Assessing Your Risk of Cardiovascular Disease | Lipid Series Part 2 | Dr Thomas Dayspring | Ep 252
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- Опубликовано: 28 июн 2024
- Last week, I sat down with Dr Thomas Dayspring to begin a three-part masterclass in atherosclerosis and blood lipids. In Episode #252, Dr Dayspring returns to continue this journey, this time shifting the focus from the causes of cardiovascular disease to more individualised applications. This episode is all about understanding where you lipids are now so you can then work out the best strategy to optimise them.
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There is so much noise online about the tests that matter, the ones that don’t, and which biomarkers to look out for. In this episode, Dr Dayspring clearly outlines the three lipid tests that you should take to best assess your risk of atherosclerotic cardiovascular disease - and importantly, the ones you don’t need.
Dr Thomas Dayspring is a Fellow of the American College of Physicians and the National Lipid Association. He is certified in internal medicine and clinical lipidology, and as we saw in last week’s episode, adept at communicating complex information in an accessible way. Make sure you watch or listen to Episode #251 first to get the background you need to better understand this conversation.
In this episode, you’ll learn about the lipid tests that matter and the ones that don’t. Dr Dayspring also explains the importance of early testing, including when to do your first lipid test and how often (if at all) you should retest. We discuss why ApoB is a superior test to LDL-C, whether LDL particle size matters, and if HDL-C is an important test.
We also cover the importance of measuring triglycerides; exactly how to request ApoB and LP(a) tests from your doctor; targeting ApoB levels for low- and high-risk patients; and how to test if someone is a hyper-producer of cholesterol and/or a hyper-absorber.
On top of all this, we walk through a few different avatars that many will find relevant and how Dr Dayspring would advise these people to proceed. Specifically, we discuss:
As we press forward with the blood lipid series, I hope you are finding value in this deep dive. This series is all about equipping you with the knowledge you need to protect yourself against the prolific disease that is atherosclerotic CVD, and the sooner you can action this knowledge, the fewer cholesterol years you will bank up. Make sure to tune in to next week’s episode, where we will cover the interventions you can make to optimise your lipids.
- 00:00 - Intro
- 02:05 - What is Lp(a), and why you need it checked?
- 20:36 - Does diet influence Lp(a)?
- 29:00 - The oxidized phospholipid test
- 31:24 - Early intervention and atherosclerosis screening for children
- 40:27 - The tests helpful in predicting cardiovascular disease risk
- 52:35 - Discordance between ApoB and LDL-cholesterol
- 1:03:14 - Normal range of ApoB levels for a healthy young person
- 1:16:52 - Does atherosclerotic plaque ever disappear?
- 1:22:15 - Triglyceride: HDL ratio vs ApoB test
- 1:29:31 - Screening women in their 30s
- 1:37:23 - Screening women in their 70s
- 1:39:25 - What causes elevated ApoB
- 1:58:55 - Do phytosterols help manage cholesterol?
- 2:07:08 - Secondary prevention
- 2:20:45 - The obviously misunderstood case of ApoB
- 2:22:35 - Outro
Connect with Dr Thomas Dayspring on Twitter at [ / drlipid ]( / drlipid .
We are also currently working on a summary PDF highlighting the key learnings from each part of the series. To receive a copy of this simply submit your email at theproof.com/lipidseries. We are also working on transcripts for these episodes, with the release date to be advised soon.
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Enjoy, friends. Simon
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The passion and knowledge of Dr Dayspring is incredible!
Dr Dayspring is a walking encyclopedia of Lipids! Awesome interview. Tom is 100% right, find a doctor who understands apo(b) and other important biomarkers. YOU need to be your own advocate. Shocking how feel doctors really understand risk. Follow Dr Attia - Longevity specialist.
This has got to be one of the best medical videos i have ever heard. Thank you both! Please interview him again, he knows so much.
Nurse here. Tom Dayspring MDis a treasure trove of evidence based information on lipids.
Mate ! What a brain, what a mouth. Rare to see the two together in one person !
Excellent series.. As a doctor i learned a lot from these podcasts.. Such a great content. Keep it up👌🏻👌🏻
It will be of great help if you make a podcast on insulin resistance
I would have liked a question about the impact of estrogen loss in peri-menopausal and menopausal women on the lipids and cardiovascular system in general, and methods of prevention, such as hormone therapy. The data on this has been known for decades, yet it’s never mentioned by these lipid specialists or cardiologists in general. I consider this neglect. Women are 50% of the population, and our risk for cardiovascular disease rises fast and steady with estrogen loss. Yet this major risk factor is ignored. Cardiovascular disease is the number one killer of post-menopausal women. Women should be informed that there is a possibility of major risk reduction if hormone therapy is initiated at the appropriate time - during the “window of opportunity”.
@@TheProofWithSimonHill Yes, Simon! I saw that episode and loved it! Thank you so much! I just find it disappointing that experts like this man seem to completely ignore this important female-specific risk factor when instead they could use this platform to draw attention to it and educate listeners.
Greetings from California! 😊
In this "man's" world, women still get overlooked (disrespected), what else is new.
@@mt4973Oh please. Women are given precedence everywhere modern society. Life was and still is hard for both genders.
What is that window of opportunity???
@@blacina9036 It refers to a timeframe of roughly 10 years around the time and after menopause, during which a woman can potentially reduce her risk of important diseases, if she starts MHT (menopausal hormone therapy) during this “window of opportunity”, although the earlier, the better, for disease prevention.
I recommend a thorough, evidence based education on menopause for all women. There are several here on RUclips, such as Dr Heather Hirsch, Dr Haver, Dr Barbara Taylor, Dr Louise Newson (my favorite 😊).
