Drug Companies Lies: Cholesterol = Heart Disease
Summary
TLDRThis video script challenges the common belief that cholesterol directly causes atherosclerosis and heart disease. The speaker, a doctor, uses logic and clinical observations to argue that high blood pressure, turbulent blood flow, and low shear stress are more likely culprits in plaque formation. They emphasize the importance of distinguishing between correlation and causation and highlight the need for a deeper understanding of the underlying mechanisms in cardiovascular health.
Takeaways
- 🧠 The traditional belief that cholesterol directly causes atherosclerosis is being challenged by the speaker, who argues that the presence of cholesterol in the blood does not uniformly lead to atherosclerosis throughout the body.
- 🔍 The speaker points out that veins, despite having the same amount of cholesterol, do not develop atherosclerosis, which contradicts the hypothesis that cholesterol alone is responsible for arterial blockages.
- 🏥 The speaker's experience in the NHS was restrictive in terms of discussing alternative views on cholesterol and atherosclerosis, prompting a move to private practice for more open patient conversations.
- 🛠 The speaker uses logic and clinical observations to argue against the simplistic view that high LDL cholesterol automatically leads to heart disease, emphasizing the complexity of the condition's development.
- 💡 The difference in pressure and flow dynamics between arterial and venous systems is highlighted as a key factor in the development of atherosclerosis, with arterial systems experiencing higher pressure and turbulence.
- 🌪️ The concept of shear stress is introduced as an important variable in vascular health, with low shear stress associated with areas of turbulence and increased risk of atherosclerosis.
- 🩸 The speaker explains that damage to arterial cells from high pressure and turbulence can lead to inflammation and the body's subsequent immune response, which involves the accumulation of LDL cholesterol as part of the repair process.
- 🛑 The speaker suggests that the presence of LDL cholesterol in arterial walls is part of a natural repair mechanism, and that its persistence in certain areas can lead to oxidative damage and plaque formation.
- 🚫 The speaker criticizes the oversimplification of medical advice and the focus on LDL cholesterol as a sole risk factor for heart disease, advocating for a more nuanced understanding of the underlying mechanisms.
- 📚 The importance of understanding the difference between correlation and causation in medical science is emphasized, with the speaker encouraging a more statistically informed approach to patient care.
- 🌐 The speaker invites viewers to consider the broader implications of diet and lifestyle on vascular health, hinting at the role of glucose and insulin resistance in the development of atherosclerosis.
Q & A
What is the common misconception about cholesterol and atherosclerosis discussed in the script?
-The common misconception is that cholesterol directly causes atherosclerosis and blocked arteries. The script challenges this by explaining that cholesterol is present everywhere in the blood, yet atherosclerosis is not found uniformly throughout the body.
Why does atherosclerosis not develop in the venous side of the vasculature, even though it has the same amount of cholesterol flowing through it?
-Atherosclerosis does not develop in the venous side due to the lower pressure and different flow dynamics compared to the arterial side. The script suggests that the pressure and shear stress in arteries are more conducive to plaque formation.
What is the role of pressure in the development of atherosclerosis?
-Pressure plays a significant role in atherosclerosis as it can cause damage to the epithelial cells lining the arteries, especially in areas of high blood pressure. This damage can lead to inflammation and the initiation of plaque formation.
What is shear stress and how does it relate to atherosclerosis?
-Shear stress is the force exerted by moving blood on the inner walls of arteries. It is critical for maintaining the integrity and flexibility of arterial walls. Areas with low shear stress, often due to turbulent blood flow, are more prone to atherosclerosis as they allow LDL particles to adhere to the arterial walls.
Why are LDL cholesterol particles more likely to accumulate in areas with low shear stress?
-In areas with low shear stress, blood flow becomes turbulent, leading to stasis and allowing LDL particles to adhere to the arterial walls. This is due to the reduced tangential force that would normally help maintain the integrity of the arterial walls and promote the release of vasodilators like nitric oxide.
What is the role of the immune system in the development of atherosclerosis?
-The immune system plays a role in atherosclerosis through the action of macrophages, which are immune cells that accumulate at the site of arterial damage. They ingest the LDL cholesterol, leading to the formation of foam cells and contributing to plaque development.
