Feel Better, Live More with Dr Rangan Chatterjee - The Real Cause of Belly Fat, How To Fix Your Metabolism & Why Your Liver Is More Important Than You Think with Professor Robert Lustig #432
Episode Date: March 6, 2024Twenty percent of obese people are in metabolically great health. Meanwhile sixty percent of supposedly ‘healthy’ weight people are metabolically unwell and at risk of a host of chronic diseases. ...With this in mind, do we need to change our thinking about what ‘being fat’ really means? Today, I’m thrilled to welcome back Dr Robert Lustig, a leading public health authority who for many years has been trying to expose the truth behind the food industry and the many myths within modern medicine. Rob is Professor Emeritus of Paediatrics, Division of Endocrinology at the University of California, San Francisco He is the author of multiple books including Metabolical: The Truth About Processed Food and How it Poisons People and the Planet.  Robert first came onto my podcast back on episode 251 when we took a deep dive into what happens inside our bodies when we consume excess sugar. In today’s conversation, we do touch again on the impact of sugar on human health but the main focus is on the three different sites in the body where we deposit fat: subcutaneous (which you can see and feel); visceral (stress-related fat around the middle), and liver fat. It’s only the first of these that you’re likely to notice on the scales – but it’s the latter two, says Rob, that really determine your health. We talk about why it’s stress not food that largely drives dangerous visceral - the fat that surrounds our organs - and Rob’s view that chronic stress underpins metabolic, mental, global and planetary health. We also discuss how a minimally processed, wholefood diet can mitigate stress and weight gain why he’s not a fan of fructose, nor the glycaemic index why he thinks that continuous glucose monitors (CGM) can help the general population, not just those with diabetes why the liver may well be the body’s most important organ when it comes to metabolic health, and some of the key tests we can do to assess our own liver health And we also talk about alcohol, fruit, honey and many more topics that will help you make empowered decisions for you and your family’s health.  Rob’s work has changed many people’s lives around the world and his message deserves to be heard loud and clear. He is knowledgeable, passionate and someone who is not afraid to say what he thinks. I always enjoy talking to him, I hope you enjoy listening. Support the podcast and enjoy Ad-Free episodes. Try FREE for 7 days on Apple Podcasts https://apple.co/feelbetterlivemore. For other podcast platforms go to https://fblm.supercast.com. Thanks to our sponsors: https://zoe.com https://drinkag1.com/livemore https://vivobarefoot.com/livemore Show notes https://drchatterjee.com/432 DISCLAIMER: The content in the podcast and on this webpage is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your doctor or qualified healthcare provider. Never disregard professional medical advice or delay in seeking it because of something you have heard on the podcast or on my website.
Transcript
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What causes belly fat?
Stress.
Stress causes belly fat.
Food? Does food cause belly fat?
Turns out, no! Food does not cause belly fat.
Stress causes belly fat.
Stress is a primary factor on its own.
And the problem is that people don't know how to mitigate their stress.
And they are actually prevented from mitigating their stress
because our society doesn't allow them to do otherwise.
It's not just getting in the way of metabolic health,
it's getting in the way of mental health,
it's getting in the way of global health,
it's getting in the way of planetary health.
It's getting in the way of everything.
Hey guys, how you doing?
Hope you're having a good week so far. My name is Dr. Rangan
Chatterjee and this is my podcast, Feel Better, Live More. 20% of obese people are in metabolically
great health. Meanwhile, 60% of supposedly healthy weight people are metabolically unwell and at risk of a variety of chronic diseases.
With this in mind, is it time we changed our thinking about what being fat really means?
For today's podcast, I'm thrilled to welcome back Dr. Robert Lustig, a leading public health authority who has for many
years been trying to expose the truth behind the food industry and the many myths within modern
medicine. Rob is Professor Emeritus of Pediatrics, Division of Endocrinology at the University of
California. He's also the author of multiple books,
including Metabolical, The Truth About Processed Foods and How It Poisons People and the Planet,
which was published back in 2021. Now, Robert first came onto my podcast back on episode 251,
when we took a deep dive into what happens inside our bodies when we consume excess sugar.
Now, if you've not heard that conversation yet, I would highly recommend that you go back and listen
when you get a spare moment. In today's conversation, yes, we do touch again briefly
on the impact that sugar can have on human health. But the main focus is on the three
different sites within the body where we deposit fat. Subcutaneous, which means under the skin,
but also visceral fat and liver fat. Now it's only the subcutaneous fat that you can actually see
and feel, but it's the latter latitude, says Rob, that really determine your
health. And in today's conversation, he tells us why. We also discuss the fascinating idea that
it's stress and not food that largely drives the dangerous visceral fat, the fat that surrounds
our organs. And Rob's view that chronic unmanaged stress
is one of the most important factors that underpin our metabolic health and our mental health.
We also discuss how a minimally processed whole food diet can mitigate both stress and weight
gain, why he's not a big fan of fructose nor the glycemic index, why he thinks
that continuous glucose monitors can help the general population, not just those with diabetes,
why the liver may well be the body's most important organ when it comes to metabolic health,
and some of the key tests we can do to assess the current state of our own liver health.
And we also talk about alcohol, fruit, honey, and many more topics that will help you make empowered decisions for you and your family's health.
Rob's work has changed so many people's lives around the world,
and his message deserves to be heard loud and clear.
He's knowledgeable, passionate,
and someone who is not afraid to say exactly what he thinks. I always enjoy talking to him.
I hope you enjoy listening.
I wanted to start off with something that you wrote in your latest book, Metabolical.
Data shows that it is your liver and visceral fat that determine your health,
not your weight or total body fat.
Stand by that. That's exactly right. It's not the fat you can see that counts. It's the fat you cannot see.
And the reason is because those fat depots have different causes, different effects, and ultimately different drainage.
The drainage is actually the important thing. So let's go through those three fat depots that you just mentioned and what causes them and what consequences there are for them. So the first fat depot is the one
that's obvious, the one you can see. Subcutaneous fat, big butt fat. Subcutaneous fat is where your body wants to store fat. And there's a lot of it.
All right. And it has big vacuoles. In other words, the place where the fat actually gets
stored inside each of the adipose tissue cells. Now, it is possible to overstuff each of those
vacuoles. And when you overstuff each of those vacuoles and you put down more and more subcutaneous fat, there is the possibility that that fat vacuole has just gotten so big,
you know, like a balloon that's about to burst. And what happens is that when that happens,
the perilipin border can't hold it anymore and the fat starts to leak out into the adipose tissue
cell, choking it off and killing it. And so now you have a dead adipose
tissue cell with a whole lot of grease that has to be cleaned up. That sends out messages to the
macrophages, the cleanup crew, which comes and then populates that fat and starts actually
cleaning up the grease. And then that sends out inflammatory cytokines. And that is and starts actually cleaning up the grease. And then that sends out inflammatory
cytokines. And that is what starts the inflammatory response. Now, when that happens,
the drainage of that adipose tissue, that subcutaneous adipose tissue goes where? It goes
into the entire systemic circulation. It goes into the inferior vena
cava and therefore circulates throughout the entire body. So the volume of distribution
is the volume of distribution of your blood supply, which is six liters.
In other words, you have to cause a lot of inflammation in a lot of adipose tissue
to be able to generate a concentration of cytokines
that's enough to actually do damage to the rest of the body. How much? Maybe 10 kilos, 22 pounds
on average, maybe a little more for certain races, maybe a little less for others. Okay. So is subcutaneous fat bad? And the answer
is when it gets super big, sure. But in general, no. In fact, that's the safe place to put the fat.
Now let's take fat depot number two, visceral fat, belly fat.
Now, what causes belly fat?
Stress.
Stress causes belly fat.
Food.
Does food cause belly fat?
Turns out, no.
Food does not cause belly fat.
Stress causes belly fat. And the reason we know this is because you can take patients who are suicidal with major depressive disorder that have to be admitted to the hospital to keep them from killing themselves, stick them in an MRI scanner, and you can see that the subcutaneous fat is going down because these are people who are anhedonic. They are not eating. They are losing weight.
Losing weight is one of the cardinal features of major depressive disorder
because you don't want to eat because you want to die.
But visceral fat is going up.
You are reapportioning the subcutaneous fat
to the visceral fat,
despite the fact that you're not eating
and you're losing weight.
So that visceral fat is driven by cortisol. It is driven by stress. It is not driven by food.
And when that fat gets too big, it starts releasing fatty acids and cytokines, and then
that goes straight to the liver because the drainage for the visceral fat
is the portal vein and it goes straight to the liver. And so what's the volume of distribution
then? Not six liters, more like 250 cc's. And so a little visceral fat will increase the
concentration reaching the liver by a lot. Okay. And how much visceral fat can you gain
before you start getting sick? About five pounds. So about 22 pounds for subcutaneous fat, about
five pounds for visceral fat. And then finally, fat depot number three, liver fat. And that liver fat
is the worst because it's actually the fat right at the center,
at the nidus of where the problem is. Because when your liver is sick, all hell breaks loose
because that's the thing that drives the hyperinsulinemia the most because the pancreas
has to basically tell the liver to do its job. And so the insulin levels go straight up based on the fat in the liver.
And how many kilos or how many pounds of fat can your liver hold before it gets sick?
About a half a pound.
So 22 pounds of subcutaneous fat versus five pounds of visceral fat versus half a pound of liver fat.
And where'd that liver fat come from?
Alcohol and sugar. So different fat depots, different risks, different drainages,
different consequences. I mean, it's fascinating. Thank you for going through those three different
fat depots. I really enjoyed reading that section in the book,
actually. And it was so striking when you pointed out, as you just have now, that,
yeah, the subcutaneous fat is where we are designed to put excess energy that we take in.
In the olden days, in the summer, we'd store the fat and it would get us through the winter,
in the olden days in the summer, we'd store the fat and it would get us through the winter,
right? That's not a problem for our health unless it goes beyond that sort of natural capacity. Then it starts to become problematic. Then you mentioned the visceral fats. Now,
hopefully listeners of my podcast have heard that term several times before, and we did touch on it in our first conversation together. But that idea that visceral fat is driven by stress and not by food,
that's quite interesting because, you know, let's say someone had no stress at all in their life.
