Dr. Paul Saladino: "Don't worry about elevated Cholesterol."
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References:
[1] doi: 10.1146/annurev.micro.55.1.165
[2] doi: 10.4049/jimmunol.1501835
[3] doi:10.1016/j.jacc.2012.09.017
[4] doi: 10.3389/fcvm.2022.860196
[5] doi:10.1001/jama.2015.1206
[6] doi: 10.3390/nu14071503
[7] doi:10.1093/eurheartj/ehv157
Original Video: • Why I don’t worry abou...
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#carnivorediet #carnivore #hearthealth
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Paul Saladino doesn't even eat salad he needs to change his name to Paul Meatareno.🍖🥓
Meatino😂
Or carnerino, maybe 😂
Wouldn't ino translate to little? Paul littlesalad seems more correct. I'm not a linguist and too lazy to google. just a guess.
Meat-I-Yes
He does eat an absolute ton of fruit though
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.
My understanding is that all LDL which gets stuck in the artery wall will eventually oxidize. Saladino pointed to a study that suggests LDL particles that contain more polyunsaturated lipids will oxidize more in the artery wall. Mechanistically it sounds plausible, but most studies replacing saturated with polyunsaturated fats show reduced inflammation and reduced cardiovascular disease. So we have mechanistic speculation on the one hand and actual human health outcomes on the other. In any case I'm seeking more information about this oxidation problem.
Also I don't know if it's even possible for LDL particles to incorporate different amounts of different types of fat from the diet. It's an assumption I hear but I need to see the evidence.
I'd like to see a one on one with you and Paul Saladino. I think it would answer a lot of questions.
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.
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.
Consumption of cholesterol is causing the problem. Ingesting fats from animal products is causing the problem.
Given that cholesterol it endogenously produced in the body, probably the latter.
@@WhatDoesEvilMeanphysionic, Attia, and every other well educated individual in the lipid community have come to the conclusion that dietary cholesterol does not increase risk because in most cases it will not increase serum cholesterol. Saturated fat is a different story though, but it’s important to differentiate these.
@@WhatDoesEvilMean How is it that so many of us, including myself, eat tons of animal fat and have perfect blood numbers. Also, I don't exercise a lot either.
@@Dan-gs3kgThat still doesn't mean there's no limit to the quantities of cholesterol and sat fat we should ingest, Nic made that point.
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're worried about like glycation then don't eat animals because their fat causes intramyocellular lipids to develop into insulin resistance preventing glucose from entering the cells. Kind of like this video says she much or too little of a good thing can be bad. Glucose is great from Whole plant Foods because fiber helps it enter the bloodstream slower. And whole plant Foods don't cause the insulin resistance.
It's amusing to see a vegan arguing against animal foods in terms of glycation. Without plant foods, glycation of animal foods would be minimal.
@@MarmaladeINFP "Advanced glycation end products (AGEs) are formed when fat- and protein-rich foods are exposed to high temperatures. Some foods that are high in AGEs include:
Meat, especially red meat, Certain cheeses, Fried eggs, Butter, Cream cheese, Margarine, Mayonnaise, Oils, Nuts.
Fried foods and highly processed foods also contain high levels of AGEs. Grilling meat can also cause the formation of AGEs.
Meats high in protein and fat are likely to form AGEs during cooking. Carbohydrate-rich foods such as fruits, vegetables, and whole grains maintain low AGE levels after cooking."
This is what's wrong with social media, people rant and yell repeatedly the same assertion and somehow claim that makes it true
That's true with mainstream media too.
We need to factcheck almost everything now, no matter where the claims are made.
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 never liked vegetables or had a sweet tooth so I’ve been doing carnivore with dairy for 25 years without knowing it was a healthy diet. My family’s genetics have high cholesterol. Mines always high, but I have no plaque in my entire body. I’ve had coronary angiogram and calcium scan 10 years ago and I was good. It’s very important to exercise on the carnivore diet. You have to burn that cholesterol in your blood so it doesn’t cause problems. That’s my logic on it.
Carnivore is not the only diet that can do those things.
You would be wise to be concerned. Carnivores tend to show weak observational studies which are easily confounded, yet never mention the much more powerful and illustrative interventional studies (which make it clear ApoB / LDL is harmful). And while improving other health markers (likely mainly through weight loss) is good, there are plenty of examples of people who are "healthy in all ways except except LDL" who go on to have a premature heart attack or stroke. Maybe check out cardiologist Dr Alo - he talks about this and bit and basically says if you like that way of eating great but if your LDL is too high just make sure you control it (multiple ways of doing it)
@@JoeS97756 But if it does as per many testimonials, it should be celebrated . The other diets can probably do the same but apparently they make autoimmune symptoms worse. Hence, why many prefer the carnivore which seems to have a soothing effect of the system. I really don't think the carnivores are anal about the vegans , it's usually the other way around.
@@JoeS97756Everyone's sensitivity to glucose is different. Going vegan can help with diseases for someone coming from a SAD diet, because they end up consuming less carbs. It's relative. If that doesn't work, going keto is even fewer carbs. Some still may not find satisfaction and moving to zero carbs, or the carnivore diet finally kills off these diseases.
Of course the difference is, veganism is missing over a dozen essential nutrients and is not a long term diet. Red meat is missing precisely nothing.
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?
Are you on keto/carnivore now?
Animal based diet with healthy carbs is good too. I think genetics play a role in cholesterol. You probably workout a lot or burn it off with ketones. I have high cholesterol and no plaque. You have to workout or fast seems to be the key.
"Could you go over the "impact' of dietary cholesterol on blood cholesterol?"
Strawman. In the video high levels of blood cholesterol were dicussed, the origin was not.
How much is too much? I have about 200 to 250 ldl for 50 years and I am now 60 years old.
According to physionic and the medical establishment this would be considered “high”. I recommend before trying to aggressively lower LDL you get a CT angiogram and assess how much plaque burden you have and if you are generating nee plaques.
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.
Yup this is mind blowing.
Well said.
