@Anthony Castore what are your thoughts of TND1128 being superior over NMN as a NAD+ precursor? The studies I’ve read indicate that TND1128 is a superior MAM+ precursor for activating SIRTUINS, help self regulate redox, with anti antioxidant and anti-inflammatory properties. That being said, all the studies were conducted on mice and we know that there’s not a direct correlation.

I thought this might be right up your alley to discuss @Anthony Castore . I am seeing the topic pick up again about why you should avoid BPC/TB due to possible increase in cancer likelihood. I can't tell if this is all just fear mongering or not. There doesn't appear to be any evidence regarding this outside of referencing a mouse study that was done: ---------------------------------------------------------------------------------------------------------------------------------------------------------- "In most solid tumors studied in mice, including fibrosarcoma, melanoma, non-small cell lung cancer (NSCLC), colon cancer, and glioblastoma, TB4 overexpression promotes tumor growth, metastasis, and angiogenesis." ----------------------------------------------------------------------------------------------------------------------------------------------------------- One person is stating that since BPC up-regulates VEGF, this would be a pathway towards cancer development (below is what they posted). ----------------------------------------------------------------------------------------------------------------------------------------------- VEGF is historically a promoting factor in oncological aspects rather than causative, but this isn't the only concern. VEGF was originally named "vascular permeability factor" for a reason. It opens gaps between endothelial cells, letting plasma proteins and fluid leak into the interstitial space. Off-target stimulation means edema in tissues that don't need increased perfusion. The problem is that VEGF receptors sit on endothelial cells throughout the entire body, not just in the tissue you're trying to help. So if VEGF reaches non-target tissues, several things go wrong. It can produce off-target angiogenesis, meaning new blood vessel growth where you do not want it. That can produce abnormal, fragile, leaky vessels rather than healthy functional ones. VEGF also increases vascular permeability, so tissue can become swollen or edematous. PMID: 35969170, 20400620

Has anyone here used ARA290?

Low energy is one of the most common complaints in medicine, coaching, and everyday life, yet it is one of the least precisely understood. People describe it as fatigue, burnout, brain fog, weakness, lack of motivation, or feeling “offline.” Athletes feel it when they cannot train. Patients feel it when they cannot work. High performers feel it when discipline no longer works. The problem is that “low energy” is not a diagnosis. It is a surface description of a system-level failure, and two people can experience nearly identical symptoms while the underlying biology is completely different. Treating them the same way helps one person and harms the other. To understand low energy correctly, you have to stop asking how to boost energy and start asking why energy is being limited in the first place. At the deepest level, there are two dominant failure modes. In one, the body cannot produce enough energy. In the other, the body is deliberately suppressing energy production. The first is mitochondrial damage, a capacity problem. The second is inflammatory inhibition, a regulatory decision. One is a broken engine. The other is a functioning engine with the brakes applied. Subjectively they feel similar. Biologically they are opposites. Everything that follows depends on recognizing which one you are dealing with. A simple model helps. Imagine the body as a car. The mitochondria are the engine. They take fuel and oxygen and convert them into usable energy in the form of ATP. Inflammation acts like the central control computer, deciding how much power the engine is allowed to produce. If the engine is damaged, pressing the accelerator does little. If the computer is limiting output, the engine could perform, but is being intentionally restrained. In both cases the car goes slow. Only one responds to pushing harder. Mitochondria exist inside nearly every cell and are responsible for producing ATP, the molecule that powers muscle contraction, nerve signaling, hormone synthesis, immune regulation, tissue repair, and cognition. Without adequate ATP, nothing in the body functions well. Energy production depends on intact mitochondrial membranes, functioning enzymes, proper redox balance, sufficient oxygen delivery, and a steady supply of micronutrients. When any part of this system is damaged, the maximum amount of energy the body can generate drops. This is not a motivational issue. It is a hard ceiling.

What protocol do you follow to minimize jet lag, avoid drops in HRV, and improve sleep after traveling to a different time zone? @Anthony Castore