콜레스테롤에 대한 이해: 오해와 핵심 지표

버그 박사의 콜레스테롤 유형에 대한 오해는 심장병 위험 요인에 대한 시청자의 오해를 불러일으킵니다.

### 콜레스테롤에 대한 이해: 에릭 버그 박사의 동영상으로 알아보는 콜레스테롤에 대한 오해 풀기
* 📊 많은 시청자가 아내의 혈액 검사에 대한 에릭 버그 박사의 논의가 혼란스럽다며 **콜레스테롤 관련 주장에 대한 명확한 설명**이 필요하다고 말했습니다.
* 📝 2018 미국 심장 협회 가이드라인에 따르면 **총 콜레스테롤은 심장 질환과 큰 관련이 없지만, 그렇다고 해서 연관성이 없는 것은 아니며 위험을 예측하는 데 가장 좋은 지표는 아니다**고 합니다.
* 🔍 식이 콜레스테롤(음식에서 섭취하는 콜레스테롤)과 혈청 콜레스테롤(혈액 내 콜레스테롤)을 구분하는 것이 중요한데, 동영상에서는 **두 가지를 잘못 혼동**하고 있습니다.
* 💡 버그 박사의 아내의 총 콜레스테롤 수치는 **261로 정상 범위인 200보다 높은 수치**를 기록했지만, **LDL 콜레스테롤의 종류에 초점을 맞추는 것**이 중요합니다.
* 🚦 작고 조밀한 LDL 입자는 위험한 것으로 간주되지만 **버그 박사의 아내는 주로 해롭지 않은 큰 LDL 입자**를 가지고 있어 콜레스테롤 유형에 대한 미묘한 이해가 필요함을 강조합니다.
* ⚖ 연구에 따르면 **입자 수(ApoB)가 입자 크기보다 심혈관 위험을 더 잘 예측**하는 것으로 나타났으며, **크고 작은 LDL 모두 죽종을 생성**할 수 있다고 강조합니다.
* 💔 심혈관 질환은 설탕 섭취량이나 콜레스테롤 수치와 같은 한 가지 측면에만 영향을 받는 것이 아니라 **혈압, 당뇨병, 염증**과 같은 다양한 요인의 영향을 받는 다인성 질환입니다.
* 🔗 건강을 개선하려면 단순히 콜레스테롤 크기를 평가하는 것보다 심혈관 위험을 나타내는 더 중요한 지표인 **ApoB와 LDL 입자 수를 낮추는 데 집중**하는 것이 중요합니다.

so we got a ton of requests from a lot of you guys to comment on this video: Dr. Eric Berg goes over his wife's blood work. I don't know why, out of all the internet content and videos, this one in particular was deemed confusing or intriguing by so many people. I guess we'll find out. Quick note before we start, and if you're a regular viewer of the channel, you probably already know this, we're going to focus only on the substance. No ad hominems, I didn't google him, I don't know anything about him, I didn't go watch a bunch of his other videos for context, nothing. Because it doesn't matter. The only thing that matters is whether the claims match the evidence. Alright, let's go. This was in 2018, the new guidelines by the American Heart Association, okay this is brand new. They say total cholesterol is not significantly associated with heart disease.

Okay, that's a new finding. They just found out. Looking at your total cholesterol doesn't really give you a lot of information in relationship to predicting heart disease. I don't know what he's talking about. Total cholesterol is not the best marker. It's a dirty marker, but it definitely associates with cardiovascular disease, with heart disease. I don't remember any American Heart Association guidelines saying that it just doesn't associate, period. Here's the 2018 American Heart Association guidelines, like he said: population studies suggest optimal total cholesterol levels are about 150. Populations with cholesterol in this range manifest low rates of atherosclerotic cardiovascular disease. Nobody's saying it's the best marker, but this is the opposite of what he's saying. I've read these guidelines. There's nothing in there about total cholesterol not associating, period. Maybe he saw something else and misunderstood it.

