Why do we develop plaque in our arteries, but not our veins?
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- Опубліковано 28 кві 2024
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Original Video: • Cholesterol debate wit...
References (Copy & Paste DOI into Search Engine)
[1] doi:10.1159/000174019
[2] doi:10.1053/pcad.2002.123471
[3] doi.org/10.1093/eurheartj/ehz962
[4] doi:10.3389/fphar.2020.613780
[5] doi:10.3389/fcvm.2022.925923
[6] doi:10.1097/MOL.0000000000000330
[7] doi:10.1097/00041433-200210000-00001
[8] doi:10.1016/s0925-4439(01)00102-8
[9] doi:10.1016/s0174-173x(86)80033-4
[10] doi:10.1093/ajh/hpy083
[11] doi:10.1002/9780470513385.ch13
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#heartdiseaseawereness #heartdiseaseprevention #heartdisease
1 AMENDMENT
AMENDMENT: I said 'CAG' for the protein name instead of 'GAG" - whoops! [Thank you to @sandrapeverelle8066 for the correction]
A simple, straightforward theory that I heard years ago, is from Linus Pauling and Dr. Rath. In my layman's translation:
Low grade, chronic scorbut or scurvy!
If you are low in vitamine C, or Ascorbic acid, you cannot maintain collagen in your blood vessel walls. The walls will eventually rupture. The biggest damage is there where the blood pressure is highest: the arteries.
Acute scurvy leads to internal bleeding and death, low grade scurvy will lead to damaged walls and the body tries to repair with plaque and stabilize the fix by calcification.
Why are we low in vitamin C? Vitamin C and Glucose use the same transporter to get into a cell. Now you'll get some 0.05-0.1 gram of vitamin C, but tens or hundreds of grams of glucose.
Guess what wins this competition?
So, if you consume more sugar, blood vessel walls will tear more easily.
The ancient human body didn't get those amounts of sugars and refined carbohydrates and our genes have not adapted to it.
We are like a cactus in a rainforest these days.
Sugars, easily oxidizing seed oils damage our blood vessels and especially the arteries.
LDL and cholesterol are not the cause, but a repair mechanism of the body that tries to limit the damage...
What's up, Physionic?
Just wanted to add that glycosaminoglycanes (GAGs) are not proteins, in fact they are complex carbohydrates (polysaccharides) and have a fundamental role in our connective tissues including the specialized ones, such as adipose, osseous, cartilage, hematopoietic and some others.
Keep up with the scientific content you are promoting and never stop fighting against healthcare misinformation. :)
See ya!
Pressure in the arteries could be a possible cause? Pressure-> cracks -> rough lining-> perfect place for ldl to stick.
Also can you explore why Japanese don’t get heart issues?
It could just be that repair mechanism on Japanese diet is better
@@PS-hy8od Exactly!
I copy/paste below my reaction that I posted in this section two months ago:
A simple, straightforward theory that I heard years ago, is from Linus Pauling and Dr. Rath. In my layman's translation:
Low grade, chronic scorbut or scurvy!
If you are low in vitamine C, or Ascorbic acid, you cannot maintain collagen in your blood vessel walls. The walls will eventually rupture. The biggest damage is there where the blood pressure is highest: the arteries.
Acute scurvy leads to internal bleeding and death, low grade scurvy will lead to damaged walls and the body tries to repair with plaque and stabilize the fix by calcification.
Why are we low in vitamin C? Vitamin C and Glucose use the same transporter to get into a cell. Now you'll get some 60 mg of vitamin C, but tens or hundreds of grams of glucose.
Guess what wins this competition?
So, if you consume more sugar, blood vessel walls will tear more easily.
The ancient human body didn't get those amounts of sugars and refined carbohydrates and our genes have not adapted to it.
We are like a cactus in a rainforest these days.
Sugars, easily oxidizing seed oils damage our blood vessels and especially the arteries.
LDL and cholesterol are not the cause, but a repair mechanism of the body that tries to limit the damage...
I'm glad you mentioned that arteries are exposed to higher blood pressure than veins. This lends credence to the hypothesis that elevated blood pressure is causative, and not merely an effect of atherosclerosis.
However, there are other differences between arteries and veins:
1) oxygen and oxyhemoglobin concentrations
2) carbon dioxide concentration and blood pH
3) glucose and nutrient concentrations
4) metabolic waste concentration
The pulse stretches the endothelium, creating spaces that can allow the LDL particles through. 60+x/minute. You don't feel your pulse in your veins, neither does your endothelium.
