@@bushpig6837Better slow than never. Of course my parents are mid 70s and on all sorts of meds but ignore any advice I give them about diet and lifestyle because it goes against their doctor. This same doctor used to prescribe me antibiotics when I was a kid and had the flu.
Oh, but the warm respectful way (even with Oreos) Nick presents his case will be hard to ignore. It will generate further investigations and discussions. L👀KING forward to the upcoming data. 📊
Dr. Nick you are a real inspiration for me. Love watching your videos and how you respectfully handled this discussion. As a physician new to the social media world we don’t see this enough and it is truly refreshing. Looking forward to more of your work in the scientific realm and your contribution to clinical medicine. All the best Drmidge!
@@nicknorwitzPhD Heloo Dr. Norwitz. I recently went on a strict ketogenic diet (was mostly meat based, low carb prior) as a means to loose weight and reduce some minor joint inflammation. Just had blood work: LDL 311, TG 71, HDL 70. I was also intentionally pushing a serious calorie deficit and lost 25 lbs in 2.5 months, eating near zero carbs and continuing to work out (20 minutes cardio + intense weightlifting 5x/week). I am 6ft tall and was 210 and now 185 with a lean but muscular build. BMI 25.6. Do you think COMBINING a ketogenic diet with rapid weight loss can further ACCELERATE the uptick in LDL? I read a study pulled from PubMed titled "The Transient Hypocholesterolemia of Rapid Weigh Loss" where participants in the study had major spikes in LDL following a 30 lb average weight loss in a short time frame. They returned to "normal" LDL after the weight loss. Sorry, don't have a "before" lipid panel to compare. Would love to hear any thoughts on this matter. Thanks.
For my class, Harvard has us to our third year rotations in our second year, and then I rolled straight through USMLE STEP1 (10/11/23) and STEP2 (11/10/23)... so what I'm saying is... now I have time to emerge. Getting named dropped on JRE was timed well, hehe!
@@nicknorwitzPhD My wife was a med student and dietician, so I will need to convince her that keto or carnivore will not cause cancer or heart disease if I do it. It sounds like you're saying that we don't know, but low carbs will help with obesity and associated co-morbidities allowing exercise and better quality of life. I need a better understanding or I'll be thrashed as she's a smart cookie.
Five years ago, I had symptoms of Sjogren's, and that alone was debilitating, but I had high blood pressure developing, risong fasted blood sugar levels, Reynauld's symptoms, migraines, horrendously painful and long periods, low Factor VIII and a load of other issues. But my cholesterol numbers were text book perfect. I now have high LDL, lower trigs and higher HDL, BUT none of the above. I stand by my choice to live with the high LDL risk (if it exists) and none of the pain etc over text book cholestrol and all the pain etc I had. My quality of life was so bad that I often considered not facing another day. Now? I get up each day wondering what joys I can find in life.
@@carinaekstrom1 Veganism/vegetarianism. Very low fat. All the shitty plant food I could stuff down my throat to eat 'according to the guidelines'. High fibre, no table sugar, lots of wholegrains and legumes. Destroyed my intestine and my gut, but my GP was happy. Ironically now as a carnivore, he wants me on a statin. No way ever.
@@kateaye3506 Yes, low fat vegan means a lot of fiber to get needed calories, and in the modern world a lot of people don't have the strong gut they need to suddenly transition from a very low fiber diet. I always suggest a higher fat vegan diet.
Point is super valid. When I was 318 lbs and eating a SAD, my TOTAL cholesterol was like 140. Recently saw a patient in consult. They were 400 lbs, brittle diabetic with A1c of 13, hypertensive etc. Their total cholesterol was in 130’s. To say they have a low cv risk because of this low cholesterol is preposterous.
@@nicknorwitzPhD I now hover at 215-220. Lipids changed with carnivore primarily. Total Chol- 347 LDL-C- 240 HDL-97 TG-51 LP(a)- 25 ApoB- 130 But I’ve recently added some small amount of fruit and some honey. Haven’t repeated labs to see how this has affected my values.
@@bushpig6837 Just experimenting. Seeing how I feel. Blood sugar response etc Also, I felt a bit too dogmatic about ketosis and carbs. I’m realizing that in all likelihood, nobody has gotten fat and unhealthy eating a sensible diet of meat and some fruit and honey. So now: meat, eggs, Greek yogurt, cottage cheese, some fruit, some honey. Not a ton of fruit and honey mind you…
@@keywestfan2503I would cut out honey, it's no better than pure white sugar. At least berries or such have vitamin C, fiber to slow glucose intake, etc. I've heard that the liver can only process something like 25g of fructose in a day before it'll start to get fatty.
The fact that this doctor lumps familial type elevated ldl and lmhr together is incredible. The two are vastly different.. I can lower my 400+ high ldl to 100 by eating 50 to 70 carbs a day for a few weeks. The familial type cant. It’s hard to understand how he doesn’t know this or acknowledge it
@@BeefNEggs057the goal is to point out that even with junk food you can lower your ldl which is a thought provocative preposition. He talks about it on his Oreo post .
57 yr old female - historically “borderline” cholesterol 200 +/- 10 pts… borderline high blood pressure… 3 years ago started running but not much change. Last year I increased my red meat intake (and meat in general over protein powders, bars etc) and I started running much, much longer distances regularly (13-32 mile events) my bp is GREAT and all my other numbers are great but dr is freaking out on me because my ldl shot up from 103ish to 144. She’s like can you eat turkey and salads? I’m so confused because I feel 100% better (not that I even felt that bad before but now I feel amazing) I am much leaner/smaller as well (lost 40 pounds over last 3 years with increased muscle strength and definition)
I actually made a reference on Derrick and Peters Video to having High LDL and mid to low HDL and high Triglycerides on a blood test while on a water fast for 3 days. I retested 3 days later at my cost after testing Dave Feldmans theory that you can shift your lipid testing dramatically by consuming nothing but fats for the 3 days. The results were low ldl, 70's normal to high HDL 80's, and triglycerides in the 40's. This was to inform the doctor on the Fragility of the testing based on your diet for the last 3 days. Im my mind, I think a study needs to be done with a Controlled diet for 3 days on large group of people with and without CVD to see if we can get stable results that show causality in a repeatable fashion that doesn't vary so significantly because of short term diet. I also want to note that my reply to a comment never showed up or was deleted for some unknown reason about me not understanding how this works "Not a Doctor". and ask Dave who had commented a few lines below my response. I also follow Derrick, and Peter and Truly believe that the truly are interested in the evolution of understanding. At 64 Quality of my remaining life seems to be more important now.
I'm not a typical LMHR either (HDL-C is borderline at about 1 mmol/L) but my CAC score is still zero at 10 years of high TC (up to 10 mmol/L) and LDL-C.
@@jacko3423 None of my pre 2010 testing should be considered baseline in my mind, due to the horror of starting as a Obese scorching diabetic. When I found out I was Diabetic it was due to losing vision 1 year after Lasik surgery and all of the sudden I could not clearly read a billboard on the highway. Thank god my eye surgeon after checking his work insisted that I got my Blood glucose checked. 480 was the results on my fasting blood glucose. Several shots of insulin later I got a ride to the hospital for 2 days. Everything was whacked out and nothing was in range on the blood work. Strict Keto, Sub 15 grams of carbs, starting on Jan 10 2020 and a year later I was fairly stable, non diabetic. "blood glucose around 70", dropped weight from 268 to 162, and Felt great with the exception of my fingers from me testing Glucose 4 times a day. post fasting test. This was not planned, during a water only fast. January 5th 2010 Doctors Orders total cholesterol was 228, LDL was 128, HDL was 52, and Triglycerides were were 152. my last test was 4 months ago and was total Cholesterol 182, LDL 140, HDL 54, and Triglycerides 59 This is on a "Dirty Keto" with approximately 50 Grams of carbs. Blood glucose testes daily @ 5 pm and eating one meal a day at 5:30-6:00 averages 65-80 As long as my Blood work stays in check, I am moving more toward a Mediterranean diet for a greater variety of healthy foods and lowering my saturated fats to a small degree. long winded reply to give context. hope this is what you wanted.
@@NickWestgate had my scan with and without contrast so plaque and calcium show up. combined score was 42 @ 62 years old. Not perfect 0 but former 45 year heavy smoker, diabetic, and party animal abusing everything. I had expected something in the 600 range based on friends testing with similar lifestyles.
@@philloderThat's pretty good considering! I probably have soft plaque and will eventually get a non-zero score (I'm only 53 now) but getting a zero keeps the doctors happy for now. Looking forward to Nick and Dave's papers so I can wave them at doctors. LDL is only part of the puzzle so I look forward to the field moving forward and finding the root cause.
As a LMHR, this exact topic has me in awe/perplexed too. Love eating low carb, beef heavy diet but am not dogmatic about it. The people need an answer to this question.. appreciate you doing the work!
Wow! This was very good. I hope People will understand that we still have to address the ApoB problem for everybody that is not a LMHR. Most people that have elevated LDLc and ApoB are not on a LC diet and don't have the triad. My patients that don't want to address their high LDLc with drugs or even supplements are in that camp. Still for the LMHR I hope you show that they don't have to worry anymore. Thanks again!
One leg of the triad may have already crumbled, the belief that high HDL cholesterol is protective. According to Dr. Dayspring who is an expert on cholesterol, HDL at 60 and above tells you nothing about what is going on in the body. It just indicates that there is too much cholesterol in the blood. He also maintains that the tg to hdl ratio is worthless.
I haven’t yet had access to an investigation that could determine whether or not any plaque has formed in my 4 years of seeing this pattern in myself since I went low carb. Because of this, I yo-yo between trusting my body and panicking about the LDL levels and the ‘area under the curve’. I follow Dr. Attia and when I heard his take on this in recent podcasts he’s been on, it was anxiety central for me. It’s reassuring to hear the issue being discussed, even if we don’t know anything for sure yet. Thanks for the video!
Thank you. Clearly, I'm not aiming to give false reassurance. But I think the discussion needs to be had and has, thus far, lacked nuance on the LMHR topic. I think I could help there and believe Peter is open-minded enough to evolve his opinion. And I would offer the same open mind and willingness to shift opinion if forced by reason and/or new data
I feel ya. I feel and operate better on low carb( good energy, low hunger, effortless weight control) but all the “science “ saying how bad it is does create some doubt. Really looking forward to the lmhr results to go to my doctor with.
My husband is in the same boat. Most of what I see is high ldl and zero CAC score. What if your score is 1300 and it went UP despite your keto diet? This is where we are and it's frightening. Husband is a LMHR and very fit. Nobody would look at him and say he was a heart attack waiting to happen...except the cardiologist. So we do olive oil and try to limit animal fats because we see the former lowers ldl, the latter raises it. He is on repatha. He caught covid earlier this year and it really kicked his butt...and he has joint pain now. I think its the low ldl. We seem to be damned if we do, damned if we don't.
@@iss8504 , Is repatha a statin? Statins could cause higher CAC score because it calcifies the soft plaque as far as I know. Olive oil can be pesky. You have to be extra diligent choosing the brand as its often adulterated with seed oils and/or oxidised.
@@lukelacey101Repartha is PCSK9 inhibitor. It does not increase calcium. It reverses plaques for many people. But it didn’t do anything for me. So I stopped taking it
I presume the major difference of LDL between LMHR and FH is the duration that each LDL particle remains in the system and thus vulnerable to oxidation. With FH, I would expect much more oxidation, and perhaps no oxidation in LMHR.
Love you men haha I feel Peter is a true scientist and he will reestructurare his opinion about LdL in LHMR in a future. Keep doing this awsome content
Attia knows all about the lmhr phenotype .He is promoting statins by saying nonsence about elevated ldl in the context of a healthy metabolism .He is delibetately deceiving people for financial reasons . The sad thing is that many people end up on statins when their metabilic health is good ....all because of the Attia types .
Dr. Attia is not a lipid expert. He will follow the lipid experts like Dr. Cromwell and Dr. Dayspring and they know that ApoB is causal for heart disease. That underscores the importance of LDL cholesterol in heart disease, since the greater the amount of LDL-C, the greater the number of ApoB particles to transport it in the blood. And those are the particles that pass through the artery wall, become oxidized and cause plaque to form. High saturated fat diets cause LDL-C to explode. Same for ApoB, increasing the risk of CD. And according to lipid experts, high levels of HDL-C are not protective. So I think this concept of the LMHR is going to self-destruct when the lipid experts get at it. Dr. Cromwell has already expressed his view in conversation with Dave Feldman that he doubts it has any value. He said he was not convinced.
According to David Diamond, the heart disease with people with FH is related to factor 8 clotting factors. According to the research that he has covered is the people with normal clotting factors do NOT have unusual heart conditions.
Yes, I was thinking about during this. We really need to understand the etiology of FH much better than we currently do. Also the hazard ratio of ASCVD/CHD is only about twice the general population (of course tragic for those people who do develop). So there any many many people with quite high LDL-Cs that never develop ASCVD! How can ApoB be so powerfully causal when this is the case? Definitely something we're missing...
