While pediatricians know that lipid screening is advisable for 9- to 11-year-olds, they may find themselves with questions, such as: “Should I test a younger child with obesity or a family history? and “How high is high?” and “Does this look like a familial disorder or poor nutrition?” This guide from June Tester, MD, MPH, a specialist in pediatric lipid management, offers useful ways to categorize testing results, insights on the potential impact of diet and exercise, notes on which meds are appropriate for kids (plus dosing strategies) and suggestions on when to retest. She also discusses how to motivate families to improve their own heart health. Bonus: Learn why a vague suggestion to try fish oil isn’t helpful and which lifestyle modifications may actually pay off.
So, um, I'm excited to talk to you today about, um, lipid management in children. I know oftentimes the topic, uh, brings a lot of questions and uncertainty in gray areas, so happy to talk and go there at the end with everyone. Um, I have no disclosures, and some objectives that we will have is, of course, to be uh familiar with current screening recommendations for hyperlipidemia in children, including the concept of universal screening. Uh, describe some key dietary recommendations, just elevator pitch style recommendations that you can make, um, and utilize basic criteria to decide whether or not to consider medical therapy and what might warrant a referral. And our general outline for today, um, you know, starting with some historical context, I think in the interest of time, I'm gonna really kind of come to the punchline, which is really, you know, the, the dawn of when did this become an issue for pediatricians. was really based on evidence that started evolving in the early 1990s, you know, statins only came on the scene in the 1980s, really only the 1950s that we started to think maybe there's a connection between high blood pressure, blood cholesterol, and cardiovascular disease, um and really emerging evidence, um, you know, from large studies showed that actually, you know, that there was a connection. Um, these are two really key ones to know as pediatricians, the Bogalusa study. Um, and also the um PA study where effectively autopsies of well, um, youth actually, you know, showed the evidence of fatty streaks in kids as young as 6, and, you know, PDay was with young adults who passed away of accidental causes, and they found they found that, you know, evidence of coverage on the inside of their vessels were linked to risk factors and And in live subjects, um, in the early 2000s, you know, evidence where you actually look at the in media thickness using, um, imaging, uh, actually showed that actually, um, you know, young adults, um, uh, with, with higher childhood cholesterol, childhood risk factors such as overweight or having had high cholesterol, were actually correlated to having thicker lining on the inside. And then really more modern evidence showing that actually if you compare um unlucky siblings that had had genetic FH familial hypercholesterolemia, just a gene that causes their cholesterol to be sky high. And you compared them to their lucky siblings who didn't happen to have FH and had normal cholesterol levels from birth, um, you know, they, uh, they found that if they followed these kids for 10 years, um, that, that you basically leveled the playing field, that the kids that had FH were no worse than we compared to their sibling that did not have sky high cholesterols earlier on. Um, and that being on a statin actually really froze things in time and they did not alter any more effect in terms of their carotid in media thickness compared to their lucky siblings. Um, the guidelines that we currently still use are really the same ones that we've had in place for a while, since about 2011, so they really haven't changed, even though, um, in that time a lot about management for uh cholesterol has changed a couple of times uh for adults in the time since then. So, um, you know, that expert panel, I'm really just gonna highlight some major pieces of it. They, they, of course, talk about continued targeted screening in younger kids 2 to 8. I think some main messages here are that, um, you know, if there is a family history of of FH that's known or just people that had early cardiovascular disease, like a male that was younger than 55 and a first degree relative, you, you really don't need to wait until the universal screening age at 9. You can start earlier, like here. As many of you know, if your children have a risk factor like obesity, you would check them earlier as well. This is uh the universal screening window that was very controversial when it first came out in 2011, um, because it is a tall order to recommend that you screen all of your children. Um, of course, the recommendation is that it need not be a fasting screen. You could do a non-fasting screen for the non-HDL where you take the total cholesterol and you subtract out the HDL and see if it's over 145, but you know, this is really, um, you know, there's a There's a, and we'll come back to this about why that age, right? But I mean, you know, obviously there's no right answer here, but, you know, this is where I often ask people to kind of reflect, um, you know, if kids in that age group kind of thinking about how often you did or didn't order a screening for them, um, and, and even in systems that are very, um, uh, organized and routine like Kaiser, where uh everyone lives in the same medical record cleanly. Um, you know, rates of screening universally are not, are not as are often lucky to be at the 50%, so this is a moving target, um, in terms of improving. This age, um, is an important one because, well, for a couple of reasons, universal screening because family history, you might, you might miss plenty of people, you might miss as many as, you know, 30 to 60% of kids that have disciplinemia if you only went on family history. Um, also realizing that those same studies that show that, um, you know, that cholesterol levels or childhood risk factors were correlated with um CIMT. Also showed that actually non-HDL was a perfectly handy, useful correlate as well. So why not use that in your screening guidelines? Most states will, you know, mandate that kids are seen at least once in that period of time. And actually, this is