Thread by @DrJackKruse

1. Lesson: Question asked

40yr old male,
6ft, 180lbs,
maternal haplotype J1, currently living at 47th latitude N
fasting insulin = 7.7 (in winter)
Good/high cholesterol numbers
Muscular, but not a shredded hypertrophied build, just solid

Without any other information can my weight and/or fasting insulin be characterized as optimal/sub optimal and can you offer a directional (you should aim to weigh more or less or have a lower fasting insulin) based on this limited information I’ve provided?

Experimenting with different meal composition/timing (Randle cycle) as well as timing/duration/temperature of cold baths in trying to understand my own body composition levers.

Thank you.

2. All you need to know about food timing.

3. Client answered: Thank you…if I’m going to eat or have coffee before sunrise (a no no, I know) in winter at 47N latitude I have noticed how using the Firewave first thing upon waking makes a difference.

Answer: Real sunlight not fake red light.

4. The Randle cycle (glucose-fatty acid cycle) perfectly slots into my decentralized light-PER2-HIF-1α framework as the downstream executor of rhythmic fuel switching, ensuring metabolic flexibility between glucose oxidation (daytime/postprandial) and fatty acid beta-oxidation (fasting/nocturnal anticipation).

Proper sunrise entrainment maintains this reciprocity for β-state efficiency; light dark desynchrony drives pseudohypoxia-like rigidity, favoring glycolysis and contributing to insulin resistance/T2D.

Fake light raise BG and insulin and fake red light lowers both but not as much as the sun does because sunlight is unpolarized. Fake lights are always polarized and this effects tissue optic chiral via CISS.

5. Healthy entrainment (morning red/IR-dominant light → PER2 amplitude ↑ → HIF-1α gated/recruited appropriately): PER2 promotes oxygen-efficient OxPhos without true hypoxia, rhythmically suppressing HIF-1α hyperactivity.

This allows Randle reciprocity:

High glucose/insulin (post-meal) inhibits fatty acid oxidation (via malonyl-CoA blocking CPT1, sparing fats).

Fasting/evening (anticipatory beta-oxidation peak) elevates acetyl-CoA/NADH from fats → inhibits PDH/PFK-1 → spares glucose for brain.

6. Circadian gating ensures timed peaks: beta-oxidation higher nocturnally (pre-fasting), glucose oxidation daytime.

SIRT3 (NAD+-dependent, boosted by PER2 redox balance) deacetylates mitochondrial enzymes, enhancing PDH flexibility and preventing hyperacetylation that locks Randle inhibition.

7. Desynchrony (poor sunrise/blue-nnEMF dominance → PER2 drop → unchecked HIF-1α → pseudohypoxia): Chronic HIF-1α mimics hypoxia signaling → PDK1 upregulation → PDH phosphorylation/inhibition → blocked pyruvate entry to TCA → forced glycolysis even with fats available (Warburg-like rigidity).

Randle cycle breaks: persistent fatty acid overflow (from lipolysis/inflammation) generates excess acetyl-CoA/NADH/citrate → sustained PDH/PFK inhibition → glucose sparing fails → hyperglycemia + ectopic lipids and the wrong enantiomers placed in tissues → insulin resistance loop.

8. This all directly ties to my GOE extensions in the blogs: Dysregulated heme (low EPO-EPOR tolerance signaling) + incoherent UPE/ROS amplify mitochondrial stress, raising NADH/NAD+ ratios that exacerbate Randle inhibition.

Nrf2/ECS buffering collapses under blue-induced disruptions, worsening redox pressure.

9. This explains T2D/obesity as lost Randle flexibility from upstream photonic desynchrony—cells "stuck" perceiving scarcity (pseudohypoxia) despite abundance, reverting to α-state inefficiency. Restoring sunrise/red exposure recalibrates PER2 → balanced HIF → rhythmic Randle switching → improved insulin sensitivity without needing primary mitochondrial "repair" (contra Seyfried).

Elegant decentralized closure: Randle as the metabolic "output" of Szent-Györgyi's ordered electronic dance, timed by sunlight's confinement of entropy.

Fuck food gurus. They are all dumb asses.

CITES

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