LDL particles (the healthy ones) are basically the "livers' delivery trucks", moving lipids around the body for fuel to make energy, the energy that can be used to "heal" things like endothelial erosion. And every healthy LDL also has a special little compartment for a stash of the actual molecule of "cholesterol" onboard, think of that as a supply bin of the "bricks and mortar" needed for cell repairs (every cell's outer membrane contains cholesterol, it's supposed to be there). As long as your LDL's are "healthy", the basic rule of thumb, as difficult as it is to accept, is "the more the better". Having an LDL on the "low end" of the scale is actually much, much, much more associated with short life and disease than having a very "high" LDL. Have an all-healthy no-small-dense LDL of 400, you're golden, and you're much better off than someone with an LDL of 100. The "100" person would likely have low energy for movement, thinking and cell repair, and an insufficient amount of "repair materials" (actual cholesterol) circulating. Around "220-280" (in American numbers) is actually the sweet spot range for lowest all cause mortality and lack of disease. Mason goes over this data in several of his videos. .
I don't quite follow this explenation on LDL, there are very little LDL in plaque and in blood clots none, the cholesterol in clots does not come from LDL(cholesterol esters) but from red blood cells(pure cholesterol) and as cholesterol crystals in clots. This disease should be called artrerie disease, and there are potentialy 100 reasons why this happens more or less in people. LDL is way down on that list! The blood cloting factor seems to be forgotten, LDL rules or apo b or all that nonsence. And the one extremely important protector i never hear the so called "expert" talk about is the Glycocalyx, who protects the endotilial cells. The process of damage vs repair are rearly talked about. This LDL debate must now come to and end. Everyone seems to feed on this LDL hypothesis, here on youtube as well, in medicine they will feed on it for 60 more years at least, 60 more years of pushing pills. Money and control is all that matters, even if the truth is the complete opposite. Just think about it, they have demonised somthing completly necessary for life and somthing that has been perfected for 100 00 0's of years. And they push more then ever. As a man with commen sense i have to pinch my arm and tell myself, how is this possible. What sadness me most are that you don't have to have very high IQ to wrap you head around this. Just basic critical and logical thinking with some reading and you are there. Roar Ellefsen
Ketovore improved my lipid panel. After 6 months, my HDL went from 46 mg/dL to 79 mg/dL, my LDL went from 105 mg/dL to 94 mg/dL, and my triglycerides went from 67 mg/dL to 63 mg/dL. I am lean also (20.4 BMI). I ate and continue to eat about 6 eggs for breakfast with about 8 ounces fatty meat, then usually either steak or ground beef for dinner and I maybe have a salad with cheese, bacon and ranch dressing every now and then. I never snack and do about 19/5 or 18/6 IF and occasionally do 36 or 72 hour water only fasts.
This is good video for people that doesn´t know anything of cholesterol. Doctor wanted to put me on statins becouse my LDL is higher than most of the people or as them book says. I said to him that i don´t have insuline resistance, t2d or inflammation after being 15 months on keto. So i don´t have the risk factors for oxodized LDL. He mumbled for while and sounded angry that i resisted of taking unnecessary pills to treat my cholesterol even that there isn´t any problem. At least here in Finland they don´t take larger scale tests that what kind of LDL you have. Also the heart hospitals guide lines from nutrition is horrible. Same goes with Finnish diabetes association. Just like ADA in US gives such a horrible knowledge of the nutrition, i don´t wonder why people doesn´t ever get cured from those diseases.
He's referring to the NMR LDL-P that measures particle size and concentration. Pheno type A is associated with larger LDL particles. LDL-P correlates with HDL TRIGLYCERIDE RATIO.
The higher the insulin resistance the higher the blood glucose which leads to higher glycation of LDL. This will result in higher than normal sdLDL. As a layperson, this is how I understood it. Please correct me if I am wrong.
