This clip is from the Huberman Lab episode "Dr. Peter Attia: Exercise, Nutrition, Hormones for Vitality & Longevity.” The full episode can be found on RUclips here: ruclips.net/video/DTCmprPCDqc/видео.html
Any doctor who tells you that you have a pharmaceutical substance deficiency and then proceeds to use a hundred logical fallacies while claiming he’s obsessed with causation and calling anyone who disagrees “idiotic” should make you RUN in the opposite direction. Check his stock portfolio.
I am about to be 82. I have been on statins for many years and always think I want to get off them. I have moderately high blood pressure which is controlled with diuretics. I have no other risk factors other than my age. My total cholesterol is around 160 and my LDL is extremely low I believe due to the statins. Watching this I am convinced by Dr. Attia to forget about getting off of statins and continue doing what I do. Eat well, get regular exercise, take my meds and get as much enjoyment out of life as I can. Thanks for these conversations.
¡Hola Profe!Going to relisten the episode! The shorter format is doing a good job to remind ,what episodes to rewatch or relisten Thank You,for all You are doing .
So much conflicting info out there. I have seen several studies that show; higher cholesterol is associated with longevity, a Korean study showed that those with very low levels (sub 150) had higher mortality than those from 200-250, more than 50% of those admitted for heart attacks have levels in the 'normal' range. With advances in medicine, stents, statins and the war on smoking, heart disease is still the number 1 killer. I just don't think we have this figured out yet.
No, it's been figured out. All studies that show higher mortality for people with low total cholesterol are demonstrating reverse causality. That is, that those people with low cholesterol probably were sick with some disease that causes low cholesterol like cancer, old age, possibly on high dose statins, etc. If you control for these alternate morbidities in low vs. high cholesterol study participants, the low cholesterol participants have lower mortality every single time.
There’s a lot of studies showing this correlation with almost everything One of the main reasons for this is people with cancer and very ill people have low cholesterol due to their illness, also after a heart attack or cardiovascular event your cholesterol drops significantly When these things are taken into account then we can see that low ApoB in healthy people are at lower risk or heart attack than those with higher levels , same association with alcohol , it’s called a J curve happens with observational studies usually referred to as a paradox, “cholesterol paradox” alcohol paradox and so on
@@dominickcruz7252yea but i remember hearing one doctor say they had a decade of research on them people or something like that. So im sure they wasn’t ill for a decade
@@dominickcruz7252 That's simply not true. A study of the 1999-2014 NHANES data adjusted for possible confounders like cancer and still found that people with lower LDL (less than 80) had a much higher hazard ratio for all-cause mortality than even those with LDLs as high as 300, which the anti-cholesterol crowd would say is basically a heart attack waiting to happen. Well, the data says otherwise.
I’m glad that you are keeping science at the forefront. Cardiovascular disease kills an American every 12 seconds and hypercholesterolemia is a profound - and eminently treatable -risk factor
Just went to the doctor in the Netherlands, she didn't know what apoB was 😂 She was looking in the system and was not able to test me on that. When I go to a blood test site I can buy a ApoB test for 30 euro, so I will do that
True, you read about ApoB everywhere and in Holland it isnt even mentioned on a general blood test. Total cholesterol, LDL, HDL, triglycerides etc, but no ApoB
Its a good argument and a good analogy, but there is a fundamental problem. Smoking is a negative intervention. Not smoking is a non-intervention. You dont have to weigh the risk of not smoking against the risk of smoking. Statins use is an active intervention, which while it does lower cholesterol, has risk of diabetes and dementia, muscle pains. In this case it does make sense to evaluate when the risk of high cholesterol becomes substantial enough to make an active intervention known to cause negative effects
Astute observation. Totally agree. Except that statins do not cause dementia--multiple studies have debunked this fear. The lipophilic statins may cause "brain fog" in some people, but it's reversible. Muscle pain is pretty common, but also reversible. These issues, therefore, should not be feared, just dealt with if they arise. But statins do increase the risk of diabetes in some people, and that's a serious concern that needs to be acknowledged and followed closely when prescribed. I eagerly await the day when PCSK9 inhibitors will be widely available, as they appear to have literally zero significant side effects--so far.
Excellent observation, sir. Also, I'm not buying yet that LDL is causally related to increase in heart disease. It's just indicative of a possibility. If your LDL is high, then why not just get your arteries checked to see if it's actually doing anything. If not, you should be good!
I am so glad to see this comment, as Peter is obviously not comparing apples to apples in his analogy. Not smoking has ZERO side effects, statins - well surely there is at least SOME side effects.
I have low LDL and low ApoB but still rather significant atherosclerosis. How come Type2 diabetes inflammation is not discussed here? No MD ever warned me about Type2 and atherosclerosis either.
How low are we talking about? Also atheroserosis is an area under the curve problem. Your apoB might be low now, but what was the lvl during the last decade? And before that?
Since the war on cholesterol, dementia and Alzheimer's have skyrocketed. I'm not gonna sacrifice my operating system for my motor. And if I'm wrong I'll die young eating the foods that make me feel the most well.
Peter Attia needs to have a debate with James Mason. The two are diametrically opposed in their claims and both extensively cite studies and resources.
I find it a bit curious that Dr. Attia calls himself "obsessive" with causality, when LDL is not the cause per se. Oxidized LDL that gets within arterial walls causes plaque, not standard LDL. The causes for atherosclerosis, then, are related to the inflammation that promotes that oxidation. We should be looking at lowering that instead of waging war on an essential molecule.
That's what I'm finding out as well. Maybe he addressed in the full lenght podcast, but I find it frustrating that he casually dismisses people that dispute the causation by saying that they're not credible without addressing this important fact.
There are all sorts of steps along the atherogenic pathway one could point to and say, "that's the cause," including oxidation of a retained LDL particle, as you point out. But the one most easily manipulated therapeutically, the most actionable one, the one most consistently and effectively shown to reduce atherosclerosis when treated is LDL (or apo B) concentration in the blood. There is a definition to the term "causal," and LDL fits it. Practically speaking, if you focus on oxidized LDL, how would you treat that? Furthermore, LDL, to my knowledge, is not essential.
Its not an either or. You need to reduce the lipoprotein numbers that are likely to get lodged in the endothelium, and you also need to also reduce inflammation in the arteries that increases risk of oxidation. Ideally you should be doing both. Cholesterol is an “essential” molecule, but you do not high amounts of it circulating thru your bloodstream. Theres no downside to loweing ApoB in the bloodstream. All of your cells manufacture cholesterol for membrane structure and other uses like hormones. It does not need to be high in the extracellular fluid of your bloodstream. Also, Peter attia isnt saying LDL is the cause. If you ever listen to his podcasts in depth, he is very clear that the main culprits are the lipoproteins that shuttle around LDL, not the cholesterol itsself.
I agree. LDL is a protein carrying essential cholesterol to the cells it is not a cause. (there is no good or bad cholesterol it is all the same). Sugar --> Inflammation --> Oxidation --> Plaque buildup --> Restriction in blood flow --> atherosclerosis IS a causal relationship whether you believe in it or not.
i've listened to the full interview as well... his talk @ancestral health symposium 2012 is a good one [again no slides], what strikes me here is he (& you) are imbibing Bayesian inference. Given a result how do we then work backwards to assess risk ?. To moi it feels like chaos theory... Did finally start on his book which i ofttimes fail to do after seeing the movie :;
I get conflicting information on whether I am ok or not. My current numbers are: Total Cholesterol 244, Triglycerides 58, HDL 106, LDL 128, ApoB 105, ApoA-1 222 mgdL. These have roughly been my numbers for years. Originally I was told not to worry about my high LDL because my HDL is high and will protect me. Now my HDL is considered too high and is not good any more. I then had my particle size tested, and the test showed low risk pattern with larger particle size and low insulin resistance. So I was considered good - no treatment necessary. Now the most important indicator appears to be ApoB. My ApoB is too high so I need treatment. I have also seen elsewhere that the most important indicator is the ratio ApoB / ApoA-1. This number is good for me due to my high ApoA-1 so I don't need treatment. My doctor is now focusing on the ApoB only and wants me on crestor. This seems to agree with what you are saying. It just seems like the parameters keep changing. I am 60, female, BMI 21, moderate exercise and eat healthy. (healthy fats, veges, some carbs, low sugar). I prefer to avoid statins.
Hi, soluble fiber is shown to decrease apob. Consider increasing fiber intake significantly - 40 gm per day. A 20 gm supplementation with psyllium husk powder can help.
I lowered mine by taking Niacin, it did lower my ApoB. I took it for 3 months but it gave me gout, so now I eat low carbs and occasionally take Niacin.
But what if the lipoproteins that carry LDL to where its needed in the body are quite essential to life, and its what causes those lipoproteins to lay down as plaque that is the ultimate cause? Addressing the lipoproteins/ldl as the cause, instead of what causes them to enter the intima and form plaque, could be an attack on the firefighter instead of the fire just because the fireman is always present at the fire! Reducing LDL that is essential to cellular function would then be just as bad as the plaque risk. What must be addressed is not LDL, but rather what is causing it to lay down plaque in the artery walls. That cause is inflammation in the arteries. And that has a wide range of causes and none are LDL. Address the cause of inflammation, and LDL will not harm you. High insulin/glucose due to bad diet is the main CAUSE of vascular disease and not LDL and its lipoproteins. Reducing LDL to reduce plaque burden could be cutting off your nose to spite your face! Instead, reduce the inflammatory factors that cause an otherwise beneficial LDL from becoming an issue.
Your exactly right. Cholesterol has been given a bad name for a long time, everyone was reducing cholesterol to such an extent that we now have dementia and alzhemirs at an all time high. Tread with caution is my motto as science is wonderful but also has made many wrong diagnosis in the past.
Great point, why would the body make something to harm itself ? It doesn't make bad cholesterol. It could be an excessive amount of sugar intake or what they feed the animals. Maybe understanding why the body does that would be more beneficial!
@@vcash1112understand the word "excess" nobody argues the value of cholesterol but in excess is the problem. The body produces glucose also so how can glucose be a problem?? the problem is when its present in "excess"
ASCVD can start and progress in the absence of inflammation as it is an independent risk factor. Make the LDLc high enough and it will produce ASCVD. If you are referencing Bart Kay please look for someone better as that guy is a muppet
@@888jucu never heard of Bart. But please explain why the level of LDL determines whether it enters the artery wall without a causal factor? Have not heard a single lipodologist be able to explain that, not even Tom Dayspring. Either the intima has to be compromised, high blood pressure prevalent, or some malady with the liver preventing its receptors from removing lipoproteins before they are reduced in particle size where they can enter through the intima. Else people of various ages would not exist who have extremely high LDL levels yet no atherosclerosis. Our bodies make LDL because it is essential to life. The level of LDL is irrelevant absent a causal factor leading to the formation of plaque. Otherwise, any level of LDL could breach of the intima. Actively reducing LDL can elevate mortality risk. Focusing on eliminating vascular inflammation instead.
My mom died at 36 from a heart attack. Her death certificate said arteriosclerosis was the cause. She drank and smoke. My apo b is 80 but lipoprotein a is 180. I’m definitely worried.
Smoking causes damage to the endothelial lining of the arteries, which results in blood clots forming. Overtime, if the damage keeps happening, these clots will build up layer by layer in the arteries thickening the artery wall until a final blood clot blocks the artery. Don't smoke! And read Malcolm Hendrick's book "The Clot Thickens."
