I Was Doing Almost Everything Right. It Wasn’t Enough.
I need to tell you something I’ve been circling around for the last four posts.
I’ve told you about the blockage. I’ve told you about the science the keto world gets wrong. I’ve told you about the tests that missed it and the fight to get the one that didn’t. But I haven’t told you this part yet: I wasn’t some guy who let himself go. I wasn’t the patient you’d look at and think, yeah, that makes sense.
I was doing almost everything right. And it wasn’t enough.
BOTTOM LINE
I had the perfect biohacker resume — three decades of training, the supplement stack, the wearables, the diet, the academic credentials, access to Mayo cardiologists. None of it caught a year-by-year arterial decline that the standard risk markers said wasn’t happening. The system isn’t built for the patients quietly accumulating damage in the gaps between the standard risk factors. This is the post where I stop telling the story and start asking why.
The Resume Nobody Expected to Fail
I’ve worked out consistently since I was fourteen years old. Athlete through high school. Personal trainer after that. Thirty years of never taking more than a week off. My body was a project I took seriously, and I was proud of the work I’d put in.
By the time the blockage was found, I had an ice bath in my garage. A Joovv red light panel. An Eight Sleep mattress that tracked and regulated my sleep temperature every night. An Oura ring on my finger and an Apple Watch on my wrist, both feeding me data on sleep, HRV, resting heart rate, and recovery. And on multiple occasions I had a glucose monitor (CGM) in my tricep just to make sure I was staying on track with metabolic health. I had been experimenting with intermittent fasting for years. I’d dabbled with NMN before most people had ever heard the letters. My supplement stack was researched and intentional, not something I grabbed off a shelf at GNC.
I read the papers. Not blogs about the papers. The actual papers. I have a graduate degree in bioinformatics from a joint program between the University of Minnesota and Mayo Clinic. I studied molecular biology, biochemistry, pharmacology, systems biology, and computational biology, then tied it all together and got published in cancer epigenetics research. Following that I decided I wanted to get into medicine and work as a board certified emergency nurse in the emergency department, while completing training to become an advanced practice provider via Duke. I work at Mayo Clinic. I doctor at Mayo Clinic. I have direct access to some of the best specialists on the planet.
All of which is to say: I wasn’t winging it.
At the end of the day, there are really only two reasons people work out. I used to say the first is to look better in a swimsuit. The second is to be healthier and hopefully live a longer life surrounded by their family and playing with grandkids. I was doing just fine for age 44 on the first one. I assumed that meant I was also doing okay on the second.
I wasn’t.
The Moment I Can’t Shake
I’ve mentioned the phone notification on the interstate. The words “critical result” and “severe, flow-limiting occlusion.” I’ve told you I pulled over. But I haven’t told you what I was actually thinking in that moment.
I thought it was wrong.
Not in the way where you’re bargaining with bad news. I genuinely, clinically believed the result was an error. I had been doing all the things we’ve been told to do with diet and exercise for thirty years. I was in the best shape of my life. I had a pristine heart artery scan only eight years earlier. Zero disease. Not a speck. So, when I spoke to my doctor the next day and he said they would need to quickly schedule an angiogram to see if I needed an immediate stent, I thought they were going to get in there and say, oops, wrong guy. Sorry for the scare. Let me send you home.
That didn’t happen. What happened was a stent and a cardiologist telling me that I was lucky to get this done when I did as only a few red blood cells at a time were making it past this block in my right coronary artery and the entire inferior part of my heart was not getting the oxygen and nutrients it required.
But the denial didn’t break in the cath lab. It broke slowly, over weeks that turned into months, as I started going back through my own data. My own choices. My own stack. And I started seeing what I hadn’t wanted to see.
The Cracks
I was doing ninety percent of things right. It’s the other ten percent that I keep coming back to.
The diet. I spent roughly a decade on a high-fat, low-carb ketogenic diet. At times full carnivore. I didn’t find keto from some Instagram ad. I found it while researching cancer metabolism during my bioinformatics work, and the science behind glucose restriction in cancer had legitimate roots. But somewhere between the Warburg effect and the occluding chunk of soft cholesterol plaque in my right coronary artery, I stopped questioning whether what was good for starving a tumor and losing bodyfat was also good for the lining of my blood vessels. The podcasters I trusted, some with MDs behind their names, said as long as my metabolic markers were clean, elevated LDL was nothing to worry about. My metabolic markers were spotless. My artery was not.
