The SHOCKING SCIENCE On How To Prevent Diabetes & LOSE WEIGHT | Dr. Ben Bikman
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In this episode of Health Theory, Dr. Ben Bikman challenges the prevailing medical paradigm that frames Type 2 diabetes and metabolic syndrome primarily as a glucose problem. Instead, he argues from his book *Why We Get Sick* that these conditions are fundamentally diseases of profound insulin resistance and hyperinsulinemia (chronically elevated insulin levels). While high blood sugar is acknowledged as pathogenic in acute scenarios like diabetic coma or kidney damage via osmolar gradients, the chronic drivers of heart disease, Alzheimer's, infertility, and erectile dysfunction are attributed to excessive insulin. Bikman explains that current treatments often lower glucose by aggressively pushing up insulin production, which paradoxically worsens metabolic health over time. He posits that shifting focus from glucose management to lowering systemic insulin is crucial for detecting and treating the root cause of these diseases decades before traditional markers like blood sugar rise. The discussion delves into specific cellular mechanisms where hyperinsulinemia causes damage, particularly through Advanced Glycation End Products (AGEs) binding to Receptors for AGEs (RAGE), which triggers chronic inflammation and cell death in nerves and capillaries. Furthermore, Bikman details how excess glucose converts into sorbitol within cells that cannot store it as glycogen; this accumulation draws water into the cells until they burst, leading to tissue degeneration. The conversation also clarifies that not all fat storage is equal: visceral fat surrounding organs becomes insulin resistant to prevent organ crushing, whereas subcutaneous fat in women's gluteofemoral regions remains sensitive due to estrogenic influences and evolutionary pressures related to pregnancy survival. This distinction explains why men typically suffer metabolic consequences from weight gain sooner than women, as testosterone promotes dangerous central storage while estrogen encourages safer peripheral storage. To reverse these pathological states, Bikman outlines four core principles: controlling carbohydrates, prioritizing animal-based protein with fat, consuming high-quality fats like eggs, and practicing intermittent fasting. He asserts that carbohydrates are not essential nutrients for humans and that a vegan diet is incompatible with long-term human survival without expensive supplementation due to inevitable deficiencies in iron, vitamin B12 (leading to pernicious anemia), and essential omega-3s like DHA and EPA. Regarding protein sources, he emphasizes the superiority of animal proteins over plant-based options because plants contain anti-nutrients like phytic acids that inhibit digestion and may concentrate heavy metals. He also highlights a unique physiological advantage in exercise: muscle cells possess insulin-independent glucose transporters activated by contraction, allowing them to clear blood sugar effectively without requiring high insulin levels, thereby lowering systemic resistance after physical activity. The dialogue addresses the limitations of current pharmaceutical approaches for diabetes, noting that drugs which block carbohydrate absorption or force glucose excretion via kidneys often result in side effects like diarrhea and increased urinary tract infections without addressing the underlying metabolic dysfunction. Bikman critiques the medical community's tendency to prescribe medications rather than advising dietary changes, arguing that treating symptoms with pills while ignoring the root cause of insulin resistance leads to a cycle of increasing drug dependence and worsening health outcomes. He shares personal anecdotes regarding diet-induced relief from chronic pain, brain fog, and migraines, reinforcing his view that many distinct medical conditions are merely branches growing from the same tree—insulin resistance—and can be pruned by cutting down this root through lifestyle modification rather than medication management.
Read the full video transcript
A vegan diet, um, well, to put it
bluntly, is incompatible with human
survival.
[music]
Everybody, welcome to another episode of
Health Theory. I am here with Ben
Bickman. Ben, welcome to the show.
Oh, Tom, my pleasure. Thanks so much.
Dude, I'm really excited to talk about
your book, Why We Get Sick,
uh, which is really interesting and it's
a take on what most people call
metabolic syndrome that I've never heard
before. Um, because I would literally,
7 minutes before beginning to research
you, I would have said the problem is
your glucose levels. And the fact that
that is the very thing that you like
swat down in the first like six words of
your book,
um,
walk walk us through that. What's the
difference? How is it possible that this
is not a glucose problem?
Yeah, yeah, so glucose, like like I
mentioned in the book, glucose is really
the sidekick, um, here of the story. And
to understand metabolic syndrome, we
need to understand the origins of that.
Uh, even the term metabolic syndrome
used to be called the insulin resistance
syndrome. And I I regret that we ever
left that title. Um, it's not that
glucose itself isn't valuable, but it's
that changes in glucose really ought to
be viewed through the lens of insulin.
And to to to defend that paradigm, let's
imagine an an individual who's
progressing from perfect metabolic
health to um, metabolic disarray. And at
the end of that would be type 2
diabetes. Type 2 diabetes really
represents the the prototypical
metabolic disease, which is itself a
disease of profound insulin resistance.
Now, to to kind of take us there on that
journey through time,
we would have an individual coming into
the clinic, and year over year, we would
be measuring their glucose. And we may
see year upon year that their glucose
levels are normal every time. And yet
other markers of of disease are getting
worse. Maybe they're gaining weight,
their blood pressure is starting to
climb, that is such a common one. Maybe
they have some fertility issues. In
women that would be PCOS, in men that
would be erectile dysfunction. But
throughout all of this, the the the
physician starts to treat the person's
infertility or they start to treat their
hypertension, but the glucose stays
normal and so they don't really pay that
any regard. However, if we had been
looking at insulin through this
timeline, we would have seen that while
glucose levels are staying normal, the
insulin levels are going up. In fact,
going up by potentially multiples. Where
by the time that 10 or 20 years later,
when we finally see the glucose starting
to change, insulin had changed
multiples. You know, it's maybe four or
five times higher than it used to be.
And if we shift the paradigm away from
glucose to insulin, we not only detect
the problem significantly sooner, indeed
potentially decades, but we also treat
the problem much much better because the
the prevailing glucose-centric paradigm
is that in type 2 diabetes, we have high
glucose and we just need to do whatever
we can to lower the glucose, including
pushing the insulin up even higher than
it was before.
That works in lowering the glucose,
but it reveals the the the problem in
that when we lower the glucose, the more
aggressively we're pushing up insulin to
lower the glucose, the more we're
literally killing these individuals.
