: it if you start your exercise in your 60s, it
- 13:36Speaker 2: doesn't work as well as if you start in your 50s.
- 13:38Speaker 2: But I don't want anyone listening to this to say, oh,
- 13:41Speaker 2: I'm too.
- 13:41Speaker 1: Fat, there's no point.
- 13:42Speaker 2: You will always get a benefit from having an exercise habit.
- 13:46Speaker 2: But it's also important, I say this to a lot
- 13:48Speaker 2: of people, when you're 80, don't push yourself as hard
- 13:51Speaker 2: as you did when you were 50 because your body
- 13:54Speaker 2: won't cope with it. And again, another thing I say,
- 13:57Speaker 2: the only joint you blow over the age of 50
- 13:58Speaker 2: is your hip or your knee. So you don't want
- 14:01Speaker 2: to push that too hard either. And that's why I
- 14:03Speaker 2: prefer an exercise bike with exercise or a cycle than
- 14:07Speaker 2: people who run on treadmills because you're really pounding your
- 14:10Speaker 2: knee and your hip when you do that. Yeah, yeah, yeah, yeah.
- 14:12Speaker 2: I agree.
- 14:13Speaker 3: And I, like you, in my 50s have given up
- 14:15Speaker 3: soccer and moved to an exercise bike.
- 14:17Speaker 1: I'm also doing a bit of crossfit.
- 14:19Speaker 2: Well, my knee made me give up soccer, which I
- 14:21Speaker 2: had replaced six years ago, unfortunately.
- 14:24Speaker 1: Yeah, well, it happens, doesn't it?
- 14:26Speaker 2: Yeah.
- 14:26Speaker 1: Just on the exercise, I want to get your.
- 14:29Speaker 3: Opinion on this, and it's probably going to be an
- 14:31Speaker 3: educated guess. So when we look into all of the,
- 14:35Speaker 3: and look, it is observational data, but they've got a
- 14:38Speaker 3: lot of it, looking at the optimal dose for exercise,
- 14:42Speaker 3: and there's that hormetic effect, right, where none is bad
- 14:45Speaker 3: for you, some is good, more is better, but there's
- 14:48Speaker 3: then the extreme exercise hypothesis.
- 14:51Speaker 2: Yep, yep.
- 14:51Speaker 3: And for cardiovascular, we know that's a shitload, right? We
- 14:55Speaker 3: know it's the triathletes and stuff. It's like 15 hours
- 14:58Speaker 3: high intensity exercise a week. That's where you lose the
- 15:02Speaker 3: benefits or start to erode them. But with resistance training,
- 15:08Speaker 3: it seems to be about 90.
- 15:11Speaker 1: Minutes a week. And I'm like, Jesus, why would that be?
- 15:15Speaker 3: Now, I have two hypotheses that are not tested, but
- 15:18Speaker 3: I wanted to run them past you. One is, We
- 15:22Speaker 3: only now have 30 years of data on resistance training
- 15:26Speaker 3: from people who started in our 30 or 40 or
- 15:29Speaker 3: 50 years for people who started in the 70s and 80s.
- 15:31Speaker 3: And most people who were doing resistance training then were
- 15:33Speaker 3: probably taking anabolic steroids.
- 15:35Speaker 1: That may have had a negative effect.
- 15:37Speaker 3: So I think that may be clouding some of the
- 15:40Speaker 3: longitudinal data. But the only thing that I can possibly
- 15:44Speaker 3: think of is the blood pressure effect that when you're
- 15:47Speaker 3: doing heavy resistance training, like your blood pressure goes through the,
- 15:51Speaker 3: especially if you're doing heavy isometrics or negatives. Have you
- 15:56Speaker 3: any inclination as to why the dose in terms of
- 16:00Speaker 3: time is much lower for resistance training than it is
- 16:04Speaker 3: for cardiovascular training?
- 16:06Speaker 2: No, no, I really can't. I can't give you any,
- 16:08Speaker 2: even an educated guess there, but, One point I'd really
- 16:11Speaker 2: like to make about all forms of exercise is that
- 16:15Speaker 2: one of the best drugs on the planet is a
- 16:17Speaker 2: thing called vasodilatation and the best vasodilator. And this is
- 16:22Speaker 2: pretty simplistic stuff, but I think it explains it well.
- 16:25Speaker 2: The best vasodilator anyone can do is exercise. And three
- 16:29Speaker 2: to five hours a week of exercise vasodilates your artery.
- 16:32Speaker 2: And this is what it does. This is why it's
- 16:33Speaker 2: so good for dementia because you're flushing blood through the
- 16:37Speaker 2: microcirculation in your brain, flushing all the toxins out. So
- 16:41Speaker 2: dementia is a vascular disease. It's just a wash down
- 16:44Speaker 2: effect from the big vessels. So I say to my patients,
- 16:47Speaker 2: just imagine a dam with the big arteries, like the
- 16:50Speaker 2: big pipes coming out of the dam. They're your carotid arteries,
- 16:53Speaker 2: your coronary arteries. The branch vessels are the pipes in
- 16:56Speaker 2: your street and the microcirculation of the pipes in your
- 16:59Speaker 2: house and the tap. So if you have some bigger
- 17:03Speaker 2: vascular disease, you get the wash down effect into the
- 17:06Speaker 2: smaller vessels. So you get sludge in the smaller vessels.
- 17:09Speaker 2: So Every time you have a thought or an emotion,
- 17:11Speaker 2: you create a waste product that has to be washed out.
- 17:14Speaker 2: So as you get older, your immune system in the brain,
- 17:17Speaker 2: the glial cells don't work as well. The microcirculation becomes sluggish.
- 17:21Speaker 2: So all of these toxic proteins accumulate in your brain
- 17:24Speaker 2: and destroy your neurons, thus Alzheimer's disease. So vasodilatation that
- 17:29Speaker 2: you get from exercise, one of the most important things
- 17:32Speaker 2: you can do. Now, again, on my radio show a
- 17:35Speaker 2: couple of weeks ago, I spoke about a major study
- 17:38Speaker 2: on what I call vitamin V and vitamin C. Vitamin
- 17:42Speaker 2: V and C are Viagra and Cialis. And this study
- 17:45Speaker 2: showed that men over the age of 40, who were
- 17:48Speaker 2: the highest end users of Viagra and Cialis, had, well,
- 17:52Speaker 2: this is quite extraordinary, a three-year study, had a 56%
- 17:56Speaker 2: reduction in all-cause death, a 55% reduction in dementia. And
- 18:02Speaker 2: this study showed a 36% reduction in heart attack and stroke,
- 18:05Speaker 2: but in other studies, a 50% reduction in in cardiovascular events.
- 18:09Speaker 2: And there's even pointers that it reduces cancer. And I
- 18:11Speaker 2: think the reason for this is that they're vasodilators. They
- 18:16Speaker 2: don't just open up the most important artery in the
- 18:18Speaker 2: male body. They open up all other arteries as well.
- 18:21Speaker 2: So that's why I'm now encouraging all of my male
- 18:24Speaker 2: patients over the age of 50 to use these drugs
- 18:27Speaker 2: as often as they like, because you get the benefits.
- 18:30Speaker 2: But don't see it as a replacement for excise. Excise
- 18:32Speaker 2: is easily the best vasodilator. I hope there is never
- 18:36Speaker 2: a pill that replaces exercise because we need to get
- 18:40Speaker 2: out and do it. And we need that three to
- 18:42Speaker 2: five hour a week commitment. And to get back to
- 18:44Speaker 2: what you were saying, people who are very high level athletes,
- 18:49Speaker 2: there's a subgroup of them who will develop more coronary calcification,
- 18:53Speaker 2: the more exercise they do. And just think of it,
- 18:56Speaker 2: they're just pounding those arteries just too much. And the
- 18:58Speaker 2: more you pound the arteries, the more you lay down
- 19:01Speaker 2: plaque in the wall of your arteries from going overboard.
- 19:04Speaker 2: But you see, this is what I say all the time, Paul,
- 19:06Speaker 2: Every single condition is genetic. Your genes load the gun,
- 19:11Speaker 2: your environment puts the trigger. So in 47 years of
- 19:15Speaker 2: being a doctor, I've never seen one person who had
- 19:18Speaker 2: a heart attack, stroke, stent, bypass, who wasn't under some
- 19:22Speaker 2: form of stress at the time, but that's with genetic predisposition.
- 19:26Speaker 2: So I tell the story about my fat mate, who's
- 19:30Speaker 2: a 71-year-old retired pediatric surgeon. He's a human vacuum cleaner,
- 19:35Speaker 2: this guy. He loves food. Hates exercise. But his diabetic
- 19:40Speaker 2: hypertensive is on 20 pills for these things. And his
- 19:43Speaker 2: coronary calcium score is four. He's got almost nothing in
- 19:46Speaker 2: his arteries. Now, I'm not saying that justifies his obesity
- 19:49Speaker 2: or his diabetes because his body's a wreck from obesity,
- 19:53Speaker 2: but I'm saying he probably won't have a major heart
- 19:55Speaker 2: attack because his calcium score is so low. I said probably.
- 19:59Speaker 2: I'm not saying definitely won't. But the worst coronary calcium
- 20:04Speaker 2: score I have, now we have a gradient in these
- 20:06Speaker 2: calcium scores. Anything above 400 is serious. is a 68-year-old
- 20:10Speaker 2: man in the fitness industry, doesn't have an ounce of
- 20:13Speaker 2: body fat, normal cholesterol, blood pressure, never smoked, not diabetic,
- 20:19Speaker 2: and no family history. So none of the five major
- 20:23Speaker 2: risk factors for heart disease, but his lipoprotein did lay
- 20:26Speaker 2: as high. Ah, yes. His coronary calcium score at the
- 20:30Speaker 2: age of 68 was 8,100. Holy guacamole. The biggest I've
- 20:33Speaker 2: ever seen. And he needed bypass surgery 12 years ago.