@@davidgrimes4726 Yes. This is what drives me crazy about the climate change people. Nearly all of the variables relationships to each other and temperature are virtually unknown. Feldman is filling in another brick of the wall for sure. I’ve seen other evidence that injured blood vessels are what signal the body to apply a bandage of cholesterol and we know for a fact that cholesterol is used for healing. William Davis of Wheat Belly fame has shown evidence of reversing cardiac plaques.
Absolutely need more clarity on FH. Attia says it's defined as LDL above 190; Dr. Casey Means says it's only above 300. ? And why do we assume any high LDL must have genetic causes? Appreciate Nick's passion for lmhr, but the larger cohort of FH also needs some attention.
Such a great video and, so respectfully done. Many people are looking to pick a side in an argument, so it's great to see someone so interested in finding the truth. Nice job, sir.
Plaque accumulates in damaged sections of the coronary arteries. This is where the pressure is highest. The particles are forced between the layers of the arterial walls. So, for plaque to form, that portion of the artery would already need to be damaged. Once the artery is compromised, any particulates in the blood stream become potential plaque media.
Stuff like nicotine, high blood sugar, blood pressure, and more can cause arterial damage, plaque is essentially scar tissue buildup from chronic damage.
@mikafoxx2717 - Dk you think oxidized fats being transported by LDL could be scarring the arteries? So the issue wouldn't be the LDL itself, but the types of fat being transported? Could even be a certain Fatty Acid
@@NutritionPolice It's the carrier of the cholesterol, the ApoB lipoprotein that gets oxidized, causing plaques to form. The ApoB particles can pass through the artery wall and get stuck there. They then get oxidized. This is the origin of heart disease and it's causal. LDL-C doesn't predict heart disease well. ApoB can diverge from cholesterol and is a good predictor. Nor is inflammation required as a precondition. Eat a diet high in saturated fat and your risk of heart disease will shoot up, as your ApoB # does the same. That's the danger of high saturated fat diets- they lead to an explosion of LDL-C AND Apob particles. I don't believe that HDL-C is protective. A high level is not good, it just indicates that there is too much cholesterol in the blood. I think Dr. Norwitz and his colleagues are wrong for believing that high HDL cholesterol is protective.
Love the work your putting in Nick. I'd listen to you all day talk about cholesterol than Dr Attia. Great job getting your details across, easily understood.
The thing I can't stand about Attia, in this interview, is he keeps saying that LDL is "causal", when it's clearly not causal. It's one of a plethora of signs someone has when they do have CVD. But by his own admission not everyone with high LDL has or will develop CVD. It's like that recent study released talking about erythritol being bad for you, when they didn't test for intake, they only checked sick people for erythritol, who's bodies are known to naturally produce more of it. So you take a sick body, you find something in it, and you then call it causal? That is not above board, that sounds more like p-hacking to me.
Appreciate your efforts to get to the truth. So discusted these days that so much "science" is financially motivated. 56 years old and from 7/1/22 to 11/30/23 have lost 124lbs eating between 10-20 total carbs per day, and managed to add muscle at the same time. My lipid panel shows exactly what you have described with elevated LDL/HDL and lower triglycerides. Never high LDL when my diet was terrible and I was in terrible health and shape. Doctor mentioned Statin at last physical and I declined informing him of how my diet was direct cause and I currently wasnt very concerned. Looking forward to showing him the final results of the oreo/statin study, because I believe I know what the results will be. Will stay tuned, thanks again.
Peter Attia looks and talks seemingly professional, but he is trapped in his own dogma, which makes it hard for him to understand the lipid energy model.
This is lovely. Thanks for sharing Nick. I'm a lmhr and flip flop between thoughts a lot ! Aka Nuance. Its such a nuisance but we'd be no where without it. Keep up the fantastic work ❤
I love both you and Peter for how much you love science and how much effort the two of you put into educating the public. I appreciate how precise you both are and the attention to nuances. I have genetic lipid dysfunctions(APO E4 and very high lp(a)). My lipid numbers were bad on ordinary diet, and my ldl-c skyrocketed even higher after I went on ketogenic diet with very low triglycerides and high HDL-c. I am lean and I work out. So I suppose I have both the genetic FH (my dad is in the same situation) and LMHR phenotype. So learning from the two of you have helped me find a lifestyle that I am comfortable with. I take Fenofibrate to control my lp(a) and continue my ketogenic diet to control inflammation. Saturated fat is good for my lp(a). And since Fenofibrate normalized my APO B, now I can eat a high saturated-fat ketogenic diet without any fear.
Thank you for the information you put forth. Being on a keto diet for a year my last test came back with LDL as "high" with high HDL and low Triglycerides, my doctor was very concerned and I was shocked to see the result, previous tests being "normal". Your information is helping me understand that there is more to it than meets the "normal" eye
I am very interested about this as well after reading Dr. Kendrick's "The Clot Thickens", where he presents some evidence and histological samples that appear contrary to the hypothesis that LDL is atherogenic. I don't feel comfortable dismissing mainstream medicine, *especially* as a layperson, but they don't do a great job presenting their case either. Even Dr. Attia, who is a great communicator, hasn't presented particularly convincing evidence -- Mendelian randomization has caveats that he doesn't address, for example.
I also recommend Kendrick's book! He explains that LDL is identical to another lipoprotein called LPa except LPa has an additional protein scarf on its' surface called Apo(a). LPa goes to sites of damaged arterial linings and helps plug up the defect along with other blood clotting factors. It also stabilizes the clot so we don't bleed to death. There is a special tissue stain which can be done in the lab on removed plaque to look for Apo(a). Sadly, it isn't ordered, so doctors don't know.
there's no such thing because that's not it works, inflammation causes arterial damage and over time arteriosclerosis. Reduce carbs and fructose as a start, they're causal agents
Taking your bike to work, is fairly common here in Denmark. A part of this is getting a flat tire now and then. The more you ride your bike, then more punctures you will experience. Is riding your bike causal? Demonstrably, biking less would result in fewer punctures, but so would better and cleaner bike lanes. Almost 10 years ago, did Attia launch a video, Straight Dope on Cholesterol. He CLEARLY states, that if there is no room in the subendothelium, you don't have atherosclerosis. So, what causes this "room"? What causes endothelial dysfunction? Why do diabetics have higher risk? The arrow seems to point very much at glucose (and possibly our ability to clear it). Dietary glucose seems to be considered as necessary as breathing, but could it be the degenerating agent through lifelong exposure by elevating your bloodsugar 3-5 times a day?
Glucose may be necessary but the level of glucose seems to be strongly managed to be between 70 and 140 with consequences for going under 60 or over 180. "Nourished by Science" suggests that if you keep your BG between 70 and 140 you are probably fine. This suggests that BG over 180 for extended periods likely has some seriously bad health effects, certainly I know from experience that going below 60 does.
@@capnkirk5528can you disclose what bad health effects you had from going below 60 BG? I assume that you are a carb burner as I have never heard of fat burners with bad effects from BG numbers below 60 due to high ketone production.
@@francisvlatko2834 Reactive hypoglycemia". I believe it's common, but I don't actually know (except I know it's common in MY family). Extreme hunger, shakiness, sweating, pallor, tachycardia. If I'm driving I have to stop (not always possible) and eat something sweet like a diabetic, but I'm not diabetic. I can trigger it with lots of things - easiest is a double bowl (2 pkgs) of Maple Cinnamon Instant Oatmeal with no other food. Spikes my BG WAY up and then I will almost always crash below 60, and if I'm not careful I WILL pass out. Repeatable. And yeah, that's carb-burner. I have to fast for at least 24 hours to even start to get into ketosis, and eating ANYTHING seems to knock me back out.
Diets high in saturated fats lead to cholesterol synthesis and increases in the ApoB lipoproteins that transport it in the blood. Those ApoB particles can pass through the artery wall, get stuck there and become oxidized, leading to plaques being formed. No other condition has to be present for this to occur.
New subscriber. started following you through Dr Ken Berry interview. You are a shooting star and I want to watch your career. Thank you for doing what you do. BTW, I'm 62 with congenital heart issue (HCM obstructive) I'm doing great now on carnivore, labs are beautiful except slightly high LDL. I'm in for the long haul now as I've had a lot of other things clear up and go away with this eating plan. :)
New subscriber! I appreciate your calm, non judgmental presentation about facts. I watched some of their conversation and I found it very judgmental, as in a “why do those people even think that, they are so willfully blind” kind of way.
Peter Attia does not know how molecular causality works, which makes sense, med students are not taught like phd students when it comes to statistics and necessity vs. sufficiency; spoiler alert, for a factor to be *causal*, it must be both necessary AND sufficient, not just necessary (what he claims LDL holds); another spoiler alert....causality has to do with wound healing responses (local inflammation) and immune cell activation, which triggers plaque formation....it helps (more plaque and future narrowing) if that plaque formation cannot be recycled once the inflammation ends, which has to do with certain genetic issues, carcinogens/xenobiotics, immune cell defects
Peter can take that Mendelian randomization and get outta here. It is firmly contradicted by real world results. In the most simplistic analysts, when 2/3 of heart attack victims have normal LDL, that should be a strong hint.
@@nicknorwitzPhD Agreed, yet I see PA and TD setting forth MR as the final answer, end of debate, no need to look at any other evidence, and those who discuss further are ‘deniers’ (or some other pejorative). And as an added bonus, ignoring harms.
Thank you Dr Norwitz for your high level analysis and research into this fascinating and potentially ground-breaking area of medicine. I have a very personal interest in this field of study as I am a 65 year old LMHR woman. My CAC score at age 63 was 0. I am fit, healthy and have no reason to change my low carb, high fat diet from a quality of life perspective. My well-meaning physician is a fan of Dr Attia and continues to want to lead me in the direction of taking a statin. I have no intention of trying to fix something that is not currently broken. After 10 years of eating this way I believe that if high LDL was directly associated with cardiovascular disease I would have demonstrable features of it by now. I may agree to another CAC score in another few years but it would be more from an academic perspective than from anxiety around my way of eating.
Thank you Nicholas Appreciate the civil discourse, regarding LMHR, 1- in my understanding there's a meta analysis of 12 RCTs that showed increasing HDL without lowering apoB doesn't reliably reduce cardiovascular events, also mednelian randomization have shown that neither low HDL nor high HDL alone affect cardiovascular risk Study name : (Effect of HDL-Raising Drugs on Cardiovascular Outcomes: A Systematic Review and Meta-Regression) 2- for triglycerides we have an RCT that showed that reducing TG by 26% also did not affect cardiovascular disease Study name (Triglyceride Lowering with Pemafibrate to Reduce Cardiovascular Risk) from these points i understand that both HDL and TG are mere bystanders when it comes to cardiovascular disease While we agree that apoB is causal So why would LMHR, which raise HDL and lower TG (bystanders) but increased apoB (causal) Not increase cardiovascular disease risk ? Feel free to correct any misconceptions or assumption i made
You can't just assume that raising HDL or lowering triglycerides via drugs should have the same (positive) effects as increased HDL or reduced triglycerides from changes in diet/physical activity/exercise/body composition. And so you can't conclude that if those drugs don't show benefits that it's evidence that increased HDL or reduced triglycerides from diet/exercise are bad indicators of CVD risk.
You can't conclude either that high HDL-C is protective. Dr. Dayspring, a lipid expert has said that high HDL-C, which he defined as 60 or above tells you nothing about what is going on in the body, except that there is too much cholesterol in the blood, and that is what happens when uou get an explosion in LDL-C on a high saturated fat diet.
Found you via Anthony Chaffee. Amazing, data driven, real science and communication. Opinions and assumptions need to be countered with facts and evidence based science. Awesome work man, I have struggled with some of Peter’s opinions and beliefs around food and cholesterol. Exercise and VO2Max is indeed important, but not as important as what we eat and drink etc. cheer N, keep rolling, it’s well needed.
I thank you so much for your prospective that as far as I can see is right on . Your extra training with your PHD has been a help in explaining many mysteries that the medical community does not seem interested in . I have been low carb for 3 years now and I feel so much better than before . Keep up the good work .
Wondering you're aware of the alternate hypothesis of the mechanism of atherosclerosis as elaborated by Dr. V Subbotin. Looks like it could account for many of the contradictions in cholesterol-heart theory, such as why LDL has such weak correlation with events. If we have the initiating process wrong, no good solution will be found.
You have the initiating process wrong, but like most commenters don't know that there is overwhelming evidence for how the process of heart disease is caused by ApoB lipoprotein particles passing through the artery wall and getting oxidized. I described it in another long reply.
