jet

• At 11, Super Size Me gave Josie a sense that she had control over her health.
• At 13, a PETA tent at Vans Warped Tour led Josie to watch Earthlings and change her diet overnight.
• Josie became vegan immediately because she believed it was healthiest, most ethical, and best for her skin.
• In hindsight, Josie knew something was wrong with the Standard American Diet, but moved in the wrong direction.

Fourteen Vegan Years and Illness

• Josie stayed vegan for 14 years without cheating and moved from meat substitutes to whole-food plant-based eating.
• During those years, Josie had weight swings, dry skin, rosacea, poor mental health, and low self-esteem.
• After about 10 years vegan, ulcerative colitis hit with diarrhea 10 to 20-plus times a day and heavy blood in stool.
• Josie was hospitalized twice, and one doctor told her the severe episode could have killed her.
• Doctors told Josie it was genetic, lifelong, medication-dependent, and incompatible with full-time work or having children.

Breaking Point and Animal Foods

• In 2021, after another severe flare and years of avoiding medication, Josie tried bone broth.
• Within a week, digestion and skin improved enough for Josie to see a workable path.
• Over about six months, Josie reintroduced animal products in steps because she was still afraid of them.
• After four to five months, colitis symptoms were mostly in remission before beef returned.
• With beef and a meat-based diet, digestion, skin, inflammation, weight, and mental health improved further.
• Carnivore finished the process: normal digestion returned after nearly a decade, and plant-food tests still bring symptoms.

Identity and Social Response

• Reintroducing animal foods created a full identity crisis after a decade of vegan commitment.
• Health gains overrode guilt and social pressure because Josie's body was improving quickly and drastically.
• Friends and acquaintances were shocked, but their reactions did not change Josie's decision.
• Josie's fiancé started carnivore with her, improved too, and added white rice only because strict carnivore made him lose too much weight.

Current Diet and Routine

• Dinner is usually steak, ground beef, eggs, salmon, shrimp, or poultry, with red meat as the base.
• Red meat is about 60 to 70% of Josie's diet because she feels best eating steak and ground beef.
• Josie usually eats two meals a day, sometimes one meal when she is busy.
• Coffee stays in the routine: organic coffee with heavy cream, butter or beef tallow, and salt.
• Compared with vegan eating, cravings and food noise are gone, and a smaller amount of food brings complete satiety.

Current Commitment and Advice

• After about four and a half years carnivore, Josie has no desire to go back.
• Small additions like organic hot sauce or avocado usually bring brain fog or skin irritation.
• For people starting, Josie recommends a 30-day carnivore trial and a gradual transition when needed.
• Josie would step down from processed foods and excess sugar first, then vegetables, then fruit.
• Josie shares the journey, recipes, experiments, and Coming Around to Carnivore through The X Plant Eater platforms.

References

• [00:15] Super Size Me — https://morganspurlock.com/work/super-size-me/
• [01:02] Earthlings — https://www.nationearth.com/earthlings
• [23:03] Coming Around to Carnivore: From Skeptic to Thriving — https://www.barnesandnoble.com/w/coming-around-to-carnivore-josie-lieder/1148793261

• The mitochondrial-metabolic model links cancer to chronic damage in oxidative phosphorylation as the origin of malignant behavior.
• The somatic mutation theory is weakened by tumor nuclei regaining regulated growth in normal cytoplasm, while tumor cytoplasm drives death or dysregulated growth.
• Nuclear-transfer experiments in frogs, medulloblastoma mice, and melanoma mice place the decisive cancer defect outside the nucleus.
• The National Cancer Institute definition keeps cancer inside a genetic-disease view, while the lecture places the core defect in mitochondrial energy production.

Energy metabolism and tumor growth

• Warburg identified insufficient respiration and compensatory fermentation through glucose-derived lactate.
• Glutamine fermentation adds a second major fuel stream, producing succinate in damaged mitochondria.
• Glucose and glutamine supply ATP, carbons, and nitrogen for membranes, proteins, nucleotides, lipids, and other biomass.
• Lactic and succinic acid create an acidic microenvironment that supports invasion and weakens drug and immune effects.
• Reactive oxygen species arise downstream from damaged respiration and can produce the mutations seen in tumor genomes.

