Episode #206
In this Fasting Q&A episode, hosted by Coach Lisa Chance, Dr. Jason Fung answers questions from the TFM Community:
- Are there common strategies that help to avoid the common pitfalls of Ramadan, like late night eating, overeating, or accidentally doing OMAD for too long and slowing down the metabolic rate? [01:07]
- Concerns about off-label use of GLP-1s. Some medical professionals seem to be prescribing GLP-1 medications for anti-aging/longevity purposes in people who aren't overweight or diabetic. What do you think about the trend of “microdosing” GLP-1s as a preventative health measure? [02:36]
- Are there further short and long-term side effects of GLP-1s coming to light? [06:36]
- Are there ethical concerns around supply issues with GLP-1s due to increased demand from off-label use? [ 10:12]
- Are there bioethical concerns about GLP-1s that doctors should be discussing with patients? [12:03]
- Can you address how people with Type 1 diabetes can develop insulin resistance similar to those with Type 2, sometimes referred to as ‘double diabetes’? [16:21]
- How concerning is an elevated Lp(a) and how can you lower it? [20:47]
- Do you know of research or trials with fasting to reduce prostate size? [26:28]
- Can someone who is considering kidney donation fast/fat fast? [29:08]
- I'm seeing many reputable sources saying that the claims against seed oils aren't actually based in the science. I'm curious whether Dr. Fung's opinion has evolved on this? [30:51]
Links
A Conversation with Dr. Tro Kalayjian
https://youtu.be/2Vuhip2UlTs?si=fxHBpgNkcI65SOrV
Cholesterol Ration Calculator - Omni Calculator
https://www.omnicalculator.com/health/cholesterol-ratio
Please note that you need to be a member of the TFM Community to submit questions to the Q&A webinars with Dr. Fung but you can submit questions to our regular Q&A episodes here: https://bit.ly/TFMPodcastQs
Transcripts of all episodes are available on the Podcast page at www.thefastingmethod.com
Sign Up to the How to Fat Fast Masterclass with Dr. Nadia Pateguana here:
https://www.thefastingmethod.com/masterclasses-and-live-workshops-2025/#FFMC
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Summary Timestamps
00:00 Intro
01:07 Fasting Strategies for Ramadan
02:36 GLP-1s for Off-Label Use
06:36 Side Effects of GLP-1s
10:12 Ethical Concerns with GLP-1 Supply Issues
12:03 Bioethical Concerns GLP-1s
16:21 Type 1 Diabetes and IR
20:47 Lp(a)
29:08 Kidney Donation
Mark as Played
Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
(00:00):
The most powerful predictor,
the strongest association, by far
and away is the HDL and triglycerides.
And that is the one that is the
most affected by diet,
specifically, carbohydrates.
So, if you reduce your carbohydrate
intake, you can reduce your triglycerides
(00:20):
and raise your HDL, which is extremely,
extremely powerful in predicting
heart disease. [music]
Hello everyone, my name is Lisa Chance
and I'm a fasting coach here at The Fasting
Method, and we are here today with our very
own Dr. Jason Fung for our monthly
(00:42):
Q&A.
This is a monthly Q& A with Dr. Fung
where he answers questions submitted
by our TFM Community members.
Hello to our podcast listeners that will be
able to listen to this a few weeks after
our Community members.
All right, so I'm going to dive right in.
Good morning, Dr. Fung.
Hi. Good morning.
(01:03):
It's great that you're here.
I've got several questions for you.
One is, "Are there common strategies that
help to avoid the pitfalls of
Ramadan (01:12):
late night eating,
overeating, or accidentally doing OMAD
for too many days in a row
and slowing down the
metabolic rate?"
I mean, just the usual precautions you
have to take about overeating.
The main thing is-- you know, a lot of people
during Ramadan, you don't eat during the day
(01:32):
and then you eat at night.
So what happens is that some people tend to
prepare a huge meal and stuff, which is
sort of one of the big pitfalls, right?
Because if you're not eating during the day,
you're allowing your body to use up the
calories, but then eat a huge meal at night
with lots of sugary stuff and
refined foods and so on, then you're sort of
(01:52):
undoing a lot of the good.
So you want to eat as normally as
possible. So it's the same idea,
like, just try to make it a routine.
And the good thing about doing it for a month
is that, if you can do it for month, then it
sort of establishes a new habit.
Eating late at night is not a great
idea anyway, so it's good to
try and keep that as low as possible because,
(02:13):
of course, you eat all that and then you go
to sleep. Well, what is your body gonna do
with it, right? It's difficult for it to do
anything other than store it, which is a
problem.
That's my pitfall.
When I eat late at night, Dr. Fung,
that's when I gain the weight.
And when I stop eating late at
night, that's when I lose the weight, so
it's, for me, it's a big one of the five
(02:35):
pillars.
This next person has several concerns
about the off-label use of
GLP-1 receptor agonists.
And I broke it down.
It was a long question, and so I broke
it down into five points.
So I'm going to address them one at a time
and have you answer or comment on them.
The first one is, "Medical professionals
(02:57):
are using and prescribing these medications
for anti-aging or longevity
purposes in people who aren't overweight
or diabetic.
Do you have a comment on that?
"
I don't know that there's a lot
of data on that.
So the whole of longevity medicine,
honestly, has very little actual
(03:18):
evidence.
There's a lot of potentials,
but it's very hard to do studies
because you don't want to treat somebody
who's 40 and then follow them for the next
40 years to see whether it worked or not.
So it's just difficult to do
studies on it, which leads to a lot of
people saying, "This is great for longevity,"
(03:39):
but, you know, most of the time
it's like they're either trying to sell you
something or just trying to get you to do
something else. So if they're saying, "Oh,
we're doing it for longevity," then you
really have to be a little bit more careful
about what the claim actually is.
There are some studies-- you can do a
biological age which is this sort of
(03:59):
artificial measure of what your age is,
and you see this on social media sometimes,
you know, there's a few of these longevity
experts and so on.
And what they do is try to do this biological
age and see if it reverses.
There's some data with fasting,
specifically the fasting mimicking diet.
So the way they do the fasting is sort
(04:19):
of a five-day, modified fast once a month.
And then there's data that you can reverse
that. But with GLP-1s, I haven't
seen any of the data that says that it
reverses biological age.
But keep in mind, too, that, you know, it's a
surrogate end point, right?
So they do a bunch of measurements, and,
from that, they interpret what your age
is, but it doesn't actually
(04:41):
mean that's going to translate into a longer
life or whatever.
So it's better than nothing, I suppose,
but the GLP-1 agonist,
could it work? I don't know about the
microdose. I mean, I think a lot of the
issues are driven by hyperinsulinemia.
So if you're taking a regular dose
of GLP-1s, I think that if you
(05:02):
have hyperinsulinemia, then
it's going to be better, right?
So this is the thing, right?
So GLP-1s, they suppress your appetite,
they reduce insulin because you're not eating
much. When you eat, insulin goes up, so,
therefore, if you eat less, insulin is going
to go up less.
So it's a great drug to reduce
hyperinsulinemia, which is the same
thing as insulin resistance.
(05:22):
If you look at the prevalence of
hyperinsulinemia in U.S.
adults, it's probably like 50 or 60%.
It's probably higher actually.
So therefore, since most adults have
hyperinsulinemia, when you treat somebody,
when you treat an unselected
population with a drug that lowers insulin,
since half of the people probably have too
(05:43):
much insulin, you're actually gonna see a
benefit. So could it work? Absolutely.
And this is why you're starting to see a lot
of this data with GLP-1s,
in terms of renal protection, in terms of
heart protection. So they'll say, "Oh, it
reduced heart failure, even people without
diabetes." It's like, yeah, because they had
hyperinsulinemia, which is a much earlier
stage than full-on
(06:04):
type 2 diabetes.
So could it work?
Absolutely. I just don't know that there's
any data in it.
So I don't see any problem if you
want to do it, but, again, I would be
careful. If, for example, you measure your
C-peptide, or hyperinsulinemia, or
pre-diabetes, or have one of these measures
that you're really sure that insulin is high,
(06:25):
then lowering it makes sense and that would
be expected to, you know, make you better.
You covered the second question here which
is on preventative health so I'm going to go
to the next one which is, "Potential unknown
short and long-term side
effects - are more coming to light?"
There's more coming to light because
more people are using it.
(06:47):
There have been certain rare--
so there are rare side effects, right?
And you don't see those until you start to
put them into widespread practice.
So there's been a few that have been
mentioned in the news.
