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.