What fibre is and whether we need it

• Carbohydrates include glucose, fructose and galactose as monosaccharides; sucrose, lactose and maltose as disaccharides; and starch and glycogen as digestible polysaccharides.
• Fibre is the indigestible polysaccharide fraction, with water-soluble forms in foods such as oats and beans and insoluble forms such as bran. Its passage through the bowel does not itself establish a health benefit.
• The 2005 macronutrient panel gives zero as the lower limit of dietary carbohydrate when fat and protein are adequate; dietary carbohydrate is not strictly necessary for survival. [1]
• The 2015–2020 American dietary guidelines classify fibre as nonessential. Nonessential status does not establish whether fibre has beneficial effects. [2]

How the fibre belief arose

• Sylvester Graham linked meat to lust and masturbation and promoted plant foods; Ellen G. White of the Seventh-day Adventists connected animal foods with moral corruption.
• John Harvey Kellogg, who typeset White's writings as a child, adopted objections to meat and masturbation and a belief that fibre cleansed the body; Graham crackers and cornflakes emerged from this milieu.
• Surgeon Denis Burkitt associated higher-fibre populations with lower frequencies of diabetes, obesity, heart disease and cancer and popularised the connection between small stools and large hospitals.
• Belinda Fettke traced opposition to Gary Fettke's low-carbohydrate advice through Australian dietitians and cereal manufacturer Sanitarium to Seventh-day Adventist influence.
• An Adventist-authored 2018 paper documents the church's global influence on plant-based eating; this history connects the movement with later fibre and plant-food promotion. [3]

Guidelines, targets and the cost of reaching them

• The 1977 McGovern dietary goals encouraged vegetables and whole grains alongside less fat, without a numerical fibre target. [4]
• Fibre received repeated attention in the 2000 US guidelines; by 2005 the target was 14 g per 1,000 calories, including for young children and reaching roughly 34 g for young men. [5][6]
• British guidance also uses 30 g for adults; the fibre targets and the earlier five-a-day message lacked supporting evidence predating their introduction. [7]
• The January 2019 Reynolds review postdates the earlier fibre target and cannot supply evidence that existed before the target was established. [8]
• The Guardian linked the review to criticism of low-carbohydrate diets; the illustrative 30 g fibre menu contained about 175 g carbohydrate, 44 g sugar and nearly half a woman's daily calories. [9]
• This distinction concerns sugar molecules and the food source and disputes excluding fruit and milk sugars when comparing sugar intake.
• High-fibre bran cereals have high fibre density but may also contain added sugar; pursuing a fixed fibre target can direct food choices toward processed cereal products.

What the intervention and observational evidence shows

• The 1997 Bristol stool scale identifies types 3 and 4 as desirable stool forms. [10]
• The DART randomised trial followed 2,033 men after heart attacks for two years and tested fish, fat and advice to eat about 18 g fibre daily. Mortality outcomes were numerically higher with fibre advice but not statistically significant. [11]
• Three Cochrane reviews cover fibre and cardiovascular disease, whole-grain cereals and cardiovascular disease, and whole grains and type 2 diabetes; each identifies a need for stronger long-term intervention evidence. [12][13][14]
• Observational evidence dominates the field. A 2018 umbrella review assessed 21 outcomes and classified evidence as convincing for three: all-cause mortality, cardiovascular mortality and pancreatic cancer. [15]
• Reynolds found roughly 15% lower relative all-cause mortality with about 30 g versus 5 g daily fibre; the result is an observational association and cannot by itself establish causality. [8]
• Bradford Hill's causation criteria involve an approximate twofold relative-risk threshold for examining causality. [16]
• Yang's 2015 analysis gives an approximately 16% relative difference; the numerical contrast of 63 and 73 illustrates the smaller absolute gap. [17]
• One cohort in the Reynolds evidence had lower-fibre participants with about twice the alcohol use and roughly 1.5 times the obesity, inactivity and low education; adjustment for measured variables leaves potential lifestyle confounding.
• The central distinction is between fibre as a cause of better health and fibre intake as an indicator of healthier overall behaviour.

The carbohydrate–fibre matrix

• The four-box matrix separates low-carbohydrate/low-fibre foods (C: meat, fish, eggs, dairy); low-carbohydrate/high-fibre foods (A: non-starchy vegetables, lower-sugar fruit, nuts and seeds); high-carbohydrate/high-fibre foods (B: legumes, starchier vegetables, sweeter fruit and whole grains); and high-carbohydrate/low-fibre foods (D: refined grains and junk).
• High- versus low-fibre epidemiological comparisons mostly contrast Box B with Box D, with few comparisons involving meat-based Box C diets.
• Many older cohorts began around 1968, when low-fibre consumption is linked to poorer-quality diets, distinct from modern low-carbohydrate patterns.
• Box B includes higher income, education and activity and less smoking or drinking; Box D includes fewer socioeconomic advantages. An increase to 30 g fibre would not itself remove those differences.

Proposed benefits and their mechanisms

• Fibre can slow carbohydrate absorption, while reduced intake of digestible carbohydrate also lowers the incoming glucose load; whole foods and refined carbohydrate differ in their effects.
• Fibre-rich foods and some plant oils contain plant sterols that compete with intestinal cholesterol absorption and lower circulating cholesterol. Plant-sterol-associated cholesterol lowering is linked to adverse heart-disease and cancer outcomes. [18]
• Weight-loss and energy-intake mechanisms draw on reviews including Aune's 2016 analysis; an apples-versus-apple-juice comparison does not isolate the effect of fibre from other food differences. [19]
• A synthesis of seven clinical studies examined fibre, weight loss and C-reactive protein: food-based dietary changes coincided with lower C-reactive protein, while the psyllium-husk supplementation study did not show a reduction. [20]
• Faster bowel transit can limit contact with potentially carcinogenic substances; avoiding their consumption is the corresponding dietary approach.
• Fibre-related changes in transit can affect absorption of magnesium, copper, calcium, iron, potassium and sodium; longer transit allows more time for nutrient extraction.
• An empty bowel alone is insufficient as a disease-prevention mechanism; fasting would also empty the bowel.

The microbiome does not depend on fibre alone

• Gut flora is influenced by parental health, vaginal birth and breastfeeding before later dietary choices.
• Antibiotics and antacids can damage the microbiome; real foods, herbs and spices support it, and junk food can harm it.
• Raw milk, unpasteurised cheese, live yoghurt and kefir contain microorganisms without dietary fibre; beans on toast is unlikely to determine microbiome quality by itself.
• A 1991 experiment measured intestinal gas in ten volunteers consuming 200 g baked beans daily, including methane production in some participants. [21]

When fibre causes problems

• In a constipation study, participants had bloating, bleeding, pain and straining on habitual diets; continued high-fibre intake showed little improvement, lower fibre improved symptoms, and zero fibre had the greatest improvement. [22]
• Fibre does not have uniform effects in digestive disorders; a one- to two-week fibre reduction can serve as a symptom trial for people with IBS or related difficulties.
• Adding a swelling fibre gel during constipation is compared to putting more material into a blocked sink; a universal 30 g target is rejected.

What is really driving the advice, and the low-carb solution

• With protein at about 15% of energy and fat capped at 30%, carbohydrate supplies about 55%, matching the high-carbohydrate direction of the 1977 goals. [4]
• Fibre promotion supports high-carbohydrate Box B over refined-junk Box D, while low-carbohydrate Box C receives criticism; cereal manufacturers, vegan advocates and Adventist groups reinforce this approach.
• Box A combines low carbohydrate with high fibre through flax and alfalfa seeds, blackberries with full-fat yoghurt, asparagus and salmon, Jerusalem artichokes, cabbage and cauliflower; such meals can approach 30 g fibre.
• The lower-carbohydrate 30 g-fibre example is calculated at roughly one-third the calories, one-quarter the carbohydrate and one-fifth the sugar of the Guardian example.
• Harvard's benchmark of at least 1 g fibre per 10 g carbohydrate can be met more easily with Box A foods than Box B foods; low carbohydrate intake need not mean low fibre intake. [23]
• Fibre is nonessential; universal intake targets lack convincing long-term trial support; the proposed mechanisms do not resolve the question; fibre can aggravate bowel symptoms; and low-carbohydrate diets can contain substantial fibre.

References

1. [03:42] Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids — https://doi.org/10.17226/10490
2. [04:21] Dietary Guidelines for Americans, 2015–2020 — https://www.dietaryguidelines.gov/about-dietary-guidelines/previous-editions/2015-dietary-guidelines
3. [08:12] The Global Influence of the Seventh-Day Adventist Church on Diet — https://doi.org/10.3390/rel9090251
4. [08:41] Dietary Goals for the United States (1977) — https://www.govinfo.gov/app/details/CPRT-95SPRT23395O
5. [08:58] Dietary Guidelines for Americans, 2000 — https://www.dietaryguidelines.gov/about-dietary-guidelines/previous-editions/2000-dietary-guidelines-americans
6. [09:12] Dietary Guidelines for Americans, 2005 — https://www.dietaryguidelines.gov/about-dietary-guidelines/previous-editions/2005-dietary-guidelines-americans
7. [09:28] SACN Carbohydrates and Health Report (2015) — https://www.gov.uk/government/publications/sacn-carbohydrates-and-health-report
8. [10:41] Carbohydrate quality and human health: a series of systematic reviews and meta-analyses — https://doi.org/10.1016/S0140-6736(18)31809-9
9. [11:03] Blow to low carb diet as landmark study finds high fibre cuts heart disease risk — https://www.theguardian.com/lifeandstyle/2019/jan/10/high-fibre-diets-cut-heart-disease-risk-landmark-study-finds
10. [12:35] Stool form scale as a useful guide to intestinal transit time — https://doi.org/10.3109/00365529709011203
11. [13:18] Effects of changes in fat, fish, and fibre intakes on death and myocardial reinfarction: DART — https://doi.org/10.1016/S0140-6736(89)90828-3
12. [14:15] Dietary fibre for the primary prevention of cardiovascular disease — https://doi.org/10.1002/14651858.CD011472.pub2
13. [14:23] Whole grain cereals for the primary or secondary prevention of cardiovascular disease — https://doi.org/10.1002/14651858.CD005051.pub3
14. [14:29] Whole grain foods for the prevention of type 2 diabetes mellitus — https://doi.org/10.1002/14651858.CD006061.pub2
15. [15:02] Dietary fiber and health outcomes: an umbrella review of systematic reviews and meta-analyses — https://doi.org/10.1093/ajcn/nqx082
16. [16:22] The Environment and Disease: Association or Causation? — https://doi.org/10.1177/003591576505800503
17. [16:55] Association between dietary fiber and lower risk of all-cause mortality: a meta-analysis of cohort studies — https://doi.org/10.1093/aje/kwu257
18. [22:49] Plant sterols lower cholesterol, but increase risk for coronary heart disease — https://doi.org/10.3844/ojbsci.2014.167.169
19. [23:37] Whole grain consumption and risk of cardiovascular disease, cancer, and all cause and cause specific mortality: systematic review and dose-response meta-analysis of prospective studies — https://doi.org/10.1136/bmj.i2716
20. [24:26] The effects of dietary fibre on C-reactive protein, an inflammation marker predicting cardiovascular disease — https://doi.org/10.1038/ejcn.2009.8
21. [27:57] Investigation of normal flatus production in healthy volunteers — https://doi.org/10.1136/gut.32.6.665
22. [28:46] Stopping or reducing dietary fiber intake reduces constipation and its associated symptoms — https://doi.org/10.3748/wjg.v18.i33.4593
23. [33:48] Identifying whole grain foods: a comparison of different approaches for selecting more healthful whole grain products — https://doi.org/10.1017/S1368980012005447

Early signs, secrecy, and early adulthood

• As a high-school freshman, Robyn experienced isolation, low self-worth, and persistent suicidal thoughts without acting on them. Her older sister knew and helped her; concern about stigma kept her symptoms hidden from others.
• School clubs, leadership roles, and lettering in football coincided with severe distress when Robyn was alone. Maintaining different outward and internal experiences was exhausting, and the outward activity concealed her symptoms.
• During college, suicidal thoughts became less prominent while anger, jealousy, unfavorable social comparisons, academic struggles, and severe anxiety increased. A routine request to choose chips for friends led to a panic episode.
• Robyn completed a degree in environmental education, served with Maryland's conservation corps, and worked in outdoor education and at a residential school for boys, where she taught math and met Matt. She rarely shared her emotional difficulties.
• The conversation includes direct questions about suicidal thoughts, their frequency, and another person's safety. External activity and apparent social functioning can coexist with severe internal distress.