What Ozempic does is basically slows down
how quickly your stomach empties,
right. So it slows everything right down.
(07:07):
So some get bad constipation, for example.
And by slowing it down, you keep people
from feeling hungry because the stomach is--
everything's just sort of sitting in the
stomach, right? So you feel full, you can't
eat. So that's how it works.
The problem is if it goes too far and
you get complete stasis (that is your
colon, your stomach is not moving), it can be
(07:27):
actually dangerous, could be a
life-threatening situation.
So there's been case reports of that.
And there's also been, I think something
like 86 deaths that have been
reported due to side effects of Ozempic.
I saw that in one of the newspapers in the UK
[claim made by The Times].
So keep in mind that, when you compare that
to the millions of people who are using it,
it's still a reasonably safe
(07:50):
drug, but it's not free
of side effects.
So this is the thing you have to keep in
mind. If you have a disease where you're
going to be expected to benefit,
so if you have diabetes, you have
pre-diabetes, if you have hyperinsulinemia
(which is a lot of people), there's a good
reason to think that that will improve
things. Then you can take the risk of
side effects, right? And they're relatively
(08:11):
rare. If you're just using it--
you know, if your 20 years old and just
trying to lose a bit of weight, which is
where we're seeing a lot of the growth and
people using it, right?
"Oh, I need to lose five pounds because I
want to look better." So giving the Ozempic.
Well, then it doesn't make sense because
you're treating a lot of people who are not
expected to benefit, so the risk-benefit
ratio really changes and it's more risky
(08:33):
than anything else.
So, you know, short and long-term side
effects, yes, there's a lot of side effects.
That's already known.
There's rare, serious side effects that
we're starting to find out, but, in general,
it's a relatively safe medication.
I think it was in the UK, I'm not sure where,
there was a ophthalmology
clinic and they noticed that
(08:55):
their people were getting blindness and
then the common factor was that they
were all on a GLP-1.
I'd have to do more research on that.
I can't even quote where it was.
I don't remember if it was the United States
or UK or what.
[music]
[promotion] Hi, this is Dr. Nadia and I am so
excited to be hosting the Fat Fast
(09:16):
Masterclass once again.
This is a three-day masterclass.
On day one, we will be talking about what
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On date two, I will go over
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I will be giving you an
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(09:36):
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be finally talking about when to fat fast.
I will also be with you for three
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as join you in the exclusive
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I am so excited to go over
(09:58):
what to eat with you, and why
fat fasting is the most appropriate
fast-mimicking diet.
See you there! [music]
The next part of this question is,
"What ethical concerns are
there around supply issues?
People with diabetes or obesity,
the struggle with that due to increased
(10:21):
demand for off-label use."
Yeah, this was a bigger issue probably a year
ago. So there wasn't enough for
the people who used it for
diabetes because all the people were
using it for weight loss.
So they allowed, I think, some of the
compounding pharmacies to make GLP-1s
and stuff. It's more or less over.
(10:43):
So about a year, year and a half ago,
I had people who would come back and they
would say, "Oh, my pharmacy said they're out
of it," so they just couldn't get it, but I
haven't heard that for like six months.
And the reason, of course, is that
the drug companies make a lot of money by
selling drugs, and you can only sell a lot
drugs if you make a lot a drugs.
[laughs] So they've invested very heavily
(11:03):
in making these drugs available.
And so that concern was
an important one, but it's probably
mostly faded now.
I think anybody who wants it can
more or less get it.
The bigger issue is the cost of the
drug. You know, they're making huge profits
on it. So is that ethical?
(11:24):
I mean, that's a different debate, as opposed
to availability.
The availability part is more
or less solved. And honestly, I think it's
only gonna get easier to get the drug from
here. We have-- there are newer drugs.
There are other companies jumping into the
space.
So, you know there's Ozempic, there's
Mounjaro, but every
(11:44):
company [laughs]
practically every drug company on earth is
looking to bring their own out, right?
It's sort of like how statins did and,
you know, every company had their
own statin. Eventually, one or two
will end up being used heavily and
that's about it.
And the last part of this question, "What are
the bioethical considerations that
(12:06):
doctors should practice when discussing
going on a GLP-1 receptor with
a client, with a patient?"
You know, I think it's all about risks
versus benefits.
And I think that certainly it's
a reasonable drug in
a lot of cases, so
(12:26):
type 2 diabetes and so on.
It's better than insulin, for example, right?
So it's a much better drug in terms of how
it's used. It causes weight loss as opposed
to weight gain. So it's a lot better than in
insulin, right? But, on the other hand,
if you're not using it for those reasons,
then what's the risk-versus-reward benefit?
The other thing, of course, is the weight
regain, right?
So if you take it, you lose weight.
(12:49):
If you stop it, all that weight comes back.
So if you're going to take it for the rest
of your life, like some of these type 2
diabetics will-- obviously, diet
is the best thing, if you can.
If you can't, then it's still better than
not taking it, right?
But are you gonna take that for the rest of
your life? So this was the big thing
about the pediatrics.
(13:10):
So it sort of blew a lot of
people's mind that the American Academy of
Pediatrics basically said you should
consider it for anybody over 12.
I'm like, what, you're gonna put a
12-year-old on drugs for the
rest of his or her life?
Are you serious?
That doesn't make any sense at all.
And they had some rationale, but
(13:32):
most of the rest of us were like, man, they
must have been donating a lot money to the
American Academy of Pediatrics [laughs] to
get that kind of endorsement.
And of course the problem is that there
were no studies saying that it was
useful in children in any way.
So they basically made it up,
you know, and pretended it was supported by
(13:53):
evidence when it wasn't.
So, yeah, the ethical concern is mostly
around people who don't have a
good indication for it,
because everything's risk versus reward.
So say you take it, you're 15 years
old, you take and then you stop it.
You know, what good have you actually done?
Like, have you gotten any good?
(14:13):
And if you haven't gotten any health benefit,
could you have used that money that you
spent on Ozempic,
on, you know, weight-loss programs,
or-- you know, there's a huge amount of other
things you can do - exercise programs,
gym memberships, right?
So there's huge amount of other things you
could do with that money instead of
(14:35):
drugs, right? You can try and do-- you
know, get people counseling, you can get them
cognitive behavioral therapy.
There's so many other things that are useful,
that take time, that take money.
And if you're taking it away, there's an
opportunity cost that's taken away.
So, yeah, absolutely. I don't think that it's
the right answer in every single case.
I think that it does help a lot of people,
(14:57):
but it's-- at this point,
in that sort of-- we just way
overused it in people.
Like, you take the group of people
who benefit, and you extrapolate it to the
entire population, right?
And it's like there's no benefit when you
give it to everybody. Anyway...
I have several clients that are on it.
And I like what Dr. Ben Bikman
(15:18):
has said, which is when you use it as a
bridge. And so they use it is
a bridge and they practice the things
we teach (which is time-restricted eating and
no snacking, getting your insulin
down, learning how to fast), and
then they can make that transition on over
because they've changed their lifestyle, and,
as you said, addressed these
(15:40):
cognitive behavior issues.
Exactly. That's exactly how you should think
of it, because you
learn all this stuff, you build in
the healthy habits that are now going to
sustain you, then you gradually pull
back. And then you don't have that weight
regain once you do it.
That's a very reasonable thing
(16:01):
to do. It makes a lot of sense to me.
But if your whole game plan is
take this drug for the rest of your life
(and sad to say, that's like 95%
of doctors, that's how they prescribe it),
then, no, it's not that useful for
people.
Thank you, Dr. Fung.
This is my question.
[laughs] I slipped one in here.
(16:21):
In the March issue of 'Diabetes,
Obesity, and Metabolism', they had an
article entitled 'The Rise in Prevalence
of Obesity in Youth with Type
1 Diabetes'.
And it got me thinking, all
right, would you address how type 1
diabetes can develop into insulin
resistance similar to type 2 diabetes,
(16:44):
sometimes referred to as 'double
diabetes'.
Yeah, that's a good question.
So type 1 diabetes is,
in a matter of fact, opposite of type 2
diabetes. So type 1 diabetes is too little
insulin, type 2 diabetes is too much insulin.
What's striking is that the
prevalence of type 1 diabetes,
(17:05):
not just in kids, but also in adults
too, has gone up substantially
in the last few decades.
It used to be extremely rare.
So if a kid had diabetes, it was almost
always type 1 diabetes.
Now it's sort of half and half type 1 and
type 2. And that's only because type 2 has
gone up so much.
Type 1 itself has actually gone up but
(17:27):
not as much as type 2.
