Wellness by Designs - Practitioner Podcast

Ubiquinol: The Missing Link in Cardiovascular Health with Dr Ross Walker

• Designs for Health • Episode 131

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Is Ubiquinol the Missing Nutrient for Lifelong Heart Health?

In this eye-opening episode of Wellness by Designs, Dr Ross Walker, a renowned cardiologist with 25 years dedicated to preventative medicine, challenges the conventional approach to heart disease, statins and cholesterol management. Central to the discussion is ubiquinol, the active form of CoQ10, essential for mitochondrial energy production and a powerful antioxidant. Dr Walker explains how our natural production of ubiquinol begins declining around age 30 and drops sharply by 50, contributing to fatigue and reduced cardiovascular resilience.

Dr Walker explores why many patients with “normal” cholesterol still develop significant coronary artery disease, arguing that coronary calcium scoring offers a far superior risk assessment tool than standard cholesterol tests. Dr Walker also addresses statin-associated muscle symptoms, recommending 150 mg of ubiquinol daily for statin users, citing research showing a 50% reduction in muscle problems, and up to 300 mg for those with heart failure to support cardiac function and endothelial health.

From mitochondrial health to protection against oxidative stress, this episode highlights why ubiquinol may be a cornerstone in maintaining cardiovascular wellness and why a more personalised, evidence-based approach is needed to truly prevent heart disease.

Connect with Dr Walker: Home - Dr Ross Walker


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DISCLAIMER: The Information provided in the Wellness by Designs podcast is for educational purposes only; the information presented is not intended to be used as medical advice; please seek the advice of a qualified healthcare professional if what you have heard here today raises questions or concerns relating to your health




Speaker 1:

This is Wellness by Designs, and I'm your host, andrew Whitfield-Cook, and joining us today is Dr Ross Walker, an esteemed cardiologist who has dedicated the past 25 years of his career to prevention, and today we're going to be discussing the role of ubiquinol in cardiovascular health. Welcome to Wellness by Designs, ross. How are you?

Speaker 2:

Andrew, it's always a great pleasure to talk with you at any opportunity I get.

Speaker 1:

Thank you, sir. It's been a long time between chats.

Speaker 2:

Now Ross.

Speaker 1:

I think the first thing we need to cover is what exactly is ubiquinol?

Speaker 2:

Yeah, well, ubiquinol is the active version of coenzyme Q10. And coenzyme Q10 has a number of roles in the body. One is basically, it's a very strong antioxidant. It's a fat-soluble antioxidant, but also it's very, very important in mitochondrial health. It's a vital part of the mitochondrial energy production. And so without good levels of ubiquinol not ubiquinone, which is inactive, it's got to be ubiquinol the mitochondria doesn't work as well, doesn't work as well.

Speaker 1:

And so where, if we're talking about CoQ10, you know the old CoQ10, the ubiquinone where let's say there's still the lion's share of research is done on. Admittedly, in the olden days I guess there was the doses were way lower than what we're using now, and now we've swapped to ubiquinone the active. Tell us about that sort of journey of research, if you like, from ubiquinone the low-dose stuff. I mean. I'm sure you'll remember when in Australia the only product we could get was ubiquinone and it was 10 milligrams.

Speaker 2:

Yeah, and really didn't do much at all. And the problem is that with the whole CoQ10 story is that you really don't get enough in your diet. Whether it's ubiquinone or ubiquinol, there's just not enough in the diet. I think you've got to have something like a kilo and a half of steak to get 30 to 50 milligrams of ubiquinol in your system, and so much broccoli you'd be eating it for about three or four weeks to get that small amount. So, yes, when CoQ10 was first released, it was only in the ubiquinone or ubicarinone form and it was in very, very low doses, so it didn't really do much. I think this is really really a good example of the history of evidence based supplementation. Orthodox medicine wants hard data. They want science behind what anyone does, and so when you're using almost homeopathic doses of something that's inactive, you're not going to get much response. I mean it takes me back to the whole vitamin E nonsense that we've heard from years ago.