- 20:41Speaker 2: He sent me an email a few years back with
- 20:43Speaker 2: a picture of him and his mates winning their latest
- 20:45Speaker 2: basketball grand final. And tragically, he died last year from
- 20:49Speaker 2: pulmonary fibrosis, which is unrelated to his heart disease. But
- 20:53Speaker 2: had he been a profligate self-abuser, had he stressed his body,
- 20:57Speaker 2: he probably would have died from his lousy genes 20
- 20:59Speaker 2: years before. So even though you might have lousy genes,
- 21:04Speaker 2: you can do something about the lousy genes. You can
- 21:07Speaker 2: change the phenotype. not the genotype.
- 21:10Speaker 3: Yeah, look, 100%. I know all my genetics have been tested,
- 21:13Speaker 3: as have my family's. We are shocking for diabetes. My
- 21:16Speaker 3: mother and brother have diabetes. I don't because of the
- 21:20Speaker 3: hard work, right? And I always say you either do
- 21:23Speaker 3: the hard work in terms of the lifestyle, I mean
- 21:25Speaker 3: the five keys that you talk about, when you're doing
- 21:28Speaker 3: their hard, but you either do the hard work now
- 21:30Speaker 3: or you pay the hard consequences later on.
- 21:32Speaker 2: Absolutely. It's choose your heart, right? I don't walk into
- 21:35Speaker 2: this room every day and go, wow, I'm about to
- 21:38Speaker 2: get my excise bike, how exciting. But at the end
- 21:41Speaker 2: of it, I feel a sense of achievement. And if
- 21:43Speaker 2: I don't do it, Paul, I feel dreadful. I feel
- 21:45Speaker 2: guilty and I think I've got to do the excise.
- 21:47Speaker 2: So it's become such an important part of my life.
- 21:50Speaker 1: And do you know another thing?
- 21:51Speaker 3: I think there is a neurobiological mechanism that's going on here, right?
- 21:57Speaker 3: Something called the mid anterior cingulate cortex is the part
- 22:02Speaker 3: of the brain that's associated with doing hard things.
- 22:05Speaker 1: And when people who do.
- 22:07Speaker 3: Hard things, that part of the brain grows. And people
- 22:10Speaker 3: who have a larger part of that brain, that part
- 22:13Speaker 3: of the brain, have more persistence, more grit, and they
- 22:16Speaker 3: put in more effort. This is the challenge muscle in
- 22:19Speaker 3: the brain. And every time you or me are jumping
- 22:22Speaker 3: on an exercise bike when we don't want to, we
- 22:24Speaker 3: are exercising and developing that part of the brain. I
- 22:28Speaker 3: think it's use it or lose it. And I think
- 22:30Speaker 3: that's an underappreciated thing effect of when you said earlier
- 22:35Speaker 3: on i hope they don't have an exercise pill because
- 22:39Speaker 3: i think an underappreciated effect is the impact on those
- 22:43Speaker 3: neurobiological areas that that get you to do hard things
- 22:48Speaker 3: totally that's hugely important.
- 22:50Speaker 2: I completely agree i mean look you and i both
- 22:52Speaker 2: ex-soccer players and i it was one of my joys
- 22:55Speaker 2: turning i was the captain of the team sweeper at
- 22:57Speaker 2: the back and i never I used to love breaking
- 22:59Speaker 2: forwards legs. And I've lost that joy. When I drive
- 23:03Speaker 2: past a soccer field and see these old farts playing soccer,
- 23:06Speaker 2: I think, oh, I'd love to be back on there.
- 23:08Speaker 2: But after the knee replacement, one bad tackle and I'm gone.
- 23:12Speaker 2: So therefore, I've lost that joy. And I don't get
- 23:15Speaker 2: anywhere near the same joy when I sit in the
- 23:17Speaker 2: excise bike, of course, because that mateship and just the
- 23:21Speaker 2: skills and everything else that goes with it was such
- 23:23Speaker 2: so wonderful. But I think this is the problem with
- 23:25Speaker 2: getting old. you have to accept certain things that you
- 23:29Speaker 2: could have done 20, 30 years ago that you can't
- 23:31Speaker 2: do now and just adjust to it. And I think,
- 23:34Speaker 2: I think life is so precious and I love life.
- 23:37Speaker 2: I love every aspect of it that I just think
- 23:39Speaker 2: I want to live for another, well, I'm 70 now.
- 23:42Speaker 2: I want to live for another 30 years.
- 23:45Speaker 1: Get the three digits.
- 23:47Speaker 3: Let's come back to stress because you've, you've hinted at
- 23:50Speaker 3: it about stress in the cardiovascular system. Um, I often
- 23:55Speaker 3: talk about this research paper by Professor Mark Seary from
- 23:59Speaker 3: the University of Buffalo. And it's all about psychology. It's
- 24:02Speaker 3: about psychophysiology. It's about challenging threat when we are faced
- 24:06Speaker 3: with adversity. But he was the first to show, this
- 24:09Speaker 3: has actually been replicated, that if me and you are
- 24:13Speaker 3: presented with the same potential stressor, you make an immediate
- 24:19Speaker 3: decision in your brain that this is a challenge. And
- 24:21Speaker 3: I make the decision that this is a threat, right?
- 24:23Speaker 3: It's just called a stress appraisal. It happens like that.
- 24:27Speaker 3: Mark's theory shows you activate the fight part of your
- 24:30Speaker 3: fight or flight nervous system. You activate adrenaline and noradrenaline,
- 24:34Speaker 3: which opens up, vasodilates the cardiovascular system. When I view
- 24:39Speaker 3: something as a threat, it releases cortisol, which constricts the
- 24:43Speaker 3: cardiovascular system. And that, for me, is one of the
- 24:47Speaker 3: reasons why this chronic stress that's to do with hypercortisolemia
- 24:53Speaker 3: really impacts on heart disease.
- 24:55Speaker 2: Yeah, but even, I'll quote some studies from really elegant
- 25:00Speaker 2: work done by Professor Geoffrey Toffler from Royal North Shore
- 25:03Speaker 2: in Sydney, where he showed, and I talk about the
- 25:05Speaker 2: five categories of stress, so I'd like to go through those.
- 25:08Speaker 2: Category number one is emotional stress. So Jeff showed that
- 25:12Speaker 2: within two hours of you getting acutely angry or anxious
- 25:16Speaker 2: about anything, you increase your risk for a heart attack
- 25:19Speaker 2: eight times or any cardiac event eight times. So the
- 25:23Speaker 2: first is emotional stress. The second is mental stress. So
- 25:28Speaker 2: from the Whitehall studies that have been going on for
- 25:31Speaker 2: 30 years, and interestingly, they found that it was the
- 25:34Speaker 2: middle managers who copped it. So they copped it from
- 25:37Speaker 2: a thing called job strain, which is high demand, low control.
- 25:40Speaker 2: It has much more cardiovascular disease, hypertension.
- 25:45Speaker 1: Lack of autonomy, right?
- 25:46Speaker 2: Yeah, yeah. And number three, you've already alluded to, which
- 25:50Speaker 2: is excessive physical stress. Now, physical stress isn't just too
- 25:54Speaker 2: much exercise. We all hear about the people who drop
- 25:57Speaker 2: dead in marathons or running the city to surf or whatever,
- 26:00Speaker 2: but that's unusual. It's much more dangerous to sit at
- 26:03Speaker 2: home and do nothing and be a fat slob. You're
- 26:05Speaker 2: going to drop dead much more from that. But what
- 26:08Speaker 2: I'm saying is if you do physical stress, especially under
- 26:11Speaker 2: extremes of environment. So I had a 78-year-old man, thought
- 26:14Speaker 2: it was a good idea on a 45-degree Celsius day
- 26:17Speaker 2: to play singles tennis and ended up with a stent
- 26:20Speaker 2: in his artery. So he obviously had the underlying coronary disease,
- 26:24Speaker 2: but just the extra environmental stress just tipped him over
- 26:27Speaker 2: with the exercise. Or like these fools who go running
- 26:30Speaker 2: when it's heavy days of pollution or bushfires, any of
- 26:33Speaker 2: these things, or even freezing cold. Now, we all know
- 26:36Speaker 2: the benefits of, say, cold water swimming, but not if
- 26:39Speaker 2: your body's not used to it. If you just jump
- 26:41Speaker 2: into freezing cold when you don't do it that often,
- 26:43Speaker 2: I've seen people get severe coronary vasospasm and have myocardial
- 26:47Speaker 2: infarctions as a consequence. We all know, just going back
- 26:49Speaker 2: to the emotional stress, the old Takotsubo's cardiomyopathy from emotion-induced
- 26:54Speaker 2: severe vasoconstriction. So number three, physical stress. Number four, and
- 26:59Speaker 2: people don't talk about this as much as they should,
- 27:01Speaker 2: is pharmacologic stress.
- 27:03Speaker 3: Yeah.
- 27:04Speaker 2: So if you've got a lot of plaques in your
- 27:06Speaker 2: arteries and even a heavy night on the grog can
- 27:09Speaker 2: do it, and a lot of people don't realize this,
- 27:12Speaker 2: one of the studies have shown that within two hours
- 27:15Speaker 2: of smoking one joint, you increase your risk for a
- 27:18Speaker 2: heart attack five times. Jesus. Yeah, when I hear this
- 27:22Speaker 2: nonsense about smoked marijuana is just recreational and good for you, crap.
