Hi. Thanks for the presentation. Could there be discordance between ApoB number and the risk for atherogenic particles? For example, could the ApoB be in mid 90s (say, 94) but the actual risk be very very low because most of the ApoB LDL-carriers will be not atherogenic ? From this lecture I understand that the number of particles is what's matters, but can't the ApoBs be further divided to risky ApoB and non-risky ApoB ? (meaning, the total ApoB number might not be the final number to base treatment...)
The graphics tell the story better than the transcript :) So looking at the history (which adds context) it does seem the advances in instrumentation are what must proceed better hypothesis. I did bill harris lipo [precursor] profile ... data data everywhere but not an oil droplet of water to drink !!. messin with HMG-COA while interesting in 100 yrs may look like a left turn in the field.
The lipoproteins are there because of inflamation. The inflammation is there from injury. The endothelial injury is from chronically high glucose and insulin. The lipoproteins are trying to help, but it doesnt work that way and things go wrong. Need to lower glucose and insulin with diet. If you do, your triglycerides will go below 80 as he says is optimum. High LDL and Apo B is a red herring. That is why half or more MI patients have low or normal LDL. Tim Russerts LDL was below 100 at the time of his fatal MI. Risk ratio of high LDL is 1.2 at best. Then there is the argument that this stuff doesnt come in through the endothelial wall, but from the backside via the vaso vasorum. The endothelial wall is really 30 cells thick around the heart, not one cell as typically modeled. Ask a good pathologist who really gets to see all this. Good point that the liver can make LDL directly.
"The lipoproteins are there because of inflamation" Lipoproteins are there because of your genes and lifestyle on top of that. You can have very, very low CRP and very, very high lipoproteins. You can also have that with low glucose and insulin levels. "That is why half or more MI patients have low or normal LDL." That is completely irrelevant. What matters are LDL levels throughout whole life, not during one episode of MI (when LDL is lowered by the organism by the way).
please, as all pathologists apparently have failed to find even one particle in mid traverse , will you please show evidence of at least one microscopic slide in human existence ? , instead of only an illustration portraying only an infant's like , simple thin epithelium ... ...the microscopic image of LDL in the proggress of transversing across the thirty or more layers thick epithelium from the inner arterial lining before it arrives at the outside of that very dense & thick lining , accumulating in a cholesterol mass of a swelling plaque thrombosis,, in and around the vicinity of all the smooth muscle and capillaries surrounding the lining . for all the plaques in the world .not every LDL particle could have magically and instantaneously been transported across thirty + bound together layers of epithelium . please help Dr. Subbotin find the first example in medical history of a proof that a magic transport of LDL outward from within the very thick layers exists , before accumulation and burst after has resulted to allow it's passage , prior to build up of the plaque pressure causes the rupture. . cholesterol transport via enterocytes in the gut , does not suffice for an explanation of lipoproteins never showing up, in act of traversing a vastly thick barrier by comparison in arteries .
Excellent talk.
Thanks for this.
So glad Dr Dayspring teamed up with Dr Attia. I’ve followed both for many years.
Great talk, learned a lot.
Hi. Thanks for the presentation. Could there be discordance between ApoB number and the risk for atherogenic particles? For example, could the ApoB be in mid 90s (say, 94) but the actual risk be very very low because most of the ApoB LDL-carriers will be not atherogenic ?
From this lecture I understand that the number of particles is what's matters, but can't the ApoBs be further divided to risky ApoB and non-risky ApoB ? (meaning, the total ApoB number might not be the final number to base treatment...)
Apob is not causal but downstream of inflammation
The graphics tell the story better than the transcript :) So looking at the history (which adds context) it does seem the advances in instrumentation are what must proceed better hypothesis. I did bill harris lipo [precursor] profile ... data data everywhere but not an oil droplet of water to drink !!. messin with HMG-COA while interesting in 100 yrs may look like a left turn in the field.
The lipoproteins are there because of inflamation. The inflammation is there from injury. The endothelial injury is from chronically high glucose and insulin. The lipoproteins are trying to help, but it doesnt work that way and things go wrong. Need to lower glucose and insulin with diet. If you do, your triglycerides will go below 80 as he says is optimum. High LDL and Apo B is a red herring. That is why half or more MI patients have low or normal LDL. Tim Russerts LDL was below 100 at the time of his fatal MI. Risk ratio of high LDL is 1.2 at best.
Then there is the argument that this stuff doesnt come in through the endothelial wall, but from the backside via the vaso vasorum. The endothelial wall is really 30 cells thick around the heart, not one cell as typically modeled. Ask a good pathologist who really gets to see all this.
Good point that the liver can make LDL directly.
Nice! The Glycocalyx is the gatekeeper of the endothelium..
"The lipoproteins are there because of inflamation"
Lipoproteins are there because of your genes and lifestyle on top of that. You can have very, very low CRP and very, very high lipoproteins. You can also have that with low glucose and insulin levels.
"That is why half or more MI patients have low or normal LDL."
That is completely irrelevant. What matters are LDL levels throughout whole life, not during one episode of MI (when LDL is lowered by the organism by the way).
Nope.
If all cells can produce cholesterol themselves, what's the objective of liver to secret cholesterol wrapped in lipoprotein to the blood?
please, as all pathologists apparently have failed to find even one particle in mid traverse , will you please show evidence of at least one microscopic slide in human existence ? , instead of only an illustration portraying only an infant's like , simple thin epithelium ... ...the microscopic image of LDL in the proggress of transversing across the thirty or more layers thick epithelium from the inner arterial lining before it arrives at the outside of that very dense & thick lining , accumulating in a cholesterol mass of a swelling plaque thrombosis,, in and around the vicinity of all the smooth muscle and capillaries surrounding the lining . for all the plaques in the world .not every LDL particle could have magically and instantaneously been transported across thirty + bound together layers of epithelium . please help Dr. Subbotin find the first example in medical history of a proof that a magic transport of LDL outward from within the very thick layers exists , before accumulation and burst after has resulted to allow it's passage , prior to build up of the plaque pressure causes the rupture. .
cholesterol transport via enterocytes in the gut , does not suffice for an explanation of lipoproteins never showing up, in act of traversing a vastly thick barrier by comparison in arteries .
Nurse here.. He is spectacularly great with the knowledge of lipids.
is this lesson 20 years old?
Title say it's from September 24th of 2020
At least 😂
What is new? Other lipoprotein (a)
Use a better microphone next time. I can barely understand the guy. The speaker was also rude to the person who tried to point it out.