July 3, 2025 • 43 mins
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.
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Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Speaker 1 (00:12):
This is Wellness by Designs, and I'm your host,
andrew Whitfield-Cook, andjoining us today is Dr Ross
Walker, an esteemed cardiologistwho has dedicated the past 25
years of his career toprevention, and today we're
going to be discussing the roleof ubiquinol in cardiovascular
health.
Welcome to Wellness by Designs,ross.
How are you?
Speaker 2 (00:33):
Andrew, it's always a great pleasure to talk with you
at any opportunity I get.
Speaker 1 (00:38):
Thank you, sir.
It's been a long time betweenchats.
Speaker 2 (00:42):
Now Ross.
Speaker 1 (00:42):
I think the first thing we need to cover is what
exactly is ubiquinol?
Speaker 2 (00:48):
Yeah, well, ubiquinol is the active version of
coenzyme Q10.
And coenzyme Q10 has a numberof roles in the body.
One is basically, it's a verystrong antioxidant.
It's a fat-soluble antioxidant,but also it's very, very
important in mitochondrialhealth.
It's a vital part of themitochondrial energy production.
(01:12):
And so without good levels ofubiquinol not ubiquinone, which
is inactive, it's got to beubiquinol the mitochondria
doesn't work as well, doesn'twork as well.
Speaker 1 (01:23):
And so where, if we're talking about CoQ10, you
know the old CoQ10, theubiquinone where let's say
there's still the lion's shareof research is done on.
Admittedly, in the olden days Iguess there was the doses were
way lower than what we're usingnow, and now we've swapped to
(01:46):
ubiquinone the active.
Tell us about that sort ofjourney of research, if you like
, from ubiquinone the low-dosestuff.
I mean.
I'm sure you'll remember whenin Australia the only product we
could get was ubiquinone and itwas 10 milligrams.
Speaker 2 (02:02):
Yeah, and really didn't do much at all.
And the problem is that withthe whole CoQ10 story is that
you really don't get enough inyour diet.
Whether it's ubiquinone orubiquinol, there's just not
enough in the diet.
I think you've got to havesomething like a kilo and a half
of steak to get 30 to 50milligrams of ubiquinol in your
(02:23):
system, and so much broccoliyou'd be eating it for about
three or four weeks to get thatsmall amount.
So, yes, when CoQ10 was firstreleased, it was only in the
ubiquinone or ubicarinone formand it was in very, very low
doses, so it didn't really domuch.
I think this is really really agood example of the history of
(02:45):
evidence based supplementation.
Orthodox medicine wants harddata.
They want science behind whatanyone does, and so when you're
using almost homeopathic dosesof something that's inactive,
you're not going to get muchresponse.
I mean it takes me back to thewhole vitamin E nonsense that
we've heard from years ago.
In 2004, a guy called EdgarMiller wrote an editorial in the
(03:09):
Annals of Internal Medicinesaying that vitamin E was not
only of no benefit but it waspossibly harmful.
And this is what does my headin a bit about orthodox medicine
.
They're still quoting thevitamin E data using
DL-alpha-tocopherol, which isthe inactive version of vitamin
D, from a thing called theFinnish Smokers Trial.
(03:32):
Now, the clue is in that titlethere.
But 29,000 Finnish smokers werestudied and were given
placebo-controlled eithervitamin E, dl alpha-tocopherol,
so a synthetic version ofvitamin E 50 international units
and 15 milligrams of syntheticbeta-carotene.
(03:54):
And this stuff shouldn't beused.
It doesn't work and in fact, itcan cause more harm.
But so people like Edgar Millerare still coming out were
coming out in 2004 sayingvitamin E may be harmful.
Well, of course it may beharmful if you use the crappy
synthetic stuff.
So again, this is what'shappened with medicine.
All the time they go back tothese silly studies that
(04:16):
disprove the benefits of, ordisprove any benefits from,
supplements because they've usedthe wrong dose of the wrong
stuff.
And again, with the initialubicarinone stuff, we're using
10, 30 milligrams of an inactivesubstance.
And here's the problem when youhit 30, and the 30 is the peak
(04:37):
of our life.
So it's a bit depressing foryou and I, but our body was
designed to wander around ajungle for 30, 40 years with a
spear and then die, had yourhead ripped off by a
saber-toothed tiger or you diedof some infection.
So when you hit 30, the peak ofyour life, things start to wear
out.
That's when osteoporosis starts, sarcopenia, loss of muscle
(04:58):
that all starts at age 30.
But also your ability toconvert ubiquinone to ubiquinol
starts to drop off a little bitat age 30.
And then at age 50, the enzymediaphoresis just goes boom.
So you just don't get theamount of active CoQ10 or
ubiquinol in the mitochondriathat you need over the age of 50
(05:21):
, which in many ways is one ofthe reasons why many people over
the age of 50 are starting tofeel tired, because their
mitochondria just aren't workingas well, and I think one of the
reasons is they're losing oneof the main drivers of their
mitochondria, which is ubiquinol.
Speaker 1 (05:42):
So just a point there about tiredness in in, you know
, around the age of 50 sort ofthing.
Obviously there's many, manyfactors, you know.
But would it be wise, therefore, for a wellness approach to
start thinking about the use ofubiquinol, the active coq10, as
part of the regimen?
(06:03):
Obviously there's exercise andgood sleep and things like that.
I get it, but the use ofubiquinol in a reasonable dosage
and I'll question you aboutthat as part of their wellness
program.
Speaker 2 (06:15):
Oh, absolutely.
And I've got to say, when Italk about wellness, wellness
isn't just the absence ofdisease, which is an important
component.
Of course you know you want tohave some illness because you
will be unwell, but what I callultimate wellness is, one, the
absence of disease.
Two, very good energy levels,which you do get from ubiquinol,
(06:40):
and also, I think, themagnesium orotate aspartate
combinations.
And there are other reasons whywe lose energy.
I mean, sleep apnea is a bigone, because all adult males
have sleep apnea, allpostmenopausal females have
sleep apnea to some extent, andas you get older the sleep apnea
gets worse and that makes youtired as well.
But there are many other reasonsfor fatigue and if anyone's
(07:02):
listening to this, I wouldn'twant you to start swallowing
ubiquinol if you're tiredwithout figuring out why you're
tired in the first place,because it may.
I mean, the commonest cause offatigue in our society is you're
working too hard, playing toohard, not sleeping well, but
then after that there'sendogenous depression that can
also make you tired.
Then there's sleep apnea, whichwe've mentioned.
(07:24):
When you've hit 50 and you'regoing through the pauses either
menopause or andropause youstart to get tired.
So that may be another factor.
But then finally, there couldbe a medical reason.
You could be losing blood, irondeficient, you could have a
thyroid problem, something wrongwith your kidneys, your liver,
your heart.
To give an example, one of thefirst presentations of a
(07:44):
ruptured plaque is incrediblefatigue.
So I wouldn't want anyone to goand say, oh, I'm tired.
Therefore, I'm going to takeubiquinol.
What I say, you're tired, findout why you're tired first, but
then, once you've had allserious conditions excluded, by
all means take now here's the toanswer your question 150
(08:05):
milligrams of ubiquinol, which Ithink is the standard dose for
people for energy.
I take it.
I'm 14 months off 70 and I'vegot a zero coronary calcium
score and I'm not on a statin,because anyone's got a zero
calcium score shouldn't goanywhere near a statin, which
we'll get to a bit later on.
But I just take the 150milligrams every day of
(08:26):
ubiquinol just to keep my energygoing and I've got pretty good
energy for someone in my agegroup.
Speaker 1 (08:32):
Firstly, you mentioned cholesterol.
So let's go there Withcholesterol and the coronary
artery calcium score.
The Australian New ZealandCollege of Cardiologists says
they sort of.
I remember when you werementioning this decades ago,
ross, by the way, and back thenthere was total denial about the
usefulness.
And now the college has got astatement saying those who have
(08:54):
low cholesterol and when I saythe word cholesterol I think we
all need to make to to realizethat we're not talking about the
molecule of cholesterol, we'retalking about lipoproteins.
But anyway, when we've got highor dysfunctional supposedly
lipoprotein profiles, that thosepeople who have got low or
(09:17):
normal cholesterol quotationmarks levels that they don't
need a coronary artery calciumscore, those people that are
mid-range could benefit, I knowcould benefit and those people
that are high have high anyway,so they should be on a statin.
What's your take on thatstatement?
Speaker 2 (09:36):
That statement is complete and utter nonsense.
And let me just give you ananecdote 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 calciumscore I have noting that
anything above 400 is serious isa 68-year-old man in the
(10:01):
fitness industry.
Doesn't have an ounce of bodyfat.
Old man in the fitness industrydoesn't have an ounce of body
fat, has a normal cholesterol,blood pressure, never smoked,
not diabetic and Andrew, waitfor this no family history of
heart disease.
So therefore, by that criteriayou just mentioned, there's no
point in him having a coronarycalcium score.
But he has and we could getinto this discussion because
(10:23):
he's one of my hobby horses.
He has an elevated lipoprotein,little a, which doctors have
been measuring for the last twoor three years because we're now
developing drugs for it.
I've been measuring it andtreating it for 30 years.
