I want to understand this more… I currently believe we have been so mislead/bamboozled by the food industry and that medicine has been corrupted by the pharmaceutical companies. Any ability to further understand biology and make informed decisions is a gift in these confusing times.
I wish every one could present material as clearly as this Dr did in this video. I actually understood everything he said, and it was presented without prejudice for a position. Very well done....Thank You!
Love your lecture been watching long, long time. I have degrees in health ed. So I understand most of your lectures. Some above my pay grade. I have had chronic fatigue syndrome 30 yrs. I keep abreast of all current studies and find most newer studies are agreeing on one thing, that cortisol levels are very low in chronic fatigue syndrome and covid. I understand it has to do with fatigue but never knew does more like appetite, brain fog and depression and anxiety salt craving etc. Would really appreciate a lecture on the way cortisol does all this. Thanks.
Love that you’re deep diving apoB, was super excited u covered the Feldman phenomena last week & eagerly await this series thank u dr bean!🙏👍 I’ve heard tons on lipids lately but how they mechanistically cause atherosclerosis leaves me with more questions than answers usually, great start tho!
It's nice to see you get up to date with the LDL-science. You should really try to get Harvards Chris Palmer on your show. He has done groundbreaking work on figuring out the root causes of all mental health issues, and he is successfully treating all of them with the ketogenic diet. People with treatment resistant schizophrenia have achieved complete remission with the diet, and it all comes down to our mitochondrial health. It's the same stuff Dave Feldman talks about, but in the context of mental health. Insulin resistance and oxidative stress slowly but surely damages your mitochondria, which causes them not be able to produce ATP from glucose the way they normally do, which leads to parts of your brains to become energy deficient (which causes the illness). This can be circumvented by providing the mitochondria an alternative fuel source, ketones, which are way more easily used by the mitochondria. This restores your mental health. On top of that, ketosis promotes mitochondrial biogenesis, which recycles and repairs your faulty mitochondria + autophagy, which restores your dead cells. Autophagy is the cause why the guy who has the record fast of +380 days didn't have any loose skin after his massive weight loss; your body reused the excess skin.
Like everything else, I’m sure that the cause of schizophrenia is not as simple as this. My son became ill at the young age of 14....he had a good diet and was not insulin resistant. Also, is identical twin brother has the same diagnosis, although he be became ill years later. And my sons would NEVER be able to go on a ketogenic diet, like I am. The meds never work 100% and drugs, smoking and food all provide some comfort and relief from residual symptoms of the illness.
@@guitajose It is as "simple" as this. It's just that many different things cause mitochondrial dysfunction on top of a poor diet. You can hop on google scholar and search about schizophrenia and mitochondrial dysfunction; the evidence is quite clear. "He had a good diet." So, a carb rich diet? Seed oils? Both are a massive cause. That's exactly the problem. And yeah, your both sons have poor mitochondria genes, which is why they developed schizophrenia - and it takes time for their mitochondria to break down. Would NEVER be able to? Why? Sure, you might feel like that, but I bet your kids would rather live an illness free life than eat carbs. Kind of a bold and rude statement when the diet could literally put their illness into complete remission without all the awful side effect drugs have. You have no idea what people with serious mental health illnesses are willing to do to get better.
Hi Dr been nice to see apob talk. My ldl was high in 200s and my apob is 98. My trig's, HDL,hba1c and other stuff were all low. I got worried about Apob for awhile because already have heart issues. The diet though makes me feel better than any others. If I eat any carbs heavy foods and lay down my heart palpitations are insane.
Yes, I am interested in the $3.99 monthly fee. I rely on you to explain things I can basically understand. Almost all my knowledge of our body and medicine started just 4 years ago with the response to Covid.
Thank you, great topic! Would be interesting to collect studies that look at the correlation of lack of sleep and apoB levels. There seems to be one study (2018) with results that indicate that SHORT SLEEP duration is strongly associated with an increased risk of elevated apoB levels in women. However, the results seem to be different for men, which raises the question of differences between women and men. Looking forward to the lectures!
My non HDL is 189 My apoB is 125 My LDL 170 I intermittent fasting everyday for 22 hours , I am keto. I exercise 7 days a week , doing HIIT twice a week and weight training 3x at least. I eat Whole Foods, mostly organic grass fed. I am 47 , 127lbs. Really not understanding how my levels can me this high.