They they get fatter and sicker and die
more by trying to push down the glucose
while pushing up the insulin. Again, the
paradigm should be this is a high
insulin state, which is insulin
resistance. We need to lower that not
and then let the glucose take care of
itself.
Yeah, so this is interesting because um
I'll start poking at the predictions
that your hypothesis makes.
[clears throat]
So,
if I could lower sugar without
increasing insulin,
then I should be able to um abate the
problem because I still like glucose is
still an issue, I'm assuming, right?
Um
oh, absolutely. Um and I don't want to I
don't want to um derail that the point
you're trying to make. Yes, and so I'll
keep it brief. Glucose is an issue, but
when type 2 diabetics are dying from
heart disease and and kidney failure and
other diseases and have a substantially
increased risk of Alzheimer's, it's not
the glucose that's doing that. It's the
insulin resistance. But that's not to
say hyperglycemia isn't pathogenic. It
is, but all the prototypical problems,
other than maybe the blindness that we
associate with diabetes, those are
really insulin problems.
So, what's cool about the hypothesis, so
um
you know, for anybody playing at home,
of course the thing I'm talking about to
lower your glucose without um
upregulating your insulin is diet. So,
avoid things that have glucose in them
and suddenly your blood glucose goes
down. Um
so, all right, that paradigm is
interesting. So, I can pull my glucose
down, it keeps my insulin down, and I'm
going to be healthier. So, it'll be
interesting to walk through um what the
problems are that insulin creates, but
first I actually want to understand
better what the problems are that
glucose creates. So, why is elevated
glucose a problem? Why does the body
work so hard? Because if I understand
right, the difference between uh normal
and somebody who's diabetic is a quarter
of a teaspoon Yep. of sugar in the
bloodstream, which is crazy when you
think about how much blood you have in
you, and it's that fine finely
regulated. So, if my body is willing to
pour this ultimately damaging hormone,
at least in in um
too high a level,
what is it that becomes the pathological
problem if I just let my sugar be
elevated?
Yeah, well boy, Tom, you're you're
bringing up a lot of very interesting
and relevant points here. So, gluco-
hyperglycemia is acutely acutely lethal
and chronic
chronically lethal or long-term lethal.
And acutely, um hyperglycemia can cause
a coma, a non-ketotic coma it's called
where if your glucose levels get too
high, and this would it depends on the
person, but it's typically around 200 mg
per deciliter. At around that range, you
are now you have a glucose amount in
your blood that the kidneys cannot
reabsorb. So, as you have all the blood
passing through the kidneys, um the
glucose will get filtered out and then
it will get pushed right back into the
blood. It'll get reabsorbed through
these glucose transporters that are
unique to the kidney.
However, once we've gotten to that, you
know, around 200, low 200s,
now what gets filtered out into the
urine or what would become urine cannot
get reabsorbed. And so, now we have
created an what's called an osmolar
gradient. Basically, this pull pressure,
whereas the kidneys are now pulling in
too much glucose and keeping that
glucose, they are demanding a certain
amount of water
to maintain a concentration that would
keep it somewhat comparable with the
rest of the body. And so, now the person
starts urinating out profound amounts of
of water. It's almost like a pressure
valve where the body knows that the
long-term consequences of the glucose
are going to be disastrous and I'll I'll
are they? I I want to really understand
that. So, why am I having why am I going
into a coma? Like, what's happening at a
cellular level? Yeah, so that is the
acute one. Um and that is that when when
you're urinating out too much water,
all of that water's coming from the
blood, what's called the plasma of the
blood, which represents the majority of
of what we call blood. And so,
naturally, as volume as the volume of
blood starts to go down, so too does
pressure. Pressure will go with volume,
just that fundamental physical
principle. And so the volume's coming
down, pressure goes down, and we are a
big column of water. And the one tissue
that that is most susceptible to
reductions in blood pressure is the one
tissue at the top of this column of
water, namely the brain. If we don't
have enough pressure in the in the
cardiovascular system, we literally
cannot get blood up to the brain, and
now the person will go unconscious and
will stay unconscious.
let me chase that what that hypothesis
would predict is if I could somehow keep
my blood pressure elevated, I could
tolerate
um more blood sugar. Is that accurate?
You absolutely could. Now, but that
would lead us to the long-term
consequences, which is the damage to
nerves and and and capillaries. There
are two distinct mechanisms whereby
hyperglycemia or chronically elevated
glucose is going to damage cells in
capillaries and and nerves in
particular. They appear to be very
susceptible to this. One is the
activation of a receptor on all cells.
All cells have this, and it's called the
receptor for advanced advanced glycation
end products or rage. That's the clever
little acronym.
Advanced glycation end products are
literally just molecules of of taking a
glucose and binding it to amino acids
that are just circulating in the blood.
So what ends up happening is that these
advanced glycation end products will
bind to these rage, these receptors, and
then they activate inflammation. Rage
actually is just what's called a pattern
recognition receptor. It will recognize
all kinds of things that are generally
viewed as noxious stimuli. So
essentially, rage is just waiting there
to be activated if something messy comes
around. And then it will say, "Hey,
you're Yeah, like like like bacteria.
Bacteria are a big one. So kind of
infectious or harmful agents in the
body. Rage is just waiting there to
activate the immune system. And then
what happens when we have chronically
elevated glucose, we have advanced
glycation end products chronically
elevated and now the body is is
essentially activating inflammatory
pathways within cells all the time. And
if a cell is activating those pathways
for too long, it will activate
apoptosis. It'll basically say, I can't
I can't do this anymore. I need to die.
And the second mechanism is is actually
somewhat related to the topic I
mentioned earlier about osmolar um
gradients and trying to balance fluids.
When when you have such a high level of
glucose, many cells of the body have
open doors for glucose. It where the
glucose just comes in. If there's a
higher amount of glucose outside the
cell than in, then it just can't help
but pulling keep pulling the glucose in.
But that overwhelms the cells' capacity
to burn the glucose. And cells can't
most cells can't store glucose like the
liver can. It can store glucose as
glycogen. The muscle can do that, too.