How does the script explain the formation of atherosclerotic plaques?
-The script explains that atherosclerotic plaques form due to a combination of high pressure, turbulent blood flow, and low shear stress, which leads to endothelial damage and the accumulation of LDL cholesterol particles in the arterial walls.
Outlines
🧠 Challenging the Cholesterol-Atherosclerosis Hypothesis
The speaker begins by questioning the widely accepted belief that cholesterol is the primary cause of atherosclerotic plaques and blocked arteries. They point out the logical inconsistency in this theory by highlighting that cholesterol is present throughout the bloodstream but atherosclerosis predominantly affects arteries, not veins. The speaker also mentions their intention to explain the actual mechanisms of arterial blockages and their departure from the NHS to work privately, where they can dedicate more time to patients without being influenced by pharmaceutical interests. The summary emphasizes the need to reassess the cholesterol theory and the importance of understanding the true causes of atherosclerosis.
🌡️ Blood Pressure and Shear Stress in Arterial Health
This paragraph delves into the role of blood pressure and shear stress in the development of atherosclerosis. The speaker explains that the aorta, being the first vessel to receive blood from the heart, is under the most pressure, making its cells more susceptible to damage from hypertension. They introduce the concept of shear stress, which is the force exerted by blood flow on the arterial walls, and how it is crucial for maintaining vascular health. The speaker also discusses the differences in blood pressure throughout the vascular system, from the high-pressure arterial side to the low-pressure venous side, and how this pressure gradient contributes to the uneven distribution of atherosclerosis. The summary underscores the importance of understanding fluid dynamics and the impact of blood pressure on arterial health.
🔬 The Role of LDL Cholesterol in Vascular Damage
The speaker explores the role of LDL cholesterol in the context of vascular damage and atherosclerosis. They explain that high pressure and turbulent blood flow can cause gaps between vessel cells, allowing LDL particles to become lodged. The speaker clarifies that LDL cholesterol is not inherently harmful but is involved in the repair of damaged cells. However, in cases of chronic hypertension, these LDL particles can become oxidized and contribute to atherosclerosis. The speaker also touches on the impact of glucose and insulin resistance on vascular health. The summary highlights the complex interplay between blood pressure, LDL cholesterol, and vascular damage, and challenges the oversimplification of LDL cholesterol as the sole cause of atherosclerosis.
📚 Clinical Evidence and the Misunderstanding of Cholesterol's Role
In this paragraph, the speaker discusses the clinical evidence that supports the mechanistic understanding of atherosclerosis and criticizes the oversimplification of cholesterol's role in heart disease. They emphasize that atherosclerotic plaques are found only in areas of low shear stress and turbulent flow, not throughout the entire vascular system. The speaker also addresses the importance of distinguishing between correlation and causation in medical understanding and practice. The summary points out the need for a more nuanced view of cholesterol, recognizing its evolutionary purpose and the context in which it may contribute to disease.
Mindmap
Keywords
💡Atherosclerosis
💡Cholesterol
💡Veins
💡Arteries
💡Shear Stress
💡LDL Cholesterol
💡Inflammation
💡Pressure
💡Turbulent Blood Flow
💡Glycation
💡Insulin Resistance
Highlights
Cholesterol's role in atherosclerosis is questioned, challenging the traditional belief that high cholesterol causes blocked arteries.
The presence of cholesterol in both arterial and venous blood suggests it is not the direct cause of atherosclerosis, as veins do not develop the condition.
The speaker proposes an alternative mechanism for atherosclerosis, involving high blood pressure and turbulent blood flow.
Shear stress and its impact on arterial health are introduced, with low shear stress linked to atherosclerosis development.
The speaker explains the difference in pressure between arterial and venous systems, which affects the likelihood of atherosclerosis.
The role of inflammation in arterial damage and the subsequent development of atherosclerosis is discussed.
The importance of understanding the difference between correlation and causation in medical theories is emphasized.
The speaker shares personal experiences from the NHS, highlighting the limitations in discussing alternative theories of atherosclerosis.
The impact of diet, specifically carbohydrate intake, on glucose levels and its potential role in atherosclerosis is briefly mentioned.
