Regarding cardiovascular risk, we need to focus on *diet and lifestyle,* not LDL or ApoB. All animals have cholesterol. It is vital to all animal life processes. LDL cholesterol will not cause strokes, heart attacks, or atherosclerosis unless we have *metabolic dysfunction,* which occurs with chronic glycation, inflammation, oxidative stress, obesity, visceral fat, hypertension, hyperinsulinemia, insulin resistance, high triglycerides, and low HDL. We can avoid every one of these, and avoid strokes and cardiovascular disease, by avoiding fast food and processed food, and avoiding inflammatory seed oils (e.g. canola) and avoiding sugar, including starches (e.g. rice, bread, pasta & potatoes). Proper lifestyle means stress management, plus regular exercise. Big Pharma does not want you to think about diet and lifestyle. Pharma wants to sell you statins and PCSK9 inhibitors. Therefore pharma wants you to only focus on reducing LDL numbers, including ApoB numbers. *This is deadly.* No matter how low your LDL numbers become, you will have a stroke or heart attack if you have a poor diet and lifestyle. If you have metabolic dysfunction, then high LDL is a liability. On the other hand, if you have metabolic *health,* then high LDL is a *benefit.* You will live longer, with far fewer infections. Cholesterol is your friend until you make it your enemy. Don’t worry about cholesterol or ApoB. Focus on improving your diet and lifestyle.
I agree with Konrad 100% . One thing I would add is that there are a growing number of studies that actually show a low LDL number increases morbidity. This means more deaths, but not all from heart events, many are from cancer and other illness's that Cholesterol is beneficial for. So long story short, reducing cholesterol to reduce your heart events does nothing for you if you die from cancer! I agree that diet and exercise are the key, and for me Carnivore diet has saved my life, which is from eliminating sugars / carbohydrates. The meat is not what does this, but you also need to maintain muscle if you are going to live past your 80's, so I eliminated carbs with a protein based diet and wish I would of discovered it in my 30's. (63 now).
This is an excellent video. After receiving a recommendation from my GP for statins, I looked into the issue. I told the doctor that I wanted to isolate lifestyle factors before taking a new pharmaceutical and its potential side effects. When the doctor scheduled a follow up lab test 6 months out to recheck levels, having done my research I asked: "Would it be possible to test for ApoB levels as well?" The response: "Oh yes, we can add that," at which point the GP updated the already-completed form to add that factor. I consider this doctor to be intelligent and competent so I was a bit astounded: if it is that simple and easy, why would you not gather more information before recommending a pharmaceutical?? I guess it is just hard for GPs to keep up on the medical science for a range of different medical conditions when they are by nature generalists.
Tom, it's simple, really. Statins are the most profitable pharmaceutical in the history of pharmaceuticals. $$$ has tipped the scale to the extent that even the most ethical and virtuous of doctors have been swept up in the tide, because they have to adhere to the 'Standard of Care', which, ultimately, is dictated by Big Pharma. But you are correct. in my six+ years of researching the subject of the pathogenesis of atherosclerosis, this is a groundbreaking video. In fact, I had a blood draw today, and made sure that NMR particle size was spelled out on the order. Best of luck to you wading through the BS!
I agree with you 100%. Unfortunately, our primary care doctors can't be experts on everything so we need to be our own advocates for the health of ourselves and our families. All I can recommend is to spend as much time as you can educating yourself. Over the last 3 years (since my coronary calcium scan put me in the 'severe" group despite no discernable risk factors or symptoms) I've reviewed a ton of information in books and videos and will be the first to say there's a lot of poor information out there. Some of the best science-based RUclips channels I'd recommend are Nutrition Made Simple with Dr. Gil Carvalho, The Drive with Dr. Peter Attia, and The Proof with Simon Hill. If you want to understand more about blood lipids than even your cardiologist, listen to the 7 hours (or maybe just the 2 hours more recently) Peter Attia did with Dr. Thomas Dayspring. He's the expert to the experts.
I’ve learned more in this comment section than 100 videos on this subject! Thanks to all of you! Absolutely amazing! Great video also. Much love and wishing EVERYONE excellent health. Cheers to a long and happy life ❤🎉
@@ExaltusCa maybe the algorithm has become enough smart to understand that a dead user is not fruitful so he is trying to keep us alive suggesting science based health videos.
The most informative way to measure the particle size & density of LDL-C is called the Lipidelectrophoresis test. VLDL_C is not an atherogenic risk. The root cause of atherosclerosis is the oxidation & glycation of healthy LDL-C large/fluffy particles by seed oils and carbohydrates, which also damage the glycocalyx allowing the foam cells containing the small, dense LDL-C particles to enter the arterial walls. So, LDL-C is not the arsonist, its the fireman. Calcification ensues as time goes on and can be measured by the CAC test.
So have the serum spun, in centrifuge, and type the particles A1, A2, B3,4,5,6,7. A1 and A2 are healthy, buoyant, and B are small dense, sometimes glycated.
I have extremely low LP little a but high Apo B and extremely high Apo A1. I'm 74, lean and healthy and don't have elevated risk. The video is misleading. Apo B isn't the whole story.