@@newyorkguy158 I know very well the process proposed by Subbotin is not the conventional one. But it explains the actual pathology better, ie. the conventional explanation is wrong. The actual concentration gradient of LDL particles is opposite to that predicted by the narrative you subscribe to. V Subbotin has proposed that neovascularization of the tunica intima is the source of the lipid particle, rather than penetration of the endothelium. Another failing of the conventional narrative is explaining why the particles only pass through coronary endothelium but nowhere else. www.ncbi.nlm.nih.gov/pmc/articles/PMC3492120
I am 18.5 bmi/ LDL 160, HDL 94, triglycerides 52. I have been on the ketogenic diet with a daily fasting window of 18 hrs. for approximately 4 years. I wish I knew what my lipid panel numbers were before I started the Ketogenic diet but I have no idea. I am experiencing the common push from my doctors to begin a statin due to my LDL. Interesting that there is never an acknowledgement or seemingly a recognization of my HDL/ triglycerides ratio. We sure have a way to go but I am so thankful for the powerful research your team is doing. I feel fairly confident in refusing the prescription for low does statin especially concerning my predisposition to Alzheimer's. Thanks! Looking forward to more data to come!!
This is exactly the situation that I am in. "High" LDL (150 to 200), HDL consistently about 80, and Triglycerides range from 40 to 60. I.F. for 7 years, Keto for 25 years this month. My doctor thinks that when I refer to my excellent Triglyceride and HDL values, I'm merely trying to say that those two things mitigate against my high LDL. But that's not the point. The point is the low Trig/HDL ratio is an indicator that the LDL is of a different type (large particle, non-oxidized,..) that is not even statistically associated with disease. In fact, I've had that independently checked, and, yes, my LDL is the large particle type.
I don't think the triglycerides to HDL ratio means anything. Dr. Dayspring, a leading lipid expert has said that HDL 60 and above is too high and only means that there is too much cholesterol in the blood. I don't think HDL is regarded any longer as protective against heart disease since the Eli Lilly HDL raising drug in clinical trials failed to prevent heart attacks and strokes and was rejected by the FDA. You need to lower your ApoB by restricting saturated fat and taking a statin.
@@newyorkguy158 That's a good point you bring up about the HDL. But I think HDL is a good marker of good health if it happens naturally. I don't know what else the HDL-raising drug does besides raise a person's HDL.
@@TheFrankHummer According to Dr. Thomas Dayspring, a well-known lipid expert, who has written chapters in medical texts on lipids, HDL tells you nothing about what is going on in the body. I would look him up on YT. He has given a lot of lengthy interviews. See Dr. Carvalho, MD & PhD on his channel, Nutrition Made Simple and Simon Hill for some very informative interviews.
Awesome video. I've watched Drs Peter Attia's, Ken Berry's, Roy Taylor's, and Robert Lustig's videos and am in awe of the research, discussions and professionalism in the questioning of the status quo, even if it turns out that the status quo remains the same. I expect that new research will impact future cardiac and type 2 diabetes clinical guidelines.
There are 2 kinds of doctors and health experts. The first group are guys like Dr. Berry and Richard Johnson. They completely understand humans were created by evolution, and see health and health science through that perspective. The others are what I call "science chasers." Guys like Layne Norton, Peter Attia and Jack Kruse look purely at science, and scientific principles to understand health. They only look at studies, draw conclusions, and make decisions based on scientific principles and evidence. The problem with this way of thinking is that biology is too complicated to understand it completely. There is, and always will be too many unknown variables that can completely destroy your hypothesis... Most all animals that are free of genetic diseases and mutations are perfectly healthy when they live and eat in their natural environment. That's what instincts are for, and why they adapted to be that way...we do best when we adopt an appropriate diet and live in our natural environment which our instincts were adapted for... There is no substitute for living a natural life when it comes to metabolic health...
you're wrong in fact, the likes of Peter don't use science, they use junk science known as observational studies to perpetuate their lies. We need to be really clear what it is that they're doing, they're lying to the public!
I’m not sure I believe the claim that animals are completely healthy in their natural environment eating their natural diets… is there data on this? Don’t most wild animals die from other causes?
Greeting Nick, I was hoping you would address these issues. From my perspective, the FH definition is advantageous to prescribing statins, if the condition is labeled genetic that helps the doctor convince the unaware that they should have one or more statins, (which provide lifelong profits and cause even worse health outcomes and even more drugs etc.) I am a LMHR, my LDL peaked at 230 which required me to change my carnivore diet. I started eating around half a cup of potato pre work out and, dropped all tallow and have been using avocado oil (per your online comment). I work out around 7-9 days straight then take one day off. At 68 years old this is getting challenging for recovery. A recent LabCorp test: Absolute Triglycerides 23, Absolute HDL Cholesterol 111, VLDL 4, Total Cholesterol Cal 229, and the Calculated LDL Chol (NIH) 114. I do not understand the math behind the LDL number, seems high per the 229 total. Can LDL be lower than HDL in some extreme cases? Is the lab algorithm forced to generate a higher LDL number? Regards and thanks!
@@nicknorwitzPhD By that reasoning, it would seem platelets would also be causal, and further along the line of reasoning, blood, heart and a brain signaling to that heart, and by further extension, anything that leads to that brain being on, is causal to heart disease. If you have a group of hikers coming in with shattered shin bones, except for one that comes in with a bloody hammer, you don't blame the hiking.
I hope someone can give me some advice. I'm kind of confused on if I'm good or bad with the cholesterol. Here is my breakdown. I have spent alot of time on my health and nutrition the last 4 years. 4 years ago my basic numbers were.... over weight, 5'6 210 lbs. 25.75 bmi. 36 waist Pre-diabetic, reactive hypoglycemia, always tired, fatigued, depressed, joint pains always, plantar warts all over my feet. Dry and itchy skin and sinus and nasal drip every morning. Also would almost pass out upon waking in morning because of reactive hypoglycemia. Strangely, although I always felt horrible and having a glucose of 110 on average and borderline high blood pressure my cholesterol wasn't too bad. It was 120 LDL, 120 trigs and 50 hdl. Total was about 190-200. Here are my new numbers after training, studying nutrition and going on a low carb keto/carnivore program. 5'6 152 lbs. 23 bmi (sometimes lower). 31 inch waist. All ailments gone. No more pre diabetes...a1c is 4.9. No more reactive hypoglycemia, no more sinus or nasal drip or dryness or itching. All plantars warts are gone. They disappeared less than 6 months on keto. No more achy joints. Tons of energy and feel great. 2 meals a day with int fasting 8 hr time frame not 6. It actually didn't work as well. Never tired. No more depression. Ok....here we go... Trigs dropped to 67 and hdl went up to 77. But.... which I wasn't too surprised the LDL went up to 170. Ofcourse the Doctor freaked about LDL and could care less about the hdl and trigs. I decided to pursue a naturalpathic doctor instead and he set me up for some tests. Advanced lipid panel. Low lipoprotein (a). Cholesterol pattern A large fluffy not small. Homocysteine low and excellent. Hs-crp very low and excellent no inflamation. All kidney and liver tests excellent. Had several inflamation markers done all great. Had ekg and stress test...all good. Even had a Cac score of 0. Have one every year and 0 the last 3 years. Out of everything only questions I have is any advice on the high LDL and high apo b which I heard coincide with eachother.
Nick thanks for these videos. I was going crazy with fasting, eating clean all because my total cholesterol (230) and LDL (154) were going up test after test. Once I watched your videos and realized I don't care because every successive blood test my other levels for TG (65), HDL (65), VLDL (11) were going down. This all started to happen when I hit my mid 40s.
Incredible video Nicholas. It make me wish i was smarter lol. Dr. Attia is a smart man but doesn't have every single answer. Its great seeing guys like you challenge great minds like Attia. I subscribed.
Fundamentally, Peter says LDL is causal. I would like to see what he is looking at. Dont studies show 1.2 risk ratio at most with many studies showing a lower than 1 risk ratio. If you agree high LDL is causal, you concede to Peter's position. High LDL in our case just indicates healthy energy transport.
Have a read of: Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel
High numbers of ApoB particles CAUSE heart disease. The more cholesterol that is synthesized from saturated fats, the greater the number of ApoB particles needed to transport the cholesterol in the blood. These particles pass through the artery wall, become oxidized and form plaques, leading to inflammation.
We just started keto 6 weeks ago because my husband came up with high cholesterol. We got his new blood work done and he has even higher LDL but his triglycerides normalized. I suspect he is LMHR. His pill pusher Dr is mad he didn't take his statins (a decision we made based on risk factor analysis). Our original plan was to do Keto for 6 months and see where we are and re-assess statins then, but its all more complicated than that. We are going to make an appointment with a keto doctor in our state to help us make sense of his charts and tweak our diet.
Your husband's case is typical of what happens to people's cholesterol when they go an a high saturated fat diet and I believe it is extremely dangerous.
@@newyorkguy158 no, experimentally very high saturated fats lowers LDL (and TG) as a result of adipose anabolism. The cell membranes consume the LDL and TG to grow in size to store more fat. The reverse is true when hypocaloric or when MBR upregulates (ie, low torpor dieting, or high activity), LDL, HDL ramp up, and TG normalises, as the adipose shrinks. HDL increases due to high LDL turnover.
@newyorkguy158 -- you think it's dangerous because you're wrong and misinformed all throughout this thread. You're on statins and low fat, I get why you're depressed but keep your ill informed bs to yourself
indeed, even accounting for LDL levels dropping following a CVD event, it doesn't change the fact that we are talking about a bell curve instead of a progressive line / curve
@@llicit1833 it's a bell curve, not a dose response, so very little to do with LDL, as long as you have other issues damaging your endothelium, the only safe level would be zero, and that would kill you
So fascinating. When I was a heavy drinker on a SAD diet, I have labs with LDL around 150-200 mg/dl; 10 years later on Carnivore or Keto, I can get my LDL as high as 500-600 mg/dl. This obviously made me severely skeptical of focusing purely on one data point. I'm 6'1, and have never been over 190 lbs. I love the work you and your team are doing!
I'm pretty much in the same boat. But my LDL is still high even increasing carbs and reducing fat, especially sat fat. My labs always say suspected FH but genetic testing says I'm not genetically predisposed to CVD risk. I figure I'm a LMHR but suspect I should be on a statin.
@@6789uiop If I eat a paleo/animal based diet with carbs from fruit, tubers, veggies etc, I'll have a total cholesterol of about 300-350. I'm currently trying a bastardized version of "slow carb" with red yeast rice supplementation and will be getting labwork in the next few weeks. I'm just trying to lower LDL to get more life insurance. If that doesn't work i'll try the Feldman protocol and then quit caring about LDL in isolation forever. BTW I tested negative for FH and have a CAC score of 0.
@@IH8CA Grats on that CAC zero! My Tot CHO is ok w/ Dr's because my HDL is always 58-60. My trig:HDL is just above 1 too. The gene test I did, Color, stated no FH but gave a big qualifier on it as well as for apo-B. I was researching red yeast rice but as it's actually Lovastatin I felt I'd get a more accurate and purer dose if I just took the Lovastatin. There's probably USP red yeast rice tho. I never did take it. I took Atorvastatin for a couple weeks and my calves cramped so bad I couldn't walk. Many years ago Feldman did an n=1 protocol for lowering cholesterol for say... presentable labs purposes. Me, I just quit fat for a while and it dropped to high normal and I got insurance in the country we now live in. LDL 171, HDL 59, TG 60, TOT CHO 223 fwiw, blood sugar great, vit D 84
Glad to hear Peter is facilitating connections between some of the movers and shakers in this field and the emerging data and science around LMHR. I am completely open to ezetimibe or other compounds to drastically reduce ldl/apob, assuming I can maintain my current therapeutic benefit and get a net win on ACM. Let's see how LMHR shakes out first though, being in my early 30's I still feel comfortable with a bit of risk in this regard considering how otherwise healthy I feel.
As a person who eats Keto-Carnivore partially for mental health, it is frustrating to see people put on stains and then medication for their depression or anxiety, etc. due to the side effects of the statins...
What I find fascinating is that they don't see the similarities between LDL to atherosclerosis and oxygen to fire. Oxygen is causal but not sufficient for fire. They too would never accept firemen to answer the question " What caused my house to burn down?" with "Oxygen in the air caused the fire." But with CVD,.. "LDL-C caused your atherosclerosis." is considered completely acceptable. I know, fire is a stupid analogy,.. but really,... It is not. It just makes the LDL-C argument look stupid.
Yes, but also the fire cannot exist without the oxygen. So, remove oxygen from the scene and fire will neither start nor spread. All kinda arguments out there. 😊😊
Higher levels of cholesterol lead to increased ApoB particles to transport it in the blood. The ApoB cause heart disease in a process I have described in other replies.
12:46 I heard Cardiologist Nadir Ali speaking about how insulin spike has something to do with lowering LDL which might be the case when consuming Orea cookies. Sugar and Fat mixed together.
Thank you for your excellent presentation. I was unaware of LMHR and appreciated your clear explanation and analysis. Keep up the great work, Nicholas!
Thank you for such a measured and intelligent perspective. There seem to be a lot of folks out there speaking with certainty on topics where we probably don't have enough data to make a perfect decision. And I think there is definitely a big difference between "the data we have so far seems to suggest" versus "you're taking big risks with your health if you do this".
