I was on Statins for a few years. My lipid panel became perfect (T:40 HDL:50 LDL:80) but I felt like crap and developed many chronic diseases... A year ago I stopped all prescription drugs. Went LCHF and OMAD. Now I'm a LMHR (T:55 HDL:79 LDL:262) and feeling great! Reversed my prediabetes. Got BP back to normal. Latest lab results show all health markers (except LDL) to be in normal range. Even if higher LDL really is a risk factor as most doctors want us to believe, I'm having absolutely no regret!
Good luck man. Maybe you could do some genetic testing and pinpoint the issue, so you could do more targeted treatment. I've heard some people who overproduce PCSK9, for instance, can just end up supplementing berberine and return to normal levels.
@@Boss_Scaggz Thanks for the suggestion. I did some research on berberine supplement and it seems promising. I'll give it a try. My current A1C is 5.4% and fasting blood glucose is 90-95 mg/dL. I'll provide update in a few weeks on fasting blood glucose. I'll order another lab work in 6 months to see how lipid panel and the rest of the health markers are doing. Hopefully this will be the LDL-lowering solution for me, and useful information for others in similar situation.
Seems like a really sensible call to me, especially if you look at the research instead of the marketing materials. But how is it going with your experiment now 10 months later?
Peter has bought into the Lipid-Heart hypothesis, but fails to explain a key point: If LDL causes heart disease, then decreasing LDL must by definition prevent heart disease. However, even in the best studies for the Lipid-Heart hypothesis (which appear to be manipulated in favor of the drug manufacturers), there is only a 1 percent reduction in cardiovascular events for patients who significantly reduce LDL. In fact, about 2/3 of people who show up at the E.R. with a heart attack have normal LDL. The inescapable conclusion is that LDL is not the cause of CVD, but accompanies CVD in the same way that bandages accompany cuts but bandages do not cause cuts. To clarify, Peter hypothesizes that LDL causes atherosclerosis. If that hypothesis is true then reducing LDL must reduce atherosclerosis. But it does not, so the hypothesis is false. Another question Peter does not answer is why the liver is producing "excess" LDL if it is not needed for any purpose and is simply causing CVD. Is the liver committing suicide? I don't think so. Peter also seems to want to ignore the massive toxic effects of cholesterol lowering medication (statins), including liver damage, kidney damage, mitochondria damage, cognitive decline, brain fog, destruction of the myelin sheath, ALS, muscle wasting, thinning of the cardiac muscle leading to congestive heart failure, and others. Overall I find Peter's treatment of this subject largely non-intellectual, like so many other big pharma physicians. But the most absurd point that Peter makes is that Lipidologists / Cardiologists do NOT have the burden of proving that LDL causes heart disease. Why not? They are prescribing highly toxic statins to lower LDL with no proof that LDL is the cause of heart disease at all. It is unethical for doctors to expose their patients to dangerous toxins without proving that the dangerous toxins (statins) prevent heart disease. Yet they offer no proof that LDL is the cause of heart disease, and indeed we already know that LDL is not the cause of heart disease because when LDL is lowered, heart disease still exists in very large numbers. In addition, it appears that Peter is hostile to the LCHF diet. Is he now promoting the AHA low fat diet? Finally, at the risk of this being interpreted as a personal attack, if the advice of lipidologists like Tom Dayspring is sound, and Feldman is wrong, then why is Dayspring obese and decrepit while Feldman is healthy and vibrant? The lipidologist's advice did not work for the lipidologist, so why would it work for me?
Yes the voice of reason! So many LDL limiting drugs, or even cholesterol lowering drugs in general has shown to have massive complications in other systems too. That high LDL or cholesterol in general is STILL considered some kind of dysregulation by the liver and not a symptom of an underlying issue is mindboggling.
YES. Related: some interventions that have been shown to reliably reduce LDL, such as consuming plant sterols as a supplement, or replacing dietary SFA with PUFA, have also been shown to reliably reduce _lifespan_ I mean, f@&#-#&$ If that doesn't convince people that, at a minimum, it's not as simple as "LDL increases cardiac risk", then I don't know what will.
Excellent commentary Daniel. Remember that Peter is an M.D., a point that he thinks he's stressing. Remember that 32% of Americans are on statins, yet the epidemic of CVD continues. The other point where Peter disagrees is the that immune function of the LDL particle is minimized, and he cannot really explain why people over 60 live longer lives with higher LDL levels.
Peter looks to be the opposite of “truth seeker” and too much confirmation bias at play. But he is knowledgeable and I get that we shall be on the caution side, ldl correlates with low cvd. I am not a keto guy, i dont have elevated cholesterol, but I am interested in the topic. So consider me neutral :)
Let me please add: perhaps Dr Attia, rather than being 'directionally inaccurate', might be more aptly characterised as being 'misdirectionally accurate' ... with the misdirection being inadvertent, hopefully ... Let's hope for him to be properly integrating the facts, and then for goodness sake zoom out a little to look at the big picture. Let's talk more about immune function and examine all cause mortality more rigorously, rather than tickle some hypothetical lipoprotein particles in some hypothetical low-carbohydrate ingesting human and fancifully posture in concern for them (far from saying the real ones lack flaws, glossing over details beyond food, like electromagnetic i. e. light exposure ... structure and stress intersecting at vagus etc.) ... good luck to him. Peace.
In the show notes, Dayspring at 2h40min states about the lipid energy model that Feldman should "Publish It". Dave did publish it last year, and Dayspring slammed him as having no credentials and no background in lipidology". Meanwhile Dayspring made ZERO attempt to address the science or the publication itself. Credential shaming while ignoring the science put forth is in itself anti-science. Why does Peter look up to Dayspring who himself is clearly dogmatic and anti-science; refusing to accept change which is required in science for it to progress? Cromwell taught Dayspring a lot of what he understand in lipidology, and Cromwell recognizes that the Oreo cookie experiment demonstrates that the lipid hypothesis cannot explain the results. The pettiness of Dayspring is repugnant, I hope everyone recognizes him as a sham and an old dog who cannot learn new tricks. If Peter cannot get out from under his cloud of admiration for Dayspring, he may well fall into the same category as being a worthless resource who cannot bend his mind around new data that disagrees with old dogma.
this was incredible. Honestly, its a tough battle going up against an expert like Attia, but Dave did a good job. I have to say though, Attia's point that the hyper-responder is synthesizing more cholesterol is hard to combat.