The speaker outlines the step-by-step process of atherosclerotic plaque formation, providing a logical sequence of events.
Clinical observations are presented to support the alternative theory of atherosclerosis, showing real-life manifestations.
The speaker argues against the oversimplification of LDL cholesterol as the sole cause of heart disease.
The importance of considering mechanical damage in the initiation of atherosclerosis is highlighted.
The speaker discusses the role of immune system cells in the atherosclerotic process and the body's response to arterial damage.
The impact of chronic hypertension on the development of atherosclerosis and the importance of managing blood pressure are discussed.
The speaker refutes the idea that cholesterol is inherently harmful, arguing that our bodies have evolved to utilize it for repair.
The limitations of medical education in teaching statistics and the importance of understanding association versus causation are critiqued.
The speaker concludes by summarizing the key points and reinforcing the need to question traditional beliefs about cholesterol and atherosclerosis.
Transcripts
so if you think cholesterol is what
causes atherosclerotic plaques and and
blocked arteries which I did too by the
way because that's what I was taught at
school and University then I'd like you
to explain the following if cholesterol
really does cause it first off on the
hypothesis that cholesterol equals
blocked arteries or
atherosclerosis we have to ask where is
cholesterol obviously it's in the blood
but specifically it's in the hole of the
blood right it's everywhere so if it's
every then that hypothesis of
cholesterol equals atherosclerosis would
mean that atherosclerosis is also
everywhere because the blood is but is
it if it is and obviously that
hypothesis could be deemed as probably
correct but it's it's not the case okay
I'll get a picture on screen now of the
body's vasculature the Via side uh side
of the veins doesn't develop
atherosclerosis even though it has you
know the same amount of cholesterol
csing through it as the arterial side
why is
if cholesterol equals
atherosclerosis then why is it not in
the veins when it's it's there too in
exactly the same amount as the arteries
clearly that theory needs banishing from
our education system frankly and I'm
going to show you the exact step-by-step
mechanism as to how the
blockages actually occur uh as can be
seen and predicted consistently in
clinical practice like with my own
patients now when I spent time in the
NHS which is the National Health servy
for those not in the UK I couldn't have
these conversations with my patients
because I think I'd have been fired for
saying things which are outside of
what's taught in medical school but I
left that and and and all hospital work
and I only work privately now um where I
can spend longer amounts of time with
each patient and I can actually treat
them properly without saying or doing
things that are designed to make money
for big pharmaceutical companies as the
priority so I'm going to work through
the AOS scerotic plat or as cvd
atherosclerotic cardiovascular disease
pathophysiology how it comes about from
start to finish and I'm going to use
basic logic at every stage to show you
that you honestly don't have to be a
doctor even though I am one to to take
control of your own health to start with
I'll get a a diagram here of of the
vasculature the side with veins the
Venus side is going to be much lower
pressure than the arterial side the
arterial side is supplied by the left
ventricle of the heart this might be
right on camera that's the bit which
generates enough Force to get it all
around the body where the arteries
become veins here we have capillaries
that deliver oxygen to the cells that
need it and they're low pressure too and
they're also really small to reach into
Tiny Places as you can imagine once the
Oxygen's been offloaded the deoxygenated
blood then makes its way back to the
heart and there it gets sent uh by the
right ventricle to the lungs to pick up
oxygen again before repeating the
cycle taking um a big picture look at at
this diagram I'll say it again there's
no artherosclerosis or heart disease or
vessel disease in the Venus side it's
all arterial this is the first
mechanistic step in disputing the
thought that LDL cholesterol or
cholesterol in general has a causal link
to blockages if the same cholesterol or
blood is everywhere then that theory
should give this blockage issue
everywhere as well this is why we can
safely say that there's no direct
causality between these two things and
that's pretty much the end of the
argument be honest when I've had this
conversation with fellow doctors at you
know conferences or in clinics even
cardiologists by the way they have no
response to this logic that I put
forward to them now that doesn't mean
that LDL cholesterol isn't involved in
some way it could still be a
contributing factor whilst we're still
working our way through this step by
step and and thought by thought but our
next step in this logic is to ask well
what's different then between the
arterial and the Venus sdes well the
actual epithelial cells that line the
vessels and actually contact the blood
you know these these vessels AR aren't