THE FIRST BIOREGULATION Plasma triglycerides below 0.6 mmol/L (50 mg/dl). Vitamin D (calcifediol): 140-240 ng/mL (350-600 nmol/L) or more subject to need, with precautions and according to protocol. Parathyroid hormone (PTH intact) 5-25 pg/mL (0.5-2.5 pmol/L), if needed around the lower reference range. Love for more oxytocin hormone.
@@aleksandarstojceski3139 Да прашај по лабораториите, само да не се уплашат од овие мои нови сознанија. Yes, ask in the laboratories, let them not be afraid of my new knowledge.
Chylomicrons have a half life of about 15 minutes so the only time they will be measurable is immediately after eating a meal. In an hour or two later at the most, they're no longer in the blood so an apoB measurement won't include them if someone fasts before this bloodwork, which is usually the case. LDL, on the other hand, has a plasma residency time of 3-5 days so will still be counted if the patient is fasting.
@@asarcadyn2414 Each HDL has 1-4 Apo A1 particles, which are not atherogenic. A different lipoprotein, ApoB, is attached to each chylomicron (actually ApoB-48), VLDL, IDL, and LDL (these have ApoB-100). A number of years ago the small LDLs were thought to be more atherogenic but more recently it was determined that the reason they were associated with higher risk was that, for any given level of LDL cholesterol measured, if the particles were small, there had to be a lot more of them than if the particles were large in order to carry the same amount of cholesterol. Once the researchers adjusted for particle number, the effect of size was found immaterial. Risk follows the number of particles (which ApoB measures) and not the particle size.
Life Extension, and there are others include it in a female or male panel. It tests many things for around $200. They have an annual sale in the Spring also.
It is best to fast for at least 12 hours before having blood drawn for a lipid panel. The lipid panel is meant to gauge LDL, VLDL and HDL from your liver. If you do not fast, then you will distort your lipid measurements. Your cholesterol numbers will be skewed by transient chylomicrons from your intestines.
01:10 "We use the mass of LDL-C to estimate the number of lipid carriers" Cholesterol, by itself, cannot travel in the blood stream. Cholesterol requires the LDL carrier to be transported. So how is the mass of cholesterol calculated? After drawing the patient's blood, is the cholesterol separated from the LDL carrier? 🤔
LP(a) is a triple threat: atherogenic, pro-inflammatory, and pro-thrombotic. My score is 300, about 4-5 times the 'recommended' value. The idiots haven't been ordering the test BECAUSE THEY DON'T YET HAVE A DRUG TO SELL YOU, so they figure it's a waste of time and money. But there are several clinical trials that are set to wrap up soon. Dr Sam Tsimiakas at UCSD is one of the top LP(a) guys in the country, if not the world. As already indicated, there are several good videos out there. It pays to educate yourself. The medical community surely won't!
Apo A1 is related to HDL particles. However I would not recommend this ratio as a valuable marker. There is only one ApoB particle on each chylomicron, VLDL, IDL, LDL and Lp(a), all which are atherogenic. However, there many be between one and four Apo A1 particles on an HDL particle so you can't tell how many HDL particles are in the measurement. Additionally, HDL particles are only one part of the reverse cholesterol transport system. HDLs will also transfer their cholesterol to LDL particles which can return it to the liver in what is known as indirect reverse cholesterol transport (as opposed to direct reverse cholesterol transport where the HDL's return cholesterol to the liver). The most current research indicates that measurement of HDL particles and HDL cholesterol are at this time not considered useful as measurements of risk or goals of therapy for this reason. In fact, interventions to deliberately raise HDL cholesterol have been abandoned because the results were higher levels of disease. Regarding LP(a), it is considered even more atherogenic than the other ApoB particles so it's important to measure it by itself. Fortunately, it is genetically determined so you only need to get it tested once in your life. Either you have high Lp(a) or you don't. If you want to learn a lot about cardiovascular disease and it's relationship to blood lipids, watch or read anything from Dr. Thomas Dayspring. He's the expert to the experts and keeps abreast of the cutting edge research in this field. Simon Hill just released on his RUclips channel, ("The Proof" with Simon Hill") the first of a 3-part series of interviews with Dr. Dayspring and it's excellent.
@@markbodine9298 "Remarkably, one-quarter of the centenarians had high Lp(a) serum levels even though they never suffered from atherosclerosis-related diseases." 1998 G. Baggio.
@@dwights1464 Dwight, I've known about Thomas Dayspring for many years, and when I tell the Cardiologist or GP I'm see that Dayspring himself said that ldl by itself is useless, or nearly useless, as a marker of cardiovascular risk, most of the time, their eyes glaze over, and they stand there with a smirk on their faces. Then I fire them.
The argument is flawed, as the Apo-B number does not distinguish between small dense and large LDL, and also VLDL. What is required is a test that gives the numbers of small dense and large (uninflamed) LDL. These numbers are given in the NMR test.