I don't know anyone living in... I was going to say, I'd like to meet them.
But let's just, you know, hypothetically speaking, someone has, you know, minimal stress in their I was going to say, I'd like to meet them.
Hypothetically speaking, someone has minimal stress in their life,
but they are consuming energy in the form of food to excess.
Are you saying that in your view, unless there's also some kind of chronic stress on boards, then that food, that excess energy
will be stored as subcutaneous fat or potentially liver fat, but it won't be stored as visceral fat
without the stress? Exactly. That's exactly what I'm saying. And the reason is because
in order for that visceral fat to accumulate the fat, there has to be something wrong with
the sympathetic nervous system. So that sympathetic nervous system is what's driving that adipose
tissue fat depot. Now think about this. This is actually very important. The visceral adipose
tissue has the beta-3 adrenergic receptor. Every single cell has the beta-3 adrenergic receptor.
So it is taking information
from the sympathetic nervous system.
Okay?
And every cell has an adrenergic innervation.
So when you are acutely stressed,
acutely,
message goes from the locus coeruleus in the brain
via the intermedial lateral cell column of the spinal cord
out to the various peripheral nerves
like the celiac nerve and the superior mesenteric nerve
to the visceral fat and sends a norepinephrine signal. And that norepinephrine signal
says to that fat cell, give up your fat because we are in a stressful situation and we need energy.
And so stop accumulating fat energy and start releasing it.
And so you hit the pause button on lipoprotein lipase,
which is making the fat,
and you hit the go button on the hormone sensitive lipase,
which allows for the extrusion of free fatty acids,
non-esterified fatty acids from that visceral
fat, which then goes into the circulation, goes to the liver and can either be manufactured into
glucose or ketones for energy for the rest of the body. Okay. That's the acute stress response.
So the acute stress response by stimulating norepinephrine causes the visceral fat to give up fat.
It is lipolytic.
It is, you know, fat losing in the visceral compartment.
But chronic stress does the opposite.
Now, how does chronic stress do the opposite? Why does chronic stress do the opposite. Now, how does chronic stress do the opposite?
Why does chronic stress do the opposite? Chronic stress causes that visceral fat to accumulate
instead. So number one, chronic stress has cortisol. Acute stress, you haven't gotten a
cortisol bump. It takes 10 minutes to generate a cortisol bump in response to an acute stress, you haven't gotten a cortisol bump. It takes 10 minutes to generate
a cortisol bump in response to an acute stressor. It's a norepinephrine response. And your adrenal
gland doesn't have any cortisol stored. It has to make cortisol de novo from scratch,
from cholesterol, because there's no storage place for cortisol. So cortisol is always a delayed response.
It comes in around 10 minutes. So for those first 10 minutes of an acute stress, the lion chasing
the pygmy on the savanna, that's all norepinephrine. And so you're going to get all
hormone sensitive lipase activation. You're going to get all hormone sensitive lipase activation.
You're going to get all that fat rushing out of the visceral adipose in order to generate the energy that the body needs to run away from the lion.
All right.
But then cortisol kicks in.
And cortisol does something very different.
Cortisol alters mitochondrial function.
Cortisol also increases the enzymes that then lay down fat.
And then something even more remarkable happens.
I'm sure you're aware, Rangan, that every adrenergic neuron in the body,
whether it's in the brain or in the periphery, releases norepinephrine.
neuron in the body, whether it's in the brain or in the periphery, releases norepinephrine,
and it also releases a second neuromodulator, a neuropeptide. And that neuropeptide is called neuropeptide Y, NPY. And they always are co-localized and they always are co-secreted.
It turns out NPY is the break on the adrenergic nervous system. So the adrenergic
nervous system is telling that fat cell, release, release, release, release. And then NPY
is co-released. And it basically tells that fat cell and every other organ in the body,
calm down, I'm the break. If you keep doing this,
we're going to get into trouble. And so NPY binds to the Y2 receptor on that visceral fat cell
and actually stops the process and actually starts promoting lipogenesis again.
and actually starts promoting lipogenesis again. So in the face of chronic stress,
you've got cortisol and you've got NPY antagonizing that lipolysis, and it actually converts it to lipogenesis. And that's why acute stress and chronic stress are virtual opposites.
Chronic stress are virtual opposites.
Yeah, it's absolutely fascinating.
And there's a wider point for me.
In the modern world today, in 2024,
there are so many different factors that are working against us when it comes to health.
You bet.
It's easy to put it all in one area
and, for example, say it's the food. Now,
I don't deny that the food is a huge problem, but as well as a lot of us having access to energy
dense, very tasty, nutrient poor foods, which we know and we'll definitely be covering in this
conversation again, we're also not moving much at all because of our jobs and the way we travel and move around.
We're sleep deprived, which we know in and of itself can cause insulin resistance. Sleep
deprivation is a stressor. Cortisol rise. Exactly. It's a stressor in and of itself. And so if that's
chronic sleep deprivation, that is a chronic stressor on the body. But then you also have,
just looking around, people feel rushed. They feel busy. They don't feel they have time.
Six, seven years ago, the World Health Organization put on their website that stress is
the health epidemic of the 21st century. It's no wonder that people are struggling. It's no wonder that people are sick,
because it seems as though for many of us, every single input coming into our bodies
from our environment is not exactly helping us, is it? It's actually getting in the way
of our overall health. But I guess fundamental to what you're writing about in your book,
it's getting in the way of metabolic health, which really is health.
I hate to tell you, but it's not just getting in the way of metabolic health. It's getting
in the way of mental health. It's getting in the way of global health. It's getting
in the way of planetary health. It's getting in the way of everything.
So I'm glad you brought this up because I wanted to talk about this with you. So, this is reciprocal. So, this is good.
to study in Paris. And I had two jobs. One, unfortunately, when COVID did hit, I had to leave and go back to the US. But the second project has continued online two hours at a time,
two days a week for the last four years. So I have been working with a French colleague,
So I have been working with a French colleague, and he is very interesting.
His name is Professor Philippe Gossier, and he is both a robotics professor and neuroscientist at the Université de Sergie-Pontoise, which is about 17 miles northwest of Paris, in a little town called Sergie.
And he has a very unique skill set, no? I mean, robotics and neuroscience. And his job, his goal, is to make robots behave more like humans, so that they would
be more acceptable to humans. Now, in order for him to do that, he has to understand emotion.
And so, there are all of these, you know,
neuroscientists out there studying the anterior fossa and, you know, neural networks and cognitive
function and learning and, you know, machine learning and AI and what have you. But almost
nobody is studying the posterior fossa, the emotion part of the brain. And so we went out to build a computational
model of the limbic system. And we have. And it's taken us four years, but it's pretty darn good.
And it actually works. And it's pretty cool when you actually look at it, because what we've come to realize
through the building of this model is that it's really about one area of the brain, the amygdala.
Now, the amygdala, for your audience, is the fear center of the brain. It is the stress
center of the brain. And here we are talking about chronic stress. It is about amygdala
dysfunction. And the point is, it's not the amygdala that is dysfunctional. The amygdala
is actually doing its job. But what we've learned is that there are four brakes on the amygdala.
And those brakes are not doing their job. They're what's dysfunctional.
So think of it this way.
You have a car, okay?
And the car has four wheels and each wheel has a brake.
So there are four brakes on the car.
You step on the brake in the cabin and all the wheels stop at the same time and you stop and then you go.
All good.
Now imagine one of those breaks fails.
You hit the break.
What happens?
Are you going to stop?
Yeah, you'll stop, but it's going to be a pretty rough ride.
Yeah.
Now imagine two breaks fail.
You're going to stop.
Yeah, you'll still stop.
If the two breaks that fail are in the back,
you'll glide to a stop.
If the two brakes that fail are in the front,
you're going to lurch to a stop.
But what if the two brakes are on either side of the car?
You're going to do a 360 and possibly damage.
All right, now what if three brakes fail?
Are you going to stop? You're going to capsize, but you'll stop. Yeah. And what if all four breaks fail at the same time?
You are over the precipice and into the abyss, like the last scene of Thelma and Louise.
of the abyss, like the last scene of Thelma and Louise. Well, that's what's happening to us because all four breaks on the amygdala are failing at the same time. So what are those
four breaks and why are they failing? So the first one is prefrontal cortex reasoning. And the reason for the failure, both cortisol and dopamine, which are both just gigantically elevated in our society.
The second break, the hippocampus memory.
Why is that failing?
Also cortisol.
Cortisol causes increased energy need, and it's not being supplied.
And so you've got hippocampal atrophy.
Third break, the afferent vagus.
The afferent vagus normally conducts neural impulses from the entire abdomen, including the gut, all the way up to the nucleus tractus solitarius,
and then a way station up to the amygdala.
Well, what is that?
That is where the serotonin goes from the gut up to the brain.
And so that is part of what we call interoception, your body's being able to actually monitor
itself.
your body's being able to actually monitor itself. Problem is, if you're eating ultra-processed food,
those microbes can't make serotonin right. And if you're eating ultra-processed food and you're insulin resistant, your liver's taking the tryptophan and turning it into chiurinine instead
of serotonin, and you're not even getting levels up into the brain that you need. So basically, no tryptophan, no serotonin, no serotonin,
no break. And then finally, number four, which is really exciting, oxytocin. So everybody thinks of
oxytocin as the love hormone or the reproduction hormone or the milk ejection hormone. That's all of those
things, but it's also the safety hormone. It's the thing that transduces the feeling of safety
and it's epigenetic because the oxytocin receptor is the most easily methylated protein in the brain.