The LDL I ignored. My LDL cholesterol ran between 130 and 150 for most of my adult life. Occasionally it touched 160. I always attributed it to the diet. I had a genetic test done: no familial hypercholesterolemia. My fasting glucose was excellent. HbA1c was clean. hsCRP was rock bottom. The internet consensus in the communities I followed was clear: if you’re metabolically healthy, LDL doesn’t matter. I believed that for a long time. Ten years, roughly. Ten years of particles entering my arterial wall while I was being told the door was locked.
The blood pressure I dismissed. My blood pressure hovered in the low 130s over mid-80s. Sometimes upper 80s on the diastolic side. Not horrible. Not the kind of numbers that automatically got you a prescription. Just… not optimal. I knew what the guidelines said. I knew what optimal looked like. I wrote it off as white coat effect or stress or just close enough. It was always “close enough.”
The training I never adapted. I was doing the same thing at 44 that I’d been doing at 22. Resistance training. High intensity intervals. Go hard, recover, repeat. No such thing as Zone 2 in my vocabulary. No long, slow cardio sessions. No meditation. No yoga. Just hard effort, four to five days a week, thirty years straight. I used to joke that I was on the “still look good naked in front of the mirror” workout plan. It was funny because it was true. Everything about how I trained was oriented around how I looked and how I performed in the gym. Not around what was happening inside my arteries at a cellular level.
None of these are catastrophic failures on their own. A lot of people reading this probably have numbers that look like mine did. That’s exactly the point.
The Math That Doesn’t Add Up
Here’s what I keep coming back to, and I don’t have an answer yet.
I went from a pristine scan at 39 to a 80% blockage requiring a stent at 44. LDL in the 130s. Blood pressure in the low 130s. No family history of early heart disease, metabolically healthy, rock bottom hsCRP, and all backed up by genetic testing. Never smoked. Worked out for thirty years. None of these numbers, alone or together, should produce that kind of progression in eight years.
I know how to look for root causes. It’s literally what I was trained to do. In my bioinformatics program, you don’t study diseases. You study the molecular machinery underneath them: why a cell changes, what pathway breaks, what upstream signal went wrong. I spent years studying histone modifications as a root cause of cancer drug resistance. That kind of thinking doesn’t turn off when you leave the lab. When something doesn’t add up, you dig until it does.
I’ve been digging for a just over a year now. I am just now starting to get closer to something. And I’m doing it largely on my own, because the medical system, even at the number one hospital in the world where I work, doesn’t have a mechanism for this. The stent went in. The artery is open. Repeat CTCAs look great. EKGs are perfect. Repeat stress echo passes with flying colors. And my ApoB, a more advanced measure of cholesterol that we’ll get into in a future post, is rock bottom. The acute problem is solved and the easy culprits to point a finger at are solved. But, nobody is asking why a 44-year-old with borderline numbers went from zero to critical in less than a decade and when I press, there is no solid answer. What was the true molecular cause allowing this to happen so quickly? Unfortunately the medical system isn’t built to always easily answer that question.
I think about that a lot. I have the training to look for root causes at the molecular level. I have clinical experience that lets me connect what I see at the bedside to what’s happening inside a cell. I have access to the best specialists in the world. And even with all of that, it took me a year to start getting close.
Now think about the guy who doesn’t have any of that. The 42-year-old who works out, eats what he thinks is right, gets told his numbers are “fine,” and never gets the scan because nobody thinks he needs it. What’s his version of this story?
That’s what this newsletter is about. That’s what I’m building toward.
Something was accelerating the damage inside my arteries that doesn’t show up on a standard blood panel. Something biological. Something deeper than the risk factors my doctors were trained to look for. I don’t know exactly what it is yet. But I’m getting closer, and I’m going to take you with me.
Next week, I’m starting with the crack that haunts me the most: the diet I thought was protecting me.
If you have borderline numbers and a doctor who told you everything is fine, I want to hear from you. If you pushed for a test that changed everything, I want to hear that too. Hit reply or find me on LinkedIn or X.
This is not medical advice. It’s one clinician-scientist’s reckoning with his own data. Discuss your health decisions with your physician.