Video Blog: Lipids
Welcome back to Empallo Heart-to-Heart! In this series, we explore common questions about heart health and cardiac care that don’t always get the time they deserve during a typical cardiology visit.
In this episode, Claire Beskin (CEO, Empallo), Dr. Dana Weisshaar (Medical Director, Empallo), and Joe Lemay (CEO, Longevity Athlete) discuss lipids and cholesterol, including LDL, HDL, ApoB, and Lp(a). They explore what these markers mean for cardiovascular health and longevity, how diet and lifestyle can influence cholesterol levels, and when additional testing or medication may be worth considering.
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Check out the episode on Youtube. Enjoy!
Claire Beskin: Hello and welcome to Empallo Heart to Heart. Today we're talking about lipids, cholesterol, and what they mean for our heart health and longevity. I'm Claire Beskin, founder and CEO of Empallo. I'm joined by Dr. Dana Weisshaar, medical director at Empallo, and Joe Lemay, founder and CEO of Longevity Athlete. This series is about discussing questions that commonly come up in cardiac care, but don't always have the time to be fully explored in a typical cardiology visit. Our goal is to answer these questions, clear up misconceptions, and introduce ideas that our listeners and viewers may not have thought about before. Few topics create more confusion than lipids. We hear terms like cholesterol, HDL (High density lipoprotein), LDL (low density lipoprotein), ApoB, Lp(a). And many people don't always know what these measurements mean, which ones matter most, and what we can do about them. Dr. Dana, let's start with the basics. What are lipids, and why do cardiologists pay so much attention to them?
Dana Weisshaar, MD: Well, lipids are a normal, important compound in our body. They're organic compounds that have an integral function in the makeup of our cells and we use them to transport nutrients, vitamins throughout our body. So I think it's important to realize that lipids are not actually a bad thing but hyperlipidemia too many lipids is a bad thing. So when I was thinking about this discussion, I wanted to make sure that we understand that lipids is not a bad word. They're actually important structural and functional molecules in our bodies. We all have them and we need them. We just don't want them in excess. So cardiologists care. Well, we all should care. And it's not just cardiologists, but your primary care doc cares about what your lipid levels are because if they're elevated, they convey long-term risk for deposition and disease and worsening mortality, shortening of your longevity.
Claire Beskin: So lipids per se, not a bad thing, but lipids in excess are bad. What is sort of the threshold to be concerned about?
Dana Weisshaar, MD: So you can't feel your lipids. It's a silent issue. The only way to know whether you have excessive lipids is with a blood test called a lipid panel. Typically, we do a fasting lipid panel, which means you don't eat for at least eight hours before you get your blood drawn because some of the tests in a lipid panel, particularly the triglycerides, are affected by what we eat. And so our levels will go up and down based on whether we have, for instance, a fatty meal or lots of oils with our meal. So we do a fasting lipid panel and it's currently recommended that all individuals have a lipid panel in early adulthood. I don't know exactly when most primary care docs will do that, but early 20s is a good time to generally start screening. And we screen children whose parents have premature coronary artery disease or have a diagnosis of severe hyper lipidmia because there are genetic conditions which even raise the risk of severe high cholesterol or hyper lipidmia in children that needs to be treated.
Claire Beskin: And we hear cholesterol, we hear lipids. Are they the same? What's the difference between the two?
