I remember the moment clearly. A hot July day, standing at my mailbox, opening an envelope from a genetic testing company. I expected reassurance. Instead, I saw a result sitting in the bright red end of the risk continuum. As far from “OK” as it could get.

Years earlier, my son had mentioned that his 23andMe test showed he carried a gene that might lead to Alzheimer’s “when he was old.” It didn’t sound worrisome. Many people develop Alzheimer’s late in life. It wasn’t until a decade later, when the gene had a name, that I paid attention.

APOE4.

My son had one copy. I now understood where it came from. I had two.

APOE4 is the strongest common genetic risk factor for late-onset Alzheimer’s disease. With two copies, I’m in the roughly 1 to 2 percent of people whose odds are estimated to be 10- to 12-fold higher than those with the most typical genotype. I was 64 when I discovered this, right around the age when Alzheimer’s symptoms often begin to appear.

Looking back, there were clues. For years, my LDL cholesterol stayed elevated despite a strict adherence to a heart-healthy diet and exercise regimen. My high cholesterol wasn’t extreme, but it was resistant in a way that didn’t match my lifestyle. In retrospect, I wish now those long-standing cholesterol abnormalities would have prompted a deeper investigation.

My father had a heart attack at 65. He survived, but later developed cognitive issues. I dismissed his confusion and failing memory as normal aging. Taking a hard look back, my assumption feels misguided.

For some time, medical societies have advised against APOE testing in asymptomatic people. The American College of Medical Genetics and Genomics is one example. The reasoning was straightforward in 2011: APOE status does not diagnose disease and cannot predict it with certainty. Without a clear treatment pathway, the potential psychological burden was thought to outweigh clinical value.

That logic made sense in 2011. It doesn’t fully hold up in 2026.

When I received my result, no protocol was included in the report and no counseling was offered. Just the hard facts.

My physician listened thoughtfully. “You don’t have dementia,” he assured me. “We’re having a coherent conversation.” I nodded, and he handed my genetic report back to me. “If you start to have symptoms, we’ll revisit this.”

Too anxious for a wait-and-see strategy, I started searching for ways to reduce my risk on my own. I was motivated but uninformed. I found myself doom-scrolling the internet, influenced by influencers and persuaded by salespeople. I made mistakes. I learned the hard way that panic is not prevention.

Eventually I found a clinician who specializes in APOE4, and my approach became more structured. I learned APOE4 doesn’t only affect the brain. APOE4 is associated with differences in lipid metabolism that may help explain why some carriers have higher baseline LDL cholesterol and respond differently to standard interventions. My long-standing “unexplained” LDL levels started to look less like a mystery and more like part of an underlying issue.

My APOE status led to a thorough examination of my cardiovascular health. A coronary artery calcium scan revealed calcification I would not have otherwise detected. My father’s first sign of heart disease was a heart attack. Mine was a scan.

Despite years of focusing on healthy lifestyle habits, genetic headwinds had still left me vulnerable. I adopted stricter dietary controls, a more focused exercise routine, and optimized my medications. My biomarkers improved, led by a 50 percent reduction in LDL cholesterol. Before long, a question crystallized in my mind: If knowing APOE4 status changes how we manage our health, why are we telling people not to learn it?

The prevention landscape has evolved. In 2024, the Lancet Commission on Dementia Prevention, Intervention, and Care added elevated LDL cholesterol as a modifiable risk factor for dementia. The commission estimated that addressing known risk factors could prevent or delay up to 45 percent of cases globally.

Whether clinicians recommend it or not, patients are already getting tested. Since the FDA authorized direct-to-consumer APOE reporting through 23andMe in 2017, large numbers of people have learned their status outside the health care system, often without clinical guidance. The trigger for my own test wasn’t a doctor’s recommendation. It was a casual comment from my son.

This is not an argument for universal screening. APOE testing carries real psychological and interpretive challenges. It should be paired with education and genetic counseling.

But the current posture, which often discourages testing even for informed, motivated individuals, is increasingly difficult to defend. Both heart disease and Alzheimer’s disease develop over decades. The window for intervention is long, and it opens early. For people willing to act on uncertain information, who want a clearer sense of their risk and understand its limits, APOE genotyping can be useful. Not because it predicts the future, but because it can prompt action.

My father had his heart attack at 65. I had spent decades trying to avoid his fate and found out I had atherosclerosis anyway. A scan, prompted by my genetics, found what the routine blood tests had missed. I now have an official diagnosis and a cardiologist who tells me my heart is functioning well. I believe him and am living my life cautiously but without fear. That is what knowing allows me to do.

Ron Carr is a patient advocate.