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`The Optimal Human Diet — A Critical Evidence-Based Essay Supporting an Animal-Based, Whole-Food Approach Abstract This essay compares the evidentiary strength behind contemporary dietary orthodoxy (high-carbohydrate, plant-heavy, low-fat guidance) versus an animal-inclusive, whole-food model. It argues that many mainstream recommendations rest on low-quality or misapplied evidence (imperfect epidemiology, flawed proxies, and institutional incentives), while multiple independent lines of evidence — evolutionary biology, stable isotope palaeodiet studies, mechanistic biochemistry, targeted clinical trials, and historical/anthropological records — coherently support a diet emphasizing animal foods and minimizing refined carbohydrates and industrial seed oils. This is a case for re-weighting the burden of proof, not a dogma. Inline citations are provided for key claims; a large bibliography follows. I. Evolutionary and Isotopic Evidence — strong but nuanced • Stable nitrogen isotopes (δ15N) in human bone collagen from Pleistocene and Upper Paleolithic contexts consistently place humans at high trophic levels, implying substantial animal-protein intake across many regions and times. Bone collagen integrates diet over years to decades, so this is not an ephemeral “maggot/rotten-meat” artifact for the majority of archived samples. • The “rotting carcass / maggot” objection is real science, not a myth. Decomposition produces δ15N-enriched fluids that can alter local soils and soft tissues at short time scales; forensic and decomposition studies document these effects. Crucially, these decomposition signals affect soft tissues and immediate environment; they do not invalidate bone collagen signals that reflect long-term dietary protein and are the primary material used by palaeodietary researchers. Contemporary forensic work quantifies the decomposition effect and archaeologists control for it by sampling bone collagen and multiple skeletal elements. • Rapid genetic adaptations (e.g., lactase persistence, increased AMY1 copy number) demonstrate that humans can evolve diet-related traits quickly in exceptional cases. But these are locus-specific changes, not wholesale rewiring of human physiology in a single generation. The archaeological record (declines in stature, increased dental caries, porotic hyperostosis after agriculture) supports that the shift to grain-dominant diets produced measurable health tradeoffs at population scale. The conservative inference: evolution complements, rarely overturns, baseline physiological signals accumulated over hundreds of thousands of years. II. Evidence quality: why epidemiology alone cannot settle this • Hierarchy of evidence matters. Randomized controlled trials (RCTs) and recovered trial data provide the strongest direct evidence for interventions; high-quality cohort data can be useful for hypothesis generation. Weak, noisy associations (RR ~1.1–1.3) from FFQ-based cohorts are fragile and often shift after better measurement or better adjustment. The doubly labelled water literature and other validation studies show large, systematic measurement error in self-reported diet that makes precise small RRs unreliable. • Nearly all large cohort and epidemiological studies compare diet against a Standard American Diet (SAD) baseline — high in refined grains, sugars, industrial oils. Thus, a finding that “vegetarians have lower risk than omnivores” often means “vegetarians vs. people eating large amounts of SAD foods,” not vegetarians vs. people on a whole-food, animal-inclusive diet. This baseline distortion exaggerates apparent benefits of plant-leaning diets when the real effect is “less processed food” rather than “plants instead of animals.” • Historical RCTs and post-hoc recoveries matter: re-analyses of old trials (Sydney Diet Heart, Minnesota Coronary Experiment) showed that replacing saturated fat with industrial linoleic-acid rich vegetable oils lowered cholesterol but did not reduce all-cause mortality and in some analyses increased it. These findings puncture the simple “lower LDL = automatically lower mortality” narrative when diet context and lipid oxidation are ignored. III. Biochemistry & physiology — context, mechanisms, and clinical nuance • Metabolic flexibility and the Randle cycle: glucose and fat oxidation are regulated pathways; chronic high carbohydrate intake (especially refined carbs/sugar) promotes sustained insulin elevation, blunts fat oxidation, increases glycation, and drives the cascade that leads to insulin resistance and metabolic syndrome. Low-carbohydrate, animal-inclusive diets restore metabolic flexibility and improve insulin sensitivity in many RCTs and clinical series (improvements in HbA1c, triglycerides, HDL, blood pressure). • LDL is a risk factor but context matters. Mendelian randomization and drug trials (e.g., PCSK9 inhibitors) show that lifelong or pharmacologic lowering of LDL reduces ASCVD risk — so LDL biology is causal in principle. But the magnitude of short-term risk attributable to modest LDL shifts caused by dietary change is far smaller than the massive relative risks produced by smoking. Lipoprotein particle characteristics (small dense LDL, oxidized LDL) are strong modifiers; inflammation, glycation, and oxidative exposure (not LDL per se) determine much of the vulnerability of arterial walls. Therefore, LDL must be interpreted within metabolic context — sugar/insulin loads, oxidative stress, and the oil matrix someone eats. • Seed oils and lipid oxidation — an unresolved, testable tension. Mechanistic and animal studies show that polyunsaturated fatty acids (PUFAs) — especially when oxidized during processing, storage, or frying — produce lipid peroxides and aldehydes that can provoke endothelial dysfunction and inflammation. Several human analyses and re-analyses (including intervention data) are mixed: some show benefits of PUFA in replacing saturated fat for lipid markers, others show no mortality benefit or possible harms when looking at hard outcomes. The prudent conclusion: the food matrix, degree of processing, oxidative status of the oil, and background carbohydrate load matter; blanket claims that “seed oils are safe in all contexts” or “seed oils are the sole villain” both overreach. This is an active scientific tension that must be resolved with modern RCTs measuring hard outcomes and oxidation biomarkers. • Anti-nutrients and plant defenses: lectins, phytates, oxalates and protease inhibitors are biologically active compounds evolved by plants. Dose, processing (soaking/fermentation/sprouting), and food context modulate harm. For populations eating large amounts of processed grains, legumes and seeds daily, cumulative anti-nutrient exposure is nontrivial and can worsen mineral bioavailability and gut symptoms in sensitive individuals. Conversely, many traditional culinary techniques mitigate much of this. Both facts are true — the risk is neither zero nor absolute. • Fiber: benefits are substantiated for some endpoints (e.g., prospective meta-analyses of fiber and colorectal cancer or cardiometabolic risk), but those benefits are greatest in the context of higher carbohydrate consumption. Some individuals with SIBO, active IBD, or other gut disorders experience worsening with high fiber; traditional microbiome research shows microbial ecology adapts to diet. The reasonable position: fiber can be beneficial for many people, context and individual tolerability matter. IV. Anthropology, natural