ApoB100 - the address for re-uptake of LDL by the liver. Oxidized LDL cannot be absorbed by the liver. I believe inflammation is also evidently a huge culprit when it gets to oxidation and damage to the LDL. My last blood works look pretty good, but as in 2023, my CRP levels remain stubbornly high; around 10 mg/l. My trigs are fine (I was not fasted) and my HDL-C is a super high 1.9 mmol/l.
Question is: why can’t VLDL and/or IDL not oxydise? They don’t have an APOB-100 molecule? Does that APOB-100 suddenly appear on a LDL particle. And what causes oxidation?
My brother had all the ultrasound and calcium scans after only 18 months on carnivore. There was no longer any occlusions or any other signs of plaques.He had bypass surgery a year before carnivore and had a couple more stents installed after that. He also went from 250#s to 165#s. I think it depends on how damaged you are and how dedicated you are to getting off the SAD and how sick you are. He had congestive heart disease as well as blockages. He is now traveling with his wife and enjoying walking and sight seeing rather than eating garbage and being so close to death he couldn't travel far from his home. Walking up his stairs was agony.
Why would you have oxidized LDL if you do NOT eat sugar or seed oils? Are there other risk factors one can work on? Can the fats in whole nuts and seeds also be damaged?
@@ML-yf2dl are you getting the health benefits that you are looking for with this diet? I would suggest keeping your carbohydrates to less than 25 g that's total carbs not net carbs. In nature, the vast majority of foods are either carb plus fat or protein plus fat. Very few foods have carb plus protein plus fat. Nuts are one such food. The combination of carbohydrate plus fat is not good, so you should limit consumption of nuts and seeds. Be extremely careful if you eat anything that comes in a wrapper with an ingredients list, even if it says it's keto friendly. Always check the ingredients list for anything untoward. There are hundreds of different names given to different types of sugar.
I never eat anything with strange ingredients. I do produce ketones, so I don’t think I eat too many carbs. You are right about nuts though, will try to reduce that.
@@ML-yf2dl if your ketones are higher than 0.5, (you are in ketosis) and you are not consuming seed oils you should have no need to worry about your LDL.
My GP (over the phone ) suggested statins as my total Chol was 6 mmmol/l. She seemed baffled when I said "Based on one biomarker in an otherwise healthy person you would prescribe a life-changing drug?" I then asked how long I would be on this drug? Answer: Until you're 80! Huh, as age is a risk factor for CVD, then I would be more at risk at 80 years of age! I ended this ridiculous conversation with "I'll do my research".
I pity the prisoners that are picked to be vegans. The food in prisons in Illinois is all soy fake meat and the prisoner were suing because many of them were suffering joint pain and other problems of digestion caused by those plants.
One day at a time. Start today. Lots of us have transformed our health by going carnivore. Thousands of stories for motivation. Nothing special about me or anyone else. You can do it also.
Stop eating seed oils and also be very selective about which "polyunsaturated" fats you eat in general. Eliminating all nuts and nut butters that have high polyunsaturated fat content would be a good idea. Walnuts and pecans are "allowable" in small quantity, they have a fair ALA (plant based) Omega 3/6 ratio, and higher saturated fat content. High quality organic peanuts/peanut butter actually has a fat profile very close to Olive oil, but there are still a fair amount of "double bonds" in the fat chain so it's not harmless either. Macadamias are great (mostly saturated fat content) but are expensive. Fish is polyunsaturated fat but is beneficial because of marine based Omega 3, DHA and EPA fats, so have (fresh) fish a couple times a week. The only way you can "get rid of" seed oil fat (polyunsaturated) in your body is to be "in fat burning mode" first, which means KETOGENIC. If most of your diet is fat, and keeping carbs as low as possible, then you have a chance of BURNING some of the polyunsaturated seed oil fats currently in the fat stores of your body, along with the new "good fats" (saturated fats) that you are eating in your diet. If you aren't even in "fat burning mode" to begin with (because your body is busy burning carbohydrates first), then you can never hope to get rid of the seed oil fats, so they will sit their in your fat stores and continue to "oxidize" and create free radicals and aldehydes. Probably the most effective and fastest way to rid the body of some of the seed oil fats would be to "extended fast", so that they body has no choice but to be in fat burning mode and consume body fat (some of which will be the seed oil polyunsaturated fats) for energy production. But if you're not overweight with a "storehouse" of fat that might not be the best course of action.