So anyhow, this guy came to seeme, sent him downstairs for a
coronary calcium score because Ihave a radiology practice under
(10:46):
my building.
It's not my practice and hiscoronary calcium score?
Wait for this.
I hope you're sitting down.
You are sitting down 8,100.
Hi so his arteries were likeporcelain pipes.
He had bypass surgery 10 yearsago.
He sent me an email a few yearsago with a picture of him and
his mates winning the latestbasketball grand final.
So he'll now live to his 100after he's bypassed, but under
(11:10):
those criteria he wouldn't havehad a coronary calcium score.
Now let's get to the science,not just to a story.
I believe and I've been sayingthis for 26 years when I
introduced coronary calciumscoring into Australia in
conjunction with the SydneyAdventist Hospital in Wurundjeri
and Dr David Grout, one of mycardiologic colleagues.
I've been saying this for 26years that all men at 50, all
(11:33):
women at 60 should have aroutine coronary calcium score.
But the goalposts change.
If, for example, you said to meoh, my dad had a bypass at 45.
Well, I'd do your coronarycalcium score at 35, as one
example.
But I don't like to overirradiate people below the age
of 50 because in my view thereare only three reasons, three
benefits of being over 50,andrew.
(11:54):
Number one is wisdom.
Number two is grandchildren ifyou got them and I have nine.
And number three is you losethe cancer risk from medical
radiation.
So the less radiation you havebefore age 50, the better off
you are.
So anyhow, to give you somescience now behind the coronary
calcium score and itsrelationship, especially to
(12:16):
statin drugs.
Firstly, it's been shown thatif you have a coronary calcium
score and you compare that tostandard risk factors for heart
disease, the calcium score hasmarked benefit in improving your
level of risk.
So there are so many people whoappear to be at high risk
because of standard risk factorprofiles and they'd be all put
(12:39):
on a statin.
Then you do their coronarycalcium score and they've got a
zero calcium score.
It markedly plummets their risk.
So I'll give you again anotherstory.
I saw a woman who was 58 yearsold with a lifelong cholesterol
of 9.5, because cholesterol hasgot nothing to do with what you
eat.
It's all to do with geneticsand metabolism.
(12:59):
So women hit menopause, theircholesterol goes up because
their metabolism changes,because they lose estrogen.
So anyhow, every time she'd seea GP or any other doctor,
scaremongering doctors say toher if you don't take Lipitor
you're going to die, which isscaremongering, nonsense.
She'd take Lipitor because shewas worried about dying, of
course, because her cholesterolwas 9.5.
(13:20):
And after a few days shecouldn't lift her muscles, they
were just killing her.
So anyhow, after seeingmultiple doctors, she heard
about me, came to see me, sentit 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 yourarteries, so forget about it.
(13:42):
Live a healthy lifestyle.
No one should eat a bad diet,not just because of the
cholesterol issue but because ofmany other factors.
But please, you don't need astatin.
So anyhow, over the next eightyears, she listened to me and
not to the scaremongeringdoctors, and she came back to
see me, age 66 now, with acholesterol of 9.5 because it's
(14:04):
genetic, sent it downstairs foranother calcium score.
It had rocketed from zero up tozero, 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.
So a study of 13,500 peoplebetween the ages of about 50 up
(14:26):
to 70 followed for 10 years thebenefits of them taking a statin
based on their calcium scoreZero.
Calcium score zero benefit.
Calcium score below 100.
So a 55-year-old male goes intoa doctor with a calcium score
of 60.
The doctor says oh, you've gotatherosclerosis, you must be on
a statin.
(14:47):
No, the evidence isn't there.
This study showed calcium scorebelow 100, p-value 0.095.
So no statistically significantbenefit from being on a statin.
But the number needed to treat,which I think is a better
number.
Here you had to treat 100people for five years to prevent
(15:08):
one heart attack and nodifference in death rate.
So who in their right mindwould take a strong synthetic
metabolic regulator for 10 yearsto prevent one heart attack out
of 100 people?
I mean for five years, oneheart attack.
It's just nonsense.
But once you get to a calciumscore above about 100 for your
(15:31):
age so if you're 60 and yourcalcium score is 150, then
that's where the benefits kickin.
The number needed to treat isonly 12, highly statistically
significant.
So to me, when people makethese comments, they've got to
have some science behind whatthey say.
The calcium score is easily thebest predictor for heart
(15:52):
disease risk.
And here's another hobby horseof mine, andrew before we should
start talking about ubiquinolsoon.
But there's a thing called a CTCori angiogram, and a CT Cori
angiogram is done on the sametechnology as the calcium
scoring still a CT coriangogram,and a CT coriangogram is done
on the same technology as thecalcium scoring still a CT but
the calcium scoring just takes asnapshot of your arteries.
(16:12):
The CT coriangogram you'reinjected with dye and you do not
qualify by Medicare for thestudy if you have no symptoms
and you haven't seen acardiologist.
So many GPs are saying, oh, aCT chorioangiogram gives you
better pictures than a calciumscore, which it does Beautiful
(16:34):
pictures of the chorio arteries.
So therefore I'll get you tohave that test done.
It costs people an extra $500 or$600 to have that test and a
study was done in the Journal ofthe American College of
Cardiology looking at thepredictive risk of coronary
calcium scoring versus CTchorangiography, or in other
words atherosclerosis versusblockages two different things.
(16:58):
So anyhow, the coronary calciumscore was a much better
predictor and it costs you $500or $600 less.
You don't glow in the dark forthree or four days afterwards
and you're not given anintravenous injection that you
potentially could have ananaphylactic reaction to or even
damage your kidneys.
So it just does my head in whenI see GPs and ignorant
(17:20):
cardiologists ordering these CTcoriangigrams on people who are
asymptomatic.
Now I do them on people who'vegot symptoms and an equivocal
stress echo.
That's the criteria to have aCT choriangiogram, not just to
see what your arteries are doing.
That's the calcium score End ofsermon Just now.
Speaker 1 (17:43):
we're going to continue it.
So, just regarding the coronaryartery calcium score, that's
calcification which is, you know, progressed, which is further
along the line of dysfunction ofendothelial dysfunction.
Advanced endothelial dysfunction?
Yeah.
What about earlier predictorslike, for instance, fibrinogen
or you know?
You mentioned lipoprotein,little a, you know, and again, I
(18:06):
remember you talking about thisdecades ago when it was.
It was lambasted and then therewas this sort of admittal that
maybe in women only.
I think that's right, there wasa certain age population or
something and that's it.
And now it's like, oh, now thatwe're developing drugs for it,
(18:27):
yeah, sure.
So what about the function ofusing earlier predictors of
endothelial dysfunction,homocysteine?
Speaker 2 (18:42):
Yeah, yeah, well, look, can I say I don't think
it's either, or I think age 50is a good time to start, If you
don't have a rampant familyhistory or a rampant cholesterol
.
I'll tell you another story.
I think anecdotes areinteresting.
They don't prove anything,they're just stories.
But I saw a 38-year-old man whosome fool had put on a statin
10 years before, at the age of28, just because he had a high
(19:05):
cholesterol and his uncle had aheart attack at 55.
That was the justification.
So this fellow faithfully tookhis 40 milligrams of
atorvastatin for 10 years.
But then he went on to tell mehow his wife had been through
wait for this for 10 years.
But then he went on to tell mehow his wife had been through
wait for this 10 unsuccessfulcycles of IVF, until it twigged
(19:27):
in his head Maybe it's theLipitor I'm taking that's
pulverizing my testicles andstopping my wife from getting
pregnant.
So he stops the Lipitor, shegets pregnant naturally within
six months.
Now, andrew, that is medicalnegligence To put someone on a
drug that really wasn'tindicated and causing them
$100,000 worth of IVF, and noteven forgetting about the money,
(19:49):
the psychological misery ofgoing through IVF, and a lot of
people also don't realize.
If you've had failed IVF, youdouble your risk for
cardiovascular disease in thenext 10 years because you're
fiddling around with people'shormones and when it doesn't
take, there's a double the riskfor heart disease.
So I think we've got to bereally careful here what we do
to people.
And there are times look, I'vegot again another anecdote.
(20:11):
I've got a 32-year-old womanwhose father died at 31 of a
heart attack and her cholesterolis 12.4 because it's all
genetic, it's familialhypercholesterolemia in her case
.
I did a calcium score on herand it was already 48.
Now 48 is not much, but for a32-year-old it means she's got
very advanced atherosclerosis ather age.
I'm hammering her with thehighest dose of statin and
(20:35):
ezetrol because she probablywill die if I don't treat her
cholesterol.
So this is the pointCholesterol, as you say, it's
not just cholesterol, it's allthe LDLs that go with it.
But there are four basiccomponents of the whole
cholesterol story.
There is small LDL, there islarge LDL, small HDL, large HDL.
(20:58):
Here, andrew, is where size isimportant.
The larger your LDL, the largeryour HDL, the healthier you are
.
So it's the small LDL that'spro-arthrogenic, puts fat in
your arteries and that's the bitthat gets very oxidized and
that's where ubiquinol stopsbeing oxidized.
Of course the large LDL is goodfor you.
(21:19):
It builds healthy cellmetabolism, cell membranes.
It's the basic ring of steroidmetabolism, bile salt, vitamin D
metabolism.
So we need large LDL.