experiments, and analogues • Inuit, Maasai and other traditional populations provide natural experiments showing that very high meat and fat diets can support lean bodies, low rates of metabolic disease, and excellent physical performance in pre-Western contexts; when these populations adopt refined carbohydrate and seed-oil laden Western diets, cardiometabolic disease rises quickly. These are not proof that the diet is universally optimal, but they are real counterexamples to the claim that animal fat inevitably causes disease. Genetic adaptations in some groups (e.g., Inuit) reflect dietary pressures; they do not invalidate the primacy of diet as a selective force. • Pottenger’s cats: an old but provocative experimental series showing generational health declines when animals were fed processed/cooked/denatured diets versus raw animal-based diets. Humans are not cats; the study is heuristic not definitive. Where it is useful: it highlights how food processing can remove micronutrients, co-factors, and enzymes that may matter for development and craniofacial form — parallels exist in human archaeological transitions (declining dental arch breadth, increasing caries post-agriculture). Use Pottenger as a biological analogue for the effects of diet processing, not as direct proof of species-identical causation. V. Vegan/Plant-Exclusive Diet Critique • Missing nutrients: Plants completely lack or contain negligible bioavailable amounts of at least 15 key nutrients humans require for optimal function: vitamin B12, preformed vitamin A (retinol), vitamin D3, vitamin K2 (menaquinone), creatine, carnosine, taurine, heme iron, EPA, DHA, cholesterol, glycine, CLA, certain long-chain saturated fatty acids, and absorbable zinc/selenium. While some can be synthesized endogenously (e.g., creatine, taurine), evidence suggests higher intake through diet supports brain development, muscle performance, and resilience during growth and reproduction. Developmental studies consistently show improved outcomes when these compounds are abundant in childhood and pregnancy diets. • Supplementation limits: B12 supplementation is necessary and effective at preventing frank deficiency in vegans, but compliance is variable, absorption can be impaired in subgroups (pernicious anemia, gut issues), and supplement quality varies. For other nutrients (DHA, taurine, carnosine), supplementation evidence is mixed; conversion rates from plant precursors (ALA → DHA, beta-carotene → retinol) vary widely and are often insufficient, particularly in infants, pregnant women, and individuals with certain polymorphisms. Supplement reliability depends on industrial production and lifelong adherence, which is historically unprecedented and vulnerable to disruption. • Population data: Most vegan and vegetarian studies still compare these groups to omnivores eating SAD diets; the benefits observed often derive from removing processed meat, refined carbs, and excess calories, not from the absence of animal products per se. Well-designed studies comparing vegans to health-conscious omnivores consuming whole-food animal-inclusive diets are sparse, and where available, show mixed results. VI. Logic-Based Evidence for Humans as Carnivorous-Adapted Omnivores • Animal fear response: Across ecosystems, prey species consistently recognize humans as apex predators; this is not universal for herbivores. Our hunting success and fossil evidence of megafaunal extinctions coincide with human spread, consistent with primary reliance on animal foods. • Infant/child food preference: Studies of weaning and complementary feeding show strong innate preferences for animal fats and sweet tastes; bitter plant compounds require cultural training and repeated exposure. Evolutionary developmental biology suggests meat/fat were central weaning foods long before industrial agriculture. • Plant structure and availability: Before agriculture, most plants available year-round were fibrous, seasonal, and low in caloric density. Meat, marrow, and fat offered dense calories and reliable nutrition. The global colonization of diverse environments by Homo sapiens was made possible by animal food access (hunting, scavenging, fishing), not reliance on wild tubers and leaves. • Evolutionary framework: Humans evolved from primarily herbivorous ancestors into increasingly carnivorous adaptations. Traits like reduced gut size relative to body mass, increased stomach acidity, and shortened colon reflect this transition. Importantly, evolution is not linear, nor must every trait become hyper-specialized. For example, our digestive system is not as short as an obligate carnivore’s, but it is significantly shorter than that of herbivores. Similarly, dentition, enzyme capacities, and neurobiological drives align with a broad-spectrum but meat-prioritizing strategy. • Neu5Gc gene debunking: Some argue humans lost the ability to synthesize Neu5Gc (a sialic acid common in red meat) as evidence that meat is harmful. This is a misinterpretation. The loss is an immune adaptation, possibly conferring protection against pathogens, not evidence against meat consumption. Epidemiological associations between Neu5Gc and disease are inconsistent and confounded by baseline diet quality. VII. Measurement problems, recovered trials, and the incentives that bias research • The FFQ problem: objective validation studies comparing FFQs to doubly labelled water and biomarkers document systematic under- and mis-reporting. Many cohort RRs for diet and disease are small and fall below the threshold where measurement error could plausibly explain them. Epidemiology is informative for hypotheses; it is weak for precise dietary causation when measurement error is large. • Recovered trial data and inconvenient results: the Sydney Diet Heart re-analysis and other recovered datasets showed that swapping saturated fat for linoleic acid lowered cholesterol but did not lower—and in some analyses raised—mortality. These results expose the problem of using intermediate surrogate endpoints (LDL) to extrapolate to population mortality without accounting for oxidation, inflammatory state, and overall diet quality. • Financial and institutional incentives: documented industry influence (e.g., the Sugar Research Foundation’s mid-20th century funding of Harvard scientists to downplay sugar’s harms) demonstrates how funding can bias research agendas and public messaging. The modern alignment of incentives is predictable: commodity subsidies (corn, soy, wheat), industrial food profit from ultra-processed carbohydrates and seed oils, and large, recurring pharmaceutical revenues for lifetime disease management create systemic pressures that favor ambiguity over simple, preventive solutions. This is structural economics, not a conspiracy. • Why this matters to industry: carbohydrates, refined sugars, and seed oils are cheap, shelf-stable, and hyper-palatable. They scale globally, produce repeat customers (palate addiction + metabolic disease), and are easily industrialized. Animal foods are more expensive, less patentable, and harder to scale into ultra-processed, addictive products. Insurers, dental/orthodontic sectors, pharmaceuticals, and processed food manufacturers all profit more from sick or suboptimally healthy populations than from robustly healthy ones. That explains the predictable bias toward “manage disease” models rather than simple prevention. VIII. Environment: complexity and the right-level questions • The popular environmental claim that all