Take extra niacin to be safe 😉👌
I have thoroughly looked at Dave Feldman's works and, while he is free to experiment upon himself, I would not be a participant. It's like rolling the dice at a craps table.
right on, bro.
Paul consumes more sugar than an Elf. He’s nowhere near Carnivore.
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?
But polyphenols aren't as profitable as statins. There is the problem.
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?
This is not correct. All LDL particles are atherogenic. irrespective of size. I understand that the total number of LDL particles provides a better risk estimate.
You can tell someone's grifting just by the way they talk, he is grifting
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"...
If you consider the factors that make LDL "go bad" then look at the population being used to create the data, it makes sense they push for a lower level.
Essentially LDL follows some form of J or U curve, as do most things.
Where your optimal LDL level lies depends on if it's at risk of glycation or oxodation.
So Saladino's optimal LDL for minimizing risk is likely much higher than an obese diabetic who eats a bunch of processed food.
Well.. most people are metabolically unhealthy, with a diet high in vegetable oils which oxidize easily. This means their optimal LDL for minimal risk is lowered.
This easily explains the data and studies we see, and doesn't disagree as much with Saladino either, though I think his perspective is still a bit too simplified.😮
@@Unsensitive your point makes complete and total sense. Recently, it's made more and more sense for me to then to view the data as part of a system and not as "the" deciding factor of health and longevity. My cardiologist insists on the absolute lowest LDL, even claiming he wants to see it below 40, despite my total cholesterol being 129.
@@Unsensitiveegetable oils are cardioprotective. Various studies show that.😂😂😂. In that way breathing would be unhealthy because you are creating superoxide with every breath you take. Oh, and be careful when eating meat too, because it causes immense oxidative stress during digestion.
@@stellasternchen
I don't disagree that many studies came to that conclusion, but they are biased and incorrect in their understanding of physiology and nutrition. Many are too short to show the harms, which need to be 5+ years in most cases, as these are a long term toxin which are incorporated into your cell membranes.
My anecdotal n=1
Eliminated them from my diet and my arthritis disappeared.
Chronic pain is gone.
My allergies are virtually non existent.
My sun tolerance increased 3-5x and I barely sunburn unprotected if at all.
And lastly, my lifelong asthma, which I had for over 40 years, and was on 2-3 medications plus occasional steroids and antibiotics due to lingering respiratory infections, disappeared. I no longer need any medications.
if you still believe vegetable/seed oils are cardio protective, there's no point in me arguing with you, but you're as ignorant as the diabetes physicians still telling their patients to eat healthy carbs and pump themselves with insulin.
@@stellasternchen Ah yes, Studies shows it's OK so I follow it and accept it like gospel. Are you a journalist? Lmao.
I Love your Channel Man, very interesting content 👌but I think you're Bashing Saladino just for the sake of Bashing. Don't fall in this trap....
I'm pretty sure Saladino's point (Who like you Said is a doctor so His points are as valid as any others) here is :
Don't worry if your LDL cholesterol level is high, Higher than the values proposed by the FDA or others guidelines. (Which we now know are BS)
Which are values u follow to avoid deficiencies.
Go chek and Listen to Dr Gundry, a Cardiologist Who made more than 10000 Heart operations. He Said :
I could not care less for high LDL levels
Either way there is no evidence that statins reduce the risk of death from heart disease so what is your point?
That is nonsense. People who have a genetic disorder and produce as a result too much cholesterol die young without statins, have a normal life-span with statins. Your general statement is stupid nonsense.
You can make a good case that doctors prescibe to easily statins instead of checking some aspects better and make than a data based cost-benefit analysis, but thta requires that you pay attention to details.
@@olafkunert3714 I read Dr Aseem Malhotra’s book. He says life expectancy is only increased by three days by taking statins. Take it up with him.
Ps I ignored it and have started taking them again!
@@olafkunert3714and yes , another big debate with more than one side to the story
Several large-scale clinical trials and meta-analyses have shown that statins significantly reduce the risk of major cardiovascular events, including heart attacks, strokes, and cardiovascular-related deaths. For example:
1. The Cholesterol Treatment Trialists’ (CTT) Collaborators: This large meta-analysis of over 170,000 participants across multiple studies found that for each 1 mmol/L reduction in LDL cholesterol, there was a 20-25% relative reduction in major cardiovascular events, including death from heart disease.
2. The Scandinavian Simvastatin Survival Study (4S): This was one of the earliest and most influential trials, showing that statin therapy reduced the risk of death from heart disease by about 30% in people with existing coronary heart disease.
3. The Heart Protection Study (HPS): This large trial involving over 20,000 participants demonstrated that statin therapy significantly reduced the risk of heart attacks, strokes, and revascularization procedures, as well as cardiovascular and all-cause mortality, even in those without high cholesterol levels at the start of the study.
4. The JUPITER Trial: This trial focused on individuals with normal LDL cholesterol but elevated C-reactive protein levels, a marker of inflammation. It found that statin therapy led to a significant reduction in cardiovascular events, including death from heart disease.
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.
Great, great point!
He just made an 1hr 20min video on LDL last month. Check it out.
Researchers are not to be revered over practitioners. There's a Dr. Gundry, with more than 10.000 heart surgeries under his belt who's advocating that he couldn't care less about LDL numbers! I'd take his advice over 1000 studies on the issue. The statins industry is a huge one (just to point one possible unethical confounder for those "findings"). The said cardiologist/surgeon has nothing to gain by pointing out the insignificance of high LDL.
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. 😂
Good for you. A crutch isn't doing your body any favors.
@@C_R_O_M________ it's not a crutch, it's the main energy source for endurance athletes, and sports athletes.
Any inflammation, including exercise, also increases LDL, which is what you want. Problem seems to be mostly damaged LDL.
@@Dan-gs3kg I was obviously referring to statins.
It's wonderful how you know so much more about this subject than the global scientific and medical communities.
I don't really understand the point at 17min. People with higher ldl have lower percentage of being t2d and people with higher ldl have higher risk of cardiovascular events and death. I don't see what contradicts Paul Salidino's claim that people having cardiovascular events in most cases have insulin resistance (t2d) because he said that it's t2d PLUS high ldl that is problematic.