I learned the importance of Apo-b in 1918 from an Italian book written by the journalist Adriano Panzironi but no mention was made at the time of the two different forms of it (48% 0r100%) From today's lecture it would appear that only the 100 form od Apo-b is susceptible to oxidation in such a way to promote plaques formation, is this a correct assumption? 🤔 It also would appear from different studies that also the Liver's receptors can no longer recognise the oxidised LDLs so instead of being reabsorbed and recycled they remain in circulation undetected. I hope all this will be discussed soon Dr. Mobeen 🙏
Both forms are susceptible to oxidative damage. However, ApoB-48 is present in larger (chylomicron) particles. These larger particles do not enter the blood vessel walls.
This was my question as well. Are there lab tests available to distinguish between ApoB 48 and 100? If there is a mix of ApoB 48 and 100 in the blood stream and only the 100 is contributory to vessel wall plaque formation, how would the test be helpful in determining how much risk there is to health versus a standard LDL test? I'm also wondering if heat shock proteins would be effective in repairing the oxidation of the ApoB cells in the serum, via NIR therapy/PBM.
I saw a few studies on sertraline causing higher triglycerides and changes in cholesterol. Mine has been affected. I'm only taking 12.5 so it's hard to imagine it affected it. But something upped it. I'm trying to eat more healthy and increase my walk to 3 miles from one.
ApoB is on the high end of normal, ldl on high end too. triglycerides low, crp normal, lp(a) low, hdl normal. What are my risks as 60+ & female. I eat low carb (mostly meat & veges) and avoid toxins. Getting cac score soon.
Love your lectures…not in the medical field, just interested in many of your lectures. Would be very interested in subscribing to your $3.99 month plan. Am a senior trying to maintain good health😀
Just a clarification on your drawing of the ApoB 48 and 100 with the ribosome transcribing the mRNA, wouldn't the stop signal be inside the nucleus coming toward the ribosome rather than at the start of the transcription? And wouldn't the Carboxy terminal be at the end of the transcription rather than at the beginning as you have depicted? Also on the second drawing with the ApoBEC-1 enzyme how does the enzyme make the conversion of the CAA to the UAA inside the nucleus before it hits the ribosome to cause the transcription to stop at that point and terminate for the ApoB-48?
I have lipoprotein A high levels, 100X higher than normal. I read it is genetic, and you are born with it. Can you discuss lipoprotein A? Thank you so much! I live your videos, I'm a natural health enthusiast. I would love to have a consultation with you,if that's possible
layperson trying to remember: the thrombogenic theory of atherosclerosis says: lipo proteins carry cholesterol in the form of cholesterol esters. the 'cholesterol' found at the sites of atheroma are pure cholesterol crystals. cholesterol esters cannot convert back to pure cholesterol crystals. the only cell carrying large amounts of pure cholesterol that could form crystals are red blood cells. the remnants of red blood cells and their payload of cholesterol crystals are found in abundance in atheroma, as they are forming the equivalent of internal scabs to heal wounds. If this is true, and the type of cholesterol found in atheroma, cannot come from the cholesterol esters in lipoproteins then it seems unlikely that high-level of lipoproteins are going to be problematic. so the cholesterol theory is wrong.
So if we have first inflammation, that inflammation oxidizes ApoB, and then we blame the original unoxidized ApoB for all the trouble. This is like blaming collagen for the damage in cartilages produced by the inflammation that degraded the collagen in the first place. Maybe someone should start producing a drug that reduces collagen, so that there is less collagen that can be attacked by inflammation. ApoB is following the same path LDL followed, once it became harder and harder to blame cholesterol alone.
You are correct that we are missing the matchsticks (inflammatory molecules) that set ApoB on fire (deform it to produce new immunogenic epitopes.) Inflammation becomes an even bigger problem when you consider that about 60% of Americans live with at least one chronic condition. So, 60% of Americans are walking around with increased risk of atherosclerosis due to these inflammatory molecules.