my my favorite little, uh, pearls to share is really if you took a kid and you check their cholesterol every year on their happy birthday, like, happy birthday, here's, let's check your cholesterol. And you were to plot it, there really is actually change over time in any given individual where there is really, you know, around 9 or 10, you're gonna have this peak. It's gonna dip uh during early adolescence. A lot of times, you know, there's a lot of thoughts behind that, but just having to do with growth. Then around the time that they're 17 again, it'll it'll even out to be kind of where, what, you know, where they're gonna be. And so that's why checking 9 to 10 is useful. But that being said, um, you know, the guidelines also, you know, mention if there's someone that wasn't screened during that earlier period of time, you can screen them again, and also, you know, they recommend a screening period for those 17 year olds because that again is going to be a more reflective of where you might biologically be in terms of your set point per se. Um, we're not gonna go over this algorithm here. I just really wanted to highlight a couple things. Really, when you think about the algorithms, I like to tell people just think of it in buckets. Think about it as LDL in a bucket of 100/130 over 160, or over 190, and what we're gonna do about kids that fall into those buckets. And also just really, you know, where where where do those numbers even come from? And part of this is related to this question of how high is high. So I often like to illustrate this with parents and say, listen, imagine you've got 100 kids and you line them all up from the one with the lowest cholesterol to the one with the highest cholesterol. And if you, you know, when you get it, someone tested in the lab, the lab will flag it as high if it's over 110%, because that corresponds to the 75th percentile. So that I would say that would mean your child is one of the 25 in the front of the line. If it's 130, uh, it's category is high because it is at the 95th percentile where you're one of the 5 in the front of the line. And if that kid, you know, if it's over 160, you just kind of say to them, listen, that would you be that one kid out of 100 for the most part that's got the highest LDL comparatively. And over 190, sometimes like just an easy way of description is just off the charts, that would be the estimate of, you know, estimated 1 in 250 people have FH or just genetically high cholesterol in that range and even despite a good diet would be kind of in that range. Now, and the guidelines also talk about a non-HDL of 145, and the reason is because 145 corresponds to 90th percentile for non-HDL, and that is why the guidelines use that as a cutoff for saying if you're in office non-HDL that you calculated or had them do with non-fasting labs is over that, then you should repeat with a fasting uh set cause then you're, it is worth your time having them go back to the lab and do it. So again, uh, thinking about those buckets, right, there are risk factors also in this algorithm. There are high level risk factors and then there are moderate level risk factors, high level being the family history of early cardiovascular disease and a first degree relative. It's not on the guidelines per per se, but LP little A, which is an independent risk factor if it's present, maybe 1 out of 20 people, some say it's 1 out of 10, have a high LP little A, that's considered a high level risk factor. Um, as well as the other things on this list, um, moderate level risk factors in the algorithm, generally you will require more moderate level risk factors to push you towards, uh, yes, they should be on a statin. Those include things like BMI over 95, um, or, you know, someone who had Kawasaki, but regressed aneurysms, for example. And so buckets, like I said, right, if they're in that bucket of 130 to 160, you know, this is basically what the algorithm will boil down to. You can say to them, let's repeat it in 6 months. But honestly, um, I, I tell people, you know, you can, if you start someone on a medicine for cholesterol or radically change their diet, you can generally see a change in their lipid profile in 4 to 6 weeks. You don't need to wait a full 6 months. You could wait just a couple and have them come back while they're motivated and curious. Um, if it's in this range, you're gonna wanna ask family history, you're really wanting to kind of get into how many high or moderate risk factors are we talking about for my patient. Even though it seems crazy, a pretty high constellation of risk factors actually could warrant needing to be on a statin. For example, what if your patient has two high level factors, say they have diabetes, and they have another, they have a family member who had a stroke at 40. Those two categories, those two factors would actually mean that in their, in this category, they probably should be on a statin. The other piece I wanna say is though, it's not in the guidelines just between you and me. You would be surprised how many patients in this range can improve, and it's actually, we'll talk later about referral criteria, but this is actually why I do see patients with with LDL in this range, but I generally will ask that they you've repeated it at least once because, you know, often that, you know, the guidance that you give will lead to change in a few months already without having to see a specialist. If they're in the 160 and 190 bucket, um, you know, the guidelines do say read it repeat in a few months, you're gonna dig into family history, think about those risk factors, and some people, if they just have one high level risk factor on the left side of that slide or two of the moderate ones, you know, that would put them in this category. So, you know, of, of being a satin recommended category. Generally speaking, in the LDL over 190, um, you know, the reason it's written up that that that it's this way is it is really hard to inflate your cholesterol just with an imperfect diet or being overweight and to this degree. Although I have seen it happen. I mean, you know, truly if your patient is, is having ice cream 4 times a week and, and, and, um, pizza every day, I mean, it is actually physically possible to get up there, but it's not common. So of course if your patient is in that range, you would always