Speaker 2:

In 2004, a guy called Edgar Miller wrote an editorial in the Annals of Internal Medicine saying that vitamin E was not only of no benefit but it was possibly harmful. And this is what does my head in a bit about orthodox medicine. They're still quoting the vitamin E data using DL-alpha-tocopherol, which is the inactive version of vitamin D, from a thing called the Finnish Smokers Trial. Now, the clue is in that title there. But 29,000 Finnish smokers were studied and were given placebo-controlled either vitamin E, dl alpha-tocopherol, so a synthetic version of vitamin E 50 international units and 15 milligrams of synthetic beta-carotene. And this stuff shouldn't be used. It doesn't work and in fact, it can cause more harm. But so people like Edgar Miller are still coming out were coming out in 2004 saying vitamin E may be harmful. Well, of course it may be harmful if you use the crappy synthetic stuff. So again, this is what's happened with medicine. All the time they go back to these silly studies that disprove the benefits of, or disprove any benefits from, supplements because they've used the wrong dose of the wrong stuff.

Speaker 2:

And again, with the initial ubicarinone stuff, we're using 10, 30 milligrams of an inactive substance.

Speaker 2:

And here's the problem when you hit 30, and the 30 is the peak of our life. So it's a bit depressing for you and I, but our body was designed to wander around a jungle for 30, 40 years with a spear and then die, had your head ripped off by a saber-toothed tiger or you died of some infection. So when you hit 30, the peak of your life, things start to wear out. That's when osteoporosis starts, sarcopenia, loss of muscle that all starts at age 30. But also your ability to convert ubiquinone to ubiquinol starts to drop off a little bit at age 30. And then at age 50, the enzyme diaphoresis just goes boom. So you just don't get the amount of active CoQ10 or ubiquinol in the mitochondria that you need over the age of 50, which in many ways is one of the reasons why many people over the age of 50 are starting to feel tired, because their mitochondria just aren't working as well, and I think one of the reasons is they're losing one of the main drivers of their mitochondria, which is ubiquinol.

Speaker 1:

So just a point there about tiredness in in, you know, around the age of 50 sort of thing. Obviously there's many, many factors, you know. But would it be wise, therefore, for a wellness approach to start thinking about the use of ubiquinol, the active coq10, as part of the regimen? Obviously there's exercise and good sleep and things like that. I get it, but the use of ubiquinol in a reasonable dosage and I'll question you about that as part of their wellness program.

Speaker 2:

Oh, absolutely. And I've got to say, when I talk about wellness, wellness isn't just the absence of disease, which is an important component. Of course you know you want to have some illness because you will be unwell, but what I call ultimate wellness is, one, the absence of disease. Two, very good energy levels, which you do get from ubiquinol, and also, I think, the magnesium orotate aspartate combinations. And there are other reasons why we lose energy. I mean, sleep apnea is a big one, because all adult males have sleep apnea, all postmenopausal females have sleep apnea to some extent, and as you get older the sleep apnea gets worse and that makes you tired as well.

Speaker 2:

But there are many other reasons for fatigue and if anyone's listening to this, I wouldn't want you to start swallowing ubiquinol if you're tired without figuring out why you're tired in the first place, because it may. I mean, the commonest cause of fatigue in our society is you're working too hard, playing too hard, not sleeping well, but then after that there's endogenous depression that can also make you tired. Then there's sleep apnea, which we've mentioned. When you've hit 50 and you're going through the pauses either menopause or andropause you start to get tired. So that may be another factor. But then finally, there could be a medical reason. You could be losing blood, iron deficient, you could have a thyroid problem, something wrong with your kidneys, your liver, your heart. To give an example, one of the first presentations of a ruptured plaque is incredible fatigue.

Speaker 2:

So I wouldn't want anyone to go and say, oh, I'm tired. Therefore, I'm going to take ubiquinol. What I say, you're tired, find out why you're tired first, but then, once you've had all serious conditions excluded, by all means take now here's the to answer your question 150 milligrams of ubiquinol, which I think is the standard dose for people for energy. I take it. I'm 14 months off 70 and I've got a zero coronary calcium score and I'm not on a statin, because anyone's got a zero calcium score shouldn't go anywhere near a statin, which we'll get to a bit later on. But I just take the 150 milligrams every day of ubiquinol just to keep my energy going and I've got pretty good energy for someone in my age group.

Speaker 1:

Firstly, you mentioned cholesterol. So let's go there With cholesterol and the coronary artery calcium score. The Australian New Zealand College of Cardiologists says they sort of. I remember when you were mentioning this decades ago, ross, by the way, and back then there was total denial about the usefulness. And now the college has got a statement saying those who have low cholesterol and when I say the word cholesterol I think we all need to make to to realize that we're not talking about the molecule of cholesterol, we're talking about lipoproteins. But anyway, when we've got high or dysfunctional supposedly lipoprotein profiles, that those people who have got low or normal cholesterol quotation marks levels that they don't need a coronary artery calcium score, those people that are mid-range could benefit, I know could benefit and those people that are high have high anyway, so they should be on a statin. What's your take on that statement?

