Estimating My Heart Disease Risks

Details of my attempts to understand and deal with high cholesterol

May 7, 2021

Estimating My Heart Disease Risks

Updated: May 7, 2021


My LDL (“bad”) cholesterol has been high (well above 150 mg/dL) since I started measuring it in my mid-20s. While my HDL-C (“good”) levels, and even the ratio between them has always been in the healthy range, my recent unexplained drop in Apple Watch VO2 Max levels has me wondering if I should revisit the affect this has on my heart health.

My History of High Cholesterol

I have no family history of cardiovascular disease. Both my parents are in their 80s and healthy. My grandparents who lived into their 90s died of other ailments. There are some strokes in the family, but always in people well over 80 years old.

My blood cholesterol levels have been high since I began measuring in my 20s. During my 40s, after marriage and children reminded me of my obligations to my family, I became convinced that I should control my high levels through statins, and for about ten years I took 20mg of simvastatin, with great results.

R Sprague Cholesterol over time

A major factor in my decision to take statins was the landmark “4S” study that showed a decrease in all-cause mortality statin users. The study convinced me because unlike many so-called “proofs” of statin effectiveness, this was a large randomized trial that looked at overall death rates, including from seemingly unrelated causes. In other words, even if statins come with unknown unexpected side effects, the consequences still result in longer life among those who take them compared to those who don’t. Case closed.

Or so I thought. Eventually as I became more skeptical of drug interventions in general, I noticed an important caveat in the study: the trial participants all had a history of heart disease – many of them quite serious. But that’s not me, and it’s not my family either, so out of a general sense of caution about the long-term consequences of taking powerful medications, I stopped taking the statin. The history of medicine is littered with examples of “expert” advice that turned out later to be incorrect, and it seemed to me that, despite the good evidence that statins are safe and effective, it was dangerous to spend a lifetime taking a powerful therapeutic without good understanding of the root cause for my high cholesterol. Given my healthy family history, is it possible that such a powerful intervention might actually cause other problems, especially if taken daily over a lifetime?

Is My Heart Okay?

It’s important to remember to care about the heart, not cholesterol. A blood test, at best, is an indirect measure of health. If high blood cholesterol is a factor in heart disease, it is only because it has an effect on the heart itself, or on the rest of the circulatory system through hardening or blockage of the arteries. Rather than an indirect measure like LDL-C, wouldn’t it be better to measure those effects directly?

Fortunately, there are many low-cost ways to find evidence of arterial blockage or thickening. For under $100, I found a local imaging center that could test me.

A CT calcium scan is a simple procedure where you lie down, fully clothed, as an expensive machine scans your body for signs of calcium that can form in blood vessels, presumably from long exposure to calcifying cholesterol. The resulting coronary artery calcium (CAC) score is a simple estimate of how hardened the arteries are.

I’ve tested a few times, before and after ending statins and found that my CAC is quite low. Measured on the Agatston scale, my numbers were always well under 50, probably ten times lower than you’d expect if there were problems.

CT Scan Results

Another test, Carotid Intima-Media Thickness (CIMT), showed similarly very clear arteries (under 0.50 mm).

These results, combined with my lack of other risk factors, made me feel vindicated for having given up statin therapy. I discussed my situation with several different doctors. While nobody was happy with my high LDL-C levels, they agreed that long-term therapies have other consequences; given my otherwise healthy lifestyle, nobody could make a case for why one risk significantly outweighed the other. I continued to get regular exercise, maintaining a healthy diet and weight, and of course kept my regular schedule of annual physicals and frequent contact with my doctor.

Based on evidence that the standard measurements of LCL-C don’t show the whole picture, I tested two other components with contradictory results.

  • Apolipoprotein B (ApoB) 141 mg/dL (“dangerously high”).
  • Lipoprotein(a): 22 nmol/L (“optimal”)

Meanwhile, my high HDL-C (“good”), low triglycerides, and the various ratios that appear to matter all seemed to point toward “no problem”. I wasn’t going to worry about it.