Then you say, no. Or no, thank you. Or "for the last time, no, thank you, I'll drop some research off to you as I see you are too busy seeing patients to keep up ...
How old is this one? He's not onto the damaged LDL and vaso vasorum thing anymore, from what I can tell. He's on Dr. M Kendrick's program now - clotting - for atherosclerotic plaque. With that said, lipids do appear roughly where the vaso vasorum reach into blood vessels. But is it all LDL as implied here? I don't think so. Some of this could be - and no one seems to be investigating this - "creative" fat storage among hypertrophic people who generally can't make new fat cells in adulthood. Fat is stored all over the place, in these people, when they are heavy carb eaters. And quite possibly in arterial walls. At this point we just don't know.
These topics are not inconsistent. And remember, this is an interview that he's responding to. As for ubiquitous fat deposits, generally doctors dismiss pericardial fat as benign-not that this is correct or negates further inquiry, but there it is. LDL is transported everywhere throughout the circulation system, for good reason. The trouble is the ROS, in the form of damaged LDL and free radicals, and what it does to the glycocalyx, which protects the intima. Once the ROS and glycation destroy this protection, then the cholesterol, good and bad, along with the macrophagic foam cells, have the opportunity, indeed are directed to the arterial wall to repair this damage, and thus form the atherosclerotic plaque. More disturbing than Dr. Mason's choice of emphasis here is WebMD's advice for mitigating this condition: less saturated fats, more fruit and vegetable carbohydrates.
A lot of Doctors don't find the HDL to TRIG ratio to be reliable or overly important in the context of arterial inflammation. High blood pressure, not discussed here, is often seen to be the main culprit for CAD. No doubt better to have high HDL and low TRIG but not as important as having HBP.
@@rogerpakrat800 - Than you have an incomplete understanding of the issue. The HDL/ TRIG ratio is almost irrelevant if for example one is prone to a hyper absorption of LDL/ Apob.
Glycation is sugars sticking to the protiens in the particle and messing it up and making it unable to bind to ldl receptors in the liver. Oxidation is when any free radical source comes in contact with the particle, tending to unravel it to some degree. High blood sugars affects the first and eating already oxidized or easily oxidized polyunsaturated seed oils affects the second.
You're contradicting yourself in this video. You made a video suggesting the Thrombogenic model, proposed by Dr Malcolm Kendrick in his book "The Clot Thickens" was a more likely model. And your comment about the Vaso Vasorem falls down because veins have a vaso vasorem, susceptible to oxidised LDL, but veins don't get atherosclerosis in them. So, it ain't that. Oxidised LDL may get into the artery wall when the endothelium is damaged by high blood pressure and an abrasive.
Veins do get sclerotic and may collapse, upon which the deoxygenated blood is normally rerouted through still healthy veins; problematic, but not imminently critical. But there is such a thing as deep vein thrombosis, which is caused by obesity and inflammatory bowel disease among other things, and can be critical.
@@hektor6766 Atherosclerosis is artery inflammation and narrowing. That isn't what you are describing. Thrombosis is a clotting of blood inside the (typically) vein. This happens when blood isn't "moved on" in the leg due to lack of motion for some time, or if you have heart fibrillation, so blood isn't moved on efficiently, or the clot from a plaque rupture moves from the site of a large vessel to a smaller vessel, as in a pulmonary thrombosis or a stroke.
True about "large fluffy" LDL (chylomicrons), true about "small" (just "unloaded of their lipids") LDL's, but small "dense" (damaged by glycation/oxidation) LDL has massive effect on heart/artery health. Your knowledge of this is incomplete. The liver will not "re-uptake" small dense LDL (because the liver recognizes them as "damaged"), so they remain in the blood stream, raising the basic total LDL count, and the particles are free to bang around in the bloodstream causing damage to the endothelium. Mason expounds on these differences in this very video, and accurately refers to the "small dense" LDL in particular, but you seem to have been oblivious to it. Mason is more than aware of these differences, he's the guy that's brought all of this to the surface in the health/nutrition sphere. He has numerous long, deep videos on this topic.