- 27:28Speaker 2: this is going to surprise you, Paul, but you've got
- 27:29Speaker 2: a couple of things in your body called your lungs.
- 27:32Speaker 2: They were strangely designed for a thing called breathing, not
- 27:35Speaker 2: to put a stick in your mouth and suck the
- 27:37Speaker 2: smoke in, whether it's cigarettes, vaping, or marijuana. It is
- 27:41Speaker 2: not good for you. And THC, the active component, of course,
- 27:45Speaker 2: of marijuana, is an endothelial cell killer. So it really
- 27:49Speaker 2: destroys the endothelium if you get THC in it.
- 27:52Speaker 3: So the people who are thinking, all right, I'll stop
- 27:55Speaker 3: the vape and I'll get on the gummies.
- 27:57Speaker 1: The THC still has an effect, right?
- 28:00Speaker 2: Of course it does.
- 28:00Speaker 1: Even if it's not smoked.
- 28:01Speaker 2: If the gummies are high in THC, I have no
- 28:04Speaker 2: problems with medical cannabis where there's a little bit of
- 28:07Speaker 2: THC to balance the CBD. So there's two receptors, CB1
- 28:11Speaker 2: and CB2. You need them balanced with a bit of THC,
- 28:15Speaker 2: a bit of CBD, but it's the high dose THC
- 28:18Speaker 2: that's the problem. And that's what damages the endothelium. But also,
- 28:22Speaker 2: I'll give you another example. I had a guy in
- 28:24Speaker 2: his 30s with a strong family history of heart disease.
- 28:27Speaker 2: went out one night in a box and I'd had
- 28:28Speaker 2: a few lines of coke, wiped out half his heart
- 28:31Speaker 2: from a major infarct.
- 28:33Speaker 3: So is it true, sorry, just while we're on, Jogs,
- 28:38Speaker 3: is it true that the worst drug for the heart
- 28:41Speaker 3: is cocaine?
- 28:42Speaker 2: Yeah, yeah. Cocaine is dreadful. And crystal meth's not much better,
- 28:47Speaker 2: but cocaine is, and crystal meth's worse for all the
- 28:50Speaker 2: other things it does. But But people shouldn't be using
- 28:52Speaker 2: illegal drugs. They're just disgraceful. And what they do to
- 28:55Speaker 2: people's health is outrageous. But I'll tell you, the commonest
- 28:59Speaker 2: used drug on the planet, which you and I have
- 29:01Speaker 2: probably had today, is coffee. And a couple of cups
- 29:04Speaker 2: of coffee a day is actually good for you. So
- 29:07Speaker 2: the studies show, beyond a doubt, a couple of cups
- 29:09Speaker 2: of coffee a day reduce risk for gallstones, kidney stones, Parkinson's, Alzheimer's,
- 29:14Speaker 2: many common cancers, type 2 diabetes, depression. and heart failure
- 29:19Speaker 2: and stroke. So there's nothing wrong with having a couple
- 29:21Speaker 2: of cups of coffee a day, but I had a
- 29:22Speaker 2: 35-year-old guy, he doesn't know why I did this, but
- 29:26Speaker 2: in the space of an hour, had three double-shot cappuccinos
- 29:30Speaker 2: and sent his heart into overdrive atrial fibrillation.
- 29:35Speaker 3: Ross, I've heard of teenagers like drinking heaps of cans
- 29:39Speaker 3: of mother.
- 29:41Speaker 1: And you know.
- 29:42Speaker 3: There's something like 160 milligrams of caffeine in one of those.
- 29:47Speaker 3: And I know teenagers who have three cans a day.
- 29:50Speaker 3: That's like one here at four. That's over 600 milligrams
- 29:55Speaker 3: of caffeine.
- 29:57Speaker 2: That's horrible. You see, again, It's like anything. I mean,
- 30:00Speaker 2: all the studies with alcohol, it's like who the alcohol
- 30:03Speaker 2: is hanging around with. So for example, if you look
- 30:06Speaker 2: at all the alcohol studies, and I'll come back to
- 30:09Speaker 2: the energy drinks in a second, but if you look
- 30:10Speaker 2: at all the alcohol studies out of America, absolutely no benefit,
- 30:14Speaker 2: except for one study in Boston where the male doctors
- 30:18Speaker 2: in Boston had a glass of red wine a day,
- 30:20Speaker 2: had an 80% reduction in sudden cardiac death. But they're
- 30:24Speaker 2: combining that with a better diet. But if you look
- 30:26Speaker 2: at the standard crappy American diet, If you combine alcohol
- 30:30Speaker 2: with that, you're really looking for trouble. But when you
- 30:33Speaker 2: look at the Mediterranean data where they combine, say, a
- 30:37Speaker 2: couple of glasses of red wine with Mediterranean-style food, 50%
- 30:41Speaker 2: reduction in heart disease and cancer in those people. But
- 30:45Speaker 2: if you look at the spirits, when you look to, say,
- 30:47Speaker 2: the Copenhagen Heart Study, a couple of spirits a day
- 30:50Speaker 2: compared with teetotalers, 30% increased risk for heart disease and cancer.
- 30:55Speaker 2: And if you drink alcohol because you're lonely or depressed,
- 30:59Speaker 2: you're combining a toxic chemical with other toxic chemicals in
- 31:02Speaker 2: your skull. That's alcohol. But when you look at caffeine, again,
- 31:08Speaker 2: it depends on who the caffeine is hanging around with.
- 31:10Speaker 2: If the caffeine is in with the polyphenols of coffee
- 31:13Speaker 2: or the polyphenols of tea, you'll probably get a benefit.
- 31:16Speaker 2: But the lack of polyphenols and the sugar and all
- 31:20Speaker 2: the other crap that's in standard soft drinks and in
- 31:23Speaker 2: energy drinks, which I think energy drinks should be banned,
- 31:26Speaker 2: but that aside– what you're saying, these teenagers who think
- 31:30Speaker 2: they're great and they keep them all hyped up and focused,
- 31:32Speaker 2: it's so dangerous. And we're going to be seeing increasing
- 31:36Speaker 2: rates of things like atrial fibrillation and other problems in
- 31:41Speaker 2: these teenagers who are using these drinks, not to mention
- 31:44Speaker 2: the phosphoric acid, which is the food acid in all
- 31:47Speaker 2: these soft drinks and energy drinks, which rip the calcium
- 31:49Speaker 2: out of your bones.
- 31:50Speaker 1: Yeah, it destroys your bones.
- 31:52Speaker 2: It's outrageous. And the final stressor is infective stress. So
- 31:59Speaker 2: during COVID, we saw a marked increased risk for myocarditis,
- 32:05Speaker 2: heart attack, atrial fibrillation, pericarditis. To quote the Donald, I
- 32:10Speaker 2: don't like quoting the Donald, but the initial China virus.
- 32:14Speaker 2: So the Wuhan strain had a 3% death rate and
- 32:18Speaker 2: huge cardiac complications. And they did a big study in
- 32:22Speaker 2: American veterans. I think it was about 153 American war vets.
- 32:26Speaker 2: followed them for 12 months. Those who had COVID versus
- 32:29Speaker 2: those who didn't have COVID had about a 50% increased
- 32:33Speaker 2: risk for all cardiovascular complications. But it's not just COVID,
- 32:37Speaker 2: it's any infective stress. So within days to weeks of
- 32:41Speaker 2: you having a virus or you having pneumonia or a
- 32:44Speaker 2: urinary tract infection or a tooth abscess, or even just
- 32:48Speaker 2: bad dentition, there's a marked increased risk for cardiovascular disease.
- 32:51Speaker 2: So those five stressors.
- 32:53Speaker 1: Sorry, Ross, is that because of the inflammation?
- 32:56Speaker 2: Yes, absolutely. So you see, I see cardiac disease and
- 33:00Speaker 2: most diseases really, genes at the top, underneath that is
- 33:04Speaker 2: chronic inflammation. So chronic inflammation, as I said before, We're
- 33:09Speaker 2: designed to only live 30, 40 years and then die
- 33:11Speaker 2: from either trauma or infection. So our immune system has
- 33:15Speaker 2: only really evolved to deal with trauma or infection. Our
- 33:19Speaker 2: immune system hasn't evolved to deal with chronic stimuli. So
- 33:23Speaker 2: in my field, in cardiology, you have the small oxidized
- 33:27Speaker 2: LDL crosses into the endothelium and then follows in there
- 33:31Speaker 2: as the macrophage. So it's basically... the stuff shouldn't be
- 33:35Speaker 2: there in the first place so all the chronic inflammation
- 33:37Speaker 2: is due to stuff that shouldn't be there in the
- 33:39Speaker 2: first place so the macrophage follows it in swallows it
- 33:43Speaker 2: and says gee this tastes nice and then the macrophage
- 33:46Speaker 2: becomes fat like human beings become fat doing this and
- 33:49Speaker 2: they turn into these things called foam cells and the
- 33:51Speaker 2: foam cells get bigger and bigger and bigger and rupture
- 33:54Speaker 2: more macrophages come in same process vicious circle and so
- 33:58Speaker 2: basically it's the chronic inflammatory response to the stuff that
- 34:03Speaker 2: shouldn't be there in the first place, which is small
- 34:05Speaker 2: oxidized LDL. It's a vicious circle. And then calcium grows
- 34:09Speaker 2: into the plaque to act as a scaffold to stop
- 34:12Speaker 2: it from breaking down. So that's a reparative response by
- 34:16Speaker 2: the body, but then your arteries get stiffer over time.