But the question is why?
So type 2 is a dietary disease.
It's often related to carbohydrates and
refined foods, but type 1
is an autoimmune disease.
So it's your own immune system that's
attacking the pancreas and, therefore, not
producing enough insulin.
So why is that going up?
That's a good question.
(17:47):
Nobody really knows the answer to that.
It's the same as, say, gluten sensitivity,
celiac disease. That's also an autoimmune
disease, the prevalence of which is going
way up. And some people might say, "Well,
it's just because you're recognizing it
more." And for celiac disease,
no, it is not because they've done a study
where they went back into some old
blood work that they had on people.
(18:09):
I think they were in the Korean War or
something like that. They drew everybody's
blood. They had archived it. They tested it,
and, sure enough, there just was not a lot
of celiac disease back then.
And now there is, right?
So that's why gluten-free is a much bigger
thing because a lot people absolutely
do suffer from this.
Same as type 1 diabetes, it's a real
increase. So for some reason, there's
(18:31):
something screwing up the autoimmunity
and nobody really knows what it is.
So type 1 is going up.
The thing about type 1 diabetes is, if
you look at a normal person,
a normal person produces probably
around 15 units of insulin per day.
So a type 1 diabetic who's newly diagnosed,
he only needs a bit of insulin, like 10, 15
(18:52):
units a day. The problem is, over time, they
develop insulin resistance.
So then they need not just 15, they need
20, 30, 40, 50, 60, 70
units. And they keep getting all type 1, but
they actually have both type 1 and type 2.
So they have type 1 because their own
pancreas produces no insulin, but they
have type 2 because, with all that exogenous
(19:13):
insulin, they actually have hyperinsulinemia.
So remember what insulin does is it tells
your body to store sugar,
you know, store calories, tells you to store
it as body fat or store as sugar, like
glycogen. And if you're taking too much
insulin with too much sugar over time, even
if that insulin comes from the
injection as opposed to your own pancreas,
(19:34):
you do get this insulin
overload, which is type 2 diabetes.
So now you have type 1 diabetes and type 2
diabetes, which is double diabetes.
So in a sense, you have both type
1 (which is increasing over time
for an unknown reason), you have type 2
(which is increasing for a dietary reason),
and then you get that double diebetes.
It's just all over bad.
(19:56):
I've been working my way through your
interviews, your conversations with
The Fasting and Longevity Summit 2.0.
I noticed you're not called Brad anymore!
[laughter] So congratulations on
that, fixing that with YouTube.
Yeah, that was something!
But I loved your interview with Dr. Tro,
and I can't say his last name.
(20:17):
He talked about the type of calories
that we're consuming is what is
leading us to wanting more calories,
usually a more problematic type of
calories also.
So I'm going to put the link to that in
the podcast show notes, but he
also went on to address these things
like you were talking about - autoimmune,
(20:38):
etc. It was a really good interview.
I really liked that. It's so neat to see you
asking the questions.
This
person would like you to talk about Lp(a)
and how concerning is an elevation
in that lab level, how
to lower it, and is there a relationship
between the gut microbiome
(21:00):
and small-particle LDL?
So Lp(a) is
supposed to be-- so you know we measure, in
the cholesterol panel, the
LDL which is always considered the 'bad'
cholesterol.
Technically, it's not a great term, but, you
know, when it's high, that's what people
focus on. Then there's the HDL, which the
'good' cholesterol, which is-- again,
(21:21):
you want it to be high because it's good,
right? And LDL is bad because it is bad, so
you want to be low.
That's how the standard cholesterol panel
is set up.
It's not ideal.
So they do this lipoprotein (a), which is
really looking at a more specific
marker of the sort of bad cholesterol
particles. So, when you do association
(21:41):
studies, it appears to be more powerful than
the LDL, so it
may be useful. So can you lower Lp(a)?
There actually was a new drug that
just got tested, which showed that you
can actually lower it quite significantly,
right? So we're talking about0-- if you lower
LDL, so with statins, for example, you lower
everything (you lower LDL, you lower Lp(a),
(22:04):
you'll lower HDL too), which is probably why
it's probably not as good as people think
it is. So that's sort of interesting because
what you have to do is you have to lower the
Lp(a) and then see if they survive longer.
So they're only at step one where they've
given the drug and they're like, yes, we can
lower Lp(a).
Now, you have to say, "Does that actually
(22:24):
do any good?" Because remember, if you think
about the cholesterol panel, there's
three things. There's the HDL (the good
cholesterol), which goes with the
triglycerides. So triglycerides and HDL
is sort of their opposite, right?
So when triglycerides go up, when you
eat a lot of carbs, triglycerides go up and
HDL goes down, right?
So there's
(22:48):
the HDL/triglyceride, there's the LDL (whichis the statin), and then there's
the Lp(a), which is that new drug.
So the most powerful predictor,
the strongest association, by
far and away, is the HDL and triglycerides.
And that is the one that is the
most affected by diet,
specifically carbohydrates.
So if you reduce your carbohydrate
(23:09):
intake, you can reduce your triglycerides
and raise your HDL, which is extremely,
extremely powerful in predicting
heart disease.
What if you just give a drug to lower HDL?
Well, they've done that.
It lowers your HDL just fine.
The problem is that you die
more frequently.
(23:29):
So it did nothing, and why?
Because you didn't actually change your diet.
The HDL was just a marker of having a
good, low-carbohydrate diet, probably not
having all that hyperinsulinemia.
LDL... You know, we go on ad nauseam
about statins and LDL and
then Lp(a).
Does diet affect Lp(a)?
Not really.
(23:50):
Same as LDL, not really.
That's the thing about LDL and Lp(a)
is that it's like a drug maker's dream
because, if you have a high LDL, there's
almost nothing you can do from a dietary
standpoint to lower it.
So what do you have to do?
You have to take drugs.
All you have do is convince people that LDL's
the sort of 'be all and end all'
(24:10):
of everything, and then you can get
them to take drugs, because there's actually
nothing they can do.
Diet, lifestyle, exercise, I don't care what
you do, you probably won't change your LDL
much. The only way you can actually change it
is with the drugs, so it's a drug maker's
dream.
And the funny thing is that (I pointed out
on Twitter) there's been two studies
(24:31):
in The New England Journal of Medicine, which
is the most important journal in
medicine, actually, it's the most
prestigious.
One just a few months ago and one,
I think, last year.
And they looked at risk factors for heart
disease. So they looked at five risk factors,
basically, and they say, "What if we reduce
smoking? How many years of life
can you save?" and all this sort of stuff.
(24:52):
And the super interesting
thing is that all these things that
were important
(stopping smoking and all of this sort
stuff), all of them showed a
real benefit, but the one thing that
didn't show practically any benefit
was lowering of the LDL
cholesterol.
(25:13):
So this is that new study.
So I tweeted it out (let me just see when I
did that) April 2nd.
So if you stop smoking, you'll save about
five years of life.
If you have diabetes, if you get rid of it,
you'll save about four years of life.
If you control your blood pressure, about 1.3
years of life saved.
If you lower your cholesterol, you'll
actually lower your life expectancy
(25:35):
[laughs] by about 0.4 to 1.3
years, which is like insane.
So all these other things - stopping smoking,
diabetes, blood pressure control - they all
help you, but the one thing that doesn't help
you is actually lowering your cholesterol,
which is, like, wow.
I don't know why more people didn't
think, "Oh, this is really an important
thing," but nobody else seems to care
(25:58):
in the medical field, right, when you point
stuff out like this. Even when it's in The
New England Journal, it doesn't get any
traction because everybody's so brainwashed
and thinking that it's all about the LDL.
I'm not saying that statins have no place,
but I think their place has just been
like Ozempic, just been expanded.
Because you could treat it, it became
this sort of 'everything is
(26:20):
cholesterol' when it's like, you know, it's
only about, as a risk factor, it is like this
important compared to diet, which is much
more important.
Do you know of research or trials
with fasting being used to reduce
prostate size?
Also, is there a medical database
that this person could subscribe to
so they could keep track of
(26:42):
any research studies being done on that?
I don't know of anywhere that you can go.
The only thing I do is just, if that
specifically is what you want, search
it every so often.
The best place to search is PubMed.
What I would put in as a search term is
something like 'fasting', 'prostate size',
[unintelligible] 'PubMed'.
That way you don't get all the sort of other
(27:03):
stuff that other people write and you just
get the studies.
And they're pretty good.
PubMed has a lot of stuff, right?
So if there's any studies-- and they'll go
back, you know, many years.