Many cells of the body don't have that
capacity. And so that glucose sits
around and then it gets converted
eventually non-enzymatically. It's just
this sort of process of the glucose
changing into a molecule called
sorbitol.
And sorbitol is membrane impermeable.
Once you have sorbitol in a cell, it
literally can't go anywhere. And so you
have more and more of this sorbitol
accumulating in say the endothelial
cells of blood vessels and then the
these cells start pulling in more and
more water and then they burst um
through this degeneration process. They
basically get so full of water that they
pop.
I love understanding this stuff at the
cellular level and look, I'm so wildly
ignorant. Like it's crazy to me that
I've gotten to my age without having
heard any of what you're talking about
right now. Um so now walk us through
what that looks like as pathology and
then my next question will be
why the cell cells start to get annoyed
and start making it impossible to feed
them the glucose.
Yeah, yes. That this is great. This is a
great progression. One let me make one
other comment though that you you'd
touched on
or we were almost getting to and then
you'd mentioned well
if if I need ever more insulin to
control my glucose, why don't I just put
less glucose in the system? That
strategy is so obvious
that it has led to multiple drugs being
developed that do nothing more than
there there's two classes of drugs. One,
it'll block the glucose from digesting.
There there's this class of drug that
will you can eat starch and you take
this pill and it doesn't allow your
intestines to absorb the glucose. And so
the glucose stays in your guts and you
sure you might get some diarrhea but
then it never it never moves the glucose
into your bloodstream. Alternatively, in
that same family of drug, you have one
that you can take that will actually
force the kidneys to excrete more of the
glucose. It essentially accelerates that
natural limit or that that that it
lowers that threshold
making the kidneys more readily dumping
out that glucose. It's not going to mess
with my blood pressure though? Well,
sure you have to drink a lot more water
but it will work. It'll lower your
glucose and that helps your insulin come
down but Tom, you touched on it so
accurately at the beginning. If I'm
taking a drug that is going to block my
glucose from coming in and give me
diarrhea or I'm taking a drug that's
going to force the glucose into my
kidneys potentially
well, drastically increasing urinary
tract infections and maybe even
increasing bladder cancer because cancer
and infections all love glucose. Why
don't I just take the rational
so obvious approach of just eating less
glucose? But that's the one conclusion
so many in this diabetes space like
genuine and educated and even smart
individuals, they they cannot they
cannot get themselves to that step. They
can nod and write prescriptions for for
glucose
inhibitors for digestion and glucose
pushers into the kidneys and yet never
just take a step back and say, "Maybe I
should just tell the person to eat less
glucose." That is really the logical
conclusion that's just being wait it's
just waiting for the person to come to.
And and you all you've already come to
with this idea of frame of reference.
Like everybody has a frame of reference
and I've heard you speak to this with
doctors. You said, "Look, a doctor's job
is not to go research all this stuff. A
doctor's job is to treat a patient." And
when your frame of reference from
schooling from just the society that you
grow up in is, "Hey, there's a drug for
that."
That's, you know, that's what you reach
for. And that's exacerbated and now
welcome to sort of, you know, as as we
all have ones that we love that struggle
profoundly with um food relational
issues. I won't go all the way to
addiction, but I think that would be
also a fair characterization. Mhm. Um
you see them, you know, doing themselves
uh great harm in terms of longevity, in
terms of quality of life, inflammation,
um just the level of adiposity that
they're carrying around. And you can
tell them, whether you're the doctor or
someone that loves them, whatever, "Hey,
by the way, just don't eat
carbohydrates." And they won't do it.
And so I imagine if you're a doctor day
after day after day, your frame of
reference is already drugs and you see
the people, the vast majority just can't
or won't make those changes, you just
Yeah, there it is.
Yeah, no, I think you're absolutely
right. And I never intend to to paint
all medical practitioners with such a
broad in such broad strokes. Uh
in fact, that's part of the tragedy of
this all, isn't it? Where where we're
we're describing this such a such an
obvious conclusion, which is just eat
fewer carbohydrates. And and yes, that
is such a simple idea, but that doesn't
mean it's easy to put in practice
because to your point, when you start
asking someone to change habits, you are
probably asking them to do the most
difficult thing they can do. It's just
so much simpler to take a pill and
consequences be damned. Yes, and here's
one insight that I think a lot of people
don't have. They don't recognize how
much of their life is tied to diet. And
I recently so I've I've been on that
train for
15 years. Thankfully just encountered
the right information at the right time.
This does not make me clever. It just
very luckily got onto that early. And
even I about I don't know 12 months ago
ish. Um I got into this thing where I
was making this like pecan pudding
thing.
Dude, it was so good and
I all of a sudden I was like, oh man,
I've got like crazy brain fog and I'm
tired all the time, but it was happening
at a time where I was stressed and I was
just sort of losing my enthusiasm for
life. And so I was just like, oh man,
you know, I've I've got to change
something so we you know, what's going
on? What's happening in my life? And I
was like, okay, what advice would you
give to somebody if they came to you
with this problem? And I would say, it's
your diet, man. And so I'm like, is it
your diet? Like you know about this
stuff, but is it your diet? And so I was
like, what am I eating a lot of?
I'm like, I'm eating a lot of pecans.
Let's cut them out. Literally 48 to 72
hours later, gone. So I was just like,
oh my god,
pain,
uh joint pain especially,
headaches, fatigue. Man, often times it
comes down to diet. And so like, when I
hear people who are are in chronic pain,
I'm just like, I'm telling you, start
with your diet. And so anyway, just
super super interesting. I have all the
empathy in the world for people
struggling with that. Like no judgment,
but um you know, I just want to see more
of them realize, okay, I can experiment
with my diet and make this pain go away.
Yeah, yeah, it's this this kind of
empowering idea. And that was very much
part of my intention when I decided to
kind of roll up my sleeves and get that
book all together. I I imagined an
individual who would be going to their
medicine cabinet every morning and they
would pull out a medication for their
hypertension, a medication for their
migraines, a medication for their
infertility, and or even their diabetes.
And then and at the end of this at the
end of this this like this conversation
when they realize wait, so many of these
problems, literally everyone I just
mentioned, but so many of these chronic
diseases that we're all afraid of, they
seem like they're distinct problems, but
to varying degrees they're all trees,
they're all branches from the same tree.
