Don’t Worry About “Bad” Cholesterol, Says Dr. Paul Saladino

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foreign because this is common misconception I have a family member who recently was diagnosed with high LDL and the first thing the doctor went to is we need to put you on a Statin in perpetuity right and when I look at her yes she's up there in age uh late 60s early 70s but has the health of an average probably 45 or 50 year old but just sees this one marker on a test and we now think that she should be on Statin so can we talk about is LDL high LDL cholesterol bad and also are statins problematic in any way what are statins and what is LDL right right this is a super important question I'll do my best to make it palatable but it's not going to be in 60 seconds so that clock we don't even need the clock um so LDL cholesterol is low density lipoprotein it's a balloon it's a it's a spherical molecule in your body that has a single lipid monolayer and it carries cholesterol and triglycerides it's essentially like a bus that moves from your liver the bus station to other tissues of your body and supplies them with building blocks so now we've already seen that the LDL has a functional positive role in the human body those building blocks being cholesterol and triglycerides cholesterol yes is a valuable nutrient in your body it's the backbone of your steroid hormones so all progesterone estrogen pregnant alone testosterone is built from a cholesterol backbone is any steroid backbone it travels on an LDL bus to tissues of your body now there's buses that go back and LDL can go back or HDL buses can usually go back to the liver this is obviously an oversimplification there's lots of buses that move around your body on bus routes and so the LDL is carrying past passengers they get off at certain stops other passengers can get on and move back to the liver generally speaking now in in in the LDL particle there are these other molecules triglycerides and cholesterol but we think of cholesterol as misnomer because cholesterol is the steroid molecule but LDL is a type of cholesterol but LDL is not cholesterol in any way shape or form it's just a bus that carries a cholesterol molecule so LDL canonically has been thought of as bad but let's reframe it let's just back up and think why would a molecule that is essential for human life be bad for us it doesn't make a lot of sense to me um and we know there are genetic syndromes where you don't make enough cholesterol because of an enzymatic genetic defects in the cholesterol synthesis pathway the liver makes a lot of cholesterol you eat cholesterol and the liver makes cholesterol and the liver exports it on the bus to other parts of the body but there's a condition called Smith lemly opposite syndrome where one of the enzymes in the synthesis of cholesterol in the body is broken and you don't make a lot of cholesterol these kids have depression they have sleep issues a lot of them die in utero and they have massive susceptibility to infections and they're given egg yolks as a therapy for their disease so they're given basically a bag of cholesterol which is an egg yolk to treat their disease we know that in animal models if you deplete an animal a rat or a mice a mouse of cholesterol of LDL cholesterol they're more susceptible to infections if you give a rat or a mouse more LDL cholesterol they have more resilience to infectious insults we know that in humans and this has been studied at many different levels those humans with higher levels of LDL tend to resist infections and have less Hospital admissions and in the elderly in elderly cohorts 75 and above I believe those with the highest levels of LDL live the longest and have the most longevity so there's a real conundrum here in Our Minds when 99 perhaps of doctors would tell you that LDL is bad how can this be and I think it's because the LDL molecule gets associated with increased levels of heart disease so often in tests and humans whether these are observational epidemiology studies and we say those people in some people as the level of LDL Rises in the body we see an increase in cardiovascular disease cardiovascular disease being this process of atherosclerosis right the formation of a plaque in the arterial wall so atherosclerosis heart disease is in the arterial wall you have an artery and if you cut that artery in this direction and you're looking down the center of the pipe the wall of the artery is where all the action happens for atherosclerosis atherosclerosis and there are levels of cells in the arterial wall there's an endothelium which is the inside there's an intima there's a media and so sub intimally between the intima and the media is generally where the atherosclerotic plaque happens and in people who have higher levels of cholesterol at a very basic high level you may see an association between more LDL in the blood higher levels of heart disease but if you look deeper it gets really interesting because in many population studies uh and Hanes which is a population or Framingham study if you break that relationship down and I almost need a whiteboard to explain this but you let's look at a relationship on the x-axis you have the the amount of LDL cholesterol in the human body and say it's running from 100 to 150 to 200 milligrams per deciliter and then above 200 and on the y-axis you have incidence of cardiovascular disease the percentage of people or the relative risk of developing a heart attack or the precursors meaning this atherosclerosis in the vessel wall if you look at the Framingham data overall as you go up it's a it's a straight line that kind of goes up to the right meaning the more cholesterol the more heart disease but if you break the cohort down by a third variable and that variable gives you some indication of your metabolic health or your insulin sensitivity a very different pattern emerges and you get four lines based on the metric that I've seen used as HDL cholesterol so HDL is canonically thought of as good cholesterol but it's much more complicated than that but in this case HDL is a good proxy for insulin sensitivity because generally people who are more insulin resistant which is synonymous with pre-diabetes and diabetes have lower HDL diabetics tend to waste HDL it's just human physiology that a pre-diabetic or diabetic State results in higher triglycerides and lower HDL so if you so if you sub fractionate the total cohort of the Framingham study by HDL you get four lines right HDL less than 25 or 25 or less HDL 25 to 50 HDL 50 to 75 or HDL above 75 you can choose whatever cutoffs you want and and the people with the highest HDL there's essentially these are people who are going to have generally