I still have a VERY hard time believing that a particle the size of LDL can simply pass through the arterial endothelium, and then pass back again. If that were true, then red blood cells, plasma cells and anything else in our bloodstream that is smaller than LDL should be able to just leave the vessel. If that were the case, we would bleed to death in seconds and life would cease. The endothelial cells are cells like any other. They have a membrane that prevents things from entering unless it is specifically allowed - water, ions, etc. Once inside the cell, things that do not belong are destroyed by lysosomes and presented on the cell's surface indicating that something is wrong. Nor is it possible for things to pass through the tight junctions between the endothelial cells. Dr. Been, this is not a criticism of you. This whole lipid hypothesis is full of holes. There is no LDL receptor on the endothelium. Even if there were, the LDL would still need to get past the glycocalyx. This drives me crazy. Those who tout this lipid hypothesis never describe the mechanism that is supposed to allow this magic movement of LDL through the endothelium. There are a number of doctors who are advocates of a realistic theory of clot formation - glycocalyx damage, endothelial exposure, endothelial damage, clot formation, clot repair that includes endothelial progenitor cells that cover the repair, making it SEEM like the LDL particles and foam cells (macrophages) can pass through the endothelium. Continued damage by hypertension, environmental pollutants, hyperglycemia, etc. pile up the damage and repair until that artery is occluded. The same concentration of LDL particles is present in veins, but there is never any plaque formation in veins. AGAIN, this whole lipid hypothesis is full of holes.
Peter Attia believes in this type of magic. Dr. Malcolm Kendrick elegantly explains a much more plausible explanation, and a non-magical mechanism for plaque formation in his book, "The Clot Thickens". This fantasy based lipid hypothesis must end. This sort of thinking (LDL can magically pass through endothelium unmolested) is rubbish.
You mean the blood vessel endothelial cells (not intestinal) I guess. LDLs are just a little bigger than the tight junctions, and about 100x smaller in diameter than RBCs. It happens when the endo cells are renewed/replaced and by caveolae-mediated transcytosis. See eg PMC2755980 . Yes blood pressure pressing&damaging and amount of stress on endo cell plays into the rate of this processes and also makes arteries much more susceptible vs veins.
Firstly LDL can transcytose through the endothelial cells. (www.ncbi.nlm.nih.gov/pmc/articles/PMC7951609/). Secondly, LDL are 22nm-28nm. In the nanometer scale an RBC is 7000nm-8000nm. Thirdly, if there was no LDL or cholesterol, or ApoB getting into the blood vessel walls then there will be no atherosclerotic plagues. Fourthly, the LDL receptor based transport is mainly to internalize the LDL into the cell and not to offer a trans-cellular passage. LDL receptor based transport and transcytosis are two entirely different events with different outcomes.
@@xcast1 Yup. I was typing away and didn't check my work. 🙂 BTW, thank you for the reference PMC2755980. It still seems like magic to me and fails to explain why other molecules aren't piling up in the intima. But, that is likely my bias.
@@DrBeenMedicalLectures Thank you for your response! Trancytosis seems like magic to me. I will read the article. There must be some mechanism causing damage or disruption since this sort of thing should kill us all and humanity would cease to exist if it were so easily accomplished.
My non HDL is 189 My apoB is 125 My LDL 170 I intermittent fasting everyday for 22 hours , I am keto. I exercise 7 days a week , doing HIIT twice a week and weight training 3x at least. I eat Whole Foods, mostly organic grass fed. I am 47 , 127lbs. Really not understanding how my levels can me this high.
I want to understand this more… I currently believe we have been so mislead/bamboozled by the food industry and that medicine has been corrupted by the pharmaceutical companies. Any ability to further understand biology and make informed decisions is a gift in these confusing times.
I wish every one could present material as clearly as this Dr did in this video. I actually understood everything he said, and it was presented without prejudice for a position. Very well done....Thank You!
3,99 a momth for general public is a great idea Dr. Been!
Thank you. Will share the link.
Dr Been, your medical lectuers are so very invaluable!
Thank you!
Love your lecture been watching long, long time. I have degrees in health ed. So I understand most of your lectures. Some above my pay grade. I have had chronic fatigue syndrome 30 yrs. I keep abreast of all current studies and find most newer studies are agreeing on one thing, that cortisol levels are very low in chronic fatigue syndrome and covid. I understand it has to do with fatigue but never knew does more like appetite, brain fog and depression and anxiety salt craving etc. Would really appreciate a lecture on the way cortisol does all this. Thanks.
Thank you for your note. Yes, will record a lecture on this topic.
