High cholesterol isn’t just a number on a lab report. It’s a silent threat that builds up over years, quietly narrowing your arteries until something critical happens-a heart attack, a stroke, or worse. The truth? Most people with high cholesterol feel absolutely fine. No chest pain. No dizziness. No warning signs. That’s why it’s called a silent killer. By the time symptoms show up, the damage is often already done.
What Exactly Is Hypercholesterolemia?
Hypercholesterolemia is the medical term for having too much cholesterol in your blood. Cholesterol itself isn’t bad. Your body needs it to build cells, make hormones, and digest food. But when levels get too high-especially the type called LDL, or "bad" cholesterol-it starts sticking to the walls of your arteries. Over time, this builds into plaque. That plaque hardens, narrows your blood vessels, and makes it harder for blood to flow. That’s how heart disease starts.
The numbers matter. According to the American Heart Association, about 93 million American adults have total cholesterol above 200 mg/dL. That’s nearly 40% of the adult population. But it’s not just the total number that counts. LDL cholesterol is the real concern. If your LDL is over 190 mg/dL, you’re in the severe range. If it’s between 160 and 189 mg/dL and you have other risk factors like high blood pressure or smoking, you’re already at elevated risk.
Familial vs. Acquired: Two Different Causes
Not all high cholesterol is the same. There are two main types: familial (inherited) and acquired (lifestyle-driven).
Familial hypercholesterolemia (FH) is genetic. It’s caused by a mutation in one of your genes-usually the LDLR gene-that stops your liver from clearing LDL cholesterol properly. This means you’re born with high levels. About 1 in 250 people have this condition, but most don’t know it. People with FH often have LDL levels above 190 mg/dL from childhood. In severe cases, especially with homozygous FH, levels can hit 450 mg/dL or higher. These individuals are at extreme risk. Without treatment, men with FH often have heart attacks before age 40. Women aren’t much safer-many face events by age 50.
Physical signs can give it away. Look for fatty lumps on the tendons of your heels or knuckles-these are called tendon xanthomas. Yellowish patches around the eyelids, known as xanthelasmas, are another red flag. These aren’t just cosmetic. They’re visible proof that cholesterol is building up in your body.
On the other hand, acquired hypercholesterolemia comes from what you eat, how you live, or other health problems. Eating too much saturated fat, being sedentary, or carrying extra weight can push your cholesterol up. So can conditions like hypothyroidism, diabetes, or chronic kidney disease. Some medications, like certain diuretics or steroids, can also raise LDL. The good news? This type often responds well to changes in diet and exercise.
Why You Can’t Just "Eat Less Fat" and Call It Done
Many people think cutting out eggs or butter will fix high cholesterol. It helps-but not enough. Studies show dietary changes alone typically lower LDL by only 10-15%. The Portfolio Diet, which combines nuts, plant sterols, oats, and legumes, does better-reducing LDL by up to 30% in clinical trials. But even that isn’t enough for people with FH.
Here’s the hard truth: if you have familial hypercholesterolemia, lifestyle changes alone won’t cut it. You’ll need medication-often multiple medications-to get your LDL down to safe levels. The European Atherosclerosis Society says untreated FH can shorten life expectancy by 30 years. That’s not an exaggeration. It’s based on decades of tracking patients.
How Doctors Test and Diagnose It
A simple blood test called a lipid panel measures your cholesterol. It checks total cholesterol, LDL, HDL (the "good" kind), and triglycerides. You don’t even need to fast anymore-the U.S. Preventive Services Task Force updated guidelines in 2022 to reflect that. That makes testing easier and more accessible.
Who should get tested? Everyone between 40 and 75, especially if they have other risk factors. But if you have a family history of early heart disease or if you notice physical signs like xanthomas, get tested earlier-even as a teenager. The Dutch Lipid Clinic Network Criteria, introduced in 2022, helps doctors spot FH with 94% accuracy by combining family history, cholesterol levels, and physical signs.
What Treatments Actually Work
Statins are still the first line of defense. Drugs like atorvastatin (Lipitor) and rosuvastatin (Crestor) can cut LDL by 50% or more. They’ve been proven in massive trials like IMPROVE-IT to reduce heart attacks and deaths. But not everyone tolerates them. About 7-29% of people experience muscle pain or other side effects.
For those who can’t take statins-or need more help-there are other options. Ezetimibe (Zetia) blocks cholesterol absorption in the gut and lowers LDL by about 18%. Then there are the PCSK9 inhibitors-alirocumab and evolocumab. These are injectable drugs that can slash LDL by another 50-60% on top of statins. They’re expensive, but for people with FH, they can be life-saving.
And now there’s something new: inclisiran (Leqvio). Approved by the FDA in 2021, it’s an RNA-based therapy that works differently. Instead of daily pills, you get two shots a year. It lowers LDL by half and improves adherence dramatically. For someone who forgets pills, this could be a game-changer.
For severe FH, doctors often use triple therapy: a high-intensity statin, ezetimibe, and a PCSK9 inhibitor. It sounds intense, but for someone with LDL over 300 mg/dL, it’s not optional.
The Real Problem: People Aren’t Taking Their Medicine
Here’s the uncomfortable part: even when doctors prescribe the right drugs, people stop taking them. Only about half of statin users are still on their medication after a year. CVS Health found that many quit because they feel fine-or they’re scared of side effects. But here’s the thing: if your cholesterol is high and you’re not treating it, you’re gambling with your life.
Adherence is even worse in women and minority groups. NHANES data shows only 49% of women and 42% of Black adults receive statin therapy, even when they qualify. That’s not just a health gap-it’s a survival gap.
What the Future Holds
Research is moving fast. Scientists now use polygenic risk scores to find people at risk even if they don’t have FH. These scores look at hundreds of tiny genetic variations to predict who’s likely to develop high cholesterol over time. That means we could start treating people in their 20s or 30s, long before plaque forms.
Public health efforts are also shifting. The American Heart Association’s 2030 goal aims to improve cardiovascular health by 20%. That includes better access to testing, more affordable medications, and policies to reduce saturated fat in processed foods. Because the truth is, we can’t treat our way out of this crisis. We need to prevent it.
What You Can Do Today
If you’ve never had your cholesterol checked, get tested. It takes five minutes. If you’re over 40, or have a family history of early heart disease, don’t wait. If you’ve been told you have high cholesterol, don’t ignore it. Talk to your doctor about what type you have-and whether you need more than just diet changes.
Medication isn’t a failure. It’s a tool. And for many people, it’s the difference between a long life and a shortened one. The science is clear: lowering LDL saves lives. Every 39 mg/dL reduction means a 22% lower risk of heart attack or stroke. That’s not a small gain. That’s life-changing.
High cholesterol doesn’t announce itself. But you can stop it before it stops you.