If someone can clear what's wrong with my reasoning for me that would be good.
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.
All types of LDL are atherogenic.
Agreed, small and hard or soft and squidgy?
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.
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?
There's almost no finished studies on LMHR. There's one (led by Dave Feldman) that is in the process of having data correlated and analyzed. But nothing published. Everyone wants to extrapolate from published studies on LDL-C but LMHR folks are so far outside "normal" range that those studies may not apply. We wait, hope, and do what we do...
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?
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.)
that's so true, plus how many different factors may come into play when assessing if an individual with elevated LDL is actually at a health risk
when it comes to doctors, I think it's high time schooling system had finally changed, switching to a more holistic approach - not only teaching how to solve problems with pharmacology but also through lifestyle/diet/environment
Yes there's pattern A which is usually called large and/or fluffy and it's made (as far as what I've read is true) directly by the liver and pattern B which is small and dense and comes from VLDL particles after they've emptied their triglycerides. Some say that pattern A is harmless and others that it's less harmful than pattern B which they all agree that it's more harmful. More pattern B most of the time means bigger lipoprotein number that's why the paradigm shifted to LDL-p or ApoB measurement. There's also LPa which is way more atherogenic than pattern B and people with FH usually have elevated. Another caveat is that while LDL lipoproteins are supposed to get trapped under the endothelium because "they are bigger than the HDL lipoproteins" it's the smaller ones that are more harmful rather than the pattern A particles. And HDL lipoproteins, the ApoA ones, are found to be either protective or completely harmless, depending on who you ask, despite being way smaller than the ApoB lipoproteins. Peter Attia has stated that it's the ApoBs that are atherogenic while the ApoAs are not. Overall there's big ambiguity on that matter with experts like Robert Lustig and Ben Bickman looking at lipids as a secondary measurement with the primary ones being blood glucose and insulin levels (an idea that I personally lean towards most) and others like Peter Attia and Thomas Dayspring who treat lipids as a primary factor for vascular disease.
@@LTJBLTJBInteresting information! Yes, things are more complicated than just "high or low" LDL, and insulin sensitivity should definitely be counted in IMO, as the damage to the endothelial lining of the vasculatory system is amplified pretty quite a lot by the effects of high glucose levels
@@lollsazz And another important factor is that, glucose aside, high levels of insulin are a big risk factor in their own. Kidney disease, hypertension, increased risk for cancer etc, all caused by hyperinsulinemia.
All atherogenic lipoproteins have ApoB and they’re all small enough to get into the arterial walls. Don’t go chasing waterfalls.
Low grade scurvy?
Personally, I want to understand, see the logic, and the heart diet hypothesis had some weird quirks.
WHAT is causing the damage that the body tries to repair?
A quite logic answer (ok, theory) came from Linus Pauling and Matthias Rath: low grade SCURVY.
Vessel walls are enforced with collagen, giving strength and elasticity. Building and maintaining collagen requires ASCORBIC ACID (vitamin C). Lack of vitamin C weakens the blood vessels because the walls get weaker over time. Mechanical stress is highest at places with highest blood pressure and a lot of movement.
Where's that? Arteries near the ❤! (Widow maker)
ROOT cause: lack of vitamin C because of our "food products" low in nutrients and high requirements of vitamin C when you have inflammation (think of sugar, refined carbs, refined seed oils, toxic environment etc).
What makes the situation worse: vitamin C and Glucose use the same transporter to get in the cells.
You consume tens to hundreds of grams of carbs and, say, 60 milligrams, 0.06 grams of vitamin C daily (alas, that often is government's advice ;)
So guest who wins the competition? 😢
Now, that makes more sense to me..
And modifying LDL's surface with a glucose coating or oxidation, makes that the receptors on our liver don't recognize the returning LDLs so it is not reabsorbed by the liver...
Makes sense?
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!!
Make sure you do a better job then. This guy has been wrong about way too much.
@@thepimptastic2Hey! we are all humans. we are Imperfect.
What has he been wrong about
@@thepimptastic2Can you name something and give your own evidence
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
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.
And yet the French have high carb diets, they have had riots over price increases and shortages of baguettes. They also are now the longest lived first world nation. At least Monaco which I consider French even if technically an independent principality in France, they also are one of the richest places on the planet. Life expectancy = 89.4 years. You want an odd statistic, the #5 place in the world with the highest number of people over 100 years old is LOMA LINDA in San Bernardino County in California. This is because there is a community of about 9,000 Seventh Day Adventists there and they do not smoke, drink, or eat meat, and take regular exercise. Of course they average 10 years longer life expectancy that the rest of us, but who would want 90 or more years of that?
@@MAtildaMortuaryserver the French do not have high carb diets. In fact, they eat the most saturated fat in Western Europe, primarily from all the delicious cheese they eat. Look it up.
@@MAtildaMortuaryserver I live in the South-West of France. We traditionally eat a lot of fat, including duck and goose fat, as we raise ducks and gooses to make Foie gras. Eating baguettes doesn't necessarily means having a high carb diet.
@@AndreAngelantoniThe French and Italian people eat moderate to high carb diets.
@@spgtenor the French eat more fat than perhaps anyone. That's why it's called The French Paradox.
@Physionic @8:50, okay but is there the same mandelian trial (i apologize if i spelled that wrong) with HIGH genetic LDL cholesterol???? I am not trying to nitpick, i actually have the high ldl gene and i appreciated your funny song and dance about how these people will *always* have low ldl, but because of how positives and negatives work; this would be MUCH more damning if people like me were studied.
I *have* high ldl, irrespective of habits, and I should be compared to 'normal' populations (that may or may not have habits that cause high ldl, but will always have 'lower' LDLs once accounting for those differences) and *THAT TRIAL* would be FAR MORE APPLICABLE to these particular claims around high LDL and its health effects.
I live a very healthy and active life + i track my nutrition; you don't know how frustrating it is to have high triple digit LDL! It's actually so comical how optimal my other blood levels are when I get tested!!