@@DrBeenMedicalLectures Then I will send thanks now. I would really appreciate it and sure others would be glad to hear also.
Love that you’re deep diving apoB, was super excited u covered the Feldman phenomena last week & eagerly await this series thank u dr bean!🙏👍 I’ve heard tons on lipids lately but how they mechanistically cause atherosclerosis leaves me with more questions than answers usually, great start tho!
Great info. This is very important. Your cartoons help me to learn. Good teaching technic. Thanks. ❤
Thanks again.
BTW, so glad I'm still in the control group.
Thank you 🙏 have been looking for podcasts on this topic this past week! Devine timing I guess ❤
👍
It's nice to see you get up to date with the LDL-science. You should really try to get Harvards Chris Palmer on your show. He has done groundbreaking work on figuring out the root causes of all mental health issues, and he is successfully treating all of them with the ketogenic diet. People with treatment resistant schizophrenia have achieved complete remission with the diet, and it all comes down to our mitochondrial health. It's the same stuff Dave Feldman talks about, but in the context of mental health.
Insulin resistance and oxidative stress slowly but surely damages your mitochondria, which causes them not be able to produce ATP from glucose the way they normally do, which leads to parts of your brains to become energy deficient (which causes the illness). This can be circumvented by providing the mitochondria an alternative fuel source, ketones, which are way more easily used by the mitochondria. This restores your mental health. On top of that, ketosis promotes mitochondrial biogenesis, which recycles and repairs your faulty mitochondria + autophagy, which restores your dead cells. Autophagy is the cause why the guy who has the record fast of +380 days didn't have any loose skin after his massive weight loss; your body reused the excess skin.
Like everything else, I’m sure that the cause of schizophrenia is not as simple as this. My son became ill at the young age of 14....he had a good diet and was not insulin resistant. Also, is identical twin brother has the same diagnosis, although he be became ill years later. And my sons would NEVER be able to go on a ketogenic diet, like I am. The meds never work 100% and drugs, smoking and food all provide some comfort and relief from residual symptoms of the illness.
@@guitajose 😮🙏
@@guitajose It is as "simple" as this. It's just that many different things cause mitochondrial dysfunction on top of a poor diet. You can hop on google scholar and search about schizophrenia and mitochondrial dysfunction; the evidence is quite clear.
"He had a good diet." So, a carb rich diet? Seed oils? Both are a massive cause. That's exactly the problem. And yeah, your both sons have poor mitochondria genes, which is why they developed schizophrenia - and it takes time for their mitochondria to break down.
Would NEVER be able to? Why? Sure, you might feel like that, but I bet your kids would rather live an illness free life than eat carbs. Kind of a bold and rude statement when the diet could literally put their illness into complete remission without all the awful side effect drugs have. You have no idea what people with serious mental health illnesses are willing to do to get better.
Yes on the monthly subscription for series. Great idea
Cool. Will get it set up and share the link.
Hi Dr been nice to see apob talk. My ldl was high in 200s and my apob is 98. My trig's, HDL,hba1c and other stuff were all low. I got worried about Apob for awhile because already have heart issues. The diet though makes me feel better than any others. If I eat any carbs heavy foods and lay down my heart palpitations are insane.
Yes, I am interested in the $3.99 monthly fee. I rely on you to explain things I can basically understand. Almost all my knowledge of our body and medicine started just 4 years ago with the response to Covid.
Thank you. Will share the link.
Thank you, great topic! Would be interesting to collect studies that look at the correlation of lack of sleep and apoB levels. There seems to be one study (2018) with results that indicate that SHORT SLEEP duration is strongly associated with an increased risk of elevated apoB levels in women. However, the results seem to be different for men, which raises the question of differences between women and men. Looking forward to the lectures!
As always excellent video. Count me in on your proposed new monthly plan.
I think the option of $3.99 a month would be a good idea. I am not a medical professional but am interested in healthspan and lifespan topics.
My non HDL is 189
My apoB is 125
My LDL 170
I intermittent fasting everyday for 22 hours , I am keto. I exercise 7 days a week , doing HIIT twice a week and weight training 3x at least. I eat Whole Foods, mostly organic grass fed. I am 47 , 127lbs. Really not understanding how my levels can me this high.
Top notch graphics
Thank you Mobeen :) !