The difficulty I have with any claims about the low level of adverse effects from statins, other cholesterol lowering drug, and for all drugs for that matter is that the system for identifying and reporting adverse effects operates in a way that ensures adverse effects will be under reported as long as a significant number of people are not dying as a result of the drug. Statins and other cholesterol lowering drugs are perhaps among the most egregious examples of under reporting adverse effects. First, initial clinical trials and subsequent research exclude any test participant who shows any sign of adverse effects during the pre-trial run up period. That is a logical thing to do, because it is important to have participants who have a high probability of being able to participate for the full run of the research effort. However, in calculating and reporting adverse effects the pharma companies and researchers then exclude data for pre-trial participants who were removed from the research. It is impossible to know the impact on adverse effects reports from drug trials and drug company sponsored research because the drug companies do not release their datasets for independent researchers or the FDA to examine. The datasets are treated as confidential proprietary information. Second, because of the low incidence of adverse effects reported from the clinical trials and an almost cult-like belief among pharma companies and doctors that claims by patients of adverse effects from statins are not real, doctors do not report statin adverse effects from clinical practice to the FDA at anything close to their rate of actual occurrence. Instead, pharma companies claim and doctors attribute patient reported adverse effects from statins as being either normal aging or the nocebo effect. Third, patients do not take advantage of the opportunity they have to self-report adverse effects from statins or other drugs. In the case of statins, doctors significantly under inform patients about potential side effects. Doctors do not appear to inform patients that if they experience adverse effects there is an FDA reporting procedure patients can use to report the adverse effects they experence. As a result of the flaws in the system for reporting adverse effects, doctors such as Peter Attia and many others, can make statements about statins' benefits outweighing their [supposedly] minimal risks and do so with a straight face.
Peter is quite misguided on this matter. There has been a real failure of his to acknowledge gaping holes in the apob concentration hypotheses. Over the years he as completey ignored the DATA on FH. There are indeed studies that analyzed the longevity of FH homozygous carriers. These studies do not indicate a shorter life span overall. This then is a problem that Peter seems to continuously ignore. In a population of so-called, very high risk, you would expect to the majority to parrish at leaat by middle-age. NOPE. A number of studies/ analyses have clearly shown that although there are some people who die in the first 2 or 3 decades of life, life expectancy actually goes up. By the time these FH carriers are in their 60s their life expectancy goes up. This is also true of people in the general population. Hmmmm How do you explain a drop in mortality with those with FH ( very high apob) in there 60s, 70s and 80s? Peter is married to his hypothesis and is a victim of his own preaching and teachings of evaluating the evidence base. Confirmationly bias. A failure to explore and properly evaluate the nuances within the FH community is quite revealing. A complete failure to recognize that there are sub populations of FH patients and these segments need to be examined independently is of significant importance. It doesn't allow for proper context. Peter has left out important elements and the nuance. This is the stuff a strawman is made of. If Peter bothered to do this or actually listened to others that have conveyed a well articulated response to Peter's view of FH, he would have likely changed his mind or at least considered it. People with FH aren't all created equally. There are subgroups with known genetic variants in the clotting cascade. FH carriers have the same risk profile as those without FH. This is quite a bit more nuanced than the way Peter has characterized it. I encourage all to look at the FH studies It is worth investigating those studies to evaluate for yourself the differences within the fh community. What accounts for these differences between fh subgroups? Please have a look at the data 🙏 One thing I have not heard Peter address ( he may have and I haven't found it yet)is the polymorphisms found in a subset of people with polymorphisms genes/proteins involved in the clotting cascade. There is data that shows polymorphic changes that a subset of fh carriers are inclined to have, and this is an independent risk factor for coronary events. This and other variables not discussed by Peter need to be considered inorder to properly evaluate the problem. Peter simply hasnt considered the entire picture. You can evaluate for yourself by lookong at the data.
Yeah, that part confused me. He and Dave Feldman had a long conversation (I think on his podcast?) where they talked and somewhat debated all of this for quite a while and at no point did he claim LDL was causal to CVD. They even discussed how that hadn't been specifically proven, but he used that "necessary but not sufficient" phrase to back up his general reasoning on the subject. IDK how in such a short time he's made that leap unless there's been massive research published since then that nobody's talking about.
@nicknorwitzPhD Have always been curious about Mendelian Randomization argument from Attia. Are there any Mendelian Randomization results for other conditions (outside of the area of heart disease) that have not ultimately demonstrated causality? Meaning, MR showed two correlations that independently appeared to lead to the same pathology, but it was later found there was some other root cause not related to that presumed causal agent? For heart disease, is there something in FH that is causing the heart disease independent of elevated LDL? ALSO: of all the genetic conditions that are associated with lower or higher LDL, do they 100% show that low LDL always is protective against heart disease and high LDL always leads to heart disease?
@lls66 Mendelian randomization addresses some of the challenges of observational studies (e.g., calculating correlations among a large number of variables from a large cohort of people followed for 5 or 10 years). But MR suffers from its own wide array of potential confounds and limitations. It is a statistical technique for attempting to draw inferences about plausible cause-effect relationships. It is, for this very reason, only as good as its underlying data collection and only as good as the assumptions made by the human investigators. Genes can cause multiple effects under diverse metabolic states. Sorting this out is a nightmare. Gene interactions can vary widely under different metabolic states. Again, this very quickly becomes incredibly complex - and hard to sort out. In the case of LDL, diet, and population data, we are faced with one very obvious challenge: genetic expression changes quite dramatically between ketogenic states and non-ketogenic states (I use the plural for both because there are many dietary combinations that will get you into either of these states). Not only gene expression differs widely, but gene-gene interactions appear to differ quite widely as well. If we are to use observational cohort data to run MR in the hopes of sorting out LDL-CVD linkages, our cohort must, by definition, include a sufficiently large number of ketogenic persons, across the relevant demographic ranges. Lacking these people, no statistical method in the universe can sort out the question of whether the ketogenic state uniquely alters patterns of genetic expression and whether these patterns *cause* uniquely protective or pathogenic effects. Dr Peter Attia seemed to imply that MR had "closed the book" on -CVD causality. Without a ketogenic cohort, which his data must have lacked (since no such cohort has yet been investigated), he must know that MR on people in other metabolic states cannot exclude the possibility that high LDL observed in a long-term ketogenic state, is either benign or even outright atheroprotective. MR is a statistical technique that can supplement observational studies and generate hypotheses with regard to the specific types of people/metabolic states included in the data collection. MR is not an experimental technique and cannot substitute for experimental hypothesis testing.
Blood is also necessary to have CVD. Should be reduce all things that are associated with CVD? LDL is certainly not causal and you will never find or have a study that shows a causal relationship. Clearly Attia has lost the plot.
There are several distinct lines of evidence that indicate it is. Have a look at: Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel
QQQ please ! ... 1: What proportion of LMHR's started on Keto/Ketovore/Carnivore due wholly or partially to some degree of obesity as part of their reason and what proportion didn't have any obesity issues but went low-carb for other reasons such as Autoimmune issues ? 2: Before they went Low-carb, were any of them Binge-eaters wolfing down tons of crap or were they all eating crap but in moderate amounts ? 3: How long do LMHR's remain LMHR's ? ... I recall hearing that some LMHR's see their LDL gradually reduce over time as though their LDL levels were being suppressed when the carbs, seed oils and plant allergens/toxins were present but then significantly increased to replenish/repair/replace what was perhaps previously deficient and/or damaged for years/decades upon cleaning up the diet !
If you have a survey send me the link. 1> I was 233, went very low carb high fat and lost 60 lbs in 4 months 2> I snacked a lot and had three meals a day as well. Binge eating, true but normal USA eating style. Now I am Carnivore and eat OMAD. 3> Sill LMHR go in and out depending on time of year. I tend to have triglycerides above the limit when I eat a lot of berries or honey in the summer. I think my LDL number may be going down slowly but that could just be because I have not fasted for a year. A good question to answer would be what effect does serious fasting have on Hypercholesterolemia?
I'm a little confused on the wording and agreement here. ApoB is necessary though not sufficient. You have a causal marker that is necessary you can't develop CVD without it, though its not sufficient you can have it and not develop CVD... When a factor is necessary but not sufficient, it means that while that factor is required for the effect to happen, other conditions or factors must also be present for the effect to manifest. This situation highlights the need for multiple factors or conditions to achieve a particular outcome. So at best, its part of the cause??
Part of the effect. ApoB is a consistent element when we observe atherosclerosis, but its involvement may be entirely induced by other, preceding factors. Insulin resistance is always observed in type 2 diabetes. Insulin resistance is "necessary" to the diagnosis of T2D. It is not causal, though, but rather the effect of preceding factors. ApoB's role in CVD pathology may prove to be an intermediate effect of a set of preceding factors. The question at the moment is, if this is the case, then does a whole-food ketogenic diet prevent the initiation of those preceding factors? Direct experimentation with long-term ketogenic individuals will help sort some of this out.
New subscriber. For the "new guy" in the space, you are AMAZING! Got a question - has there EVER been a valid, quality, interventional study on the efficacy of statins as a secondary preventative measure in heart attack survivors?
I am also a fellow graduate from Harvard Medical School (and therefore you are a like minded thinker) who has had elevated cholesterol since age 29 (discovered when I got life insurance). My total cholesterol level has always been averaging 225-275 (only once was 199). I am likely a LMHR phenotype, had a negative CT Heart scan (zero score) at age 40 and at age 53 last year. Thank goodness I never subscribed to Statin therapy- not everyone with high cholesterol needs a statin- which your work will ultimately prove. Keep up the great work and dialogue. Of course, Big Pharma does not want those with high cholesterol to understand/know this.
I’m usually on board with Attia, but I’m with you on this. I wonder if big pharma took him to the woodshed over not taking statins. Hundreds of of billions $$
It's fascinating to watch a widely-held paradigm actually shift in real time...
It's frustrating when it's so slow, when the rest of us can see it as clear as day. It's like waiting for a glacier to melt.
@@bushpig6837Better slow than never. Of course my parents are mid 70s and on all sorts of meds but ignore any advice I give them about diet and lifestyle because it goes against their doctor. This same doctor used to prescribe me antibiotics when I was a kid and had the flu.
It is indeed ☺️
It sure seems like watching a glacier in real-time but I'm pretty sure you are a much more optimistic person than me.
Oh, but the warm respectful way (even with Oreos) Nick presents his case will be hard to ignore. It will generate further investigations and discussions. L👀KING forward to the upcoming data. 📊
I'm a borderline zealot on the lipid theory of ASCVD, but this was an excellent, nuanced discussion. Kuddos, doc.
Thank you. Appreciate this a lot.
Nick you will be bigger than Attia before too long.
Unlikely... I've tried overfeeding macadamia to >5000kCal per day but I'm a hard gainer ;)
@@nicknorwitzPhD I should have expressed myself better. You will have a bigger following. 🤦🏼♀️
@@suecosser I'm just messing around ;)
I know 😊
Believe it too... but I am not inline with Attia (enough said).
Dr. Nick you are a real inspiration for me. Love watching your videos and how you respectfully handled this discussion. As a physician new to the social media world we don’t see this enough and it is truly refreshing. Looking forward to more of your work in the scientific realm and your contribution to clinical medicine. All the best Drmidge!
Thank you very much for the kind words!
@@nicknorwitzPhD Heloo Dr. Norwitz. I recently went on a strict ketogenic diet (was mostly meat based, low carb prior) as a means to loose weight and reduce some minor joint inflammation. Just had blood work: LDL 311, TG 71, HDL 70. I was also intentionally pushing a serious calorie deficit and lost 25 lbs in 2.5 months, eating near zero carbs and continuing to work out (20 minutes cardio + intense weightlifting 5x/week). I am 6ft tall and was 210 and now 185 with a lean but muscular build. BMI 25.6. Do you think COMBINING a ketogenic diet with rapid weight loss can further ACCELERATE the uptick in LDL? I read a study pulled from PubMed titled "The Transient Hypocholesterolemia of Rapid Weigh Loss" where participants in the study had major spikes in LDL following a 30 lb average weight loss in a short time frame. They returned to "normal" LDL after the weight loss. Sorry, don't have a "before" lipid panel to compare. Would love to hear any thoughts on this matter. Thanks.
Excellent framing and well-articulated discussion. Thank you, Nick, for all you do. I can’t imagine juggling these projects during 3rd year rotations!
For my class, Harvard has us to our third year rotations in our second year, and then I rolled straight through USMLE STEP1 (10/11/23) and STEP2 (11/10/23)... so what I'm saying is... now I have time to emerge. Getting named dropped on JRE was timed well, hehe!
@@nicknorwitzPhD My wife was a med student and dietician, so I will need to convince her that keto or carnivore will not cause cancer or heart disease if I do it. It sounds like you're saying that we don't know, but low carbs will help with obesity and associated co-morbidities allowing exercise and better quality of life. I need a better understanding or I'll be thrashed as she's a smart cookie.
Five years ago, I had symptoms of Sjogren's, and that alone was debilitating, but I had high blood pressure developing, risong fasted blood sugar levels, Reynauld's symptoms, migraines, horrendously painful and long periods, low Factor VIII and a load of other issues. But my cholesterol numbers were text book perfect.
I now have high LDL, lower trigs and higher HDL, BUT none of the above.
