• Fermentation is a key ancestral food processing technique that enhances nutrition, detoxifies foods, and improves shelf life.
• Plants were a significant part of human diets long before meat was introduced, and they continued to be consumed alongside meat.
• The domestication of plants has led to a reduction in their natural defense mechanisms, making them more susceptible to pests and diseases.
• Modern agricultural practices often strip plants of their natural toxins, which can be harmful if consumed in large quantities or improperly processed.
• The Blue Zones diet, often misrepresented as plant-based, actually includes a significant amount of animal products and fermented foods.
• Salt has been an important part of human diets since ancient times, with high-quality, mineral-rich salts being the most beneficial.
• Traditional diets were highly diverse and seasonal, with a focus on locally available and hyper-seasonal plants and animals.
• The modern industrial food system has led to a loss of diversity in diets, with a focus on a limited range of crops and animal products.
• The role of plants in traditional diets was multifaceted, including nutrition, entertainment, medicine, and poison.
• The misrepresentation of the Blue Zones diet has led to a misunderstanding of the importance of animal products and fermented foods in traditional diets.

Video Summary — EAT-Lancet “Planetary Health Diet” & “Misinfluencer” Campaign

Context

• The video discusses the EAT-Lancet “Planetary Health Diet” (PHD)—its goals and scientific basis—and a new “misinfluencer” campaign launched around the forthcoming EAT-Lancet 2.0 update.
• Guest: Dr. Georgia Ede (named in the campaign) responds to the label and critiques the report’s methods and conclusions.

What EAT-Lancet Proposes (as described in the video)

• A global dietary pattern intended to be healthy for humans and environmentally sustainable by 2050.
• Core recommendation: minimize or eliminate animal-source foods; emphasize grains, legumes, nuts, with supplements and fortified processed foods filling nutritional gaps.

Methodological Concerns Raised in the Video

• Heavy reliance on nutrition epidemiology (observational associations) rather than:
  • Randomized controlled trials
  • Clinical experiments
  • Human biology/mechanistic evidence
• Evidence that would challenge or nuance conclusions is dismissed, excluded, or downplayed.
• The report’s broad, universal prescription is questioned given heterogeneity in human needs and contexts.

Nutrient Adequacy & Supplementation (quotations/paraphrases from the report cited in the video)

• The report acknowledges shortfalls for at least four key nutrients on the recommended pattern:
  • Calcium, **Vitamin B12, Iron, Iodine
• States that B12 intake is already low globally and would be further reduced without optimization.
• Advises supplementation and fortified processed foods to cover gaps.
• The video emphasizes that these nutrients are most easily—or sometimes only—reliably obtained from animal foods.

Populations of Concern (as stated in the video)

• The report itself flags risks for:
  • Women, children, malnourished/impoverished populations, and older adults.
• The video stresses heightened vulnerability for women and children, who may be more likely to adopt such guidance and more susceptible to nutrient deficits.

Risk Framing

• The video characterizes the recommended diet as “incredibly risky” if broadly prescribed, due to:
  • Dependence on supplements/fortification
  • Potential nutrient insufficiencies
  • Lack of strong experimental evidence underpinning sweeping global recommendations

Environmental Framing

• The video argues it’s overly simplistic to label animal agriculture as inherently worse and plant agriculture as inherently better for the environment.
• Notes industrial production of both plant and animal foods raises distinct environmental concerns not fully addressed by the report.

“Misinfluencer” Campaign (as described in the video)

• Ahead of EAT-Lancet 2.0, an organized communications effort labeled critics as “misinfluencers.”
• Georgia Ede (guest) was listed; the video says the campaign names people and claims but does not substantively rebut their specific arguments.
• The campaign is presented as an attempt to discredit dissent rather than engage with evidence.

Protein & Brain Health (discussion points)

• The video raises concerns about adequacy of high-quality protein (and specific fatty acids) for brain development and function within the recommended pattern.
• Emphasizes biological needs that may not be fully met without animal-source foods or targeted supplementation.

Bottom Line from the Video

• A single global diet prescription is portrayed as unsupported by robust experimental evidence and potentially unsafe for many, especially vulnerable populations.
• The video calls for higher-quality evidence (RCTs, clinical and mechanistic studies) and nuanced, context-specific guidance rather than one-size-fits-all recommendations.

Referenced Paper(s) with DOI

• Food in the Anthropocene: the EAT–Lancet Commission on healthy diets from sustainable food systems (2019, The Lancet) — https://doi.org/10.1016/S0140-6736(18)31788-4

Video Summary: Low-Carb/Ketogenic Diet Evidence vs. Common Misrepresentations

Core Message

• Media headlines and some academic papers frequently misrepresent or overstate findings that appear to undermine low-carb/ketogenic diets.
• These distortions discourage patients and clinicians despite evidence that low-carb approaches can benefit type 2 and type 1 diabetes.
• Careful reading of methods and figures often reveals problems (misclassification, poor diet formulation, invalid comparisons, or design flaws).

Case Study 1 — “Ketogenic diet causes insulin resistance/obesity” (mouse paper)

• A 2025 Science Advances paper claimed a ketogenic diet caused worsening glucose regulation and other harms in mice.
• Video’s critique:
  • Animal model & generalizability: Findings are in a specific mouse model, not humans; appetite control and metabolic regulation differ fundamentally.
  • Internal inconsistency: Even Figure 1 shows outcomes (e.g., body fat gain vs. controls) that complicate the headline narrative when inspected closely.
  • Takeaway: Mouse data were publicized as if they overturn human clinical evidence for low-carb diets; they do not.

Referenced paper (from the video):

• A long-term ketogenic diet causes hyperlipidemia, liver dysfunction, and glucose intolerance from impaired insulin secretion in mice. Science Advances (2025). https://doi.org/10.1126/sciadv.adx2752

Case Study 2 — 2021 metabolic-ward crossover trial (Nature Medicine)

• A 2021 Nature Medicine randomized, inpatient, ad libitum crossover trial compared a plant-based low-fat diet vs. an animal-based ketogenic diet.
• Public messaging framed it as strong evidence against the carbohydrate-insulin model, with high-profile endorsements.
• Video’s critique (why the trial’s conclusions were misleading):
  • Diet formulation issues: The so-called “animal-based ketogenic” diet menu composition (e.g., “fried chicken on salads,” etc.) did not reflect a well-formulated ketogenic diet as typically practiced for metabolic health.
  • Crossover design without adequate adaptation: Rapid diet switching can produce carryover effects; metabolic and hormonal adaptations require time. Short periods bias results against low-carb/keto when no keto-adaptation phase is allowed.
  • Outcome interpretation: Reported differences in ad libitum energy intake were over-interpreted; design/implementation flaws undercut the headline claims.
  • Ongoing controversy: Despite the methodological concerns, the paper has not been retracted.

Referenced paper (from the video):

• Effect of a plant-based, low-fat diet versus an animal-based, ketogenic diet on ad libitum energy intake. Nature Medicine (2021). https://doi.org/10.1038/s41591-020-01209-1

Common Patterns of Distortion Highlighted

• Observational misclassification: “Low-carb” exposure defined via food-frequency questionnaires or composite scores rather than actual carbohydrate percent, leading to misleading comparisons.
• Inadequate keto adaptation: Short trials or abrupt crossovers ignore physiologic adaptation, biasing against ketogenic arms.
• Headline amplification: Press and social media spread simplified narratives that obscure methodological caveats.