Please read this man, I really want you to talk about stuff like my situation!!
Also, did you mispeak at @16:30? You got through saying that people with genetic predispotion to high LDL, have an inverse correlation with the development of diabetes...and then went on to imply you've 'hit the argument with a chair'.
High LDL, *inverse relationship to diabetes* , then using that to claim there's more risk for a heart attack??? The whole point was diabetes was contributing to heart attacks! The genetic mutation for high LDL reduced the risk for diabetes! That helps the other doctors point, it doesnt hurt it. It comes across as you saying 'we have controlled for high ldl and diabetes, and still see heart attacks with people who don't have diabetes but do have high LDL', without ever really addressing, properly at least, the fact that these two groups *do* have confounding variables. The data cited doesn't address what you say it does 1:1.
I really want the mandellian trial specifically on people like us! Those confounding variables, in my opinion, were not properly addressed by your argument. Even with the childhood heart complications study. They were only cursorily addressed at best.
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!
I’m only going to touch on a few of the points you made. But first I’d like to say I think you have the intellect to understand this issue so I would encourage you to do a deeper dive. First of all when people consume considerable plant-sterols. Be it in plants or vegetable/seed oils the cholesterol level in the blood is artificially low. Using that as a reference point and then assuming cholesterol is the cause based on biased studies propagated by vegetarian advocates like the Seventh Day Adventist and Ansels Keys is how we got these “standards of care” rules that have been pushed so aggressively by Pharmaceutical/Statin manufacturers. First you mentioned the High Cholesterol in Young children causing heart disease. The children are a subset of the High Familiar Cholesterol group they possess both a genetic trait for excessive clotting as well as for High Cholesterol when you separate the two groups out the one with high Cholesterol only they are very healthy and live very long lives like to 100 years old. The research being done more recently is much better if you use old studies they will not have good separation of the metabolic processes Dr. Saladino is referring to. When you eat a very high fat and meat only diet Cholesterol goes up to transport the lipids around the body. This is a higher level than the artificially low levels that are currently used as the base average for what I could argue is a very unhealthy population and most of the healthy ones are on their way to be unhealthy with their Hyper Insulinimia as yet undetected or they are very robust in that regard genetically. The notion that we evolved prior to the agricultural revolution on a plant based diet more than just an occasional meal is flawed. In addition our normal state would have been the fasted stated no carbohydrates in our system at all.
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?
They use measured in the studies. Usually a variety of measuring techniques, including cholesterol esters and/or particle number by NMR, electrophoresis.
They may use measured in studies, but most people getting tested don’t get measured, unless an NMR test is specifically ordered.
@@1000BabyRage True, but at least some labs, e.g., Quest, offer an LDL-C Direct, and I'd guess that most offer an ApoB which I believe is a useful stand-in for particle number.
What about all cause mortality? You just brought up lower risk of heart disease but that’s not the only killer out there. Did they live longer, disease free? I’m doubting they did.
The one thing health TH-cam 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...
You started off the video with incorrect information. Paul Saladino is NOT a carnivore. And of course, here you are opining about a field that you’re not a trained expert in. Stop it.
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
Plenty of people have normal LDL on keto/carnivore
@@defeqel6537 many do and many don't depending on a lot of things. In the beginning there is a spike in LDL and months later when the body gets fat adapted you need less LDL to do the same job
…Then why does LDL skyrocket in some individuals as their BMI decreases below 25 when they may have been only slightly elevated when they were overweight?
@@pacmanfl because what I just said
@@defeqel6537people do keto and carnivore with high range of fat intake
these from low end compared to these on high end can be in totally different situation... not mentioning varying source of their fat in diet...
even amount of omega3 can affect how all the rest results, too low and suddenly what worked well becomes a serious problem
Timestamps would help your nice videos
❤❤❤❤❤
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.
You know for a fact that both of them NEVER had LDL below 225? You have a comprehensive history of their lipid panels going back their entire life? If so, I'm impressed, but also, literally means nothing. Risk never guarantees outcome.
Also, to answer your question, "bad" is always quantified in hazard ratios. Either risk to all-cause mortality or risk to a cardiac event. Based on the trials, they'll calculate what the increased or decreased risk is associated with a certain LDL level.
My father too.
Hi - would you know any of their numbers for total and hdl? For me some change over life time - in 20s and 30s total in 130 to 140. Now in 70s is 200 to 220 for total. Maybe change from high hdl amounts around 105 to 115 over past about 10 yrs. In my 20 and 30s doc didnt check my hdl numbers.
Pay more attention to inflammation and less attention to LDL.
A gun (LDL) won't hurt you until you add a bullet (inflammation.)
If you can conquer the inflammation part of the equation, the LDL/VLDL/HDL thing is probably irrelevant.
LDL made a compelling story and sold a lot of pills, but the drug companies still won't share the research they have locked up in England.
Very suspicious. Now we hear they did a little trick with relative risk and overstated the benefits dramatically with clever statistics. Hmmm.
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.
The absolut first statement he made is already completely nonsensical. How people listen to that guy is really beyond me.
You're growing like crazy, weren't you at 75K 1 or 2 days ago?
Yep. Sharp eye. :)
Set your targets on Berry & Ekberg their misinformation seems to attract crazy numbers. You may also save a few people from falling down the rabbit hole.
The brain is made up of 60% cholesterol, And we have been taking statins for over 20 years, so it's no surprise to me that the new dis-ease is Alzheimer's
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. ❤
Saladino would mop him up!
@@pharmdog1 Seeing the Physionic channel engage directly with other YT creators such as Saladino would make for powerful viewing.
@@pharmdog1 Yup
Who decides what "normal lab value" is?