I stand by my choice to live with the high LDL risk (if it exists) and none of the pain etc over text book cholestrol and all the pain etc I had.
My quality of life was so bad that I often considered not facing another day. Now? I get up each day wondering what joys I can find in life.
POWERFUL!
i must wonder how you got your "text book perfect" numbers of LDL/ApoB under 70? Statins or diet?
@@carinaekstrom1 Veganism/vegetarianism. Very low fat. All the shitty plant food I could stuff down my throat to eat 'according to the guidelines'. High fibre, no table sugar, lots of wholegrains and legumes. Destroyed my intestine and my gut, but my GP was happy. Ironically now as a carnivore, he wants me on a statin. No way ever.
@@kateaye3506 Yes, low fat vegan means a lot of fiber to get needed calories, and in the modern world a lot of people don't have the strong gut they need to suddenly transition from a very low fiber diet. I always suggest a higher fat vegan diet.
What's your current diet like that's raised your LDL and cured all those problems? Carnivore?
Point is super valid. When I was 318 lbs and eating a SAD, my TOTAL cholesterol was like 140.
Recently saw a patient in consult. They were 400 lbs, brittle diabetic with A1c of 13, hypertensive etc. Their total cholesterol was in 130’s. To say they have a low cv risk because of this low cholesterol is preposterous.
Have you gone LCHF, lost weight and only after losing lots of weight from 318 see LDL rise in a lot TG/HDL context?
@@nicknorwitzPhD I now hover at 215-220. Lipids changed with carnivore primarily.
Total Chol- 347
LDL-C- 240
HDL-97
TG-51
LP(a)- 25
ApoB- 130
But I’ve recently added some small amount of fruit and some honey. Haven’t repeated labs to see how this has affected my values.
@keywestfan2503 may I ask the reason for reintroducing carbs/honey?
@@bushpig6837 Just experimenting. Seeing how I feel. Blood sugar response etc
Also, I felt a bit too dogmatic about ketosis and carbs. I’m realizing that in all likelihood, nobody has gotten fat and unhealthy eating a sensible diet of meat and some fruit and honey.
So now: meat, eggs, Greek yogurt, cottage cheese, some fruit, some honey. Not a ton of fruit and honey mind you…
@@keywestfan2503I would cut out honey, it's no better than pure white sugar. At least berries or such have vitamin C, fiber to slow glucose intake, etc. I've heard that the liver can only process something like 25g of fructose in a day before it'll start to get fatty.
Loving this burst of top tier content lately!
These are exciting times to be alive.
The fact that this doctor lumps familial type elevated ldl and lmhr together is incredible. The two are vastly different.. I can lower my 400+ high ldl to 100 by eating 50 to 70 carbs a day for a few weeks. The familial type cant. It’s hard to understand how he doesn’t know this or acknowledge it
Attia doesn’t seem to know half of what he thinks or pretends to know.
@@stx7389 Why does that matter? Should we eat Oreos so we can have low average APOB? Seems silly but you do you.
I’ll be testing this on me for next few weeks and go retest .
@@BeefNEggs057the goal is to point out that even with junk food you can lower your ldl which is a thought provocative preposition. He talks about it on his Oreo post .
@@BeefNEggs057 a lot of what he is asserting is contradicted by research done and presented by David Diamond here in RUclips
57 yr old female - historically “borderline” cholesterol 200 +/- 10 pts… borderline high blood pressure… 3 years ago started running but not much change. Last year I increased my red meat intake (and meat in general over protein powders, bars etc) and I started running much, much longer distances regularly (13-32 mile events) my bp is GREAT and all my other numbers are great but dr is freaking out on me because my ldl shot up from 103ish to 144. She’s like can you eat turkey and salads? I’m so confused because I feel 100% better (not that I even felt that bad before but now I feel amazing) I am much leaner/smaller as well (lost 40 pounds over last 3 years with increased muscle strength and definition)
Well said... we are with you and Dave all the way! Thank you!!
I actually made a reference on Derrick and Peters Video to having High LDL and mid to low HDL and high Triglycerides on a blood test while on a water fast for 3 days. I retested 3 days later at my cost after testing Dave Feldmans theory that you can shift your lipid testing dramatically by consuming nothing but fats for the 3 days. The results were low ldl, 70's normal to high HDL 80's, and triglycerides in the 40's. This was to inform the doctor on the Fragility of the testing based on your diet for the last 3 days.
Im my mind, I think a study needs to be done with a Controlled diet for 3 days on large group of people with and without CVD to see if we can get stable results that show causality in a repeatable fashion that doesn't vary so significantly because of short term diet.
I also want to note that my reply to a comment never showed up or was deleted for some unknown reason about me not understanding how this works "Not a Doctor". and ask Dave who had commented a few lines below my response.
I also follow Derrick, and Peter and Truly believe that the truly are interested in the evolution of understanding. At 64 Quality of my remaining life seems to be more important now.
Hey, your comment caught my attention since I also have high triglycerides and low HDL. Can I ask what was your baseline and post fasting readings?
I'm not a typical LMHR either (HDL-C is borderline at about 1 mmol/L) but my CAC score is still zero at 10 years of high TC (up to 10 mmol/L) and LDL-C.
@@jacko3423 None of my pre 2010 testing should be considered baseline in my mind, due to the horror of starting as a Obese scorching diabetic. When I found out I was Diabetic it was due to losing vision 1 year after Lasik surgery and all of the sudden I could not clearly read a billboard on the highway.
Thank god my eye surgeon after checking his work insisted that I got my Blood glucose checked. 480 was the results on my fasting blood glucose. Several shots of insulin later I got a ride to the hospital for 2 days. Everything was whacked out and nothing was in range on the blood work.
Strict Keto, Sub 15 grams of carbs, starting on Jan 10 2020 and a year later I was fairly stable, non diabetic. "blood glucose around 70", dropped weight from 268 to 162, and Felt great with the exception of my fingers from me testing Glucose 4 times a day.
post fasting test. This was not planned, during a water only fast. January 5th 2010 Doctors Orders
total cholesterol was 228, LDL was 128, HDL was 52, and Triglycerides were were 152.
my last test was 4 months ago and was total Cholesterol 182, LDL 140, HDL 54, and Triglycerides 59
This is on a "Dirty Keto" with approximately 50 Grams of carbs. Blood glucose testes daily @ 5 pm and eating one meal a day at 5:30-6:00 averages 65-80
As long as my Blood work stays in check, I am moving more toward a Mediterranean diet for a greater variety of healthy foods and lowering my saturated fats to a small degree.
long winded reply to give context. hope this is what you wanted.
@@NickWestgate had my scan with and without contrast so plaque and calcium show up. combined score was 42 @ 62 years old. Not perfect 0 but former 45 year heavy smoker, diabetic, and party animal abusing everything. I had expected something in the 600 range based on friends testing with similar lifestyles.
@@philloderThat's pretty good considering! I probably have soft plaque and will eventually get a non-zero score (I'm only 53 now) but getting a zero keeps the doctors happy for now. Looking forward to Nick and Dave's papers so I can wave them at doctors. LDL is only part of the puzzle so I look forward to the field moving forward and finding the root cause.
As a LMHR, this exact topic has me in awe/perplexed too. Love eating low carb, beef heavy diet but am not dogmatic about it. The people need an answer to this question.. appreciate you doing the work!
Wow! This was very good. I hope People will understand that we still have to address the ApoB problem for everybody that is not a LMHR. Most people that have elevated LDLc and ApoB are not on a LC diet and don't have the triad. My patients that don't want to address their high LDLc with drugs or even supplements are in that camp. Still for the LMHR I hope you show that they don't have to worry anymore. Thanks again!
One leg of the triad may have already crumbled, the belief that high HDL cholesterol is protective. According to Dr. Dayspring who is an expert on cholesterol, HDL at 60 and above tells you nothing about what is going on in the body. It just indicates that there is too much cholesterol in the blood. He also maintains that the tg to hdl ratio is worthless.
Nick, you are a gift to this world. Ty! ❤
I haven’t yet had access to an investigation that could determine whether or not any plaque has formed in my 4 years of seeing this pattern in myself since I went low carb. Because of this, I yo-yo between trusting my body and panicking about the LDL levels and the ‘area under the curve’. I follow Dr. Attia and when I heard his take on this in recent podcasts he’s been on, it was anxiety central for me.
It’s reassuring to hear the issue being discussed, even if we don’t know anything for sure yet. Thanks for the video!
Thank you. Clearly, I'm not aiming to give false reassurance. But I think the discussion needs to be had and has, thus far, lacked nuance on the LMHR topic. I think I could help there and believe Peter is open-minded enough to evolve his opinion. And I would offer the same open mind and willingness to shift opinion if forced by reason and/or new data
I feel ya. I feel and operate better on low carb( good energy, low hunger, effortless weight control) but all the “science “ saying how bad it is does create some doubt. Really looking forward to the lmhr results to go to my doctor with.
My husband is in the same boat. Most of what I see is high ldl and zero CAC score. What if your score is 1300 and it went UP despite your keto diet? This is where we are and it's frightening. Husband is a LMHR and very fit. Nobody would look at him and say he was a heart attack waiting to happen...except the cardiologist. So we do olive oil and try to limit animal fats because we see the former lowers ldl, the latter raises it. He is on repatha. He caught covid earlier this year and it really kicked his butt...and he has joint pain now. I think its the low ldl. We seem to be damned if we do, damned if we don't.
@@iss8504 , Is repatha a statin? Statins could cause higher CAC score because it calcifies the soft plaque as far as I know. Olive oil can be pesky. You have to be extra diligent choosing the brand as its often adulterated with seed oils and/or oxidised.
@@lukelacey101Repartha is PCSK9 inhibitor. It does not increase calcium. It reverses plaques for many people. But it didn’t do anything for me. So I stopped taking it
Such a great video, its nice to see someone who truly is trying to understand something regardless of the outcome. Subscribed!
There's no shame in being wrong, as long as you're true to the scientific process
I love Nick's disciplined approach. Very much looking forward to seeing how the evidence unfolds. He restores my aspiring citizen scientist awe.
Thank you, Dr. Norwitz! The discussion is encouraging.
I presume the major difference of LDL between LMHR and FH is the duration that each LDL particle remains in the system and thus vulnerable to oxidation. With FH, I would expect much more oxidation, and perhaps no oxidation in LMHR.
Excellent point
Thank you for being curious, intelligent and willing to do the hard work for answers! I'm impressed!
Cheers :)
Love you men haha I feel Peter is a true scientist and he will reestructurare his opinion about LdL in LHMR in a future. Keep doing this awsome content
I hope so.
Attia knows all about the lmhr phenotype .He is promoting statins by saying nonsence about elevated ldl in the context of a healthy metabolism .He is delibetately deceiving people for financial reasons . The sad thing is that many people end up on statins when their metabilic health is good ....all because of the Attia types .
Dr. Attia is not a lipid expert. He will follow the lipid experts like Dr. Cromwell and Dr. Dayspring and they know that ApoB is causal for heart disease. That underscores the importance of LDL cholesterol in heart disease, since the greater the amount of LDL-C, the greater the number of ApoB particles to transport it in the blood. And those are the particles that pass through the artery wall, become oxidized and cause plaque to form. High saturated fat diets cause LDL-C to explode. Same for ApoB, increasing the risk of CD. And according to lipid experts, high levels of HDL-C are not protective. So I think this concept of the LMHR is going to self-destruct when the lipid experts get at it. Dr. Cromwell has already expressed his view in conversation with Dave Feldman that he doubts it has any value. He said he was not convinced.
According to David Diamond, the heart disease with people with FH is related to factor 8 clotting factors. According to the research that he has covered is the people with normal clotting factors do NOT have unusual heart conditions.
Yes, I was thinking about during this. We really need to understand the etiology of FH much better than we currently do. Also the hazard ratio of ASCVD/CHD is only about twice the general population (of course tragic for those people who do develop). So there any many many people with quite high LDL-Cs that never develop ASCVD! How can ApoB be so powerfully causal when this is the case? Definitely something we're missing...
@@davidgrimes4726 Yes. This is what drives me crazy about the climate change people. Nearly all of the variables relationships to each other and temperature are virtually unknown. Feldman is filling in another brick of the wall for sure. I’ve seen other evidence that injured blood vessels are what signal the body to apply a bandage of cholesterol and we know for a fact that cholesterol is used for healing. William Davis of Wheat Belly fame has shown evidence of reversing cardiac plaques.
Absolutely need more clarity on FH. Attia says it's defined as LDL above 190; Dr. Casey Means says it's only above 300. ? And why do we assume any high LDL must have genetic causes? Appreciate Nick's passion for lmhr, but the larger cohort of FH also needs some attention.
Such a great video and, so respectfully done. Many people are looking to pick a side in an argument, so it's great to see someone so interested in finding the truth. Nice job, sir.
Plaque accumulates in damaged sections of the coronary arteries. This is where the pressure is highest. The particles are forced between the layers of the arterial walls. So, for plaque to form, that portion of the artery would already need to be damaged. Once the artery is compromised, any particulates in the blood stream become potential plaque media.
oh, I like this...stealing it
Stuff like nicotine, high blood sugar, blood pressure, and more can cause arterial damage, plaque is essentially scar tissue buildup from chronic damage.
