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    Rev Up Health Podcast

    Ep058 Heart Health Redefined: Why Your Standard Lipid Panel is Only Half the Story

    Cardiovascular disease remains the world’s #1 killer, yet the standard "total cholesterol" test often misses the real risks. In this episode of the RevUp Health Podcast, Dr. Mark and Tandi Hechler go beyond the basics to explain what truly drives heart disease: inflammation, particle size, and metabolic health. They break down the "missing" markers your doctor might not be ordering, like ApoB and Lp(a), and explain why your Triglyceride-to-HDL ratio is a critical window into your insulin sensitivity. You’ll also learn about the CAC (Calcium Artery Score), an affordable $75 scan that reveals…

    Episode Transcript

    Hello, hello, and welcome to this episode of the Rev Up Health Podcast. Today we're going to be talking about cardiovascular disease. It's February — National Heart Month — and cardiovascular disease is the number one killer, plus Valentine's Day is this month, so we've got to love it.

    Heart disease is the big number one killer — more than all the cancers combined — so we get a lot of questions about it. Quite frankly, it's one of the more complex topics to discuss, with a lot of controversy and ideas, but we'll try to give you some education and insight into the details.

    The Standard Lipid Panel

    One of the things your primary care doctor tests every year is your lipid panel. There's a lot of variety there, and some of it boils down to what order was actually placed by your provider. A typical panel includes total cholesterol, which is made up of HDL, LDL, VLDL, and triglycerides — basically different-sized lipid particles. Generally, the larger particles are better than the smaller ones — that's where the "good cholesterol" and "bad cholesterol" idea comes from.

    Just like your total weight isn't as good a picture as what makes up your weight — body composition matters more than the big number on the scale — the same principle applies to your lipid panel. Total cholesterol isn't always giving you the answer; it's about the components that make up that number.

    The main drivers are LDL and HDL. LDL are the delivery particles — think of them delivering cholesterol to the tissues. HDL are the transporters that give us metabolic insight and carry cholesterol from the tissues back to the liver to be broken down. That's why HDL is the "good" cholesterol (getting it out of the tissues) while LDL is the "bad guy" (taking it to the tissues).

    But before we go too far with good guys and bad guys, we need cholesterol. It's a necessary component that helps produce vitamin D, supports our immune system, and is essential for hormone production — testosterone and estrogen. Triglycerides are another picture of metabolic health and are often looked at as a metabolic marker. We use the triglyceride-to-HDL ratio frequently to get insight into insulin resistance and what your dietary actions look like. Ideally, your HDL and triglycerides should be as close to the same as possible, or your HDL should be higher than your triglycerides — keep that triglyceride number under your HDL. The way to raise HDL is more activity, movement, and sustained exercise, whether zone 2, HIIT, or even resistance training.

    What the Standard Panel Misses

    Some particles aren't drawn in routine lipid panels. One is ApoB, which estimates how many truly atherogenic particles are on your LDL — the actual components that can create the atherosclerotic plaque buildup in the arteries. That's why some people may have an okay LDL number but a higher ApoB. We really want to know your ApoB, because it's the true driver of your atherosclerosis risk. Remember, too, that LDL rises from the good healthy fats we encourage people to eat — olive oil, avocados, coconut — so knowing the difference between LDL and ApoB is helpful.

    Another number that's rarely drawn — and usually only needs to be drawn once — is Lp(a) ("LP little a"). Think of Lp(a) as an ApoB with an extra sticky protein on it. About 20% of the population has elevated Lp(a), and those individuals are more at risk for heart disease because of its sticky nature — it's about six times the atherogenic effect of typical LDL. So you may have normal-ish LDL, but if your Lp(a) is high, you're still at higher risk. It's a genetic marker, so you probably only have to have it drawn once to know if you're predisposed. We don't typically draw Lp(a) unless there's a need to look further or someone requests it.

    The Inflammatory Piece

    You need more than just cholesterol particles floating around to create cardiovascular disease. It's more than just having the pie — you've got to eat the pie, too. Chronic inflammatory processes in your system oxidize those particles — essentially "rusting" them inside the endothelial lining of the arteries, which leads to thickening and plaque buildup. So it's not just because you have LDL or ApoB; you need the other component to have the problem. That's why just taking a statin without changing your lifestyle isn't a free ticket — it helps a little, but there's more to it.

    The main inflammatory marker we look at is hs-CRP (high-sensitivity C-reactive protein). It's elevated in some individuals due to that chronic inflammatory process. It doesn't tell us where the inflammation is coming from, but it hints that there's an inflammatory response going on. One snapshot doesn't tell the whole story — CRP can be elevated for other reasons, like running a marathon or having an infection. So if someone comes back with a high CRP, we monitor how it trends and ask what they did recently. Transient elevations are one thing; chronic, long-term elevations are the problem — that's like always sprinkling gas on the fire. Numbers up to three are considered normal, but we like to see CRP under one in someone without an ongoing inflammatory process.

