#79: My calcium score was terrible. My friend’s was perfect. He might be the one who should worry.

A friend called me a few weeks ago, sounding relieved. He is 48. His doctor had ordered a coronary calcium scan and the score came back zero. In his mind, that settled it. His LDL cholesterol (the “bad cholesterol”) has been sitting around 150 mg/dL for years (higher than the 100 mg/dL that is recommended for most healthy people), but the calcium scan was clean. Why worry?

I understood the relief. In 2015, my own calcium score came back at 266, the 98th percentile for my age. I would have given anything for a zero.

And yet, here is the strange truth I have come to believe. My 266 may have saved my life by forcing me to act. His zero, if it gives him false reassurance, could keep him from acting. In this post (#79), I get into the details of why.

The Basics of plaque, calcium scans and calcium scores

In order to better understand why a zero calcium score is reassuring but not sufficient evidence of a plaque-free or risk-free heart, let’s get into the basics. Stay with me through three minutes of fundamentals. They make the study’s findings easier to follow.

What is plaque, really? Plaque is not something that coats the inside of your arteries like grease in a pipe. It builds inside the artery wall itself. The process starts when LDL particles slip out of the bloodstream and get stuck in the wall. Your immune system treats them as intruders and sends in cleanup cells, which swell up, die, and pile up. Over years, this becomes a soft, fatty deposit buried in the wall. It starts surprisingly early. Autopsies routinely find the first fatty streaks in people in their 20s.

Particles getting stuck in the artery wall is a probability game. The probability depends particularly on how many cholesterol-carrying particles are circulating. ApoB estimates their number; LDL cholesterol measures the cholesterol they collectively carry. The two usually rise together, which is why LDL works as an everyday estimate, but when they disagree, apoB tends to reflect risk more accurately. And more particles means more chances for one to get stuck, the way more vehicles on a road raise the odds of an accident without guaranteeing one.

Where does calcium come in? Late, at least in visible form. Calcium is not the disease. It is part of the body’s healing and remodeling response to plaque that has sat there a long time, like the hard callus over an old wound. Noncalcified plaque generally develops years before enough calcium accumulates to show up on a scan. So a person can have plaque even when the calcium score is zero.

Here is an analogy I will use for the rest of this post. Think of a car driven every winter on salted roads. Corrosion starts under the paint, quietly, years before anything shows. By the time you can see rust, the damage has been building for a long time. The salt is your LDL and apoB particles. The rust is the calcification. The corrosion under the paint is the plaque that has not yet turned into visible calcium.

What does the scan actually do? A coronary artery calcium scan, or CAC, is a low-radiation CT scan of your chest. It takes about ten minutes, involves no needles or dye, and uses a low dose of radiation, commonly around 1 mSv, though this varies by scanner and protocol. Many centers offer it for a modest out-of-pocket price, typically $100 to $200 in the US or a few thousand rupees in India. The scanner does one thing: it detects hardened, calcified plaque in the arteries that feed your heart, not the soft plaque that has not yet calcified. In our analogy, the scan is you walking around the car looking for rust. It cannot see the corrosion under the paint.

What does the score mean? Zero means no detectable hardened calcium. One to 99 is mild, 100 to 399 is moderate and the level where treatment decisions get unambiguous, and above 400 is extensive. The raw score is generally the stronger predictor of future events, but your percentile adds context, especially when you are younger. A score of 50 may be common at 70 but is highly unusual at 45, and at either age it confirms that coronary plaque is present. My 266 at the age of 43 put me in the 98th percentile, meaning 98 percent of men my age had less rust than I did.

So the score is easy to read in one direction. Higher score, more risk. The tricky part is the other direction. A zero means no rust is visible today. It does not tell you how much salt the car has already been through.

Which brings me back to my friend. His zero may be fine, but it needed a double click given his high LDL load over the years. A new study from one of the longest-running heart projects in the world helps quantify this exact scenario.

The CARDIA Study

Researchers went back to CARDIA, a landmark study that enrolled several thousand healthy adults aged 18 to 30 and followed them for 35 years, measuring cholesterol over and over. Calcium scans were done at year 15, when participants averaged 40, and again at year 25, around age 50.

The researchers asked a clear question. Among people with a calcium score of zero, did lifetime cholesterol exposure still predict future heart attacks and strokes? In the analogy: among cars with no visible rust, do the winters driven on salt still predict which cars break down?