Then there's small HDL, which ispro-inflammatory.
That's bad for you as well.
Large HDL sucks fat out of yourarteries.
(21:40):
It's involved in reversecholesterol transport, takes the
cholesterol out of the arteriesand back into the bloodstream.
It's broken down harmlessly bythe liver.
So it's not about cholesterol,this nonsense about focusing on
cholesterol.
You focus on the atherogenicpart and the inflammatory part
of cholesterol, the small bits,and you do something about that
(22:00):
so you don't just pulverizecholesterol.
I saw a woman yesterday in mypractice cholesterol of 7.5,
triglycerides of 0.7, hdl of 2.5, and the GP was desperate to
put her on a statin Coronarycalcium score.
Of course nothing.
She doesn't need a statin.
(22:21):
She needs to be congratulatedfor being what we call a lean
hyper-responder.
Speaker 1 (22:28):
A lean hyper-responder.
Okay, I'll have to write thatone down.
Speaker 2 (22:31):
That's what we call these people, Thin people with
high cholesterol, high HDL, lowtriglyceride, zero calcium
scores, are leanhyper-responders.
They've got very goodmetabolism.
They're being protected.
But you mentioned the LP littlea.
That is 20% of heart disease.
70% of heart disease is due toinsulin resistance.
(22:52):
So 90% of atherosclerotic heartdisease is explained by two
genes insulin resistance geneand lipoprotein delay.
Speaker 1 (23:03):
Let's just talk a little bit about that
endothelial function and howubiquinol works.
We've spoken about protectingthe molecule of LDL.
What about endothelial function?
How does ubiquinol help thereand can it regress
atherosclerosis, existingatherosclerosis?
Speaker 2 (23:23):
like a high coronary artery score.
Yeah, can I make the point thatthe first thing that goes wrong
in atherosclerotic heartdisease?
So the progressive buildup offat, inflammatory tissue, and
then calcium, and calcium is notthe problem.
So imagine a donut like thisthe blood's going through the
hole, the fat's building up inthe wall.
(23:44):
As the fat builds up in thewall, the body throws in calcium
to act as a scaffold to stop itfrom 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 yourartery is most stable.
It's just telling you there'satherosclerosis throughout the
(24:05):
arteries.
So the endothelium is the firstbarrier to all the muck coming
through your arteries.
So if you have endothelialdysfunction so, for example,
there are still some people whosmoke cigarettes.
So within an hour of smokingone cigarette, you reduce your
endothelial function by 50%.
So what is endothelial function?
Firstly, it's the ability toact as a barrier.
Secondly, it's the ability toopen and close with different
(24:29):
stimuli.
So if you're in the middle of adeep sleep, the last thing you
need is torrential blood flow toyour heart and your muscles, so
the system closes down and yourbody has a rest, so a thing
called endothelin is releasedthat constricts down the
arteries, but then, when youneed blood flow to your muscles,
the endothelium releases nitricoxide, the ubiquitous
(24:51):
vasodilator, and that's whatopens up.
Now what does ubiquinol do?
Ubiquinol firstly acts as anantioxidant to stop the small
LDL being oxidized and gettinginto your arteries, but it also
has a direct effect on nitricoxide metabolism through a thing
called nitric oxide synthase,and so it basically generates
(25:13):
more nitric oxide, which keepsthose arteries open, which is so
important for you.
Speaker 1 (25:18):
And that all comes from a thing called L-arginine
which is part of one of theamino 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 shownwith evidence to be of most
(25:43):
benefit for people?
Yeah, what doses?
We might use that sort of thing, sure.
Speaker 2 (25:49):
Okay, well, firstly, we've spoken about endothelial
function and the studies areshowing clearly anywhere between
100 to 200 milligrams ofubiquinol will improve
endothelial function by itseffects on nitric oxide synthase
and working as an antioxidant,et cetera, et cetera.
So that evidence is rock solidthat ubiquinol is terrific for
endothelial function.
(26:09):
But let's go to the next level.
There's evidence to show thatubiquinol can convert you from
small LDL to large LDL.
Studies have come out and shownthat as well, confirmed that
one.
But then there's the wholething about whether ubiquinol
should be used for people whoare taking statins and I put all
of my patients on statins, on acombination of ubiquinol and a
(26:31):
magnesium orotate aspartatecombination, because the orotate
and the aspartate lift up theCoQ10 in the mitochondria.
And also what happens when youtake a statin there's a thing
called complex three in themitochondria.
So basically to explainmitochondria, they've got these
little turbines that are pushingprotons through and helping to
(26:53):
generate this ATP.
So ATP is, of course, the unitof energy in the body and
ubiquinol works on complex three, especially complex two,
complex three, to help generatemore of this ATP.
Now statins completelypulverize complex three and stop
the generation of ATP, which iswhy people get.
(27:14):
I'd say about 20% of people getproblems with muscle pain,
stiffness, weakness, crampingand, over time, loss of muscle
bulk, which we call, of course,atrophy, and it's about 20%.
If you look at the randomizedcontrolled clinical trials,
people only get muscle problemsless than 5% of cases.
But the problem with that,andrew, is that they have a
(27:35):
strict definition of myalgia,which is muscle pain with a CK
that's three times the normallevel.
That's the definition.
So of course that's less than5%.
But I work in the real worldwhere I actually see things
called human beings, and thehuman beings that I see it's
about 20% get that just muscleweakness or they just get a lot
(27:58):
of cramping and they mightn'thave the muscle pain that gives
them the criteria for myalgia.
So what I do is I try to preventthat by giving everyone
ubiquinol and the magnesiumorotate aspartate and vitamin D
is very good as well.
I think everyone should betaking vitamin D.
A thousand units, two a day.
You should be doing that justroutinely, but some people on
(28:18):
statins need 1,000 units, two aday.
You should be doing that justroutinely, but some people on
statins need about 4,000 units aday.
So I stylize my therapy for theindividual, but it's just
routine for me for everyone tobe given the ubiquinol in that
dose 150 milligrams, who aregoing in any form of statin, and
I don't use fat-soluble statins, lipitor and Zocor, or
(28:39):
Atorvastatin, simvastatin,because I believe they cause
more problems than theResuvastatin and the Pravastatin
.
Speaker 1 (28:48):
Right, so the Resuvastatin and the Pravastatin
are water-soluble, correct.
Speaker 2 (28:52):
Yeah, yeah.
Speaker 1 (28:54):
And so they don't cross the.
Speaker 2 (28:56):
So this is perhaps membranes as much right.
Speaker 1 (28:59):
So this is perhaps why the original big trial with
reserva statin was at thejupiter trial.
Speaker 2 (29:05):
Um was looking at decrease in um c-reactive
protein oh yeah, but all statinshave been shown to reduce
c-reactive protein around 30 Imean statins.
And look, I'm not anti statin.
I don't want anyone to thinkthat that I'm I'm an anti-statin
campaigner.
I'm against the inappropriateuse of statins for people who
don't need them.
(29:25):
So your calcium score is below100, you don't need a statin.
But if your calcium score ishigh or you've had a heart
attack, stent or a bypass, I usestatins all the time.
So I spend half my week puttingpeople on statins who don't
want to take them, the otherhalf taking people off statins
who don't need them.
So to me it's just logical.
Speaker 1 (29:44):
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 type2?
Is it a type 2?
That's the worst risk.
Speaker 2 (29:59):
I think you're talking about when you do the
subfraction analysis, aren't you?
Speaker 1 (30:04):
Yes, for giving me subfractions.
Yes, yeah, so you're looking atsubfractions so basically
you're measuring small LDLversus large LDL.
Speaker 2 (30:14):
So you're measuring that.
And look, the only time I everdo that is when I can't give
someone a good explanation forwhy they have heart disease.
So if someone's got a highlipoprotein delay, I'm going to
treat them anyhow.
Someone's insulin resistant?
I'm going to treat them anyhow.
But I have the occasionalpeople that seem to have a
(30:34):
relatively normal cholesterolprofile, everything else is
going okay and they still haveearly heart disease.
So then I'll go off and huntdown their sub-fractions to see
whether we need to be monitoringand measuring those.
But really, for example, mostcases of small LDL have a high
triglyceride, low HDL.
(30:55):
So, for example, someone'scholesterol 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 cholesterolis pretty good.
(31:16):
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 showthat people who take statins,
who are given ubiquinol, itreduces their muscle pain and
weakness by around 50%.
(31:36):
So there is an evidence basebehind that as well.
But then one of the big thingsnow for ubiquinol.
It's been used in peoplepost-infarct and whatever.
I think that's its benefits onendothelial function.
But then there's the wholething about myocardial function.
Now you mentioned beforecongestive cardiac failure and
(31:57):
there really are two types ofheart failure.
There's heart failure withreduced ejection fraction, where
your heart's like a floppy bagand just not pumping well, the
commonest cause of that ofcourse, being recurrent heart
attacks that have scarred yourheart.
But there's also dilatedcardiomyopathy and we saw this a
lot during COVID.
People who got COVID hadsignificant myocarditis.
(32:19):
Some people with the RNAvaccines got myocarditis, but
it's much more with COVID thanthe RNA vaccines.
But there are other causes ofdilated cardiomyopathy Alcohol,
for example.
