Type 2 diabetes is a disease of insulin excess and resistance — not insulin deficiency — which means the century-old standard of care (high-carb diet + more insulin) has been treating the wrong problem and driving the epidemic rather than reversing it.
2
The ACCORD trial (10,000 diabetics, intensive insulin therapy) was halted early because more people died and had heart attacks in the aggressive-treatment arm — yet the ADA's answer remains 'not aggressive enough.'
3
The Verta Health trial showed that nutritional ketosis — zero carb restriction policy, continuous physician support — put Type 2 diabetes into full remission and improved 20+ cardiovascular biomarkers simultaneously, without drugs.
4
93.2% of Americans are metabolically unhealthy by at least one insulin-resistance marker; the current GLP-1 agonist craze mirrors the 1922 insulin euphoria, with unknown long-term consequences including muscle loss, rebound weight gain, and fetal programming risks.
Protocols
Concrete recipes — what, when, how much, and why
7 items
T2D reversal via nutritional ketosis with medication taper
WhatEliminate all refined carbohydrates, starch, and sugar; shift macros toward fat and adequate protein (typically <20-50g net carbs/day). Simultaneously taper glucose-lowering medications under physician supervision as blood sugar normalizes.
WhenFor Type 2 diabetics or pre-diabetics seeking remission. Medication taper begins within days as diet lowers blood sugar; physician supervision required to avoid hypoglycemia from over-medication.
DoseVerta Health used continuous ketosis monitoring via blood/breath ketone measurement. Clinical response (A1C improvement) typically seen within weeks; full metabolic normalization in 2-3 months for compliant patients. Continue indefinitely — remission is diet-dependent.
For whomOverweight Type 2 diabetics and pre-diabetics. Less appropriate for naturally thin individuals who lose too much weight on strict keto.
WhyT2D is a disorder of carbohydrate metabolism driven by chronic hyperinsulinemia. Removing the dietary substrate that drives insulin secretion removes the cause rather than managing the symptom. There are no essential dietary carbohydrates.
CaveatsMedication taper requires medical supervision — blood sugar drops rapidly with dietary change, creating hypoglycemia risk if drug doses are not simultaneously reduced. Some lean individuals or specific lipid responders may need individualized fat quality guidance.
The Verta Health trial demonstrated that patients on escalating drugs achieved A1C from 11 to 5.5 in months and improved all 20+ cardiovascular biomarkers. Hyman's clinical replication: patient with triglycerides >300, HDL very low, total cholesterol >300 — after keto: 20 lbs lost, cholesterol -100, triglycerides -200, HDL +30, blood sugar normalized. The Look AHEAD trial established that weight loss via low-fat calorie restriction alone does not achieve this — carbohydrate removal is the active ingredient.
Mechanism
Dietary carbohydrate is the primary insulin secretagogue. Removing it drops circulating insulin, releases the block on lipolysis, allows fat mobilization for fuel, reduces hepatic glucose output, and over time improves insulin receptor sensitivity. Beta cells recover when not chronically overstimulated.
If you stop eating the toxin you don't need the antidote. It's a disorder of carbohydrate metabolism — tell them not to eat it, they do fine.
Also said
“For patients who comply with the diet they seem to put this progressive chronic disease into remission. So it's not a progressive chronic disease — it's only a progressive chronic disease if you're eating the toxin.”— The clinical verdict of the Verta trial: remission is achievable, not merely management.
WhatPair a ketogenic diet (<20-50g net carbs/day) with the minimum insulin dose required to maintain normoglycemia. Eliminate carbohydrate spikes that require large correction boluses. Monitor blood glucose continuously and adjust basal dose downward as carbohydrate intake drops.
WhenApplicable to any Type 1 diabetic seeking to minimize insulin dose, reduce glycemic variability, and avoid weight gain and cardiovascular risk of high-dose insulin.
DoseSome Type 1 physicians on ketogenic diets maintain on 1-2 units/day vs 100+ on standard high-carb diet. Dose reduction begins immediately with dietary change; stabilization in days to weeks.