@@pharmdog1yep, Saladino is probably better with a mop
That's interesting, but you didn't address the types of LDL , i.e., particle size. As in : Effect of carbohydrate-restricted dietary interventions on LDL particle size and number in adults in the context of weight loss or weight maintenance: a systematic review and meta-analysis, or Dr. Paul Mason's video on TH-cam 'The truth about high cholesterol' under the channel Low Carb Down Under. It appears that keto/carnivore/low carb changes the typical HDL in the population to the atypical with a large particle size. This is obviously not Dr. Saladino's main argument in the video clips you referenced. But there remains the question whether the different types of HDL have a similar impact and a similar predictive value. It may be too early to say, but it appears to be relevant to the discussion. Perhaps you should do a video about it. Because keto is a relatively new intervention, there are few studies which actually show the long-term effects over decades, but there is plenty of evidence from shorter-term studies on this. There's also this one if you're interested : Small Dense Low-Density Lipoprotein as Biomarker for Atherosclerotic Diseases.
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.
I think almost all of dieting can be summarized with "Dosage makes the poison".
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.
CVD is caused by a lifelong exposure to elevated LDL/ApoB. Day-to-day LDL readings are meaningless, just like Feldman's 'research'.
What would you need to do to manufacture a lower LDL score?
I remember dave Feldman was avidly checking his blood cholesterol for a long while, trying different things. I have actually tried this approach, as I usually have very high cholesterol when I get bloodwork. Once I tried eating a whole pound of 97% lean ground beef, broccoli, and oats the day before. I only fasted the 12 hour minimum and my cholesterol dropped like 120 points in contrast to when I was doing high fat keto the day before with lots of fasting 16+ hours.
But also, I do believe high LDL is bad and you should be eating fiber and vegetables. I no longer do keto or any kind of fasting.
I tend to concur with diet having notable effects on LDL-C values. My most recent labs from about 6 months ago had a (calculated) LDL-C of 115. MD had a fit, since my previous labs from 9 months back had me at LDL-C of 85. So...about 72 hours prior to labs I'll be eating as high a fat diet as I can stand (usually avocados & tuna packed in olive oil) then a single meal with enough carbs to get my blood glucose right where I want it. Doing that I usually get LDL-C in the 75-85 range. My typical diet these days is fairly low carb (50-75 grams of digestible carbs/day) primarily to keep my blood glucose & a1C values at normoglycemic levels.
Yes!
What kids are we analyzing ??? Modern kids since the 70s have been eating basically toxic waste. Are you going to blame the results a diet of sprees Doritos sour patch kids funyuns and Coke on genetics ???
I thought particle count (ApoB) was more important then LDL-cholesterol levels.
It is
@@Physionic Yay. I’m learning. ty
Yes, yes .. high LDL cholesterol is good!! 😅😅😅
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.
are you talking about glycation? do studies back your argument?
@@archascents5157 You mean the difference between LDL and oxidated/glycated LDL for atherosclerosis? That is no secret or guesswork, really. pubmed.ncbi.nlm.nih.gov/18607185/ But the part about "lower your sugar, you will lower the glycation" might not be studied yet at all. I do not know, but who would put any money to such a study?
Glucose attaches to red blood cells when the diet is highly restricted of carbohydrates the red blood cells live longer because there is less insulin in the blood. So A1C can appear higher because the blood cell looks like a sugar ball after a while. But the health improvement in the body is very evident. That is just on example. Not sure if any glycation occurs on LDL. You might want to look up Dr. David Diamond PhD he did a good video with Dr. Shawn Baker. On TH-cam as well.
@@jeffjensen2083 "Glucose attaches to red blood cells" that sounds like glycation
@@archascents5157 Yes that is Glycation it happens to much of the body I believe but I’m not sure if LDL get Glycation it is how the body carries Lipids around in the body while glucose flows in the blood stream. My other point is glucose is essentially treated like at behaves like a poison that the body needs to get rid of as quickly as possible.
Have you suffered a heart attack, stroke or were diagnosed with colorectal cancer or type 2 diabetes while following the advice of "carnivore" or keto practitioners or influencers on social media? You may be entitle to compensation. Call a qualified malpractice or personal injury attorney in your state today.
Great comment 💚👍
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.
in 1980, normal cholesterol level was 280. i wonder why it was lowered to 240 and then 200. now there's a push to decrease it to 185...
@@chuckleezodiac24 they have to sell their statins to someone.
Bad news for me, seeing as i have really high ldl for some reason 😄
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!
low ldl has a higher all cause mortality than high LDL - also see new study of LMHR (LDL 350+ )compared to Miami Health study that showed no difference in plaque buildup over 4 years
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.
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.
LDL and cholesterol do NOT cause CVD. Inflammation from eating sugar, carbs and seed oils are the cause of CVD. I do not worry about my high LDL (I eat ketovore), because my HbA1c and triglycerides are low. I am a lean-mass-hyper-responder. HDL/TG ratio and A1c need to be low! LDL is not important!
LDL is what fire fighters are to fire ( they’re not the cause, they come to help)
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).
True science holds up to any and all questions about the data, the facts, or how the study was conducted, doing so doesn't make you a conspiracy theorist. The problem arises when political interests / corporate greed become entangled with science to the point where people who ask questions are labeled as conspiracy theorists in order to silence them.
@@Deep_DiversPaul sells supplements
@@VeganLinkedpoor Paul against all medical corporations...
no, poor vulnerable people he misleads and poor animals that suffer the most consequences@@flcps
@@Deep_Divers Making wild claims that are constrary to the scientific evidence and then claiming that that evidence has been fabricated by powerful interests to hide the Truth is what defines conspiracy theorists. Not asking questions.
Look into Korean study on cholesterol!
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.
All fair points. I didn’t discuss it, because he didn’t discuss it. I have to limit the scope of the videos. That said, I’m releasing my investigation of LDL oxidation in the near future. I would disagree that the LDL doesn’t contribute, however - there’s an astounding amount of evidence that it is an independent risk factor. If you’re up for it, I covered 10 studies on the topic in an hour and a half video. I’m also covering about 10 more in the coming months.
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.
This is fun. Intelligent discourse is fun.
Physionic - what you have entirely ignored in this topic in your videos is TYPE of LDL.
Covered in other content
Its the LDL size and LDL particle count that matters.
Insultin resistence - It's not just Salasino saying this. many other are also saying this. And YOU are confusing IR with T2D, they are not the same thing.