If you like it more “nerdy”, you could check out the 2020 scientific statement by the American Heart Association - “Menopausal Transition and Cardiovascular Risk: Implications for Timing of Early Prevention”
Hope this helps!
Wow, one of the most incredible and valuable podcasts that I've heard, along with the first one with Dr. Dayspring, can't wait for the third. Yes, a lot of this is hard to digest for the lay person, but a lot of it isn't, and, well, if we really want to digest all of it well, it's just a matter of going back and taking notes, etc.
I appreciate the question regarding secondary prevention. Most videos, including this one, concentrate on primary prevention, maybe because it's presumed that the people who already have diagnosed disease don't have questions, they are just following what their doctors prescribe - at least as far as medicine goes. But especially given the complexities of cholesterol metabolism, LP(a), etc., I want to do everything I can do lower risk. My LDL has basically been in the 30s for 4 years since my heart attack, and my APO B when measured a couple of years ago was in the low 50s (mg/dL), trigs have always been 80s or lower.
As far as, LP(a), I've gotten this measured multiple times. First was in 2014 when it was 61 (nmol/l) in 2014, about 8 months after my first stent and also 8 months after going on a Statin. I actually got it measured again in 2019 after a my heart attack in order to see if I was a candidate for the drug trial. I got it taken 3 times that year and it ranged from 73 to 88 nmol/l. So a bit more elevated than in 2014, but I'd been taking statins at that point for 5+ years.
In any case, Dr. Dayspring mentioned some mail order test to get genetic markers for cholesterol absorption/synthesis which I'm very interested in getting, since while my numbers are great right now (on a WFPB very low oil diet for 5+ years), when I was on the high-meat low-carb diet back in the 14 years proceeding my heart issues, my LDL initially shot up as high as 250, and never got lower than 156, and given the family history of heart disease on my dad's side at least, it seems likely that there are some genetic abnormalities at play. Would appreciate it if you could get the link to the lab that does these genetic marker tests.
Thanks again for such a great interview, it is such a fantastic reference for anyone who wants a serious deep dive into the subject but doesn't have the motivation or money to buy a textbook. It's like reading the cliff notes (do they have those in Australia?)! I am so grateful for you and your channel, Simon, and for Dr. Dayspring for sharing his incredible wealth of knowledge with us!
Yes that lab would be helpful
I have learned more from this series about cholesterol than I did during 4 years of pharmacy school. Thanks for all you do!
Absolutely the best video Simon again with Dr. Thomas D. So much info to take in. Thank you.
Thanks to both. He is so humble for all he has done.
Excellent discussion, the clinical pearl new to me was the algorithm construction for insulin resistance score on a Labcorp NMR Lipoprofile Test (1:24:47). I recently saw claims that the NMR test uses flawed methodology and the LPP® (Lipoprotein Particle Profile) is a better tool for determining risk of CVD. ITs so confusing, as Dr. Dayspring mentions, sometimes very difficult to understand who is a subject matter expert and sort out all the biases held (consciously or unconsciously) and financial stakes in particular behind these claims. Just because a lab claims their technique better (because obviously they want you to buy their test) their financial interest does not automatically make their claim false. Maybe LPP is better than NMR. But as a clinician, not a laboratory science person, I don't have the tools necessary to understand who is right. (and maybe it doesn't matter). Its like the folks who don't understand their is something better than LDL-C: ApoB. It's exhausting to be on the cutting edge/early adopter.
Again, thanks Simon and Dr. Dayspring.
Can't wait for part 3. Thank you so much SImon and Thomas for a wonderful interview and discussion. I've learned so much.
@@TheProofWithSimonHill thabk you too Simon, as a person in the third world country with not the best healthcare, educating ourselves is the best way to be saved. Not one place offers the ApoB test, i really wish i got the safe range for the non HDL from the interview.
🤯 I need a nap after listening to this on the podcast. Fantastic info
What a wonderful and informative guest !!
Excellent interview. I watched the whole thing and took notes to take to my doctor next month.
amazing! again... beautiful work you are doing Simon!
Interesting interview. After watching the podcast, I did a Google scholar search and found a paper that suggested that tocotrienols found in unprocessed palm oil placed in the diet of pigs with high apoB or dyslipidemia helped to reduce apoB levels. Of course more research especially in humans is needed. Good to know that lactobacilli can help with conditions for improving apoB lipid profiles.
Update: ApoB result was 27. Not bad for an old lady. Strong fam hx of cardiovascular disease. Lp(a) was 6. On HRT and exercise regularly. Eat a varied diet. 50 in a few months. My grandfather was dead at 47 from MI. Dad has three stents and has come under my tuttilege for his labs as well and he is ready to beat the walls for his labs to be up to date.
Excellent results….working on mine…. but ma’am 50 definitely isn’t deserving of old lady status!! We are rocking 50!!!!! 🎉
@@trudywilson9634 Yeah, 50 will seem young when you reach 70 like me!
I’ve said it before, and I’ll say it again: I absolutely love his energy. The info he presents is very pertinent to me. Heart disease runs in my family. A recent echo revealed I have a couple valves that are mildly regurgitating (tricuspid and mitral), and a CT scan showed I have fatty liver. I also have elevated LDL and total cholesterol. I’ve been eating plant-based for 3 years and do intense structured training on my bike 3 days per week and strength training 5 days per week. I’ll be getting the tests he recommends. I’m in the middle of changing doctors because my current one won’t work with me to look into my abnormal echocardiogram and fatty liver results.