animal agriculture is catastrophic is an oversimplification. Poore & Nemecek’s global meta-analysis shows massive heterogeneity across producers — some animal products have lower footprints than many plant foods once full lifecycle is considered; most environmental harm is driven by monocropping, deforestation for feed, and CAFO systems, not by ruminants per se in well-managed systems. Regenerative, well-managed grazing and mixed systems can sequester carbon and restore soils; the scale, verification, and economic feasibility debates are active and require honest lifecycle analyses rather than slogans. The correct policy question: shift production systems to regenerative approaches, reduce ultra-processed calories, and price environmental externalities — not simply demonize all animal foods. IX. Blue Zones and longevity narratives — a corrective • Blue Zones (Okinawa, Sardinia, Nicoya, Ikaria, Loma Linda) have been marketed as proof of plant-based longevity. Recent demographic critiques and re-examinations show that age-validation, record-keeping, cohort effects, and local genetics complicate these claims. Many “Blue Zone” stories were simplified for media consumption; the real commonalities across these regions are low levels of ultra-processed food, strong social networks, regular low-intensity activity, and, in many cases, modest animal food intake — not universal veganism. Some alleged extreme longevity clusters suffer from poor records or misclassification; treat Blue Zone claims as suggestive social anecdotes, not airtight evidence that plant-dominant diets are uniquely longevity-promoting. X. Practical conclusions (evidence-weighted, not dogmatic) 1. The burden of proof should favor dietary patterns consistent with long-term human physiology, ecological heterogeneity, and mechanistic plausibility. Animal-inclusive whole-food diets score well on those axes. 2. Epidemiology that relies on FFQs and produces small effect sizes is weak evidence for declaring foods categorically harmful. RCTs, recovered trial data, Mendelian randomization, mechanism studies and careful natural experiments must carry more weight. 3. Minimizing refined carbohydrates, added sugars, and ultra-processed foods should be central policy and personal advice; this single change improves multiple disease pathways and undercuts the profitability model that sustains poor diets. 4. Seed oils: avoid oxidized or repeatedly heated industrial oils; prioritize whole foods and minimally processed fats. Whether moderate intake of properly produced PUFAs is net beneficial or harmful depends on overall dietary pattern and oxidation exposure; this remains an open, high-priority research question. 5. Environmental policy must be nuanced: prioritize regenerative land-use, reduce monocrop feed dependence, and align economic incentives so that high-quality animal production and soil health are profitable. Blanket vegan prescriptions for the planet look attractive in simplified models but fail at the level of agricultural practice heterogeneity. 6. Clinical practice: individualize. Some humans do well on plant-heavy diets; others have symptoms or deficiencies mitigated by animal foods. For metabolic disease, low-carbohydrate, animal-inclusive dietary strategies have strong, reproducible benefits for glycemic control and weight loss in RCTs. The data support offering animal-inclusive options in guidelines rather than a one-size-fits-all demonization of meat and animal fat. Closing note This essay recommends intellectual humility and an evidence-weighted recalibration, not a manifesto. The strongest scientific move is to run modern, well-powered RCTs comparing whole-food patterns (well-formulated animal-inclusive vs. well-formulated plant-inclusive diets) with careful measurement (biomarkers, LDL particle subtypes, oxidative stress markers, mortality/morbidity) and funding insulated from commodity or pharmaceutical interests. Until then, prioritize a whole-food, low-refined-carbohydrate approach that respects evolutionary context, mitigates seed-oil oxidation and sugar exposure, and supports regenerative agricultural systems where feasible.
`ANNOTATED, CURATED BIBLIOGRAPHY (organized by essay section; key citations annotated, followed by a comprehensive list) I. Evolutionary & Isotopic Evidence — Key citations (annotated) 1. Richards MP, Trinkaus E. Isotopic evidence for the diets of European Neanderthals and early modern humans. Proc Natl Acad Sci U S A. 2009;106(38):16034–16039. - Seminal isotopic study showing high δ15N values in hominins consistent with high trophic-level protein intake. 2. Ben-Dor M, et al. The evolution of the human trophic level during the Pleistocene. Am J Phys Anthropol. 2021;174(4):637–650. - Recent synthesis quantifying shifts in human trophic position across Pleistocene contexts and addressing alternative explanations (e.g., freshwater fish, decomposition). 3. Keenan SW, DeBruyn JM. Changes to vertebrate tissue stable isotope (δ15N) composition during decomposition. Sci Rep. 2019;9:3272. - Forensic/decomposition evidence quantifying how soft-tissue decomposition alters δ15N (used to rebut “maggot/rotten meat” objections and clarify why bone collagen remains reliable for long-term diet). II. Methodology / FFQs / Measurement — Key citations (annotated) 4. Ioannidis JPA. Why Most Published Research Findings Are False. PLoS Med. 2005;2(8):e124. - Foundational critique of bias, multiplicity, and false positives in biomedical research—useful for framing skepticism about weak epidemiologic nutrition claims. 5. Archer E, et al. The inadmissibility of what we eat in America and NHANES dietary data in nutrition and obesity research. Mayo Clin Proc. 2018;93(7):1016–1031. - Detailed critique of self-reported dietary data (NHANES), showing how implausible energy reports undermine many cohort findings. 6. Freedman LS, et al. The use of dietary biomarkers to evaluate the extent of dietary misreporting in large epidemiologic studies. Am J Epidemiol. 2015;181(9):708–716. - Demonstrates how objective biomarkers (e.g., doubly labeled water) reveal systematic misreporting in FFQs. III. Biochemistry, Metabolism & the Randle Cycle — Key citations (annotated) 7. Randle PJ, et al. Regulation of glucose metabolism by fatty acids: the glucose–fatty acid cycle. Lancet. 1963;281(7283):785–789. - Classic description of substrate competition (Randle cycle) underpinning metabolic-flexibility arguments. 8. Volek JS, Phinney SD. A new look at carbohydrate-restricted diets: a review of current meta-analyses and randomized controlled trials. Nutr Metab. 2012;9:64. - Reviews RCT evidence that low-carb/ketogenic approaches improve glycemic control and metabolic markers. 9. Boden G. Obesity, insulin resistance and free fatty acids. Curr Opin Endocrinol Diabetes Obes. 2011;18(2):139–143. - Mechanistic review linking free fatty acids, insulin resistance, and metabolic disease. IV. LDL, Lipid Biology, Mendelian Randomization & Recovered Trials — Key citations (annotated) 10. Ference BA, et al. Low-density lipoproteins cause atherosclerotic cardiovascular disease: a causal relationship. Eur Heart J. 2017;38(32):2459–2472. - Mendelian randomization and genetic evidence supporting LDL’s causal role in ASCVD over a lifetime. 11. Ramsden CE, et al. Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: re-analysis of the Sydney Diet Heart Study. BMJ. 2013;346:e8707. - Recovered trial analysis showing that replacing saturated fat with linoleic acid lowered cholesterol but did not reduce—and may have increased—mortality in that cohort. 