It's not often I come across a serum lab panel like the one below and see Lp(a) drop. 103.3 down to 15.1 nmol/L. An 85% drop. That's rare because Lp(a) typically doesn't budge. Changing up your diet won't do it. Exercise certainly won't do it, and statins aren't reducing it either. Historically, I've only consistently seen it drop with nandrolone, but in this case, no nandrolone was in place. And truth be told, it's really what prompted me to write this newsletter. Testosterone, methenolone enanthate (Primobolan) and drostanolone enanthate (Masteron) were included. The first time I came across a change like this, I was confused and thought it was a lab error. It wasn't. Naturally, my thought process went something like: "whoa, drugs are cool, I'm intrigued, now how does this work?" Before we get to how, here's a quick Lp(a) 101. A quick lesson on Lp(a) Lp(a) is an LDL particle with an extra protein attached, called apolipoprotein(a), or apo(a). (That's about as much science as we really need to know here.) It's largely genetically determined and an independent predictor of heart disease and calcific aortic stenosis. One large analysis estimated a single Lp(a) particle is about 6 times as harmful as a regular LDL particle. Your Lp(a) level is set mostly by one gene, LPA. Diet, training and statins don't meaningfully move it, so it's widely accepted you really only need to test it once. The risk cutoff is generally 50 mg/dL, or 125 nmol/L, depending on which unit your lab uses. A lean, fit 35-year-old with great LDL can still carry a high Lp(a) and have no idea- so this is your sign to check it if you haven't. That said, I’ve seen the same avatar who eats like a boring bodybuilder all year round, and still has a higher LDL-c, because Lp(a) is high. And don't confuse apo(a) with ApoA. ApoA (Apo capital A) lives on HDL, the "good cholesterol." Apo(a) (Apo little a) lives on Lp(a). It would be wonderful if the names weren't also confusing, but here we are, I don't make the rules.

Spent some time reflecting on body dysmorphia, the coaching space, and some of the philosophies I have about coaching in this one. I hope you enjoy! Side note, I'm working on a visual aid to help with the lectures I'm building. I'm a visual learner, and I think illustrating that as I discuss different mechanisms might help them land.

This is an ongoing log I will keep for my own progress and transparency. I'm leaving absolutely nothing out. Feel free to use this thread to ask specific questions related to the log itself or questions about what I'm doing. Please save any other non-log related questions for outside of this thread.

This is part 1 of my post-show labs taken back in June. I never recorded this previously but figured it would be useful to start doing here. I say it's part one because these labs weren't taken at peak doses during my post-show push. These were done post show just to see how things were looking and I was pretty happy with how they turned out. I'll be drawing my labs here again real soon and will compare them to these labs here. I'll do my best to walk you through what my thoughts are as I dive into these and help me ultimately decide what my next move is. Let me know if you like this and would enjoy seeing more! https://www.loom.com/share/3431c4d30e184ce998f78f3c27ae4c45

I just posted a new classroom course on LDN! I was going to keep it here, but it felt more appropriate in the course module. I'll likely be adding even more to it because there's really a ton of data that can be shared. I'll keep the carousel post here to reference though. Overall, the TLDR; The potential upside is high, and the downside is inconsequential. This alone makes it worth considering for those who deal with chronic pain or have an autoimmune condition like Hashimoto's. By no means is this a cure or a silver bullet, but mechanistically the theory is sound and grounded in evidence. Have you heard of LDN or Naltrexone at all?