communicate to them, we want to improve your habits, let's let's do what we can, but the likelihood that they are just somebody who is wired to be a cholesterol producer is just that much higher in that range. So, question, you can all answer yourselves, uh, you know, LDL cholesterol is 132. This represents a value at the 95th percentile. We're gonna pretend we all have eye clickers here. Um, the algorithm also speaks to triglycerides, and, um, you know, I will say that one of the things that I, I like to simplify the overall messages in terms of your buckets, think of it as above or below 100 in a kid under 10 or above or below 130 in a teen in in a kid older than one of your patients who's older than 10. And like before, you know, you're gonna want to repeat something in general to to make sure, you know, to see if they respond to your changes, right, your recommendations, but if it's in the 200 to under 500 range, it's reasonable to consider fish oil, and we will talk more about that though, cause I do have a lot of heated things to say about that. Um, and if it's over 500, it's absolutely appropriate to just refer to, to lipid clinic even if there's just a single time in that range. Here is an example. I guess it's a dated example of a patient regarding lifestyle optimization. And so this is somebody who over time, you can see what we have them do between November of 2018 and August of 2019, they reduced the frequency of eating out, they cut their Starbucks drinks, and they had a 17% reduction in their LDL and cut triglyceride by roughly half. As a general rule of thumb, um, a person with a kind of typical American diet, so to speak, that includes probably, you know, some fast food, a little bit more than we want, some convenience foods, and they improve it. You can for the most part see up to maybe about a 25% improvement in that LDL. Um, you know, people who have an LDL of 300, uh, having them improve their diet is not gonna be enough, right? But just as a guideline, I mean, 25% for most people, and maybe if their baseline diet is particularly high in saturated fat at baseline, you might see them be able to shave that off by about a third. Um, triglyceride is, is much more variable in terms of how much it can be more inflated and, and likewise how much it can respond, and we'll talk more about that later too. So specifically LDL cholesterol, um, uh, as a big picture, we kind of remember that there is exogenous sources, right? What you eat, you, you consume it, it's in the intestines, it's absorbed into big blebs called chylomicrons, and you go through this process of recycling them, chipping away at them. Being away at them until they're kind of ending up in your storage pathways. We also endogenously on our own produce cholesterol. I like to sometimes tell people we're like red meat on two legs. We produce cholesterol. Some of us produce more than others. Now, um, so just other ways of thinking about that. There's of course diet cholesterol, fat from diet, and then endogenously there are some people who have extreme patterns, right, where there's monogenic um LDL receptor mutations up here which I'm covering on this part of the graph, or different mutations, kind of lesser versions or less pathogenic versions of mutations and those same exact genes, right? And there's also influence in other parts of this pathway. You might, we kind of wave our hands and say polygenic mutations, meaning this is people where there's a genetic setup for it, we're having kind of combined hyperlipidemia under suboptimal dietary conditions, so to speak, um, they might be able to change it more, and this is of course much more common. Another way of kind of thinking all of this is to say, OK, so how I'm gonna translate this and this big kind of concept of a pathway between exogenous and endogenous production from more extreme genes, less extreme genetic patterns. I will say this. First of all, cholesterol in our blood comes in part from food that we eat, but our bodies producing recycled cholesterol. Most of the cholesterol in our blood is actually from what we make. I think that's a key concept to kind of point that out, like a lot of that is actually from what that LDL that we've produced. Some people have a rare genetic problem where they just cannot recycle the cholesterol that they produce, so it builds up. Um, this is like a, it's like a garbage truck problem really. They just don't they don't have the receptors that actually help them chip away and recycle properly, the, you know, metabolize properly, the different um intermediate cholesterols that get produced. More people have a different genetic setup, so it's a setup. Their LDL cholesterol will run high compared to the next person eating the same food, but it's manageable. And like I said earlier, lifestyle can generally speaking improve LDL by up to about 25%. So you could have a patient where their LDL was 130, and they made a lot of improvements. They didn't make their diet perfect, but they made a lot of meaningful improvements and you could see them come down to something like a 98. Um, you know, the guidelines include, uh, you know, dietary recommendations, and I know it, it's very, uh, formalized to see it written as child-1 and 2. The child 1 diet is really just how everyone should be eating, and this is where school lunch programs and and federalized programs actually get their general diet. guidelines from, right? This, this general advice. No more than 25 to 30% of your calories should come from saturated fat. Saturated fat's the main driver that's gonna push up your LDL cholesterol, and that general recommendation at this level is to say no more than 10% of calories from a specific food should be high in saturated fat. Um, Uh, there is a recommendation written in there for 300 mg of cholesterol a day, keeping in mind that an egg yolk is 180 mg. I do not, and, and most of us do not spend time in actually um counseling too directly about cholesterol because it's becoming increasingly increasingly clear that Limiting dietary cholesterol intake is not really where the money is, and there's a lot more improvement in reducing the saturated fats in the diet, rather than nickeling and diming them on how many eggs do they eat. Um, So some examples to kind of put those skills in practice, right, 10% is kind of what we zero