There's not any that I actually know of,
because, remember, fasting hasn't had a lot
of data in it.
It's possible though.
I actually think that a lot of these may
require regular fasting.
(27:24):
So, you know, with fasting, there's this
whole thing about autophagy and, also,
you know, not just that, but insulin is
not just a metabolic hormone, it's
a growth factor, right?
So, if you have hyperinsulinemia, the thing
is that you may have a lot of these other
growth factors being increased.
And one of them could affect the
prostate size, obviously, because you
(27:46):
just don't want it to grow.
So if you have insulin, which is a growth
factor, and high insulin is going to lead
to more growth.
So, therefore, it makes sense that, hey,
this might be an intervention that was very
useful, but that's just a hypothesis.
I don't have any proof that
actually happens.
You know, on the other hand, if you wanted
to wait for the proof, [laughs] you might be
(28:08):
waiting, like, 20 years, in which case
you might not be worried about your prostate
at that point, right?
20 years is a long time to wait.
So the whole thing is that,
at some point, you have to say, well, either
you just go ahead and do it and hope for the
best, or you can wait for that data.
Because that data is-- it takes time,
it take money, it takes people who are
(28:28):
interested in fasting.
I mean, the initial fasting studies that were
done were just really bad.
They were like, "Oh, fast on one day
and eat double the next day." I'm like, okay,
but that's not gonna give you very good
results. Like, you don't have to be a genius
to figure that out, right?
You're not gonna do very well.
So, of course, they didn't do very well and
they said, "Fasting doesn't work." It's like,
(28:48):
no, you did it all wrong.
When are you supposed to allow your body to
use up your calories if you're just gonna
double up the next day?
So anyway, the whole point is that I would
just check it on PubMed (that's the best
thing to do) and then you'll find everything
you need.
I'm navigating this question carefully
because I don't want it to be a medical
question. But this person would appreciate
(29:09):
your opinion on somebody who's a
65-year-old woman who's considering
donating her kidney.
Would fasting or
fat fasting help around
that time period?
It can, but it doesn't affect the kidney
function so much.
So fasting is good for a lot of things.
The kidney isn't probably one of the ones
(29:29):
that gets affected a lot.
I mean, in chronic kidney disease, and we've
talked about CKD, there is
a study on chronic kidney disease and
fasting. It was from the fasting-mimicking
diet people, because, again, because they
have a product, they're actually more
interested in sponsoring research on it.
So a lot research has started to come out
from them. It does reduce chronic kidney
(29:50):
disease. Of course, it can reduce diabetes,
both of which are important. If you're going
to donate your kidney and you have
diabetes, you will get turned down right away
because people are like, "Well, you have a
diabetes, your kidneys will be at risk in the
future, so we can't take your one kidney
because you could need it in the future."
So it could help certainly around that
by reducing the sugars.
(30:11):
And then, again, if you have any kidney
disease at all, they will refuse to
take that kidney as well.
So it could be worthwhile to get those
sugars right down and also help to reserve
the kidney function.
And fasting increases your glomerular
filtration rate too, doesn't it?
I don't know if that would help with the
kidney transplant.
Yeah, I mean, some of the data is--
(30:33):
the glomerular filtration rate is basically
how well your kidney is working.
Most people are normal so it doesn't matter
how much you are filtrating.
But if it starts to go down, then,
when you get kidney disease, you'll see a
lower filtration rate.
And that's where fasting can sometimes help
with that, actually. So that can be useful.
And by the way, I get a lot of people who
(30:54):
send me articles for you to read.
That doesn't work that way, you guys.
[laughs] He's already read it.
But they were wondering if you had read
the latest article in The New York
Times about the processed
seed oils. It seems like this is coming
up for debate again.
And, you know, they're saying they have seen
(31:15):
multiple, reputable sources.
I personally question the
type of research that they're doing.
Is it questionnaire or
is it randomized control study?
Do you have anything to say about
seed oils being avoided, on account of
them being more processed, rather than
(31:36):
something like olive oil or butter?
Yeah, so this one
is actually an important
one because seed oils are highly,
highly processed, right?
The problem when you process stuff is that
you purify certain things, in this case,
the polyunsaturated fats, right?
And the problem with polyunsaturated fats is
that, because there's a lot of unsaturated
(31:58):
bonds, they're less stable than saturated
fats.
Because they're less stable, they're prone to
oxidation and stuff, which then, if they
become oxidized, then they could cause a lot
of inflammation. So everybody thinks they
could be highly inflammatory, which I
think is certainly possible, but it's always
hard to put a link one-to-one
with it. You can do studies linking,
(32:19):
say, linoleic acid and polyunsaturated
acids to certain diseases,
but, when you do it over large populations,
then everybody does it differently
(everybody's eating different seed oils and
stuff).
So you have a potential
mechanism which is plausible,
that is too much of this process
seed oils gives you too many unsaturated
(32:40):
which are unstable oils which leads
to increased inflammation.
So that's a very plausible hypothesis.
The problem is going from that
hypothesis to actual proof
is much more difficult.
It takes a lot of studies and
the studies are sort of like here and there.
So there are a lot of people who say that
(33:02):
eating a lot of vegetable oils is good,
and now there's a lot of people saying that
eating a lot vegetable oils is bad.
To me, it's very hard to
argue because the data is just so sparse
in terms of actual causal
data.
So it's hard to say that it's
true and it's hard to say that it's false.
(33:22):
So, in that case, I always
fall back and say, "Well, what's
the smartest thing to do for myself?"
The smartest thing would be to eat the
oils that have always been eaten.
So, if you look back, what have people
naturally eaten? What are the natural fats?
Olive oil has been used for thousands of
(33:43):
years, coconut oil has used for thousand of
years, butter has been used for thousands
years.
So those are what I eat.
Vegetable oils have been around since about
1900.
They really increased a lot
in the 60s, 70s,
80s.
Around the same time, you saw all these
autoimmune diseases popping up, right?
(34:04):
So is it plausible that
the seed oils are causing inflammation,
which is causing all these autoimmune
diseases, which is inflammation, right,
inflammatory diseases?
Yes, it's possible.
I don't know that it's true, but
what do I do?
Am I going to wait 20, 30, 40 years?
In 40 years, I really won't care.
(34:27):
[laughs] It'll be way too late for me.
So what do I do? I eat butter, I eat coconut
oil, I eat olive oil because those are
natural fats that I know people have eaten
for a long time, so I'm pretty
sure that they won't be harmful to me.
I'm not so sure that eating a lot of
vegetable oils is bad for me.
I actually think that there's two things with
(34:47):
vegetable oils. One, I try not to eat too
many. And two, I try not
to eat them in fried foods.
Deep-fried seed oils are probably the
worst thing you can do because the oil
is not stable, chemically stable.
Like there's-- you know, you can argue a lot
of things, but, if you look at saturated
versus unsaturated, unsaturated is
(35:08):
much less stable in heat.
So when you do high-temperature seed
oils, like deep frying your foods in
seed oils, if it's gonna be bad,
if the seed oil is gonna be bad, the high
temperature is gonna be like 10 times as
bad, right? So putting a little canola
oil in your dressing, I'll accept that
if I have to.
I try not to, I almost always use olive oil,
(35:31):
but deep frying in vegetable oils is
like super bad for you.
So when you go to McDonald's, when you got to
any of the other places, yeah, the deep
fried foods are probably bad for you, but it
might not have been the fat, it might have
been the seed oil and it might have been the
fact that it's deep fried.
So those are the things to really watch out
for. So, to me, it's like I can't make any
100%, this is what's true, this is what's
(35:53):
not true, but I can only say that
the smartest-- what I think is the most
logical path is to
avoid deep-fried seed oils,
definitely, and then seed oils
I try to limit, but it's not always
possible. Like, other people use it and,
you know, I'm not gonna say no, but if
you look at what's in my kitchen, I have
(36:15):
olive oil and butter for
practically everything.
I would use coconut oil, but my kids actually
don't like it at all, so they won't eat
anything-- it has a strong flavor.
I love coconuts, so I put coconut in
everything.
Me too. It helps my migraines too, I think.
I think it's because it's a saturated fat, I
think, it helps my migraines, but that's a
(36:37):
whole other story.
But really it's all butter or olive oil
in my kitchen, and I don't have any problems,
right? I deep fry-- I don't deep fry, I use
the air fryer more
and more just because it's a lot easier, but
I pan fry stuff and, you
know, they have this new olive oil that you
can pan fry in.