Practical Implications (as stated in the video)

• Patients may be discouraged from trying dietary approaches (e.g., well-formulated low-carb/keto) that could substantially improve glycemic control.
• Clinicians might hesitate to recommend low-carb strategies due to high-visibility but methodologically weak or misinterpreted findings.

Bottom Line

• Evaluate study design, diet formulation, population/model, and figures before accepting headline claims that “debunk” low-carb/ketogenic diets.
• The cited mouse paper and the 2021 metabolic-ward trial do not invalidate evidence that properly implemented low-carb/ketogenic diets can benefit metabolic health.

• Context & Participants

  • Discussion on GLP-1 medications (e.g., Wegovy/Ozempic [semaglutide], Zepbound/Tirzepatide) and how we may be “talking about GLP-1s all wrong.”
  • Guest: Dr. Robinson — board-certified in psychiatry and addiction medicine — sharing her personal and clinical perspective.

• Personal Background

  • Long history of weight fluctuation; previously tried WeightWatchers, Jenny Craig, MetaFast.
  • On low-carb for ~11 years with strict avoidance of sugar and starch.
  • During a major life stressor (mother in hospice and passing), gained ~20 lbs, then another ~20 lbs despite unchanged intake.
  • Began a GLP-1; has been on it for ~1 year and 3 months at the time of the conversation.

• Why GLP-1s (for some low-carb patients)

  • Even with consistent low-carb, some people need additional assistance to control appetite/cravings and “food chatter.”
  • GLP-1s can help adherence to dietary changes rather than replace them.

• Addiction-Medicine Analogy

  • In opioid use disorder, psychotherapy alone leads to ~85% returning to use within a year; combining with medications (e.g., methadone, buprenorphine) dramatically improves outcomes.
  • By analogy, GLP-1s can be a medication “bridge” that enables behavior change (e.g., CBT skills, low-carb adherence) for those who need it.
  • Emphasis on avoiding stigma or shaming toward people who benefit from medication support.

• Effects & Day-to-Day Experience

  • Marked appetite reduction, especially after dose increases.
  • Easier time entering and maintaining ketosis on GLP-1s; could lower protein somewhat and still achieve ketosis compared with pre-GLP-1.
  • Continues resistance training (lifting twice weekly). Notes some **

Why Doctors Aren’t Taught Nutrition — Dr. Nick Norwitz Exposes The Truth

Participants: Dr. Eric Westman (host) and Dr. Nick Norwitz (guest)

Norwitz’s background & health story

• Undergraduate at Dartmouth (cell biology & biochemistry); PhD at Oxford; admitted to Harvard Medical School.
• Developed severe inflammatory bowel disease with debilitating GI symptoms.
• Attempted standard medical approaches without adequate relief.
• Adopted a Mediterranean-leaning ketogenic diet (fatty fish, olive oil, vegetables; low carbohydrate) and experienced rapid, substantial improvement and recovery.

Why doctors aren’t taught much nutrition

• Medical training is designed primarily for diagnosing and treating disease with medications and procedures; prevention and nutrition receive little curricular time.
• “Evidence-based medicine” is valuable but can be limited by:
  • Overreliance on narrow hierarchies that discount mechanistic and patient-level evidence.
  • Institutional incentives (e.g., drug-centric frameworks) that don’t translate well to diet and lifestyle.
• Practical nutrition education is often missing, leaving clinicians without clear frameworks or tools.

Models of obesity & metabolism discussed

• Calories In/Calories Out (CICO): Critiqued as a near tautology—describes weight change but offers limited mechanistic guidance.
• Carbohydrate-Insulin Model (CIM): Presented as an alternative framework emphasizing hormonal regulation (insulin) and carbohydrate quality/quantity as drivers of fat storage and appetite.

Clinical practice considerations raised

• Many patients achieve meaningful improvements (weight, metabolic health) with low-carb/keto patterns; individual responses vary.
• Randomized trials and mechanistic studies both matter, but patients ultimately need safe, n=1 experimentation with clinician support.
• Clinicians are comfortable prescribing FDA-approved drugs (e.g., GLP-1 agonists, SGLT2 inhibitors), but comparable, scalable guidance for nutrition is rarely taught despite potential benefit.

Statins, GLP-1, and emerging evidence

• A highlighted human controlled trial reported that statin therapy markedly reduced circulating GLP-1 levels over ~16 weeks, raising questions for primary prevention scenarios with isolated LDL elevation.
• Framed as hypothesis-generating rather than definitive clinical guidance; underscores the need for open, nuanced discussion about trade-offs.

Westman’s reflections (host)

• Early clinical encounters with patients succeeding on very low-carb or carnivore-leaning diets challenged prior assumptions.
• Longstanding experience suggests such diets can be safe and effective for many, but academic acceptance lagged amid debates over mechanisms.

Takeaways

• Nutrition is underemphasized in medical education relative to its potential impact on chronic disease.
• Competing models (CICO vs. CIM) shape how clinicians and researchers interpret evidence and craft guidance.
• More practical, patient-centered nutrition training and better translational frameworks are needed alongside pharmacologic options.

Papers referenced in the discussion (DOIs)

• Carbohydrate-Insulin Model overview: Ludwig DS et al. “The carbohydrate-insulin model: a physiological perspective on the obesity pandemic.” Am J Clin Nutr (2021). https://doi.org/10.1093/ajcn/nqab270
• Statins & GLP-1 (human controlled trial): She J et al. “Statins aggravate insulin resistance through reduced blood glucagon-like peptide-1 levels in a microbiota-dependent manner.” Cell Metabolism (2024). https://doi.org/10.1016/j.cmet.2023.12.027
• Low-carb/keto for T2D (Virta 2-year trial referenced): Athinarayanan SJ et al. “Long-Term Effects of a Novel Continuous Remote Care Intervention Including Nutritional Ketosis for the Management of Type 2 Diabetes: A 2-Year Non-randomized Clinical Trial.” Front Endocrinol (2019). https://doi.org/10.3389/fendo.2019.00348

“The Future of Mental Health Care: Training Doctors in Ketogenic Therapy” — Summary

Participants

• Host introduces Metabolic Mind interview with Deanna Kelly, PharmD, BCPP (University of Maryland).
• Discussion credits and mentions: Denise Potter, RDN, CDCES; Dr. Chris Palmer; Shebani (Shebani) Sethi, MD; Albert Danan, MD; Charlie Foundation; Keto-Mojo.

Core Topic

• “Live It, Launch It”: a capacity-building project to train clinicians to use ketogenic therapy for mental illness by having them live the diet briefly themselves, then launch it in practice.

Why This Is Needed

• Growing patient demand; the guest previously had a waitlist of ~16–17 families seeking clinicians who could implement ketogenic therapy.
• Clinicians report interest but low confidence/competence implementing ketogenic therapy safely alongside standard care.