Motherhood, psychiatric diagnoses, and the cost of sedation

• After the birth of Robyn's first child in 2005, isolation, financial pressure, and disrupted routines coincided with an acute crisis. She wrote about wanting to die, struggled to speak, and acknowledged thoughts of harming herself or her baby without intent to act.
• Matt took Robyn to the hospital for urgent assessment. She was observed without admission, diagnosed with postpartum depression, given antidepressants, and discharged without a substantive counseling session or specialist referral.
• Her first period on antidepressants coincided with improvement, with no clear attribution to the medication. During her second pregnancy she stopped the drug without a gradual taper after consulting a clinician, then deteriorated amid relocation and Matt's frequent absence for work.
• Robyn experienced intense anger while caring for young children, including avoiding play, holding a bedroom door closed during an overwhelmed episode, and frequent yelling. She later felt enduring guilt about how this affected them.
• Robyn resumed medication during pregnancy because symptoms became unmanageable. A marriage counselor subsequently urged hospital evaluation after an angry episode. Following a move, she stopped medication without informing her new clinicians and struggled for several years.
• Personal accounts of bipolar disorder matched Robyn's anger, periods of reduced sleep, compulsive organizing and cleaning, and disproportionate emotional reactions. A general practitioner prescribed an antipsychotic and referred her to psychiatric care.
• Her psychiatric visits involved questionnaires, repeated medication and dose changes, long travel, high costs, and little sustained exploration of her personal history. She experienced financial guilt and expected medication to remain necessary throughout her life.
• A general practitioner eventually maintained a fixed regimen. Robyn experienced profound sedation, relied on alarms for her children's school routine, slept for much of the day, and had only two or three functional waking hours, sometimes with continuing anger.
• In an Easter photograph, Robyn sat on a couch while her children hunted eggs. She had difficulty joining family activities, while Matt performed much of the household work alongside his employment and travel.
• Robyn remained active in scouting but needed significant rest around major events. During an overnight leadership camp, her evening medication caused severe impairment in speech and mobility, and other volunteers helped her with personal care and getting to bed.
• Her usual food included convenient processed meals, cereal, and nightly ice cream. Dietary changes were not raised during psychiatric care, and she initially had no awareness of nutrition as a possible influence on mental well-being.

The dietary change that began as an effort to avoid a statin

• At age 40, elevated cholesterol prompted a proposed statin, and Robyn wanted to avoid adding another medication. Her general practitioner agreed to six months of dietary change. She began Vinnie Tortorich's no-sugar, no-grains (NSNG) approach on August 6, 2017.[1]
• Robyn eliminated sugars and grains, later avoided seed oils, and initially shifted from nightly ice cream to yogurt. Matt joined her. Their approach generally avoided low-carb imitations of bread and other foods.
• After about six months, Robyn had lost approximately 25 pounds, had changes in cholesterol measurements her doctor welcomed, and had more energy for walking. She continued the same prescribed psychiatric doses and initially viewed these as separate issues.
• NSNG permits different degrees of carbohydrate restriction and does not necessarily produce therapeutic ketosis. Robyn progressed to a heavily meat-based diet, was fully carnivore for a period, and later sometimes included berries or a sweet potato.
• Robyn has never measured ketones. Her belief that she may have been in ketosis was based on her eating pattern and subjective sensations, and the timing of her mental-health improvement was not established by measurement.

Recognizing improvement and tapering psychiatric medication

• After Matt's job loss, the family moved from South Carolina to Texas. During the household transition and after the move, Robyn experienced energy, curiosity, and enjoyment of ordinary activities such as watching sunsets, without initially linking these changes to nutrition.
• A podcast conversation with Dr. Georgia Ede about ketogenic nutrition and mental health prompted Robyn to connect her changed functioning with her diet. She and Matt involved their children in monitoring any deterioration during a possible medication reduction.
• With a general practitioner's oversight, Robyn gradually reduced her antipsychotic and antidepressant around 2018–2019. Missing doses had previously caused severe disturbances, so she used a planned taper and accepted the possibility that medication might become necessary again.
• Robyn has not resumed those psychiatric drugs since tapering. She became active in walking, yoga, and strength training and experienced greater awareness of her surroundings and participation in family life.
• The medication taper followed an established dietary change, involved family monitoring, and was supervised by a medical prescriber. Unsupervised psychiatric medication discontinuation carries potential rebound effects, which Robyn specifically cautioned against.

High LDL, Hashimoto's, and the sweet-potato experiment

• Robyn initially had improved cholesterol measurements during weight loss but later experienced a sharp LDL increase while lean. The lean mass hyper-responder pattern combines high LDL, high HDL, and low triglycerides after carbohydrate restriction; the lipid energy model seeks to explain this response.[2][3]
• Several physicians recommended statins, which Robyn declined amid uncertainty about her individual cardiovascular risk. She also pursued thyroid symptoms and markedly elevated thyroid antibodies, with both parents having undergone thyroid removal.
• An earlier clinician declined to pursue Robyn's thyroid antibodies until a nodule developed. Dr. Tro Kalayjian subsequently identified Hashimoto's and addressed the high LDL with both conventional statin risk factors and uncertainty about carbohydrate-restriction-associated lipid elevations.
• David Feldman's 2018 white-bread-and-processed-meat self-experiment reduced LDL to 83 mg/dL over roughly seven days; Nick Norwitz later conducted an Oreo-based carbohydrate self-experiment. These interventions examined short-term LDL responsiveness, not long-term cardiovascular outcomes.[4][5]
• Dr. Kalayjian offered a daily choice of rice, oatmeal, or sweet potato to test LDL reduction with carbohydrate reintroduction. Robyn ate a palm-sized sweet potato at her first meal without added fat for about three months, and her LDL decreased.
• Robyn experienced renewed sugar cravings after adding sweet potato. She stopped yoga and, after approximately two further months at half a potato daily, experienced declining exercise, a wish to return to bed on waking, and depressive symptoms.
• Reducing to one-quarter of a sweet potato daily did not resolve Robyn's symptoms. Anger and daytime sleep increased, and during COVID illness she still maintained the food intervention until Matt urged her to stop.
• Robyn stopped the sweet-potato intervention, resumed carnivore eating, and did not restart psychiatric medication. Returning to her earlier level of comfort took approximately four months of sustained effort, renewed exercise and yoga, and outside support.
• Robyn prioritizes daily mental functioning and family relationships over lowering LDL through a dietary change she associated with psychiatric deterioration. She acknowledges unresolved cardiovascular risk and has declined statin therapy without establishing that high LDL is harmless.

The KETO-CTA research and its disputes

• The KETO-CTA prospective study enrolled 100 lean mass hyper-responders and near-hyper-responders for coronary calcium and CT angiography at baseline and one year. All 100 participants completed follow-up, producing 200 scans for examining coronary plaque progression.[6]
• The April 7, 2025 KETO-CTA publication used the initial Cleerly coronary-plaque analysis. Public criticism followed while additional quantitative analyses of the same scans were pending.[7]
• HeartFlow and QAngio analyses of the same scans yielded broadly consistent findings that differed from Cleerly. Median plaque progression was low, and some participants had plaque regression while LDL remained high. Longer-term cardiovascular outcomes remain unknown.[8]
• The team repeatedly requested and offered to fund Cleerly quality-control checks or a new analysis, without obtaining the requested re-analysis. The disagreement involved legal consultation and delayed the research process while data validation continued.
• A five-year follow-up was under planning, with some original participants willing to return. The proposed work included tighter contracts, blinding procedures, quality control, and data collection safeguards.
• Cardiovascular risk evidence frequently comes from metabolically unhealthy populations and is applied to otherwise metabolically healthy individuals. This raises questions about the ability of statistical adjustments to capture differences between these populations.
• The lipid energy model and the lipid hypothesis each require evaluation across their predictions and exceptions. Prospective population-specific data, transparent methods, and reproducibility are central to testing the competing explanations.
• The documentary and research center on people using carbohydrate restriction for substantial health concerns, beyond weight loss alone. The focus is on the relationship between LDL measurements and cardiovascular outcomes in the recruited population.
• Drug studies have finite observation periods, possible run-in phases, and differences in adverse-event monitoring. GLP-1 medicines can have benefits while longer-term outcomes and adverse effects require continued study.
• Clinical communication about incomplete evidence includes known effects, uncertainties, and patient choices. Robyn's carbohydrate-reintroduction trial with Dr. Kalayjian involved this kind of shared decision-making.

Advocacy, food behavior, and maintaining change

• Robyn became active in Vinnie Tortorich's online community and launched the Ketobiography interview podcast to share everyday experiences of low-carb and ketogenic living, including less dramatic examples.[9]
• Robyn associates higher carbohydrate intake with rapid deterioration and therefore maintains strict dietary habits. She also explores how people without immediate symptom changes sustain adherence, since simple dietary rules do not eliminate cravings or behavioral difficulties.
• Robyn's father maintained NSNG during cancer care and experienced a strong therapeutic response alongside substantial side effects. She attributes part of his resilience to his dietary habits but does not regard low-carb eating as protection from every illness.
• Dave Feldman sometimes uses informal 30-day low-carb trials with family and friends, comparing bloodwork before and after, and estimates a success rate around 50%. Energy changes vary, as do individual reasons for carbohydrate restriction.
• Weight loss can fluctuate over time without following a straight downward slope, as in Amy Berger's illustration. Comparing individual progress with unusually rapid transformations can create unrealistic expectations, and experiences may differ between women and men.
• Dietary consistency involves individual food triggers, persistent habits, and resuming routines after setbacks. Certain low-carbohydrate snacks can still prompt overeating, and short-term outcomes may not capture longer-term changes.

Long-term adaptation, movement, and changing health needs

• Dave uses poker as an analogy for outcome variability: the example of roughly 2,000 hours of play illustrates how short observation periods can mislead. Short-term fluctuations can also complicate interpretation of diet outcomes.
• In a 2018 self-experiment, Dave gained 19 pounds over approximately six weeks while tracking lipids, body composition, and respiratory exchange ratio. His later usual body weight remained about six to seven pounds above his earlier baseline.[10]
• Robyn maintained her dietary pattern while the unexpected death of her mother and other stresses disrupted her exercise over approximately two to three years. She experienced sustained grief with some similarities to depression but distinguished it from her earlier psychiatric illness.
• A trainer helped Robyn resume strength training, which was followed by more walking, outdoor activity, and improved subjective well-being. She maintains nutrition as a foundation while also valuing movement, sleep, sunlight, and routines.
• Robyn investigated possible indoor environmental factors, including mold, purchased air-cleaning equipment, and experienced better sleep and breathing. She did not establish a causal explanation through testing.
• Metabolic Mind's THINK+SMART program helped Robyn identify missing elements of her former routine, particularly exercise, and resume those practices.[11]
• At age 48, Robyn is focusing on perimenopause, hormonal changes, and maintaining thyroid function while living with Hashimoto's and a family history of thyroid surgery. She has read Amy Alkon's Going Menopostal and consults her clinician about options.[12]

Making metabolic mental-health support accessible

• Robyn participated in The Cholesterol Code documentary about LDL changes and coronary research after carbohydrate restriction. Her psychiatric history and dietary experience are part of the context for her medical decisions.
• Metabolic Mind brings together research, clinicians, and personal experiences; the Coalition for Metabolic Health connects people with experts; and Metabolic Collective is an independent grassroots organization organized around peers and families.
• Metabolic Collective developed through community focus groups and volunteers and supports community-led projects, including storytelling training, connections between podcast hosts and advocates, and the MAMAS family-support initiative drawing on an Al-Anon model.
• The organization's work centers on access to information, lived experience, peer support, and individualized decisions about metabolic strategies alongside clinical care, without a single required dietary pattern or assured outcome.