insulin sensitivity they're going to be metabolically healthy right people with the lowest HDL most likely to be diabetic pre-diabetic insulin resistant okay follow me so far yep people with the highest HDL in the Framingham cohort have basically a straight line that's flat they don't have any connection between the amount of LDL in their body and the incidence of coronary heart disease oh wow the people with or like a very very small upslope very small okay people with the lowest HDL looks like this meaning that the more higher your LDL the more heart disease you have and there are multiple studies that show this in humans who have high HDL and low triglycerides which is a clear marker of insulin sensitivity and metabolic Health there is very little if any relationship between the amount of LDL in your blood and the incidence of cardiovascular disease but in both instances that LDL bus is going to be consistently traveling it's always traveling and so that's what makes us say it's correlated with that the LDL is always there yeah but what we see is that when you if you if you stratify Studies by insulin sensitivity we know that the single greatest risk factor I would argue for determining whether your LDL is going to be connected with heart disease is your insulin sensitivity but most most people don't understand that so when you're when your family member had her cholesterol checked I'm willing to bet a very nice delicious ribeye steak that they did not check a fasting insulin they they probably did zero metrics to look at her fasting insulin or her metabolic health so we know very clearly in medicine that your metabolic health is the context by which we should evaluate the risk of your LDL load but doctors don't do that so we're Flying Blind we're only using half the variables that we should be using there's no contextualizing because Western medicine isn't good at contextual Nuance at all we just want to say you have high LDL we know that in a population if we give you a Statin and I'll talk about statins in a moment we will slightly reduce your risk especially if you've had a heart attack if you haven't had a heart attack there's not a lot of great data for statins and primary prevention but so their Western medicine is not good at individualizing care for humans they're they're okay at looking at a population swath but for anyone who's listening to this podcast or thinking about these things with Nuance or making intentional decisions with regard to their food and lifestyle Western medicine is not really going to serve you with the level of like Clarity and like specificity that you really need and so they're not even going to check what her insulin sensitivity is they're not going to say you're metabolically healthy and if we look at the data someone who's metabolically healthy with your level of LDL actually doesn't have an increased risk of heart disease so why would we give you a Statin which we know interrupts the synthesis of cholesterol and the human body and has tons of side effects because when we're interrupting the synthesis of cholesterol we're also interrupting the synthesis of coenzyme Q10 which is a key part of an electron transport chain which is how all the energy in the body gets processed and translated into useful currencies ATP and things like that so many people who take statins get muscle aches because they because because they're we've we've abrogated we've basically stopped their production of critical nutrients that are in the same pathway as cholesterol and so Western medicine says oh it's okay we'll just give you more coenzyme Q10 well what about the squalene or these other you know nutrients that the human body is making in the cholesterol pathway we're not supplementing all of those and how bioavailable is this coenzyme Q10 that they're giving you and if a doctor gives you coins on Q10 when you have muscle aches on a Statin that's a very astute position in the first place most of them will just say stay on the Statin the most important thing is that I don't get sued for you getting a heart attack with this LDL so it's a very complex situation but let's just back up again and really kind of summarize what we're dealing with here here's the question that I would ask because there are a lot of really well-intentioned super smart people in the space who believe that something called APO B which is a lipoprotein that identifies that sits on LDL another bus called vldl another bus called chylomicrons so they say APO B containing particles are atherogenic they create atherosclerosis that doesn't make sense to me that a particle that exists in the human body that carries this apoprotein would inherently be damaging to the endothelium the inside of our blood vessels and initiate atherosclerosis and so the question I always ask these people is if LDL if APO B containing the proteins like LDL are atherosclerotic meaning they have the ability to generate atherosclerosis on their own by damaging the inside of the blood vessel then why don't we get atherosclerosis in veins and why is it only in arteries so when you're when when the blood goes out of your heart into your tissues that's in arteries when it returns from your tissues to your heart that's in veins you can see veins on the surface of my skin they're blue you can't see the arteries they're deeper a lot of track marks there so the veins are coming back right we never see atherosclerosis in veins in humans only arteries and why is that because the same amount of LDL cholesterol is circulating in my veins as in my arteries it's contiguous system there are capillaries here the blood gets pumped out of my heart to my brain and arteries to my legs and arteries all over my body it's an arteries and then it goes to capillaries and it switches and it comes back around makes a U-turn and comes back to my heart that's how it works so veins don't develop don't develop atherosclerosis only arteries why is that if able B is initiating atherosclerosis doesn't make any sense to me and the answer is that in arteries you have higher pressure you know average blood pressure is 120 over 80 millimeters of mercury because arteries are more muscular they have a an outer layer a muscularis layer that is much bigger than a vein but the inner part the endothelium is exactly the same so arteries are much more muscular because they must carry more pressure to push the blood which means that when there's more pressure there's more denuding of the endothelium which means there's more damage just by being an artery because the pressure in there is higher so my argument is apob containing particles like LDL are not atherosclerotic you need endothelial damage to initiate atherosclerosis and then if