80 percent of ldl are large puffy not to be worried about a long with your cholesterol. It's your Apoe B and Lpa you need checked. And perhaps your triglyceride/hdl ratio.
@@nancyevans5176 I actually did end up getting those checked (ApoB & Lp(a))! Both were moderately elevated as I suspected they might.
There is zero truth to the statement that you have nothing to worry about with large fluffy LDL. It is irrelevant that dense LDL may be more harmful when both types are atherogenic. Although you do see that sort of misinformation circulating on RUclips.
Soooo awesome. Thanks for this great interview.
This is a great masterclass on lipids! Simon, have you already done a similar episode series about insulin resistance?
Very interesting discussion. I got my apob tested jul-22 on the back of one of your earlier podcasts. Apob was 81, LDL was 117. Had it done again yesterday, and Apob down to 62, LDL 78. Interesting that the proportional change wasn’t the same for LDL and apob, but ties in with discussion you had (ldl and apob are related, but don’t move in lockstep). Still waiting for my lp(a) - that one had to go to Jakarta so will take a few days. Wish I had had this info earlier in life, but better late than never! Thanks for all of your work and sharing your knowledge!
are you taking medicine to make it lower ?
@@Youssef-1911 no. The only “non food” things I take are creatine, B12 and amla. I think the amla is helping, but I did have my cholesterol this low previously without amla, but I was eating a lot better then, so I think the amla is helping.
@@grasmi thats great but i think as long as you are taking b12 you are following vegan diet,right ? you did great job
@@Youssef-1911 yes, mainly whole food plant based, but I do eat some fish and have the occasional steak / burger with friends.
@@grasmi thanks you were so helpful
What's up Simon. Great podcast mate, I've been reviewing all of the content. I really appreciated the highlighted graphics during this series. very helpful in understanding the complex lipid mechanisms discussed. Thank you for your work
Great to hear!
This lesson should be taught to everyone.......salute
Thank you for all this information Simon and Dr Dayspring . Fantastic info !
Our pleasure!
Thanks so much Dr. TS, I wish you to live 120 and hear this lecture/talk from you again, God bless what a great contribution to our understanding. Thanks you both for your commitment to health a and public education,
Listened to the whole series and it was fantastic. Thanks so much
Fantastic discussion! A lot of interesting info.
Fantastic! Such a wonderful, informative guest. Here's hoping medical guidelines catch up to scientific knowledge and start making ApoB testing the norm
Thank you Dr. Dayspring. I have listened to all 3 episodes in this series and learned so much. My lipids have been a puzzle for years. So frustrating. Tried keto and my lipids were still elevated. LDL/TC/Trigs. No diabetes or high blood pressure. Weight good. Visceral fat low. Watched 100 hrs of videos. Settled on Mediterranean with IF. Less saturated fats. Dr wanted to try zeti which I had never heard of but could not tolerate tricore so didn’t want to try statin yet. Had already been on vacipa and niacin. After 4 weeks in zeti my LDL dropped 70% to 54 and Trigs 86 60% and TC 111 60%!! So I assume I am a hyper absorber. This info is so interesting and helpful. Wish I had this info years ago when zeti came out. Thank you!
The Dr is amazing ❤
I love this man: 'i'm 77 i want to live to 100!!'. True inspiration !
Wow, I am an Anatomy and Physiology professor and I learned so much! I was wondering if Dr. Dayspring knows by what mechanism coffee raises LDL- C. I saw on Nutritionfacts that paper filtered coffee once was thought not to raise cholesterol does raise LDLs. I love my coffee.
Filtered coffee doesn't raise LDL...unfiltered does
@@markgarcia5845 how much? Can you get an assay locally? Not me, but...I know my D levels are great. I take about 5500iu daily, 5'9, BMI 23, WHtR 43, 40yrs...
"Vitamin D levels had linear relation with their Homocysteine levels (t = -2.40, df = 302, p = 0.017). For every 1 ng/mL increase in vitamin D, there was a 0.04277 uM decrease in homocysteine, on average."
Thank you for all this information Dr Dayspring and Simon! Learnt a lot of new stuff, especially that some microbes can be beneficial in preventing cholesterol absorption. It was surprising to hear that people like Dr Dayspring don't have much of an influence on the guidelines, since I thought that the committees who created them were composed of people like him, who are on top of the latest science.
Why do you care of your ApoB number if you have high LDL ?!? He thinks putting on statins is the solution and most doctors would do it to patients with high LDL anyway… and he said no downside from the drug… 🤔I thought I would get something new!!
Dr dayspring is amazing!
I've been monitoring my ApoB for about 5 years now. My ratio of ApoB/non-HDL has varied from 0.62 to 0.78. I am not discordant, but that's a pretty wide range if you are borderline, like I am. In the US, I've been able to purchase the ApoB test on a discount site for $35, but you need to hunt around.
WHAT IS AN ACCEPTABLE Adobe non hdl ratio?
If that's the ratio then why they keep saying that if apob is not available you can look at non hdl instead?
This episode will save many lives! Such important information. I've been vegan for 7 years but often ate "junk vegan foods" containing palm and coconut oils. Now in my 50's my TC & ApoB are elevated. I also have Lp(a). This episode scared me. I've been 100% WFPB no sugar or oil for 6 weeks and I'm ready to get my ApoB tested again. If still high I will go on medication, which is devastating to me. From this episode I'm really understanding that I have no choice if my healthy lifestyle can't bring my numbers down.
6 weeks might not be long enough for that intervention. If you get dissapointing results keep it up and test again in 6 months.
Make sure you get plenty of fermented foods and probiotics in your diet. Lactobacilli seems to help.