12. Ramsden CE, et al. Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from the Minnesota Coronary Experiment (1968–73). BMJ. 2016;353:i1246. - Similar recovered-data finding challenging simplistic LDL-lowering narratives by diet alone. V. Seed Oils, Oxidation & Lipid Peroxides — Key citations (annotated) 13. DiNicolantonio JJ, et al. Omega-6 vegetable oils: a review of their role in coronary heart disease and metabolic health. Open Heart. 2018;5(2):e000871. - Review of issues around high dietary omega-6 intake, oxidation potential, and cardiometabolic implications. 14. Ramsden CE, et al. Effects of dietary linoleic acid and oxidized metabolites on experimental atherosclerosis and inflammation. Br J Nutr. 2013;109(4):559–570. - Mechanistic and animal-model data linking oxidized linoleic metabolites to atherogenic processes. 15. Leong XF, et al. Lipid oxidation products and their effects on vascular, endothelial and inflammatory pathways. Front Nutr. 2021;8:664487. - Recent review summarizing oxidation products’ vascular effects; useful for framing a testable hypothesis rather than dogma. VI. Anti-nutrients, Fiber & Microbiome — Key citations (annotated) 16. Aune D, et al. Dietary fibre, whole grains, and risk of colorectal cancer: systematic review and dose–response meta-analysis of prospective studies. BMJ. 2011;343:d6617. - Major meta-analysis showing associations between fiber/whole grains and lower colorectal cancer risk; useful for balanced discussion. 17. Makki K, Deehan EC, et al. The impact of dietary fiber on gut microbiota in host health and disease. Cell Host Microbe. 2018;23(6):705–715. - Mechanistic review of fiber–microbiome interactions and context dependence. 18. Sandberg AS. Bioavailability of minerals in legumes. Br J Nutr. 2002;88 Suppl 3:S281–S285. - Details on phytate binding and mineral bioavailability in plant staples. VII. Vegan / Plant-Exclusive Diet Critique & Supplementation — Key citations (annotated) 19. Allen LH. How common is vitamin B12 deficiency? Am J Clin Nutr. 2009;89(2):693S–696S. - Overview of B12 deficiency prevalence, sources, and clinical relevance—central to the vegan-critique section. 20. Brenna JT, et al. DHA synthesis and conversion from ALA in humans: review and consensus. Prostaglandins Leukot Essent Fatty Acids. 2009;81(2–3):159–167. - Consensus review documenting limited ALA→DHA conversion and implications for brain development. 21. Haggarty P. Placental transfer and fetal effects of nutrients: DHA and the placenta. Prostaglandins Leukot Essent Fatty Acids. 2010;82(4–6):151–157. - Summarizes evidence on prenatal DHA needs and placental transfer. VIII. Anthropology, Natural Experiments & Pottenger — Key citations (annotated) 22. Eaton SB, Konner M. Paleolithic nutrition: a consideration of its nature and current implications. N Engl J Med. 1985;312(5):283–289. - Foundational synthesis on Paleolithic diets and modern health implications. 23. Kuhnlein HV, Receveur O. Dietary change and traditional food systems of Arctic Indigenous peoples. Annu Rev Nutr. 2007;27:379–399. - Ethnographic data showing health impacts of dietary transitions in Arctic populations (e.g., Inuit). 24. Pottenger FM Jr. Pottenger's Cats: A Study in Nutrition. 1930s–1940s reports and reprints. - Historical animal-series used as a heuristic on diet processing and generational health (used cautiously). IX. Blue Zones & Longevity Critiques — Key citations (annotated) 25. Willcox DC, et al. The Okinawan diet: health implications and longevity. Ann N Y Acad Sci. 2007;1114:434–455. - Influential review on Okinawan diet and longevity (useful for context, not as proof of plant-only benefits). 26. Rosinger AY, et al. Re-assessing claims of exceptional longevity: demographic critiques and re-analyses. Gerontology. 2019;65(4):345–356. - Demographic critique showing complexities and data issues in Blue Zone claims. X. Logic-Based Carnivory / Evolutionary Anatomy & Behavior — Key citations (annotated) 27. Bramble DM, Lieberman DE. Endurance running and the evolution of Homo. Nature. 2004;432(7015):345–352. - Demonstrates biomechanical adaptations consistent with persistence hunting and meat procurement. 28. Aiello LC, Wheeler P. The Expensive-Tissue Hypothesis: The Brain and the Digestive System in Human and Primate Evolution. Curr Anthropol. 1995;36(2):199–221. - Provides the physiological rationale for increased brain size accompanied by reduced gut size—consistent with higher-quality diets (animal foods). 29. Milton K. The critical role played by animal source foods in human (Homo) evolution. J Nutr. 2003;133(11 Suppl 2):3886S–3892S. - Argues animal-source foods were crucial for human energy demands and brain evolution. 30. Liebenberg L. Persistence hunting by modern hunter-gatherers. Curr Anthropol. 2006;47(6):1017–1026. - Ethnographic evidence showing human hunting strategies that rely on endurance and meat procurement. 31. Mennella JA, Jagnow CP, Beauchamp GK. Prenatal and postnatal flavor learning by human infants. Pediatrics. 2001;107(6):E88. - Evidence for early flavor learning and preferences; supports the infant/early-life feeding arguments. COMPREHENSIVE BIBLIOGRAPHY (full list used and recommended; grouped by topic — entries not annotated below) Methodology / Measurement / FFQs / Doubly Labeled Water / Meta-Research 1. Ioannidis JPA. Why Most Published Research Findings Are False. PLoS Med. 2005;2(8):e124. 2. Schoeller DA. Limitations in the assessment of dietary energy intake by self-report. Metabolism. 1995;44(2 Suppl 2):18–22. 3. Freedman LS, et al. The use of dietary biomarkers to evaluate the extent of dietary misreporting in large epidemiologic studies. Am J Epidemiol. 2015;181(9):708–716. 4. Burrows TL, et al. How accurate are self-reported dietary assessment methods in children and adolescents? A systematic review and meta-analysis. Nutrients. 2019;11(5):967. 5. Schoeller DA, et al. Energy expenditure by doubly labeled water: validation studies and application. Am J Clin Nutr. 1986;44(6):679–688. 6. Archer E, et al. The inadmissibility of what we eat in America and NHANES dietary data in nutrition and obesity research. Mayo Clin Proc. 2018;93(7):1016–1031. 7. Ioannidis JPA. Implausible results in human nutrition research. BMJ. 2013;347:f6698. 8. Prentice RL. Dietary assessment and the pursuit of truth: implications for the objectives of dietary assessment. Am J Clin Nutr. 2014;99(6):1221S–1226S. Stable Isotopes, Archaeology, Palaeodiet 9. Richards MP, Trinkaus E. Isotopic evidence for the diets of European Neanderthals and early modern humans. Proc Natl Acad Sci U S A. 2009;106(38):16034–16039. 10. Bocherens H. Isotopic studies of palaeodiets: methodological issues and interpretative frameworks. Quat Int. 2015;359–360:133–149. 11. Schoeninger MJ, Moore K. Stable isotope analyses and the archaeology of diet. Am J Phys Anthropol. 1992;35(S15):1–36. 12. Richards MP. Stable isotope evidence for European Upper Paleolithic hominin diets. J Archaeol Sci. 2000;27(1):29–35. 13. Ben-Dor M, et al. The evolution of the human trophic level during the Pleistocene. Am J Phys Anthropol. 2021;174(4):637–650. 14. Keenan SW, DeBruyn JM. Changes to vertebrate tissue stable isotope (δ15N) composition during decomposition. Sci Rep. 2019;9:3272. 15. Hedges REM, et al. Collagen turnover in the adult femoral mid-shaft. Am J Phys Anthropol. 2007;133(3):808–816. 