Interview with Dr Josh Lindsley DO, Physcian, DABOM, ABEM, Highland Longevity

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Interview with Dr Josh Lindsley DO, Physcian, DABOM, ABEM, Highland Longevity

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This interview is with Dr Josh Lindsley DO, Physcian, DABOM, ABEM, Highland Longevity.

For readers meeting you for the first time, how do you describe your clinical focus and the patients you help at Highland Longevity?

I’m a board-certified emergency medicine and obesity medicine physician who founded Highland Longevity, a concierge longevity and wellness clinic in Fort Worth, Texas.

My clinical focus sits at the intersection of metabolic health, body composition, and healthspan optimization. I help patients who are done chasing quick fixes and want a data-driven approach to how they age. That typically means busy professionals in their 40s, 50s, and 60s who have noticed the old playbook has stopped working—the weight creeps up, energy declines, and recovery takes longer than it used to.

Part of my motivation came from the ER. After years of seeing patients in late-stage disease—the heart attacks, the diabetic foot wounds, the strokes—I kept thinking there has to be a better way to do medicine. Instead of pulling people out of the deep end, I wanted to teach them how to swim. That meant building a practice around accurate, science-backed, gold-standard measurements for longevity and preventive medicine—not the fad treatments or experimental protocols you see at medspas and cash-grab businesses.

At Highland Longevity, we use DEXA scans to measure body composition, RMR testing to prescribe diets, and VO2 max testing to prescribe exercise. We offer medical weight loss with GLP-1 therapy, hormone optimization, and peptide protocols—all with strict clinical standards using only FDA-approved medications or reputable 503A and 503B compounding pharmacies.

I’ve also lived this journey myself. I lost over 100 pounds total, but along the way, I learned that the scale alone is a terrible metric. I lost muscle mass initially and had to redesign my approach to preserve lean tissue while losing fat. That experience shapes how I treat every patient—we optimize body composition, not just body weight.

What pivotal experiences moved you from emergency medicine into obesity and longevity care?

In the ER, I kept seeing the same story on repeat: the 54-year-old with his first heart attack, the diabetic who ignored the warning signs until she couldn’t feel her feet, and the family receiving the news that their loved one’s stroke was devastating and largely preventable. Emergency medicine is heroic work, but it’s fundamentally reactive. By the time patients reach me, the damage is often done. I started thinking there has to be a better way to practice medicine—one that intervenes before the crisis, not after.

The personal piece hit closer to home. I was overweight for years, and I understood the struggle from the inside. When I finally committed to change, I lost 87 pounds with GLP-1 medications. However, I also lost significant muscle mass in the process—something I didn’t fully appreciate until I looked at my own body composition data. The scale indicated success, but my physiology told a different story. I had to redesign my entire approach, ultimately losing over 100 pounds total while learning to preserve lean tissue and optimize metabolic health, not just chase a number.

That combination—watching preventable disease destroy lives in the ER while navigating my own metabolic transformation—made the pivot inevitable. I returned and became board-certified in obesity medicine because I wanted the clinical rigor to match my conviction. I wanted to stop pulling people out of the deep end and start teaching them how to swim.

Highland Longevity is the result. We use gold-standard measurements—DEXA, RMR, VO2 max—to build personalized, evidence-based plans. No fads, no experimental protocols, no shortcuts. Just science-backed preventive medicine for people who want to take control of how they age.

Starting with GLP-1 therapy, what is the biggest mistake you see in real-world use?

The biggest mistake I see is treating the scale as the only metric that matters.

Patients celebrate a 30-pound loss, but when we run a DEXA scan, the picture changes. Studies on semaglutide show that up to 40% of weight lost can be lean mass. That’s not a minor side effect; it’s a fundamental problem with how these medications are prescribed.

Muscle isn’t just for aesthetics. It’s your glucose sink, your primary driver of resting metabolic rate, and one of the strongest predictors of longevity we have. Lose enough of it, and you’ve traded one disease risk for another—hitting your goal weight but ending up metabolically fragile and primed to regain.