Disadvantages and Limitations of NMR spectroscopy is that it requires expensive equipment. I've never seen that option on my cholesterol REQUISITION test. (CANADA)
Dr. Peter Attia debunked that over 10 years ago. Studies have clearly shown that the LDL particle size, i.e. whether it follows a Pattern A or B, does not matter when ApoB is taken into account. So even if you have an “optimal” triglyceride/HDL ratio but test high for ApoB, sorry your risk is still elevated despite what the low-carb docs say.
@@robocar I'm a good example of what you're talking about. My triglycerides were 90 and HDL-C was 56, giving me a healthy triglyceride to HDL-C ratio of 1.6 in 2019. Unfortunately, I had a CAC scan a week previous to the blood test showing an Agatston score of 435, putting me in the 79th percentile (to the worse) for my age. I didn't know about ApoB then but had a NMR LDL-Particle count and it was a high 1413 (ideal is
@@robocar I disagree. An optimal trig / HDL ratio signifies metabolic health, which is the *sole determinant* of cardiovascular risk. With metabolic health (achieved via proper diet and lifestyle) high LDL numbers and ApoB numbers are benefits, not liabilities.
Yes the NMR test measures particle size and prescribing statins without having this test means your doctor is not up to date on this data. Find a doctor that understands NMR tests.
Hi there! Thanks for your patience. We're happy to announce that the second video has now been released: ruclips.net/video/KjjxpWlzDik/видео.html. Hope you find it helpful!
Try to correlate that total particle number with actual heart risk across a large population and I believe you end up with no correlation. The same thing happens with total cholesterol
For all practical purposes, yes. They both count the number of atherogenic particles although ApoB includes VLDLs and IDLs in addition LDLs. However, the plasma residence time for VLDLs and IDLs is short (a few hours as opposed to days for LDLs) so LDLs are most of the atherogenic particles. ApoB seems to be the more favored measurement presently because, I believe, the measurement process for it has become more standardized.
What causes lipoproteines to get trapped in the vessel lining? Can this happen in healthy vessels or only in unhealthy inflamed vessels? Inflamed by sugar, seed oils, smoking, alcohol?
Yes you are spot on, this is why HDL:Triglycerides is the ultimate health marker. The higher the triglycerides level the higher the inflammation, due to bad diets. In addition long carbon chain fatty acids is also a contributing factor.
Lipoproteins only get trapped in arterial walls if there is *inflammation.* Your body does this to protect you. *Plaque is your friend until you make it your enemy.* Plague is like scar tissue. If you abuse your body enough with poor diet and lifestyle, then this “scar tissue” will cease to protect you, and will eventually kill you. Liver fibrosis is another kind of scar tissue. In extreme cases (e.g. liver cirrhosis) it will kill you. *THEREFORE* the key is to lower inflammation by any and all means possible. Don't worry about LDL or ApoB. With no inflammation, these take care of themselves.
You know they said " don't use a lipid panel "because it measures only LDL and triglycerides. But then they are saying apoB measures all of the LDL's together, and since LDL is the higher number out of all of the LDL's it is the way to measure. Does not make sense, they are saying using apoB is basically the same as doing a Lipid panel, but adds in lipids that are not bad for you as part of the count. So sounds like another way to make your count high and justify....wait for it.....more statin's. Do a LIpoprotein anylysis NMR test, this will tell you all of it, count and sizes, look it up on line.
A much better measure than Apo B is the ratio of Apo B to Apo A1. Apo B can be large but if it's small in relation to Apo A1 it is not correct to assume elevated risk.
LDL is ony atherogenic in the presence of metabolic dysfunction caused by poor diet and lifesyle. Metabolic dysfunction means chronic glycation, inflammation, oxidative stress, obesity, visceral fat, hypertension, hyperinsulinemia, insulin resistance, high triglycerides, and low HDL. All these are easily avpoided via proper diet and lifestyle. If there is no metabolic dysfunction, then regardless of LDL numbers or ApoB numbers, high LDL is a benefit, not a liability, and there is *no risk* of stroke, heart attack, or cadiovascular disease.
Thank you for this. I'm trying to find some good studies that state this. My doctor insists that my high LDL is bad even though all of my other numbers (HDL, BMI, blood pressure, Triglycerides) are good. She wants me on statins but I refuse. @@konradx498
So, my Tri is 31 and my HDL is 50... Is this OK? My LDL is high - always has been - 224. Total C is 288. Been animal based only since Dec. Dropped 64lbs and now 181lbs (52 yr old guy)...my Dr is freaking out - he hates the whole keto/animal based stuff. Eeeek
@@Crushin123 i've started keto, 3 wks now. My TG went from 63 up to 94mg/dl, LDL went from 84 to 184, HDL from 42 to 55. Got both very high apoB 177mg/dl (this was shock) and apoA1 179. I'll give it another couple of months to see how its going
@@agustind5744 oddly enough, add a tiny bit more carbs and your ldl and TGs will go down a tad. If you're exercising before blood tests, your ldl will increase as well.
@@agustind5744 3 weeks is a short time, triglycerides do go up initially for some. Few factors your body releasing more fat is known about. Carbs arent the answer but balancing fat/protein ratio can be. Adding carbs just mwans your eating less Fat or Protein which you could just change the ratio for instead.
