Paul Saladino doesn't even eat salad he needs to change his name to Paul Meatareno.🍖🥓

This is what's wrong with social media, people rant and yell repeatedly the same assertion and somehow claim that makes it true

This video did not address subgroups, other than the genetic differentiators. For those without the gene "snips" , there are basically two reasons why people have higher than average LDL particle counts; one is because the Apo-B particles get damaged; they get too oxidized, glycated, or small because of other problems, and the liver fails to recognize and recycle them, so they float aimlessly in the bloodstream, liable to get in trouble including building plaque. The other is that a person's individual metabolism is adapted to using triglycerides as a major fuel source, so more Apo-B particles are put into circulation as VLDL packed with triglycerides, which eventually become a higher number of LDL particles after they've delivered the triglycerides. Such particles, however, are recognized and recycled by the liver. This video completely ignores the issues of LDL/Apo-B particle size and health, which is the elephant in the room that any honest evaluation of the role of LDL in atherosclerosis should be focusing on. Perhaps Physionic might take up Dave Feldman's challenge of producing a good study that finds a high risk of atherosclerosis in people with ultra-high LDL but also with low fasting triglycerides and healthy HDL levels. There is a reward of thousands of dollars in the challenge. There is also the fact to consider that in the NHANES database, the 5 most long-lived people had very high LDL by current mainstream standards, and this was not measured in their final days, but was recorded as "high" for many years. Lumping very different people together based on a single, independent characteristic is not the best way to do science, as it allows false proxies to contaminate the data and conclusions. The fact is, total LDL count has so little association with atherosclerosis, that many heart risk calculators don't even ask LDL levels; the other factors are just so much more predictive, that many calculators don't bother to ask. I've played with various calculators, some of which do ask for LDL counts, and none of them changed their predictive risk as much when you changed LDL counts, as when you changed other parameters. The point that many LDL-catastrophe deniers are making is not that there is never an *individual* correlation between LDL counts or particle numbers and atherosclerosis; the point is that there are good or neutral reasons, and clearly bad reasons, why LDL might be elevated. Those which are elevated because of triglyceride delivery in a fat-burning metabolism do not have to worry about LDL if their HDL and triglycerides are healthy. If this is true, then LDL is worthless as a marker for health, and concerns of disease should concentrate on damaged LDL which does not get recycled by the liver, and not all forms of LDL.

Correct me if I'm wrong, but isn't only _oxidized_ LDL (and not standard, healthy molecules of LDL) that actually turns into plaque within arteries' walls? My biggest concern would be with inflammation that helps promote that oxidation.

Either way there is no evidence that statins reduce the risk of death from heart disease so what is your point?

This LDL controversy is what concerns me the most about the carnivore diet. However, the association shown is some studies are always in the range of 00% to 30% max, which is relevant, but not really that high, considering it's only association, not straight forward causality. Also, if carnivore diet manages to reduce body fat massively, normalize blood pressure, soothe inflation, make glicemy super low - among many other benefits, I think it's safe to assume that overall coronary desease risk should go down substantially, even if LDL level is increased.

I just passed my entrance celular bio exam and I’m in awe with your content, (I’m a med student) and I aspire to one day do research of my own, thank you for the amazing content!!

Glad to find this scientific based channel! I just subscribed!

I'd like to see a one on one with you and Paul Saladino. I think it would answer a lot of questions.

I have heard that sugar in the bloodstream can scratch up the walls of the arteries and that scratched surface provides the means by which ldl (sdldl) will adhere to the artery walls. Additionally, calcium at some point becomes encased in the sdldl particles, so there is the hardening ( calcofication) process. Would you care to address this postulation, as well as D3, K2, calcium supplementation, slsl, and elevated triglycerides ?