Association, causation- theory Vs axiom... Lung cancer statistics show that lung cancer prevalence is increasing every year, in spite of the fact that smoking has been declining dramatically over the years. How do you explain that as smoking being declared as the one of the main culprits of lung cancer???
Judging from the comments, it seems there’s a lot of confusion about apo B and Peter’s approach. First, context matters. Keep in mind that he treats people whose goal is to live as long as possible-to never have a heart attack or stroke. If that’s not your goal, then there’s no need to be so aggressive with your apo B levels. The average American male has his first heart attack at age 65, and if you’re OK with that, then don’t worry about it. But if, like Peter’s patients, you don’t want your first MI before your 100th birthday, your best bet is to stop the underlying pathology (ASCVD) as soon as possible. Healthy lifestyle, low insulin, low blood pressure, high HDL, and excellent metabolic health are essential, for sure, but insufficient for many people. The most reliable way to stop plaque progression is to drive apo B as low as possible, much lower than current guidelines recommend, and much lower than most trials have achieved. This claim is beyond evidence-based medicine because no trial has been designed to test it directly. But it’s evidence-informed: all the interventional, observational, and Mendelian randomization data suggest that if you drive your apo B below a certain threshold (probably about 40 or 50 mg/dL for most people), you cannot grow plaque. In theory, it’s the closest thing to a guarantee that you will never have that heart attack. If you don’t trust the data, experiment on yourself. Get a CCTA or CAC to see if you’ve got plaque. Then do your lifestyle interventions, keto diet, or favorite supplements, and repeat it in two years to see if you’ve stopped disease progression. If you have, fantastic! But if you haven’t, take the drugs and get your apo B as low as a baby’s, then check again in another year or two. For those who think Peter Attia is unreliable because he believes cholesterol causes heart disease, I’d encourage you to open your mind and try to steel-man his argument yourself. Dive into the literature and do your best to debunk the influencers online who claim the establishment narrative is a lie. Don’t take their word for it, but don’t take Peter’s word for it, either. Do your own research with an open mind. For example, why do some observational studies show people with low LDL are at higher risk of death? Why do the statin trials show only modest benefit? Who makes money off statins today? You have to know how to read and interpret scientific articles, but the answers are out there. Until you understand that literature as well as he does, I don’t think you’re in a position to dismiss his conclusion. (Hint: the answer to that last question is no one.) The case against cholesterol (LDL or apo B, more specifically) has been studied exhaustively for over 50 years and is about as conclusive as anything in medicine.
No one makes money off statins?? Lipitor is considered to be the biggest selling drug of all time, with an estimated 131 Billions generated from sales. Billions.
@@mfkleven you mean no one makes money off the patent. The companies that manufacture and sell statins make plenty of money off them. Billions to be exact.
“Billions” is not exact, lol. Nor is it directionally accurate, although I don’t have numbers to argue. But you’re right in principle that generic drug manufacturers make some profit producing generic statins, if that’s your point. My point is that nobody’s “pushing” statins for financial gain, which is a common accusation from the anti-statin movement. Even when Lipitor was branded, doctors who prescribed it weren’t getting anything more than a plastic pen for doing so.
What was interesting for me in this discussion, was that Peter focussed on apoB levels, without even mentioning their VO2max level, which he largely has said is the single-most important determinant of life expectancy, or health span. Specifically, if someone has a 95th% VO2max, AND a high apoB, how does that affect life expectancy?
Points well taken, but smoking is NOT a good metaphor for ApoB. Smoking is not a natural part of the human body. It is completely and totally foreign. ApoB and cholesterol IS natural, normal and in fact, a REQUIRED part of our physiology. Therefore, it becomes a much more nuanced and complex question than smoking. Another question. Are we sure that higher ApoB is causal with regard to higher risk? Is it possible that the genes for lower ApoB also affect something else that actually lowers cardiovascular events? In other words, do the people with genetically lower ApoB also have lower inflammation, glucose and insulin, for example? I wouldn’t question this, except that I want to be sure. I just started a low dose statin, and I’m not crazy about the possible side effects.
I am healthy/physically fit 61 year old male. My ApoB came back at 150. Cardiologist prescribed 10 mg of Crestor(statin). Seems like Dr Attia favors statins now.
If your specific case warrants it, then yes. I've never heard him say that everyone should be on statins. The evidence is just abundantly clear that high LDL and ApoB is causal for negative cardiovascular health outcomes, so the side effects of statins are easily better than the alternatives in terms of longevity.
@@nichtsistkostenlos6565not really, there are other tests, like your HDL and triglycerides ratio. If you have 1 to 1 the likelihood of having a cardiac event goes down to pretty much zero.. there might be a few events but not many.. plus Statins cause more issues ie., Dementia, diabetes, Rhabdomyolysis in cases... plus Stains do not stop you from getting clogged arteries. It just slows the progression
Agreed, plus he doesn't speak of what people are eating.. do not consume, oils, processed foods, limited carbs... Eat real food... Meat, veggies if you like them.. some fruit if you like them..
Yes there is causality, nature already randomized some people with familiar hypercolesrerolemy, those are the mendelian randomization studies that he mentioned
@DiogenesNephew that is incorrect. See eg 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
Hi, I'm dealing with high lpa. Because of that obviously my apob is also high, nevertheless I reduced my ldl which can be a good strategy until pcsk9 or new meds are finally coming out for the public.
6:00 That's the most idiotic comparison I have ever heard! Even if I didn't know anything else about LDL (I do), the comparison of smoking with LDL is ridiculous on its own. First of all... most of the LDL in your blood is produced by your liver; "Smoke" or other carcinogenic components are not, save some excepcionally rare conditions. Secondly, smoking has zero benefits, while LDL is actually necessary to the production of testosterone and estrogen, so clearly... the "right amount of LDL cholesterol can't be zero, while smoking can and should. On the other hand, although his "causal" corollary is one I agree with, i.e: "You should focus in causation instead of correlation", that is exactly what the so called "evidence" about LDL and heart disease suggests... There's plenty of proof of it's correlation, but pretty much zero proof on its causation. In fact... what seems to be the case is that OXIDIZED LDL increases the risk of CVD. And what causes LDL to oxidize? Insulin resistance and a diet high in carbs, especially sugar.
I believe Peter's overall message is something many people need to hear. However, to Peter's credit to being a doctor and scientist, the way we see data has the same flaws all humans are subject to: we judge others by their actions, not their intent, because we cannot observe it. Data can show a system is not working and what is causing it to not work, but not the original intent of a system.
There are shepherds who live high in the mountains of europe and they smoke a lot. They get very little lung cancer. But, they take in a lot of goat cheese where the goats are eating weeds. And that cheese is very very high in anti-oxidants.
i have high Apo-B but my HDL, triglycerides, insulin, CRP and insulin are all normal. my CAC score is 1.5 & i am 56 y/o. my PCP just now puts me on ezetimibe after long debate on taking myself on statin. it only lowered my LDL a little and side effects were very bad on me. I quit cold turkey on it for 17 yrs. I also was put on Repatha but I had severe migraine, nausea and swollen fingers.
My guess is that while smoking may have brought you to the point where you might even in years show signs of the cancer, I'm not certain there isn't a point beyond which cancer will develop even if you give up (referring to 1:30). Some damage can heal very well and quickly, but DNA damage that is going to almost ensure cancer develops is not easily reversed.
I've watched a ton of RUclips doctors. Attia is the best. I always feel like I'm getting a modern, nuanced, agnostic take on how to increase my odds of remaining healthy.
Depends on what kind of fats you eat. The healthy version of keto (salmon, olive oil, nuts, seeds, avocado) will probably lower risk. But mainstream keto (bacon, cheese, red meat) is a heart hazard in my professional opinion
You have to watch out for insulin resistance meaning control your blood sugar. Level of your Lipids is only one of the many factors. If you only look at your Lipids and disregard your blood sugar control you will still end up with heart disease due to atherosclerosis. The reason is a high blood sugar leads to production of Advance Glycation end products (AGEs) these AGEs can react with proteins and lipids and even with other sugars when it does that AGEs increases inflammation and Reactive oxygen species (ROS) production both are one of the main drivers in Atherosclerosis. It does matter if your Cholesterol is 200-300mg/dl as long as you control your blood sugar you can avoid excess AGEs that can lead to heart disease. LIPIDS themselves doesn't cause Atherosclerosis the oxidation of lipids from ROS making oxidised Lipids due to AGEs makes them sticky and signals the macrophages to eat this Oxidized lipids leading to atherosclerosis. Yes LDL-c still matters but you should watch out for your Triglycerides more if you don't test for level of Apo-B. Red meat is not a hazard Saturated fats are less likely to be oxized than seed and vegetable oils that are high in polyunsaturated fats. PUFAs are more likely to be oxidized because their double bonds are more likely to react with ROS unlike SFA. This is basic Biochemistry. If you are gonna be animal-based diet just avoid processed meat and avoid process sugars High fat and protein diet should combine with a high sugar/carb intake because like i said it leads to production od AGEs. Keep your blood sugar in control so they don't react with the LDL-C in your blood that leads to oxidized LDL (oxLDL) that is then taken up by macrophages creating Foam cells and these Foam cells deposits in the lining of your blood vessels if the process happen to often it leads to plaque build up and thus atherosclerosis.
I’m confused. He says that high ApoB and LDL does not cause atherosclerosis, but later says he would treat someone with ApoB in the 130s. Can someone please explain to me what he means? I’ve been on a carnivore diet and my ApoB is high now.
Glycation and the resulting cardiovascular disease is the driver and when you have elevated damaged LDL and elevated triglycerides this is the key factor showing you have elevated glyation
So what's Dr A's conclusion??? It was cut short. The biggest question is if there was therapy to reduce ApoB levels, would that translate to a benefit? So far we have not got the answer to that.
LDL-cholesterol correlates pretty closely with apo B, so all the treatments used to lower LDL-C will also lower apo B (statins, PCSK9 inhibitors, ezetimibe, bempedoic acid). And the evidence showing their effectiveness is abundant and consistent: the degree of ASCVD risk reduction tracks linearly with apo B (or LDL-C) reduction.
@@0861USMC Those are associations, observations at a point in time; they do not show causation. We observe the same phenomenon with blood pressure: the lower the BP, the higher the mortality. Yet no one would argue that higher BP is protective. We all know hypertension is quite harmful and lower BP is protective. But in advanced illness, frailty, and toward the end of life, both BP and LDL-C drop, and death follows. That these declines precede death does not mean they cause it.
I thank the doctor for putting this much thought into cardio vascular health BUT the CAC score is a 5-10 year MACE risk assessment so I’m curious as to what steps he believes are needed with raised Apob and LDL? Statins have been linked to increased insulin resistance which cause inflammation and are said to be precursors of heart disease! I’m struggling with weather to take a statin at 57 years young, my second 5 year CAC is 0 my LDL is 250, a1c has been a steady 5.3 for the last 5 years my fasted glucose is always around 90 but my particulate count came back high for Apob my HDL is great and I follow a KETOvour diet…
CAC only shows calcified plaque, but newer, uncalcified plaque may still be present and is more unstable and dangerous. You can still follow a low carb diet without eating a lot of saturated fat, if you prefer low carb. Obviously, if you have some extra weight to lose, do that as well. If I were you, I'd take the statin. It was popular for a while to claim that we don't need to worry about LDL, but that idea has started to fade recently (and that's a good thing!). There really are mountains of evidence about the danger of high LDL.