- 34:19Speaker 2: And then if you do rupture a fatty plaque, a
- 34:22Speaker 2: clot forms to try and block the rupture up, but
- 34:25Speaker 2: that clot then blocks the artery. So The only thing
- 34:28Speaker 2: that's wrong is the LDL being there. Everything else is
- 34:30Speaker 2: a reparative response to the LDL that's being there.
- 34:34Speaker 3: Now, that's a beautiful segue to LDL. So let's talk
- 34:37Speaker 3: all things cholesterol. So I think my sort of view
- 34:42Speaker 3: on this, I want to road test this against you,
- 34:44Speaker 3: is that just looking at your LDL, at a population level,
- 34:50Speaker 3: we get it, but at an individual level is really suboptimal.
- 34:54Speaker 3: You should be looking at, The particle size, whether it's oxidized,
- 34:58Speaker 3: you should be looking at ApoB and LpA, which you.
- 35:01Speaker 2: Mentioned earlier on.
- 35:02Speaker 3: Because you can have high LDL. Like me, I've got
- 35:06Speaker 3: quite high LDL. But when I got my particle size measured,
- 35:10Speaker 3: it's all big, fluffy LDL.
- 35:12Speaker 1: There's no small, dense LDL.
- 35:14Speaker 2: There's no oxidized LDL.
- 35:16Speaker 3: So what are my cardiovascular risks or someone like that?
- 35:20Speaker 3: versus somebody who's got relatively low LDL, but it's all small, dense,
- 35:25Speaker 3: and oxidized, and it's got high LP little a and
- 35:28Speaker 3: high ApoB. So can you go through this, talk through this.
- 35:32Speaker 2: For our listeners? Oh, sure, sure. And look, in 1999,
- 35:36Speaker 2: I introduced into Australia in conjunction with the Sydney Advanced
- 35:39Speaker 2: Hospital in Wurundjeri, one of my colleagues, Dr. David Grout,
- 35:42Speaker 2: a test called coronary calcium scoring. So I was one
- 35:45Speaker 2: of the pioneers of that in Australia. We had the
- 35:48Speaker 2: first machine. And I still believe 27 years later that
- 35:54Speaker 2: that is still the best predictive test for the degree
- 35:57Speaker 2: of atherosclerosis. So that tells you how bad your disease is.
- 36:01Speaker 2: It's never wrong. If you've got a zero score, you
- 36:04Speaker 2: have low level coronary atherosclerosis. Everybody living in this society
- 36:08Speaker 2: who has a cholesterol above three and a blood pressure
- 36:11Speaker 2: above 100, which is almost everybody, has a degree of atherosclerosis.
- 36:16Speaker 2: But the coronary calcium score tells you how bad it is.
- 36:20Speaker 2: And you can still have a heart attack with a
- 36:21Speaker 2: zero score or a low score, but I believe it's
- 36:24Speaker 2: a different type of heart attack. So that tells you
- 36:28Speaker 2: where you are, but it doesn't tell you what's put
- 36:30Speaker 2: it there. What tells you what's put it there is
- 36:33Speaker 2: how much atherogenic particles you have. And you get the
- 36:37Speaker 2: best indication of atherogenic particles because ApoB, apolipoprotein B, carries
- 36:43Speaker 2: all of the atherogenic particles that it gets from the
- 36:47Speaker 2: atherogenic bits of LDL cholesterol, VLDL cholesterol, LP little a,
- 36:51Speaker 2: occasionally IDL, which is not as important. But all of
- 36:54Speaker 2: these things then give you this atherogenic LDL. Now, again,
- 36:58Speaker 2: you've mentioned the size of your LDL, and there's very
- 37:01Speaker 2: good work to show that it is small, dense LDL
- 37:04Speaker 2: that is atherogenic, whereas the large, buoyant LDL, in most cases, Paul,
- 37:09Speaker 2: not in all, in most cases is not so atherogenic.
- 37:13Speaker 2: But for example, one of the big exceptions there is
- 37:17Speaker 2: a condition that people rabbit on about so much, but
- 37:19Speaker 2: it's only really one in 250 people who get it.
- 37:22Speaker 2: Whereas with L-pillet lay, it's one in five people have
- 37:25Speaker 2: a high L-pillet lay. But in this condition, familial hypercholesterolemia,
- 37:29Speaker 2: it's only one in 250. And again, it's often misdiagnosed
- 37:34Speaker 2: even by cardiologists. So for example, Your cholesterol might sit
- 37:37Speaker 2: at 7.5, but your triglycerides are 0.5 and your HDL
- 37:43Speaker 2: is 2.5 and your chlorine calcium score is zero. And
- 37:46Speaker 2: people say, oh, you have familial hypercholesterolemia. No, you don't.
- 37:50Speaker 2: You're what we call a lean hyper-responder. You don't have
- 37:54Speaker 2: an issue. Your large LDL particles are being processed well
- 37:57Speaker 2: by the liver. If they're not particularly atherogenic, don't worry
- 38:01Speaker 2: about it. You don't need a statin. Forget about it.
- 38:04Speaker 2: But You also might have familial hypercholesterolemia where your cholesterol
- 38:08Speaker 2: sits at 7.58, but your HDL is only one and
- 38:12Speaker 2: your triglycerides might be normal at one or 1.2. But
- 38:15Speaker 2: your LDL, even though it's large, mainly large, it's a
- 38:19Speaker 2: different configuration and doesn't fit into the standard receptor as well.
- 38:23Speaker 2: And it's still very atherogenic. So that's where the calcium
- 38:26Speaker 2: score tells you. Now, here's the thing about FH, that 50%
- 38:29Speaker 2: of people with FH will have a vascular event by
- 38:34Speaker 2: age 50. But if you're an optimist, 50% of people
- 38:38Speaker 2: with FH won't have a vascular event. That's where I
- 38:42Speaker 2: use the calcium score. So I'll give you one great example.
- 38:44Speaker 2: This is just an anecdote, not a clinical trial.
- 38:47Speaker 3: Sorry, Russ, how does that compare with the population who
- 38:50Speaker 3: doesn't have familial hypercholesterolemia what percentage of those would have
- 38:55Speaker 3: a cardiovascular event by 50?
- 38:56Speaker 2: Yeah, that's a great question. And the answer to that
- 38:59Speaker 2: is very difficult. At a population level, you can say
- 39:03Speaker 2: up to the age of 50, it's probably only 1%
- 39:05Speaker 2: to 2% of those people as opposed to 50%. But
- 39:08Speaker 2: once you get to 60%, 70%, 80%, I mean, the
- 39:10Speaker 2: greatest risk for heart disease is getting old. Is it age? Yeah, yeah.
- 39:13Speaker 3: So you're talking a 20% to 25% increase if you.
- 39:17Speaker 1: Have a medial hyperplasia.
- 39:18Speaker 2: If you've got FH. But I saw a woman age 58.
- 39:21Speaker 2: whose lifelong cholesterol was 9.5, triglycerides 1, HDL 1. And
- 39:26Speaker 2: every scaremongering doctor said, to her, if you don't take
- 39:30Speaker 2: a statin, you're going to die. And so she'd take
- 39:32Speaker 2: the statin for three days. In her case, just couldn't
- 39:35Speaker 2: lift her arms. And it's my clinical experience of having
- 39:38Speaker 2: used these drugs for 35 years that around 20% of
- 39:41Speaker 2: people who take statins get muscle symptoms.
- 39:44Speaker 1: Now, The research says seven, doesn't it?
- 39:47Speaker 2: Well, even less than that. But let me tell you why.
- 39:49Speaker 1: The pharmaceutical-sponsored research.
- 39:52Speaker 2: Yeah, to an extent. But even the non-pharmaceutical-sponsored even said
- 39:57Speaker 2: even less than 5%. But this is why. Their definition
- 40:00Speaker 2: of myalgia is muscle pain with a CK three times
- 40:05Speaker 2: the normal range. So what I'm saying to you, mate,
- 40:09Speaker 2: is that the 20% of people that I see with
- 40:11Speaker 2: muscle symptoms get muscle pain, stiffness, weakness, cramping, and even
- 40:16Speaker 2: loss of muscle bulk, often with a normal CK. So
- 40:19Speaker 2: they don't fit the definition. So I'm talking, I practice
- 40:23Speaker 2: in the real world, not in the rarefied research environment
- 40:26Speaker 2: where these guys don't actually see patients. I talk to
- 40:30Speaker 2: people and these people tell me, doctor, I was on
- 40:33Speaker 2: these drugs and I stopped them. The pain went away
- 40:35Speaker 2: within a day. Now, is that all in their head?
- 40:37Speaker 2: I don't think so. So anyhow, this woman came to
- 40:40Speaker 2: see me I organized the coronary calcium score, came back
- 40:43Speaker 2: a big fat zero. And I said, look, you've gone
- 40:46Speaker 2: 58 years with your 9.5 cholesterol not spilling into your arteries.
- 40:52Speaker 2: You've got very low level disease with a zero score.
- 40:55Speaker 2: If it was me, I'd practice the five keys. I'd
- 40:58Speaker 2: take some supplements, but I wouldn't take a statin.
- 41:00Speaker 3: Okay.
- 41:01Speaker 2: For the next eight years, Paul, every scaremongering GP said, well,
- 41:05Speaker 2: if you don't take a statin, you're going to die.
- 41:07Speaker 2: She listened to me, not to the GP. Came back
- 41:10Speaker 2: eight years later. I told her to come back five years,
- 41:12Speaker 2: but she came back eight years later for another coronary
- 41:14Speaker 2: calcium score. She's now 66. It had rocketed from zero
- 41:18Speaker 2: to zero. And so I said, look, you've made it
- 41:22Speaker 2: 66 years without a vascular problem. The statins knock your
- 41:25Speaker 2: body around. And she probably qualifies for that. PCSK9 inhibitors.