Then, in the summer of 2020, despite my regular exercise, I began to notice a disturbing trend in both my self-perceived levels of fitness and in the VO2 Max estimates made by my Apple Watch. Climbing stairs quickly never bothered me, but even my wife began to notice how winded I appeared to get after such a simple activity. And I noticed a decisive plunge in my VO2 Max:

Sprague VO2Max Estimate from Apple Watch

Because my Apple Watch tracks my heart rate along with my movement, it’s possible to roughly estimate my overall fitness as measured by the maximum volume (V) of oxygen (O2) my lungs can handle, the so-called “VO2 Max”. Considering the exercise I do, my numbers were mysteriously never all that great for my age, but the recent steep drop was enough for me to consult with my doctors again.

Not only that, but I noticed a long-term increase in my resting heart rate. Apple Watch shows a clear year-over-year pattern:

Year-Over-Year Changes in My Resting Heart Rate

A cardiologist couldn’t detect anything unusual in his careful examination of my heart at rest. But he emphatically insisted that I return to statin therapy immediately. While there are always outliers, my very high LDL-C combined with my body’s tolerance for statins, made this a no-brainer, he said. My low CAC wasn’t necessarily a good indication of my risks, particularly for stroke, since a CT scan won’t see the “soft” cholesterol deposits that haven’t yet formed into calcium. A blood vessel could be 80% blocked, he said, without showing signs of calcification.

So I began taking statins again. The cardiologist recommended atorvastatin (aka Lipitor), at a more aggressive 40mg dose. After a month of daily use, my cholesterol declined, and after two months it was back to the levels I’d seen when I’d used statins a decade before.

Cholesterol levels since 2020

Incidentally, as expected note how my LDL-C rises dramatically when eating a low-carb, high-fat (“Ketogenic”) diet.

One more incidental observation: the significantly lower results from the April 1 test followed three days of heavy eating on my version of the Feldman protocol: more than 3K calories/day, at least half of which were fat.

The Case for Statins

The most up-to-date (updated 2019) guidelines from the American College of Cardiology are clear for somebody like me with LDL-C > 200. I am at high risk, period, and should be on aggressive statin therapy regardless of other risk factors.

In patients with severe primary hypercholesterolemia (LDL-C level ≥190 mg/dL aka ≥4.9 mmol/L), without calculating 10-year ASCVD risk, begin high-intensity statin therapy. If the LDL-C level remains ≥100 mg/dL (≥2.6 mmol/L), adding ezetimibe is reasonable. If the LDL-C level on statin plus ezetimibe remains ≥100 mg/dL (≥2.6 mmol/L) and the patient has multiple factors that increase subsequent risk of ASCVD events, a PCSK9 inhibitor may be considered, although the long-term safety (>3 years) is uncertain and economic value is uncertain at mid-2018 list prices.

Years of taking 20mg of simvastatin lowered my LDL-C below 100, so probably I don’t need the extra ezetimibe boost.

American College of Cardiology Lifetime ASCVD Calculator says my lifetime risk is 50% based on my Sept 2020 blood test results.

American College of Cardiology Risk Assessment

The dangerous association between high LDL cholesterol and heart disease is abundantly clear. For example, see this lengthy review in Goldstein and Brown (2015):

summarizes the scientific evidence that converged from multiple disciplines to implicate cholesterol-carrying low-density lipoprotein (LDL) as the instigator of atherosclerotic plaques and high dietary fat as the major cause of pathologic LDL levels

Cochrane Reviews (2013) concludes that statins are a good idea for preventing heart attacks:

Of 1000 people treated with a statin for five years, 18 would avoid a major CVD event which compares well with other treatments used for preventing cardiovascular disease. Taking statins did not increase the risk of serious adverse effects such as cancer. Statins are likely to be cost-effective in primary prevention.

There are exceptions. For example, a 2016 Review (Ravnskof et al) says that, among people over age 60, LDL appears not to make a difference in mortality. My 80-year-old mother, who with my same blood type is still healthy and well despite cholesterol levels similar to mine.

The Case Against Statins

But maybe LDL-C isn’t the whole story. I’ve tested a few other parameters, so what do they say about my overall risk?