I learned the importance of Apo-b in 1918 from an Italian book written by the journalist Adriano Panzironi but no mention was made at the time of the two different forms of it (48% 0r100%) From today's lecture it would appear that only the 100 form od Apo-b is susceptible to oxidation in such a way to promote plaques formation, is this a correct assumption? 🤔 It also would appear from different studies that also the Liver's receptors can no longer recognise the oxidised LDLs so instead of being reabsorbed and recycled they remain in circulation undetected. I hope all this will be discussed soon Dr. Mobeen 🙏
Both forms are susceptible to oxidative damage. However, ApoB-48 is present in larger (chylomicron) particles. These larger particles do not enter the blood vessel walls.
@@DrBeenMedicalLectures Thank you dearest Mobeen, you are special ❤
My pleasure.
This was my question as well. Are there lab tests available to distinguish between ApoB 48 and 100? If there is a mix of ApoB 48 and 100 in the blood stream and only the 100 is contributory to vessel wall plaque formation, how would the test be helpful in determining how much risk there is to health versus a standard LDL test? I'm also wondering if heat shock proteins would be effective in repairing the oxidation of the ApoB cells in the serum, via NIR therapy/PBM.
Yes...3.o9 a mo.....even a soc sec recipient can afford it!!!!!! THANK YOU FOR YOUR KIND OFFER!!!!!❤❤❤❤❤????
Great video, sir… I have a question are you vegetarian or vegan? I just found you on UA-cam and I really enjoy watching your videos!
So what induces the ROS, .... insulin resistance.
Thanks ❤
I saw a few studies on sertraline causing higher triglycerides and changes in cholesterol. Mine has been affected. I'm only taking 12.5 so it's hard to imagine it affected it. But something upped it. I'm trying to eat more healthy and increase my walk to 3 miles from one.
ApoB is on the high end of normal, ldl on high end too. triglycerides low, crp normal, lp(a) low, hdl normal.
What are my risks as 60+ & female. I eat low carb (mostly meat & veges) and avoid toxins.
Getting cac score soon.
Thank you Dr. Been, I really appreciate this information!
Yes, I'd be interested in a low cost monthly subscription.
Thank you. Will share the link soon.
What are the differences between La and ApoB?
Love your lectures…not in the medical field, just interested in many of your lectures. Would be very interested in subscribing to your $3.99 month plan. Am a senior trying to maintain good health😀
Thank you. Will share the link.
Just a clarification on your drawing of the ApoB 48 and 100 with the ribosome transcribing the mRNA, wouldn't the stop signal be inside the nucleus coming toward the ribosome rather than at the start of the transcription? And wouldn't the Carboxy terminal be at the end of the transcription rather than at the beginning as you have depicted? Also on the second drawing with the ApoBEC-1 enzyme how does the enzyme make the conversion of the CAA to the UAA inside the nucleus before it hits the ribosome to cause the transcription to stop at that point and terminate for the ApoB-48?
I have lipoprotein A high levels, 100X higher than normal. I read it is genetic, and you are born with it. Can you discuss lipoprotein A? Thank you so much! I live your videos, I'm a natural health enthusiast. I would love to have a consultation with you,if that's possible
So normal LDL shot up, doc prescribes statin, but does that help if this is what is actually happening?
How do you remove the plaque
Thanks, but I think Dr Malcolm Kendrick's explanation is more plausible.
Wow!
UAA is the stop codon
Fixed.
I wish you could look into joe tippens protocol and perhaps break down possible mechanisms for helping cancer patients.
Wow 😳
layperson trying to remember:
the thrombogenic theory of atherosclerosis says:
lipo proteins carry cholesterol in the form of cholesterol esters.
the 'cholesterol' found at the sites of atheroma are pure cholesterol crystals.
cholesterol esters cannot convert back to pure cholesterol crystals.
the only cell carrying large amounts of pure cholesterol that could form crystals are red blood cells.
the remnants of red blood cells and their payload of cholesterol crystals are found in abundance in atheroma, as they are forming the equivalent of internal scabs to heal wounds.
If this is true, and the type of cholesterol found in atheroma, cannot come from the cholesterol esters in lipoproteins then it seems unlikely that high-level of lipoproteins are going to be problematic.
so the cholesterol theory is wrong.