Attia schooled him like a boy premed. The insight of clinical experience is something one can't learn from self study and self experiments. Attia the GOAT
I think the rising level of anger that you shown to your guest as the podcast evolved only can mean you were scared of what was being said. Anger=fear and Peter you can’t hide the anger
@@Boss_Scaggzhe clearly tried to intimidate and belittle Dave by the end of the interview saying he needs to spend more time around lipid experts which a degree of hostility. It was uncalled for, he should have just stayed friendly and encouraged him to do more research to find support and/or falsify his research. Instead he suggested that the lipid hypothesis is the null hypothesis, that the science is already settled, which is absurd, because a null hypothesis is always, that there is no effect. The past 50 years of lipid research and the nutritional guidelines that followed have been a disaster.
Dave's model appears to be more and more correct each day. He will be publishing soon. 👌 Even his baseline data in fact does appear to prove that persistently (over the course of years) high ldl is not "sufficient" to be causative of cvd. But lifelong statin takers may find out eventually that it is not "necessary" either. Thanks to this rigid stance on lipidology and longevity, im sure there will be those that bottom out their cholesterol for most of their lives (and yet die of cvd sooner than one of these LMHR types). That is the really unfortunate other side of the coin. Something else is clearly causing the dysfunction. Statins and PCSK9 inhibitors dont adress that.
Attia is a hypochrondiac with ocd. So much for healthspan over lifespan. The more time elapses and I read about this model, the more I realize what a frustrated joyless creature Dr. Attia is. To his credit, he eludes to this himself with his transparency about his past issues with anger management. The man is driven by fear due to the loss of family members to CVD which is tragic, but his obsession with longevity is fuelled by an obsession to avoid negative emotions. The pursuit of the avoidance of an early grave has become more important than enjoying life. By the end of this discussion he for no reason other than a lifelong investment in the lipid hypothesis, starts attacking Dave who has been nothing but humble and open to falsification of his own model. “You need to spend more time around the “experts” to get brainwashed like I have been.” Totally uncalled for. Dave is fundraising his research while the likes of Ferrence et al. have big pharma sponsors behind them. The next few years will be interesting.
I always felt that if you study the actual science of something, then you could derive a better idea of how to fix its problems.... Please correct me if I'm wrong: ** LDL is needed for all the cells of the body for proper functioning...as was listed before in previous posts... it is very important. **Plaque formation starts its cascade of events when there is damage to the endothelium lining...LDL tries to repair this damage...but it draws in the rest of the gang of immune cells, monocytes, etc. also... so, in all their combined efforts to repair this damage- they form a plaque mound under the endothelium which protrudes into the lumen of the artery... **So, if there is no endothelium damage, then there should be no reason for LDL to try to repair it..therefore, LDL will continue travelling thru the artery to finish its main job of supplying nutrients and fuels to all the cells... **It seems that LDL gets oxidized 'after' it enters the crack in the endothelium... but it has been said that 'native' LDL in the artery interacts with oxygen to become oxidized, and that this oxidized LDL is the culprit in burrowing into healthy smooth endothelium?? My understanding is that LDL only digs into damaged artery walls and becomes oxidized under the endothelium... ** It then seems that if you can keep the endothelium lining smooth with no damage, then LDL would not even be a factor... ** There are many nutritional ways to keep the artery smooth that can eliminate the need of LDL and the gang going in there to heal it. * Vitamin C is known to form a light film of collagen to repair any cracks in the endothelium without the need of the gang of immune cells...so it's fixed without a plaque mound formation... ** Statins are blocking LDL at its birthplace in the liver before it even gets to any cracks in the artery...is it bad coming right out of the liver...statins are blocking essential food, fuel, and nutrients from getting to the cells of the body where needed to perform a valuable function... ** So statins block essential LDL coming right out of the liver for fear that it might become a 'bad' LDL much further downstream while trying to repair a damaged artery... ** An analogy would be like a bank who blocks their customers ( with deposit money) from coming into the bank for fear that one of them might rob the bank...sure, there are no robberies, but the bank gets no money..... just sayin...
The amount of strawmen Peter built in this conversation is unbelievable. I think Peter himself confirmed Dave's point, that LDL is not causal in first hour of that 'debate' making analogy to oxygen and fire. Oxygen is necessary, but not sufficient to cause fire. Same with ldl, it is necessary, buy not sufficient to create a plaque. This is exactly what Dave is trying to prove. Oxygen is not CAUSING fire and LDL is not CAUSING atherosclerosis, how simple is that?
The whole necessary but not sufficient argument towards LDL works for an interesting masters thesis, but is not practical in a clinical setting. Attia has to worry about people dying and lawyers coming after him if he makes a wrong diag. Going against 50 years of lipid research is too much of a risk. Until there's more science, going with consensus is the correct approach for patients. Sure Ketp/LC works for you, but still having elevated levels of LDL? It's not good because that puts a patient in that risk category for CVD.
@@crimpers5543when you adjust ApoB for ApoC-III, it’s association with heart disease disappears. I would say LMHRs phenotypically are sitting in the first decile of ApoC-III. Same goes for LDL-TG, with discordance at 80th percentile, association between ApoB and CVD becomes non-significant, and I suspect that it would be further attenuated if adjusted for lp(a) and/or high polygenic risk score. There is a paucity of evidence for lipid lowering therapy in metabolically healthy patients and the evidence that I have seen gives me concerns about potential harm. In other words, I think Peter needs to get his head out of Dayspring’s ass 😂
I think everybody is understanding this analogy. The problem is, that we have genetic evidence, in the form of mendelian randomization studies showing it is causal independent of other factors. If we want to pinpoint it down further we can even determine that it is the ApoB on the LDL, that is the causal part. I‘ve read an article recently, why brown bears, although having severe dyslipedemia before hibernation, do not get arteriosclerosis. Because their ApoB protein on the LDL has not such a high affinity to bind to artery walls as the human one does. It needs to be some factor like that, different in LMHR for there to be some truth to this. What could that be? LDL particles are in serum for a shorter time, thus do have less chance to get stuck in the artery wall LMHR have a genetic mutation in ApoB, thus it is less binding to the artery wall The artery wall of LMHR are less stiff and thinner, so LDL particles are less likely to bind. My theory is they do have a connective tissue defect. This makes them appear lean - due to muscle weakness, but hypermobile, and so are their vessels. Adipose tissue is connective tissue so this kind of defect might influence lipid metabolism.