@@juliebrown8375 I will refine your definition of the CAC score as I understand, it is a measure of risk of a cardiovascular event happening in the next 5-10 years, a 0 score means the lowest possible risk, not 0 risk. You are correct that by the time you register a calcium score that an event has already happened, not a heart attack per se but inflammation that has eventually calcified hence I’m happy I did a CAC (against my doctors wishes so I paid for it myself) 5 years ago to form a baseline, despite my low carb/fasting lifestyle I’ve not increased risk of a cardiovascular event at all. The medical industry must face up to the fact they have not honored the “first, do no harm” oath and should be ashamed of themselves.
"Linked with insulin resistance" doesn't mean causal, but let's say it's causal. How many people do you think die of direct side effects of insulin resistance compared to cardiovascular disease related to high ApoB? High cholesterol kills more people than anything else and many other causes combined. It's not hard to choose which is worse.
@@nichtsistkostenlos6565 In my experience (retired PCP), I saw very few people with heart disease who were not either diabetic/pre-diabetic or smokers. Furthermore, controlling blood sugar also improved lipids. Diabetics mostly die of heart disease. Familial hyperlipidemia is rare compared to DM. So I don't think you can really separate the two.
How do we know that LDL, specifically, is causully related to atherosclerosis? Why does he not bring up the examples of people that have genetically extremely high LDL over 600 but these people never develop atherosclerosis?
Science... High cholesterol and LDL are important risk factors for heart disease. That would contradict over 100 years of confirmed data which apparently you and others think doesn't exist. And it's scientific data that combines literally every single possible type of study you can imagine whether it's epidemiologically finding that people with the highest intakes of saturated fat have the highest levels of heart disease, -to the blinded experiments (which are extremely hard to do in nutrition) back in the 60's and 70's where saturated fat was replaced with unsaturated fat to specifically see if it prevented heart disease and it DID, -to studies where people were given intestine bypass surgeries to surgically drop their LDL by Henry Buckwald back decades ago showing that those who had the surgery, dropped their LDL and so too did their heart disease risk, -to genetic studies (there are some people who have genetically high cholesterol no matter what you do and those people if they are unlucky enough to be homozygous having both high cholesterol genes will have LDL levels 5-8 times as high as a normal person and they die in their teenage years of heart attacks). So not sure what you are talking about that they never develop atherosclerosis? -and then there were studies looking at the opposite, people who have genetically low LDL and they almost never get heart disease and live and average of about 10 years longer than their peers. There are endless studies, including the most powerful studies: The statin studies.
He did, indirectly. Like a lifelong smoker who doesn’t get lung cancer, you can find people with high LDL who don’t seem to develop heart disease. That doesn’t mean apo B doesn’t cause it, simply that it doesn’t always cause it in everyone. We know that LDL causes atherosclerosis because the mechanisms involved have been thoroughly established, but mostly because large interventional trials over several decades consistently show that ASCVD risk reduction tracks linearly with the dose and duration of LDL lowering.
@@mfklevenThere aren't any trials that do that conclusively. Which ones do you mean? I'm pretty sure they don’t show LDL-C causes atherosclerosis in a healthy body.
@@asarcadyn2414 The simplest example is familial hypercholesterolemia. There are kids having heart attacks simply because their apo B is extremely high. They are metabolically healthy, they don't smoke, they have great triglycerides, they're physically active, not obese, yet they still have aggressive ASCVD. So we know that apo B alone, when it's high enough, can be sufficient to drive disease. Just like smoking can be sufficient to drive lung cancer. However--and this where language needs to be precise--that does NOT mean that everyone with high apo B grows plaque. Many people, even some with FH, don't. It's not clear why some are protected. But most smokers also never get lung cancer. To your point, high LDL-C is certainly less likely to cause disease in a healthy body. But it may.
The mistake guys like Attia make is what I call being a "science chaser." All animals, including humans are not created by science. We were created by evolution. Also, our bodies are not just a bunch of parts like a car. We are one complete biological unit, and every part of the body has an effect on every other part. We don't completely even understand the science we think we know, and there are always unknown biological variables that may completely invalidate any of our scientific opinions... We evolved cholesterol for a reason, and guys like Attia need to pull back from the science a little bit, and see us for what we really are...evolutionary beings. The answers to health lie in evolutionary thought, not just scientific numbers...
Ok that is all fine and good i too debate the causality of events in my head on a daily basis 🙃and this might be the wrong video to pose this question but what do i eat? 🥩or🥦🥑or🍐🍏
High cholesterol, not low, is associated with greater longevity. Half the people who have a heart attack have low cholesterol. The key is to determine if the cholesterol is oxidized or damaged by requesting an advanced lipid panel. This will tell you particle size of cholesterol (damaged is smaller, and that is dangerous). Large buoyant cholesterol particles are not dangerous. They are necessary for proper hormone generation. That is why some doctors are using the carnivore diet (high cholesterol) to help people with infertility (they produce more sex hormones when their cholesterol is higher). People with higher cholesterol not only live longer, but they have less incidence of cancer.
Absolutely brother, my TC is 443 and LDL 378....TGL 51 and HDL 62, Uric acid 5.5 BP perfect 113/65 and RHR 42bpm, maxes out 192bpm and I'm 55....A CAC scan is £500 in Scotland, ApoB test £160....I bike 6-800km a month and would rather spend the money on bike parts or rib-eyes...If I drop dead on my bike one day I'll die a happy man and quality trumps quantity every time. Bad news for everyone I'm afraid, none of us gets out alive......
You don't get to choose unfortunately. Same process could just as easily see you end up in stroke ward for example. "atherosclerosis affects many other arterial beds [15-17] in ways that develop slowly over many years. Atherosclerosis causes disability and death from its contributions to: • Cerebral vascular accidents and cerebral ischemia • Dementia • Peripheral arterial disease • Heart failure • Renal artery stenosis • Carotid artery stenosis and embolization • Kidney failure • Hypertension • Aortic disease • Mesenteric artery disease • Erectile dysfunction • Frailty • Poor aging"
And there are many people who get lung cancer who have never smoked. So there must be other causative factors? Likewise ApoB?? Is there something that causes ApoB to oxidise? Or is it high levels of ApoB, period?
What you're saying is a logical fallacy. Yes some people who dunt smoke get lung cancer but a disproportionate number of lung cancer sufferers were smokers and that is statistically significant and leads us to know that smoking causes lung cancer. Whether some people get lung cancer for other reasons is a completely separate issue.
It is the right time to step in PRECISION MEDICINE based on deep understanding rather than basics models which are most of the time non relevant and wrong. Thanks for this sharing and experience. Thumb up Dr 's.
How well informed are you about your health really? You say non diabetic; how do you know? Have you had your glucose and insulin levels observed? Other biomarkers?
hmmm I don't totally agree. CVD is multifactorial, includes genetics, lifestyle, insulin resistance and many things we don't yet understand. Lung cancer is different there are likely 3 things that cause lung cancer; smoking (pollution), radon, and genetics. Apo(b) for sure is a risk but just that. So many other factors come into play with CVD.
All the common risk factors may be sufficient to drive ASCVD, but only hyperlipidemia is necessary. In other words, if you don’t have enough apo B particles flowing through your blood, you can’t grow plaque. Lowering apo B below that threshold, therefore, is the most reliable way to stop plaque progression. The same cannot be said of any other risk factor.
@@mfkleven Long discussion implying HTN, Insulin resistance, aging, Lp(a) aren't part of that equation? Certainly not saying that Apo(b) isn't a risk. But it one risk not necessary causal as smoking is to lung ca. Or Lp(a) is to aortic calcification. Are you saying if you drove Apo(b) to less than 30 there would never be any CVD?
@@dralexbrothers Yes, but with the simple caveat that there are no guarantees in medicine. There may be contexts in which 30 mg/dL may not be low enough to completely arrest atherogenesis. Lp(a) may be one such context. The combination of diabetes, smoking, and pre-existing advanced ASCVD may be another. But speaking generally, if the entire population maintained an apo B concentration of 30 mg/dL for life, heart disease would become a rare curiosity. From the article linked below: “Although the answer to this question in humans is not definitively known, several lines of evidence point to plasma LDL levels
Ok, in reference to the early discussion of ApoB. First, you have EPIDEMIOLOGICAL associations shown between ApoB and atherosclerosis, you do NOT have cause and effect. Note that the epidemiology of the cigarette case was FAR more clear cut as a causal factor than ApoB is. Second, the studies that show an association between ApoB and heart disease are being done on populations already compromised by poor metabolic health. In other words, just because metabolically unhealthy people (the norm in our society these days) shows an association between ApoB count and heart disease does NOT mean that the same association is valid when applied to a metabolically healthy individual.
In Puerto Rico there’s no even a APoB lab test. My cholesterol is at 240. I just had an electro and a stress test and everything is perfect. I’m going to the gym and have a low carb diet. What should I do?
Both law and medicine need legal and physical conditions to remain profitable. It's illogical to expect the beast to act one way when the actors within the beast act differently from outside expectations of the beast. My doctor and my lawyers need their boats and lakeside mansions. It is not to their benefit to have a sane, humane or fair system.
How does someone eati g carnivore for years and years have a CAC score of zero? Is this the same as a smoker never getting lung disease? Maybe chronic elevated insulin levels, insulin resistance, and inflammation are the cause? Maybe chloresterol is present to put the fire out?
But that doesnt factor in benefits of not treating it. I am not an expert on this at all but it wouldn't surprise me to hear that there could be some stuff ldl causes that is good, and also besides that treatment has some cost to it as well.
Garbage. To use two numbers to predict longevity is ridiculous. Modelling is not proof. "Association is not causation". It's all speculation and conjecture. Low cholesterol and ApoB measurements can be useful, but only in context of an individual's other health markers such as CAC, HBA1C, Homar-IR, blood pressure etc. Most would-be health influencers get big headed and start advising us on topics outside their knowledge base.
I’m surprised that he’s emphasizing LDL. All the recent analysis from studies, says that triglycerides to hdl ratio is most important. Plus, ldl below 120 triples all cause mortality compared to those over 250.
It's so popular these days to pretend that serum LDL cholesterol is just not a good enough or valid measure of heart disease. And it's like...uhh...YES it is. Just like high blood pressure is. It's a simple, very old fashioned and basic test, but they both are just as valid. And no, people who die of diseases such as cancer etc, can often times have a cholesterol level that drops, and it will remain until the cancer is treated. Same with hepatitis or infection. The disease comes first and causes the cholesterol to drop, not the other way around.
You are absolutely correct. Triglycerides is the problem. It leads to high super small LDL. Only super small LDL is associated with cardiovascular diseases.
LDL levels can be reduced by a number of diseases. So those observational studies showing higher mortality with lower levels, can just be a "sick man effect". If you specifically go in and reduce LDL levels then heart disease rates drops. The genetic condition familial hypercholesterolema specifically causes high LDL-C levels and sufferers of this have substantially reduced lifespans (15-30 years) if left untreated. A more severe form of this lifelong high LDL-C (homozygous FH) can see children as young as 5 having impacts, events in the teens, and sometimes death in 20's. People eating a carnivore diet can have LDL-C levels similar to those with homozygous FH! 😕 Severe Dyslipidemia Mimicking Familial Hypercholesterolemia Induced by High-Fat, Low-Carbohydrate Diets: A Critical Review, 2023
So a 24 year old sub 10% bodyfat . Doesn’t smoke or drink, use any drugs . Exercises 5 days a week. Works construction , eats all Whole Foods. Has high APO b. So I have atherosclerosis? Makes no sense
Any doctor who tells you that you have a pharmaceutical substance deficiency and then proceeds to use a hundred logical fallacies while claiming he’s obsessed with causation and calling anyone who disagrees “idiotic” should make you RUN in the opposite direction. Check his stock portfolio.