And rather than continuing to prune
these individual branches that all
inevitably grow back with the
medications we're taking, let's just cut
the whole tree down. Let's just get
right to the roots of this thing and get
rid of the problem. And and
so it was this idea that it might be
empowering that rather than hopelessly
taking medications every day knowing
that the only the only future is
increasing the dose of those
medications,
let's actually address the true origins
of the problem, which again to varying
degrees is often going to be insulin
resistance.
So now walk me into that pathology cuz
this is where the story really starts to
get interesting. Cuz so many things that
I had no idea were related to insulin
are direct results of insulin. Yeah.
Yeah, so insulin resistance, which is my
focus as a scientist, is is very likely
the single most common health disorder
in the world.
A paper published in 2018 found that 88%
of adults in the US were considered
metabolically unfit. In other words,
they had some aspect of the metabolic
syndrome. And again, as I mentioned
earlier, that's really the insulin
resistance syndrome. So it doesn't take
too much of a logical step to say well
then 88% of adults has have some
manifestation of insulin resistance. So
can we make that really simple and say
metabolically unfit just means it
you're forcing your system to pump too
much insulin?
Yeah, in fact, exactly. In fact, that's
a perfect segue to just defining the
villain. So, insulin resistance is the
villain and it's all the rage nowadays
to have a movie about the origins of of
villains. So, let's let's describe it.
So, insulin resistance is is two
problems. And this is so essential.
Those especially for those that are in
the low-carb space where the term
insulin resistance
I believe gets invoked a very
inappropriately in certain
settings.
Um and you have to have both of these
phenomena occurring for it to be insulin
resistance. One is the insulin
resistance itself. And that is defined
um at the level of the cell.
What is insulin? How is insulin acting
at the cell? Once upon a time, one
molecule of insulin was capable, say, of
of moving this many molecules of glucose
into the cell. And that's one of
insulin's main most famous actions where
insulin comes to the door of a cell,
knocks on the door, allows the glucose
to then come in once it's opened those
glucose doors.
Um so so insulin can't do that as well.
That's part of the what we call insulin
resistance. So, insulin resistance is
that some cells of the body, but not
all, aren't responding to insulin as
well as they used to. And that is a
particular problem in light of the
second aspect, the second side of this
coin that we're calling insulin
resistance, which is the
hyperinsulinemia, or in other words, the
chronically elevated insulin levels. You
That is the part that's overlooked.
People will only want to mention the
insulin resistance part of it, maybe the
elevated glucose levels,
which again is really selling insulin
short as it has its hand in thousands of
biochemical reactions throughout the
body. But even still, you cannot pull
that apart from the chronically elevated
insulin. There is no situation of
insulin resistance in the body that that
lacks the the other side of this, namely
the hyperinsulinemia. And that is the
pathological side, which we're talking
about now, where someone is noticing
their blood pressure going up or he's
noticing his erectile dysfunction. Those
are very much consequences of the
insulin resistance.
But do we have And that's that's the
pathological insulin resistance. But
there are states of physiological
insulin resistance where the body is
deliberately pushing up its insulin and
changing the efficacy of the insulin
throughout the body in order to do
something. So it's serving a useful or a
physiological purpose. But that only
happens in two instances. It's puberty
and pregnancy. In those instances where
the the elevated the the substantial
increases in insulin are facilitating a
substantial growth.
And in pregnant mom, it is basically her
body's way of saying
"I'm about to undergo this metabolic
marathon growing this little human in my
belly, and I need to make sure I have
enough fat to go through that whole
process if for some reason food became
scarce." And so it really does serve a
purpose for mom to get fat in the
elevated insulin in that
pregnancy-related insulin resistance
help that helps that happen. But also
mom's elevated insulin helps the baby
grow and the baby get fat. And a baby
must be fat when it's born to be
healthy. In fact, if a baby is too
skinny, um it's very likely the baby
will suffer from learning um
disabilities as the baby grows as he or
she grows because a baby In fact, Tom,
it's a this I I hate that I'm getting
off topic, but you steer me back if we
need to. Humans are the only land-based
mammals that are born obese. And we are
the only animal that is born with a
brain and head a skull that is bigger
than the birth canal, much to mom's
chagrin. But we have these massive
metabolic um demands in our brain. And
the baby must have enough fat to make
enough ketones to feed the brain. And if
baby doesn't have enough fat when baby's
born, say because baby's premature,
um then then we need to make sure we can
fatten that baby up as quickly as
possible. Otherwise, it's it's very very
likely the baby's going to have learning
disorders because it just wasn't getting
enough ketones to to fuel this
incredible growth of the brain during
those newborn years. Okay, God, there's
so much there.
Um I want to go back. You had mentioned
that not all cells get insulin
resistant. What cells do not get insulin
resistant? Yeah, that's a great
question. In fact, I I like to present
this sort of paradigm when I teach this
idea to my students. You have some cells
on one end, um like like uh muscle
cells. Muscle cells can become very
insulin resistant. That's a problem
because now they're not pulling in
glucose as well. It's a problem because
insulin isn't defending the proteins,
and now you could be break breaking down
muscle proteins, um and then just
releasing those amino acids, but for no
for no reason. It's just that the
insulin isn't working. Then you have a
tissue like the liver, um which uh
can can some of its aspects become
insulin resistant and some of the
liver's processes stay insulin
sensitive. And then, you have some types
of fat cells,
like, for example, the the the the fat
cells that a woman will have on her butt
and hips, the what's called the
gluteofemoral fat depot or fat pad.