Program Overview (“Live It, Launch It”)

• Pilot site: Maryland.
• Cohort size: ~40 clinicians (set at 40; ~40 consented).
• Format:
  • Asynchronous online education (~4 hours), including a keto mastery class for psychiatry (developed with the Charlie Foundation and experts).
  • Four-week dietary intervention in which participating clinicians personally follow a ketogenic diet.
  • Weekly group meetings with dietitians for Q&A, troubleshooting, and peer support.
  • Before/after assessments evaluating knowledge gains and self-rated competence to apply therapy with patients.
  • Data collection tools used weekly to capture what may work for specific patient scenarios.
• Logistics/support:
  • Participants across many U.S. states.
  • Lab slips provided; Keto-Mojo meters mailed to participants with a starter packet.
• Goal: graduate clinicians who both understand and feel competent to add ketogenic therapy as an adjunct to standard care for psychiatric conditions, with attention to medication and metabolic safety.

Clinical Context Discussed

• Serious mental illness (e.g., schizophrenia, bipolar disorder, major depression) often coexists with metabolic dysfunction (weight gain, insulin resistance), partly due to psychotropic medications.
• GLP-1 agonists (e.g., semaglutide) were discussed in the context of a recent randomized controlled trial in patients on antipsychotics; benefits for metabolic parameters noted, but negative symptoms of schizophrenia and broader functional outcomes may remain unmet by GLP-1s alone.
• Ketogenic therapy is positioned as adjunctive, potentially addressing psychiatric symptoms and metabolic health together; does not require FDA approval to implement clinically under appropriate supervision.

Evidence Mentioned (from the conversation)

• Publications by Shebani Sethi and Albert Danan were cited as evidence that ketogenic therapy can improve psychiatric symptoms (including in schizophrenia) and metabolic markers.
• Quantitative examples referenced in the conversation:
  • In metabolic disease literature, reports of ~69% decreases in HOMA-IR and >80% blood sugar normalization with ketogenic approaches were cited in passing.
• An earlier inpatient schizophrenia ketogenic program in Maryland was referenced as having been shut down by the Maryland Department of Health; the guest provides an update on related activities.

Who It’s For

• Clinicians (psychiatrists, prescribers, therapists, dietitians, etc.) wanting structured training to safely integrate ketogenic therapy with standard psychiatric care.
• Patients/families indirectly benefit as trained clinicians expand capacity in this area.

KETO-CTA Study — Findings Presented by Dave Feldman (Interview with Dr. Ken Berry)

Core Questions Raised

• Does high LDL cholesterol or high ApoB, especially on ketogenic/carnivore diets, accelerate coronary plaque formation?
• What happens to plaque burden when people maintain very high LDL for years on low-carb diets?

Study Overview (as described)

• Design: Coronary CT angiography (CCTA) scans analyzed for plaque burden; scans compared across time.
• Cohort size: ~100 participants discussed.
• Diet: Low-carb / ketogenic (includes lean-mass hyper-responders).
• Exposure duration mentioned: Multi-year follow-up; “nearly half a decade” (~4.5 years) cited in discussion for average exposure at very high LDL levels.
• Baseline CAC: Majority reported as CAC=0 at baseline.
• Age: Average age stated as ~55 years.

LDL/ApoB & Who Elevates Most on Keto

• LDL/ApoB rises are most prominent in leaner individuals; a “1–5%” subgroup can see marked increases (lean-mass hyper-responders).
• Overweight individuals starting keto more often see LDL fall or change minimally as metabolic health improves.

Imaging & Analysis Pipelines Used

• Multiple, independent quantification routes were used on the same CCTA datasets:
  • Cleerly (AI plaque quantification).
  • HeartFlow.
  • QAngio.
  • A semi-quantitative visual method.
• Quality control / usability rates differed by tool on identical scans:
  • Example figures mentioned: HeartFlow ~6.3%, QAngio ~39.8% (context: differing pass/fail or exclusion proportions across analyses).
• Key metric emphasized: Percent Atheroma Volume (PAV); also total plaque volume and non-calcified vs calcified plaque were discussed.
• A specific change example cited: Cleerly ~+23.3 mm³ (small absolute change) in a reported plaque volume metric.

Main Findings Reported

• Progression signals were low overall across the cohort despite very high LDL/ApoB levels on long-term low-carb/keto.
• Some participants showed regression (less plaque at follow-up than baseline).
• Results were directionally consistent across analysis methods, despite different exclusion/quality rates.
• Emphasis that non-calcified plaque (considered more concerning) did not show worrisome acceleration cohort-wide.

Clinical Events Mentioned

• Among ~100 people followed/discussed, no heart attacks were reported within the study’s observation window.

Radiation & Practical Notes on CCTA

• Modern CCTA was described as low-dose radiation, with a figure around ~0.6 mSv mentioned.
• Dosing framed as roughly ~1.5× a mammogram (comparative remark).
• Procedure described: IV contrast to opacify coronary lumens; modern detectors/software reduce needed dose.

Limitations Acknowledged (as discussed)

• Not a randomized trial; observational cohort with multi-tool re-analysis for robustness.
• Different software pipelines yield different exclusion rates and require careful quality control.
• Calls for larger, head-to-head prospective studies (e.g., vegan vs carnivore cohorts) were explicitly voiced.

Takeaways Stated in the Video

• In a keto/carnivore cohort with very high LDL/ApoB and ~4.5 years average exposure, plaque progression was minimal on average, with some regressors, and no heart attacks recorded in the observed period.
• Multiple independent analytic methods—despite differing QC pass rates—converged on low progression signals.

Video Summary

Speaker: Dr. Tony Hampton
Topic: Using food as a lever to calm rheumatoid arthritis (RA), how to measure remission, and how to taper medications safely with data.

Opening patient stories

• A patient reported her RA pain vanished after cutting out sugar.
• The same patient also reversed type 2 diabetes with diet, bringing A1C to 5.1; some clinicians were skeptical of diet as the cause.

What RA is and why measurement matters

• RA is an immune-mediated arthritis that inflames and, if uncontrolled, damages joints.
• Treatment aims for remission, not just “less pain.”
• Remission is defined with composite scores (e.g., swollen joint count, tender joint count, patient global assessment, and CRP):
  • Boolean remission: very strict; thresholds summarized as “≤ 1.”
  • Index cutoffs: SDAI < 3.3 or CDAI < 2.8 → in plain terms, almost no swollen or tender joints.
  • DAS28-CRP also referenced and used in trials.

Food patterns discussed

• Low-carb / ketogenic (and even carnivore for some):
  • Aim for roughly 20–50 total carbs/day (unless doing strict carnivore).
  • Typical foods: non-starchy vegetables, fish, eggs, meat, dairy (if tolerated), olives, avocado, extra-virgin olive oil.
• Mediterranean-like (anti-inflammatory) approach:
  • Emphasizes extra-virgin olive oil, oily fish, herbs, nuts, leafy greens.
  • Caveat mentioned: still avoid a lot of grains (i.e., a lower-carb Mediterranean pattern).
• Fasting / time-restricted eating also discussed as helpful tools for some.

Mechanistic note

• Ketone bodies (e.g., beta-hydroxybutyrate)—which rise on low-carb/keto—can directly inhibit the NLRP3 inflammasome, a key immune alarm pathway driving inflammation.