Holy 💩. Higher LDL associated with reversal of plaques.!!! That’s jaw dropping information 👍
LDL particles (the healthy ones) are basically the "livers' delivery trucks", moving lipids around the body for fuel to make energy, the energy that can be used to "heal" things like endothelial erosion. And every healthy LDL also has a special little compartment for a stash of the actual molecule of "cholesterol" onboard, think of that as a supply bin of the "bricks and mortar" needed for cell repairs (every cell's outer membrane contains cholesterol, it's supposed to be there). As long as your LDL's are "healthy", the basic rule of thumb, as difficult as it is to accept, is "the more the better". Having an LDL on the "low end" of the scale is actually much, much, much more associated with short life and disease than having a very "high" LDL. Have an all-healthy no-small-dense LDL of 400, you're golden, and you're much better off than someone with an LDL of 100. The "100" person would likely have low energy for movement, thinking and cell repair, and an insufficient amount of "repair materials" (actual cholesterol) circulating. Around "220-280" (in American numbers) is actually the sweet spot range for lowest all cause mortality and lack of disease. Mason goes over this data in several of his videos. .
@@ericeric9208 👍😎
It is a pity my cardiologist, and my GP, do not seem to understand this...
Surgeons and scientists know more than an MD, stay away from cardiologists there nothing but drug pushers.. .
I don't quite follow this explenation on LDL, there are very little LDL in plaque and in blood clots none, the cholesterol in clots does not come from LDL(cholesterol esters) but from red blood cells(pure cholesterol) and as cholesterol crystals in clots. This disease should be called artrerie disease, and there are potentialy 100 reasons why this happens more or less in people. LDL is way down on that list! The blood cloting factor seems to be forgotten, LDL rules or apo b or all that nonsence. And the one extremely important protector i never hear the so called "expert" talk about is the Glycocalyx, who protects the endotilial cells. The process of damage vs repair are rearly talked about. This LDL debate must now come to and end. Everyone seems to feed on this LDL hypothesis, here on youtube as well, in medicine they will feed on it for 60 more years at least, 60 more years of pushing pills. Money and control is all that matters, even if the truth is the complete opposite. Just think about it, they have demonised somthing completly necessary for life and somthing that has been perfected for 100 00 0's of years. And they push more then ever. As a man with commen sense i have to pinch my arm and tell myself, how is this possible. What sadness me most are that you don't have to have very high IQ to wrap you head around this. Just basic critical and logical thinking with some reading and you are there.
Roar Ellefsen
worse still, they aren't interested in it either...
Very well explained, thanks Paul!
Ketovore improved my lipid panel. After 6 months, my HDL went from 46 mg/dL to 79 mg/dL, my LDL went from 105 mg/dL to 94 mg/dL, and my triglycerides went from 67 mg/dL to 63 mg/dL. I am lean also (20.4 BMI). I ate and continue to eat about 6 eggs for breakfast with about 8 ounces fatty meat, then usually either steak or ground beef for dinner and I maybe have a salad with cheese, bacon and ranch dressing every now and then. I never snack and do about 19/5 or 18/6 IF and occasionally do 36 or 72 hour water only fasts.
😊👍👍 -70SomethingGuy
This is good video for people that doesn´t know anything of cholesterol. Doctor wanted to put me on statins becouse my LDL is higher than most of the people or as them book says. I said to him that i don´t have insuline resistance, t2d or inflammation after being 15 months on keto. So i don´t have the risk factors for oxodized LDL. He mumbled for while and sounded angry that i resisted of taking unnecessary pills to treat my cholesterol even that there isn´t any problem. At least here in Finland they don´t take larger scale tests that what kind of LDL you have.