References

1. [01:13] Vinnie Tortorich, What Is NSNG? — https://vinnietortorich.com/what-is-nsng/
2. [01:34] Are You a Lean Mass Hyper-responder? — https://cholesterolcode.com/are-you-a-lean-mass-hyper-responder/
3. [01:35] The Lipid Energy Model: Reimagining Lipoprotein Function in the Context of Carbohydrate-Restricted Diets — https://doi.org/10.3390/metabo12050460
4. [01:44] White Bread and Processed Meat Experiment — https://cholesterolcode.com/the-tandem-drop-experiment-part-2-carbs/
5. [01:44] Oreo Cookie Treatment Lowers LDL Cholesterol More Than High-Intensity Statin Therapy in a Lean Mass Hyper-Responder on a Ketogenic Diet: A Curious Crossover Experiment — https://doi.org/10.3390/metabo14010073
6. [01:54] The Impact of Carbohydrate Restriction-Induced Elevations in Low-Density Lipoprotein Cholesterol on Progression of Coronary Atherosclerosis: The Ketogenic Diet Trial Study Design — https://doi.org/10.1097/MCA.0000000000001395
7. [02:00] Longitudinal Data From the KETO-CTA Study: Plaque Predicts Plaque, ApoB Does Not (retracted in 2026) — https://doi.org/10.1016/j.jacadv.2025.101686
8. [02:06] The Impact of Sustained LDL-C Elevation on Plaque Changes: Primary Coronary Plaque Progression Results From the Keto CTA Study (2026 preprint, not peer-reviewed) — https://doi.org/10.64898/2026.01.15.26343955
9. [02:27] Ketobiography — https://shows.acast.com/less-of-me-success-stories/about
10. [02:45] Weight Gain Experiment (2018), Experiment List — https://cholesterolcode.com/experiment-list/
11. [03:18] Metabolic Mind, What Is THINK+SMART? — https://www.metabolicmind.org/thinksmart/what-is-think-smart/
12. [03:19] Amy Alkon, Going Menopostal — https://www.amyalkon.net/

Before low-carb: diabetes care without remission

• For 25 years, type 2 diabetes care focused on blood sugar prescriptions without investigating the causes; chronic disease care frequently misses underlying causes.
• Repeat prescriptions dominated while patients developed ulcers, amputations and escalating medication regimens; the work became management of decline.
• Before 2012, drug-free remission was absent in the practice; higher doses, additional drugs and eventually insulin were the usual progression.
• An NHS low-carb programme later achieved remission in approximately half of participating patients, a major change from earlier outcomes. [1]
• Severe dyslexia made medical training difficult despite a strong commitment to helping people; better patient outcomes renewed that purpose.

Publishing outcomes in a normal NHS surgery

• The first 18-patient low-carb case series documented major improvements and triggered hostility among some dietitians, endocrinologists and doctors. [2]
• Public heckling and hate mail led to baseline measurements, weekly follow-up, inclusion of poor outcomes and continuous programme audit.
• These audits improved clinical methods; observational data follow actual patients, with similar work emerging in multiple countries.
• A subsequent 186-patient NHS service evaluation found about 50% remission without expensive concierge care or a large dedicated team. [1]

How low-carb advice works

• Norwood Surgery diet sheets and protocols are available in BMJ Nutrition papers; no single carbohydrate limit applies to every patient. [1][3]
• With insulin resistance, glucose processing is impaired; lowering foods that raise blood sugar and increasing protein and healthy fats addresses this.
• Research commonly defines low-carb as under 130 g/day, while the effective level depends on individual glucose response.
• Goals and baseline HbA1c, weight, waist or CGM values guide reassessment; drug-free remission requires HbA1c under 48 mmol/mol (6.5%).
• Initial remission or satisfactory weight and long-term maintenance are distinct challenges.

Maintenance through feedback and psychology

• Longer participation at Norwood Surgery coincides with continued average HbA1c improvement; Jen Unwin's psychology input supports maintenance.
• Progress checks around six weeks and immediate CGM feedback connect glucose spikes with recently eaten foods, without waiting three months.
• The DiRECT programme achieved nearly 50% remission after one year, declining to approximately 12% after five years. [4]
• Birthdays, Christmas, holidays, bereavement and stress contribute to lapses, and almost everyone eventually needs renewed support.
• Persistent pressure to eat carbohydrates in the wider food environment makes ongoing support essential.

Food addiction and long-term adherence

• Failure to ask about food addiction left it unrecognized alongside the absence of remission; questioning patients revealed substantial cravings for bread and other carbohydrates.
• A food-addiction study connected addiction with a 670% greater likelihood of type 2 diabetes, making screening important. [5]
• Jen Unwin's CRAVED questionnaire sometimes identifies carbohydrate addiction throughout groups of approximately 30 people with diabetes.
• Severe mental-health symptoms can motivate sustained ketosis, while food addiction can interfere with ketogenic adherence, as Iain Campbell has observed.
• Moderation of bread, potatoes and other problem foods can fail for affected patients; abstinence can be more effective.

Growing acceptance and visible glucose responses

• An initially isolated and unpopular low-carb approach now has an international network, dozens of annual talks, thousands of attendees and continuing critics.
• CGMs expose glucose responses; a small bowl of cereal doubles Unwin's blood glucose and causes illness in his own type 2 diabetes.
• Some criticism attributes low-carb benefits entirely to weight loss, while other data indicate effects on diabetes beyond weight reduction.
• Approximately 30 papers have been published by the team, alongside clinical learning shared across countries.

GLP-1 drugs: benefits, limits and combinations

• Low-carb often lowers hunger and body weight; Isabella Cooper's work links nutritional ketosis to higher endogenous GLP-1. [6]
• Unwin's roughly 15 years of GLP-1 prescribing include reduced cravings for ultra-processed foods and alcohol alongside severe adverse outcomes.
• Two patients required intensive care: one nearly died of pancreatitis, and another needed removal of most of the bowel after stasis and necrosis.
• A minimal effective GLP-1 dose for limited duration with a discontinuation plan addresses escalating doses, adverse effects and weight regain.
• GLP-1 therapy offers an interval for reducing addictive foods and increasing protein, beyond simply decreasing portions of junk food.
• One patient lost 1 kg over five years with a GLP-1 drug and 27 kg over two years with low-carb; efficacy varies for both approaches.
• Real-world GLP-1 evidence indicates up to 50% discontinuation within two years, requiring plans beyond initial weight loss.
• For severe food addiction and poorly controlled diabetes, combining CGM, GLP-1 therapy and low-carb with collaborative decisions can improve adherence.

Medication safety during carbohydrate reduction

• Insulin, sulfonylureas and SGLT2 inhibitors need medication review as carbohydrates fall; practical clinician guidance is available in a published paper. [7]
• With CGM and close support, initial insulin dose reductions of 50%, followed by further reductions, have enabled some long-term users to stop insulin.
• SGLT2 inhibitors can cause euglycemic ketoacidosis, making hydration important on low-carb; doses are sometimes halved and eventually discontinued.
• Glucose in urine can lead to severe thrush; metformin and GLP-1 drugs are compatible with low-carb without intrinsic hypoglycemia risk.
• Individualized, clinician-led adjustments with monitoring are necessary.

The changing food environment

• In earlier medical training, type 2 diabetes was uncommon and absent among patients younger than 60; it now affects younger people.
• Limited genetic change over forty to fifty years implicates the changed food environment in the diabetes epidemic.
• Changing the food environment and addressing underlying causes could make type 2 diabetes rare again without relying only on medication.
• Low-carb is not appropriate for everyone, but ordinary NHS care has yielded remission, lower medication use and savings.

References

1. [04:52] What predicts drug-free type 2 diabetes remission? Insights from an 8-year general practice service evaluation of a lower carbohydrate diet with weight loss — https://doi.org/10.1136/bmjnph-2022-000544
2. [07:40] Low carbohydrate diet to achieve weight loss and improve HbA1c in type 2 diabetes and pre-diabetes: experience from one general practice — https://doi.org/10.1002/pdi.1835
3. [11:14] Insights from a general practice service evaluation supporting a lower carbohydrate diet in patients with type 2 diabetes mellitus and prediabetes: a secondary analysis of routine clinic data including HbA1c, weight and prescribing over 6 years — https://doi.org/10.1136/bmjnph-2020-000072
4. [15:32] 5-year follow-up of the randomised Diabetes Remission Clinical Trial (DiRECT) of continued support for weight loss maintenance in the UK: an extension study — https://doi.org/10.1016/S2213-8587(23)00385-6
5. [18:19] Food addiction is strongly associated with type 2 diabetes — https://doi.org/10.1016/j.clnu.2023.03.014
6. [26:21] Ketosis Suppression and Ageing (KetoSAge) Part 2: The Effect of Suppressing Ketosis on Biomarkers Associated with Ageing, HOMA-IR, Leptin, Osteocalcin, and GLP-1, in Healthy Females — https://doi.org/10.3390/biomedicines12071553
7. [32:40] Adapting diabetes medication for low carbohydrate management of type 2 diabetes: a practical guide — https://doi.org/10.3399/bjgp19X704525

Early illness and unresolved digestion

• For years Mark followed bodybuilding-style macro targets, usually capping fat around 70 g a day despite enjoying steak and butter.
• On September 26, 2025, at age 37, Mark went to hospital with glucose around 337 and received a type 1 diabetes diagnosis; his HbA1c exceeded 14%.
• Mark had lifelong digestive problems that became severe around diagnosis. He connected them with autoimmunity and possible high-glucose injury to the vagus nerve, including gastroparesis.
• An endocrinologist, primary-care physician, and gastroenterologist explored differing possibilities, including SIBO, gastroparesis, or psychological causes. Digestive enzymes, fiber, probiotics, and kiwi did not resolve his symptoms, even after glucose control improved.

Why carnivore initially seemed absurd

• Mark logged food-related gut symptoms, including problems with foods common in plant-based or Mediterranean diets. Carnivore initially seemed to him like the "Tide Pod challenge" of diets, not a serious intervention.
• Videos by Shawn Baker, Ken Berry, Anthony Chaffee, and other ketogenic-diet advocates challenged Mark's assumptions about meat, cholesterol, and saturated fat. He remained skeptical of cardiologists calling saturated fat protective, while continuing to feel ill despite following medical advice.
• On May 14, Mark switched abruptly to beef, bacon, and eggs, despite previously struggling to tolerate eggs. His aim was relief of gut symptoms, not discontinuation of insulin; he saw the diet as a reversible experiment.

Weight loss and diabetes diagnosis

• Before diagnosis Mark weighed about 200 lb, ate roughly 2,500 calories and 265 g of carbohydrate daily, and adjusted intake around training. His weight continued falling as he increased calories.
• Mark progressively raised intake to 3,000, 4,000, 5,000, and perhaps 7,000 calories a day, adding bagels, chips, cookies, ice cream, juice, and other sugar-rich foods. His weight fell to around 150–155 lb; he initially connected the fat loss with training.
• Hospital staff initially called the condition "pancreatic overload" and were uncertain whether Mark had type 2 diabetes. Ketosis and inadequate insulin were identified, while his initial medication included metformin and very little insulin.
• Mark's primary-care team ordered GAD65 antibodies and C-peptide. Strongly positive GAD65 and C-peptide of 0.26, against a lower normal value he recalled as 0.85, supported type 1 diabetes; his primary-care clinician arranged insulin and continuous glucose monitoring urgently.
• With diabetes management Mark lowered HbA1c from above 14% to 5.9% and then 5.7% within roughly three to six months, before carnivore. Metformin ended because of digestive symptoms, and improved glucose numbers did not restore his gut health.

