Does anyone have a DR that prescribe and will work with compounding pharms like VPI or CRE8? My knees are in poor shape after years of abuse training Martial Arts. Appreciate your help and this community.

I’ve been running 250mcg SLU-PP-332 fasted AM 5x weekly. Taken with NR, Urolithin A, Fatty15. I’m going to be increasing my dose to 500mcg and curious if people are having more success going with a bolus dose and taking the full 500mcg AM, or splitting it 250 AM and 250 afternoon?

Here’s a StoryBrand-style rewrite of your promo (clear problem → guide → plan → success → call to action): Most people who hear about new compounds like SLU-PP332 get stuck in two places: 1. The science feels too complicated. 2. The real-world application is missing. That’s frustrating, because you want to know if this tool can actually help you perform better, recover faster, and think clearer. Tomorrow morning at 10 a.m. Eastern, I’ll guide you through exactly what you need to know about SLU-PP332. You’ll get:• The backstory of where it came from and why it matters.• A simple explanation of how it works inside your cells.• Real-world dosing strategies you can actually use.• Objective and subjective ways to track if it’s working.• The key things you need in place to make it most effective. This isn’t about hype. It’s about clarity. When you understand both the science and the strategy, you stop guessing and start building momentum with confidence. Join us live tomorrow at 10 a.m. Eastern. The link is in the community calendar. Be part of the group that learns to use this breakthrough the right way while everyone else is still confused by the noise.

We’ve talked about what FGF21 is, when it rises, how it changes your mitochondria, and what science has shown us. Now let’s put it all together into something you can actually use. FGF21 isn’t a hormone you want blasting all the time. It works like a reset button short pulses of it help your mitochondria adapt and stay flexible. The key is to create the right contrast: some days that push it high, and other days that let it fall so your body stays sensitive. Here are the main levers you can pull: 1. Strategic sugar or carb surges. On training days, especially when you’re lifting hard or doing intervals, a surge of carbs with very low fat can spike FGF21. This is like revving your engine on purpose—it makes the mitochondria split into more units (fission) to keep up with demand. 2. Low-calorie or fasting days. On recovery or rest days, pulling calories back especially carbs and protein helps mitochondria repair (fusion) and recycle damaged parts (mitophagy). This is like parking the car in the shop so it can get tuned up. 3. Exercise. Whether it’s cardio, strength training, or even just a brisk walk, exercise is a universal trigger for FGF21. It’s like the master switch that makes sure your cells are ready to handle whatever fuel you throw at them. 4. Environmental stressors. Cold showers, sauna, or even just walking outside in the winter can bump up FGF21. These little stressors teach your mitochondria to stay resilient. 5. Support stack. Peptides like MOTS-c or SS-31, nutrients like CoQ10 and carnitine, and lifestyle choices like good sleep all improve how your body responds to FGF21. Think of these as the supporting cast that make the conductor’s job easier. Sample Weekly Calendar (200-lb man, 4 training days) Monday (Training – Fission Day)High carbs, low fat, lean protein. Example: fruit, juices, honey during the day; lean chicken and veggies at night. Tuesday (Rest – Fusion Day)Low calorie, higher fat, lots of vegetables. Example: salad with salmon and olive oil, roasted broccoli, eggs.

Glucose matters, but so does the ability to switch away from it. Metabolic flexibility, the capacity to toggle between carbohydrate and fat oxidation as conditions change, is a core health trait. Loss of this flexibility (leaning chronically on any single fuel, whether glucose or fat) drives mismatch between fuel supply and oxidation, promotes ectopic lipid or glycogen accumulation, and sets up insulin resistance, mitochondrial stress, and redox imbalance [4,5,6]. Beyond ATP, glucose feeds the pentose phosphate pathway (PPP) to make NADPH, which maintains the glutathione system and broader antioxidant defense. In states of high oxidative demand or low oxygen, routing glucose through glycolysis/PPP supports redox homeostasis; starving these pathways can impair cellular repair and antioxidant capacity. Recent Cell Metabolism work highlights glycogen->PPP flux as an "extramitochondrial redox hub" sustaining cytosolic NADPH [1,2,3]. The Randle (glucose-fatty acid) cycle shows that sustained dominance of one substrate suppresses the other for example, high fatty acid oxidation inhibits glucose oxidation and vice versa [4,5]. Over time, this competitive inhibition, combined with nutrient excess, leads to intramyocellular lipid accumulation, impaired PDH activity, and insulin resistance - classic metabolic inflexibility [5]. Exercise restores the switch: training induces tissue-specific adaptations (PGC-1alpha programs, mitochondrial biogenesis, improved substrate transport) that enhance the ability to alternate between fuels and improve cardiometabolic health. Physical inactivity does the opposite, leading to glycogen overaccumulation, reduced oxidative capacity, and impaired redox balance [6,7]. Bottom line, glucose isn't the villain; chronic overreliance on glucose (or fat) is. Protect redox by preserving the switch - periodize intake and training so the system regularly uses both glycolysis/PPP and fat oxidation, rather than locking into one lane.