Does pulse stretching or the endothelium also allow other types of particles through?
It's certainly both a cause and an effect.
It makes more sense that in high pressure environments you'll get some microtears which serve as a starting point for the plaque accumulation.
Yeah, but it's probably the pressure mashing everything together. Like a highway with no speed limit filled with oil tankers, and never closing down a lane to clear up the debris and crash sites.
With the heartbeat isn’t there an actual stoppage of movement in arterial flow maybe even a slight reversal. Whereas vein blood flow is constantly moving forward. If so couldnt this stop of flow allow for particles to stop and stick. Complete layman here pondering
The mechanical stresses are greater in arteries due to higher pressure, but more importantly due to being a larger diameter. The larger the diameter, the greater the hoop stresses.
When the wall is damaged due to diabetes, smoking, etc, the risk of rupture is much higher in arteries, and the body responds accordingly by thickening the artery wall.
Seems like a good mechanism to keep us alive by the human body.
Veins have a wider lumen diameter than arteries, especially the coronary arteries, which are prone to blockage because they are narrow.
@@mattermat1925 Thank you for sharing. Arteries are much thicker than veins, so I assured the outside diameter must be larger as well. I wonder if anyone has done a FEA stress comparison of arteries vs veins
Exactly it's a rather miracle people don't die within a week or month of smoking, plaque development only halts the inevitable.
now think about cancer...what if its simply the body's last survival attempt in a toxic environment
@@prozac5314 interesting hypothesis. Inflammation is the root of heart disease and cancer.
I'm curious you didn't discuss "arteries carry oxygenated blood and veins carry deoxygenated blood."
I would expect to learn plaque development to require the presence of certain concentrations if oxygen. What is that mechanism?
So we can easily fight atherosclerosis just removing oxygen from arterial blood 😂
@gz625 no duh but OXIDATION is more likely when there is MORE OXYGEN so they have a good point
Extreme breath holding, ex. David Blane clears plaque? Caution side effects include neural degradation, ...
@@caljerm it's a joke mate. No oxygen == death 😅
But it isn't free floating oxygen, it's bound to the hemoglobin inside red blood cells. So I doubt it has any effect. (Btw you don't require oxygen for oxidation, just need an electron acceptor)
Another factor not being discussed is that arteries contain oxygen-rich blood that contributes to more oxidation of LDL particles
Great video, thank you Nic. I appreciate the vulnerable and openminded look that you've taken at the issue.
There are several reasons why plaque tends to form more frequently in arteries than in veins:
1) Blood Pressure: Arteries carry oxygen-rich blood away from the heart to the rest of the body, and they are subjected to higher blood pressure compared to veins, which carry deoxygenated blood back to the heart. The higher pressure in arteries can damage the inner lining of the blood vessels, making it easier for plaque to accumulate.
2) Shear Stress: Arteries are exposed to greater shear stress, which is the frictional force exerted by the flowing blood on the arterial walls. This stress can lead to damage and inflammation in the arteries, making them more susceptible to plaque formation.
3) Oxygen Content: Arteries carry oxygen-rich blood, which contains higher levels of oxidized low-density lipoprotein (LDL) cholesterol. Oxidized LDL is more likely to contribute to the formation of plaque compared to the less oxygenated blood found in veins.
4) Structural Differences: Arteries and veins have different structures and functions. Arteries have thicker walls and more muscular tissue to withstand the higher pressure of blood flow. Veins, on the other hand, have thinner walls and contain valves to prevent the backward flow of blood. These structural differences may influence the development of plaque.
While plaque buildup is less common in veins, it can still occur under certain conditions, such as in individuals with venous diseases or conditions that affect blood flow in the veins. However, atherosclerosis primarily affects arteries due to the unique physiological and hemodynamic characteristics of the arterial system.
The veins should in theory have the same fluid shear stress? The same amount of blood/fluid passes. Maybe veins are smaller is diameter? If they are similar diameters to arteries, the fluid shear stress should be the same since the flow rates are the same (same amount of fluid/minute in and out in a closed system). Maybe the density and/or viscosity of the blood changes with different amounts of dissolved O2 and CO2? Then the shear stress would be different.
Thanks chat gpt!
Flow rate is different, they differ in diameter @@yodaiam1000
@@kevingibrayel160 In that case, It is a higher velocity and Shear stress but same average flow rate. The total amount of fluid moved coming in is the same as going out unless there is a serious issue. But it is interesting to know that the arteries are more narrow.