And all of these stresses like adverse childhood experiences and traumas
and what have you, all end up methylating that oxytocin receptor so that you can't get the
feeling of safety. You are under constant and chronic threat. And that is the fourth
break on the amygdala. And that's what everyone's complaining about, is that they don't
feel safe. And so all four breaks are failing at the same time. And so the amygdala has run
hog wild. And it is the driver of our systemic health crisis through all the processes we just discussed, the mental health crisis,
the depression, the PTSD, the global health crisis in terms of social disparities and
corporate determinants of health. And there was also the driver of the planetary health crisis in terms of inequality, war, and climate change.
I mean, thank you for sharing that. That's so, so interesting.
As you were describing those four breaks that no longer work well at all for many of us,
I was thinking about a thought experiment that I often do. I, a few years
ago, set out this model of the four pillars of health, right? Food, movement, sleep, and stress
being the four areas that not only have the most impact on our short-term and long-term health,
but also they're four areas that we have, you know, a fair degree of control over, although that is arguable depending on your life circumstance.
And I often ask myself, which is the most important?
And I know it's a bit of a ridiculous one because they're all important, right?
And it's going to depend on the individual as to what's going on in their life,
which is the pillar that they probably need to address the most.
But often I come to the conclusion that
for many people, stroke most people, the stress pillar might be the most important one. And the
way I sort of justify that is not only does chronic stress impact every single organ system in the
body negatively, you know, we could spend half an hour just talking
about what chronic stress does to the body. Absolutely.
But also, if we think about food, well, these days, we're not always eating because of physical
hunger. We're often eating because of emotional hunger. So chronic stress is driving us to comfort
eat and eat more of these so-called unhealthy foods than if we weren't feeling so
stressed. So what I'm trying to get to, Rob, is this idea that being under chronic stress drives
so many problematic behaviors. You've spent a lot of your career raising awareness about the problems of too much sugar,
the problems of highly processed foods. How do you think about food and stress
in terms of their relative importance?
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more. The fact of the matter is that virtually everyone, including myself, are stress eaters.
Yeah, there are a few people out there who are, you know, who stop eating because of stress, but most people are actually stress eaters. And there's a reason is because there's a, there's a pathway of reward suppressing
stress. Okay. This is one of the pathways in the nucleus accumbens to calm it down. So dopamine,
dopamine is an excitatory neurotransmitter, and it sends the pericary in the ventral tegmental area of the
back of the brain, and it sends the processes to two places, just two places. The first is the
nucleus accumbens, the reward center, so you get a feeling of reward. And then the second is the
prefrontal cortex. Okay, now the prefrontal cortex is then supposed to send information back to the nucleus
accumbens, basically calming it down. Okay. Yeah. I love this chocolate, but you know what? I don't
need to eat any more of that. All right. That's, that's the reciprocal relationship that's supposed
to occur between the reward system and the reasoning system. Well, that is broken. And what broke it? Cortisol. Because
cortisol causes the atrophy, the cell death and atrophy of those neurons in the prefrontal cortex.
You can actually see it on magnetic resonance imaging. You can actually see the reduction in volume in the face of chronic
stress and in the face of obesity. So we know that this level of cognitive inhibition that normally
controls that reward system has basically been, you know, taken offline.
Yeah.
And that's the whole point.
That's one of the four breaks that you're describing.
So this is not surprising or even remarkable for that matter.
And this has actually been known for 40 years.
of work Robert Sapolsky did way back in the 1980s when he realized that the hippocampus was the most vulnerable part of the brain to energy deprivation and that those neurons
would die quickest.
And the reason is because the mitochondria are being altered by cortisol so that they
do not produce as much ATP. So they need more glucose in order
to be able to survive. And so that's one of the reasons why you keep eating when you're stressed
is because you're basically trying to feed those hippocampi to keep them from dying.
Yeah. You know, Rob, I think the first time I really became aware of this, and it's interesting hearing you
talk about these three fat depots in the body, because I'm drawn to several previous patients,
and they all had a particular pattern. And maybe this is about 10 years ago when I first started
to see this and observe this and go, wow, stress is really playing a role here in terms of fat
accumulation on the body. And it would typically be women, I would say in their mid to late 40s,
who I was seeing, often they were mothers. And of course, yes, that is a time when they could
be going through hormonal changes and premenopausal and menopausal, for sure. But what I would see with these particular patients
is that they were eating pretty well, actually.
They were trying their best to eat well,
but they had a stressful life, a very busy life,
and they were pushing themselves at the gym
with lots of intense cardio.
And I remember with one patient once thinking,
okay, look, this just feels like
there's too much of a stress load on your body. And I remember one patient in particular who I
advised to stop doing intense cardio. And I said, honestly, I feel that you need something more
relaxing for your movement like yoga. And she was quite skeptical at first, but within weeks of
stopping the intense cardio and doing, I think it was two
yoga classes a week she would do after work on the way home, the weight around her belly started
to come off. And I remember seeing that pattern. And I think that was very, very common. And I
think, you know, in this era of health information overloads with people consuming, you know,
all the time podcasts and YouTube videos and
trying to learn, which I think is great on one level. I think one of the downsides sometimes
is that people think they need to keep doing more and more. Wow, I need to do that exercise.
I need to add that in to an already busy life. They're adding in more and more stress. So,
you know, it kind of fits in with what you just described, right?
So, you know, it kind of fits in with what you just described, right?
We didn't see it.
We studied it.
We had a whole study here at UCSF called the SHINE study where we did just that.
We took peri- and postmenopausal women with metabolic syndrome, and we divided them up into three groups. One, a standard exercise regimen.
One, a mindfulness-based stress reduction regimen.
Okay, so basically meditation.
Okay, i.e. yoga.
And number three, control.
And asked the question, what happened?
And it turned out that weight did not change.
We were hoping weight would change. Weight did not change. But what did change was visceral fat,
waist circumference, and insulin sensitivity. And we're well, you know, we had papers in JAMA, Bottom line is we know that stress is the bad guy.
It's not the only bad guy.
There are other bad guys.
I mean, bad food is a bad guy.
And stress basically makes you eat bad food too.
But stress is a primary factor on its own.
And the problem is that people don't know how to mitigate their
stress. And they are actually prevented from mitigating their stress because our society
doesn't allow them to do otherwise. In Metabolical, in the chapter where you
write about the eight subcellular pathologies that underpin pretty much all of the chronic diseases
that we have, you know, glycation, oxidative stress, mitochondrial dysfunction, insulin resistance,
etc, etc. I underline a section in the insulin resistance parts, which I think really relates
to this part of our conversation. You wrote this, even those who are overweight and those who are under stress
don't exhibit metabolic syndrome if their diet is unprocessed.
Yeah.
That's really interesting because look, as you say, you know, stress, too much stress for too
long a period of time will drive us to eat poor quality food.
At the same time, eating lots of poor quality food is a stressor on the body.
So why is it that even if you're under chronic stress and you're overweight,
why is it that people don't develop metabolic syndrome in the absence of these ultra processed foods?
I can sum it up in one word. Reactive oxygen species. You have to be able to handle your
reactive oxygen species. Every one of these things, including cortisol, generates reactive
oxygen species. Mitochondria generate reactive oxygen species. The cytokines that are
released from visceral fat bind to their receptors and activate NADPH oxidase to generate reactive
oxygen species. Those reactive oxygen species do damage, the damage of metabolic syndrome.
And it can be whether you're thin or whether you're fat. Now, you got to get rid of the reactive oxygen species because they're the mover in terms
of the damage.
Okay.
And they are part of life.
You can't get rid.
The only way to get rid of reactive oxygen species is to be dead.
All right.
They are going to be manufactured.
You know, it is part of energy metabolism.
It is part of energy metabolism. It is part of protein metabolism. It is part of
lipid metabolism to generate reactive oxygen species. All right? Little oxygen radicals,
little hydrogen peroxides running around your cells. Okay? Turns out those change energy
metabolism. So you got to clear the ROSs. Well, where do you clear the ROSs?
And subcellular organ in the cell called the paroxysome. That's where the antioxidants are.
So the paroxysome is where ROSs go to die. That's where you quench the effect of the
reactive oxygen species.
It turns out that every mitochondrion is next to a peroxisome on purpose to be able to basically get rid of that ROS before it does damage.
Because that ROS will peroxidate a lipid or it'll denature a protein or whatever.
It's going to cause cellular dysfunction.
or it'll denature a protein or whatever.
It's going to cause cellular dysfunction.
Now, let's say you don't have enough antioxidants to cover your ROS burden,
that your ROSs are greater than your antioxidant capacity.
Now you can't clear them.
So where do they go?
They go to the endoplasmic reticulum,
which is where proteins, as you know, get built.
There's a little, you know, assembly line of adding amino acids.
The transfer RNA is bringing the amino acids, you know, using the genetic code in order
to build up proteins and then fold them, right?
Well, if you don't fold them right because of the ROSs, you have what we call ER stress, endoplasmic reticulum stress, also known as the unfolded protein response, also known as the pathogenesis of metabolic syndrome.
Those three terms are synonymous.
So if you can't fold your insulin molecule, you got type two diabetes.
If you can't fold your insulin receptor molecule, you've got metabolic syndrome,
insulin resistance, and possibly Alzheimer's and possibly cardiovascular disease, possibly fatty
liver disease, et cetera, et cetera. So getting rid of the ROSs is super
important. And there's only one way to get rid of the ROSs, antioxidants. And there's only one way
to get the antioxidants. You can't breathe them in. Ain't no antioxidants in the air.
in the air, you got to get it in your food. So when you eat food, you can mitigate that metabolic syndrome pathology. But unfortunately, ultra-processed food only, because it's
antioxidant-poor, only contributes to an increase in reactive oxygen species. Because you're bringing on all of this carbohydrate,
you're bringing on all of these trans fats,
you're bringing on all of these things that generate ROSs
without bringing on the antioxidants that can quench them.
When you say antioxidants,
and you get these antioxidants from foods,
and from real foods.
And in particular, fruits and vegetables.
You know, I mean, that's the primary, you know, source of antioxidants.
I mean, you know, there are amino acids that are antioxidant,
but what you really need are, you know, the biotin, the anthocyanins, the flavonoids, the various other things that come from a, shall we say, real food diet.