is there anything in the description that he links as a reference? okay, two links to journals, that's good. american heart association journal, that's probably it, let's click here, alright, sweet, um wait this is the scientific advisory for dietary cholesterol. no way. no way don't tell me this guy's confusing... wow. wow. yep, here's the passage he's referring to, oh my god generally no significant association with cardiovascular disease risk but this document is the scientific this is the science advisory on dietary cholesterol. i think most people understand the difference but just in case: dietary cholesterol is the cholesterol content of your food, if you eat eggs or some butter there's going to be some cholesterol in there. serum cholesterol is the level of cholesterol in your blood when you go to the doctor, when you get some blood work, that's your serum cholesterol levels.

they're two different things. You could have high blood cholesterol levels and not eat any cholesterol. It's possible. It's like saying there's potassium in foods and then there's my blood potassium levels that I see in my blood work with the reference ranges. They're two very different things. He's talking about serum cholesterol. Total cholesterol refers to the total amount of cholesterol in your blood, in your serum. He has the levels right there on the board, levels of serum cholesterol. And the video is called Dr. Berg's Wife Has Crazy High Cholesterol. That's referring to her serum cholesterol levels. So he's talking about blood cholesterol levels, but the thing he just mentioned with the American Heart Association and the document he linked is on dietary cholesterol. It says right there and there and in the title. It's the first word of the title of the paper he linked. Okay, so I just went over the document to make sure I didn't miss anything.

because it's honestly a bit hard to believe, but yeah, he just confused the two. He probably heard something vague about cholesterol, and he conflated it with serum cholesterol. Either he's not super clear on the difference, or he didn't pay attention to this reference that he linked. So, total cholesterol, serum cholesterol, alright? It does associate with cardiovascular disease risk, but there are better markers. LDL cholesterol is better, non-HDL cholesterol is even better (that's non-HDL cholesterol, not HDL cholesterol, alright?), and many other things associate, but the best marker, causal marker, is ApoB, and we've made entire videos about it, and I'll link it at the end. Now, dietary cholesterol associates with cardiovascular disease risk in some studies but not others because it depends on a number of factors, but that's not even what he's referring to, the whole

thing's a misunderstanding, so I guess let's just move on. I don't know what to expect now, honestly this is a stunning start, I'm a little speechless. Her total cholesterol was 261. Normal is below 200. So this is too high, right? Yeah, see, he's talking about serum cholesterol all the way, the whole dietary cholesterol was a complete sidetrack. I still can't believe it, nobody checked this video before it went out, nobody checked the reference. This total cholesterol is not the cholesterol that's floating through your arteries, it can't, it doesn't mix well with blood, it has to be packaged in a protein. Okay, this is all good stuff, lipids travel in lipoproteins because they're hydrophobic, in an aqueous medium like plasma they would clump up so they need that protein shell to be transported and it's very important, it's very good to shift the conversation

about cardiovascular disease to lipoproteins. Why? Because the public discourse around heart disease always focuses on lipids, cholesterol, and good cholesterol and bad cholesterol, but at the end of the day, it's high lipoproteins that raise cardiovascular risk. So, lipoproteins are the vehicle, and cholesterol is the passenger traveling inside that vehicle, and it's the number of vehicles on the road that causes traffic jams. And we said a minute ago that apob is the best metric; this is exactly why. Apob is a direct measurement of the number of vehicles. Everything else, the lipids, the total cholesterol, LDL-cholesterol, those are measurements of the passengers, so they can give you a rough indirect guestimate of the number of vehicles, but they're not as good. Apob measures directly the number of vehicles, and that's why it's the best causal marker of risk. Make sense? Alright, moving on. This is looking up, this is getting better, let's go.