Too much alcohol can induce adilated cardiomyopathy, a
familial cardiomyopathy with avirus tipping you over the edge
and giving you a severe dilatedcardiomyopathy.
(32:40):
So there's all of that.
That's reduced ejectionfraction.
And a number of studies have nowshown that just standard CoQ10
by itself can improve the heartevents.
So there was a study calledQ-symbio where they used I think
it was from memory about 400milligrams a day of CoQ10, so
(33:03):
200 milligrams twice a day ofCoQ10.
And in a number of people itwas a big study and it showed
that over two years there was a50% reduction in death and hard
cardiac events just from usingstandard CoQ10.
But then when you look at thepeople who switched from CoQ10
to ubiquinol because theyhaven't done the study with
(33:26):
ubiquinol yet they should.
But when they switch peopleover from CoQ10 to ubiquinol,
their ejection fraction, whichis how well the heart pumps,
markedly improves from goingfrom ubiquinone to ubiquinol and
a lot of the evidence isshowing that ubiquinol is so
good to improve cardiac function.
So in all my patients who havecardiac failure I certainly put
(33:50):
them on 300 milligrams ofubiquinol with the magnesium
orotate aspartate combination.
But also what I haven'tmentioned is the other form of
heart failure, which is heartfailure with preserved ejection
fraction.
So the heart's pumping well butit's not relaxing properly and
really up to the last five yearswe haven't really had any
(34:12):
treatment for that.
Now we're getting things calledSGLT2 inhibitors, which are very
good drugs for that condition,and also the flavor of the
decade, the GLP-1 receptoragonists, things like
ozempicators, mates.
They're also very good for thatcondition and this is just a
slight deviation but it'sinteresting for people to hear
(34:34):
this.
The reason why the GLP-1receptor agonists work, it's not
just the reduction in fat inyour gut.
It takes fat out of your organs.
So if you do an autopsy onsomeone who's died, who's
significantly overweight, halftheir heart is full of fat and
obviously that's going to altercardiac function and make your
(34:55):
heart a lot stiffer.
And so the GLP-1 receptoragonist take the fat out of the
heart and restore the heart to amore elastic state.
Now, interestingly, there was astudy done where they used a
combination of D-ribose andubiquinol in people with heart
failure with preserved ejectionfraction, and showed significant
(35:16):
parameters of benefit, soreduced BNP, better exercise
function, et cetera, nomortality rates.
But the study wasn't big enoughto cover mortality.
Speaker 1 (35:28):
Just a point about ribose and thinking about
substrates of the electrontransport chain Nicotinamide
ribose NR.
Have you ever used that?
Have you got any data on that,Any benefits?
Speaker 2 (35:44):
Oh, yeah, yeah, yeah, I'm using well, I use more NMN
than NAD riboside, which is whatyou're talking about, but I
think they're about the same.
So I think anything that's anNAD plus feeder, such as NMN,
NAD riboside what you've justsaid and nicotinic acid, and
I've got to say I've been takingfor five years I obviously
(36:08):
won't mention products on air,but I've been taking an
NMN-based product for the lastfive years and I also take
immediate release nicotinic acidas well every day.
The reason I do this is becauseit is an activated B3, like an
NAD plus.
But I've been using nicotinicacid in its immediate release
(36:29):
form in my patients for over 30years and what I was noticing
with all of these people is theywere having incredible
longevity, just things weren'thappening to them, they weren't
having the cardiac events theyshould be having, and so I
thought, well, there's somethingweird about this.
And I started reading allaround nicotinic acid and the
(36:50):
studies that said that nicotinicacid didn't work were done on
the slow release form.
And you see, I think this is oneof the keys to good health,
Andrew, it's a thing calledvasodilatation.
So what's one of the bestvasodilators on the planet?
It's a thing called exercise.
So I think the way exerciseworks.
One of the ways it works ispumps blood through the body and
(37:11):
flushes crap out.
But nicotinic acid does asimilar thing makes you go
bright red, opens up yourarteries, flushes all the crap
out of the system.
There's another drug, anothercouple of drugs, that does the
same thing, what I call vitaminV, otherwise known as Viagra,
and a study of 72,000 men over14 years showed that those who
(37:35):
were the highest end users ofViagra versus those men who
didn't Viagra and Cialis I'm notjust picking on one of the
drugs had weight for this Notonly the benefit of not falling
out of bed, but also thebenefits of a 55% reduction in
cardiac events, a 50% reductionin all-cause death, a reduction
(37:55):
in dementia and bowel cancer,and I believe this is because of
the vasodilatation.
So that's one of the big keyshere.
That's what ubiquinol does.
It's a good vasodilator becauseof its effects on nitric oxide.
So vasodilatation, I think, isone of the keys to good health.
Speaker 1 (38:13):
Just going back as a last question for dosage range
with ubiquinol, you know, likeyou mentioned, what is it?
150 twice a day or something?
150, just standard, 150milligrams, 150.
150 milligrams for anextraordinary healthy.
Speaker 2 (38:32):
I was going to say for an extraordinary.
Speaker 1 (38:36):
But then you've got people who have problems, who
have an increased coronaryartery calcium, who have maybe
cardiomyopathy from COVID CCF.
Congestive cardiac failure whatdosage range do you go up to?
Myalgic myeloid encephalitischronic fatigue what dosage
range do you go up to?
Yeah, look, I go up to about300.
Speaker 2 (38:55):
And I always give it in the morning because it does
give you energy, you don't sleepas well.
So I wouldn't go a BD dose.
I do 150 milligrams as just amaintenance dose for energy or
if you're on statins.
But once you get to the heartfailure component of it, 300
milligrams in the morning andlook, you can go up to 600
(39:15):
milligrams.
I've got a good mate who'sabsolutely mad.
He runs marathons and I tellanyone who runs marathons,
there's a perfectly good busservice, so why anyone would do
it is just beyond me.
But anyhow he takes, before hedoes a marathon, 600 milligrams.
So he's powered by ubiquinolwhen he does his marathons and
(39:38):
he's a very good marathon runner.
But look, you could do that.
But it just becomes a veryexpensive exercise and this cost
of living crisis.
It is expensive but you've gotto pay for quality.
So I think, if you can getpeople out of it as cheaply as
possible, 150 milligrams in themorning for just a good standard
dose, 300 milligrams if you'remuch sicker with
(39:59):
cardiomyopathies or you've gotlong COVID.
You see, I believe and this isanother sort of left field thing
, but I believe chronic fatiguesyndrome, fibromyalgia, long
COVID is all due to gutdysbiosis and I think the gut's
been knocked off and a lot ofubiquinol is made by the gut, so
(40:21):
I give people, especially inthe throes of their acute
symptoms, 300 milligrams for afew months until they get back
on their feet.
Then I'll drop it back to 150.
Speaker 1 (40:32):
Dr Ross Walker, every single time I speak with you, I
learn something of value andsomething new.
So thank you so much for takingus through the benefits of
ubiquinol in cardiac healthtoday, and I look forward to our
next podcast when we're goingto go through some of the other
things that you use in yourpractice.
You know one.
A couple of things I didn'teven question you about was
(40:52):
vitamin k2 and berberine, butthat's probably for another time
, very, very good well, I tellyou what, just as a quick
snippet, because I can't wastethis opportunity.
Vitamin k2 when do you use?
At what dose?
Berberine when do you use it,what does?
Okay?
Speaker 2 (41:13):
vitamin k2 I.
180 micrograms daily is thebasic dose, although if you've
got renal disease, a higher dosebecause you do need more.
And I, when do I use it?
Everyone with coronarycalcification takes the calcium
out the arteries, puts it backin the bones, um and uh.
And I I mean I take it myself,even though I've got a zero
(41:34):
calcium score.
I take it just to give myselfstrong bones.
So I take it for a preventionof osteoporosis, based on work
out of the rotterdam Heart Studywhich showed there was an
improvement in bone strength andalso improvement in arterial
flexibility.
Berberine is something I don'tuse myself, so I've not
prescribed it, but I'm startingto see over the last, especially
(41:55):
six to 12 months, a lot of goodevidence that berberine may
have added benefits.
To be frank with you, mate, Itake 40 pills in the morning and
15 in the evening, allpreventative stuff.
Berberine is not one of them atthe moment, but I've the work
I'm seeing on berberine, evenwith weight loss and better
metabolic syndrome.
I'm starting to think maybe Ishould be thinking about that
(42:17):
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 andabout 50 in the evening and
monitors everything he does.
I think you should smell theroses, not analyse the damn
things.
But, andrew, can I say mate,every time I have a chat with
you it's just a great pleasurefor me.
(42:37):
You do a wonderful service toeveryone who listens to you.
You're incredibly intelligentand eloquent and I really love
talking with you.
So thank you very much, mate.
Speaker 1 (42:47):
Ross, thank you so much.
Thank you, that's made my day.
And thank you once again, drRoss Walker, for joining us
today, and I really do.
Every single time this man Iattend his lectures or his talks
, I'll learn something of valuefor patients.
It's a brilliant man and hequestions everything.
I love you, so thank you somuch for taking us through the
(43:09):
benefits of ubiquinol today and,of course, everybody, thank you
for joining us today.
You can catch up on all theother podcasts and on the
Designs for Health website.
I'm Andrew Whitfield-Cook.