in, look at the look at the um fats and look at the saturated fat, and is it above or below 10%. It's above 10%, it's a high in saturated fat food, and you can see coconut oil is a perfect example. It's, it's on par or sometimes higher than butters, and actually there's no way to get a dietician at a cholesterol conference more fired up than to bring up cholesterol or bring up coconut oil, because it's uh it's one of those foods that seems to always have this healthy sheen and yet it's actually quite high when it comes to cholesterol. Ina's ice cream cause it's frequently in this in this range of about 50% of the calories from saturated fat. It's kind of like um 80/20 ground beef is about that too, yeah, it's 40, 45, 50%. Um, you look at this example here, almonds, saturated fat, yes, they do have fat. You take them, you squish them on paper, you get oil oil markings. They, they have fat, but the saturated fat is actually under 10%, it's only 5%, and they are nice and high in other. Unsaturated fats, which are beneficial fats. And so I always like to make sure to be very clear with people, it isn't, you know, not all fats are bad. There's different types of fats and, um, you know, if you see the, the longer the word is, polyunsaturated monoaccentuated, usually those are the better ones. Um, fiber, so half of the conversation is really what to cut out from the diet in order to improve your cholesterol, right? And so, you know that patients didn't need to take time out of their day, out of school, out of work, to have a doctor say, don't eat at McDonald's 5 days a week, right? But that is the part of the equation that is, that makes sense, is always very logical to people that I should reduce the fat I consume. The part that is the other half of the equation is really increasing fiber, especially soluble fiber. Um, you know, in theory, you know, patients should be eating about 20 to 25 g a day of fiber, to put that in perspective of how much you have to have, a half a cup serving of broccoli has about 4 g of fiber, and on Quaker oatmeal, you know, the advertisements for years have always talked about how their heart healthy, you know, and they're and they're not lying and actually where that comes from is 4 g a day. Of viscous soluble fiber can reduce LDL by up to about 10%. Um, and so I'll sometimes tell people, you know, there's different kinds of fiber, you know, when you make oatmeal, you know how there's that gel that forms on the outside between the oatmeal and the bowl, that is soluble fiber, that's the good stuff and that's actually why oatmeal is healthy, and that's why okra is particularly look at just the the soluble fiber, the viscous fiber. Child 2 just really relates to that higher level of guidelines where you're basically shaving off even more. And, um, you know, I've only, I've highlighted in red what's different from child 1, which is that, you know, the, the saturated fat line is technically lower. I will be honest, I actually do not convey this message because it is hard enough to just, I think it's, it's enough to just be. about 10% of calories from saturated fat. Um, patients who are adults and heart attack survivors and on, um, they are, they are canceled with a very strict line of 7% um calories from saturated fat and the lower 200 instead of 300 line for cholesterol. In theory, also other things that you can add are plants, dental esters, um, uh, which, you know, these are basically animals make cholesterol, plants make their own kind of cholesterol, and plant cholesterol competes in the intestinal brush border with animal cholesterol, so that is actually why it adding plants down esters like what you would get in Beneol. You know, you would normally not think something in a tub is gonna be recommended, but the idea is plant cholesterol outcompees the animal cholesterol when you're absorbing it, and that's the theory for why that is helpful. Um, I don't actually use the plants dentals. Um, we don't have as many really good products that are easily able for patients to find in any kind of quantities. Other countries like England, there are a lot more options and it's a more feasible thing to go with. Um, however, I do actually frequently enough, um, talk to patients about psyllium fiber, which is basically Metamucil. Because 6 g a day or 3 level teaspoons uh actually can lower LDL by about 7 to 10%. Um, and this can be a handy tool, especially for patients where um they're too young for a statin, um, you know, we're not really gonna go there and we've already, they've already got a pretty good diet, really tried everything else and um there's only so many vegetables you can get them to eat in a day. So adding soluble fiber that you dissolve in water for them to drink and consume is actually, um, you know, decently effective and, and I mean, I know it seems some kids genuinely don't mind and they add it into their lifestyle and other kids try it once and they just refuse, so it's it's something to consider. So, audience question, the food in this mystery item, uh, is not a good choice for someone looking to improve their high cholesterol because the total fat is higher than 10%, true or false, as we're all jumping up and saying no, that's false. These are almonds. They are very low in saturated fat, but full of very desirable polyunsaturated and mono unsaturated fats. Um, medications to lower LDL cholesterol. Um, obviously in medical school, everybody learned about HMG coase reductase inhibitors or statins which block cholesterol production, um, and also decreased synthesis internally leads to upregulation of more of those LDL receptors and greater clearance. Um, I'm always very careful to explain statins reduce the cholesterol that you produce. They're not aaser. They do not erase what you've consumed from the diet because again, if you think back to the nerdy pathway, statins reduce endogenous production of of of lipids. They do not reduce exogenous production or exogenous consumption or absorption. Um, there are, uh, favorable side effect profiles for certain ones that I prefer to use or that we prefer to use in pediatrics because they are water soluble. So, you know, they basically don't cross the blood brain barrier, pravastatin and Crestor. Most of your patients' parents are on atorvastatin because that was off patent much earlier and so has been