Speaker 2:

That statement is complete and utter nonsense. And let me just give you an anecdote just to show you how that is just such nonsense. This is not a clinical trial, but then I'll get on to the clinical trials. The worst coronary calcium score I have noting that anything above 400 is serious is a 68-year-old man in the fitness industry. Doesn't have an ounce of body fat.

Speaker 2:

Old man in the fitness industry doesn't have an ounce of body fat, has a normal cholesterol, blood pressure, never smoked, not diabetic and Andrew, wait for this no family history of heart disease. So therefore, by that criteria you just mentioned, there's no point in him having a coronary calcium score. But he has and we could get into this discussion because he's one of my hobby horses. He has an elevated lipoprotein, little a, which doctors have been measuring for the last two or three years because we're now developing drugs for it. I've been measuring it and treating it for 30 years. So anyhow, this guy came to see me, sent him downstairs for a coronary calcium score because I have a radiology practice under my building. It's not my practice and his coronary calcium score? Wait for this. I hope you're sitting down. You are sitting down 8,100.

Speaker 2:

Hi so his arteries were like porcelain pipes. He had bypass surgery 10 years ago. He sent me an email a few years ago with a picture of him and his mates winning the latest basketball grand final. So he'll now live to his 100 after he's bypassed, but under those criteria he wouldn't have had a coronary calcium score. Now let's get to the science, not just to a story.

Speaker 2:

I believe and I've been saying this for 26 years when I introduced coronary calcium scoring into Australia in conjunction with the Sydney Adventist Hospital in Wurundjeri and Dr David Grout, one of my cardiologic colleagues. I've been saying this for 26 years that all men at 50, all women at 60 should have a routine coronary calcium score. But the goalposts change. If, for example, you said to me oh, my dad had a bypass at 45. Well, I'd do your coronary calcium score at 35, as one example. But I don't like to over irradiate people below the age of 50 because in my view there are only three reasons, three benefits of being over 50, andrew. Number one is wisdom. Number two is grandchildren if you got them and I have nine. And number three is you lose the cancer risk from medical radiation. So the less radiation you have before age 50, the better off you are. So anyhow, to give you some science now behind the coronary calcium score and its relationship, especially to statin drugs. Firstly, it's been shown that if you have a coronary calcium score and you compare that to standard risk factors for heart disease, the calcium score has marked benefit in improving your level of risk. So there are so many people who appear to be at high risk because of standard risk factor profiles and they'd be all put on a statin. Then you do their coronary calcium score and they've got a zero calcium score. It markedly plummets their risk. So I'll give you again another story.

Speaker 2:

I saw a woman who was 58 years old with a lifelong cholesterol of 9.5, because cholesterol has got nothing to do with what you eat. It's all to do with genetics and metabolism. So women hit menopause, their cholesterol goes up because their metabolism changes, because they lose estrogen. So anyhow, every time she'd see a GP or any other doctor, scaremongering doctors say to her if you don't take Lipitor you're going to die, which is scaremongering, nonsense. She'd take Lipitor because she was worried about dying, of course, because her cholesterol was 9.5. And after a few days she couldn't lift her muscles, they were just killing her. So anyhow, after seeing multiple doctors, she heard about me, came to see me, sent it downstairs for a calcium score. It came back a big fat, nothing. And I said look, in your case, your cholesterol and all of its mates are not spilling into your arteries, so forget about it. Live a healthy lifestyle. No one should eat a bad diet, not just because of the cholesterol issue but because of many other factors. But please, you don't need a statin. So anyhow, over the next eight years, she listened to me and not to the scaremongering doctors, and she came back to see me, age 66 now, with a cholesterol of 9.5 because it's genetic, sent it downstairs for another calcium score. It had rocketed from zero up to zero, still zero. So I just said to her look, cholesterol is not an issue for you, don't have it checked again, don't listen to doctors worrying you about it. And she hasn't had a problem.