@mikafoxx2717 - Dk you think oxidized fats being transported by LDL could be scarring the arteries?
So the issue wouldn't be the LDL itself, but the types of fat being transported? Could even be a certain Fatty Acid
Nicotine?
@@NutritionPolice It's the carrier of the cholesterol, the ApoB lipoprotein that gets oxidized, causing plaques to form. The ApoB particles can pass through the artery wall and get stuck there. They then get oxidized. This is the origin of heart disease and it's causal. LDL-C doesn't predict heart disease well. ApoB can diverge from cholesterol and is a good predictor. Nor is inflammation required as a precondition. Eat a diet high in saturated fat and your risk of heart disease will shoot up, as your ApoB # does the same. That's the danger of high saturated fat diets- they lead to an explosion of LDL-C AND Apob particles. I don't believe that HDL-C is protective. A high level is not good, it just indicates that there is too much cholesterol in the blood. I think Dr. Norwitz and his colleagues are wrong for believing that high HDL cholesterol is protective.
Love the work your putting in Nick. I'd listen to you all day talk about cholesterol than Dr Attia. Great job getting your details across, easily understood.
The thing I can't stand about Attia, in this interview, is he keeps saying that LDL is "causal", when it's clearly not causal. It's one of a plethora of signs someone has when they do have CVD. But by his own admission not everyone with high LDL has or will develop CVD. It's like that recent study released talking about erythritol being bad for you, when they didn't test for intake, they only checked sick people for erythritol, who's bodies are known to naturally produce more of it. So you take a sick body, you find something in it, and you then call it causal? That is not above board, that sounds more like p-hacking to me.
Yes.. he lost me at causal. A correlation maybe.. and then we can debate
Oh my. Anyone who call himself an expert and doesn’t understand the difference between correlation and causation should work in some other field.
It depends what they mean by causal. If they mean necessary and sufficient then of course not.
@@isaacgarzams Got it. Thanks.
I want you as my defense lawyer@@isaacgarzams
Appreciate your efforts to get to the truth. So discusted these days that so much "science" is financially motivated. 56 years old and from 7/1/22 to 11/30/23 have lost 124lbs eating between 10-20 total carbs per day, and managed to add muscle at the same time. My lipid panel shows exactly what you have described with elevated LDL/HDL and lower triglycerides. Never high LDL when my diet was terrible and I was in terrible health and shape. Doctor mentioned Statin at last physical and I declined informing him of how my diet was direct cause and I currently wasnt very concerned. Looking forward to showing him the final results of the oreo/statin study, because I believe I know what the results will be. Will stay tuned, thanks again.
Thank you for this. And I cannot wait for the research coming out, as an LMHR!
I love your approach to this topic. You're definitely positioned in the right place. I'm looking forward to more from you in this space.
You will go very far young man! Please keep up the great work.
Peter Attia looks and talks seemingly professional, but he is trapped in his own dogma, which makes it hard for him to understand the lipid energy model.
He finds it hard to believe what he has learned is wrong.
His book Outlive sucked too. Very pointless compared to many other, better books on the topic.
And Attia is friend of dayspring. What I can expect as a scientist.
This is lovely. Thanks for sharing Nick. I'm a lmhr and flip flop between thoughts a lot ! Aka Nuance. Its such a nuisance but we'd be no where without it. Keep up the fantastic work ❤
I love both you and Peter for how much you love science and how much effort the two of you put into educating the public. I appreciate how precise you both are and the attention to nuances. I have genetic lipid dysfunctions(APO E4 and very high lp(a)). My lipid numbers were bad on ordinary diet, and my ldl-c skyrocketed even higher after I went on ketogenic diet with very low triglycerides and high HDL-c. I am lean and I work out. So I suppose I have both the genetic FH (my dad is in the same situation) and LMHR phenotype. So learning from the two of you have helped me find a lifestyle that I am comfortable with. I take Fenofibrate to control my lp(a) and continue my ketogenic diet to control inflammation. Saturated fat is good for my lp(a). And since Fenofibrate normalized my APO B, now I can eat a high saturated-fat ketogenic diet without any fear.
I'm ApoE4/4 and have high Lp(a) from my dad's side... sounds like we have quite a bit in common. Thanks for the kind words
I’m heading to LA for my second LMHR study visit in a couple of days. Given all the improvements in my health, the low carb
Thank you for the information you put forth. Being on a keto diet for a year my last test came back with LDL as "high" with high HDL and low Triglycerides, my doctor was very concerned and I was shocked to see the result, previous tests being "normal". Your information is helping me understand that there is more to it than meets the "normal" eye
Nic, never loose the awe.
You have a great future ahead of you. Keep up this fascinating work.
Could you please point out the studies that show _how_ LDL particles (or ApoB) generate atherosclerosis?
I am very interested about this as well after reading Dr. Kendrick's "The Clot Thickens", where he presents some evidence and histological samples that appear contrary to the hypothesis that LDL is atherogenic.
I don't feel comfortable dismissing mainstream medicine, *especially* as a layperson, but they don't do a great job presenting their case either. Even Dr. Attia, who is a great communicator, hasn't presented particularly convincing evidence -- Mendelian randomization has caveats that he doesn't address, for example.
Wait, let me look...sorry couldn't come up with anything
I also recommend Kendrick's book! He explains that LDL is identical to another lipoprotein called LPa except LPa has an additional protein scarf on its' surface called Apo(a). LPa goes to sites of damaged arterial linings and helps plug up the defect along with other blood clotting factors. It also stabilizes the clot so we don't bleed to death.
There is a special tissue stain which can be done in the lab on removed plaque to look for Apo(a). Sadly, it isn't ordered, so doctors don't know.
there's no such thing because that's not it works, inflammation causes arterial damage and over time arteriosclerosis. Reduce carbs and fructose as a start, they're causal agents
Taking your bike to work, is fairly common here in Denmark. A part of this is getting a flat tire now and then. The more you ride your bike, then more punctures you will experience. Is riding your bike causal? Demonstrably, biking less would result in fewer punctures, but so would better and cleaner bike lanes.
Almost 10 years ago, did Attia launch a video, Straight Dope on Cholesterol. He CLEARLY states, that if there is no room in the subendothelium, you don't have atherosclerosis. So, what causes this "room"? What causes endothelial dysfunction? Why do diabetics have higher risk? The arrow seems to point very much at glucose (and possibly our ability to clear it).
Dietary glucose seems to be considered as necessary as breathing, but could it be the degenerating agent through lifelong exposure by elevating your bloodsugar 3-5 times a day?
AHS12 Peter Attia, MD - The Straight Dope on Cholesterol
The statement is about 19 : 30 into the video.
Glucose may be necessary but the level of glucose seems to be strongly managed to be between 70 and 140 with consequences for going under 60 or over 180. "Nourished by Science" suggests that if you keep your BG between 70 and 140 you are probably fine.
This suggests that BG over 180 for extended periods likely has some seriously bad health effects, certainly I know from experience that going below 60 does.
@@capnkirk5528can you disclose what bad health effects you had from going below 60 BG? I assume that you are a carb burner as I have never heard of fat burners with bad effects from BG numbers below 60 due to high ketone production.
@@francisvlatko2834 Reactive hypoglycemia". I believe it's common, but I don't actually know (except I know it's common in MY family).
Extreme hunger, shakiness, sweating, pallor, tachycardia. If I'm driving I have to stop (not always possible) and eat something sweet like a diabetic, but I'm not diabetic.
I can trigger it with lots of things - easiest is a double bowl (2 pkgs) of Maple Cinnamon Instant Oatmeal with no other food. Spikes my BG WAY up and then I will almost always crash below 60, and if I'm not careful I WILL pass out. Repeatable.
And yeah, that's carb-burner. I have to fast for at least 24 hours to even start to get into ketosis, and eating ANYTHING seems to knock me back out.
Diets high in saturated fats lead to cholesterol synthesis and increases in the ApoB lipoproteins that transport it in the blood. Those ApoB particles can pass through the artery wall, get stuck there and become oxidized, leading to plaques being formed. No other condition has to be present for this to occur.
New subscriber. started following you through Dr Ken Berry interview. You are a shooting star and I want to watch your career. Thank you for doing what you do. BTW, I'm 62 with congenital heart issue (HCM obstructive) I'm doing great now on carnivore, labs are beautiful except slightly high LDL. I'm in for the long haul now as I've had a lot of other things clear up and go away with this eating plan. :)
@nicknorwitzPHD
BIG QUESTION to Dave Feldman, Dr Budoff or Norwitz:
The criteria for LMHR is
- LDL >200
- HDL >80
- TRG
New subscriber! I appreciate your calm, non judgmental presentation about facts. I watched some of their conversation and I found it very judgmental, as in a “why do those people even think that, they are so willfully blind” kind of way.
Peter Attia does not know how molecular causality works, which makes sense, med students are not taught like phd students when it comes to statistics and necessity vs. sufficiency; spoiler alert, for a factor to be *causal*, it must be both necessary AND sufficient, not just necessary (what he claims LDL holds); another spoiler alert....causality has to do with wound healing responses (local inflammation) and immune cell activation, which triggers plaque formation....it helps (more plaque and future narrowing) if that plaque formation cannot be recycled once the inflammation ends, which has to do with certain genetic issues, carcinogens/xenobiotics, immune cell defects
What do you think would happen if someone with LMHR were to take Berberine?
Peter can take that Mendelian randomization and get outta here. It is firmly contradicted by real world results. In the most simplistic analysts, when 2/3 of heart attack victims have normal LDL, that should be a strong hint.
MR have their place. But causal ≠ sufficient, and congenital/genetic ≠ metabolic response.
@@nicknorwitzPhD Agreed, yet I see PA and TD setting forth MR as the final answer, end of debate, no need to look at any other evidence, and those who discuss further are ‘deniers’ (or some other pejorative). And as an added bonus, ignoring harms.
Normal in a society where the biggest killer is heart disease. Just means the levels need to be set lower.
Just curious as LDL-C is not a true indicator of heart disease. It is sdLDL or ApoB, what was their ApoB level in those analyses?
Thank you Dr Norwitz for your high level analysis and research into this fascinating and potentially ground-breaking area of medicine. I have a very personal interest in this field of study as I am a 65 year old LMHR woman. My CAC score at age 63 was 0. I am fit, healthy and have no reason to change my low carb, high fat diet from a quality of life perspective. My well-meaning physician is a fan of Dr Attia and continues to want to lead me in the direction of taking a statin. I have no intention of trying to fix something that is not currently broken. After 10 years of eating this way I believe that if high LDL was directly associated with cardiovascular disease I would have demonstrable features of it by now. I may agree to another CAC score in another few years but it would be more from an academic perspective than from anxiety around my way of eating.
Have you done any interim CIMT ultrasounds (like cardiorisk dot come) does to look at intimal thickness in the carotid artery?
Doctors sure spend a lot of time looking for something to treat.
Fantastic - Thank You!
Thank you Nicholas Appreciate the civil discourse,
regarding LMHR,
1- in my understanding there's a meta analysis of 12 RCTs that showed increasing HDL without lowering apoB doesn't reliably reduce cardiovascular events, also mednelian randomization have shown that neither low HDL nor high HDL alone affect cardiovascular risk
Study name : (Effect of HDL-Raising Drugs on Cardiovascular Outcomes: A Systematic Review and Meta-Regression)
2- for triglycerides we have an RCT that showed that reducing TG by 26% also did not affect cardiovascular disease
Study name (Triglyceride Lowering with Pemafibrate to Reduce Cardiovascular Risk)
from these points i understand that both HDL and TG are mere bystanders when it comes to cardiovascular disease
While we agree that apoB is causal
So why would LMHR, which raise HDL and lower TG (bystanders) but increased apoB (causal)
Not increase cardiovascular disease risk ?
Feel free to correct any misconceptions or assumption i made
You can't just assume that raising HDL or lowering triglycerides via drugs should have the same (positive) effects as increased HDL or reduced triglycerides from changes in diet/physical activity/exercise/body composition. And so you can't conclude that if those drugs don't show benefits that it's evidence that increased HDL or reduced triglycerides from diet/exercise are bad indicators of CVD risk.
You can't conclude either that high HDL-C is protective. Dr. Dayspring, a lipid expert has said that high HDL-C, which he defined as 60 or above tells you nothing about what is going on in the body, except that there is too much cholesterol in the blood, and that is what happens when uou get an explosion in LDL-C on a high saturated fat diet.
Found you via Anthony Chaffee. Amazing, data driven, real science and communication. Opinions and assumptions need to be countered with facts and evidence based science. Awesome work man, I have struggled with some of Peter’s opinions and beliefs around food and cholesterol. Exercise and VO2Max is indeed important, but not as important as what we eat and drink etc. cheer N, keep rolling, it’s well needed.
I thank you so much for your prospective that as far as I can see is right on . Your extra training with your PHD has been a help in explaining many mysteries that the medical community
does not seem interested in . I have been low carb for 3 years now and I feel so much better than before . Keep up the good work .