Evidence referenced (from the video)

• Mediterranean-style RCTs showed lower disease activity, improved function, and less stiffness versus control.
• ADIRA trial (Sweden): improved DAS28-CRP and patient-reported outcomes on an anti-inflammatory Mediterranean-like diet.
• Classic Lancet trial: a short fasting phase followed by a plant-based diet lowered RA activity for months.

What to reduce/avoid

• Sugar highlighted as a driver that can worsen inflammation and RA risk; removing sugar is framed as a step that can help earn the right to taper medicines.

“Playbook” / data to track for clinic visits

• Track DAS28-CRP, SDAI, or CDAI; aim for Boolean remission if possible.
• Use labs that move with inflammation: CRP (and ESR).
• Don’t chase RF or anti-CCP for activity (helpful for diagnosis but often remain positive).
• Consider ultrasound to rule out silent synovitis.
• Document function (e.g., a daily diary or HAQ-DI).
• If relevant to your case, bring metabolic markers (e.g., A1C) showing dietary progress.

Tapering guidance mentioned

• After ~6 months of sustained remission, it’s reasonable to consider dose reduction of disease-modifying therapy—not abruptly stopping.
• “Don’t ghost your meds.” Earn your taper with objective data and work with your clinician.

Summary

This comprehensive discussion with Gary Taubes, an investigative science journalist, delves deeply into the complexities, challenges, and misinterpretations surrounding nutrition science, obesity research, and the broader scientific method. Taubes shares his extensive experience spanning over four decades investigating scientific controversies, including cold fusion and nutrition epidemiology, exposing how deeply ingrained biases, poor experimental design, and sociopolitical factors can distort scientific progress.

Taubes begins by recounting the cold fusion episode as a case study in bad science—initially hyped discoveries that diminish over time but never fully disappear due to human belief and financial incentives. This example sets the stage for understanding similar dynamics in nutritional science, where simplistic hypotheses like “gluttony and sloth” dominate despite anomalous observations that suggest more complex physiological mechanisms govern fat storage and obesity.

He reflects on his evolution from physics journalism to nutrition and public health, highlighting the stark contrast between the rigor and falsifiability of physical sciences versus the murky, politically charged, and often poorly controlled world of nutritional epidemiology. Taubes emphasizes the importance of hypothesis testing and notes that many nutrition studies fail to rigorously disprove hypotheses or openly acknowledge negative results due to funding pressures and cultural biases.

Taubes then provides a detailed historical overview of obesity research, tracing shifting paradigms from 19th-century ideas about energy balance toward more nuanced fuel partitioning and neuroendocrine models of fat storage. He explains how political, cultural, and historical events—especially post-World War II American dominance and the rise of psychological explanations—pushed the field toward simplistic energy balance and behavioral models. These models obscure the reality that fat accumulation can occur independently of calorie intake, governed instead by hormonal and neurological regulation.

The conversation explores the carbohydrate-insulin model as a modern iteration of the fuel partitioning hypothesis. Taubes and his interlocutor discuss how insulin’s role in fat storage, carbohydrate quality, and metabolic health underlie obesity and related chronic diseases. They highlight the failures of the calorie-centric “energy balance” hypothesis, which is tautological and unable to explain many clinical observations.

Taubes shares personal anecdotes about his own weight struggles and how low-carbohydrate, high-fat diets profoundly altered his physiology and hunger cues, challenging prevailing dogma. He also discusses the psychological and sociological dimensions of scientific belief systems—how people see and interpret evidence through their cognitive biases and cultural lenses, making paradigm shifts difficult.

The interview concludes with reflections on the need for better scientific practices, transparency, preregistration of hypotheses, and humility to accept negative results. Taubes underscores the importance of engaging with dissenters thoughtfully and testing hypotheses rigorously, illustrating this with historical cases from physics and medical research.

Highlights

• 🔥 Cold fusion exemplifies how scientific hype can persist despite disproven claims due to human belief and financial incentives.
• ⚖️ The energy balance model of obesity is tautological and fails to explain many anomalous observations about fat storage.
• 🧬 Fat accumulation is regulated by complex neuroendocrine and hormonal mechanisms, not simply by how much one eats.
• 🍞 The carbohydrate-insulin model links dietary carbohydrates, insulin secretion, and fat storage, providing a compelling alternative hypothesis.
• 🧠 Scientific paradigms are strongly influenced by cultural, political, and psychological factors that shape what evidence is accepted.
• 📉 Nutrition science often suffers from poor experimental design, funding biases, and reluctance to publish negative results.
• 💡 Rigorous hypothesis testing, preregistration, and open critique are essential for scientific progress but are often lacking in nutrition and epidemiology.

Key Insights

• 🔬 Science’s Messy Reality: Cold Fusion and Nutrition as Case Studies
  Taubes uses cold fusion as a metaphor for how scientific enthusiasm can outpace evidence, leading to premature claims that persist despite refutation. This mirrors issues in nutrition science where initial simplistic models (e.g., gluttony causes obesity) dominate despite contradictory physiological evidence. The human tendency to believe in “miracle” explanations and the financial incentives surrounding such narratives impede objective evaluation.

• ⚖️ Energy Balance Hypothesis: A Circular and Inadequate Explanation
  The calorie-in-calorie-out model is fundamentally tautological: weight gain is assumed to result from overeating because weight gain is observed, not because overeating is objectively measured first. This circular reasoning prevents meaningful falsification. Taubes highlights historical metabolic studies showing that obese individuals often do not eat more than lean individuals, challenging the core premise of energy balance.

• 🧬 Fuel Partitioning and Neuroendocrine Regulation: The Forgotten Paradigm
  Before WWII, European scientists understood obesity as a disorder of fuel partitioning regulated by hormones and the nervous system, where fat cells’ tendency to store or release fat is governed by insulin and other signals. This nuanced understanding was lost in the post-war American focus on behaviorism and psychological explanations (gluttony and sloth), leading to the dominance of simplistic calorie-centric models.

• 🍞 Carbohydrate-Insulin Model and Its Implications
  The carbohydrate-insulin model posits that high carbohydrate intake elevates insulin, which promotes fat storage and reduces fat mobilization. This model better explains the rise in obesity and diabetes seen during global nutrition transitions involving increased processed carbohydrate consumption. It also aligns with observed metabolic syndrome features, insulin resistance, and the clinical success of low-carb diets.

• 🧠 Scientific Belief Systems and Paradigm Entrenchment
  Taubes emphasizes that what scientists observe is filtered through preexisting beliefs, cultural norms, and funding pressures. Paradigm shifts are resisted because new models challenge deeply held assumptions and threaten reputations and funding. This is compounded by the “you have to trust the science” mantra that discourages critical scrutiny and open debate.

• 📉 Limitations of Nutritional Epidemiology and Publication Bias
  Nutritional epidemiology relies heavily on observational cohorts with self-reported data, leading to confounding and unreliable associations. Further, negative findings are often hidden or spun positively to justify funding, impeding true scientific progress. Taubes advocates for preregistration of hypotheses and transparent reporting of both positive and negative results to improve rigor.