Cancer hallmarks from damaged mitochondria

• Cell-cycle disorder follows mitochondrial effects on nuclear gene expression and regulatory control.
• Loss of contact inhibition follows calcium and adhesion defects at the tumor-cell surface.
• Angiogenesis follows HIF-1 alpha and c-MYC opening glucose and glutamine transport pathways.
• Failed apoptosis follows dysfunction in the organelle that normally controls programmed cell death.
• Metastasis follows fusion between a cancer stem cell and a macrophage-like immune cell, creating a mobile glucose- and glutamine-driven cell.

Metabolic management strategy

• Management requires lowering glucose and glutamine while raising fatty acids and ketones.
• Cancer cells cannot rely on fatty acids or ketone bodies when glucose and glutamine are unavailable.
• Water-only fasting, calorie restriction, low-carbohydrate diets, ketogenic diets, ketone supplements, exercise, stress control, hyperbaric oxygen, and pulse drugs fit this strategy.
• The glucose ketone index tracks the glucose-to-ketone ratio, with values near or below 2.0 used as the therapeutic zone.
• Press-pulse therapy uses chronic metabolic pressure plus timed pulses against glucose and glutamine dependence.

Preclinical evidence

• In an aggressive mouse brain-tumor model, 40% calorie restriction on the same high-carbohydrate diet reduced tumor size by 65% to 80%.
• Higher blood glucose tracked with larger and faster tumors, while lower glucose tracked with slower tumor growth, lower inflammation, fewer abnormal vessels, and more tumor killing.
• Calorie-restricted ketogenic diet plus pulsed DON produced far better survival in late-stage experimental glioblastoma than either diet or DON alone.
• A juvenile high-grade glioma model used restricted ketogenic diet, mebendazole, and glucose-glutamine targeting, with longer survival and better quality of life.

Human and animal cases

• Glioblastoma outcomes have barely improved, and standard surgery, radiation, chemotherapy, and steroids can increase glucose, glutamine, inflammation, and metabolic stress.
• The Alexandria glioblastoma case combined fasting, restricted ketogenic diet, awake craniotomy, modified standard care, and hyperbaric oxygen, with 24-month follow-up publication.
• Brittany Maynard is used as a standard-care contrast case: young glioblastoma patient, steroid effects, and medically assisted death in 2014.
• Pablo Kelly used ketogenic metabolic therapy without chemotherapy or radiation, tracked glucose and ketones for years, and lived 122 months after diagnosis.
• The Greece glioblastoma study pairs standard care with ketogenic metabolic therapy; four of six adherent patients lived at least three years versus one of twelve in the standard-care group.
• Triple-negative breast cancer, lung cancer, prostate cancer, and canine mast-cell tumor examples are used as broader applications of the same metabolic strategy.

Closing thesis

• Cancer management should avoid fatalistic terminal language when metabolic options remain.
• Mitochondria, not the nucleus, belong at the center of cancer origin and management.
• Substrate-level phosphorylation through glucose and glutamine fermentation drives dysregulated growth.
• The future cancer program is press-pulse metabolic therapy: lower glucose and glutamine, elevate ketones, and use coordinated metabolic tools.

