I know, I KNOW, we are omnivores (you, me, maybe not our llm friends, but most of us)... but that doesn't quite line up with biological necessity.

I would argue we are facilitative omnivores, but obligate carnivores. We can eat plants for efficiency (famines and whatnot), but they are not necessary for life. Meat, however, is necessary - at the very least we would have b vitamin deficiencies without meat, and babies wouldn't develop into healthy humans without it.

People will argue, and i love you all for it, that maybe this applies historically but in the modern food environment we can engineer our way out of this obligation - sure, that's true, but when speaking of our species appropriate and native diet - we would still be obligate carnivores

 

As two physicians who have independently questioned many of the conventional recommendations surrounding nutrition and metabolic health, we have a fascinating conversation about what led us to rethink what we were taught in medical school and what the research actually tells us about the foods we eat. Dr. Berry shares his personal journey from struggling with obesity and prediabetes to discovering low-carb nutrition and the carnivore diet. We discuss the limitations of traditional diabetes dietary recommendations, the influence of food industry sponsorship on nutrition guidelines, and why so many doctors receive surprisingly little education about nutrition.

We also dig into some of the biggest controversies in nutrition, including plant-based versus animal-based diets, whether grains and carbohydrates are really necessary for optimal health, and what happens when we look beyond the headlines of published nutrition studies. We take a closer look at research involving plant-based diets and type 2 diabetes, the importance of sustainable dietary changes, and why calorie restriction and short-term improvements don't necessarily tell the whole story.

generated summary

Medical training and a failed conventional diet

  • Lies My Doctor Told Me [1] centers on nutrition advice repeated by physicians and the role of confirmation bias in making repeated dietary assumptions feel certain.
  • Dulaney moved from long-term plant-based cardiology toward carnivore eating after developing health problems, challenging entrenched dietary beliefs.
  • Berry graduated in 2000 after a half-semester nutrition class with 175 students; its predominantly plant-based instructor implied he had type 1 diabetes and used steel-cut oats and whole-grain pasta as examples of managing it.
  • Residency, emergency-room shifts and convenience food coincided with Berry reaching 297 lb and an HbA1c of 5.9, creating a conflict between his own health and the weight-loss advice he gave patients.
  • Ninety days of following an American Diabetes Association diet handout and jogging two or three times weekly coincided with an increase to 300 lb and an HbA1c of 6.1, motivating a change in dietary approach.
  • Robert Atkins's Diet Revolution, Mark Sisson's The Primal Blueprint and Loren Cordain's The Paleo Diet [2][3][4] introduced low-carbohydrate approaches absent from Berry's medical-school instruction.

Plant-based beliefs and medical authority

  • Berry's earlier diet was roughly 70–85% plant-based, with lean meat, reduced-fat dairy and fewer egg yolks. He also promoted blueberries as having "magic in plants" despite lacking evidence for that belief.
  • A couple planted three blueberry bushes after Berry's community lecture, an example of nutrition advice affecting patient behavior even without a scientific basis.
  • Dulaney's former plant-based diet was influenced by animal welfare, John Robbins's Diet for a New America [5], saturated-fat concerns and fears of animal-derived toxins. Her household garden did not produce enough vegetables to sustain her.
  • Food-industry sponsorship of nutrition organizations adds a source of bias to conventional dietary guidance.
  • Presumed comprehensive medical expertise is the central misconception: physicians lack complete nutrition and health knowledge, while strong patient trust can contribute to harmful advice.
  • Medical instruction contains errors and uncertainty, captured by Berry's professor warning that half of the instruction could be wrong; clinical knowledge requires revision and candor about gaps.
  • Nutrition research spanning archaeology, anthropology and non-English scientific literature expands the evidence available beyond English-language dietary research.
  • USDA food-composition data [6] list zero vitamin C for red meat, in some cases by assumption, while Nordic, Japanese, European and British tables include roughly 1–3 mg in a substantial meat serving; extensive cooking reduces this amount.
  • Medical professionals have an obligation to investigate nutrition evidence before giving confident advice; false answers delivered in professional practice can constitute "lies".

Grains, family history and food identity

  • Grains are used to fatten farm animals yet are widely perceived as wholesome human staples, embedded in family customs, poverty diets, religion and inherited beliefs.
  • Berry's great-grandmother lived mainly on cornbread and beans and died of pellagra, a B-vitamin deficiency, despite her community's positive view of that homegrown diet.
  • Dulaney previously attributed her grandmother's diabetes to lard while giving less attention to bread, dumplings and sugar, illustrating the selectivity of dietary beliefs.
  • The effects of Esselstyn's plant-based cardiac program cannot be isolated from accompanying changes in smoking, exercise and body weight; the effects of kale alone remain uncertain.

Diabetes research, hunger and sustainability

  • A 24-week randomized trial involving Brenda Davis combined a whole-food plant-based diet with provided meals, exercise and classes during the first 12 weeks; weight and HbA1c improved during the early phase [7].
  • By week 24, early changes in glucose, insulin, HOMA-IR and cholesterol were no longer maintained. Animal products and junk food returned as eating became less restricted, with hunger and renewed satiety central to the explanation.
  • Hunger and eating until full are normal physiological functions; wild mammals eat their typical diets to satiety. Restricting intake can cause short-term weight loss but is difficult to maintain with persistent hunger.
  • Ancel Keys's Minnesota starvation experiments documented food fixation and psychological distress during sustained underfeeding; energy restriction can temporarily reduce body weight and blood glucose [8].
  • Virta Health's five-year ketogenic diabetes follow-up included ongoing participation, weight loss and reduced diabetes medication with carbohydrate restriction [9].
  • Dulaney sought an egg-like sandwich made from tofu during her plant-based years; animal-food imitations can coexist with cravings for familiar animal foods and their nutrients.