Speaker 2:

So a study of 13,500 people between the ages of about 50 up to 70 followed for 10 years the benefits of them taking a statin based on their calcium score Zero. Calcium score zero benefit. Calcium score below 100. So a 55-year-old male goes into a doctor with a calcium score of 60. The doctor says oh, you've got atherosclerosis, you must be on a statin. No, the evidence isn't there. This study showed calcium score below 100, p-value 0.095. So no statistically significant benefit from being on a statin. But the number needed to treat, which I think is a better number. Here you had to treat 100 people for five years to prevent one heart attack and no difference in death rate. So who in their right mind would take a strong synthetic metabolic regulator for 10 years to prevent one heart attack out of 100 people? I mean for five years, one heart attack. It's just nonsense. But once you get to a calcium score above about 100 for your age so if you're 60 and your calcium score is 150, then that's where the benefits kick in. The number needed to treat is only 12, highly statistically significant. So to me, when people make these comments, they've got to have some science behind what they say. The calcium score is easily the best predictor for heart disease risk.

Speaker 2:

And here's another hobby horse of mine, andrew before we should start talking about ubiquinol soon. But there's a thing called a CT Cori angiogram, and a CT Cori angiogram is done on the same technology as the calcium scoring still a CT coriangogram, and a CT coriangogram is done on the same technology as the calcium scoring still a CT but the calcium scoring just takes a snapshot of your arteries. The CT coriangogram you're injected with dye and you do not qualify by Medicare for the study if you have no symptoms and you haven't seen a cardiologist. So many GPs are saying, oh, a CT chorioangiogram gives you better pictures than a calcium score, which it does Beautiful pictures of the chorio arteries. So therefore I'll get you to have that test done.

Speaker 2:

It costs people an extra $500 or $600 to have that test and a study was done in the Journal of the American College of Cardiology looking at the predictive risk of coronary calcium scoring versus CT chorangiography, or in other words atherosclerosis versus blockages two different things. So anyhow, the coronary calcium score was a much better predictor and it costs you $500 or $600 less. You don't glow in the dark for three or four days afterwards and you're not given an intravenous injection that you potentially could have an anaphylactic reaction to or even damage your kidneys. So it just does my head in when I see GPs and ignorant cardiologists ordering these CT coriangigrams on people who are asymptomatic. Now I do them on people who've got symptoms and an equivocal stress echo. That's the criteria to have a CT choriangiogram, not just to see what your arteries are doing. That's the calcium score End of sermon Just now.

Speaker 1:

we're going to continue it. So, just regarding the coronary artery calcium score, that's calcification which is, you know, progressed, which is further along the line of dysfunction of endothelial dysfunction.

Speaker 1:

Advanced endothelial dysfunction? Yeah. What about earlier predictors like, for instance, fibrinogen or you know? You mentioned lipoprotein, little a, you know, and again, I remember you talking about this decades ago when it was. It was lambasted and then there was this sort of admittal that maybe in women only. I think that's right, there was a certain age population or something and that's it. And now it's like, oh, now that we're developing drugs for it, yeah, sure. So what about the function of using earlier predictors of endothelial dysfunction, homocysteine?

Speaker 2:

Yeah, yeah, well, look, can I say I don't think it's either, or I think age 50 is a good time to start, If you don't have a rampant family history or a rampant cholesterol. I'll tell you another story. I think anecdotes are interesting. They don't prove anything, they're just stories. But I saw a 38-year-old man who some fool had put on a statin 10 years before, at the age of 28, just because he had a high cholesterol and his uncle had a heart attack at 55. That was the justification. So this fellow faithfully took his 40 milligrams of atorvastatin for 10 years. But then he went on to tell me how his wife had been through wait for this for 10 years. But then he went on to tell me how his wife had been through wait for this 10 unsuccessful cycles of IVF, until it twigged in his head Maybe it's the Lipitor I'm taking that's pulverizing my testicles and stopping my wife from getting pregnant. So he stops the Lipitor, she gets pregnant naturally within six months.

Speaker 2:

Now, andrew, that is medical negligence To put someone on a drug that really wasn't indicated and causing them $100,000 worth of IVF, and not even forgetting about the money, the psychological misery of going through IVF, and a lot of people also don't realize. If you've had failed IVF, you double your risk for cardiovascular disease in the next 10 years because you're fiddling around with people's hormones and when it doesn't take, there's a double the risk for heart disease. So I think we've got to be really careful here what we do to people. And there are times look, I've got again another anecdote. I've got a 32-year-old woman whose father died at 31 of a heart attack and her cholesterol is 12.4 because it's all genetic, it's familial hypercholesterolemia in her case. I did a calcium score on her and it was already 48. Now 48 is not much, but for a 32-year-old it means she's got very advanced atherosclerosis at her age. I'm hammering her with the highest dose of statin and ezetrol because she probably will die if I don't treat her cholesterol. So this is the point Cholesterol, as you say, it's not just cholesterol, it's all the LDLs that go with it.