You are not thinking I'm terms of risk. Oxygen doesn't cause fire (by itself), but an oxygen rich environment will make things burn much easier faster and hotter. LDL increases risk of atherosclerosis. The mechanism is known, not just the association, which is extremely strong. People who say their high LDL does not put them at risk are like smokers who talk about the 80 year old lady who has smoked all her life. That's not science.
During my gap year I’ve been preparing for medical school (I start in the fall)... I’ve designated an entire notebook (entitled Dr. Peter Attia notes) which is filled with information I’ve learned from your podcasts... it will for sure be my go to source for HIGHLY RELEVANT CLINICAL INFORMATION... I’ll do my best to share your podcast (and it’s content) with my premed friends and professors faculty...
This is the most adversarial interview I’ve listened to by Dr Attia so far. I found him after reading and appreciating the work of Dave Feldman so the tone was a little jarring. The science is vary hard to follow I assume the show notes would make that easier. I’m considering paying the twenty bucks Dr Attia wants to view them(and all the other notes for show I’ve listened to). I still respect the work Dave is doing but Peter has given me some healthy perspective on it.
Very hard to follow, mostly thanks to Dr Attia's obfuscation ... otherwise, while complex, nonetheless sufficiently straightforward - when knowledge is presented without bias and without unjustifiably outlandish interpretations. Though admittedly, invoking complexity without undue generating complication is generally all too uncommon, such that Dr Attia represents more the rule than the exception, regrettably. Well-meaning person though he may be, undoubtedly.
@@yl1487I found Dr Attia's responses very appropriate and to the point. To confirm or disconfirm hypotheses that involve biochemical pathways, one must be able to discuss biochemical pathways. Not everything can be oversimplified, sometimes one needs to discuss things properly. As a scientist, but not a lipidologist, I found this conversation very informative.
@@Sobchak2 biochemical pathways? Let's take an example where extra facts are subtly removed from context and thereby lose the significance attributed to them: combusting food in a chamber, measuring 'calories' and then assuming relevance to biological metabolism. Before invoking the complexity of these systems and claiming relevance of a multitude of facts, understanding the fundamental weirdness of magnetic flux electrons and the electron transport chain, thermodynamics. I'm claiming contrary to what you seem to be thinking I'm expressing. I claim the system to be far more complex than anything that can be reduced to arbitrarily numerous facts, and thus the complex system remains uncomplicated. Information is contained in the surfaces. If one forgets that magnetic fields are generated by ATP synthases spinning at the mitochondrial membrane, one easily continues to produce a whole bunch of babbling that isn't even wrong. But, chemical pathways before physics, right?
@@Sobchak2intelligent people exposed to relevant facts, that they haven't considered before, will take the new facts into account. For one who doesn't even know that one doesn't know squat about electrons - the fine line between bringing up relevant facts and babbling becomes seemingly non existent. How many ATP molecules are synthesized by ATP synthase? Does it even matter that the answer is far from clear cut? Comprehending mitochondrial coupling will make isolated discussions of pathways not even theoretical or idealized, but as irrelevant as measuring calories from combusting in an isolated chamber to understand an open biological system.
The straight dope on cholesterol was particularly insightful... it’s quite fortunate how experts in these fields can do years and years of hard work and research... just to share the key information with viewers in the matter of a couple of hour through a podcast... and given that most of those viewers are probably physicians and other medical professionals, they can then share that information with all their patients who’ll pass on that information to their friends and loved ones... like it’s an incredibly efficient format and method to distribute state of the art medical science to the general population
5:00 the most frustrating thing about this is that while you're clearly way above my level of expertise here, you don't get into subfractions at all, and seem to be dismissing the idea that high LDL can mean a lot of small, dense, oxidized LDL, or very little of the same.. and that the difference goes to the heart (no pun intended) of the debate. I don't have a strong opinion on the overall validity of Dave's energy model or of the idea that LMHR is an inherently safe place, but if there's one thing he's convinced me of, it's that not all LDL is equal and the differences are crucial. So, yeah.. in the context of a population eating the SAD where everyone is inflamed and has high trigs, high LDL is probably high small, dense, oxidized LDL, and you're SOL, but assuming we all operate in that context is, put mildly, highly unwise.
Cool name, appreciating your Herbertian nod. Far from above your level, perhaps in some regards below yours. Ivory tower lipidologists hardly bring any value to the table with these kind of discussions, and Dr Attia himself, who I would have imagined is with some on the ground experience and less ivory tower syndrome, still wishes to take an apologist's stance when it comes to mentors for whom he appears to hold excessive, partially blind respect and admiration, in my opinion. Peace.
The more Peter Attia tries to upstage Dave Feldman, the wiser Dave will get, which benefits us Citizen Scientists. Self experimentation is VASTLY superior to general population studies, because we can see EXACTLY how our health changes with changes in dietary inputs. This is the future, Crowd Sourced Data! PS, Peter. Your disdain for the low carb movement is showing....
You're what Attia refers to when he's talking about low-carb zealots. If you had done your homework, mr "Citizen Scientist" (lmao) you'd know that he was on a keto diet for years, so the most low carb you can get, completely debunking your dumb take. Not to mention he does experiment on himself except he actually knows what he is doing contrary to wannabe scientists like yourself
You know what's even more powerful than self experimentation? The knowledge that comes with working experimenting not only on yourself but with hundreds of patients first hand in a clinical setting and seeing the quantified results of many different approaches and many different phenotypes.
