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💪🏼 I help people become the best versions of themselves 🥑 A ketogenic fasting approach to health, fitness & nutrition ⬇️ Sign up – LIMITED SPOTS

Nordrhein-Westfalen, Deutschla
Joined February 2021
Photo by ketOntrack (@ketontrack)Photo by ketOntrack (@ketontrack)Photo by ketOntrack (@ketontrack)Photo by ketOntrack (@ketontrack)Photo by ketOntrack (@ketontrack)Photo by ketOntrack (@ketontrack)Photo by ketOntrack (@ketontrack)Photo by ketOntrack (@ketontrack)Photo by ketOntrack (@ketontrack)
Why keto is still debated 1.Glucose metabolism has been investigated for the last 300 years when we still didn't know how respiration was working. There was a number of scientists from Lavoisier to Warburg and Krebs who established the foundation of our current understanding. 1/
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🚨👋I’m launching a Substack to write about metabolism, sports performance, mitochondrial function, metabolic health, cancer metabolism, longevity... I’m starting with two pieces!. The first addresses the recent review “Much Ado About Zone 2.” My position is simple: the debate between Zone 2 and HIIT is largely artificial. In real training environments, both intensities coexist and always have. The second article explains the physiology behind Zone 2, something that is often simplified or misunderstood. Zone 2 is not just a training label. It reflects a specific metabolic state defined by redox balance, mitochondrial flux, and lactate shuttle equilibrium. Thirty years working with elite athletes and metabolic patients led me to this framework. Links below: Article 1 — Why the Zone 2 vs HIIT debate is largely misguided inigosanmillan.substack.com/… Article 2 — The cellular physiology that actually defines Zone 2 inigosanmillan.substack.com/… If this topic and others interests you, feel free to subscribe. I’ll be writing regularly about metabolism, performance, metabolic health, mitochondrial function, cancer metabolism...Thank you!😉
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For about a decade, I’ve been showing these two slides at conferences. Two hunter-gatherer populations (Hadza and Tsimane), likely the closest living humans to our Paleolithic ancestors. Diet: • 65–70% carbohydrates • 15-20% protein • 10–15% fat • ~13% lower daily caloric intake than the US population Daily movement: • 115–135 minutes per day • 6–12 km of walking Health outcomes: • Obesity: ~2% • Type 2 diabetes: ~1% • Cardiovascular disease: among the lowest ever observed This is not a low-carbohydrate population. The difference is metabolic fitness. When mitochondria are continuously stimulated by daily movement, carbohydrates can be oxidized (burnt). When movement disappears, fuel oxidation fails and metabolic disease emerges. The debate should not be low-carb vs high-carb. That debate has failed to solve obesity or type 2 diabetes for decades. The real question is: Can your mitochondria still do their job? #MitochondrialFunction #MetabolicFitness #MetabolicFlexibility #PhysicalActivity
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Context: a few months ago I wrote (link in next comment) about how the triple agonist retatrutide appears to "work" via mechanisms in common with the state of ketosis. In the article I also pointed to @garytaubes ' article pointing out that previous GLP-1RAs already appear to induce fuel partitioning. Today I learned that there is evidence from @JohnSpeakman4 and his group that semaglutide via AMPK (shared pathway with ketogenic diets) is also improving osteoarthritis. My feeling is that this kind of research is good news for both nutritional ketogenic therapies and for GLP-1RAs. As we get better and better ketosis mimetics it will help clarify what each can and cannot do, how they are different and how they are the same. cell.com/cell-metabolism/abs…
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It will take some time until the algorithm gets kicked off again. But how much time? – at Düsseldorf, Germany
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There is one good thing with hospitals. They serve all three meals at the same time. 8-12-17. That is almost a 16-hour fast - want it or not. Water in between and one coffee after breakfast. – at Düsseldorf, Germany
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And you sleep proper hours. No mobiles, lights and the likes – at Düsseldorf, Germany
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Replying to @ketontrack
1.) N-telopeptide and C-telopeptide in blood and/or urine (bone breakdown markers) 2.) Urinary pH, citrate, ammonium and calcium 3.) High Resolution CT scan of the bone (cortical bone thinning and/or decrease in cortical bone porosity) 4.) Serum CO2/bicarbonate (usually won’t be clinically low but lower end of normal) 5.) BUN, cystatin C, albumin 6.) PaCO2 (ventilatory compensation during acidosis)
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HIGH ANIMAL PROTEIN (without base) can lead to NEGATIVE CALCIUM BALANCE, BONE BREAKDOWN and increased PROPENSITY for VASCULAR CALCIFICATIONS
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ketOntrack retweeted
A single night of sleep can now predict 130 future diseases with up to 93% accuracy. Stanford researchers just released SleepFM. This is a multimodal foundation model trained on 585,000 hours of physiological data from 65,000 participants. And it's actually insane: (1/5)
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Suppose you eat some bread in the morning and sushi 🍣 at 12 pm. What fuel would you be burning at 4 pm? Carbs , fat, mix ? And how would you measure it? – at Düsseldorf, Germany
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4-5h of walking a day on 1,850kcal... no weight loss. CICO defeated once again🤣
Anywhere from 4-5 hours depending how fast he was walking. 1,850kcals But hey, he’s not autistic or anything and he didn’t track lol. Just more steps and lessss food!
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Everyone wants the shortcut to longevity. Pills, powders, boosters, activators, molecules that promise to “hack” aging. But let’s be honest: 👉 There’s no solid scientific evidence that almost any of these supplements extend human lifespan or healthspan. Most studies are mechanistic, in mice, or rely on surrogate markers, not real-world outcomes. And here’s the paradox: The people who live the longest on this planet have never heard of NMN, NAD⁺, or rapamycin. They walk daily, eat natural unprocessed food, have purpose, strong community ties and low chronic stress. Longevity doesn’t come from a capsule. It comes from metabolic health, movement, connection, and consistency; the same foundations that modern science is still trying to replicate in pill form. Longevity isn’t hacked. It’s earned.
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Common experience on Carnivore that scaling back the protein in favour of beef fat trimmings can be a game changer in brain function. Also, yes, high protein often causes nocturia.
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New POST - The ability, to produce energy without treating everything as a crisis, is the essence of metabolic health. What happens if you don't? ketontrack.substack.com/p/me… 1/
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A metabolically flexible person can increase energy output while keeping this buffering under control, CO₂ rises gradually, breathing stays calm. An inflexible metabolism (RER close to 1) relies on glycolysis too early resulting in many problems. 4/
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Your mitochondria are always answering the same question: What substrate do I need to deliver this task. What substrate are you using?
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This would explain why fructose is a huge problem if you're PUFA'd, but not if you're metabolically well. Lesson for Peaters: deplete linoleic acid for a couple years until you're confirmed low. Then you can indulge in sugar. "Fructose activates oxidative stress. If membranes contain enough omega-6 polyunsaturated fatty acids derived from linoleic acid, sufficient aldehydes will be produced to activate AR — and thus the polyol pathway. The vicious cycle closes and becomes increasingly self-reinforcing."
The Vicious Cycle Causing Obesity More detailed explanation. This is a model of obesity development. The base image comes from a study on mouse obesity. At the end, there’s a large “WG,” meaning weight gain. doi.org/10.1016/j.redox.2021… 1/16
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