Carnivore adaptation, glucose, and insulin

• Mark began carnivore for digestion and initially expected indefinite insulin use. He identified close glucose and insulin monitoring as essential during the first weeks for type 1 diabetes, connecting that period with glycogen loss, "oxalate dumping", and cortisol changes.
• Mark's gut began improving within a couple of weeks. Around six weeks he experienced major improvements in digestion, mood, and energy, which he linked to fat adaptation; he also regained tolerance for eggs.
• At the start Mark's continuous glucose monitor averaged about 116, and within the first weeks his HbA1c was around 5.6%. Large one-meal-a-day portions seemed incompatible with digestive trouble and fear of further weight loss, so he experimented with meal size and frequency.
• By about six weeks, Mark's average glucose moved toward 105 and roughly two daily units of long-acting insulin began causing lows, sometimes requiring honey. His long-acting dose fell to zero.
• Mark's fast-acting insulin also fell in stages from roughly 8–10 units daily to six, then four to six, three to five, two to four, and eventually about 1.5–2 units. His insulin requirements had already been unusually low and declining before carnivore.
• Coffee coincided with a worse glucose response and a temporary increase in insulin use, leading Mark to suspect an autoimmune trigger. Chicken wings twice coincided with rises from around 90 to 170, so he eliminated them and returned to basic animal foods.
• Resistance training sometimes raised Mark's glucose to 120–160, yet even half a unit of insulin could later pull it near 75. Ten-minute post-meal walks and ordinary movement increased his concern about lows.
• Mark stopped insulin around October 18 because the smallest dose available to him, half a unit, no longer felt safe. At interview time he was using neither insulin nor metformin, had continuous-monitor glucose averaging around 95–100, and was tracking ketones.
• By six weeks Mark's lifelong digestive symptoms had essentially disappeared; hunger and fullness signals returned, food noise diminished, and energy became steady. He also eliminated energy drinks.

Meals, strength, and clinical uncertainty

• Mark's wife joined him after seeing the changes, although she initially worried about their cholesterol tests. Both enjoy the food.
• Mark eats two substantial meals: a morning meal of roughly 8–10 eggs, ham, four to six slices of bacon, and a little olive oil and sauerkraut, then 1–2 lb of beef or sometimes salmon around 1–2 p.m. He includes olive oil because of research on polyphenols and autoimmunity; his diet is not literally animal-only.
• Mark still lifts four or five days per week, but sessions have shortened from about an hour to 35–40 minutes, often with heavier weights and fewer sets. He experiences greater strength and more consistent energy at roughly 165–170 lb than around 200 lb.
• The doctors saw positive antibodies and very low C-peptide as consistent with classic type 1 diabetes, but Mark needed unusually little insulin even while eating carbohydrates; his long-acting dose had fallen from ten to six, four, and eventually only two or three units.
• Mark contrasted his doses with his estimate of common type 1 requirements of roughly 24–30 units of long-acting insulin plus mealtime doses, perhaps 60 units total daily. Doctors raised the "honeymoon phase" as a possible explanation because some beta-cell function can remain.
• Mark's C-peptide rose from 0.26 to 0.37 in June, soon after beginning carnivore, but remained below normal. Its subsequent trajectory and the reason for his lower insulin requirements remain unknown; his antibody results and the possibility of a honeymoon phase leave major questions open.
• Mark sees autoimmunity and gut dysfunction as closely intertwined and wants diabetes care to address nutrition and these symptoms more directly. His endocrinologist left the practice, and neither specialist nor primary care had a clear explanation for his course.
• Mark plans repeat C-peptide testing and has sought parasite testing and intervention along with other investigations, sometimes paying himself. His priorities are answers, lasting relief, and health and energy for his three children.

Cholesterol criticism and practical advice

• Friends and family question the diet and Mark's elevated cholesterol number, but he gives greater weight to how he feels and to work by doctors such as Anthony Chaffee on emerging research. He sees his critics as less active and energetic than he wants to be.
• For Mark, resistance to giving up processed carbohydrates reflects the appeal of sugary foods. He linked sugar and cocaine to overlapping dopamine pathways and acknowledged his own reliance on sweets before diagnosis.
• Mark also experienced relief from longstanding insomnia and more consistent daytime energy. Those improvements changed his response to other people's seemingly exaggerated success stories.
• Mark would not advise most beginners to switch overnight. His own abrupt change came from desperation; without similar urgency or discipline, he favors carnivore dinners first, then lunches, while gradually eliminating ultra-processed foods.
• Mark favors three meals over an immediate shift to one meal a day, with time for increased fat intake and microbiome changes, and an experiment of around 120 days. His examples include people who needed to discontinue blood-pressure or type 2 diabetes medication during that period.

Why lowering LDL has not eliminated heart disease

• Heart disease remains a leading cause of death despite decades of increasingly powerful LDL-lowering medications. Coronary bypass surgery is still needed when blockages become too advanced for less invasive procedures, and heart surgeons remain in demand despite predictions that cholesterol drugs would make their work obsolete.
• LDL lowering reduces some cardiovascular events, but the observed reduction is smaller than expected under a model in which LDL dominates atherosclerosis. Some patients take statins for decades, meet cholesterol targets, and still require bypass surgery.
• Lowering LDL earlier, further, and for longer does not by itself resolve why disease persists. Additional metabolic factors, including insulin resistance, are relevant to the broader disease process.
• LDL remains a possible contributor to atherosclerosis. The question is how its substantial reduction relates to the more limited reduction in cardiovascular disease.
• Advanced heart disease is common with aging, while preventing its progression to the point of surgery remains an important objective.

Cardiovascular endpoints, mortality, and trial design

• Cardiovascular event reduction and longer overall survival are distinct outcomes. Improvement in a cardiovascular endpoint need not demonstrate an all-cause mortality benefit, and deaths from other causes remain relevant to patients.
• Lifelong genetically lower LDL, including PCSK9 loss-of-function variants, and Mendelian randomization findings raise questions about overall longevity as well as cardiovascular outcomes. The findings cited in the conversation do not establish longer lifespan through lower LDL alone.
• Early termination of trials after cardiovascular or composite endpoints can leave mortality questions unresolved. In the FOURIER PCSK9-inhibitor trial, the intervention arm had numerically more all-cause deaths, without a statistically significant difference. [1]
• Randomization strengthens clinical evidence, while selection, duration, endpoints, run-in periods, subgroup differences, and statistical adjustments influence interpretation. Statins can also have anti-inflammatory effects beyond LDL reduction.
• Evidence obtained mainly in metabolically unhealthy populations or patients with established cardiovascular disease does not directly establish identical effects in metabolically healthy people with elevated LDL.

Metabolic health and individualized risk

• KETO-CTA examines people with very high LDL after carbohydrate restriction and otherwise favorable metabolic markers, using coronary imaging to investigate the LDL-risk relationship in this distinct physiology. [2]
• Insulin resistance receives less attention than cholesterol in routine cardiovascular care. Smoking is an established cardiovascular risk, and glucose and insulin dysfunction are additional factors warranting direct measurement.
• The cited subgroup analyses of statin and PCSK9 trials associate lower insulin resistance with smaller observed medication benefits. Direct study of metabolically healthy groups can provide information not available from adjustments across mixed populations.
• Decisions for metabolically healthy low-carbohydrate patients with high LDL can incorporate inflammation, glucose control, insulin resistance, lipoprotein characteristics, and actual arterial disease alongside LDL.
• Coronary imaging allows assessment of existing disease and subsequent changes. Monitoring arterial plaque and metabolic health can inform decisions about cholesterol medication in selected patients.

Making prevention practical

• Stay Off My Operating Table focuses on avoiding advanced heart disease and surgery; Stay Off My Kitchen Table develops the associated dietary and practical approach. [3][4]
• Medical interventions and prescriptions can leave patients dependent on healthcare while dietary advice remains ineffective. Prevention involves understanding and improving metabolic health through everyday choices.
• Calorie restriction, exercise instructions, and low-fat diets can be difficult to sustain when they produce persistent hunger. Whole-food, low-carbohydrate eating can improve satiety, energy, and adherence.
• Lifestyle coaching and follow-up can support behavioral change, with successful preventive care eventually reducing the need for ongoing medical supervision.
• Medical care often addresses advanced damage after disease develops, while long-term dependence on that care remains common.

Diabetes and the hospital food contradiction

• Substantial improvement or remission of type 2 diabetes through carbohydrate restriction has been demonstrated in Virta Health's clinical work, while hospital meals commonly contain substantial carbohydrate.
• Postoperative glucose control matters because elevated glucose is associated with worse cardiac-surgery outcomes. Patients may receive intravenous insulin while also consuming carbohydrate-heavy hospital meals.
• Lower carbohydrate intake can reduce glucose exposure and insulin requirements. A trial comparing carbohydrate restriction with standard postoperative glucose management would examine the consequences of these different approaches.
• Richard Bernstein's low-carbohydrate approach to type 1 diabetes uses smaller carbohydrate loads and insulin doses. Ovadia's brother, who has longstanding type 1 diabetes, has also used less insulin after carbohydrate restriction.
• Joseph Kraft's insulin-testing work is associated with a high prevalence of insulin resistance among heart-attack patients that conventional diabetes diagnosis or LDL measurement can miss. Historical dietary priorities focused more on saturated fat and cholesterol than John Yudkin's concerns about sugar.

Why metabolic risk cannot be reduced to LDL

• LDL of 40 mg/dL with HbA1c of 7% does not automatically indicate better metabolic or cardiovascular health than LDL of 130 mg/dL with HbA1c of 5%. Very low LDL does not eliminate risk associated with metabolic syndrome.
• Patients can substantially lower HbA1c with carbohydrate restriction while experiencing higher LDL. Decisions focused solely on the LDL rise may overlook improvements in other metabolic markers.
• David Unwin's low-carbohydrate primary-care data showed little mean LDL change alongside metabolic improvements, while individual LDL responses differed.
• A meta-analysis of 41 randomized trials, involving 1,379 participants over an average 19.4 weeks, linked lower BMI to larger LDL increases, intermediate BMI to little average change, and the highest BMI to LDL decreases. [5]
• The 2025–2030 US dietary guidelines give greater prominence to real foods, meat, and full-fat dairy while retaining a saturated-fat limit. The combined guidance creates tension with older dietary messages centered on cholesterol. [6]

Meat, plants, and dietary individualization

• The EAT-Lancet focus on predominantly plant-based eating does not establish that plant-only whole-food diets are superior to whole-food diets containing meat. Meat provides important nutrients and can contribute to optimal nutrition. [7]
• Vegan diets can support health with careful planning and supplementation, including B12, while requiring continued attention to nutritional adequacy.
• Carnivore eating can function as an elimination diet. Removing multiple foods may reduce symptoms, and gradual reintroduction can help identify individual intolerances.
• Reintroduction of fruit, vegetables, or other carbohydrates does not independently establish that carnivore eating was unsuccessful. Dietary tolerance, activity, glucose regulation, and preferences vary between people.
• Greater insulin resistance can require tighter carbohydrate restriction than the intake tolerated by a lean, highly active individual. Dietary suitability depends on individual outcomes.

Continuous glucose monitoring

• A two-week continuous glucose monitor can identify individual meal responses and reveal glucose patterns not captured by general dietary advice.
• Normal glucose regulation permits temporary post-meal increases followed by a return toward baseline, such as under 100 mg/dL within roughly two to three hours. Persistent elevation is a different pattern.
• Responses to potatoes, strawberries, and other carbohydrate-containing foods differ between individuals. Measurements can help define a sustainable carbohydrate intake.
• Better metabolic flexibility and glucose regulation may have implications for cardiovascular, brain, and cancer-related health beyond changes in LDL.

What cardiac surgery actually involves

• Ovadia wanted to become a surgeon in childhood and completed general and cardiothoracic training despite predictions that cholesterol medications would reduce demand for cardiac surgery.
• Cardiopulmonary bypass permits a stopped heart while blood circulates through equipment that supplies oxygen and removes carbon dioxide. John Gibbon developed the heart-lung machine following his experience with a fatal pulmonary embolism.
• Cardiopulmonary bypass may use continuous, nonpulsatile circulation despite normal pulsatile blood flow. The comparisons mentioned do not establish a clear advantage for pulsatile circulation during surgery.
• Ventricular assist devices can maintain continuous blood flow in severe heart failure, with kidney, stroke, and other complications remaining possible.
• Major cardiac operations involve substantial physiological disruption, intensive care, ventilation, chest tubes, and recovery. Prevention can avoid burdens that even successful surgical care cannot eliminate.