cheaper longer. And it's just, you know, common and well known, but uh for children we really prefer to use pravastatin, which you can use in someone who's at least 8, and you can get about a 30% reduction in LDL and this is one of those that because of the short half life, it's like one of the more earlier statins that were developed where You know, we think you produce more cholesterol at night, and that's why the statins that when they were taken at night and correspond to peak blood levels at night, seem to work better, and it's cheap. It's been around for a long time. Um, Crestor took longer to come off patent, but it is now and it's perfectly easy enough to get. Um, you can use it for your patients who are over 10. And as a more potent statin, you can actually see up to about 50% reduction in LDL. You can take any time of day, whatever is gonna be easier for them to remind, remember taking and it has because it has a longer half life. Um, and I think one message I think that is very helpful, um, I actually, I, I maybe it's just cause I've been doing it for a long time, but I actually enjoy the process of, um, when it's clear that a kid needs to be on a statin of kind of working towards getting everyone on board. Um, and, uh, one of the, you know, one of the key differences is with a double patients, say your patient is a 65 year old man and you don't know if they're gonna have a heart attack before you see them in your office next. You do not waste time, and in adults. You know, you, you, the newer guidance basically puts people in risk categories and certain high risk patients, you just move to a high dose of a statin immediately without, you know, there's no negotiating, right? With kids, we have time. Nothing is gonna happen on my watch. And, and so a lot of this is really this process of starting at a low dose and working up, and that is very different from adult management in terms of style and and just um how that plays out. Fundamentally, um, side effects, so specifically myopathies or um, uh, out of the blue muscle soreness, for example, are dose dependent. And that's another really important part because a lot of times adults might have had a bad personal experience where their doctor identified that they needed to be on a statin, and they put them immediately on 80 mg of atorvastatin, and they had a bad experience and then they don't take them out and they don't go back to that doctor. Right? So kind of preparing people for the idea that yes, there are different side effects and they are dependent on dose. I have, I can count on the few fingers of one hand, the kids who I actually think have had side effects and in the end, and even to this day, it's not even clear if it was true. Um, the statins do not avoid their do not reduce their ability to get pregnant. Of course they need to avoid becoming pregnant while on a statin. Um, and so, you know, that is, that is always an important piece of the conversation for people to know that, and, and as crazy as it seems, as bug-eyed as everyone gets when you're talking to a 15 year old about, you know, you basically, at some point, you know, when they are planning to, or they may accident. have, you know, become pregnant, they need to be not taking their statin daily at that point. Um, but it's also important that they know as a point of advocacy that they need to get back on their statin when they are someday done breastfeeding, because there are a lot of women who get forgotten about after they are pregnant, have a baby, and don't get put back on their statin. Um, at this point in time for the, you know, we are really only putting um kids who have, you know, true FH on a statin, um. There are for the kids who have high LDL and it's up in that range and say it's 160, and it's just stubbornly hanging out that way. They don't have another risk factor, um, you know, most pediatric lipidologists are, are not necessarily putting them on statins quite yet. I, I, I sometimes do, and it's just very case by case. Um, there are studies that were happening right before the pandemic that have had some Difficulties and some setbacks, but just in general the jury is is still out somewhat on whether or not to put, put, you know, globally kids on stands if they meet those other criteria. Um, PCSK inhibitors are good to know about. Um, they are a completely different way of skinning this cat. Um, they are actually developed based on experience realizing that people who had PCSK9 uh mutation actually We really lucky with a super low cholesterol, so they realized how to mimic the opposite, um, and actually use that to their advantage. And so, since 2021, um, these injected medications every other week or every month have been approved for kids who are over 10 who have heterozygous or homozygous FH, um, You know, chances are you will not have um it's very rare for kids to need to be on this, um, so, but I'm happy to talk more if people are curious and and understanding more, you probably will, you probably don't realize it, but you have some patients' parents who are on this. Azimi is a non-statin pill that actually works on the other side of that, uh, table, that picture, right, the exogenous um absorption. It works at the brush border of intestinal cells and inhibits absorption. And it's usually used as an adjunct after already being on a statin, um, and you can, you know, It's you can use it in younger kids and actually this is an important, this is the one way that this may come up. If you have patients of mine and they're on two medications, it is because we are stopping at the kind of recommended pediatric level for their statin rather than going all the way to the top dose. And adding this as a second medication. It is extremely helpful and it's just very, very well tolerated, just you rarely use it on its own because the statins are more potent comparatively. So, how about this patient? So, um, uh, take a look at their numbers, a single set really only tells part of the picture. You can see this kid, um, their LDL cholesterol was 203 at this point, um, and then Check them again, and you look back in their records and you see, gosh, before a bunch of weight gain their LDL was 101 and 10101 again around that, you know, about 5 or 6 years prior to that. And this is an example of somebody where I um where you can see that actually if