Over-simplified and convoluted logic. If a cop (LDL in this case) happens to be present near a place where a crime (atherosclerosis in this case) is conducted, does not imply that the cop was responsible for the crime! The atherosclerosis process is far more complex - oxidized LDL is one actor but there is much more to this story!
I just can’t get behind the broad very vague brush that’s being painted with. Yes, under certain circumstances ApoB is destructive. But there is so much data that demonstrates that metabolically healthy adults with elevated LDL levels do not benefit from “medical intervention”. The other risk factors he spoke about, blood pressure, insulin sensitivity, endothelial health. These things, when at dangerous stages cause LDL to become the means whereby atherosclerosis begins and proliferates. *Elevated to a certain extent… Not LDL at 300 or greater… That is an issue and may demonstrate an issue at the genetic level.
Metabolically healthy adults are at lower risk of heart disease, for sure. But plenty of metabolically healthy people still grow plaque and have heart attacks. All you need for atherosclerosis to develop is sufficient apo B particles flowing through your blood, and the more of them you have, the more likely you are to grow plaque. But there’s no need to guess about risk, either. If you have elevated LDL but are otherwise healthy, get a CCTA or CAC and see if you’re growing plaque. If not, then you may not need to treat your lipids right now. But if you’re growing plaque, the most reliable way to stop it is to get your apo B as low as possible.
This is so poorly argued. With smoking, we know the actual mechanics of how it causes lung cancer. By contrast, Peter is using statistics and statistics alone to try to argue that cholesterol "causes" heart disease. He doesn't explain the disease mechanism. Why? Because most experts agree it's poorly or incompletely understood. It is not plaque formation per se that leads to serious cardiac events; it is unstable (or "vulnerable") plaque. And it's not cholesterol generally that ends up in that plaque; it's oxidized cholesterol. Cholesterol is not the villain. It's more systemic issues like inflammation, metabolic syndrome, etc.
To my point, to quote the Johns Hopkins website: "It's not clear exactly how atherosclerosis starts or what causes it." Cholesterol is listed as one among many "risk factors." That's not the same as definitively arguing for causation.
Who cares? If an individual takes statins events go down for that individual. Straw man arguments. Doesn't matter if we know the causes of lung cancer or not.
If smoking is causally related to lung cancer, then 100% of people who smoke would get lung cancer. Maybe you could quibble about “well, this guy only had 20 cigs his whole life…” vs “2 packs a day for 20 years…”. But if it is causal it is causal. The word has a meaning. If less than 100% of people who smoke get lung cancer (and it is less than 70) then it is not causal.
He addressed this in the clip. Obviously not 100% of all smokers will get lung cancer (some will be carried off by one of the plethora of other smoking related diseases) but the correlation is sufficiently significant as to consider it causal.
@@turbobros_online1561we can quibble over terminology but the facts are that smoking increases your risk of cancer to a staggering extent. Though if I were a smoker I’d be more worried about other health consequences. I think your definition of causal is rather simplistic but I’m not really fussed
@@sivikasi I think people manipulate language to their benefit. What part of the "smoking" is causal for lung cancer? Is it the actual smoking like the actual act of smoking caused cancer or is it caused by a secondary effect of smoking such as physical or chemical damage to the lung tissues? Wouldn't that be fundamentally different? Ya know if I were to shoot a propane tank with a tracer round of ammo, that would "cause" that tank to explode. What if I emptied the tank first and then shot it? It wouldn't explode right? So was shooting the full tank the "cause" of the explosion? Or did the shot create a condition(source of combustion/heat combined with flammable/combustible gas and oxygen) that caused the explosion? Shooting the tank created a condition that caused the explosion. If you really look at the available research with scrutiny, you see it doesn't show causality, only correlation. No one has ever shown how APO-B is causal in CVD because you see people with high APO-B and no signs on CVD and you see people who have died from CVD complication that had low APO-B and low overall cholesterol.
Does Attia believe that humans were born with cigarettes in their mouths? LDL is part of us from inception, so tampering with its level may or may not be the best for us, and cannot be compared to a foreign substance such as smoke.
I'd really love to know just how many "health conscious" people there are on these sites who are obsessed with all these numbers, facts and figures that have willingly taken the mRNA clot shots? Must be a lot of ticking time bombs worrying about LDL while having mini clots, TIA's, myocardial damage from these bio-weapons???
So he’s saying that there is a genetic statin deficiency? 😂😂😂 inhaling a toxic smoke is not the same as a particle produced by our bodies. MDs have gotten so robotic in this country. 😊
You completely missed the plot. It’s an apt analogy that compares how the medical system currently approaches preventative care, and the timeline used. Attia is presenting the idea that we should approach causal, modifiable risk much earlier than we do now. Smoking CAUSES lung cancer, so we say don’t smoke at all. Elevated LDL CAUSES atherosclerosis, so we should apply the same metric and keep LDL low as soon as possible for as long as possible. Also, genetic statin deficiency was never mentioned the video and makes no sense. A statin is a medication, not something your body synthesizes. You can’t be genetically deficient in something that your body doesn’t produce. People have genetic conditions that cause them to have extremely low LDL and vice versa. It’s clearly shown that lower LDL leads to less and less cardiac events.
I have to disagree that we should intervene and prevent activities that are causal to mortality. If we assume there is some utility from the activity, like eating steak, and has low ldl and others factors, the benefit of eating the steak might be of more value than a forecast for a longer life.
I think Peter would agree that you’re certainly allowed to make that judgment call. He’s simply arguing for informed consent-as patients, we should all be aware of what causes heart disease, and that treating the underlying cause early is the best way to avoid having to treat the disease itself later. If we know that and still feel steak is worth the risk, great. However, I also don’t think he’d fault you for eating steak anyway. He’s noted in other places that the risk of saturated fat is easily mitigated pharmacologically when appropriate.
@@hamadax97 Of course there are many benefits to eating steak, including high quality protein, abundant micronutrients, zero spike in blood glucose, and of course taste. You might argue the risks outweigh them, but the benefits are quite real.
When the numbers for high ApoB and CVD are of a similar size to cigarette smoking and lung cancer I might take Attia seriously but until then he is simply scare-mongering.
He is simply wromg wbout cholesterol. Low cholesterol is associated with increased mortality, even compared to high cholesterol. In womrn high cholesterol is assiciated with lower mortality. Attia is turning into a clown
"for most people no meaningful benefit and a lfie of pain and misery"?? Where do you even come up with this non-sense. Statins are EXTREMELY impactful on health outcomes and most people barely have any side effects.
well, his approach evolved with the new study data came in, just because he is not following the trend now does not make him bad, I used to do fasting keto and stuff, now I have a much more moderate approach to it.
@@richardzhang8312 I absolutely agree with you. Live your life as n=1 experiment, keep an open mind, try different things with support from Doctors and published Research, until you find what works best For You. But don't go around saying things like As far as I'm concerned everyone over 19 should be on a statin, as some doctors are doing currently. This Lazy, one-size-fits-all approach, with the drug script pad and the differential diagnosis, is one of the worst trends in modern medicine, where patients tend to be treated not as individuals, but as an amorphous mass of identical people. It ignores a significant number of patients for whom the magic cure of the moment causes harm instead of good, as you would've no doubt seen with the side effects of the vaccine for the unidentified-virus-of-unknown-origen, for which they now have filed a Class Action. This example is no different.
This clip is from the Huberman Lab episode "Dr. Peter Attia: Exercise, Nutrition, Hormones for Vitality & Longevity.” The full episode can be found on RUclips here: ruclips.net/video/DTCmprPCDqc/видео.html
Any doctor who tells you that you have a pharmaceutical substance deficiency and then proceeds to use a hundred logical fallacies while claiming he’s obsessed with causation and calling anyone who disagrees “idiotic” should make you RUN in the opposite direction. Check his stock portfolio.
I am about to be 82. I have been on statins for many years and always think I want to get off them. I have moderately high blood pressure which is controlled with diuretics. I have no other risk factors other than my age. My total cholesterol is around 160 and my LDL is extremely low I believe due to the statins. Watching this I am convinced by Dr. Attia to forget about getting off of statins and continue doing what I do. Eat well, get regular exercise, take my meds and get as much enjoyment out of life as I can. Thanks for these conversations.
No one over 75 should be on a statin for prevention.
@@sellmavwhat about PCSK9 inhibitors? (Assuming one can afford it).
Why is it that I could listen to these two all day long speak while in a meditative state? You both are mesmerizing. 🎉
The analogy make no sense. With out APOB we would die. It is needed and natural. Smoking it not needed or natural.
¡Hola Profe!Going to relisten the episode! The shorter format is doing a good job to remind ,what episodes to rewatch or relisten Thank You,for all You are doing .
Such a Privilege to listen and learn from these two amazing gentlemen.
Yet NO REFERENCES LISTED IN THE SHOW NOTES !
Another smooth talker WITH ZERO PROOF !
Until data is published HE CAN POUND SAND !
So much conflicting info out there. I have seen several studies that show; higher cholesterol is associated with longevity, a Korean study showed that those with very low levels (sub 150) had higher mortality than those from 200-250, more than 50% of those admitted for heart attacks have levels in the 'normal' range. With advances in medicine, stents, statins and the war on smoking, heart disease is still the number 1 killer. I just don't think we have this figured out yet.
No, it's been figured out. All studies that show higher mortality for people with low total cholesterol are demonstrating reverse causality. That is, that those people with low cholesterol probably were sick with some disease that causes low cholesterol like cancer, old age, possibly on high dose statins, etc. If you control for these alternate morbidities in low vs. high cholesterol study participants, the low cholesterol participants have lower mortality every single time.
There’s a lot of studies showing this correlation with almost everything
One of the main reasons for this is people with cancer and very ill people have low cholesterol due to their illness, also after a heart attack or cardiovascular event your cholesterol drops significantly
When these things are taken into account then we can see that low ApoB in healthy people are at lower risk or heart attack than those with higher levels , same association with alcohol , it’s called a J curve happens with observational studies usually referred to as a paradox, “cholesterol paradox” alcohol paradox and so on
@@dominickcruz7252yea but i remember hearing one doctor say they had a decade of research on them people or something like that.
So im sure they wasn’t ill for a decade
No thinking , we definitely do not. Don’t sell yourself short
@@dominickcruz7252 That's simply not true. A study of the 1999-2014 NHANES data adjusted for possible confounders like cancer and still found that people with lower LDL (less than 80) had a much higher hazard ratio for all-cause mortality than even those with LDLs as high as 300, which the anti-cholesterol crowd would say is basically a heart attack waiting to happen. Well, the data says otherwise.
I’m glad that you are keeping science at the forefront. Cardiovascular disease kills an American every 12 seconds and hypercholesterolemia is a profound - and eminently treatable -risk factor
Just went to the doctor in the Netherlands, she didn't know what apoB was 😂
She was looking in the system and was not able to test me on that.