@@Crushin123 my story's similar. Lost 30lbs over the past year. Went on statins only for 4 months but surprisingly today (1 year later) my CARDIO said they're optional since my numbers were halved. Try a new CARDIO??
Measuring ApoB is expensive and unnecessary. You want to know how much ApoB is DAMAGED and for that, there are already datapoints in your lab values: A1c and triglycerides/HDL. These two numbers should be low, the lower, the better. The higher the worse your cardiovescular risk. Why does this work? ApoB is a protein and Glucose attatches to it in roughly the same amount than hemoglobine. And when ApoB is attached with glucose, it becomes damaged. The liver does recycle LDL molecules with an undamaged ApoB. It refills them and sends them again on their way. If ApoB is damaged, the liver ignores it. These damaged LDL have to be recycled by macrophages. And where reside most of these? In the walls of the arteries. Here is the catch with LDL: it is not the total mass of LDL, which damages your arteries and your heart IT is the LDL molecules which have no functioning ApoB anymore. What we would like to know is the ratio of damaged LDL vs good LDL. And here comes triglycerides/HDL into play: it correlates highly with this ratio (about 0.9 which is as good as it gets, a correlation of 1 would be perfect). Get your fscking blood sugar down, eat healthy fats (not the plant based crap... put that into your Diesel engine). Do not take statins. At all! These do more harm than good.
A better way to measure risk is signs of insulin resistance, measured OxLDL, low HDL, high TG. ApoB and LDL are poor markers and the hazard ratios for them are really low.
This is the current war, isn't it, between most YT doctors who claim that TG is a better determinant of AVDSC vs. APOB. My doctor still believes it's the latter.
You are absolutely right. The underlying cause of elevated APO-B is sensitivity to insulin, that is if you have higher insulin resistance in your body your APO-B will tend to be higher. Good saturated fat like lauric acid is a powerful super nutrient provided by nature to increase our body sensitivity to insulin.
HDL:Triglycerides ratio is the ultimate health marker. The higher the triglycerides level the higher the inflammation, due to a bad diet. In addition long carbon chain fatty acids is also a contributing factor.
This is why HDL:Triglycerides ratio is the ultimate health marker. The higher the triglycerides level the higher the inflammation, due to bad diet. In addition long carbon chain fatty acids is also a contributing factor.
ApoB is not The Better Way to Measure Cardiovascular Risk. And even if ApoB would be causal, then it would be able to cause damage in any place, right? So, does it damage all arterial system? And does it harm venous system too? Something seems incomplete here.
Regarding cardiovascular risk, we need to focus on *diet and lifestyle,* not LDL or ApoB.
All animals have cholesterol. It is vital to all animal life processes. LDL cholesterol will not cause strokes, heart attacks, or atherosclerosis unless we have *metabolic dysfunction,* which occurs with chronic glycation, inflammation, oxidative stress, obesity, visceral fat, hypertension, hyperinsulinemia, insulin resistance, high triglycerides, and low HDL.
We can avoid every one of these, and avoid strokes and cardiovascular disease, by avoiding fast food and processed food, and avoiding inflammatory seed oils (e.g. canola) and avoiding sugar, including starches (e.g. rice, bread, pasta & potatoes).
Proper lifestyle means stress management, plus regular exercise.
Big Pharma does not want you to think about diet and lifestyle. Pharma wants to sell you statins and PCSK9 inhibitors. Therefore pharma wants you to only focus on reducing LDL numbers, including ApoB numbers. *This is deadly.* No matter how low your LDL numbers become, you will have a stroke or heart attack if you have a poor diet and lifestyle.
If you have metabolic dysfunction, then high LDL is a liability. On the other hand, if you have metabolic *health,* then high LDL is a *benefit.* You will live longer, with far fewer infections. Cholesterol is your friend until you make it your enemy.
Don’t worry about cholesterol or ApoB. Focus on improving your diet and lifestyle.
I agree with Konrad 100% . One thing I would add is that there are a growing number of studies that actually show a low LDL number increases morbidity.
This means more deaths, but not all from heart events, many are from cancer and other illness's that Cholesterol is beneficial for. So long story short, reducing
cholesterol to reduce your heart events does nothing for you if you die from cancer! I agree that diet and exercise are the key, and for me Carnivore diet has
saved my life, which is from eliminating sugars / carbohydrates. The meat is not what does this, but you also need to maintain muscle if you are going to
live past your 80's, so I eliminated carbs with a protein based diet and wish I would of discovered it in my 30's. (63 now).
@@markfrazer7706 Interesting. Could you include a link to study showing that?