Speaker 2:

But there are four basic components of the whole cholesterol story. There is small LDL, there is large LDL, small HDL, large HDL. Here, andrew, is where size is important. The larger your LDL, the larger your HDL, the healthier you are. So it's the small LDL that's pro-arthrogenic, puts fat in your arteries and that's the bit that gets very oxidized and that's where ubiquinol stops being oxidized. Of course the large LDL is good for you. It builds healthy cell metabolism, cell membranes. It's the basic ring of steroid metabolism, bile salt, vitamin D metabolism. So we need large LDL.

Speaker 2:

Then there's small HDL, which is pro-inflammatory. That's bad for you as well. Large HDL sucks fat out of your arteries. It's involved in reverse cholesterol transport, takes the cholesterol out of the arteries and back into the bloodstream. It's broken down harmlessly by the liver. So it's not about cholesterol, this nonsense about focusing on cholesterol. You focus on the atherogenic part and the inflammatory part of cholesterol, the small bits, and you do something about that so you don't just pulverize cholesterol. I saw a woman yesterday in my practice cholesterol of 7.5, triglycerides of 0.7, hdl of 2.5, and the GP was desperate to put her on a statin Coronary calcium score. Of course nothing. She doesn't need a statin. She needs to be congratulated for being what we call a lean hyper-responder.

Speaker 1:

A lean hyper-responder. Okay, I'll have to write that one down.

Speaker 2:

That's what we call these people, Thin people with high cholesterol, high HDL, low triglyceride, zero calcium scores, are lean hyper-responders. They've got very good metabolism. They're being protected. But you mentioned the LP little a. That is 20% of heart disease. 70% of heart disease is due to insulin resistance. So 90% of atherosclerotic heart disease is explained by two genes insulin resistance gene and lipoprotein delay.

Speaker 1:

Let's just talk a little bit about that endothelial function and how ubiquinol works. We've spoken about protecting the molecule of LDL. What about endothelial function? How does ubiquinol help there and can it regress atherosclerosis, existing atherosclerosis?

Speaker 2:

like a high coronary artery score. Yeah, can I make the point that the first thing that goes wrong in atherosclerotic heart disease? So the progressive buildup of fat, inflammatory tissue, and then calcium, and calcium is not the problem. So imagine a donut like this the blood's going through the hole, the fat's building up in the wall. As the fat builds up in the wall, the body throws in calcium to act as a scaffold to stop it from breaking down. So I see people say, oh doctor, all my calcium's in the LAD, I'm in real trouble. No, no, no, that's where your artery is most stable. It's just telling you there's atherosclerosis throughout the arteries.

Speaker 2:

So the endothelium is the first barrier to all the muck coming through your arteries.

Speaker 2:

So if you have endothelial dysfunction so, for example, there are still some people who smoke cigarettes. So within an hour of smoking one cigarette, you reduce your endothelial function by 50%. So what is endothelial function? Firstly, it's the ability to act as a barrier. Secondly, it's the ability to open and close with different stimuli. So if you're in the middle of a deep sleep, the last thing you need is torrential blood flow to your heart and your muscles, so the system closes down and your body has a rest, so a thing called endothelin is released that constricts down the arteries, but then, when you need blood flow to your muscles, the endothelium releases nitric oxide, the ubiquitous vasodilator, and that's what opens up. Now what does ubiquinol do? Ubiquinol firstly acts as an antioxidant to stop the small LDL being oxidized and getting into your arteries, but it also has a direct effect on nitric oxide metabolism through a thing called nitric oxide synthase, and so it basically generates more nitric oxide, which keeps those arteries open, which is so important for you.

Speaker 1:

And that all comes from a thing called L-arginine which is part of one of the amino acids, of course, talking more about heart disease, different types of heart disease, so, for instance, you know, congestive heart failure. Where do you stop? Can you go through? Where ubiquinol has been shown with evidence to be of most benefit for people? Yeah, what doses? We might use that sort of thing, sure.

Speaker 2:

Okay, well, firstly, we've spoken about endothelial function and the studies are showing clearly anywhere between 100 to 200 milligrams of ubiquinol will improve endothelial function by its effects on nitric oxide synthase and working as an antioxidant, et cetera, et cetera. So that evidence is rock solid that ubiquinol is terrific for endothelial function. But let's go to the next level. There's evidence to show that ubiquinol can convert you from small LDL to large LDL. Studies have come out and shown that as well, confirmed that one. But then there's the whole thing about whether ubiquinol should be used for people who are taking statins and I put all of my patients on statins, on a combination of ubiquinol and a magnesium orotate aspartate combination, because the orotate and the aspartate lift up the CoQ10 in the mitochondria. And also what happens when you take a statin there's a thing called complex three in the mitochondria. So basically to explain mitochondria, they've got these little turbines that are pushing protons through and helping to generate this ATP. So ATP is, of course, the unit of energy in the body and ubiquinol works on complex three, especially complex two, complex three, to help generate more of this ATP. Now statins completely pulverize complex three and stop the generation of ATP, which is why people get.