somebody has genetic monogenic FH they have a gene that is causing their cholesterol to be high. Generally speaking, it has always been that high. Um, and so when you have older information from before, you can actually see that, well, right, if they're this high now, it's probably more that there's that perfect setup, perfect storm, so to speak, of maybe some genetic setup to have a higher cholesterol than the next person, but not FH all in and of itself, you know, high cholesterol that they've been pumping out since the day they were born. How about this patient? You can see this one, and you go like, OK, well, their LDL is 158, but without knowing the whole story, actually, this particular person actually did need to be put on a statin. They actually, when we did more testing, did have one of the monogenic FH genes, and because of their knowledge of their Super, super strong family history, every generation with a person identified having early heart attacks and, and cholesterol. This kid was just on a picture perfect diet, and this number was just as low as could humanly be. But, um, but it, they really needed to be more appropriately on on statin treatment, which they initiated just like everyone else. So. Um, so question, children should always only be started on pravastatin for LDL lowering, true or false. False. It's not necessarily wrong to start with pravastatin, but if they're over 10, and it's clear that you're gonna need to be lowering them more than that 30% range that you could expect from a low potency statin like Pravastatin, it's reasonable to start with a higher potency statin. And so most of your patients of mine that I've seen and started on statins if they're over 10, um uh would be started on resuvastatin. Um, triglycerides. Uh, so back to our kind of general concept of metabolism, I think some keynotes to know is really there are genes and then there are genes. So for example, there's different types of genes where you can have basically uh what is a fundamental complete loss of function. These people basically have familial chilomicronnemia syndrome because they eat food. It comes into colomicrons, big labs that they're producing, you know, that that we all have to kind of package up the dietary fats that they cannot because they lack lipoprotein lipase fundamentally completely, they lack the to break those chylomicrons down and so their triglycerides are always super super high, and actually it doesn't matter if they're fasting and it comes down, you know, whatever they ate the day before just was really, really slow to come down because it's just not being recycled in the right way. Then there's other people where, well, maybe they have often the same exact genes, but just there's a variant and it's not the pathogenic variant, and so there's different penetrances or just other stuff. So this is like the other one where we say polygenic pattern, multifactorial hypertriglyceridemia, right, where people, you know, this might be your patient where uh on a bad day their triglyceride can hit 8 or 900, but really for the most part it's more like in the 400s or something like that. Um, the other thing that's really key is, we'll see all of these little parts of the of the reactions, right? Everywhere you see a LPL lipoprotein lipase to triglyceride chipping away, chipping away. Insulin resistance impairs lipoprotein lipase activity. So you have those other people with the extreme situation where they just have no lipoprotein lipase and they are just completely stuck the chilomicronnemia syndrome always, but insulin resistance to increasing degrees mess it up, messes up lipopropy lipase activity here and here and here, and you get the idea such that insulin resistance. Decreases lipoprotein lipase activity, and you end up with buildup of triglyceride rich BLDL and other atherogenic intermediates, right, when you have that whole readout of the LDL, the IDL, you know, all of the other ones that are kind of on this pathway of big stuff getting smaller, right? The intermediates before they get chipped away to be an LDL. So insulin insulin resistance is bad. So, so to put this in translation for kind of easier to digest sentences for your patients, triglyceride is a fat in blood that our body makes not only from fats we eat, but also from extra sugar and starch that we didn't need. Some people have genes that make them wired to be sky high over 5 times normal, even with a pretty good diet. Some people have a setup in their genes, right? Such that even if they don't have a good diet, and especially if they have extra weight, their levels will blossom to be 2 or 3 times normal. These are your patients where it might be 300, you know, but their sibling or someone else might not have it to be so so high, right? But anyway. Regardless of their genes or exotic genes, this or that, getting it, regardless of those will have triglyceride that goes up with poor diet and no exercise because of the relationship between insulin resistance just in general along every way of the pathway and how that can affect your lipids. So dietary fat, of course, certainly increases triglycerides. Those are the ingested chylomicrons, right? And um but added sugars and refined starches drive up triglyceride levels because of the end the endogenous side of the equation. It's the hepatic VLDL production. And so just kind of take a second for that cause that's important, right? So that's why I like patients with a really classic, you know, chlamyronemia syndrome, they do not have lipoprotein lipase receptors. They have the same advice that everyone gets, which is you have to be careful about your drinks and your starches, but they actually have a limit on their total dietary fat that they can have because they do not they do not have the capacity to break them down and recycle them. Um, so, uh, other kind of things to keep in mind, beverages is like by far the quickest way to help somebody improve their triglycerides and likewise their prediabetes. And I say even 100% fruit juice is is the only permitted sweetened beverage according to most guidelines, but even that should be no more than 4 ounces a day, just the size of the little tiny juice boxes that they get at school, cause you can count that as a fruit as a serving of fruit. Um, but just in other words, don't, right? Just there's they don't