Dana Weisshaar, MD: It's a little complex biochemically and I don't want to get too geeked out, but cholesterol is a compound that our bodies use in making our sex hormones and some of our other proteins that our bodies use. So, they're related, but they're not all-encompassing. So cholesterol is part of the lipid profile, but it's one of the lipids of a whole variety of lipids that our bodies have and make. Would it help if I showed you a picture of an LDL? So, I gave a lecture u to some medical students back in March of 2026 and I have a slide deck and it has a small picture that might be helpful. Okay, so basically this is a cartoon of an LDL. We'll talk a little bit about what LDL means, but lipids are these really interesting organic compounds that have what I think of as a head and a tail. So it looks a little bit like a squid in my opinion. And the head is what we call hydrophilic, meaning it's attracted to water or it can be surrounded or submerged in like the plasma and the blood. Whereas the tails are what we call hydrophobic. So you hear the term oil and water don't mix. Well, oil is hydrophobic. It's afraid of the water, if you will. So it doesn't mix. So we use lipids called phospholipids to create these packages, these lipoproteins that carry hydrophobic or kind of oily if you will substances around our body because our bodies will use things like triglycerides for energy storage. In fact, that's why if we have too many triglycerides, we deposit those in fat stores or adipose tissue for later use. But you can see there's also cholesterol esters in here that could be carried to other cells to be used in the manufacturer of the cell wall or the manufacturer of certain hormones. So I think about lipids as this really important community of compounds that have an important function. And I think the lipoproteins that carry these packages are kind of like your delivery driver, right? So they carry whatever you need to your doorstep. So they carry things around your body to your cells and provide them. So they have a really important function. However, once you've kind of saturated the need in the body for these things, you have excess. So some of them you deposit into your fat cells and others like these, if you can't clear the carrying container, the LDL, the low density lipoprotein, if you can't clear that out at the liver level, then you've got too many of these floating around. they start to deposit into tissues. And so the reason we care about an excess of these is that they deposit everywhere. They deposit in our arteries. The normal artery is nice and smooth. And when we start depositing them underneath the lining of the artery, we get atherosclerosis. So you get this plaque buildup that clogs these arteries in the heart, we call it coronary artery disease. If the arteries are in the brain or in the carotid, call it carotid atherosclerosis, or if it's in the aorta, aortic atherosclerosis, so it can happen in any and all blood vessels. The ultimate risk is if it either impinges the blood flow or it ruptures and causes a clot. Then we have inadequate blood flow to our heart which we call ischemia or angina or we close it off completely and we have a heart attack or a myocardial infarction. If these blood vessels are to the brain we have a TIA, a transient ischemic attack in the brain or a stroke. What a lot of people don't understand is that hyper lipidmia doesn't just affect our coronary arteries. It is also linked to causing hypertension. We talked about atherosclerosis and ischemic stroke and it can cause brain hemorrhage and we talked about coronary arteries. It also can deposit in the liver and cause fatty liver. It can cause hyperglycemia or pre-diabetes which leads to diabetes over time. And then thrombus which is this clot formation is also associated with hyperlipemia. So that's why cardiologists and like all physicians and why we all should care what our cholesterol levels are.
Claire Beskin: I've heard of these terms good cholesterol and bad cholesterol. Can you talk a bit about the difference between the two?
Dana Weisshaar, MD: A great question. So it's an oversimplification of course because we need all of these lipids and all of these lipoprotein particles to do their jobs. And so let me go back to this picture and say that this carrying case, if you will, actually is created in the liver and it starts out with a really large lot more triglycerides in it called a chylomicron. And that chylomicron then as it deposits or delivers its wares around the body gets smaller and smaller and then becomes an intermediate sized particle and gets smaller and then we get these things called low density lipoproteins. So that's an LDL particle and its LDL particle’s job is still to keep delivering stuff and it continues to try to deliver stuff even when the delivery market is saturated. So that's why it starts in a metaphor and starts to look for other places to deposit if you will. Whereas an HDL is even smaller. So if this has gotten rid of more of its stuff, it loses its ApoB molecule which is kind of the tracking to find where to deposit stuff molecules and now it gets an ApoA molecule and it becomes an HDL, a high density lipoprotein. It's got a different marker on its surface. It hones back to the liver and delivers the vehicle back to the liver that then kind of reuses it and remakes it and then fills it back up again and sends it back out. So that's why we consider HDL good cholesterol as it tends to take these lipoproteins from the periphery and return them back to the liver to be recycled. Whereas LDL is still more of a delivery and it will find places to deposit if it can't find someplace to deliver its wares. Does that analogy kind of work for you?