Surrogate cholesterol outcomes and coronary interventions

  • Short-term reductions in cholesterol on a Portfolio Diet do not establish long-term effects on mortality or heart attacks; LDL and total cholesterol are surrogate outcomes.
  • Stent placement is influenced by clinical practice and procedural incentives, limiting its value as a health outcome. Sham-controlled stenting trials [10] subsequently tested benefits of coronary intervention; earlier preventive stenting could include 30–50% blockages.
  • Bypass grafts on moderately narrowed arteries can fail, and a high number of bypass grafts or stents does not necessarily indicate full resolution of coronary disease.
  • In a recent three-diet trial covered by JAMA, a ketogenic diet reduced liver fat and improved metabolic measures more than Mediterranean and very-low-fat plant-forward diets at similar weight loss [11]. Carbohydrate intake, not dietary fat, is the central dietary explanation for fatty liver here.

Lipid panels, HbA1c and individual physiology

  • Dulaney's total cholesterol rose from approximately 180 to 315 and then 407 mg/dL after adopting a very-low-carbohydrate, meat-heavy diet; her LDL was 278, HDL 125 and triglycerides 52, consistent with a lean-mass hyper-responder pattern.
  • A 10-year ApoB–HDL cardiovascular-risk study [12] linked higher HDL with a weaker association between elevated ApoB and cardiovascular events, supporting combined interpretation of HDL, triglycerides and ApoB.
  • Low triglycerides, high HDL, fasting insulin near 3–7, HbA1c below 5.7 and normal hs-CRP form a metabolic profile in which ApoB, LDL and total cholesterol carry little risk significance.
  • Dulaney's HbA1c remained 5.9 with fasting glucose around 110, insulin 3, C-peptide near 1 and negative autoimmune diabetes antibodies, a pattern inconsistent with adult-onset autoimmune diabetes.
  • Glycated albumin tests were no longer available through Berry's laboratories, while Dulaney's fructosamine was normal despite an elevated HbA1c.
  • Red blood cells normally circulate for roughly 110 days, and longer survival of about 115–125 days, potentially from less cell damage, could allow more glycation and a mildly elevated HbA1c in some lean carnivores even when fructosamine and insulin are low.
  • The dawn effect can temporarily increase glucose on waking through cortisol and adrenaline; checking glucose one or two hours later can yield a lower value.
  • Ketones differ between individuals and circumstances: Dulaney's rise with more fat or running, while Berry has values around 0.5–0.7 mmol/L after a three-day fast and his wife can exceed 2 after a brief meal delay. Isolated ketone or glucose readings are an incomplete metabolic picture.

References

  1. [01:03] Lies My Doctor Told Me — https://drberry.com/products/lies-my-doctor-told-me
  2. [07:26] Dr. Atkins' Diet Revolution — https://books.google.com/books/about/Dr_Atkins_Diet_Revolution.html?id=Cp-ozwEACAAJ
  3. [07:32] The Primal Blueprint — https://www.primalkitchen.com/pages/primal-blueprint
  4. [07:35] The Paleo Diet, Revised Edition — https://thepaleodiet.com/the-paleo-diet-revised-edition/
  5. [13:45] Diet for a New America — https://redwheelweiser.com/book/diet-for-a-new-america-9781932073546/
  6. [19:01] USDA FoodData Central — https://fdc.nal.usda.gov/
  7. [30:07] A whole-food, plant-based intensive lifestyle intervention improves glycaemic control and reduces medications in individuals with type 2 diabetes: a randomised controlled trial — https://doi.org/10.1007/s00125-024-06272-8
  8. [34:00] The Biology of Human Starvation (Volume I) — https://www.upress.umn.edu/9780816672349/the-biology-of-human-starvation/
  9. [34:33] 5-Year effects of a novel continuous remote care model with carbohydrate-restricted nutrition therapy including nutritional ketosis in type 2 diabetes: An extension study — https://doi.org/10.1016/j.diabres.2024.111898
  10. [38:01] Percutaneous coronary intervention in stable angina (ORBITA): a double-blind, randomised controlled trial — https://doi.org/10.1016/S0140-6736(17)32714-9
  11. [39:48] 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
  12. [41:47] Interplay of HDL cholesterol and apoB and the risk of incident atherosclerotic cardiovascular disease in UK Biobank — https://doi.org/10.1093/eurjpc/zwag400
 

generated summary

How I found carnivore and what changed

  • A friend's experience around 2017 led to interviews with Shawn Baker and Jordan Peterson on Joe Rogan, including Peterson's daughter Mikhaila's experience. Strict carnivore is a deeply ketogenic way of eating. [1][2]
  • Strict carnivore began in January 2020 at age 52. Within six months, weight fell by 65 lb, and borderline diabetes, severe ulcerative colitis, Hashimoto's thyroiditis, plantar fasciitis, and knee pain cleared; skin also looked younger.
  • Carnivore remained the usual diet, with occasional deviations. Chicken noodle soup containing vegetables could trigger a rapid colitis recurrence; grilled cheese caused glucose spikes on a continuous monitor and required four or five days of recovery.
  • This experience reversed an earlier preference for limiting red meat. Health biomarkers improved, with LDL cholesterol a possible exception, and strict adherence may slow some visible changes associated with aging.

The immune system, sugar, and chronic infection

  • Stanford bioengineering research on innate immunity, infection, Alzheimer's, and Parkinson's underlies a hypothesis linking chronic infection and immune dysregulation to autoimmune and neurological diseases. Human research connects Epstein-Barr virus with multiple sclerosis. [3]
  • Sugar drives inflammation and impairs innate immunity involving neutrophils, macrophages, and natural killer cells. A 1973 experiment found reduced neutrophil activity for roughly five hours after sugar ingestion; frequent carbohydrate intake could prolong impaired immune function. [4]
  • Impaired immunity allows persistent pathogen growth. Candida albicans proliferates with sugar and may support anaerobic bacteria such as Porphyromonas gingivalis; these processes may connect with inflammatory bowel disease, skin disorders, eye inflammation, and neurological illness.
  • Kelly Hogan experienced regrowth of receding gums after carnivore, as did Annalise Barron. Strict animal-based eating with intermittent fasting, one or two meals in a five- or six-hour window, allows low-glucose and low-insulin periods associated with immune repair and tissue regeneration.
  • Beef, eggs, salt, water, and sometimes pork for vitamin B1 form a sufficient diet for Annalise Barron, while vegetables irritate her gut. Many drugs and vaccines may disrupt immune function, and restoring it can enable recovery from nearly any illness short of advanced cancer.