I made this mistake myself. I lost 87 pounds on GLP-1 therapy and thought I was succeeding. Then I saw my body composition data and realized I’d lost significant muscle in the process. I had to redesign my entire approach to lose additional fat while preserving lean tissue.

Now that’s the standard at my clinic. Every GLP-1 patient gets a DEXA scan so we know exactly what they’re losing. We prescribe protein targets based on lean mass, push resistance training, and reframe the goal: optimize body composition, not just body weight. The scale is one data point—not the finish line.

On the diagnostic side, when you read a DEXA scan during weight loss, which metric do you treat as the key decision-maker?

Honestly, there’s no single metric that matters most. That’s the whole point of running the scan—it tells me which number to prioritize for this specific patient.

Take two people who both weigh 200 pounds. One has adequate muscle mass but elevated fat. The other has low muscle and high fat—what we call sarcopenic obesity. Same weight, completely different clinical picture. For the first patient, a GLP-1 medication and caloric deficit might be straightforward. For the sarcopenic patient, that same approach could make things worse. They can’t afford to lose more muscle, so the entire strategy shifts: higher protein targets, aggressive resistance training, slower rate of loss, possibly reconsidering whether a GLP-1 is even the right tool.

In a patient with underlying cardiovascular or metabolic disease, I might focus on visceral adipose tissue first—the fat packed around the organs that drives inflammation and insulin resistance. Reducing visceral fat can move the needle on disease risk faster than total weight loss.

That’s why I don’t treat DEXA scans like a scorecard with one winning number. It’s a diagnostic tool that tells me where the problems are and how aggressive I can safely be. The initial scan sorts patients into buckets. Follow-up scans tell me if the plan is working or needs adjustment.

No cookie-cutter protocols. The measurement is standardized. The treatment that follows is fully custom to the individual.

From there, how do you turn a resting metabolic rate test into a simple daily calorie plan a patient can follow?

The RMR test gives me the real number—not an estimate from an online calculator, but the actual calories that the specific patient burns at rest.

Those calculators exist everywhere, and they’re fine as rough guides. But if they’re off by even 300-400 calories per day, that’s the difference between losing a pound a week and losing nothing. A 500-calorie daily deficit produces about a pound of fat loss per week—3,500 calories. Cut that margin in half with a bad estimate and the patient stalls, gets frustrated, and assumes their body is broken. It’s not broken. The starting number was just wrong.

But here’s the real key—RMR alone isn’t enough. The power is in combining measurements. I pair RMR with DEXA data to set a protein floor based on actual lean mass, usually 0.7-1 gram per pound. I look at labs to understand metabolic health, insulin sensitivity, and hormone status that might affect how aggressively we can push a deficit. I also use VO2 max testing to prescribe exercise at the right intensity—not guessing based on age-predicted heart rate zones, but targeting their actual physiological thresholds.

Each test answers a different question. Together, they create a plan that’s truly individualized—not a template with their name on it.

What I hand the patient is simple: a calorie target, a protein target, and exercise parameters. These are guardrails they can adapt to real life.

The other piece is tracking over time. As patients lose weight, adaptive thermogenesis kicks in—the body downregulates metabolism to conserve energy. Rechecking RMR lets me adjust the plan based on what’s actually happening, not what a formula predicts.

Shifting to hormones, which lab abnormality most often changes your weight-loss strategy in midlife patients?

Testosterone in men and menopause in women are the two factors that change my approach most often.

In men, low testosterone is rampant and underdiagnosed. By age 45, a significant percentage are walking around with levels that make building or even maintaining muscle an uphill battle. They’re doing everything right—protein intake is adequate, they’re lifting weights, and the calorie deficit is reasonable—but they are still losing lean mass. When I check labs and see total testosterone levels in the 200s or low 300s accompanied by corresponding symptoms, that’s a strategy changer. Trying to preserve muscle during weight loss while fighting that hormonal headwind is nearly impossible. These are the patients most at risk for sarcopenic obesity—losing fat and muscle simultaneously until they’re lighter but weaker and metabolically fragile.