This is Wellness by Designs.
This is Wellness by Designs, and I'm your host,
andrew Whitfield-Cook, andjoining us today is Dr Ross
Walker, an esteemed cardiologistwho has dedicated the past 25
years of his career toprevention, and today we're
going to be discussing the roleof ubiquinol in cardiovascular
health.
Welcome to Wellness by Designs,ross.
How are you?
Speaker 2 (00:33):
Andrew, it's always a great pleasure to talk with you
at any opportunity I get.
Speaker 1 (00:38):
Thank you, sir.
It's been a long time betweenchats.
Speaker 2 (00:42):
Now Ross.
Speaker 1 (00:42):
I think the first thing we need to cover is what
exactly is ubiquinol?
Speaker 2 (00:48):
Yeah, well, ubiquinol is the active version of
coenzyme Q10.
And coenzyme Q10 has a numberof roles in the body.
One is basically, it's a verystrong antioxidant.
It's a fat-soluble antioxidant,but also it's very, very
important in mitochondrialhealth.
It's a vital part of themitochondrial energy production.
(01:12):
And so without good levels ofubiquinol not ubiquinone, which
is inactive, it's got to beubiquinol the mitochondria
doesn't work as well, doesn'twork as well.
Speaker 1 (01:23):
And so where, if we're talking about CoQ10, you
know the old CoQ10, theubiquinone where let's say
there's still the lion's shareof research is done on.
Admittedly, in the olden days Iguess there was the doses were
way lower than what we're usingnow, and now we've swapped to
(01:46):
ubiquinone the active.
Tell us about that sort ofjourney of research, if you like
, from ubiquinone the low-dosestuff.
I mean.
I'm sure you'll remember whenin Australia the only product we
could get was ubiquinone and itwas 10 milligrams.
Speaker 2 (02:02):
Yeah, and really didn't do much at all.
And the problem is that withthe whole CoQ10 story is that
you really don't get enough inyour diet.
Whether it's ubiquinone orubiquinol, there's just not
enough in the diet.
I think you've got to havesomething like a kilo and a half
of steak to get 30 to 50milligrams of ubiquinol in your
(02:23):
system, and so much broccoliyou'd be eating it for about
three or four weeks to get thatsmall amount.
So, yes, when CoQ10 was firstreleased, it was only in the
ubiquinone or ubicarinone formand it was in very, very low
doses, so it didn't really domuch.
I think this is really really agood example of the history of
(02:45):
evidence based supplementation.
Orthodox medicine wants harddata.
They want science behind whatanyone does, and so when you're
using almost homeopathic dosesof something that's inactive,
you're not going to get muchresponse.
I mean it takes me back to thewhole vitamin E nonsense that
we've heard from years ago.
In 2004, a guy called EdgarMiller wrote an editorial in the
(03:09):
Annals of Internal Medicinesaying that vitamin E was not
only of no benefit but it waspossibly harmful.
And this is what does my headin a bit about orthodox medicine
.
They're still quoting thevitamin E data using
DL-alpha-tocopherol, which isthe inactive version of vitamin
D, from a thing called theFinnish Smokers Trial.
(03:32):
Now, the clue is in that titlethere.
But 29,000 Finnish smokers werestudied and were given
placebo-controlled eithervitamin E, dl alpha-tocopherol,
so a synthetic version ofvitamin E 50 international units
and 15 milligrams of syntheticbeta-carotene.
(03:54):
And this stuff shouldn't beused.
It doesn't work and in fact, itcan cause more harm.
But so people like Edgar Millerare still coming out were
coming out in 2004 sayingvitamin E may be harmful.
Well, of course it may beharmful if you use the crappy
synthetic stuff.
So again, this is what'shappened with medicine.
All the time they go back tothese silly studies that
(04:16):
disprove the benefits of, ordisprove any benefits from,
supplements because they've usedthe wrong dose of the wrong
stuff.
And again, with the initialubicarinone stuff, we're using
10, 30 milligrams of an inactivesubstance.
And here's the problem when youhit 30, and the 30 is the peak
(04:37):
of our life.
So it's a bit depressing foryou and I, but our body was
designed to wander around ajungle for 30, 40 years with a
spear and then die, had yourhead ripped off by a
saber-toothed tiger or you diedof some infection.
So when you hit 30, the peak ofyour life, things start to wear
out.
That's when osteoporosis starts, sarcopenia, loss of muscle
(04:58):
that all starts at age 30.
But also your ability toconvert ubiquinone to ubiquinol
starts to drop off a little bitat age 30.
And then at age 50, the enzymediaphoresis just goes boom.
So you just don't get theamount of active CoQ10 or
ubiquinol in the mitochondriathat you need over the age of 50
(05:21):
, which in many ways is one ofthe reasons why many people over
the age of 50 are starting tofeel tired, because their
mitochondria just aren't workingas well, and I think one of the
reasons is they're losing oneof the main drivers of their
mitochondria, which is ubiquinol.
Speaker 1 (05:42):
So just a point there about tiredness in in, you know
, around the age of 50 sort ofthing.
Obviously there's many, manyfactors, you know.
But would it be wise, therefore, for a wellness approach to
start thinking about the use ofubiquinol, the active coq10, as
part of the regimen?
(06:03):
Obviously there's exercise andgood sleep and things like that.
I get it, but the use ofubiquinol in a reasonable dosage
and I'll question you aboutthat as part of their wellness
program.
Speaker 2 (06:15):
Oh, absolutely.
And I've got to say, when Italk about wellness, wellness
isn't just the absence ofdisease, which is an important
component.
Of course you know you want tohave some illness because you
will be unwell, but what I callultimate wellness is, one, the
absence of disease.
Two, very good energy levels,which you do get from ubiquinol,
(06:40):
and also, I think, themagnesium orotate aspartate
combinations.
And there are other reasons whywe lose energy.
I mean, sleep apnea is a bigone, because all adult males
have sleep apnea, allpostmenopausal females have
sleep apnea to some extent, andas you get older the sleep apnea
gets worse and that makes youtired as well.
But there are many other reasonsfor fatigue and if anyone's
(07:02):
listening to this, I wouldn'twant you to start swallowing
ubiquinol if you're tiredwithout figuring out why you're
tired in the first place,because it may.
I mean, the commonest cause offatigue in our society is you're
working too hard, playing toohard, not sleeping well, but
then after that there'sendogenous depression that can
also make you tired.
Then there's sleep apnea, whichwe've mentioned.
(07:24):
When you've hit 50 and you'regoing through the pauses either
menopause or andropause youstart to get tired.
So that may be another factor.
But then finally, there couldbe a medical reason.
You could be losing blood, irondeficient, you could have a
thyroid problem, something wrongwith your kidneys, your liver,
your heart.
To give an example, one of thefirst presentations of a
(07:44):
ruptured plaque is incrediblefatigue.
So I wouldn't want anyone to goand say, oh, I'm tired.
Therefore, I'm going to takeubiquinol.
What I say, you're tired, findout why you're tired first, but
then, once you've had allserious conditions excluded, by
all means take now here's the toanswer your question 150
(08:05):
milligrams of ubiquinol, which Ithink is the standard dose for
people for energy.
I take it.
I'm 14 months off 70 and I'vegot a zero coronary calcium
score and I'm not on a statin,because anyone's got a zero
calcium score shouldn't goanywhere near a statin, which
we'll get to a bit later on.
But I just take the 150milligrams every day of
(08:26):
ubiquinol just to keep my energygoing and I've got pretty good
energy for someone in my agegroup.
Speaker 1 (08:32):
Firstly, you mentioned cholesterol.
So let's go there Withcholesterol and the coronary
artery calcium score.
The Australian New ZealandCollege of Cardiologists says
they sort of.
I remember when you werementioning this decades ago,
ross, by the way, and back thenthere was total denial about the
usefulness.
And now the college has got astatement saying those who have
(08:54):
low cholesterol and when I saythe word cholesterol I think we
all need to make to to realizethat we're not talking about the
molecule of cholesterol, we'retalking about lipoproteins.
But anyway, when we've got highor dysfunctional supposedly
lipoprotein profiles, that thosepeople who have got low or
(09:17):
normal cholesterol quotationmarks levels that they don't
need a coronary artery calciumscore, those people that are
mid-range could benefit, I knowcould benefit and those people
that are high have high anyway,so they should be on a statin.
What's your take on thatstatement?
Speaker 2 (09:36):
That statement is complete and utter nonsense.
And let me just give you ananecdote 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 calciumscore I have noting that
anything above 400 is serious isa 68-year-old man in the
(10:01):
fitness industry.
Doesn't have an ounce of bodyfat.
Old man in the fitness industrydoesn't have an ounce of body
fat, has a normal cholesterol,blood pressure, never smoked,
not diabetic and Andrew, waitfor this no family history of
heart disease.
So therefore, by that criteriayou just mentioned, there's no
point in him having a coronarycalcium score.
But he has and we could getinto this discussion because
(10:23):
he's one of my hobby horses.
He has an elevated lipoprotein,little a, which doctors have
been measuring for the last twoor three years because we're now
developing drugs for it.
I've been measuring it andtreating it for 30 years.
So anyhow, this guy came to seeme, sent him downstairs for a
coronary calcium score because Ihave a radiology practice under
(10:46):
my building.