Ovadia's metabolic recovery and clinical approach

• Ovadia previously experienced obesity and prediabetes. Calorie counting and increased exercise initially reduced weight, followed by regain.
• A gluten-free dietary experiment with his wife in 2013 also reduced bread and pasta intake, improved energy, and initiated a sustained dietary change.
• Gary Taubes's lectures and the books The Case Against Sugar and Good Calories, Bad Calories contributed to Ovadia's revised view of obesity and metabolic disease. He subsequently achieved and maintained substantial weight loss. [8][9]
• Carbohydrate restriction and intermittent fasting now coincide with more consistent energy during six- to eight-hour operations than Ovadia experienced when younger and metabolically unhealthy.
• A roughly 30-day carbohydrate-restriction trial, with measurements before and after, can reveal changes in glucose, triglycerides, appetite, and energy. Subjective improvement can support long-term adherence.
• Ovadia's preventive practice, education, books, and podcast developed from a desire to reduce progression to advanced disease and surgery.

Why prevailing medical ideas are difficult to change

• Ovadia's medical training centered on the cholesterol hypothesis, with little exposure to John Yudkin's work on sugar. Training can establish a dominant model without extensive examination of competing explanations.
• Career incentives, funding, and publication practices can favor established research questions. Work on lean mass hyper-responders may be viewed as professionally risky by early-career researchers.
• Clinicians and researchers may have invested substantial professional effort in prevailing assumptions. Revising those assumptions requires reevaluating earlier advice and decisions.
• Scientific and media gatekeeping can give conventional interpretations greater visibility and restrict the circulation of dissenting work without requiring coordinated action.
• Cardiac surgical techniques have changed through repeated technical advances. Cardiovascular prevention can also evolve when observations conflict with established expectations.

Insulin resistance, GLP-1 drugs, and lipid quality

• GLP-1 medications improve cardiometabolic outcomes without LDL reduction being their main mechanism. Their cardiovascular effects are relevant to metabolic dysfunction beyond cholesterol.
• GLP-1 drugs can help some patients initiate difficult lifestyle changes, while durable improvement also depends on diet and behavior.
• Small-dense LDL proportion, oxidation, glycation, and inflammation may have associations with risk that differ from total LDL and ApoB concentrations. A high absolute particle count need not correspond to identical risk in every metabolic context.
• Systemic metabolic dysfunction can alter both the lipid profile and cardiovascular risk, producing an association between the two without resolving every causal contribution.
• The 2017 European Atherosclerosis Society consensus supports a causal role for LDL in atherosclerosis. Its application to metabolically healthy carbohydrate-restricted groups with unusually high LDL is the question examined here. [10]

KETO-CTA: the cohort and its central question

• KETO-CTA includes about 100 metabolically healthy ketogenic participants, many lean, with markedly elevated LDL, low triglycerides, high HDL, low inflammation, and favorable glucose markers.
• Mean age was approximately 55 years, and ketogenic dieting had continued for roughly four to five years. Six participants had LDL at or above 400 mg/dL, with the highest near 595 mg/dL.
• Some participants had high absolute numbers of small-dense LDL particles even when these represented a low proportion of total LDL particles. The cohort allows examination of predictions based on absolute ApoB exposure.
• Longitudinal KETO-CTA used coronary CT angiography about one year apart. In the analyses described, LDL and ApoB were not associated with plaque progression in the manner predicted by a simple lipid-centered model. [11]
• The earlier KETO publication found low baseline plaque levels in the high-LDL ketogenic cohort and included a comparison with Miami Heart participants. [12]
• Small baseline plaque volumes increase the difficulty of distinguishing biological change from measurement variability, making imaging precision and blinding important.

The conflicting coronary image analyses

• The Cleerly quantitative dataset contained unusual findings: progression in all participants, regression in none, and an average increase in plaque volume of approximately 50% in one year.
• Participants with calcium scores of zero had greater measured plaque progression than participants with positive calcium scores in that dataset.
• Feldman's inspection of anonymized raw measurements identified further irregularities, and the original Cleerly analysis was found not to have been fully blinded.
• Blinded HeartFlow measurements and prespecified Medis QAngio measurements aligned more closely with semi-quantitative findings than with the Cleerly measurements.
• Multiple quality-control efforts preceded the decision to exclude the delivered Cleerly dataset. The concern centered on that dataset rather than the general utility of quantitative coronary imaging.
• Medical decisions depend on the reliability of image interpretation. Disagreement between methods creates a need to examine both the underlying images and measurement processes.

Reading plaque measurements correctly

• Coronary CT angiography reconstructs coronary anatomy, semi-quantitative methods grade affected arterial segments, and quantitative methods estimate plaque volume.
• Heart motion, scan timing, changing vessel geometry, and low plaque volumes can produce measurement differences without corresponding biological progression.
• The smallest detectable change at a specified confidence level differs from the smallest numerical change produced by software. Feldman's approximate HeartFlow figure was 60 mm³, leaving smaller changes difficult to distinguish from noise.
• Percent atheroma volume is plaque volume divided by vessel volume. A decrease in vessel volume can increase this ratio despite an absolute reduction in plaque.
• A patient's maximum left anterior descending stenosis changed from 81% to 82%, while the length of severe narrowing contracted from several millimeters to a pinpoint. The maximum percentage alone missed the anatomical improvement.
• Severe stenosis in an asymptomatic patient does not automatically require stenting. Imaging interpretation must account for symptoms, actual anatomy, and disease progression.

Long-term uncertainty, lean mass hyper-responders, and mechanisms

• Under a simple cumulative LDL-exposure model, the cohort's lifelong exposure would predict more disease than was observed at baseline. Children with homozygous familial hypercholesterolemia provide a contrasting high-LDL example.
• Repeat imaging after five or six years could establish whether plaque progression accelerates and whether LDL or ApoB becomes associated with its rate. The existing observation period cannot resolve lifelong risk.
• Carbohydrate restriction and the lean mass hyper-responder phenotype do not eliminate the possibility of heart attacks. Some cardiovascular events can occur as a cohort of 55-year-olds ages, while isolated cases cannot quantify population risk.
• Prospective enrollment using predefined metabolic criteria reduces the selection problems of retrospectively assembled cases. Narrow ranges of normal glucose, blood pressure, and inflammation also limit correlations detectable within the cohort.
• A five-patient Journal of Clinical Lipidology case series included features such as markedly elevated triglycerides and xanthomas. Those characteristics differ from the classic metabolically healthy lean mass hyper-responder pattern. [13]
• The classic lean mass hyper-responder pattern includes LDL at least 200 mg/dL, HDL at least 80 mg/dL, and triglycerides no greater than 70 mg/dL. LDL responses form a continuum and may vary with body composition and weight-loss history. [14]
• Atherosclerosis includes active interactions among lipoproteins, arterial endothelial cells, and transport into the vessel wall. The 2020 European Atherosclerosis Society mechanistic paper addresses processes beyond passive cholesterol accumulation. A fuller model of cardiovascular disease incorporates more than increasingly intensive LDL reduction. [15]

References

1. [00:22] Evolocumab and Clinical Outcomes in Patients with Cardiovascular Disease — https://doi.org/10.1056/NEJMoa1615664
2. [00:27] The impact of carbohydrate restriction-induced elevations in low-density lipoprotein cholesterol on progression of coronary atherosclerosis: the ketogenic diet trial study design — https://doi.org/10.1097/MCA.0000000000001395
3. [00:39] Stay Off My Operating Table — https://ifixhearts.com/books/somot/
4. [00:40] Stay Off My Kitchen Table — https://ifixhearts.com/books/somkt/
5. [01:12] Increased low-density lipoprotein cholesterol on a low-carbohydrate diet in adults with normal but not high body weight: A meta-analysis — https://doi.org/10.1016/j.ajcnut.2024.01.009
6. [01:17] Dietary Guidelines for Americans, 2025–2030 — https://realfood.gov/guidelines
7. [01:21] Food in the Anthropocene: the EAT-Lancet Commission on healthy diets from sustainable food systems — https://doi.org/10.1016/S0140-6736(18)31788-4
8. [02:20] The Case Against Sugar — https://www.penguinrandomhouse.com/books/213737/the-case-against-sugar-by-gary-taubes/
9. [02:21] Good Calories, Bad Calories — https://www.penguinrandomhouse.com/books/176680/good-calories-bad-calories-by-gary-taubes/9781400033461/
10. [03:00] Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies — https://doi.org/10.1093/eurheartj/ehx144
11. [03:02] RETRACTED: Longitudinal Data From the KETO-CTA Study: Plaque Predicts Plaque, ApoB Does Not — https://doi.org/10.1016/j.jacadv.2025.101686
12. [03:32] Carbohydrate Restriction-Induced Elevations in LDL-Cholesterol and Atherosclerosis: The KETO Trial — https://doi.org/10.1016/j.jacadv.2024.101109
13. [03:43] Ketogenic diets, not for everyone — https://doi.org/10.1016/j.jacl.2020.10.005
14. [03:45] Elevated LDL Cholesterol with a Carbohydrate-Restricted Diet: Evidence for a Lean Mass Hyper-Responder Phenotype — https://doi.org/10.1093/cdn/nzab144
15. [03:54] Low-density lipoproteins cause atherosclerotic cardiovascular disease: pathophysiological, genetic, and therapeutic insights — https://doi.org/10.1093/eurheartj/ehz962

From carbohydrate orthodoxy to low-carbohydrate eating

• Noakes's Lore of Running taught carbohydrate loading, while Waterlogged addressed excess drinking and exercise-associated hyponatremia. Dulaney began long-distance running using those guidelines. [1][2]
• A recent paper coauthored by Noakes and Andrew Koutnik centers the endurance benefit of carbohydrate on maintaining blood glucose during exercise, rather than replenishing depleted muscle glycogen; Dulaney subsequently changed her fueling. [3]
• Noakes grew up eating meat, fish, and farm foods in Zimbabwe, adopted the low-fat advice from his 1970s medical training, switched to grains, and subsequently gained weight and developed insulin resistance.
• Swedish muscle-biopsy research in 1967 shifted endurance physiology from liver glycogen and blood glucose toward muscle glycogen depletion; Noakes taught that model for decades. [4]
• Bruce Fordyce recovered his pace late in the Comrades Marathon after drinking Coca-Cola with added sugar; Noakes subsequently introduced glucose polymers to his regimen and helped develop an early endurance carbohydrate gel with Bernard Rose.
• Industry funding supported sports-drink research, while advice to drink heavily coincided with exercise-associated hyponatremia. Noakes's research connected dangerous cases with overhydration, preceding his departure from prevailing fueling and hydration guidance. [5]
• After an unusually exhausting short run, Noakes read The New Atkins for a New You, revised his nutrition advice after 33 years, and switched to a low-carbohydrate, high-fat diet in 2010. [6]
• Noakes has maintained that diet for about 16 years, identifies his type 2 diabetes as being in remission though not fully normalized, and connects his personal risk to his father's severe diabetes and early death.

Dulaney's parallel path through endurance sport and plant-based eating

• Dulaney expected that remaining lean through marathons, Ironman races, and ultramarathons would protect her from her family's diabetes and heart-disease history; abdominal fat and symptoms accumulated despite extensive running.
• Carbohydrates before running triggered recurring shakiness and sweating, while gels coincided with repeated energy highs, crashes, nausea, and difficulty continuing without additional sugar.
• She initially rejected Noakes's low-carbohydrate approach and adopted a low-fat plant-based diet based on the idea that removing dietary fat could prevent insulin resistance.