Claire Beskin: It's helpful. Yes.
Dana Weisshaar, MD: Okay. So, when we have a low HDL high LDL ratio, it puts us at higher risk of cardiovascular disease than if we have a high HDL low LDL ratio.
Claire Beskin: Can your lipid levels be too low? What happens if you go too low on the HDL LDL?
Dana Weisshaar, MD: That's a really interesting question. There growing data that really it's not clear that there's a low LDL level and it's not necessarily that super high HDL levels are helpful either. There's concern that when we get to really high HDL levels, the good cholesterol levels, they might not be quite so functional, which is why there's so many of them circulating. So there's no specific floors or ceilings that we look for. We look for targets generally speaking for asymptomatic patients who've never had a heart attack, a stroke or clinical atherosclerosis, fatty liver, things like that. We target an LDL level less than 100 and we shoot for much lower targets less than 55 in particular in patients who have severe atherosclerosis or previous heart attacks, things like that. So there are three main targets. There's less than 100 for most people who we deem need lipid lowering therapy. There's less than 70 for people at intermediate (to high) risk. And then there's less than 55 for people who are at highest risk.
Claire Beskin: How do people figure out if they're at high risk or intermediate risk?
Dana Weisshaar, MD: So there's what we call the prevent risk calculator from the American Heart Association. And this first page tells all about how it was designed and developed in 2023. But the online calculator is pretty self-explanatory. So it gives three levels. So the cardiovascular disease risk, the specific atherosclerotic cardiovascular disease risk and the heart failure risk. So it calculates that risk in 10-year or 30-year risk. When we think about hyperlipidemia or high blood pressure or anything else as far as cardiac risk, we think about primary prevention and secondary prevention. The secondary prevention is: we already know you have coronary disease or atherosclerosis or had a prior stroke or prior heart attack and so we're not trying to prevent the disease but we're trying to prevent heart attacks and strokes or subsequent sequelae of the disease. So in those patients that's called secondary prevention and so all of those patients warrant lipid lowering therapy and it's just a matter of the degree to which we lower the LDL.
Dana Weisshaar, MD: This tool is for primary prevention. So patients who we don't have a diagnosis of atherosclerosis and we want to assess their risk of atherosclerosis. So let's for [snorts] example just take a man who's 62 years old who's got a blood pressure that's mildly elevated let's say 128 and has a total cholesterol of 220, HDL that's a little bit low, and eGFR is an estimate of renal dysfunction so let's just give him good renal function. Let's say he's got a eGFR of 100. Let's make him a little bit overweight. He's not diabetic. He doesn't smoke currently. He's not currently on medication for blood pressure or lipid lowering. There are three additional risk markers they have in the calculator. You can add the zip code as an estimate of social deprivation which raises cardiovascular risk. hemoglobin A1C which is a marker of insulin resistance and diabetes and UACR is urine albumin-to-creatinine ratio and this is another marker of renal function that has to do with whether or not your kidney leaks protein but let's say we don't have those. So we just got this guy who's got some hyperlipidemia and really not much else going on, maybe a little obesity and let's calculate his risk. So you can see that he has an 8.2% risk of developing cardiovascular disease in 10 years. So he would fall into an intermediate risk group. Over 10% is the high risk group and under 3% is the low risk group. Between three and five is considered borderline and 5 to 10 is considered intermediate. And so we would have a conversation with this patient about weight loss and consider lipid lowering therapy. So this is how we do that. Oh, and we can break it down into this overall risk. This is his risk. So he's intermediate risk still for atherosclerotic heart disease and he's at borderline risk for heart failure at 10 years. Okay. So we take these risk calculators and we have an individualized conversation with the patient about when to initiate lipid lowering therapy, when to get additional testing when you're in this intermediate group. You know, what do you need to tip the scale toward let's go ahead and treat versus let's defer treatment and just work on lifestyle modification. And that's where we get into some really interesting things like do you do additional testing? We talked in earlier podcasts about coronary calcium score. This would be a perfect patient to consider a coronary calcium score because if his coronary calcium score was more than zero, now that says now you've got demonstrable coronary disease, we need to lower that LDL cholesterol to less than 100.