I do butter. I don't do high-temperature
(36:58):
cooking. You know, it's not that
hard, right, to get away from that almost
entirely.
I haven't bought vegetable oil in like 10
years.
I use avocado oil, also.
And what shocks me is I read some
of these studies and they're still putting
all these oils together,
like avocado oil and olive
(37:19):
oil, in with the studies of the seed oils.
And it's like no you need to separate those
out.
Yeah, I think avocado oil is fine too,
it's just that I'm so used to olive oil
now. There's a little bit of flavor with the
olive oil so I like that, and I think olive
oil is just more easily available,
but avocado oil it's great too.
But really it's-- to me, it's like, I'd
(37:40):
say 80%,
85% butter and olive
oil, almost everything that I
use is that.
Sometimes I use like the drippings from beef
and stuff (you know, you get the oil), and
then I save it actually to fry in it.
That's beef oil and whatever.
But again, it's a natural fat, so that's why
I save it. Or bacon oil, I'll save
(38:02):
it and use it again.
I use bacon oil too.
Even though I'm basically plant-based, I will
save the bacon oil, bacon grease.
[laughter]
Well, thank you so much, Dr. Fung, I know I
kept you over this time.
All right, you guys, see you next month.
The most powerful predictor,
the strongest association, by far
and away is the HDL and triglycerides.
And that is the one that is the
most affected by diet,
specifically, carbohydrates.
So, if you reduce your carbohydrate
intake, you can reduce your triglycerides
(00:20):
and raise your HDL, which is extremely,
extremely powerful in predicting
heart disease. [music]
Hello everyone, my name is Lisa Chance
and I'm a fasting coach here at The Fasting
Method, and we are here today with our very
own Dr. Jason Fung for our monthly
(00:42):
Q&A.
This is a monthly Q& A with Dr. Fung
where he answers questions submitted
by our TFM Community members.
Hello to our podcast listeners that will be
able to listen to this a few weeks after
our Community members.
All right, so I'm going to dive right in.
Good morning, Dr. Fung.
Hi. Good morning.
(01:03):
It's great that you're here.
I've got several questions for you.
One is, "Are there common strategies that
help to avoid the pitfalls of
Ramadan (01:12):
late night eating,
overeating, or accidentally doing OMAD
for too many days in a row
and slowing down the
metabolic rate?"
I mean, just the usual precautions you
have to take about overeating.
The main thing is-- you know, a lot of people
during Ramadan, you don't eat during the day
(01:32):
and then you eat at night.
So what happens is that some people tend to
prepare a huge meal and stuff, which is
sort of one of the big pitfalls, right?
Because if you're not eating during the day,
you're allowing your body to use up the
calories, but then eat a huge meal at night
with lots of sugary stuff and
refined foods and so on, then you're sort of
(01:52):
undoing a lot of the good.
So you want to eat as normally as
possible. So it's the same idea,
like, just try to make it a routine.
And the good thing about doing it for a month
is that, if you can do it for month, then it
sort of establishes a new habit.
Eating late at night is not a great
idea anyway, so it's good to
try and keep that as low as possible because,
(02:13):
of course, you eat all that and then you go
to sleep. Well, what is your body gonna do
with it, right? It's difficult for it to do
anything other than store it, which is a
problem.
That's my pitfall.
When I eat late at night, Dr. Fung,
that's when I gain the weight.
And when I stop eating late at
night, that's when I lose the weight, so
it's, for me, it's a big one of the five
(02:35):
pillars.
This next person has several concerns
about the off-label use of
GLP-1 receptor agonists.
And I broke it down.
It was a long question, and so I broke
it down into five points.
So I'm going to address them one at a time
and have you answer or comment on them.
The first one is, "Medical professionals
(02:57):
are using and prescribing these medications
for anti-aging or longevity
purposes in people who aren't overweight
or diabetic.
Do you have a comment on that?
"
I don't know that there's a lot
of data on that.
So the whole of longevity medicine,
honestly, has very little actual
(03:18):
evidence.
There's a lot of potentials,
but it's very hard to do studies
because you don't want to treat somebody
who's 40 and then follow them for the next
40 years to see whether it worked or not.
So it's just difficult to do
studies on it, which leads to a lot of
people saying, "This is great for longevity,"
(03:39):
but, you know, most of the time
it's like they're either trying to sell you
something or just trying to get you to do
something else. So if they're saying, "Oh,
we're doing it for longevity," then you
really have to be a little bit more careful
about what the claim actually is.
There are some studies-- you can do a
biological age which is this sort of
(03:59):
artificial measure of what your age is,
and you see this on social media sometimes,
you know, there's a few of these longevity
experts and so on.
And what they do is try to do this biological
age and see if it reverses.
There's some data with fasting,
specifically the fasting mimicking diet.
So the way they do the fasting is sort
(04:19):
of a five-day, modified fast once a month.
And then there's data that you can reverse
that. But with GLP-1s, I haven't
seen any of the data that says that it
reverses biological age.
But keep in mind, too, that, you know, it's a
surrogate end point, right?
So they do a bunch of measurements, and,
from that, they interpret what your age
is, but it doesn't actually
(04:41):
mean that's going to translate into a longer
life or whatever.
So it's better than nothing, I suppose,
but the GLP-1 agonist,
could it work? I don't know about the
microdose. I mean, I think a lot of the
issues are driven by hyperinsulinemia.
So if you're taking a regular dose
of GLP-1s, I think that if you
(05:02):
have hyperinsulinemia, then
it's going to be better, right?
So this is the thing, right?
So GLP-1s, they suppress your appetite,
they reduce insulin because you're not eating
much. When you eat, insulin goes up, so,
therefore, if you eat less, insulin is going
to go up less.
So it's a great drug to reduce
hyperinsulinemia, which is the same
thing as insulin resistance.
(05:22):
If you look at the prevalence of
hyperinsulinemia in U.S.
adults, it's probably like 50 or 60%.
It's probably higher actually.
So therefore, since most adults have
hyperinsulinemia, when you treat somebody,
when you treat an unselected
population with a drug that lowers insulin,
since half of the people probably have too
(05:43):
much insulin, you're actually gonna see a
benefit. So could it work? Absolutely.
And this is why you're starting to see a lot
of this data with GLP-1s,
in terms of renal protection, in terms of
heart protection. So they'll say, "Oh, it
reduced heart failure, even people without
diabetes." It's like, yeah, because they had
hyperinsulinemia, which is a much earlier
stage than full-on
(06:04):
type 2 diabetes.
So could it work?
Absolutely. I just don't know that there's
any data in it.
So I don't see any problem if you
want to do it, but, again, I would be
careful. If, for example, you measure your
C-peptide, or hyperinsulinemia, or
pre-diabetes, or have one of these measures
that you're really sure that insulin is high,
(06:25):
then lowering it makes sense and that would
be expected to, you know, make you better.
You covered the second question here which
is on preventative health so I'm going to go
to the next one which is, "Potential unknown
short and long-term side
effects - are more coming to light?"
There's more coming to light because
more people are using it.
(06:47):
There have been certain rare--
so there are rare side effects, right?
And you don't see those until you start to
put them into widespread practice.
So there's been a few that have been
mentioned in the news.
What Ozempic does is basically slows down
how quickly your stomach empties,
right. So it slows everything right down.
(07:07):
So some get bad constipation, for example.
And by slowing it down, you keep people
from feeling hungry because the stomach is--
everything's just sort of sitting in the
stomach, right? So you feel full, you can't
eat. So that's how it works.
The problem is if it goes too far and
you get complete stasis (that is your
colon, your stomach is not moving), it can be
(07:27):
actually dangerous, could be a
life-threatening situation.
So there's been case reports of that.
And there's also been, I think something
like 86 deaths that have been
reported due to side effects of Ozempic.
I saw that in one of the newspapers in the UK
[claim made by The Times].
So keep in mind that, when you compare that
to the millions of people who are using it,
it's still a reasonably safe
(07:50):
drug, but it's not free
of side effects.
So this is the thing you have to keep in
mind. If you have a disease where you're
going to be expected to benefit,
so if you have diabetes, you have
pre-diabetes, if you have hyperinsulinemia
(which is a lot of people), there's a good
reason to think that that will improve
things. Then you can take the risk of
side effects, right? And they're relatively
(08:11):
rare. If you're just using it--
you know, if your 20 years old and just
trying to lose a bit of weight, which is
where we're seeing a lot of the growth and
people using it, right?
"Oh, I need to lose five pounds because I
want to look better." So giving the Ozempic.