Isn't shear stress beneficial, since they stimulate production of nitric oxide which aids vasodilation? By your logic, people who exercise regularly would have higher risk, since the shear forces are higher, but that's not the case, since regular exercise does reduce the chances of plaque formation (in addition to lowering other risks of getting one in the first place)
How about the thrombolytic theory. Hihg blood pressure causes endothelial damage which is covered over by something like a scab. Then a new endothelial layer forms over that damaged area. After continued damage in the same area the repaired or partially repaired materials are eventually drawn inward by succesive layers.
I believe this to be true. That is why we don't typically see plaque build up throughout the arteries, but at bifurcation points where the artery walls are more likely to be damaged by higher pressure/turbulent flow. There's also the whole glycocalyx thing, which is super interesting. I believe plaque is the body's way of repairing damage to the artery wall.
Malcolm Kendrick explains this in his book, The Clot Thickens. This theory explains why so many seemingly unrelated things (e.g., sickle cell disease, pollution, heavy metals, smoking, cancer medications, etc0 can cause heart disease. The unifying factor is that they all either damage the glycocalyx or they inhibit the repair processes.
I read this book also. Makes the most sense to me.
I love that you are a stickler for detail. She didn’t get all the facts correct , but he r” hack “ was mostly accurate, you clarified the important details of making it work properly. Thanks keep it coming.
Logical explanations! Well done ! Nobody has explain at this level.
Thank you for the breakdown explanation of this topic. Well done!
amazing stuff. glad to find this channel on youtube. hope to see more stuff.
Thank you SO much for addressing this podcast. When I was listening to it and they were repeating "it's the same" I was ripping off my hair screaming "blood pressure" in my head 😂
Thanks so much for answering this mystery!
You’re getting closer Nickolas! Yes, cells differentiate and dediffereniate their phenotypes according to blood pressure. Now look at the receptors on the endothelial and smooth muscle cells in response to pressure and shear stress. TRPV4! The intercellular junctions between endothelial cells are compromised when TRPV4 is activated. This leads to a break in the endothelial cell layer and mcp-1 is called in via TRP signal as TRP on monocytes cause differentiation to M1 inflammatory macrophages. At the same time lipid oxidation/peroxidation takes place as excess glucose metabolism caused by too much carb/sugar intake/metabolism leads to too much ROS by mitochondria that damages the mitochondria and cells. There much more including the production of lp(a) that attaches to the apoB. Lo(a) is not a constant value. A study in children on oxcarbazepine that increases TRPV1 and TRPV4 found that after 1 year of treatment children had a statistically significant increase in lp(a).
All of this is inflammation, hypertension and stimulation of key receptors that lead to differentiation and dedifferentiation of cells in response to physiological conditions.
In your opinion, what’s the best way to lower LPA ,as somebody that has it super elevated 400 and 500 most of the time
I read a blog that somebody said, excessive grain and carb intake with raise it, so I assume obviously sugars the same.
It would be nice to know mechanism
I think they suggested that grains increase apo a
@@hypnotiqpits13Interesting Tnx, So the small amount of Rice and Gluten Free organic Oats.. I eat..
(No other Grains.. ) Is causing Trouble! 😟
@@mystrength5640 not sure, I tried to find more information on what raises Apo protein A-levels in the body, but I can’t really find anything
Assuming this is true, why is it that people eating diets traditionally very high in whole food carbohydrate (grains, sweet potatoes, whatever) don't have extensive atherosclerosis?
@@broccoli7263 do you have serial CT angiograms of these people and 6 hour oral glucose tolerance tests with insulin and c-peptide curves etc? Are any of them on psychotropic or hypotensive drugs that cause hyponatremia?
This channel appear to my recommendation. And I glad to find it! Thanks UA-cam, great job!!
Welcome!
Great analysis.
I have thought about this hard for the last 20 years. The Arteries that branch out immediately after the heart are closest to the "Jacuzzi pump" There is higher pressure and flow rate at that point. If there is any degradation to the surface particles can penetrate and collect.
I observed this while trekking in the back country. Streams that flow crazy hard, and split, debris builds up at the split. However if the split is smooth rock there is no build up of sticks and leaves.
Meanwhile the small slow flowing creeks that branch off from the main stream do not have this debris.
I summarize that degradation to the endothelium triggers the process of particle build up within arteries.
Now I will watch the video and see what is says.
I give you props just for paying attention to the nuances of nature and applying it to other aspects of life👏🙌
The entirety of existence seems to be a manual for a life and is honestly the most important thing that has allowed me to understand the science.