When I go to a blood test site I can buy a ApoB test for 30 euro, so I will do that
True, you read about ApoB everywhere and in Holland it isnt even mentioned on a general blood test. Total cholesterol, LDL, HDL, triglycerides etc, but no ApoB
I hate doctors
I'm not getting any tests done. Screw it. I cut out all sugar, processed foods, carbs, whatever. I don't trust studies anymore.
Its a good argument and a good analogy, but there is a fundamental problem. Smoking is a negative intervention. Not smoking is a non-intervention. You dont have to weigh the risk of not smoking against the risk of smoking.
Statins use is an active intervention, which while it does lower cholesterol, has risk of diabetes and dementia, muscle pains. In this case it does make sense to evaluate when the risk of high cholesterol becomes substantial enough to make an active intervention known to cause negative effects
Astute observation. Totally agree. Except that statins do not cause dementia--multiple studies have debunked this fear. The lipophilic statins may cause "brain fog" in some people, but it's reversible. Muscle pain is pretty common, but also reversible. These issues, therefore, should not be feared, just dealt with if they arise.
But statins do increase the risk of diabetes in some people, and that's a serious concern that needs to be acknowledged and followed closely when prescribed.
I eagerly await the day when PCSK9 inhibitors will be widely available, as they appear to have literally zero significant side effects--so far.
@@mfkleven yes, I have heard pcsk9 inhibitors are too expensive
@@mfklevenstudies with how long of a duration? which ones?
Excellent observation, sir. Also, I'm not buying yet that LDL is causally related to increase in heart disease. It's just indicative of a possibility. If your LDL is high, then why not just get your arteries checked to see if it's actually doing anything. If not, you should be good!
I am so glad to see this comment, as Peter is obviously not comparing apples to apples in his analogy. Not smoking has ZERO side effects, statins - well surely there is at least SOME side effects.
Love how they boil it down to its essential essence.
I have low LDL and low ApoB but still rather significant atherosclerosis. How come Type2 diabetes inflammation is not discussed here? No MD ever warned me about Type2 and atherosclerosis either.
Do you also have low hdl
How low are we talking about? Also atheroserosis is an area under the curve problem. Your apoB might be low now, but what was the lvl during the last decade? And before that?
Since the war on cholesterol, dementia and Alzheimer's have skyrocketed.
I'm not gonna sacrifice my operating system for my motor.
And if I'm wrong I'll die young eating the foods that make me feel the most well.
Me too. I’ll never take a statin. Another scam by big pharma.
Peter Attia needs to have a debate with James Mason. The two are diametrically opposed in their claims and both extensively cite studies and resources.
With a quack? Nah
@@jxeh1442 If he's a quack, shouldn't take long to dispatch his arguments.
@@utarian7i could spend the rest of my life quickly dispatching quacks, and there would be a limitless supply of more quacks.
@@iloled2924 Though there's only one claim to dispatch, not endless.
I think you mean Dr. Paul Mason? And yes, I agree that would be a good debate.
I find it a bit curious that Dr. Attia calls himself "obsessive" with causality, when LDL is not the cause per se. Oxidized LDL that gets within arterial walls causes plaque, not standard LDL. The causes for atherosclerosis, then, are related to the inflammation that promotes that oxidation. We should be looking at lowering that instead of waging war on an essential molecule.
That's what I'm finding out as well. Maybe he addressed in the full lenght podcast, but I find it frustrating that he casually dismisses people that dispute the causation by saying that they're not credible without addressing this important fact.
There are all sorts of steps along the atherogenic pathway one could point to and say, "that's the cause," including oxidation of a retained LDL particle, as you point out. But the one most easily manipulated therapeutically, the most actionable one, the one most consistently and effectively shown to reduce atherosclerosis when treated is LDL (or apo B) concentration in the blood.
There is a definition to the term "causal," and LDL fits it.
Practically speaking, if you focus on oxidized LDL, how would you treat that?
Furthermore, LDL, to my knowledge, is not essential.
@@mfkleven spot on.
Its not an either or. You need to reduce the lipoprotein numbers that are likely to get lodged in the endothelium, and you also need to also reduce inflammation in the arteries that increases risk of oxidation. Ideally you should be doing both. Cholesterol is an “essential” molecule, but you do not high amounts of it circulating thru your bloodstream. Theres no downside to loweing ApoB in the bloodstream. All of your cells manufacture cholesterol for membrane structure and other uses like hormones. It does not need to be high in the extracellular fluid of your bloodstream.
Also, Peter attia isnt saying LDL is the cause. If you ever listen to his podcasts in depth, he is very clear that the main culprits are the lipoproteins that shuttle around LDL, not the cholesterol itsself.
I agree. LDL is a protein carrying essential cholesterol to the cells it is not a cause. (there is no good or bad cholesterol it is all the same). Sugar --> Inflammation --> Oxidation --> Plaque buildup --> Restriction in blood flow --> atherosclerosis IS a causal relationship whether you believe in it or not.
i've listened to the full interview as well... his talk @ancestral health symposium 2012 is a good one [again no slides], what strikes me here is he (& you) are imbibing Bayesian inference. Given a result how do we then work backwards to assess risk ?. To moi it feels like chaos theory... Did finally start on his book which i ofttimes fail to do after seeing the movie :;
I get conflicting information on whether I am ok or not.
My current numbers are: Total Cholesterol 244, Triglycerides 58, HDL 106, LDL 128, ApoB 105, ApoA-1 222 mgdL. These have roughly been my numbers for years.
Originally I was told not to worry about my high LDL because my HDL is high and will protect me. Now my HDL is considered too high and is not good any more.
I then had my particle size tested, and the test showed low risk pattern with larger particle size and low insulin resistance. So I was considered good - no treatment necessary.
Now the most important indicator appears to be ApoB. My ApoB is too high so I need treatment.
I have also seen elsewhere that the most important indicator is the ratio ApoB / ApoA-1. This number is good for me due to my high ApoA-1 so I don't need treatment.
My doctor is now focusing on the ApoB only and wants me on crestor. This seems to agree with what you are saying. It just seems like the parameters keep changing.
I am 60, female, BMI 21, moderate exercise and eat healthy. (healthy fats, veges, some carbs, low sugar).
I prefer to avoid statins.
You get on the Crestor yet?
Ask your doctor about Repatha or another non-statin. I dont think you levels warrant a statin but to be honest, at your age, id be on one regardless.
Hi, soluble fiber is shown to decrease apob. Consider increasing fiber intake significantly - 40 gm per day. A 20 gm supplementation with psyllium husk powder can help.
I lowered mine by taking Niacin, it did lower my ApoB. I took it for 3 months but it gave me gout, so now I eat low carbs and occasionally take Niacin.
Watch some interviews of Robert Lustig or better yet read his book.
LOVE Dr A and Andrew as well I have learned sooooo much and continue to do so
But what if the lipoproteins that carry LDL to where its needed in the body are quite essential to life, and its what causes those lipoproteins to lay down as plaque that is the ultimate cause? Addressing the lipoproteins/ldl as the cause, instead of what causes them to enter the intima and form plaque, could be an attack on the firefighter instead of the fire just because the fireman is always present at the fire! Reducing LDL that is essential to cellular function would then be just as bad as the plaque risk. What must be addressed is not LDL, but rather what is causing it to lay down plaque in the artery walls. That cause is inflammation in the arteries. And that has a wide range of causes and none are LDL. Address the cause of inflammation, and LDL will not harm you. High insulin/glucose due to bad diet is the main CAUSE of vascular disease and not LDL and its lipoproteins. Reducing LDL to reduce plaque burden could be cutting off your nose to spite your face! Instead, reduce the inflammatory factors that cause an otherwise beneficial LDL from becoming an issue.
Your exactly right. Cholesterol has been given a bad name for a long time, everyone was reducing cholesterol to such an extent that we now have dementia and alzhemirs at an all time high. Tread with caution is my motto as science is wonderful but also has made many wrong diagnosis in the past.
Great point, why would the body make something to harm itself ? It doesn't make bad cholesterol. It could be an excessive amount of sugar intake or what they feed the animals. Maybe understanding why the body does that would be more beneficial!
@@vcash1112understand the word "excess" nobody argues the value of cholesterol but in excess is the problem. The body produces glucose also so how can glucose be a problem?? the problem is when its present in "excess"
ASCVD can start and progress in the absence of inflammation as it is an independent risk factor. Make the LDLc high enough and it will produce ASCVD. If you are referencing Bart Kay please look for someone better as that guy is a muppet
@@888jucu never heard of Bart. But please explain why the level of LDL determines whether it enters the artery wall without a causal factor? Have not heard a single lipodologist be able to explain that, not even Tom Dayspring. Either the intima has to be compromised, high blood pressure prevalent, or some malady with the liver preventing its receptors from removing lipoproteins before they are reduced in particle size where they can enter through the intima. Else people of various ages would not exist who have extremely high LDL levels yet no atherosclerosis. Our bodies make LDL because it is essential to life. The level of LDL is irrelevant absent a causal factor leading to the formation of plaque. Otherwise, any level of LDL could breach of the intima. Actively reducing LDL can elevate mortality risk. Focusing on eliminating vascular inflammation instead.
I am trying to dig deep into knowledge on cholesterol. Starting w anyone speaking of it on Dr Hubermans podcast .
My mom died at 36 from a heart attack. Her death certificate said arteriosclerosis was the cause. She drank and smoke. My apo b is 80 but lipoprotein a is 180. I’m definitely worried.
Did she ate a lot of red meat?
@@kotenoklelu3471For somebody to have a heart attack in their thirties, whether they ate red meat or not wouldn't even be in the top 10 concerns.
@@nichtsistkostenlos6565 she died from it
Please resesarch studies regarding high LDL and longevity.
Smoking causes damage to the endothelial lining of the arteries, which results in blood clots forming. Overtime, if the damage keeps happening, these clots will build up layer by layer in the arteries thickening the artery wall until a final blood clot blocks the artery.
Don't smoke! And read Malcolm Hendrick's book "The Clot Thickens."
Association, causation- theory Vs axiom... Lung cancer statistics show that lung cancer prevalence is increasing every year, in spite of the fact that smoking has been declining dramatically over the years. How do you explain that as smoking being declared as the one of the main culprits of lung cancer???
Judging from the comments, it seems there’s a lot of confusion about apo B and Peter’s approach.
First, context matters. Keep in mind that he treats people whose goal is to live as long as possible-to never have a heart attack or stroke. If that’s not your goal, then there’s no need to be so aggressive with your apo B levels. The average American male has his first heart attack at age 65, and if you’re OK with that, then don’t worry about it.
But if, like Peter’s patients, you don’t want your first MI before your 100th birthday, your best bet is to stop the underlying pathology (ASCVD) as soon as possible. Healthy lifestyle, low insulin, low blood pressure, high HDL, and excellent metabolic health are essential, for sure, but insufficient for many people. The most reliable way to stop plaque progression is to drive apo B as low as possible, much lower than current guidelines recommend, and much lower than most trials have achieved.
This claim is beyond evidence-based medicine because no trial has been designed to test it directly. But it’s evidence-informed: all the interventional, observational, and Mendelian randomization data suggest that if you drive your apo B below a certain threshold (probably about 40 or 50 mg/dL for most people), you cannot grow plaque. In theory, it’s the closest thing to a guarantee that you will never have that heart attack.
If you don’t trust the data, experiment on yourself. Get a CCTA or CAC to see if you’ve got plaque. Then do your lifestyle interventions, keto diet, or favorite supplements, and repeat it in two years to see if you’ve stopped disease progression. If you have, fantastic! But if you haven’t, take the drugs and get your apo B as low as a baby’s, then check again in another year or two.
