Chris Masterjohn: Hi, Lauren.
Lauren Davis: So, hi. My questions
relate to sunflower lecithin. Taking sunflower lecithin for fatty liver
problems. Chris Masterjohn:
All right. Okay. Lauren Davis:
And I kind of am wondering whether or not there's any data, or whether or not you have a sense
of how things change over a year of taking it, particularly in terms of imaging fat in the liver,
whether or not that just disappears or if it kind of alters how it's located in the liver. Also,
does weight loss happen after taking sunflower lecithin? And if so,
does that happen more likely at the beginning or at the end of the year, or unrelated? And also,
so it sounds like if you have dietary fat then your sunflower lecithin, if you're taking that,
would kind of be tied up in taking care of the dietary fat rather than taking care of the fat
that's stored in your liver. Is that correct? Chris Masterjohn:
Can you say that last part one more time? Lauren Davis:
Sure. So if a person is taking sunflower lecithin and they're also consuming
fat in their diet... Which, everybody's going to be consuming some kind of fat.
Chris Masterjohn: Right.
Lauren Davis: I guess I'm thinking more of like a keto
diet or something, where you might be consuming a huge amount of fat. Is that counterproductive?
Chris Masterjohn: Oh, you mean is that going to
increase the fat in your liver? Lauren Davis:
Or does the sunflower lecithin get tied up? Does it just
preferentially end up taking care of the dietary fat, and not getting around to taking care of the
fat that's been stored in the liver for too long? Chris Masterjohn:
Yeah, all right. I think that, so the second part of your question is a simple one, and I'll answer
that first. So first of all, it is the case that the sunflower lecithin will help you absorb the
fat from the diet. It is not the case that that then detracts from its ability to remove fat from
the liver, because they're both getting absorbed and then they can both get repackaged. However,
it is the case that fat will increase the amount of fat that goes through your liver, and
that will then put a tax on the amount of choline that's required to remove the fat from the liver.
And so if you think about the inputs of fat into the liver, you basically have...
Well, I should back up for a second and just say, so fatty liver is basically an in-versus-out
equation where out can then be further broken into two components. One is exported, and the other
is burned for energy. So some other people might prefer to phrase it as fatty liver equals fat in
minus the sum of fat burned and fat exported, or something like that. But the point is that there's
one way fat gets into the liver, and that's for fat to come in. And there's two ways to get rid
of it, one is to export it into the blood and the other is to burn it for energy. And so choline,
which is what the sunflower lecithin is giving you, is allowing fat to come out of the liver.
And then anything that would determine the rate at which the liver would beta-oxidize
fatty acids for energy would be another way that fat would leave the liver, if it's just combusted.
And so in terms of the ways that fat get into the liver, one is from diet and the other is
from the blood. The two ways to get fat into the blood would be, eat fat, it travels to the lymph
and then gets into the general circulation, or to release stored fat from adipose tissue.
If it's coming from the visceral abdominal fat it's opening directly into the portal vein and
going into the liver, and so that's much more pro fatty liver because all of it goes through
the liver. All of your other fat depots are releasing into the general circulation,
so the diet and the general circulation, the diet and the non-visceral fat pads are both releasing
fat into the general circulation before it gets to the liver. And so it's some portion of that
fat that gets into the liver, whereas the visceral abdominal fat pad is emptying directly into the
liver, so all of it goes into the liver. So if you put those risks in perspective,
the visceral abdominal fat pad is way worse than dietary fat, and it's way worse than all of the
other fat pads that can release it, because dietary fat and all the other fat pads are going
into the blood, circulating through the whole body. Only some of it's going into the liver.
Now, in terms of other dietary inputs, then you could compare that to protein or you could compare
it to starch or you could compare it to sugar, and then you can compare different fats. And among the
different fats, the ones that are more easily beta-oxidized are the least likely to increase
fatty liver. So MCTs are the least likely, or I mean really short-chain fatty acids and then MCTs,
because those are so easily burned for energy. The longer the chain and the fats, the long-chain
fats are, are going to increase liver fat more. Polyunsaturated fatty acids, although they are bad
for the progression of fatty liver from simple fat accumulation, which is called steatosis,
to oxidative stress and inflammation which is called steatohepatitis, or NASH,
and is what drives further disease progression towards eventually in a subset of people cirrhosis
and liver failure. Polyunsaturated fatty acids are bad for that progression, but because they
are more easily beta-oxidized for energy, they are less likely to increase liver fat than long-chain
saturated fats are. So there's basically a hierarchy of long-chain saturated fats,
and monounsaturated fats are quite similar, maybe a little bit less. Then long-chain PUFAs are less,
and then medium-chain fats are even less, and then short-chain fats are even less.
And then after that basically sugar is next, because sugar can be turned into fat. But
sugar is turned into fat at a very low rate, so in humans generally between one gram and 10
grams of carbohydrate are converted to fat per day. And if you eat a low-carbohydrate
diet and you're getting about one or two grams of carbohydrate converted to fat, and if you eat a
55%-sugar diet, you're going to push that up to 10 grams. But 10 grams of carbohydrate converted
to fat is very small compared to what even someone on a low-carbohydrate... I mean on a
low-fat, high-carbohydrate diet is eating more fat than 10 grams. So converting sugar to fat
is never anywhere near as important as dietary fat, because the only exception to that rule
is when your total carbohydrate exceeds your total energy expenditure. And the only time
that ever happens is in a hotdog-eating contest, or a tribal fattening ritual.
So, no one... Even someone who's pigging out on ice cream is never going to eat more carbohydrate
than the total amount of energy that they needed for that day, because they have other things in
their diet. I mean, even ice cream, right? Only a portion of that is coming from the sugar.
