Hi all! I’m looking for advice regarding dosing and injection site recommendations for plantar fasciitis. I know it can be beneficial when injected close to the injury, but not sure how that would work sub Q on a foot. 😄 Thanks!

@Anthony Castore would love your thoughts on this video. I received it from a bunch of people. I don’t agree with his overall logic based on personal experience and that of a couple dozen others I personally know. The comments show even more. Studies never (or rarely) show micro dosing. And I also realize micro dosing has been bastardized from its original meaning to be more of a split dosing protocol. Studies typically deal with those that have T2D and/or Obesity and we know metabolically that’s not the same at all as someone just wanting a boost or reset that maybe has low-grade insulin resistance or inflammation, etc. https://youtu.be/PZtKV9DjRxQ?si=9AQiebL7MStjHOTX

I have what I believe to be an acute strain to the plantar fascia. (36 hours) Trying NOT to throw the kitchen sink at it. Readily available to me BPC-157, TB-500 GHK-CU, KPV Cartalax Red light - R+ | NIR+ wavelengths of 480nm, 630nm, 660nm, 810nm, 830nm, 850nm and 1060nm. I believe caused by increased overuse and chronic dehydration. Also fairly certain Pickleball was invented by orthopedists.

Monthly Q&A is Wed, Sept 24th at 12pm EST! Peptides, mitochondria, training, recovery, redox, nutrition nothing off limits. Can’t make it? It’s recorded. Send your questions ahead & I’ll tackle as many as possible. Don’t miss this one! Anthony Castore is inviting you to a scheduled Zoom meeting. Topic: Anthony Castore's Zoom Meeting Time: Sep 24, 2025 12:00 PM Eastern Time (US and Canada) Join Zoom Meeting https://us06web.zoom.us/j/3374982270?pwd=df4BMZNo1LubZaVOX40y7ApApJMNh1.1&omn=86062393294 Meeting ID: 337 498 2270 Passcode: 12345 --- One tap mobile +13052241968,,3374982270#,,,,*12345# US +13017158592,,3374982270#,,,,*12345# US (Washington DC) Join instructions https://us06web.zoom.us/meetings/86062393294/invitations?signature=ifWS2d8Nthqfmi1D1qiFFAu-MxuZwFKHQvHy7dxGD68

One of the most powerful ideas in cellular medicine is that the “invisible” can be made visible. The pathways and dominoes that tumble inside our cells aren’t just abstract concepts—they leave fingerprints that can be measured. Biomarkers are those fingerprints. They are the translation between mechanistic stress and clinical awareness, the way we can peer inside the dance of mitochondria, immune tone, vascular health, and repair. In kidney disease, the biomarker story tells us exactly how the first domino set the others into motion. Think first of redox balance. When mitochondria lean too heavily on glycolysis and electron flow becomes inefficient, NAD+ pools drain and NADH builds. The NAD+/NADH ratio is the gold-standard reflection of redox status, showing whether the cell is running smoothly on oxidative phosphorylation or choking on excess reducing equivalents. A low ratio means sirtuins like SIRT1 and SIRT3 are silenced, leaving DNA less protected and repair less efficient. It’s like a city that once had a thriving team of repair crews, now sitting idle because their wages dried up. Alongside this, the lactate-to-pyruvate ratio offers a more accessible proxy. High lactate with relatively low pyruvate tells us glycolysis has become dominant, confirming that cells are leaning on the quick-and-dirty survival pathway rather than efficient respiration. As the imbalance spreads outward, we can track inflammation. hsCRP is a workhorse biomarker here. Elevated levels tell us that NF-κB has been turned on, driving a persistent inflammatory tone. But hsCRP alone is blunt—it’s like knowing a fire alarm is ringing but not knowing which room the fire is in. Cytokine panels offer more nuance: IL-6 and TNF-alpha elevations confirm pro-inflammatory dominance, while low IL-10 shows that resolution is missing. In kidney disease, this trio tells us not just that inflammation is present, but that it is locked into the maladaptive side of the cycle. The vasculature offers its own set of clues. Nitric oxide metabolites can be measured directly, reflecting endothelial flexibility. Low NO levels indicate that PI3K/AKT and eNOS are faltering. Flow-mediated dilation (FMD), a functional vascular test, demonstrates whether blood vessels can widen smoothly in response to increased flow. Poor FMD is a functional echo of what is happening in the kidney’s glomeruli: rigid vessels transmitting mechanical stress downstream. Add in ICAM and VCAM, adhesion molecules that rise when endothelial walls are inflamed, and you have a detailed map of how the traffic lights of circulation are failing.