able B particles get wrapped into that perhaps as part of the repair process it could make it look like they're make it look like they're guilty right are they the firemen or are they the arsonist maybe they're arriving to the scene of the damage in the artery that is happening because of high pressure as part of the healing process and there's more of them in people who have more susceptibility to damage in their arteries like diabetics we know that people who are insulin resistant or back to that term insulin resistant they have more they have impaired wound healing we hear about this all the time in diabetics you get a amputated toe or a leg or a foot yeah they have very impaired wound healing and we know that in the artery at the level of the endothelium just by living a diabetic is damaging their endothelium just like you and I are damaging the endothelium of Our arteries by having pressure but neither you or I are diabetic neither you or I are insulin resistant so our body has the ability to repair those things properly to go in with immune cells and repair the endothelium but a diabetic someone that's insulin resistant is going to have impaired wound healing and that leaves more holes in the facade where there is damage where the LDL particles are being called and there's an immune impairment in the process of repair and that is what causes atherosclerosis does that make sense that makes sense if someone is metabolically damaged and they have decreased insulin sensitivity is that repairable it's absolutely reversible by changing the diet and so just to summarize here with respect to LDL cholesterol Dr Paul saladino is not that worried about LDL cholesterol some doctors are worried because they're afraid of being sued and so then they recommend statins which might be worrisome for many people but because of the side effects and speaking of not being sued I should remark that nothing on this podcast is medical advice and so please consult your doctor your astrologist your pet care facilities and uh your yoga instructor before implementing anything into your life don't take responsibility for yourself please Outsource it to everyone in your community because you're not responsible everyone else is responsible for your health oh my goodness the one thing I'll just add to your summary is I don't worry about LDL if someone is insulin sensitive in a diabetic do I worry about LDL yeah but fix the insulin sensitivity right I'm not the the LDL I think there's there's a lot of good evidence that we really need to have these these discussions among Physicians and and question the Dogma with regard to LDL I think just knee-jerk responses saying your LDL is high you need a Statin is is not the whole picture you have to understand the context of that and then we need to equip Physicians with education that tells them this is how you help your patients reverse their insulin resistance and we need to do research that actually creates some substance behind that recommendation so real quick because someone who goes to their doctor and their doctor says hey you have high LDL and they Panic right away right and they're like oh they want me to get on a drug and I can't possibly repeat everything that Dr saladino just said and so I just throw up my hands what is one or two sentences they can say to their doctor to say I'm not that concerned about my high LDL because I'm not diabetic did you check a fasting insulin can we can we evaluate my metabolic health you just say can we evaluate my metabolic Health the doctor will not know how to evaluate the metabolic health so you may need to ask them to check a fasting insulin and the the last piece I'll add to this is that it's very clear in human physiology that in many humans eating more saturated fat and less polyunsaturated fat raises the LDL slightly right slightly ten percent twenty percent which is why a lot of people eating in this way will go to their doctor and have a quote high LDL the last time I checked my LDL it was 130 milligrams per deciliter which is just above the normal range saying 120 but most doctors would say you have a high LDL you should eat less red meat well yes eating less red meat will lower my LDL and I could even lower my LDL more by eating canola oil but what do we know and what are the doctors missing something I've hinted at a couple times in the podcast that if you go a level deeper and you look at the predictors of cardiovascular disease in general LDL is pretty poor like we talked about what's a really good predictor oxidized LDL so you're taking the phospholipids on the outside of the LDL molecule and asking how many of them have been oxidized and we know that oxidized LDL goes up when you eat polyunsaturated fats even though your total LDL goes down because you're populating more of the outside of that LDL molecule with fragile fats these polyunsaturated fatty acids so Ox LDL goes up LP little a which is another metric of LDL oxidation because it's a particle that kind of scavenges oxidized phospholipids goes up when you eat polyunsaturated fatty acids but your LDL goes down so most Physicians are just looking surface at LDL but really we should be looking at oxidized LDL NLP little a and remember that just because eating saturated fat makes your LDL go up your oxidized LDL and your LP Little Egg go down it probably has to do with something this word is technical so I apologize in advance called the home viscous model of membrane fluidity and the the high level is that when you eat more saturated fats we know that the fats we eat become a part of our cell membranes and cells are very delicate and very specific about how they want to maintain membrane fluidity and because you're eating more saturated fats cells are probably going to raise the cholesterol in your bed in your blood to keep the membrane fluidity at a at a baseline level so more saturated fats in the body will in the diet will create uh increase in blood cholesterol because your body's trying to maintain fluidity of the cell membrane more polyunsaturated fats will probably lower the blood cholesterol because your body is trying to maintain fluid of the membrane but again it's not it's it's not a bad thing it's not pathological that when you're eating more saturated fat the LDL is going up it's your body just trying to keep homeostasis yeah that makes a lot of sense yeah did you enjoy this Standalone patreon highlight if so you can listen to full episodes of the minimalist private 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Channel: The Minimalists
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Length: 18min 57sec (1137 seconds)
Published: Thu Mar 23 2023
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