I hope everyone had a fantastic weekend! We’ve got some exciting updates this week, and I wanted to bring everything together in one post for simplicity. First, big news the Kenetik Pro Buyers Club is officially launching! If you’ve been curious about trying the supplement I personally rely on the most, ketone esters, now’s your chance. I’m thrilled to be able to offer both access and savings. I’ve put together a thread that breaks down everything you’ll need—how to order, how many bottles you’ll likely go through in a month, and pricing details. Next, a quick clarification on the upcoming free webinar. This one is going to pull back the curtain on my own protocol and thought process. You’ll get the full, no-holds-barred breakdown of what I take, why I take it, and how I pair it with training, nutrition, and lifestyle strategies. My goal is to help you see things through a systemic lens so you can craft protocols that are more precise and effective. I want this to be fun, transparent, and useful and I’ll say up front, I’m learning every day right alongside you. Feedback (positive or critical) is always welcome. My plan is to make this a monthly feature, including not just my own protocols but also other people’s, so we can grow as a community of protocol designers together. Finally, a huge thank-you to Kassem Hanson of N1. He’s been an incredible resource for me personally and for our community. I’m currently enrolled in his program design mentorship, and if you want to learn the N1 approach, I can’t recommend their online and in-person seminars enough. They teach customization and critical thinking in a way that resonates whether you’re brand-new or decades into this field. Kassem generously edited the SLU webinar from Saturday, and I’ll be posting the recording soon for anyone who couldn’t attend. I’ll also be sharing the slides here, so if you haven’t received them by email, keep an eye out for the link. Link to webinar reply Thank you all so much for your support and for the energy you bring to this community. Everything we’re building here is possible because of each of you. Please don’t hesitate to reach out if there’s something you’d like to see more of, or if you have suggestions on how I can serve you better. I’m here for you guys!

When I saw this video, sent to me by my fiancée, it really highlighted something important: a lot of health misinformation is packaged so well that it feels convincing especially when it comes from charismatic voices. The problem is, calling something like Hashimoto’s a simple ‘vitamin issue’ ignores the real science and can lead people away from the care they truly need. My goal isn’t to attack anyone, but to help people become more discerning about where they get their health information, and to equip them with the knowledge to take control of their own health with clarity and confidence. I’m sharing the link here so you can see exactly what I’m referring to. After that, I’ll walk through the facts and explain what’s really going on. https://www.instagram.com/reel/DLjIu7TtKmv/?igsh=NXh4dHdrenFiOGo1 The thyroid gland produces mostly T4 (thyroxine) and a much smaller amount of T3 (triiodothyronine). Rough ballpark: ~80–90% T4, ~10–20% T3. So the “20% T3, 80% T4” claim is somewhat misleading. The thyroid doesn’t make that much T3 directly—most circulating T3 is made peripherally, not in the thyroid gland. T4 is a prohormone. It must be converted to T3, the active form, inside tissues like liver, kidney, muscle, and brain. This conversion is catalyzed by deiodinase enzymes (D1, D2, D3), which remove an iodine atom. This is not a methylation reaction. There’s no methyl group transfer involved. The key nutrient cofactors are selenium (for deiodinase activity), iron, zinc, and adequate caloric/redox balance. Giving only T4 (levothyroxine) can be problematic in some individuals because if their deiodinase enzymes are impaired (due to stress, inflammation, nutrient deficiency, illness), they won’t convert enough T4 → T3, leaving them hypothyroid at the tissue level even if their TSH and T4 look “normal.” Giving only T3 can overshoot and create spikes, since T3 has a short half-life. That’s why some clinicians use a combination (like natural desiccated thyroid or compounded T4/T3).

The members have spoke and I listened....Most coaches talk about principles. Some share theory. Very few show you exactly what they do themselves. about to change that. I’m opening up my personal playbook, the protocol I run on myself, to show you how I structure my training, nutrition, supplementation, peptides, and recovery strategies to stay at the top of my game. This isn’t a “one-size-fits-all” plan. It’s the real system I use, built from: - Lab data and cellular feedback loops - Peptide science and mitochondrial optimization - Periodized training matched to performance goals - Nutrition timing dialed to physiology, not fads You’ll see the exact tools, dosages, timing, and reasoning I use and how I adjust based on metrics, recovery, and results. If you’ve ever wondered how a coach integrates the science into a living, breathing system… this is your chance to see it in action. Drop a 🔥 below if you want to see the full breakdown of The Coach’s Protocol.I will likely do this as a webinar. Let me know your thoughts who would be interested in seeing this to kick off our monthly case study feature.