For whomType 1 diabetics motivated to minimize insulin burden and glycemic swings; individuals developing secondary insulin resistance from high-dose insulin use.
WhyHigh carbohydrate intake requires large insulin boluses, creating glycemic variability, hypoglycemia risk, and over time insulin resistance ('double diabetes'). Tiny carb intake = tiny insulin dose = tiny dosing error = flat blood sugar curve.
CaveatsRequires active monitoring. Not appropriate for brittle patients or those with poor hypoglycemia awareness without close supervision. Dietary restriction must be sustained or glucose excursions return immediately.
Richard Bernstein developed this in the 1970s after failing to control his own Type 1 on standard high-carb protocol. Joslin held this view in the early 1920s before the field shifted toward high-dose permissiveness. The principle: let minimal carb intake dictate minimal insulin need, rather than letting carb intake dictate high doses and then trying to match them.
Mechanism
Near-zero carbohydrate intake eliminates most postprandial glucose excursion in Type 1 diabetics, making basal insulin adequate without complex bolus calculations. Fat and protein raise glucose slowly and predictably via gluconeogenesis, far less than starch and sugar.
This is was Richard Bernstein's Revelation in type one diabetes in the 70s — let's use the lowest doses and craft a diet that allows those lowest doses to be effective, which is basically lower starch and sugar and higher fat.
GLP-1 agonist safety protocol: lowest dose + mandatory protein and resistance training
WhatIf using GLP-1 agonists (semaglutide, tirzepatide), combine with: (1) dietary carbohydrate reduction to prevent rebound hunger when dose is lowered; (2) adequate protein intake (at minimum 1g/lb lean body mass) to minimize muscle loss; (3) regular resistance training to preserve lean mass throughout treatment.
WhenFrom initiation of GLP-1 therapy. Muscle preservation is critical because GLP-1 agonists cause muscle and fat loss in roughly equal proportion, but muscle is not recovered after drug discontinuation.
DoseUse the lowest dose that achieves the therapeutic goal. Protein and resistance training maintained throughout the entire treatment period — not started when weight loss stalls.
For whomClinicians prescribing GLP-1 agonists; patients on these drugs; parents of children being prescribed them. Special caution for women of reproductive age.
WhyWeight returns as fat (not muscle) when drug is stopped. Muscle lost during treatment is very difficult to regain, especially with age. This depresses metabolic rate, requiring even less food to maintain the regained higher weight.
CaveatsThe 10-20-year safety data does not exist yet. It is possible GLP-1s will prove safe at population scale; the historical lesson of insulin suggests caution about extrapolating 5-year data to lifetime use.
Taubes: 'Insulin 1922 — it's a lifesaver, it's a miracle drug. And like Ozempic in obesity patients, clearly minimizing complications for the first 5 or 10 years. But then you get to see the long-term complications.' The 60% discontinuation rate in clinical trials means safety data is biased toward tolerators. Fetal programming: mothers who regain weight during pregnancy after stopping GLP-1s may pass insulin resistance to children epigenetically. American Academy of Pediatrics is recommending these drugs for children who may be on them 50-60 years.
When you take these drugs you lose muscle and fat and you gain back the weight usually gaining back as fat and so your metabolism is slower at the end of the process than at the beginning and you need to eat less food in order to just maintain the same weight — it's a real problem unless you eat a lot of protein and do a lot of strength training while you're taking these drugs.
Metabolic health panel: screen for insulin resistance before glucose rises
WhatScreen using the full metabolic cluster: fasting insulin, fasting glucose, HbA1c, triglycerides, HDL, blood pressure, and waist circumference. Track fasting insulin trajectory year-over-year as the earliest detectable signal of insulin resistance.
WhenRoutine annual metabolic screening for any adult, especially those with weight gain, fatigue, carbohydrate cravings, or family history of T2D.
For whomAll adults; priority for overweight individuals, high-carbohydrate dietary pattern, women with PCOS, family history of T2D or cardiovascular disease.
