So thanks for having me and thanks for all the time you spent with us.
Chris (00:33:28): You're welcome. Thanks for coming on.
So I got a new client who got a heart attack five years ago and got diagnosed with FH,
and has been put on statins ever since and now she developed type two diabetes on top.
The doctor has said the dosage of statins should be so high to keep her LDLc below 50 milligrams
per deciliter. So my questions would be first- 15? One five?
50. Five zero. 50, okay.
Would you agree with that? That it's really necessary? Second question would be, is there a
functional medicine way to deal with FH without going the way of statins
and what would be your best strategy to lower insulin without rising the LDL-C?
Yeah. Okay. So first of all, just to... I know you know this, but just to preface
this with a disclaimer. I am not a doctor and not a cardiologist by any means and so
anything I say in this case is just my opinion and should be taken as such. So I think
that... And I wouldn't change anyone's medication on my advice ever, but my personal opinion is that
I think what they're doing is they see this as using the precautionary principle.
And so I think there's the general perspective that there's no point in having LDL-C
be any higher than 50; therefore, since it doesn't matter, let's provide a sufficient margin of
error where we're real confident that getting it down to 100 is great and so why
not get it down to 50? If there is any extra protection we get it and we don't lose it.
I don't believe in the "lower is better and there's no point in having cholesterol higher
than X" attitude. I'm sure they would critique my point of view as follows. I would point out that
there is evidence that having your total cholesterol below 160-ish or so
is bad for neurological health, and I believe they would counter that
the evidence isn't that great. And I agree with that, but that's because there's been
obscene amounts of money poured into researching how you can get CVD down by lowering cholesterol,
and there's been almost no money poured into researching the neurological consequences of
having cholesterol below a certain point. So I don't think it makes any sense whatsoever
to base the totality of your view on what has been researched when the reasons for
having more confidence in one point versus another is based purely on one being under-researched.
So my point of view would be, I would personally rather use a more conservative
target of lowering down to 100 or so where the confidence is actually really high,
because I'm not convinced by the lack of confidence that there's no neurological
downside to pushing it twice as low as that. So that's my general perspective and if this were me,
and it'll never be because I can't for the life of me get my total cholesterol
above 160, but if it were me I'd be lowering my dose on that out of precaution on the other side.
Now, the other part of your question is what else could you do? And... Oh, and I would note that...
I imagine a lot of people listening already know this, but CoQ10 and MK4 would be two critical
things to supplement with on the statins. So I do have a podcast on what to do about heterozygous
familial hypercholesterolemia. So if you Google my name "masterjohn heterozygous FH" or something
like that you should get that podcast up. There's a short one I did on Chris Masterjohn Lite, but
there's also a longer one that's an hour long... and actually I should bring in the chat here.
Someone was saying in the chat that FH is well addressed with PCSK9 inhibitors,
even in the absence of statins. And yeah, that's true. PCSK9 nine inhibitors though apart
from costing $140,000 a year in total healthcare burden to insurance and whoever's paying for it,
PCSK9 inhibitors are not without their side effects. I've had clients come to me
who had extreme exercise intolerance that was directly precipitated by going on PCSK9 inhibitors
and no one could do anything for it. So whatever you think might be a potential side effect of
statins, I don't at all think PCSK9 inhibitors, which do literally the same thing. Well, actually,
that's not true. Not literally the same thing. They do literally the same thing in terms of
how they lower cholesterol by increasing the LDL receptor, but they're... So consequences of
mevalonate inhibition like decreased synthesis of CoQ10 and MK4 are going to be different,
but consequences of lowering LDL cholesterol are going to be the same.