How else can we possibly understand things we have never seen or experienced based solely on the words of those who have?
This is a very impressive analogy!
@@michaels1532 Next time you are in a swimming pool, put your hand up to the water circulation jets. The strongest jet closest to the pump. Feels good at first. But keep your hand there for too long and the friction can actually begin to hurt.
@@arnoldfrackenmeyer8157 since vessels should technically have laminar flow in an ideal scenario this shouldn’t be an issue though right?
@@arnoldfrackenmeyer8157 I guess you are right though cause with such a high velocity and pressure there would be turbulent flow according to reynolds law
Thanks for educational... appreciate. ❤❤🎉🎉
Excellent question.
Thank you
Amazing job
Also I understand that plaques form at high stress points like junctions.
That appears to be true, so if it was about LDL concentration, atherosclerosis would be spread all over the artery system. Dr Malcolm Kendrick believes that atherosclerosis forms from an abrasive and high pressure damaging the endothelium and not from LDLs passing through the cellular joins. Read "The Clot Thickens" for a detailed explanation. He's been studying this for 30 years and has learned a few things. Who knew?
What an awesome video!
Thank you sir !
Nice calm informative video
Arteries experience higher blood pressure than veins and it is well known that elevated blood pressure results in greater chance of vascular disease. Higher BP damages the endothelium making it easier to transport LDL particles into the artery wall. I suspect that arteries also experience higher levels of glucose which if too high is also another source of damage to the vascular walls.
True. We can also say that for the glycating effects of excess glucose and insulin. But we can blame LDL all we like ; we still need it to live.
@@chazwymanHow much LDL do we need?
What's also interesting is that people with long term elevated blood glucose and insulin don't tend to develop focal plaques in the large arteries, but rather medial calcification of entire lengths of small arteries.
Would it be safe then to assume that blood pressure is a greater risk factor than LDL-C?
@@kinpatu hunter gather societies tend to test at about 75 LDL, while many Americans are 100-200 with over 200 being considered Very High,
Paul saladino also made the case earlier that it is the blood pressure that is more important for atherosclerosis
If pressure were the issue, then plaque would be distributed evenly.
@adriansrfr not really, arterial pressure is higher than venous pressure
@@markregan7639, veins don't get plaque at all.
@@adriansrfr I don't know, but pressure isn't distributed evenly throught the circulatory system. Arterial pressure is higher, therefore that's a potential factor.
@markregan7639 , yes, high blood pressure is a factor.
This is actually an interesting question that I never thought to ask.
Dr Rath explained this 10 years ago. Due to mechanical movement of the heart, arteries develop tiny cracks due to Vit C deficiency occur thus the liver is triggered to produce protein patches to block the cracks. The patches build up and are seen as arterial plaque. Doesn't happen in the venous system. Videos about this. Sub clinical scurvy is the cause of arterial plaqueing.
Thanks for the info/explanation. Yet another reason lower blood pressure is important.
Could there also be a mechanical contribution? If an endothelial lined tube is exposed to more pressure from the heart, could the pressure differential between the arterial & veinous tubing explain part of the conundrum? Also, the arteries are exposed to a hydraulic hammer effect from the heart that the veins do not experience. Could this hammering from the heart beat slightly open the gaps in the endothelial cells to allow micro leaks that build up over time?
Why would those things hold on, and be so abundant, to LDL if not for a reason - killing our bodies is likely not the reason?
Interesting question
If your argument is right, then blood pressure is the proximate cause not ldl.
This youtuber pushes the ldl hypothesis like he has shares in statins.
There is never a single cause. A bullet does not kill people until it’s loaded into a gun. But it’s still helpful to unload the gun or reduce the availability of bullets.
@@fool9111z i.e. bullet is not the cause, thanks for clarifying that.
Not sure that is right. We shouldn't even be talking about LDL-C as the cause of heart disease. It isn't. ApoB lipoprotein particles that transport LDL-C in the blood are the actual cause. They can pass through an undamaged artery wall by transcytosis. If there is damage, more can pass through. But there has to be a threshold level of ApoB particles present before they can pass through the endothelium and get lodged in the subspace, resulting in oxidation, immune response, macrophages, foam cells and plaque formation.