A lot of the foods that contain those wonderful compounds, as you said, are fruits and vegetables, let's say.
let's say. Blueberries, for example, would be an example of a food that is rich in all the compounds you've just mentioned, which will help dampen down the ROS, the reactive oxygen species,
right? How do you put that together with your take on fructose? So fructose is something you've
spoken about on our first podcast together about the problems of excess fructose in our diet. And of course, fruit also
contains fructose. So could you just help tease that apart for us? I genuinely want this conversation
to be helpful for people so they understand what's going on and they know what they can do.
So I think that would be quite helpful if you don't mind. All right. It's very simple. Number
one, berries, like blueberries,
they don't have much fructose. I mean, they have a little, yeah, okay, yeah, they're mildly sweet,
but not like ridiculously so, number one. Number two, they got a lot of fiber, okay, and fiber
turns out to be the antidote to sugar, and I'll show you why in a minute. And number three,
to sugar and we'll show and i'll show you why in a minute and number three they have all these antioxidants right now um sugar is the bad guy and the reason is because fructose this sweet molecule
and sugar is not glucose glucose is the energy of life every cell on the planet can you know
utilize glucose for energy.
Glucose is so important that if you don't consume it, your body makes it.
There's this process called gluconeogenesis, where fat breakdown can generate glucose in the liver.
Amino acid breakdown can generate glucose in the liver. So glucose is so essential,
you don't have to consume it. That's how essential it is. Okay. It is essential to have, it is not essential to consume.
Now, fructose on the other hand is totally non-essential.
There's no enzyme in the body that requires it.
There is no benefit to it other than the fact that it
incorporates energy, you know, has a certain amount of energy associated with it.
Okay.
But it is completely vestigial to all animal life, all the way down to the amoeba.
Okay.
I always used to say all vertebrate life, but in fact, all animal cell life. There is no reaction in any animal cell on the planet that
requires fructose. Not necessary. Completely vestigial. It's a holdover from our plant
ancestors. Now, it does have energy. I'm not saying it doesn't. If you throw it into a bomb
calorimeter, it'll burn at four calories per gram.
Yes, we can harness some of that energy.
And that's, of course, ostensibly why it's in sports drinks.
But the fact of the matter is, it is metabolized a completely different way from that of glucose.
And instead of going to either ATP and carbon dioxide or to glycogen, which is a storage form of glucose, fructose goes straight to the mitochondria. If the mitochondria are overwhelmed
and can't process all of it, then the mitochondria throw off the excess and then the cell turns that
into fat. And we have just talked about liver fat being the worst of the bunch. And fructose is a primary
driver of liver fat accumulation, and therefore a primary driver of metabolic syndrome. Oh,
and by the way, a primary driver of reactive oxygen species because of the stereochemistry
of the fructose molecule. it engages in that reactive oxygen species generation
seven times faster than glucose does.
So it is a lipogenic substrate
and it is an oxidative stress all by itself.
Now, what I said, the fruit is good, right?
I mean, you said the fruit is good.
The reason the fruit is good is because number one, it has the fiber,
and number two, it has the antioxidants.
It's not good because it has the fructose.
The fructose is what makes you eat it, but that's not why it's good.
So how does the fiber act to mitigate the negative effects of fructose?
There are two kinds of fiber, soluble and insoluble.
You need both.
So insoluble fiber is like cellulose, you know, like the springy stuff in celery.
Soluble fiber is like pectins or inulin, like what holds jelly together, right?
You need both.
Together, what happens is that the cellulose acts like a latticework, like a fishnet on the inside of your intestine. The soluble fiber, the pectins and the inulin, they plug
the holes in the fishnet. And so together they form a secondary barrier. And that prevents transport of glucose, fructose, sucrose, simple starches from the intestinal
lumen into the portal circulation so that it never reaches the liver.
And if it doesn't reach the liver, it goes further down the intestine and the bacteria
chew it up for its own purposes.
You have fed the microbiome.
You have to feed your gut.
Well, the fiber is the
food for the gut. And so it takes the pressure off your liver, so fewer ROSs, and it feeds your gut.
So your microbiome can, number one, work for you, generate short-chain fatty acids,
can number one, work for you, generate short-chain fatty acids, suppress inflammation,
maintain the intestinal barrier integrity so that you don't get inflamed, so you don't get metabolic syndrome. So yes, even though the fructose is in the fruit, the antioxidants and the fiber more than make up for it.
But as soon as you squeeze it, now the fiber is gone.
The antioxidants will still be there, that's true.
But the fiber is gone.
And so now you're going to get this big fructose load hitting your liver.
That's why I tell people, eat the fruit, don't drink the juice.
There's a couple of things which have just come up for me as you were explaining that. First one, Rob, is to do with the fact that fruit does
have fructose within it, just not that much. And your message, I think, is that it's the
excess fructose that we're consuming that's causing problems.
Especially in the absence of the reactive oxygen species and fiber.
Yeah. So let's say someone is in perfect metabolic health, and we compare that to someone
who has really poor metabolic health, like much of the US population, much of the UK population, and frankly, much of the global
population these days, is the way they're going to... Let's take a high sugar fruit like a mango,
for example. If you're in perfect metabolic health, everything's working great,
metabolic health, everything's working great, that mango is going to have one effect on you,
I'm guessing, compared to someone who has advanced metabolic syndrome and is very insulin resistant.
I guess the point I'm trying to get to is too often, I think, we're trying to say,
this is good, this is bad, this food is good, this food is bad. Context matters massively.
The state of your cellular health, the state of your mitochondrial health, the state of your insulin sensitivity, all that
plays into whether that particular fruit is going to be helpful. Because I think the truth is for
some people who've got type 2 diabetes, actually having as much fruit as they want because it
contains antioxidants, I personally haven't
seen it to be the best idea. But then people will get very black and white. You're saying
fruit is good or fruit is bad. It's like, well, no, hold on a minute. I'm saying for this individual
patient who's very, very insulin resistant and is struggling, I'm not sure they need to be having
lots of high sugar fruits. How do you see it? First of all, Rangan, I couldn't agree with
you more. You are 150% right. You have said nothing I disagree with. In fact, I subscribe
to it wholeheartedly, completely. People are black and white. People want rules. People want to be told, this is good, this is bad.
This is helpful, this is hurtful. This is good, this is evil. And it's never that simple.
It's never that simple. What we've learned is that different foods affect different people,
different ways.
That is what we have learned.
And there's absolutely no question that you take somebody who is in the prime of health,
who is completely insulin sensitive, who is a marathon runner,
and you give them a glass of orange juice, it's going to have a different effect on them metabolically
than if you take a 70-year-old sedentary type 2 diabetic
who's got vascular problems and potentially kidney problems, and you give them a glass,
the same glass of orange juice, it's going to have much worse effects. No argument, completely.
it's going to have much worse effects. No argument, completely. How do you know who you are?
How do you know whether or not this food is okay for you and that food is not? We're still in the process of trying to figure all of that out. We have some tools. There are a few things that we can do now.
Now, there are some general global things, like for instance, this thing called glycemic index,
which I hate. I think glycemic index needs to be blown up, but the dieticians still subscribe to it. Before you move on, Rob, could you explain why that is? Because a lot of people will know
that term and they'd be very interested to know why you're not a big fan of that term not a big fan is being is an understatement
okay i kill the glycemic index now right so let me explain for your audience what this is okay It is a tool that dieticians developed that tells you how high does your plasma glucose rise
after you eat 50 grams of carbohydrate in any given food. That's what glycemic index is.
And it's all standardized against the rise that you would see with white bread. White bread would have a
glycemic index of 100. So it's straight glucose. There's nothing else in it. It's polymerized
carbohydrates, straight glucose. So if you eat a piece of white bread, you're going to get a big
glucose rise in your bloodstream. And everything else is compared against that. All right.
That sounds good because when you generate a glucose response,
you also generate an insulin response. And the glucose does one thing, it causes vascular
endothelial cell dysfunction. And the insulin does another thing, it causes vascular smooth
muscle proliferation and cell growth. Okay. So they both have problems. The glucose has a problem and the insulin that
follows it has a problem. So obviously the higher the glucose goes, the worse off you are
metabolically. Now that's true. That is true. I don't say that that's not true,
but glycemic index is not the way to figure it out. And here's why.
it out and here's why. Two reasons. First, let's take carrots. Carrots are good. If you eat 50 grams of carbohydrate in carrots, their blood glucose is going to go pretty high. So carrots
have a high glycemic index. The question is how many carrots do you have to eat to get 50 grams
you have to eat 700 grams of carrots to get 50 grams of carbohydrate what's the rest fiber
so you are taking in 650 grams of fiber to get 50 grams of carbohydrate. Okay? So it's not about glycemic index,
it's about glycemic load.
Okay?
You have to eat 1.4 pounds of carrots
to get 50 grams of carbohydrate in carrots.
Okay, you tell me who does that other than Bugs Bunny.
All right?
So the concept of glycemic index is useless.
Glycemic load, that makes more sense because that takes into account the fiber issue.
So that's the first reason.
Second reason, fructose.
So remember, glycemic index is how high does your blood glucose rise?
Doesn't say anything about how high does your blood fructose rise?
Because you don't measure the blood fructose in the glucose level.
So when something is sugar, it's half glucose, half fructose, which means the blood glucose will only rise half as high because the rest is fructose, and it's not captured in the measurement. Yet fructose is seven times worse in terms of
generating reactive oxygen species and in terms of generating liver fat, both of which drive the
phenomena of metabolic syndrome. That's not captured in glycemic index because it's only
concerned about the glucose. It's not concerned about the fructose i guess the other issue is we're all highly individual aren't
we we're learning that more and more over the last what five ten years that we all have different
responses to the same food exactly and that's what levels health showed us by normal people wearing
continuous glucose monitors now the fda says don't do that and the FDA says don't do that, and the government says don't do
that. But the fact of the matter is we are learning a lot by having normal people wear
continuous glucose monitors because we are seeing the variation that occurs across populations.