In women, the transition through perimenopause and menopause creates a similar inflection point. Estrogen and progesterone decline, but what often gets missed is that women also produce testosterone, which drops significantly during this window. The result is the same: it becomes harder to maintain muscle, and easier to accumulate visceral fat. Add in sleep disruption, mood changes, and metabolic shifts, and preserving lean mass becomes a real challenge.

What’s interesting is the magnitude of difference between these hormones. We measure testosterone in nanograms and estrogen in picograms—a thousand-fold difference in concentration. Yet both have outsized effects on body composition and how patients respond to treatment.

I’m not looking to put every midlife patient on hormones. However, when labs show clear deficiencies and the clinical picture matches, optimizing hormones isn’t optional—it’s foundational. You can’t out-protein or out-train a hormonal environment that’s actively breaking down muscle. Fix the foundation first, and then the diet and exercise will actually work.

To protect muscle while losing fat, what beginner-friendly resistance training plan do you prescribe first?

The absolute gold standard is to start with a comprehensive evaluation by a physical therapist or personal trainer. Everyone comes in with different movement limitations, injury histories, and baseline strength. A professional assessment catches problems before they become injuries and builds a program around what that individual can safely do.

For a complete beginner, I recommend compound lifts targeting the full body three times per week. These include:

  • Squats
  • Deadlifts
  • Rows
  • Presses
  • Pulls

These movements recruit multiple muscle groups and joints simultaneously, delivering the most muscle-preserving stimulus for the time invested.

The evidence supports this approach. The American College of Sports Medicine recommends 2-3 days per week for novice lifters, with loads in the 8-12 rep range. A 2022 meta-analysis in Obesity Reviews found that supervised resistance training is the most effective intervention for preserving lean mass during caloric restriction—more effective than aerobic exercise alone. A recent 2025 study in Frontiers in Endocrinology showed that resistance training participants actually gained lean mass while losing fat, whereas 81% of diet-only participants and 39% of aerobic-only participants lost significant muscle.

That last point is critical. Without resistance training, research suggests 20-30% of the weight lost during caloric restriction comes from lean mass—not fat. That’s the exact outcome we’re trying to avoid.

I don’t overcomplicate it for beginners. Three days a week, compound movements, progressive overload, and adequate protein. Get the fundamentals right first. As they advance, we can refine frequency, volume, and exercise selection—but the foundation is simple, evidence-based, and effective.

When a patient is ready to taper off a GLP-1, what maintenance protocol do you use to prevent weight regain?

First, I set expectations: the data on GLP-1 discontinuation is sobering. In trials, participants regained 50-66% of lost weight within a year of stopping. That’s not failure—it’s biology. Obesity is a chronic disease, and the hormonal adaptations that drove weight gain don’t disappear just because the medication worked.

But here’s what I point patients to: the National Weight Control Registry. This is long-running data on people who lost at least 30 pounds and kept it off for at least a year—collected before GLP-1s existed. It tells us what successful maintenance actually looks like.

The key insight is that weight maintenance is a completely different game than weight loss, largely due to adaptive thermogenesis. Your body fights to regain. What the NWCR found is that maintainers share common behaviors:

  • High physical activity—often an hour a day, at least 300 minutes per week
  • Consistent eating patterns across weekdays and weekends
  • Regular self-monitoring of weight
  • Lower sedentary time

Over 87% of participants maintained at least 10% weight loss at 5 and 10 years.

The red flags for regain are equally instructive:

  • Decreases in physical activity
  • Decreases in dietary restraint
  • Less frequent self-weighing
  • Increases in sedentary behavior

These are the warning signs I teach patients to watch for.