really that different the structure is
pretty much the same the musculature you
know keeping the vessel stable which is
called smooth muscle it's a bit bigger
on the arterial side n say higher
pressure so you need a higher ability to
withstand that pressure as I'm sure you
can
understand the the walls i' say a bit
thicker too overall U we can measure
that um but we're kind of clutching up
straws here the the physical structure
is is really just not that different at
all but remember what I said before the
biggest difference is the pressure
inside the vessels we're also going to
add another concept here called sheer
stress this is to do with the turbulent
flow and how different directions of
flow can interact with each other and
the environment holding them in
position pressure is basically a measure
of how much force is being exerted on
the vessels from the blood on the inside
that's why the formula for pressure is
is force divided by area and why you get
pressure units like pound per square in
force per unit area and the aorta is
under the most pressure because it's
it's the first bit the blood goes into
after the left ventricle pumps blood out
of the heart this is why the vessel
cells here are more likely to get
damaged if there's high blood pressure
in in you as an individual they're
taking this pounding from from the the
pumping constantly and adding to the
pressure is going to give even more of a
pounding and I hope you can see too that
this isn't comp at by the way to to
understand or follow it's all pretty
logical at the end of the day so if the
pressure from the heartbeat is combined
with a raised you know Baseline blood
pressure as well then eventually you can
actually get inflammation of these cells
you know if you get punched in the face
repeatedly like a boxing match then as
the rounds go on your face is going to
look more and more swollen and inflamed
because of the physical and mechanical
damage that's done and you can imagine
the cells in the vessels getting punched
constantly from natural pressure being
increased by high blood pressure on top
of that so to to recap and try to kind
of summarize what we've gleaned from our
logic so far to create artherosclerosis
one of the things we need is some kind
of inflammation of the epithelial cells
uh lining the arteries and we can get
this by increasing the blood pressure to
then increase the physical force on the
cells to damage them and then cause an
inflammatory response which is where the
body tries to protect itself now we
don't get this on the Venus side because
we don't have this type of damage there
due to the pressure being much lower
those punches to the face just they're
not happening in the veins they are in
the
arteries so let's carry on uh let's take
a look at the the variation in blood
pressure right you get this all
throughout our vature I'll get a diagram
here that shows you the pressure when
the blood leaves the heart is being very
high and obviously it's going to be very
high at this point but as you get
further away the pressure reduces and
and the pulsatile nature of the flow
starts to reduce in size and then you
get to the smaller arteries the pulses
actually you just stop and you get this
more constant flow which is called
lamina flow this is basically like um
it's it's like a normal steady stream of
traffic instead of stop start and after
that you've got the capillary beds where
Oxygen's are floated like I said and
then you enter the Venus system the
pressure as you can clearly see is is
well hopefully depending on which
diagram I get is is lower and lower the
further you are from leaving the heart
and the closer you are to to returning
to the heart with de oxygenated blood
and this kind of shows you in a really
clear way the lack of pressure leading
to lack of damage in in the Venus side
now again I'm going to add to our logic
here I'm going to throw in the study of
fluid dynamics in simpler terms the
study of turbulent blood flow within the
arterial vessels we can't really do this
for the Venus side because the blood
there just flows like a steady stream of
traffic constantly lamina flow but in
the arterial side we've got things like
y-shaped Junctions I'll get a picture of
one on the screen here actually um this
this y-shaped Junction is termed a b
ation the initial portion just splits
into two and you get bation to things
like teeth roots where a single root can
split into two now after the split
generally get one side bigger than the
other and the arrows that hopefully you
can see on on the diagram show you the
direction of the flow of that blood when
it's in this bacation it's not that
different to what happens in the world
around us and things like Rivers you
know and how the water in them flows in
specific ways the physics principles of
fluid flow basically the same there and
here when the flow hits the Y part of
the
bifocal or swirling effect and as you'll
come to see this this turbulence is
another Factor that's needed in order to
achieve
atherosclerosis now when the blood flows
through vessels with pressure the
pressure is going to push outwards on on
the vessels okay so you got something
called sheer stress as well which I've
mentioned before um I've mentioned that
in for example my big hyaluronic acid