If you are on a keto or carnivore diet or any other diet your LDL will go high just because you need to transfer a lot of fat in your body for Energy. What Saladino usually says is that LDL is only harmfull when the cause of high LDL is insulin resistance or metabolic syndrome. Genetic problems are execeptions not the rule as you made to look

Since my cancer diagnosis 2 years ago, I developed what my husband considers an obsession with becoming healthy. I read - no, study- everything I can and make use of it in my personal life to that end. Granted, I am a test subject of 1. But here’s what happened to me. In September 2021, I had surgery for breast cancer followed by radiation therapy. I am 5’3.5” tall and weighed 160 lbs., had insulin resistance with morning fasting BG levels around 102. Blood lipids were in the normal range, though Total cholesterol was a bit over 200. However, there were questions regarding the health of my liver based those lab results. Fast forward to September 2022. Went for my annual check-up. Cancer hasn’t returned but blood work hasn’t improved, but hasn’t gotten worse either. My weight is now 165, I feel sluggish, and don’t sleep well. My cancer doc is concerned about my BP and fasting glucose. Forgot to mention that my BP was around 143/78. Typical HR was 76-78. My GP insisted I start statins. I complied, though the only lipid out of line was total cholesterol. In November, cholesterol was low enough to be considered normal but I felt even worse. Brain fog, muscle cramps. It was almost as bad as Covid. I was disgusted and determined to do everything I needed to do to get healthy. I started intermittent fasting, got rid of all sugar in my diet, had no more than 1 alcoholic drink per month (at celebrations) then started following a mostly keto diet. Again fast forward 6.5 months. My weight is now 132. A DXA scan shows visceral fat at 1.8 which is ideal. My RER is 0.71, also great. In addition, I had in-depth labs done - CardioIQ Advanced Lipid Panel and Insulin Resistance Panel with Score. Insulin resistance was gone - Ref Range is Insulin sensitive

The debate here isn't whether too much Cholesterol will kill ya. Too much anything will do that. Question is how much is too much. And is Cholesterol causing your problems or your problems causing the Cholesterol.

I think this is productive fact checking. Thanks for doing this. Also like to add that the ideas of dr saladino help strengthen or if he would have been right to rethink and develop the connections we think we know. So thanks to both of you.

Many health professionals agree with Paul S. Of course, many do not. And both sides use scientific studies to support their view. What is one to do? I weigh 139 pounds, workout, do cardio, do not drink, and am in excellent health. I switch between Paleo, Keto, Animal Foods, Carnivore, and Mediterranean diets. I will do one of these for a few months at a time. I also intermittent fast and do 3-5 day fast occasionally. I have high cholesterol and a doctor who demands I take 10 mg of a statin. My HDL is 72, total cholesterol just below 200 and LDL over 100 (currently 114 and this is what my doc is screaming about ! but LDL was much higher a few months ago). My HDL/triglyceride ratio is 0.5 (which is perfect and a good indicator to many for heart disease). I follow many different medical doctors including Paul S. and I get many different opinions from each and every one of these doctors/researchers. Again, what is one to do?

Another issue is that LDL is a calculated value. There are at least 2 types (5?) which can only be determined by direct test, and not all types cause problems. In my opinion, the calculated value should be considered a screening test only, followed up with a confirmatory direct test. And, of course, training for the doctor. (Yeah, its amazing how many doctors lack training, except perhaps on the golf course.)

What I was taught at uni was exactly in the middle of those two points of view. LDL is not what causes any problems to anyone - the problem begins when LDL binds with a sugar molecule. Such a product can no longer be a part of the lipid delivery cycle and ends up dumped on the artery walls, causing all the trouble. You can fight that issue in two ways: lower your LDL, or lower your blood glucose levels. So... the main problem I see is all the blame gets excessively put on a single culprit - although it takes two to tango. From this perspective, you can get away with higher LDL on a keto diet, or you can eat a whole cake if you have low LDL. I would not go for such extremes, though.

A question I have pertaining to LDL's is concerning the different density species of LDL's. There are different sizes of LDL's and the danger risk is associated ONLY with the lowest density species. But a standard HDL and LDL panel doesn't differentiate between those sub species. I have read that the Larger of the LDL's can make up as much as 80 of the LDL's and they are not a risk factor for CHD. So the statement that a high LDL reading (overall) isn't making that distinction. So the question I have is this: At what percentage of the total LDL reading that is from the Lowest LDL species represents a higher risk for CHD?

Wrestling analogies is the perk I like most in Nickolas' videos. Helps a lot to digest science granite.