Disdain for the low carb movement? I'm literally LCHF because of Peter (I'm not a LMHR though - neither was Peter). He was in ketosis for a period of 3 years straight way before it became trendy. He often talks about returning to a ketogenic diet, but his obsessive personality gets in his own way. Peter is also probably one the most prolific self-experimenters in the world, except he has access to far more scientifically accurate measurement tools and the expert knowledge to interpret the data. You should really look into his work more before criticizing.
Yup, Peter was even quoting a nutritional epidemiology study, which is not very reliable science. And Peter admits he cannot provide that LDL causes heart disease. He just thinks it is probable. Yet people have been researching this since 1950 and it is still unproven. Maybe it is unproven because it is untrue.
On Ivor Cummins channel (12/14/18) and on the Sigma Nutrition podcast with Alan Flanagan (#321), Dave elaborates a bit more, suggesting it's not as simple as CVD is a cholesterol retention issue vs a response to injury issue.. instead that the panel as a whole is what paints a picture of risk. For example, those with LOW ApoB100 (vldl/idl/ldl particle count) and LOW triglycerides, HIGH HDL have a HIGHER death rate than those with HIGH ApoB100!! ApoC3 declines with insulin sensitivity. Also, statins seem to be correlated with lower dementia (any kind)?!
why? Peter was pretty nice, but the model is useless, it doesn't provide any practical insights. It's an interesting analogy tool for teaching, but that's about it. Everything else was just lipid biochem 101. Peter is 100% right this guy should just sit in a NLA meeting and learn some stuff. Surprised he said they were too expensive for a wealthy soft eng who sold his startup.
Yes. I concur with your sentiment ... likewise here. I wonder if you have perchance become familiarised with Peter Dobromyslkyj's perspectives on this matter of lipoprotein and energy management / substrate transport, mitochondrial ROS signalling and such?
Hello Dr Attia, thanks for sharing this. I realise that in light of your apparent emotional stance revealed here, with an already pre-formed expectation about the 'probability' - of [you 'feeling' that you might be about to find yourself in agreement with] the ideas you may be about to be exposed to being 'correct' - being low ... ... You may consequently have an understandable and natural resistance to the idea of bringing more people who look at this same matter of energy substrate transport from perspectives distinct to yours and moreover, ensuring that you steel man rather than straw man sensible points that you may nevertheless be opposed to (fair enough - hope you are able to steel man regardless). I hope you surprise me with my own expectations here - why then, how 'bout Peter Dobromylskyj? Thanks and take care.
I have no idea what is right or wrong here, this is way out of my league, but... just because at a certain point in the regression, they took the wrong path and started researching that when in fact you need to go back and start all over? I think Peter is getting in the way of science. Maybe not though who knows.
1:20:47 does Peter not understand at least some of the pathogenesis of FH is the result of inadequate absorption of the components of lipoproteins into cells ie they are starved on energy? It’s not just the liver fella!
LDL has nothing to do with energy. Fatty acids transported from fat tissue by albumin are responsible for energy delivery. VLDL/LDL merely transport triglycerides from the liver to the adipose tissue, losing a little to the muscle.
I enjoyed most of this conversation but a couple of parts got really frustrating. "Necessary but not sufficient" is NOT the same as _causal_ and P.A. keeps using it as a backdoor into labeling it as causal. What we're trying to validate is the assertion of a dose-dependent response from LDL level to CVD with little variation due to other factors, not just that LDL plays a role, which everyone agrees on.
Does it really matter? If atherosclerosis cannot happen without apoB, and we lower our apoB levels to that of a child’s without side effects, can we eliminate atherosclerosis?
@@ApoBeef Yes. There are Pygmies, who all smoke, but have very low cholesterol (~110 total) thanks to the plant-based diet. They have zero atherosclerosis.
Low carb mean low SCFA ?.. low microbiome diversity?.. I think people eat non veg because their heart need that .. even though non veg harm all other things in body !!..
Clear as day to see that Peter has a strong bias and incentive to defend the incomplete and broken Lipid Heart Hypothesis, as he is benefitting from big pharma and cannot come to terms with the fact that his interventions in terms of medication may not be giving any benefit to his patients.
Yes ... cognitive dissonance ... good intentions though he may have. I have little envy for him in his position, must be emotionally hard to come to terms with.
AI pattern recognition will solve problems that are hindered by human demand for first principle proofs. Humans have used pattern recognition for life and establishment of science only to be discarded by the recently established rigor of science. This rigor threshold appears to be selective especially in recent virulent times.
It's time to revisit this conversation a few years later after the LMHR studies have started to been published.
I was on Statins for a few years. My lipid panel became perfect (T:40 HDL:50 LDL:80) but I felt like crap and developed many chronic diseases... A year ago I stopped all prescription drugs. Went LCHF and OMAD. Now I'm a LMHR (T:55 HDL:79 LDL:262) and feeling great! Reversed my prediabetes. Got BP back to normal. Latest lab results show all health markers (except LDL) to be in normal range. Even if higher LDL really is a risk factor as most doctors want us to believe, I'm having absolutely no regret!
Good luck man. Maybe you could do some genetic testing and pinpoint the issue, so you could do more targeted treatment. I've heard some people who overproduce PCSK9, for instance, can just end up supplementing berberine and return to normal levels.
@@Boss_Scaggz Thanks for the suggestion. I did some research on berberine supplement and it seems promising. I'll give it a try. My current A1C is 5.4% and fasting blood glucose is 90-95 mg/dL. I'll provide update in a few weeks on fasting blood glucose. I'll order another lab work in 6 months to see how lipid panel and the rest of the health markers are doing. Hopefully this will be the LDL-lowering solution for me, and useful information for others in similar situation.
@@bigcat9977 Any update?
Peter would insist that you take a statin. (wtf)
Seems like a really sensible call to me, especially if you look at the research instead of the marketing materials. But how is it going with your experiment now 10 months later?
