Drug Companies Lies: Cholesterol = Heart Disease

Summary

This 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

00:00

🧠 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.

05:00

🌡️ 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.

10:01

🔬 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.

15:02

📚 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.

Keywords

💡Atherosclerosis

Atherosclerosis is a form of arteriosclerosis involving the thickening and hardening of the arteries due to plaque build-up. In the video, it's discussed as a common misconception that cholesterol directly causes atherosclerosis, but the speaker argues that the condition is more complex and involves factors such as blood pressure and vessel damage.

💡Cholesterol

Cholesterol is a waxy substance that is essential for the body's functions but can become problematic when levels are too high. The video challenges the traditional view that cholesterol is the primary cause of blocked arteries and atherosclerosis, suggesting that its role is more nuanced and related to the body's repair mechanisms.

💡Veins

Veins are blood vessels that return deoxygenated blood to the heart. The script points out that veins do not develop atherosclerosis despite carrying cholesterol, which challenges the direct link between cholesterol and arterial blockages.

💡Arteries

Arteries are blood vessels that carry oxygenated blood away from the heart. The video discusses how the arterial side of the vasculature is subject to higher pressure and thus is more prone to atherosclerosis, unlike veins.

💡Shear Stress

Shear stress in the context of the video refers to the force exerted by the blood flow on the inner walls of the arteries. It is critical in maintaining the integrity of arterial walls, and areas of low shear stress are associated with atherosclerosis due to turbulent blood flow and increased LDL cholesterol permeability.

💡LDL Cholesterol

LDL cholesterol, or 'bad cholesterol,' is a type of lipoprotein that can contribute to plaque formation in the arteries. The video script discusses how LDL cholesterol becomes trapped in arterial walls due to high pressure and vessel damage, but its presence is part of a repair process rather than the sole cause of atherosclerosis.

💡Inflammation

Inflammation is the body's response to injury or damage and is a key part of the atherosclerosis process. The script explains how high blood pressure and vessel damage can lead to inflammation, which in turn can cause the body to trap LDL cholesterol in the arterial walls as part of a repair response.

💡Pressure

Pressure in the video refers to the force exerted by the blood on the vessel walls. It is highlighted as a significant factor in atherosclerosis, with higher pressures in arteries leading to more damage and thus a greater likelihood of plaque formation.

💡Turbulent Blood Flow

Turbulent blood flow is a type of blood flow characterized by chaotic and swirling patterns. The script explains how areas of turbulent flow in arteries can lead to low shear stress and subsequent atherosclerosis due to the increased residence time of blood components, including LDL cholesterol.

💡Glycation

Glycation is the process by which glucose attaches to proteins, such as hemoglobin, altering their structure and function. The video mentions glycation in the context of diabetes and how it can contribute to vascular damage, indirectly linking it to the development of atherosclerosis.

💡Insulin Resistance

Insulin resistance is a condition in which the body's cells do not respond properly to insulin, leading to high blood sugar levels. The script briefly touches on insulin resistance as a factor that can exacerbate vascular damage and contribute to atherosclerosis by causing glucose to linger in the blood.

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