Speaker 2:

I'd say about 20% of people get problems with muscle pain, stiffness, weakness, cramping and, over time, loss of muscle bulk, which we call, of course, atrophy, and it's about 20%. If you look at the randomized controlled clinical trials, people only get muscle problems less than 5% of cases. But the problem with that, andrew, is that they have a strict definition of myalgia, which is muscle pain with a CK that's three times the normal level. That's the definition. So of course that's less than 5%. But I work in the real world where I actually see things called human beings, and the human beings that I see it's about 20% get that just muscle weakness or they just get a lot of cramping and they mightn't have the muscle pain that gives them the criteria for myalgia.

Speaker 2:

So what I do is I try to prevent that by giving everyone ubiquinol and the magnesium orotate aspartate and vitamin D is very good as well. I think everyone should be taking vitamin D. A thousand units, two a day. You should be doing that just routinely, but some people on statins need 1,000 units, two a day. You should be doing that just routinely, but some people on statins need about 4,000 units a day. So I stylize my therapy for the individual, but it's just routine for me for everyone to be given the ubiquinol in that dose 150 milligrams, who are going in any form of statin, and I don't use fat-soluble statins, lipitor and Zocor, or Atorvastatin, simvastatin, because I believe they cause more problems than the Resuvastatin and the Pravastatin.

Speaker 1:

Right, so the Resuvastatin and the Pravastatin are water-soluble, correct.

Speaker 2:

Yeah, yeah.

Speaker 1:

And so they don't cross the.

Speaker 2:

So this is perhaps membranes as much right.

Speaker 1:

So this is perhaps why the original big trial with reserva statin was at the jupiter trial.

Speaker 2:

Um was looking at decrease in um c-reactive protein oh yeah, but all statins have been shown to reduce c-reactive protein around 30 I mean statins.

Speaker 2:

And look, I'm not anti statin. I don't want anyone to think that that I'm I'm an anti-statin campaigner. I'm against the inappropriate use of statins for people who don't need them. So your calcium score is below 100, you don't need a statin. But if your calcium score is high or you've had a heart attack, stent or a bypass, I use statins all the time. So I spend half my week putting people on statins who don't want to take them, the other half taking people off statins who don't need them. So to me it's just logical.

Speaker 1:

And what about the comprehensive test that is done at the Sydney Adventist Hospital, the lipoprint test, if people have got like what is it a type 2? Is it a type 2? That's the worst risk.

Speaker 2:

I think you're talking about when you do the subfraction analysis, aren't you?

Speaker 1:

Yes, for giving me subfractions. Yes, yeah, so you're looking at subfractions so basically you're measuring small LDL versus large LDL.

Speaker 2:

So you're measuring that. And look, the only time I ever do that is when I can't give someone a good explanation for why they have heart disease. So if someone's got a high lipoprotein delay, I'm going to treat them anyhow. Someone's insulin resistant? I'm going to treat them anyhow. But I have the occasional people that seem to have a relatively normal cholesterol profile, everything else is going okay and they still have early heart disease. So then I'll go off and hunt down their sub-fractions to see whether we need to be monitoring and measuring those.

Speaker 2:

But really, for example, most cases of small LDL have a high triglyceride, low HDL. So, for example, someone's cholesterol is 7 with a HDL of 2.5, your triglyceride at 0.7, that's good, that means large LDL, large HDL. But if your cholesterol is 4.5, your triglycerides are 1, your HDL is 1. So your triglycerides are 2, your HDL is 1, I mean the GP will say, oh, your cholesterol is pretty good. No, that's small LDL, small HDL. That's what that all means. So that's the statin part of it. And there are studies to show that people who take statins, who are given ubiquinol, it reduces their muscle pain and weakness by around 50%. So there is an evidence base behind that as well. But then one of the big things now for ubiquinol. It's been used in people post-infarct and whatever. I think that's its benefits on endothelial function. But then there's the whole thing about myocardial function.

