@garytaubes
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Author of Rethinking Diabetes, The Case for Keto, The Case Against Sugar, Why We Get Fat, Good Calories, Bad Calories, Bad Science, and Nobel Dreams
Oakland, California
Joined June 2009
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1960: < 2 million Americans with diagnosed diabetes
Today: 30 million*
Is this a problem that can be solved by drug therapy?
There must be a better way
My new book, Rethinking Diabetes, is out Jan 2
tinyurl.com/5ft2btcy
#diabetes #wefightdiabetes
* cdc.gov/diabetes/data/statis…
@diabetesdaily
@ADA_DiabetesPro
@IntDiabetesFed
@JoslinDiabetes
@diaTribeNews
@Diabetescouk
@BeyondType1
@DiabetesCanada
@ADCESdiabetes
@Diabetes_DRI
@martymakary
@samiinkinen
@bretschermd
@davidludwig
@lowcarbgp
@robbwolf
@drjasonfung
@KenDBerryMD
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gary taubes retweeted
The Endocrine Society has a new "scientific statement" on the gaps (or rather black holes) in obesity science.
@garytaubes shines cosmic light on the matter.
If you don't subscribe to his Substack, this essay alone is worth the price.
Here’s a question from my latest Substack post. It's about obesity and obesity medicine and it should be rhetorical. Regrettably, it's not:
Q. If you were going to study a disorder of excess fat accumulation (i.e., too much fat in fat cells) and the action of the drugs that so spectacularly treat it, wouldn’t you be at least vaguely interested in the physiological mechanisms that determine how much fat those fat cells will store?
1. Yes?
2. No?
Common sense (and the history of obesity science) might suggest the answer has to be yes, but the expert authors of a recent Endocrine Society Scientific Statement on “Obesity science, research gaps, and opportunities in the new era of obesity medicines,” would claim otherwise.
They put the brain at the center of obesity science and GLP-1 action, then omit (ignore?) a century of science suggesting that since it's the fat cells that get fatter in obesity, the direct neuroendocrine regulation of fat storage in those cells must be relevant.
These expert authors include @kevinhallPhD and @danielJdrucker and a half dozen others, and we can assume they know more about obesity than anyone.
They’re the experts.
But if so, why do they ignore the fat cell itself when discussing why we accumulate excess fat in fat cells, and why GLP-1 drugs do such a remarkable job of reversing that process?
What are they missing with their conviction that obesity is an "appetitive behavior" disorder?
The Black Hole at the Galactic Core of Obesity and GLP-1 Drug Science uncertaintyprinciples.substa…
Here’s a question from my latest Substack post. It's about obesity and obesity medicine and it should be rhetorical. Regrettably, it's not:
Q. If you were going to study a disorder of excess fat accumulation (i.e., too much fat in fat cells) and the action of the drugs that so spectacularly treat it, wouldn’t you be at least vaguely interested in the physiological mechanisms that determine how much fat those fat cells will store?
1. Yes?
2. No?
Common sense (and the history of obesity science) might suggest the answer has to be yes, but the expert authors of a recent Endocrine Society Scientific Statement on “Obesity science, research gaps, and opportunities in the new era of obesity medicines,” would claim otherwise.
They put the brain at the center of obesity science and GLP-1 action, then omit (ignore?) a century of science suggesting that since it's the fat cells that get fatter in obesity, the direct neuroendocrine regulation of fat storage in those cells must be relevant.
These expert authors include @kevinhallPhD and @danielJdrucker and a half dozen others, and we can assume they know more about obesity than anyone.
They’re the experts.
But if so, why do they ignore the fat cell itself when discussing why we accumulate excess fat in fat cells, and why GLP-1 drugs do such a remarkable job of reversing that process?
What are they missing with their conviction that obesity is an "appetitive behavior" disorder?
The Black Hole at the Galactic Core of Obesity and GLP-1 Drug Science uncertaintyprinciples.substa…
In the past two years, 14 studies have exploited the same remarkable natural experiment: the end of sugar rationing in Britain in 1953.
All have come to essentially the same conclusion: greater exposure to sugar early in life is associated with more chronic disease decades later—diabetes, heart disease, cancer, depression, dementia, and more.
These studies aren’t appearing in obscure journals. They’re being published in Science, the BMJ, PNAS, the American Journal of Clinical Nutrition, Nature Communications, and elsewhere.
Meanwhile, @tamarhaspel of the @washingtonpost confidently tells us in a recent column: “The real problem with sugar is simply that we like it.”
So why the confidence? And what do we do with this remarkable body of new evidence?