Well, then it doesn't make sense because
you're treating a lot of people who are not
expected to benefit, so the risk-benefit
ratio really changes and it's more risky
(08:33):
than anything else.
So, you know, short and long-term side
effects, yes, there's a lot of side effects.
That's already known.
There's rare, serious side effects that
we're starting to find out, but, in general,
it's a relatively safe medication.
I think it was in the UK, I'm not sure where,
there was a ophthalmology
clinic and they noticed that
(08:55):
their people were getting blindness and
then the common factor was that they
were all on a GLP-1.
I'd have to do more research on that.
I can't even quote where it was.
I don't remember if it was the United States
or UK or what.
[music]
[promotion] Hi, this is Dr. Nadia and I am so
excited to be hosting the Fat Fast
(09:16):
Masterclass once again.
This is a three-day masterclass.
On day one, we will be talking about what
is a fat fast and why is it so effective.
On date two, I will go over
how to fat fast with you.
I will be giving you an
omnivore fat fast list and a
(09:36):
vegan, plant-based fat fast
list. And on day three, we will
be finally talking about when to fat fast.
I will also be with you for three
live Q&A's where I will answer
all of your questions, as well
as join you in the exclusive
forum where we can chat daily.
I am so excited to go over
(09:58):
what to eat with you, and why
fat fasting is the most appropriate
fast-mimicking diet.
See you there! [music]
The next part of this question is,
"What ethical concerns are
there around supply issues?
People with diabetes or obesity,
the struggle with that due to increased
(10:21):
demand for off-label use."
Yeah, this was a bigger issue probably a year
ago. So there wasn't enough for
the people who used it for
diabetes because all the people were
using it for weight loss.
So they allowed, I think, some of the
compounding pharmacies to make GLP-1s
and stuff. It's more or less over.
(10:43):
So about a year, year and a half ago,
I had people who would come back and they
would say, "Oh, my pharmacy said they're out
of it," so they just couldn't get it, but I
haven't heard that for like six months.
And the reason, of course, is that
the drug companies make a lot of money by
selling drugs, and you can only sell a lot
drugs if you make a lot a drugs.
[laughs] So they've invested very heavily
(11:03):
in making these drugs available.
And so that concern was
an important one, but it's probably
mostly faded now.
I think anybody who wants it can
more or less get it.
The bigger issue is the cost of the
drug. You know, they're making huge profits
on it. So is that ethical?
(11:24):
I mean, that's a different debate, as opposed
to availability.
The availability part is more
or less solved. And honestly, I think it's
only gonna get easier to get the drug from
here. We have-- there are newer drugs.
There are other companies jumping into the
space.
So, you know there's Ozempic, there's
Mounjaro, but every
(11:44):
company [laughs]
practically every drug company on earth is
looking to bring their own out, right?
It's sort of like how statins did and,
you know, every company had their
own statin. Eventually, one or two
will end up being used heavily and
that's about it.
And the last part of this question, "What are
the bioethical considerations that
(12:06):
doctors should practice when discussing
going on a GLP-1 receptor with
a client, with a patient?"
You know, I think it's all about risks
versus benefits.
And I think that certainly it's
a reasonable drug in
a lot of cases, so
(12:26):
type 2 diabetes and so on.
It's better than insulin, for example, right?
So it's a much better drug in terms of how
it's used. It causes weight loss as opposed
to weight gain. So it's a lot better than in
insulin, right? But, on the other hand,
if you're not using it for those reasons,
then what's the risk-versus-reward benefit?
The other thing, of course, is the weight
regain, right?
So if you take it, you lose weight.
(12:49):
If you stop it, all that weight comes back.
So if you're going to take it for the rest
of your life, like some of these type 2
diabetics will-- obviously, diet
is the best thing, if you can.
If you can't, then it's still better than
not taking it, right?
But are you gonna take that for the rest of
your life? So this was the big thing
about the pediatrics.
(13:10):
So it sort of blew a lot of
people's mind that the American Academy of
Pediatrics basically said you should
consider it for anybody over 12.
I'm like, what, you're gonna put a
12-year-old on drugs for the
rest of his or her life?
Are you serious?
That doesn't make any sense at all.
And they had some rationale, but
(13:32):
most of the rest of us were like, man, they
must have been donating a lot money to the
American Academy of Pediatrics [laughs] to
get that kind of endorsement.
And of course the problem is that there
were no studies saying that it was
useful in children in any way.
So they basically made it up,
you know, and pretended it was supported by
(13:53):
evidence when it wasn't.
So, yeah, the ethical concern is mostly
around people who don't have a
good indication for it,
because everything's risk versus reward.
So say you take it, you're 15 years
old, you take and then you stop it.
You know, what good have you actually done?
Like, have you gotten any good?
(14:13):
And if you haven't gotten any health benefit,
could you have used that money that you
spent on Ozempic,
on, you know, weight-loss programs,
or-- you know, there's a huge amount of other
things you can do - exercise programs,
gym memberships, right?
So there's huge amount of other things you
could do with that money instead of
(14:35):
drugs, right? You can try and do-- you
know, get people counseling, you can get them
cognitive behavioral therapy.
There's so many other things that are useful,
that take time, that take money.
And if you're taking it away, there's an
opportunity cost that's taken away.
So, yeah, absolutely. I don't think that it's
the right answer in every single case.
I think that it does help a lot of people,
(14:57):
but it's-- at this point,
in that sort of-- we just way
overused it in people.
Like, you take the group of people
who benefit, and you extrapolate it to the
entire population, right?
And it's like there's no benefit when you
give it to everybody. Anyway...
I have several clients that are on it.
And I like what Dr. Ben Bikman
(15:18):
has said, which is when you use it as a
bridge. And so they use it is
a bridge and they practice the things
we teach (which is time-restricted eating and
no snacking, getting your insulin
down, learning how to fast), and
then they can make that transition on over
because they've changed their lifestyle, and,
as you said, addressed these
(15:40):
cognitive behavior issues.
Exactly. That's exactly how you should think
of it, because you
learn all this stuff, you build in
the healthy habits that are now going to
sustain you, then you gradually pull
back. And then you don't have that weight
regain once you do it.
That's a very reasonable thing
(16:01):
to do. It makes a lot of sense to me.
But if your whole game plan is
take this drug for the rest of your life
(and sad to say, that's like 95%
of doctors, that's how they prescribe it),
then, no, it's not that useful for
people.
Thank you, Dr. Fung.
This is my question.
[laughs] I slipped one in here.
(16:21):
In the March issue of 'Diabetes,
Obesity, and Metabolism', they had an
article entitled 'The Rise in Prevalence
of Obesity in Youth with Type
1 Diabetes'.
And it got me thinking, all
right, would you address how type 1
diabetes can develop into insulin
resistance similar to type 2 diabetes,
(16:44):
sometimes referred to as 'double
diabetes'.
Yeah, that's a good question.
So type 1 diabetes is,
in a matter of fact, opposite of type 2
diabetes. So type 1 diabetes is too little
insulin, type 2 diabetes is too much insulin.
What's striking is that the
prevalence of type 1 diabetes,
(17:05):
not just in kids, but also in adults
too, has gone up substantially
in the last few decades.
It used to be extremely rare.
So if a kid had diabetes, it was almost
always type 1 diabetes.
Now it's sort of half and half type 1 and
type 2. And that's only because type 2 has
gone up so much.
Type 1 itself has actually gone up but
(17:27):
not as much as type 2.
But the question is why?
So type 2 is a dietary disease.
It's often related to carbohydrates and
refined foods, but type 1
is an autoimmune disease.
So it's your own immune system that's
attacking the pancreas and, therefore, not
producing enough insulin.
So why is that going up?
That's a good question.
(17:47):
Nobody really knows the answer to that.
It's the same as, say, gluten sensitivity,
celiac disease. That's also an autoimmune
disease, the prevalence of which is going
way up. And some people might say, "Well,
it's just because you're recognizing it
more." And for celiac disease,
no, it is not because they've done a study
where they went back into some old
blood work that they had on people.
(18:09):
I think they were in the Korean War or
something like that. They drew everybody's
blood. They had archived it. They tested it,
and, sure enough, there just was not a lot
of celiac disease back then.
And now there is, right?
So that's why gluten-free is a much bigger
thing because a lot people absolutely
do suffer from this.
Same as type 1 diabetes, it's a real
increase. So for some reason, there's
(18:31):
something screwing up the autoimmunity
and nobody really knows what it is.
So type 1 is going up.
The thing about type 1 diabetes is, if
you look at a normal person,
a normal person produces probably
around 15 units of insulin per day.