Dave Feldman did some experiments years back showing how LDL strongly varied with fat intake. What that told us was that LDL isn't a good indicator of much more than fat intake a few days earlier. Using his results as a guide, you can practically get any result you want at some specific day. I'm in the camp that thinks avoiding diabetes is much more important than LDL values. And that there are more effective ways of avoiding CVD than trying to change the LDL.

Pharmacology Ph.D. here. I think you're missing an important point regarding oxidation of LDL particles, as it wasn't mentioned. There was a very good review article published on the topic: "Omega-6 vegetable oils as a driver of coronary heart disease: the oxidized linoleic acid hypothesis" (published in Open Heart, 2018). They basically conclude that it's the oxidation by-products of linoleic acid that contribute to heart disease, not the LDL itself. The important context is that high LDL must be in combination with a high linoleic acid diet to be damaging. Saladino is strongly against seed oils that contain high concentrations of linoleic acid, and all plant oils for that matter. Also, you didn't mention anything about ApoB as an alternative measurement of heart disease risk, which is currently a hot topic.

I believe the issue here is not the idea of elevated LDL, but more of the definition of elevated. It seems that as the years go by, the smaller the number that is considered "normal LDL"...

You bring up some great points. You two should debate. Yes it's a risk factor but I don't see how you explained why it's not causative which is his point.

really liked this video, you are the best science based channel ever!

Firat, I really enjoy your videos, but I disagree on this one=I'm a biochemist and you're missing some key points; you never mentioned pattern A or B which is really the key factor. You can't just say LDL is bad, just like you can't say cholesterol is bad. Plus, as you know hyperinsulinemia. manifests 10-20 years before diabetes show up. Virtually everyone in America has hyperinsulinemia because of the SAD diet. Ben Bickman and Jason Fung both address this point many times. You should have a complete lipid profile done and not just cholesterol and LDL. you never addressed the type of LDL which is very misleading.

To understand what's going on, watch "Dr. David Diamond: Should Low Carbohydrate Diet Guidelines Include Concerns Over LDL Cholesterol?" He explains that it's not the high LDL that is causing the trouble. It's the high *damaged* LDL. In one study in which the damaged LDL were removed, the remaining high LDL had no adverse effect.

Could you please name the researchers that you’re reading in your studies in the videos? It helps promote those researchers and in my opinion thanks them in a way.

I ate carnivore for a few years, I ate a high fat keto version I got my cholesterol checked regularly. It stayed low the entire time. Could you go over the "impact' of dietary cholesterol on blood cholesterol?

High LDL is not a problem if you're on a low carb diet. The LDL just floats around in your blood doing the job nature designed it to do. It only becomes a problem if you have elevated blood sugar. The sugar causes lesions, the LDL then gets layed down in a scab to try and heal that lesion. The scab reduces the size of the arterial pathway, eventually a total blockage and heart attack or stroke if the brain is starved of blood.

Outstanding analysis on LDL that even my goldfish mind was able to comprehend. As a fitness trainer focusing on people over 50, this nuanced understanding of LDL was extremely helpful. Thank you Nicolas!

😆 You're awesome man! love your wry humor. That accompanied by your clear explanations and quality in depth research is golden. I love that you get into the biochemistry details without over simplification. I come to your channel for facts and i'm enjoying it very much. Thanks.

Paul's overall message has helped me.. I used to eat vegetarian throughout the week then meat on weeknds(cause I believed meat was unhealthy but still craved it). Since discovering him I follow his "animal based" recomendations, specifically I eat mostly red meat(ground beef/steak), fish, liver, eggs, butter, fruit. I am in a lot better shape with less stomach pains compared to when I ate all veggies (brocolli, asparagus, yams, onions, mushroom was the avg meal)

On the first point, the argument is aimed at a practicing medical audience where often the paradigm is reducing LDL as low as possible to reduce MIs and CVAs. On the vein issue, he would be referring to SVG stenosis especially compared to LIMA stenosis. The argument towards insulin resistance can't be equated directly as diabetes; though the two occur together often, they don't always occur together and obesity can be an alternate presentation that can explain many of these instances of lack of diabetes.

I'm 75 years old and I have high LDL (139). I worked for 52 years and had one sick day back in 1969. Maybe there is something good about having high LDL. I am also Apoe2.