Those are fat cells that will virtually
forever maintain perfect insulin
sensitivity. Insulin will always tell
those fat cells to store more fat. But
not all fat cells. So, like a guy, fat
cells that where where they're stored
more centrally around the abdominal
area, or or even more um
relevant, the visceral fat cells, the
fat cells that are within the abdominal
space and behind our behind our abs,
behind our muscles, um around our liver
and guts and kidneys, those are those
are fat cells that can become insulin
resistant. But so we have those the glu-
the gluteal femoral fat cells, which is
which is a subcutaneous fat. That's a
fat that you can pinch and jiggle. Um
those maintain almost perfect insulin
sensitivity forever. And I don't know
why
it could be that a woman has such a
the woman is going to bear the metabolic
burden of pregnancy. And so that might
just represent a way to ensure that the
woman always has a place to store a
little extra fat should she need it. And
if you think about the cell, the fat
cells within the abdominal within the
visceral space surrounding our kidneys
and our liver and and etc. and our
intestines, if we had limitless
potential to store fat there, it would
literally crush all of those essential
organs. You know, it would be expanding
so much that it may even start to put
pressure on the lungs and the and the
heart. And so then we die. So that it's
we we it makes sense that those fat
cells would become insulin resistant
because insulin tells fat cells to grow.
And those cells essentially get to a
point of hypertrophy where they start to
tell insulin, you want me to keep
growing, but if I do, we're going to
die. So for the sake of the body, I'm
not going to listen to you anymore and
I'm going to you want me to store more
fat, I'm going to start I'm going to
become insulin resistant and I'm going
to start leaking fat. That actually
becomes a problem overall, but I would
say it's a it's a problem that we're
willing to have rather than, you know,
crush our internal organs. But when you
look at the the woman on her butt and
hips, well, there's no harm in storing
more fat there. It is literally not
going to get in the way of anything. She
might she might curse it, but but it is
a nice place to store fat. And women
store more fat in the subcutaneous fat
depots, the fat beneath the skin that
you can pinch and jiggle, than men do.
Men store relatively more of their fat,
of course, on their abdomen, but inside
in the visceral space as well.
So if you have a couple they got married
in college, now they're both gaining 10
lbs, you know, every year or so, the man
will start to suffer from the
consequences of that much, much sooner
than the woman. Women can just
as visceral fat around his organs. Yep,
that's exactly right. Women can get
than men? Do you think the reason that
nature is doing that is because we don't
have to bear children?
Oh, I I do. Yeah, in in in fact, that
that difference in how we're storing fat
is entirely under the control of sex
hormones. Androgens, testosterone, like,
are are promoting the fat storage in the
abdominal and even visceral space.
Estrogens, in contrast, are very much
stimulating the storage of fat um in
that subcutaneous space, especially the
butt and hips, but also the arms and the
breasts and all those prototypical
female spots. So, that's under the
control of the sex hormones. That's why
little Tommy and little Jane, as they
grow up through puberty, they start to
look so different. It's because the sex
hormones are telling the body where to
store the fat, not how much, though.
Insulin's telling the body how much fat
to store. The sex hormones are just
telling the body where to store it and
how and how to store it, whether to it's
growing through making new fat cells,
what's called hyperplasia, which is
what's happening on the um the fat at
the butt and hips, or whether it's
hypertrophy, which is usually what's
more happening around the abdomen or in
the visceral Okay, so now we're back to
the uh the pathology of elevated
insulin. When you were describing all
the things that I just thought of
Honestly, I defaulted to thinking of
them as a a reaction to elevated
glucose. So, um you know, damage to the
epithelial lining of the vasculature,
like things like that. What what is
happening and what is it that that what
are the properties of insulin that cause
that?
Yeah. Yeah, well, it would depend on the
specific pathology, but you mentioned
the endothelium or the epithelial lining
of the blood vessels. So, that's a a
really nice
um place to to kind of define or
identify part of what's happening with
insulin resistance. Now, to put all this
in perspective
um as one step back and then I'll step
right back into it. Um
insulin has an effect on on literally
every single cell of the body.
There is not a single cell in the body
that doesn't have insulin receptors.
Every cell will respond will respond to
insulin in some way. Doesn't matter what
it is. Now, the endothelial cells are a
fascinating
example because they have multiple ways
to respond to insulin. And and this is
um very illustrative of how insulin
resistance is virtually in every
instance the the cause of hypertension.
So, if someone listening to this has
been told they have hypertension and
they've been struggling with it for
years or they're taking a drug for it, I
can almost guarantee it's because they
have insulin resistance. It is very
uncommon for that to be an exception.
So, there there are several distinct
mechanisms, um but but I mentioned one
where insulin will come to the
endothelium
and it will it will bind to the
endothelial cells and it will induce the
production of a molecule called nitric
oxide.
Now, that is not something that happens
at other cells of the body. And so, this
is just reflective of how unique insulin
is at different cells. It will tell
different cells to do different things.
And so, it comes to the endothelial
cells, it stimulates the production of
nitric oxide, which will relax the
smooth muscles of the blood vessel, and
now we have dilation. And so, that's
changing the way we're moving blood
around. In in systemically throughout
our body, that helps the blood pressure
be a little lower because the blood
vessels are a little wider. And so, now
the pressure has gone down, but at the
say with an erection, you need that
dilation to facilitate greater blood
flow into that area. And so, that's
that's the problem. And in fact, indeed,
that is the problem in in hypertension.
Um, chronically, when someone puts on
the blood pressure cuff and they see
their blood pressure is high, part of
that problem is that insulin isn't
working well. And insulin used to induce
this vasodilation because of nitric
oxide, and now it doesn't. Insulin is
still there. It's pounding on the door
of the endothelium. The endothelium
isn't working anymore.
So, that's one effect. But then other
ways that insulin is affecting
hypertension, insulin uh amplifies the
sensitivity to catecholamines, like
epinephrine. When when epinephrine is
high, it will induce vasoconstriction.
And it will induce the heart. It will
stimulate the heart to beat harder and
faster. In in chronically elevated
insulin, the insulin is pushing up the
epinephrine in the body. So, it's
amplifying this this kind of
anxious-like state, where the blood
vessels are constricting, the heart is
beating harder, and then overall, we
have an increase in blood pressure.
Another, [snorts] maybe one more, um,
just cuz I would dominate this for too
long. Insulin also stimulates the
release of a hormone called aldosterone.
And aldosterone is the main hormone that
tells the kidneys to hold on to salt and
water. And so, if you're eating a diet
that's keeping your insulin high, that's
going to artificially push up your
aldosterone. And the consequence of that
is going to be that the kidneys are now
retaining too much salt and water. And
of course, that means blood volume goes
up, and as blood volume goes up, blood
pressure goes up. And now our blood
pressure is potentially getting high
enough that it may hurt, um, blood
vessels. So, those are several distinct
mechanisms. In fact, I ended up bringing
in, you know, multiple different angles.