• 💡 Personal Experience and Empirical Evidence in Shaping Beliefs
  Taubes shares his own experience with weight loss on a low-carb diet, illustrating how personal observation can challenge prevailing dogma. He notes that those who have not experienced obesity often resist alternative models because they lack motivation or evidence from lived experience. This highlights the importance of integrating both scientific data and individual clinical outcomes in forming health guidelines.

Extended Analysis

Gary Taubes’ narrative is a powerful critique of the scientific process as practiced in nutrition and public health. His investigation illuminates how sociology, psychology, and politics can distort what should be an objective search for truth. The cold fusion story is a cautionary tale about premature scientific claims driven by excitement and financial gain rather than reproducible evidence. Similarly, the simplistic “energy balance” explanation for obesity has been entrenched for decades despite mounting contradictory evidence.

Taubes’ detailed historical account reveals that early scientists understood obesity as a complex neuroendocrine disorder influenced by hormonal control, particularly insulin’s dominant role in fat storage. This understanding was sidelined due to geopolitical and cultural shifts, including the rise of behavioral psychology in America post-WWII, which framed obesity as a moral failing (gluttony and sloth). This reframing shaped decades of research funding and public health messaging, limiting exploration of alternative hypotheses.

The carbohydrate-insulin model emerges as a robust alternative that explains numerous clinical and population-level phenomena, including the rise of obesity and diabetes during nutritional transitions around the globe. It also explains why low-carb and ketogenic diets can lead to effortless weight loss and reduced “food noise” or intrusive hunger thoughts—an experience Taubes personally attests to.

Importantly, Taubes critiques the current research culture that prioritizes positive findings, often due to funding incentives, and discourages publication of negative results. This creates a confirmation bias that perpetuates flawed theories. His call for preregistration of hypotheses and transparent reporting could greatly improve scientific rigor.

His reflections on scientific belief systems highlight how difficult it is to change entrenched paradigms because what scientists “see” is shaped by what they expect or want to see. The example of how political ideology shapes media consumption—and thus worldview—provides a useful analogy for scientific communities. Scientists and laypeople alike may be trapped in echo chambers that confirm their biases.

Finally, Taubes’ personal journey underscores the role of experience in shifting beliefs. Those who have struggled with obesity and found success in low-carb diets are often more open to alternative explanations than those who have not. This experiential evidence complements scientific data and is crucial for changing public health narratives.

In sum, this discussion is a masterclass in the sociology of science, the history of obesity research, and the challenges of nutrition science. It advocates for humility, transparency, and openness to new ideas to overcome decades of entrenched, simplistic thinking that have impeded progress in understanding and treating obesity and chronic disease.

This detailed exploration provides a nuanced understanding of why obesity science remains controversial, why simple explanations fail, and what might be done to advance the field with more rigor, honesty, and openness. Taubes’ insights are invaluable for scientists, clinicians, policymakers, and anyone interested in the complex science of nutrition and health.

Summary

Michelle Karn, a registered and licensed dietitian and ultrarunner, shares her deeply personal and professional journey through severe anorexia nervosa, traditional dietetic training, and ultimately, her transformative experience with ketogenic and carnivore diets. Diagnosed at age 12 with anorexia nervosa, Michelle endured extreme malnutrition, psychiatric symptoms, and standard medical treatments that relied heavily on the conventional American diet and medications. Despite achieving weight restoration, her mental health struggles continued with anxiety, depression, and body dysmorphia.

As a dietitian, Michelle initially adhered to and promoted conventional nutrition guidelines focusing heavily on carbohydrates as the foundation of a healthy diet. However, during her career, she observed the limitations and failures of this approach, especially in managing chronic illnesses like type 2 diabetes and mental health disorders. Personal health crises in her late twenties, including severe fatigue, anxiety, and performance decline as an athlete, led her to question the traditional carbohydrate-heavy dietary recommendations.

Driven by intuition and desperation, Michelle adopted a ketogenic diet followed by a carnivore diet, despite initial skepticism from her partner and concerns tied to her history of eating disorders. The dietary shift resulted in profound improvements in her mental health, anxiety levels, and physical well-being, enabling her to return to ultrarunning and reclaim her life. Michelle critiques the current healthcare system’s handling of mental health and eating disorders, highlighting the influence of processed food industry sponsorships on dietary guidelines and the deep-seated dogma around carbohydrate consumption in dietetics.

Michelle emphasizes the metabolic underpinnings of psychiatric diseases, arguing that effective treatment must address metabolism alongside traditional psychiatric interventions. She advocates for ketogenic diets as a powerful, evidence-backed approach to improving mental health and metabolic function, encouraging patients and clinicians to remain open-minded and willing to integrate metabolic therapies. Her story culminates in a hopeful message about the human body’s incredible capacity for healing when provided with the right nutritional inputs.

Highlights

• 🏃‍♀️ Michelle’s journey from severe anorexia nervosa at age 12 to becoming an ultrarunner and registered dietitian.
• 🍞 Questioning the carbohydrate-centric nutritional paradigm ingrained in traditional dietetics.
• 🍖 Personal transformation through ketogenic and carnivore diets, leading to significant mental health improvements.
• 💊 Critique of the healthcare system’s failure to adequately treat metabolic aspects of mental illness.
• 🔬 Evidence supporting ketogenic diets for reversing type 2 diabetes, traumatic brain injury, and mental health conditions.
• 🧠 The importance of addressing metabolism to enable neuroplasticity and effective psychiatric treatment.
• 💡 Encouragement to approach nutrition and mental health with humility, openness, and individualized experimentation.

Key Insights

• 🧩 Eating disorders and mental health are deeply intertwined with metabolic dysfunction. Michelle’s early experience with anorexia and subsequent mental health challenges highlight that traditional approaches focusing solely on weight restoration and psychiatric medication often fail to address underlying metabolic imbalances. This suggests a need for integrated treatment paradigms that incorporate metabolic therapies.

• 🥖 The entrenched carbohydrate dogma in dietetics can hinder patient outcomes. Michelle’s training and early career were dominated by the belief that carbohydrates are essential for energy and health, leading to recommendations that sometimes worsened patients’ conditions. This reflects a systemic issue within dietetics where dogmatic adherence to outdated guidelines prevents personalized care and innovation.

• 🥩 Ketogenic and carnivore diets can dramatically improve mental health and physical performance for some individuals. Michelle’s shift to a low-carb, high-fat diet after years of struggling with anxiety, depression, and athletic decline was a turning point. Her experience aligns with growing clinical evidence that ketosis and reduced carbohydrate intake can reduce inflammation, stabilize blood sugar, and provide neuroprotective benefits.

• 🏥 Current healthcare systems often fail to integrate metabolic treatments for psychiatric disorders. Michelle critiques how mental health is often treated only with medications and therapy without addressing metabolic dysfunction. She argues this oversight leads to poor outcomes and relapse, as the brain cannot effectively engage in neuroplasticity without proper metabolic support.

• 💡 There is a significant conflict of interest influencing nutritional guidelines. Michelle points out that major dietetic organizations receive funding from processed food companies and sugar industries, which can bias dietary recommendations and suppress emerging evidence supporting low-carbohydrate diets. This raises ethical concerns about guideline development and patient care.

• 🔄 Personal intuition and open-mindedness are crucial in navigating nutrition and mental health. Michelle’s willingness to challenge conventional wisdom, try alternative diets, and learn from emerging research was essential to her recovery. This highlights the importance of humility in healthcare providers and patients, fostering experimentation and individualized treatment.