@@danguee1
Https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6367420/
@@danguee1
Do a search for this:
Association between low
density lipoprotein cholesterol
and all‐cause mortality: results
from the NHANES 1999-2014
@@danguee1 here is one:
www.ncbi.nlm.nih.gov/pmc/articles/PMC6832139/pdf/jcm-08-01571.pdf
This is an excellent video. After receiving a recommendation from my GP for statins, I looked into the issue. I told the doctor that I wanted to isolate lifestyle factors before taking a new pharmaceutical and its potential side effects. When the doctor scheduled a follow up lab test 6 months out to recheck levels, having done my research I asked: "Would it be possible to test for ApoB levels as well?" The response: "Oh yes, we can add that," at which point the GP updated the already-completed form to add that factor. I consider this doctor to be intelligent and competent so I was a bit astounded: if it is that simple and easy, why would you not gather more information before recommending a pharmaceutical?? I guess it is just hard for GPs to keep up on the medical science for a range of different medical conditions when they are by nature generalists.
My doctor did the same. Just learned about ApoB and will request additional tests before going back on statins
Tom, it's simple, really. Statins are the most profitable pharmaceutical in the history of pharmaceuticals. $$$ has tipped the scale to the extent that even the most ethical and virtuous of doctors have been swept up in the tide, because they have to adhere to the 'Standard of Care', which, ultimately, is dictated by Big Pharma. But you are correct. in my six+ years of researching the subject of the pathogenesis of atherosclerosis, this is a groundbreaking video. In fact, I had a blood draw today, and made sure that NMR particle size was spelled out on the order. Best of luck to you wading through the BS!
@@markbodine9298 Thanks for the comment - helpful and much appreciated.
Docs are compelled to adhere to ‘Standard of Care’ guidelines, hence the usual statin recommendations,etc
I agree with you 100%. Unfortunately, our primary care doctors can't be experts on everything so we need to be our own advocates for the health of ourselves and our families. All I can recommend is to spend as much time as you can educating yourself. Over the last 3 years (since my coronary calcium scan put me in the 'severe" group despite no discernable risk factors or symptoms) I've reviewed a ton of information in books and videos and will be the first to say there's a lot of poor information out there. Some of the best science-based RUclips channels I'd recommend are Nutrition Made Simple with Dr. Gil Carvalho, The Drive with Dr. Peter Attia, and The Proof with Simon Hill. If you want to understand more about blood lipids than even your cardiologist, listen to the 7 hours (or maybe just the 2 hours more recently) Peter Attia did with Dr. Thomas Dayspring. He's the expert to the experts.
I’ve learned more in this comment section than 100 videos on this subject! Thanks to all of you! Absolutely amazing! Great video also. Much love and wishing EVERYONE excellent health. Cheers to a long and happy life ❤🎉
I had to plead with my PCP to screen APOb. He finally agreed but said “I wouldn’t know what to do with it.”
Didn't expect a recommended video to be this good.
Thank you very much, Andrea! Would you mind sharing who recommended this video to you?
@@ExaltusCa it was on my RUclips recommendation.
So interesting! Thank you. We were wondering how we suddenly received so many views and comments
@@ExaltusCa maybe the algorithm has become enough smart to understand that a dead user is not fruitful so he is trying to keep us alive suggesting science based health videos.
The most informative way to measure the particle size & density of LDL-C is called the Lipidelectrophoresis test. VLDL_C is not an atherogenic risk. The root cause of atherosclerosis is the oxidation & glycation of healthy LDL-C large/fluffy particles by seed oils and carbohydrates, which also damage the glycocalyx allowing the foam cells containing the small, dense LDL-C particles to enter the arterial walls. So, LDL-C is not the arsonist, its the fireman. Calcification ensues as time goes on and can be measured by the CAC test.
Where can I get more details on the process you describe?
Can it test for sdLDL?
Focus on ApoB whis is a lipoprotein. You are still mentioning the outdated cholesterol.
Umm, thats not correct. Both small and large particles can enter the arterial walls.
Thank you for your explanation
Very comprehensive video, thanks!
Glad you enjoyed it! Thank you!
To view the second video in the series, please visit: ruclips.net/video/KjjxpWlzDik/видео.html
Best is to measure soft plaque with CIMT
So have the serum spun, in centrifuge, and type the particles A1, A2, B3,4,5,6,7. A1 and A2 are healthy, buoyant, and B are small dense, sometimes glycated.
It's also very important to test Lipo(a), which is determined genetically.
I have extremely low LP little a but high Apo B and extremely high Apo A1. I'm 74, lean and healthy and don't have elevated risk. The video is misleading. Apo B isn't the whole story.
@@whiznot3028Can you elaborate? Thanks
Salient info given so well
Thanks so much, Jay
THE FIRST BIOREGULATION
Plasma triglycerides below 0.6 mmol/L (50 mg/dl).
Vitamin D (calcifediol): 140-240 ng/mL (350-600 nmol/L) or more subject to need, with precautions and according to protocol.
Parathyroid hormone (PTH intact) 5-25 pg/mL (0.5-2.5 pmol/L), if needed around the lower reference range.
Love for more oxytocin hormone.
Zdravo, kaj nas moze da se proverat ovie parametri?
@@aleksandarstojceski3139 Да прашај по лабораториите, само да не се уплашат од овие мои нови сознанија. Yes, ask in the laboratories, let them not be afraid of my new knowledge.
ApoB counts all particles irrespective of their size. We know many particles aren’t atherogenic. Doesn’t that make it a blunt weapon as a marker?