References

• [00:00] Cancer as a Metabolic Disease: On the Origin, Management, and Prevention of Cancer — https://doi.org/10.1002/9781118310311
• [02:00] Can the Mitochondrial Metabolic Theory Explain Better the Origin and Management of Cancer than Can the Somatic Mutation Theory? — https://doi.org/10.3390/metabo11090572
• [03:00] Hallmarks of Cancer: The Next Generation — https://doi.org/10.1016/j.cell.2011.02.013
• [06:00] Transplantation of Pluripotential Nuclei from Triploid Frog Tumors — https://doi.org/10.1126/science.165.3891.394
• [07:00] Mouse Embryos Cloned from Brain Tumors — https://aacrjournals.org/cancerres/article/63/11/2733/510012/Mouse-Embryos-Cloned-from-Brain-Tumors1
• [08:00] Reprogramming of a Melanoma Genome by Nuclear Transplantation — https://doi.org/10.1101/gad.1213504
• [10:00] What Is Cancer? — https://www.cancer.gov/about-cancer/understanding/what-is-cancer
• [11:00] On the Origin of Cancer Cells — https://doi.org/10.1126/science.123.3191.309
• [18:00] The Living State and Cancer — https://doi.org/10.1073/pnas.74.7.2844
• [21:00] Cancer as a Metabolic Disease — https://doi.org/10.1186/1743-7075-7-7
• [21:00] Cancer as a Metabolic Disease: Implications for Novel Therapeutics — https://doi.org/10.1093/carcin/bgt480
• [21:00] Cancer as a Mitochondrial Metabolic Disease — https://doi.org/10.3389/fcell.2015.00043
• [22:00] The Calorically Restricted Ketogenic Diet, an Effective Alternative Therapy for Malignant Brain Cancer — https://doi.org/10.1186/1743-7075-4-5
• [23:00] The Glucose Ketone Index Calculator: A Simple Tool to Monitor Therapeutic Efficacy for Metabolic Management of Brain Cancer — https://doi.org/10.1186/s12986-015-0009-2
• [25:00] Press-Pulse: A Novel Therapeutic Strategy for the Metabolic Management of Cancer — https://doi.org/10.1186/s12986-017-0178-2
• [26:00] Therapeutic Benefit of Combining Calorie-Restricted Ketogenic Diet and Glutamine Targeting in Late-Stage Experimental Glioblastoma — https://doi.org/10.1038/s42003-019-0455-x
• [29:00] Management of Glioblastoma Multiforme in a Patient Treated With Ketogenic Metabolic Therapy and Modified Standard of Care: A 24-Month Follow-Up — https://doi.org/10.3389/fnut.2018.00020
• [30:00] Terminally Ill Woman Brittany Maynard Has Ended Her Own Life — https://people.com/celebrity/terminally-ill-woman-brittany-maynard-has-ended-her-own-life/
• [31:00] Ketogenic Metabolic Therapy, Without Chemo or Radiation, for the Long-Term Management of IDH1-Mutant Glioblastoma: An 80-Month Follow-Up Case Report — https://doi.org/10.3389/fnut.2021.682243
• [33:00] Successful Application of Dietary Ketogenic Metabolic Therapy in Patients With Glioblastoma: A Clinical Study — https://doi.org/10.3389/fnut.2024.1489812
• [35:00] Ketogenic Diet as a Metabolic Vehicle Enhancing the Therapeutic Efficacy of Mebendazole and Devimistat in Juvenile Syngeneic High-Grade Glioma — https://doi.org/10.1016/j.xcrm.2026.102845
• [35:00] Efficacy of Metabolically Supported Chemotherapy Combined With Ketogenic Diet, Hyperthermia, and Hyperbaric Oxygen Therapy for Stage IV Triple-Negative Breast Cancer — https://doi.org/10.7759/cureus.1445
• [36:00] Restricted Ketogenic Diet Therapy for Primary Lung Cancer With Metastasis to the Brain: A Case Report — https://doi.org/10.7759/cureus.27603
• [36:00] Clinical Research Framework Proposal for Ketogenic Metabolic Therapy in Glioblastoma — https://doi.org/10.1186/s12916-024-03775-4
• [37:00] Case Report: Resolution of Malignant Canine Mast Cell Tumor Using Ketogenic Metabolic Therapy Alone — https://doi.org/10.3389/fnut.2023.1157517