Why93.2% of Americans are metabolically unhealthy by at least one criterion. Standard screening (fasting glucose alone) misses the majority of the insulin-resistance spectrum until the pancreas begins to fail and glucose finally rises — by which point metabolic damage has been accumulating for years.
CaveatsFasting insulin assays vary by lab; reference ranges are set too permissively for early detection. Oral glucose tolerance test with insulin measurement is more sensitive.
Hyman opens the episode noting 93.2% of Americans are somewhere in the insulin-resistance continuum. The current diagnostic threshold (A1c ≥ 5.7% for pre-diabetes) captures only the most advanced cases. The far larger population of asymptomatic insulin-resistant individuals is not identified until disease has advanced significantly.
Recent data from the NHANES trials showed that 93.2% of Americans are metabolically unhealthy, which means there's somewhere in the continuum of insulin resistance — with high blood pressure, high blood sugar, high cholesterol, or have had a heart attack or stroke already.
Present dietary reversal as co-equal first option at T2D diagnosis
WhatWhen diagnosing T2D or pre-diabetes, explicitly present carbohydrate restriction as a co-equal alternative to drug therapy with specific outcomes data: 'Here are two paths. Path A: drugs + standard diet, likely progressive escalation, known complications. Path B: carb restriction, can go into remission, no drug side effects, requires dietary commitment.'
WhenAt diagnosis. Not as an afterthought buried in ADA guidelines but as the first conversation.
DoseThe dietary arm is indefinite — effective while maintained. The drug arm is also indefinite but carries escalating doses and compounding side effects.
For whomPhysicians, nurse practitioners, and dietitians caring for Type 2 diabetics. Patients with new diagnoses.
WhyThe ADA standard-of-care documents acknowledge carb-restricted diets but bury them among multiple equivalent options. The evidence for dietary remission is strong; the evidence that drug therapy prevents long-term complications is weaker than commonly portrayed (ACCORD, UGDP trials).
CaveatsFor patients who cannot or will not maintain dietary change, drug therapy is appropriate — but as the patient's informed choice, not the clinician's default.
Taubes frames the clinical visit: 'What if confronted with a new patient you give them the diagnosis and you say: we can treat your symptoms with drugs, you can continue to eat exactly the way you want — or you can do this diet. No bread, potatoes, sweets, sugary beverages. As far as we can tell, if you eat this way you'll be fine. No drugs, no complications of drugs, no needing more doses, no waiting for new drugs, no dialysis. It might take two or three months to get used to it. Your choice.' This is a clinical conversation that currently almost never happens.
What if confronted with a new patient you give them the diagnosis... look we can do this we can treat your symptoms with drugs you can continue to eat exactly the way you want... or you can do this diet... as far as we can tell if you eat this way you'll be fine — no drugs, no complications of drugs, no needing more doses... your choice.
Reframe carbohydrate cravings as a physiological symptom of insulin resistance, not willpower failure
WhatWhen patients report inability to stick to low-carb diets because of cravings, explain that carbohydrate cravings are a biological symptom of insulin resistance that disappears within 1-4 weeks of strict carbohydrate elimination — not a permanent character limitation.
WhenAt initiation of dietary change and whenever patients report craving-driven non-compliance.
DoseMost patients experience resolution of carbohydrate cravings within 1-4 weeks of strict carbohydrate elimination. Initial difficulty is highest in the first 1-2 weeks.
For whomAny patient who reports food cravings as the primary barrier to dietary compliance.
WhyRefined carbohydrates and sugars activate dopamine reward circuits — the same pathway activated by addictive substances, as confirmed by brain imaging. Insulin resistance drives increased carbohydrate cravings in a positive feedback loop. Removing carbohydrates disrupts the loop and brain chemistry normalizes.