Also the heart hospitals guide lines from nutrition is horrible. Same goes with Finnish diabetes association. Just like ADA in US gives such a horrible knowledge of the nutrition, i don´t wonder why people doesn´t ever get cured from those diseases.
THANK You...! 😊👍 Very Enlightening and Comprehensive -70SomethingGuy
Thank you Paul. Such a great explainer. Appreciate what you do. 🙏
One who knows his subject explains it well.
Very clear explanation thanks. My LDL is fine. Will live longer. 😉
He's referring to the NMR LDL-P that measures particle size and concentration. Pheno type A is associated with larger LDL particles. LDL-P correlates with HDL TRIGLYCERIDE RATIO.
What about Cardio IQ's Advanced Lipid Panel?
@@JasonBuckman NMR will tell you everything you need to know in correlation to your HDL TRIGLYCERIDE ratio....keep it simple.
Excellent!
A good point about the vasa vasorum being the likely source of LDL in the artery wall.
I'd love to see a citaation that supports the claim that high LDL individuals seem to have a better chance of plaque regression.
1:00 I am Jeff. I am not a bus. I am a carnivore. 🙂
The higher the insulin resistance the higher the blood glucose which leads to higher glycation of LDL. This will result in higher than normal sdLDL. As a layperson, this is how I understood it. Please correct me if I am wrong.
Great description
ApoB100 - the address for re-uptake of LDL by the liver. Oxidized LDL cannot be absorbed by the liver. I believe inflammation is also evidently a huge culprit when it gets to oxidation and damage to the LDL.
My last blood works look pretty good, but as in 2023, my CRP levels remain stubbornly high; around 10 mg/l.
My trigs are fine (I was not fasted) and my HDL-C is a super high 1.9 mmol/l.
Thank you.
Regarding the higher ldl patients had plaque regression, could you please provide the reference?
Thanks
Question is: why can’t VLDL and/or IDL not oxydise? They don’t have an APOB-100 molecule? Does that APOB-100 suddenly appear on a LDL particle. And what causes oxidation?
They can. The only difference between ldl and vldl is the amount of cargo.
Another excellent interview! I would like to send a Super Thanks, but dont see an option to select under the video.
How long on average does it take for the plaques to be reversed on carnivore.
My brother had all the ultrasound and calcium scans after only 18 months on carnivore. There was no longer any occlusions or any other signs of plaques.He had bypass surgery a year before carnivore and had a couple more stents installed after that. He also went from 250#s to 165#s. I think it depends on how damaged you are and how dedicated you are to getting off the SAD and how sick you are. He had congestive heart disease as well as blockages. He is now traveling with his wife and enjoying walking and sight seeing rather than eating garbage and being so close to death he couldn't travel far from his home. Walking up his stairs was agony.
Why would you have oxidized LDL if you do NOT eat sugar or seed oils? Are there other risk factors one can work on? Can the fats in whole nuts and seeds also be damaged?
Don't forget all carbs are sugar.
Am doing keto but not carnivore. 🤷♀️ HDL and triglyerides are good.
@@ML-yf2dl are you getting the health benefits that you are looking for with this diet?
I would suggest keeping your carbohydrates to less than 25 g that's total carbs not net carbs.
In nature, the vast majority of foods are either carb plus fat or protein plus fat.
Very few foods have carb plus protein plus fat. Nuts are one such food.
The combination of carbohydrate plus fat is not good, so you should limit consumption of nuts and seeds.
Be extremely careful if you eat anything that comes in a wrapper with an ingredients list, even if it says it's keto friendly. Always check the ingredients list for anything untoward.
There are hundreds of different names given to different types of sugar.
I never eat anything with strange ingredients. I do produce ketones, so I don’t think I eat too many carbs. You are right about nuts though, will try to reduce that.
@@ML-yf2dl if your ketones are higher than 0.5, (you are in ketosis) and you are not consuming seed oils you should have no need to worry about your LDL.
My GP (over the phone ) suggested statins as my total Chol was 6 mmmol/l. She seemed baffled when I said "Based on one biomarker in an otherwise healthy person you would prescribe a life-changing drug?"