I think the jury is out on this one. Could one wish for a friendly debate with Dr Saladino? Give the man a chance to respond to Your critizisms? Thanks.....

I heard from The Dr. Gundry Podcast that Polyphenols reduce the stickines effect in LDL, and in theory we might rather look on the levels of polyphenols in our food, rather than worry about LDL. I'm curious what your thoughts would be on this theory?

What's "excess" (or "deficient") LDL and by what criteria is it established? Then answer why ranges are changing over the years? Moreover, explain to me how was it that the egg was demonized as food, for decades, numerous studiess "proved" its detrimental effect) but now it's ok to eat dozens a week? What I'm trying to communicate with this comment is that academic knowledge (studies) aren't infallible (quite the contrary - most are for the bin) and you should always be skeptical and careful when you are reading such works and their primary assumptions (or axioms) which they could be proven arbitrary in the future. P.S. There's a cardiothoracic surgeon that has performed thousands of operations and, according to him he wouldn't bother about any number on LDL cholesterol but instead he proposes to measure triglycerides and HDL. His name is Dr. Steven Gundry. You should look him up. I'd rather follow his advice and expertise than 10.000 papers in academia.

I'd be interested to know what you think about his recent discussion with Dr Alo, a cardiologist. Dr Saladino makes some great points as they discuss the subject in detail.

Free cholesterol in the blood never was a problem until a pharmaceutical company obtained a drug that reduced it in the blood. I remember hearing a conversation, as a child, in the hospital where my father worked between several doctors about that fact...

One wildcard in this is whether the studies use measured or calculated LDL. Our blood work results use a Friedewald calculation as it saves money over actually measuring it. I have found that having a good (low) Triglyceride/HDL ratio, say below 1 tends to show a significantly higher calculated level than if using the "Iranian" LDL calculator. My Trig/HDL tends to run around 0.8-0.9 ( a measure of good insulin sensitivity) and my Friedewald LDL calculation tends to run 25-30 higher than the Iranian calculation. Any comments on this?

I would be interested in how the studies bear out the level at which LDL is considered “bad”. Both my parents died in their 90’s and never had LDL below 225 when tested.

LDL is being referenced without regard for type of LDL. ApoB little particles are dangerous. We need to learn to differentiate the two and recognize risk

This is excellent! I love your unbiased approach that is based on an analysis of reputable studies. Thanks for the fact checking on potentially harmful claims being made in other other youtube videos

I love your content and willing to pay for more. Question: Can you do a study on the impact of Zone 2 training

Being a non academic person, my simple understanding is diabetes results in obesity due to diet (sugar and processed carbs) , obesity causes inflammation, oxidation from say seed oils cause damaged LDL which combined with inflammation cause plaque which grows and causes blockages.

it seems to me as if he has many hypotheses, however I feel that he tried to skip the scientific process for the excitement of a new discovery. another great video!

Thanks for your analysis (and the bit with the chairs ... 🙂). With regards to LDL, an you comment on the phenomena related to lean mass hyper-responders? What is the relationship between exercise (in terms of both intensity and volume/ammount of exercise) and LDL? Have you looked at any studies that look at hyper-responders?

Glad there's someone out there covering some of his claims as he makes a lot of them.

Love your enthusiasm @5:00 and you're right it is super cool!

He looks incredible for 46 :) At 58 I have sky high cholesterol but a high end scan showed ZERO coronary artery deposits and low normal blood pressure. I eat no grains or legumes nor seed oils, lots of polyphenols and fibre and am keto for more than ten years. No doubt people with a normal high inflammatory diet would be all clogged up eating so much fat. I had never heard his theory that deposits were formed to soothe damage, rather I believed that deposits were made to cover inflamed regions. I don't consider insulin resistance to have much relevance. there are several new studies out discussed on youtube by a Dr Feldman.

Thank you for the very well explained VDO. One question though: What LDL-level range would typically be the sweet spot from an overall health perspective?

I guess what i tried to say with the previous post is that people with a high LDL often have this from eating a shty diet, and therefor will suffer from CVD more than people with a low LDL who will eat a overal healthier diet. If you get your high LDL from a healthy diet you might not get sick from it at all.

