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The Proof

My Plaque Protocol, and Why I Started a PCSK9 Inhibitor | Simon Hill, MSc

56 min episode · 2 min read

Episode

56 min

Read time

2 min

Topics

Fundraising & VC, Artificial Intelligence, Crypto & Web3

AI-Generated Summary

Key Takeaways

  • ✓Cumulative LDL exposure: Atherosclerosis risk is determined by lifetime ApoB exposure, not current levels. Hill carried LDL around 125 mg/dL for 30 years before shifting to a plant-based diet at age 30, dropping LDL into the 70s. Plaque accumulated during those earlier decades does not reset when diet improves, making early intervention the highest-leverage action available.
  • ✓Plaque quantification platform variance: Three platforms analyzing identical CCTA scans produced total plaque volumes of 11.5, 60, and 74 cubic millimeters — a sixfold spread. AI-based platforms (Clearly, HeartFlow) likely overestimate soft plaque versus human-reviewed QAngio. When tracking plaque serially, use one platform consistently; switching platforms between scans makes change data meaningless.
  • ✓Rapid progression threshold as the key metric: Regardless of which platform is used, the clinically meaningful benchmark is percent atheroma volume increasing by one or more percentage points per year — defined as rapid progression. All three of Hill's analyses came in well below this threshold, making that consensus the most reliable takeaway from multi-platform disagreement.
  • ✓PCSK9 inhibitor selection rationale: Hill chose Repatha (evolocumab) over a statin for three reasons: injection adherence (every two weeks versus daily pill), a favorable side-effect profile for a lean, insulin-sensitive individual, and completed cardiovascular outcomes trial data showing both LDL reduction and event reduction — including the GLAGOV imaging trial demonstrating plaque regression down to 20 mg/dL LDL.
  • ✓Scan interval validity: The American College of Cardiology recommends a minimum two-to-five-year interval between serial CCTA scans using the same scanner and settings. Hill's 16.5-month interval, combined with low absolute plaque volume, means measurement noise can easily mimic a dramatic result. The REACT study, the largest asymptomatic atherosclerosis imaging study, uses a six-to-eight-year rescan window.

What It Covers

Simon Hill, MSc, details the 16.5-month lifestyle protocol behind his coronary plaque scan results, explains why three different AI and human-reviewed analysis platforms produced wildly divergent readings of the same scans, and reveals his decision to start Repatha (evolocumab), a PCSK9 inhibitor, targeting an ApoB of 40 mg/dL.

Key Questions Answered

  • •Cumulative LDL exposure: Atherosclerosis risk is determined by lifetime ApoB exposure, not current levels. Hill carried LDL around 125 mg/dL for 30 years before shifting to a plant-based diet at age 30, dropping LDL into the 70s. Plaque accumulated during those earlier decades does not reset when diet improves, making early intervention the highest-leverage action available.
  • •Plaque quantification platform variance: Three platforms analyzing identical CCTA scans produced total plaque volumes of 11.5, 60, and 74 cubic millimeters — a sixfold spread. AI-based platforms (Clearly, HeartFlow) likely overestimate soft plaque versus human-reviewed QAngio. When tracking plaque serially, use one platform consistently; switching platforms between scans makes change data meaningless.
  • •Rapid progression threshold as the key metric: Regardless of which platform is used, the clinically meaningful benchmark is percent atheroma volume increasing by one or more percentage points per year — defined as rapid progression. All three of Hill's analyses came in well below this threshold, making that consensus the most reliable takeaway from multi-platform disagreement.
  • •PCSK9 inhibitor selection rationale: Hill chose Repatha (evolocumab) over a statin for three reasons: injection adherence (every two weeks versus daily pill), a favorable side-effect profile for a lean, insulin-sensitive individual, and completed cardiovascular outcomes trial data showing both LDL reduction and event reduction — including the GLAGOV imaging trial demonstrating plaque regression down to 20 mg/dL LDL.
  • •Scan interval validity: The American College of Cardiology recommends a minimum two-to-five-year interval between serial CCTA scans using the same scanner and settings. Hill's 16.5-month interval, combined with low absolute plaque volume, means measurement noise can easily mimic a dramatic result. The REACT study, the largest asymptomatic atherosclerosis imaging study, uses a six-to-eight-year rescan window.

Notable Moment

When Hill ran the same two CCTA scans through three separate analysis platforms, one showed 48% plaque regression, one showed 20% progression, and one showed near-zero change — meaning the headline result and its opposite both came from identical source images, exposing how unreliable short-interval plaque quantification currently is.

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Episode Transcript

A few weeks ago, I shared my own heart scans and the amount of regression was dramatic. In sixteen and a half months, the plaque in my arteries had dropped by 48%. And the top comment on this video, how did you do this? And underneath that, person after person asking the same thing. One person said the whole episode felt like a bait and switch, that they were never going to find out how to actually reduce plaque. Fair enough. That episode though was about my results. This one today is how I got them and whether that 48% was even real. Because here's the part that might seem strange. Despite that number, I've started a prescription medication to lower my blood lipids. In this episode, I'll tell you exactly which one and why. Quick housekeeping before we get into things. This, of course, is not medical advice. It's one person's process, and your numbers belong with your doctor. If you're new here, I'm Simon Hill, physiotherapist by training, masters in nutrition science from Deakin University in Melbourne, and I've interviewed hundreds of researchers and clinicians on this show since 2018. I have a particular interest in cardiovascular disease and track this disease in my own arteries, which is what today's episode is all about. I'll go as far as saying, I don't think anyone else on the Internet has had their coronary arteries analyzed this many ways and then been silly enough to publish all of it. Some might even say that this is a world's first. Take that for what it's worth, of course. It's hardly a competitive field. So a quick recap in case you missed the last episode on this topic. I've had serial coronary CT angiograms or CCTAs. These scans don't just tell you whether you have blockage. They allow you to quantify how much plaque is in your arteries and what type it is. So instead of being told that you have mild, moderate, or severe soft plaque, I got reports breaking it down. Soft plaque, calcified plaque, total volume, all in cubic millimeters. And just so we're clear, this isn't the plaque your dentist talks about. Different plaque, different body part. Though it would be pretty cool if we could floss our arteries. The first scan I had was in December 2024 at age 38, and then a follow-up scan sixteen and a half months later in April 2026 at 39. I've since turned 40. That's a whole another story, but happy birthday to me. Same imaging center both times, same scanner, same protocol at the Lundquist Institute in Los Angeles under the guidance of doctor Matthew Budoff, one of the world's experts on this type of imaging. Those scans, the baseline and the follow-up scan, were then analyzed by three different software platforms. On one of them, HeartFlow, my total plaque volume had dropped by about 48%. That's the number that ended up in the title of this episode. That's the …

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