But to varying degrees, you have this
happening in the hippocampus, which is
compromising glucose use, which is
necessary for memory and learning, which
is why they call Alzheimer's disease in
insulin resistance of the brain. You
have this happening to blood vessels in
the brain, um, where they don't dilate
as well. They don't They're aren't as
dynamic and that can lead to migraines.
And that is why people who adopt
low-carb diets can in many instances
have a complete cessation of migraines.
They may never have another migraine
again.
Um and and and and many many more
pathologies. Polycystic ovary syndrome,
which is one I've alluded to a few times
now, which is the most common
infertility in women,
that is directly a result of too much
insulin in the body preventing the
ovaries from releasing a big spike of
estrogens. And if you don't have that
estrogen spike, you do not have
ovulation. And so the woman has ovaries
that are making lots of follicles
throughout the menstrual cycle or the
ovulatory cycle getting ready to
ovulate, but the insulin is preventing
it from actually ovulating. And now all
those follicles just stick around in the
ovaries making the ovaries get bigger
and bigger and bigger.
It is It is not to be trifled with. All
right, so we have just put told
everybody how they're getting themselves
in trouble. Now, let's get them out. You
do a great job of talking people through
this. Diet, exercise, what are what are
the keys?
Yes. Yes, so in fact, let's start with
the simple one, which is exercise.
Any kind of exercise is going to be
beneficial.
And that's [clears throat] because two
two reasons. One, during exercise
itself, insulin must come down somewhat.
It's just It is incompatible even just
for survival really to be exercising and
insulin staying high.
Because the muscles are using the
glucose and therefore there's no reason
to inject the insulin.
Yeah. Yeah, in fact, yes, that's a part
of it where if insulin is up, insulin
wants to store energy. It is It is not
allowing the liver to share its glucose.
It is not allowing the fat cells to
share their fat. Um and and so that is
of course not conducive to exercising.
You need those tissues to be sharing
their energy so that the hungry muscle
can be pulling it all in. And so insulin
comes down during exercise. Now, to the
to the astute listener, they'd be
saying, "Well, wait a minute, Ben. You
You and Tom were just saying how you
need insulin to move glucose into the
muscle." Not when you exercise. That is
a genius in the design of the muscle
cell. It has insulin-independent doors
for the glucose. So, the moment you have
a muscle that is going through that
dynamic contraction and relaxation,
you open those glucose doors without
insulin ever having in come ever having
come knocked on them. So, it's an
insulin-independent mechanism. So, it
That Wow, I've never heard that before.
So,
muscle cells do not need insulin, then
why do other cells need insulin? Because
is it going back to that sort of idea of
like, "Hey, even between men and women,
we have to like, you know, move this
stuff around differently. So, we need
sort of the middle man that's going to,
you know, partition this and, you know,
send this to the right places?"
Yeah. Well, in fact, [clears throat]
let's just burst the balloon. Um very,
very few cells of the body actually need
insulin for glucose uptake. Like the
liver that I mentioned a moment ago,
insulin will tell the liver what to do
with the glucose, but it doesn't tell
the liver to take it in. Most of the
cells of the body are They can pull in
glucose without the need of insulin. And
so, that's part of the tragedy of how we
define insulin through by just nature of
what it does to glucose when the reality
is only a handful of cells actually
respond to insulin with glucose uptake.
Um and that is muscle and fat and heart
and then the some parts of the brain.
And so, in the grand scheme of things,
that's that's a profoundly small number,
but the muscle
is so hungry during exercise that it
just basically tells insulin, "Look, in
when I'm and when I'm at rest, you're
the boss,
but when I'm exercising, I'm the boss.
I'm going to get what I need." And so,
it basically pushes insulin to the side.
And again, that's a good thing cuz
insulin comes down. And now that working
muscle can clear the blood of glucose.
And so, we have that acute benefit of
insulin coming down, then we have the
long-term benefit, which is at the back
end of all of this, our glucose is going
to be better controlled because we've
been exercising, and now the insulin
doesn't have that pressure to be higher
as it is.
I wore a continuous glucose monitor for,
I don't know, probably 6 months. A, it's
super fun. Anybody watching this
episode, if you've made it this far,
trust me when I say you'd really enjoy
it. Um and I had ice cream
and my blood sugar went from like
85 to 178
in like 20 minutes. Maybe it was a
little bit longer, but it was fast. And
so I started doing air squats
and I must have done
close to 300. It It was to the point
where I was like, I'm either just going
to accept that, you know, I have this
crazy uh blood sugar spike, or I'm never
eating ice cream again cuz I don't want
to do 300 air squats again. It takes
hours.
Um and but it dropped my blood sugar
back down. I think if memory served, it
dropped it back down to either right
around 100 or even back under 100. I I
literally I had heard people say a
million times, "Hey, exercise really
helps. Like if you're pre-diabetic, go
exercise." And it's just like, "Why
would that be true?"
And in doing that and seeing like, "Oh
my god, like my muscles are obviously
gobbling up the sugar from the
bloodstream." I I was really shocked at
how
how profound
the effect the measurable effect was.
Yeah, in fact, I that's that exact
phenomenon is why, which plays out in
multiple studies in humans, is that's
why I recommend that when someone has
eaten their most starchy meal of the
day, go on a walk. Just get out and do
something. Whatever that whatever that
meal was or that that treat that spiked
your glucose, get out and walk. Just go
on a 20-minute walk or something, and
you will much more rapidly bring that
down. What might be elevated for a few
hours may only be elevated for an hour
if you get out and do something.
Yeah, it's crazy.
Um, that's super interesting. Okay, so
exercise good, muscles have a unique
door that's really going to pull in the
the glucose. So, now talk to me about
diet. Right. Right. So, this is the
elephant in the room.