Im on the side of Dr Saladina. His right Cholesterol is important in our body. The higher the cholesterol the better. Greetings all the way from Republic of Ireland filipino

thanks for your analysis and informative content

I love the way you explain things and your delivery is brilliant. 😊👍

I did not hear VLDL mentioned and how it differs in effect from LDL. Very often VLDL is referred to as simply LDL and this can be very misleading since the two are quite different. Also I did not hear anything about the HDL and the Ratios and those effects on overall health.

Total cholesterol - HDL - LDL = VLDL, if this number is

This is very interesting to me, on a personal level. Two years ago I was a fit healthy 59 year old with good dietary habits, no overweight, no smoking, very little drinking and no drugs when I had a heart attack completely unexpected. Turns out I have clogged arteries. No one can tell me why. I have zero pre-diabetes, perfect blood sugar levels but higher than average LDL-c. That last one, no one can explain other than 'genetics.' I am now looking into elevated levels of homocysteine as a possible cause, because 'genetics' doesn't really mean anything. I fortunately didn't suffer any damage to my heart and I am fine for now but I did have a stent placed and I probably need more care, although I feel perfectly fine - but I felt fine the night before the heart attack so... Your videos have a real life impact on me and I'm sure others, so thank you for this. 👍

Thanks for the analysis. Although I'm not technical in this area, I follow and appreciate your input. I recall hearing something about Triglycerides also being a factor, one possibly to be concerned about over LDL, as well. I don't recall where I heard that. Anyway, thanks for the information.

I love your videos. You are the "Data'” of the medical video world! Funny and factual. Keep making the fact checking videos!

I turned down statin therapy for my high ldl because of this paper: "Statin therapy is not warranted for a person with high LDL-cholesterol on a low-carbohydrate diet" Curr Opin Endocrinol Diabetes Obes. 2022 Oct 1;29(5):497-511. I am on a keto diet, and my hdl and triglycerides are excellent.

Great work, thanks for sharing!

Re the Mendelian randomisation studies. It works the other way also. Those that genetically have high LDL (familial hypercholesterolemia) have greatly increased heart disease levels (can reduce life expectancy 15-30 years if untreated; even more if the homozygous form). Seems like a pretty straightforward demonstration that LDL is causally implicated ...

I'm not taking Dr Saladino's side as many of his arguments are specious, but I do think part of the problems with these studies is that LDL is more complex that just LDL. The nature of the LDL profile (and triglycerides and HDL) in toto need to be taken into account. I enjoy this channel because Physionic does go into direct mechanisms and depth and does find multifactor studies to ferret out conclusions that are informed and closer to truth. I have just dipped my toes(watched 3 or 4) into the Physionic waters and I'm impressed by the thoughtfulness he brings to the casts. As a critical thinker I do note that multifactor health analysis is extremely difficult and prone to many inference errors in a multitude of studies. Physionic sifts and distills a lot of information!

Great analysis and presented respectfully. Love the humour thrown in!

I am a bit confused between this video of yours and the previous one i just saw addressing the vein vs arteries video, you seem to come to similar but somewhat different conclusions? how would the elevated blood sugar effect arteries? is the attraction of ldl or leakage is due to damage or not? how do you place the dietary and life style factors in this? how does the calcium play a role in this formation? and how would you evaluate the factor of oxidized vs large ldl (whatever it is properly called) thanks.

I read somewhere that overall LDL is not the problem, there are I think two kinds of LDL, small and large and its the small that are harmful and large beneficial (forgive me I am just a 'layman'). However most doctors just do the standard tests and not the comprehensive one. So is there a way of targeting small LDL only? I have familial hypercholesterolaemia and even when my overall levels were normal way back when I was young, my LDL was always higher.. I was on Statins from 2018 - 2022 40mg and lowered to 3 with LDL higher than HDL but in normal range; then I had a heart Scan and my CAC socre is zero, so if LDL causes calcification of arteries why is my score zero? Maybe because when I was young overall scores were in normal range, and when I stopped statins values went through the roof. How long does it take to build up? Maybe take vit K2 to take calcium to bones and not arteries will help? I now have an appointment with cardiology, they put me on urgent cat 1 appointment as they were freaking out about my cholesterol... watch this space for when I see them...