Alright, we have her name, we have the date, and we have the total cholesterol, which is 261, right? Check that out right there, and the second one that's high, LDL-C, that stands for LDL-cholesterol. It's 195. Okay, we take a look on the second page right here, look at this, the LDL is 2128, right? But let's narrow in on this one type of LDL, sdLDL, that's the small dense low-density lipoprotein. This is the one that's dangerous, and it's actually 26, within the normal range, it's optimal. So guess what this means. It means that Karen's high level of LDL is not the small dense type. It is the large buoyant type, and it's the small dense type that creates the damage. Yeah, I was hoping he wouldn't fall for this one, I hear this a lot, small dense LDL is harmful, but large LDL is

fine, it's benign, so my sky-high cholesterol is totally fine as long as my particles are large. Very common idea on social media. So it is true that if we look at two populations with the same level of LDL-cholesterol, the one with the smaller particles will tend to have a higher risk. But, and you may already be picking up on the problem here, and if not let me give you an analogy before I give away the answer. Imagine two roads. Same size, same everything, and same number of people traveling in vehicles on each road, but road A has more traffic jams. So we want to figure out why, so we run this study and we find smaller vehicles run on road A, more compact cars, whereas road B has more vans and buses. So now someone pops up and says aha, so smaller vehicles cause traffic jams. What's wrong with that logic? There's one key parameter we're leaving out. Pause

the video if you want to think through it. It's the number of vehicles, right? If we have the same number of passengers traveling in smaller vehicles, we probably have more vehicles on the road. So, we have two variables, the size of the vehicles and the number of the vehicles. It's precisely the same thing with heart disease. For the same level of cholesterol, people who have smaller vehicles, smaller lipoproteins, tend to have more of them to carry that same amount of cholesterol, right? So, we have two potential suspects present at the crime scene at the same time. So, whodunit? Who's the murderer? Particle size could be the cause of risk like he's concluding or it could be an innocent bystander. These authors explain exactly this conundrum: at a given level of LDL-cholesterol, individuals with predominantly small LDL particles (that's called pattern B) have higher risk. So

people with smaller particles have a higher risk. The seemingly reasonable conclusion would be that size matters and that clinical assessment would benefit from measuring both LDL quantity and particle size. That's precisely the logic we just heard Dr. Berg laying out. However, there is a flaw in this reasoning. At the same level of LDL-cholesterol, the pattern B individuals (that's the ones with smaller particles) also have more particles. Is the risk attributable to the fact that they have more particles or to the smaller size? So how do we solve this mystery? Well, one thing we can do is run some statistical analysis to find out which of the two parameters tracks best with risk. Which one is the best predictor: particle size or particle number? This is like running a large population study and finding that people who own ashtrays are more likely to have lung cancer, but of course, smokers are also more likely to have lung cancer. So we can do a statistical test to see which

of the two parameters, tracks best with risk, and we'll probably find it's smoking. Ashtray ownership will generally correlate with lung cancer, but not as tightly, not as closely, not as accurately, because some people might own ashtrays but not be smokers, and it's for the visitors or whatever, and some smokers might not have any ashtrays at the house, or they might smoke outside. So smoking will track much closer with risk; we'll find that it's a better predictor, and we'll probably conclude that ashtray ownership is likely a correlate, something that correlates but probably not causal, probably an innocent bystander. It's the same thing with cardiovascular disease, and this type of analysis has been done many times with LDL. So the authors explain: collectively, the results of multivariate analyses (that's what the statistical technique is called) of numerous clinical trials provide persuasive evidence that it is the number of LDL particles, not LDL size or the amount of

cholesterol, that is the principal determinant of coronary heart disease risk. So it's not about the size of your particle, it's how you use it. These scientists also explain it really well: association of LDL size with risk typically loses significance when adjusted for particle number or concentration, same thing, like ApoB. So ApoB measures particle number, as we said, and particle size will generally correlate with risk, but after you remove ApoB, after you remove particle number from the equation, particle size no longer predicts risk. It's just like the ashtray analogy. And they add two more lines of evidence: statins, which have a well-established effect of lowering risk, preferentially reduce large LDL. And number two, patients with familial hypercholesterolemia, which is a disease where people have very high cholesterol and very high risk of heart disease, they have mainly large LDLs, and they are at high risk, indicating that large LDLs are not benign.