Banting, institutional resistance, and the hearing

• Two runners who traversed the Great Wall of China ate pork fat when food was scarce; their experience helped initiate The Real Meal Revolution, which popularized the high-fat, low-carbohydrate Banting diet in South Africa. [7]
• After a parliamentary official publicly requested Noakes's autograph, university leaders criticized his diet advocacy; Noakes connected their opposition with grain and nutrition interests.
• Dietitians objected as patients rejected low-fat advice. A general tweet recommending low-carbohydrate, high-fat eating for children became the basis of a professional-misconduct complaint, without individualized advice to a specific mother.
• Noakes's former colleagues and the Health Professions Council of South Africa assembled a case against him amid opposition to departures from established nutrition guidelines.
• With pro bono legal assistance, Noakes underwent a 28-day hearing, spent nine days giving evidence and three days under cross-examination, and was ultimately found not guilty; the defense involved two years of intensive nutrition research.
• Lore of Nutrition emerged from that research and disciplinary process; Nina Teicholz and Zoë Harcombe supported the defense, and Dulaney used Teicholz's The Big Fat Surprise to reexamine low-fat dietary advice based on observational studies, selective evidence, and entrenched assumptions. [8][9]

Changes in Dulaney's practice and nutrition

• After a difficult 50-km race fueled by gels, Dulaney completed another 50-km race using small, regularly timed carbohydrate amounts, maintained her pace without bonking, and experienced little soreness the following day; Koutnik linked the reduced soreness to less glucose-related inflammation.
• Koutnik's explanation of insulin as a storage hormone led her to investigate whether repeated gels and high-carbohydrate meals reduced access to stored body fat.
• Her wellness practice followed fewer than 200 patients and taught low-calorie plant-based cooking; some patients initially lost weight, but she did not achieve complete diabetes remission with that dietary approach.
• Lean patients also developed abdominal fat, rising HbA1c, frequent hunger, post-meal sleepiness, and digestive symptoms; thinness and the absence of heart attacks coexisted with other metabolic concerns.
• Reducing carbohydrate on a plant-based diet also reduced protein from legumes and grains, leading her to reintroduce eggs, fish, and other animal foods after family and practice consultations.
• After reading Michael Crawford's work on DHA and the brain, she measured omega-3 profiles in herself, relatives, and patients, found very low DHA, and introduced fish or supplements to address limited conversion from flax, chia, or hemp ALA.
• Dulaney initially used Noakes's Banting green/yellow/orange/red food lists as a starting guide for patients while her own approach developed.

CGM observations during running and ultramarathons

• Continuous glucose monitoring showed that Dulaney's shaky symptoms after carbohydrates began as glucose fell from a peak, without a measured glucose low.
• She completed 267 miles over 16 days, averaging about 17 miles daily, consuming almost no carbohydrate beyond traces in an electrolyte drink, with steady energy and little cumulative soreness.
• Despite years of extensive running, fasting glucose increased to roughly 103–105 mg/dL; HbA1c reached 5.9% with insulin of 4.9, and she eventually reduced carbohydrates to under 10 g daily.
• During a 100-mile race lasting 33 hours, she consumed some carbohydrate, including a cheeseburger bun, and CGM peaks increased from about 150 to above 200 mg/dL, returning toward baseline roughly eight hours after finishing.
• Without food, morning five- or six-mile runs elevated CGM glucose to 130–150 mg/dL, occasionally 180 at higher heart rates, with one to two hours to settle; heat and greater effort coincided with larger rises.

The liver, insulin resistance, and carbohydrate balance

• Exercise-associated glucose increases can result when liver glucose output exceeds muscle uptake; glucagon, cortisol, epinephrine, and exercise intensity are possible contributors.
• Slower exercise has reduced Noakes's glucose spikes; greater exertion can coincide with increased glucose in an insulin-resistant person, although the specific mechanism is unresolved.
• Ben Bikman's alpha-cell insulin-resistance hypothesis involves abnormal glucagon release, which could explain the glucose rises and can be tested through direct glucagon measurements.
• Noakes and Philip Prins are developing a carbohydrate-balance model: daily carbohydrate is oxidized or stored, and glycogen-filled muscles are associated with higher insulin, carbohydrate oxidation, and reduced fat oxidation; related hypotheses had existed in 1970s–1980s research.
• Muscle and liver glycogen are repeatedly used rather than permanently retained; Dulaney's very-low-carbohydrate intake and regular running make excess muscle glycogen an insufficient explanation for persistent glucose spikes.
• A recent randomized comparison of ketogenic, Mediterranean, and very-low-fat plant-forward diets found the largest reductions in liver fat, de novo lipogenesis, and impaired hepatic glucose regulation with ketogenic eating at comparable weight loss. [10]
• Years of high carbohydrate intake can increase liver fat production and insulin resistance, with ketogenic eating producing the greatest hepatic improvements among the three diets.
• Dulaney suspects that some very thin long-term plant-based advocates have elevated insulin and reduced muscle; Noakes concurs that normal-range HbA1c alone cannot settle this question.
• Brain activity and stress also affect glucose control: Noakes's fasting CGM readings rose from about 5.2 to 6.2 mmol/L during a stressful period, then returned over roughly a week.

Protein, dietary fat, and ketone responses

• Dulaney, weighing about 113 pounds, consumes roughly 100 g protein daily and questions whether her protein-to-fat ratio contributes to elevated glucose despite minimal carbohydrate intake.
• Noakes experiences gradual glucose rises after protein-rich meals and invokes the nearly all-fat diets used for type 1 diabetes before insulin availability as historical examples of dietary glucose control.
• Dulaney observes a steadier glucose trace with sardines packed in oil than with less-fatty foods and experiments with greater fat relative to protein.
• Dulaney's blood ketones are often around 0.4–0.5 mmol/L in the morning and sometimes about 1.4 later; Noakes links low readings during exercise to greater ketone use and experiences higher levels with fasting and exercise.
• An exogenous ketone drink lowered Noakes's glucose by roughly 1 mmol/L; Dulaney used exogenous ketones during her 100-mile race without her familiar shaky or sleepy symptoms and observed a downward afternoon glucose trend during later use.
• Both favor testing exogenous ketones when glucose remains elevated during carbohydrate restriction, with metabolic responses varying between individuals.

Body weight, ultramarathon fueling, and ongoing work

• Dulaney's calorie-restricted plant-based approach did not produce weight loss in her severely obese patients; some patients with previously stalled weight loss are now losing weight after dietary changes.
• Substantial weight-loss cases included approximately 100 pounds in one year and 80 kg in 28 weeks for a man in Cape Town, demonstrating the magnitude of the observed changes.
• For an upcoming 100-mile race, Noakes advises that dietary fat need not be carried as exercise fuel: stored body fat supplies muscle energy, while carbohydrate during prolonged exercise serves mainly to maintain brain-accessible blood glucose.
• Ketone adaptation can increase tolerance of lower glucose without symptoms, while eating during a race can also address hunger, comfort, and morale; Arthur Newton's mid-race meals and the runners' late-race meals serve as examples.
• Collaboration with Andrew Koutnik and Philip Prins sustained Noakes's research career and the Noakes Foundation's educational work, while the dietary change renewed Dulaney's clinical practice.

References

1. [00:00] Lore of Running — https://us.humankinetics.com/products/lore-of-running-4th-edition?variant=12335071690813
2. [00:00] Waterlogged: The Serious Problem of Overhydration in Endurance Sports — https://us.humankinetics.com/products/waterlogged-epub
3. [00:01] Carbohydrate Ingestion on Exercise Metabolism and Physical Performance — https://doi.org/10.1210/endrev/bnaf038
4. [00:04] Diet, Muscle Glycogen and Physical Performance — https://doi.org/10.1111/j.1748-1716.1967.tb03720.x
5. [00:07] Water Intoxication: A Possible Complication During Endurance Exercise — https://doi.org/10.1249/00005768-198506000-00012
6. [00:08] The New Atkins for a New You — https://www.simonandschuster.com/books/The-New-Atkins-for-a-New-You/Dr-Eric-C-Westman/Atkins/9781439190272
7. [00:14] The Real Meal Revolution — https://www.quivertreepublications.com/product/the-real-meal-revolution/
8. [00:21] Lore of Nutrition: Challenging Conventional Dietary Beliefs — https://thenoakesfoundation.org/lore-of-nutrition-out-now/
9. [00:22] The Big Fat Surprise — https://www.simonandschuster.com/books/The-Big-Fat-Surprise/Nina-Teicholz/9781451624434
10. [00:41] Effect of Diet Macronutrient Content on the Cardiometabolic Response to Weight Loss: A Randomized Clinical Trial — https://doi.org/10.1016/j.cmet.2026.07.020

Bacon, nitrate and cancer

• Beetroot has about 40 times the nitrate of bacon; the cancer question concerns nitrosamines formed from nitrite.
• In a 1991 experiment, more than 4,000 rats drank nitrosamines for roughly 2.5 years and developed liver and oesophageal tumours. The lowest carcinogenic cumulative dose was about 9 mg/kg. [1]
• The "bacon equivalent" calculation equates the rat dose to 126,000 kg of bacon over 2.5 years for a 70 kg human, or 138 kg per day, far beyond ordinary intake.
• Rats are unusually sensitive to these nitrosamines: mice and hamsters needed about five times the exposure, and human liver DNA-repair activity is about 8-10 times higher than in rats. Endogenous nitrosamine production is equivalent to roughly 200 kg of bacon daily; credible evidence of nitrosamine-caused human cancer is lacking.
• "No added nitrate" bacon commonly uses celery powder, whose nitrate is converted by added bacteria such as Staphylococcus into nitrite; the resulting curing chemistry is the same as conventional bacon.
• Oral bacteria convert salivary nitrate into biologically active nitrite that helps lower blood pressure; antibacterial mouthwash may disrupt that pathway.
• Nitrosamine exposure from bacon can be reduced with ventilated cooking below about 160°C, including air frying, and by discarding rendered grease, where they concentrate. Many evaporate during cooking; microwaving is another option.
• A 2007 study of 27 ileostomy patients found that adding 1 g vitamin C or vitamin E during red/processed-meat feeding did not significantly reduce measured N-nitroso compounds in ileal output. American bacon already requires added antioxidants such as vitamin C. [2]

Vitamin C, organ meat and the historical meat-only experiment

• Meat contains vitamin C, particularly organ meat. In the 1953 Sheffield vitamin-C deprivation experiment with about 20 people, 10 mg daily prevented or reversed scurvy; intake recommendations are higher: initially 30 mg, now 45 mg in Australia and 90 mg for US men or 75 mg for women. [3]
• About 40 g pork liver or 43 g lamb liver supplies 10 mg vitamin C; spleen and lung are richer still, while obtaining that much from muscle meat could need up to 1 kg. A modest quantity of offal increases vitamin C intake on carnivore.
• Vilhjalmur Stefansson lived with Arctic peoples for 11 years and said he spent more than five years eating only meat and water; contemporary physicians expected meat-only diets to cause scurvy, kidney damage, hypertension and other disease.
• In a supervised follow-up, Stefansson ate only meat for 375 days and Karsten Andersen for 367, initially under hospital observation and subsequently monitored through ketones. No vitamin deficiencies or kidney deterioration emerged; Andersen's blood pressure went from 140/80 to 120/80. [4]
• Their diet included liver, kidney, brain, marrow and substantial fat, not just lean muscle. Roughly 40 g of liver daily could supply the minimum vitamin C needed to avoid scurvy alongside other animal foods.
• During a lean-meat phase of the experiment, Stefansson developed weakness, nausea and diarrhoea within a week, then recovered rapidly when fat was restored. On modern carnivore diets, inadequate fat can contribute to diarrhoea; increasing fat has helped some patients. [4]
• Higher-fat carnivore choices include 18-20%-fat mince, marbled or fattier cuts with fat retained, and tallow or lard added to leaner foods.
• Amber O'Hearn connects vitamin C-dependent carnitine synthesis with dietary meat carnitine, potentially reducing the need for vitamin C in that pathway. Animal experiments also connect carnitine deficiency with fatigue and weakness resembling some scurvy symptoms.
• Vitamin C also functions as an antioxidant, and meat provides other antioxidants such as B12. In a 1993 guinea-pig experiment without vitamin C, controls died at 21-22 days, whereas animals given glutathione ester survived to day 40, indicating that other antioxidants can affect outcomes during deficiency. [5]
• Vitamin C blood samples degrade rapidly without proper collection and transport; falsely low laboratory results can therefore occur.
• Scurvy on ketogenic diets is possible: published cases involve children with epilepsy or autism on restricted, inadequately supplemented diets. Vitamin C intake depends on diet composition, organ foods and fresh-meat juices; adequate vitamin C cannot be assumed for every keto or carnivore diet. [6][7][8]

HbA1c, glucose spikes and insulin physiology

• Blood donation can lower measured HbA1c by increasing the proportion of young red blood cells, even without lower glucose, because HbA1c depends on glucose exposure over each cell's roughly 120-day lifespan.
• Reticulocyte counts assess red-cell turnover, and two stable haemoglobin measurements four to six weeks apart help determine whether changing cell production affects HbA1c.
• Glucose falling from about 15 to below 5 mmol/L after three days of low-carbohydrate, one-meal-a-day eating is plausible for blood glucose but not as an equivalent three-day HbA1c reversal; glucose can change rapidly with fasting and carbohydrate restriction.
• Insulin and sulfonylurea use requires medical supervision during major carbohydrate restriction or fasting because unchanged doses can cause dangerous, potentially fatal hypoglycaemia.
• An active viewer has HbA1c around 5.5%, normal fasting glucose and a 12-15 mmol/L rise after a sandwich. A slice of bread contains roughly 15 g carbohydrate whereas circulating blood holds only about 4-5 g glucose; post-meal insulin responses are relevant even with normal fasting values.
• Weight gain alongside these spikes can fit insulin resistance, where muscle and liver respond poorly to insulin but adipose tissue still stores energy. High glucose with inadequate insulin can indicate insulin deficiency, including autoimmune diabetes, often associated with weight loss.
• A Kraft-style oral glucose-tolerance test measuring insulin alongside glucose separates high-insulin resistance from low-insulin production. Some people diagnosed with type 2 diabetes have an autoimmune component and may need insulin even with ketogenic eating.
• A 2013 study followed about 400 nondiabetic Japanese Americans for around 10 years: those whose insulin peaked at 30 minutes had 3.2% diabetes incidence versus 47.8% when it peaked at 120 minutes, roughly a twelvefold adjusted odds ratio. [9]
• Continuous glucose monitors are useful for relative rises and recovery patterns but can be unreliable for absolute glucose, so finger-prick testing helps confirm readings. A brief rise to about 8 mmol/L after oatmeal differs from a prolonged elevation.
• Spike size depends on portion, muscle mass, exercise, glycogen reserves, gastric emptying and food order; one reading cannot identify the mechanism by itself.