The NLRP3 inflammasome and rapid pain relief

  • The NLRP3 inflammasome is a protein assembly activated by pathogens or their debris, oxidative stress, toxins, and physical injury. Its inflammatory signaling connects with pain, mental illness, Alzheimer's, Parkinson's, MS, and performance anxiety.
  • Postmortem Alzheimer's brains, especially the hippocampus, have more NLRP3 activity and downstream interleukin-18 with greater disease involvement. The protein machinery forms visible ASC specks as part of this inflammatory pathway. [5]
  • Beta-hydroxybutyrate, a ketone produced during ketosis, blocks NLRP3 activation. This mechanism connects with accounts of knee or joint pain disappearing by the third day of strict carnivore, before meaningful weight loss. [6]
  • Exogenous ketones or MCT oil may supply fuel to neurons with impaired mitochondria, but high glucose and insulin continue to hinder immune function. Sustained ketosis and immune restoration are distinct from taking ketone supplements.

Mental illness and the Stanford ketogenic research

  • A $20.4 million NIH grant application was submitted on June 15, 2026, for a 200-person trial of fewer than 20 g of carbohydrates daily. Participants would have serious depression, bipolar disorder, or schizophrenia alongside metabolic dysfunction; a funding decision was pending.
  • Psychiatrist and obesity-medicine specialist Shebani Sethi observed improvements among patients with eating disorders using ketogenic diets. Psychiatric symptoms may involve metabolic illness, neuroinflammation, and sometimes chronic infection.
  • Sethi's Stanford pilot enrolled 23 people; 21 completed a ketogenic intervention identified here as 12 weeks. Their metabolic disorders resolved, 79% had major psychiatric symptom improvements, and stricter adherence corresponded to better outcomes. [7]
  • The pilot also tracked inflammatory biomarkers, including NLRP3, with reduced inflammasome signaling. Contact after publication led to a zero-carbohydrate proposal and collaboration on a larger NIH application.
  • Medication adjustments in psychiatric illness require careful supervision, as do blood-pressure medication changes after dietary improvements. Starting or discontinuing psychiatric drugs can cause serious problems.
  • Robert F. Kennedy Jr. may have approached Sethi about leadership of the National Institute of Mental Health. A Science article covered the possible appointment, which remained pending, amid anticipated resistance from pharmaceutical interests. [8]

Multiple sclerosis: mechanism and recovery stories

  • MS is strongly linked with Epstein-Barr virus, which most adults carry. The virus persists, and a strict high-fat carnivore diet with intermittent fasting may rebalance immune activity and reduce continuing neurological injury. [3]
  • MS symptoms may improve within two or three weeks, while substantial gains can take six months or longer. Existing MRI lesions may remain, while progression and new lesions may stop; medication reductions occur gradually.
  • Diane Ladd's Boston Carnivore channel includes approximately 15 or 16 MS interviews covering diagnosis, medication, diet adherence, and symptom changes. Diane and Rebecca in Spain both recovered from severe symptoms, with a more difficult course for Rebecca; a planned book combines their experiences and the immune mechanism.

Alzheimer's and Parkinson's: longer recovery horizons

  • At least three Alzheimer's recovery accounts occur on Dave's channel. Judy Snideman's MoCA score increased from 14 out of 30 to at least 28 after approximately one year of carnivore and exercise.
  • Cognitive recovery is linked here to strict carnivore, patience, at least 7,000 walking steps per day, and supplements such as vitamin D3, magnesium, and curcumin for immune support.
  • Mimi Morgan had serious Parkinson's symptoms, ate keto for two years, discontinued Parkinson's medication, and then adopted carnivore and strength training. She now helps other people with Parkinson's using keto or carnivore and exercise.
  • Lars Konge's Genesis for PD program followed an improvement in a physician's Parkinson's symptoms with carnivore and exercise. The program now includes about 200 people, with approximately 37 experiencing substantial symptom reversal within its first two years.
  • These accounts are self-selected and may omit people without benefit. Dave and Annalise Barron have encountered no strict, sustained carnivore case without improvement, although some gains occur slowly and dietary lapses can produce setbacks.

Diabetes, medical resistance, and next steps

  • Approximately 88% of American adults have poor metabolic health, and type 2 diabetes remission is an especially rapid improvement associated here with carnivore. One interview involved a man with HbA1c of 14 whose diabetes came under control with diet. [9]
  • Some medical colleagues remain skeptical, including a periodontology professor and Stanford's dean of medicine. Conventional medicine manages separate diseases with specialized drugs, including steroids and expensive biologics, without correcting the proposed shared underlying cause.
  • Broad assertions about reversing MS, Alzheimer's, and Parkinson's lack strong clinical proof and create professional risk if published. Books, scientific writing, and additional recovery histories could clarify the mechanisms and the range of people who benefit.