need juice, right? And as an example here, everything in the Denny's Grand Slam except for the black coffee will contribute to increased triglycerides directly. Um, sometimes it's helpful to have some label reading, and sometimes I'll frame it to kids as, especially kids who are old enough to be doing things like word problems and math. I say this, it's like a word problem. Every 4 g of sugar is a teaspoon. So if you want to look smart, you can look at a label and find what's in a serving and go to the sugar number and divide it by 4. Just divide by 4, divide by 4, and you can look, and you could show off and say this has blah blah teaspoons, right? So this 16 ounce boba has 52 g of sugar, which is 13 teaspoons. Now, the recommendation is that added sugar should not exceed 6 to 9 teaspoons a day, but there's a lot of studies that show that there's American teenagers who get like 30 teaspoons a day and in higher, so. Sky is the limit, right? Um, a really helpful and important thing is to level set of um how the relationship between exercise and your lipids. Now, with triglycerides, exercise, even in the absence of weight loss, is helpful with lowering triglycerides. And so it's almost like you think of it like a dial and exercise just will turn that dial down. And as an example, you know, they've had, um, you know, studies, laboratory based. Studies where they have individuals that have to be living in a facility for like a week while they study them metabolically. And if you have somebody on a treadmill and you can actually, you know, you can actually measure their like take sample their triglycerides every 15 minutes or 30 minutes, you can actually show that bout of really vigorous exercise can lower postprandial triglycerides up to 36 hours later. So talk about turning that dial down in terms of what those triglyceride levels are. So, you know, exercise, even if weight loss doesn't happen, is still very helpful for lowering triglycerides. Weight loss, of course, results in even more. I don't know if I have the parallel, yeah, yeah, this is the next slide that's important that the part two of that, because this is kind of different from exercise and LDL. Now for LDL, I think it's always important to emphasize exercise is extremely important, your heart is a muscle, it needs to be exercised and technically speaking, however, exercise alone doesn't really bring down LDL that much unless it is exercise that brings a reduction in adiposity. So that's really that's really important because a lot some of your patients, you know, um, a normal weight patient who has an LDL of 200 and is told, OK, just exercise more let's see where you go, it's not, it's not an appropriate expectation because they do not have weight to lose, and so therefore that is not a winning game for them. Um, how are we doing on time? It's 1:14. I got 15 minutes. Um, OK. Hypertriglyceridemia, the guidelines frequently have this magical above or below 500, above or below 500, and where that comes from is if patients have a fasting triglyceride in the over 500 range, they are at a higher risk of having an attack of acute. Pancreatitis. Um, and it's, it's, there's a lot of kind of factors that, that feed into this. There's kind of inflammation. It's not just blockage, but sometimes I will say it's almost like a heart attack in a way, but kind of related to the pancreas, but it's something serious, something that's painful, and it's a serious emergency, you have to be admitted for it. I will say it doesn't mean that when someone's triglycerides hit 500, that they're a walking risk, they're the walking time bomb. Generally speaking, people who have attacks of acute pancreatitis, it doesn't usually happen until they're like more like in the 1000 plus range. So, but the fasting and 500 and above is often a useful marker because, well, they're 515 because, you know, in a lab when they were fasting, imagine what they are after dinner, and I could think of as an example. For example, a girl that, um, you know, usually her triglycerides were kind of in the 500 range, and then one time we caught her and it on a Sunday morning and it was 2500, and it was because she was at a quinceanera the night before, because people who have impaired triglyceride processing, even if they're fasting, it isn't cleared from the day before, like it would be for other people. Um, so, yeah, so exactly. So hyper hypertriglyceridemia, you're basically not preventing a heart attack in the future, or you're preventing, you know, something that could happen tomorrow, right? And so, you know, acute pancreatitis is low. This is one, you know, cause of pancreatitis is not, of course, the only cause of pancreatitis, but, you know, it is gonna be a greater fraction of course in in youth, right? Um, and I think I said this already. These are some pictures I sometimes show patients just to kind of illustrate the fact that triglycerides are fat and blood, and this would be a tube of, you put it on ice, it's like a stew where the fat rises and solidifies, and this would be, this would correspond to somebody with like a triglyceride of like a 2000 kind of range. Um, oh, we are almost done. OK. So some notes about fish oil. So first of all, um, the omega 3 is the active ingredient, and DHA and EPA are the components that are important. And so if you tell your patient just generally, go buy omega 3 from the store, go buy fish oil. I guarantee you almost, the kind that they will come home with is something akin to this, which is uh generally the cheapest one that they're they're gonna find, which is 1000 mg that have 300 mg of omega 3. It's really just actual omega 3 in a capsule is only 300 mg, and the rest is literally just fish fat, OK? And so this is important because, and actually gummies, forget it, there's nothing, there's no, there's no gummies have any kind of meaningful amount of omega 3 if you're going there for a therapeutic route. Now, the, the reason that's important is because the kinds of amounts of omega 3 that you actually need to have therapeutic benefit is really high. So, you know, I, I will say that, you know, that I even somewhat disagree. The guidelines even will sometimes say, oh, you can try, you know, if borderline high, you can tell them to take fish oil, and, and I, I just, I will say that generally speaking in order the the the the