If still high, what medication you will be in? Statins? Thanks
@@chiyerano Prebiotics > probiotics. It's the fiber that does the magic.
@@Joseph1NJ Just going by what was mentioned by the guest during the interview.
This was great fun. Now I know what to ask of my cardiologist next visit. Cheers!
Thank you Simon for this expansive lipid picture ( part 1,2&3) with the fascinating Dr Dayspring . His “am 77 and want to live to 100. I enjoy Life” is a testament to a contagious “joue de vivre’ and his passion for furthering the science of lipidology is fascinating . So grateful to both! 🙏
Good questions!
Is the only reason for testing ApoB vs LDL the 20% discordance or is there another consideration?
So much passionate knowledge and wisdom here!Thank you both for articulating a much needed content with total grace .
That was great. Statin + Ezetimibe works very well for me. ApoB stays around 30mg/dL.
what statin are u taking? what is ezetimibe?
People on STATINs with low LDL cholesterol still end up with CVD.
There is a growing number of physicians who disagree with the Lipid Theory of Heart Disease and a growing body of evidence the LDL is not a good marker for predicting CVD, and that it has more to do with sticky platelets and abnormal clotting and/or insulin resistance. I would love to see Dr. Dayspring debate Dr David Diamond and or Dr. Ovadia.
I think I have the same thinking as you, eating plant food grains no fats as Not helped everyone, He says he would fight insulin resistance if he new he had it , I think sugars are the problem. Cholesterol is vital. dr sten Eckberg videos
I think a healthy level of all markers is my target not just cholesterol
That is nonsense. LDL has been proven causal, you can read the ESC consensus paper with the overwhelming evidence of it. Just because the rate of insulin resistance is rising and thus we of course have a bigger comorbidity with cardiovascular disease then in the past, does not mean that insulin resistance directly causes cardiovascular disease. The existance of people with familial hypercholesteremia, while being metabolically healthy, still having heart attacks at a very young age. Also if abnormal blood clotting would be the main problem - not saying it does not play a part, you would see abnormal values in blood tests, which would be acted upon - pulmonary embolism, deep vein thrombosis is no fun - we would have solved the problem long ago. We have a pleithra of anticoagulants to choose from, and there has been primary prevention with aspirin. Studies showed only a small benefit in a certain age group.
It might very well be that people on statins get CVD is funny, because people on statins already have CVD. We actually might use them far to late. The disease starts when you are young, so Dr. Dayspring is advocating to test people when they are young to actually prevent disease from happening. Prescribing statins for prevention is still debated if LDL-C is not astronomically high hinting at familial hypercholestemia. You can find that in the guidlines.
If you watched the video, you would know, that there is a difference between LDL- the particles and the marker LDL-C - the cholesterol. Dr Dayspring agrees that LDL-C is not the best marker and proposes to rather meassure LDL by meassuring the protein on each particle called ApoB.
I agree that LDL-C is not that great, but it is what is currently available to most. It unfortunatley underestimates the risk - not overestimates it. It can happen that LDL-C is low, but LDL particles are high -they just are small and do not carry much cholesterol. That happens in genetic mutations for example. You would see that with ApoB as the marker - so we are missing those.
And as he explaided we are also missing people with high Lipoprotein a, an other genetic variant, if we don't test for it.
LDL-C does not overestimate risk though. high LDL-C means a higher number of particles. It might vary from person to person how much the risk increase is, but there is one.
If you want to see a debate between a pro LDL-C MD and researcher and Dr. Ovadia, head over to Nutrition made simple! Dr. Gil Carvalho debated him, maybe it answers some questions for you. Nutrition made simple is pretty neutral, I have no idea what Dr. Carvalho is eating or prefering as a diet.
As far as Dr. Diamond goes, he unfortunatley has a habit of misquoting studies, books or people. I invite you to check his references. He claimed Dr. Ancel Keys had no education to conduct the studies he did. A quick check of the wikipedia article or google search will show you otherwise. He was a biologist with a degree in physiology. Would be easy to debate him for any real expert, if he is doing such things during a debate.
It is really infuriating how much misinformation is out there on the web - for money, for fame - that you don't detect if you are a layperson.
@@kevinbrannan8347 Huh? Then you got the wrong message. The diet reccomended as a heart healthy diet is in no way low fat. It is the one keys advocated for - the mediteranean diet with arround 40% fat. There is also a low carb and keto version if that suits you better.
And then there are general reccomendations if that is not what works for you. Whole food diet, high in fiber, low in refined carbs, low in saturated fat, high in omega 3 and polyunsaturated fat. I think Dr Eckberg talks about refined vs. complex carbs and fiber too.
Sugars are part of the problem - they are refined carbs, make you hungry and overeat. If you can handle eating sugar in moderation and not eat more calories then you should, it is not that big of a problem.
The same is to be said about saturated fat. There are studies hinting at that. Did you notice junk foods are often a combination of saturated fat and refined carbs? Fat tends to be the least satiating macronutrient, while protein is the most and carbs come in between.
For me foods like beans, lentils and chickpeas fill me up very quickly, they are starches combined with protein and fiber.
I think Dr. Eckberg might be right in many things - but I disagree with him in others. Mainly seed oils and saturated fat. saturated fat might be no problem short term, but certainly long term. Not for all, some people have genetics that does not make them react to saturated fat by raising LDL-C. I am not so lucky, I do react.