References

  1. [00:20] Joe Rogan Experience #1050 - Dr. Shawn Baker — https://www.youtube.com/watch?v=Yj_Bc9hdHa0
  2. [00:24] Joe Rogan Experience #1139 - Jordan Peterson — https://www.youtube.com/watch?v=9Xc7DN-noAc
  3. [05:52] Longitudinal analysis reveals high prevalence of Epstein-Barr virus associated with multiple sclerosis — https://doi.org/10.1126/science.abj8222
  4. [11:13] Role of sugars in human neutrophilic phagocytosis — https://doi.org/10.1093/ajcn/26.11.1180
  5. [20:13] Increased expression of inflammasome signaling genes and proteins in selective brain regions in the intermediate stage of Alzheimer's disease — https://doi.org/10.1111/bpa.70086
  6. [22:01] The ketone metabolite β-hydroxybutyrate blocks NLRP3 inflammasome–mediated inflammatory disease — https://doi.org/10.1038/nm.3804
  7. [31:38] Ketogenic Diet Intervention on Metabolic and Psychiatric Health in Bipolar and Schizophrenia: A Pilot Trial — https://doi.org/10.1016/j.psychres.2024.115866
  8. [36:15] Kennedy rejects NIH director's pick for mental health institute — https://doi.org/10.1126/science.aen6354
  9. [52:25] Prevalence of Optimal Metabolic Health in American Adults: National Health and Nutrition Examination Survey 2009–2016 — https://doi.org/10.1089/met.2018.0105
 

Alex McDonald has embraced a low carb high fat (LCHF) lifestyle since January 2010. Initially, he planned a one-month test of low carb and then expected to return to his original diet. The drastic improvements in his well-being during that first month were so compelling that returning became impossible.

For over a decade, Alex has delved deep into the research underpinning low carbohydrate and ketogenic diets, including the completion of Sports Nutrition and LCHF Advisor Training through the Nutrition Network and attendance at several global LCHF conferences.

Although he briefly engaged in running during his late twenties and completed three half marathons, more than a decade had passed without participating in long-distance events. In 2023, Alex decided to prove the science of low carb nutrition by running five marathons in five days while completely fasted.

generated summary

The finish line and what led me there

  • At kilometer 38 of the 35°C Sydney Marathon, Alex McDonald passed a collapsed runner, ambulances, and stretchers; 26 runners were taken to hospital. He continued toward the finish.
  • The Sydney race was his fifth marathon in five days, after 110 hours without food, with only water and salt. In September 2023, at age 42, he became the first person on record to complete 211 km in five fasted marathons, having never previously run one.
  • McDonald was a Sydney father, not a doctor, dietitian, or established athlete. In 2010, Art De Vany inspired him through fitness into his seventies, activity with his grandchildren, and eating foods available before modern agriculture.
  • McDonald moved from paleo to keto to carnivore, avoiding grains and processed food and increasing fat and protein. He experienced progressively better well-being, encountered objections, and spent about ten years studying the topic.

The fuel-access problem

  • Dietary carbohydrates are not essential nutrients. The available glycogen reservoir contains about 2,000 calories, less than a marathon requires; fat adaptation permits use of the much larger body-fat reservoir.
  • His DEXA scan showed 14% body fat, estimated at 100,000 calories: roughly 50 times his carbohydrate reservoir and the equivalent of approximately 25 marathons, despite his lean body composition.
  • An average Australian man carries an estimated 227,000-plus calories in body fat, equivalent to roughly 55 marathons. The distinction is between stored energy and access to that energy.
  • Stephen Phinney used the analogy of a fuel tanker running out of petrol. Carbohydrates raise insulin, which promotes fat storage and inhibits fat burning; lower insulin permits greater access to stored fat.
  • Carbohydrate loading can support performance while requiring planned refuelling; insufficient intake can lead to hitting the wall, and excess intake can cause gastrointestinal problems. McDonald sought to test endurance without this refuelling.

Designing and training for the five-marathon fast

  • The attempt consisted of five 42.2-km marathons in five days without food. Lead doctor Paul Mason and a medical team supported it, with continuous glucose monitoring, blood ketones three times daily, blood testing, and pre/post DEXA scans.
  • Preparation involved seven months, 77 runs, and 700 km, often starting at 4 a.m.; every run was fasted, followed by food. His diet comprised meat, seafood, eggs, and some dairy, with almost no carbohydrate.
  • Fat adaptation took weeks, while the seven-month preparation conditioned his legs. The pacing plan aimed for a heart rate below 140 bpm, approximately zone two, and completion over speed.
  • On day one he spent nearly five hours in zone three or higher. Days two to four followed the lower-intensity plan, while day five included three and a half hours in zone three or higher, with one hour above 164 bpm.
  • The five days included about eight and a half hours of moderate-to-high-intensity running without food. Speed was not the measured question; he was both the fastest and slowest recorded finisher of this particular challenge.

Glucose, ketones, and sustained energy

  • Across the 121-hour fast with water and salt but no food, continuous glucose measurements were generally 4–6, including during running. Glucose was produced internally through gluconeogenesis.
  • Glucose dipped below 4 several times from day three, reaching 3.5 overnight. There was no experienced energy collapse or hitting the wall.
  • The highest glucose reading, 7.7, occurred after the final finish, attributed to heat and stress. Blood ketones increased from 0.1 on day-one morning to 4.3 on day-five afternoon.
  • Glucose remained broadly steady as ketones rose. The five fasted marathons were completed without exhaustion of available energy.

Heat, injuries, fluid balance, and finishing

  • Day four combined 38°C heat, nearly 170 km already run, pain in ligaments and tendons, and loops around a barbecue-filled food festival. Fat adaptation supported fuelling but did not prevent physical wear.
  • Following excess water intake in the heat, he had two sprained ankles, pitting oedema, and a 1.6-kg increase in one day; after four marathons and four food-free days, his weight equalled his starting weight.
  • Paul Mason identified further overhydration as a greater danger than dehydration for the fifth marathon. McDonald elevated his feet, slept poorly, and received a 47/100 recovery score, while morning glucose was 4.3.
  • In the 35°C Sydney Marathon, he finished on two sprained ankles with his second-fastest time of the week, while other runners required ambulances. Heat, fluid balance, and injuries were the limiting problems, not an energy shortfall.

