I love talking about longevity tools. Sauna, strength training, cold exposure, CGMs, red light therapy, better sleep, better protein, better recovery. These are all useful conversations.

But sometimes I think we skip over the most obvious thing.

You have to not die from heart disease first.

That may sound blunt, but it is clinically important. Cardiovascular disease is still the #1 cause of death in the U.S. It is also one of the areas where we often have time to intervene. 

Most people are used to getting a basic cholesterol panel once a year. Maybe their LDL is a little high. Maybe their doctor says it is “fine for now.” Maybe blood pressure is checked quickly at the beginning of a visit. If there are symptoms, maybe an EKG or stress test gets ordered.

Those tools have a place. They are not wrong. They are just not always enough.

I have seen patients with “normal” labs who still had cardiovascular disease. I have seen people with reassuring cholesterol numbers who had risk hiding in other markers. I have also seen patients with strong family histories who were told not to worry because their standard labs looked okay. This is where I think medicine has to become more individualized.

Guidelines are built for population health. They have to consider cost, access, safety, and what makes sense across millions of people. That is necessary. But population-level guidance does not always answer the question a patient is really asking, which is:

“What is my actual risk?”

For longevity, that question matters.

Why standard labs can miss the bigger picture

A basic lipid panel usually includes total cholesterol, LDL, HDL, and triglycerides. These are helpful starting points, but they do not tell us everything about plaque risk.

LDL matters, but LDL alone does not always show how many atherogenic particles are circulating. Inflammation matters, but it is not part of the standard cholesterol panel. Genetics matter, but many inherited risk markers are never checked. Blood sugar matters, but some patients have insulin resistance years before diabetes is diagnosed.

That is why someone can look “low risk” on a standard report and still have a meaningful cardiovascular risk profile. There is also a timing issue. Many conventional tests are better at detecting disease once it is more established.

An EKG can tell us about rhythm changes or prior heart damage, but it does not screen for early plaque. A stress test can be helpful when symptoms are present or when there is concern about blood flow, but it often identifies disease once it is advanced enough to limit circulation under stress. By that point, we may have missed years of opportunity.

In longevity medicine, I am much more interested in the earlier window. The period when a patient feels well, but risk may be starting to build.

That is when we can change the most.

The markers I wish more patients knew about

When I am looking more deeply at cardiovascular risk, there are a few blood markers I often want to understand.

Lp(a)

Lp(a), or lipoprotein(a), is one of the most important inherited cardiovascular risk markers. Many people have never heard of it, and many have never had it checked. That is a problem.

Elevated Lp(a) can increase the risk of heart attack, stroke, plaque buildup, and aortic valve disease. It is especially important in patients with a family history of early heart disease.

The tricky part is that Lp(a) is mostly genetic. You do not usually lower it very much with diet and exercise alone. That can be frustrating for patients who are already doing a lot right.

It is also important to know that there are currently no FDA-approved medications specifically designed to lower Lp(a) and reduce Lp(a)-driven cardiovascular risk. However, several Lp(a)-lowering medications are now in late-stage clinical trials, including Phase 3 studies. If these therapies prove effective and receive regulatory approval, they could become an important option for patients with elevated inherited risk in the coming years.

But knowing about it still matters.

If Lp(a) is elevated, we can be more intentional about lowering other risks. We may want LDL and ApoB lower than we otherwise would. We may monitor more closely. We may think differently about imaging. We may involve cardiology earlier.

ApoB

ApoB stands for apolipoprotein B. It helps us estimate the number of particles in the blood that can contribute to plaque. This is different from LDL cholesterol.

LDL tells us how much cholesterol is being carried. ApoB helps tell us how many plaque-forming particles are carrying it. Sometimes those line up. Sometimes they do not.

I pay close attention to ApoB in patients with insulin resistance, elevated triglycerides, metabolic syndrome, PCOS, diabetes risk, or a strong family history. It can reveal risks that LDL alone may underestimate. If I had to choose one advanced lipid marker that deserves more attention, ApoB would be high on the list.

hs-CRP

hs-CRP is a marker of inflammation.

It is not specific to the heart, which is important. A high hs-CRP does not automatically mean there is plaque in the arteries. It can be elevated because of infection, autoimmune disease, poor sleep, stress, excess visceral fat, gut inflammation, dental disease, or many other causes.

But inflammation is part of the cardiovascular story.