My apoB is between 140 mg/dL (Sep 2020) and 170 (Feb 2019) which “constitutes a risk-enhancing factor”. Although I should be careful relying on this number because some labs may not measure it reliably, different labs show consistent results for me, so I think it’s likely I’m at risk. According to Grundy et al (2019):

Because apoB is the major apolipoprotein embedded in LDL and VLDL, several investigators identify strength of association between apoB and ASCVD

Still, InsideTracker (2021) thinks ApoB is not yet worth measuring:

there is not currently enough research to determine an optimal zone or specific recommendations to be developed for particle size and ApoB, which are both necessary for a biomarker to join the InsideTracker platform. Because of the continued need for further research, InsideTracker does not include LDL particle size or number in our lipid panels just yet.

On the other hand, my Lp(a) is around 22 nmol/L, out of the risk range.

an Lp(a) ≥50 mg/dL or ≥125 nmol/L, Lp(a) may be considered a risk-enhancing factor

Still, the guidelines suggest you only bother testing Lp(a) if you’re unsure about the other risk factors.

Similarly, coronary artery calcium (CAC) is useful for borderline cases, but any Agatston score above 0 “favors statin, especially after age 55”. My scores hover below 50, but never 0, so once again this is a case for statin therapy.

It’s not hard on the internet to find credentialed cardiologists who think LDL-C by itself isn’t especially predictive. For example Dr. Mark Houston is a cardiologist who says

If you look at total LDL you cannot predict anything about risk, what the treatment is going to do and how far you need to drive the LDL down. So total levels, no matter whether you’re looking at, HDL or LDL, to my reading, are non useful information.

Instead, he thinks insulin response is more important. (Mine insulin levels are fine).

Cholesterol Code

Dave Feldman is a fellow software engineer and, like me, a curious amateur, who proposes a condition he calls Lean Mass Hyper Responder (LMHR), characterized by people just like me with lipids:

  • LDL of 200 mg/dL (5.17 mmol/L) or higher
  • HDL of 80 mg/dL (2.07 mmol/L) or higher
  • Triglycerides of 70 mg/dL (0.79 mmol/L) or lower

His Cholesterol Code Report shows I’m at low risk on every one of the studies he tracks. I remain at low risk even after after a Keto Diet, where my LDL-C shot up to 300 nmol/dL.

I’m now following their 6K+ member Facebook group for more detailed discussions.

Echo Stress Test

The ultimate test of heart health is an echo stress test, and so in March 2021 I found myself on a treadmill, plugged into an EGK and blood pressure cuff. Under carefully controlled conditions, I ran as hard as I could so a specialist could study my heart with a live ultrasound.


The stress test said my heart is fine:

  • Stress ECG findings: No chest pain or ECG changes of ischemia noted. Exercise time: 12:37 min on Bruce protocol. Duke treadmill score = +12, which predicts a low risk for future adverse cardiac events at 5 years.
  • Arrhythmias: No significant arrhythmias.
  • Hemodynamic findings: Blunted BP response to stress
  • Stress Echo findings: There are no stress induced wall motion abnormalities with an adequate exercise workload. Stress echo is negative for ischemia.
  • Risk: This study predicts a low short-term risk for future major adverse cardiac events
  • Functional aerobic impairment (FAI): < -20 %
  • Age equivalent: 36 years

It completely contradicts the Apple Watch-estimated VO2Max that was driving my recent concerns.

Exercise capacity: Overall, the patient’s exercise capacity was excellent. The estimated VO2 max is 45.09 ml/min/kg.

and, based on the performance of others who’ve taken this test, it computes:

  • Workload achieved: 12.8 METS
  • Baseline heart rate: 85 bpm
  • Baseline blood pressure: 110/70 mmHg
  • Peak heart rate: 182 bpm
  • Peak blood pressure: 130/60 mmHg
  • Target heart rate: 139 bpm
  • % of max predicted heart rate achieved: 112%
  • Max predicted heart rate (220-Pt age): 163 bpm
  • Estimated VO2 max: 45.09 ml/kg/min
  • One minute heart rate recovery: 160 bpm

In other words, I passed the functional heart test with flying colors.


Other than stubbornly-high total and LDL cholesterol levels, I find it difficult to make a case for why I should be concerned about cardiovascular disease, at least in my current healthy state. I worry about my high LDL, but I worry about the long-term effects of a statin too.

For now I’ll continue taking the 40mg atorvastatin, but study other dietary ways to lower my cholesterol, such as reduced eating of saturated fats.