Speaker 2:

Now you mentioned before congestive cardiac failure and there really are two types of heart failure. There's heart failure with reduced ejection fraction, where your heart's like a floppy bag and just not pumping well, the commonest cause of that of course, being recurrent heart attacks that have scarred your heart. But there's also dilated cardiomyopathy and we saw this a lot during COVID. People who got COVID had significant myocarditis. Some people with the RNA vaccines got myocarditis, but it's much more with COVID than the RNA vaccines. But there are other causes of dilated cardiomyopathy Alcohol, for example. Too much alcohol can induce a dilated cardiomyopathy, a familial cardiomyopathy with a virus tipping you over the edge and giving you a severe dilated cardiomyopathy. So there's all of that. That's reduced ejection fraction.

Speaker 2:

And a number of studies have now shown that just standard CoQ10 by itself can improve the heart events. So there was a study called Q-symbio where they used I think it was from memory about 400 milligrams a day of CoQ10, so 200 milligrams twice a day of CoQ10. And in a number of people it was a big study and it showed that over two years there was a 50% reduction in death and hard cardiac events just from using standard CoQ10. But then when you look at the people who switched from CoQ10 to ubiquinol because they haven't done the study with ubiquinol yet they should. But when they switch people over from CoQ10 to ubiquinol, their ejection fraction, which is how well the heart pumps, markedly improves from going from ubiquinone to ubiquinol and a lot of the evidence is showing that ubiquinol is so good to improve cardiac function. So in all my patients who have cardiac failure I certainly put them on 300 milligrams of ubiquinol with the magnesium orotate aspartate combination.

Speaker 2:

But also what I haven't mentioned is the other form of heart failure, which is heart failure with preserved ejection fraction.

Speaker 2:

So the heart's pumping well but it's not relaxing properly and really up to the last five years we haven't really had any treatment for that.

Speaker 2:

Now we're getting things called SGLT2 inhibitors, which are very good drugs for that condition, and also the flavor of the decade, the GLP-1 receptor agonists, things like ozempicators, mates. They're also very good for that condition and this is just a slight deviation but it's interesting for people to hear this. The reason why the GLP-1 receptor agonists work, it's not just the reduction in fat in your gut. It takes fat out of your organs. So if you do an autopsy on someone who's died, who's significantly overweight, half their heart is full of fat and obviously that's going to alter cardiac function and make your heart a lot stiffer. And so the GLP-1 receptor agonist take the fat out of the heart and restore the heart to a more elastic state. Now, interestingly, there was a study done where they used a combination of D-ribose and ubiquinol in people with heart failure with preserved ejection fraction, and showed significant parameters of benefit, so reduced BNP, better exercise function, et cetera, no mortality rates. But the study wasn't big enough to cover mortality.

Speaker 1:

Just a point about ribose and thinking about substrates of the electron transport chain Nicotinamide ribose NR. Have you ever used that? Have you got any data on that, Any benefits?

Speaker 2:

Oh, yeah, yeah, yeah, I'm using well, I use more NMN than NAD riboside, which is what you're talking about, but I think they're about the same. So I think anything that's an NAD plus feeder, such as NMN, NAD riboside what you've just said and nicotinic acid, and I've got to say I've been taking for five years I obviously won't mention products on air, but I've been taking an NMN-based product for the last five years and I also take immediate release nicotinic acid as well every day. The reason I do this is because it is an activated B3, like an NAD plus. But I've been using nicotinic acid in its immediate release form in my patients for over 30 years and what I was noticing with all of these people is they were having incredible longevity, just things weren't happening to them, they weren't having the cardiac events they should be having, and so I thought, well, there's something weird about this. And I started reading all around nicotinic acid and the studies that said that nicotinic acid didn't work were done on the slow release form.

Speaker 2:

And you see, I think this is one of the keys to good health, Andrew, it's a thing called vasodilatation. So what's one of the best vasodilators on the planet? It's a thing called exercise. So I think the way exercise works. One of the ways it works is pumps blood through the body and flushes crap out. But nicotinic acid does a similar thing makes you go bright red, opens up your arteries, flushes all the crap out of the system.

Speaker 2:

There's another drug, another couple of drugs, that does the same thing, what I call vitamin V, otherwise known as Viagra, and a study of 72,000 men over 14 years showed that those who were the highest end users of Viagra versus those men who didn't Viagra and Cialis I'm not just picking on one of the drugs had weight for this Not only the benefit of not falling out of bed, but also the benefits of a 55% reduction in cardiac events, a 50% reduction in all-cause death, a reduction in dementia and bowel cancer, and I believe this is because of the vasodilatation. So that's one of the big keys here. That's what ubiquinol does. It's a good vasodilator because of its effects on nitric oxide. So vasodilatation, I think, is one of the keys to good health.