For those who think Peter Attia is unreliable because he believes cholesterol causes heart disease, I’d encourage you to open your mind and try to steel-man his argument yourself. Dive into the literature and do your best to debunk the influencers online who claim the establishment narrative is a lie. Don’t take their word for it, but don’t take Peter’s word for it, either. Do your own research with an open mind. For example, why do some observational studies show people with low LDL are at higher risk of death? Why do the statin trials show only modest benefit? Who makes money off statins today? You have to know how to read and interpret scientific articles, but the answers are out there. Until you understand that literature as well as he does, I don’t think you’re in a position to dismiss his conclusion. (Hint: the answer to that last question is no one.)
The case against cholesterol (LDL or apo B, more specifically) has been studied exhaustively for over 50 years and is about as conclusive as anything in medicine.
No one makes money off statins?? Lipitor is considered to be the biggest selling drug of all time, with an estimated 131 Billions generated from sales. Billions.
@@phantomguard71 Lipitor came off patent years ago. Today, all statins (except Livalo) are generic. No one makes money off statins.
@@mfkleven you mean no one makes money off the patent. The companies that manufacture and sell statins make plenty of money off them. Billions to be exact.
“Billions” is not exact, lol. Nor is it directionally accurate, although I don’t have numbers to argue. But you’re right in principle that generic drug manufacturers make some profit producing generic statins, if that’s your point. My point is that nobody’s “pushing” statins for financial gain, which is a common accusation from the anti-statin movement. Even when Lipitor was branded, doctors who prescribed it weren’t getting anything more than a plastic pen for doing so.
This makes too much sense.
This is good health info.
What was interesting for me in this discussion, was that Peter focussed on apoB levels, without even mentioning their VO2max level, which he largely has said is the single-most important determinant of life expectancy, or health span. Specifically, if someone has a 95th% VO2max, AND a high apoB, how does that affect life expectancy?
Points well taken, but smoking is NOT a good metaphor for ApoB. Smoking is not a natural part of the human body. It is completely and totally foreign. ApoB and cholesterol IS natural, normal and in fact, a REQUIRED part of our physiology. Therefore, it becomes a much more nuanced and complex question than smoking.
Another question. Are we sure that higher ApoB is causal with regard to higher risk? Is it possible that the genes for lower ApoB also affect something else that actually lowers cardiovascular events? In other words, do the people with genetically lower ApoB also have lower inflammation, glucose and insulin, for example?
I wouldn’t question this, except that I want to be sure. I just started a low dose statin, and I’m not crazy about the possible side effects.
Interesting stuff.
I am healthy/physically fit 61 year old male. My ApoB came back at 150. Cardiologist prescribed 10 mg of Crestor(statin). Seems like Dr Attia favors statins now.
If your specific case warrants it, then yes. I've never heard him say that everyone should be on statins. The evidence is just abundantly clear that high LDL and ApoB is causal for negative cardiovascular health outcomes, so the side effects of statins are easily better than the alternatives in terms of longevity.
@@nichtsistkostenlos6565not really, there are other tests, like your HDL and triglycerides ratio. If you have 1 to 1 the likelihood of having a cardiac event goes down to pretty much zero.. there might be a few events but not many.. plus Statins cause more issues ie., Dementia, diabetes, Rhabdomyolysis in cases... plus Stains do not stop you from getting clogged arteries. It just slows the progression
Agreed, plus he doesn't speak of what people are eating.. do not consume, oils, processed foods, limited carbs... Eat real food... Meat, veggies if you like them.. some fruit if you like them..
Yes there is causality, nature already randomized some people with familiar hypercolesrerolemy, those are the mendelian randomization studies that he mentioned
@DiogenesNephew that is incorrect. See eg 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
Let's first start with defining LONGEVITY and is it always a benefit?
No need
Any thoughts on LPa as a cardiovascular target?
Hi, I'm dealing with high lpa. Because of that obviously my apob is also high, nevertheless I reduced my ldl which can be a good strategy until pcsk9 or new meds are finally coming out for the public.
Yes to Causality !! Medical training should include tools such as Causal Networks
6:00 That's the most idiotic comparison I have ever heard! Even if I didn't know anything else about LDL (I do), the comparison of smoking with LDL is ridiculous on its own. First of all... most of the LDL in your blood is produced by your liver; "Smoke" or other carcinogenic components are not, save some excepcionally rare conditions. Secondly, smoking has zero benefits, while LDL is actually necessary to the production of testosterone and estrogen, so clearly... the "right amount of LDL cholesterol can't be zero, while smoking can and should. On the other hand, although his "causal" corollary is one I agree with, i.e: "You should focus in causation instead of correlation", that is exactly what the so called "evidence" about LDL and heart disease suggests... There's plenty of proof of it's correlation, but pretty much zero proof on its causation. In fact... what seems to be the case is that OXIDIZED LDL increases the risk of CVD. And what causes LDL to oxidize? Insulin resistance and a diet high in carbs, especially sugar.
I believe Peter's overall message is something many people need to hear. However, to Peter's credit to being a doctor and scientist, the way we see data has the same flaws all humans are subject to: we judge others by their actions, not their intent, because we cannot observe it. Data can show a system is not working and what is causing it to not work, but not the original intent of a system.
My father’s cholesterol was 180 his entire life. My mom’s has been 220-250 and she’s 87. My father passed in 2007.
There are shepherds who live high in the mountains of europe and they smoke a lot. They get very little lung cancer. But, they take in a lot of goat cheese where the goats are eating weeds. And that cheese is very very high in anti-oxidants.
i have high Apo-B but my HDL, triglycerides, insulin, CRP and insulin are all normal. my CAC score is 1.5 & i am 56 y/o. my PCP just now puts me on ezetimibe after long debate on taking myself on statin. it only lowered my LDL a little and side effects were very bad on me. I quit cold turkey on it for 17 yrs. I also was put on Repatha but I had severe migraine, nausea and swollen fingers.
Peter, what about lipoprotein (a)?
My guess is that while smoking may have brought you to the point where you might even in years show signs of the cancer, I'm not certain there isn't a point beyond which cancer will develop even if you give up (referring to 1:30). Some damage can heal very well and quickly, but DNA damage that is going to almost ensure cancer develops is not easily reversed.
I've watched a ton of RUclips doctors. Attia is the best. I always feel like I'm getting a modern, nuanced, agnostic take on how to increase my odds of remaining healthy.
Curious how ApoB levels measure in people following the Keto diet. Does the lipid fuel movement and consumption cause heart and cardiovascular issues?
Depends on what kind of fats you eat. The healthy version of keto (salmon, olive oil, nuts, seeds, avocado) will probably lower risk. But mainstream keto (bacon, cheese, red meat) is a heart hazard in my professional opinion
You have to watch out for insulin resistance meaning control your blood sugar. Level of your Lipids is only one of the many factors. If you only look at your Lipids and disregard your blood sugar control you will still end up with heart disease due to atherosclerosis. The reason is a high blood sugar leads to production of Advance Glycation end products (AGEs) these AGEs can react with proteins and lipids and even with other sugars when it does that AGEs increases inflammation and Reactive oxygen species (ROS) production both are one of the main drivers in Atherosclerosis.
It does matter if your Cholesterol is 200-300mg/dl as long as you control your blood sugar you can avoid excess AGEs that can lead to heart disease. LIPIDS themselves doesn't cause Atherosclerosis the oxidation of lipids from ROS making oxidised Lipids due to AGEs makes them sticky and signals the macrophages to eat this Oxidized lipids leading to atherosclerosis.
Yes LDL-c still matters but you should watch out for your Triglycerides more if you don't test for level of Apo-B.
Red meat is not a hazard
Saturated fats are less likely to be oxized than seed and vegetable oils that are high in polyunsaturated fats. PUFAs are more likely to be oxidized because their double bonds are more likely to react with ROS unlike SFA. This is basic Biochemistry.
If you are gonna be animal-based diet just avoid processed meat and avoid process sugars
High fat and protein diet should combine with a high sugar/carb intake because like i said it leads to production od AGEs.
Keep your blood sugar in control so they don't react with the LDL-C in your blood that leads to oxidized LDL (oxLDL) that is then taken up by macrophages creating Foam cells and these Foam cells deposits in the lining of your blood vessels if the process happen to often it leads to plaque build up and thus atherosclerosis.
@@The_Average_RUclips_Enjoyerbecause I just started this animal based diet after being vegan for years
I’m confused. He says that high ApoB and LDL does not cause atherosclerosis, but later says he would treat someone with ApoB in the 130s. Can someone please explain to me what he means? I’ve been on a carnivore diet and my ApoB is high now.
Glycation and the resulting cardiovascular disease is the driver and when you have elevated damaged LDL and elevated triglycerides this is the key factor showing you have elevated glyation
Why do you focus on apo b rather then the apo b + a1 ratio?
So what's Dr A's conclusion??? It was cut short.
The biggest question is if there was therapy to reduce ApoB levels, would that translate to a benefit? So far we have not got the answer to that.
LDL-cholesterol correlates pretty closely with apo B, so all the treatments used to lower LDL-C will also lower apo B (statins, PCSK9 inhibitors, ezetimibe, bempedoic acid). And the evidence showing their effectiveness is abundant and consistent: the degree of ASCVD risk reduction tracks linearly with apo B (or LDL-C) reduction.
The lower LDL, the higher the mortality.
@@0861USMC No. Low or high LDLs confer increased mortality. There is a normal one should aim for.
@@creativesource3514
No, research shows elderly patients with higher than average LDLs live longer.
@@0861USMC Those are associations, observations at a point in time; they do not show causation. We observe the same phenomenon with blood pressure: the lower the BP, the higher the mortality. Yet no one would argue that higher BP is protective. We all know hypertension is quite harmful and lower BP is protective. But in advanced illness, frailty, and toward the end of life, both BP and LDL-C drop, and death follows. That these declines precede death does not mean they cause it.
I thank the doctor for putting this much thought into cardio vascular health BUT the CAC score is a 5-10 year MACE risk assessment so I’m curious as to what steps he believes are needed with raised Apob and LDL? Statins have been linked to increased insulin resistance which cause inflammation and are said to be precursors of heart disease! I’m struggling with weather to take a statin at 57 years young, my second 5 year CAC is 0 my LDL is 250, a1c has been a steady 5.3 for the last 5 years my fasted glucose is always around 90 but my particulate count came back high for Apob my HDL is great and I follow a KETOvour diet…
CAC only shows calcified plaque, but newer, uncalcified plaque may still be present and is more unstable and dangerous. You can still follow a low carb diet without eating a lot of saturated fat, if you prefer low carb. Obviously, if you have some extra weight to lose, do that as well.
If I were you, I'd take the statin. It was popular for a while to claim that we don't need to worry about LDL, but that idea has started to fade recently (and that's a good thing!). There really are mountains of evidence about the danger of high LDL.
@@juliebrown8375 I will refine your definition of the CAC score as I understand, it is a measure of risk of a cardiovascular event happening in the next 5-10 years, a 0 score means the lowest possible risk, not 0 risk. You are correct that by the time you register a calcium score that an event has already happened, not a heart attack per se but inflammation that has eventually calcified hence I’m happy I did a CAC (against my doctors wishes so I paid for it myself) 5 years ago to form a baseline, despite my low carb/fasting lifestyle I’ve not increased risk of a cardiovascular event at all. The medical industry must face up to the fact they have not honored the “first, do no harm” oath and should be ashamed of themselves.