So a type 1 diabetic who's newly diagnosed,
he only needs a bit of insulin, like 10, 15
(18:52):
units a day. The problem is, over time, they
develop insulin resistance.
So then they need not just 15, they need
20, 30, 40, 50, 60, 70
units. And they keep getting all type 1, but
they actually have both type 1 and type 2.
So they have type 1 because their own
pancreas produces no insulin, but they
have type 2 because, with all that exogenous
(19:13):
insulin, they actually have hyperinsulinemia.
So remember what insulin does is it tells
your body to store sugar,
you know, store calories, tells you to store
it as body fat or store as sugar, like
glycogen. And if you're taking too much
insulin with too much sugar over time, even
if that insulin comes from the
injection as opposed to your own pancreas,
(19:34):
you do get this insulin
overload, which is type 2 diabetes.
So now you have type 1 diabetes and type 2
diabetes, which is double diabetes.
So in a sense, you have both type
1 (which is increasing over time
for an unknown reason), you have type 2
(which is increasing for a dietary reason),
and then you get that double diebetes.
It's just all over bad.
(19:56):
I've been working my way through your
interviews, your conversations with
The Fasting and Longevity Summit 2.0.
I noticed you're not called Brad anymore!
[laughter] So congratulations on
that, fixing that with YouTube.
Yeah, that was something!
But I loved your interview with Dr. Tro,
and I can't say his last name.
(20:17):
He talked about the type of calories
that we're consuming is what is
leading us to wanting more calories,
usually a more problematic type of
calories also.
So I'm going to put the link to that in
the podcast show notes, but he
also went on to address these things
like you were talking about - autoimmune,
(20:38):
etc. It was a really good interview.
I really liked that. It's so neat to see you
asking the questions.
This
person would like you to talk about Lp(a)
and how concerning is an elevation
in that lab level, how
to lower it, and is there a relationship
between the gut microbiome
(21:00):
and small-particle LDL?
So Lp(a) is
supposed to be-- so you know we measure, in
the cholesterol panel, the
LDL which is always considered the 'bad'
cholesterol.
Technically, it's not a great term, but, you
know, when it's high, that's what people
focus on. Then there's the HDL, which the
'good' cholesterol, which is-- again,
(21:21):
you want it to be high because it's good,
right? And LDL is bad because it is bad, so
you want to be low.
That's how the standard cholesterol panel
is set up.
It's not ideal.
So they do this lipoprotein (a), which is
really looking at a more specific
marker of the sort of bad cholesterol
particles. So, when you do association
(21:41):
studies, it appears to be more powerful than
the LDL, so it
may be useful. So can you lower Lp(a)?
There actually was a new drug that
just got tested, which showed that you
can actually lower it quite significantly,
right? So we're talking about0-- if you lower
LDL, so with statins, for example, you lower
everything (you lower LDL, you lower Lp(a),
(22:04):
you'll lower HDL too), which is probably why
it's probably not as good as people think
it is. So that's sort of interesting because
what you have to do is you have to lower the
Lp(a) and then see if they survive longer.
So they're only at step one where they've
given the drug and they're like, yes, we can
lower Lp(a).
Now, you have to say, "Does that actually
(22:24):
do any good?" Because remember, if you think
about the cholesterol panel, there's
three things. There's the HDL (the good
cholesterol), which goes with the
triglycerides. So triglycerides and HDL
is sort of their opposite, right?
So when triglycerides go up, when you
eat a lot of carbs, triglycerides go up and
HDL goes down, right?
So there's
(22:48):
the HDL/triglyceride, there's the LDL (whichis the statin), and then there's
the Lp(a), which is that new drug.
So the most powerful predictor,
the strongest association, by
far and away, is the HDL and triglycerides.
And that is the one that is the
most affected by diet,
specifically carbohydrates.
So if you reduce your carbohydrate
(23:09):
intake, you can reduce your triglycerides
and raise your HDL, which is extremely,
extremely powerful in predicting
heart disease.
What if you just give a drug to lower HDL?
Well, they've done that.
It lowers your HDL just fine.
The problem is that you die
more frequently.
(23:29):
So it did nothing, and why?
Because you didn't actually change your diet.
The HDL was just a marker of having a
good, low-carbohydrate diet, probably not
having all that hyperinsulinemia.
LDL... You know, we go on ad nauseam
about statins and LDL and
then Lp(a).
Does diet affect Lp(a)?
Not really.
(23:50):
Same as LDL, not really.
That's the thing about LDL and Lp(a)
is that it's like a drug maker's dream
because, if you have a high LDL, there's
almost nothing you can do from a dietary
standpoint to lower it.
So what do you have to do?
You have to take drugs.
All you have do is convince people that LDL's
the sort of 'be all and end all'
(24:10):
of everything, and then you can get
them to take drugs, because there's actually
nothing they can do.
Diet, lifestyle, exercise, I don't care what
you do, you probably won't change your LDL
much. The only way you can actually change it
is with the drugs, so it's a drug maker's
dream.
And the funny thing is that (I pointed out
on Twitter) there's been two studies
(24:31):
in The New England Journal of Medicine, which
is the most important journal in
medicine, actually, it's the most
prestigious.
One just a few months ago and one,
I think, last year.
And they looked at risk factors for heart
disease. So they looked at five risk factors,
basically, and they say, "What if we reduce
smoking? How many years of life
can you save?" and all this sort of stuff.
(24:52):
And the super interesting
thing is that all these things that
were important
(stopping smoking and all of this sort
stuff), all of them showed a
real benefit, but the one thing that
didn't show practically any benefit
was lowering of the LDL
cholesterol.
(25:13):
So this is that new study.
So I tweeted it out (let me just see when I
did that) April 2nd.
So if you stop smoking, you'll save about
five years of life.
If you have diabetes, if you get rid of it,
you'll save about four years of life.
If you control your blood pressure, about 1.3
years of life saved.
If you lower your cholesterol, you'll
actually lower your life expectancy
(25:35):
[laughs] by about 0.4 to 1.3
years, which is like insane.
So all these other things - stopping smoking,
diabetes, blood pressure control - they all
help you, but the one thing that doesn't help
you is actually lowering your cholesterol,
which is, like, wow.
I don't know why more people didn't
think, "Oh, this is really an important
thing," but nobody else seems to care
(25:58):
in the medical field, right, when you point
stuff out like this. Even when it's in The
New England Journal, it doesn't get any
traction because everybody's so brainwashed
and thinking that it's all about the LDL.
I'm not saying that statins have no place,
but I think their place has just been
like Ozempic, just been expanded.
Because you could treat it, it became
this sort of 'everything is
(26:20):
cholesterol' when it's like, you know, it's
only about, as a risk factor, it is like this
important compared to diet, which is much
more important.
Do you know of research or trials
with fasting being used to reduce
prostate size?
Also, is there a medical database
that this person could subscribe to
so they could keep track of
(26:42):
any research studies being done on that?
I don't know of anywhere that you can go.
The only thing I do is just, if that
specifically is what you want, search
it every so often.
The best place to search is PubMed.
What I would put in as a search term is
something like 'fasting', 'prostate size',
[unintelligible] 'PubMed'.
That way you don't get all the sort of other
(27:03):
stuff that other people write and you just
get the studies.
And they're pretty good.
PubMed has a lot of stuff, right?
So if there's any studies-- and they'll go
back, you know, many years.
There's not any that I actually know of,
because, remember, fasting hasn't had a lot
of data in it.
It's possible though.
I actually think that a lot of these may
require regular fasting.
(27:24):
So, you know, with fasting, there's this
whole thing about autophagy and, also,
you know, not just that, but insulin is
not just a metabolic hormone, it's
a growth factor, right?
So, if you have hyperinsulinemia, the thing
is that you may have a lot of these other
growth factors being increased.
And one of them could affect the
prostate size, obviously, because you
(27:46):
just don't want it to grow.
So if you have insulin, which is a growth
factor, and high insulin is going to lead
to more growth.
So, therefore, it makes sense that, hey,
this might be an intervention that was very
useful, but that's just a hypothesis.
I don't have any proof that
actually happens.
You know, on the other hand, if you wanted
to wait for the proof, [laughs] you might be
(28:08):
waiting, like, 20 years, in which case
you might not be worried about your prostate
at that point, right?
20 years is a long time to wait.
So the whole thing is that,
at some point, you have to say, well, either
you just go ahead and do it and hope for the
best, or you can wait for that data.
Because that data is-- it takes time,
it take money, it takes people who are
(28:28):
interested in fasting.