Wondering you're aware of the alternate hypothesis of the mechanism of atherosclerosis as elaborated by Dr. V Subbotin. Looks like it could account for many of the contradictions in cholesterol-heart theory, such as why LDL has such weak correlation with events. If we have the initiating process wrong, no good solution will be found.
You have the initiating process wrong, but like most commenters don't know that there is overwhelming evidence for how the process of heart disease is caused by ApoB lipoprotein particles passing through the artery wall and getting oxidized. I described it in another long reply.
@@newyorkguy158 I know very well the process proposed by Subbotin is not the conventional one. But it explains the actual pathology better, ie. the conventional explanation is wrong.
The actual concentration gradient of LDL particles is opposite to that predicted by the narrative you subscribe to. V Subbotin has proposed that neovascularization of the tunica intima is the source of the lipid particle, rather than penetration of the endothelium. Another failing of the conventional narrative is explaining why the particles only pass through coronary endothelium but nowhere else.
www.ncbi.nlm.nih.gov/pmc/articles/PMC3492120
I am 18.5 bmi/ LDL 160, HDL 94, triglycerides 52. I have been on the ketogenic diet with a daily fasting window of 18 hrs. for approximately 4 years. I wish I knew what my lipid panel numbers were before I started the Ketogenic diet but I have no idea. I am experiencing the common push from my doctors to begin a statin due to my LDL. Interesting that there is never an acknowledgement or seemingly a recognization of my HDL/ triglycerides ratio. We sure have a way to go but I am so thankful for the powerful research your team is doing. I feel fairly confident in refusing the prescription for low does statin especially concerning my predisposition to Alzheimer's. Thanks! Looking forward to more data to come!!
This is exactly the situation that I am in. "High" LDL (150 to 200), HDL consistently about 80, and Triglycerides range from 40 to 60. I.F. for 7 years, Keto for 25 years this month. My doctor thinks that when I refer to my excellent Triglyceride and HDL values, I'm merely trying to say that those two things mitigate against my high LDL. But that's not the point. The point is the low Trig/HDL ratio is an indicator that the LDL is of a different type (large particle, non-oxidized,..) that is not even statistically associated with disease. In fact, I've had that independently checked, and, yes, my LDL is the large particle type.
@@TheFrankHummer yes, mine as well.
I don't think the triglycerides to HDL ratio means anything. Dr. Dayspring, a leading lipid expert has said that HDL 60 and above is too high and only means that there is too much cholesterol in the blood. I don't think HDL is regarded any longer as protective against heart disease since the Eli Lilly HDL raising drug in clinical trials failed to prevent heart attacks and strokes and was rejected by the FDA. You need to lower your ApoB by restricting saturated fat and taking a statin.
@@newyorkguy158 That's a good point you bring up about the HDL. But I think HDL is a good marker of good health if it happens naturally. I don't know what else the HDL-raising drug does besides raise a person's HDL.
@@TheFrankHummer According to Dr. Thomas Dayspring, a well-known lipid expert, who has written chapters in medical texts on lipids, HDL tells you nothing about what is going on in the body. I would look him up on YT. He has given a lot of lengthy interviews. See Dr. Carvalho, MD & PhD on his channel, Nutrition Made Simple and Simon Hill for some very informative interviews.
Well articulate Nick
We love you too!!!! thanks for your dedication and hard work 🥰
Awesome video. I've watched Drs Peter Attia's, Ken Berry's, Roy Taylor's, and Robert Lustig's videos and am in awe of the research, discussions and professionalism in the questioning of the status quo, even if it turns out that the status quo remains the same. I expect that new research will impact future cardiac and type 2 diabetes clinical guidelines.
There are 2 kinds of doctors and health experts. The first group are guys like Dr. Berry and Richard Johnson. They completely understand humans were created by evolution, and see health and health science through that perspective.
The others are what I call "science chasers." Guys like Layne Norton, Peter Attia and Jack Kruse look purely at science, and scientific principles to understand health. They only look at studies, draw conclusions, and make decisions based on scientific principles and evidence.
The problem with this way of thinking is that biology is too complicated to understand it completely. There is, and always will be too many unknown variables that can completely destroy your hypothesis...
Most all animals that are free of genetic diseases and mutations are perfectly healthy when they live and eat in their natural environment. That's what instincts are for, and why they adapted to be that way...we do best when we adopt an appropriate diet and live in our natural environment which our instincts were adapted for...
There is no substitute for living a natural life when it comes to metabolic health...
you're wrong in fact, the likes of Peter don't use science, they use junk science known as observational studies to perpetuate their lies. We need to be really clear what it is that they're doing, they're lying to the public!
I’m not sure I believe the claim that animals are completely healthy in their natural environment eating their natural diets… is there data on this? Don’t most wild animals die from other causes?
Greeting Nick, I was hoping you would address these issues. From my perspective, the FH definition is advantageous to prescribing statins, if the condition is labeled genetic that helps the doctor convince the unaware that they should have one or more statins, (which provide lifelong profits and cause even worse health outcomes and even more drugs etc.) I am a LMHR, my LDL peaked at 230 which required me to change my carnivore diet. I started eating around half a cup of potato pre work out and, dropped all tallow and have been using avocado oil (per your online comment). I work out around 7-9 days straight then take one day off. At 68 years old this is getting challenging for recovery. A recent LabCorp test: Absolute Triglycerides 23, Absolute HDL Cholesterol 111, VLDL 4, Total Cholesterol Cal 229, and the Calculated LDL Chol (NIH) 114. I do not understand the math behind the LDL number, seems high per the 229 total. Can LDL be lower than HDL in some extreme cases? Is the lab algorithm forced to generate a higher LDL number? Regards and thanks!
Causal? I don't think that has been established at all
Stop coming across as rational
Causal, yes. It's part of the causal pathway. But it's not sufficient.
@@nicknorwitzPhD By that reasoning, it would seem platelets would also be causal, and further along the line of reasoning, blood, heart and a brain signaling to that heart, and by further extension, anything that leads to that brain being on, is causal to heart disease. If you have a group of hikers coming in with shattered shin bones, except for one that comes in with a bloody hammer, you don't blame the hiking.
I hope someone can give me some advice. I'm kind of confused on if I'm good or bad with the cholesterol. Here is my breakdown. I have spent alot of time on my health and nutrition the last 4 years. 4 years ago my basic numbers were.... over weight, 5'6 210 lbs. 25.75 bmi. 36 waist Pre-diabetic, reactive hypoglycemia, always tired, fatigued, depressed, joint pains always, plantar warts all over my feet. Dry and itchy skin and sinus and nasal drip every morning. Also would almost pass out upon waking in morning because of reactive hypoglycemia. Strangely, although I always felt horrible and having a glucose of 110 on average and borderline high blood pressure my cholesterol wasn't too bad. It was 120 LDL, 120 trigs and 50 hdl. Total was about 190-200. Here are my new numbers after training, studying nutrition and going on a low carb keto/carnivore program. 5'6 152 lbs. 23 bmi (sometimes lower). 31 inch waist. All ailments gone. No more pre diabetes...a1c is 4.9. No more reactive hypoglycemia, no more sinus or nasal drip or dryness or itching. All plantars warts are gone. They disappeared less than 6 months on keto. No more achy joints. Tons of energy and feel great. 2 meals a day with int fasting 8 hr time frame not 6. It actually didn't work as well. Never tired. No more depression. Ok....here we go... Trigs dropped to 67 and hdl went up to 77. But.... which I wasn't too surprised the LDL went up to 170. Ofcourse the Doctor freaked about LDL and could care less about the hdl and trigs. I decided to pursue a naturalpathic doctor instead and he set me up for some tests. Advanced lipid panel. Low lipoprotein (a). Cholesterol pattern A large fluffy not small. Homocysteine low and excellent. Hs-crp very low and excellent no inflamation. All kidney and liver tests excellent. Had several inflamation markers done all great. Had ekg and stress test...all good. Even had a Cac score of 0. Have one every year and 0 the last 3 years. Out of everything only questions I have is any advice on the high LDL and high apo b which I heard coincide with eachother.
LDL-C and ApoB can diverge. ApoB number is more important. Reducing saturated fat and taking a statin will reduce ApoB.
Thanks for all your work. Keep it up!!
I hope you can grow your channel ! Excellent video, thanks.
Brilliant clear nuanced and compelling. Thank you
Welcome
Nick thanks for these videos. I was going crazy with fasting, eating clean all because my total cholesterol (230) and LDL (154) were going up test after test. Once I watched your videos and realized I don't care because every successive blood test my other levels for TG (65), HDL (65), VLDL (11) were going down. This all started to happen when I hit my mid 40s.
Incredible video Nicholas. It make me wish i was smarter lol. Dr. Attia is a smart man but doesn't have every single answer. Its great seeing guys like you challenge great minds like Attia. I subscribed.
Fundamentally, Peter says LDL is causal. I would like to see what he is looking at. Dont studies show 1.2 risk ratio at most with many studies showing a lower than 1 risk ratio. If you agree high LDL is causal, you concede to Peter's position. High LDL in our case just indicates healthy energy transport.
The LDL levels plummeting after introducing a small amount of carbohydrate would support this idea also.
Have a read of: Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel
High numbers of ApoB particles CAUSE heart disease. The more cholesterol that is synthesized from saturated fats, the greater the number of ApoB particles needed to transport the cholesterol in the blood. These particles pass through the artery wall, become oxidized and form plaques, leading to inflammation.
So thorough and thoughtful. Thanks.
We just started keto 6 weeks ago because my husband came up with high cholesterol. We got his new blood work done and he has even higher LDL but his triglycerides normalized. I suspect he is LMHR. His pill pusher Dr is mad he didn't take his statins (a decision we made based on risk factor analysis). Our original plan was to do Keto for 6 months and see where we are and re-assess statins then, but its all more complicated than that. We are going to make an appointment with a keto doctor in our state to help us make sense of his charts and tweak our diet.
Drs get paid for prescribing 🤑🤑. You lost him money
If LDL is that bad, just tell your husband to eat a few oreos before the blood test.
Your husband's case is typical of what happens to people's cholesterol when they go an a high saturated fat diet and I believe it is extremely dangerous.
@@newyorkguy158 no, experimentally very high saturated fats lowers LDL (and TG) as a result of adipose anabolism. The cell membranes consume the LDL and TG to grow in size to store more fat.
The reverse is true when hypocaloric or when MBR upregulates (ie, low torpor dieting, or high activity), LDL, HDL ramp up, and TG normalises, as the adipose shrinks. HDL increases due to high LDL turnover.
@newyorkguy158 -- you think it's dangerous because you're wrong and misinformed all throughout this thread. You're on statins and low fat, I get why you're depressed but keep your ill informed bs to yourself
I don’t know if Dr Attia addressed the low levels of LDL in almost half the CVD cases. How would be explain that?
Or cancer.
Is that a trick question?
indeed, even accounting for LDL levels dropping following a CVD event, it doesn't change the fact that we are talking about a bell curve instead of a progressive line / curve
Just means that the safe levels of LDL have been set too high. Normal in societies where the leading cause of death is CVD is not actually normal
@@llicit1833 it's a bell curve, not a dose response, so very little to do with LDL, as long as you have other issues damaging your endothelium, the only safe level would be zero, and that would kill you
Love your take - I'm LMHR my self
Nick, I am a patient of Dr Nadir Ali the low carb cardiologist in Webster TX. You should talk to him about your medical career plans.
So fascinating. When I was a heavy drinker on a SAD diet, I have labs with LDL around 150-200 mg/dl; 10 years later on Carnivore or Keto, I can get my LDL as high as 500-600 mg/dl. This obviously made me severely skeptical of focusing purely on one data point. I'm 6'1, and have never been over 190 lbs. I love the work you and your team are doing!
I'm pretty much in the same boat. But my LDL is still high even increasing carbs and reducing fat, especially sat fat.
My labs always say suspected FH but genetic testing says I'm not genetically predisposed to CVD risk. I figure I'm a LMHR but suspect I should be on a statin.
@@6789uiop If I eat a paleo/animal based diet with carbs from fruit, tubers, veggies etc, I'll have a total cholesterol of about 300-350. I'm currently trying a bastardized version of "slow carb" with red yeast rice supplementation and will be getting labwork in the next few weeks. I'm just trying to lower LDL to get more life insurance. If that doesn't work i'll try the Feldman protocol and then quit caring about LDL in isolation forever. BTW I tested negative for FH and have a CAC score of 0.
@@IH8CA Grats on that CAC zero! My Tot CHO is ok w/ Dr's because my HDL is always 58-60. My trig:HDL is just above 1 too. The gene test I did, Color, stated no FH but gave a big qualifier on it as well as for apo-B.
I was researching red yeast rice but as it's actually Lovastatin I felt I'd get a more accurate and purer dose if I just took the Lovastatin. There's probably USP red yeast rice tho. I never did take it. I took Atorvastatin for a couple weeks and my calves cramped so bad I couldn't walk.
