Nathan Ball Z Personal Training

Two particles can carry the exact same amount of cholesterol and do very different damage to an artery. The blood test almost everyone gets measures the cholesterol. It does not measure the thing that actually varies: what kind of particle is carrying it.

Every particle that can build plaque, whether it is LDL, a triglyceride-rich remnant, or lipoprotein(a), carries exactly one molecule of a protein called apolipoprotein B, or apoB. One particle, one apoB.

That is what makes apoB useful: it is a direct headcount of how many plaque-causing particles are in your blood. A standard cholesterol panel does something different. It weighs the total cholesterol those particles are hauling, not how many particles there are. Most of the time the two line up. When they do not, decades of data say the same thing: risk follows the particle count, not the cholesterol number. This is the finding that reframes the whole panel, because it means a normal LDL cholesterol can sit on top of a high particle count, and the standard test will read reassuring while the risk is real.

The next question is whether every particle in that count is equally dangerous, and it is not.

LDL is the baseline. It enters the artery wall, can lodge there, and drives plaque, and because it is the most common apoB particle, it makes up the bulk of the count for most people. It is the reference against which the others are judged.

Remnants are worse, particle for particle. These are the leftovers of triglyceride-rich lipoproteins, larger particles that have dropped their fat and are on their way to being cleared. They are retained in the artery wall more readily than LDL, they carry more cholesterol per particle, and they provoke inflammation and foam-cell formation once they are stuck. They contribute to cardiovascular risk beyond what LDL cholesterol captures, which is why someone with normal LDL cholesterol but high triglycerides, common with insulin resistance and metabolic syndrome, can be carrying a risk their panel understates.

Lipoprotein(a), or Lp(a), is the one that does far more damage, and it is different in kind, not just degree. It is an LDL particle with an extra protein tail, apo(a), wrapped around it, and that tail resembles a clotting protein, adding a pro-thrombotic dimension the other particles do not have. The evidence that it causes disease is not just association. Genetic studies, which track people who inherited high Lp(a) from birth, show it is a direct causal driver, and high levels predict roughly a two- to threefold increase in the risk of heart attack, peripheral artery disease, and calcific aortic valve stenosis. And here is the part that matters for anyone reading this: your Lp(a) level is set almost entirely by your genes, diet and exercise barely move it, and roughly one in five people carry a high level. It is one of the strongest inherited cardiovascular risk factors there is, and it is measured with a single blood test that most people have never had ordered.

Particle count and particle type sharpen risk assessment, but they do not replace the rest of the picture, blood pressure, smoking, and the standard lipids still matter, and no single marker decides an individual's fate. And identifying a high-risk particle is not the same as having a proven way to lower the risk it carries. LDL and remnants respond to established therapies, but targeted Lp(a)-lowering drugs are still in trials, and until those trials report, a high Lp(a) is information that sharpens prevention rather than a number with its own treatment. The practical reframe stands anyway. The standard panel counts cholesterol and treats every apoB particle as interchangeable. They are not. Two of the three particles that matter most, remnants and Lp(a), are the ones a routine cholesterol number is least equipped to see.

Glavinovic et al., J Am Heart Assoc 2022
Cantey & Wilkins, Curr Opin Endocrinol Diabetes Obes 2018
Pinto et al., Clin Investig Arterioscler 2023
Kamstrup, Clin Chem 2021

Nobody warns you that your 20s lie to you.

You can skip the gym for a month, eat like garbage, cancel plans with people you care about, and stay stuck doing the same easy version of your life — and nothing happens. You feel fine.

You look fine. So you assume that's just how it works.

Then one day it isn't. The body stops absorbing the neglect quietly. The relationships you never invested in aren't there when you need them. The hobbies you never picked up leave you with nothing but work. It doesn't happen all at once. It happens slowly enough that you don't notice until you look up and the bill's due.

None of the basics feel urgent in the moment. Lifting weights. A weekly night with your spouse.

A smaller circle of people who actually know you. A hobby that's yours and nobody else's. Skip any one of them today and nothing breaks.

But they're not optional. They're just deferred.

-Coach Jon

The mechanism is not disputed. Every cardiologist alive agrees an LDL particle has to oxidise before the artery wall traps it. Every chemist alive agrees a saturated fat cannot perform that reaction, because there's nothing on the molecule to oxidise.

Only polyunsaturated fats can. Linoleic acid is the one on the shelf.

Butter cannot do the chemistry. Sunflower oil is designed for it.

The public health advice for fifty years has been to swap the fat that cannot cause the disease for the fat that mechanistically must.

The Lancet paper in 1994 said this plainly. Nobody in charge reconsidered a single guideline.

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Our light exposure has changed drastically over the past 20 years, with the introduction of energy-efficient LED light bulbs. Now, we’re discovering how they're short on red wavelengths, which messes with our mitochondria, contributing to diabetes, dementia and more.

Doing hard things in the gym prepares you for hard things in life.

Physical and mental training is a process of building tolerance to one’s intolerances.

Said another way:

Sh*t’s gonna happen. Get strong so you can deal with it.

-Coach Jon