I then asked how long I would be on this drug? Answer: Until you're 80!
Huh, as age is a risk factor for CVD, then I would be more at risk at 80 years of age!
I ended this ridiculous conversation with "I'll do my research".
Have a research of Vegan vs Carnivore for 5 years in Prisoners as part of their rehabilitation
I pity the prisoners that are picked to be vegans. The food in prisons in Illinois is all soy fake meat and the prisoner were suing because many of them were suffering joint pain and other problems of digestion caused by those plants.
Cannot immagine prisons providing acarnivore diet to inmates😂😂😂
You clearly have a rose-tinted view of prisons.
The prisoners would LEAP at consenting to a rib eye in place of potato mush and grey unidentifiable blobs of muck.
How do i get rid of 40 years of eating seed oils
One day at a time. Start today. Lots of us have transformed our health by going carnivore. Thousands of stories for motivation. Nothing special about me or anyone else. You can do it also.
Carb and sugar free. Use Ghee and Avocado oil. Intermittent fasting.
Nattokinase could help.
Stop eating seed oils and also be very selective about which "polyunsaturated" fats you eat in general. Eliminating all nuts and nut butters that have high polyunsaturated fat content would be a good idea. Walnuts and pecans are "allowable" in small quantity, they have a fair ALA (plant based) Omega 3/6 ratio, and higher saturated fat content. High quality organic peanuts/peanut butter actually has a fat profile very close to Olive oil, but there are still a fair amount of "double bonds" in the fat chain so it's not harmless either. Macadamias are great (mostly saturated fat content) but are expensive. Fish is polyunsaturated fat but is beneficial because of marine based Omega 3, DHA and EPA fats, so have (fresh) fish a couple times a week. The only way you can "get rid of" seed oil fat (polyunsaturated) in your body is to be "in fat burning mode" first, which means KETOGENIC. If most of your diet is fat, and keeping carbs as low as possible, then you have a chance of BURNING some of the polyunsaturated seed oil fats currently in the fat stores of your body, along with the new "good fats" (saturated fats) that you are eating in your diet. If you aren't even in "fat burning mode" to begin with (because your body is busy burning carbohydrates first), then you can never hope to get rid of the seed oil fats, so they will sit their in your fat stores and continue to "oxidize" and create free radicals and aldehydes. Probably the most effective and fastest way to rid the body of some of the seed oil fats would be to "extended fast", so that they body has no choice but to be in fat burning mode and consume body fat (some of which will be the seed oil polyunsaturated fats) for energy production. But if you're not overweight with a "storehouse" of fat that might not be the best course of action.
Yet your doctor, with a smile: "Here, take this statin."
😡🤦♂️
Then you say, no. Or no, thank you. Or "for the last time, no, thank you, I'll drop some research off to you as I see you are too busy seeing patients to keep up ...
So transcytosis is not a mechanism? What is the evidence that LDL c is delivered to the sub endothelial space and intima via the vaso vasorum.
How old is this one? He's not onto the damaged LDL and vaso vasorum thing anymore, from what I can tell. He's on Dr. M Kendrick's program now - clotting - for atherosclerotic plaque. With that said, lipids do appear roughly where the vaso vasorum reach into blood vessels.
But is it all LDL as implied here? I don't think so. Some of this could be - and no one seems to be investigating this - "creative" fat storage among hypertrophic people who generally can't make new fat cells in adulthood. Fat is stored all over the place, in these people, when they are heavy carb eaters. And quite possibly in arterial walls. At this point we just don't know.
These topics are not inconsistent. And remember, this is an interview that he's responding to.
As for ubiquitous fat deposits, generally doctors dismiss pericardial fat as benign-not that this is correct or negates further inquiry, but there it is. LDL is transported everywhere throughout the circulation system, for good reason. The trouble is the ROS, in the form of damaged LDL and free radicals, and what it does to the glycocalyx, which protects the intima. Once the ROS and glycation destroy this protection, then the cholesterol, good and bad, along with the macrophagic foam cells, have the opportunity, indeed are directed to the arterial wall to repair this damage, and thus form the atherosclerotic plaque. More disturbing than Dr. Mason's choice of emphasis here is WebMD's advice for mitigating this condition: less saturated fats, more fruit and vegetable carbohydrates.