"Linked with insulin resistance" doesn't mean causal, but let's say it's causal. How many people do you think die of direct side effects of insulin resistance compared to cardiovascular disease related to high ApoB? High cholesterol kills more people than anything else and many other causes combined. It's not hard to choose which is worse.
@@nichtsistkostenlos6565 In my experience (retired PCP), I saw very few people with heart disease who were not either diabetic/pre-diabetic or smokers. Furthermore, controlling blood sugar also improved lipids. Diabetics mostly die of heart disease. Familial hyperlipidemia is rare compared to DM. So I don't think you can really separate the two.
@@juliebrown8375 you are correct.
How do we know that LDL, specifically, is causully related to atherosclerosis? Why does he not bring up the examples of people that have genetically extremely high LDL over 600 but these people never develop atherosclerosis?
Science... High cholesterol and LDL are important risk factors for heart disease. That would contradict over 100 years of confirmed data which apparently you and others think doesn't exist.
And it's scientific data that combines literally every single possible type of study you can imagine whether it's epidemiologically finding that people with the highest intakes of saturated fat have the highest levels of heart disease,
-to the blinded experiments (which are extremely hard to do in nutrition) back in the 60's and 70's where saturated fat was replaced with unsaturated fat to specifically see if it prevented heart disease and it DID,
-to studies where people were given intestine bypass surgeries to surgically drop their LDL by Henry Buckwald back decades ago showing that those who had the surgery, dropped their LDL and so too did their heart disease risk,
-to genetic studies (there are some people who have genetically high cholesterol no matter what you do and those people if they are unlucky enough to be homozygous having both high cholesterol genes will have LDL levels 5-8 times as high as a normal person and they die in their teenage years of heart attacks). So not sure what you are talking about that they never develop atherosclerosis?
-and then there were studies looking at the opposite, people who have genetically low LDL and they almost never get heart disease and live and average of about 10 years longer than their peers. There are endless studies, including the most powerful studies: The statin studies.
He did, indirectly. Like a lifelong smoker who doesn’t get lung cancer, you can find people with high LDL who don’t seem to develop heart disease. That doesn’t mean apo B doesn’t cause it, simply that it doesn’t always cause it in everyone.
We know that LDL causes atherosclerosis because the mechanisms involved have been thoroughly established, but mostly because large interventional trials over several decades consistently show that ASCVD risk reduction tracks linearly with the dose and duration of LDL lowering.
@@mfklevenyou should have your own channel, you explain this better than Attia
@@mfklevenThere aren't any trials that do that conclusively. Which ones do you mean? I'm pretty sure they don’t show LDL-C causes atherosclerosis in a healthy body.
@@asarcadyn2414 The simplest example is familial hypercholesterolemia. There are kids having heart attacks simply because their apo B is extremely high. They are metabolically healthy, they don't smoke, they have great triglycerides, they're physically active, not obese, yet they still have aggressive ASCVD. So we know that apo B alone, when it's high enough, can be sufficient to drive disease. Just like smoking can be sufficient to drive lung cancer.
However--and this where language needs to be precise--that does NOT mean that everyone with high apo B grows plaque. Many people, even some with FH, don't. It's not clear why some are protected. But most smokers also never get lung cancer.
To your point, high LDL-C is certainly less likely to cause disease in a healthy body. But it may.
Doesnt all cause mortality go up, the lower your cholesterol gets?
I just found out that my apo b is 107. I have work to do.
I don't know who he is "treating" because when you go on his website he is not accepting new consults.
Those are his patients, so you're never going to know who he is treating. And he's not accepting new patients because his clinic is already full.
How do I get (in the US) a prescription for a statin if my dr. thinks my apoB-100 isn't high enough (in the 25%ile for my age)? That's 99 mg/dL.
@@jsherrier1196 Thanks. I'll look into that. Either way, I'm probably going to have to ditch the doc.
@@jsherrier1196 Wow! Took a look at Push Health. Had no idea it existed. Again, thanks!
@@toddboothbee1361 do you know what the average increase in life expectancy is with statins vs w/o statins? It's 4 days. Yep 4 whole days......
The mistake guys like Attia make is what I call being a "science chaser."
All animals, including humans are not created by science. We were created by evolution.
Also, our bodies are not just a bunch of parts like a car. We are one complete biological unit, and every part of the body has an effect on every other part.
We don't completely even understand the science we think we know, and there are always unknown biological variables that may completely invalidate any of our scientific opinions...
We evolved cholesterol for a reason, and guys like Attia need to pull back from the science a little bit, and see us for what we really are...evolutionary beings. The answers to health lie in evolutionary thought, not just scientific numbers...
Ok that is all fine and good i too debate the causality of events in my head on a daily basis 🙃and this might be the wrong video to pose this question but what do i eat? 🥩or🥦🥑or🍐🍏
High cholesterol, not low, is associated with greater longevity. Half the people who have a heart attack have low cholesterol. The key is to determine if the cholesterol is oxidized or damaged by requesting an advanced lipid panel.
This will tell you particle size of cholesterol (damaged is smaller, and that is dangerous). Large buoyant cholesterol particles are not dangerous. They are necessary for proper hormone generation. That is why some doctors are using the carnivore diet (high cholesterol) to help people with infertility (they produce more sex hormones when their cholesterol is higher). People with higher cholesterol not only live longer, but they have less incidence of cancer.
The Perdue-funded meat lobby has entered the chat. Hi guys!
What is the obsession with longevity? Ideally, I want to live a healthy life, and then die quickly. A heart attack seems like the best option.
Not everyone wants to die quickly.
Absolutely brother, my TC is 443 and LDL 378....TGL 51 and HDL 62, Uric acid 5.5 BP perfect 113/65 and RHR 42bpm, maxes out 192bpm and I'm 55....A CAC scan is £500 in Scotland, ApoB test £160....I bike 6-800km a month and would rather spend the money on bike parts or rib-eyes...If I drop dead on my bike one day I'll die a happy man and quality trumps quantity every time. Bad news for everyone I'm afraid, none of us gets out alive......
You don't get to choose unfortunately. Same process could just as easily see you end up in stroke ward for example. "atherosclerosis affects many other arterial beds [15-17] in ways that develop slowly over many years. Atherosclerosis causes disability and death from its contributions to:
• Cerebral vascular accidents and cerebral ischemia
• Dementia
• Peripheral arterial disease
• Heart failure
• Renal artery stenosis
• Carotid artery stenosis and embolization
• Kidney failure
• Hypertension
• Aortic disease
• Mesenteric artery disease
• Erectile dysfunction
• Frailty
• Poor aging"
And there are many people who get lung cancer who have never smoked. So there must be other causative factors? Likewise ApoB?? Is there something that causes ApoB to oxidise? Or is it high levels of ApoB, period?
What you're saying is a logical fallacy. Yes some people who dunt smoke get lung cancer but a disproportionate number of lung cancer sufferers were smokers and that is statistically significant and leads us to know that smoking causes lung cancer.
Whether some people get lung cancer for other reasons is a completely separate issue.
Saying something is causal, doesnt mean it's the only cause available.
It is the right time to step in PRECISION MEDICINE based on deep understanding rather than basics models which are most of the time non relevant and wrong. Thanks for this sharing and experience. Thumb up Dr 's.
Somebody get Bart Kay
So how did end up with a 90% RCA blockage? Non-smoker, mountain biker, eats well, not overweight, not diabetic.
Probably because of high ApoB...
How well informed are you about your health really? You say non diabetic; how do you know? Have you had your glucose and insulin levels observed? Other biomarkers?
so is APO B the same as LDL
It's a good proxy. Or better yet Non-hdl c
Low Cholesterol & ApoB Levels Are Critical for the medical-industrial complex to make billions every year.
i'm curious if more ppl vape today in the US than smoke tobacco .
hmmm I don't totally agree. CVD is multifactorial, includes genetics, lifestyle, insulin resistance and many things we don't yet understand. Lung cancer is different there are likely 3 things that cause lung cancer; smoking (pollution), radon, and genetics. Apo(b) for sure is a risk but just that. So many other factors come into play with CVD.
I don't think the above doctors discussion disagrees with your statement.
Well Attica says causal. Too many things with CVD are causal to say one is the main thing likely not the case.
All the common risk factors may be sufficient to drive ASCVD, but only hyperlipidemia is necessary. In other words, if you don’t have enough apo B particles flowing through your blood, you can’t grow plaque. Lowering apo B below that threshold, therefore, is the most reliable way to stop plaque progression. The same cannot be said of any other risk factor.
@@mfkleven Long discussion implying HTN, Insulin resistance, aging, Lp(a) aren't part of that equation? Certainly not saying that Apo(b) isn't a risk. But it one risk not necessary causal as smoking is to lung ca. Or Lp(a) is to aortic calcification. Are you saying if you drove Apo(b) to less than 30 there would never be any CVD?
@@dralexbrothers Yes, but with the simple caveat that there are no guarantees in medicine. There may be contexts in which 30 mg/dL may not be low enough to completely arrest atherogenesis. Lp(a) may be one such context. The combination of diabetes, smoking, and pre-existing advanced ASCVD may be another. But speaking generally, if the entire population maintained an apo B concentration of 30 mg/dL for life, heart disease would become a rare curiosity.
From the article linked below: “Although the answer to this question in humans is not definitively known, several lines of evidence point to plasma LDL levels
Brilliant guy, but he'll never say that multiple covid reinfections are causally relayed to bad long-term health 😊
Ok, in reference to the early discussion of ApoB. First, you have EPIDEMIOLOGICAL associations shown between ApoB and atherosclerosis, you do NOT have cause and effect. Note that the epidemiology of the cigarette case was FAR more clear cut as a causal factor than ApoB is. Second, the studies that show an association between ApoB and heart disease are being done on populations already compromised by poor metabolic health. In other words, just because metabolically unhealthy people (the norm in our society these days) shows an association between ApoB count and heart disease does NOT mean that the same association is valid when applied to a metabolically healthy individual.
no... there are plenty interventional studies looking at this...
What happens when you have high LPa but low APOb?
Doctor Erik Berg and Doctor Sten Ekberg, among many other experts have different opinions on this topic. I cannot make up my mind who to believe.
Agree 💯
I have listened to them as well. I don’t know who is correct.
In Puerto Rico there’s no even a APoB lab test. My cholesterol is at 240.
I just had an electro and a stress test and everything is perfect.
I’m going to the gym and have a low carb diet.
What should I do?
Fly to US
Don't overindulge in red meat. People on keto diet had higher mortality if they ate too much red meat
Is there a study that shows this? @@kotenoklelu3471
@@kotenoklelu3471That needs a study. Do you have the name of it?
I'd keep on doing what you are doing and ignore Attia.
Both law and medicine need legal and physical conditions to remain profitable.
It's illogical to expect the beast to act one way when the actors within the beast act differently from outside expectations of the beast.
My doctor and my lawyers need their boats and lakeside mansions. It is not to their benefit to have a sane, humane or fair system.
How does someone eati g carnivore for years and years have a CAC score of zero? Is this the same as a smoker never getting lung disease?
Maybe chronic elevated insulin levels, insulin resistance, and inflammation are the cause? Maybe chloresterol is present to put the fire out?