Body composition and comparison with fasting research

  • After five days and 211 km, body weight fell by 3 kg. DEXA indicated a loss of 1 kg fat and 2 kg lean mass; lean mass includes water and glycogen as well as muscle.
  • For a fasting-only comparison, a 2025 Norwegian study followed 13 people during a seven-day water-only fast without marathons. [1]
  • The Norwegian group lost about 8% of fat mass compared with his 9.5%, and about 8% of lean mass compared with his 3%, despite his 211 km of running. [1]
  • The comparison differed in participant age, fat adaptation, seven versus five fasting days, and scan timing: the Norwegian group was still fasting, while McDonald had eaten for two days. His lean-mass change was smaller. [1]

Muscle damage, laboratory results, and gut tolerance

  • His blood tests showed exertional stress, including an approximately twentyfold increase in muscle-damage markers and high inflammation, after 211 km as a first-time marathon runner.
  • In a study of 32 trained ultrarunners who ate during a 200-km race, muscle-damage markers rose nearly one hundredfold and inflammation more than twentyfold. His measurements were within that exercise-related range. [2]
  • His kidney markers and electrolytes were normal, fasting insulin declined from 5 to 2, and no gastrointestinal problems occurred during the event.
  • Carbohydrate-fuelled runners plan gels, drinks, and feeding schedules, sometimes with digestive issues. Water and salt eliminated food and gel scheduling for McDonald, and he experienced no digestive disruption.

A second fasted endurance test in 2024

  • In October 2024, he entered a backyard ultra with a 6.7-km loop every hour until elimination. Nearly 300 started; he completed 15 hours and 100 km, outlasted about two-thirds, and finished in the top quarter.
  • The 100 km exceeded twice his previous longest single-day distance and was completed fasted with water and salt, while other runners carried substantial race fuel.
  • Continuous glucose and continuous ketone monitors showed stable glucose and ketones rising from zero at the start to above 4 at the finish, paralleling the five-marathon pattern.

The wider point

  • The fast eliminated food intake during the event as an energy source. The central distinction is stored energy versus access to it: body-fat stores supported prolonged exertion without dietary carbohydrates.
  • Marathons served as a demonstration. The intended everyday outcome is sufficient energy for activity, including playing with grandchildren into older age, as exemplified by Art De Vany.
  • McDonald serves on the board of the Australasian Metabolic Health Society to support practitioner education and broader access to metabolic-health knowledge.

References

  1. [14:48] Effects of seven days' fasting on physical performance and metabolic adaptation during exercise in humans — https://doi.org/10.1038/s41467-024-55418-0
  2. [16:13] Creatine kinase isoenzyme activity during and after an ultra-distance (200 km) run — https://doi.org/10.5604/20831862.1163384
 

Recorded at the Public Health Collaboration annual conference in London, UK, on 11th May 2019.

generated summary

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
 

Recorded at the Public Health Collaboration annual conference in Manchester, UK, on 20th June 2017.

zoeharcombe.com/2017/06/dietary-fat-guidelines

::: spoiler generated summary

Food composition and dietary-fat arithmetic

  • Nearly all natural foods supply protein; pure sugar and pure fats are the exceptions, while butter still has some protein.
  • Natural foods largely separate carbohydrate-and-protein foods—fruit, vegetables, grains and pulses—from fat-and-protein foods—meat, fish, eggs and dairy; nuts, seeds and avocado are uncommon mixed examples.
  • Meat and fish are generally carbohydrate-free, eggs have traces, and fluid dairy can contain 5–10 g carbohydrate per 100 g; processed foods combine fat and carbohydrate in highly palatable products.
  • With real-food protein typically around 15% of calories, a 30% fat ceiling leaves about 55% for carbohydrate; a 25% fat target leaves 60%, while low-carbohydrate eating requires more fat.
  • Every fat-containing food includes saturated, monounsaturated and polyunsaturated fats; among ordinary food groups, dairy has more saturated than unsaturated fat.
  • USDA food data put a typical sirloin steak at about 2% saturated fat, while oily fish has twice its total fat and 1.5 times its saturated fat; olive oil has 14 times the total fat and seven times the saturated fat of that steak. [1]
  • One tablespoon of olive oil contains more saturated fat than a 100 g pork chop, and lard is predominantly monounsaturated; simplified warnings about meat, eggs and saturated fat do not match these food-composition comparisons.

How the guidelines emerged

  • The 1977 US McGovern committee introduced dietary-fat goals, incorporated into the 1980 Dietary Guidelines for Americans; Britain followed with NACNE proposals in 1983 and the COMA cardiovascular document in 1984. [2][3][4]
  • Earlier medical advice identified floury, vegetable and sugary foods as fattening, illustrated by an 1869 Tanner quotation reproduced in Gary Taubes's Good Calories, Bad Calories. [5]
  • The new recommendations shifted the dietary focus to ceilings of 30% of calories from total fat and 10% from saturated fat; those limits necessarily raised the carbohydrate share without evidence establishing that level as healthy or safe.
  • Coronary heart disease motivated the policy. In the US in 1950, annual all-cause mortality was about 1.45%, and about 589 people per 100,000 died from heart disease: roughly 0.59% of the population but about 40% of deaths.
  • Those measures convey different risks; heart disease accounting for 40% of deaths does not mean 40% of living people die from it each year.
  • Early Russian pathologists fed cholesterol-rich animal material to rabbits and observed arterial damage, although rabbits do not naturally eat animal foods; this model differs substantially from human diets.
  • Ancel Keys tested dietary cholesterol in people in the early 1950s; in a 1954 symposium he concluded that dietary cholesterol did not affect human blood cholesterol or atherosclerosis. These findings clear animal foods of raising blood cholesterol or causing atherosclerosis, while fat remained the focus. [6]