I mean, the initial fasting studies that were
done were just really bad.
They were like, "Oh, fast on one day
and eat double the next day." I'm like, okay,
but that's not gonna give you very good
results. Like, you don't have to be a genius
to figure that out, right?
You're not gonna do very well.
So, of course, they didn't do very well and
they said, "Fasting doesn't work." It's like,
(28:48):
no, you did it all wrong.
When are you supposed to allow your body to
use up your calories if you're just gonna
double up the next day?
So anyway, the whole point is that I would
just check it on PubMed (that's the best
thing to do) and then you'll find everything
you need.
I'm navigating this question carefully
because I don't want it to be a medical
question. But this person would appreciate
(29:09):
your opinion on somebody who's a
65-year-old woman who's considering
donating her kidney.
Would fasting or
fat fasting help around
that time period?
It can, but it doesn't affect the kidney
function so much.
So fasting is good for a lot of things.
The kidney isn't probably one of the ones
(29:29):
that gets affected a lot.
I mean, in chronic kidney disease, and we've
talked about CKD, there is
a study on chronic kidney disease and
fasting. It was from the fasting-mimicking
diet people, because, again, because they
have a product, they're actually more
interested in sponsoring research on it.
So a lot research has started to come out
from them. It does reduce chronic kidney
(29:50):
disease. Of course, it can reduce diabetes,
both of which are important. If you're going
to donate your kidney and you have
diabetes, you will get turned down right away
because people are like, "Well, you have a
diabetes, your kidneys will be at risk in the
future, so we can't take your one kidney
because you could need it in the future."
So it could help certainly around that
by reducing the sugars.
(30:11):
And then, again, if you have any kidney
disease at all, they will refuse to
take that kidney as well.
So it could be worthwhile to get those
sugars right down and also help to reserve
the kidney function.
And fasting increases your glomerular
filtration rate too, doesn't it?
I don't know if that would help with the
kidney transplant.
Yeah, I mean, some of the data is--
(30:33):
the glomerular filtration rate is basically
how well your kidney is working.
Most people are normal so it doesn't matter
how much you are filtrating.
But if it starts to go down, then,
when you get kidney disease, you'll see a
lower filtration rate.
And that's where fasting can sometimes help
with that, actually. So that can be useful.
And by the way, I get a lot of people who
(30:54):
send me articles for you to read.
That doesn't work that way, you guys.
[laughs] He's already read it.
But they were wondering if you had read
the latest article in The New York
Times about the processed
seed oils. It seems like this is coming
up for debate again.
And, you know, they're saying they have seen
(31:15):
multiple, reputable sources.
I personally question the
type of research that they're doing.
Is it questionnaire or
is it randomized control study?
Do you have anything to say about
seed oils being avoided, on account of
them being more processed, rather than
(31:36):
something like olive oil or butter?
Yeah, so this one
is actually an important
one because seed oils are highly,
highly processed, right?
The problem when you process stuff is that
you purify certain things, in this case,
the polyunsaturated fats, right?
And the problem with polyunsaturated fats is
that, because there's a lot of unsaturated
(31:58):
bonds, they're less stable than saturated
fats.
Because they're less stable, they're prone to
oxidation and stuff, which then, if they
become oxidized, then they could cause a lot
of inflammation. So everybody thinks they
could be highly inflammatory, which I
think is certainly possible, but it's always
hard to put a link one-to-one
with it. You can do studies linking,
(32:19):
say, linoleic acid and polyunsaturated
acids to certain diseases,
but, when you do it over large populations,
then everybody does it differently
(everybody's eating different seed oils and
stuff).
So you have a potential
mechanism which is plausible,
that is too much of this process
seed oils gives you too many unsaturated
(32:40):
which are unstable oils which leads
to increased inflammation.
So that's a very plausible hypothesis.
The problem is going from that
hypothesis to actual proof
is much more difficult.
It takes a lot of studies and
the studies are sort of like here and there.
So there are a lot of people who say that
(33:02):
eating a lot of vegetable oils is good,
and now there's a lot of people saying that
eating a lot vegetable oils is bad.
To me, it's very hard to
argue because the data is just so sparse
in terms of actual causal
data.
So it's hard to say that it's
true and it's hard to say that it's false.
(33:22):
So, in that case, I always
fall back and say, "Well, what's
the smartest thing to do for myself?"
The smartest thing would be to eat the
oils that have always been eaten.
So, if you look back, what have people
naturally eaten? What are the natural fats?
Olive oil has been used for thousands of
(33:43):
years, coconut oil has used for thousand of
years, butter has been used for thousands
years.
So those are what I eat.
Vegetable oils have been around since about
1900.
They really increased a lot
in the 60s, 70s,
80s.
Around the same time, you saw all these
autoimmune diseases popping up, right?
(34:04):
So is it plausible that
the seed oils are causing inflammation,
which is causing all these autoimmune
diseases, which is inflammation, right,
inflammatory diseases?
Yes, it's possible.
I don't know that it's true, but
what do I do?
Am I going to wait 20, 30, 40 years?
In 40 years, I really won't care.
(34:27):
[laughs] It'll be way too late for me.
So what do I do? I eat butter, I eat coconut
oil, I eat olive oil because those are
natural fats that I know people have eaten
for a long time, so I'm pretty
sure that they won't be harmful to me.
I'm not so sure that eating a lot of
vegetable oils is bad for me.
I actually think that there's two things with
(34:47):
vegetable oils. One, I try not to eat too
many. And two, I try not
to eat them in fried foods.
Deep-fried seed oils are probably the
worst thing you can do because the oil
is not stable, chemically stable.
Like there's-- you know, you can argue a lot
of things, but, if you look at saturated
versus unsaturated, unsaturated is
(35:08):
much less stable in heat.
So when you do high-temperature seed
oils, like deep frying your foods in
seed oils, if it's gonna be bad,
if the seed oil is gonna be bad, the high
temperature is gonna be like 10 times as
bad, right? So putting a little canola
oil in your dressing, I'll accept that
if I have to.
I try not to, I almost always use olive oil,
(35:31):
but deep frying in vegetable oils is
like super bad for you.
So when you go to McDonald's, when you got to
any of the other places, yeah, the deep
fried foods are probably bad for you, but it
might not have been the fat, it might have
been the seed oil and it might have been the
fact that it's deep fried.
So those are the things to really watch out
for. So, to me, it's like I can't make any
100%, this is what's true, this is what's
(35:53):
not true, but I can only say that
the smartest-- what I think is the most
logical path is to
avoid deep-fried seed oils,
definitely, and then seed oils
I try to limit, but it's not always
possible. Like, other people use it and,
you know, I'm not gonna say no, but if
you look at what's in my kitchen, I have
(36:15):
olive oil and butter for
practically everything.
I would use coconut oil, but my kids actually
don't like it at all, so they won't eat
anything-- it has a strong flavor.
I love coconuts, so I put coconut in
everything.
Me too. It helps my migraines too, I think.
I think it's because it's a saturated fat, I
think, it helps my migraines, but that's a
(36:37):
whole other story.
But really it's all butter or olive oil
in my kitchen, and I don't have any problems,
right? I deep fry-- I don't deep fry, I use
the air fryer more
and more just because it's a lot easier, but
I pan fry stuff and, you
know, they have this new olive oil that you
can pan fry in.
I do butter. I don't do high-temperature
(36:58):
cooking. You know, it's not that
hard, right, to get away from that almost
entirely.
I haven't bought vegetable oil in like 10
years.
I use avocado oil, also.
And what shocks me is I read some
of these studies and they're still putting
all these oils together,
like avocado oil and olive
(37:19):
oil, in with the studies of the seed oils.
And it's like no you need to separate those
out.
Yeah, I think avocado oil is fine too,
it's just that I'm so used to olive oil
now. There's a little bit of flavor with the
olive oil so I like that, and I think olive
oil is just more easily available,
but avocado oil it's great too.
But really it's-- to me, it's like, I'd
(37:40):
say 80%,
85% butter and olive
oil, almost everything that I
use is that.
Sometimes I use like the drippings from beef
and stuff (you know, you get the oil), and
then I save it actually to fry in it.
That's beef oil and whatever.
But again, it's a natural fat, so that's why
I save it. Or bacon oil, I'll save
(38:02):
it and use it again.
I use bacon oil too.
Even though I'm basically plant-based, I will
save the bacon oil, bacon grease.
[laughter]
Well, thank you so much, Dr. Fung, I know I
kept you over this time.
All right, you guys, see you next month.
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