The Chart

How Can I Tell If I'm Metabolically Healthy?

Stephen Strong, M.D. · September 2026

It's easy to get lost in health these days. There's a new test or measurement almost daily, it seems.

Fortunately, figuring out whether you're metabolically healthy, and whether something needs to change, is simpler than the noise suggests.

Let's simplify things a bit.

"Metabolic health" could mean a lot of things. For our purposes, we're talking about three: how your body processes energy, whether you're insulin resistant, and whether you're carrying visceral fat that's actively generating disease.

Three principles before we start.

Principle one: everyone's body is different. Some people's genetics are more forgiving than others. For better or worse, someone doing most things right may get penalized for a bit of excess body fat, while someone with worse habits skates by.

Principle two: no single measurement is perfect. Body fat percentage, BMI, waist size. They measure different things, and none of them is a clean readout of metabolic health. What they do is point you in a direction.

Principle three: skeletal muscle is anti-metabolic disease. Up to a point, building muscle mass is the best thing you can do to fend off metabolic disease.

Now, how do you tell? There are two routes: what you can measure on your body, and what shows up in your blood.

What you can measure on your body

BMI. Easy. All you need is height and weight.

Also limited. Some people with a normal BMI carry very little muscle and are metabolically unhealthy, a pattern sometimes called sarcopenic obesity, or "skinny fat." Others have a high BMI, a lot of muscle, and are metabolically fine. BMI doesn't know the difference between a pound of muscle and a pound of visceral fat.

Waist to height ratio. The rule is about as simple as it gets: your waist should measure less than half your height.

Measure your bare waist midway between your lowest rib and the top of your hip bone, at the end of a normal breath out. Divide by your height. Under 0.5 is where you want to be, 0.5 to 0.6 deserves attention, above 0.6 is a red flag.

It beats BMI because it cares where the fat is, and fat around the middle is the fat sitting on your organs. Two caveats. Measure the same way every time or you're tracking noise instead of fat. And if you're of South or East Asian descent, trouble tends to start below 0.5.

Body fat percentage. Harder to pin down precisely. You can eyeball an estimate from appearance, use an impedance device, or get a DEXA scan if you want real numbers. From a body composition standpoint, this is about as close as we can get.

Roughly 18 to 24 percent for men and 20 to 28 percent for women is a good place to be. But again, different bodies have different tolerances.

What shows up in your blood

The pathway to metabolic disease, with early and later clues A vertical sequence from energy surplus through fat storage overflow, ectopic fat, and compensatory hyperinsulinemia to beta cell failure. Early clues such as waist-to-height ratio, triglycerides, ALT and ApoB appear during the compensated phase. Later clues such as fasting glucose, A1C, hsCRP and imaging findings appear only after compensation fails. Energy surplus Genetics, inactivity, sleep Storage capacity exceeded Fatty acids spill over Ectopic fat Liver, muscle, viscera Hyperinsulinemia Beta cells compensate Beta cell failure Glucose finally rises Early clues Years before glucose moves Waist past half your height Triglycerides up, HDL down ALT drifting upward ApoB high, LDL-C normal Later clues Compensation has failed Fasting glucose rises A1C above 5.7% hsCRP elevated Fatty liver, plaque on imaging
Metabolic disease develops over years. The clues on the right appear long before blood sugar does.

A quick word on order. The tests below aren't equally early. Some of them move years before anything is wrong with your blood sugar. The one everybody screens for moves last. That's worth knowing before you take comfort in a normal glucose.

Triglycerides. Triglycerides are fatty molecules, and fasting triglycerides work as a barometer of metabolic health, which is why I'm starting here instead of with the sugar.

Here's what's actually happening when they rise. Insulin normally does two things. It tells your liver to stop pumping out fat carrying particles, and it switches on the enzyme that clears them from your blood. When you become insulin resistant, you lose both. Your liver overproduces while your clearance slows down, and the fat coming out of your fat cells keeps feeding the process. So a rising triglyceride level isn't really a record of what you ate last week. It's a signal that insulin has stopped being listened to.

Strength training, healthy fats, and improved body composition all bring these down. Fructose in particular, more than starch generally, drives them up.

A useful trick: look at your triglycerides divided by your HDL. A high ratio is one of the better early signals of insulin resistance, often before the A1C has moved at all. One caveat. It works well in some populations and poorly in others. Black patients frequently have genuine insulin resistance with normal triglycerides, so this ratio will miss them.

Hemoglobin A1C and fasting glucose. The most familiar route, and the latest one.

A1C measures how much blood sugar has molecularly attached itself to the hemoglobin inside your red blood cells. Those cells circulate for about 90 days, which is why A1C gives a three month average instead of a snapshot. It's almost like taking a tissue sample of your body.

An A1C above 5.6% almost always means insulin resistance. But notice where it sits on the diagram above. Your pancreas will pour out extra insulin for years to hold that number down, and it succeeds, right up until it doesn't. A normal A1C tells you your beta cells are still winning. It doesn't tell you the fight isn't happening.