First review: randomized trials available when policy began

  • The February 2015 analysis included six historical randomized trials involving 2,467 men, nearly all already ill; none tested both the 30% total-fat and 10% saturated-fat targets. [7]
  • Headlines vindicating butter or crediting fat with longer life went beyond the review: it tested evidence for the guidelines, not butter or fat's effects on lifespan.
  • They included the Rose Corn Oil trial, LA Veterans trial, Oslo Diet-Heart Study and Sydney Diet-Heart Study; one trial was released after the 1977 committee met. [8][9][10][11]
  • Pooled all-cause deaths were 370 versus 369, with no significant difference; coronary-heart-disease mortality likewise did not improve, and the forest-plot estimates lay on the line of no effect.
  • The Sydney intervention reached the 10% saturated-fat target alone, but had significantly more deaths in its intervention arm; its original authors also warned about possible toxicity of the vegetable oil.
  • Blood cholesterol fell in both trial arms and more in the diet-intervention arms, yet this did not coincide with fewer heart deaths; cholesterol reduction alone did not establish improved mortality in these trials.
  • Plant sterols in vegetable oils can compete with cholesterol absorption and lower blood cholesterol without improving heart-disease outcomes; a 2014 paper identified a possible adverse coronary effect, leading to advice against large vegetable-oil intakes. [12]
  • The 1965 Research Committee trial concluded that a low-fat diet had no role after myocardial infarction, and the Rose Corn Oil trial cautioned that corn oil might cause harm. [13][8]
  • Dietary advice was nevertheless applied to about 276 million Britons and Americans on the basis of trials involving fewer than 2,500 mostly ill men; that population offered no direct evidence for healthy people or women.

Second review: observational evidence before the guidelines

  • The review of six prospective cohorts available before the UK recommendations included only men, mostly healthy, followed for roughly four to 20 years. [14]
  • The Western Electric, London Banks and Busmen, F. Heart, Honolulu and Seven Countries cohorts found no association between total fat and coronary-heart-disease deaths. [15][16][17][18]
  • Only the Seven Countries Study linked saturated fat and heart-disease deaths, through a between-country correlation, not a within-population relationship; other cohorts identified smoking and paternal age.
  • Some cohorts found inverse associations between alcohol and heart disease, potentially reflecting affluence and its benefits, not a benefit from drinking; Keys found no association with smoking, activity or body weight in his study.
  • The Seven Countries Study enrolled about 13,000 men aged 40–59 from 1956 and linked saturated fat to cholesterol and cholesterol to coronary disease; its original conclusions concerned associations, not demonstrated causation. [18]
  • In a 25-year follow-up, Menotti and Keys obtained a cholesterol–heart-disease correlation of 0.72 (R²≈0.52); a reanalysis yielded a stronger latitude correlation of 0.96 (R²≈0.92), with sunlight/vitamin D as a possible explanation across 16 cohorts. [19]
  • The stronger latitude relationship points toward sunlight and vitamin D, with lower exposure in Finland and higher exposure nearer the equator; country comparisons also differ in climate, history and wealth.
  • Across the historical cohorts, all-cause mortality was just under 5% and coronary mortality around 1%; in Seven Countries, five-year coronary mortality was 21% with pre-existing coronary disease versus 1% without it.
  • Neither the six observational cohorts nor the randomized evidence supported those population-wide fat limits.

Third and fourth reviews: more recent trials and cohorts

  • Updating the randomized evidence to ten trials and about 62,000 participants added women, healthy people, and studies lasting one to eight years, including Minnesota, DART and the Women's Health Initiative. [20][21][22][23]
  • The pooled results remained null for all-cause and coronary-heart-disease mortality despite larger cholesterol reductions in nine of the ten intervention comparisons.
  • Only the Minnesota Coronary Survey included healthy men and women together, but they were institutionalized psychiatric patients who might have been taking cardiovascularly relevant medication, limiting applicability to the general population.
  • Even these later trials never directly tested both official fat limits; STARS came closest at 27% total fat and 8–10% saturated fat, but it enrolled only 55 people and its initial positive result lost significance with Fisher's exact test. [24]
  • The updated prospective-cohort review identified seven cohorts, six usable in meta-analysis, with the Kushi cohort excluded; its pooled results again found no significant association between total or saturated fat and coronary deaths. [25]
  • Four isolated positive cohort findings failed Bradford Hill causal criteria, and the combined results of these four reviews gave no support for the fat guidelines.

Other research and the Cochrane controversy

  • A 20-year vegetarian history preceded the research; its findings favored animal foods despite an initial inclination away from meat.
  • Skeaff and Miller's 2009 review combined 28 studies and about 280,000 people without a significant effect; Siri-Tarino's 2010 analysis of about 350,000 people likewise found no saturated-fat association with coronary disease. [26][27]
  • Mozaffarian's 2010 review found a benefit when saturated fat was exchanged for polyunsaturated fat, while Hooper's 2011 Cochrane review contained one positive result amid eleven nonsignificant results. [28][29]
  • Chowdhury's 2014 review found a significant association for trans fats but not saturated, monounsaturated or polyunsaturated fats; Schwingshackl and Hoffmann's review also found no significant effects. [30][31]
  • Hooper's 2015 saturated-fat Cochrane update was a 150-page review with a single significant signal: cardiovascular events after lowering saturated fat; seven other outcomes, including all-cause, cardiovascular and coronary mortality, heart attacks and strokes, were nonsignificant. [32]
  • Ravnskov and colleagues criticized the Mozaffarian analysis for excluding the Rose Corn Oil and Sydney trials while including a Finnish Mental Hospital study that was neither randomized nor adequately controlled. [33][8][11]
  • The Cochrane cardiovascular-event estimate pooled eleven trials although only one documented an actual exchange of saturated for polyunsaturated fat; the others intended dietary changes without verifying them.
  • The positive signal depended on adding unpublished heart-event data from four studies originally about skin cancer, high cholesterol, insulin resistance or diabetes, involving only 646 additional people.
  • Those extra data were not peer reviewed; study heterogeneity was high (I²=65%), and the positive cardiovascular-event signal lost statistical significance in sensitivity analysis.
  • No trial contributing to that Cochrane result studied healthy men and women together, limiting its applicability to the general population.
  • Malhotra, Redberg and Meier's 2017 editorial challenged the saturated-fat artery-clogging theory, while the Hooper 2015 cardiovascular-event result remained central to criticism of that view. [34]