And what kinds of things actually influence the glucose excursions,
which we know have information in them,
and we also know have pathology in them.
And the goal is to keep your glucose down,
in part because keeping your glucose down means less endothelial cell dysfunction.
And also, if you keep your glucose down, it means keeping your insulin down.
And that means less cell growth,
less chance for chronic metabolic disease also.
So knowing how your body responds to a specific food
turns out to actually be quite important.
And there's no way to know that
unless you're wearing a monitor.
It's interesting that you said that you're looking at normal people wearing cgms wearing continuous glucose
monitors and seeing how they respond to certain foods the word normal is quite interesting isn't
it because there's no one's normal you know 88 we we we hear of the u the US population have a degree of- No, 93.
93% has gone up.
And metabolically dysfunctional.
So when you wrote Metabolical, and the first time you came on my podcast,
I think the figure was 88%. So already in the space of, what, a year or two, that's gone up to 93%.
Right.
There were two papers.
The first paper was 2019, Araujo et al.
And it was at 88%.
paper was 2019, Araujo et al. It was at 88%. Then the next paper from Mozaffarian's group out of Tufts actually categorized it in 2021 at 93%. Maybe it was COVID that did that, I don't know.
Well, let's just pause on that for a minute, because for anyone who's watching this
or listening to this conversation and they haven't heard our first one, just explain what that means. 93% of the US population have a degree of metabolic dysfunction. Are
you able to very succinctly summarise what is metabolic dysfunction and why should people
be worried about that statistic?
Before we get back to this week's episode, I just wanted to let you know that I am doing my
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So many people tell me that health feels really complicated, but it really doesn't need to be.
In my live event, I'm going to simplify health and together we're going to learn the skill of
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Sound good?
All you have to do is go to drchatterjee.com forward slash tour.
I can't wait to see you there.
This episode is also brought to you by the Three Question Journal,
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So metabolic dysfunction means mitochondrial dysfunction. That's what it means. So mitochondria are the little energy burning factors inside each of your cells. Mitochondria are how you turn
chemical compounds into energy to power cells.
That's what mitochondria do.
Mitochondria are refurbished bacteria.
Okay.
They have their own DNA.
They made an alliance with us back,
you know,
5 billion years ago to basically be our powerhouse.
If we gave them safety and comfort. It's basically the way it worked.
It was a symbiotic relationship between the animals and the plants because bacteria came
from plants. So it's the prokaryote, eukaryote. But they have their own DNA. They act on their own. And what we have to do is we have to be nice
to our mitochondria. And that means not exposing them to toxins that can hurt them.
And it means not exposing them to overwhelming nutrients that basically overwhelm them okay we have to be nice to our mitochondria our mitochondria
have a set of proteins in order to maintain their proton gradient to allow
them to work and they're called complex one complex two complex three complex
four complex five and turns out there's this
one at the end, which is sort of the molecular motor of the mitochondria, and it's called ATP
synthase. And all of the food you eat, ultimately the electrons from that food end up going through
the mitochondria and coming out as ATP through this ATP synthase.
So when your mitochondria work, you can efficiently turn food into energy. But when
your mitochondria are not working, and there are ways to knock your mitochondria off their game,
off their game, stress, cortisol will do it. Toxins in the environment will do it.
The wrong fatty acids will do it because the mitochondria are made of fatty acids.
There are a whole bunch of things that can basically make your mitochondria not work right.
And a lot of them are toxins in the environment. And unfortunately,
stress is a big one, as we've talked about. So when your mitochondria are working subpar,
you are not turning chemical energy into motor energy to power the cell properly. That will generate the reactive oxygen species that will damage the cell that will ultimately make you feel lousy and tired
because you don't have the energy that you think you should have. And this is, of course,
what happens in aging. This is what happens in stress. This is what happens in eating bad food.
Yeah.
So all of these things are inexorably tied
to how well your cells work
and ultimately how well your mitochondria work.
So maintaining mitochondrial integrity has to be job one.
Yeah.
You know what I'd love to see?
And I'm not aware of any studies or research where they've done this.
You might be, I hope you are.
But what I'd love to see is, you know, in some of the populations around the world
where historically they would have 80% of their diet from carbohydrates,
but whole food carbohydrates. Let's say the Okinawans, maybe not the new generation,
but the few decades ago, the generations who were eating whole foods and were having those
purple sweet potatoes. I'd just love to know if they were wearing a CGM, what on earth was going
on with their blood sugars? Because
it would be quite interesting in that very low stress environment where they're moving lots and
they're getting good amounts of sleep and they've got strong community. When they're having these
whole food sweet potatoes, what is that doing? Is their sugar curve relatively flat? I don't wear a CGM all the
time. I probably wear one for two weeks, I would say every few months. So I don't personally want
to get overly reliant on it or too obsessed, but I use it maybe two or three times a year. I put
it on for two weeks just to see where I'm at and give me an idea of the regular foods I'm consuming, what are they doing? And one of the things I discovered is that sweet potato wedges shoot my blood sugar
pretty high. So the thing we've learned, Rangan, and Levels Health is to be credited with this.
And full disclosure, I'm an advisor to
levels and one of the reasons is because I recognize that this is an important
component of metabolic health is maintaining you know your glucose
homeostasis in a good place because that basically translates into functioning
mitochondria and that's what I'm really espousing here.
But having said that, and not that it's an advertisement for levels, but the bottom line is
everybody has their, shall we say, bad food, their problem food, The food that they think is good for them, which turns out not to be so much.
All right.
Everyone's got one.
And, you know, everyone says oatmeal is good.
Yeah.
But for oatmeal, you know, like 25% of the population spikes like crazy.
Okay.
Even though it's supposed to be something that's supposed to give you a consistent and non-spiky glucose excursion.
That turns out not to be true for a lot of people.
Different people, different problems.
And so the only way to answer these questions is for you to do it yourself.
Yeah, that's super interesting, Rob.
for you to do it yourself. Yeah, that's super interesting, Rob.
What do you say to opponents of continuous glucose monitors who say that looking at these blood sugar excursions, and again, for someone who's never used one of these
before, essentially, you basically see in real time what your blood
glucose is doing and you can very quickly extrapolate, oh, when I eat this kind of food
or this quantity of this type of food, this is what happens to my blood sugar. Now, it's not
universally accepted that this is a good thing, right? Some opponents would say that getting
obsessed with these blood sugar ups and downs is pathologizing
a normal physiological response. What do you say to that, Rob?
I'm sure. So there is no question that we have this thing out there now called orthorexia.
called orthorexia. So, orthorexia is basically a pathological hypervigilance about food,
okay, and that anything can hurt you. And some people have actually, you know, accused me of contributing to this phenomenon and, you know, concept of orthorexia.
You know, look, there's always going to be the pendulum swinging one way and the other. When we didn't
care about what our food did, look what happened.
If you care too much about what your food does,
that's a problem too. Somehow we have to find
the place in the middle. There are probably some people that should not wear. Because just because you gather
data doesn't mean it actually is data you can use. You have to be able to integrate it. And then you
have to be able to disseminate it to the patient in a meaningful way that they can understand.
So three separate phenomena, acquisition, integration, dissemination.
And you have to be able to do all three accurately and correctly and for the right patient.
You know, the fact is we've had this problem throughout all of medicine.
Ultimately, it is something you need to discuss with your doctor because your doctor knows you best.
discuss with your doctor because your doctor knows you best. But the idea that you shouldn't use it because, yeah, some people might consider it a problem is, you know, that's how you get into
trouble, actually. So, no, I'm not okay with that. Yes, I agree. We need to take this down to the per patient level. This shouldn't be a blanket recommendation
across all populations.
And I think sort of opponents to CGMs also,
I think sometimes they make quite a black and white
extreme argument, which is,
yeah, if you eat just bacon three times a day,
seven days a week,
you'll have a completely perfect
blood glucose stable response, right?
But nobody's saying that only blood glucose matters.
No, no.
And that's correct.
So first of all, there are a whole bunch of carnivores out there, okay?
And carnivores will have the most stable of blood glucoses.
And the reason is because they're not running on glucose,
they're running on ketones because they're carnivores.
The fact is that the glucose excursion does matter and the reduction in the glucose excursion
can provide metabolic safety to some extent.
Now, having said that,
what if a patient with familial hypercholesterolemia
decides to go carnivore? That's a really bad idea. That's a really bad, that's a great way to end up
with cardiovascular disease really quick. Again, it's which patient are you and what's going on with you? And you have to do this individually.
Now, one of the knocks against CGMs is, well, you don't have diabetes.
Why do you need a CGM?
It's actually because you don't have diabetes that you actually do need the CGM.
Because it will give you information to prevent diabetes, not just treat it. And that's
what we've learned is, you know, super important, especially when, you know, 45% of America is now
pre-diabetic because they're insulin resistant. So how do you fix that? Well, glucose is one channel. It's one way. It's only one. It's
not all of them. Okay. So ultimately we're going to need more channels. And I agree with that. We
need ketones, we need lactate, and ultimately the one we need the most is insulin. We need an
in real time insulin monitor to basically tell us how high does your insulin go when you eat
certain foods. Now, the problem with insulin is because it's a peptide and because it's extremely
low concentration, it's much harder to measure in real time, but people are working on that.
We'll probably have it in about four to five years. Does that mean we shouldn't be using
glucose in the meantime? No, it just means that research will catch up to it and we'll have a better answer five years from
now than we do today. But we still have an answer now. Yeah. I mean, anything generally speaking
that you can do to educate yourself about your own individual responses, I think by and large,
for most people is a good thing, but it's a question of balance. I think our
personality plays a role here as well. Some of us are more likely to become anxious and obsessed.
Other people can look at the data in a much more distant way without affecting every single food
decision they make throughout the day. But one person's obsession is another person's care and attention, right?
So it's very hard to say what is right for another person, I think.
Having personal medical technology available to individual patients
is, of course, going to have benefits, and it's also going to have drawbacks.
Okay?
It's a tool.