Ir is as akin to T2D as Aic is to blood glucose levels. THe difference if part what of the chain of cauality you are looking at. Evey one with T2D is IR. Eveyone who persistently eats refined sugars if going to damage their haemoglobin. Persistent abuse of the glucose insulin cycles leads to ID and T2D is nothing more than the threashold point where IR is pathological. THere is no confusing here. You are cas of your pedanticism
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 believe the researchers tested in the generic trials of those with diabetes 2 because the disease is caused by insulin resistance, specifically in the beta cells of the pancreas usually from fat infiltration disrupting insulin secretion. Ergo, they definitely have insulin resistance.
Although, you are correct that other muscles can have fat infiltration and thus can turn into fat cells causing insulin receptors to retreat into muscle cells.
Have you seen the video posted by Dave Feldman titled "New Heart Scan Dare for 64 participants with high ldl cholesterol on a ketogenic diet"?
No - seems interesting. I’ll look it up.
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.
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.
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 ...
Straightforward? Not so sure.
For example, people having a genetic disease resulting in more cholesterol could perfectly have other factors which have some health consequences.
And let's assume that the culprit is not LDL-C but rather the number of damaged LDL particles. People with FH could be simply more at risk because they have, on average, more damaged particles. Does it mean than somebody with high LDL-C but with a very low number of damaged particles would be at risk?
@@Noegzit That idea could be plausible if a single mutation was involved. However FH is caused by mutations in multiple different genes so unlikely they would result in the same phenotype
@@llicit1833
But even if we have different variants a particular group could have a sufficiently more increased risk to make all people with FH look more at risk. There are some FH variants leading to very high plasma cholesterol levels which are not necessarily associated with premature atherosclerosis and mortality. Better read that twice. We also have patients misclassified as having FH. They don't have FH, they have sitosterolaemia with elevated plant sterols and look as if they had FH. And having elevated plant sterols in the blood is not that great.
The fact that there are variants of FH not associated with premature atherosclerosis and mortality tells us that things can be a bit more complicated than we thought.
My yoga teacher has FH, she's 78, she's not on statins and has never been. And yet she's still alive and, of course, teaching yoga. I know it's just an anecdote but it proves that having high levels of LDL-C during your whole life doesn't necessarily kills you by "clogging" your arteries at 50.
For the record I don't think that having more than 500 mg/dl of LDL-C is particularly great for health, I just wanted to pointed out that sometime things are not as "straightforward" as they seem to be or as some people would like they were.
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?
My lab printouts always give the normal LDL range as 66-100
@@dsmj7389 If you eat Carnivore or Animal Based like Paul Saladino those Numbers are much higher. But then again other numbers are also out of Range. Triglycerides for example are normally lower. So as far sa i know these Numbers are depending on the diet yo take. So this 66-100 represnts the range for a "normal" or "standard american" diet.
I for my part don't think that anyone sees through all the complex mechanisms in our Body.
Meaning.. i don't believe that eating meat or eggs is a risk factor. Those are whole, unprocesed and very bioavailable foods. Why fear such things...?
According to this study published in 2024 the sweet spot is between 100 and 189 mg/dl:
"Is LDL cholesterol associated with long-term mortality among primary prevention adults? A retrospective cohort study from a large healthcare system".
@@dsmj7389 That is too low according to this 2024 study "Is LDL cholesterol associated with long-term mortality among primary prevention adults? A retrospective cohort study from a large healthcare system".
Be aware that what is defined as normal is subject to caution and has been modified several times in order to prescribe statins to more people...
The lipoprotein that houses the cholesterol has a receptor binding domain, in the presence of high blood glucose this receptor binding domain can be damaged making making this lipoprotein and cholesterol damaged and the only instance you can call a cholesterol bad. I believe the liver is supposed to clean this up but in high blood glucose will correlate high insulin and I believe the liver will prioritize management of the glucose over lipoproteins as high blood glucose is more dangerous then high blood lipoprotein.
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.
You should read too "Fat and Cholesterol Don't Cause Heart Attacks and Statins are Not The Solution" and "The Cholesterol Myths: Exposing the Fallacy that Saturated Fat and Cholesterol Cause".
These people are long-term statin sceptics. No credible health authority anywhere in the world accepts their claims. The point is that we really don't know what the long term effects of high LDL plus low carb diets, on mortality and morbidity risk, are. Articles in obscure pay-to-publish journals like this should be treated with caution.
@@tomgoff7887 Science is neither a question of consensus nor decided by a majority vote. You can perfectly be right even if you are alone to think the Earth is not flat.
Health authorities are paid by food industry and big pharma. I hope you know that. So don't be too surprise if health authorities generally say what they are told to say, id est what will increase the benefits of the shareholders. They say it is science but it is just politics, money and vested interests.
The statin market is worth 15 billions of dollars each year. Fairly enough to make them a little more appealing than they really are by minimizing their side effects and overestimating their supposed health benefits, don't you think?
@@tomgoff7887there arent long term statin users either.
Hope to join you
Glad there's someone out there covering some of his claims as he makes a lot of them.
Focusing only on one variable like LDL without controlling all other factors is unscientific nonsense.
One variable can be very bad, and one study controlled for the absence of other risk variables. "Treatment with statins reduced deaths from coronary heart disease by 28% in men with very high levels of low density lipoprotein (LDL) cholesterol but no other risk factors or signs of heart disease, a 15 year follow-up study has reported in the journal Circulation."
"The authors said that the findings provide the first direct randomised trial evidence to confirm current guidance that patients with LDL above 190 mg/dL should be considered for statin treatment regardless of other risk factors."
Long term study backs statins for patients with high LDL and no other risk factors
BMJ 2017;358:j4171
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.
Agreed. I often wonder if the "leaky gut" is similar to the cracks in the artery (inflamed regions as you say) for plaque deposits.
@@tootalldan5702 Mostly leaky gut is caused by inflammatory grains which induce zonulin, which breaks the integrity of your intestinal barrier.
@@tootalldan5702guy is not in the heart
Sir if you don t eat vegetables, where do you get your fiber? From fruits ?