After the guidelines: obesity and the sources of dietary fat

  • Mark Hegsted and legislators acknowledged in 1977 that the evidence lacked proof and scientific consensus, yet the committee asserted that the recommended dietary changes could cause no physical or mental harm. [2]
  • UK obesity rose from about 2.7% in 1972 to 25% by the end of the century; US obesity accelerated around the 1976–1980 guideline transition. The timing raises a question about a possible connection.
  • The 2015 US dietary-guideline charts attribute much saturated fat intake to pizza, desserts, candy, chips, tortillas, sauces, mixed ready meals and processed meat, before reaching cheese, milk, butter, nuts and seeds. [35]
  • The UK Family Food figures likewise place pastries, cakes, biscuits and sweets prominently among fat sources; real meat, fish and eggs account for only 7%, with substantial intake also coming from dairy, added fats and processed products. [36]
  • Processed food, not saturated fat itself, is the main dietary target; the central public-health guidance is to eat real food.

References

  1. [06:13] USDA FoodData Central — https://fdc.nal.usda.gov/
  2. [07:44] Dietary Goals for the United States (1977) — https://www.govinfo.gov/app/details/CPRT-95SPRT23395O
  3. [07:50] Nutrition and Your Health: Dietary Guidelines for Americans (1980) — https://www.dietaryguidelines.gov/about-dietary-guidelines/previous-editions/1980-dietary-guidelines-americans
  4. [08:07] Diet and Cardiovascular Disease: COMA Report (1984) — https://assets.publishing.service.gov.uk/media/5bab9af640f0b60633988006/Diet_and_Cardiovascular_Disease__1984_.pdf
  5. [08:20] Good Calories, Bad Calories — Gary Taubes — https://www.penguinrandomhouse.com/books/176680/good-calories-bad-calories-by-gary-taubes/9781400033461/
  6. [13:04] Symposium on Atherosclerosis (1954), including Ancel Keys — https://doi.org/10.17226/20269
  7. [14:11] Evidence from randomised controlled trials did not support the introduction of dietary fat guidelines in 1977 and 1983 — Harcombe et al. (2015) — https://doi.org/10.1136/openhrt-2014-000196
  8. [15:42] Corn Oil in Treatment of Ischaemic Heart Disease — Rose et al. (1965) — https://doi.org/10.1136/bmj.1.5449.1531
  9. [15:43] A Controlled Clinical Trial of a Diet High in Unsaturated Fat in Preventing Complications of Atherosclerosis — Dayton et al. (1968) — https://doi.org/10.1016/S0140-6736(68)91531-6
  10. [15:44] Effect of Diet on Five-Year Mortality in the Oslo Diet-Heart Study (1970) — https://doi.org/10.1161/01.cir.42.5.935
  11. [15:47] Dietary Prevention of Coronary Heart Disease: The Sydney Diet Heart Study — Woodhill et al. (1978) — https://doi.org/10.1007/978-1-4684-0967-3_18
  12. [18:35] Plant sterols lower cholesterol, but increase risk for coronary heart disease — Harcombe and Baker (2014) — https://doi.org/10.3844/ojbsci.2014.167.169
  13. [19:51] Low-fat Diet in Myocardial Infarction: A Controlled Trial — Research Committee (1965) — https://doi.org/10.1016/S0140-6736(65)91469-8
  14. [20:19] Evidence from prospective cohort studies did not support the introduction of dietary fat guidelines in 1977 and 1983 — Harcombe et al. (2016) — https://doi.org/10.1136/bjsports-2016-096409
  15. [20:50] Diet and Coronary Death: The Western Electric Study — Shekelle et al. (1981) — https://doi.org/10.1056/NEJM198101083040201
  16. [20:52] Diet and Heart: A Postscript — Morris et al. (1977), London banks and busmen — https://doi.org/10.1136/bmj.2.6098.1307
  17. [20:54] Framingham Heart Study — Official research milestones — https://www.framinghamheartstudy.org/fhs-about/research-milestones/
  18. [20:56] Seven Countries Study — Official publications archive — https://www.sevencountriesstudy.com/study-findings/publications/
  19. [23:41] Inter-cohort Differences in Coronary Heart Disease Mortality in the 25-Year Follow-up of the Seven Countries Study — Menotti et al. (1993) — https://doi.org/10.1007/BF00209531
  20. [27:15] Evidence from Randomised Controlled Trials Does Not Support Current Dietary Fat Guidelines — Harcombe et al. (2016) — https://doi.org/10.1136/openhrt-2016-000409
  21. [27:54] The Minnesota Coronary Survey (1989) — https://doi.org/10.1161/01.atv.9.1.129
  22. [27:57] Diet and Reinfarction Trial (DART) (1989) — https://doi.org/10.1016/S0140-6736(89)90828-3
  23. [27:59] Low-Fat Dietary Pattern and Risk of Cardiovascular Disease: Women’s Health Initiative (2006) — https://doi.org/10.1001/jama.295.6.655
  24. [29:48] St Thomas’ Atherosclerosis Regression Study (STARS) (1992) — https://doi.org/10.1016/0140-6736(92)90863-x
  25. [30:35] Evidence from Prospective Cohort Studies Does Not Support Current Dietary Fat Guidelines — Harcombe et al. (2016) — https://doi.org/10.1136/bjsports-2016-096550
  26. [32:18] Dietary Fat and Coronary Heart Disease: Summary of Evidence from Prospective Cohort and Randomised Controlled Trials — Skeaff and Miller (2009) — https://doi.org/10.1159/000229002
  27. [32:41] Meta-analysis of Prospective Cohort Studies Evaluating the Association of Saturated Fat with Cardiovascular Disease — Siri-Tarino et al. (2010) — https://doi.org/10.3945/ajcn.2009.27725
  28. [32:56] Effects on Coronary Heart Disease of Increasing Polyunsaturated Fat in Place of Saturated Fat — Mozaffarian et al. (2010) — https://doi.org/10.1371/journal.pmed.1000252
  29. [32:59] Reduced or Modified Dietary Fat for Preventing Cardiovascular Disease — Hooper et al., Cochrane (2011) — https://doi.org/10.1002/14651858.CD002137.pub2
  30. [33:11] Association of Dietary, Circulating, and Supplement Fatty Acids with Coronary Risk — Chowdhury et al. (2014) — https://doi.org/10.7326/M13-1788
  31. [33:24] Dietary Fat Intake and Risk of Cardiovascular Disease and All-Cause Mortality — Schwingshackl and Hoffmann (2014) — https://doi.org/10.1136/bmjopen-2013-004487
  32. [33:44] Reduction in Saturated Fat Intake for Cardiovascular Disease — Hooper et al., Cochrane (2015) — https://doi.org/10.1002/14651858.CD011737
  33. [34:07] The Questionable Benefits of Exchanging Saturated Fat with Polyunsaturated Fat — Ravnskov et al. (2014) — https://doi.org/10.1016/j.mayocp.2013.11.006
  34. [37:30] Saturated Fat Does Not Clog the Arteries: Coronary Heart Disease Is a Chronic Inflammatory Condition — Malhotra, Redberg and Meier (2017) — https://doi.org/10.1136/bjsports-2016-097285
  35. [39:20] Dietary Guidelines for Americans, 2015–2020 — https://www.dietaryguidelines.gov/about-dietary-guidelines/previous-editions/2015-dietary-guidelines
  36. [40:08] Family Food Statistics — UK Government — https://www.gov.uk/government/collections/family-food-statistics