- 41:30Speaker 3: That was going to be my next question is statin
- 41:32Speaker 3: versus PCSK9.
- 41:33Speaker 2: Okay. And I'll explain that to you as well, but
- 41:36Speaker 2: she probably qualifies for them, but why bother with a
- 41:39Speaker 2: zero calcium score? So now this is the thing. Everyone thinks, oh,
- 41:42Speaker 2: it's a needle. It's an injection, the PCSK9. It's got
- 41:45Speaker 2: to be stronger.
- 41:46Speaker 3: No.
- 41:48Speaker 2: Statins are easily the best drugs to lower vascular risk.
- 41:51Speaker 2: They're not as powerful as lifestyle, but they're still the
- 41:55Speaker 2: best drugs we have that lowers your vascular risk. maybe
- 41:58Speaker 2: not lower the LDL as much as, say, Repatha, the
- 42:01Speaker 2: fortnightly injection. I think that's Evalucumab, but it's the fortnightly
- 42:06Speaker 2: injection of this PCSK9 inhibitor, markedly lowers your LDL, but
- 42:11Speaker 2: only reduces your vascular risk maybe 20%, 30%, statins maybe 30%.
- 42:17Speaker 2: So statins are better than the PCSK9s at lowering vascular risk.
- 42:21Speaker 2: But I just think there's more side effects with statins.
- 42:24Speaker 2: And I think, really, The public gives statins far too
- 42:27Speaker 2: much pain. The medical profession gives statins far too much power.
- 42:31Speaker 2: It's an extra layer of protection if you're at high risk.
- 42:34Speaker 2: So who do I use statins in? I use them
- 42:36Speaker 2: in people who have high coronary calcium scores, so well
- 42:39Speaker 2: above 50%, the 50th percentile for your age. So for example,
- 42:44Speaker 2: a 70-year-old male, the average calcium score for a 70-year-old
- 42:48Speaker 2: male is 200. Now I'm 70, my calcium score is zero,
- 42:52Speaker 2: but that's just pure genetics. My fat mate, four. But
- 42:56Speaker 2: if I see a male who's 70 with a high
- 42:59Speaker 2: cholesterol and his calcium score is 150, there's no way
- 43:02Speaker 2: I'd give him a statin. So if you're below the 50%
- 43:04Speaker 2: off range, I don't use statins. But if you already
- 43:08Speaker 2: had heart attack, stent, or a bypass, and you have
- 43:11Speaker 2: known atherosclerosis, then I'd definitely use a statin in that situation.
- 43:16Speaker 2: But somebody, for example, who's got a low calcium score
- 43:19Speaker 2: and had a heart attack for another reason, maybe plaque
- 43:21Speaker 2: erosion or something, or SCAD or something else, there's no
- 43:25Speaker 2: way I'd use a statin. But my colleagues all use
- 43:27Speaker 2: statins once you've had a heart attack, stent, or a bypass.
- 43:30Speaker 2: I prefer to individualize my management for the patient.
- 43:32Speaker 3: Now, I've read research, and that was years ago, so
- 43:35Speaker 3: this may be out of date, that in terms of
- 43:38Speaker 3: the efficacy of statins, that they only are effective in
- 43:43Speaker 3: producing cardiovascular death in people who've had a previous MI.
- 43:47Speaker 1: They may reduce your risk of vascular disease.
- 43:50Speaker 3: But it was only basically people who had a previous
- 43:53Speaker 3: MI that they would prevent death significantly.
- 43:56Speaker 1: Is that true?
- 43:57Speaker 2: Yeah, yeah, yeah. Right.
- 43:58Speaker 3: But there is a vascular benefit outside of the death prevention.
- 44:02Speaker 2: So if you look at your risk for heart attack,
- 44:05Speaker 2: a non-fatal heart attack, it's definitely reduced by statins, about 20, 30%.
- 44:09Speaker 2: The evidence is overwhelming.
- 44:11Speaker 1: So coronary events.
- 44:12Speaker 2: But there's still residual risk. There's significant residual risk due
- 44:16Speaker 2: to the fact that no one is really addressing LP
- 44:18Speaker 2: little a, and I've been, Look, doctors have been measuring
- 44:21Speaker 2: LP little a, which is, for the people who don't
- 44:23Speaker 2: know what it is, it's an ApoB molecule attached to
- 44:28Speaker 2: an apolipoprotein little a protein. So the ApoB puts fat
- 44:31Speaker 2: in your arteries. The apolipoprotein little a protein thickens the blood.
- 44:36Speaker 2: So two things you don't want to do. And doctors
- 44:39Speaker 2: have been measuring it for two or three years because
- 44:41Speaker 2: we're now developing drugs to lower LP little a.
- 44:44Speaker 1: I've seen them and they're astounding, aren't they?
- 44:46Speaker 2: Astounding results. Yeah. Yeah, but what we have to see...
- 44:49Speaker 2: For example, there's a yearly injection that lowers LP to
- 44:53Speaker 2: the late 90%, but we want to make sure that
- 44:56Speaker 2: that then lowers coronary events. There's no point lowering a
- 44:58Speaker 2: number in your bloodstream. It's not going to do anything.
- 45:02Speaker 2: And I've got to say, the two-year data on this
- 45:04Speaker 2: stuff doesn't look that promising. But we've got to look
- 45:07Speaker 2: at the five-year data to see what it does.
- 45:09Speaker 3: Yeah, I just saw this study came out, and it
- 45:12Speaker 3: was like, well, it's not that promising at the minute.
- 45:14Speaker 1: But as you say, we need more data.
- 45:17Speaker 3: So somebody who's going in, right, who's pretty healthy, but
- 45:23Speaker 3: their LDL is pretty high. The GP is gone. You
- 45:26Speaker 3: need to go on a statin. They might have a
- 45:29Speaker 3: little bit of calcium, right? So they're in their, say me,
- 45:33Speaker 3: in their 50s, but fit and healthy. Like, would they
- 45:39Speaker 3: be better off on a statin or would they be
- 45:40Speaker 3: better off taking Viagra or the other option that you
- 45:44Speaker 3: talked about?
- 45:45Speaker 2: Vitamin V and vitamin C, Viagra, Cialis. No, look, I
- 45:49Speaker 2: think what they're better off, I certainly wouldn't give someone
- 45:52Speaker 2: a statin under those circumstances, whereas most of my colleagues would.
- 45:55Speaker 2: And the reason being, I base it on a major
- 45:58Speaker 2: study done by a guy called Mitch Folleans out of Philadelphia, 2018,
- 46:01Speaker 2: the Journal of Merit and College of Cardiology, where he
- 46:05Speaker 2: took a 13,000 people over 10 years between the ages
- 46:10Speaker 2: of 50 to 75. And he looked at the benefits
- 46:13Speaker 2: of them being on a statin based on their calcium score,
- 46:16Speaker 2: not based on their cholesterol. And he found if you
- 46:19Speaker 2: have a zero calcium score, there is zero benefit from
- 46:23Speaker 2: being on a statin. You get no benefit at all.
- 46:26Speaker 2: If your calcium score is below 100, which typically is
- 46:30Speaker 2: below the 50th percentile, there is no statistically significant benefit.
- 46:35Speaker 2: The number needed to treat there is 100 people for
- 46:37Speaker 2: five years to prevent one heart attack with no difference
- 46:41Speaker 2: in death rate. But once you get well above 100,
- 46:45Speaker 2: then the number needed to treat becomes 12. The p-value
- 46:50Speaker 2: is less than 0.001. So it shows that once you
- 46:54Speaker 2: have a significant atherosclerotic load, then that's where the statin
- 47:00Speaker 2: benefit kicks in. And this is interesting. A lot of
- 47:02Speaker 2: my colleagues now believe that this CT coriangigram, where you
- 47:06Speaker 2: squirt people with dye, is better than a coronary calcium score,
- 47:10Speaker 2: and that's nonsense.
- 47:11Speaker 3: I actually had a cardiologist on who was talking about that. Now,
- 47:15Speaker 3: he was a big fan of CT, because he said
- 47:19Speaker 3: you can look inside, it's like a 3D model of
- 47:22Speaker 3: the heart.
- 47:22Speaker 2: Of course you can. It gives you beautiful pictures of
- 47:24Speaker 2: the coronary arteries. But a guy called Mortensen, I think
- 47:28Speaker 2: it was a few years back, again in the Journal
- 47:30Speaker 2: of the American College of Cardiology, compared the two in
- 47:33Speaker 2: asymptomatic patients. People will often... quote what's called the Scott trial,
- 47:37Speaker 2: SCOT trial, or it could be the ASCOT trial, which
- 47:42Speaker 2: showed in people who were symptomatic, there's a definite benefit
- 47:45Speaker 2: of CT coronary angiography. I don't dispute that. But in
- 47:48Speaker 2: people who are asymptomatic, when you compare the two, so
- 47:52Speaker 2: the coronary calcium score is a measure of the degree
- 47:54Speaker 2: of atherosclerosis, whereas the CT angiogram is a measure of
- 47:57Speaker 2: the degree of blockages that you have. Yes. That the
- 48:01Speaker 2: degree of atherosclerosis easily beats finding a few blockages in
- 48:05Speaker 2: your arteries. So again, I focus on the coronary customer school,
- 48:10Speaker 2: but there is a caveat here. Coming into Australia soon,
- 48:14Speaker 2: it's already available in some centers in America, and I
- 48:17Speaker 2: think there's a couple of people in Australia doing this.
- 48:19Speaker 2: They're now doing, with CT coronary angiogram, plaque analysis. So
- 48:24Speaker 2: even the soft plaques, they can analyze the plaques look
- 48:27Speaker 2: for features like lower tenuators.