Diet shifts and liver enzymes

• A viewer moved from carnivore to vegan after unfavourable bloodwork. Higher carbohydrate consumption may increase triglycerides and ALT, while dietary change alone cannot explain every illness or laboratory abnormality.
• Carnivore eating does not eliminate infections or other causes of symptoms and abnormal tests.
• Elevated ALT need not always result from fatty liver or damaged liver cells. Excess glucose metabolism can increase mitochondrial pyruvate, conversion to alanine and ALT activity; elevated ALT has occurred in some vegan patients.

Uric acid, ketosis and gout

• A viewer on carnivore for 18 months reduced allopurinol, then saw uric acid rise from 299 to around 600 without another gout attack. High urate alone is not the same as symptomatic gout.
• During ketosis, renal ketone clearance competes with urate excretion, potentially increasing blood urate; the rise can settle over roughly four to six weeks, with individual variation.
• In a 2019 12-week ketogenic-diet study of 35 overweight or obese adults, uric acid moved downward by the end of the intervention. High urate during carnivore eating has not necessarily coincided with gout attacks in clinical observations. [10]

Dental infection and unexplained IgE elevation

• A patient with otherwise unremarkable tests has elevated IgE and an abscessed tooth scheduled for extraction. A hidden dental infection may contribute to elevated IgE.
• In a 1984 dental-abscess investigation, IgE fell after dental intervention in seven of eight patients with before-and-after samples. [11]
• A 2019 pilot randomized study of 10 children aged 6-16 with gingivitis and dust-mite allergy compared periodontal scaling and root planing in five children with five controls; six months later IgE fell in all five who received the procedure. [12]
• A panoramic dental X-ray may find only about a third of occult infections; intraoral films around half and cone-beam CT about 90%. Cone-beam CT radiation is roughly three to six weeks of natural background exposure. The patient's IgE can be monitored after extraction.

Maternal anaemia and infant brain development

• An observational study of 394 South African mother-infant pairs used repeat MRI scans from three months to two years. Infants of anaemic mothers had brains about 4% smaller at 12 months and 6% smaller at 24 months; this association does not prove causation. [13]
• Iron contributes to brain development and synthesis of neurotransmitters such as dopamine and serotonin; trials in selected groups have linked iron supplementation to higher IQ. Anaemia can also arise through B12 deficiency, which affects neurological development.

Antifungal therapy in inflammatory bowel disease

• A 2026 study compared oral nystatin with systemic fluconazole for patients with Crohn's disease or ulcerative colitis and oral Candida albicans; the fluconazole group had more favourable microbiome changes and some improvement in bowel disease activity. [14]
• Nystatin and amphotericin B are poorly absorbed and usually act locally, limiting systemic adverse effects. Fluconazole acts systemically and may be used more often in patients with both inflammatory bowel disease and Candida, with systemic adverse-effect potential.
• The study compared nystatin with fluconazole, not a combination. Combining topical and systemic drugs may be feasible without evident harm, but the study did not evaluate that approach.
• Azoles inhibit fungal ergosterol synthesis and can interfere with human cholesterol synthesis. Dietary cholesterol absorption continues; cholesterol-rich foods such as prawns and eggs are used alongside fluconazole in this practice, with fewer observed side effects, without providing fungal ergosterol.
• Blood LDL measurements concern lipoprotein particles containing cholesterol, other lipids and proteins, not isolated cholesterol molecules; LDL and cholesterol are distinct entities.

Video-production clarification

• Both speakers are real people. Riverside software uses AI eye-contact correction when speakers look at one another on screens rather than the camera; this enhancement may make their faces look artificial.

References

1. [01:24] Effects on 4080 Rats of Chronic Ingestion of N-Nitrosodiethylamine or N-Nitrosodimethylamine: A Detailed Dose-Response Study — https://aacrjournals.org/cancerres/article/51/23_Part_2/6415/497270/Effects-on-4080-Rats-of-Chronic-Ingestion-of-N
2. [08:14] The effect of haem in red and processed meat on the endogenous formation of N-nitroso compounds in the upper gastrointestinal tract — https://doi.org/10.1093/carcin/bgl192
3. [10:36] The Sheffield Experiment on the Vitamin C Requirement of Human Adults — https://doi.org/10.1079/PNS19530054
4. [14:46] Clinical Calorimetry: XLV. Prolonged Meat Diets with a Study of Kidney Function and Ketosis — https://doi.org/10.1016/S0021-9258(18)76842-7
5. [22:52] Glutathione ester delays the onset of scurvy in ascorbate-deficient guinea pigs — https://doi.org/10.1073/pnas.90.1.317
6. [25:12] Case report: scurvy in an epileptic child on a ketogenic diet with oral complications — https://doi.org/10.1007/BF03262627
7. [25:12] No Longer A Historical Ailment: Two Cases of Childhood Scurvy with Recommendations for Bone Health Providers — https://doi.org/10.1007/s00198-019-05264-4
8. [25:12] Florid Scurvy in an Autistic Child on a Ketogenic Diet — https://doi.org/10.1097/PEC.0000000000001695
9. [38:24] Patterns of Insulin Concentration During the OGTT Predict the Risk of Type 2 Diabetes in Japanese Americans — https://doi.org/10.2337/dc12-0246
10. [49:25] Weight loss, improved physical performance, cognitive function, eating behavior, and metabolic profile in a 12-week ketogenic diet in obese adults — https://doi.org/10.1016/j.nutres.2018.11.007
11. [52:47] Concentrations of Immune Complexes, IgG, IgM, IgE, and C3 in Patients with Acute Apical Abscesses — https://doi.org/10.1016/S0099-2399(84)80262-9
12. [53:13] Effect of scaling and root planing on level of immunoglobulin E and immunoglobulin G4 in children with gingivitis and house-dust mite allergy: A pilot randomised controlled trial — https://doi.org/10.1142/S2214607519500020
13. [56:33] Antenatal maternal anaemia and infant brain structure: high-field (3 T) and ultra-low-field (64 mT) MRI findings from South Africa — https://doi.org/10.1093/braincomms/fcag318
14. [59:06] Antifungal therapy improves microbiome dynamics in inflammatory bowel disease — https://doi.org/10.1038/s41591-026-04616-y

From plant-based eating to carnivore

• Judy ate plant-based for 12 years, developed an eating disorder and severe depression, and attributed these problems to stress and weight concerns rather than food.
• Following her first child, a breakdown led to an involuntary psychiatric hold and memory loss; antidepressants and antipsychotics stabilized her behavior before her memory returned.
• The recovery center offered therapy and coping skills but permitted plant-based eating while prohibiting low-carb diets, reinforcing her belief that food was not the problem.
• She investigated her brother's butter-heavy ketogenic diet expecting heart risks, then tried plant-based keto with olive and avocado oils, with only limited improvement.
• Sweet foods, including artificially sweetened foods, still triggered binge cycles; during a severe episode she decided to try the all-meat diet a friend had mentioned.
• After two weeks on carnivore, her urge to binge and constant food noise disappeared; therapy remained necessary for changing emotionally driven food habits.
• She regretted years lost to illness, studied nutrition for her sons and encountered Weston A. Price and saturated-fat teachings that changed her earlier views.
• Her management-consulting experience became carnivore pyramids and portion infographics intended to help people with mental illness or disordered eating avoid prolonged suffering.

Nine years of recovery, skepticism and medication

• Her husband initially feared meat-related heart disease but became convinced as her secret bingeing, nighttime eating and withdrawal from parenting ended; she has eaten this way for nearly nine years.
• Others praised her when she was extremely thin and plant-based yet questioned her healthier look over fiber and cholesterol; one supportive person can help sustain dietary change.
• Being available to her children motivated her dietary change, and helping others with chronic illness became her purpose as her health improved.
• She received high-dose Zoloft and antipsychotics including Zyprexa and Rexulti; fear of weight gain led her to stop the antipsychotics, and she later tapered Zoloft herself.
• Her family observed emotional flattening on Zoloft, with less happiness and sadness despite greater outward mood stability.

Eating-disorder care and the medical model

• Her eating-disorder program required three meals, two snacks plus an at-home snack, and processed sugary challenge foods after meals; refusing these foods was classified as disordered behavior.
• She believes frequent processed carbohydrates and sweets aggravated blood-sugar fluctuations and anxiety, with additional psychiatric drugs sometimes used for persistent distress.
• She favors meat and ketones for stable nourishment and mood, links THC-related anandamide in fatty red meat with calming effects, and regards psychological work as necessary for emotional food coping.
• Her psychiatrist dismissed diet as a factor and focused on prescriptions; she worries about medication-centered incentives, adverse effects and antidepressant withdrawal difficulties.
• Patient education about bodily warning signals is central to her approach; medication can relieve symptoms without resolving the underlying imbalance.
• She attributes nutritional deficits and gut dysfunction, mood disturbances and intensified food-seeking to plant-based eating, with medication addressing the symptoms.

Building a practice beyond diet alone

• Carnivore Cure [1] grew from questions about fiber, vitamin C, plant antinutrients and glyphosate; her subsequent coaching developed into functional-medicine work.
• Therapy helped her connect poor boundaries with family and work to comfort eating, making behavioral change and nervous-system regulation parts of recovery.
• Empower Functional Health begins with carnivore to reduce processed foods, seed oils and potentially reactive plants and to supply absorbable animal nutrients before pursuing other causes.
• The Carnivore Elimination Protocol [2] serves as a starting point; persistent symptoms prompt further examination of the gut, environmental exposures and mind-body factors.
• Her first check when progress stalls is adequate intake: strong satiety on carnivore can mask under-eating, with thyroid and other hormonal problems emerging after roughly three to six months in her experience.
• Half a pound of meat for an entire day may be insufficient; she sometimes eats another half-pound and plentiful fat at dinner despite lacking hunger.
• With adequate intake, her team investigates small intestinal bacterial or fungal overgrowth and other illnesses while retaining carnivore or mostly meat as the dietary foundation.

Inflammation, environment and stress physiology

• Inflammation Fix [3] draws on experience with thousands of clients, from four-month-old infants to people in their 90s, and prioritizes major drivers of persistent illness over minor biohacks.
• Its foundation is personal health education: acute inflammation is useful, but chronic inflammation can persist, and food, immune function and toxins interact.
• Carnivore elimination is a possible healing phase without mandatory lifelong strictness; bowel movements, waste removal, mold, Epstein-Barr, Lyme, heavy metals and parasites are additional areas.
• The hypothalamus coordinates thyroid signaling through TRH, TSH and T4/T3 and stress signaling through CRH, ACTH and cortisol, linking stress with hormones and autonomic responses.
• Blood-sugar problems, environmental irritants, difficult work and relationships can sustain stress signaling; undernourishment can lead the body to use its own tissues for survival.
• Rumination about danger without an immediate threat can trigger physical fight-or-flight responses; she views many thyroid and sex-hormone problems as downstream effects of ongoing stress or inflammation.
• Similar thyroid problems in families may involve shared diets and stress patterns alongside genetics; small changes involving pepper or coffee may be less consequential.
• The book aims to help people navigating conflicting specialist and online advice identify larger causes of persistent illness through knowledge of their bodies.