Hey Physionic, I love your videos, you focus a lot on health, sleep, exercise, diabetes, and obesity. All of these things apply to me.. I would love to see some study analysis on sleep apnea and its real scientific effects on our bodies. I know having sleep apnea is not good, but I can't help but feel a lot of these studies/experts may be overstating how bad a typical case of sleep apnea really is on an individual. If sleep apnea is so extremely bad, why is it not taken more seriously for health concern? You almost never hear about sleep apnea and its risks unless you go and seek it out. Would love to see what you dig up, thanks! Love the videos.
hey, on sleep Apnea, try sleeping grounded. Good health to you.
Does it have anything to do with the motor motion of the heart ?
CAGS?? Nice.. my head is spinning hard.. But excellent video I should say. The body is truly wonderfully dynamic in every sense.
This demonstrates the need to be quantitative - hammered into me by several tutors.
One "Some" is not equal to another "some".
Any comments on the glycocalyx and its function toward protecting the arteries? Thanks
It is well known that high blood pressure is more closely linked to atherosclerosis than LDL. ARBs and ACE-I reduce atherosclerosis in clinical trials and some animal models (no idea why nobody pays attention to that). Veins are not subjected to the same levels of blood pressure unless you use them for a bypass. Actually it is intriguing that it is very common for plaque to form in the same place of the carotid artery where pressure is sensed by the autonomic nervous system. Is it so hard to imagine that blood pressure changes membrane protein expression in the endothelium by stretching the artery wall triggering atherosclerosis?
I feel like you just repeated what I said in the video :) we're on the same page. I agree, blood pressure is a major contributor to atherosclerosis, and I agree it tracks better than LDL.
@@Physionic jajaja, yes, but I didn´t get to watch that part before I wrote that. Its an idea that I´ve had for years. That is why I have been looking into the effects of angiotensin 2 type 1 Receptor blockers on atherosclerosis. But I never realized about the vein paradox
Questions….
Does the increase in blood pressure while resistance training have the same relationship to a person who is prone to HBP?
Does the oxidation of LDL happen before or after entering the endothelium?
Does elevated glycation of hemoglobin cause oxidation.
If bp really tracked then resistance trainers would all be dead of heart attacks. My guess is that you cannot separate bp from other lifestyle factors that are more causal.
Subscribed... and took my Crestor.
only thing missing is that adjusted for LDL levels Blood Pressure is still a risk factor (as are others), and arteries experience higher BP
Ya Learned me somethin!
It is flow, when veins are used in coronary grafts they get blocked with plaque.
Plaques are more likely to develop at junctions and branch take offs.
Flow and turbulence changes gene expression at those points
@physionic are there any current human trials you are interested in that try to reverse plaque? -- thanks
The pharmaceutical industry keep stamping all over that territory. Vitamin K2 trials and Natto Kinase trials.
There have been studies showing their efficacy. Pharma have then done studies with vastly reduced doses and shown no improvement - shocker. They also select patients that have little to no coronary plaque in the first place.
Natural products don't make them money.
Oxygen somthing to do with it ?
Wouldn't the higher pressure in arteries cause more LDL to be deposited through the endothelium without any change in CAGs?
It is my understanding that the higher arterial pressure 120/80 mmHg causes microtears, these expose subenthothelial tissues and PG to the LDL and bind it. In veins the low pressures 8/0 mmHg dont cause tears, therefore no atherosclerosi. As soon as a vein is placed in the arterial higher pressure it will develop the micro-tears and eventually acquire athsc.
I take 10mg Crestor and eat a meditation diet and do cardio and weights for my veins, lots of blueberries, kale, fruits and veggies and wild salmon and chicken breast
The first thing that came to my mind blood pressure. But my thought process was, maybe the higher pressure in arteties forces the LDLs past the endothelial layer. It would also explain the plaque formation seen in grafted veins.
But this gene expression theory makes a lot more sense..
Linus Pauling had some great views on this question back in the 90's.
I assumed it was because of the pressure difference, arteries being high pressure and when you move a vein into the artery or high pressure side they get plaque. I also assume the high pressure arterial side is more susceptible to damage and the body uses cholesterol to repair the damage.
Have you listened to or read anything from Dr. Malcolm Kendrick?
Thanks for the great video. Based on how accurate the interaction theory between the proteoglycans and LDL is, this may give us the two hands it takes to clap. If so, the next thing we need to figure out is what causes the rise of these proteoglycans and how do lean mass hyper responders (Dave Feldman) not get plaque. Could this be the villain instead of LDL as has been hypothesized so far?
I thought that high blood pressure contributed to blocked arteries?
it does
But really really high pressure unblocks them, like how urinating after 6 beers can pop out a kidney stone. I think.