In fact, far far more relevant than
exercise. As much as I am an advocate of
exercise,
there are even exercise studies that
find that if you exercise and then you
follow that up with high-carb meals,
then you mitigate, you undo the
insulin-sensitizing effect of the
exercise itself. Just touching on the
fact that if you try to compare diet to
exercise, diet will beat the hell out of
exercise
as a variable for insulin resistance.
Now, when it comes to diet, the
principles I think there are, to me,
I've I've attempted to sort of distill
these ideas to four principles. And they
are so simple, but again, at the very
beginning of our conversation, we both
realized and acknowledged that doesn't
mean they're easy.
But,
assuming that someone would want to hear
them anyway, and then they can make
their own choice, I would say the very
first principle needs to be control
carbohydrates. Now, I'm not saying you
don't eat any, but carbohydrates are not
essential to humans. So, put that in
perspective then when when you're
looking at a big spread of of
carbohydrate-heavy foods,
um, this is that is the macronutrient
that is the biggest offender. It will
spike
live my entire life and never eat a
carbohydrate and be fine? Are we
prepared to stand by that statement?
Oh, to 100%. In fact, indeed, Tom, even
the most dogmatic dietitian has to even
reluctantly admit that. Um, it is it is
literally the stuff of dietitian and
dietetics textbooks. Carbohydrates are
not essential to humans. Again, that's
an unpopular sentiment nowadays,
especially, but it doesn't change the
reality of humans. There is no such
thing
get unless I eat
Well, yeah, yeah, that's a good
question. So,
there there are certainly and so let me
be nuanced here.
There are plants that can be beneficial
and part of a healthy diet, but that
does in no way mean they're essential.
There is there there's certainly no such
thing as an essential carbohydrate.
That's so In fact, we know people, I
know I'm friends with Shawn Baker.
Everyone knows about him. I mean, talk
about a beast. That guy literally eats
nothing but steak. Yeah, that's crazy.
The the whole carnivore thing is really
interesting to me. But all things being
equal, I don't care.
Right? So, as long as everything's being
done ethically and the animals are, you
know, treated well and free range and
all that stuff. And the only bad day
they have is the day they die and you
make that as wonderful as as you
possibly can.
Um
I don't care. So, I just want to know
what's going to help me be healthier
longer.
And I know you have some interesting
concerns about a vegan diet and I would
love to to hear
what you think it's missing if anything.
I don't want to put words in your mouth.
Yeah, yeah. Yeah, in fact, that this
plays well still into that first rule
with controlling carbohydrates. But
a vegan diet
Um well, to put it bluntly, is
incompatible with human survival. Um and
and so I like to get real specific.
Yeah, yeah, so now that's not to say
there could be a vegan listening to this
and they're saying, "Well, forget you,
Ben. I'm doing fine." But it is a
privilege of the elite. You have to be
educated enough to know what your
deficiencies are and you have to be
wealthy enough to afford the
supplements. Now, the deficiencies are
going to be iron and someone could say,
"I'm getting all my iron from my
plants." No, you're not. That doesn't
work. You you cannot get iron from from
from broccoli to to any measurable
amount or even the right kind that's
going to influence your iron. So, you
have vegans who will suffer from iron
deficiency anemia almost all the time.
They will suffer from vitamin B12
deficiencies, which are is impossible to
get from any plant whatsoever. And and
that leads to something called
pernicious anemia, and that is something
that vegan mom actually can pass on to
vegan baby. But the baby will be
identified as failure to thrive. If the
baby won't be meeting normal kind of
growth metrics and and cognitive metrics
because of the lack of B12 in mom's
diet, which is then passed into the milk
or not passed into the milk. But you
need vitamin B12 for cells to divide.
And so, the newborn baby, which is
experiencing such explosive growth, a
lot of that growth is happening because
of hyperplasia cells dividing. And we
The reason we tell a mom to get folate
is so that the cells of the fetus, that
little growing baby can divide. But if
you don't have B12, the folate can't
work in the first place. That's sort of
the other side of this concern. Folate
and B12 work hand in hand to allow cells
to divide. And you cannot get B12 from
plant sources. It it It's impossible.
You have to get it from animal-sourced
foods. So, that those So, pernicious
anemia and and any disease related to a
failure of cells to divide would follow
that. And then just one last one would
be the essential omega-3s for the brain,
DHA and EPA. And and a vegan would say,
"Well, I'm getting
alpha-linolenic acid or linolenic acid,
ALA, which is the the plant-based
omega-3." And I would say that's all
fine and dandy.
You cannot Humans can't convert enough
of that over to constitute the omega-3s
of EPA and DHA, which are so essential
for brain development. In fact, that
goes back to the growing baby and the
developing baby and baby's brain as
well, which has a very high need for
omega-3s. Um and so, so there are
multiple deficiencies, and those are
just um some of the obvious ones.
Very interesting. Okay, so we are
controlling carbohydrates. We're having
some animal protein for sure. Yep, in
fact that's the second one. We're
getting fat.
Yep, yeah, that's the second point.
Prioritize protein and it has to come
from animal sources.
In my mind it's very clear. There's no
question animal sources are superior.
It is it is I think very unfortunate
this growing trend of trying to get
protein from plants. Now I know this is
delicate cuz some people have a lot of
strong feelings about this kind of
thing, but the consequences when you're
trying to get your protein from plants
is you very often will become protein
deficient because the plants won't have
the full complement of amino acids or in
the right levels. Um, they are not as
bioavailable. This is documented. You
aren't moving those in as well. And part
of that could be that plant proteins
have honest-to-goodness molecules in
them that inhibit the digestion of the
proteins. Phytic acids, tannins, trypsin
inhibitors, these are things that just
occur in in these plants. They're in
peas, they're in soy. And when we take a
thousand peas and concentrate them to
get one serving of protein,
the protein's what we want. What we
don't want is all the other stuff coming
with it. Like these molecules that block
digestion. We also get potentially
dangerous levels of heavy metals like
lead and arsenic because plants, these
seeds of the plants, will naturally
concentrate these minerals from the
ground. Now if you and I just ate a
handful of peas, that's in such an
inconsequential amount as to not be
relevant. But it's also an
inconsequential amount of protein. So if
we want to try to get enough protein
from peas, we end up getting these other
things that we don't want. But
nevertheless, prioritize protein and
then if you're getting it from animal
sources it's going to come with fat
because in nature the best proteins
always come with fat. And that's good
because it helps us digest the protein
better. And fat and protein are more
anabolic than protein alone. So, there's
something anabolic about the fat. And
so, don't fear fat. And then the fourth
principle
Really fast before you move off that one
and we get to the fourth one. Um where
do you come down on eggs?