Exactly my point. The video does not actually explain WHY ApoB is a better way to measure cadiovascular risk.
Actually apoB *is* what puts the cholesterol in your arterial wall and this has been demonstrated repeatedly in multiple studies
Chylomicrons have a half life of about 15 minutes so the only time they will be measurable is immediately after eating a meal. In an hour or two later at the most, they're no longer in the blood so an apoB measurement won't include them if someone fasts before this bloodwork, which is usually the case. LDL, on the other hand, has a plasma residency time of 3-5 days so will still be counted if the patient is fasting.
@@dwights1464 So HDL and any size LDL is atherogenic? I thought HDL wasn’t and only the smallest LDL particles could stick in the epithelial layer?
@@asarcadyn2414 Each HDL has 1-4 Apo A1 particles, which are not atherogenic. A different lipoprotein, ApoB, is attached to each chylomicron (actually ApoB-48), VLDL, IDL, and LDL (these have ApoB-100). A number of years ago the small LDLs were thought to be more atherogenic but more recently it was determined that the reason they were associated with higher risk was that, for any given level of LDL cholesterol measured, if the particles were small, there had to be a lot more of them than if the particles were large in order to carry the same amount of cholesterol. Once the researchers adjusted for particle number, the effect of size was found immaterial. Risk follows the number of particles (which ApoB measures) and not the particle size.
What about the potentially offsetting effects of ApoA1 on ApoB?
CAC Scan is the best option. BTW, Cholesterol doesn¨t cause CAD. Inflamation is the cause.
very well done, thanks
So what is a good ApoB level?
Peter Attia has stated that he considers an ApoB level of less than 80 mg/dL to be optimal.
If you have never had a CV event around 80. But if you have had a CV event around 40
Great video.
Turns out my health insurance company won't pay for an ApoB blood test.
Pretty sad when such a test exists but isn't covered.
Mine does
and since it's supposedly the NUMBER ONE DETERMINANT of HEART DISEASE, shouldn't it be done every few months on patients who are worried?
Life Extension, and there are others include it in a female or male panel. It tests many things for around $200. They have an annual sale in the Spring also.
Do we fast if we’re also doing a lipid panel at the same time?
It is best to fast for at least 12 hours before having blood drawn for a lipid panel. The lipid panel is meant to gauge LDL, VLDL and HDL from your liver. If you do not fast, then you will distort your lipid measurements. Your cholesterol numbers will be skewed by transient chylomicrons from your intestines.
Thank you so much for this video. It helps me understand. I need more information though.
Is the lab test called Apo-B?
Need this done soon.
yes, it's part of your CHOLESTEROL LIPIDS test but your doctor must check off APO B as well.
At NYU it is listed as Apolipoprotein B (ApoB only pulls up genetic tests...)@@MsElke11
01:10 "We use the mass of LDL-C to estimate the number of lipid carriers"
Cholesterol, by itself, cannot travel in the blood stream. Cholesterol requires the LDL carrier to be transported.
So how is the mass of cholesterol calculated? After drawing the patient's blood, is the cholesterol separated from the LDL carrier? 🤔
Does this factor the ratio of APO B to APO A1? it has been recommended on several channels, also what is the value of testing LPa
ruclips.net/video/cBDrK3xOZ7U/видео.html
Deep dive postcast if you are interested.
LP(a) is a triple threat: atherogenic, pro-inflammatory, and pro-thrombotic. My score is 300, about 4-5 times the 'recommended' value. The idiots haven't been ordering the test BECAUSE THEY DON'T YET HAVE A DRUG TO SELL YOU, so they figure it's a waste of time and money. But there are several clinical trials that are set to wrap up soon. Dr Sam Tsimiakas at UCSD is one of the top LP(a) guys in the country, if not the world. As already indicated, there are several good videos out there. It pays to educate yourself. The medical community surely won't!
Apo A1 is related to HDL particles. However I would not recommend this ratio as a valuable marker. There is only one ApoB particle on each chylomicron, VLDL, IDL, LDL and Lp(a), all which are atherogenic. However, there many be between one and four Apo A1 particles on an HDL particle so you can't tell how many HDL particles are in the measurement. Additionally, HDL particles are only one part of the reverse cholesterol transport system. HDLs will also transfer their cholesterol to LDL particles which can return it to the liver in what is known as indirect reverse cholesterol transport (as opposed to direct reverse cholesterol transport where the HDL's return cholesterol to the liver). The most current research indicates that measurement of HDL particles and HDL cholesterol are at this time not considered useful as measurements of risk or goals of therapy for this reason. In fact, interventions to deliberately raise HDL cholesterol have been abandoned because the results were higher levels of disease. Regarding LP(a), it is considered even more atherogenic than the other ApoB particles so it's important to measure it by itself. Fortunately, it is genetically determined so you only need to get it tested once in your life. Either you have high Lp(a) or you don't. If you want to learn a lot about cardiovascular disease and it's relationship to blood lipids, watch or read anything from Dr. Thomas Dayspring. He's the expert to the experts and keeps abreast of the cutting edge research in this field. Simon Hill just released on his RUclips channel, ("The Proof" with Simon Hill") the first of a 3-part series of interviews with Dr. Dayspring and it's excellent.