How Your Body Chooses Fuel (And How to Tilt the Odds Toward Fat) By now, you’ve mobilized fat from storage (Part 1) and learned how to support the mitochondria so they can burn it efficiently (Part 2). But here’s the question that matters most: How does your body decide whether to burn fat or sugar? The answer isn’t random—it’s governed by tightly regulated signaling systems. And if you understand how they work, you can bias your metabolism toward fat oxidation without starving yourself or overtraining. At any given time, your body can use glucose, fatty acids, or ketones for fuel. Protein can be used too, but that's not ideal unless you’re undernourished or extremely glycogen-depleted. The fuel you burn depends on your internal environment mainly energy status, hormone levels, and cellular signaling. The primary switch that tilts metabolism toward fat burning is AMPK (AMP-activated protein kinase). AMPK is activated when energy is low like during fasting, exercise, or calorie deficits. It tells the cell: “We’re short on energy. Start breaking down fat, stop building things, and prioritize survival.” When AMPK is activated, several things happen: - It increases fatty acid uptake and oxidation - It downregulates mTOR (the growth/building pathway) - It enhances mitochondrial biogenesis and function - It inhibits anabolic processes like fat storage and protein synthesis This is the environment where fat is preferred over sugar as a fuel source. On the flip side, mTOR (mechanistic Target of Rapamycin) is a nutrient-sensing signal that turns on when energy and nutrients especially amino acids and insulin are abundant. It tells the body: “We’re good on energy. Let’s build, grow, and repair.” That’s great for hypertrophy or recovery but it shuts down fat oxidation. mTOR and AMPK work in opposition. You can't fully activate both at once. This is why timing matters. If you activate mTOR right after waking up with a large carb-heavy meal, you blunt the AMPK-driven fat-burning window you had from fasting overnight. But if you train fasted or push your first meal later (and keep it moderate in carbs), you extend the AMPK window and shift fuel use toward fat.

https://www.instagram.com/p/DM21Ta2PFWv/?utm_source=ig_web_copy_link Fat loss doesn’t start with cardio. Or fasting. Or even a calorie defecit it starts with a signal. That signal tells your body, “We need fuel. Tap into the reserves.”But unlocking stored fat is only half the story. The real challenge is getting that fat where it needs to go so it can actually be burned. Let’s break it down clearly: before fat can be used as energy, it has to go through two critical steps lipolysis and transport. Without both, there is no true fat loss. Fat is stored in your adipose tissue as triglycerides three fatty acids bound to a glycerol backbone. These are compact, stable, and metabolically inert. To use them for fuel, the body first breaks them apart. This is called lipolysis. Lipolysis is triggered when insulin is low and counter-regulatory hormones like adrenaline, cortisol, and growth hormone rise. Exercise, fasting, cold exposure, and stimulants can all push this button. The result: free fatty acids and glycerol are released into the bloodstream. But—and this is crucial—those fatty acids aren’t automatically burned.They’re just mobilized. Now they’re floating around, waiting to be used… or re-stored. If the next step transport doesn’t happen efficiently, those fatty acids never make it to the mitochondria. They get recycled, turned back into fat, or contribute to inflammation To reach the mitochondria, long-chain fatty acids require a shuttle system.That shuttle is carnitine. Carnitine binds to fatty acids and helps escort them across the inner mitochondrial membrane. This process is called the carnitine shuttle, and it’s the rate-limiting step in fat oxidation. If this system is underpowered, you’ll struggle to lose fat no matter how “in a deficit” you are. There are different forms of carnitine, each with unique properties. L-carnitine tartrate is used in performance and recovery settings. Acetyl-L-carnitine (ALCAR) crosses the blood-brain barrier and supports both mental energy and mitochondrial function. Carnitine fumarate adds cardiovascular support and works well in metabolic dysfunction. Injectable carnitine bypasses gut absorption issues and results in higher blood and tissue concentrations, making it especially effective when timed around fasted cardio or training.