And so if you look at, if you think of the sunflower lecithin as providing choline
that is meant to export fat from the liver, then the way that that is getting taxed is by
increasing the amount of fat in the liver. And so any fat from the diet is going to be the principal
thing in the diet that is increasing liver fat. ... the principle thing in the diet that is
increasing liver fat, even though it's not anywhere near as bad as the abdominal fat pad,
and even though there are other things, such as sugar. Protein in the diet is generally
going to increase the amount of choline that you have, because some of it is synthesized
from protein, not just gotten from the diet. So, generally, protein is anti fatty liver. And in
fact, old animal experiments from the first half of the 20th century showed that protein, sulfur
amino acids, and choline were the three things that would totally cure fatty liver, whether it
was caused by alcohol, sugar, or fat. And that's because protein provides sulfur amino acids,
sulfur amino acids synthesize choline, choline is choline. And so if you provide the precursors or
the choline, that's the anti fatty liver effect. Starch is neutral. Sugar is slightly pro fatty
liver. Fat is pro fatty liver. Long-chain saturated fats are the most pro fatty liver. And
short-chain and medium-chain fats are the least. Polyunsaturated fats are in the middle.
When I say pro fatty liver, I just mean that in the equation of fatty liver equals fat in minus
the sum of fat burned and fat out, then that's increasing the fat in part of the equation.
But as long as you are increasing the other parts of the equation, fat burned or fat exported,
then you don't wind up with fatty liver, if that sums to zero or negative. Right? So
if that sums to zero, your liver is as fat as it is currently and it doesn't change.
If that equation sums to negative, then you're reversing fatty liver over time.
Now, in terms of how long that would take, that all depends on how negative that equation is.
Right? So if fatty liver, I should say fatty liver progression or the delta of fatty liver, equals
fat in minus the sum of fat burning plus fat exported. If delta fatty liver is .01% per day,
then it's going to take you a lot longer to reverse fatty liver than if
delta fatty liver equals negative 30% per day. And so I wouldn't want to be on 30% per day because
that's too much stress on the body, to move anything in that quantity, that fast.
But the point is that it could take weeks to reverse fatty liver, it could take years,
depending on how negative that equation is. And if you look at studies that revert,
that's caused fatty liver by withdrawing choline from the diet, or like on TPN, where they caused
fatty liver by not having choline in the TPN and reversed it, you're generally looking at it taking
weeks to reverse fatty liver, or cause it, if you are kind of putting the pedal to the metal on that
dietary change that you're making. Lauren Davis:
What's TPN? Chris Masterjohn:
I'm sorry, total parenteral nutrition, or TPN, is when you are fed a diet completely
intravenously. And that's done when there are extreme situations where you're unable to eat.
Lauren Davis: Okay. And anything about imaging
the liver, its fat and liver. Chris Masterjohn:
Yeah. I mean, those studies are based on imaging the liver. And so in studies where
imaging the liver was an endpoint and they set the threshold that whatever they set it at, probably
5% or something like that, then in a matter of weeks, you can change the imaging to have more
fat or less fat, and you can cross that threshold. Now, crossing that threshold obviously depends on
how far you are away from that threshold as well. So if you say greater than 5%
represents some steatosis, and you've gone to 7% in three weeks, it's probably going to take
you three weeks to get back to under 5%, by just reversing whatever dietary change that was. If you
push that to a much higher fat percentage, it's going to take longer, obviously.
But if something is taking longer than a matter of weeks to show any change on imaging,
it is either working very slowly or it's not working. And it would be... If it is working,
it's working more slowly than you want it to, if you're expecting to see a change and you don't.
Lauren Davis: Okay.
Chris Masterjohn: The other part of your question was, "Is
dietary fat detracting from it?" It's not that you can't eat dietary fat and reap the benefits of it,
but you are raising the choline requirement when you have more fat in the diet. And other animal
experiments that were done many decades ago, there was one that showed that if you feed an animal
butter or corn oil, you're increasing the choline requirements substantially when you feed butter.
And even though butter is probably good for you, and even though corn oil in the context
of fatty liver actually causes animals to go from simple steatosis to NASH, which is
going from a predisposition to a disease state to an active disease state, it is still the case that
corn oil, because its PUFAs is beta-oxidized at a higher rate than saturated fats.
And so in the equation of delta fatty liver equals fat in minus some of fat burned plus fat exported,
it's fat in, but it's also amping up the fat burned part of that equation more than the
butter is. And so what you see is it requires a higher choline intake to prevent fat accumulation
in the liver there. And so it's just a matter of the relative balance of those things. So, yeah,
I think a high fat diet is going to require considerably more choline to export
the the fat from the liver. Lauren Davis:
Okay. And just incidentally, does any sort of a supplement that is called phosphatidylcholine,
if one needed to take something other than sunflower lecithin for a while,
should it react the same, if you're gauging your dose on how much choline
is in it? Chris Masterjohn:
Yes, but you want to keep in mind that, whereas in the past I've stated that sunflower lecithin
has roughly the lecithin of an egg yolk, which is like 136 milligrams of choline,
if you're using a capsule that says the amount of phosphatidylcholine on it, you have to...
Basically 8% of that is choline. Lauren Davis:
I think it's 15%. Chris Masterjohn:
Is it? Lauren Davis:
I thought you had said 15- Chris Masterjohn:
Yeah, yeah. You know, you might be right. I defer to what I said before. I might have been switching
around what you multiply by versus what you divide by. So, whatever it says in the Cliff Notes is the
right one. Yeah. Lauren Davis:
All right. So, as long as you calculate it based on the amount of choline, then you can substitute.
Chris Masterjohn: Yeah, yeah,
yeah. Lauren Davis:
Thank you so much. Chris Masterjohn:
You're welcome, Lauren. Thank you for your question.