For eastbound travel, the goal is to advance the clock only as fast as the nervous system can tolerate. On arrival morning, wake on local time but prioritize calm over performance. Take 10–20 g of ketone monoester on waking with water and electrolytes to stabilize energy and reduce oxidative and inflammatory load from sleep loss. If ketones create anxiety or agitation, reduce the dose rather than pushing through. Within the first hour, get gentle outdoor light paired with very light movement such as walking or mobility, stopping before fatigue rises. This anchors the central clock only if the nervous system feels safe enough to receive the signal. Eat your first meal early on local time, but keep it small and protein-forward if digestion feels off. Do 5–10 minutes of easy walking after meals to support peripheral clock alignment without metabolic stress. If energy or HRV drops midday, a small second ketone dose of 5–10 g can be used as temporary support, but only if it does not delay evening sleep pressure. Dinner should be early and light, food stopped at least three hours before bed, with strict avoidance of bright light at night. If sleep remains fragmented, do not escalate stimulation; reduce inputs and allow recovery to lead entrainment. For westbound travel, the goal is to delay the clock without overstimulation. Wake slightly later if needed, but still begin the day with hydration and 10–20 g of ketone monoester to stabilize energy and blunt inflammatory signaling. Delay light exposure and movement until later morning or early afternoon, keeping intensity low and rhythmic. Delay the first substantial meal until later in the day, keeping portions modest if digestion is slow. Walk briefly after meals to help muscle and liver clocks adapt. If an afternoon crash occurs, use a small ketone dose (5–10 g) instead of stacking caffeine. Dinner can be slightly later but should remain light, and food should still stop three hours before bed. In both directions, hydration with electrolytes is continuous and non-negotiable, especially in the first 48 hours. Avoid high-intensity training, long endurance work, and alcohol until HRV and resting heart rate normalize. Ketones are used as scaffolding, not as a way to override fatigue. If ketones maintain alertness but sleep depth does not rebound after two nights, reduce dosing rather than increasing it. Evening ketones are generally avoided; in rare cases of extreme sympathetic activation, a very small early-evening dose (3–5 g) can be tested once and discontinued immediately if sleep worsens.

I would not use GLOW at all, regardless of whether it’s mixed or injected separately. It’s a blended peptide product, which already creates problems at the level of chemistry, dosing precision, and signal control. You’re not administering a defined molecule with a known pharmacokinetic profile. You’re injecting a variable system where stability, relative ratios, and degradation pathways are not controlled. That alone makes it a non-starter for me. On glutathione injections, my concern is not limited to whether it degrades GHK when physically mixed. The deeper issue is redox signaling. Glutathione is not just an antioxidant. It is a dominant intracellular redox buffer. When you inject it exogenously, especially repeatedly or at higher doses, you can push the system into an artificially reduced state. That suppresses the very redox gradients that peptides like GHK-Cu rely on to signal repair, remodeling, and gene expression. Tissue regeneration is a redox-regulated process. Blunting ROS too aggressively interferes with adaptive signaling, not just oxidative damage. GHK’s biological activity depends on metal coordination dynamics (especially copper), redox cycling, and localized oxidative signaling. Glutathione has a strong affinity for copper and participates in thiol-based redox reactions. Whether or not the two are in the same syringe, elevated extracellular or intracellular glutathione shifts copper availability, alters redox tone, and can blunt GHK’s downstream effects. So while direct chemical degradation is most obvious when mixed in solution, functional antagonism can still occur even when injected separately. So the problem is not simply “does glutathione degrade GHK if mixed?” The real problem is that glutathione changes the signaling environment that GHK and other regenerative peptides require to work properly. GLOW is flawed because blended peptides remove control and introduce instability and signal noise. Injectable glutathione often disrupts redox signaling rather than supporting it. Even when injected separately, glutathione can blunt or counteract peptide-driven repair by flattening redox gradients and interfering with metal-dependent signaling.

Great question and I’m glad you asked for clarification.I should have been clearer in my wording, GHK-Cu by itself is fine, and yes, it has been part of my toolbox. That hasn’t changed. What I’m referring to when I say I avoid “both” is the practice of blending peptides or pairing GHK-Cu with exogenous glutathione, especially in injectable form. Those are very different decisions than using GHK-Cu on its own. I almost never use exogenous glutathione. Not because it’s “bad,” but because it forces redox in one direction and can mask whether the system actually has the capacity to handle repair and signaling. In many people, it creates short-term relief at the cost of long-term signaling clarity. GHK-Cu is different. It’s a context-dependent signal, not a blanket reducer. Used appropriately, it can support tissue repair, copper trafficking, and ECM remodeling without artificially flattening redox gradients. That said, I don’t treat it as a default either. Its use depends on the redox state, inflammatory tone, mitochondrial capacity, and timing within a broader protocol.There aren’t really hard rules here other than DON’T MIX PEPTIDES (I feel pretty strongly about that 😉). I try not to think in terms of “always” or “never.” Decisions should be built around context and redox, not dogma. I appreciate the thoughtful question this is exactly the kind of nuance that tends to get lost online. I hope this clears it up.

@Drew Wurst Thank you 🙏

@Anton Sh there isn’t a recording, but inside the Circle community I’ll be breaking down and critiquing my previous protocol (there’s a lot I’d do differently now), then walking through my current approach, how I evaluate effectiveness, and the decision-making behind tool selection, cycling, and lifestyle support.

That is definitely not me. I will find out who this is and get them booted and report them to Skool. Thank you again!

Thank you 🙏 I will have to be more selective about who I let in the community. It is unfortunate these spammers are out there

In plain physics terms, water is weakly diamagnetic, and the magnetic fields you can realistically put around a household pipe are far too small and inconsistent to create a stable, persistent “re-structured” state once the water leaves the field. Any short-lived changes in dissolved gas, microbubbles, temperature gradients, flow turbulence, or mineral precipitation will dominate what you perceive as “different” water. If you notice an effect, it’s likely from: 1. degassing/CO₂ changes 2. temperature 3. mineral scaling/precipitation behavior 4. flow rate/shear 5. taste changes from the pipe material itself. Mist people will get pretty far if they prioritize what actually changes physiology: low contaminants + correct minerals + good CO₂/temperature + consistent intake. Neutral osmolytes can be helpful as well.

Great question. I do take Pollack’s work seriously, and I don’t dismiss EZ water as a concept. I think where people go wrong is treating EZ water as something separate or magical that you “add” to the body. My view is that EZ water formation is more of a downstream outcome of good cellular conditions, not a primary lever you pull directly. In other words, the body naturally forms structured water when proteins are properly folded, membranes are healthy, mitochondria are working efficiently, redox balance is good, and inflammation is low. If those things are off, trying to force EZ water with external hacks misses the point. So yes, promoting conditions that favor EZ water formation absolutely makes sense things like light exposure, proper mineral balance, healthy membranes, good mitochondrial function, and reduced oxidative stress. I’m less convinced by approaches that focus on EZ water as the starting point rather than the result. My stance isn’t anti-EZ water; it’s that fixing the biology that allows EZ water to form is the more reliable strategy.