I believe most people in the comments are right.The simplest explanation is usually right.The differences in degree of atherosclerosis must have to do with blood content rather than structural differences of blood vessels. My theory is this:
Vein blood contains more carbon dioxide and less oxygen.The higher carbon dioxide levels make the blood pH more acidic .CO2 reacts with water to form carbonic acid which in turn gives bicarbonate ions.This is key because bicarbonate ions react with calcium to give calcium carbonate which is insoluble and a major component of atheromatic plaque .The calcium carbonate then probably aggregates with organic components such as cholesterol, collagen ,elastin etc to contribute to plaque deposits
The higher arterial pressure should increase the LDL incursion rate into the blood vessel wall, if it's a "small" molecule squeezing through a porous barrier as indicated in your pictures.
What's worse beef tallow l animal fat or seed oils?
Would like to see some more analysis of nicotinamide riboside, particularly the chloride form used in Tru Niagen , as well as pentadecanoic Acid (C15:0) aka Fatty 15. Many thanks.
Gil Carvalho did a video on this topic a while back, perhaps Saladino (that was him wasn't it?) might want to watch it.
I have questions please
Why arterial construction decrease the blood flow but venous construction ( like in the lower limp by skeletal muscles) improve it
this begs to further study what the vasculature regulation/gene expression is controlled from and by. another vid Nick.
Question.., LDL , is it the problem or is it the oxidized LDL that is the problem. Or does it matter?
That oxidized LDL would then be traveling through the veins, and should, per that hypothesis, fix to the venous walls. Yet it doesn't.
In the veins, OxLDL shifts back to LDL form in lower oxygen and higher CO2 environment. Makes sense? Someone can do a study on this.
@@alexsingyuchu1955 thanks for the imput
I’m glad SOMEONE is explaining this so well for “non-science” people like me. I’m also very concerned by the way the “carnivore” community in particular (and I am speaking as a meat and fish eater!) is so eager to cling-on to every on-line sound-bite that dismisses the significance of LDL cholesterol as a COMPONENT of atherosclerosis and CVD. Wishful thinking? Time will hopefully tell, one way or another. In the meantime, lets procede with science-led (hopefully unbiased!) caution.
These diet communities are a dietary equivalent of astrology. They start with a fallacious argument and every scientific evidence that happens to coincide with their worldview is somehow a proof of their theory.
There's no such thing as unbiased science.
@@garbajful I did say “hopefully”…because I try to remain hopeful!
@@stevelanghorn1407 Time has already told us whether or not carnivore diet is healthy. Hundreds of thousands of years of human history was completely dependent on predatory hunting. Quite literally, our species would have been extinct long ago if they had to rely on plant matter for sustenance.
@@garbajfulthat has been proven false by several different types of studies & archeological explorations.
Meat eating mainly only increased during glacial maximums.
Prior to that we have millions of years of ancestry subsisting mostly on vegetation.
We didnt just magically appear as a completely new species dependent on the opposite of everything we actually evolved from.
The guy defeated his own argument when he emphasized that only veins grafted into the arterial circulation develop atherosclerosis.
A much more credible difference is that the blood pressure is higher in arteries, and they are therefore more likely to be damaged by irritants, and have to form a scab. This will happen over and over again if the irritants are repeatedly introduced by a bad diet or smoking.
Axel Haverich did interesting studies in micro circulation and how high blood pressure causes aerterosclerosis. This could be an answer to this question.
it has to be the higher flow rate in arteries causing a nidus for the atherosclerotic plaque to form. then, it's accentuated by turbulent flow, further causing endothelial damage and more exposure of the intima, reinforcing the cycle. without the same level of shear forces in veins, the damage can't really begin in the same manner. this explains why veins will become atherosclerotic when exposed to arterial levels of pressure, for example, the saphenous coronary artery bypass. I wonder what the exact rate is, and if veins have any sort of "defense mechanism", where they are able to stretch to accommodate more fluctuations in pressure and not receive damage as quickly in arterial flow. who knows
Couldn't the grafted veins get the cags (or gags) diffused into them by the system of arteries that they now are directly connected to? Or do they have to be grown by the vein's RNA itself after the graft?
Could this suggest that veins which are under consistent hypertension (from/during whatever cause/disease, e.g. portal vein hypertension) are more susceptible to developing plaques?
You mean arteries?
@Physionic I mean veins. IIUC, you said that there are more proteoglycans in subendothelian layer of arteries which are under bigger pressure and that using venous graft in arterial circulation can increase the amount of proteoglycans in the used vein part as well. Now I wonder would the pressure increase due to venous hypertension conditions cause similar effect (or maybe it would't cause big enough difference to match effects of arterial pressure).