Okay? Every tool has its good and bad side. going to have benefits and it's also going to have drawbacks okay it's a tool okay every tool
has its good and bad side okay nuclear power can be a tool right in terms of generation of electricity or it can be a downside it can be you know nuclear bomb okay a hammer can hammer a nail
it can also hammer a skull. So just because
something's a tool doesn't make it good or bad. It depends on the user. It depends on the purpose.
This is a tool. So for the right patient, it can be a good tool. Now, there are a lot of doctors
out there who don't know how to use it. They were never trained on it. They don't understand it. They never learned about this. And so they're going to be faced with somebody
walking into their office, you know, with all of this data saying, explain this to me, and they're
not going to be able to, and they're going to be like, screw this, right? We already see this,
you know, we have these people who are coming into cardiologist's office with oral rings you
know oh my god i threw a vpc what am i going to do now it turns out vpcs are normal can you just
explain what a vpc is for the audience ventricular premature contractions where your heart goes
you know like that um turns out you know until we aura rings, we didn't know how common they were, but they're common.
So, yes, this stuff happens.
So we have to ultimately determine, you know, like what's normal, what isn't.
And, you know, that expecting physicians to be able to, you know, sit down with all of these data and be able to interpret this for any given patient might be
asking too much of them. So the question is, how do you then democratize this? How do you
ultimately allow patients to be in possession of their own information so that they can utilize it
properly? Well, that's the hard part. We can absolutely get people to be in charge of their own information.
The question is, how do we know that they will utilize it properly?
And that's where guardrails are needed.
Yeah, for sure.
All right?
Okay.
The bottom line is, we have needed guardrails in our society for all sorts of things.
Let me give you an example of what happens when guardrails work
and when guardrails don't. Okay. In the last 75 years, there have been five major scientific
breakthroughs that have changed the world. Five. Here they are. Nuclear weapons weapons as soon as they were used everyone went straight to
the table because they saw the immense disaster that would could could be
coming and so they established guardrails and those guardrails for the
most part are still in place aren't they number two recombinant DNA back in the
70s 80ss. Okay.
Everybody said, oh my God, you know, we're going to unleash, you know, some virus.
Maybe, you know, maybe we've already seen it.
I don't know that that's to be determined.
But what did they do?
They established guardrails.
And now, you know, all this work is done in P4 facilities, you know, very specifically to keep it from getting out.
Number three, CRISPR. Okay.
CRISPR developed, you know, recently, and that Chinese doctor made two designer babies and
everybody rushed to the table and established guardrails for how to be able to utilize this,
you know, so that we don't actually, you you know re-engineer the human race number four
social media how'd we do with that one not so hot no guard rails and look what happened
and now we got number five ai i don't know what we're going to do about that. Bottom line is every one of these has the
potential for basically helping people because they are tools or hurting people if they are,
you know, basically democratized into the wrong hands. We need guardrails for these things. Well,
we need guardrails for CGMs too. We need guardrails for virtually everything we do in medicine. Okay, so I'm for patients owning their data. I am for patients understanding what's happening to them. I am for patients taking control of their own health within guidelines and within the guardrails that need to be set up for
it. So that's how I feel. We started off this conversation, Rob, talking about
the different fat depots, right? The three places where we can store fat subcutaneous visceral and liver and what was so interesting about that is that we can tolerate much more fat accumulation
subcutaneously you said 22 pounds on average before it starts to cause a problem whereas
visceral fats we can only tolerate about five pounds or so before it starts causing real harm to us.
Whereas with the liver, it's only 0.3 pounds. Now, just to make sure everyone's following along
with this, the subcutaneous fats we were saying was from consuming excess, and your body will
store that excess in a relatively safe place unless it gets too much.
You were saying stress is ultimately the key driver of visceral fat, which we know is really,
really problematic. What is the key driver of liver fat? I think you mentioned it was sugar
and alcohol, or I should say fructose. Well, is sugar as a term problematic? Because
when we use the term sugar, we know that people will say sugar is essential for life,
and they might be talking about glucose, or they might be saying blood sugar. And I sometimes say
blood sugar when I mean blood glucose. Are we at a stage where we need to be a bit more precise? Because the term sugar
can be so misleading, can't it? Oh, I so agree. You have hit me right where I live.
The fact is that there are corporate interests that ultimately misuse all sorts of verbiage
for their own purposes. Example, weight. Okay. What kind of weight are we
talking about? You know, body weight, fat weight, fat. Are we talking dietary fat? Are we talking,
you know, liver fat? Are we talking visceral fat? Sugar. Right. Exactly. Are we talking dietary
sugar? Are we talking blood sugar, which is really blood glucose. Ultimately, a sugar is not a sugar.
A fat is not a fat.
A pound is not a pound.
A calorie is not a calorie.
A fiber is not a fiber.
A protein is not a protein.
An amino acid is not an amino acid.
And down the line, of course, we should be more exact.
And I endeavor and strive to be more exact. Unfortunately, the population has not been educated into what these things are. So it tends to regress back to the mean. And so, and of course, because corporations actually hide behind this because they say, well, a sugar is a sugar. Therefore, I can put any amount of sugar I want in this thing.
this because they say, well, a sugar is a sugar, therefore I can put any amount of sugar I want in this thing. It is a problem. So yes, educating the public has been a major component of my work.
So when we then are talking about what drives liver fat specifically, you're saying alcohol.
And when you say sugar, do you essentially mean excess fructose?
I mean fructose. I don't mean glucose. I mean fructose. But because fructose is half of dietary
sugar and there is no fructose alone in nature, it always comes with fiber, except in honey.
But how much honey are you eating? But pretty much everywhere else, it comes with fiber.
Let's just pause on honey for a minute because many people will consume honey as a healthier
option because it's natural compared to, let's say, table sugar or refined sugar. Now,
I'm putting this out there just to get your view on this. The Hadza tribe in Tanzania,
hunter-gatherer tribe that has been very, very
well studied by lots of different groups, are well known to gorge on honey when it is available.
If they're on a hunt and they come across honey, from what I understand, they will often gorge on
that honey. Now, I'm also aware that these guys have great gut microbiomes. They're very, very physically
active. They do not touch ultra processed food. It's all food from nature, et cetera, et cetera.
So they're consuming potentially on occasion, large volumes of honey.
For the regular urban dweller who is listening to us chat now, should they learn anything from the headset about honey?
Or for us, is it completely different?
If you want to gorge on honey, have at it.
All right? And the reason is because honey is so freaking expensive
that if you gorge on it, you're going to be broke.
You're not going to be able to afford it.
The big problem with honey is not honey.
The big problem with honey is the fraud of honey
because almost all of the honey in the store
is not honey my colleague mitchell weinberg actually set up a uh uh check and balance system
on honey to keep uh honey fraud off the market almost all of the honey that you buy in commercial grocery stores,
unless you buy them in very artisan shops, is actually a conglomeration of glucose syrup and
fructose and some artificial flavors. Honey fraud is the single biggest fraud item in food worldwide.
Wow.
There are other things too.
There are wine fraud, there's fish fraud,
there's scotch fraud.
That's a big one.
But honey is one of the biggest.
And so they've actually developed a method
for determining whether or not the honey you're eating is actually honey.
First of all, I didn't know that.
That's really, really interesting and slightly concerning.
In our first conversation, you explained that table sugar is sucrose, which is made up of glucose and fructose.
Okay.
What is natural, real honey? Like, what is that up of glucose and fructose okay what is natural real honey like what is that made off assuming what we were buying or let's say what the hads are gorging on in nature right what is
that made up of it's made up of sucrose it's made up of glucose and fructose and it's got a couple
of other bioactive compounds now Now, those bioactive compounds have
never been shown to do anything. They may do something, but not usually in the amounts and
concentrations that people consume them in. There are a lot of people who say, well, honey is good
for you. Show me. Show me the data that shows that honey is good for you. There are a lot of people
who say it. I'm still waiting to see the data. Are you essentially saying that for someone
who is probably not in the best metabolic health, which is most people, consuming honey from a metabolic health perspective is pretty much the same thing
as consuming table sugar? Yeah. The good thing about honey is because it's expensive and because
it has its own unique flavor, people tend to use less of it. And anything that makes you use less
of it, as far as I'm concerned, is good. But from the standpoint of gram for gram, ounce for
ounce, calorie for calorie, it's basically no different from sucrose. Okay. So let's go back
to liver fat for a minute then. So liver fat, it doesn't take much liver fat accumulation,
0.3 pounds, as you mentioned, to start causing problems. Now that doesn't sound like much at all. And you're saying that excess fructose and alcohol are the two main drivers of that.
One of the other, there's a third, there are two other drivers of it as well.
Trans fats did that like crazy. But as we learned that, and in 2013, the FDA banned trans fats in
foods. So that's good, except by the way, the FDA banned trans fats in foods.
So that's good, except, by the way, there are still trans fats in foods.
Because of the FDA rules here in the United States,
let's say if you are below 0.5 grams of trans fat, you can say zero.
You get to round down. So if you have 0.49, you get to say zero.
Now we have learned that two grams of trans fats
are cardiovascularly toxic.
If you consume two grams of trans fats per day,
you're gonna get heart disease.
So if you consume four candy bars,
let's say that they have no trans fats in them,
there's a good chance that you will have gotten the equivalent of two grams.
So just because it says none doesn't mean it's none.
This is one of the other subterfuges of the food industry.
So that's one thing.
And then the fourth thing that causes this liver fat is branched chain
amino acids so leucine isoleucine valine now these three branched chain amino acids
are common they are 20 percent of muscle so if you if i took a muscle biopsy and I subjected it to amino acid analysis,
okay, 20% of the amino acids in muscle are branched chain amino acids. And all three of
those branched chain amino acids are essential amino acids. You have to consume them. You can't
make them. So leucine, isoleucine, valine, you have to consume them.
It's not like you can make your diet branch chain amino acid free. You need them. But
if you consume excess branch chain amino acids and you're not laying down muscle,
so you have no place to put the branched chain amino acids into.
And you consume excess.
Where's the excess go?
So they go to the liver.
The liver takes the amino group off.