Peter has bought into the Lipid-Heart hypothesis, but fails to explain a key point: If LDL causes heart disease, then decreasing LDL must by definition prevent heart disease. However, even in the best studies for the Lipid-Heart hypothesis (which appear to be manipulated in favor of the drug manufacturers), there is only a 1 percent reduction in cardiovascular events for patients who significantly reduce LDL. In fact, about 2/3 of people who show up at the E.R. with a heart attack have normal LDL. The inescapable conclusion is that LDL is not the cause of CVD, but accompanies CVD in the same way that bandages accompany cuts but bandages do not cause cuts. To clarify, Peter hypothesizes that LDL causes atherosclerosis. If that hypothesis is true then reducing LDL must reduce atherosclerosis. But it does not, so the hypothesis is false.
Another question Peter does not answer is why the liver is producing "excess" LDL if it is not needed for any purpose and is simply causing CVD. Is the liver committing suicide? I don't think so. Peter also seems to want to ignore the massive toxic effects of cholesterol lowering medication (statins), including liver damage, kidney damage, mitochondria damage, cognitive decline, brain fog, destruction of the myelin sheath, ALS, muscle wasting, thinning of the cardiac muscle leading to congestive heart failure, and others. Overall I find Peter's treatment of this subject largely non-intellectual, like so many other big pharma physicians.
But the most absurd point that Peter makes is that Lipidologists / Cardiologists do NOT have the burden of proving that LDL causes heart disease. Why not? They are prescribing highly toxic statins to lower LDL with no proof that LDL is the cause of heart disease at all. It is unethical for doctors to expose their patients to dangerous toxins without proving that the dangerous toxins (statins) prevent heart disease. Yet they offer no proof that LDL is the cause of heart disease, and indeed we already know that LDL is not the cause of heart disease because when LDL is lowered, heart disease still exists in very large numbers.
In addition, it appears that Peter is hostile to the LCHF diet. Is he now promoting the AHA low fat diet?
Finally, at the risk of this being interpreted as a personal attack, if the advice of lipidologists like Tom Dayspring is sound, and Feldman is wrong, then why is Dayspring obese and decrepit while Feldman is healthy and vibrant? The lipidologist's advice did not work for the lipidologist, so why would it work for me?
Yes the voice of reason!
So many LDL limiting drugs, or even cholesterol lowering drugs in general has shown to have massive complications in other systems too.
That high LDL or cholesterol in general is STILL considered some kind of dysregulation by the liver and not a symptom of an underlying issue is mindboggling.
YES. Related: some interventions that have been shown to reliably reduce LDL, such as consuming plant sterols as a supplement, or replacing dietary SFA with PUFA, have also been shown to reliably reduce _lifespan_
I mean, f@&#-#&$
If that doesn't convince people that, at a minimum, it's not as simple as "LDL increases cardiac risk", then I don't know what will.
Excellent commentary Daniel. Remember that Peter is an M.D., a point that he thinks he's stressing. Remember that 32% of Americans are on statins, yet the epidemic of CVD continues. The other point where Peter disagrees is the that immune function of the LDL particle is minimized, and he cannot really explain why people over 60 live longer lives with higher LDL levels.
Peter looks to be the opposite of “truth seeker” and too much confirmation bias at play. But he is knowledgeable and I get that we shall be on the caution side, ldl correlates with low cvd. I am not a keto guy, i dont have elevated cholesterol, but I am interested in the topic. So consider me neutral :)
Let me please add: perhaps Dr Attia, rather than being 'directionally inaccurate', might be more aptly characterised as being 'misdirectionally accurate' ... with the misdirection being inadvertent, hopefully ...
Let's hope for him to be properly integrating the facts, and then for goodness sake zoom out a little to look at the big picture.
Let's talk more about immune function and examine all cause mortality more rigorously, rather than tickle some hypothetical lipoprotein particles in some hypothetical low-carbohydrate ingesting human and fancifully posture in concern for them (far from saying the real ones lack flaws, glossing over details beyond food, like electromagnetic i. e. light exposure ... structure and stress intersecting at vagus etc.) ... good luck to him. Peace.
In the show notes, Dayspring at 2h40min states about the lipid energy model that Feldman should "Publish It". Dave did publish it last year, and Dayspring slammed him as having no credentials and no background in lipidology". Meanwhile Dayspring made ZERO attempt to address the science or the publication itself. Credential shaming while ignoring the science put forth is in itself anti-science. Why does Peter look up to Dayspring who himself is clearly dogmatic and anti-science; refusing to accept change which is required in science for it to progress? Cromwell taught Dayspring a lot of what he understand in lipidology, and Cromwell recognizes that the Oreo cookie experiment demonstrates that the lipid hypothesis cannot explain the results. The pettiness of Dayspring is repugnant, I hope everyone recognizes him as a sham and an old dog who cannot learn new tricks. If Peter cannot get out from under his cloud of admiration for Dayspring, he may well fall into the same category as being a worthless resource who cannot bend his mind around new data that disagrees with old dogma.
this was incredible. Honestly, its a tough battle going up against an expert like Attia, but Dave did a good job. I have to say though, Attia's point that the hyper-responder is synthesizing more cholesterol is hard to combat.
I guess he’ll have to prove it.
Attia schooled him like a boy premed. The insight of clinical experience is something one can't learn from self study and self experiments. Attia the GOAT
I think the rising level of anger that you shown to your guest as the podcast evolved only can mean you were scared of what was being said. Anger=fear and Peter you can’t hide the anger
1. I detected no anger from Peter in this podcast. 2. Peter has spoken at length about his extremely intense anger issues in the past.
@@Boss_Scaggz Is that why he did not finish his surgical residency?
@@danielmccarthyy I don't know anything about that.
@@Boss_Scaggzhe clearly tried to intimidate and belittle Dave by the end of the interview saying he needs to spend more time around lipid experts which a degree of hostility. It was uncalled for, he should have just stayed friendly and encouraged him to do more research to find support and/or falsify his research. Instead he suggested that the lipid hypothesis is the null hypothesis, that the science is already settled, which is absurd, because a null hypothesis is always, that there is no effect. The past 50 years of lipid research and the nutritional guidelines that followed have been a disaster.