Conventional medicine and connected body systems

• Judy's anger at doctors softened through clinical collaboration; brief visits, debt and specialty divisions burden well-meaning clinicians, and she believes physicians have the highest occupational suicide risk.
• Brain, gut, heart and lung functions interact: salivation at the sight of food and stress-related blood-pressure increases illustrate connections that isolated specialties may overlook.
• Asthma inhalers can relieve immediate symptoms, but she worries about black-box warnings for some inhalers, bone and childhood growth effects, and steroid-related glucose problems when causes go unexplored.
• Symptom relief can be temporary, like covering a crack in a wall; identifying what caused the problem may require examining food and environmental triggers.

Starting carnivore and sustaining change

• Phase one of her strictest elimination protocol is beef, salt and water, but the starting method depends on individual personality and sustainable adherence.
• Abrupt carbohydrate removal suited her all-or-nothing tendencies; gradual reduction and temporary inclusion of manageable foods may suit a more moderate eater.
• For someone keeping blueberries, she might place half a cup after a one-pound steak to reduce the glucose effect relative to eating the berries first.
• Beginners can start with enjoyable meats, including convenient beef sticks, reduce carbohydrates promptly and refine meat quality and fat intake after establishing a stable routine.
• Consistent, less-strict carnivore is preferable to five strict days followed by two off-plan days; symptom changes and personal knowledge guide decisions while preserving individual authority over health.

References

1. [23:36] Carnivore Cure — https://carnivorecure.com/
2. [26:44] Carnivore Elimination Protocol — https://www.nutritionwithjudy.com/carnivore-cure-elimination-diet-cheat-sheet/
3. [30:06] Inflammation Fix — https://www.nutritionwithjudy.com/inflammation-fix/

Clinical mission — test medical dogma against patient outcomes

• Tro Kalayjian reached 350 lb and experienced fatigue and pain; calorie counting was ineffective. He lost 150 lb with ketogenic eating, reconsidered conventional nutritional guidance and shifted his career toward chronic metabolic disease remission.
• Kalayjian is an internal- and obesity-medicine physician, SMHP board member and Toward Health chief medical officer. The remote practice combines physicians, coaches, messaging, CGMs, connected scales, blood-pressure monitoring and individualized feedback, alongside general medicine, hormones, microbiome problems and cancer prevention.
• Disease remission and medication deprescribing are explicit clinical goals. Continuous care operates between visits through repeated support and monitoring, while published clinical observations enable wider clinical use.
• Institutional guidance is challenged through published observations that patients and clinicians can use when evaluating withheld care options. The studies were self-funded, conflicts and affiliations were disclosed, and one collaborator was employed by a pharmaceutical company.
• Two recent studies examine AHA PREVENT-estimated cardiovascular risk and strong LDL reductions after ezetimibe among ketogenic patients. [1][2]
• Other ketogenic clinical trials cover metabolic psychiatry, heart failure, weight loss and deprescribing, with further randomized results pending and a growing body of evidence.

Diabetes and triglycerides — metabolic improvement without major weight loss

• The ADA focused on weight loss for diabetes improvement. In early clinical cases, HbA1c decreased from about 12% to 6% after four months of ketogenic eating and intermittent fasting, all diabetes drugs were stopped, and weight loss was only a few pounds; glycemia improved before substantial weight loss. The early data received little interest from the ADA and were subsequently published. [3]
• The National Lipid Association warned against ketogenic diets in severe hypertriglyceridemia because high fat intake might elevate triglycerides and induce pancreatitis. The annual pancreatitis-risk estimates cited were 10% at 1,000 mg/dL and 50% at 5,000 mg/dL. [4]
• Carbohydrate restriction lowers insulin and fasting triglycerides. A two-patient series found severe triglyceride values around 800–1,000 mg/dL or higher decreasing below 200 mg/dL within weeks of ketogenic eating and intermittent fasting, contrary to that contraindication. [5]

Food addiction and binge eating — dietary change with psychological support

• Some psychiatrists and mental-health professionals associated restriction with worsening binge eating and equated keto or fasting with eating disorders. A 2020 case series found marked improvement in binge-eating and food-addiction symptoms when food addiction was still controversial. [6]
• In a larger 2025 TOWARD cohort of about 50 people, approximately 40% experienced significant food-addiction symptom improvement and 34% experienced binge-eating symptom improvement during carbohydrate-restricted continuous care. [7]
• The ketogenic care model combines coaching, group visits, biofeedback and psychological support. Its binge-eating improvement was similar in magnitude to published stimulant-drug effects; GLP-1 drugs may produce larger improvements, while underlying psychological concerns and nutritional adequacy remain important.
• Jen Unwin's low-carbohydrate and psychoeducational work found sustained food-addiction improvement at one year, with possible two-year follow-up. Nutritional and psychosocial care were combined. [8]

Durable weight loss — continuous care and medication reduction

• A six-month employer-wellness pilot published in 2022 was followed by a 2025 one-year study of 50 manufacturing employees. Average weight loss was 15.5%, similar in magnitude to semaglutide; unpublished 24-month clinic data showed nearly comparable weight loss. [9][10]
• At one year, 80% continued losing weight, 82% remained engaged and 92% had lost at least 5% of initial body weight. These results support an employer-based scalable continuous-care approach combining diet with ongoing clinical support. [10]
• About two medications per participant were stopped and eight were initiated across the cohort when needed. Medication management was individualized, with deprescribing an important outcome. [10]

PREVENT — the AHA's risk scorecard versus its dietary guidance

• The AHA placed ketogenic diets in the lowest dietary-alignment tier in 2023. The ranking assessed compatibility with nutritional guidance on grains, fruit and fats, not outcomes from a clinical trial of this care model. [11]
• The AHA introduced cardiovascular-kidney-metabolic (CKM) syndrome, which Kalayjian viewed as a renamed version of insulin resistance and metabolic syndrome, and called for disruptive CKM care models. The clinic evaluated its outcomes with the AHA risk calculator. [12]
• PREVENT estimates 10- and 30-year probabilities of total cardiovascular disease, ASCVD and heart failure in people without known cardiovascular disease. Inputs include age, sex, blood pressure, total and HDL cholesterol, kidney function, diabetes, smoking and BMI, with optional HbA1c, urine albumin and social deprivation. These are calculated probabilities, not observed cardiovascular events. [13]
• The intervention combined physician-led continuous care, remote monitoring, coaching, messaging, group support, specialized curricula, an app and AI-assisted clinical tools. Its ketogenic diet targeted fewer than 30 g of carbohydrate daily, limited grains, legumes, starches and fruit, favored animal proteins and fats, avoided seed oils and allowed olive oil, avocado oil, tallow, butter and coconut oil.
• The cohort included 120 employees enrolled in 2022–2023; 91 reached about one year, around 90 had paired 10-year estimates and 73 qualified for 30-year calculations. Mean age was 52, and the 30-year findings were still unpublished. [1]
• After one year, estimated 10-year total cardiovascular risk decreased 28%, ASCVD risk 29% and heart-failure risk 42%. These were relative changes in PREVENT risk calculations, not measured cardiovascular events. [1]
• The risk changes persisted in sensitivity analyses holding medication use, diabetes status, cholesterol or kidney function constant, consistent with changes across multiple metabolic measures. [1]
• Median weight decreased 12.2%, systolic blood pressure decreased 10.7%, HbA1c decreased 0.48 percentage points amid medication deprescribing, triglycerides also decreased and 13 participants achieved medication-free diabetes remission. [1]
• Across separate publications, the 29% estimated ASCVD-risk reduction was similar to one-year bariatric-surgery findings, compared with roughly 15% for statins or semaglutide and about 13% for DASH. These were indirect, non-head-to-head comparisons, while surgery entailed much greater expense and invasiveness. [14]
• The design was an observational before-and-after analysis, not a randomized dietary trial or a cardiovascular-events trial. The AHA PREVENT equations were applied to a ketogenic care model whose diet differs substantially from AHA guidance. [1]

LDL — two ways to manage ketogenic hypercholesterolemia

• LDL is a major unresolved issue in ketogenic diets. A Soto-Mota and Ludwig meta-analysis associated larger LDL increases with lower BMI, with stable or decreased LDL more common at higher BMI. [15]
• Earlier lean-mass hyper-responder research found that adding approximately 25–50 g of carbohydrate could substantially lower elevated LDL in some lean ketogenic patients, providing a dietary management option. [16]
• A non-statin LDL-lowering option was investigated for people continuing ketogenic eating, including those with high cardiovascular risk or difficulties with statins. The statin concerns included muscle and liver effects, mitochondrial function, insulin resistance and potentially reversible cognitive symptoms.
• Fourteen ketogenic patients with high cholesterol who used ezetimibe were examined, including 12 receiving monotherapy. Clinical assessments also included coronary calcium, genetic markers and cholesterol absorption or synthesis indicators such as campesterol, beta-sitosterol and lanosterol. [2]
• Median LDL decreased from about 254 to 127 mg/dL, approximately two to three times the usual manufacturer-listed response. HDL remained broadly stable, and triglycerides decreased slightly with uncertain causation. [2]
• Conventional genetic variants and sterol markers did not predict response. Low insulin increasing intestinal cholesterol absorption is a proposed mechanism for unusually large effects from ezetimibe's absorption blockade, not an established explanation. [2]
• Marked ketogenic LDL elevation was uncommon in the clinic and concentrated among very lean people or those with major weight loss. Modest carbohydrate reintroduction and ezetimibe were two potential LDL-management options. [2][16]

Closing thesis — make observations reproducible

• The studies form a strategy of publishing clinical findings to challenge established medical assumptions, improve disease remission and medication reduction, and expand options available for clinical evaluation.
• Other clinics can calculate PREVENT scores, examine ezetimibe responses, compare findings and publish results. The SMHP's Journal of Metabolic Health has published a therapeutic carbohydrate-reduction consensus guideline, and collaboration can expand the evidence base. [17]

References

1. [03:32] One-year change in PREVENT-estimated cardiovascular risk during telehealth metabolic care centered on a therapeutic ketogenic diet — https://doi.org/10.1016/j.ajpc.2026.102087
2. [03:35] Increased LDL-C reduction with ezetimibe in ketogenic diet-induced hypercholesterolemia — https://doi.org/10.1186/s12944-026-03034-w
3. [09:00] Treating Diabetes Utilizing a Low Carbohydrate Ketogenic Diet and Intermittent Fasting Without Significant Weight Loss: A Case Report — https://doi.org/10.3389/fnut.2021.687081
4. [09:51] Review of current evidence and clinical recommendations on the effects of low-carbohydrate and very-low-carbohydrate (including ketogenic) diets for the management of body weight and other cardiometabolic risk factors: A scientific statement from the National Lipid Association Nutrition and Lifestyle Task Force — https://doi.org/10.1016/j.jacl.2019.08.003
5. [10:42] Reversal of severe hypertriglyceridemia with intermittent fasting and a very-low-carbohydrate ketogenic diet: a case series — https://doi.org/10.1097/MED.0000000000000566
6. [11:52] Treating binge eating and food addiction symptoms with low-carbohydrate Ketogenic diets: a case series — https://doi.org/10.1186/s40337-020-0278-7
7. [12:47] TOWARD: a metabolic health intervention that improves food addiction and binge eating symptoms — https://doi.org/10.3389/fpsyt.2025.1612551
8. [14:39] Low carbohydrate and psychoeducational programs show promise for the treatment of ultra-processed food addiction: 12-month follow-up — https://doi.org/10.3389/fpsyt.2025.1556988
9. [15:13] A Company Is Only as Healthy as Its Workers: A 6-Month Metabolic Health Management Pilot Program Improves Employee Health and Contributes to Cost Savings — https://doi.org/10.3390/metabo12090848
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