What my own genes taught me about cholesterol (even though I'm the Nutritional Therapy Practitioner)

I've spent years telling clients that food is information — that what we eat talks to our bodies, and our bodies talk back. I did not expect my own body to talk back this loudly, or for me to cry over a lab report.

Late last year, I started training to become a 3X4 Genetics Practitioner. Part of that process is learning to read your own genetic results, so I ran mine — not out of worry, honestly, more out of curiosity. I wanted to understand the tool before I used it on clients. What I found instead was an answer to something I'd quietly wondered about for years: why my LDL always seemed to teeter toward "higher than ideal" no matter what I did, even while my HDL stayed genuinely great.

I carry one copy of APOE E4.

Here's the plain-language version: APOE comes in three common variants — E2, E3, E4 — and we each carry two, one from each parent. I'm E3/E4. The E4 variant is associated with a steeper LDL response to dietary saturated fat than the more common E3/E3 pattern. It's not that saturated fat is toxic for E4 carriers. It's that the dose-response curve is steeper. The same amount of cheese or eggs that barely moves someone else's numbers moves mine more. My husband can eat a carnivore-leaning diet and thrive on it. I add a little fat back into mine and my numbers climb. That's not a willpower difference. That's biology.

In April, I ran an LDL panel. Both LDL and HDL were elevated — LDL particularly gave me pause. I thought seriously about going back to fully plant-based eating right then. I didn't. Protein has always been my personal nutrition Achilles' heel — I genuinely struggle to get enough of it — and cheese, eggs, and yogurt were doing a lot of that work for me. I told myself I "needed" them. I'm putting that in quotes on purpose, because looking back, what I needed was protein. What I chose was the easiest source of it, even after my own body had already told me, gently, that it didn't love that source. So instead of cutting them, I added berberine. I tried psyllium husk. I figured I was managing it.

Ninety days later, I retested. This time I also ran Lp(a) for the first time in my life.

I cried when I saw those results.

Here's what ninety days of "managing it" actually looked like. In March, my total cholesterol was 214 and my LDL was 129. In July — after the berberine, after the psyllium, after telling myself I had it handled — my total cholesterol was 227 and my LDL was 138. Not better. Higher. My ApoB, which counts the actual particles ferrying cholesterol through my arteries, came back at 117; optimal is under 90. And my Lp(a) — the one I'd never run in my life — came back at 141 nmol/L. Anything over 125 is the high-risk category.

And here's what made it confusing: plenty of it looked great. My triglycerides dropped from 95 to 74. My HDL came in at 72. My inflammation marker was practically pristine. By every number I'd been quietly proud of, I was doing beautifully. I know it's dramatic to call it a betrayal by my own body. It still felt like one.

Not because I was afraid of a number. I actually had to sit with that for a minute — heart attack and stroke were not on the list of things I normally worry about. I've spent years feeling like I had that part handled. What actually broke me open was smaller and harder: the proof, right there on the page, that I had not been moving the needle the way I thought I was. That everything I know, everything I teach, still applies fully to me — and I had ignored what my own body was telling me anyway.

That's the part I want to be honest about, publicly, because I think it matters more than the numbers themselves. People assume that because I study this, because I can tell you why the red-tinged ends of an onion are worth saving for their quercetin, that I am automatically the picture of health, immune to my own advice. Mostly, I am healthy. But I also have a genetic factor I have to actively manage, and I still, sometimes, make choices that work against my own body — usually for reasons that feel completely reasonable in the moment. I was managing other people's health while quietly ignoring a signal in my own. That's a hard thing to admit out loud. I'm choosing to anyway.

This week, I went back to fully plant-based eating. I'm having a grapefruit daily — there's actual research behind that one. A 2006 study out of Hebrew University, published in the Journal of Agricultural and Food Chemistry, followed 57 people with stubbornly high cholesterol — people whose levels hadn't responded well to statins — as they added fresh grapefruit to their diet for 30 days. The group eating red grapefruit saw meaningful drops in total cholesterol, LDL, and especially triglycerides.¹ It's a small study in a specific group, and it's no substitute for the bigger dietary shift I'm making — but it's a real, evidence-backed piece to lean on, not just folklore. I'm also working psyllium husk back in (a better delivery method this time), and I've kept exactly one thing: a bit of yogurt on my oatmeal each morning, because protein is still protein, and I'm not interested in solving one problem by creating another.

Why I'm telling you all of this

Two things came out of this that matter more than my own story.

Lp(a) testing matters, and almost nobody gets it. Unlike LDL, Lp(a) is largely genetically determined — it doesn't move much in response to diet or lifestyle for most people, but it changes your overall cardiovascular risk picture significantly. It's rarely included in a standard lipid panel unless you specifically ask for it. If you have a family history of early heart disease, or your LDL isn't responding the way it "should" to the changes you're making, this is worth a direct conversation with your provider.

Genetic testing gave me information I couldn't have gotten any other way. My APOE result also carries a second piece of information, unrelated to cholesterol: E4 is the variant most studied in relation to Alzheimer's risk. Having one copy raises relative risk somewhat — it is not a diagnosis, and plenty of E3/E4 carriers never develop dementia. Of everything my genetics point to, it's honestly the one I'm least afraid of. My mother lived with early-onset Alzheimer's, and she also lived for decades with heavy alcohol use — a very different lifestyle than mine. I can't know for certain what drove her path, but I know I'm not walking it the same way. (I wrote more about her, and about why family history is a tendency and not a verdict, in You Are Not Your Genes.) The lipid side of this gene, on the other hand, is the one actively shaping my choices every day, because I have the data and I know exactly what to do with it.

That's the real lesson underneath all of this, and it's one I already believed but now understand differently: there is no single right way to eat, and knowing the theory is not the same as living the practice. My husband does genuinely better on a carnivore-leaning, plant-supported way of eating than he ever did plant-based. I do better fully plant-based, informed by markers he doesn't need to think about. Neither of us is right in some universal sense. We're both right for our own biology — and I'm still learning to actually listen to mine, instead of just teaching other people to listen to theirs.

I'm not writing this from a place of doom. I'm writing it because I'd rather you see the whole picture — the credentials and the crying-over-a-lab-report moment, both. That's what personalized nutrition actually looks like. Not a marketing phrase. A woman with a mostly-figured-out relationship to food, one genetic curveball, and a psyllium husk habit she's genuinely trying to stick with this time.