This question keeps me worried all the time. Alex Kikel mentioned it multiple times. That through receptors crass-talk it can do it. What's your personal opinion on it? Is it possible technically ? Do you know someone who suffered from gyno caused by SLU ?

@Anthony Castore As far as the nutrition on certain days https://youtu.be/roB4KfR-_hg?si=ry06iHvv5ta2Y2q3

I’m wondering where everyone gets their injectible peptides from? Anthony, does SSRP have a preferred source that us in the community could purchase from? Any online clinic where a virtual consult could be done and the peptides prescribed from a compounding pharmacy and shipped to our residence? I have a functional medicine doctor in miami but he requires you pick them up and they are already reconstituted which affects their expiration.

Sleep is not passive. It is one of the most energy-demanding things the body does. Repair, detoxification, memory consolidation, immune recalibration, and cellular cleanup all require ATP. This is where aging quietly sabotages sleep. As cells lose efficiency, sleep becomes harder to enter and harder to sustain. Children sleep well because their mitochondria are powerful, flexible, and responsive. Energy production is efficient. Waste is cleared quickly. Signals are clean. Adults carry years of oxidative stress, inflammation, and metabolic strain. Mitochondria still work, but they work at a higher cost. Every cell has to decide how to allocate energy. When energy is abundant, repair is prioritized. When energy is scarce or inefficient, survival comes first. Sleep sits downstream of that decision. As mitochondria age, several things happen at once. Electron transport becomes less efficient. More reactive oxygen species are generated per unit of ATP. Redox balance shifts. The cost of maintaining membrane potential rises. Cells become more sensitive to stress. This matters because sleep requires coordinated downshifting across the entire system. If cells are struggling to maintain basic function, they resist the drop in activity that sleep demands. Think of it like an old engine. When it runs well, you can idle smoothly. When it is worn, idling causes stalling. The system compensates by keeping the RPMs slightly elevated. That compensation feels like light sleep, fragmentation, or early waking. Inflammation further disrupts sleep. As people age, low-grade inflammation becomes more common. Inflammatory signals stimulate the brain and alter neurotransmitter balance. The brain becomes more reactive. Sleep becomes lighter. Children have lower baseline inflammation. Their immune systems are adaptive, not chronically activated. Adults carry unresolved immune activation from stress, poor sleep, infections, gut issues, and metabolic disease. Sleep both suffers and contributes to this cycle.

Most conversations about mitochondria start in the wrong place. They start with energy production, ATP output, or how to “boost” mitochondria. That framing misses the real problem. Mitochondria don’t usually fail because they can’t make energy. They fail because the physical structure that allows energy to be made cleanly and efficiently becomes unstable. Once structure is compromised, every attempt to push energy production creates more noise, more oxidative stress, and more dysfunction. This is why people can have “normal” labs yet feel exhausted, wired, inflamed, or unable to recover. The issue isn’t fuel. It’s architecture. To understand this, we need to zoom in to the level of mitochondrial structure. Inside every mitochondrion is an inner membrane that folds inward into structures called cristae. These folds are not random. They are precisely shaped, tightly regulated, and essential for efficient energy production. Cristae dramatically increase surface area, but more importantly, they organize the electron transport chain into coherent, functional units. The electron transport chain is not just a series of enzymes floating in space. It is a spatially organized system embedded in the inner membrane. Distance between complexes, membrane curvature, lipid composition, and membrane tension all matter. A helpful analogy is an accordion. When the folds are evenly spaced, elastic, and well aligned, air flows smoothly and predictably. When the folds become stiff, warped, or collapsed, airflow becomes turbulent and inefficient. The same thing happens with electrons inside mitochondria. Electrons enter the electron transport chain and move through complexes I, II, III, and IV. As they move, they pump protons across the inner membrane, creating a proton gradient called membrane potential. ATP synthase then uses that gradient to produce ATP. When cristae structure is intact, electrons flow smoothly, protons are distributed evenly, ATP is produced efficiently, and reactive oxygen species remain low. When cristae structure is compromised, electrons leak, protons accumulate unevenly, membrane potential becomes excessive or unstable, and reactive oxygen species rise.