true therapeutic benefit is actually when you're finally at least in this range or higher of 1 to 2 g of actual omega 3. You, you, I mean, 4 regular fish oils only gives you 1.2 g if those, you know, those ones that are 300 per. And that's a lot, right? Because the true better like the like when people are actually using it as a prescription or Lovaza, which is pharmaceutical grade omega 3, most everything in that 1000 mg capsule is actual omega 3. Um, you know, that is really, when I have patients that I do actually intentionally put on fish oil, I am only really technically bothering with it with using Lovaza in patients whose insurance will cover it because they already have diabetes and they're on CCS. Otherwise, nobody's insurance is ever going to cover it, and the only other way you can do this is by getting triple strength, and for a long time this was all that was available. Actually now there are ones that are sold at Costco even now and in a black bottle. The main message is really triple strength makes it lovaza strength because regular is teeny tiny. And so I usually have a policy of either not having them on omega 3 at all, or I have them on a really high dose and I'm super picky about making them stick with it. Sometimes I might just get have them get the equivalent of Lavasa from Costco, the triple strength one, and I will have them and only take one, but I will make them promise and I nag them and nag them that that is their medication. I want them always on it so that I actually know if it's making a difference, right? Because, um, because here's the thing is actually if you, if you, a lot of people, you know, will, will get put on it and then they'll take a bottle, and then that's it, and they'll kind of never in the end it was just an experience and they took it and you never really had any kind of sense of did they really need to be do it. And to be honest, I always tell People, the amount of triglyceride lowering you're going to get from your own efforts is generally speaking, even more than what they're going to get from being on a supplement. So see what they can do without on their own first, and you have to be clear about what amount you're recommending. Like I said, being really anal and telling them it's like their prescription, right? And also, if you start it, treat it like you mean it and monitor for improvement, right? Otherwise, why are they taking it, right? Uh, if not to just make you feel better. Half-hearted recommendation is going to be half-hearted compliance. Fibrates, if triglycerides are truly over 500, and I've tried optimizing omega 3, it's just not enough to kind of get them safely below 500. That's when I will have them on fibrates, and I don't have enough time to talk as much as I would love to, but fibroids are a great medication, you know, some of you may have patients of mine that are on them. Um, and, uh, they basically, uh, they basically increase triglyceride metabolism and they decrease hepatic production. That's the main thing if you remember that kind of picture of exogenous and endogenous production, it's really they just decrease how much that that person produces. Um, so just to kind of remind us of sort of a kind of a boiled down version of what is in the guidelines, if it's 100 to 200, lifestyle recommendations, just repeat it next year. 200 to 500. Kind of, I like to convey to people in terms of how many fold normal is it they're double normal, they're triple normal. Let's make these changes, and actually the heavy hitters are of course the beverages, reducing carbohydrates, exercising, cause exercise explicitly, you know, partic particularly decreases the triglycerides, um, and let's recheck soon, and I bet you can bring this down to normal, and you'd be just so pleased to see how many people are are motivated to see if they can, right? Over 500, we really need some serious effort. We're gonna recheck to see whether we're gonna, you know, whether omega 3 would be enough or whether you need something stronger. Over 1000, uh, you know, I think it's important for them to know. I mean, they are really super high risk, uh, we need to address this, and uh, you know, if you end up in the ER I'll also tell them please know to bring it up that you have this issue that could be a part of your abdominal pain. And I'll kind of convey to them. I'm not saying you're gonna need this for the rest of your life, but for now, um, you know, it is not safe for you to not be on a fibrate with your triglyceride that high. So, that you do a lipid screen on your new patient who's 10, they had a triglyceride of 205. You should recommend that they take a fish oil and come back and recheck their lipids at next year's physical. Well, and like again, you know, everybody is happy if they go home from the doctor with a prescription. OK, I'm being prescribed fish oil to fix my triglycerides. But this kid with barely elevated triglycerides probably make one lifestyle change and consistent and would probably reduce their triglycerides much more than the kind of teeny tiny amount that omega 3 that they're gonna get from that first bottle that they purchase, and they're gonna stop getting it anyway because they finished the bottle and then then. Right? So, um, always, always, always say, give your where I have it here it is. Give your patients the gift of feedback. It is people really, really get a lot of benefit out of being able to see how much they've been able to improve in that interval of time. Don't wait too long because people can only behave well for so long. And if they've seen how much it made a difference that they really worked on their like lifestyle in a couple months, there's more incentive to keep going versus if you don't check until a year later, maybe they were perfect and they were on it and they got their numbers normal after 2 months, but they slid and they went back up again, and then they feel hopeless and you feel hopeless a year later. So changes you may wish to make, fasting or non-fasting lipid in all kids in this age range, familiarize yourself with those cutoffs, like I was saying, those buckets, 130, 160, 190 for the lipids and above or below 500 for triglycerides, and, and just, you know, recheck. All right, and that's it. We're barely with time, so let me stop sharing my screen and um let's take a look at questions.