But that doesnt factor in benefits of not treating it. I am not an expert on this at all but it wouldn't surprise me to hear that there could be some stuff ldl causes that is good, and also besides that treatment has some cost to it as well.
Huh. How about low LDL smokers ?
how to lower ApoB ?
lower LDL-P
The analogy make no sense. With out APOB we would die. It is needed and natural. Smoking it not needed or natural.
Garbage. To use two numbers to predict longevity is ridiculous. Modelling is not proof. "Association is not causation". It's all speculation and conjecture. Low cholesterol and ApoB measurements can be useful, but only in context of an individual's other health markers such as CAC, HBA1C, Homar-IR, blood pressure etc. Most would-be health influencers get big headed and start advising us on topics outside their knowledge base.
So he's basically saying keep cholesterol levels low ?
I’m surprised that he’s emphasizing LDL. All the recent analysis from studies, says that triglycerides to hdl ratio is most important. Plus, ldl below 120 triples all cause mortality compared to those over 250.
He said apoB, which is a more precise metric than both LDL or LDL ratios
It's so popular these days to pretend that serum LDL cholesterol is just not a good enough or valid measure of heart disease. And it's like...uhh...YES it is. Just like high blood pressure is. It's a simple, very old fashioned and basic test, but they both are just as valid.
And no, people who die of diseases such as cancer etc, can often times have a cholesterol level that drops, and it will remain until the cancer is treated. Same with hepatitis or infection. The disease comes first and causes the cholesterol to drop, not the other way around.
Poor mico
You are absolutely correct. Triglycerides is the problem. It leads to high super small LDL. Only super small LDL is associated with cardiovascular diseases.
LDL levels can be reduced by a number of diseases. So those observational studies showing higher mortality with lower levels, can just be a "sick man effect". If you specifically go in and reduce LDL levels then heart disease rates drops. The genetic condition familial hypercholesterolema specifically causes high LDL-C levels and sufferers of this have substantially reduced lifespans (15-30 years) if left untreated. A more severe form of this lifelong high LDL-C (homozygous FH) can see children as young as 5 having impacts, events in the teens, and sometimes death in 20's. People eating a carnivore diet can have LDL-C levels similar to those with homozygous FH! 😕
Severe Dyslipidemia Mimicking Familial Hypercholesterolemia Induced by High-Fat, Low-Carbohydrate Diets: A Critical Review, 2023
when Attia asks a question, he can certainly elaborate
Get Bart Kay
Yes! We need his voice in amongst all this ridiculous misinformation
So a 24 year old sub 10% bodyfat . Doesn’t smoke or drink, use any drugs . Exercises 5 days a week. Works construction , eats all Whole Foods. Has high APO b. So I have atherosclerosis? Makes no sense
Hmmm runs rather counter to all the carnivore doctors out there. My cholesterol is high but triglycerides are almost zero...
it runs against common sense and human evolution too. I would not trust Attia at all
this guy is very logical and makes sense
just because there are outliers you would still be best to take the general advice
British Medical Association ....founded 1832 , high cholesterol means you live longer. Look it up
Any doctor who tells you that you have a pharmaceutical substance deficiency and then proceeds to use a hundred logical fallacies while claiming he’s obsessed with causation and calling anyone who disagrees “idiotic” should make you RUN in the opposite direction. Check his stock portfolio.
Talk about people hearing what they want to hear...
Over-simplified and convoluted logic. If a cop (LDL in this case) happens to be present near a place where a crime (atherosclerosis in this case) is conducted, does not imply that the cop was responsible for the crime! The atherosclerosis process is far more complex - oxidized LDL is one actor but there is much more to this story!
Smoking what?
I just can’t get behind the broad very vague brush that’s being painted with. Yes, under certain circumstances ApoB is destructive. But there is so much data that demonstrates that metabolically healthy adults with elevated LDL levels do not benefit from “medical intervention”. The other risk factors he spoke about, blood pressure, insulin sensitivity, endothelial health. These things, when at dangerous stages cause LDL to become the means whereby atherosclerosis begins and proliferates.
*Elevated to a certain extent… Not LDL at 300 or greater… That is an issue and may demonstrate an issue at the genetic level.
Metabolically healthy adults are at lower risk of heart disease, for sure. But plenty of metabolically healthy people still grow plaque and have heart attacks. All you need for atherosclerosis to develop is sufficient apo B particles flowing through your blood, and the more of them you have, the more likely you are to grow plaque.
But there’s no need to guess about risk, either. If you have elevated LDL but are otherwise healthy, get a CCTA or CAC and see if you’re growing plaque. If not, then you may not need to treat your lipids right now. But if you’re growing plaque, the most reliable way to stop it is to get your apo B as low as possible.
This is so poorly argued. With smoking, we know the actual mechanics of how it causes lung cancer. By contrast, Peter is using statistics and statistics alone to try to argue that cholesterol "causes" heart disease. He doesn't explain the disease mechanism. Why? Because most experts agree it's poorly or incompletely understood. It is not plaque formation per se that leads to serious cardiac events; it is unstable (or "vulnerable") plaque. And it's not cholesterol generally that ends up in that plaque; it's oxidized cholesterol. Cholesterol is not the villain. It's more systemic issues like inflammation, metabolic syndrome, etc.
To my point, to quote the Johns Hopkins website: "It's not clear exactly how atherosclerosis starts or what causes it." Cholesterol is listed as one among many "risk factors." That's not the same as definitively arguing for causation.
Who cares? If an individual takes statins events go down for that individual. Straw man arguments. Doesn't matter if we know the causes of lung cancer or not.
@@f.b.9143 Take drugs! Take drugs! Take drugs!
If smoking is causally related to lung cancer, then 100% of people who smoke would get lung cancer. Maybe you could quibble about “well, this guy only had 20 cigs his whole life…” vs “2 packs a day for 20 years…”. But if it is causal it is causal. The word has a meaning. If less than 100% of people who smoke get lung cancer (and it is less than 70) then it is not causal.
He addressed this in the clip. Obviously not 100% of all smokers will get lung cancer (some will be carried off by one of the plethora of other smoking related diseases) but the correlation is sufficiently significant as to consider it causal.
@@sivikasi so you don't understand what causal means then do you?
@@turbobros_online1561we can quibble over terminology but the facts are that smoking increases your risk of cancer to a staggering extent. Though if I were a smoker I’d be more worried about other health consequences. I think your definition of causal is rather simplistic but I’m not really fussed
@@sivikasi I think people manipulate language to their benefit. What part of the "smoking" is causal for lung cancer? Is it the actual smoking like the actual act of smoking caused cancer or is it caused by a secondary effect of smoking such as physical or chemical damage to the lung tissues? Wouldn't that be fundamentally different?
Ya know if I were to shoot a propane tank with a tracer round of ammo, that would "cause" that tank to explode. What if I emptied the tank first and then shot it? It wouldn't explode right? So was shooting the full tank the "cause" of the explosion? Or did the shot create a condition(source of combustion/heat combined with flammable/combustible gas and oxygen) that caused the explosion? Shooting the tank created a condition that caused the explosion.
If you really look at the available research with scrutiny, you see it doesn't show causality, only correlation. No one has ever shown how APO-B is causal in CVD because you see people with high APO-B and no signs on CVD and you see people who have died from CVD complication that had low APO-B and low overall cholesterol.
3:30
Does Attia believe that humans were born with cigarettes in their mouths? LDL is part of us from inception, so tampering with its level may or may not be the best for us, and cannot be compared to a foreign substance such as smoke.
I'd really love to know just how many "health conscious" people there are on these sites who are obsessed with all these numbers, facts and figures that have willingly taken the mRNA clot shots? Must be a lot of ticking time bombs worrying about LDL while having mini clots, TIA's, myocardial damage from these bio-weapons???
Good question.
So he’s saying that there is a genetic statin deficiency? 😂😂😂 inhaling a toxic smoke is not the same as a particle produced by our bodies. MDs have gotten so robotic in this country. 😊
You completely missed the plot. It’s an apt analogy that compares how the medical system currently approaches preventative care, and the timeline used. Attia is presenting the idea that we should approach causal, modifiable risk much earlier than we do now. Smoking CAUSES lung cancer, so we say don’t smoke at all. Elevated LDL CAUSES atherosclerosis, so we should apply the same metric and keep LDL low as soon as possible for as long as possible.
Also, genetic statin deficiency was never mentioned the video and makes no sense. A statin is a medication, not something your body synthesizes. You can’t be genetically deficient in something that your body doesn’t produce. People have genetic conditions that cause them to have extremely low LDL and vice versa. It’s clearly shown that lower LDL leads to less and less cardiac events.
I have to disagree that we should intervene and prevent activities that are causal to mortality. If we assume there is some utility from the activity, like eating steak, and has low ldl and others factors, the benefit of eating the steak might be of more value than a forecast for a longer life.
I think Peter would agree that you’re certainly allowed to make that judgment call. He’s simply arguing for informed consent-as patients, we should all be aware of what causes heart disease, and that treating the underlying cause early is the best way to avoid having to treat the disease itself later. If we know that and still feel steak is worth the risk, great.
However, I also don’t think he’d fault you for eating steak anyway. He’s noted in other places that the risk of saturated fat is easily mitigated pharmacologically when appropriate.
@@hamadax97 Of course there are many benefits to eating steak, including high quality protein, abundant micronutrients, zero spike in blood glucose, and of course taste. You might argue the risks outweigh them, but the benefits are quite real.
@@hamadax97you got that backwards, there is no benefit of eating anything other than steak
Get your hands off my God given right to enjoy vivid dreams.😊
Still.....love y'alls work.❤
thx
When the numbers for high ApoB and CVD are of a similar size to cigarette smoking and lung cancer I might take Attia seriously but until then he is simply scare-mongering.
He is simply wromg wbout cholesterol. Low cholesterol is associated with increased mortality, even compared to high cholesterol. In womrn high cholesterol is assiciated with lower mortality.
Attia is turning into a clown
So Peter, take statins to get your 'bad' LDL for most people no meaningful benefit and a life of pain and misery. Your tune is changing...shame
I have great respect for Dr. Attia, but is he working for Big Pharma now?
@@jaimemedina7422he must be
"for most people no meaningful benefit and a lfie of pain and misery"?? Where do you even come up with this non-sense. Statins are EXTREMELY impactful on health outcomes and most people barely have any side effects.
LMHR shows LDL is safe if people have no insulin resistance
This guy used to be all about keto food, fasting and exercise. Now he's just a statin salesman
well, his approach evolved with the new study data came in, just because he is not following the trend now does not make him bad, I used to do fasting keto and stuff, now I have a much more moderate approach to it.
@@richardzhang8312 I absolutely agree with you.
Live your life as n=1 experiment, keep an open mind, try different things with support from Doctors and published Research, until you find what works best For You.
But don't go around saying things like As far as I'm concerned everyone over 19 should be on a statin, as some doctors are doing currently.
This Lazy, one-size-fits-all approach, with the drug script pad and the differential diagnosis, is one of the worst trends in modern medicine, where patients tend to be treated not as individuals, but as an amorphous mass of identical people.
It ignores a significant number of patients for whom the magic cure of the moment causes harm instead of good, as you would've no doubt seen with the side effects of the vaccine for the unidentified-virus-of-unknown-origen, for which they now have filed a Class Action.
This example is no different.
Statins are generic now so there isn't much money selling them!
Kamala also is evolving
To equate smoking to a lipid particle is more idiotic than anything he thinks is “idiotic”
This was not helpful at all