The following is AI slop. Be warned!

1) First principles (systems model)

  • Energy handling & signaling

    • Mitochondrial ETC flux → ROS byproducts. ROS are signals at low levels and damaging at high; damage risk scales with membrane PUFA content and antioxidant network sufficiency (tocopherols/tocotrienols, glutathione system, NADPH).
    • Membrane composition → insulin signaling. High palmitic:oleic in phospholipids increases viscosity and can impair insulin receptor signaling; sterols/cholesterol buffer fluidity but only partly compensate.
    • Lipoprotein trafficking sets vascular exposure to oxidizable lipids. Lowering ApoB/LDL particle burden (diet, lifestyle; pharmacologic if needed—PCSK9 where appropriate) reduces substrate for oxidation and immune activation.

  • Oxidation cascade

    • Initiation (ROS abstracts a hydrogen from PUFA) → propagation (lipid peroxyl radicals) → termination (chain-breakers like tocopherols). BHT/tocopherols stop propagation, not initiation; lowering LA-rich PUFA lowers both initiation probability and damage propagation.

  • Immunology & barrier integrity

    • Prolamines (e.g., gliadin) and certain plant defense molecules (lectins, saponins, glycoalkaloids) can increase gut permeability and chemotaxis (e.g., CXCR3 signaling) in susceptible people → innate/adaptive activation → systemic inflammatory tone, insulin/leptin signaling perturbations.
    • Casein-derived opioidergic peptides cross the BBB variably; effects depend on permeability and individual immune reactivity—not universal.

  • Epistemics

    • Separate weight-loss effects (lipid-soluble toxin mobilization, transient dyslipidemia) from ingredient effects: use weight-stable testing when isolating variables.
    • Triangulate mechanism + n-of-1 challenge/rechallenge + biomarkers rather than relying on single study designs.

2) Practical dietary pattern (default)

Core template: meat / eggs / shellfish + fruits / roots / tubers / shoots + low-PUFA fats; optional white rice paired with micronutrient & Nrf2 support.

  • Proteins (nutrient density first): ruminant meat, organs (liver sparingly but regularly), shellfish (zinc/copper/iodine), eggs. Collagenous cuts or glycine (5–10 g/d) to balance methionine. Choline target \~500–1,000 mg/d (eggs, liver).
  • Carbohydrates: whole fruit and cooked roots/tubers as primary; white rice is “just starch”—pair with ETC cofactors (B1/B2/niacin/lipoic acid, minerals) and Nrf2 inducers (crucifers/alliums, herbs/spices) to mitigate redox burden.
  • Fats: minimize linoleic acid (LA) to blunt peroxidation (practical target ≤2–4% energy); prefer MUFA/SFA from ruminants, dairy fat (if tolerated), high-oleic olive/avocado oil, cocoa butter; use coconut/palm for high-heat. DHA/EPA \~250–1,000 mg/d for neuronal/immune signaling while keeping total PUFA modest.
  • Plants to trial-eliminate if symptomatic: gluten-containing grains (prolamines), some legumes (lectins/saponins), nightshades (glycoalkaloids), A1-dominant casein, FODMAPs. Reintroduce systematically.

3) Micronutrient & redox architecture

  • Fat-soluble vitamins: A, D, K2, E in physiologic balance (avoid single-nutrient megadosing). Animal foods plus sun; consider K2 (MK-7/MK-4) if dairy-free.
  • Minerals: Magnesium 400–600 mg/d, potassium-rich tubers/fruit/veg, iodine via seafood, zinc–copper balance (oysters + liver), selenium (seafood/eggs).
  • Antioxidant network: tocopherols/tocotrienols with low-LA background; build endogenous capacity (glycine → glutathione; riboflavin/niacin → NADPH; sulfur amino acids; Nrf2 foods) rather than relying on synthetic chain-breakers alone.

4) Lipids, membranes, and metabolic syndrome

  • Membrane MUFA (oleate) supports fluidity; excessive palmitate in phospholipids raises viscosity → insulin resistance. Stearate is less reactive than LA; context matters.
  • PUFA management: Lower dietary LA lowers oxidizable substrate in LDL and membranes, reducing ox-LDL, foam-cell formation, and sterile inflammation.
  • Lipoproteins: If ApoB/LDL-C remain high despite diet/lifestyle—and risk is high—PCSK9 inhibitors are coherent with the model. Track ApoB rather than LDL-C alone.

5) Insulin/leptin resistance levers

  • Energy balance with satiety: high-protein, minimally processed food matrix, circadian alignment, adequate sleep.
  • Lower LA and improve membrane oleate to enhance insulin action; avoid high-PUFA + high-heat cooking.
  • Avoid simultaneous surges of saturated fat + refined starch in a highly palatable matrix; favor whole-food carbs with micronutrient support.
  • Leptin: reduce inflammatory tone (gut antigens, LA, sleep debt), normalize adipocyte signaling (magnesium, DHA/EPA in modest doses), maintain resistance training.

6) Gut & immune protocol (test, don’t guess)

  1. Eliminate suspected antigens for 3–6 weeks: gluten grains → legumes → nightshades → A1 dairy (sequence by likelihood).
  2. Rechallenge one by one while weight stable; track symptoms and CRP, WBC, fecal calprotectin when relevant.
  3. Optional tests in stubborn cases: celiac serology, lactulose–mannitol permeability, IgE (for true allergy), stool markers.

7) Cooking & sourcing

  • Fry/sauté with saturated or low-PUFA fats; save EVOO for low-heat/cold uses. Avoid repeatedly heated seed oils.
  • Favor ruminant fats (low LA) and high-oleic variants across the food chain when possible (including animal feed).

8) Biomarker panel & decision rules

  • Core: fasting insulin or C-peptide, glucose, HbA1c; ApoB, non-HDL-C; TG/HDL; ALT/AST/GGT; hs-CRP; ferritin + transferrin saturation; RBC fatty acids (%LA, %DHA/EPA); thyroid panel (TSH, fT3).

  • Interpretation heuristics:

    • High ApoB + high RBC-LA → tighten LA, consider MUFA/SFA swap; if persistent → pharmacologic discussion.
    • High insulin/C-peptide at normal glucose → membrane/lipid environment and circadian/behavior targets.
    • Elevated GGT/ALT with high LA → redox/PUFA load; prioritize mitochondrial cofactors and LA reduction.
    • Symptom flares after reintroduction → keep antigen out for 3–6 months and retest.

9) Special cases & cautions

  • Rapid fat loss mobilizes lipophilic toxins; use gradual deficits; support bile flow (protein, choline), fiber from tolerated plants, adequate minerals.
  • Ketosis can increase oxidative demand transiently; ensure riboflavin/niacin, minerals, and sleep adequacy.
  • White rice is acceptable fuel only when paired with micronutrients/Nrf2 support.

10) Minimalist implementation checklist

  • Remove: seed oils high in LA; gluten grains; suspect legumes/nightshades; A1 dairy if reactive.
  • Base meals on: ruminant meat/eggs/shellfish + fruit/tubers + low-PUFA fats.
  • Weekly: liver (small), shellfish; crucifers/alliums.
  • Daily targets (adjust clinically): protein 1.6–2.2 g/kg LBM; LA ≤2–4% kcal; DHA+EPA 250–1,000 mg; magnesium 400–600 mg; choline 500–1,000 mg; glycine 5–10 g.