Joe Lemay: I'm curious when it comes to my cholesterol. I know cholesterol is essential. It's like a precursor for testosterone and other hormones and other things in the body, but too much is a problem. So, how much can I manage it through lifestyle interventions like diet, like exercise, things like that before I need to start thinking about a statin if I want to avoid medications?
Dana Weisshaar, MD: Fabulous question. The answer is about 20%. So there are a number of triggers you can pull to lower your cholesterol to lower your LDL and only about 20% of our cholesterol comes from our diet. So people say ah but doc how can I have high cholesterol? I am a vegan and I don't eat any oils and I exercise regularly. So about 20% comes from our diet and 80% comes from our liver. 80% is your genetics basically. But if you're following a great diet and you're overweight, you can work to lose that excess body fat. That is an additional trigger you can pull. So components of a healthy lifestyle have multiple triggers or levers we can pull. Diet is one part of it. Exercise, moving, improving the vascular tone of our blood vessels improves or lessens their susceptibility to atherosclerosis and becoming stiff related to the atherosclerosis. Reducing our body fat, improving our mental state, so stress reduction, all of these things make up a healthy lifestyle. All of which can help to reduce hyper lipidmia and development of atherosclerosis. So the American Heart Association (AHA) calls it life's essential 8. Okay. So life's essential eight from the American Heart Association. So basically it says we should focus on our diet and here there are two diets in particular that have shown excellent control over lipids. One is the Mediterranean diet which basically focuses on very little red meat. It's fish particularly oily fish that has a lot of omega-3 fatty acids in it, chicken, but very vegetable forward. Using olive oil rather than any tropical oils. And so it's based on legumes, lean proteins, high-fiber foods, and unsaturated rather than saturated fats. The other diet, very similar, but cutting out the animal proteins, is a whole food plant-based diet where we use whole grains, plant-based proteins rather than animal proteins. exercise. The American Heart Association and therefore I recommend at least 30 minutes of cardiovascular exercise at least 5 days a week. Blood sugar control. So if you have insulin resistance or diabetes, make sure that your blood sugar is under excellent control. Weight management, maintaining a healthy weight, which for most populations is a BMI less than 25, but for Asian populations a BMI less than 23. Controlling your lipids. We talked about those goals. Controlling your blood pressure, ideally all blood pressure readings under 18, 130 over 80. Avoid toxins. This is not just smoking. It's all nicotine. It's some things that those of us who live in urban centers can't avoid, like air pollution. People with high risk jobs like people who work in factories with heavy metals or firefighters who are exposed to fire smoke. and also more and more information about avoiding disposable plastics, drinking our water out of reusable BPAfree bottles. And then I talked a little bit about stress management and getting good sleep. And so treating sleep apnea if you have it is also part of a healthy heart lifestyle. So these are the triggers. And when we're talking about lipids, we can generally with a great diet reduce our lipids by up to 20%. And if we have any of these other things that are out of balance, maybe be able to pull your lipids down another 10% or so. So if you start with an LDL cholesterol of 160,
you're probably not going to be able to get your LDL less than 100, which is the ideal range with just lifestyle changes. So you might need to then consider medical therapy.
Joe Lemay: It seems that a lot of problems related to heart and heart disease actually are accelerated by sugar consumption. If I were to eat more sugar, would something change in my blood work that you would see? How does someone connect the dots?
Dana Weisshaar, MD: What I hear is that the increased sugar we know is a trigger for inflammation. The excess calories need to be stored and if we don't use them all, we store them as triglycerides in our fats. So they're tied in that reducing our sugars also helps us reduce our body fat which also helps us then reduce our atherosclerotic risk. So they're all tied together. The diets that I mentioned, the Mediterranean diet and the whole food plant-based diet both are low in high glycemic foods. So, we're using whole grains, which take more energy to digest and package up into the carbs that we actually use in our bodies, avoiding sugary drinks, refined sugar, and the higher glycemic index foods.