Study Findings

At age 40, the answer was unclear. Cardiac events were rare in this young group, so the study did not have enough of them to detect a pattern.

By age 50, the pattern was unmistakable. The researchers split the zero-calcium group into four tiers of lifetime LDL exposure. The lowest tier had averaged about 76 mg/dL over 25 years, the highest about 140. The highest tier had 3.4 times the risk of a cardiovascular event. Same zero score for everyone. Very different outcomes.

The absolute numbers stayed modest: 3.9 percent of the high-exposure group had an event over roughly 10 years versus 1.3 percent of the low-exposure group, so a zero still marks a lower-risk group overall. But within it, the cars that spent 25 winters on salt broke down at three times the rate of the others. Visible rust or not, the salt left its mark.

It is not speculation. Studies using CT angiography, a scan that can see soft plaque, found uncalcified plaque in 5 to 28 percent of people with a calcium score of zero, the low end in healthy screening populations, the high end in people with symptoms or heavy risk factors. Corrosion under the paint.

Here is the concept I want you to take away. Doctors measure smoking damage in pack-years, packs per day multiplied by years smoked. Your arteries work the same way. What matters is not your LDL cholesterol today but your LDL cholesterol multiplied by every year you have carried it. Call them cholesterol-years. An LDL of 140 mg/dL for 25 years is a very different disease than 140 for 2 years, even if the lab report looks identical. A calcium scan cannot measure cholesterol-years. Your past blood tests reveal the exposure, and CT angiography can reveal some of the plaque that accumulated along the way.

Why age changes the meaning of zero

Here is the part people often miss. The same zero means different things at different ages.

A car driven on salted roads for 40 years with no rust has proven something. A 5-year-old car with no rust tells you much less. There has just not been enough time. Same with arteries. A zero at the age of 70 is unusually strong evidence of low risk. A zero at 45 is still good news for the near term, but it says less about lifetime risk, because plaque may not yet have accumulated enough calcium to become visible. This is even more true for women, whose plaque tends to calcify later than men’s. A woman in her 40s or 50s can carry meaningful soft plaque with a spotless calcium score.

If your score is zero but your lifetime cholesterol exposure is high, the logical next conversation with your doctor is whether your overall risk warrants treatment despite the zero. In selected cases, particularly if symptoms or real diagnostic uncertainty remain, your doctor may consider a CT angiogram. I covered both tests in Post #60 and Post #71.

And if your score is not zero

The flip side is not ambiguous at all. Fewer than 1 in 10 people in their early 40s have any detectable calcium. If you are one of them, like I was at 43 with a score of 266, you are seeing rust on a young car.

Two terms before the numbers. Coronary events mean trouble in the heart’s own arteries, mainly heart attacks and deaths from them. Cardiovascular events cast a wider net that also counts strokes and other major blood vessel problems. Every coronary event is cardiovascular, but not the reverse.

To make the numbers easy to compare, I will use the same yardstick throughout: out of 100 people, how many have an event over roughly a decade. The baseline is people the same age with a score of zero. In CARDIA, 1 to 4 of every 100 zero-scorers had a cardiovascular event over a decade, depending on lifetime LDL exposure. Against that baseline, any calcium at all around age 40 was associated with about three times the risk of a cardiovascular event over the following 12 years, and about five times the risk of a coronary event in that same window. These are not lifetime numbers; risk keeps compounding even after the study window closed. A score of 100 or more at that age was outright dangerous: in that small group, about 22 percent died over 12.5 years of follow-up, ten of the thirteen deaths adjudicated as coronary events. Thirteen deaths is a small number, so the exact percentage is imprecise, but the signal is striking. My 266 at 43 put me in exactly this group. It was the wake-up call that started everything I now write about.

By the early 50s, the gap remains wide. These numbers come from a second large study, MESA, which reports ten-year risk, the same window your doctor’s risk calculator and the statin guidelines use, and its events include strokes as well as heart attacks. Among participants aged 45 to 54 with a zero score, about 1.7 in 100 had a major event over a decade. A score of 1 to 100 roughly doubled that, to 3.8 in 100. A score above 100 pushed it to roughly 15 to 16 in 100, a level that strongly supports lipid-lowering therapy.