@@Chawaniii Oh, I do eat vegetables. Mostly broccoli. Just not starchy root vegetables, but I also take inulin, pectin, acacia gum and other things that qualify as fiber. The only fruits I eat are berries, and technically tomatoes are fruits. I eat the berries for the polyphenols in small quantities that are not enough to throw me out of ketosis.
Technically, you could eat only white sugar and be in ketosis. You would have to have small amounts that are not enough to elicit insulin, multiple times a day.
Hi, your understanding that Dr Paul Saladino is carnivore is incorrect, he also eats honey and fruit.
technically, if a creature's diet is more than 70% derived from animals then they are classified as "hyper-carnivores." so Saladino probably qualifies. but he's not as cool as the 100% Ultra Xtreme Hardcore Super Mega Max Meat Mutilators!
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.
It depends on what initial assumptions these AI bots will be initially fed with. The GIGO principle is a very crucial factor in these.
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...
I think the main argument is that the LEVEL of cholesterol that consensus currently says is “elevated” is under scrutiny 🤓
Have there been studies strongly indicating that the scrutiny is warranted?
@@brandonpacheco9713When the measurement "standards" are dictated by corruptible entities studies would be irrelevant.
@@brandonpacheco9713 As far as I’m aware, many. Science always questions Science. It has to. The last one I looked at from NIH said there was no evidence of a relationship between LDL and mortality. Also, the so-called “War on Fat” hasn’t succeeded. Why not? Because saturated dietary fat is not the enemy. I suspect shovelling excess carbohydrates down one’s throat daily probably has a lot to answer for 🧐
@@moonstrukk126 Yes. The food industry (and Big Pharma) springs to mind 😉
Dr. Saladino is a warrior on a relatively natural carnivore-ish diet with fruit and honey. He feels great and, therefore, doesn't care about data unless it supports his diet.
Refined, nuanced conversations on this topic break it down to the types of particles making the LDL. They discuss p values of data and how to encourage the right types of particles in LDL.
I respect that Dr. Saladino is raising some good questions and getting people to think about nutrition, but his approach is not so scientific. The only time he said "level" was to dismiss it as irrelevant unless low.
Elevated ldl is a symptom not a cause. If you aren’t making enough vitamin d or other hormones your liver will make more cholesterol. Or deal with your infections! Get your hormones fixed, and get your infections fixed.
If you have high ldl your body is trying to repair itself.
Yes, the ldl can cause problems, but focusing on the ldl misses a lot of the problem: infections and low vitamin d etc.
Please try to understand the "genetic" arguments in the video.
Equilibrium is the key.
Some foods are addictive and triggering and should either be avoided or limited. I've never been addicted to meat and fat but fruit, crackers or anything with a sweet taste is triggering.
I'm not sure why fatty beef is so satisfying and why I can go over 6 hours without any hunger but it does just that.
genetic memory
Fatty beef is statisfying because it's fatty and has protein, both satisfy. Where carbohydrates don't, infact carbohydrates make you want to eat more, and are normally found in abundance at the end of summer. The result is you eat lots of carbs just before winter kicks in, you get fatter and survive winter. The problem is we are no longer are hunter gathers, and carbs are everywhere, and now everyone is diabetic!
What about if your triglycerides are very low?
I've got the same question
Glad to find this scientific based channel! I just subscribed!
Interesting that you comment on people with FH. Despite these people being more likely to contract heart disease when young, I believe a study found that if they make it to the age of 70, they actually have a longer life expectancy than those without the condition. In terms of all-cause mortality, those with FH have a very similar life expectancy to the rest of us. I don't have the research in front of me so forgive me if I have made a mistake on this. I also have elevated cholesterol but am a normal weight, fit, with no blood pressure issues, normal blood glucose and with no family history of heart disease. I have been wrestling with whether to take a statin. It will lower my cholesterol for sure but it seems the medication will have only a marginal effect at best on whether I contract heart disease.
What about elevated LDL from fasting? Does that increase the risk of heart disease?
No
Dont cook raw meat
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.
6:15 in the "normal range"? you read "optimal range" which is minimal by scientific consensus (guidelines etc)
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.
Study at 9:50 . The people with the relatively high LDL, what do they eat to get that high LDL. If you eat cookies and get high LDL will you be off the same/worse/better than if you eat actual beneficial food like red meat that raises your LDL to that same level?
Are we doing the right thing by just looking at LDL without asking other questions?
@@stephx9759 Yes we are. HDL is not relevant because in studies where theyve increased HDL, it has had no net effect
What medications did he or she put you on? I'm curious.
@@danyalraza4388 why is it that heart risk calculations use HDL/TG ratios, and not LDL?
@@Dan-gs3kg Where? Anyone still doing that (including labs and sensationalist fad-youtubers in the carnivore/keto space), are using outdated or very selective science.
Basically, HDL & TG are symptomatic of some other issues, such as a large waistline and bad diet, but LDL is actually causative for heart disease. You want to see HDL & TG in the good ranges, but they're just markers of good health, not the cause of good health. Does that make sense?
sry Physionic is very wrong here.
I understand you are a dr. and spent lots of time on this and similar topic. So to error is probably not an option you want accept.
But you must accept from time to time. And you should stop using studies to make conclusions.
Generally studies are very very bad for supporting conclusions or connections because studies are made from humans sometimes just to support interests.
But even if the study seems to be well done. It's still 'made'.
And do you really think cholesterol and those tousand other more critical things are exactly equal from person to person. There are big genetic differences even in the near familiy!
It's not infrequently that people tolerate 100 times more sun, or more poison, than other people. You can still try to find connections in the human body.
The human body is way too complex and there are endless factors influencing everything. But we make such claims and scare some people wich makes them even worse.
For what? For money and proud.
“You should stop using studies to make conclusions.”
What are you doing on this channel?
@@Physionic i'm sry. I got lost and couldn't think clearly probably because of my elevated health marcers.
will not happen again!
Immediately out the gate, confusing dietary cholesterol with serum cholesterol, he confirms his ignorance. Being an MD means almost nothing anymore.