Joe Lemay: Trigger more insulin spikes that would come with it and drive triglycerides and then of course weight gain.
Dana Weisshaar, MD: Right.
Claire Beskin: We've talked about LDL and HDL. Some other lipids that come up are ApoB, Lp(a). They're not in a typical lipid panel
Dana Weisshaar, MD: Right. They're lipoprotein. So apo lipoprotein B or ApoB for short and lipoprotein little A or Lp(a) for short are adjuncts. Remember I showed you the picture of the LDL molecule and it had an ApoB molecule attached. So it's kind of like an identifier for an LDL molecule. So your ApoB is related to your LDL and it's not related in a onetoone fashion but it's related. So when we have people who have elevated LDL in that intermediate or borderline range, we can test the apo lipoprotein B as one of those things that might tip the scale. If your ApoB is elevated, then it tips the scale toward we should lower your cholesterol. We should put you on lipid lowering therapy. The same with Lp(a) except that Lp(a) has been shown to have an independent risk for atherosclerosis. The problem is we have not yet developed a treatment that targets lowering Lp(a). It's coming. It's in clinical trials and it's showing pretty promising results, but we don't at this point have Lp(a) targeted therapies. If the Lp(a) is elevated, we again use lipid lowering therapy targeting an LDL less than 100 in order to modify the risk of developing atherosclerosis. So those tests have to be ordered separately separate from a fasting lipid profile and we do those when patients have an intermediate or borderline risk and we're trying to tip the scale one way or the other. If the ApoB and the Lp(a) and a third one called a high sensitivity CRP are low then we can defer medical therapy focus on life's essential eight to optimize our cardiac health, reduce our LDL over time and perhaps avoid medical therapy. Whereas if your ApoB or your Lp(a) are elevated or your high sensitivity CRP is elevated, then that would tip us toward let's treat now to reduce your risk. High sensitivity CRP, I mention it together because I think of them when I order them together as all kinds of additional weights that I could put on this scale to help me figure out treat or not treat. But high sensitivity CRP is a marker of inflammation. And so this is the other thing that your physician is considering when discussing lipids that we hadn't touched on yet, which is what other risk factors. If you have an inflammatory disease, psoriasis, rheumatoid arthritis, HIV disease, other kinds of chronic inflammatory conditions that increase your risk and may indicate that we not only treat your underlying condition to reduce the inflammation in your body, but treat your lipids earlier. So, a high sensitivity CRP in someone who doesn't have a frank diagnosis of an inflammatory disease can be an indicator that there's a lot of inflammation going on in the body and may be a helpful trigger to treat.
Claire Beskin: That's helpful and interesting. Social media may have figured me out because it feeds me a lot of content about health and wellness and recently I've seen content about ApoB, Lp(a) and I'm not sure how much that's just a function of this niche little bubble that I'm in or maybe reflective of a wider conversation that's happening in longevity circles for example. So I'm curious, Joe, in the circles you're in. How much conversation is there around lipids cholesterol ApoB, Lp(a), how do you think about these?
Joe Lemay: Yeah, I think that there's a number of doctors who are getting really aggressive on things like ApoB for example. I don't know if the word is yet, but it's not yet a standard of care that's made its way out to most doctors, but some doctors are being very aggressive about it. I think another theory, I think it's still more in the theory zone than consensus or standard of care is that you mentioned high sensitivity CRP measures of inflammation. So even though that's an imperfect measure of inflammation, it is one of the ones that we have. And the theory is that it's really the inflammation that is more of a root cause as some doctors have explained to me. The plaques that are coming onto your endothelial cells are sort of more like the ambulance coming to heal the insult from inflammation. And it's really the underlying inflammation that should be managed before that and more of a root cause. So watching out for your inflammation in various ways is one of the theories that I'm hearing from a few doctors or on the internet.