Now they're a branched chain organic acid.
And now they go into the Krebs cycle, go into the tricarbosilk acid cycle and the mitochondria.
And now they go into the Krebs cycle, go into the tricarbosilic acid cycle and the mitochondria.
You've now added extra substrate that the mitochondria can't process.
It overloads it.
And so you're going to throw off that citrate and that citrate is going to end up undergoing de novo lipogenesis.
And you're going to make liver fat out of the amino acids because you didn't need them
so branched chain amino acids if you're a bodybuilder are great and so that's why bodybuilders you know scoop protein powder you know when they make their smoothie shakes
and you know if you're a bodybuilder that's okay But if you're not a bodybuilder and you're taking
excess branched chain amino acids, all you're doing is increasing your liver fat. And that's
what we're seeing. And so the question is, all right, where is Joe Schmo getting his branched
chain amino acids from? And the answer is corn. Corn fed beef, chicken, and fish, which here in the United States is virtually all of our protein supply.
So that's different from grass-fed.
Exactly. Grass-fed has less branched-chain amino acids.
It sounds, Rob, to me, if I sort of try and zoom out and take a big picture look at this,
I feel like the liver needs some better PR, right? Because we are excited about brain health and
heart health and muscle health. No one's getting excited about liver health.
Liver needs love.
Liver needs love, right? The liver's the heart. It's arguably the most important organ when it
comes to metabolic health. I don't know if you disagree with that.
When it comes to metabolic health, it is the organ of record. Yes.
Come on. Pretend you're doing PR for the liver at the moment, Rob. Tell us,
why should we care about the liver?
Because when your liver works right, every other cell in your body works right.
And we've actually looked at this.
This is one of the reasons why in metabolical, I, you know, espouse to protect the liver.
Okay.
Promote metabolism, suppress inflammation.
So those are the two things that you have to do to be metabolically healthy.
Promote metabolism, suppress inflammation.
Promote metabolism where?
Well, the liver, because that's what does the metabolism.
That's where virtually all the metabolism in your body gets done.
It's where detoxification of poisons comes in. It's what ultimately sends
out energy to the rest of the body because the liver is in charge of turning that energy into
stuff that the rest of the body can use, whether it be ketones or glucose. It is the thing that
ultimately impacts on your blood glucose control because it's where insulin works. Insulin works
at the liver. That's why the pancreas is in
series with the liver. That's why the pancreatic vein drains into the portal vein to go to the
liver, not to the entire general circulation because the liver is ground zero. Good liver,
good body. And all the data shows that when you screw up the liver, everything upstream of the liver
gets worse. That's what we've shown. So yes, you got to protect your liver.
And what do you have to protect it from? Well, you have to protect it from toxins.
And what are those toxins? Well, the big one is fructose. Not the only one, but it's the big one. Okay. Are there others? Sure. Cadmium, arsenic, you know, a lot of heavy metals are, you know, big ones there.
And of course, alcohol is the other, you know, huge one.
And if your liver works right, you will be healthy.
What is the best way for someone to assess the state of their liver?
So that's a little bit harder and it's a little more complicated. The easiest way, the cheapest
way, the free way, if you will, but unfortunately not the specific way, is a waist circumference.
not the specific way, is a waist circumference. So that anyone can do. But unfortunately,
it doesn't necessarily tell you everything you need to know. But it's a good start.
And what do you look for?
Well, if you're a male over 40 inches, if you're a female over 35,
means probably have a liver problem.
But that's, can I just say on that, that's interesting. And you've also said that it's not perfect. If I think about that through the lens of myself, I'm naturally slim.
Now, yes, I do look after myself and I pay close attention to the way I live my life,
but I would say I'm naturally slim. If I got up to, I would say a 37 inch waist,
I would say a 37 inch waist, that would be huge for me, right? So the reason I'm bringing that up is purely for the fact that 40 inches, it kind of depends on your starting point as well.
Because I would even argue if I got to 36, 36.5, I would say for me, I'm carrying extra fat around
my abdomen. So- No question. No question. This is racially determined as well.
You know, Asians will have liver fat at a much lower BMI. Yeah. African-Americans will have
liver fat at a much higher BMI. So it's very, it's very individual and it's got race dependency
and sex dependency and age dependency.
So that's one of the reasons why it's not that easy to use.
Number two, lab tests.
All right, what lab tests?
Well, the easiest lab test and the one that pretty much everyone gets once a year is an ALT. Yeah.
Alanine aminotransferase. Now, the problem with alanine aminotransferase
is it's sensitive but not specific. If your ALT is high, it usually means you have liver fat.
Doesn't tell you why you have liver fat, but it usually means you have liver fat.
But the question is, what's the cutoff? And this is where things get a little dicey.
Because the doctor will look at the lab slip and say, oh, your ALT is 30. You're fine. And the
reason is because the upper limit of normal is 40 on the lab slip. Like hell it is. The upper limit of ALT should be 25. When I entered medical
school in 1976, the upper limit for ALT was 25. Yeah. And it should be 20 for African-Americans.
Okay. 25. But today it's 40. Did they change the assay? They changed the name, but they didn't
change the assay. Are they changing what, but they didn't change the assay.
Are they changing what they're measuring?
No, they're still measuring the same thing.
So why is it that 50 years ago, the upper limit for ALT was 25,
and today the upper limit is 40?
Very simple, because everyone has fatty liver now.
45% of the American population have fatty liver. So if you take 100,000 lab specimens
from 100,000 people who say they're healthy,
and you run the ALT and you measure the mean,
and then you measure two standard deviations from the mean,
and that's where you draw the line for what's abnormal,
the entire curve has shifted to the right because everyone's got fatty liver.
And so two standard deviations from the mean is now 40. So that's what they put on the lab slip.
So if your doctor's reading off the lab slip, oh, your ALT is 30, so you're fine. No, you're not
fine. You're not fine at all. Okay. You're consistent with the general population,
but the general population is not fine either. Yeah. So you have to be able to interpret the
number properly. So that's the problem there. And then once you get past ALT, now we're getting into the rarefied air and the expensive stuff and the imaging like ultrasound or the magnetic resonance spectroscopy or the elastography.
There's this calculation called FibroScan that will give you a little bit better answer.
But now we're talking like real money.
Yeah. I think the first two you mentioned there
are so accessible and cheap, right? Waist circumference, anyone can do that themselves
at home just to get an idea. Even if they track that themselves over time, every six months,
let's say you put it in your diary, you track it and you see which way it's going. That would be something really helpful to give you
an indication of what might be going on inside, something that you can't see potentially.
But also the ALT test. Now I know people watch and listen to the show all over the world,
but for anyone in the UK, that is available on the NHS.
I mean, you can get that.
Any adult can go in pretty much and get an ALT.
It's a very, very cheap test.
Standard test on a standard chem profile.
The only thing to admonish your listeners,
do not take normal for an answer.
Yeah, find out what it is.
Get the number.
Get the number and then maybe track it once a year
and see which direction it's going in.
And if you're concerned, discuss it with your doctor.
I think that's really useful.
I mean, that's how you can look for it in yourself,
but it's a pretty reasonable assumption
that most of us, most of the population have got
more liver fat than they would want. Is that a fair assumption?
That is a very fair assumption. Much more common than anyone realized.
Yeah, because you can't see it. And you know what else is common?
Non-alcoholic fatty pancreas disease.
Wow.
Whoa.
Not fatty liver, fatty pancreas disease.
Okay, now, how do you find that?
Well, you have to set the MRI in a very special way to be able to actually see that.
But we did that. And we found non-alcoholic fatty pancreas disease, and it correlated with insulin release negatively. So the more fat in the pancreas,
the less insulin released. So it's very possible that the fat being laid down in the pancreas is
actually one of the drivers of diabetes, which of course is responsive to sugar.
I mean, if we had another hour, I'd love to go down that rabbit hole, but we'll save that for
part three, Rob. That is really interesting. But there's a wider point there for me. I was
thinking about this today. In our first conversation, we spoke at length about non-alcoholic
fatty liver disease. I thought the term's interesting.
You know, we're kind of not really saying what it is. We're saying non-alcoholic, right? So
we could say fructose-driven liver disease, or sugar-driven liver disease, couldn't we? Or,
you know, something else, or ultra-processed food-driven liver disease, but we just say non-alcoholic.
So it kind of doesn't quite land for us that what we're doing may be impacting our liver fats.
So the hepatologists here in the United States, in their infinite wisdom,
have rebranded the disease. They've got a new name for it.
Okay.
the disease. They've got a new name for it. What is it? Okay. It is ready. M-A-S-L-D.
Massled. Instead of Naffled, it's Massled. And what is Massled? Metabolic associated steatotic liver disease. Now, which one of those two, NAFLD or MASLD, tells you what's going on?
Neither. Neither. I would like to call it processed food fatty liver disease. That's
what I would call it. But that's not on the table, unfortunately.
How early does this liver fat start to accumulate? Are we seeing it in children now,
for example? Oh yeah. No, we can see it in five-year-olds.
I've seen it in three-year-olds. And hold on a minute. Let's just be really clear here.
Should we be having zero
liver fat? Is that what normal is? Normal is zero. Right. Okay. So up to 5% usually means no damage.
But really, we should be aiming for zero, ideally. Ideally, zero to maybe 0.5%.
So if we just go back to
again the opening question right the three fat depots which really
appears to have been the theme of this entire conversation this time around
is it possible then if if theoretical question. If excess fructose and alcohol and yes, trans fats and excess branch
chain amino acids, if you're not working out regularly, if those are the key drivers of liver
fats, right? Is it in theory possible then if you are having a completely whole food diet,
but you're probably eating a little bit
too much of that whole food diet for your daily needs, and you have low to non-existing stress
levels, so you're not driving visceral fats, and you're not having excess fructose, and you don't
drink alcohol, is it in theory then possible that you will have subcutaneous fats, but no visceral fats,
no liver fats, and therefore be metabolically healthy?