So the decision table is simple. Zero plus low lifetime LDL cholesterol provides genuine reassurance, and if you are older with low apoB too, you are in a good place. The scan is most trustworthy when everything else points the same way. Zero plus high LDL or high apoB under the age of 55 is the exact trap this study exposes. The scan looks clean precisely because you are young, so keep a close watch, and depending on your overall risk and whether treatment is deferred, your doctor may suggest repeating the scan in roughly three to seven years. Do not let the zero talk you out of treating the lipids. The salt is still salt. And anything above zero at the age of 40 or 50, act now.

So what should you consider doing next?

First, know your LDL cholesterol number, and know it early. The study group that got into trouble averaged 140 mg/dL. That is a number many people walk around with for decades because no one calls it an emergency.

Second, and this is the strongest recommendation in this post, get an apoB test at your next blood draw, not once you already have a problem. As we saw earlier, apoB counts the particles that actually cause plaque, and it can disagree with LDL cholesterol. Two people with identical lipid panels can carry very different particle counts. The mismatch is especially common in South Asians, people with insulin resistance or diabetes, and anyone with high triglycerides. Which describes a large share of the people reading this. The test is cheap, and the 2026 guidelines give apoB a larger role in identifying residual risk and deciding whether lipid-lowering treatment should be intensified, something I covered in Post #71. European guidelines and many prevention-focused physicians use approximate apoB goals below 100, 80, or 65 mg/dL as cardiovascular risk rises (I recently saw a lab report that listed an apoB range of 50 to 132 mg/dL as acceptable!). These are not universal targets, so discuss the right goal with your doctor.

Third, get your Lp(a) tested once in your life. Lipoprotein(a), pronounced “L-P-little-a”, is a cousin of LDL set almost entirely by your genes. Roughly 1 in 5 people worldwide carries an elevated level, though prevalence and risk vary across ancestral groups, and diet and exercise barely move it. In our analogy, high Lp(a) is a car that left the factory with thin paint. The same salt corrodes it faster. For most people, one properly measured result settles the question, because Lp(a) is largely genetically determined and stays relatively stable through life. A high result is not helplessness, it is clarity: you manage everything you can control, your apoB, blood pressure, and blood sugar, more aggressively.

Fourth, remember that every year counts. Lowering your LDL and apoB at the age of 45 instead of 60 is like moving to a state with no road salt 15 years earlier. The car ages differently from that point on. I substantially changed my risk trajectory after 2015 with food, exercise, and yes, medication when the numbers called for it.

As for my friend, I sent him the study the day after our call. He is getting his apoB and Lp(a) tested at his next physical. His zero is still good news. But now he knows what it does and does not mean. References are attached below if you would like to read further.

As always, I would love to hear your thoughts and experiences in the comments.

References

Peng AW, Razavi AC, Wilkins JT, et al. Impact of LDL-Cholesterol When the Coronary Artery Calcium Score Is 0: Long-Term Cardiovascular Events. Journal of the American College of Cardiology. 2025;86(9):676-680. doi:10.1016/j.jacc.2025.06.053
Friedman GD, Cutter GR, Donahue RP, et al. CARDIA: study design, recruitment, and some characteristics of the examined subjects. J Clin Epidemiol. 1988;41(11):1105-1116.
Nasir K, Cainzos-Achirica M, Valero-Elizondo J, et al. Coronary Atherosclerosis in an Asymptomatic U.S. Population: Miami Heart Study at Baptist Health South Florida. JACC Cardiovasc Imaging. 2022;15(9):1604-1618.
Carr JJ, Jacobs DR Jr, Terry JG, et al. Association of Coronary Artery Calcium in Adults Aged 32 to 46 Years With Incident Coronary Heart Disease and Death. JAMA Cardiology. 2017;2(4):391-399.
Budoff MJ, Young R, Burke G, et al. Ten-year association of coronary artery calcium with atherosclerotic cardiovascular disease events: the Multi-Ethnic Study of Atherosclerosis (MESA). Eur Heart J. 2018;39(25):2401-2408.

Nickhil Jakatdar is the CEO of GenePath Diagnostics and the founder of PreventiveHealth.ai, working to make advanced diagnostics and credible health guidance more accessible, affordable, and actionable. A PhD in EECS from UC Berkeley and the youngest recipient of the UC Berkeley Distinguished Alumnus Award, he has founded and led multiple tech companies. He holds 60 patents, and serves on several academic, healthcare, and innovation boards. To follow his thinking on preventive health, technology, and systems that scale expertise, join his private WhatsApp community and subscribe to his Substack.

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