Dana Weisshaar, MD: Yeah, I think inflammation is part of it. Even in patients who don't have frank inflammatory markers, we still deposit these cholesterol plaques that begin to develop. What exactly the inciting factor is for it to develop at that point in the artery is not 100% understood.
Joe Lemay: Mhm. And then there's the whole topic of toxins and how that might drive inflammation. There's like an endless number of vectors of toxins to get into us. You know, if you eat anything that comes out of a package and it's packaged in plastic, if you know, I saw a cup of tea the other day and someone served it in a plastic tea bag and I was like, "Oh my god, that's crazy." Uh, but it's just like everywhere. And I mean, my table in front of me is plastic, right? Everything is plastic. And what of this is releasing toxins? like it's very hard to figure out, but we can try to get rid of our plastic cutting boards and all of this stuff, but it sort of seems like we can't eliminate it unless we move out into the woods and just use glass and wood. But one of the things like having some therapies to try to accelerate how we take toxins out of our body. So, there's a lot of talk about saunas. There's a lot of talk about combining NAC (N-acetylcysteine) with glutathione and glycine and things like that to accelerate just how our bodies can process and remove toxins from our body is just another way to to help assist with that. These are the types of things that I'm hearing a little bit about these days.
Dana Weisshaar, MD: Yeah. Well, and some of the simplest things to do to avoid toxins, and I still see a lot of it. Don't smoke, don't vape, don't use nicotine. You know, there's still an awful lot of toxins that we expose our bodies to electively rather than just collectively in our society. We have a lot of plastics. So, I agree. It's great for us to start to remove some of these toxins that have seeped into our collective experience like packaged foods and things like that. But to start with, let's not add toxins intentionally. That's smoking anything.
Joe Lemay: Thanks for addressing some of my questions. Sometimes it's a little bit awkward talking to a real doctor because a lot of what I'm absorbing from information is like stuff on podcasts and on Reddit, you know, it's like it's kind of like “bro science” as they call it, right? And so now to bring this to you and ask you questions about it, some of it might become standard of care and it might take a few years, but some of it might be complete nonsense. And so I'm just bringing it to you to help me understand what if this smells legit versus smells like nonsense.
Dana Weisshaar, MD: You know, you make a great point that all of this knowledge that we have or that I've shared with you today has started with theory and testing and some of it becomes truth and some of it becomes, you know, lore. And so I like your term “bro knowledge”. Some of that makes sense and so it's reasonable to do. I think of it as “yes and”. And so yes, here's what I know scientifically and organizations with great minds like the American Heart Association and American College of Cardiology have put together the best recommendations we have in 2026 based on hard scientific data. And here are the things that have a reasonable basis in science and theory that are apparently safe that you can also do. Don't ignore this part, but you can supplement with some of these other anti-inflammatory agents and things like that if you have the means and you're not overwhelmed by pill burden and you're not overwhelmed by supplement burden and things like that, you can do both. It's not one or the other. It's “yes and”.
Joe Lemay: That's good. Thank you.
Dana Weisshaar, MD: You're welcome.
Claire Beskin: This has been a great conversation. We are coming up on time today. We've talked about lipids, cholesterol, things in our environment that we can modify like our diet, environmental toxins. To wrap this up, Dr. Dana, if someone were to remember only one thing about lipids, what should it be?
Dana Weisshaar, MD: I would say understand that sometimes even if you have the best lifestyle, the best diet, the best intentions, you do everything right, you might still have high cholesterol and it's not your fault. It's genetic and it's rampant in our society. And treating hyper lipidmia is a key way to improve our well-being and our longevity. So it's not just about living longer, it's about living better for a longer time. So medications are not the enemy.
Claire Beskin: Thank you, Dr. Dana. Thank you, Joe.
Dana Weisshaar, MD: All right. Thanks, guys.
Joe Lemay: Thank you, Dr. Dana.
Dana Weisshaar, MD: Great to see you.
This content is for general informational purposes only and is not medical advice. Talk with your healthcare provider before making any decisions about your health.