Hyman: 'When you do the right thing, their brain chemistry changes, their hormones change, their metabolism changes, and they don't actually have those cravings — it's not like they use willpower to fix it, use science.' Taubes draws the smoking parallel: 'There was a period in my life where I couldn't imagine going through my life without a cigarette. After a while you won't miss cigarettes.' Carbohydrate addiction has a biological substrate and a withdrawal curve, not a permanent state.
Mechanism
Refined carbohydrates stimulate dopamine release in the nucleus accumbens. Chronic activation sensitizes the reward circuit, increasing craving intensity. Removing the stimulus allows circuit reset; improving insulin sensitivity simultaneously reduces the metabolic drive for carbohydrates.
When you do the right thing their brain chemistry changes their hormones change their metabolism changes and they don't actually have those cravings — it's not like they use willpower to fix it, use science.
Evidence-based audit of diabetes guidelines: ask 'what was actually proven?' before each recommendation
WhatApply the investigative method Taubes used in 'Rethinking Diabetes': go back to primary literature and clinical case records, asking 'What was actually shown in trials versus what was assumed from clinical lore?' Identify where current guidelines rest on 1920s assumptions never formally tested.
WhenRelevant for researchers, guideline-writers, and clinicians who sense a disconnect between patient outcomes and guidelines.
For whomResearch investigators, clinical guideline writers, physicians dissatisfied with the chronic-progressive-disease trajectory of their patients.
WhyThe entire edifice of diabetes drug therapy rests on an assumption (uncontrolled blood sugar causes complications; therefore lower it with insulin) established by clinical lore before randomized trials existed — and directly falsified by ACCORD. The ADA's annual-revision model cannot produce paradigm shifts; it only adjusts the existing paradigm incrementally.
Taubes: 'The physicians who crafted that philosophy had a thousand piece jigsaw puzzle and they had maybe 50 pieces... Now you can get 950 pieces. You can see everything they should have seen but didn't.' Reading 100-year-old textbooks and original case reports revealed decisions made on 50-piece information that now look obviously wrong with 950 pieces. The insulin era shifted clinical consensus so completely that the 120-year dietary consensus disappeared without any trial being done to compare dietary and drug therapy head-to-head.
Now you can get say 950 pieces of that thousand piece jigsaw puzzle — you can see everything they should have seen but didn't. You can go back and not only describe what they did but what they missed.
What's new
Personal practice updates, fresh positions, predictions
8 items
T2D was routinely reversed on ketogenic diet before insulin was discovered
~10 min
From 1797 to 1921, European and American diabetes specialists used a high-fat, near-zero-carbohydrate 'animal diet' as the only effective treatment for what we now recognize as T2D. Patients' symptoms effectively vanished on this regimen; the diet became the standard of care across Germany, Italy, France, and Britain.
Why this matters: Reframes low-carb/keto not as a fringe 21st-century hack but as a 120-year-old medical standard that was abandoned for logistical reasons after insulin discovery, not because it stopped working.
Background
Colonel Meredith, the first well-documented case in 1797, recovered on a diet of fatty meat prescribed by British physician John Rollo. By the mid-19th century the diet consisted of fatty meat and green leafy vegetables, effectively what we now call keto-paleo.
The diet dominated European diabetes care for over 100 years. Swedish specialist Petren was feeding patients 95% fat diets. Elliott Joslin kept his own diabetic mother alive on a high-fat carbohydrate-restricted regimen, and she outlived all her healthy relatives. When insulin arrived in 1922, the practical problem of preventing hypoglycemia — the most dangerous side effect of insulin — led physicians to mandate carbohydrate intake as a buffer, and almost overnight the 120-year dietary consensus evaporated without a clinical trial being done.
By the mid 19th century this animal diet... basically just becomes fatty meat and green leafy vegetables. So it is in effect a ketogenic diet, paleo keto is, and as a time it becomes a standard of care for treating diabetes. So it could keep patients with type 2 diabetes alive indefinitely.
