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.

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## 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](https://pmc.ncbi.nlm.nih.gov/articles/PMC3388522/). Reintroduce systematically.

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## 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.

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## 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.

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## 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.

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## 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.

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## 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).

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## 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.

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## 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.

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## 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.

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