I also believe better medical decision making starts with context, not fear. A1c can mislead in endurance athletes. AST and ALT can rise from training load rather than liver disease. A DEXA scan can be useful, but a T-score alone does not tell the whole fracture-risk story. The righ…

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Why “normal” lab values aren’t really normal at all, and what optimal ranges actually look like for metabolic health. Standard reference ranges are based on population averages — not on what’s optimal.

This series teaches you to read your labs through a metabolic health lens and spot dysfunction before it becomes disease.

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Before we get into the science, I want to share a few numbers that explain why I care about this topic as much as I do. Bone is not a lifeless scaffold. It provides your body with the calcium and phosphate it needs. It also serves as an endocrine organ that has distant effects throughout the body. Yes, as an Orthopedic Surgeon, I’m biased… but bones are awesome— until they’re not.

The Scary Statistics… Men— This Affects You Too.

After age 50, approximately 1 in 3 women and 1 in 5 men will sustain an osteoporosis-related fracture in their remaining lifetime. Women will spend more time in a hospital for osteoporosis-related fractures than for breast cancer and heart disease combined. That statistic is worth reading twice. Breast cancer and heart disease are the two conditions that dominate the public conversation about women’s health, yet osteoporotic fractures generate more hospital days than both of them put together. A hip fracture in someone over 65 carries a one-year mortality rate of approximately 20 to 30 percent, and roughly half of those who survive are never functionally independent again. These are not rare outcomes. These are the numbers that drive my clinical practice every week and are why I talk about bone health so often.

Men!! You are not exempt. Up to a third of men over 50 have either osteopenia or osteoporosis, and most of them have no idea because men are rarely screened and bone health is culturally framed as a women’s issue. It is not a woman’s issue; it is a human issue, and the fracture consequences in men are at least as severe.

This is why the test we are about to discuss matters so much, and why understanding what it can and cannot tell you is worth your time.

Here is what you need to know going in. Your skeleton is not the steel frame of a building. It is a living organ that is being dissolved and rebuilt continuously by specialized cells that never stop working. Right now, as you sit here reading this, osteoclasts are carving small trenches into your bone, dissolving the mineral matrix with acid and enzymes, and osteoblasts are following behind them, laying down fresh collagen and orchestrating its mineralization with calcium and phosphate crystals. Your entire skeleton turns over roughly every ten years. Some regions, like the vertebrae in your spine, turn over much faster than that.

That mineralization process is worth understanding because it is exactly what the DEXA scanner measures. When osteoblasts lay down new bone, they first create a collagen scaffold, a protein framework called osteoid. That scaffold is structurally important but mechanically soft. What makes bone hard, what enables it to resist compression and absorb impact, is the deposition of hydroxyapatite crystals within and around the collagen matrix. Hydroxyapatite is a calcium phosphate mineral, and it accounts for roughly 65 percent of your bone’s dry weight. The calcium and phosphorus that make up those crystals are not just structural materials sitting quietly in your skeleton. They are metabolically active elements in constant conversation with the rest of your body.

Your skeleton stores approximately 99 percent of your body’s calcium and about 85 percent of its phosphorus. Calcium is essential for muscle contraction, nerve transmission, cardiac rhythm, and blood clotting. Phosphorus is a component of ATP, your cells’ primary energy currency, and of the DNA and cell membranes in every tissue. When blood levels of either mineral drop below what the body needs to keep those systems running, the skeleton is the bank the body draws from. Parathyroid hormone signals osteoclasts to dissolve bone and release the stored minerals into the bloodstream. When levels are restored, the withdrawal stops and the remodeling system resumes maintenance work.

This is why I said in Part 1 that skeletal health and metabolic health are inseparable. Your bones are not passive scaffolding. They are a mineral reservoir that the rest of your body depends on, and the balance between deposits and withdrawals is what determines whether the reservoir stays full or quietly empties over the decades. That delicate balance is off in nearly 50% of people by midlife.

This is why determining your bone density is imperative. Given how common osteoporotic fractures are, scanning bone density should be at least as common as scans for heart disease. The science behind determining bone density measurements and interpreting them is changing. Hopefully, this post helps you put all of this into perspective.

The DEXA scan you get every two years is essentially a photograph of your reservoir’s balance. And like any photograph, it captures something real, but it does not capture everything. Let me walk you through what it shows, what it misses, and what I actually use it for in my own office.

What DEXA Actually Measures

DEXA stands for Dual-Energy X-ray Absorptiometry. The technology works by passing two low-dose X-ray beams of different energies through the body. Bone absorbs these beams differently from soft tissue, allowing the scanner to calculate the bone's mineral content in the scanned region.

What it produces is a measurement called areal bone mineral density, the amount of mineral per square centimeter of bone area as seen on a two-dimensional image. The result is expressed in grams per square centimeter. Remember those hydroxyapatite crystals I described a moment ago, the calcium phosphate deposits that make bone hard? The DEXA is measuring how much of that mineral is packed into the area it can see. More minerals per square centimeter means higher density. Fewer minerals means the remodeling balance has been tipping toward withdrawal, and the reservoir is running lower than it should be.