Its the LDL size and LDL particle count that matters.

Interesting point about LDL and heart attack risk. I'll have to chew on that for a while. Although, I am still staying away from statins given the other risks such as dementia, Parkinson's, muscle aches, fatigue... while I can understand that extremely high LDL could directly harm the endothelial cells as can sickle cells as can a constant barrage of high insulin levels and high blood pressure.... I am still extremely skeptical that reducing LDL's with drugs that have such harmful side effects is the way to go.

How many ways can you damage the endothelial wall? Have you ever seen a scab form where there's no injury? Injury occurs through many different mechanisms. Mechanical, chemical, infection. Clearly, diabetes is not the only way you can damage arteries.

Also, you are well read and research and I would like for you and Dr. Paul Saladino to actually have a gentlemanly debate and discuss the research. That would be amazing. ♥️🤗

Interesting. Most don’t look at cancer rates esp colon and longterm high meat and or animal protein intake. Also studies on effect of IGF1 (certain healthy level -not too high or low) and pesticides/fertilizer etc concentrated/ stored in animal fat.

An important consideration is any fasting diet also raises LDL. Why? The LDL is an energy transportation molecule. Once you need to transport FATS to energy rather than glucose LDL will elevate to transport this secondary energy system. My doctor was shocked when my yearly check showed a complete change and LDL was elevated. I had lost weight blood glucose down. Triglycerides down. He still wanted to prescribe Statins! I told him as he didn’t have time to do research on new studies in his field I would. Still not taking statins. 😂

Interested layman here. The LDL was measured but what were the HDL and TG levels? Surely they provide a wider context?

Amazing content, keep it up!

The one thing health KZfaq is lacking is mano a mano debate. People who have guests on their channel always pick people drinking the same Kool-aid. Would love to see an hour debate between you and Paul Saladino, Shawn Baker or.... Peter Attia on areas of disagreement...

I think we should take into consideration that the reference ranges for cholesterol have been constantly lowered by the science community in the last 30 years. I remember when I was doing my faculty education the limit for overall cholesterol was 6, now it is 5. We do have to wonder if this is only due to new emerging studies or something else (and no, I am not a conspiracy theoriest).

I think almost all of dieting can be summarized with "Dosage makes the poison".

Moderation in everything and everything in moderation.

It would be interesting if Dr. Saladino chose to respond to this video, which I found extremely compelling by the way. I’m learning a lot from you. I still think it would be interesting to hear Saladino’s rebuttal, however. ❤

I like your rebuttal of the (hypo)theses of dr. Saladino. Still I wonder if current guidelines are set correctly. Of course water is healthy, but deadly if we drink 30l/day, but also it is better to drink 3l than 2l. What about the cholesterol? How can we be sure that slightly increased levels are not better than "normal" as we know it? How were the tables creatred? Just my 5 cent for a potentially very insightful and interesting new video topic that we would be happy to hear you commenting on!

Great video, thank you! Insulin resistance and diabetes are precursors to stroke and heart attack. Unfortunately, most docs do not know how to correctly diagnose metabolic issues, which means many people will have an event before they are correctly diagnosed.

As the body makes the majority of our cholestrol you'd have to wonder why it does that. I think the problem with the scientific community generally is myopia and not very good at thinking outside the boxes nor challenging dogma or possibly just happy to get a grant studying something for confirmation bias. I also wonder why cholesterol 'sticks' to some parts of the arterial wal .... but not others yet science not interested in answering those questions. Is high blood pressure ever caused by the body making too much blood?

The words, "relative vs absolute" made this video well worth watching and heeding. THANK!!! YOU!!! I've had a great amount of frustration over the last couple years, because of the seemingly well informed, and researched based presenters of information on CAD, were contradicting eachother on this particular point. Thanks again. I'm 67, and have a relatively low calcium score for a man my age, BUT, I have one particular coronary artery that is "50-70% occluded." perhaps 50% isn't what I was hoping for, but it's hell of a lot better than 70% Needless to say I am concerned. With family history of CAD, I want to be sure I'm not misinformed. Thus far, instead of a stent, my cardiologist and I have opted for the higher dosis of the cholesterol meds. So.... There it is. scary reality.