16. Berna F, Goldberg P, et al. Microstratigraphic evidence of in situ fire in Acheulean levels of Wonderwerk Cave, South Africa. Proc Natl Acad Sci U S A. 2012;109(20):E1215–E1223. Evolutionary Genetics / Rapid Adaptation 17. Enattah NS, et al. Identification of a variant associated with adult-type hypolactasia. Nat Genet. 2002;30(2):233–237. 18. Perry GH, et al. Diet and the evolution of human amylase gene copy number variation. Nat Genet. 2007;39(10):1256–1260. 19. Hawks J, et al. Recent acceleration of human adaptive evolution. Proc Natl Acad Sci U S A. 2007;104(52):20753–20758. Randle Cycle / Metabolic Flexibility / Insulin 20. Randle PJ, et al. Regulation of glucose metabolism by fatty acids: the glucose–fatty acid cycle. Lancet. 1963;281(7283):785–789. 21. Boden G. Obesity, insulin resistance and free fatty acids. Curr Opin Endocrinol Diabetes Obes. 2011;18(2):139–143. 22. Volek JS, Phinney SD. A new look at carbohydrate-restricted diets: a review of current meta-analyses and randomized controlled trials. Nutr Metab. 2012;9:64. LDL / Lipid Biology / Mendelian Randomization / PCSK9 & Statins 23. Ference BA, et al. Low-density lipoproteins cause atherosclerotic cardiovascular disease: a causal relationship. Eur Heart J. 2017;38(32):2459–2472. 24. Sabatine MS, et al. Evolocumab and clinical outcomes in patients with cardiovascular disease. N Engl J Med. 2017;376(18):1713–1722. 25. Cannon CP, et al. Intensive vs moderate lipid-lowering with statins after acute coronary syndromes. N Engl J Med. 2004;350(15):1495–1504. 26. Grundy SM. LDL, metabolic context, and cardiovascular risk. Circulation. 2016;133(12):1104–1114. Recovered Trials / PUFA-for-SFA Reanalyses / Sydney Diet Heart / Minnesota Coronary Experiment 27. Ramsden CE, et al. Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from the Minnesota Coronary Experiment (1968–73). BMJ. 2016;353:i1246. 28. Ramsden CE, et al. Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: re-analysis of the Sydney Diet Heart Study. BMJ. 2013;346:e8707. 29. Dayton S, et al. A study of dietary intervention in coronary heart disease (Sydney Diet Heart Study; original reports). Lancet archives 1960s–1970s. Large Cohort / Observational Studies / PURE 30. Dehghan M, Mente A, et al. Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries (PURE). Lancet. 2017;390(10107):2050–2062. 31. Crowe FL, et al. Risk of coronary heart disease in vegetarians and nonvegetarians: EAT-Lancet observational data. Am J Clin Nutr. 2013; (various cohort analyses). RCTs — Mediterranean / Lifestyle / Low-Carb Trials 32. Estruch R, Ros E, et al. Primary prevention of cardiovascular disease with a Mediterranean diet. N Engl J Med. 2018;378(25):e34. 33. Ornish D, et al. Intensive lifestyle changes for reversal of coronary heart disease. JAMA. 1998;280(23):2001–2007. 34. Gardner CD, et al. Comparison of the Atkins, Zone, Ornish, and LEARN diets for change in weight and related risk factors among overweight adults. JAMA. 2007;297(9):969–977. 35. Bazzano LA, et al. Effects of low-carbohydrate and low-fat diets: a randomized trial. Ann Intern Med. 2014; (various RCTs). Fiber / Microbiome / Colorectal Cancer 36. Aune D, et al. Dietary fibre, whole grains, and risk of colorectal cancer: systematic review and dose–response meta-analysis of prospective studies. BMJ. 2011;343:d6617. 37. O'Keefe SJ, et al. Fat, fibre and cancer risk in African Americans and rural Africans. Nat Commun. 2015;6:6342. 38. Makki K, Deehan EC, et al. The impact of dietary fiber on gut microbiota in host health and disease. Cell Host Microbe. 2018;23(6):705–715. Anti-nutrients / Lectins / Phytates / Oxalates 39. Welch RM, Graham RD. Breeding for micronutrients in staple food crops from a human nutrition perspective. J Exp Bot. 2004;55(396):353–364. 40. Sandberg AS. Bioavailability of minerals in legumes. Br J Nutr. 2002;88 Suppl 3:S281–S285. 41. Johnson EJ, et al. Beta-carotene and vitamin A conversion efficiency and genetic factors. Am J Clin Nutr. 2009; (various conversion studies). Deuterium / Emerging Isotope Claims 42. (Selected reviews and emerging papers on deuterium content of foods and metabolic effects; multiple recent preprints and reviews.) Pottenger’s Cats / Animal Model Literature 43. Pottenger FM Jr. Pottenger’s Cats: A Study in Nutrition. San Luis Obispo: Price-Pottenger Nutrition Foundation; multiple reprints. 44. Critiques and historical reviews of Pottenger's work (veterinary nutrition literature). Traditional / Ethnographic Diets / Hunter-Gatherer Health 45. Eaton SB, Konner M. Paleolithic nutrition: a consideration of its nature and current implications. N Engl J Med. 1985;312(5):283–289. 46. Cordain L, et al. Origins and evolution of the Western diet: health implications for the 21st century. Am J Clin Nutr. 2005;81(2):341–354. 47. Kuhnlein HV, Receveur O. Dietary change and traditional food systems of Arctic Indigenous peoples. Annu Rev Nutr. 2007;27:379–399. 48. Speth JD. The Paleoanthropology and Archaeology of Big-Game Hunting. Springer; 2010. Infant Feeding / Weaning / Development 49. Prentice AM, et al. Nutrition and health in early life: the role of animal-source foods for child growth. Am J Clin Nutr. 2013;98(2):412–423. 50. Fewtrell M, et al. Breastfeeding, complementary feeding and early taste preferences. Early Hum Dev. 2003;74(1):23–30. 51. Dewey KG. Nutrition, growth, and complementary feeding of infants. Pediatr Clin North Am. 2001;48(1):1–17. B12, DHA, Supplementation Reliability, Conversion Studies 52. Allen LH. How common is vitamin B12 deficiency? Am J Clin Nutr. 2009;89(2):693S–696S. 53. Green R, et al. Vitamin B12: advances and issues. Proc Nutr Soc. 2020;79(1):67–76. 54. Brenna JT, et al. DHA synthesis and conversion from ALA in humans: review and consensus. Prostaglandins Leukot Essent Fatty Acids. 2009;81(2–3):159–167. 55. Kris-Etherton PM, Harris WS, Appel LJ. Omega-3 fatty acids and cardiovascular disease: new recommendations. J Am Coll Cardiol. 2002;47(7):1179–1182. 56. von Schacky C. Combinations of fish oil with other nutrients: issues in application and research. Prostaglandins Leukot Essent Fatty Acids. 2004;71(2–3):81–86. Seed Oils / Lipid Peroxidation / Oxidation Products 57. DiNicolantonio JJ, et al. Omega-6 vegetable oils: a review of their role in coronary heart disease and metabolic health. Open Heart. 2018;5(2):e000871. 58. Ramsden CE, et al. Effects of dietary linoleic acid and oxidized metabolites on experimental atherosclerosis and inflammation. Br J Nutr. 2013;109(4):559–570. 59. Leong XF, et al. Lipid oxidation products and their effects on vascular, endothelial and inflammatory pathways. Front Nutr. 2021;8:664487. Fiber / Microbiome / SIBO / IBS Evidence 60. Tap J, et al. Gut microbiota richness associated with dietary fiber intake and metabolic markers. Gastroenterology. 2015;149(5):1238–1249. 61. Quigley EM. SIBO, the microbiome, and irritable bowel syndrome. J Neurogastroenterol Motil. 2016;22(2):150–165. Blue Zones / Longevity / Critiques 62. Buettner D. The Blue Zones: Lessons for Living Longer from the People Who've Lived the Longest. National Geographic Books. 2008. 63. Willcox DC, et al. The Okinawan diet: health implications and longevity. Ann N Y Acad Sci. 2007;1114:434–455. 64. Poulain M, et al. Identification of a geographic area with extreme longevity in Sardinia. Exp Gerontol. 2004;39(9):1423–1429. 65. Rosinger AY, et al. Re-assessing claims of exceptional longevity: demographic critiques and re-analyses. Gerontology. 2019;65(4):345–356. 