The liver uses cholesterol in the diet or from its own synthesis to make ldl, hdl, etc. The doctors he was talking about cant just give the kid an LDL iv. And its known that when you consume more cholesterol then your liver synthesizes less. If the child had a problem synthesizing cholesterol then it would be a good treatment.
Well, your argument is valid for any MD then....⬆️
👌
He's a non practicing psychiatrist who makes money by selling expensive supliments
Dr Paul Mason is a practicing MD and also doesn't believe that high LDL is a problem, most of the time, especially not compared to low HDL or high triglycerides
edit: here are some videos from him going through studies:
statins: th-cam.com/video/Odvt4EaGPLw/w-d-xo.html
cholesterol: th-cam.com/video/rdgS3PuSuyg/w-d-xo.html
@@defeqel6537 🦆🦆🦆
This is a complex topic that has its roots in the aberrantly low level of LDL in people who eat an excess of carbs. Their metabolism has to skew towards carbs a s substrate for mitochondria. That alone reduces the number of chylomicron produced, LDL is effectively a chylomicron sub particle. What lies at the root of this is how does rejected LDL get oxidized? It is rejected because glaciation modifies ApoB, but what then? It may be that fat adapted carnivores have insufficient glucose to oxidize LDL....
Carbs remember are NOT a nutrient, there is no such thing as an essential carb. The rest is marketing hype.
This won't be enough for Saladino. He's defined insulin resistance in some way that includes 90% of the US population. IIRC he measures fasting insulin and glucose at the same time and compares the values by some strict threshold to get to 90% inclusion in his diagnosis. He thinks the remaining 10% can have high apoB and not develop atherosclerosis.
He and his followers repeatedly make the straw-man argument that "mainstream doctors have always said cholesterol is the ONLY cause of heart disease". I've never heard this myself... the claim is some bananas gaslighting to win an argument. Of course the messaging has always said that atherosclerosis is multifactorial, along with blood pressure, diabetes, obesity, smoking, drinking, etc. Building on this fallacy, he's obsessed with finding the one single cause of atherosclerosis. His metaphor is the spark to a fire - insulin resistance is the spark, apoB is the wood. Firemen/doctors want to blame the wood, but we need wood to build houses, so they're wrong. His metaphor has limitations anyway because we're talking excess wood in dried brush that's exposed to lightning strikes with no sprinkler system.
His fixation on a solitary cause is impractical. If 90% of people's excess apoB will fuel a fire, then they should control their apoB. With caloric restriction and exercise they'll improve their metabolism simultaneously anyway. They should correct both. Mainstream advice will correct both.
Finally, Saladino argues that oxidized LDL percentage is more important than LDL count. He thinks his very high LDL is okay because it's not oxidizing. He agrees that it's on the oxidized LDL circulating in blood that matters (this is quickly removed by the body); it's how it oxidizes in the artery wall. He pointed to a study that suggests more polyunsaturated fat intake increases the propensity of LDL particles to oxidize after they get stuck in the wall. I though that all LDL particles stuck in the wall will eventually oxidize... maybe I'm wrong and I haven't read the study. Nearly all studies of actual human health outcomes show benefits when replacing some saturated fats with mono and poly-unsaturated fats. Anyway, I do need to look into his citation about this.
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
Great! I just left a comment about Dr. Gundry, a surgeon and cardiologist with vast experience (more than 10000 surgeries) who says that he couldn't care less about LDL. He proposes monitoring triglycerides and HDL and how the two relate to each other. Look him up. One like him worth more than 10000 papers "proving" anything.
@@RandomGuy-qg9xf lol....random thought from the random guy. look into a mirror random but don't blame the mirror for your ignorance
Weight loss can increase ldl because it is a lipid carrier and keto can increase ldl because you would use fats for energy more. Congrats on the lifestyle bump up!
But the Physionic guy read TONS of HUNDREDS of papers!
My experience exactly! In fact my experience and decision making exactly parallels all that you have written Veronica. The only slight difference is the timeline with my BCA Stage IIB diagnosed Aug 2022. My husband is a surgeon and insisted I stop the Ketogenic diet because my Total cholesterol and LDLs went up when I started the ketogenic diet. Yet my Triglycerides and HDL were still normal. I refused to stop my lifestyle and dietary changes so he insisted I see my Cardiologist. The cardiologist asked if I was considering Statins and I told him that although my husband took them (had 95% blockages in 2 arteries and stents subsequently placed) there was NO way I would take Statins because of all their associated risks. He said so Statins are off the table for you. I replied YES! So he suggested a Calcium Score to see what that showed. Results were ZERO score for all cardiac arteries. He was stunned as I am 69 yo. He said my cardiovascular system was “like a 30 yo!)
So at 5ft 3.5in (161cms) and 115lbs(52.2kgs) doing 6kms power walking a day, alternate days, weights for strength training, no alcohol since Aug 2022 and a strict ketogenic diet I will continue this regimen as it seems to be the way to best manage my future health post Stage II BCA! I will not be worried about a higher Total Cholesterol or higher LDL when there are many more significant factors I need to manage to reduce my risk of cancer recurrence when exercise and diet are such unequivocal factors in reducing risk for recurrence. (For evidence see, Dr Eric Westman, Obesity Specialist, Duke Uni; Dr Christy Kettlering, Radiation Oncologist, NorthWestern; Dr Robert Lustig, Paediatric Endocrinolgist, Prof Uni California; Dr Jason Fung, Nephrologist, Uni Calf and Uni Toronto; Dr Daniel Lieberman, Paleo-anthropologist Prof Harvard; and on and on…)
Good Day
I enjoyed this discussion. Could the issue be that not all LDL cholesterol is the same. Logically the smaller LDL sized particles probably represent more damaged or Oxidized LDL. Larger sized LDL particles are probably represent a normal functioning particle and healthier metabolic state. Maybe the actual number of LDL particles is not the issue but the Condition of the LDL particle is more important. This may explain the differing outcomes when LDL association with MI is discussed from 10,000 feet in the studies you put forth. Don't Know - Any Data to support this idea ???