Also said
“It becomes richer and richer with fat because again patients show up in the doctor's office having lost a lot of weight and if they're type one and they're young they're emaciated so the doctors thought we want to put weight back on them and we want to feed them as much food as we can and since you can't give them carbohydrates we can give them fat.”— Explains the clinical logic that led to the high-fat pre-insulin diet and then its abandonment after insulin made carb coverage possible.
The ACCORD trial: intensive insulin therapy increased heart attacks and deaths
~20 min
ACCORD and two companion trials (10,000 diabetics total) were halted early because the arm receiving the most aggressive blood sugar control via high-dose insulin suffered significantly more deaths and heart attacks than the standard-care arm — the opposite of the intended result.
Why this matters: This trial directly falsified the foundational assumption of modern diabetes management: that aggressive blood-sugar lowering via insulin prevents cardiovascular complications. Yet the ADA's response was not to question insulin-centric care but to argue doctors were 'not treating aggressively enough.'
Background
The prevailing theory since the 1920s held that diabetic complications — blindness, kidney disease, neuropathy, atherosclerosis — resulted from uncontrolled blood sugar, so more aggressive insulin should prevent them.
Hyman draws the lesson from his own training: 'We saw these patients come in who were eating a lot of carbohydrates and they were taking 100 or 200 units of insulin and we thought that was fine... but it never occurred to me: what was the normal amount of insulin produced by the pancreas? It's like 20 to 60 units.' By forcing insulin beyond physiological range to cover a high-carb diet, clinicians were compounding hyperinsulinemia rather than addressing it. Patients on high insulin doses then developed weight gain, high triglycerides, high blood pressure, and cholesterol abnormalities — each requiring another drug.
There was a trial that happened that got me completely switched in my thinking — it was called the ACCORD trial — and what they said was look, sugar is the problem, so if we really want to fix diabetes we need to be very aggressive in controlling blood sugar. The consequences of that therapy were that more people died and more people had heart attacks.
Also said
“ACCORD was one of three similar trials; all of them found the same thing. So basically we're talking about a disease that we have been treating in the wrong way.”— Three independent trials converged on the same damning result, ruling out a single-study artifact.
Verta Health trial: nutritional ketosis reversed T2D and improved 20+ cardiovascular markers
~80 min
A multi-year trial by Steve Phinney, Jeff Volek, and Sarah Halberg at Verta Health put Type 2 diabetics on continuous-ketosis dietary therapy with smartphone-based telemedicine support and medication adjustment. Compliant patients achieved remission — A1C normalization, weight loss, and improvement in over 20 cardiovascular biomarkers — without drug escalation.
Why this matters: Directly challenged the 'chronic progressive disease' framing: T2D is only progressive if you keep eating the substance that drives it.
Background
The trial was catalyzed by Sarah Halberg being assigned to run an obesity clinic at Indiana Health with no conventional tools that worked. She trained with Eric Westman at Duke, then joined Steve Phinney and Jeff Volek.
The mechanism: 'It's a disorder of carbohydrate metabolism — tell them not to eat it, they do fine. If you don't take the toxin you don't need the antidote.' In Hyman's clinical practice he replicated these results: a patient with triglycerides over 300, very low HDL, total cholesterol over 300 tried keto — lost 20 pounds, cholesterol dropped 100 points, triglycerides dropped 200 points, HDL rose 30 points, blood sugar normalized. All 20+ cardiovascular biomarkers in the Verta cohort moved beneficially, refuting the concern that high-fat diets worsen cardiovascular risk in diabetics.
For patients who comply with the diet they seem to put this progressive chronic disease into remission. So it's not a progressive chronic disease — it's only a progressive chronic disease if you're eating the toxin.
Also said
“I've seen that over and over again — people just on insulin, get off insulin; on meds, get off meds; normalize your weight, normalize your metabolism. Their A1C goes down, they went from 11 to five and a half in a few months.”— Hyman's direct clinical replication of the Verta findings.
There are no essential dietary carbohydrates
~90 min
Unlike essential fatty acids and essential amino acids, the body has no dietary carbohydrate requirement. The body produces all needed glucose via gluconeogenesis from protein and fat. This metabolic fact has never been incorporated into standard diabetic dietary recommendations.