here's a visual that really helps put all of this in perspective: small dense LDLs are roughly 20 nanometers in diameter. One nanometer is a million times smaller than a millimeter. Now, large LDLs are a little larger. Duh, right? A little over 20 nanometers. But then in the same family of lipoproteins, we have IDLs. So LDL stands for low-density lipoprotein, and IDL for intermediate-density lipoprotein, and IDLs also carry ApoB, this protein that identifies all of these particles that cause plaque and heart disease. And the diameter of IDLs is in the mid-20s. Then in the same family, we have the VLDLs, very low-density lipoproteins, but there are many sizes of VLDLs, many different models. The small ones are sometimes called VLDL remnants because they're what's left of the larger ones. VLDLs can go up to 60 nanometers, which

is already three times larger than LDLs, and they can be even larger, over 70 nanometers, and all of these are ApoB lipoproteins. Now, here's the kicker: there's a threshold. Lipoproteins that are too big can't get into the artery wall and can't contribute to plaque and heart disease, and that threshold is 70 nanometers. All ApoB lipoproteins less than 70 nanometers in diameter, including VLDL remnants and LDLs, freely flux across the endothelial barrier (that's the lining of the artery wall) where they can become retained. So, the key threshold is all the way over here: the largest LDLs are too big to get in, and they're not atherogenic; they don't cause atherosclerosis. Everything else is atherogenic. So, in the grand scheme of things, LDLs are dwarves. The difference between small and large LDLs is relatively minor; they can both get into

the artery wall and contribute to plaque, as can much larger particles that carry apob. And this gets even more mind-blowing because all of these under 70 nanometers are thought to be equally atherogenic. Particle for particle, they all represent the same risk of heart disease. They've shown this with genetic experiments. So, we all carry different genetic variants. That's why we're all a little bit different. Some are taller, some have green eyes, some have larger feet. And just like our genes can influence those traits, they can also influence our lipoproteins. So, they looked at gene variants affecting LDL particles and other gene variants affecting VLDL particles. And the results suggested that all apop-containing lipoprotein particles, including VLDLs and their remnants, as well as LDLs, have approximately the same effect on risk of cardiovascular disease per particle. Alan Sniderman breaks it down here: It was demonstrated that the decrease in risk

per VLDL particle decrease was the same as the decrease in risk per LDL particle decrease. The conclusion that follows is that a VLDL and an LDL pose equal cardiovascular risk. Now, it's important to point out these genetic studies are considered a causal test, a more reliable test of cause and effect, because the correlations we looked at earlier, that experimental approach has some caveats that the genetics improve upon. So, all ApoB particles under 70 nanometers are harmful. Even VLDLs, which are way larger than the largest LDLs, so we want to keep all of these lipoproteins in the healthy range, not just some of them and let the other ones go off the charts, that's the misconception. Okay, one last citation to drive this home and then we'll move on. Because these authors summarize everything we talked about so far. The large cholesterol-rich LDL is the predominant

type in familial hypercholesterolemia, as we saw earlier, and it is firmly established that this LDL is responsible for their premature atherosclerosis. So large and small LDL are both atherogenic, and it's not possible to judge which, if any, is more harmful overall. So particle number determines risk; particle size is probably just a correlate, kind of like the ashtrays and lung cancer. So saying that my ApoB is very high but I'm fine because my LDLs are not small dense is like saying that I smoke like a chimney but I'm totally fine because I got rid of all the ashtrays. It's overvaluing a correlation that is likely not causal while undervaluing the likely real causal factor; it's a huge mistake. So the important parameters here in the blood work that he shows are LDL-P; he mentions it in passing, and ApoB, which I don't think he even mentioned, and those two are almost