AST and ALT. We've been talking about visceral fat this whole time. Here's where you can actually see it. When your body has extra calories for long enough, that energy finds its way into and around your organs. When it happens in the liver, your liver enzymes, ALT especially, go up.

This is one of the early ones, and it's on every basic panel you've ever had. An ALT drifting up over the years, still inside the "normal" range, is one of the most commonly ignored findings in medicine.

What is LDL?

LDL is a particle in your blood that carries fats, including cholesterol.

That's really it. It's a carrier. Your body needs cholesterol to build cells and make hormones, your liver makes most of it, and LDL particles are how it gets delivered where it's needed. You have millions of them moving through you right now, doing a job you would miss if they stopped.

The trouble is that these particles can push into the wall of an artery and get stuck there. Most of them drift back out. Some don't. Over years, the ones that stay begin to pile up, and that pile is what we call plaque. Plaque is what narrows an artery and causes heart attacks and strokes.

So the disease is not really about cholesterol. It's about particles getting stuck.

What does a high LDL mean?

It means you're carrying a lot of cholesterol around in your blood.

That by itself isn't bad. Cholesterol isn't a poison and you can't live without it. The problem is volume. The more particles you have moving through your arteries, the more chances there are for one of them to push into a wall and stay there.

So it's a numbers game, played over a long stretch of time. Generally speaking, the higher your LDL, and the longer it stays high, the greater your odds of building plaque.

That's why this one number gets so much attention. Not because cholesterol is evil, but because it's one of the few things on your lab report that we know contributes to the disease directly, and one of the even fewer we can actually do something about.

One more thing, because it matters for the rest of this article. Your LDL number measures the cholesterol being carried, not the number of particles carrying it. For most people those two rise and fall together. In someone who is insulin resistant they can come apart, and the number can look reassuring while the particle count climbs.

What sets your LDL in the first place

Mostly genetics. The vast majority of the cholesterol in your body was made by your body, not eaten. How much you make, and how efficiently you clear it back out of circulation, is largely inherited. So is how much you absorb from your gut.

Diet matters, but less than most people assume, and saturated fat matters considerably more than dietary cholesterol does. This is why one person can eat eggs and red meat daily and have an unremarkable panel, while another eats carefully and doesn't.

There's one pattern worth naming because you'll run into it online. Some lean, well trained people eating very low carbohydrate diets watch their LDL climb dramatically, sometimes past 200. It's a real phenomenon and the mechanism is reasonably well understood. Whether that particular version of a high LDL carries the same risk as any other is genuinely unsettled, and I wouldn't assume in either direction. In that situation I'd rather look at the arteries directly than argue about the number.

The rest of the cholesterol panel

ApoB. The test that counts the particles directly. Every one of them carries a single ApoB protein on its surface, so measuring ApoB tells you how many are in circulation rather than how much cholesterol they're hauling.

For most people this agrees with the LDL number and adds nothing. It earns its keep in the roughly one in five where the two disagree, and that group is disproportionately people with high triglycerides, extra weight around the middle, or diabetes. If that's you, this is the one worth asking for.

Non-HDL cholesterol. If you can't get ApoB, this one is already sitting on the panel you had last year. Total cholesterol minus HDL. It captures every particle capable of causing plaque, and unlike the calculated LDL it stays reliable when triglycerides are high.

Lp(a). Worth a paragraph because it's the exception to most of what I've said.

About one in five people carries an elevated Lp(a). It's almost entirely genetic, it barely moves with diet or training or body composition, and it raises your risk of heart attack and aortic valve disease on its own. It's a once in a lifetime test, since the number doesn't meaningfully change, and most people have never had it. If there's early heart disease in your family that nobody has ever been able to explain, this is frequently the explanation.

HDL cholesterol. Roughly the opposite story. Healthy muscle mass and good insulin sensitivity both associate with a higher HDL, along with genetics. A high HDL is generally a sign of healthy metabolic status.

Read that as a readout, though, not a target. Every drug that raised HDL directly failed to prevent a single heart attack, and very high levels, above 80 or 90, actually associate with worse outcomes. HDL is a thermometer, not a thermostat. It tells you the metabolic room is warm. Breaking the thermometer doesn't heat the house.

A few bonus signals

Elevated serum bicarbonate. Often a sign of obstructive sleep apnea. Not metabolic syndrome exactly, but it causes plenty of problems of its own, and the two travel together.

Elevated hemoglobin. Same story.

hsCRP. A marker of systemic inflammation. It doesn't tell you plaque is there, but elevated levels track with cardiovascular risk and warrant attention, especially alongside anything else on this list. If you want to know whether plaque is actually present, that's a coronary calcium score, not a blood test.

What to do with all this

You don't need every one of these. If your waist is under half your height, your A1C is under 5.7%, your triglycerides are low and your liver enzymes are normal, you're almost certainly fine.

If two or three of them are off, that's not four separate problems. It's one problem showing up in four places, and the fix is largely the same regardless of which number got your attention. Build muscle, cut the refined starch, sleep, and reassess in three months.

— Stephen

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