Ultimately, the question is one we’ve been arguing about for decades: Should we treat sugar as a chronic toxin—or as a benign indulgence that becomes harmful only because it provides excess calories?
Is Sugar Toxic? Can It Cause Cancer? CHD? Frailty? Dementia?
Read the post on Uncertainty Principles
uncertaintyprinciples.substa…
Do GLP-1 drugs work by inhibiting appetite or by prioritizing fat oxidation over storage--changing metabolic fuel partitioning, in the lingo?
Most researchers (and X influencers) will insist it's the former, but they'll do so because they don't think deeply about the alternative.
Maybe the new paper by Friedman & Lund will help. 🤞
Well, this is nice to see.
And from Sam Klein of all people. He was a co-author on two major Atkins studies in the 00s, but seemed to be stumbling blindly over the results.
He seems to have his eyes open now.
Signs of a paradigm shifting?
When we were dating, my engineer now-husband was floored that I didn’t trust Scientific American’s take on nutrition.
After we were married my husband adopted Keto and lost his T2 diabetic dawn effect and fatty liver disease. On Keto, eventually his labs made him appear to be non-diabetic
Now, 14 years since I first objected to nutrition à la Scientific American it looks like the magazine is finally coming around 😊
I have @garytaubes to thank for the insights in his book, Good Calories, Bad Calories, that started my low carb journey. Nicely done, Gary Taubes 🌸
@sciam
scientificamerican.com/artic…
gary taubes retweeted
Excited to see the evidence base for ketogenic therapies as a treatment for severe mental illnesses and neurocognitive disorders continue to advance!
This systematic review and meta-analysis includes 73 studies.
More are on the way!
nature.com/articles/s41398-0…
I've never been a fan of the American Heart Association's version of the diet-heart hypothesis.
But what if they're right?
Shouldn't we all work diligently to lower our LDL by diet?
Let's work through the numbers and see what we have to gain.
If you're curious about how a public health campaign acknowledging "negligible benefit" for most of us became the foundational proposition of our dietary wisdom, read on...
Lowering LDL: Surely, a “Heart-Healthy” Diet is Worth the Effort. Isn’t it? uncertaintyprinciples.substa…
gary taubes retweeted
We recently hosted a Capitol Hill briefing on how nutrition can address chronic disease, improve health outcomes, and reduce healthcare costs in the era of GLP-1s.
Watch highlights featuring @RepDavids, Dr. Maya Maroto, @bschermd, @DoctorTro, and Dr. Caroline Roberts.
Question of the day: Why would you ever eat a fad diet?
1. Because you’re a frivolous person, and this is the kind of thing frivolous people do.
2. Because you lack the critical skills necessary to understand why our nutrition authorities don’t take such a diet seriously?
3. Because you’ve been living with an intractable diet-related health issue for far too long, and the conventional dietary approaches have failed you.
4. Because a relative, friend, co-worker, TikTok influencer, or maybe even (heaven forbid) your doctor suggested it might cure what ails you, and so, what the hell? Why not?
NY Times writers will invariably suggest 1 or 2. Maybe because I think conventional diets are doomed to fail, and I eat a fad diet, I’m going with 3 and 4.
Now RKF Jr and his Republican colleagues (or cronies, depending on your political affiliation) are eating a meat-and-sauerkraut diet.
Why would they do such a thing? And how do you think the Times reported it? How about the WSJ?
Blah Health Journalism: Meat, Sauerkraut and Politics Edition. uncertaintyprinciples.substa…
And please listen to this, too.
We tend to forget that treating the symptoms of obesity and diabetes does precious little or nothing to prevent their appearance.
At our congressional briefing, @RepDavids explains why the U.S. healthcare system must do more to prevent chronic disease before people get sick.
Watch to learn about bipartisan efforts to expand Americans' access to fresh produce, nutrition counseling, and more.
Please Listen. 5 minutes of your time.
Obesity researchers believe the brain defends body weight by regulating how many calories we consume and expend. It monitors our fat stores, turning hunger up or down as necessary to keep them stable.
Decades ago, though, researchers in the field of physiological psychology, who actually study the physiological basis of hunger, reached a very different conclusion.
They concluded that the brain doesn't care about how fat we are, or how much we’ve just eaten, but is monitoring the energy status of our cells—whether they are producing energy or depleting it.
Remember ATP from high school biology? The “molecular unit of currency” for moving energy around the body? Unlike fats and carbohydrates, ATP cannot be stored. An animal deprived of food survives for days or longer; an animal whose ATP production is shut down by a toxin survives for seconds.
Both theory and evidence were compelling, but the obesity researchers knew nothing about it, and they still don’t. (They didn’t read the physiology journals, and the physiological psychologists—PhDs, not MDs—weren’t presenting at obesity conferences.)