@@markbodine9298 "Remarkably, one-quarter of the centenarians had high Lp(a) serum levels even though they never suffered from atherosclerosis-related diseases." 1998 G. Baggio.
@@dwights1464 Dwight, I've known about Thomas Dayspring for many years, and when I tell the Cardiologist or GP I'm see that Dayspring himself said that ldl by itself is useless, or nearly useless, as a marker of cardiovascular risk, most of the time, their eyes glaze over, and they stand there with a smirk on their faces. Then I fire them.
The argument is flawed, as the Apo-B number does not distinguish between small dense and large LDL, and also VLDL. What is required is a test that gives the numbers of small dense and large (uninflamed) LDL. These numbers are given in the NMR test.
Disadvantages and Limitations of NMR spectroscopy is that it requires expensive equipment. I've never seen that option on my cholesterol REQUISITION test. (CANADA)
Dr. Peter Attia debunked that over 10 years ago. Studies have clearly shown that the LDL particle size, i.e. whether it follows a Pattern A or B, does not matter when ApoB is taken into account. So even if you have an “optimal” triglyceride/HDL ratio but test high for ApoB, sorry your risk is still elevated despite what the low-carb docs say.
@@robocar I'm a good example of what you're talking about. My triglycerides were 90 and HDL-C was 56, giving me a healthy triglyceride to HDL-C ratio of 1.6 in 2019. Unfortunately, I had a CAC scan a week previous to the blood test showing an Agatston score of 435, putting me in the 79th percentile (to the worse) for my age. I didn't know about ApoB then but had a NMR LDL-Particle count and it was a high 1413 (ideal is
@@robocar I disagree. An optimal trig / HDL ratio signifies metabolic health, which is the *sole determinant* of cardiovascular risk. With metabolic health (achieved via proper diet and lifestyle) high LDL numbers and ApoB numbers are benefits, not liabilities.
Yes the NMR test measures particle size and prescribing statins without having this test means your doctor is not up to date on this data. Find a doctor that understands NMR tests.
Are you sure ApoB is atherogenic? How do you know
Where is the next video please!
It's coming soon! We're just adding a few finishing touches. :)
Hi there! Thanks for your patience. We're happy to announce that the second video has now been released: ruclips.net/video/KjjxpWlzDik/видео.html. Hope you find it helpful!
Try to correlate that total particle number with actual heart risk across a large population and I believe you end up with no correlation. The same thing happens with total cholesterol
Is ApoB the same as LDL Particles in NMR or fractionation test?
APO B is so missing from our health discussions and yet it's one of the main determinants of HEART DISEASE. Tell us more about APO B, doctors!!
For all practical purposes, yes. They both count the number of atherogenic particles although ApoB includes VLDLs and IDLs in addition LDLs. However, the plasma residence time for VLDLs and IDLs is short (a few hours as opposed to days for LDLs) so LDLs are most of the atherogenic particles. ApoB seems to be the more favored measurement presently because, I believe, the measurement process for it has become more standardized.
What causes lipoproteines to get trapped in the vessel lining? Can this happen in healthy vessels or only in unhealthy inflamed vessels? Inflamed by sugar, seed oils, smoking, alcohol?
Yes you are spot on, this is why HDL:Triglycerides is the ultimate health marker. The higher the triglycerides level the higher the inflammation, due to bad diets. In addition long carbon chain fatty acids is also a contributing factor.
Lipoproteins only get trapped in arterial walls if there is *inflammation.* Your body does this to protect you. *Plaque is your friend until you make it your enemy.* Plague is like scar tissue. If you abuse your body enough with poor diet and lifestyle, then this “scar tissue” will cease to protect you, and will eventually kill you. Liver fibrosis is another kind of scar tissue. In extreme cases (e.g. liver cirrhosis) it will kill you. *THEREFORE* the key is to lower inflammation by any and all means possible. Don't worry about LDL or ApoB. With no inflammation, these take care of themselves.
You know they said " don't use a lipid panel "because it measures only LDL and triglycerides. But then they are saying apoB measures all of the LDL's together, and since LDL is the
higher number out of all of the LDL's it is the way to measure. Does not make sense, they are saying using apoB is basically the same as doing a Lipid panel, but adds in lipids
that are not bad for you as part of the count. So sounds like another way to make your count high and justify....wait for it.....more statin's.
Do a LIpoprotein anylysis NMR test, this will tell you all of it, count and sizes, look it up on line.
A much better measure than Apo B is the ratio of Apo B to Apo A1. Apo B can be large but if it's small in relation to Apo A1 it is not correct to assume elevated risk.
It is not the MASS you are measuring, it is the amount. Mass is a measure of the amount of matter in a substance.
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Wait for LMHR
Not so sure LDL has been shown to be athrogenic. Please share evidence.