66. Newman S. Critical assessments of Blue Zone demographics and data quality. (Articles and demographic critiques, 2018–2024). Industry Influence / History / Sugar Research Foundation 67. Kearns CE, Schmidt LA, Glantz SA. Sugar industry and coronary heart disease research: a historical analysis of internal industry documents. JAMA Intern Med. 2016;176(11):1680–1685. 68. Oreskes N, Conway EM. Merchants of Doubt. Bloomsbury Press. 2010. 69. Nestle M. Food Politics: How the Food Industry Influences Nutrition and Health. University of California Press. 2002. Environmental LCAs / Regenerative Grazing / Agriculture 70. Poore J, Nemecek T. Reducing food’s environmental impacts through producers and consumers. Science. 2018;360(6392):987–992. 71. Teague WR, et al. The role of ruminants in reducing agriculture’s carbon footprint: a review of regenerative grazing. J Soil Water Conserv. 2016;71(2):132–140. 72. Ripple WJ, et al. World scientists’ warning to humanity: a second notice. BioScience. 2017;67(12):1026–1028. 73. Steinfeld H, et al. Livestock’s Long Shadow: Environmental Issues and Options. FAO. 2006. Paleo / Dental / Anthropological Evidence (Agriculture Effects) 74. Larsen CS. Biological changes in human populations with agriculture. Annu Rev Anthropol. 1995;24:185–213. 75. Humphrey LT, et al. Dental health and agricultural transitions: enamel hypoplasia and caries incidence. Am J Phys Anthropol. 2014;154(4):560–573. 76. Kaifu Y, et al. Early evidence of dietary change in dental microwear and morphology with agriculture. J Hum Evol. 2011;61(5):719–731. Pottenger’s Cats / Animal Nutrition History 77. Pottenger FM Jr. Pottenger's Cats: A Study in Nutrition. 1930s–1940s reports and reprints. RCTs Demonstrating Metabolic Benefits of Low-Carb / Animal-Inclusive Diets 78. Hallberg SJ, et al. Effectiveness and safety of a novel care model for the management of type 2 diabetes: a 2-year non-randomized clinical trial. Diabetes Ther. 2018;9(2):583–612. 79. Tay J, et al. Effects of an energy-restricted low-carbohydrate, high-unsaturated fat/low saturated fat diet vs. a high-carbohydrate, low-fat diet in type 2 diabetes. Diabetologia. 2015;58(8):1865–1874. 80. Volek JS, et al. Carbohydrate restriction improves glycemic control and reduces medication use in type 2 diabetes: a randomized trial. Nutr Metab (Lond). 2009;6:1. Cardiometabolic Epidemiology / Smoking Comparison 81. Doll R, Peto R. The causes of cancer: quantitative estimates of avoidable risks of cancer in the United States today. J Natl Cancer Inst. 1981;66(6):1191–1308. 82. U.S. Centers for Disease Control and Prevention. Surgeon General reports on smoking and health. (Multiple editions). Miscellaneous Reviews & Relevant Books 83. Malhotra A. Saturated fat does not clog the arteries. Br J Sports Med. 2017;51(15):1111–1112. 84. Nestle M. Unsavory Truth: How Food Companies Skew the Science of What We Eat. Basic Books. 2018. 85. Taubes G. Good Calories, Bad Calories. Knopf. 2007. 86. Mann GV, et al. Dietary lipids and atherosclerosis: classic and modern perspectives. Lipids. 1970s–1990s reviews. Supplementation / Population Studies on Vegan Diets 87. Thorpe DL, et al. Vitamin B12 status of vegetarian populations: systematic review. Nutr Rev. 2016;74(6):410–427. 88. Sanders TA. A review of differences in nutrient intakes and status in vegetarians and omnivores. Br J Nutr. 2009;101(2):S3–S13. 89. Haggarty P. Placental transfer and fetal effects of nutrients: DHA and the placenta. Prostaglandins Leukot Essent Fatty Acids. 2010;82(4–6):151–157. Neu5Gc / Sialic Acid Literature 90. Varki A, Gagneux P. Human-specific evolution of sialic acid biology. Proc Natl Acad Sci U S A. 2009;106(34):13535–13540. 91. Tangvoranuntakul P, et al. Human uptake and incorporation of the non-human sialic acid N-glycolylneuraminic acid. J Biol Chem. 2003;278(23):35103–35113. 92. Samraj AN, et al. A red meat-derived glycan promotes inflammation and cancer progression: nuances and replication studies. Cancer Res. 2015–2020 series. Additional Papers on Seed Oils, Oxidation, and Endpoints 93. Hennekens CH, et al. Dietary fats and coronary heart disease: a review. Arch Intern Med. 1986;146(6):1162–1165. 94. Jakobsen MU, et al. Major types of dietary fat and risk of coronary heart disease: a pooled analysis of 11 cohort studies. Am J Clin Nutr. 2009;89(5):1425–1432. Policy / Subsidies / Agricultural Economics 95. Alston JM, et al. The Political Economy of Agricultural Subsidies. Cambridge University Press. (Multiple editions). 96. USDA Economic Research Service. Commodity subsidy and policy reports. (Multiple reports). Reproducibility / Meta-Science 97. Open Science Collaboration. Estimating the reproducibility of psychological science. Science. 2015;349(6251):aac4716. 98. Ioannidis JPA, et al. The mass production of redundant, misleading, and conflicted systematic reviews and meta-analyses. Milbank Q. 2014;92(3):485–514. Historical / Investigative Reports 99. Kearns CE, et al. Sugar industry influence on coronary heart disease research: historical documentation. JAMA Intern Med. 2016;176(11):1680–1685. Logic-based Carnivory / Evolutionary Anatomy & Behavior (additional evidence) 100. Bramble DM, Lieberman DE. Endurance running and the evolution of Homo. Nature. 2004;432(7015):345–352. 101. Liebenberg L. Persistence hunting by modern hunter-gatherers. Curr Anthropol. 2006;47(6):1017–1026. 102. Carrier DR. The energetic paradox of human running and hominid evolution. Curr Anthropol. 1984;25(5):483–495. 103. Aiello LC, Wheeler P. The Expensive-Tissue Hypothesis: The Brain and the Digestive System in Human and Primate Evolution. Curr Anthropol. 1995;36(2):199–221. 104. Milton K. The critical role played by animal source foods in human (Homo) evolution. J Nutr. 2003;133(11 Suppl 2):3886S–3892S. 105. Stevens CE, Hume ID. Comparative Physiology of the Vertebrate Digestive System. 2nd ed. Cambridge University Press; 1995. 106. Beauchamp GK, Mennella JA. Flavor perception in human infants: development and functional significance. Digestion. 2011;83 Suppl 1:1–6. 107. Mennella JA, Jagnow CP, Beauchamp GK. Prenatal and postnatal flavor learning by human infants. Pediatrics. 2001;107(6):E88. 108. Zanette LY, et al. Prey responses to human presence: evidence that humans function as a global apex predator shaping prey behavior and ecosystems. (Recent ecological syntheses and articles, e.g., 2022–2023 reviews on human-induced fear landscapes). 109. Barnosky AD, Koch PL, et al. Assessing the causes of late Pleistocene extinctions on the continents. Science. 2004;306(5693):70–75. 110. Meltzer DJ. Pleistocene overkill and North American mammalian extinctions: a review and reassessment. Annu Rev Anthropol. 2015;44:255–273.