- 48:29Speaker 3: That's what this guy was talking about because he was
- 48:31Speaker 3: an American dude and he said that they were the
- 48:33Speaker 3: latest advent of the CT coronary angiogram.
- 48:36Speaker 2: Yeah, well, I don't disagree with him. And when that
- 48:38Speaker 2: becomes available, and the good thing is there's only three
- 48:41Speaker 2: advantages of being over 50, Paul. One is wisdom. Two
- 48:46Speaker 2: is grandchildren, if you have them. And three, you lose
- 48:50Speaker 2: the cancer risk from medical radiation. So everyone worries about radiation,
- 48:54Speaker 2: but over the age of 50, it doesn't matter. You're
- 48:55Speaker 2: not going to get a cancer out of you. having
- 48:58Speaker 2: a ct cori angiogram but if you start throwing radiation
- 49:00Speaker 2: at 30 year olds right 20 years down the track
- 49:03Speaker 2: the cancer risk does rise so i i won't have
- 49:07Speaker 2: any problems at all using the ct cori angiogram as
- 49:10Speaker 2: a better predictive risk when i can do plaque analysis
- 49:14Speaker 2: yeah gotcha It's not really freely available yet in Australia.
- 49:18Speaker 3: That's what this guy was talking about, right, which is
- 49:20Speaker 3: the latest advent of the CT. That makes perfect sense.
- 49:23Speaker 3: So let's jump and talk about nutrition. What, in your view,
- 49:31Speaker 3: are the biggest do's and don'ts for heart health and nutrition?
- 49:36Speaker 3: I love this because I have a preventative cardiologist, who's
- 49:40Speaker 3: on here talking about nutrition, who's very experienced in it.
- 49:44Speaker 2: Yeah. Firstly, and this is so obvious, everybody eats too much.
- 49:49Speaker 2: So basically we were designed to wander around the jungle
- 49:52Speaker 2: with a spear. You killed the beast. You ate it
- 49:54Speaker 2: straight away because there was no prehistoric Kelvinators. And you
- 49:57Speaker 2: stored a bit of fat around your belly for the
- 49:59Speaker 2: next big feed two or three days away. And in
- 50:02Speaker 2: the meantime, I had a few nuts and berries off
- 50:03Speaker 2: the trees and water out of the watering hole. No
- 50:06Speaker 2: one does that. And let's face it, that sucks. So
- 50:09Speaker 2: people think it's their God-given right to have breakfast, lunch, dinner,
- 50:12Speaker 2: and sit in their bums all day. They wonder why
- 50:14Speaker 2: they get fat. So I say to people, you've got
- 50:17Speaker 2: to just cut back down. No one should eat unnecessary food. Now,
- 50:21Speaker 2: what's unnecessary food? Snacking. People say, well, doctor, I get
- 50:26Speaker 2: starving by 10.30. Get over it. My mate David Sinclair
- 50:30Speaker 2: is the world anti-aging guru from Harvard. He said, Look,
- 50:34Speaker 2: hunger is actually good for you. It's good to feel
- 50:37Speaker 2: a bit hungry. You don't always have to have your
- 50:39Speaker 2: belly fed. If you feel hungry, celebrate it. Enjoy it.
- 50:43Speaker 2: Don't get there and say, oh, no, this is wrong.
- 50:45Speaker 2: I've got to eat. So firstly, don't eat so much.
- 50:48Speaker 2: That's the first point I make to people. Cut back
- 50:50Speaker 2: your calories and don't eat unnecessary food. Number two, I've
- 50:54Speaker 2: already mentioned it, fruit and vegetables. Two or three pieces
- 50:57Speaker 2: of fruit, three to five servings of vegetables, servings about
- 51:00Speaker 2: a half a carrot. And then what we shouldn't be
- 51:03Speaker 2: eating is What I call white death. So any form
- 51:07Speaker 2: of sugar, white bread, salt, and to a lesser extent, pasta, potatoes,
- 51:13Speaker 2: and rice. We should be minimizing our intake of that rubbish.
- 51:16Speaker 2: And also the process package muck masquerading as food. It's
- 51:22Speaker 2: not food. It's empty calories. So if it's in a box...
- 51:25Speaker 2: or a container with the use by date. And people say,
- 51:27Speaker 2: you should always read the labels. If it's got labels
- 51:29Speaker 2: on it, you shouldn't be eating the damn thing.
- 51:32Speaker 1: We're very aligned.
- 51:33Speaker 3: I'd talk about low HI diet, which is human interference.
- 51:36Speaker 2: Human interference, yeah. I use that term as well. And
- 51:39Speaker 2: also this nonsense about saturated fat. Yes. There's a study
- 51:43Speaker 2: called the PURE study. 220,000 people followed for nine years
- 51:48Speaker 2: in 50 different countries showed that those who had the
- 51:51Speaker 2: highest intake of saturated fat, meat, eggs, and dairy, compared
- 51:55Speaker 2: with those who had the lowest incidence, had a 25%
- 51:58Speaker 2: reduction in death and cardiovascular disease. And I'm not suggesting
- 52:02Speaker 2: people should swim in red meat, dairy products, and eggs.
- 52:05Speaker 2: I'm not suggesting that. But just don't give me this rubbish.
- 52:08Speaker 1: Don't be scared of it.
- 52:10Speaker 3: You know, this is the thing, Ross, that I have
- 52:12Speaker 3: a major issue with in nutrition is is that these people,
- 52:17Speaker 3: and dieticians in Australia are still banging on about saturated fat,
- 52:20Speaker 3: which is ridiculous.
- 52:21Speaker 2: As are major cardiology institutions around Australia.
- 52:25Speaker 3: It's like, for me, if you're going to change the
- 52:31Speaker 3: ancestral diet or change the recommendations that we shouldn't eat
- 52:35Speaker 3: what humans have been eating for for millions of years,
- 52:37Speaker 3: for hundreds of thousands of years, you need overwhelming scientific
- 52:42Speaker 3: evidence and there is nowhere near overwhelming scientific. I mean,
- 52:47Speaker 3: all this, the studies that they promote that says we
- 52:50Speaker 3: should reduce saturated fat and produce with it.
- 52:52Speaker 1: They're flawed. They're highly flawed. I mean, you can talk.
- 52:55Speaker 2: Also, mate, they were done in animals. A lot of
- 52:57Speaker 2: these are animals who are used to eating something and
- 53:00Speaker 2: then you totally change their diet. It's a bit like
- 53:02Speaker 2: going to an Eskimo and saying, okay, from now on,
- 53:05Speaker 2: we're going to give the same food we give to
- 53:06Speaker 2: someone who lives in the equator. They haven't evolved for this,
- 53:09Speaker 2: and animals haven't evolved for our crappy diets.
- 53:11Speaker 3: And I think the other thing is that a lot
- 53:14Speaker 3: of the stuff where they measure the blood and they
- 53:16Speaker 3: talk about it is saturated fat in blood is not
- 53:20Speaker 3: caused by eating saturated fat. It's caused by eating processed carbohydrates.
- 53:24Speaker 3: This is what people do not understand, right? And then
- 53:27Speaker 3: they're going, hey, there's saturated fat in blood, and that's bad,
- 53:30Speaker 3: therefore saturated fat's bad. No, it's the freaking sugar and
- 53:33Speaker 3: the processed carbs that are driving it up.
- 53:35Speaker 2: And in fact, this all started because of a lunatic
- 53:38Speaker 2: called Ansel Keys.
- 53:39Speaker 3: Yes.
- 53:39Speaker 2: Who, I think in the 60s, brought out the seven
- 53:43Speaker 2: country studies where he looked at 22 countries and released
- 53:46Speaker 2: the results of six in the seven country studies. Because
- 53:49Speaker 2: the six fitted his hypothesis was that fat caused heart disease.
- 53:54Speaker 2: At the same time, a guy called John Yudkin, who
- 53:57Speaker 2: was from the UK, came out and said, no, no, no.
- 53:59Speaker 2: What causes heart disease is sugars. Sugar, that's right. And
- 54:02Speaker 2: the dairy industry, the sugar industry shut him down because
- 54:06Speaker 2: he was saying what they didn't want to hear. And
- 54:09Speaker 2: so since we've switched to this low-fat, high-carb diet, we've
- 54:14Speaker 2: seen the rates of obesity and the true pandemic of
- 54:17Speaker 2: the 21st century is not COVID, it is diabesity, which
- 54:21Speaker 2: has come from all of this rubbish, this processed package
- 54:24Speaker 2: rubbish from the refined carbohydrates that people are eating far
- 54:28Speaker 2: too much of. And just a bit of a segue
- 54:31Speaker 2: back to cholesterol, that when you look at someone's cholesterol,
- 54:35Speaker 2: you might have a cholesterol of 7, HDL of 2.5,
- 54:37Speaker 2: triglyceride of 0.5. As I said, lean hyper-responder, healthy. Your
- 54:41Speaker 2: saturated fat might make that a little bit more accentuated.
- 54:44Speaker 2: But if your cholesterol is 4.5 and your triglycerides are
- 54:48Speaker 2: 2.5 and your HDL is 0.9, your doctor will say,
- 54:52Speaker 2: you've got a better cholesterol. No, you haven't. That's all
- 54:55Speaker 2: small LDL. That's what that's telling you. It's atherogenic.
- 55:00Speaker 3: So one thing, by the way, we're on violent agreement
- 55:03Speaker 3: on nutrition. And I love that you called him a lunatic,
- 55:06Speaker 3: Ansel Keys, because that's fraudulent research that has affected nutrition.
- 55:11Speaker 1: More than anything else.
- 55:12Speaker 2: Absolutely. Absolutely.