Arteries are high pressure. Veins are low pressure. The high pressure of the blood in the arteries is what "forces" the ldl particles into the vessel wall. This is why hypertension itself also causes atherosclerotic cardiovascular disease.
What about the 90-year-olds that have high LDL all their life and have no heart disease
Where did they find enough of these 90-year-olds, considering blood lipoprotein concentration screening was just becoming commonplace in the 1980s?
reverse cholesterol transport, HDL
Who cares? They are obviously outliers and outliers are of little importance. There are people who have smoked their whole lives and dont get lung cancer, but that means nothing and certainly doesn't mean smoking is not harmful for lungs
The data has shown that the older people who live longer have higher LDL levels.
@@The_Kirk_LazarusDon't know if that is true. You don't cite anything, but doesn't matter, since LDL-C is not the cause of heart disease, ApoB particles are the cause and they don't necessarily track LDL-C.
I have heard that it is not LDL but rather phytosterols (plant cholesterol). Is it confirmed to be ldl or are we guessing this based on the shape of the scarring that is left over?
Perhaps the pulsating pressure in arteries from Heart cause LDL to build up in arteries ??
Good reminder nothing simple or as you say static about humans/our body. All life is dynamic and exquisitely complex w/still yet to be fully understood intelligence.
Arteries on the pump side veins on the return line side. See similar in hydronic heating. Who knows
I was always curious how veins heal after needl poke? It uses plaque as patch?
Cholesterol arrives at damaged areas to affect repair. Since arteries have higher pressure by nature they are the ones that experience more damage usually due to other factors. High Blood pressure is caused by other factors like diet and lifestyle habits and sometime misalignment in the c1-c2 vertebrae ie causing reduced pressure to the Brain and the Brain signals to increase pressure. (a factor that 99 percent of “MDs” ignore or are unaware of) The repaired site (Plaque buildup) can also contribute to higher blood pressure but is not the initial cause.
5:19
It's not clear from this figure/narration, whether we're comparing affinities of different GAGs to LDLs or their respective amounts in different vessels. But either way, i can't see how it can be concluded that the GAG with the highest affinity to LDLs is also the one found in the highest amounts in arteries....
One theory about plaque development and blood clots is loss of exclusion zond (EZ) water. Supposedly, that is what primrily protects the arterial membrane and maintains the negative charge to keep the blood flowing. But I'm not sure what would be the hypothesis for the difference between arteries and veins.
As a biologist, surely the obvious hypothesis is that it’s related to the pressure within each vessel type, especially with the known fact that hypertension increase rate of arterial plaque buildup.
Hi @Physionic thank you as always for such clarity! I am puzzled as to why folks still want to push the micro tears and endothelial damage theory of atherosclerosis? When you've explained so well that the main variable here is the amount and nature of the GAGS - Glycosaminoglycans within the arteries. People want to attribute High blood pressure and turbulent flow as the proximate cause but this is conflating what is actual cause. But from your explanation it is the artery walls responding (naturally) to these pressures (natural pressures even at normal B.Ps) by incorporating structural proteoglycans with the sticky GAGs that is the cause. Meaning people in denial will want to refute the ApoB carriers and associated LDL getting trapped by the GAGs as the cause. You might need to further clarify this misconception else the same confusions that Dr Saladino has will be passed on to those with self reinforcing prior beliefs. Causation vs correlation. Your explanation now makes it very clear at least to me that the main explanation is the ApoB retention hypothesis (Lipid retention hypothesis) within the arterial walls. Which then makes it purely a function of prevailing levels of ApoB being shuttled in and out of the sub endothelial layer (maybe passively but could also be actively via transcytosis but still a function of the available amount in lumen). Which also means that even at healthy Blood pressures, as long as the LDL carriers the ApoB particles are above certain physiological levels they will get retained and atherosclerotic plaques will form. And it just so happens that Artery walls are the ones that are subject to more blood pressure and mechanical hydrostatic forces than veins, hence will have more of the sticky GAGs - because as you explain blood vessels are living cells and respond to forces and stimulii. So unless one is those very lucky folks that naturally clear LDL's and ApoB's very efficiently or have more LDL receptors than others or don't recycle them as fast as others then even at normal BP's their atherosclerosis will be a function of the quantities of cholesterol, LDL and triglycerides being trafficked over time - hence getting into contact with the GAGs in the intima. Anyway that's now my understanding, thanks as always - Corrections are welcome and any misconceptions here are purely mine! 😀
In my college biochem lab we did an experiment that showed how pressure would cause cholesterol to precipitate out of solution. Arteries are subject to higher pressures than veins.