LDL is ony atherogenic in the presence of metabolic dysfunction caused by poor diet and lifesyle. Metabolic dysfunction means chronic glycation, inflammation, oxidative stress, obesity, visceral fat, hypertension, hyperinsulinemia, insulin resistance, high triglycerides, and low HDL. All these are easily avpoided via proper diet and lifestyle. If there is no metabolic dysfunction, then regardless of LDL numbers or ApoB numbers, high LDL is a benefit, not a liability, and there is *no risk* of stroke, heart attack, or cadiovascular disease.
Thank you for this. I'm trying to find some good studies that state this. My doctor insists that my high LDL is bad even though all of my other numbers (HDL, BMI, blood pressure, Triglycerides) are good. She wants me on statins but I refuse. @@konradx498
The key ratio is Triglycerides to HDL less than 2 in mg/dl units.
So, my Tri is 31 and my HDL is 50... Is this OK? My LDL is high - always has been - 224. Total C is 288. Been animal based only since Dec. Dropped 64lbs and now 181lbs (52 yr old guy)...my Dr is freaking out - he hates the whole keto/animal based stuff. Eeeek
@@Crushin123 i've started keto, 3 wks now. My TG went from 63 up to 94mg/dl, LDL went from 84 to 184, HDL from 42 to 55. Got both very high apoB 177mg/dl (this was shock) and apoA1 179. I'll give it another couple of months to see how its going
@@agustind5744 oddly enough, add a tiny bit more carbs and your ldl and TGs will go down a tad. If you're exercising before blood tests, your ldl will increase as well.
@@agustind5744 3 weeks is a short time, triglycerides do go up initially for some. Few factors your body releasing more fat is known about.
Carbs arent the answer but balancing fat/protein ratio can be.
Adding carbs just mwans your eating less Fat or Protein which you could just change the ratio for instead.
@@Crushin123 my story's similar. Lost 30lbs over the past year. Went on statins only for 4 months but surprisingly today (1 year later) my CARDIO said they're optional since my numbers were halved. Try a new CARDIO??
It is very simple, low level of plasma triglycerides means low number of LDL-P, apoB100 and apoB lipoproteins
I have also heard that low triglycerides are directly correlated with low , small dense LDL-P.
Measuring ApoB is expensive and unnecessary. You want to know how much ApoB is DAMAGED and for that, there are already datapoints in your lab values: A1c and triglycerides/HDL. These two numbers should be low, the lower, the better. The higher the worse your cardiovescular risk. Why does this work? ApoB is a protein and Glucose attatches to it in roughly the same amount than hemoglobine. And when ApoB is attached with glucose, it becomes damaged. The liver does recycle LDL molecules with an undamaged ApoB. It refills them and sends them again on their way. If ApoB is damaged, the liver ignores it. These damaged LDL have to be recycled by macrophages. And where reside most of these? In the walls of the arteries. Here is the catch with LDL: it is not the total mass of LDL, which damages your arteries and your heart IT is the LDL molecules which have no functioning ApoB anymore. What we would like to know is the ratio of damaged LDL vs good LDL. And here comes triglycerides/HDL into play: it correlates highly with this ratio (about 0.9 which is as good as it gets, a correlation of 1 would be perfect). Get your fscking blood sugar down, eat healthy fats (not the plant based crap... put that into your Diesel engine). Do not take statins. At all! These do more harm than good.
A better way to measure risk is signs of insulin resistance, measured OxLDL, low HDL, high TG. ApoB and LDL are poor markers and the hazard ratios for them are really low.
Im sure the video assumes HDL is a maximum of high-normal (under 2.5 mmol/L) and Triglycerides are normal (less than 1.7 mmol/L)
yeah, being overweight has the potential to create all those problems
This is the current war, isn't it, between most YT doctors who claim that TG is a better determinant of AVDSC vs. APOB. My doctor still believes it's the latter.
You are absolutely right. The underlying cause of elevated APO-B is sensitivity to insulin, that is if you have higher insulin resistance in your body your APO-B will tend to be higher. Good saturated fat like lauric acid is a powerful super nutrient provided by nature to increase our body sensitivity to insulin.
HDL:Triglycerides ratio is the ultimate health marker. The higher the triglycerides level the higher the inflammation, due to a bad diet. In addition long carbon chain fatty acids is also a contributing factor.
This is why HDL:Triglycerides ratio is the ultimate health marker. The higher the triglycerides level the higher the inflammation, due to bad diet. In addition long carbon chain fatty acids is also a contributing factor.
What is the ratio of HDL 48 and TRIGLYCERIDES of 53? Is that at risk? Working on raising my HDL currently.
I strongly dislike doodle or what ever the writing programme is called and never ever watch vids in this format.
ApoB is not The Better Way to Measure Cardiovascular Risk. And even if ApoB would be causal, then it would be able to cause damage in any place, right? So, does it damage all arterial system? And does it harm venous system too? Something seems incomplete here.
Add in excess glucose and insulin as well as possible stress and then you may have the answer. But the fix there is diet and not a money making drug.
@@johnsonpaul1914 whole food low carb diet may be the answer for most of the people. The main problem is concentrating on specific blood markers.
No ApoB but triglyceride which is caused by bad diet.
I ALSO HATE DOODLE GOOD BYE AUFWIEDERSEHEN