- 55:14Speaker 3: But just to come back to what you said, can
- 55:16Speaker 3: you please explain the... triglyceride to HDL ratio the impact
- 55:22Speaker 3: on insulin and the broader conversation around metabolic syndrome and
- 55:27Speaker 3: secondly do you think that if you just looked at
- 55:32Speaker 3: HDL triglyceride ratio versus LDL cholesterol which one would be
- 55:37Speaker 3: a better predictor because.
- 55:38Speaker 1: You're not allowed to do both you're just allowed to
- 55:40Speaker 1: pick one.
- 55:40Speaker 2: Okay a better predictor I think is the the triglyceride
- 55:43Speaker 2: to HDL ratio because that is a marker for small LDL.
- 55:47Speaker 2: And small LDL is the most atherogenic component of your
- 55:51Speaker 2: lipid profile. So certainly triglyceride HDL, because that's just telling
- 55:56Speaker 2: you you've got a lot of small LDL.
- 55:58Speaker 1: Yeah, without actually paying the expensive test.
- 56:00Speaker 2: Getting back to metabolic syndrome, a lot of people don't
- 56:03Speaker 2: understand this. As I said, right at the start, everything's genetic.
- 56:06Speaker 2: So 30% of Caucasians are born with the gene for
- 56:10Speaker 2: insulin resistance. 50% of Asians... and close to 100% of
- 56:14Speaker 2: people with dark or olive skin are born with the
- 56:17Speaker 2: gene for insulin resistance. That's why we've never seen a
- 56:20Speaker 2: skinny Tongan. They're the world champions of insulin resistance and
- 56:24Speaker 2: the world champions of obesity. So as soon as you
- 56:26Speaker 2: expose anyone who's insulin resistant to Western crap, that's when
- 56:30Speaker 2: they bulk up. And the four features of insulin resistance
- 56:33Speaker 2: are tendency to or frank diabetes, high blood pressure, high triglyceride,
- 56:39Speaker 2: low HDL, what we were just talking about there, and
- 56:42Speaker 2: it's really easy to put fat around the belly. And
- 56:45Speaker 2: so once you've got a couple of those, we call
- 56:47Speaker 2: it metabolic syndrome. So insulin resistance is the cause of 70%
- 56:51Speaker 2: of heart disease, 20% LP little a, and throw on
- 56:55Speaker 2: top of that, which we mentioned before, we haven't really
- 56:57Speaker 2: discussed the MTHFR gene abnormalities, but all of these things
- 57:01Speaker 2: cause about 90% of heart disease, 10% from the less
- 57:04Speaker 2: common genetic abnormalities like FH and a few other things. Wow.
- 57:08Speaker 1: Interesting.
- 57:09Speaker 3: Let's talk about what's known in certain circles colloquially as
- 57:14Speaker 3: the motherfucker gene. Because you've mentioned the MTHFR gene. What
- 57:19Speaker 3: is it and what are the risks if you have
- 57:24Speaker 3: one or more variants of it?
- 57:26Speaker 2: Okay, well, the MTHFR gene is the major gene that
- 57:29Speaker 2: codes this methyl tetrahydrofolate reductase enzyme, which is one of
- 57:34Speaker 2: the major checkpoints for folate in your diet. being incorporated
- 57:39Speaker 2: into DNA, RNA, and protein. And tragically, one in two people,
- 57:44Speaker 2: and I've got the worst mutation, have one of the
- 57:47Speaker 2: mutations in this gene or possibly even two. One in two? Yeah,
- 57:50Speaker 2: one in two people.
- 57:51Speaker 1: I didn't think it was that much.
- 57:52Speaker 2: No, it's that high. And just for people who don't
- 57:56Speaker 2: understand this, genetics 101, every gene is paired, one from mum,
- 58:00Speaker 2: one from dad. That's how we are who we are.
- 58:03Speaker 2: So this MTHFR gene, you either have two normal genes
- 58:07Speaker 2: or you have– either two Cs, which is the worst,
- 58:10Speaker 2: the C allele is the worst one, I've got two
- 58:13Speaker 2: of those, two As, which is much less significant, or
- 58:17Speaker 2: what we call a combined heterozygote, the C and the A. Now,
- 58:22Speaker 2: this is the interesting thing, that if you've got two Cs,
- 58:25Speaker 2: your methyl tetrahydrofolate reductase enzyme is down about 80%, 70
- 58:30Speaker 2: to 80%. So as you get older, you're not getting
- 58:36Speaker 2: high quality folate into your DNA, RNA and protein. So
- 58:39Speaker 2: up goes your homocysteine level, which is toxic to the
- 58:43Speaker 2: lining of your blood vessels. And here's where all the
- 58:45Speaker 2: trials have been bunkum because they've used folic acid, which
- 58:50Speaker 2: is a poison for someone who's got an MTHFR gene abnormality.
- 58:54Speaker 2: They've used folic acid, B12 and synthetic B6, which is pyridoxine.
- 59:00Speaker 2: And this is why we're now seeing all these pyridoxine
- 59:03Speaker 2: toxicities because 10 to 20% of the population can't metabolize
- 59:08Speaker 2: inactive B6, pyridoxine, to active B6, which is pyridoxal 5-phosphate.
- 59:14Speaker 2: And so therefore, people are going out and taking their
- 59:17Speaker 2: multivitamins because they think they're good for them, which are
- 59:20Speaker 2: full of folic acid and pyridoxine, and they're not good
- 59:23Speaker 2: for you. That's why the studies aren't showing any benefits
- 59:26Speaker 2: in people in high homocysteine who are given these poisons. Yes.
- 59:30Speaker 2: what I'm doing now is I'm looking at the MTHFR gene.
- 59:33Speaker 2: If people have my mutation or one of my mutations,
- 59:36Speaker 2: which is the CLL, so I've got two of them,
- 59:38Speaker 2: I take activated folate, five prime methyl tetrahydrofolate, which then
- 59:44Speaker 2: directly bypasses that mutation and feeds into DNA, RNA, protein,
- 59:48Speaker 2: and lowers your homocysteine. Yeah.
- 59:51Speaker 1: And do you take activated B vitamins as well as
- 59:53Speaker 1: the activated folate?
- 59:55Speaker 3: Yeah.
- 59:55Speaker 2: So I do that as well. And I think That's
- 59:58Speaker 2: really important for all of us, the one in two
- 1:00:00Speaker 2: of us who've got this. And interestingly, and this is
- 1:00:03Speaker 2: a really interesting study, there's a study called the Aspirin
- 1:00:06Speaker 2: Folic Acid Colonic Polyp Study, where they studied, I think
- 1:00:10Speaker 2: it was three or 4,000 people over 10 years. And
- 1:00:13Speaker 2: they gave them five milligrams a day of folic acid
- 1:00:17Speaker 2: and 100 milligrams a day of aspirin. I think it
- 1:00:20Speaker 2: was a two by two vectorial design. And they found
- 1:00:23Speaker 2: that there was no reduction in polyps at all. But
- 1:00:27Speaker 2: in the men taking the folic acid, there was a
- 1:00:30Speaker 2: triple risk for prostate cancer. And I believe the reason
- 1:00:34Speaker 2: being is that probably the ones who had, the one
- 1:00:36Speaker 2: in two people who've got an MTHFR gene abnormality, the
- 1:00:39Speaker 2: folic acid couldn't be metabolized, increases in the bloodstream in
- 1:00:43Speaker 2: what we call strangely unmetabolized folic acid, and that damages
- 1:00:47Speaker 2: the immune system. And so this is why All of
- 1:00:51Speaker 2: the doctors who don't understand any of this, the conservative
- 1:00:53Speaker 2: doctors don't understand how this works. They say, oh, all
- 1:00:56Speaker 2: you get with vitamins is expensive urine. No, you get
- 1:01:00Speaker 2: dangerous urine if you use the crappy vitamins. So I
- 1:01:03Speaker 2: have a plea out there to all of the supplement companies,
- 1:01:07Speaker 2: get folic acid out of it. So pregnant women should
- 1:01:10Speaker 2: not be taking folic acid or one in two of
- 1:01:12Speaker 2: them shouldn't. They should be taking folate, activated folate. Or
- 1:01:16Speaker 2: if you've got the allele, I use folinic acid. So
- 1:01:20Speaker 2: folic acid. And that targets the ALL, whereas activated folate
- 1:01:26Speaker 2: targets the CLL.
- 1:01:28Speaker 3: Ah, no, I didn't know that. I didn't know there
- 1:01:30Speaker 3: was one that was better for the ALL. Because I
- 1:01:32Speaker 3: get the ALL, my wife has one of the CLLs, right?
- 1:01:36Speaker 3: And this is an issue because folic acid has been
- 1:01:40Speaker 3: put in things like bread and stuff.
- 1:01:42Speaker 1: Like that, right?
- 1:01:43Speaker 2: It should be taken out.
- 1:01:44Speaker 3: Yeah, and that's why, you know, go and get yourself
- 1:01:48Speaker 3: a proper artisan sardo that doesn't have any shit rather
- 1:01:52Speaker 3: than supermarked breads that as well as being a completely
- 1:01:56Speaker 3: different species, they often have folic acid in them, which
- 1:02:00Speaker 3: in one in two of you might be actually damaging
- 1:02:02Speaker 3: rather than helpful.
- 1:02:03Speaker 2: Yeah, causing you issues. And this is, again, the whole
- 1:02:05Speaker 2: concept of supplements is that not all supplements are created equal.