It's not my practice and hiscoronary calcium score?
Wait for this.
I hope you're sitting down.
You are sitting down 8,100.
Hi so his arteries were likeporcelain pipes.
He had bypass surgery 10 yearsago.
He sent me an email a few yearsago with a picture of him and
his mates winning the latestbasketball grand final.
So he'll now live to his 100after he's bypassed, but under
(11:10):
those criteria he wouldn't havehad a coronary calcium score.
Now let's get to the science,not just to a story.
I believe and I've been sayingthis for 26 years when I
introduced coronary calciumscoring into Australia in
conjunction with the SydneyAdventist Hospital in Wurundjeri
and Dr David Grout, one of mycardiologic colleagues.
I've been saying this for 26years that all men at 50, all
(11:33):
women at 60 should have aroutine coronary calcium score.
But the goalposts change.
If, for example, you said to meoh, my dad had a bypass at 45.
Well, I'd do your coronarycalcium score at 35, as one
example.
But I don't like to overirradiate people below the age
of 50 because in my view thereare only three reasons, three
benefits of being over 50,andrew.
(11:54):
Number one is wisdom.
Number two is grandchildren ifyou got them and I have nine.
And number three is you losethe cancer risk from medical
radiation.
So the less radiation you havebefore age 50, the better off
you are.
So anyhow, to give you somescience now behind the coronary
calcium score and itsrelationship, especially to
(12:16):
statin drugs.
Firstly, it's been shown thatif you have a coronary calcium
score and you compare that tostandard risk factors for heart
disease, the calcium score hasmarked benefit in improving your
level of risk.
So there are so many people whoappear to be at high risk
because of standard risk factorprofiles and they'd be all put
(12:39):
on a statin.
Then you do their coronarycalcium score and they've got a
zero calcium score.
It markedly plummets their risk.
So I'll give you again anotherstory.
I saw a woman who was 58 yearsold with a lifelong cholesterol
of 9.5, because cholesterol hasgot nothing to do with what you
eat.
It's all to do with geneticsand metabolism.
(12:59):
So women hit menopause, theircholesterol goes up because
their metabolism changes,because they lose estrogen.
So anyhow, every time she'd seea GP or any other doctor,
scaremongering doctors say toher if you don't take Lipitor
you're going to die, which isscaremongering, nonsense.
She'd take Lipitor because shewas worried about dying, of
course, because her cholesterolwas 9.5.
(13:20):
And after a few days shecouldn't lift her muscles, they
were just killing her.
So anyhow, after seeingmultiple doctors, she heard
about me, came to see me, sentit 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 yourarteries, so forget about it.
(13:42):
Live a healthy lifestyle.
No one should eat a bad diet,not just because of the
cholesterol issue but because ofmany other factors.
But please, you don't need astatin.
So anyhow, over the next eightyears, she listened to me and
not to the scaremongeringdoctors, and she came back to
see me, age 66 now, with acholesterol of 9.5 because it's
(14:04):
genetic, sent it downstairs foranother calcium score.
It had rocketed from zero up tozero, 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.
So a study of 13,500 peoplebetween the ages of about 50 up
(14:26):
to 70 followed for 10 years thebenefits of them taking a statin
based on their calcium scoreZero.
Calcium score zero benefit.
Calcium score below 100.
So a 55-year-old male goes intoa doctor with a calcium score
of 60.
The doctor says oh, you've gotatherosclerosis, you must be on
a statin.
(14:47):
No, the evidence isn't there.
This study showed calcium scorebelow 100, p-value 0.095.
So no statistically significantbenefit from being on a statin.
But the number needed to treat,which I think is a better
number.
Here you had to treat 100people for five years to prevent
(15:08):
one heart attack and nodifference in death rate.
So who in their right mindwould take a strong synthetic
metabolic regulator for 10 yearsto prevent one heart attack out
of 100 people?
I mean for five years, oneheart attack.
It's just nonsense.
But once you get to a calciumscore above about 100 for your
(15:31):
age so if you're 60 and yourcalcium score is 150, then
that's where the benefits kickin.
The number needed to treat isonly 12, highly statistically
significant.
So to me, when people makethese comments, they've got to
have some science behind whatthey say.
The calcium score is easily thebest predictor for heart
(15:52):
disease risk.
And here's another hobby horseof mine, andrew before we should
start talking about ubiquinolsoon.
But there's a thing called a CTCori angiogram, and a CT Cori
angiogram is done on the sametechnology as the calcium
scoring still a CT coriangogram,and a CT coriangogram is done
on the same technology as thecalcium scoring still a CT but
the calcium scoring just takes asnapshot of your arteries.
(16:12):
The CT coriangogram you'reinjected with dye and you do not
qualify by Medicare for thestudy if you have no symptoms
and you haven't seen acardiologist.
So many GPs are saying, oh, aCT chorioangiogram gives you
better pictures than a calciumscore, which it does Beautiful
(16:34):
pictures of the chorio arteries.
So therefore I'll get you tohave that test done.
It costs people an extra $500 or$600 to have that test and a
study was done in the Journal ofthe American College of
Cardiology looking at thepredictive risk of coronary
calcium scoring versus CTchorangiography, or in other
words atherosclerosis versusblockages two different things.
(16:58):
So anyhow, the coronary calciumscore was a much better
predictor and it costs you $500or $600 less.
You don't glow in the dark forthree or four days afterwards
and you're not given anintravenous injection that you
potentially could have ananaphylactic reaction to or even
damage your kidneys.
So it just does my head in whenI see GPs and ignorant
(17:20):
cardiologists ordering these CTcoriangigrams on people who are
asymptomatic.
Now I do them on people who'vegot symptoms and an equivocal
stress echo.
That's the criteria to have aCT choriangiogram, not just to
see what your arteries are doing.
That's the calcium score End ofsermon Just now.
Speaker 1 (17:43):
we're going to continue it.
So, just regarding the coronaryartery calcium score, that's
calcification which is, you know, progressed, which is further
along the line of dysfunction ofendothelial dysfunction.
Advanced endothelial dysfunction?
Yeah.
What about earlier predictorslike, for instance, fibrinogen
or you know?
You mentioned lipoprotein,little a, you know, and again, I
(18:06):
remember you talking about thisdecades ago when it was.
It was lambasted and then therewas this sort of admittal that
maybe in women only.
I think that's right, there wasa certain age population or
something and that's it.
And now it's like, oh, now thatwe're developing drugs for it,
(18:27):
yeah, sure.
So what about the function ofusing earlier predictors of
endothelial dysfunction,homocysteine?
Speaker 2 (18:42):
Yeah, yeah, well, look, can I say I don't think
it's either, or I think age 50is a good time to start, If you
don't have a rampant familyhistory or a rampant cholesterol
.
I'll tell you another story.
I think anecdotes areinteresting.
They don't prove anything,they're just stories.
But I saw a 38-year-old man whosome fool had put on a statin
10 years before, at the age of28, just because he had a high
(19:05):
cholesterol and his uncle had aheart attack at 55.
That was the justification.
So this fellow faithfully tookhis 40 milligrams of
atorvastatin for 10 years.
But then he went on to tell mehow his wife had been through
wait for this for 10 years.
But then he went on to tell mehow his wife had been through
wait for this 10 unsuccessfulcycles of IVF, until it twigged
(19:27):
in his head Maybe it's theLipitor I'm taking that's
pulverizing my testicles andstopping my wife from getting
pregnant.
So he stops the Lipitor, shegets pregnant naturally within
six months.
Now, andrew, that is medicalnegligence To put someone on a
drug that really wasn'tindicated and causing them
$100,000 worth of IVF, and noteven forgetting about the money,
(19:49):
the psychological misery ofgoing through IVF, and a lot of
people also don't realize.
If you've had failed IVF, youdouble your risk for
cardiovascular disease in thenext 10 years because you're
fiddling around with people'shormones and when it doesn't
take, there's a double the riskfor heart disease.
So I think we've got to bereally careful here what we do
to people.
And there are times look, I'vegot again another anecdote.
(20:11):
I've got a 32-year-old womanwhose father died at 31 of a
heart attack and her cholesterolis 12.4 because it's all
genetic, it's familialhypercholesterolemia in her case
.
I did a calcium score on herand it was already 48.
Now 48 is not much, but for a32-year-old it means she's got
very advanced atherosclerosis ather age.
I'm hammering her with thehighest dose of statin and
(20:35):
ezetrol because she probablywill die if I don't treat her
cholesterol.
So this is the pointCholesterol, as you say, it's
not just cholesterol, it's allthe LDLs that go with it.
But there are four basiccomponents of the whole
cholesterol story.
There is small LDL, there islarge LDL, small HDL, large HDL.
(20:58):
Here, andrew, is where size isimportant.
The larger your LDL, the largeryour HDL, the healthier you are
.
So it's the small LDL that'spro-arthrogenic, puts fat in
your arteries and that's the bitthat gets very oxidized and
that's where ubiquinol stopsbeing oxidized.
Of course the large LDL is goodfor you.
(21:19):
It builds healthy cellmetabolism, cell membranes.
It's the basic ring of steroidmetabolism, bile salt, vitamin D
metabolism.
So we need large LDL.
Then there's small HDL, which ispro-inflammatory.