Why this matters: If there are no essential carbs, then recommending that diabetics consume 50% of calories from carbohydrates is prescribing the substance that causes their disease.
Taubes: 'There are essential fatty acids, there are essential amino acids, there are no essential carbohydrates — the body actually does not need them biologically to thrive.' Hyman adds the clinical nuance: humans have adapted to diets from the near-zero-carb Inuit to the 80% carbohydrate Pima Indians — but the Pima diet consisted of high-fiber, nutrient-dense whole plant foods, not refined starch. The modern diet represents carbohydrate exposure levels the human genome has never previously encountered.
There are essential fatty acids, there are essential amino acids, there are no essential carbohydrates — the body actually does not need them biologically to thrive, even though it's our main fuel source.
GLP-1 agonists (Ozempic/Wegovy) mirror the 1922 insulin euphoria — including unknown long-term risks
~60 min
Taubes draws an explicit parallel between the explosive adoption of GLP-1 agonists today and the 1922 insulin miracle: both were genuine lifesavers for the most severe cases, both were rapidly extended to the general population, and in both cases the long-term complications only became visible a decade later.
Why this matters: Key unknowns: what happens after 10-30 years of use; what happens during pregnancy; whether weight regain after stopping represents permanent metabolic damage.
Background
The University Group Diabetes Program (1960-1970) was the first randomized trial in diabetes pharmacology. It found oral hypoglycemics no better than diet alone — and the drugs carry an FDA blackbox warning for cardiovascular events.
When GLP-1 agonist users stop, weight returns predominantly as fat while muscle lost during treatment is not recovered. This depresses metabolic rate, requiring even less food to maintain a higher weight. The fetal programming concern: mothers who regain weight during pregnancy (after stopping the drug) may pass metabolic dysfunction to children epigenetically. American Academy of Pediatrics is now recommending these drugs for children who may take them for 50-60 years.
What do you do if the drug helps 80% of the patients and causes intractable harm to 20% and you don't find out for 10 years whether you're in the 80% or the 20%.
Also said
“When you take these drugs you lose muscle and fat and you gain back the weight usually gaining back as fat and so your metabolism is slower at the end of the process than at the beginning and you need to eat less food in order to just maintain the same weight.”— Quantifies the metabolic downshift from GLP-1 cycling — a structural risk not captured by 2-year trials.
Richard Bernstein's low-dose insulin protocol: Type 1 diabetics on keto need only 1-2 units/day
~75 min
In the 1970s, Richard Bernstein pioneered minimizing insulin doses in Type 1 diabetes by simultaneously minimizing carbohydrate intake. Hyman knows a physician with Type 1 who manages on just 1-2 units of insulin daily on a ketogenic diet, versus the 100+ units commonly used in standard care.
Why this matters: Demonstrates that even Type 1 — a disease of absolute insulin deficiency — benefits dramatically from dietary carbohydrate restriction, reducing dose requirements and hyperinsulinemia side effects.
Bernstein's insight echoed Elliott Joslin's original approach before the carb-permissive era: minimize doses, use diet to make those minimal doses sufficient. The low-carb approach reduces both the amplitude and variability of blood glucose swings, which is the source of most insulin-dosing error and hypoglycemia risk.
This is was Richard Bernstein's Revelation in type one diabetes in the 70s — let's use the lowest doses and craft a diet that allows those lowest doses to be effective, which is basically lower starch and sugar and higher fat.
Also said
“We have a friend in common who is a type 1 diabetic who's a doctor who basically uses one or two units of insulin a day because she's on a ketogenic diet. So she needs very very low doses — she needs a little but not that much.”— Real-world proof of concept: a physician managing their own Type 1 on 1-2 units versus 100+ in standard care.