You should watch the first part of the series, Dr. Dayspring agrees with you that cholesterol is vital, and that's why every cell has the ability to make their own. What is circulating in the blood stream is just additional cholesterol manufactured in the liver to mostly keep the lipoproteins (LDL, HDL VLDL etc...) stable, in order to transport the fat you ate from the intestines to the cells for energy production. But you don't really need that for cell walls, hormone productions etc, since the cells just produce it when they need it.
But of course it is important to stay healthy overall, not just focus on one thing.
@@stellasternchen From my perspective…LDL has not been proven to cause atherosclerosis. So we can agree to disagree on this point. I’m glad you do agree LDL-C is not a good biomarker for Heart Disease. Dr Lustig argues that the ratio of TG/HDL is a much better predictor of future Heart Attacks or Stroke.
And you have to know that most people with Hypercholesterolemia (heterozygous) live a normal healthy life. Which begs the question….what is different about the small percentage of them that experience Heart Attacks or Stroke at a young age. Perhaps it is that they also have the Lpa snip, or one of the other clotting issues. This would be an interesting study…to figure this out.
Ancel Keyes found two factors correlated to Heart Disease…cholesterol and insulin resistance or Type 2 Diabetes. David Diamond and his team removed insulin resistance as a factor, and found there was no correlation between LDL cholesterol and Heart disease.
What many of us are suggesting is that it was never cholesterol…and our maniacal focus on it driven by STATIN profits have prevented us from better understanding what actually causes CVD. Plus the side effects of STATINs have been downplayed (for obvious reasons), but they are significant. Patients must understand the true risk-benefit before they take any medications…including STATINs. I appreciated the fact that Dr. Dayspring was not quick to prescribe a STATIN …rather considered a broader patient history.
@@DrJK-wm9ec I don‘t know the study of David Diamond, do you have the DOI of it? I’d like to take a look. As far as I know Keys only measured cholesterol, not LDL cholesterol, and we know now that HDL particles are not harmful in physiological amounts. They basically transport fatty acids to tissues in order for them to burn them. So using total cholesterol including HDL cholesterol is inaccurate.
It is kind of strange though to stratify for insulin resistance, it is not an independent factor, it increases LDL-C and LDL particles as well. They are connected, not independent.
That‘s the problem with correlation. You can‘t say if there is an other factor causing the correlation.
Keys study findings showed basically that not all fat is bad, like many colleagues believed, but there is nuance. Some fats do increase the risk some decrease it.
He advocated for a diet with 35-40% of fat, not a low fat diet because of that, the Mediterranean diet. It might be anecdotal, but he lived longer then most people - he diet at 100.
I know that the Framingham heart study is a perfect example, why relying only on correlations is not always a good idea. LDL-C had only shown a weak correlation with cardiovascular events, but a strong with HDL-C.
Drugs have been developed to increase HDL-C, but showed no cardiovascular risk reduction at all, so trying to increase HDL-C for example with a low carb diet, does not reduce your risk either of heart disease.
For LDL-C lowering drugs, we see a risk reduction. Don‘t be fooled by the small absolute risk. Absolute risk does not tell you anything.
I‘ll explain. Let‘s say we have the hypothesis that driving with a seat belt on Leads to less chance of injury during a car crash. So we have an intervention group of 100 people with seat belt and an control group with no seat belt.
Let‘s say for convenience sake we had 3 car accidents in each group.
1 injured person in the intervention group, 2 in the control group.
So we have 1% risk of injury in the intervention group and 2% risk in the control group, meaning we have an absolute risk reduction of 1%. So in this example seat belts would be pretty useless, right? I mean most of the time you drive you won‘t have a car accident anyways.
Not if you look at relative risk. Relative risk in this example would be the risk of injury in case of an accident. If we calculate that we get a risk reduction of 50%
So yeah, in 99% of the times you drive in this scenario, you would not really need a seat belt, but do you know when you need it. But if you have it on in the case of an accident, there is a 50% risk reduction of injury. Would you put it on?
The same principle applies to relative risk and absolute risk with statins.
We can not predict 100% wether somebody is going to have a heart attack or not, so we have to depend on risk calculation who should get medication or not. The downside of this method is that we only can calculate 10 year risk of cardiovascular risk, not 30 or 40. Disease development of arteriosclerosis takes decades, thus at the moment we just treat it, not preventing it from even developing.
For prevention guidelines set focus on lifestyle interventions and treating other risk factors like high blood pressure, diabetes, obesity, tell the patient to stop smoking and exercise regularly and reduce LDL-C.
Despite the lack of exercise, all those risk factors are damaging vessel walls. Including LDL-Particles. The higher the blood pressure, those LDL spheres are shooting like bullets through the arteries and sometimes crash full speed into the vessel walls for example at bifurcations like in the coronaries. The weaker the vessel wall, the higher the risk that this might happen, the more particles there are, the more frequent are the crashes.
If they get stuck, the immune system reacts - they do not belong there after all- creating inflammation setting up a detrimental cascade of chronic inflammation. The body only can put out that fire, by sealing away that inflammation and reinforcing the seal when necessary. That is the calcification we see, and that calcification is actually a good thing, reducing the risk for strokes and heart attacks, but unfortunately can severely block the arteries, which in turn can increase the risk for heart attack and strokes by impairing perfusion.
As I‘m trying to explain, the disease process is an interplay of all the risk factors.
Statins have the additional effect of stabilizing unstable soft plaques by promoting their calcification. This protects from blood cults forming or parts of the still soft plaque getting ripped off. You can see the effect of statins probably - study is still going on- in an increased CAC.
Sorry I hope you are not bored - it is easier to understand why those meds are used and when, and what else is taken into consideration.
But drug trials can be biased - like you hint by pharmaceutical companies.