Dave's model appears to be more and more correct each day. He will be publishing soon. 👌 Even his baseline data in fact does appear to prove that persistently (over the course of years) high ldl is not "sufficient" to be causative of cvd.
But lifelong statin takers may find out eventually that it is not "necessary" either. Thanks to this rigid stance on lipidology and longevity, im sure there will be those that bottom out their cholesterol for most of their lives (and yet die of cvd sooner than one of these LMHR types). That is the really unfortunate other side of the coin.
Something else is clearly causing the dysfunction. Statins and PCSK9 inhibitors dont adress that.
Attia is a hypochrondiac with ocd. So much for healthspan over lifespan. The more time elapses and I read about this model, the more I realize what a frustrated joyless creature Dr. Attia is. To his credit, he eludes to this himself with his transparency about his past issues with anger management. The man is driven by fear due to the loss of family members to CVD which is tragic, but his obsession with longevity is fuelled by an obsession to avoid negative emotions. The pursuit of the avoidance of an early grave has become more important than enjoying life. By the end of this discussion he for no reason other than a lifelong investment in the lipid hypothesis, starts attacking Dave who has been nothing but humble and open to falsification of his own model. “You need to spend more time around the “experts” to get brainwashed like I have been.” Totally uncalled for. Dave is fundraising his research while the likes of Ferrence et al. have big pharma sponsors behind them. The next few years will be interesting.
Why would Dave gets better on CIMT while having high LDL?
Peter, you need to have Dave on again to discuss the stunning results of his LMHR study. But somehow I think your pride won't allow it.
I agree that Attia won't admit he was wrong.
I always felt that if you study the actual science of something, then you could derive a better idea of how to fix its problems....
Please correct me if I'm wrong:
** LDL is needed for all the cells of the body for proper functioning...as was listed before in previous posts...
it is very important.
**Plaque formation starts its cascade of events when there is damage to the endothelium lining...LDL tries to repair this damage...but it draws in the rest of the gang of immune cells, monocytes,
etc. also... so, in all their combined efforts to repair this damage- they form a plaque mound under the endothelium which protrudes into the lumen of the artery...
**So, if there is no endothelium damage, then there should be no reason for LDL to try to repair it..therefore, LDL will continue travelling thru the artery to finish its main job of supplying nutrients and fuels to all the cells...
**It seems that LDL gets oxidized 'after' it enters the crack in the endothelium...
but it has been said that 'native' LDL in the artery interacts with oxygen to become oxidized, and that this oxidized LDL is the culprit in burrowing into healthy smooth endothelium?? My understanding is that LDL only digs into damaged artery walls and becomes oxidized under the endothelium...
** It then seems that if you can keep the endothelium lining smooth with no damage, then LDL would not even be a factor...
** There are many nutritional ways to keep the artery smooth that can eliminate the need of LDL
and the gang going in there
to heal it.
* Vitamin C is known to form a light film of collagen
to repair any cracks in the endothelium without the need of the gang of immune cells...so it's fixed without a plaque mound formation...
** Statins are blocking LDL at its birthplace in the liver
before it even gets to any cracks in the artery...is it bad coming right out of the liver...statins are blocking essential food, fuel, and nutrients from getting to the cells of the body where needed to perform a valuable function...
** So statins block essential LDL coming right out of the liver for fear that it might become a 'bad' LDL much further downstream
while trying to repair a damaged artery...
** An analogy would be like a bank who blocks their customers ( with deposit money) from coming into the bank for fear that one of them might rob the bank...sure, there are no robberies, but the bank gets no money.....
just sayin...
When is Dave's study going to be published in a Journal?
The amount of strawmen Peter built in this conversation is unbelievable. I think Peter himself confirmed Dave's point, that LDL is not causal in first hour of that 'debate' making analogy to oxygen and fire. Oxygen is necessary, but not sufficient to cause fire. Same with ldl, it is necessary, buy not sufficient to create a plaque. This is exactly what Dave is trying to prove. Oxygen is not CAUSING fire and LDL is not CAUSING atherosclerosis, how simple is that?
The amount of sound reasoning based on actual knowledge on this topic, you mean.
The whole necessary but not sufficient argument towards LDL works for an interesting masters thesis, but is not practical in a clinical setting. Attia has to worry about people dying and lawyers coming after him if he makes a wrong diag. Going against 50 years of lipid research is too much of a risk. Until there's more science, going with consensus is the correct approach for patients. Sure Ketp/LC works for you, but still having elevated levels of LDL? It's not good because that puts a patient in that risk category for CVD.
@@crimpers5543when you adjust ApoB for ApoC-III, it’s association with heart disease disappears. I would say LMHRs phenotypically are sitting in the first decile of ApoC-III. Same goes for LDL-TG, with discordance at 80th percentile, association between ApoB and CVD becomes non-significant, and I suspect that it would be further attenuated if adjusted for lp(a) and/or high polygenic risk score.
There is a paucity of evidence for lipid lowering therapy in metabolically healthy patients and the evidence that I have seen gives me concerns about potential harm.
In other words, I think Peter needs to get his head out of Dayspring’s ass 😂
I think everybody is understanding this analogy. The problem is, that we have genetic evidence, in the form of mendelian randomization studies showing it is causal independent of other factors. If we want to pinpoint it down further we can even determine that it is the ApoB on the LDL, that is the causal part.
I‘ve read an article recently, why brown bears, although having severe dyslipedemia before hibernation, do not get arteriosclerosis. Because their ApoB protein on the LDL has not such a high affinity to bind to artery walls as the human one does.
It needs to be some factor like that, different in LMHR for there to be some truth to this.
What could that be?
LDL particles are in serum for a shorter time, thus do have less chance to get stuck in the artery wall
LMHR have a genetic mutation in ApoB, thus it is less binding to the artery wall
The artery wall of LMHR are less stiff and thinner, so LDL particles are less likely to bind. My theory is they do have a connective tissue defect. This makes them appear lean - due to muscle weakness, but hypermobile, and so are their vessels. Adipose tissue is connective tissue so this kind of defect might influence lipid metabolism.