interchangeable, they're both measures of particle number, and they're both very high in her case. That is the focus to lower risk. And we can lower apob with medications or with lifestyle. I'll link a video at the end with all the information on this. I'm sorry if this video turns out to be a bit repetitive, but this isn't the simplest topic in the world, which is why we have rampant misunderstandings, and I don't blame people. So I'm trying to make this as simple as possible, but you give me feedback below if we succeeded or if it's still super confusing. I tried. Now, what I usually tell people who ask me about particle size is it's probably not going to change anything. But if you for some reason are bent on having large particles and you have a way to do it, I don't see a problem, as long as it's not at the expense of particle number, right? As long

as your total particle number, your apob, stays constant or comes down, playing with particle size, I don't see an issue. Alright, moving on. As I always recommend when you get a cholesterol test, you get an advanced lipid profile, an advanced test that measures the two different types of ldl. Yeah, it's the second time he's said that, but the reason these aren't routinely done when you go to the doctor is that they usually don't add that much useful information. Because the different size ldls are all problematic, knowing if my ldls are a bit larger or a bit smaller doesn't really change course of action, we still want to keep the total number of apob lipoproteins in the healthy range. It's explained here: the burden of proof for any newly proposed risk factor is that it must add to risk assessment by current measurements or it must be more economical. Ldl

subtyping (which is looking at the different LDL sizes) does not meet either of these expectations. And: LDL subclass measurement does not add independent information to that conferred by LDL concentration (so, number of particles ApoB), along with the other standard risk factors (things like diabetes, smoking, blood pressure, family history). So, if you want to get these advanced tests and you don't mind spending the extra money, I don't think it hurts, just don't let all those numbers distract you from what really matters, and that's ApoB. Now, many people don't know their ApoB, and your LDL-cholesterol and your non-HDL cholesterol give you a rough estimate, but in a percentage of the population, they can be off. So, when in doubt, get your ApoB. Alright, moving on the small dense type, it's one of the better markers for predicting heart problems.

It's one of the best indicators for detecting inflammation. Yeah, this is an interesting point. It's an important point. Small dense LDLs are markers for a number of issues. They associate with diabetes, with insulin resistance, with obesity, so no wonder they associate well with heart disease. They're a marker for all kinds of metabolic issues. As some people say, particle size is a marker, not a maker. But none of these associations mean that larger LDLs are benign. This is why we have to be very careful with correlations and not assume causality. That's the trap he's falling into. Correlations can indicate causality or not. They can be a wild goose chase, so we have to dig deeper with the analyses, with the genetics, with the clinical trials, right? We have to go above and beyond. By themselves, the associations are very slippery terrain. Alright, moving on. Goes the

inside of your artery to that much glucose. Wow, that's a really cool animation. It looks like he's inside the vessel. That clot breaks off, goes up to your brain, and starts shutting off oxygen into your brain. You get a stroke, and so all of this can be completely prevented just by getting the sugar out of the diet. Sure, excess refined sugar is a risk factor for cardiovascular disease, but that's an oversimplification. Getting sugar out of the diet can make things better or not; it depends on what you replace it with. In fact, this exact question has been investigated, and we've known the answer for a number of years now. Replacing refined carbs (so that's table sugar, candy, white bread, cookies, pizza, etc.) with unrefined carbohydrate from whole grains is associated with lower cardiovascular risk. Whole grains would be oats, brown rice, whole wheat bread.

etc. now, replacing refined carbs with unsaturated fats also lowered risk, especially polyunsaturated. monounsaturated tended to be lower but was not statistically significant. unsaturated fats would be things like nuts and seeds, most vegetable oils, and fatty fish. and replacing refined carbohydrates with saturated fat (so fatty meats, butter, coconut oil, etc.) was not significantly different. and these findings are corroborated by other data from clinical trials, for example. so moderating refined sugars, added sugars, absolutely, everybody agrees with that, but we should emphasize, try to replace them with something more health-promoting so you actually get that upgrade, like whole grains or sources of unsaturated fat. that's not to say that a healthy diet can't contain some red meat or some butter, it can, but it's about the proportions. if you take the bulk of refined carbohydrates and you replace that calorie for calorie with saturated fat, it's a lateral move, you're not going to

