One of the most common questions I get is which lab tests or other metrics matter the most to track for long-term health, and how to interpret them. Here is a list (in no order) of 5 numbers we deem important to know:
1. Lipoproteins/LDL
The number one killer in the U.S. is cardiovascular disease, and it’s pretty easy to argue that it’s also the most preventable of the major chronic diseases. Therefore, it warrants a lot of our attention, which is why the first three metrics on this list are all relevant to cardiovascular disease. The most clearly causal modifiable risk factor for atherosclerosis, the main mechanism of cardiovascular disease, is low-density lipoprotein (LDL). This molecule, a protein that carries cholesterol around in the bloodstream, is what starts the cascade of atherosclerotic cardiovascular disease (ASCVD) in the artery wall, and is necessary for it to take place.
It is not all that necessary for us to survive and thrive, though. We have plenty of other lipoproteins that can shuttle cholesterol through the body that won’t go setting off three-alarm fires everywhere. In fact, some people are born with naturally low LDL. For example, there are those with mutations in a gene called PCSK9, coding for an enzyme that degrades LDL receptors in the liver, that render the enzyme minimally functional. If you don’t have this enzyme, you have significantly more LDL receptors because they aren’t being degraded, allowing you to pull more LDL out of the circulation. These people are not only free from complications with very low LDL, but they are largely free of cardiovascular disease and general ill health as well.
The conclusion? We should be quite liberal in hammering our LDL down as low as we can, because it is pretty much only harmful to us, and we have fantastic options for lowering it. The cheapest and most common are statins, which inhibit the enzyme responsible for the first step in cholesterol synthesis in the liver. The liver senses a decrease in cholesterol and decides to pull more cholesterol out of the bloodstream, and upregulates LDL receptors to clear more LDL. These drugs have gotten some unfair press in the past for a number of adverse effects that did not have any real validity, but they are certainly among the most studied drugs in history, and it clearly appears they are safe. The only real side effect that people may get are muscle aches, but if someone is struggling to tolerate a statin, they can easily switch to a different one. With the low cost and easy accessibility, I think there’s virtually no reason not to start this lipid-lowering therapy from a young age to decrease total lifetime exposure to LDL, and chances of forming an atherosclerotic plaque. I have been taking one myself for years without issue. There are several other options outside of statins, including drugs that directly inhibit that PCSK9 enzyme, like Praluent and Repatha, though these drugs are currently quite expensive. It shouldn’t be (although it sometimes is) hard to work with your doctor to find a lipid-lowering therapy regimen that works for you.
Lastly, a lot of providers measure LDL as LDL cholesterol (LDL-C), which is a decent indicator of risk, but not as good as the LDL particle number (LDL-P) or ApoB (a protein on every atherosclerosis-inducing lipoprotein particle, including LDL but also others), which are the best predictors. LDL-C simply gauges the cholesterol content across all the LDL particles in the bloodstream, whereas LDL-P and ApoB actually give the number of lipoprotein particles floating around that can kick off that atherosclerotic cascade. These tests are quite cheap to do, but they are rarely the default tests in the U.S. Try and ask your provider, or see if you can get one done at a third-party testing center.
2. Blood sugar patterns
Another critical component of cardiovascular and overall longitudinal health is metabolic function, which can generally be approximated by someone’s blood sugar regulation. Like many things in medicine, we have an unfortunate situation at present, where this is treated as a binary: you do not have diabetes and are “not at risk,” or you have diabetes and are “at risk.” The reality is that diabetes (at least type 2 diabetes, by far the most common and the clearly modifiable form) is a spectrum based on one’s sensitivity or resistance to insulin, a hormone that tells cells to take up sugar from the bloodstream, lowering blood sugar. The healthiest end of the spectrum, where we want to stay, is with low/normal blood sugar, and low levels of insulin required to maintain that. Moving in the wrong direction on the spectrum, the first sign of metabolic disease is not elevations in blood sugar; it’s an increasing amount of insulin necessary to maintain the same blood sugar levels, because our cells start to become resistant to insulin’s signaling to lower blood sugar. Eventually, we become so resistant that even very high levels of insulin are insufficient to keep blood sugar down. Only then, late in the game of the disease process, would you start to see elevations in blood sugar. If this spectrum of diabetes seems a bit confusing, check out this video we posted recently, which outlines it visually in a little more detail.
Understanding this, as well as the volatile nature of blood sugar already across a day, it becomes evident why just measuring one’s blood sugar at one static point in time does not tell us a whole lot. If it did, we would probably want it to be fasting, but even so there is great variability based on hormone levels at various times of the day, like a cortisol spike in the morning that can make our sugars run high. It actually would be much more informative to see a fasting insulin than a fasting blood sugar, since again insulin is what rises first in the disease course. The next step up would be a hemoglobin A1C, which essentially approximates our average blood sugar over a three-month period based on the amount of glucose bound to hemoglobin on our red blood cells. This is still far from an ideal metric due to variation in people’s hemoglobin molecules and an unclear sense of the individual’s blood sugar variability, just the average they run at (and blood sugar spikes matter just as much as an average). However, at least a lot of clinics will offer it and it provides some sense of long-term insight, so for now this is an okay option accessibility-wise.
Our top recommendations for truly understanding one’s glucose regulation, though, are two-fold: oral glucose tolerance testing (OGTT) and continuous glucose monitoring (CGM). Starting with the former, a proper OGTT involves giving someone a set amount of glucose solution to drink, then measuring both blood sugar and insulin at 30 minute intervals for two hours (starting at t=0). This allows someone to see how both their blood sugar and insulin behave in response to a major challenge of sugar, which is ideally the extreme we would ever encounter in our diet. It actually should be a quite affordable and accessible test, yet it is rarely performed in clinical practice due to time constraints and our ingrained reliance on things like the A1C. Additionally, it is often performed incorrectly when it is done, which is usually just for women around pregnancy to assess for something different called gestational diabetes. When clinicians do perform this test, they typically just look at blood sugar before and two hours after the glucose challenge. This fails on two fronts: the frequency, and the lack of insulin tracking. In almost all cases, two hours after a meal comes after the peak of someone’s postprandial blood sugar spike, so we would not really know just how high they got. Plus, as we have already noted, if we don’t track insulin, we’re going to miss everyone for a huge early chunk of their developing pathology. We’ll only catch them when it’s super late in the game, and the high insulin can’t handle the glucose demand. It can be tough to arrange logistically sometimes, but this should be quite a simple and cheap test to get done at a third party lab source if your provider is strongly resistant.
The other top-tier assessment for glucose regulation is continuous glucose monitoring (CGM). Sensors produced by companies such as Dexcom, Abbott, and Medtronic are the predominant ones in the market, and work by just punching a little bandage-like monitor onto the skin. The monitor has a tiny wire about the size of a hair, which goes just under the skin, not even into the bloodstream, to sample glucose levels from the interstitial fluid every 5 minutes. This approximates blood sugar very closely, and essentially allows us to see how our glucose behaves for a 10-day or maybe 2-week period. Even just wearing one of these sensors for 10 days provides significant insight into our metabolic health, as we get a strong sense for how we respond to every sort of stimulus we put our body through across a day: eating, sleeping, exercising, etc. We don’t yet have access to something like continuous insulin monitoring, but this could be on the horizon and allow us to be even more ahead of the curve with detecting metabolic dysregulation. For now, though, CGM is a powerful tool to have accuracy without ambiguity in regard to our blood sugar dynamics.
Stay tuned for part 2 coming soon, where we dive into our next three most important metrics to know and why.
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