If this is the case, would it be logical to expect LDL as a precipitate out of cholesterol to show up more in arteries than veins?
Following on from this, it is plausible that we have been barking up the wrong tree by focussing on LDL as a causative component??
Interesting! So veins can change the expression of certain proteins as their environment changes which of course makes sense. I wonder if there are people with certain gene variants who naturally produce fewer of the LDL attracting GAGs in their arteries. If that's the case it would mean that genetic predisposition should also be included in the heart disease debate.
I'm 63 and just completed a 12-day water fast, then I watched a video interview with you where you pointed out the dark side of autophagy. Would you consider doing a video on age and fasting, including some insights on autophagy? I also do keto and OMAD. I'm wondering if I'm really wasting my time or maybe doing some damage.
If you do animal food based keto, then yes, you're doing damage.
BS @@k.h.6991
If you don't do animal food based keto, then yes, you're doing damage. In fact, if you don't do animal based any diet, you're doing damage. Even a vegetarian diet is only healthy to the degree it includes eggs and dairy.
As for fasting, there is no advantage to fast beyond 3 days. After that, you're not getting any additional benefit and likely just causing harm. If you simply do OMAD and/or some moderate extended fasting a few times a year, you'll do fine as long as you get plenty of animal fat.
What about the elasticity of those two are different?
What if the difference in glucose concentration between the arterial and the venous circulation plays a role?
Just wondering, is concentration of CO2 in vein protecting it for plaque?
whaddabout the vascular endothelial glycocalyx
it isn't shown in your diagram
Could it be as simple as our cells supplied w/ arterial flow are filtering out the plaque materiel so that the venous blood flow lacks the necessary components for plaque to form?
Without going to the end of the video, I'll speculate that there are two major differences - very high pressure in arteries (compared to very low pressure in veins) that causes great infusion of the low dense particles in the arteries walls, next thing is oxygen rich red blood cells that maybe help with the process.
Also I'm thinking because arteries are under more pressure, there are more mechanical reasons that ldl can get deposited inside their inner lining especially if the walls have become more cracked or brittle with age or diabetes
Maybe the cyclic change of pressure in the artery makes it react differently to a vein, which has a steadier pressure.
I think cholesterol acts in the arteries like fix a flat acts in a multi ply tire that starts separating. Arteries are under pressure and if the inner wall becomes damaged (due to inflammation?) then they are likely to leak. Cholesterol tries to plug the leaks perpetuating a very compromising set of complicating and confounding issues.
Good analogy. A simple “plug” would be good. The trouble is that , like most plugs, if the root cause is not alleviated, it’s in vain. However, given that in this analogy, the plaque formation is a response by the body to heal a break, then it obviously is not the cause. So, the cause is…?
I'm really shocked that on this channel there is so much misinformation and ignorance concerning the real cause of plaque formation and heart disease. It's NOT LDL-C. It's the ApoB lipoprotein particles that transport the LDL-C in the blood. When there are too many of these particles, more than the physiological needs of the body, they readily pass through the endothelium. Those that get lodged in the subspace, that is, retained there, are the source of the problem, because they get oxidized and provoke the immune response that leads to plaque formation and inflammation. Inflammation can occur at this point, it doesn't have to precede the process. That is a fallacy promulgated by a lot of youtube doctors.
I think the two major differences between the arterial circulation & the venal circulation is that:
1. The blood pressure is much greater in the arterial circulation
2. The inner lining of the arteries are much thicker than the inner linings of the veins,
What about the particle type of LDL ? Type a or Type b LDL actually matters , type b being the more damaging one.
anyone who has thoughts about ldl passing from the luminal side of arteries or rather from the vasa vasorum?
All conditions in arteries exist in veins (high glucose, smoking contamination, cholesterol, LDL particles, etc.) the difference is the amount of blood pressure. High blood pressure damages the walls of the artery; the existence of other factors exacerbates the damage. Even high level athletes who do not smoke, do not have high glucose, monitor their choleslterol develop atherosclerosis almost certainly because they experience regular very high blood pressure.
What about the arteries in the pulmonary circulation? They generally don't have plaque buildup.
I was just wondering about this. Those two doctors were focused on cholesterol, but what about other aspects of blood chemistry? (oxygen levels, glucose levels, etc) Would any of that play a role?
Definitely :)