If it’s true, though, it changes radically how we think about obesity, hunger, and, yes, food noise—and why the GLP-1 drugs so famously shut that down. It puts our livers at the center of the metabolic universe, not our brains.
(And even Karl-Anthony Towns comes into this story.)
Karl-Anthony Towns, Food Noise, and Why GLP-1 Drugs Quiet the Brain open.substack.com/pub/uncert…
gary taubes retweeted
Mental health and metabolic health are deeply interconnected, and the science is advancing rapidly.
Join us virtually for this Harvard Medical School-accredited CME/CE course September 16–19, 2026.
We'll explore the latest research and practical clinical applications related to mental health, metabolism, nutrition, lifestyle interventions, and integrated care models.
Only 9 days left to take advantage of the early registration discount.
I hope you'll join us!
learn.hms.harvard.edu/progra…
I'm looking forward to LowCarbUSA in San Diego next month.
This year I'll be talking about why anyone would do a diet as extreme as keto or carnivore if it wasn't necessary.
The new code is 'JulySavings'.
Should be fun and informative, as always.
There's a moment, for a lot of people, when the story they've been told about food, weight, and metabolic health stops making sense…
For many in this community, Gary Taubes is the person who lit the match.
The science journalist behind Good Calories, Bad Calories; Why We Get Fat; The Case Against Sugar; The Case for Keto; and Rethinking Diabetes has been part of LowCarbUSA from the very first San Diego event 11 years ago.
This August, he returns to the stage.
That shift — from a dozen physicians a quarter century ago to tens of thousands today — didn't happen because the theoretical debate was won.
It happened because clinicians and patients witnessed what changed:
- weight loss
- falling A1C
- lower blood pressure
- reduced hunger
In San Diego, Taubes is weighing two talks: the lost history of obesity science, or the clinical case for ketogenic diets — and why the popular "ultra‑processed" label may be too broad to explain what foods actually do to blood sugar, insulin, hunger, and fat storage.
Read the full story and join the movement.
buff.ly/iN5Bjef
2026 Symposium for Metabolic Health
📍 Wyndham San Diego Bayside
🗓️ August 13–16
Final days — use code SummerSavings for 10% off your full registration, only through July 4.
buff.ly/iWurpuV
#TheSMHP #MetabolicHealth #MHP #NeverStopLearning #SymposiumForMetabolicHealth #GaryTaubes #EvidenceBasedMedicine #TCR
gary taubes retweeted
Proud to share a study lead by PI Judy Ford which I was a co-investigator at @UCSF on: the first randomized controlled trial of ketogenic therapy in schizophrenia-spectrum and bipolar disorders, out now in Schizophrenia Bulletin.
Key results: keto was feasible, metabolic markers improved significantly at 1 month, and the 4-month extension showed significant psychiatric symptom reduction and better cognition.
58 participants at UCSF. 1-month RCT + optional 4-month keto extension.
Early evidence — but a real step toward metabolic treatments for serious mental illness.
Paper: doi.org/10.1093/schbul/sbag0…
Does this make any sense to you? Evolution (or your deity of choice) goes through all that trouble to induce us to procreate and assure the survival of our genes and our species, and then it makes the actual act of giving birth so painful, prolonged, and dangerous that it can kill or disable both mother and child just for going through with it.
Now that a new study may have killed the conventional explanation of the Obstetrical Dilemma, maybe we should consider the unconventional. Dare we suggest diet matters?
Shouldn’t Giving Birth Be (Reasonably) Easy? open.substack.com/pub/uncert…
gary taubes retweeted
Results of the first-ever randomized controlled trial testing ketogenic therapy in people living with schizophrenia and bipolar disorder were just published in Schizophrenia Bulletin.
Here's what was found 🧵
gary taubes retweeted
They expected to learn more about digestion.
What they found changed the history of diabetes.
In 1889, Oskar Minkowski and Joseph von Mering at the University of Strasbourg surgically removed a dog’s pancreas.
They were studying the pancreas’ digestive enzymes and their role in fat digestion.
What happened next surprised them.
The dog developed polyuria, and its urine contained glucose.
The experiment provided the first compelling evidence that the pancreas played a critical role in preventing diabetes, decades before insulin was discovered.
You can read more about it in @garytaubes’ excellent book Rethinking Diabetes.
gary taubes retweeted
The Futility of Calorie Counting:
“You could put sawdust into a bomb calorimeter and you would get basically 4 calories per gram.... If you’re a termite, yes, you’ll get calories from it. But humans won’t.”
apnews.com/article/calories-…