:::

 

Cancer progression is frequently accompanied by systemic inflammation and host-wide disturbances, including neuroinflammation-associated cognitive impairment, yet interventions that simultaneously target tumor growth and host dysfunction remain limited. Here we show that a ketogenic diet suppresses tumor growth while improving emotional and cognitive deficits in tumor-bearing mice. The diet elevates circulating and intratumoral uridine and enriches Flavonifractor plautii, a gut bacterium that contributes to host uridine availability. In tumor cells and patient-derived organoids, uridine cooperates with β-hydroxybutyrate to promote cytosolic DNA accumulation and activate cGAS–Sting signaling, consistent with enhanced antitumor immune activity. In parallel, ketogenic diet, uridine supplementation and F. plautii transplantation reduce systemic and hippocampal inflammatory readouts and improve neurobehavioral phenotypes. These findings identify a diet–microbiota–metabolite axis that links ketogenic metabolism to tumor immune signaling and reduced peripheral-to-brain inflammation in preclinical cancer models.

Full Paper - https://doi.org/10.1038/s41467-026-78868-0

 

what happens when a midlife dietary change collides with decades of diagnosis, stigma, and trial-and-error? Guest Robyn Dobbins (lived-experience advocate, podcast host, health coach, and community coordinator at the nonprofit Metabolic Collective) makes the case for why personal narratives matter in metabolic mental-health advocacy—covering early symptoms, postpartum struggles, routines and relationships, low-carb/keto tradeoffs, community building, and how cholesterol conversations show up along the way.

generated summary

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/

 

Type 2 diabetes is often treated as a chronic, progressive disease, but Dr. David Unwin has spent years showing that, for many patients, remission is possible through low-carb nutrition and a different approach to care.

In this episode, Dr. Bret Scher speaks with Dr. Unwin about how his work as an NHS primary care physician changed after he began focusing on insulin resistance, carbohydrate intake, and the underlying drivers of type 2 diabetes rather than blood sugar alone.

Dr. Unwin shares how his approach to care evolved and discusses published real-world findings on type 2 diabetes remission among patients who chose a low-carb approach. He also explains why long-term maintenance became just as important as achieving remission in the first place, and how he uses continuous glucose monitors to support that process. He also describes his approach to behavioral support, including addressing food addiction.

generated summary

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
 

One of my favorite programming books.

Filled with gems like this:

Numbers that fool the Fermat test are called Carmichael numbers, and little is known about them other than that they are extremely rare. There are 255 Carmichael numbers below 100,000,000. the smallest few are 561, 1105, 1729, 2465, 2821, and 6601. In testing primality of very large numbers chosen at random, the chance of stumbling upon a value that fools the Fermat test is less than the chance that cosmic radiation will cause the computer to make an error in carrying out a “correct” algorithm. Considering an algorithm to be inadequate for the first reason but not for the second illustrates the difference between mathematics and engineering.

Full Text - https://web.mit.edu/6.001/6.037/sicp.pdf

 

Marc talks about his journey on the carnivore diet.

generated summary

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.

 

can heart disease prevention be asking the wrong question? Dave sits down with Philip Ovadia, MD, cardiothoracic surgeon, as the guest makes the case for looking beyond LDL alone. They discuss bypass surgery, why cholesterol-lowering hasn’t erased heart disease, insulin resistance, trial design, statins and PCSK9 drugs, real-food diets, CGMs, and how clinicians think about risk in practice.

generated summary

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
 

n this episode, I have the incredible opportunity to sit down with one of my lifelong mentors in both medicine and endurance running, Dr. Tim Noakes. I first discovered his work when I started running marathons in 1999, and his books completely shaped the way I thought about endurance training, hydration, and fueling. But Dr. Noakes' story is also a story of changing your mind when the evidence and your own experience tell you that something isn't working.

We talk about his evolution from promoting high-carbohydrate fueling to questioning that approach, his own experience with type 2 diabetes and metabolic health, and the research that changed the way he thinks about endurance performance. We also dive into my own journey with insulin resistance, continuous glucose monitoring, low-carbohydrate endurance training, and what happened when I began experimenting with how I fueled my ultramarathons. This is a conversation about being willing to question what you've been taught, examine your own experience, and keep learning as the science evolves.

generated summary

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
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