video when I talked about the
manufacturing of it but you get it in
vessels as well it's the force exerted
by the moving Blood on the inner walls
of the arteries basically as a blood
flows it creates this tangental force
that acts parallel to the surface of the
arterial wall and that's critical in
regulating vascular function and health
if you have that you help maintain the
integrity and flexibility of the
arterial walls um and you can promote
release of things like nitric oxide that
keeps them dilated and areas like this
have no atherosclerosis surprise
surprise but if you have low sha stress
then you do have
aerosis when you look at the diagram you
can see there there'll be areas where
the blood turbulently swells like in
bipoc instead of flowing parallel to the
vessels now these swirly areas have low
sha stress and as you can see the areas
highlighted then have a higher adhesion
of of monocytes which are selles from
the immune system and a higher
permeability to LDL cholesterol
particles so to recap I know this you
might need to watch this more than once
but to recap we've got damage from high
pressure as well as increased amount of
turbulence which then gives us lower
shear stress this then allows that blood
to hang around instead of making its way
straight through and it seems like this
is what allows the LDL to then Place
itself in the small gaps that appear
from damage between the vessel cells
right the high pressure seems to cause
damage that makes this small Gap like a
sort of break or fracture if you like
and once this happens we can get
inflammatory markers which can then
increase the permeability even more okay
at this point you know even more sdl
particles can get stuck in there and
these are are small dense ldls um you
also have lb which is large buoyant LDL
the fact that they're a large means that
they can't fit into the same Gap and B
buoyant means they they float so they
aren't going to be possible to to tie
down in the same way now don't don't to
jump to conclusions so right just the
actual getting stuck in the Gap isn't
necessarily the issue that they're
positioned there now because the
underlying cells have been damaged and
they need repairing if you're going to
rebuild or repair cells then you need to
make the membrane which cells are made
of and take a guess what that membrane's
made of amongst other things cholesterol
and how convenient is it that some has
just landed there ready to help out and
donate some building blocks to repair in
a normal situation that repair it just
just takes place and then the LDL can be
released and everyone's happy but in the
abnormal situations you know we have a
different situation we in an abnormal
situation or an AB normal situation
sorry that was so bad uh but we have
longer term blood pressure or chronic
hypertension to use a medical
terminology these LDL particles they
just they never get released and and and
we get oxidative damage over time where
the ldls stay there for ages and and the
oxygen flowing past you know that can
cause oxidation of the LDL matter and
this is another Factor why we don't see
in in Venus sides because the veins
don't carry oxygenated blood now we can
also get damage from glucose because
glucose glyc hates things which is where
it kind of attaches onto stuff and
prevents that stuff from doing its job
like a nagging child that's attached to
you and slowing you down at work and
when we measure something called a hba1c
on a blood test we're measuring the
glycation of hemoglobin glycation is is
not a good thing the glucose attaching
to the hemoglobin and and it can cause
lots of harm if it happens to hemoglobin
then it can't deliver the oxygen to your
cells as well I won't going into diet
and glucose too much in the video but I
will say that this is one reason why
watching carbohydrate intake is so
important and if you get to the point
where you can't be where you can be
considered as you know having a glucose
uptake into C or not having glucose
uptake into cells even with insulin
round which is what we call insulin
resistance to make it easy that glucose
lingers in the blood even longer and it
can cause even more damage you know as
as a carnivore I'll never have to worry
about this because I just don't eat
carbs my body makes glucose from fatty
acids or amino acids when needs so it'll
always make the exact amount it needs uh
it's not going to make so much it causes
damage to itself obviously we wouldn't
have evolved that way now if if this
process with the vessel damage um and
LDL placement goes on and on then the
body starts to create an immune response
too right you get these things called
macrofagos which are the cells of the
immune system and they turn up like
police at a crime scene right and now
this is full on
atherosclerosis our bodies have have put
that LDL there for a particular purpose
it's supposed to be be there why would
we make something that causes us to
react badly as soon as it's made we
would have died out long ago as a
species if that happened you know there
there are many things I can say about
diet here and and its role in this
pathophysiology I'll leave it for
another video because this there's still
people out there that think veganism is
is really healthy it is in the short