Inflamed blood vessels are more vulnerable. Plaque biology is influenced by inflammation. So when hs-CRP is elevated, especially alongside other risk factors, I want to understand why.

When imaging is worth considering

Blood work can tell us about risk. Imaging can tell us more about whether plaque is already present. One common option is a coronary artery calcium score. This is a CT scan that looks for calcified plaque in the coronary arteries. It is often less expensive than other imaging.

It can be useful, but it has limitations.

A calcium score looks for hard, calcified plaque. It does not show soft plaque. That means a score of zero can be reassuring, but it is not a guarantee that there is no cardiovascular risk.

This is especially important for certain patients, including those with elevated Lp(a), autoimmune or inflammatory conditions, strong family history, or other concerning markers.

Another option is a CT coronary angiogram. 

This uses contrast to look at the coronary arteries in more detail and can identify both calcified and non-calcified plaque. There are also newer technologies, including Cleerly, that use AI to analyze coronary CT angiography and characterize plaque in a more detailed way. This is one of the more exciting areas in preventive cardiology. 

No test is perfect. CT imaging involves radiation. CT angiograms require contrast, which is not appropriate for everyone, especially patients with certain kidney issues or contrast allergies.

But for the right patient, imaging can be incredibly helpful.

It can answer a question that labs cannot always answer: “Is plaque already there?”

Who should think about deeper testing?

Not everyone needs advanced cardiovascular testing. I do not believe in ordering every test on every person just because it exists.

But there are certain patients where I think it is worth a deeper conversation.

That includes people with:

  • Family history of early heart disease
  • Elevated LDL cholesterol
  • Elevated ApoB
  • Elevated Lp(a)
  • High blood pressure
  • Diabetes or prediabetes
  • Insulin resistance
  • Obesity or excess visceral fat
  • Smoking history
  • Autoimmune or inflammatory conditions
  • Chronic inflammation on labs
  • History of preeclampsia or gestational diabetes
  • Normal basic labs but strong concern based on family history
  • A proactive longevity mindset

The last point matters. Many patients do not want to wait until something is obviously wrong. They want to know what they can do now to preserve health for the next 20, 30, or 40 years.

What we do with the information

Testing is only useful if it changes what we do next.

If advanced labs or imaging show elevated risk, the plan depends on what we find. Sometimes the next step is lifestyle. Sometimes it is medication. Sometimes it is a supplement strategy. Sometimes it is cardiology. Often, it is a combination of options.

For most patients, that means consistent cardiovascular exercise. A general goal is at least 150 minutes per week of zone 2 or moderate-intensity cardio. I also like to see some higher-intensity work when appropriate, even if it is a smaller amount each week.

Strength training matters too for metabolic health and healthy aging.

Nutrition is another major lever. I usually start with a whole-foods approach: enough protein, plenty of plants, healthy fats, minimal ultra-processed food, and enough fiber. Around 30 grams of fiber per day is a helpful target for many people. Then, we individualize.

If LDL or ApoB is high, we may discuss medication. Statins can be very effective. Ezetimibe, PCSK9 inhibitors, and other therapies may be appropriate depending on risk and response. For some patients, medication is one of the best tools we have to prevent a future event.

Supplements can also be useful in the right context, but they need to be treated with the same respect as medication. Berberine may help with glucose and lipid metabolism for some people. Red yeast rice can lower LDL, but it can act similarly to a statin and quality control is an issue. CoQ10 is often considered for patients on statins, since statins can reduce CoQ10 levels.

The right plan depends on the labs, the imaging, the family history, and the full picture.

The Timmons Wellness perspective

At Timmons Wellness, cardiovascular health is one of the first places I look.

There are many exciting things happening in longevity medicine right now. I love that patients are more interested in prevention, performance, recovery, and living well longer. But we cannot talk seriously about longevity while ignoring the number one thing most likely to shorten it.

That is why I want patients to understand their cardiovascular risk earlier. Advanced cardiovascular testing is about being appropriately curious. Some questions I consider: 

  • What is your inherited risk?
  • How many plaque-forming particles are in circulation?
  • Is inflammation part of the picture?
  • Is there already plaque present?
  • Are we doing enough to reduce future risk?

The goal is to live longer with a strong heart, healthy vessels, stable metabolism, and the best possible chance of avoiding disease. Because you can do all the biohacks in the world.

But first, you have to not die from heart disease.