Insulin is a fat-storage hormone — giving more insulin to insulin-resistant patients worsens obesity
~40 min
Fat cells are the most insulin-sensitive cells in the body. The tiniest circulating insulin signal halts lipolysis completely. High-dose insulin therapy in T2D patients — already hyperinsulinemic — drives weight gain and locks stored fat in adipose tissue, worsening the underlying disorder.
Why this matters: Explains why patients on insulin routinely gain 40-80 pounds and why 'double diabetes' (Type 1 developing insulin resistance from high-dose coverage of high-carb diets) is a clinical reality.
German and Austrian researchers established in the 1950s: fat cells respond primarily to insulin, not to total caloric intake or exercise. Raise insulin → drive fat accumulation, block fat mobilization. A Type 1 diabetic untreated can eat 10,000 calories and still lose weight because without insulin, fat cannot be stored. The implication — that treating T2D with high insulin doses while allowing high carbohydrate intake is metabolically incoherent — was never tested in a controlled trial.
Insulin is a fat storage hormone. And apparently no cell in the body is as sensitive to insulin as a fat cell. So if there's the tiniest bit of insulin in your circulation it's going to shut down mobilization of fat.
The Look AHEAD trial ($200 million): weight loss via low-fat diet did not reduce diabetic complications
~85 min
Look AHEAD was a $200 million trial designed to show that weight loss in T2D patients reduces cardiovascular complications. Participants lost meaningful weight on a conventional low-fat diet — and their complication rates were no better than controls. The trial was halted for futility.
Why this matters: Invalidates the 'just lose weight' prescription if weight is lost via low-fat calorie restriction. The mechanism matters, not just the pounds — carbohydrate removal, not calorie restriction, is the active ingredient.
Taubes had warned investigators before the trial: add a low-carb arm. They refused because low-carb was still considered fringe. The result proved the wrong diet, regardless of weight lost, does not fix the underlying metabolic dysfunction. David Nathan of Harvard called for 'an adult conversation about this' in the New York Times — which never happened.
They do this huge Look AHEAD trial — $200 million — to demonstrate that if you lose weight you'll reduce diabetic complications. They get them to lose weight and it doesn't make a damn bit of difference. Trial was ended for futility.
Recommendations
Products, supplements, and tools mentioned in the episode
2 items
The Big Fat Surprise by Nina Teicholz
Book
Teicholz's investigative book on the origins of the dietary fat hypothesis and the weak evidence behind low-fat dietary guidelines — a companion to Taubes's work from a different investigative angle.
Teicholz is Taubes's co-author on the Unsettled Science newsletter and applies the same evidence-audit methodology to dietary fat guidelines. Hyman's endorsement signals alignment with the broader intellectual project of questioning nutrition-science orthodoxy through rigorous historical and clinical-trial review.
Nina Teicholz who wrote a book called The Big Fat Surprise — also another great book.
A pediatrician-turned-medical-historian's account of Elliott Joslin's patient records from the early insulin era, documenting the 'tidal wave of diabetic complications' that emerged in insulin-treated patients in the 1930s.
Taubes credits Feudtner's research with illuminating the pattern: patients 'thriving' on insulin therapy would deteriorate rapidly over one or two years from multi-system vascular disease. Feudtner could not conclusively answer whether the complications resulted from high blood sugar, high insulin doses, high carbohydrate diets, or some combination — because no trial had been done to separate them. The lesson: the history of insulin therapy contains a cautionary signal about treating metabolic disease with hormone replacement without addressing the dietary substrate.
There was a wonderful book by a pediatrician turned medical historian named Chris Feudtner called 'Bitter Sweet' where he got a hold of Joslyn's records from his early years and these patients would be thriving and then over the course of a year or two their bodies would just fail them.
A historical investigative work tracing how the modern standard of care for diabetes was built on 50-piece jigsaw-puzzle evidence from the 1920s — and what the now-950-piece picture actually shows about dietary reversal.
DisclosureGuest's own book, explicitly promoted throughout the episode.