- 1:02:10Speaker 2: And many people just go into a health food store
- 1:02:12Speaker 2: and say, this has been advertised for this condition and
- 1:02:15Speaker 2: take it. And they don't realize in their case, it
- 1:02:17Speaker 2: may be causing problems. And also these days with polypharmacy,
- 1:02:22Speaker 2: many drugs that doctors use interact with some supplements and
- 1:02:26Speaker 2: can cause issues. So you just got to be really
- 1:02:28Speaker 2: careful what you're doing with all this. Yeah, you do.
- 1:02:32Speaker 3: And that's why integrative doctors like you, and I know
- 1:02:35Speaker 3: lots of integrative doctors, that they're the ones to talk
- 1:02:38Speaker 3: about or well-qualified naturopaths who or nutritionists who understand the
- 1:02:43Speaker 3: genetics and the nutrigenomics, I think that's really, really important. So, Ross,
- 1:02:49Speaker 3: I'm aware of your time, but what do you think
- 1:02:52Speaker 3: that we are now talking about in terms of cardiovascular
- 1:02:56Speaker 3: health that in 20 years we're going to be going, geez,
- 1:02:59Speaker 3: why were we saying that?
- 1:03:01Speaker 2: Yeah, well, I think in 20 years' time, we're now
- 1:03:05Speaker 2: talking about things like gene therapy and to change people's lipids. So,
- 1:03:10Speaker 2: for example, there's been a couple of studies that have
- 1:03:11Speaker 2: been released recently, I think in the New England Journal
- 1:03:14Speaker 2: of Medicine, where they just gave one gene therapy with
- 1:03:18Speaker 2: a viral vector to completely change people that had, say,
- 1:03:23Speaker 2: LDL receptor defects with familial hypercholesterolemia. So one therapy, 18
- 1:03:27Speaker 2: months later, their cholesterol was back to normal. And they're
- 1:03:31Speaker 2: even working on a vaccination against heart disease, which would
- 1:03:34Speaker 2: be dreadful for people like me out of a job.
- 1:03:37Speaker 2: But imagine being able to be vaccinated against oxidized small
- 1:03:41Speaker 2: LDLs so it just doesn't become a problem. So they're
- 1:03:44Speaker 2: the sort of things I think we're working towards in cardiology.
- 1:03:47Speaker 2: And also a lot of the techniques where you need
- 1:03:51Speaker 2: your valve replaced or whatever, we're now doing transcutaneous valve replacements.
- 1:03:56Speaker 2: We can do that with aortic valves and mitral valves
- 1:03:59Speaker 2: and even now things like dissected aortas or widening aortas,
- 1:04:03Speaker 2: just putting stents in. So- I think the jobs of
- 1:04:06Speaker 2: cardiac surgeons are going to drop right off. And also,
- 1:04:09Speaker 2: once we work on the preventative side of things, whether
- 1:04:12Speaker 2: it is better ways to lower cholesterol or whatever, once
- 1:04:15Speaker 2: we do all of that, we'll see much less people
- 1:04:18Speaker 2: having the severe presentations of coronary artery disease. So my
- 1:04:22Speaker 2: hope still is that people realize And we finish off
- 1:04:26Speaker 2: with a positive note on things like the blue zones. Now,
- 1:04:28Speaker 2: I know there's some people who've been disputing whether the
- 1:04:30Speaker 2: blue zones are actually real. And I think we can
- 1:04:33Speaker 2: debunk the debunking of the blue zones because I think
- 1:04:36Speaker 2: the evidence is pretty solid for them. But in the
- 1:04:38Speaker 2: blue zones, they've never heard of Crestor or Lipitor to
- 1:04:43Speaker 2: lower your cholesterol. They've never heard of gyms. They basically
- 1:04:46Speaker 2: don't smoke. They eat buckets of fruits and vegetables, as
- 1:04:49Speaker 2: we've stressed today. They live on the side of hills,
- 1:04:52Speaker 2: so they're moving up and down the hill all day.
- 1:04:54Speaker 2: They have a very strong sense of family and community.
- 1:04:57Speaker 2: And they're the people who have the greatest longevity on
- 1:04:59Speaker 2: the planet. So I hope we don't see that marvels
- 1:05:03Speaker 2: of modern medicine is replacing what to me is the
- 1:05:06Speaker 2: most important thing, which is a healthy lifestyle, especially based
- 1:05:10Speaker 2: around human connection, which is absolutely vital.
- 1:05:14Speaker 3: Yeah, absolutely. Oh, one last question. personal question here, because
- 1:05:18Speaker 3: you know about my condition. I think most of the
- 1:05:21Speaker 3: listeners know I had open heart surgery for a bicuspid
- 1:05:24Speaker 3: aortic valve that I was born with. And then something
- 1:05:27Speaker 3: chewed up a chunk of my basal septum on my
- 1:05:30Speaker 3: left ventricle. Um, which we think might be.
- 1:05:33Speaker 1: A one-off infarct.
- 1:05:34Speaker 3: But do you think, because I've been reading some research
- 1:05:39Speaker 3: about the potential of stem cells to regenerate dead cardiac tissue,
- 1:05:44Speaker 3: do you think that that's a possibility on the horizon?
- 1:05:47Speaker 2: Look, I've been following stem cell therapy and have visited
- 1:05:50Speaker 2: some clinics in Thailand when they were doing this 15
- 1:05:52Speaker 2: years ago. A lot of hype, not a lot of
- 1:05:55Speaker 2: science yet. And the problem is that once you inject
- 1:05:57Speaker 2: stem cells anywhere, they're chewed up by the immune system
- 1:06:01Speaker 2: almost immediately. So they're talking more about it being a
- 1:06:04Speaker 2: paracrine effect rather than the stem cells. The public sort
- 1:06:09Speaker 2: of gets the idea that the stem cells get implanted
- 1:06:12Speaker 2: in the arteries and regrow new cells and everything's wonderful.
- 1:06:15Speaker 2: But they haven't been able to do that yet. Maybe
- 1:06:17Speaker 2: that will happen in the future. There's been some work
- 1:06:20Speaker 2: with spinal cord injuries with some benefits there with pancreatic transplants.
- 1:06:24Speaker 2: So these things are showing promise. But they're still not
- 1:06:27Speaker 2: prime time. So I'm hoping that one day we'll be
- 1:06:30Speaker 2: able to do that. Maybe there'll be other techniques, genetic techniques,
- 1:06:33Speaker 2: where we can regrow myocardium. I'm sure that's another way
- 1:06:36Speaker 2: of doing it as well. Maybe not stem cells. But
- 1:06:38Speaker 2: there will be something in the not too distant future,
- 1:06:42Speaker 2: maybe 10 or 15 years away. But again, I've been
- 1:06:44Speaker 2: talking about this for 15 years, that may be able
- 1:06:47Speaker 2: to do that.
- 1:06:48Speaker 1: Yeah, cool.
- 1:06:49Speaker 2: I'll just check.
- 1:06:50Speaker 1: It's like that.
- 1:06:51Speaker 3: We've just got to hang on another 10 or 15 years, right?
- 1:06:53Speaker 3: And then there'll be so many more advances.
- 1:06:56Speaker 2: But Paul, the best way to do that is to practice.
- 1:06:59Speaker 1: The five keys.
- 1:07:02Speaker 2: Oh, 100%.
- 1:07:02Speaker 3: We are in violent agreement about those five keys for sure.
- 1:07:06Speaker 1: And in pretty much everything that you've talked about.
- 1:07:09Speaker 3: And actually, it's been great because it's opened my eyes
- 1:07:11Speaker 3: and cleared up some things that I was a little
- 1:07:14Speaker 3: bit confused about.
- 1:07:15Speaker 1: So, mate, this has been awesome.
- 1:07:17Speaker 3: I don't think anybody could have listened to this and
- 1:07:19Speaker 3: not learned an absolute ton.
- 1:07:22Speaker 2: I don't care who they are.
- 1:07:23Speaker 1: So, mate, thank you for your life's work.
- 1:07:26Speaker 3: And, mate, I hope to interview you in another 10
- 1:07:29Speaker 3: or 15 years when you're still practicing the five keys,
- 1:07:33Speaker 3: fit as a virtuous dog.
- 1:07:34Speaker 2: I'm about to release my new service called W Life,
- 1:07:38Speaker 2: which W obviously for Walker, but also W Life, which
- 1:07:42Speaker 2: is an anti-aging service. So we haven't even got into
- 1:07:45Speaker 2: the whole topic of anti-aging. But again, anti-aging is still 80-10-10.
- 1:07:50Speaker 2: So there's a bucket of supplements you can swallow for anti-aging.
- 1:07:54Speaker 2: You don't practice the 80%, forget it.
- 1:07:56Speaker 1: Yeah, yeah, no, 100%.
- 1:07:57Speaker 3: Where can people go to find out more about you
- 1:08:01Speaker 3: to buy– One of your seven books.
- 1:08:03Speaker 1: And when is your book number eight going to be out?
- 1:08:05Speaker 2: Healthspan will be coming out probably early next year. So
- 1:08:10Speaker 2: not yet. The other books are out of date, really.
- 1:08:12Speaker 2: I haven't written a book for about 13 years. So
- 1:08:14Speaker 2: this is the new one, which is my latest tome.
- 1:08:17Speaker 2: And I'm working on another book called Medicine Versus Healing,
- 1:08:20Speaker 2: which is something else we could talk about on another occasion.
- 1:08:23Speaker 2: So if anyone's interested, it's drrosswalker.com and also wlife.co.
- 1:08:32Speaker 1: RossWalker.com and WLife.co.
- 1:08:35Speaker 2: Brilliant.
- 1:08:36Speaker 1: Excellent. Ross, this has been awesome. Thanks very much for
- 1:08:40Speaker 1: your time.
- 1:08:42Speaker 2: Thanks, mate.