That's bad for you as well.
Large HDL sucks fat out of yourarteries.
(21:40):
It's involved in reversecholesterol transport, takes the
cholesterol out of the arteriesand back into the bloodstream.
It's broken down harmlessly bythe liver.
So it's not about cholesterol,this nonsense about focusing on
cholesterol.
You focus on the atherogenicpart and the inflammatory part
of cholesterol, the small bits,and you do something about that
(22:00):
so you don't just pulverizecholesterol.
I saw a woman yesterday in mypractice cholesterol of 7.5,
triglycerides of 0.7, hdl of 2.5, and the GP was desperate to
put her on a statin Coronarycalcium score.
Of course nothing.
She doesn't need a statin.
(22:21):
She needs to be congratulatedfor being what we call a lean
hyper-responder.
Speaker 1 (22:28):
A lean hyper-responder.
Okay, I'll have to write thatone down.
Speaker 2 (22:31):
That's what we call these people, Thin people with
high cholesterol, high HDL, lowtriglyceride, zero calcium
scores, are leanhyper-responders.
They've got very goodmetabolism.
They're being protected.
But you mentioned the LP littlea.
That is 20% of heart disease.
70% of heart disease is due toinsulin resistance.
(22:52):
So 90% of atherosclerotic heartdisease is explained by two
genes insulin resistance geneand lipoprotein delay.
Speaker 1 (23:03):
Let's just talk a little bit about that
endothelial function and howubiquinol works.
We've spoken about protectingthe molecule of LDL.
What about endothelial function?
How does ubiquinol help thereand can it regress
atherosclerosis, existingatherosclerosis?
Speaker 2 (23:23):
like a high coronary artery score.
Yeah, can I make the point thatthe first thing that goes wrong
in atherosclerotic heartdisease?
So the progressive buildup offat, inflammatory tissue, and
then calcium, and calcium is notthe problem.
So imagine a donut like thisthe blood's going through the
hole, the fat's building up inthe wall.
(23:44):
As the fat builds up in thewall, the body throws in calcium
to act as a scaffold to stop itfrom 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 yourartery is most stable.
It's just telling you there'satherosclerosis throughout the
(24:05):
arteries.
So the endothelium is the firstbarrier to all the muck coming
through your arteries.
So if you have endothelialdysfunction so, for example,
there are still some people whosmoke cigarettes.
So within an hour of smokingone cigarette, you reduce your
endothelial function by 50%.
So what is endothelial function?
Firstly, it's the ability toact as a barrier.
Secondly, it's the ability toopen and close with different
(24:29):
stimuli.
So if you're in the middle of adeep sleep, the last thing you
need is torrential blood flow toyour heart and your muscles, so
the system closes down and yourbody has a rest, so a thing
called endothelin is releasedthat constricts down the
arteries, but then, when youneed blood flow to your muscles,
the endothelium releases nitricoxide, the ubiquitous
(24:51):
vasodilator, and that's whatopens up.
Now what does ubiquinol do?
Ubiquinol firstly acts as anantioxidant to stop the small
LDL being oxidized and gettinginto your arteries, but it also
has a direct effect on nitricoxide metabolism through a thing
called nitric oxide synthase,and so it basically generates
(25:13):
more nitric oxide, which keepsthose arteries open, which is so
important for you.
Speaker 1 (25:18):
And that all comes from a thing called L-arginine
which is part of one of theamino 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 shownwith evidence to be of most
(25:43):
benefit for people?
Yeah, what doses?
We might use that sort of thing, sure.
Speaker 2 (25:49):
Okay, well, firstly, we've spoken about endothelial
function and the studies areshowing clearly anywhere between
100 to 200 milligrams ofubiquinol will improve
endothelial function by itseffects on nitric oxide synthase
and working as an antioxidant,et cetera, et cetera.
So that evidence is rock solidthat ubiquinol is terrific for
endothelial function.
(26:09):
But let's go to the next level.
There's evidence to show thatubiquinol can convert you from
small LDL to large LDL.
Studies have come out and shownthat as well, confirmed that
one.
But then there's the wholething about whether ubiquinol
should be used for people whoare taking statins and I put all
of my patients on statins, on acombination of ubiquinol and a
(26:31):
magnesium orotate aspartatecombination, because the orotate
and the aspartate lift up theCoQ10 in the mitochondria.
And also what happens when youtake a statin there's a thing
called complex three in themitochondria.
So basically to explainmitochondria, they've got these
little turbines that are pushingprotons through and helping to
(26:53):
generate this ATP.
So ATP is, of course, the unitof energy in the body and
ubiquinol works on complex three, especially complex two,
complex three, to help generatemore of this ATP.
Now statins completelypulverize complex three and stop
the generation of ATP, which iswhy people get.
(27:14):
I'd say about 20% of people getproblems with muscle pain,
stiffness, weakness, crampingand, over time, loss of muscle
bulk, which we call, of course,atrophy, and it's about 20%.
If you look at the randomizedcontrolled clinical trials,
people only get muscle problemsless than 5% of cases.
But the problem with that,andrew, is that they have a
(27:35):
strict definition of myalgia,which is muscle pain with a CK
that's three times the normallevel.
That's the definition.
So of course that's less than5%.
But I work in the real worldwhere I actually see things
called human beings, and thehuman beings that I see it's
about 20% get that just muscleweakness or they just get a lot
(27:58):
of cramping and they mightn'thave the muscle pain that gives
them the criteria for myalgia.
So what I do is I try to preventthat by giving everyone
ubiquinol and the magnesiumorotate aspartate and vitamin D
is very good as well.
I think everyone should betaking vitamin D.
A thousand units, two a day.
You should be doing that justroutinely, but some people on
(28:18):
statins need 1,000 units, two aday.
You should be doing that justroutinely, but some people on
statins need about 4,000 units aday.
So I stylize my therapy for theindividual, but it's just
routine for me for everyone tobe given the ubiquinol in that
dose 150 milligrams, who aregoing in any form of statin, and
I don't use fat-soluble statins, lipitor and Zocor, or
(28:39):
Atorvastatin, simvastatin,because I believe they cause
more problems than theResuvastatin and the Pravastatin
.
Speaker 1 (28:48):
Right, so the Resuvastatin and the Pravastatin
are water-soluble, correct.
Speaker 2 (28:52):
Yeah, yeah.
Speaker 1 (28:54):
And so they don't cross the.
Speaker 2 (28:56):
So this is perhaps membranes as much right.
Speaker 1 (28:59):
So this is perhaps why the original big trial with
reserva statin was at thejupiter trial.
Speaker 2 (29:05):
Um was looking at decrease in um c-reactive
protein oh yeah, but all statinshave been shown to reduce
c-reactive protein around 30 Imean statins.
And look, I'm not anti statin.
I don't want anyone to thinkthat that I'm I'm an anti-statin
campaigner.
I'm against the inappropriateuse of statins for people who
don't need them.
(29:25):
So your calcium score is below100, you don't need a statin.
But if your calcium score ishigh or you've had a heart
attack, stent or a bypass, I usestatins all the time.
So I spend half my week puttingpeople on statins who don't
want to take them, the otherhalf taking people off statins
who don't need them.
So to me it's just logical.
Speaker 1 (29:44):
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 type2?
Is it a type 2?
That's the worst risk.
Speaker 2 (29:59):
I think you're talking about when you do the
subfraction analysis, aren't you?
Speaker 1 (30:04):
Yes, for giving me subfractions.
Yes, yeah, so you're looking atsubfractions so basically
you're measuring small LDLversus large LDL.
Speaker 2 (30:14):
So you're measuring that.
And look, the only time I everdo that is when I can't give
someone a good explanation forwhy they have heart disease.
So if someone's got a highlipoprotein delay, I'm going to
treat them anyhow.
Someone's insulin resistant?
I'm going to treat them anyhow.
But I have the occasionalpeople that seem to have a
(30:34):
relatively normal cholesterolprofile, everything else is
going okay and they still haveearly heart disease.
So then I'll go off and huntdown their sub-fractions to see
whether we need to be monitoringand measuring those.
But really, for example, mostcases of small LDL have a high
triglyceride, low HDL.
(30:55):
So, for example, someone'scholesterol 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 cholesterolis pretty good.
(31:16):
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 showthat people who take statins,
who are given ubiquinol, itreduces their muscle pain and
weakness by around 50%.
(31:36):
So there is an evidence basebehind that as well.
But then one of the big thingsnow for ubiquinol.
It's been used in peoplepost-infarct and whatever.
I think that's its benefits onendothelial function.
But then there's the wholething about myocardial function.
Now you mentioned beforecongestive cardiac failure and
(31:57):
there really are two types ofheart failure.
There's heart failure withreduced ejection fraction, where
your heart's like a floppy bagand just not pumping well, the
commonest cause of that ofcourse, being recurrent heart
attacks that have scarred yourheart.
But there's also dilatedcardiomyopathy and we saw this a
lot during COVID.
People who got COVID hadsignificant myocarditis.
(32:19):
Some people with the RNAvaccines got myocarditis, but
it's much more with COVID thanthe RNA vaccines.
But there are other causes ofdilated cardiomyopathy Alcohol,
for example.