You are not thinking I'm terms of risk. Oxygen doesn't cause fire (by itself), but an oxygen rich environment will make things burn much easier faster and hotter. LDL increases risk of atherosclerosis. The mechanism is known, not just the association, which is extremely strong. People who say their high LDL does not put them at risk are like smokers who talk about the 80 year old lady who has smoked all her life. That's not science.
I hope you do an update
This is the kind of discussion we need 😊
During my gap year I’ve been preparing for medical school (I start in the fall)... I’ve designated an entire notebook (entitled Dr. Peter Attia notes) which is filled with information I’ve learned from your podcasts... it will for sure be my go to source for HIGHLY RELEVANT CLINICAL INFORMATION... I’ll do my best to share your podcast (and it’s content) with my premed friends and professors faculty...
This is the most adversarial interview I’ve listened to by Dr Attia so far. I found him after reading and appreciating the work of Dave Feldman so the tone was a little jarring.
The science is vary hard to follow I assume the show notes would make that easier. I’m considering paying the twenty bucks Dr Attia wants to view them(and all the other notes for show I’ve listened to).
I still respect the work Dave is doing but Peter has given me some healthy perspective on it.
Very hard to follow, mostly thanks to Dr Attia's obfuscation ... otherwise, while complex, nonetheless sufficiently straightforward - when knowledge is presented without bias and without unjustifiably outlandish interpretations. Though admittedly, invoking complexity without undue generating complication is generally all too uncommon, such that Dr Attia represents more the rule than the exception, regrettably. Well-meaning person though he may be, undoubtedly.
@@yl1487I found Dr Attia's responses very appropriate and to the point. To confirm or disconfirm hypotheses that involve biochemical pathways, one must be able to discuss biochemical pathways. Not everything can be oversimplified, sometimes one needs to discuss things properly.
As a scientist, but not a lipidologist, I found this conversation very informative.
@@Sobchak2 biochemical pathways? Let's take an example where extra facts are subtly removed from context and thereby lose the significance attributed to them: combusting food in a chamber, measuring 'calories' and then assuming relevance to biological metabolism. Before invoking the complexity of these systems and claiming relevance of a multitude of facts, understanding the fundamental weirdness of magnetic flux electrons and the electron transport chain, thermodynamics. I'm claiming contrary to what you seem to be thinking I'm expressing. I claim the system to be far more complex than anything that can be reduced to arbitrarily numerous facts, and thus the complex system remains uncomplicated. Information is contained in the surfaces. If one forgets that magnetic fields are generated by ATP synthases spinning at the mitochondrial membrane, one easily continues to produce a whole bunch of babbling that isn't even wrong. But, chemical pathways before physics, right?
@@yl1487 bunch of babbling, you say
@@Sobchak2intelligent people exposed to relevant facts, that they haven't considered before, will take the new facts into account. For one who doesn't even know that one doesn't know squat about electrons - the fine line between bringing up relevant facts and babbling becomes seemingly non existent. How many ATP molecules are synthesized by ATP synthase? Does it even matter that the answer is far from clear cut? Comprehending mitochondrial coupling will make isolated discussions of pathways not even theoretical or idealized, but as irrelevant as measuring calories from combusting in an isolated chamber to understand an open biological system.
The straight dope on cholesterol was particularly insightful... it’s quite fortunate how experts in these fields can do years and years of hard work and research... just to share the key information with viewers in the matter of a couple of hour through a podcast... and given that most of those viewers are probably physicians and other medical professionals, they can then share that information with all their patients who’ll pass on that information to their friends and loved ones... like it’s an incredibly efficient format and method to distribute state of the art medical science to the general population
listen to Dave at Denver low carb Conference
One of the best interrogatory discussions on lipids - that is also informative
Please invite Dr David Diamond to talk about statins and statistics.
... Statinstics? Kidding aside, second that. Diamond as guest - yes.
5:00 the most frustrating thing about this is that while you're clearly way above my level of expertise here, you don't get into subfractions at all, and seem to be dismissing the idea that high LDL can mean a lot of small, dense, oxidized LDL, or very little of the same.. and that the difference goes to the heart (no pun intended) of the debate. I don't have a strong opinion on the overall validity of Dave's energy model or of the idea that LMHR is an inherently safe place, but if there's one thing he's convinced me of, it's that not all LDL is equal and the differences are crucial. So, yeah.. in the context of a population eating the SAD where everyone is inflamed and has high trigs, high LDL is probably high small, dense, oxidized LDL, and you're SOL, but assuming we all operate in that context is, put mildly, highly unwise.
Cool name, appreciating your Herbertian nod. Far from above your level, perhaps in some regards below yours. Ivory tower lipidologists hardly bring any value to the table with these kind of discussions, and Dr Attia himself, who I would have imagined is with some on the ground experience and less ivory tower syndrome, still wishes to take an apologist's stance when it comes to mentors for whom he appears to hold excessive, partially blind respect and admiration, in my opinion.
Peace.
The more Peter Attia tries to upstage Dave Feldman, the wiser Dave will get, which benefits us Citizen Scientists. Self experimentation is VASTLY superior to general population studies, because we can see EXACTLY how our health changes with changes in dietary inputs. This is the future, Crowd Sourced Data!
PS, Peter. Your disdain for the low carb movement is showing....
You're what Attia refers to when he's talking about low-carb zealots. If you had done your homework, mr "Citizen Scientist" (lmao) you'd know that he was on a keto diet for years, so the most low carb you can get, completely debunking your dumb take. Not to mention he does experiment on himself except he actually knows what he is doing contrary to wannabe scientists like yourself
You know what's even more powerful than self experimentation? The knowledge that comes with working experimenting not only on yourself but with hundreds of patients first hand in a clinical setting and seeing the quantified results of many different approaches and many different phenotypes.
Disdain for the low carb movement? I'm literally LCHF because of Peter (I'm not a LMHR though - neither was Peter). He was in ketosis for a period of 3 years straight way before it became trendy. He often talks about returning to a ketogenic diet, but his obsessive personality gets in his own way. Peter is also probably one the most prolific self-experimenters in the world, except he has access to far more scientifically accurate measurement tools and the expert knowledge to interpret the data. You should really look into his work more before criticizing.