Many years ago Feldman did an n=1 protocol for lowering cholesterol for say... presentable labs purposes. Me, I just quit fat for a while and it dropped to high normal and I got insurance in the country we now live in.
LDL 171, HDL 59, TG 60, TOT CHO 223 fwiw, blood sugar great, vit D 84
Very respectfull comments! Congrats!
Glad to hear Peter is facilitating connections between some of the movers and shakers in this field and the emerging data and science around LMHR. I am completely open to ezetimibe or other compounds to drastically reduce ldl/apob, assuming I can maintain my current therapeutic benefit and get a net win on ACM. Let's see how LMHR shakes out first though, being in my early 30's I still feel comfortable with a bit of risk in this regard considering how otherwise healthy I feel.
As a person who eats Keto-Carnivore partially for mental health, it is frustrating to see people put on stains and then medication for their depression or anxiety, etc. due to the side effects of the statins...
Thank you for what you do!
Really good piece Nicholas, all very humbly and articulately framed. You have a new subscriber to add to your no doubt quickly growing cohort.
Thank you very much!
What I find fascinating is that they don't see the similarities between LDL to atherosclerosis and oxygen to fire.
Oxygen is causal but not sufficient for fire.
They too would never accept firemen to answer the question " What caused my house to burn down?" with "Oxygen in the air caused the fire."
But with CVD,.. "LDL-C caused your atherosclerosis." is considered completely acceptable.
I know, fire is a stupid analogy,.. but really,... It is not.
It just makes the LDL-C argument look stupid.
Yes, but also the fire cannot exist without the oxygen. So, remove oxygen from the scene and fire will neither start nor spread. All kinda arguments out there. 😊😊
I think it is a great analogy!
O2 is necessary, but not causal. The faulty electrics (or whatever) are causal.@@yoso585
Higher levels of cholesterol lead to increased ApoB particles to transport it in the blood. The ApoB cause heart disease in a process I have described in other replies.
12:46 I heard Cardiologist Nadir Ali speaking about how insulin spike has something to do with lowering LDL which might be the case when consuming Orea cookies. Sugar and Fat mixed together.
Seeking truth, no finer vocation on the planet. And you don't have to dump on alternate views to implement. Keep up the good work.
Thank you for your excellent presentation. I was unaware of LMHR and appreciated your clear explanation and analysis. Keep up the great work, Nicholas!
Awesome commentary - great questions ... and, as important - respectful!
Thank you for such a measured and intelligent perspective. There seem to be a lot of folks out there speaking with certainty on topics where we probably don't have enough data to make a perfect decision. And I think there is definitely a big difference between "the data we have so far seems to suggest" versus "you're taking big risks with your health if you do this".
The difficulty I have with any claims about the low level of adverse effects from statins, other cholesterol lowering drug, and for all drugs for that matter is that the system for identifying and reporting adverse effects operates in a way that ensures adverse effects will be under reported as long as a significant number of people are not dying as a result of the drug.
Statins and other cholesterol lowering drugs are perhaps among the most egregious examples of under reporting adverse effects.
First, initial clinical trials and subsequent research exclude any test participant who shows any sign of adverse effects during the pre-trial run up period. That is a logical thing to do, because it is important to have participants who have a high probability of being able to participate for the full run of the research effort. However, in calculating and reporting adverse effects the pharma companies and researchers then exclude data for pre-trial participants who were removed from the research. It is impossible to know the impact on adverse effects reports from drug trials and drug company sponsored research because the drug companies do not release their datasets for independent researchers or the FDA to examine. The datasets are treated as confidential proprietary information.
Second, because of the low incidence of adverse effects reported from the clinical trials and an almost cult-like belief among pharma companies and doctors that claims by patients of adverse effects from statins are not real, doctors do not report statin adverse effects from clinical practice to the FDA at anything close to their rate of actual occurrence. Instead, pharma companies claim and doctors attribute patient reported adverse effects from statins as being either normal aging or the nocebo effect.
Third, patients do not take advantage of the opportunity they have to self-report adverse effects from statins or other drugs. In the case of statins, doctors significantly under inform patients about potential side effects. Doctors do not appear to inform patients that if they experience adverse effects there is an FDA reporting procedure patients can use to report the adverse effects they experence.
As a result of the flaws in the system for reporting adverse effects, doctors such as Peter Attia and many others, can make statements about statins' benefits outweighing their [supposedly] minimal risks and do so with a straight face.
Peter is quite misguided on this matter. There has been a real failure of his to acknowledge gaping holes in the apob concentration hypotheses. Over the years he as completey ignored the DATA on FH. There are indeed studies that analyzed the longevity of FH homozygous carriers. These studies do not indicate a shorter life span overall. This then is a problem that Peter seems to continuously ignore. In a population of so-called, very high risk, you would expect to the majority to parrish at leaat by middle-age. NOPE.
A number of studies/ analyses have clearly shown that although there are some people who die in the first 2 or 3 decades of life, life expectancy actually goes up. By the time these FH carriers are in their 60s their life expectancy goes up. This is also true of people in the general population. Hmmmm
How do you explain a drop in mortality with those with FH ( very high apob) in there 60s, 70s and 80s?
Peter is married to his hypothesis and is a victim of his own preaching and teachings of evaluating the evidence base. Confirmationly bias.
A failure to explore and properly evaluate the nuances within the FH community is quite revealing. A complete failure to recognize that there are sub populations of FH patients and these segments need to be examined independently is of significant importance. It doesn't allow for proper context. Peter has left out important elements and the nuance. This is the stuff a strawman is made of.
If Peter bothered to do this or actually listened to others that have conveyed a well articulated response to Peter's view of FH, he would have likely changed his mind or at least considered it.
People with FH aren't all created equally. There are subgroups with known genetic variants in the clotting cascade.
FH carriers have the same risk profile as those without FH.
This is quite a bit more nuanced than the way Peter has characterized it. I encourage all to look at the FH studies
It is worth investigating those studies to evaluate for yourself the differences within the fh community. What accounts for these differences between fh subgroups?
Please have a look at the data 🙏
One thing I have not heard Peter address ( he may have and I haven't found it yet)is the polymorphisms found in a subset of people with polymorphisms genes/proteins involved in the clotting cascade.
There is data that shows polymorphic changes that a subset of fh carriers are inclined to have, and this is an independent risk factor for coronary events. This and other variables not discussed by Peter need to be considered inorder to properly evaluate the problem. Peter simply hasnt considered the entire picture. You can evaluate for yourself by lookong at the data.
Yeah, that part confused me. He and Dave Feldman had a long conversation (I think on his podcast?) where they talked and somewhat debated all of this for quite a while and at no point did he claim LDL was causal to CVD. They even discussed how that hadn't been specifically proven, but he used that "necessary but not sufficient" phrase to back up his general reasoning on the subject. IDK how in such a short time he's made that leap unless there's been massive research published since then that nobody's talking about.
Can you share these studies
Really well explained and presented, Nicholas. Keep up the good work. Hopefully the data coming out soon will clarify things.
@nicknorwitzPhD Have always been curious about Mendelian Randomization argument from Attia. Are there any Mendelian Randomization results for other conditions (outside of the area of heart disease) that have not ultimately demonstrated causality? Meaning, MR showed two correlations that independently appeared to lead to the same pathology, but it was later found there was some other root cause not related to that presumed causal agent? For heart disease, is there something in FH that is causing the heart disease independent of elevated LDL? ALSO: of all the genetic conditions that are associated with lower or higher LDL, do they 100% show that low LDL always is protective against heart disease and high LDL always leads to heart disease?
@lls66 Mendelian randomization addresses some of the challenges of observational studies (e.g., calculating correlations among a large number of variables from a large cohort of people followed for 5 or 10 years). But MR suffers from its own wide array of potential confounds and limitations. It is a statistical technique for attempting to draw inferences about plausible cause-effect relationships. It is, for this very reason, only as good as its underlying data collection and only as good as the assumptions made by the human investigators. Genes can cause multiple effects under diverse metabolic states. Sorting this out is a nightmare. Gene interactions can vary widely under different metabolic states. Again, this very quickly becomes incredibly complex - and hard to sort out.
In the case of LDL, diet, and population data, we are faced with one very obvious challenge: genetic expression changes quite dramatically between ketogenic states and non-ketogenic states (I use the plural for both because there are many dietary combinations that will get you into either of these states). Not only gene expression differs widely, but gene-gene interactions appear to differ quite widely as well.
If we are to use observational cohort data to run MR in the hopes of sorting out LDL-CVD linkages, our cohort must, by definition, include a sufficiently large number of ketogenic persons, across the relevant demographic ranges. Lacking these people, no statistical method in the universe can sort out the question of whether the ketogenic state uniquely alters patterns of genetic expression and whether these patterns *cause* uniquely protective or pathogenic effects.
Dr Peter Attia seemed to imply that MR had "closed the book" on -CVD causality. Without a ketogenic cohort, which his data must have lacked (since no such cohort has yet been investigated), he must know that MR on people in other metabolic states cannot exclude the possibility that high LDL observed in a long-term ketogenic state, is either benign or even outright atheroprotective.
MR is a statistical technique that can supplement observational studies and generate hypotheses with regard to the specific types of people/metabolic states included in the data collection. MR is not an experimental technique and cannot substitute for experimental hypothesis testing.
Oh... forgot to mention my blood pressure is now consistently 105/70. I'm actually wondering if thats too low? My avg heart beat is 62-65.
I really love your respectful and nuanced response. I've watched a few or your vids -- you have a new sub.
Thank you :)
We love you too Nick 😊
❤️
Blood is also necessary to have CVD. Should be reduce all things that are associated with CVD? LDL is certainly not causal and you will never find or have a study that shows a causal relationship. Clearly Attia has lost the plot.
There are several distinct lines of evidence that indicate it is. Have a look at: Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel
10:00 We should have some more clues on that as of 8th December. Keep an eye on Dave Feldman for details.
QQQ please ! ...
1: What proportion of LMHR's started on Keto/Ketovore/Carnivore due wholly or partially to some degree of obesity as part of their reason and what proportion didn't have any obesity issues but went low-carb for other reasons such as Autoimmune issues ?
2: Before they went Low-carb, were any of them Binge-eaters wolfing down tons of crap or were they all eating crap but in moderate amounts ?
3: How long do LMHR's remain LMHR's ? ... I recall hearing that some LMHR's see their LDL gradually reduce over time as though their LDL levels were being suppressed when the carbs, seed oils and plant allergens/toxins were present but then significantly increased to replenish/repair/replace what was perhaps previously deficient and/or damaged for years/decades upon cleaning up the diet !
If you have a survey send me the link.
1> I was 233, went very low carb high fat and lost 60 lbs in 4 months
2> I snacked a lot and had three meals a day as well. Binge eating, true but normal USA eating style. Now I am Carnivore and eat OMAD.
3> Sill LMHR go in and out depending on time of year. I tend to have triglycerides above the limit when I eat a lot of berries or honey in the summer. I think my LDL number may be going down slowly but that could just be because I have not fasted for a year.
A good question to answer would be what effect does serious fasting have on Hypercholesterolemia?
I'm a little confused on the wording and agreement here. ApoB is necessary though not sufficient. You have a causal marker that is necessary you can't develop CVD without it, though its not sufficient you can have it and not develop CVD... When a factor is necessary but not sufficient, it means that while that factor is required for the effect to happen, other conditions or factors must also be present for the effect to manifest. This situation highlights the need for multiple factors or conditions to achieve a particular outcome. So at best, its part of the cause??
Part of the effect. ApoB is a consistent element when we observe atherosclerosis, but its involvement may be entirely induced by other, preceding factors. Insulin resistance is always observed in type 2 diabetes. Insulin resistance is "necessary" to the diagnosis of T2D. It is not causal, though, but rather the effect of preceding factors.
ApoB's role in CVD pathology may prove to be an intermediate effect of a set of preceding factors. The question at the moment is, if this is the case, then does a whole-food ketogenic diet prevent the initiation of those preceding factors?
Direct experimentation with long-term ketogenic individuals will help sort some of this out.
@@ketolomics thank you for the information!
The FH is thought to sometime have at the same time a high rate of a clotting factor and that is actually what is going on with the plaque increase
New subscriber. For the "new guy" in the space, you are AMAZING!
Got a question - has there EVER been a valid, quality, interventional study on the efficacy of statins as a secondary preventative measure in heart attack survivors?
I am also a fellow graduate from Harvard Medical School (and therefore you are a like minded thinker) who has had elevated cholesterol since age 29 (discovered when I got life insurance). My total cholesterol level has always been averaging 225-275 (only once was 199). I am likely a LMHR phenotype, had a negative CT Heart scan (zero score) at age 40 and at age 53 last year. Thank goodness I never subscribed to Statin therapy- not everyone with high cholesterol needs a statin- which your work will ultimately prove. Keep up the great work and dialogue. Of course, Big Pharma does not want those with high cholesterol to understand/know this.
Great job!
Thank You !!!
I’m usually on board with Attia, but I’m with you on this. I wonder if big pharma took him to the woodshed over not taking statins. Hundreds of of billions $$