Speaker 1:

Just going back as a last question for dosage range with ubiquinol, you know, like you mentioned, what is it? 150 twice a day or something? 150, just standard, 150 milligrams, 150. 150 milligrams for an extraordinary healthy.

Speaker 2:

I was going to say for an extraordinary.

Speaker 1:

But then you've got people who have problems, who have an increased coronary artery calcium, who have maybe cardiomyopathy from COVID CCF. Congestive cardiac failure what dosage range do you go up to? Myalgic myeloid encephalitis chronic fatigue what dosage range do you go up to? Yeah, look, I go up to about 300.

Speaker 2:

And I always give it in the morning because it does give you energy, you don't sleep as well.

Speaker 2:

So I wouldn't go a BD dose. I do 150 milligrams as just a maintenance dose for energy or if you're on statins. But once you get to the heart failure component of it, 300 milligrams in the morning and look, you can go up to 600 milligrams. I've got a good mate who's absolutely mad. He runs marathons and I tell anyone who runs marathons, there's a perfectly good bus service, so why anyone would do it is just beyond me. But anyhow he takes, before he does a marathon, 600 milligrams. So he's powered by ubiquinol when he does his marathons and he's a very good marathon runner.

Speaker 2:

But look, you could do that. But it just becomes a very expensive exercise and this cost of living crisis. It is expensive but you've got to pay for quality. So I think, if you can get people out of it as cheaply as possible, 150 milligrams in the morning for just a good standard dose, 300 milligrams if you're much sicker with cardiomyopathies or you've got long COVID. You see, I believe and this is another sort of left field thing, but I believe chronic fatigue syndrome, fibromyalgia, long COVID is all due to gut dysbiosis and I think the gut's been knocked off and a lot of ubiquinol is made by the gut, so I give people, especially in the throes of their acute symptoms, 300 milligrams for a few months until they get back on their feet. Then I'll drop it back to 150.

Speaker 1:

Dr Ross Walker, every single time I speak with you, I learn something of value and something new. So thank you so much for taking us through the benefits of ubiquinol in cardiac health today, and I look forward to our next podcast when we're going to go through some of the other things that you use in your practice. You know one. A couple of things I didn't even question you about was vitamin k2 and berberine, but that's probably for another time, very, very good well, I tell you what, just as a quick snippet, because I can't waste this opportunity.

Speaker 1:

Vitamin k2 when do you use? At what dose? Berberine when do you use it, what does? Okay?

Speaker 2:

vitamin k2 I. 180 micrograms daily is the basic dose, although if you've got renal disease, a higher dose because you do need more. And I, when do I use it? Everyone with coronary calcification takes the calcium out the arteries, puts it back in the bones, um and uh. And I I mean I take it myself, even though I've got a zero calcium score. I take it just to give myself strong bones. So I take it for a prevention of osteoporosis, based on work out of the rotterdam Heart Study which showed there was an improvement in bone strength and also improvement in arterial flexibility.

Speaker 2:

Berberine is something I don't use myself, so I've not prescribed it, but I'm starting to see over the last, especially six to 12 months, a lot of good evidence that berberine may have added benefits. To be frank with you, mate, I take 40 pills in the morning and 15 in the evening, all preventative stuff. Berberine is not one of them at the moment, but I've the work I'm seeing on berberine, even with weight loss and better metabolic syndrome. I'm starting to think maybe I should be thinking about that one yet another one on top of it. I'm not as bad as brian john, the lunatic in America, who takes 50 in the morning and about 50 in the evening and monitors everything he does. I think you should smell the roses, not analyse the damn things. But, andrew, can I say mate, every time I have a chat with you it's just a great pleasure for me. You do a wonderful service to everyone who listens to you. You're incredibly intelligent and eloquent and I really love talking with you. So thank you very much, mate.

Speaker 1:

Ross, thank you so much. Thank you, that's made my day. And thank you once again, dr Ross Walker, for joining us today, and I really do. Every single time this man I attend his lectures or his talks, I'll learn something of value for patients. It's a brilliant man and he questions everything. I love you, so thank you so much for taking us through the benefits of ubiquinol today and, of course, everybody, thank you for joining us today. You can catch up on all the other podcasts and on the Designs for Health website. I'm Andrew Whitfield-Cook. This is Wellness by Designs.