So we have correlation and Pharma funded RCT‘s right?
But we do have more, we have genetic evidence for high LDL causing CVD.
Those trials are called Mendelian randomization studies. They do look at genetic mutations increasing HDL or decreasing LDL and the cardiovascular risk of those individuals. And the LDL lowering mutations showed risk reduction, while the HDL increasing mutations did not, which is in line with our drug trials. This method of studying eliminates almost every confounding factor and looks at the factor independently. The genes are there from birth - there is almost no outside factor able to change them, interference is very unlikely.
If there are Mendelian randomization trials looking at diabetes and cardiovascular risk I honestly don‘t know, type 2 - in type 1 there is usually no insulin resistance - can also be genetic.
And can there be cardiovascular disease without insulin resistance?
I can tell you yes two times.
Let‘s start with the anecdotal evidence. I have somebody in my extended family, who is lean, female, was an very active person, had no signs of being insulin resistant getting a stroke at 47 and a heart attack at 52.
My second example is a sad condition called homozygote familial hypercholesteremia. Those young children have extremely high LDL due to genetic mutations and do get heart attacks sometimes already still in childhood. It is not really associated with insulin resistance, not even when statins are taken, there have been studies looking into that.
If statin producers had so much influence on the guidelines, why don‘t they say to prescribe every patient with high LDL -C over the threshold a statin instead of calculating the individual risk to decide on a treatment plan. I don‘t quite get the logic behind the theory.
Like I said statins are prescribed very late, when there are already signs of arteriosclerosis. Before that‘ it is debatable. Since they are not something you can take like candy and there are risks. It is still difficult to estimate if the risk reduction in low risk to intermediate risk is worth the risk of side effects.
Although there are also a bit of fearmongering. Some people claim that statins do cause dementia - which has not been shown in studies from independent researchers.
Kidney and Liver - problems are possible though and you have to pay attention to.
I do need to take a medication, that unfortunately can harm the kidneys, I understand that people only want to take them when there is a benefit.
There are alternatives to statins as well, but of course they come with their own risks.
I‘m kind of in the situation where my LDL-C is not elevated yet but borderline. But I think in my situation, it might not be worth the risk to take something, since I‘m otherwise healthy - not that somebody told me to, but I had my own thoughts about it.
But I agree with you on one thing - it would be great to know which people with high cholesterol are the ones getting heart attacks and which not, maybe we will find a yet unknown pattern in the future.
1:18:00- Dear Simon, what life style changes did you make to cause your LDL fall from 120 to 80?😊
1:46:00- an oversyntasizer?
1:47:00- an hyperabsorber?
Nice haircut Simon!;)
Thumbs up and subscribed!
Great discussion. I would also though love to hear more about Glycocalyx. Interesting info on pub med about it. I had not heard about it prior. Would love more discussion on this.
Thank you for bringing clarity to this perpetually confusing topic! As a nurse practitioner I’m always learning and love this conversation. Can’t wait to get the guide you’re putting together.
I really like this doctor I’ve seen him on Peter Attila’s podcast also. Thank you
This guy describes it all so well, he should be teaching
What do you think he is doing now? This video can reach thousands where a classroom might be limited to fewer than a hundred.
Thank you for this series!! I just had my LPa tested, 101.5 NMole/liter and an APOB of 82 mmole/liter. Contacted my Dr with the results, I’m 60 and concerned with Aortic calcification now. This video may have just educated me and probably saved my life from advanced dyslipidemia. Thank you!
Wow, Simon your questions are all on the point, you must know the material as well as a doctor , to ask these questions, that are well thought of, I am interested to know the books in which the Chapters of Dr. TS are published, please get the name of text books though might be found only on medical publications. thanks
How to lower ApoB??
Excellent discussion. I may have missed this point but would insulin resistance generally simply be measured by HbA1c rather than an NMR lipoprofile test? In other words, can you have insulin resistance and a normal HbA!c ?
"Thomas Dayspring consults for Abbott, GSK, Health Diagnostic Labs, Kowa Company, Eli Lilly, Merck, Genentech, The Roche Group, Genzyme, and Omthera. He is on the Lecture Bureau for Abbott, GSK, Health Diagnostic Labs, Kowa, Eli Lilly, LipoScience, Merck." No?
Things that make you go hmmmm....
Hard to be a consultant for big Pharma and discourage drug peddling...
@@b.h.1205So let's try wooddoo.
So what. Dude knows his shit
Is he consulting for the companies that produce the tests that you, your doctor are requesting? It would be good to now.
so is the ApoB test available in the standard lipid profile in Australia? I'm having trouble finding that information.
Simon, have you looked into photobiomodulation and how this affects arterial scolorosis?
I would like to know why most doctors only focus on 10 year risk, even for young adults. I would only be interested in my 10 year risk if I were 90 years old.
Dr. Thomas Dayspring gives the same energy as Richard Kind.
So how do you lower ApoB?
At 1:39:42 you raised the subject of dietary cholesterol but after the re-absorption discussion that followed, no conclusion on dietary cholesterol was explicitly stated. Can we conclude that that absorption of dietary cholesterol is always insignificant compared to re-absorption of endogenously produced cholesterol? Therefore the person eating all of those eggs can continue to do so knowing that it won't be affecting their LDL levels significantly?
That would be logical.
Where’s part 1? Anyone please..
It would be interesting to know if people who live in the Arctic and/or have an ancestral history of cholesterol filled diets tend to absorb less cholesterol than others.
Listening to this scares the Sh** out of me. I had my LPa tested through my naturopath and my doctor thought it was ridiculous. My results were 172. Obviously a problem but I can’t get a doctor to take it seriously. So now what am I supposed to do?