So if we have first inflammation, that inflammation oxidizes ApoB, and then we blame the original unoxidized ApoB for all the trouble. This is like blaming collagen for the damage in cartilages produced by the inflammation that degraded the collagen in the first place.
Maybe someone should start producing a drug that reduces collagen, so that there is less collagen that can be attacked by inflammation.
ApoB is following the same path LDL followed, once it became harder and harder to blame cholesterol alone.
You are correct that we are missing the matchsticks (inflammatory molecules) that set ApoB on fire (deform it to produce new immunogenic epitopes.) Inflammation becomes an even bigger problem when you consider that about 60% of Americans live with at least one chronic condition. So, 60% of Americans are walking around with increased risk of atherosclerosis due to these inflammatory molecules.
I still have a VERY hard time believing that a particle the size of LDL can simply pass through the arterial endothelium, and then pass back again. If that were true, then red blood cells, plasma cells and anything else in our bloodstream that is smaller than LDL should be able to just leave the vessel. If that were the case, we would bleed to death in seconds and life would cease.
The endothelial cells are cells like any other. They have a membrane that prevents things from entering unless it is specifically allowed - water, ions, etc. Once inside the cell, things that do not belong are destroyed by lysosomes and presented on the cell's surface indicating that something is wrong. Nor is it possible for things to pass through the tight junctions between the endothelial cells.
Dr. Been, this is not a criticism of you. This whole lipid hypothesis is full of holes. There is no LDL receptor on the endothelium. Even if there were, the LDL would still need to get past the glycocalyx. This drives me crazy. Those who tout this lipid hypothesis never describe the mechanism that is supposed to allow this magic movement of LDL through the endothelium.
There are a number of doctors who are advocates of a realistic theory of clot formation - glycocalyx damage, endothelial exposure, endothelial damage, clot formation, clot repair that includes endothelial progenitor cells that cover the repair, making it SEEM like the LDL particles and foam cells (macrophages) can pass through the endothelium. Continued damage by hypertension, environmental pollutants, hyperglycemia, etc. pile up the damage and repair until that artery is occluded.
The same concentration of LDL particles is present in veins, but there is never any plaque formation in veins.
AGAIN, this whole lipid hypothesis is full of holes.
Peter Attia believes in this type of magic.
Dr. Malcolm Kendrick elegantly explains a much more plausible explanation, and a non-magical mechanism for plaque formation in his book, "The Clot Thickens".
This fantasy based lipid hypothesis must end. This sort of thinking (LDL can magically pass through endothelium unmolested) is rubbish.
You mean the blood vessel endothelial cells (not intestinal) I guess. LDLs are just a little bigger than the tight junctions, and about 100x smaller in diameter than RBCs. It happens when the endo cells are renewed/replaced and by caveolae-mediated transcytosis. See eg PMC2755980 . Yes blood pressure pressing&damaging and amount of stress on endo cell plays into the rate of this processes and also makes arteries much more susceptible vs veins.
Firstly LDL can transcytose through the endothelial cells. (www.ncbi.nlm.nih.gov/pmc/articles/PMC7951609/).
Secondly, LDL are 22nm-28nm. In the nanometer scale an RBC is 7000nm-8000nm.
Thirdly, if there was no LDL or cholesterol, or ApoB getting into the blood vessel walls then there will be no atherosclerotic plagues.
Fourthly, the LDL receptor based transport is mainly to internalize the LDL into the cell and not to offer a trans-cellular passage. LDL receptor based transport and transcytosis are two entirely different events with different outcomes.
@@xcast1 Yup. I was typing away and didn't check my work. 🙂
BTW, thank you for the reference PMC2755980. It still seems like magic to me and fails to explain why other molecules aren't piling up in the intima. But, that is likely my bias.
@@DrBeenMedicalLectures Thank you for your response! Trancytosis seems like magic to me. I will read the article. There must be some mechanism causing damage or disruption since this sort of thing should kill us all and humanity would cease to exist if it were so easily accomplished.
Great talk. . Bet hi meat and dairy consumption is still the killer
My non HDL is 189
My apoB is 125
My LDL 170
I intermittent fasting everyday for 22 hours , I am keto. I exercise 7 days a week , doing HIIT twice a week and weight training 3x at least. I eat Whole Foods, mostly organic grass fed. I am 47 , 127lbs. Really not understanding how my levels can me this high.