Yup, Peter was even quoting a nutritional epidemiology study, which is not very reliable science. And Peter admits he cannot provide that LDL causes heart disease. He just thinks it is probable. Yet people have been researching this since 1950 and it is still unproven. Maybe it is unproven because it is untrue.
@@danielmccarthyy 😁
On Ivor Cummins channel (12/14/18) and on the Sigma Nutrition podcast with Alan Flanagan (#321), Dave elaborates a bit more, suggesting it's not as simple as CVD is a cholesterol retention issue vs a response to injury issue.. instead that the panel as a whole is what paints a picture of risk. For example, those with LOW ApoB100 (vldl/idl/ldl particle count) and LOW triglycerides, HIGH HDL have a HIGHER death rate than those with HIGH ApoB100!! ApoC3 declines with insulin sensitivity. Also, statins seem to be correlated with lower dementia (any kind)?!
Hmm, statins are most certainly correlated with "compliance" with a lot of people having very adverse effects discontinuing treatment.
Best talk ever on this subject. Needs a second round.
why? Peter was pretty nice, but the model is useless, it doesn't provide any practical insights. It's an interesting analogy tool for teaching, but that's about it. Everything else was just lipid biochem 101. Peter is 100% right this guy should just sit in a NLA meeting and learn some stuff. Surprised he said they were too expensive for a wealthy soft eng who sold his startup.
Especially now.
It’s good to know where somewhat of the leading edge is on this topic.
Wish I would've watched this all the way through a year ago. Thanks Dr. Attia, I needed to hear this.
Good discussion as always.
While I don't agree with Peter entirely, I also know my knowledge in this area is insufficient.
Time to keep learning.
Yes. I concur with your sentiment ... likewise here. I wonder if you have perchance become familiarised with Peter Dobromyslkyj's perspectives on this matter of lipoprotein and energy management / substrate transport, mitochondrial ROS signalling and such?
You think Attia knows what he’s talking about wrt lipids?
Sheesh, this is, quite literally, like Dave vs Goliath lmao
@Anita Martini sounds like it's just way over your head
Hello Dr Attia, thanks for sharing this. I realise that in light of your apparent emotional stance revealed here, with an already pre-formed expectation about the 'probability' - of [you 'feeling' that you might be about to find yourself in agreement with] the ideas you may be about to be exposed to being 'correct' - being low ...
... You may consequently have an understandable and natural resistance to the idea of bringing more people who look at this same matter of energy substrate transport from perspectives distinct to yours and moreover, ensuring that you steel man rather than straw man sensible points that you may nevertheless be opposed to (fair enough - hope you are able to steel man regardless).
I hope you surprise me with my own expectations here - why then, how 'bout Peter Dobromylskyj? Thanks and take care.
I have no idea what is right or wrong here, this is way out of my league, but... just because at a certain point in the regression, they took the wrong path and started researching that when in fact you need to go back and start all over? I think Peter is getting in the way of science. Maybe not though who knows.
The economics of Big Pharma tends to do this. Sound familiar?
Arterial sclerosis & blood pressure, glycocalyx need to be considered
1:20:47 does Peter not understand at least some of the pathogenesis of FH is the result of inadequate absorption of the components of lipoproteins into cells ie they are starved on energy? It’s not just the liver fella!
LDL has nothing to do with energy. Fatty acids transported from fat tissue by albumin are responsible for energy delivery. VLDL/LDL merely transport triglycerides from the liver to the adipose tissue, losing a little to the muscle.
OMG, what a lively, lovely banter!
Dave, carry your charger with you!
Dave's point about ldl n vit e is brilliant
This discussion should be rehashed again
I enjoyed most of this conversation but a couple of parts got really frustrating. "Necessary but not sufficient" is NOT the same as _causal_ and P.A. keeps using it as a backdoor into labeling it as causal.
What we're trying to validate is the assertion of a dose-dependent response from LDL level to CVD with little variation due to other factors, not just that LDL plays a role, which everyone agrees on.
Oxygen is necessary but not sufficient for arson 😜
Does it really matter?
If atherosclerosis cannot happen without apoB, and we lower our apoB levels to that of a child’s without side effects, can we eliminate atherosclerosis?
@@ApoBeef Yes. There are Pygmies, who all smoke, but have very low cholesterol (~110 total) thanks to the plant-based diet. They have zero atherosclerosis.
@@erastvandoren Most people cannot get their apoB levels below 40 mg/dl on any diet. Pharmacological solutions are the only way for them (and myself).
@southviet890 Who says 40? 50 is normally enough. The majority can reach 50 with the WFPB diet.
After hearing the podcast, I confirmed my hypothesis that he is a def ** :)
If this was recorded in the UK we would say "Feldman got Paxoed" you've gotta be a Brit to get it...unless, of course you know who Jeremy Paxman is 😜
Peter Attia is the culture!!! Amazing quote to and from him
Low carb mean low SCFA ?.. low microbiome diversity?..
I think people eat non veg because their heart need that .. even though non veg harm all other things in body !!..
Clear as day to see that Peter has a strong bias and incentive to defend the incomplete and broken Lipid Heart Hypothesis, as he is benefitting from big pharma and cannot come to terms with the fact that his interventions in terms of medication may not be giving any benefit to his patients.
Yes ... cognitive dissonance ... good intentions though he may have. I have little envy for him in his position, must be emotionally hard to come to terms with.
Excellent Podcast 🙂👍
Thomas Dayspring fails the visual test. If he doesn’t look smart he ………………….
Attia trying to be the Sam Harris of health. Then Sam Harris is just an entitled self righteous………
AI pattern recognition will solve problems that are hindered by human demand for first principle proofs. Humans have used pattern recognition for life and establishment of science only to be discarded by the recently established rigor of science. This rigor threshold appears to be selective especially in recent virulent times.
When Bro Science runs head first into Real Science.
@InmanRoshi real science has been proven wrong over n over since the beginning.