Man you read a lot! Well, I think Dr. Saladino also reads a lot. Given he is 45 and he looks remarkably healthy despite his elevated Cholesterol levels. I suspect he is stronger maybe than most people 25. I guess we need to define what is elevated, because what is an accepted reference range maybe defined on an otherwise unhealthy population. Reading is one thing, practice is the other. You can read all the books in the world but the question is can you be as healthy as Dr. Saladino when you are 45?

You bring up some valid points regarding FH and early development of atherosclerosis, but I would like to bring your attention to the inverse association outlined here 16:29 . A review of FH patients “Importance of Coagulation Factors as Critical Components of Premature Cardiovascular Disease in Familial Hypercholesterolemia” by David Diamond and colleagues show that most of the risk for early development of atherosclerosis in these patients has to do with abnormal coagulation that is inherited and can be worsened with lifestyle. They demonstrated that patients with FH that did not have these abnormal coagulation patterns lived as long if not longer than patients with normal cholesterol levels. Also the inverse association can be contributed to the patients knowing they have FH and actively changing their lifestyle to ensure they are healthy well into the future.

I thought particle count (ApoB) was more important then LDL-cholesterol levels.

I remember reading study that showed little correlation between LDL and CVD after age 55, and another study that showed an inverse correlation between LDL and all-cause mortality (with a high optimum level). "LDL-C does not cause cardiovascular disease: a comprehensive review of the current literature" "Burgess et al., ‘Power, linkage disequilibrium, pleiotropy, canalization and population stratification have all been recognized as potential flaws in the Mendelian randomization approach’"

This is fun. Intelligent discourse is fun.

How much is too much? I have about 200 to 250 ldl for 50 years and I am now 60 years old.

What about lower cholesterol,but risk for neurodegenerative? My husbands family has “normal” cholesterol, only to spend the last 15 years going downhill with Parkinson’s.

I really appreciate that about the same time I want to start yelling at a video, you basically make the point I want to. I imagine most of your audience is the same way. Thank you for moderated analysis and sharing with us all.

Out of an overall population you can have groups with different characteristics. You can prove that the overall population is overall aided by lower cholesterol. But that doesn't mean that it applies all subsets of the population. For instance, those specifically on Keto diet may not have the same disease or malfunction vectors that those not on Keto diet and there characteristics of the LDL are shaped differently. I believe AI's are going to eventually sort out much of these subset issues and we will get much closer to individualized and specific medicine based on the entirety of an individuals lifestyle. There are a large number of tracking apps are gathering daily information from individuals health decisions and I believe ultimately AI's are going access and sift this data for a huge advance in determining correlations and causations.

6:15 in the "normal range"? you read "optimal range" which is minimal by scientific consensus (guidelines etc)

Would people who have genetically lowered LDL, which we discussed has a myriad of health functions, potentially suffer from other issues (morbidity and even mortality) first before suffering from a cardiovascular issue? I think of the U-shaped curve that pops up in certain health markers and how too low and too high areas of the curve can indicate confounding variables in health.

What about elevated LDL from fasting? Does that increase the risk of heart disease?

How many of the patients in the studies that you read were in permanent nutritional ketosis on a zero carb diet? None of them, I believe. As Dr. Saladino says, context is everything.

Great video. I appreciate your objectiveness in addressing this issue. Three things: 1. You have researched multiple studies regarding the relationship between elevated LDL & heart disease. Keep in mind that the studies funded by Big Pharma could be biased. 2. There are studies that also show an inverse relationship between between elevated LDL & heart disease. The lower the LDL, the greater the association with all cause mortality. Those studies are routinely ignored. 3. People generally develop insulin resistance LONG before diabetes manifests. That may explain why people with Hypercholesterolemia do NOT have diabetes (but they are still insulin resistant). Dr. Paul Saladino never mentioned diabetes, only insulin resistance. Therefore, his hypothesis is still valid. I don’t have a dog in this hunt. Just sifting through the data that is out there.

You can tell someone's grifting just by the way they talk, he is grifting

I think the main argument is that the LEVEL of cholesterol that consensus currently says is “elevated” is under scrutiny 🤓