My friend's 72 year old mother had a stroke a year ago and recently tried ketones (not the kind you recommend, but the one pictured) and her aides said it made her difficult and anxious. I'm curious as to why or how this could do that. Do you think she needed a smaller dose to start with or is the electrolytes in this formulation the cause of throwing her off balance?

Hi Anthony, I recently saw this rodent study done by Ben Bikman's lab on BHB and 1,3 BD. https://www.mdpi.com/2072-6643/18/4/675 This study found: "1,3 BD induces significant hepatic stress characterized by ATP depletion, oxidative stress, and lipid accumulation. These results align with and extend recent findings by Ari and D’Agostino demonstrating formulation-dependent hepatic outcomes of chronic ketone supplementation, where ketone salts preserved liver health while BD-based ketone esters and precursors drove inflammation and steatosis" What are your thoughts on their findings? Does their study design bias the outcome? Are there similar studies that show that 1,3 BD is neutral in its effects? Does KineticPro or KE4 use ketones that are different than what was studied here? (It looks the same to my naive and uninformed eyes, so that's why I'm asking.)

VISION, POSTURE, COGNITION, AND PERFORMANCE: HOW MEMBRANES GOVERN THE WHOLE ORGANISM Up to this point, we’ve stayed mostly at the cellular and membrane level. Conductors, buffers, mitochondria, failure modes. That work matters, but if it stays abstract it risks feeling disconnected from lived experience. So in this part, we zoom out. Membrane health doesn’t just determine what happens inside cells. It determines how an organism perceives the world, organizes its body, and decides how much stress it can tolerate. This is where DHA stops being a biochemical curiosity and becomes something you can see in posture, feel in cognition, and observe in performance. Let’s start with vision. Vision is often treated as a sensory add-on. Something that delivers information to the brain, where the “real work” happens. That framing is backwards. Vision is a primary regulator of autonomic tone. The retina is not just detecting light. It is converting photons into electron movement. That electron movement sets timing signals that propagate through the nervous system. These signals influence circadian rhythm, arousal state, muscle tone, and spatial orientation. The retina is one of the most DHA-dense tissues in the human body for a reason. Phototransduction is a high-frequency, high-precision process. Light hits photoreceptors, electrons move, ion channels open, and signals propagate in milliseconds. The system must respond quickly and reset just as fast. Any noise or delay degrades perception and increases stress. DHA allows retinal membranes to maintain signal fidelity under constant flux. It improves signal-to-noise and shortens recovery time between inputs. When DHA is insufficient, or when membranes are oxidatively unstable, the retina becomes noisy. The system compensates by increasing sympathetic tone. The body becomes more vigilant, more guarded, less adaptable. This is not psychological. It is electrical. From the retina, this tone propagates. Visual instability increases neck and jaw tone.

DHA, PLASMALOGENS, AND MITOCHONDRIAL MEMBRANE POTENTIAL: POWER WITHOUT INSTABILITY At this point in the series, one thing should be clear: membranes are not passive. They are active regulators of signal timing, electron flow, and system stability. Nowhere is that more consequential than in the mitochondria. Most conversations about mitochondria focus on output. ATP. Energy. Fuel utilization. Fat versus glucose. Those discussions matter, but they start too late in the causal chain. Mitochondria do not fail because they lack fuel. They fail because electron flow becomes unstable. To understand why DHA and plasmalogens matter here, we need to talk about mitochondrial membrane potential, often abbreviated as ΔΨm. ΔΨm is usually described as voltage. A battery. A charge gradient across the inner mitochondrial membrane. That description is technically accurate, but conceptually incomplete. ΔΨm is not just how much charge exists. It is how controlled that charge is. A stable membrane potential means electrons move smoothly through the electron transport chain, protons are pumped predictably, and ATP synthase can operate efficiently. An unstable membrane potential means electrons back up, leak, and react with oxygen in places they shouldn’t. This is where most mitochondrial dysfunction actually begins. The inner mitochondrial membrane is not just a lipid barrier. It is a highly specialized electrical interface. It contains densely packed protein complexes, curved membrane structures, and unique lipid compositions. Its job is not to hold charge. Its job is to manage electron flow under load. DHA and plasmalogens directly influence how well it does that job. DHA alters the dielectric properties of the membrane. In practical terms, it changes how electric fields behave within the membrane. It reduces resistance to lateral electron movement and improves the probability that electrons move forward through the chain instead of backing up. This matters at Complex I and Complex III in particular, where electron congestion commonly occurs.

Hey friends, I’m reaching out because I’m walking through something really scary right now, and I would really appreciate your wisdom, experience, and prayers. About three weeks ago, I was hit with a really rough virus. I thought I was on the mend… and then about a week ago I suddenly started losing vision — first in my left eye, then in my right. I ended up in the hospital terrified and confused, not understanding what was happening to my body. While I was there, they ran a ton of tests — full blood panels, autoimmune workups, MRI, and even a lumbar puncture. Most of the autoimmune conditions they tested for have been ruled out, but I’m still waiting on a few more results that take longer, including the GFAP panel. Right now I’m sitting at about 50% vision loss in both eyes, which has been one of the most emotional and humbling experiences of my life. The neuro-ophthalmologist said ischemic optic neuropathy is still a possibility, but there are signs that make him hopeful it could instead be post-/para-infectious optic papillitis — inflammation of the optic nerve triggered by the virus I had. This is treatable, but recovery can be slow, sometimes taking a month or more before improvement begins. I’ve been on steroids for a week now with no major changes yet. I’m also feeling some nerve pain behind my right eye, which can happen during healing, but it’s hard not to worry when you’re living it. To support myself, I’ve been using: - Steroids - BPC-157 - Anti-inflammatory + gut support - Rest and as much calm as possible But this community has so much collective wisdom, especially around peptides, neuro repair, and post-viral healing — so I’m reaching out. If you have experience with optic nerve inflammation, optic neuritis, nerve repair, or post-infectious healing — what peptides, supplements, or approaches would you consider supportive right now? (ARA-290, TA-1, SS-31, MOTS-c, glutathione, SPMs, NAC, high-dose omega-3s, etc.) This whole situation has really tested me but I’m doing everything I can to support healing while staying safe. Any insight, personal experiences, or encouragement would mean the world to me right now.