Ketogenic Diet and HLA-B27: My n=1 Inflammation Experiment

In January, I ran a structured experiment on myself.

I carry HLA-B27 and, for a long time, I’ve dealt with a familiar pattern: morning stiffness, nagging hip and lower back pain, regular fatigue — including the kind of “crash” where motivation disappears and all you want is to lie in a dark room — and sleep that tends to break in the middle of the night.

After hearing compelling arguments about ketogenic diets in inflammatory conditions, I decided to stop theorizing and actually test it. Not casually. Properly. I wanted to know: if I went all-in on ketosis, would my symptoms shift in a meaningful way?

The setup

For a little over four weeks, I ate around 2000 kcal per day with fewer than 30 grams of carbohydrates. Protein was high (around 185 grams daily), and most of my fat sources were what you’d call “healthy fats” — olive oil, salmon, and avocado — although I also ate more saturated fat than usual. I had three eggs per day (which is worth mentioning, because it likely contributed to what happened later).

I kept the routine consistent: four meals a day (pre-workout, breakfast, lunch, dinner), with my last meal around 17–18. I supplemented with electrolytes and creatine in the morning and magnesium in the evening. Training stayed stable too: four strength sessions per week and two runs.

This wasn’t “trying keto.” It was a controlled, repeatable month with the same inputs — because I wanted to be able to trust the signal.

What changed — quickly

The first thing I noticed was how fast things shifted. Within weeks, the symptoms I’d been using as my personal inflammation dashboard basically disappeared. Morning stiffness was gone. Joint pain resolved. The fatigue crashes — which had felt like a recurring tax on my life — didn’t happen at all. I had stable energy throughout the day, felt satisfied after meals, and I didn’t need anti-inflammatory medication.

Even though symptom relief is subjective, the objective markers pointed in the same direction. My HRV improved, resting heart rate dropped, and my Whoop recovery metrics reflected lower physiological stress. Sleep was also noticeably better in the beginning.

Metabolically, I felt excellent. And from an inflammation perspective, the effect was hard to ignore.

The trade-off

But the story didn’t stay simple.

After a few weeks, sleep changed. I still fell asleep quickly, but I started waking up a lot — and when I woke up, I felt unusually alert. Not anxious, necessarily. Just… switched on. Wired.

More importantly, my LDL increased significantly. I may actually fit the Lean Mass Hyper Responder (LMHR) profile. And because I have elevated Lp(a), this isn’t something I can brush aside as a “temporary downside” or a debate topic. Even if keto is anti-inflammatory for me, cardiovascular risk still matters.

That’s the tension.

Ketosis felt like it gave me my body back — but it also raised a long-term trade-off I’m not willing to gamble with. I don’t optimize for three months. I optimize for decades.

Where I am now

I’ve reintroduced carbohydrates and I’m no longer keto. Inflammation and fatigue have returned slightly, but not at the same level as before. The crash pattern is less frequent. The baseline feels better than it did pre-experiment.

So where do I land?

Right now, my takeaway is that a ketogenic diet can be a powerful short-term anti-inflammatory intervention for some people with HLA-B27. It may reduce symptoms fast, and the improvements can show up both in how you feel and in recovery metrics.

But for anyone with elevated Lp(a) or increased cardiovascular risk, the trade-off deserves real caution and proper monitoring.

The real question may not be “keto or not.”

It may be: how do we combine the inflammation benefits of ketosis with metabolic flexibility — and long-term cardiovascular safety?

This isn’t medical advice. It’s one structured experiment in one body.

And I’m continuing to refine.