But anyway, so dietarily, I think that the best thing that you can do is, first of all,
do a dietary experiment to see what are the most sensitive things that control cholesterol levels
in that person. And most likely those are going to be either saturated fat or dietary cholesterol
although you could screen for other problems. So inflammation is a factor. Thyroid health
is a factor and so on, but assuming all those other ducks are in order,
this person's eating decently and has a good microbiome, they have a healthy thyroid level
and they don't have a systemic inflammation problem driven by something besides this issue
then assuming that, you're probably going to find that are very responsive to dietary cholesterol,
whereas you might expect that most people wouldn't be. But I think people with FH are generally going
to be much more sensitive to dietary cholesterol and they are probably very responsive to saturated
fat, particularly if they have... If they are sensitive to increasing their cholesterol output
in response to saturated fat, then their blood levels will probably be responsive because
remember in someone with FH the problem is they're not clearing it from the blood. So anything that
gets into the blood in the first place, it is going to not be cleared as effectively.
So dietary cholesterol, yeah, it might have the feedback loop of suppressing cholesterol
synthesis but it's still making it into the blood, and if you can't clear it from the blood,
it's going to be a factor. Saturated fat, whether it boosts cholesterol is going to depend on other
genes involved in cholesterol synthesis, but if it does, they're going to have trouble clearing that.
So although I'm not a big fan of restricting saturated fat and cholesterol from a nutrition
perspective, I think if your goal is to treat FH without statins or PCSK9 inhibitors,
then most likely you're going to have to go on a low fat, low... Oh, that's the other thing.
In general... So the molecular biology behind this is complicated, but carbohydrate and insulin
act as PCSK9 inhibitors in people who are insulin sensitive and act as PCSK9 stimulators in people
who are insulin resistant. And that relates to the fact that in people with insulin resistance,
they generally have selective hepatic insulin resistance,
which makes the lipid synthesis pathway in the liver not resistant
and the carbohydrate-metabolizing pathway in the liver resistant.
So the person winds up with hyperlipidemia that gets worse with carbohydrate because the
lipid synthesis pathway is not resistant and with hyperglycemia in response to carbohydrate because
the carbohydrate-metabolizing pathway is resistant. If you look at those pathways,
that basically works out so that the mix of those responses to insulin lead to PCSK9 inhibition when
things are working properly and leads to PCSK9 stimulation when things are messed up in that way.
So I think for someone who's overweight and insulin resistant
carbohydrate is not going to be a helpful thing,
but if they get those other things in line, and so they're lean, healthy body composition, insulin
sensitive, generally more carbohydrate is going to lead to PCSK9 inhibition. And on top of that,
more carbohydrate is going to lead to increased thyroid activity within the normal range.
So by shifting the diet away from fat and toward carbohydrate, you are going to get more thyroid
activity, less PCSK9 activity. So a low-fat, low-saturated fat, low-cholesterol diet that is
rich in healthy, unrefined, whole-food starches is probably going to be the diet that's going to help
manage that most without a statin. And when I'm looking at that, that has obvious implications of
you're probably going to have to mostly clear out eggs. You're probably going to have to
mostly clear out dairy fat, and so other people might not think that's an issue at all. Whereas
in our circle, we understand that that has nutritional implications.
So there's a lot of things that you're going to have to compensate for, biotin and choline,
and so on and so forth because of the things that you'd have to clear out of the diet in that way.
But "if you can achieve natural LDL receptor upregulation and PCSK9 inhibition with diet
and lifestyle, why not do that first?" is how I would see that.
Well, she's pretty lean for her age but the diet is very crappy. So
lots of processed sugars, lots of- Which means that there's-
... coffee. Very little protein. So my point was how do you raise really protein intake without
taking out all the meat and fat and probably getting her to consume too much carbohydrates?
Well, so I think you get protein up with lean proteins, and so that means like
white fish, poultry, and low-fat milk instead of whole eggs and full-fat milk and beef.
So that's... And again, that's not my standard dietary approach, but it has its place in the tool
belt and this is a case where that is relevant. And then carbohydrates, I think you want to cut
out the junk, but if you have someone who's got stable blood sugar and is metabolically healthy,
at that point, it becomes an advantage to increase the whole-food starches in that person, yeah.
Okay. Cool. Thank you very much. You're welcome. Thank you, Christian.