get an improvement. The key realization here is that cardiovascular disease is a multifactorial condition, just like most chronic diseases of the western world; multiple factors affect it. It's not all one thing. Every time you hear 'heart disease is all about this one thing', get your guard up. Apob is a major factor, but blood pressure matters, diabetes, not smoking, inflammation matters, exercise, healthy body weight, right? They're all factors, they're all pieces of the puzzle. Hey, before you go real quick. Okay, that's pretty much it, so you see why in our videos we never go after the individual. First of all, it's completely inappropriate; second, it's a distraction, distracts you from the things that really matter. But also, here's a super likable guy, charming guy, right? Good delivery, calm, it almost felt soothing to watch him. He's got a very good

calming quality. Unfortunately, most of the ideas have very little scientific substance because the bulk of the evidence is stacked in exactly the opposite direction. And these aren't new ideas. I hear this stuff on the internet all the time, and my guess is he's exposed to these online, and he kind of cobbled this together, but he didn't really bother to properly fact-check things. I mean, it's obvious from the way he started the video, right? With just a colossal misunderstanding of the fundamentals. It was his opener; that's what he planned to start the video with, and he didn't even read the thing he linked. So, this is a very clear example that we can't rely on how friendly or how trustworthy or how genuine someone seems. It hinges a hundred percent on the evidence, not the packaging, not the presentation, not the messenger. There's just no way around that. This also confirms my general impression that I've always had. I have a lot of colleagues who are very

frustrated, and they say, ah, all this misinformation on the internet, people just lying to the public. I never thought that explanation was convincing. I think it's much more likely that people are repeating things that they do believe in, and I think that's clearly the case here. I mean, he's talking about his own wife's health. Of course, he wants her to be safe and healthy. I don't question that. So, I think it's very obvious that he believes this. The problem is he's getting these ideas from unreliable sources and then uncritically accepting them. Dr. Berg, if you're watching this one day (you never know, a few months ago you guys asked us to comment on one of the videos from what I've learned, and that was a massive channel, had like a million subscribers, and within the same day, within an hour of the video being released, the creator hit me

up on social media, he says he sometimes watches our videos, so you never know) and if somebody's in touch with Dr. Berg, hit him up. So, Dr. Berg, if you're watching, what will lower your wife's risk is lowering that LDL-P and ApoB. The particle size is mostly a distraction. Now, a good specialist, cardiologist, or lipidologist will probably check her for familial hypercholesterolemia because her numbers are pretty high, depends also if they just got high or if they've always been high, and they might also check her for some other lipid disorders. But in most regular people that don't have an underlying genetic condition, ApoB can be lowered very quickly, almost overnight. It can be done with meds or it can be done with lifestyle, and we've actually made a whole video showing exactly how to do this, all based on peer-reviewed literature, and you can check that out right here.

and here's more on apob and what each number on your blood work means. Take care, see you next week.

Dr. Eric Berg gets fact-checked by MD PhD doctor

Nutrition Made Simple!

에릭 버그 박사의 아내의 혈액 검사에 관한 동영상은 심장병에서 콜레스테롤의 역할에 대한 혼란을 불러일으켰습니다.

2018년 미국심장협회 가이드라인에 따르면 총 콜레스테롤은 심장병과 큰 관련이 없다고 하지만, 발표자는 이를 잘못 해석한 것이라고 주장합니다.

이 동영상은 서로 다른 개념인 식이 콜레스테롤과 혈청 콜레스테롤을 연결하여 주장에 혼란을 더하고 있습니다.

콜레스테롤과 심혈관 질환에 대한 이해

총 콜레스테롤과 혈청 콜레스테롤을 혼동하는 경우가 많지만 LDL 및 비HDL 콜레스테롤이 심혈관 질환 위험에 대한 더 나은 지표입니다.

ApoB는 지단백질 운반체의 수를 직접 측정하는 가장 좋은 인과관계 마커입니다.