    What Damages the Endothelium

    Endothelial damage is a driving factor that sets the stage for the oxidation and plaque buildup. First on the list is high blood pressure, which creates shear stress damage to the endothelial lining. High blood sugar or diabetes weakens the endothelial tissue over time. Smoking introduces harmful substances and toxins that accelerate oxidation and damage. High cholesterol increases risk — but knowing which parts of your cholesterol are high is key. And any inflammatory process creates oxidative stress and reactive oxygen species, which can reduce the production of nitric oxide — our ability to have vascular elasticity so our blood vessels can relax.

    Lifestyle factors matter too. Physical inactivity and sedentary behavior lower your HDL, and obesity and poor diet lead to structural changes. This metabolic dysregulation is a significant driver of cellular dysfunction and disease progression.

    The Coronary Artery Calcium Score

    The next thing on our list is a coronary artery calcium score — an actual CT scan that shows if you have plaque. It's super fast, takes just minutes, and is very inexpensive; in our situation it's a $75 out-of-pocket test. A lot of insurance may not cover it, which is why we often order it on a self-pay basis. You like to see that calcium score close to zero. When it starts sneaking up into the 125-plus range, that's when you have more significant calcium buildup in the arteries.

    Treatment Options

    What do we do about lipid problems? Lifestyle changes are a big contributing part to reducing risk, but there are also statins, one of the main pharmaceutical go-tos to reduce LDL. In the right individual, the benefits are important, but there are associated risks: muscle symptoms — painful muscles or a hit to the substance of the muscle that can cause generalized weakness (sometimes the only thing a person notices is "I'm just not as strong as I used to be"). Statins can also affect liver enzymes, potentially reduce HDL, carry a slight diabetic risk, and sometimes affect cognition. It's not that one statin is worse than another, but some people don't get the response they need from a statin in general.

    The other pharmaceutical type is the PCSK9 inhibitors. Statins reduce the *production* of LDL particles, whereas PCSK9 inhibitors reduce LDL by absorbing it into the liver — number one, we don't produce it; number two, we absorb it. The disadvantage is they're pricey and given as an injection every couple of weeks, so they're for someone who really can't tolerate a statin. Statins are first line pharmaceutically.

    Then there's the question of *when* you should take a statin. There are a lot of schools of thought. Some people don't want to or can't tolerate the medication. Knowing your calcium artery score can give you more assurance that maybe you can address your lifestyle inputs to reduce your risk instead. This is a very personal choice — look at the whole picture and decide which way to go. Some people have a genetic predisposition that means they have to do something, but you also have choices: put the cigarette down, get moving.

    A statin may be a bridge to get you from where you are to where you want to be. If you start one, be mindful about also changing your lifestyle. We have patients who've been on a statin so long they don't even know what their lipids were before starting, so we don't know what they'd be without it — they may not even need it now that their insulin resistance or pre-diabetic tendency is under control. It all plays into a multi-spoked wheel where all the spokes keep it rolling.

    For people on a statin having muscle fatigue, pain, or aches, there's research suggesting that annatto tocotrienols and geranylgeraniol can help improve the body's ability to make CoQ10, since people on statins have a reduced ability to make it — which helps cellular health and reduces oxidation.

    What to Do Next

    If you don't know what your lipids are, get them drawn — that's first line and common in any standard annual lab draw. But understand the difference between normal and optimal: it's not optimal to have triglycerides above your HDL; ideally they're closer to one-to-one. Getting the answer "it's normal" isn't necessarily acceptable. And an LDL a little over normal may not be all that bad — it's not a sentence, it's a marker. All these labs are markers that help us take a snapshot of where we are and what we need to change.

    I'd suggest people consider having their provider draw an ApoB or Lp(a) to see their risk factors, since those are much better indicators of heart disease risk than total cholesterol alone. Consider getting a calcium artery score to see what's happened over the previous decades, and consider a CRP to look for inflammatory drivers.

    Then there are the many lifestyle strategies within your control that can really change your cardiovascular risk: strength training, zone 2, sleep, stress management, avoiding smoking, and minimizing ultra-processed foods. Sleep is frequently overlooked — it's not just lying down for seven or eight hours; you need good quality sleep. If you or your partner has obstructive sleep apnea, you're not getting the quality your body needs to repair and heal.

    Wrapping Up

    Hopefully we've given you a little clarity. This isn't all-inclusive, but it's something you can start to digest so you have a road map to reduce your risk burden and the inflammatory processes you have control over. You do have control over your LDL, HDL, totals, and triglycerides, and lifestyle changes are a good place to start. This isn't meant to be fear-inducing — just to give you information and things to think about. Reach out if you have any questions, and we hope you have a healthy day.

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