term um but yeah I won't go on now I
want to show you the actual formation of
these plaques so you can actually see
for yourself the real life
manifestations of all these logical
steps we've gone through today and also
see for yourself that these logical
steps we've gone through are actually
correct I'll get a diagram of an
arterial bation on on screen for you now
you should be able to see the areas with
high and low sha stress and we can see
then the the actual plaque formation
sites too what I want you to take from
this is the fact that the real life
observations completely back up
everything in these logical steps that
we've gone through today we we we've you
gone through in a systematic and
methodical and predictable way along
with common sense some reasoning behind
why these plaques and blockages might be
happening and now we can see what
actually happens in real life clinical
practice to in a completely predictable
and formulaic way I see these things in
my own patients when we get a let's say
a CAC or CAC scan done of the vessels in
fact part of the reason I'm making this
video is so my patients don't have to
remember everything I say and they can
just watch this back instead as a
reference because they always they
always ask me about cholesterol
you other portions of the vasculature
have the same blood with the same
cholesterol with the same oxygen with
the same glucose and clearly no plaques
there at all should be obvious now that
clearly some kind of mechanical damage
is 100% required for atherosclerosis to
initiate if you're wondering why a tiny
bit of plaforms at the split point of
the bipoc by the way it's because the
currents and turbulence change once you
have plaques built up in the bigger
areas first and then it can have a knock
on effects elsewhere
too to expand on this real life clinical
practice view so that we can test all
the step-by-step logic that we've gone
through here there's a diagram uh which
I'll get up um of the areas where we
actually find artherosclerotic plex
surprise surprise it's only in the
larger arterial vessels and if we
distill what's going on even further
it's only in the areas where we have low
shear stress in these places as a result
of turbulent flow which allows some form
of blood to hang around
stasis and the areas where there's
higher shear stress where it's flowing
past nicely there's no pathophysiology
there's no pathology going on there so I
hope you guys see why it's so ridiculous
to say the blanket statement LDL
cholesterol is the cause of
atherosclerosis it's actually quite
Incorrect and hopefully as you'll see
now um I I I couldn't care less about my
lipid panel or my blood tests which show
that I have very high LDL cholesterol
our bodies have genes that have evolved
over millions of years to protect us if
cholesterol was bad how would we have
evolved to still be alive now makes no
sense that our bodies would do something
that you know that ends up killing us so
also while looking at blood results and
lab tests to a certain extent in some
cases can be a useful exercise you know
we've hopefully now completely dispelled
the lotion for you that cholesterol
equals heart disease I could go on and
talk about APO B which I know a lot of
you are worried about because people
like Peter attia say it needs to be low
however we we can go through this exact
same exercise of making logical step-by
step distillations to come to the same
thought about a b
too you don't need to worry about it
your body's put it there for a reason
maybe that'll be a video for another day
you know there's there's different
doctors that will always say different
things because in medical school or
dental school or nursing school whatever
we don't get taught things like
statistics to to any meaningful degree
I'm saying that from a personal
experience of University and as a result
clinicians don't understand the
importance of understanding the
difference between Association or
correlation and actual cause and effect
which is what we can derive as direct
risk you also don't pay attention to
making sure there's a sound basis of
control over independent variables which
is more complex than it sounds for most
I appreciate that now I'm not saying
also that that I'm any better I'm not a
statti statistician by any means but I
do try and remind myself of Association
versus causality and risk whenever I can
and and through videos like this I like
to show actual Mech mechanistic steps
which you can see for yourself and and
that can also be tested in clinical
practice for veracity every day seeing
what I've shown here in in my clinical
practice with real patients shows me
that what's been shown here which isn't
100% of the subject by the way is true I
know some may disagree with with certain
bits and that that's always going to
happen but I'm saying it as someone that
actually sees patients with this exact
phenomenon day in day out now please
understand that this video is once again
not designed to convey the whole subject
in its absolute entirety there's a
reason medical SCH is years there are
indeed things I've left out because I
don't want it to be longer than it
already is but I hope you've learned
something from it
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