• ⚙️ Metabolism is fundamental to brain function and mental health recovery. Michelle emphasizes that to benefit from therapy and psychiatric interventions, the brain must be metabolically healthy. Ketogenic diets provide an alternative fuel source (ketones) that may improve brain metabolism, reduce anxiety and depression, and facilitate neuroplasticity, offering a promising adjunct or alternative to pharmacological treatments.

Expanded Summary and Analysis

Michelle Karn’s narrative begins with a harrowing experience of anorexia nervosa diagnosed at just 12 years old. Severely underweight and malnourished, she was hospitalized and subjected to tube feeding formulas composed of maltodextrin, soy protein, canola oil, and corn syrup—the very components of a standard American diet high in sugars and refined carbohydrates. This aggressive refeeding precipitated intense gastrointestinal distress, psychiatric symptoms including OCD, anxiety, and depression, and a reliance on multiple medications to manage side effects, reflecting the challenges and shortcomings of conventional inpatient care for eating disorders.

Despite achieving weight restoration, Michelle’s mental health remained precarious. She describes a persistent internal battle with anxiety, depression, and body dysmorphia, feeling as though she was on the sidelines of her own life. Her early exposure to nutrition inspired her to become a dietitian, driven by the hope that food could be a key to healing both body and brain. However, during her dietetic training, she encountered a rigid orthodoxy emphasizing carbohydrates as essential energy sources. This framework conflicted with her intuition, especially when witnessing the adverse health trajectories of patients with metabolic diseases like type 2 diabetes, where carbohydrate restriction could logically be beneficial.

Michelle’s critical turning point came in her late twenties when she faced a severe decline in athletic performance, accompanied by worsening anxiety, fatigue, and other systemic symptoms. Traditional medical evaluations and nutritional advice failed to yield improvement, and increasing carbohydrate intake only exacerbated her symptoms. Desperate and disillusioned, she experimented with a ketogenic and eventually carnivore diet, drastically reducing carbohydrates and increasing fats and proteins. Although initially challenging due to side effects and a lack of proper guidance on electrolyte balance, this dietary shift brought profound improvements in her mental clarity, anxiety reduction, and physical health.

Her partner’s observation that Michelle’s anxiety was the lowest it had been in over a decade underscores the dramatic impact of this change. Michelle’s experience is supported by a growing body of scientific literature documenting the anti-inflammatory, neuroprotective, and metabolic benefits of ketogenic diets in conditions ranging from diabetes to bipolar disorder and traumatic brain injury. She also highlights the potential for ketones to serve as a more efficient brain fuel, particularly in individuals with impaired glucose metabolism, which is common in psychiatric disorders.

Michelle critiques the healthcare system for its failure to integrate metabolic interventions into mental health treatment, often relying solely on medications and therapy that do not address the underlying biological dysfunction. She stresses that the brain must be metabolically healthy to engage effectively in neuroplasticity and benefit from therapeutic interventions. Without addressing insulin resistance, dysregulated blood sugar, and metabolic inflammation, patients are likely to relapse or experience suboptimal recovery.

A significant insight Michelle offers is the influence of industry funding on nutritional guidelines, which perpetuates carbohydrate-centric recommendations despite mounting evidence to the contrary. She calls for humility and openness within the dietetic profession and among health practitioners to consider alternative dietary approaches tailored to individual metabolic needs.

As an ultrarunner now, Michelle has integrated a strategic use of carbohydrates to fuel her athletic performance while maintaining a primarily ketogenic dietary framework. She acknowledges the powerful hold of sugar addiction both personally and societally, emphasizing the importance of discipline and saying no to foods that trigger mental health symptoms.

Ultimately, Michelle’s story is one of resilience, transformation, and advocacy for a paradigm shift in how mental health and nutrition are approached. She encourages others to explore metabolic therapies with an open mind and asserts the human body’s extraordinary ability to heal when given the right nutritional inputs.

Conclusion

Michelle Karn’s journey from a severely malnourished adolescent with anorexia to a thriving ultrarunner and dietitian who has embraced ketogenic nutrition provides a compelling case for reevaluating the role of metabolism in mental health treatment. Her experience challenges entrenched dietary dogmas, exposes systemic conflicts of interest, and advocates for more integrative, individualized approaches to care that address both brain and body. Her insights emphasize the critical need for metabolic health in achieving lasting recovery from psychiatric and eating disorders, offering hope and a roadmap for others facing similar struggles.

Detailed summary — "The Real Cause of Clogged Arteries and how fasting can help"

• Core claim: Atherosclerosis (clogged arteries) is primarily driven by chronic inflammation, not merely passive cholesterol deposition, and plaque is a metabolically active, inflammatory process that can rupture and cause heart attacks.

• Primary triggers that cause vascular inflammation:

  • Metabolic dysfunction (insulin resistance, prediabetes) which promotes harmful lipid profiles including small, dense LDL.
  • Dietary factors (processed foods, high omega‑6 intake, advanced glycation end products) that drive inflammation and oxidative stress.
  • Toxins and impaired detoxification, which increase systemic inflammatory burden.
  • Gut problems (e.g., leaky gut / dysbiosis) that seed inflammation systemically.
  • Lifestyle stressors (poor sleep, chronic stress) that amplify inflammatory cascades.

• Nature and consequence of plaque: Plaque is described as an inflammatory, metabolically active lesion; when plaque becomes unstable and ruptures the ensuing clot formation leads to heart attacks — so reducing inflammation and stabilizing plaque is central to preventing acute events.

• How fasting counteracts the causes (mechanisms):

  • Lowers insulin levels, improving insulin sensitivity and reducing production of small, dense LDL, thereby decreasing a major driver of inflammation and atherogenesis.
  • Stimulates autophagy and mitophagy, promoting cellular and mitochondrial cleanup which reduces oxidative stress and inflammatory signaling.
  • Supports detoxification by enhancing liver processing and elimination of toxins that contribute to vascular inflammation.
  • Resets gut health, helping reduce inflammation originating from a leaky or dysbiotic gut.
  • Promotes ketogenesis and fat mobilization during extended fasting, which is framed as anti‑inflammatory and metabolically beneficial.
  • Overall effect: fasting lowers measurable inflammatory markers, improves metabolic health, and creates conditions that can halt or reverse drivers of plaque progression.

• Practical fasting approaches recommended:

  • Time‑restricted feeding as a daily lifestyle (example: 18:6, eat within 6 hours, fast 18 hours).
  • Periodic prolonged fasts (example: a 3‑day water fast done periodically — cited as helpful for metabolic reset, stem cell mobilization and deeper detoxification; suggested timing varies by individual needs).
  • Use of fasting to achieve ketosis for added anti‑inflammatory and fat‑mobilizing effects.

• Overall strategy and expectations: Adopt an anti‑inflammatory lifestyle (fasting, improved diet, sleep, stress management, and addressing toxins/gut health) to manage plaque — the goal is usually to prevent progression and rupture rather than promise complete elimination of existing plaque; with these measures individuals can often live with plaque without experiencing fatal events.