Hyman: 'I've been savoring it every night — it's like a mystery novel about the history of diabetes and what's gone wrong in our approach.' The book is structured as a narrative with detective-story framing, designed to be read by clinicians who believe the current consensus and need their assumptions shaken. The epilog covers the history of the evidence-based medicine movement and how even EBM failed to ask the right questions about diabetes therapy.
I have loved this book — I've just been savoring it every night, it's like a mystery novel about the history of diabetes and what's gone wrong in our approach to this condition.
The foundational book arguing that insulin, not total calories, regulates fat metabolism — and that carbohydrate quality is the primary driver of obesity, T2D, and cardiovascular disease.
DisclosureGuest's prior work, mentioned multiple times as foundational context.
Taubes: 'The argument I began making in Good Calories Bad Calories — that fat storage is regulated independently from how much you eat and exercise — it's still with me in this one because it's to me clear as day.' The book was controversially criticized in the New York Times by Gina Kolata, who said 'diabetes specialists have proven that a calorie is a calorie.' Taubes wrote back citing basic endocrinology: every macronutrient produces a different hormonal response — a point any diabetes specialist actually understands.
The argument I began making in Good Calories Bad Calories — as you point out it's been in every one of my books and it's in this one too because it's to me clear as day.
Unsettled Science newsletter on Substack (Gary Taubes + Nina Teicholz)
Service Sponsored · disclosed
A newsletter providing an alternative point of view on nutrition science co-authored with Nina Teicholz, author of The Big Fat Surprise.
DisclosureGuest's own newsletter, promoted at the close of the episode.
Hyman frames both Taubes and Teicholz as investigative journalists who bring the evidence-based question 'why do we do this, what's the evidence?' to nutrition science — a discipline historically driven by expert consensus rather than rigorous clinical trial data. The newsletter extends the method of 'Rethinking Diabetes' to ongoing nutritional science controversies.
I would encourage you to check out his newsletter called Unsettled Science on Substack — he writes it with Nina Teicholz who wrote a book called The Big Fat Surprise — and it's a great way to sort of get another point of view about nutrition that you might not be hearing through conventional channels.
Lines worth pulling out — contrarian, specific, or perfectly phrased
6 items
If you don't take the toxin you don't need the antidote. It's a disorder of carbohydrate metabolism — tell them not to eat it, they do fine.
The cleanest restatement of the episode's central thesis: T2D is caused by a substance; stop the substance, stop the disease.
Recent data from the NHANES trials showed that 93.2% of Americans are metabolically unhealthy, which means there's somewhere in the continuum of insulin resistance.
Reframes the metabolic crisis at full scale: this is not a minority problem, it is the dominant state of the American population.
Insulin is a fat storage hormone. And apparently no cell in the body is as sensitive to insulin as a fat cell. So if there's the tiniest bit of insulin in your circulation it's going to shut down mobilization of fat.
The physiological mechanism explaining why prescribing more insulin to insulin-resistant patients worsens obesity rather than improving it.
There was a trial that happened that got me completely switched in my thinking — it was called the ACCORD trial — the consequences of that therapy were that more people died and more people had heart attacks than who didn't have the intensive therapy.
The most clinically important single data point in the episode — three trials converged on this finding and the field still has not changed its paradigm.
What do you do if the drug helps 80% of the patients and causes intractable harm to 20% and you don't find out for 10 years?
The epistemic challenge to GLP-1 agonist enthusiasm: the long-term safety data does not exist yet, and the history of miracle diabetes drugs is not reassuring.
When you do the right thing their brain chemistry changes their hormones change their metabolism changes and they don't actually have those cravings — it's not like they use willpower to fix it, use science.
Reframes dietary compliance from a moral contest to a physiological prediction: fix the biology, the cravings go with it.
Sign in to share feedback
Tell us if this brief hit the mark or missed it — feedback feeds back into the next iteration of the prompt.
Reading is free for everyone. A free account adds the personal layer: save protocols, follow experts, and see how the other experts weigh in on this same topic.
Educational summary of the cited expert source — not medical advice. Open the source recording linked above and consult a qualified physician before acting on any protocol.