• Metabolic psychiatry adds glucose, insulin, inflammation, oxidative stress, and mitochondrial energy to the older neurotransmitter-centered model of psychiatric illness.
• High glucose and high insulin can drive brain inflammation, oxidative stress, advanced glycation end products, and neurotransmitter disruption.
• Excess inflammation and oxidative stress can push glutamate far above baseline and damage proteins, lipids, DNA, mitochondria, the blood-brain barrier, and the hippocampus.
• Brain glucose entry is insulin independent, but brain glucose use depends on adequate brain insulin.
• Chronic high insulin can make the blood-brain barrier insulin resistant, so the brain can receive too little insulin while glucose remains high.
• Cerebral glucose hypometabolism is the energy deficit that links metabolic dysfunction to late-onset Alzheimer’s disease and serious psychiatric illness.
• Ketones cross into the brain even when insulin resistance is severe and burn well in a low-insulin environment.
• Ketogenic therapy can bridge the brain energy gap when more glucose or more insulin would worsen the metabolic problem.

Clinical evidence and active trials

• Alzheimer’s disease has long-standing metabolic evidence, including the type 3 diabetes model from Brown University and earlier insulin-signaling work.
• Cynthia Calkin’s bipolar depression trial used metformin to reverse insulin resistance, and mood improvement occurred in the patients whose insulin resistance reversed.
• Ketogenic diet research in psychiatry is expanding across bipolar disorder, schizophrenia, depression, alcohol withdrawal, autism, Alzheimer’s disease, ADHD, and anorexia.
• The alcohol-withdrawal randomized trial found that people on a ketogenic diet required about half as much benzodiazepine and had fewer alcohol cravings.
• Albert Danan’s inpatient ketogenic diet analysis involved 31 severe, therapy-resistant patients with depression, bipolar disorder, and schizophrenia.
• In Danan’s adherent inpatient group, all 28 patients improved psychiatrically and metabolically, 43% reached clinical remission, and 64% left on less psychiatric medication.
• Ian Campbell’s bipolar pilot enrolled euthymic outpatients for an 8-week ketogenic diet and found strong adherence, average ketones around 1.3 mmol/L, and symptom links with ketone levels.
• Campbell’s spectroscopy data showed a large reduction in brain glutamate-related signal, with several participants refusing to stop the diet after the protocol ended.
• Shebani Sethi’s Stanford pilot placed outpatients with bipolar disorder or schizophrenia on a ketogenic diet for 4 months and found clinically meaningful psychiatric improvement in most participants.
• Randomized trials are still needed for serious mood and psychotic disorders, and new studies are underway or planned at Oxford, UC San Diego, Stanford, and other sites.

Clinical use and ketone targets

• Psychiatric ketogenic therapy needs clinician oversight when patients have serious symptoms, take psychiatric medications, or have anorexia risk.
• Medication interactions matter because antipsychotics and some anticonvulsants can make ketone production harder.
• For low ketones, insulin is the control knob: lower total carbohydrates, sometimes below 20 g; count total carbs; regulate protein; avoid snacking; and add resistance exercise.
• Whey, casein, dairy excess, sweeteners, frequent eating, and excess protein can keep insulin high even when glucose does not rise.
• A practical starting target is blood ketones between 1.0 and 3.0 mmol/L most of the time.
• Some patients improve with simple low carbohydrate intake and low glucose, while others need sustained ketones in a tighter or higher range.
• A fair trial requires consistent therapeutic ketosis for weeks, not occasional late-day ketone readings.

Q&A applications

• GLP-1 agonists can reduce appetite, glucose, and insulin and may help some patients bridge into ketogenic therapy, but responses can be positive, neutral, or counterproductive.
• Continuous ketone monitors may be most useful for patterns, timing, overnight changes, food responses, and hidden gaps in daily ketosis.
• Gut symptoms matter in psychiatric ketogenic care, and persistent constipation should lead to food-choice review after the adaptation period.
• High-fiber foods, cruciferous vegetables, nuts, seeds, chia, cheese, and dairy can be hard to digest for some patients.
• The quiet diet approach uses paleo, keto, or carnivore versions designed to be gentler on the gut.
• Fiber requirements for the microbiome are cast as untested, and many people with serious gastrointestinal symptoms improve when fiber is reduced.
• Mediterranean-style diet changes can help depression when they replace a junk-food diet, but the metabolic piece may require lower carbohydrate intake.
• Type 1 diabetes makes ketosis harder because injected insulin suppresses ketone production, so exercise and careful monitoring become more important.
• Women may have more difficulty entering ketosis during perimenopause and menopause because falling estrogen can worsen insulin resistance.
• Estrogen replacement may help some women improve metabolic flexibility, while progesterone may push metabolism in the opposite direction.
• Early Alzheimer’s patients who remain hyperglycemic and out of ketosis on low carbohydrate intake may need lower protein and higher fat intake.