• Takeaway (concise): Targeting systemic inflammation and metabolic dysfunction — with fasting as a central tool among dietary and lifestyle interventions — is presented as the most effective approach to preventing plaque progression and reducing risk of heart attacks.

• Brain aging follows a nonlinear trajectory with distinct phases, including a critical window in midlife (ages 40-60) where metabolic interventions may be most effective.
• The onset of brain aging is marked by increased insulin resistance, which disrupts neuronal glucose metabolism and contributes to cognitive decline.
• Ketones, which bypass insulin resistance, can stabilize brain networks and potentially reverse early aging effects, particularly in the midlife critical window.
• The study identifies specific genes (GLUT4, MCT2, APOE) associated with brain aging patterns, highlighting the role of neuronal insulin resistance and ketone transport.
• Brain network destabilization accelerates after age 40, with the most rapid changes occurring between ages 60-70, indicating a critical period for intervention.
• The effects of ketones on brain network stability are most pronounced in individuals aged 40-59, suggesting a limited window for effective metabolic intervention.
• The study suggests that early metabolic stress in neurons, due to insulin resistance, can lead to irreversible damage if not addressed promptly.
• Gene expression analysis supports the role of insulin resistance in brain aging, with GLUT4 and MCT2 emerging as key factors.
• The study's findings align with broader aging biomarkers, linking molecular mechanisms to neurobiological outcomes.
• The research emphasizes the importance of early intervention in brain aging to prevent or delay cognitive decline and neurodegenerative diseases.

0:00 – Intro & welcome
0:34 – Disclosures & background on the Keto-CTA study
1:01 – Study design & lean mass hyper-responder criteria
1:45 – CT scans, imaging methods & data acquisition
2:10 – Semi-quantitative vs quantitative analysis explained
3:06 – Timeline of analyses & initial expectations
3:29 – First Cleerly results & early concerns
4:11 – Shared findings: baseline plaque & lack of LDL/ApoB association
5:21 – Paper publication & critics’ reactions
6:07 – Prespecified methodology: why QAngio matters
6:59 – Social media debates & misinterpretations
7:33 – The “limited contrast” argument emerges
8:33 – Breaking down claims about “all high LDL”
9:42 – Visualizing the actual LDL spread
11:01 – LDL variability: 49 mg/dL to 591 mg/dL
12:30 – Problems with the “limited exposure” critique
13:08 – Revisiting the lipid hypothesis: dose-dependent effects
14:07 – Are these the “healthiest” participants? Context & caveats
15:14 – Participant risk factors: CAC scores, A1C, glucose, hs-CRP
16:33 – Why Dave reduced public debates for a time
17:01 – Issues discovered in Cleerly’s dataset
18:13 – Introducing HeartFlow: a blinded independent analysis
19:05 – Why a fourth analysis was critical
20:02 – Record-breaking multi-analysis study design
20:34 – Preliminary results warning
21:04 – Non-calcified plaque volume % change: conflicting findings
22:00 – Absolute vs relative change: why it matters
22:28 – Total plaque volume & percent atheroma volume
23:17 – How HeartFlow & QAngio compare to reference studies
24:40 – Top-level observations & agreements
25:07 – Plaque regression: the star of the show
26:14 – Direct verification of regression by Dr. Budoff
27:00 – Red flags in Cleerly’s data: no negative values
28:33 – The “noise floor” problem explained
30:28 – Why multiple analyses were necessary
31:15 – Every imaging study shows regression — except Cleerly
32:02 – Statistical implausibility of Cleerly’s results
32:37 – Final conclusions on regression evidence
33:29 – Does regression imply safety for lean mass hyper-responders?
34:11 – No association of LDL/ApoB with plaque presentation or progression
35:02 – What’s next: study extension & Triad study
35:38 – Reflecting on six years since Keto-CTA’s conception
36:32 – Acknowledgments & closing remarks

Summary

The speaker, an engineer and founder of the Citizen Science Foundation, presented a detailed overview of the ketoCTA study, which investigates the effects of a ketogenic diet on cholesterol and coronary plaque development. Initiated in 2015, the study followed 100 individuals who exhibited increased cholesterol levels after adopting a ketogenic diet, a phenomenon the speaker termed "lean mass hyper-responder" (LMHR). These participants were selected based on specific cholesterol criteria (LDL ≥190, HDL ≥60, triglycerides ≤80) and underwent coronary CT angiography (CTA) scans at baseline and after one year (totaling 200 scans).

The study employed multiple methods of analyzing the scans: semi-quantitative expert reviews, and various quantitative analyses using AI and algorithms, including platforms named Clearly, Qangio (the prespecified methodology), and HeartFlow. Early results revealed notable discrepancies between the different analyses, particularly with the Clearly platform, which showed no instances of plaque regression—a finding at odds with both the other analyses and established scientific knowledge that some plaque regression is expected even in healthy populations.

The speaker emphasized the broad variation in LDL cholesterol levels among study participants, ranging from very low to extremely high (including cases of homozygous familial hypercholesterolemia), countering criticisms that there was insufficient LDL variability (“limited contrast”) to assess LDL’s impact on plaque progression. Despite the large spread and high LDL levels, none of the analyses demonstrated an association between LDL cholesterol or ApoB levels and the progression or presence of coronary plaque in this cohort, challenging aspects of the lipid hypothesis within this specific group.

The speaker also addressed social media critiques and the challenges faced during the study, including delays and disagreements over data analysis and interpretation. Due to concerns over the Clearly analysis, a blinded quality control review was requested but not completed, leading the team to commission an additional independent analysis via HeartFlow. The HeartFlow and Qangio analyses showed close agreement and revealed instances of plaque regression in some participants, which was independently verified by expert readers.

The talk concluded with a balanced message: while some participants showed plaque regression despite high LDL levels, this does not imply that being a lean mass hyper-responder guarantees low cardiovascular risk. The cohort was generally healthier than average but included individuals with various risk factors and pre-existing conditions. The study’s findings are preliminary, with ongoing efforts to analyze further data and extend the study. The speaker expressed gratitude to the research team, contributors, and participants and highlighted the significance of this milestone in the journey that began nearly six years ago.

Highlights

• 🩺 Study of 100 keto diet adopters with elevated cholesterol tracked over one year using coronary CT angiography.
• 🧬 Multiple independent methods analyzed the same 200 scans, revealing discrepancies between analysis platforms.
• 🔍 No association found between LDL cholesterol/ApoB levels and plaque progression in this cohort.
• 📊 Study population demonstrated an exceptionally wide range of LDL cholesterol, including extreme familial hypercholesterolemia.
• 🔄 Evidence of plaque regression verified by multiple analyses and expert readers, contradicting one major analysis (Clearly).
• 🛑 Challenges with data quality and analysis led to commissioning additional independent review (HeartFlow).
• ⚠️ Regression does not guarantee low cardiovascular risk; cohort includes individuals with varying health statuses.

Key Insights

• 🧪 Multi-modal imaging analysis reveals complexity and variability in plaque progression assessment:
  The ketoCTA study uniquely employed four independent analyses on the same set of 200 coronary CT scans, including semi-quantitative expert reads and three AI-driven quantitative platforms (Clearly, Qangio, HeartFlow). This multi-layered approach highlighted how different methodologies can produce divergent results, particularly in measuring plaque regression or progression. It underscores the importance of using multiple analytical tools and blinded quality controls to validate imaging studies, especially in novel cohorts.