In addition my LDL is 109
What about ogtt test for insulin ?
Hello Friends,
I'm curious to know which part of the conversation you found the most insightful and engaging. Also, if you have any other questions related to this subject, please post them below this comment. I'll make sure to include them in our next discussion.
The fiber thing surprises me. Most plant based sources suggest fiber does block absorption of cholesterol. So more on that would be great.
If one is on a PSK9 inhibitor like Repatha, which I take, does one need to worry about one's lipoprotein (a) level?
The question is what is the magnitude of the contribution of damage free migration of ApoB attached LDL into the endothelium to atherosclerosis?
I’m in Canada and paid for my own APOB-about $100. Most people don’t know you can do this.
You've gone thru when a statin or Bempedoic Acid is beneficial and when Ezetimibe is beneficial, but when is the Pcsk9 prohibitor most beneficial?
If you've low HDL and probably not likely to be a hyperabsorber thru your guts, can a high LDL and low HDL indicate insulinresistens to be the cause of your lipid disturbances?
And what's the best way to get more insulin sensitive?
LDL particles are part of the immune system. They can help in dealing with paracites, fungi, viruses, etc.
These are problems you won't likely encounter in research settings.
So it would be interesting to know what people with extremely low LDL, die of.
1. Where do the PCSK9 inhibitors fit into the absorption vs synthesis topic? 2. If your on Zetia and repatha, would that 99.00 test for sterols be skewed if I’m on these current meds?
sO FAR i'VE HAD MY apoB tested 3n times and each time it has tracked to be exactly the same as my LDL..... is that a normal occurrence?
What I'm interested to know is. Early 20th century there was practically no heart disease and people were eating plenty of meat and dairy and I'm sure they had high APOB etc also populations like the American Inuit and other examples.
Average life expectancy was only in the high 40's at that time. Without detailed autopsies or the advanced scanning techniques we have today, there is no way of knowing what condition their arteries were in. They were also not eating animal protein from the commercial practices of today so it was much lower in saturated fat and they were far more active on a daily basis than 90% of the populations today. So early 20th century is not a relevant comparison to today.
@@garydublanko4098 Life expectancy is tied to infant mortality as well. Children died much more frequently during this time period. Most people do not know this. There were many people who lived long lives back then.
@@scotterickson9091yeah I heard if they account for infant mortality life expectancy was similar to now
I'm sure they ate less meat and dairy. It's an upward curve throughout the 20th century. Remember: this is the time of the world wars and the economic crisis of the 30s. Most people could not afford all that many animal products. They ate the proverbial beans and rice.
Does red yeast rice lower ApoB? If so, by which mechanism (i.e., synthesis or absorption)?
Just saw a Dr. Alo post on this. The answer is ‘yes’, but the efficacy is only a fraction of what a statin can provide, and that’s assuming the supplement is what is the label says it is.
I'm a hyper absorber of sterols but my doctor won't prescribe me ezetimibe.
Do I have to quit eating nuts and seeds because of their phytosterols?
So what lowers apob
Simon, I'm very confused by your Lipid Cheat Sheet document.
On page 7, bottom left corner, it notes: If ApoB is not available, use non-HDL as the best surrogate marker for ApoB. Ideal target level is
Wow- he says STOP using the triglyceride/ HDL ration? Other leaders in the field including Robert Lustig, highlight this as a significant marker, with various cutoffs for race?
Simon, after this talk, have you changed your position on recommending photosterol supplementation to your audience? Great talk!
This was interesting to me as well, it seems that the supplement is very well studied and has been proven to lower cholesterol. I'm guessing he thinks the risks outweigh the benefits?
He seemed very in favor of medicinal intervention versus supplements. I also didn't really hear the doctor speak at all in this episode about dietary and exercise intervention.
Fidosterol?
There are people who have very high Lp(a) levels but don't develop atherosclerosis. Not all Lp(a) particles sre the same; thee kringle number on the Apo a protein determines atherogenicity.
CANADA HERE. APO B: MUST YELLLLL AT THE DOC
Nattokinase or serrapeptidase?
What about super-high HDL? Mine is125 mg/dl. Wish you had addressed this. I know it is uncommon and likely genetic but I don't know whether/how much to be worried and have read exhaustively about research that should be done, but have not found anything about what to do now.
It's in the episode: HDL is not a significant marker. In lay people's terms that means you can ignore your high level. It's as relevant to heart health as the color of your hair. It's really only measured because of tradition.
Where's this channel been, nice ome
Simon what are your cholesterol levels? Do you take statins or meds? Or lifestyle, diet, exercise?
@@TheProofWithSimonHill :) So ApoB is 70... not total cholesterol. Gotcha, when listening to this interview I thought it was total cholesterol. My husband and I are working on our lifestyle and making changes. Always learning. Thanks! We need to up our weight and strength training!
@@TheProofWithSimonHill what do you think of ketogenic diet mostly in unsaturated fat, and fibre rich
Do you mean no butter no eggs no red meat …unsaturated fat keto diet?
When would there be a low risk 🎉discordance of low ApoB and high LDL-C. Could that be an explanation for the lean mass hyper responders who have low triglycerides and high LDL? Maybe there are a higher number the LDL that are larger fluffy type with higher concentration of triglycerides and less smaller dense LDL?
"Larger fluffy" and "small dense" are not actual determenants of heart disease. See it explained in detail here and check the sources: ruclips.net/video/NUTvzuDphmg/видео.html
My ApoB is so high, I'm scared to write the number here. This is helping me open to the possibility of medication. I've definitely begun changing my diet.....LOTS of FIBER!! (Mine is in the stratosphere). PS: The confusing part is that there's no plaque.