20%. 20% of obese people are just that. They are metabolically healthy obese. We even have a name for them,
MHO, metabolically healthy obese. They will live a completely normal life,
die at a completely normal age, not cost the taxpayer a dime.
They just have increased subcutaneous fat tissue. So what?
And if we were to look at their bloods,
they probably have a normal-ish HbA1c,
normal triglycerides,
normal ALT that we just spoke about.
So for all intents and purposes,
it would just be a cosmetic...
I don't even want to say issue.
It's not an issue.
It's not an issue. The way society looks at it... It's not an issue. It's not an issue.
The way society looks at it...
It's only an issue in your own head.
Yeah.
If it's an issue, it's because you made it an issue,
not because it is an issue.
But yes, unfortunately, society is very cruel.
Yeah.
And they will punish people for just about anything.
But that's interesting, isn't it?
20% are metabolically healthy.
Yeah, 20% of the obese population is metabolically healthy.
Conversely, 60% of the normal weight population is metabolically ill.
So just because you're fat doesn't mean you're sick. And just because you're thin doesn't mean you're sick and just because you're thin
doesn't mean you're healthy and this is why it's so important for people to know who they are
and what they are and what caused them to be who or what they are and that's one of the reasons
for gathering these data and figuring it out and And don't just let your doctor say,
ah, your labs are normal, go away.
I've got two kids, Rob, 13-year-olds and an 11-year-old.
Given everything you have researched throughout your career,
given all the patients you've seen,
if you were sitting in front of my children right now, and you were going to educate them
on health and the importance of how they treat their bodies,
what are the key things that you would say to them? Eat real food.
And if they say to you, Dr. Lustig, what does that mean?
What's real food?
What would you say?
So real food is what came out of the ground or animals that ate what came out of the ground.
Real food does not have a label because it doesn't need a label because it's real.
does not have a label because it doesn't need a label because it's real
in fact the only foods that have labels are foods that had had something done to it
so every label is a warning label does a radish have a label does a broccoli have a label
does a steak have a label none of them have labels because they're real food.
Now, if something's been done to it, then there's a label. So the question is, okay,
what is it that's been done to it? Maybe what was done to it was okay. Like it got, you know, it was milk that got irradiated, you know, to up the vitamin D. Maybe that's a good thing.
Maybe they added some preservatives so that it stabilized the shelf life.
Maybe that's a good thing, or maybe it's not a good thing,
because we're now learning that certain preservatives are actually mitochondrial toxins.
So it's not what's in the food. It's what's been done to the food that matters. All food is inherently good. It's what we do to the
food that's not. And that's why I wrote this book, Metabolical, is to explain to people what's been
done to their food that they don't know about because the food industry doesn't want you to know about it because if you knew what they did to it you wouldn't buy it yeah
so eat real food and the way you know you're eating real food is it doesn't have a label
that's good advice i hope i very much hope i very much hope my children know that by now
they certainly i certainly think they do know that um look if you think cheetos is food you
know all you know it's it's all over that you know we have to undo this concept you know that
people think that this is the case so So here's a question for you.
Well, we can end on this.
All right, Rangan.
Okay.
In order to understand this, you have to actually know the definition of food.
So what's the definition of food?
Well, I'll tell you right now from the dictionary okay i memorized it substrate that contributes
to either the growth or burning of an organism that is the definition of food substrate that
contributes to either growth or burning of an organism what does that mean burning of an organism. What does that mean, burning of an organism? In other words, used for
energy utilization. Burn. Okay. That's a perfectly fine definition. It is a 100% definition. Okay. I
have zero problem with that definition. Okay. So let's go to burning first. Bottom line,
first. Bottom line, fructose inhibits burning. Fructose has been added to 73% of the items in the American grocery store. Okay, that's burning. Now let's take growth.
My colleague, Dr. Afrat Monsonigo-Ornan, who is the head of nutrition at Hebrew University Jerusalem,
has actually studied this. It turns out that ultra-processed food inhibits growth. It inhibits skeletal growth, it inhibits trabecular bone growth, it inhibits cancellous bone growth,
it inhibits cortical bone growth. You can actually see it on electromicroscopy, you can see the holes eaten out of the bone. You can see the problem with the epiphyses not, you know, gaining in length.
Okay, you can measure the bone.
You can measure the tensile strength of the bone.
Basically, the bones break.
One of the reasons for osteoporosis, one of the primary reasons for osteoporosis.
So, if a substrate does not contribute to growth and does not contribute to burning is it a food
yeah we have to teach that we have to explain to people that ultra processed food is not food
just because the food industry called it that doesn't make it true.
What if a child was to say to you, Rob, okay, I get that.
Dr. Lester, this sounds really interesting.
But what happens if I want a bag of sweets once a week, right?
That's probably not food by your definition or by the definition that you're referring to.
Is that okay?
And I think what I'm trying to get to is where is the balance point for people? Because very few people are going to eat exclusively just real foods.
And so people want to know, you know, well, how much, you know,
what can I get away with as it were?
I totally understand.
I get it. I get it. So I'm going to
give you two things. One is a tool and the other is a concept. Here's the concept. I, Robert Lustig,
am for dessert. For dessert. I am not for dessert for breakfast, lunch, snacks, and dinner.
So if you're going to eat that bag of candy and that's dessert, hey, have at it. But that bag of
candy has as much sugar as the Froot Loops you ate at breakfast, And the Chinese chicken salad you ate at lunch.
And the chicken teriyaki you ate at dinner.
So in fact, you ate four desserts today.
So that's the problem.
It's not the sugar in the candy that's really the problem
because you identified it as such. The problem is the sugar in the candy, that's really the problem because you identified it as such.
The problem is the sugar in everything else.
The sugar in the 73% of the items in the grocery store that you didn't know had it, like the tomato sauce and the bread.
And so that's the concept.
Now, the tool.
My colleagues and I have developed a tool to help people at the grocery store
and it is called perfect p-e-r-f-a-c-t and you can find it online at perfect p-e-r-f-a-c-t.co
perfect.co and what it, is it's a recommendation engine.
Now, right now, it's for the United States. We would like it to be for the UK,
but it needs a branded foods database that lives online. And right now, the only one that exists
like that, that we know of is Waitrose. So we need Tesco and we need Marks and Spencer and we need,
you know, all of your other stores to sort of ante up. So for Waitrose, we can do it.
But in the United States, we can basically tell you any given food at your grocery store,
not only what's in it, but what's been done to it. And so you can apply specific
filters based on your metabolic status, whether you have metabolic syndrome, whether you're trying
to avoid carbs, whether you're trying to avoid oxalate, whether you're trying to avoid peanuts,
whether you're trying to avoid animal products because you're vegan. Okay. And you can basically filter out everything in the
store that is metabolically unhealthy for you. Yeah. And it's free. Yeah. Brilliant. Well,
we'll put that in the show notes for other people who want to check that out.
Robert, you're just doing such incredible work. You know, one of the most gratifying things about
researching your work for these conversations is if you go and watch any of your YouTube videos, the amount of comments underneath from people who
have literally said, Dr. Lustig has changed my life. Dr. Lustig got me onto a low sugar,
high fiber diet. Dr. Lustig really connects with me for the first time. He told it straight up how
it is. And that's what I needed to change my life.
I know you get a lot of naysayers, particularly as you're growing and your message is growing,
but that must be very gratifying to read and to hear from so many people what an impact you've
had on them. It is. There's no question. And I love to hear those stories because they give me purpose. They make me feel like I'm doing something valuable. What I don't like, and I truly don't like it, is when people, you know, when they think somehow I'm sort of like some rock star, you know, like, no, no.
No, no. It's the message, not the messenger. Okay. I would very much like to be anonymous.
I would very much like to basically, you know, have this problem go away, you know,
but it's not going away. And unfortunately it's going to need people like you and me to make it go away. Well, Robert, it's always a pleasure. You mentioned that eat real food is the
key message you want to give to children. I'm guessing that's the same message you want to give to adults.
Apart from that as a take home for people, is there any final bit of wisdom you want to impart
to people in terms of what they can do immediately to improve their health?
You can't solve a problem unless you know what the problem is.
And for the last 50 years, we've been told the wrong thing.
So,
what we have is,
we have a belief system.
Okay?
So, here's a new construct for you, Ryan.
Okay?
Are you Hindu?
Yeah, my family are.
I was certainly raised that way.
Okay.
Right. Do you ever think about being jewish not really no no okay because hindu work for you right okay in america in america only
when i was a kid in 1970 or so only two percent of people change religions. Today it's 24%.
Why is that?
Because whatever their religion is, it's not working for them.
Okay?
So they were taught a belief system,
and they found that the belief system ultimately did not solve their issues
or answer their questions. And so they are looking
for something else. Well, we have had a belief system called calories for the past 50 years.
And that's all it is, is a belief system. And believe it or not, it didn't work.
And it hasn't worked. And the reason is because it's not true.
And so what I'm trying to do is I'm trying to reorient people so that they can actually
understand what the truth, what the science says, and so that they can form their own narrative that
will work for them. That's what I'm trying to do. Well, Robert, you're doing a great job. I think
Metabolical is a fantastic book. Thank you for making time to come on the show again. I really
appreciate it. No, it's my pleasure, Rangan, anytime.
Really hope you enjoyed that conversation. Do think about one thing that you can take away
and apply into your own life. And also have a think about one thing that you can take away and apply into your
own life. And also have a think about one thing from this conversation that you can teach to
somebody else. Remember, when you teach someone, it not only helps them, it also helps you learn
and retain the information. Now, before you go, just wanted to let you know about Friday Five.
Now, before you go, just wanted to let you know about Friday Five. It's my free weekly email containing five simple ideas to improve your health and happiness. In that email, I share
exclusive insights that I do not share anywhere else, including health advice, how to manage your
time better, interesting articles or videos that I'd be consuming, and quotes that have caused me
to stop and reflect. And I have to say, in a world of endless emails, it really is delightful that many of you tell me
it is one of the only weekly emails that you actively look forward to receiving. So if that
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at drchatterjee.com forward slash Friday Five.
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