논의된 사례의 높은 LDL 수치는 손상을 일으키는 작은 고밀도 유형이 아닌 큰 부력 유형에서 비롯된 것입니다.

LDL 입자 크기와 심장병 위험의 관계

입자가 작을수록 심장 질환의 위험이 높아지기 때문에 LDL 입자가 크면 무해하다는 일반적인 믿음은 잘못된 것입니다.

입자 크기와 개수 모두 콜레스테롤 수송에 중요한 역할을 하며, 입자가 작을수록 도로를 달리는 차량의 수가 많아지는데, 이는 LDL 입자에서 나타나는 상관관계와 유사합니다.

통계 분석에 따르면 LDL 입자 수가 입자 크기보다 심장병 위험을 더 잘 예측하는 것으로 나타났는데, 이는 입자 크기가 아니라 입자 수가 진짜 원인일 수 있음을 시사합니다.

심장병 위험에서 LDL과 ApoB의 역할

콜레스테롤, 특히 LDL 입자는 관상동맥 심장 질환 위험을 결정하는 주요 요인이며, 입자 수(ApoB)는 크기보다 더 중요합니다.

가족성 고콜레스테롤혈증과의 연관성 및 스타틴이 큰 LDL을 우선적으로 감소시키는 것에서 알 수 있듯이 큰 LDL은 양성이 아닙니다.

70 나노미터 미만의 모든 ApoB 함유 지단백질은 동등하게 죽종 형성을 유발하여 심장 질환의 위험에 기여하는 것으로 생각됩니다.

VLDL과 LDL 입자는 그 수가 감소할수록 심혈관 질환 위험이 감소하기 때문에 동일한 심혈관 질환 위험을 초래합니다.

70나노미터 미만의 모든 ApoB 입자는 해롭기 때문에 모든 지단백질을 건강한 범위로 유지하는 것이 필수적입니다.

크기보다는 입자 수가 위험을 결정하며, LDL-P와 ApoB는 심혈관 위험을 낮추기 위해 우선적으로 고려해야 하는 입자 수의 주요 척도입니다.

심장 질환에서 LDL 아형과 ApoB의 역할

LDL 하위 클래스 측정은 LDL 농도 및 표준 위험 요인 외에 추가적인 정보를 제공하지 않습니다.

작은 고밀도 LDL은 심장 문제와 대사 문제를 나타내는 강력한 지표이지만, LDL이 크다고 해서 반드시 양성인 것은 아닙니다.

식단에서 정제 설탕을 줄이는 것은 심혈관 질환의 위험 요소이지만, 이를 통곡물의 정제되지 않은 탄수화물로 대체하는 것은 심혈관 질환 위험을 낮추는 것과 관련이 있습니다.

지방과 탄수화물이 심혈관 질환에 미치는 영향

정제 탄수화물을 불포화 지방, 특히 고도 불포화 지방으로 대체하면 심혈관 질환의 위험이 낮아지는 반면 포화 지방은 큰 영향을 미치지 않는 것으로 나타났습니다.

건강한 식단에는 붉은 고기와 버터가 일부 포함될 수 있지만, 탄수화물을 포화 지방으로 대체하여 옆으로 이동하지 말고 비율을 조절하는 것이 중요합니다.

심혈관 질환은 혈압, 당뇨병, 운동 등 여러 요인이 복합적으로 작용하는 다인자성 질환이므로 메신저가 아닌 증거에 집중하는 것이 중요합니다.

발표자는 사람들이 의도적으로 잘못된 정보를 퍼뜨리기보다는 자신이 진정으로 믿는 생각을 반복하는 경우가 많다고 생각합니다.

그들은 아내의 건강에 대한 버그 박사의 우려를 강조하며 그가 신뢰할 수 없는 출처의 아이디어를 무비판적으로 받아들이고 있음을 시사합니다.

연사는 LDL-P와 ApoB를 낮추는 것이 건강 위험을 줄이는 데 핵심이라고 조언하며, 이를 위한 추가 정보를 얻을 수 있는 리소스를 제공합니다.