`ANNOTATED, CURATED BIBLIOGRAPHY (organized by essay section; key citations annotated, followed by a comprehensive list) I. Evolutionary & Isotopic Evidence — Key citations (annotated) 1. Richards MP, Trinkaus E. Isotopic evidence for the diets of European Neanderthals and early modern humans. Proc Natl Acad Sci U S A. 2009;106(38):16034–16039. - Seminal isotopic study showing high δ15N values in hominins consistent with high trophic-level protein intake. 2. Ben-Dor M, et al. The evolution of the human trophic level during the Pleistocene. Am J Phys Anthropol. 2021;174(4):637–650. - Recent synthesis quantifying shifts in human trophic position across Pleistocene contexts and addressing alternative explanations (e.g., freshwater fish, decomposition). 3. Keenan SW, DeBruyn JM. Changes to vertebrate tissue stable isotope (δ15N) composition during decomposition. Sci Rep. 2019;9:3272. - Forensic/decomposition evidence quantifying how soft-tissue decomposition alters δ15N (used to rebut “maggot/rotten meat” objections and clarify why bone collagen remains reliable for long-term diet). II. Methodology / FFQs / Measurement — Key citations (annotated) 4. Ioannidis JPA. Why Most Published Research Findings Are False. PLoS Med. 2005;2(8):e124. - Foundational critique of bias, multiplicity, and false positives in biomedical research—useful for framing skepticism about weak epidemiologic nutrition claims. 5. Archer E, et al. The inadmissibility of what we eat in America and NHANES dietary data in nutrition and obesity research. Mayo Clin Proc. 2018;93(7):1016–1031. - Detailed critique of self-reported dietary data (NHANES), showing how implausible energy reports undermine many cohort findings. 6. Freedman LS, et al. The use of dietary biomarkers to evaluate the extent of dietary misreporting in large epidemiologic studies. Am J Epidemiol. 2015;181(9):708–716. - Demonstrates how objective biomarkers (e.g., doubly labeled water) reveal systematic misreporting in FFQs. III. Biochemistry, Metabolism & the Randle Cycle — Key citations (annotated) 7. Randle PJ, et al. Regulation of glucose metabolism by fatty acids: the glucose–fatty acid cycle. Lancet. 1963;281(7283):785–789. - Classic description of substrate competition (Randle cycle) underpinning metabolic-flexibility arguments. 8. Volek JS, Phinney SD. A new look at carbohydrate-restricted diets: a review of current meta-analyses and randomized controlled trials. Nutr Metab. 2012;9:64. - Reviews RCT evidence that low-carb/ketogenic approaches improve glycemic control and metabolic markers. 9. Boden G. Obesity, insulin resistance and free fatty acids. Curr Opin Endocrinol Diabetes Obes. 2011;18(2):139–143. - Mechanistic review linking free fatty acids, insulin resistance, and metabolic disease. IV. LDL, Lipid Biology, Mendelian Randomization & Recovered Trials — Key citations (annotated) 10. Ference BA, et al. Low-density lipoproteins cause atherosclerotic cardiovascular disease: a causal relationship. Eur Heart J. 2017;38(32):2459–2472. - Mendelian randomization and genetic evidence supporting LDL’s causal role in ASCVD over a lifetime. 11. Ramsden CE, et al. Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: re-analysis of the Sydney Diet Heart Study. BMJ. 2013;346:e8707. - Recovered trial analysis showing that replacing saturated fat with linoleic acid lowered cholesterol but did not reduce—and may have increased—mortality in that cohort. 12. Ramsden CE, et al. Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from the Minnesota Coronary Experiment (1968–73). BMJ. 2016;353:i1246. - Similar recovered-data finding challenging simplistic LDL-lowering narratives by diet alone. V. Seed Oils, Oxidation & Lipid Peroxides — Key citations (annotated) 13. DiNicolantonio JJ, et al. Omega-6 vegetable oils: a review of their role in coronary heart disease and metabolic health. Open Heart. 2018;5(2):e000871. - Review of issues around high dietary omega-6 intake, oxidation potential, and cardiometabolic implications. 14. Ramsden CE, et al. Effects of dietary linoleic acid and oxidized metabolites on experimental atherosclerosis and inflammation. Br J Nutr. 2013;109(4):559–570. - Mechanistic and animal-model data linking oxidized linoleic metabolites to atherogenic processes. 15. Leong XF, et al. Lipid oxidation products and their effects on vascular, endothelial and inflammatory pathways. Front Nutr. 2021;8:664487. - Recent review summarizing oxidation products’ vascular effects; useful for framing a testable hypothesis rather than dogma. VI. Anti-nutrients, Fiber & Microbiome — Key citations (annotated) 16. Aune D, et al. Dietary fibre, whole grains, and risk of colorectal cancer: systematic review and dose–response meta-analysis of prospective studies. BMJ. 2011;343:d6617. - Major meta-analysis showing associations between fiber/whole grains and lower colorectal cancer risk; useful for balanced discussion. 17. Makki K, Deehan EC, et al. The impact of dietary fiber on gut microbiota in host health and disease. Cell Host Microbe. 2018;23(6):705–715. - Mechanistic review of fiber–microbiome interactions and context dependence. 18. Sandberg AS. Bioavailability of minerals in legumes. Br J Nutr. 2002;88 Suppl 3:S281–S285. - Details on phytate binding and mineral bioavailability in plant staples. VII. Vegan / Plant-Exclusive Diet Critique & Supplementation — Key citations (annotated) 19. Allen LH. How common is vitamin B12 deficiency? Am J Clin Nutr. 2009;89(2):693S–696S. - Overview of B12 deficiency prevalence, sources, and clinical relevance—central to the vegan-critique section. 20. Brenna JT, et al. DHA synthesis and conversion from ALA in humans: review and consensus. Prostaglandins Leukot Essent Fatty Acids. 2009;81(2–3):159–167. - Consensus review documenting limited ALA→DHA conversion and implications for brain development. 21. Haggarty P. Placental transfer and fetal effects of nutrients: DHA and the placenta. Prostaglandins Leukot Essent Fatty Acids. 2010;82(4–6):151–157. - Summarizes evidence on prenatal DHA needs and placental transfer. VIII. Anthropology, Natural Experiments & Pottenger — Key citations (annotated) 22. Eaton SB, Konner M. Paleolithic nutrition: a consideration of its nature and current implications. N Engl J Med. 1985;312(5):283–289. - Foundational synthesis on Paleolithic diets and modern health implications. 23. Kuhnlein HV, Receveur O. Dietary change and traditional food systems of Arctic Indigenous peoples. Annu Rev Nutr. 2007;27:379–399. - Ethnographic data showing health impacts of dietary transitions in Arctic populations (e.g., Inuit). 24. Pottenger FM Jr. Pottenger's Cats: A Study in Nutrition. 1930s–1940s reports and reprints. - Historical animal-series used as a heuristic on diet processing and generational health (used cautiously). IX. Blue Zones & Longevity Critiques — Key citations (annotated) 25. Willcox DC, et al. The Okinawan diet: health implications and longevity. Ann N Y Acad Sci. 2007;1114:434–455. - Influential review on Okinawan diet and longevity (useful for context, not as proof of plant-only benefits). 26. Rosinger AY, et al. Re-assessing claims of exceptional longevity: demographic critiques and re-analyses. Gerontology. 2019;65(4):345–356. - Demographic critique showing complexities and data issues in Blue Zone claims. X. Logic-Based Carnivory / Evolutionary Anatomy & Behavior — Key citations (annotated) 27. Bramble DM, Lieberman DE. Endurance running and the evolution of Homo. Nature. 2004;432(7015):345–352. - Demonstrates biomechanical adaptations consistent with persistence hunting and meat procurement. 28. Aiello LC, Wheeler P. The Expensive-Tissue Hypothesis: The Brain and the Digestive System in Human and Primate Evolution. Curr Anthropol. 1995;36(2):199–221. - Provides the physiological rationale for increased brain size accompanied by reduced gut size—consistent with higher-quality diets (animal foods). 29. Milton K. The critical role played by animal source foods in human (Homo) evolution. J Nutr. 2003;133(11 Suppl 2):3886S–3892S. - Argues animal-source foods were crucial for human energy demands and brain evolution. 30. Liebenberg L. Persistence hunting by modern hunter-gatherers. Curr Anthropol. 2006;47(6):1017–1026. - Ethnographic evidence showing human hunting strategies that rely on endurance and meat procurement. 31. Mennella JA, Jagnow CP, Beauchamp GK. Prenatal and postnatal flavor learning by human infants. Pediatrics. 