Too much alcohol can induce adilated cardiomyopathy, a
familial cardiomyopathy with avirus tipping you over the edge
and giving you a severe dilatedcardiomyopathy.
(32:40):
So there's all of that.
That's reduced ejectionfraction.
And a number of studies have nowshown that just standard CoQ10
by itself can improve the heartevents.
So there was a study calledQ-symbio where they used I think
it was from memory about 400milligrams a day of CoQ10, so
(33:03):
200 milligrams twice a day ofCoQ10.
And in a number of people itwas a big study and it showed
that over two years there was a50% reduction in death and hard
cardiac events just from usingstandard CoQ10.
But then when you look at thepeople who switched from CoQ10
to ubiquinol because theyhaven't done the study with
(33:26):
ubiquinol yet they should.
But when they switch peopleover from CoQ10 to ubiquinol,
their ejection fraction, whichis how well the heart pumps,
markedly improves from goingfrom ubiquinone to ubiquinol and
a lot of the evidence isshowing that ubiquinol is so
good to improve cardiac function.
So in all my patients who havecardiac failure I certainly put
(33:50):
them on 300 milligrams ofubiquinol with the magnesium
orotate aspartate combination.
But also what I haven'tmentioned is the other form of
heart failure, which is heartfailure with preserved ejection
fraction.
So the heart's pumping well butit's not relaxing properly and
really up to the last five yearswe haven't really had any
(34:12):
treatment for that.
Now we're getting things calledSGLT2 inhibitors, which are very
good drugs for that condition,and also the flavor of the
decade, the GLP-1 receptoragonists, things like
ozempicators, mates.
They're also very good for thatcondition and this is just a
slight deviation but it'sinteresting for people to hear
(34:34):
this.
The reason why the GLP-1receptor agonists work, it's not
just the reduction in fat inyour gut.
It takes fat out of your organs.
So if you do an autopsy onsomeone who's died, who's
significantly overweight, halftheir heart is full of fat and
obviously that's going to altercardiac function and make your
(34:55):
heart a lot stiffer.
And so the GLP-1 receptoragonist take the fat out of the
heart and restore the heart to amore elastic state.
Now, interestingly, there was astudy done where they used a
combination of D-ribose andubiquinol in people with heart
failure with preserved ejectionfraction, and showed significant
(35:16):
parameters of benefit, soreduced BNP, better exercise
function, et cetera, nomortality rates.
But the study wasn't big enoughto cover mortality.
Speaker 1 (35:28):
Just a point about ribose and thinking about
substrates of the electrontransport chain Nicotinamide
ribose NR.
Have you ever used that?
Have you got any data on that,Any benefits?
Speaker 2 (35:44):
Oh, yeah, yeah, yeah, I'm using well, I use more NMN
than NAD riboside, which is whatyou're talking about, but I
think they're about the same.
So I think anything that's anNAD plus feeder, such as NMN,
NAD riboside what you've justsaid and nicotinic acid, and
I've got to say I've been takingfor five years I obviously
(36:08):
won't mention products on air,but I've been taking an
NMN-based product for the lastfive years and I also take
immediate release nicotinic acidas well every day.
The reason I do this is becauseit is an activated B3, like an
NAD plus.
But I've been using nicotinicacid in its immediate release
(36:29):
form in my patients for over 30years and what I was noticing
with all of these people is theywere having incredible
longevity, just things weren'thappening to them, they weren't
having the cardiac events theyshould be having, and so I
thought, well, there's somethingweird about this.
And I started reading allaround nicotinic acid and the
(36:50):
studies that said that nicotinicacid didn't work were done on
the slow release form.
And you see, I think this is oneof the keys to good health,
Andrew, it's a thing calledvasodilatation.
So what's one of the bestvasodilators on the planet?
It's a thing called exercise.
So I think the way exerciseworks.
One of the ways it works ispumps blood through the body and
(37:11):
flushes crap out.
But nicotinic acid does asimilar thing makes you go
bright red, opens up yourarteries, flushes all the crap
out of the system.
There's another drug, anothercouple of drugs, that does the
same thing, what I call vitaminV, otherwise known as Viagra,
and a study of 72,000 men over14 years showed that those who
(37:35):
were the highest end users ofViagra versus those men who
didn't Viagra and Cialis I'm notjust picking on one of the
drugs had weight for this Notonly the benefit of not falling
out of bed, but also thebenefits of a 55% reduction in
cardiac events, a 50% reductionin all-cause death, a reduction
(37:55):
in dementia and bowel cancer,and I believe this is because of
the vasodilatation.
So that's one of the big keyshere.
That's what ubiquinol does.
It's a good vasodilator becauseof its effects on nitric oxide.
So vasodilatation, I think, isone of the keys to good health.
Speaker 1 (38:13):
Just going back as a last question for dosage range
with ubiquinol, you know, likeyou mentioned, what is it?
150 twice a day or something?
150, just standard, 150milligrams, 150.
150 milligrams for anextraordinary healthy.
Speaker 2 (38:32):
I was going to say for an extraordinary.
Speaker 1 (38:36):
But then you've got people who have problems, who
have an increased coronaryartery calcium, who have maybe
cardiomyopathy from COVID CCF.
Congestive cardiac failure whatdosage range do you go up to?
Myalgic myeloid encephalitischronic fatigue what dosage
range do you go up to?
Yeah, look, I go up to about300.
Speaker 2 (38:55):
And I always give it in the morning because it does
give you energy, you don't sleepas well.
So I wouldn't go a BD dose.
I do 150 milligrams as just amaintenance dose for energy or
if you're on statins.
But once you get to the heartfailure component of it, 300
milligrams in the morning andlook, you can go up to 600
(39:15):
milligrams.
I've got a good mate who'sabsolutely mad.
He runs marathons and I tellanyone who runs marathons,
there's a perfectly good busservice, so why anyone would do
it is just beyond me.
But anyhow he takes, before hedoes a marathon, 600 milligrams.
So he's powered by ubiquinolwhen he does his marathons and
(39:38):
he's a very good marathon runner.
But look, you could do that.
But it just becomes a veryexpensive exercise and this cost
of living crisis.
It is expensive but you've gotto pay for quality.
So I think, if you can getpeople out of it as cheaply as
possible, 150 milligrams in themorning for just a good standard
dose, 300 milligrams if you'remuch sicker with
(39:59):
cardiomyopathies or you've gotlong COVID.
You see, I believe and this isanother sort of left field thing
, but I believe chronic fatiguesyndrome, fibromyalgia, long
COVID is all due to gutdysbiosis and I think the gut's
been knocked off and a lot ofubiquinol is made by the gut, so
(40:21):
I give people, especially inthe throes of their acute
symptoms, 300 milligrams for afew months until they get back
on their feet.
Then I'll drop it back to 150.
Speaker 1 (40:32):
Dr Ross Walker, every single time I speak with you, I
learn something of value andsomething new.
So thank you so much for takingus through the benefits of
ubiquinol in cardiac healthtoday, and I look forward to our
next podcast when we're goingto go through some of the other
things that you use in yourpractice.
You know one.
A couple of things I didn'teven question you about was
(40:52):
vitamin k2 and berberine, butthat's probably for another time
, very, very good well, I tellyou what, just as a quick
snippet, because I can't wastethis opportunity.
Vitamin k2 when do you use?
At what dose?
Berberine when do you use it,what does?
Okay?
Speaker 2 (41:13):
vitamin k2 I.
180 micrograms daily is thebasic dose, although if you've
got renal disease, a higher dosebecause you do need more.
And I, when do I use it?
Everyone with coronarycalcification takes the calcium
out the arteries, puts it backin the bones, um and uh.
And I I mean I take it myself,even though I've got a zero
(41:34):
calcium score.
I take it just to give myselfstrong bones.
So I take it for a preventionof osteoporosis, based on work
out of the rotterdam Heart Studywhich showed there was an
improvement in bone strength andalso improvement in arterial
flexibility.
Berberine is something I don'tuse myself, so I've not
prescribed it, but I'm startingto see over the last, especially
(41:55):
six to 12 months, a lot of goodevidence that berberine may
have added benefits.
To be frank with you, mate, Itake 40 pills in the morning and
15 in the evening, allpreventative stuff.
Berberine is not one of them atthe moment, but I've the work
I'm seeing on berberine, evenwith weight loss and better
metabolic syndrome.
I'm starting to think maybe Ishould be thinking about that
(42:17):
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 andabout 50 in the evening and
monitors everything he does.
I think you should smell theroses, not analyse the damn
things.
But, andrew, can I say mate,every time I have a chat with
you it's just a great pleasurefor me.
(42:37):
You do a wonderful service toeveryone who listens to you.
You're incredibly intelligentand eloquent and I really love
talking with you.
So thank you very much, mate.
Speaker 1 (42:47):
Ross, thank you so much.
Thank you, that's made my day.
And thank you once again, drRoss Walker, for joining us
today, and I really do.
Every single time this man Iattend his lectures or his talks
, I'll learn something of valuefor patients.
It's a brilliant man and hequestions everything.
I love you, so thank you somuch for taking us through the
(43:09):
benefits of ubiquinol today and,of course, everybody, thank you
for joining us today.
You can catch up on all theother podcasts and on the
Designs for Health website.
I'm Andrew Whitfield-Cook.
This is Wellness by Designs.
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