References

• [00:01] Change Your Diet, Change Your Mind — https://www.gcp-balance.com/titles/dr-georgia-ede-m-d/change-your-diet-change-your-mind/9781538739075/
• [00:12] Impaired Insulin and Insulin-Like Growth Factor Expression and Signaling Mechanisms in Alzheimer’s Disease – Is This Type 3 Diabetes? — https://doi.org/10.3233/JAD-2005-7107
• [00:13] Alzheimer’s Disease Is Type 3 Diabetes—Evidence Reviewed — https://doi.org/10.1177/193229680800200619
• [00:15] Treating Insulin Resistance With Metformin as a Strategy to Improve Clinical Outcomes in Treatment-Resistant Bipolar Depression (the TRIO-BD Study): A Randomized, Quadruple-Masked, Placebo-Controlled Clinical Trial — https://doi.org/10.4088/JCP.21m14022
• [00:19] Ketogenic Diet Reduces Alcohol Withdrawal Symptoms in Humans and Alcohol Intake in Rodents — https://doi.org/10.1126/sciadv.abf6780
• [00:19] Ketogenic Diet Versus Gluten Free Casein Free Diet in Autistic Children: A Case-Control Study — https://doi.org/10.1007/s11011-017-0088-z
• [00:19] Randomized Crossover Trial of a Modified Ketogenic Diet in Alzheimer’s Disease — https://doi.org/10.1186/s13195-021-00783-x
• [00:22] The Ketogenic Diet for Refractory Mental Illness: A Retrospective Analysis of 31 Inpatients — https://doi.org/10.3389/fpsyt.2022.951376
• [00:25] Pilot Study of a Ketogenic Diet in Bipolar Disorder — https://doi.org/10.1192/bjo.2023.568
• [00:27] A Pilot Study of a Ketogenic Diet in Bipolar Disorder: Clinical, Metabolic and Magnetic Resonance Spectroscopy Findings — https://doi.org/10.1192/bjo.2024.841
• [00:28] Ketogenic Diet Intervention on Metabolic and Psychiatric Health in Bipolar and Schizophrenia: A Pilot Trial — https://doi.org/10.1016/j.psychres.2024.115866
• [00:31] Metabolic Mind — https://www.metabolicmind.org/
• [00:31] Ketogenic Diets for Mental Health Resources — https://www.diagnosisdiet.com/resources
• [00:44] Impact of Glucagon-Like Peptide 1 Agonist Deprescription in Type 2 Diabetes in a Real-World Setting: A Propensity Score Matched Cohort Study — https://doi.org/10.1007/s13300-024-01547-0
• [00:52] The Effects of Ketogenic Metabolic Therapy on Mental Health and Metabolic Outcomes in Schizophrenia and Bipolar Disorder: A Randomized Controlled Clinical Trial Protocol — https://doi.org/10.3389/fnut.2024.1444483
• [01:03] Stress Dynamically Modulates Neuronal Autophagy to Gate Depression Onset — https://doi.org/10.1038/s41586-025-08807-4
• [01:21] Child Bipolar Network Ketogenic Diet Approach to Depression or Mixed Mood in Bipolar Disorder — https://clinicaltrials.gov/study/NCT06920940
• [01:21] Food for ADHD and Depression — https://www.isrctn.com/ISRCTN62698625
• [01:21] Therapeutic Ketogenic Diet in Anorexia Nervosa — https://clinicaltrials.gov/study/NCT06000774