After 7 Years, I Changed My Mind on Cholesterol Meds (Or Did I?)
🚨You'll want to read this one all the way though. Link at the end🚨
1/7) After seven years of living with astronomically high cholesterol, I’ve decided to start two medications. Not statins, but ezetimibe and bempedoic acid.
But that’s NOT the real story. The real story is WHY… and it has nothing to do with cholesterol🤨🤔...
Quick preface: “cholesterol-lowering drugs” are named for one effect, not their full biological impact.
Molecules don’t respect our labels. These drugs can influence multiple systems, including metabolism and brain health.
And in this case, they likely do.
2/7) Take ezetimibe. Beyond lowering LDL, evidence suggests it crosses into the brain and influences neurobiology.
Specifically, is disrupts the interaction between 14-3-3 and hexokinase, reducing protein aggregation.
Full video:
3/7) That means less amyloid, less tau, and even improved autophagy.
Even more interesting: retrospective analyses have found up to an ~8x lower risk of Alzheimer’s in patients on ezetimibe.
Not causal. Not definitive. But a signal worth paying attention to—especially in the right context.
4/7) Then there’s bempedoic acid. New research (Cell Metabolism, May 2026) suggests even its “inactive” form is biologically active—binding PPAR-alpha.
That matters because PPAR-alpha can shift amyloid processing toward a neuroprotective pathway.
(image modified from Norwitz et al. 2019)
5/7) So no, this isn’t a story about “I changed my mind and lower cholesterol is better.”
It’s a story about nuance, mechanisms, and staying open to new evidence. Don’t let labels or dogma do your thinking for you.
But there’s more…
6/7) But let me pause and make an important aside.
Speaking directly to those who have followed the research my colleagues and I have been doing on cholesterol, particularly in the context of the very real lean mass hyper-responder phenotype cc @PeterAttiaMD: I recognize that this work has raised a lot of questions… and just as many misrepresentations.
So let me be clear:
This is not a pivot. It’s not an attention grab.
For those who have actually been following the thread, the message has always been the same:
Interpret data with an open mind, and within your individual context.
And don’t let other people’s caricatures of what they think you believe dictate how you think.
In my case, I’m more than willing to look at molecules traditionally labeled as “cholesterol-lowering drugs,” recognize that they may have multiple biological effects, and use those effects as tools where appropriate.
That’s not inconsistency. That's perfect consistency if you've been following our work, rather than some manipulated cartoon version of it.
Now, of course, some will try to twist this message to fit their own narrative.
Because, frankly, much of modern cardiology—and medicine more broadly—still treats LDL cholesterol as the central pillar of health, rather than what it may actually be: one very small piece of a much larger and more complex system.
But let’s not let that kind of closed-mindedness spread.
Science is not settled. It never is. Stay open. Stay rigorous. And above all—stay genuinely curious.
7/7) But now, for the moment of truth. Because for nearly 7 years, I’ve been running a natural experiment: total cholesterol ~700 and off-the-charts ApoB. If conventional thinking holds, my arteries should be full of plaque.
So, let’s test it. I’m getting an advanced coronary CT angiography with expert and AI analysis.
Let’s see what the data actually say. Any guesses?
1/5) Here are four things statins do in your body.
First: A human controlled trial found statins reduced GLP-1 levels by 50% in 16 weeks.
The clinical implications aren’t fully clear—but the fact this isn’t discussed is a disservice to science and to patients.
2/5) Statins disrupt mitochondrial function.
They reduce CoQ10 synthesis (a key electron carrier) and directly inhibit Complex IV in the electron transport chain. These are biochemical effects—but they matter for informed decisions. staycuriousmetabolism.substack.com/p/the-mitochon…
3/5) Statins are sexist. Women face higher risk of muscle pain, potential muscle loss, and statin-induced diabetes.
Eating 1000 Sardines Gave Me THIS Superpower
(New 2026 Findings!)
1/8) I ran a self-experiment where I ate 1000 sardines in a month.
Sure, it made me stink—but it also gave me one epic superpower. Let me explain. 🧵 (link at the end)
We all know sardines make your breath stink and that they’re nutrient-dense.
That’s basic.
But eating that many sardines changed me. It gave me a “superpower” that had my inner Marvel nerd activated—and my scientist brain scrambling to explain it.
Eventually, I found those data.
2/8) It was new paper in a top journal turned confusion into clarity and left me in awe of how much we’re still uncovering about human physiology.
1/5) One meta-analysis of controlled human trials found that citrus bergamot extract lowers triglycerides, increases HDL, and lowers LDL — to a substantial degree.
But that’s not all... (link at the end)
2/5) More interestingly, one trial showed that while bergamot decreased small dense LDL, it increased‘large, fluffy’ LDL.
This shift towards a preponderance of large LDL vs small LDL is a metabolic fingerprint of improved metabolic health.
3/5) So how does citrus bergamot work?
Citrus bergamot isn’t a single nutrient — it’s a cocktail of polyphenolic compounds that influence multiple metabolic enzymes.
For example, the bergamot polyphenols inhibit the enzyme ACAT, contributing to downstream increase LDL receptor expression.
A strange new 2026 study suggests compounds in garlic might:
👉Extend lifespan (11.4% in animals)
👉 Improve insulin sensitivity (lower glucose and insulin levels)
👉Reduce fatty liver & reduce inflammation
Let’s break down this bizarre but compelling research.
2/7) Garlic is rich in diallyl sulfides (DAS) — sulfur compounds that increase hydrogen sulfide (H₂S) levels. H₂S acts like a hormone: it diffuses through membranes, triggering cellular pathways across the body.
Researchers fed mice a diet enriched with DAS, leading to an 11.4% increase in lifespan, more than double the effect of metformin.
3/7) Furthermore, on a glucose tolerance test, DAS-treated mice showed: Lower total glucose and much lower insulin levels
How Sleep Deprivation Causally Drives Atherosclerosis
1/5) It’s well established that poor sleep is associated with an increased risk of cardiovascular disease.
But the big question has always been: How… Exactly?
Impressive research published in Nature — one of the world’s top scientific journals — reveals a fascinating biological mechanism. (link at the end)
2/5) To test for a causal connection between sleep deprivation and atherosclerosis (the buildup of plaque in arteries), researchers sleep-deprived mice genetically predisposed to developing atherosclerosis.
Compared to well-rested healthy control mice, the sleep-deprived mice developed significantly more atherosclerotic plaque (quantified on the right).
But that’s not all…
3/5) The sleep-deprived animals also accumulated more inflammatory immune cells inside their arteries — the very cells that drive plaque formation and instability.
Below you can see a quantification of the immune cells (three types) in the arteries of sleep deprived animals (green) versus healthy controls.