You're young. Plaque buildup takes time.
@@k.h.6991 I’m 72.
What bothers me the most is the fact that an Apob of 80 should correspond an LDL-c of 70 according to ESC. Not only my LDL is 117 while Apob is 73, but from most studies I've seen LDL should be 30% higher than Apob on average. There's something seriously wrong here. Maybe at low levels Apob tend to decrease less than LDL.
There are few infos missing here: reference range for LDL are not corrected for age.
It is not said what are the corresponding LDL values for Apob.
It is not stated where those reference ranges come from: are they updated?LDL cholesterol declined by 15 points between 2000 and 2010.
@@TheProofWithSimonHill thank you. I'm European and those guidelines are bible for me but those Apob values doesn't add up, if you look at most research papers where Apob and LDL are reported, LDL is always higher than Apob, so I don't see how an LDL of 70 can be equal to an Apob of 80.
@@TheProofWithSimonHill anyway I searched on my own. If you are interested the 80th percentile of LDL is 160, corresponding to an Apob of 120. So the whole discussion you made was on a very shaky ground. I have the sense that what's reported on esc guidelines is not a percentile but a target. Can't imagine them being wrong on this. Probably they simply use Apob as a secondary threshold in case of discordance and is not to be intended as a percentile. Not questioning the knowledge of the doctor, but this should be addressed more clearly and age adjusted as well. An LDL of 150 in a 60 yo woman have not the same importance in a 35 yo one.
I don't understand something, the whole idea behind testing for apob, and the doc said it, is the *number* of particles, not the amount in total volume/weight/mass.
So why the result value is measured in mg/dl and not particles number per some plasma volume?
Unless the lab somehow strips the apob protein from the ldl lipos and returns a mass, then you'll get mg/dl...
But even then, the doc said him self that not all apob proteins are the same size, so you can't bunch them all into a single mass value.
I was recently told that due to my high cac score, performing a test such as a ct angiogram would not show any soft plaque because of the calcium reflection effects. So essentially my cardiologist said there’s no way to measure the soft plaque and left me with that. Is this correct? I find it hard to believe that there is no tests I can utilize to determine the soft plaque location and amount. Should I be looking for a different doctor? I think he’s just upset because I don’t want to take a statin yet until further testing is done.
My cardiologist's excuse for never offering any testing beyond the basis LDL Calc test is that it wouldn't change his recommendation for Statins. LDL was the shining object. I got a CAC and advanced bloodwork work on my own. I had been on statins years ago and for various reasons was deemed statin intolerant. My current regime is a pcsk9 inhibitor, very low dose crestor and niacin. They have taken my LDL down from 300 to 70. Docs want it lower. I'm not convinced that LDL/APOb are the risk factors docs like Dayspring make them out to be or that lowering them makes a hills beans of a difference but I'm playing along as I do more research. There are equally brilliant people on the other side of the argument. As for the CTA, my understanding is that it does show soft plaque as well as any obstructions irrespective of the presence of calcified plague. It's also my understanding that the CAC score represents only a small portion of overall plaque burden. If we have hard plaque, we surely have much more soft. Another test mentioned for soft plaque is the CIMT. If there's soft plaque in the carotid, it's also going to be present in the heart. Another thing to be aware of is that if you take statins, it will increase any subsequent CAC score. Researchers say they "think" this is a good thing but further research is needed.
I thought the lower the CAC score the better🤔 do you think Statins is beneficial for preventing heart disease?
N2daAIR I have heard this too. Very confusing, conflicting info out there.
Bikman looks at insulin resistance.
Ken Berry found a way to reduce body fat, get improved insulin resistance.
Each are looking at this issue from different points of view
Did you read Why We Get Sick?
Did you see all the research you keep talking about?
I am reducing carbs. I get lower blood sugars.
I did eat bacon and eggs and my blood sugar went down. (Berry suggested)
I would like to see your high carb diet.
I suppose Glucose Goddess is wrong too!
Somewhere is the way to insulin below 5, insulin resistance low, LDL clearance leading to longevity by Attia.
Every one of these people have something that works.
Now when calcium CT scan shows no injury to the blood vessels, good lipid clearance and my blood pressure which can go down to 112/69, then we need to see how more can benefit.
What works best?
No two humans are alike.
By the way, how old are you?
Completely different each decade of life.
I am 69
Ken Berry MD told why he ate like he did. It worked for his body. As long as I see improvement, I will go where my labs & glucose monitor takes me.
Your discussion of lipids is badly needed.
So you can eat carbs with a CGM and your blood sugar is steady? Congratulations, neither Berry, Bikman, Glucose Goddess nor myself get that privilege.
Carbs are the only food that needs glucose. I can't handle carbs anymore. I need fewer carbs and more protein with fats to lower blood sugar.
So if high apoB at 50 i could be on statins for 40 years? I wish u wld have asked if we ever stop taking statins/Zetia...
Just wondering...are you willing to have someone on who has opposing viewpoints? When he said there's really no downside to taking a statin, I nearly dropped from disbelief. There's good evidence, whether he believes it or not, to demonstrate statins are themselves killers. My point being, there's two sides to this coin. He presents one side, and not everyone is in agreement with his assertions.
Yes and that should make anyone cautious as to his motivations.
I asked my doctor at my last checkup for ApoB and Lp(a) tests, and he ordered the wrong test - a "Lipofit by NMR". It was just total particles and particle sizes. Frustrating that primary care doctors don't know about this stuff.