A lot of Doctors don't find the HDL to TRIG ratio to be reliable or overly important in the context of arterial inflammation. High blood pressure, not discussed here, is often seen to be the main culprit for CAD. No doubt better to have high HDL and low TRIG but not as important as having HBP.
What causes HBP? Sugar, seed oils and inflammation
@@DaveIrish66 - There is no identifiable cause for primary HBP in most people.
@@jameswarhol442 was high blood pressure a thing prior to the over consumption of sugars and seed oils? Which cause inflammation
Not surprised that a lot of doctors think that way.
@@rogerpakrat800 - Than you have an incomplete understanding of the issue. The HDL/ TRIG ratio is almost irrelevant if for example one is prone to a hyper absorption of LDL/ Apob.
❤❤❤
Please make it simple.
Too much carb in diet = bad for LDL. Lower carb intake as much as possible. At least remove the processed crap.
@@ElexyrEven more important: lower plant oil consumption or eliminate entirely
What do you mean by damaged?
Go back and watch again, Dr.Mason has explained this quite simply.
Sugar, carbs, seed oils, oxidation and inflammation.
Do keep up.
Glycation is sugars sticking to the protiens in the particle and messing it up and making it unable to bind to ldl receptors in the liver. Oxidation is when any free radical source comes in contact with the particle, tending to unravel it to some degree. High blood sugars affects the first and eating already oxidized or easily oxidized polyunsaturated seed oils affects the second.
Unlikely… 🤔
If you need to point out in the title that he is an expert, then he probably isn’t much of one.
Shrinkage? Do women know about shrinkage?
You're contradicting yourself in this video. You made a video suggesting the Thrombogenic model, proposed by Dr Malcolm Kendrick in his book "The Clot Thickens" was a more likely model. And your comment about the Vaso Vasorem falls down because veins have a vaso vasorem, susceptible to oxidised LDL, but veins don't get atherosclerosis in them. So, it ain't that. Oxidised LDL may get into the artery wall when the endothelium is damaged by high blood pressure and an abrasive.
Veins do get sclerotic and may collapse, upon which the deoxygenated blood is normally rerouted through still healthy veins; problematic, but not imminently critical. But there is such a thing as deep vein thrombosis, which is caused by obesity and inflammatory bowel disease among other things, and can be critical.
@@hektor6766 Atherosclerosis is artery inflammation and narrowing. That isn't what you are describing. Thrombosis is a clotting of blood inside the (typically) vein. This happens when blood isn't "moved on" in the leg due to lack of motion for some time, or if you have heart fibrillation, so blood isn't moved on efficiently, or the clot from a plaque rupture moves from the site of a large vessel to a smaller vessel, as in a pulmonary thrombosis or a stroke.
On this occasion this is NOT expert knowledge. He doesn't understand the mechanism. Damaged or fluffy or small LDL has NO effect on heart disease.
Except in a case of high triglycerides and low HDL. In that case LDL can be a problem
You evidently haven't bothered reading the research.
Troll.
Paul mason reviews the evidence..I trust him..
True about "large fluffy" LDL (chylomicrons), true about "small" (just "unloaded of their lipids") LDL's, but small "dense" (damaged by glycation/oxidation) LDL has massive effect on heart/artery health. Your knowledge of this is incomplete. The liver will not "re-uptake" small dense LDL (because the liver recognizes them as "damaged"), so they remain in the blood stream, raising the basic total LDL count, and the particles are free to bang around in the bloodstream causing damage to the endothelium. Mason expounds on these differences in this very video, and accurately refers to the "small dense" LDL in particular, but you seem to have been oblivious to it. Mason is more than aware of these differences, he's the guy that's brought all of this to the surface in the health/nutrition sphere. He has numerous long, deep videos on this topic.