My tapering protocol builds this infrastructure before the medication stops. Throughout treatment, I track body composition with DEXA to preserve lean mass—metabolic insurance. I establish resistance training and protein targets early. When tapering, I do it gradually over 8-12 weeks, recheck RMR to set realistic calorie targets, and increase monitoring frequency.

The through-line isn’t one “best diet.” It’s sustained behavior change plus tight feedback loops. If we build that foundation during treatment, some patients can successfully taper. Not all—but some.

Zooming out to longevity medicine, what biomarker or test do you rely on that most clinicians overlook?

Two tests, both underutilized: apolipoprotein B and the oral glucose tolerance test with insulin levels.

Apo B first. Most clinicians still rely on LDL cholesterol to assess cardiovascular risk, but LDL-C measures the cholesterol mass inside particles—not the number of atherogenic particles themselves. That distinction matters. A 2025 systematic review found that in 9 out of 9 discordance studies, Apo B was superior to LDL-C for predicting cardiovascular events. The European Society of Cardiology now states Apo B is a more accurate marker of cardiovascular risk than LDL-C or non-HDL-C. Yet most standard lipid panels still don’t include it.

Why does this matter in longevity medicine? Patients with metabolic syndrome, insulin resistance, or high triglycerides often have normal LDL-C but elevated Apo B—meaning they’re carrying more atherogenic particles than their cholesterol numbers suggest. Their risk is being underestimated. If you’re trying to prevent a heart attack 20 years from now, Apo B gives you better information to act on.

The second overlooked test is the oral glucose tolerance test with insulin levels. Standard screening relies on fasting glucose and HbA1c, but both can remain normal for years while insulin resistance quietly progresses. By the time HbA1c rises, patients have often developed significant beta-cell dysfunction. You’ve missed the early window.

An OGTT with insulin measurements shows you how hard the pancreas is working to maintain normal glucose. Dr. Joseph Kraft analyzed over 14,000 glucose-insulin tolerance tests and found that many patients classified as “normal” by glucose metrics alone were already insulin resistant. Adding insulin levels catches the problem earlier—when lifestyle intervention is most effective.

These aren’t exotic tests. They’re available, affordable, and dramatically improve risk stratification. They just aren’t part of the standard playbook most clinicians follow.

Thanks for sharing your knowledge and expertise. Is there anything else you'd like to add?

My path to longevity medicine wasn’t linear—it was personal.

I started as a personal trainer. I loved the work because I could see the impact: people getting stronger, moving better, and gaining confidence. That hands-on experience with human physiology eventually pulled me toward medicine. I wanted to understand the deeper science behind what I was seeing in the gym.

Then I lost my dad. He drowned in an accident in Costa Rica. That loss shaped everything that followed. I went into emergency medicine partly because of him—I wanted to be the person who could help when it mattered most, in those critical moments when someone’s life hangs in the balance.

Medical school and then residency at UT Southwestern were brutal. The stress, the sleep deprivation, fostering two children, and the complete absence of time for self-care—I gained a significant amount of weight. I was learning how to save other people’s lives while my own health deteriorated. The irony wasn’t lost on me.

But here’s what really changed my trajectory: working in the ER, I realized that most of the death and suffering I witnessed wasn’t from accidents like my father’s. It was from chronic disease—heart attacks, strokes, diabetic complications, and obesity-related illnesses. Conditions that were largely preventable. I kept thinking about all the years before these patients ended up in my trauma bay, all the opportunities that were missed.

That realization, combined with my own weight loss journey, pushed me toward a different kind of medicine—one I wasn’t taught in medical school. I’m grateful to voices like Peter Attia and Rhonda Patrick who helped me see what evidence-based preventive care could look like. They laid a foundation.

My goal now is to build on that foundation: to create healthcare that prevents rather than reacts; to catch disease 20 years before it becomes an emergency, not 20 minutes after. That’s what Highland Longevity is about—using gold-standard measurements and individualized protocols to help people take control of how they age, before they ever need someone like the ER doctor I used to be.

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