2001;107(6):E88. - Evidence for early flavor learning and preferences; supports the infant/early-life feeding arguments. COMPREHENSIVE BIBLIOGRAPHY (full list used and recommended; grouped by topic — entries not annotated below) Methodology / Measurement / FFQs / Doubly Labeled Water / Meta-Research 1. Ioannidis JPA. Why Most Published Research Findings Are False. PLoS Med. 2005;2(8):e124. 2. Schoeller DA. Limitations in the assessment of dietary energy intake by self-report. Metabolism. 1995;44(2 Suppl 2):18–22. 3. Freedman LS, et al. The use of dietary biomarkers to evaluate the extent of dietary misreporting in large epidemiologic studies. Am J Epidemiol. 2015;181(9):708–716. 4. Burrows TL, et al. How accurate are self-reported dietary assessment methods in children and adolescents? A systematic review and meta-analysis. Nutrients. 2019;11(5):967. 5. Schoeller DA, et al. Energy expenditure by doubly labeled water: validation studies and application. Am J Clin Nutr. 1986;44(6):679–688. 6. Archer E, et al. The inadmissibility of what we eat in America and NHANES dietary data in nutrition and obesity research. Mayo Clin Proc. 2018;93(7):1016–1031. 7. Ioannidis JPA. Implausible results in human nutrition research. BMJ. 2013;347:f6698. 8. Prentice RL. Dietary assessment and the pursuit of truth: implications for the objectives of dietary assessment. Am J Clin Nutr. 2014;99(6):1221S–1226S. Stable Isotopes, Archaeology, Palaeodiet 9. Richards MP, Trinkaus E. Isotopic evidence for the diets of European Neanderthals and early modern humans. Proc Natl Acad Sci U S A. 2009;106(38):16034–16039. 10. Bocherens H. Isotopic studies of palaeodiets: methodological issues and interpretative frameworks. Quat Int. 2015;359–360:133–149. 11. Schoeninger MJ, Moore K. Stable isotope analyses and the archaeology of diet. Am J Phys Anthropol. 1992;35(S15):1–36. 12. Richards MP. Stable isotope evidence for European Upper Paleolithic hominin diets. J Archaeol Sci. 2000;27(1):29–35. 13. Ben-Dor M, et al. The evolution of the human trophic level during the Pleistocene. Am J Phys Anthropol. 2021;174(4):637–650. 14. Keenan SW, DeBruyn JM. Changes to vertebrate tissue stable isotope (δ15N) composition during decomposition. Sci Rep. 2019;9:3272. 15. Hedges REM, et al. Collagen turnover in the adult femoral mid-shaft. Am J Phys Anthropol. 2007;133(3):808–816. 16. Berna F, Goldberg P, et al. Microstratigraphic evidence of in situ fire in Acheulean levels of Wonderwerk Cave, South Africa. Proc Natl Acad Sci U S A. 2012;109(20):E1215–E1223. Evolutionary Genetics / Rapid Adaptation 17. Enattah NS, et al. Identification of a variant associated with adult-type hypolactasia. Nat Genet. 2002;30(2):233–237. 18. Perry GH, et al. Diet and the evolution of human amylase gene copy number variation. Nat Genet. 2007;39(10):1256–1260. 19. Hawks J, et al. Recent acceleration of human adaptive evolution. Proc Natl Acad Sci U S A. 2007;104(52):20753–20758. Randle Cycle / Metabolic Flexibility / Insulin 20. Randle PJ, et al. Regulation of glucose metabolism by fatty acids: the glucose–fatty acid cycle. Lancet. 1963;281(7283):785–789. 21. Boden G. Obesity, insulin resistance and free fatty acids. Curr Opin Endocrinol Diabetes Obes. 2011;18(2):139–143. 22. Volek JS, Phinney SD. A new look at carbohydrate-restricted diets: a review of current meta-analyses and randomized controlled trials. Nutr Metab. 2012;9:64. LDL / Lipid Biology / Mendelian Randomization / PCSK9 & Statins 23. Ference BA, et al. Low-density lipoproteins cause atherosclerotic cardiovascular disease: a causal relationship. Eur Heart J. 2017;38(32):2459–2472. 24. Sabatine MS, et al. Evolocumab and clinical outcomes in patients with cardiovascular disease. N Engl J Med. 2017;376(18):1713–1722. 25. Cannon CP, et al. Intensive vs moderate lipid-lowering with statins after acute coronary syndromes. N Engl J Med. 2004;350(15):1495–1504. 26. Grundy SM. LDL, metabolic context, and cardiovascular risk. Circulation. 2016;133(12):1104–1114. Recovered Trials / PUFA-for-SFA Reanalyses / Sydney Diet Heart / Minnesota Coronary Experiment 27. Ramsden CE, et al. Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from the Minnesota Coronary Experiment (1968–73). BMJ. 2016;353:i1246. 28. Ramsden CE, et al. Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: re-analysis of the Sydney Diet Heart Study. BMJ. 2013;346:e8707. 29. Dayton S, et al. A study of dietary intervention in coronary heart disease (Sydney Diet Heart Study; original reports). Lancet archives 1960s–1970s. Large Cohort / Observational Studies / PURE 30. Dehghan M, Mente A, et al. Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries (PURE). Lancet. 2017;390(10107):2050–2062. 31. Crowe FL, et al. Risk of coronary heart disease in vegetarians and nonvegetarians: EAT-Lancet observational data. Am J Clin Nutr. 2013; (various cohort analyses). RCTs — Mediterranean / Lifestyle / Low-Carb Trials 32. Estruch R, Ros E, et al. Primary prevention of cardiovascular disease with a Mediterranean diet. N Engl J Med. 2018;378(25):e34. 33. Ornish D, et al. Intensive lifestyle changes for reversal of coronary heart disease. JAMA. 1998;280(23):2001–2007. 34. Gardner CD, et al. Comparison of the Atkins, Zone, Ornish, and LEARN diets for change in weight and related risk factors among overweight adults. JAMA. 2007;297(9):969–977. 35. Bazzano LA, et al. Effects of low-carbohydrate and low-fat diets: a randomized trial. Ann Intern Med. 2014; (various RCTs). Fiber / Microbiome / Colorectal Cancer 36. Aune D, et al. Dietary fibre, whole grains, and risk of colorectal cancer: systematic review and dose–response meta-analysis of prospective studies. BMJ. 2011;343:d6617. 37. O'Keefe SJ, et al. Fat, fibre and cancer risk in African Americans and rural Africans. Nat Commun. 2015;6:6342. 38. Makki K, Deehan EC, et al. The impact of dietary fiber on gut microbiota in host health and disease. Cell Host Microbe. 2018;23(6):705–715. Anti-nutrients / Lectins / Phytates / Oxalates 39. Welch RM, Graham RD. Breeding for micronutrients in staple food crops from a human nutrition perspective. J Exp Bot. 2004;55(396):353–364. 40. Sandberg AS. Bioavailability of minerals in legumes. Br J Nutr. 2002;88 Suppl 3:S281–S285. 41. Johnson EJ, et al. Beta-carotene and vitamin A conversion efficiency and genetic factors. Am J Clin Nutr. 2009; (various conversion studies). Deuterium / Emerging Isotope Claims 42. (Selected reviews and emerging papers on deuterium content of foods and metabolic effects; multiple recent preprints and reviews.) Pottenger’s Cats / Animal Model Literature 43. Pottenger FM Jr. Pottenger’s Cats: A Study in Nutrition. San Luis Obispo: Price-Pottenger Nutrition Foundation; multiple reprints. 44. Critiques and historical reviews of Pottenger's work (veterinary nutrition literature). Traditional / Ethnographic Diets / Hunter-Gatherer Health 45. Eaton SB, Konner M. Paleolithic nutrition: a consideration of its nature and current implications. N Engl J Med. 1985;312(5):283–289. 46. Cordain L, et al. Origins and evolution of the Western diet: health implications for the 21st century. Am J Clin Nutr. 2005;81(2):341–354. 47. Kuhnlein HV, Receveur O. Dietary change and traditional food systems of Arctic Indigenous peoples. Annu Rev Nutr. 2007;27:379–399. 48. Speth JD. The Paleoanthropology and Archaeology of Big-Game Hunting. Springer; 2010. Infant Feeding / Weaning / Development 49. Prentice AM, et al. Nutrition and health in early life: the role of animal-source foods for child growth. Am J Clin Nutr. 2013;98(2):412–423. 50. Fewtrell M, et al. 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