That density number is then compared to the average peak bone mineral density of a healthy young adult, typically a 30-year-old, and the difference is expressed as a standard deviation. That is your T-score.

A T-score of 0 means your bone density is identical to the average healthy young adult. A T-score of -1 means you are one standard deviation below the average. The WHO diagnostic categories are:

• Normal: T-score above -1.0

• Osteopenia: T-score between -1.0 and -2.5

• Osteoporosis: T-score at or below -2.5

There is also a Z-score that compares your density to age-matched peers rather than to young adults. The Z-score is particularly useful for identifying whether your bone loss is more than expected for your age, a signal that something beyond normal aging is driving it. A Z-score significantly below -2.0 in someone who is doing everything right, loading their skeleton, getting adequate calcium and Vitamin D, maintaining hormonal health, suggests a secondary cause of bone loss that warrants investigation, whether that is a medication effect, malabsorption, or an endocrine problem.

The standard scan sites are the lumbar spine (L1-L4), the hip (total hip and femoral neck), and, sometimes, the distal forearm (wrist). These sites are chosen because they are the most common fracture locations and because they contain trabecular bone, which is most vulnerable to the remodeling imbalance I described in Part 1. Part 1 really does lay the groundwork for this post… check it out.

What DEXA Does Well

DEXA is the standard of care for bone density assessment for good reasons.

It is fast, widely available, inexpensive, and delivers very low radiation, roughly equivalent to a few hours of normal background environmental radiation. A full scan takes about 10 minutes.

It is reproducible. When performed on the same machine by the same technician, serial DEXA scans can detect meaningful changes in bone density over time with reasonable precision. This makes it a useful tracking tool, not just a one-time snapshot. When I compare my DEXA from two years ago to this year’s, I am watching the remodeling balance play out in real numbers. If the density is stable, the osteoclasts and osteoblasts are matched. If it is dropping, something has shifted the balance, and I need to figure out what shifted it.

It is well-validated for population-level fracture risk prediction. Lower T-scores are associated with higher fracture risk. The FRAX tool, which combines T-scores with clinical risk factors, provides a reasonably accurate 10-year fracture probability to guide treatment decisions.

A DEXA scan can also be used to tell you something meaningful about your total body composition, lean mass, fat mass, and regional fat distribution, which goes well beyond bone. A DEXA for bone density is also effectively a body composition scan if the software is set up to analyze it that way, and I track this as part of my own annual panel.

What DEXA Misses: The Structural Problem

Here is where the picture gets more complicated, and where understanding the living biology from Part 1 really matters.

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Often enough, a runner or endurance athlete gets labs back and sees an elevated hemoglobin A1c. Their physician might warn them that they’re pre-diabetic. Quest Labs‘ interpretation will, too. This is very often wrong. Don’t panic… let’s explore this.

Hemoglobin A1c is a useful population-level marker, but it is not perfect. It reflects glucose exposure over the lifespan of red blood cells, not real-time glucose control. And that distinction matters to people who train often and occasionally train hard. Your hemoglobin A1c theoretically reflects your average glucose over the last 90 days.

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The average lifespan of a red blood cell (RBC) is 120 days. But it’s an average. Glucose, over time, will bind to hemoglobin in RBCs. The higher the glucose in your blood, the more glucose will bind to hemoglobin. So, in theory, if RBCs lived for 120 days, a rise in A1c would always be due to elevated blood glucose levels over the past 90 or so days, and reflect insulin resistance, pre-diabetes, or diabetes itself, depending on the A1c level.

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As reviewed in detail by Radin in Pitfalls in Hemoglobin A1c Measurement , A1c can be misleading in multiple common clinical scenarios. Anything that alters red blood cell lifespan or turnover can shift A1c upward or downward without any true change in insulin sensitivity.

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Endurance athletes check several boxes that can throw off A1c measurements. Many endurance athletes, myself included, have an A1c that nears “pre-diabetic” levels on routine lab testing.

Regular training increases red blood cell turnover, but paradoxically, some athletes — particularly older runners — develop a relative iron deficiency, B12 deficiency, or low-grade anemia. Iron deficiency is one of the most common causes of falsely elevated A1c, even in people with normal glucose control.

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Training itself can also skew interpretation. Long bouts of exercise increase glucose flux and transient post-exercise hyperglycemia driven by catecholamines, cortisol, and hepatic glucose output. This does not equal insulin resistance. In fact, skeletal muscle insulin sensitivity in trained athletes is usually excellent.

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Add in dehydration, relative iron deficiency, oxidative stress, altitude exposure, and frequent micro-hemolysis (breaking down RBCs) from repetitive foot strike, and the signal-to-noise ratio of A1c gets worse.

This is why A1c should not be interpreted or treated in isolation in athletes.

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