Yeah, so I think eggs are are God's if
or nature's most perfectly packaged
food. It is a one-to-one mix of protein
to fat by mass. And I think that is
Well, I joke. It's like it's a divine
mix. But, that is the exact mix that
this study that I just mentioned showed
where they had they had weightlifters
take egg white, which is egg white and
whey is the best demonstrably the best
proteins in humans. And then they had
them So, they had them take egg whites
alone and detected a significant
increase in muscle protein synthesis.
And then they had them take the whole
egg, which is by mass one-to-one.
There's an equal amount of mass of of
egg white to yolk. And now they got a
significant growth of the muscle beyond
just the egg white alone.
I eat a lot of eggs. So, I'm I'm very
happy to hear that.
Um okay, so the fourth pillar bucket
Yep. Yep, the fourth pillar is fasting.
Um and and this doesn't need to be
anything complicated. It's funny how
complicated something can be of just not
eating. That you know, we've made it so
complicated. And so, I I and I don't I
don't really try to come down on any
particular version of that. Um there are
so many different ways to do it. Um full
multi-day fasts or just within 24-hour
time-restricted eating windows. My only
advice is if someone's going to engage
in time-restricted eating, like an 18:6
where they fast for 18 hours and eat for
6, I would say when you can, try to push
that eating window to the beginning of
the day. That is better than pushing it
to the end of the day. Um there are
metabolic improvements that come with
it. There are studies that have compared
that. But, also practically speaking,
it's just so much easier to indulge in
junk food when you're eating in the
evening. But, But your eating window has
has stopped with lunch, you're you just
don't indulge. You're not as you're not
as tempted. Um but I appreciate that
socially awkward, you know, dinner at
least for me. I'm a I'm a husband. I'm a
father. Not eating dinner is just weird
because I want to have that moment with
my family. So, despite me saying that,
it doesn't I'm not trying to pretend
that it's easy to do. But but if if
someone can do it,
it's better to have the eating window be
earlier in the day than later. Yeah. I
have my last meal at about 1:15.
Mhm. Yep. Yep. That's a great way to do
it. It really is.
Honestly, for years I did it the other
way and I thought, "Oh, breakfast is,
you know, super easy to skip and so I'll
do lunch and dinner." And then I just
found myself in the mornings I'd be so
distracted and I'm like, "Oh, you know,
I hope I have like a meeting where I
have to be responsive versus where I
need to be creative." Because I can do
meetings all day in a fasted state, no
problem. But I'm not as creative and
maybe other people are, but for me it's
I'm not. And uh so finally I was like,
"Well, wait a second. I start getting
tired in the evenings anyway. Why don't
I start ending my meal much earlier? So,
because of my sleep schedule, I go to
bed very early, so I get up really
early. So, I don't eat probably for
about 4:00 to 5:00 hours in the morning
anyway, but I'm still having my first
meal at like 9:30. Um yeah. And then I
have my
That's a great way to do it. 1:15 or so.
Yeah, but you came to intuitively is
certainly supported by the data. What I
came to through a lot of pain and
suffering. I am the most [laughter] like
I have done everything from a health
perspective like the hardest, dumbest
way possible. I spent like 3 years in
rabbit starvation. I got lean, but
because all I was eating was protein, I
hurt everywhere.
And it was god awful. I mean, it was god
awful. I was lean and I looked great,
but whoa, I did not feel good. In fact,
that is so important because there is I
am I am a huge defender of protein,
but I I vehemently disagree with the
idea that you need to focus on protein
at the expense of something like fat. I
think that we are denying nature if when
we're teasing those two apart. And and I
think it's not a it's not it's
interesting that our ancestors, even
here in the United States, in the early
1900s, we didn't eat chicken.
We had the we we didn't If you look at
the consumption of meat patterns in the
United States, chicken as a meat was
almost nothing for for decades decades
decades and then it exploded in the
mid-1900s right around the time we
started vilifying saturated fat and fat
in general. And chicken meat is so lean.
We didn't used to eat the chickens, we
kept them for their eggs. And so when we
this modern focus on protein, I I do
appreciate
really the utility of protein and the
value of emphasizing it very much.
But to to pull that away from the fat
leads us to I think an unhealthy way of
eating.
So interesting. Ben, you are
fascinating. I loved your book. I have
so enjoyed my time with you. Where can
people follow you, dive in deeper, get
more insights? Where's the best place?
Yeah.
Yeah, thanks so much, Tom. This was
great. Yeah, so everyone can check out
the book. It's Why We Get Sick.
And I am fairly active on mostly on
Instagram these days and people can find
me there at Ben Bickman, PhD. And then I
invite everyone go check out two kind of
ventures I'm involved with. One is a
coaching platform just to try to create
a nice simple online low-carb coaching.
I don't do the coaching, but I helped
create the
kind of the the curriculum, I guess. And
people can find that at insulinIQ.com.
And then lastly,
just a little while ago I started a
company called Health Code and health is
spelled
People can go to that website at
gethealth hlt h.com. And that was really
just born from
my my view that as valuable as a
low-carb diet is, it's sometimes hard
for people to do it. And we've touched
on that even in this conversation. So, I
just thought no one had really done a
low carb shake that great yet. And so,
it's a low carb high fat high protein in
that one-to-one ratio, that divine ratio
that I mentioned earlier. Um and if
anyone wants to
make a purchase, please use Ben 10, um
my my name Ben 10 for a 10% off the
order.
Amazing. Dude, thank you so much. This
is wonderful. Guys, trust me, his book
Why We Get Sick absolutely phenomenal.
He's got such a unique take that you
guys just went on a ride and got to
enjoy. Uh it's amazing. You will be
richly rewarded. And speaking of things
that are rewarding, if you haven't
already, be sure to subscribe. And until
next time, my friends, be legendary.
Take care.
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