• 📉 Plaque regression occurs even among individuals with high LDL cholesterol:
  Contrary to the dominant lipid hypothesis narrative, multiple analyses in this study documented regression of coronary plaque in a subset of participants, including those with LDL levels comparable to familial hypercholesterolemia. This finding challenges the assumption that high LDL universally predicts plaque progression and cardiovascular risk, suggesting that other factors may modulate atherosclerosis in lean mass hyper-responders or ketogenic dieters.

• 📈 No correlation between LDL cholesterol/ApoB and plaque progression in this cohort:
  Despite the large variability of LDL levels (ranging from under 50 to nearly 600 mg/dL), the study found virtually no association between LDL or ApoB and either the baseline plaque burden or the change in plaque volume over one year. This lack of correlation, consistent across multiple analyses, suggests that LDL cholesterol may not be the sole or primary driver of atherosclerosis progression in this specific population, prompting a re-examination of the lipid hypothesis in diverse metabolic contexts.

• ⚖️ Wide LDL cholesterol variability refutes the “limited contrast” critique:
  Critics argued that the study’s participants all had uniformly high LDL, limiting the ability to detect dose-response relationships. However, the data showed a broad LDL distribution with a standard deviation of 84 mg/dL and a range from 49 to 591 mg/dL—arguably the widest spread in any prospective imaging study to date. This diversity provides a strong test of the LDL-plaque relationship, reinforcing the study’s conclusions.

• 🔍 Importance of absolute versus relative changes in plaque measurements:
  The speaker pointed out a critical methodological issue: relying solely on relative percent changes in plaque volume can be misleading. Absolute changes provide a clearer picture, better aligned across different analytical platforms. This distinction is crucial for interpreting imaging results and for understanding the biological significance of plaque dynamics in clinical research.

• 🛑 Data quality and transparency are vital, especially amid scientific controversy:
  The Clearly platform’s refusal to conduct a blinded quality control review after concerns were raised highlights challenges in data transparency and scientific rigor. The study’s response—to commission an additional independent analysis with HeartFlow—demonstrates a commitment to robust science and the value of independent validation, particularly in contentious areas like keto and lipid research.

• ⚠️ Plaque regression does not equate to cardiovascular safety:
  The study emphasizes that even with documented plaque regression, lean mass hyper-responders are not guaranteed protection from atherosclerotic cardiovascular disease. The cohort was healthier than average but included individuals with diabetes, obesity, hypertension, and high coronary artery calcium scores. This nuanced view cautions against oversimplified conclusions and underscores the need for ongoing research into risk stratification and mechanisms beyond cholesterol levels.

Conclusion

This presentation offers a comprehensive and transparent look at the ketoCTA study’s progress, challenges, and preliminary findings related to cholesterol, ketogenic diets, and coronary artery plaque. It highlights the complexity of interpreting advanced imaging data, the need for rigorous multi-method validation, and the evolving understanding of lipid biology in cardiovascular risk. The findings challenge conventional lipid dogma in this unique population, while also acknowledging limitations and the necessity for further research.

Methods: Three adults, ages 32–36, with major depression, generalized anxiety, other anxiety disorders, and comorbid psychiatric conditions were treated for 12–16 weeks with personalized whole food animal-based ketogenic metabolic therapy (1.5:1 ratio) in a specialized metabolic psychiatry practice. Interventions included twice-weekly visits with an experienced ketogenic registered dietitian; daily photo journaling and capillary blood BHB/glucose/GKI monitoring; virtual groups; family/friends support; nature walks and talks several times per week, and community building. Successful adoption of the ketogenic diet was defined as the achievement and maintenance of capillary BHB ≥ 0.8 mmol/L and GKI < 6. Remission was assessed by GAD-7 and PHQ-9, and quality of life was assessed subjectively and with validated scales for flourishing and self-compassion. Metabolic health was assessed by laboratories/biometric measures.

Results: Two patients achieved remission of major depression (PHQ-9 ≤ 4) and generalized anxiety (GAD-7 ≤ 4) within 7 weeks of therapeutic nutritional ketosis; one required 12 weeks. Anxiety responded and remitted more quickly than major depression. Flourishing and self-compassion increased steadily. Patients lost 10.9 to 14.8% of their initial body weight within 12 weeks and improved metabolically; one achieved optimal metabolic health.

Conclusion: Complete remission of major depression and generalized anxiety disorder occurred within 7–12 weeks of therapeutic nutritional ketosis during treatment with a personalized animal-based ketogenic diet (ratio 1.5:1) in adults with complex comorbid depression and anxiety engaged in a specialized metabolic psychiatry program.

Methods: The patient engaged in KMT with a 1.5:1 macronutrient ratio under the supervision of a treatment team consisting of a medical professional, psychotherapist, and ketogenic-informed nutrition professional through an online program that provided both individual and group support. Interventions included dietary modifications, micronutrient supplementation, and participation in a group coaching program. Outcomes were assessed using validated tools for symptom severity, including PHQ-9 for depression and GAD-7 for anxiety, at baseline, 2 months, and 4 months post-intervention. Qualitative data on patient experiences and functional improvements were also collected.

Results: The patient achieved remission of MDD within 8 weeks of initiating KMT, with PHQ-9 scores decreasing from 25 (severe depression) at baseline to 0 at 2- and 4-month assessments. GAD-7 scores decreased from 3 (minimal anxiety) to 0 over the same period. Qualitative findings revealed significant improvements in emotional regulation, energy levels, and cognitive function.

Conclusion: This case study demonstrates the potential of KMT as a non-pharmacological intervention for achieving full remission in treatment-resistant MDD. These findings suggest further research to evaluate feasibility, efficacy, and broader applicability in diverse clinical settings.

Study design: In this retrospective analysis of clinical care, 31 adults with severe, persistent mental illness (major depressive disorder, bipolar disorder, and schizoaffective disorder) whose symptoms were poorly controlled despite intensive psychiatric management were admitted to a psychiatric hospital and placed on a ketogenic diet restricted to a maximum of 20 grams of carbohydrate per day as an adjunct to conventional inpatient care. The duration of the intervention ranged from 6 to 248 days.

Study results: Three patients were unable to adhere to the diet for >14 days and were excluded from the final analysis. Among included participants, means and standard deviations (SDs) improved for the Hamilton Depression Rating Scale scores from 25.4 (6.3) to 7.7 (4.2), P < 0.001 and the Montgomery-Åsberg Depression Rating Scale from 29.6 (7.8) to 10.1 (6.5), P < 0.001. Among the 10 patients with schizoaffective illness, mean (SD) of the Positive and Negative Syndrome Scale (PANSS) scores improved from 91.4 (15.3) to 49.3 (6.9), P < 0.001. Significant improvements were also observed in metabolic health measures including weight, blood pressure, blood glucose, and triglycerides.

Conclusions: The administration of a ketogenic diet in this semi-controlled setting to patients with treatment-refractory mental illness was feasible, well-tolerated, and associated with significant and substantial improvements in depression and psychosis symptoms and multiple markers of metabolic health.