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Curious why coconut oil can raise LDL for some people yet still show up in diets that improve metabolic health, cognition, and body composition? We get clear on what coconut oil actually is—a family of saturated fats with a rare abundance of medium-chain triglycerides—and why MCTs create ketones that the brain and mitochondria can use even without fasting. Instead of stopping at cholesterol, we look at the fuller picture: insulin resistance, inflammation, triglycerides, and real-world outcomes that drive risk more than a single lab value.

We dig into the differences between MCT oil, extra-virgin coconut oil, and refined coconut oil, and when each makes sense. We compare biomarkers to hard endpoints, explain why some populations with high coconut intake have low cardiovascular disease, and explore how diet context flips the script: in a high-sugar diet, lipids can look worse; in a lower-carb, whole-food pattern, markers of metabolic syndrome often improve even if LDL nudges up. Along the way, we share insights on cooking stability, oxidative stress, and the intriguing idea that latitude and season may influence how fats signal thermogenesis and photoprotection.

You’ll leave with practical takeaways you can use today: how to choose between MCTs and whole coconut oil, how to integrate them into a low-sugar, nutrient-dense diet, and which labs to track beyond LDL, like ApoB, triglyceride-to-HDL ratio, hs-CRP, and fasting insulin. If you’ve wondered whether coconut oil is a villain or a misunderstood ally, this conversation offers a grounded, outcome-focused way to decide what fits your body and your climate.

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If pomegranates, raspberries, and walnuts could whisper a secret to your cells, it might be this: the right microbes can turn plant defense into human resilience. We dive into the journey from ellagic acid to urolithin A, mapping how polyphenols meet the microbiome to support mitochondrial function, muscle strength, and brain health. Along the way, we unpack the science of mitophagy, inflammation control, and metabolic signaling that ties colorful foods to better performance and longevity.

We share why only an estimated 20–40% of people currently convert ellagic acid to urolithin A, and what that means for your choices. You’ll hear practical ways to build a food-first foundation—pomegranate arils or juice (mind the sugar), raspberries, blackberries, and walnuts—while nurturing a diverse microbiome with fiber-rich meals. We also explore when direct urolithin A supplementation might be considered, what early trials show for strength and function, and how to think about testing—from proprietary blood kits to broader stool profiling—without getting lost in the weeds.

Throughout, we keep one principle in focus: hormesis. Whole-food antioxidants rarely overwhelm, but concentrated interventions can mute the low-level stress signals that spark repair. By pairing smart training, adequate protein, and polyphenol-rich foods, you create overlapping pathways for mitochondrial renewal and metabolic health—even if you’re not yet a “converter.” Subscribe for more evidence-led, kitchen-to-cell insights, and leave a review to tell us: are you going food-first, testing, supplementing, or blending all three?

For video, Powerpoint slides and referenced research go to www.thehealthedgepodcast.com

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A 35% drop in liver fat in under a week sounds impossible—until you see how a simple macro shift can redirect your metabolism. We dive into a Danish crossover study where calories stayed equal, protein held steady, and the only real change was carbohydrates versus fat. The result: rapid reductions in hepatic fat, lower triglycerides, improved insulin sensitivity, and clear signs of metabolic flexibility, all in four to five days. We unpack what that means for everyday eating, how to use CGM feedback to reduce glucose spikes, and why outcomes like organ fat and fat oxidation should trump a single lipid reading taken out of context.

From there, we widen the lens. Fatty liver—now recognized as a hallmark of metabolic dysfunction—is staggeringly common, yet highly responsive to nutrition quality and distribution. We break down why modest carb moderation paired with quality fats and robust protein can stabilize energy, support endogenous GLP-1 signaling, and protect lean mass. We also confront a common confusion: “high fat” isn’t a license for ultra-processed oils or low-fiber meals. When fats come from olive oil, avocado, nuts, eggs, and fish—and plants supply fiber and polyphenols—the microbiome, mitochondria, and glycemic control can all improve together.

We close with practical implications for anyone using GLP-1 medications. Pharmacology can provide short-term traction, but it doesn’t guarantee nourishment. A protein-forward, lower-glycemic template plus resistance training helps preserve muscle, sustain satiety, and potentially reduce medication reliance over time. If you’re ready to swap shaky biomarkers for meaningful outcomes—and to see changes fast—this conversation offers a clear, evidence-backed roadmap. If it resonates, follow the show, share with a friend, and leave a quick review to help more listeners find The Health Edge.

www.thehealthedgepodcast.com