The first answers a Vice story that the drugs may make your fingernails fall off. The study behind it was a questionnaire. People ticked a box, and no one examined a nail. The paper is on the site: No, GLP-1 drugs won’t detach your fingernails.

The second answers an Apple News story on whether you can stop the drug and keep the weight off. Its hopeful answer rests on a Cleveland Clinic figure of 45%, which measures something different from the trials. The trials say most of the weight comes back within a year. The paper is on the site: Can You Stop a GLP-1 Drug and Keep the Weight Off?.

The series so far:

· No, GLP-1 drugs won’t detach your fingernails

· Can You Stop a GLP-1 Drug and Keep the Weight Off?

· GLP-1 Side Effects and the Dose

· Can You Really Wean Off a GLP-1?

· Does GLP-1 Make You Blind?

· Is Taking a GLP-1 Drug Cheating?

There seems to be a common bias against using GLP-1 drugs, for a reason I don’t know. If you have thoughts on this, please add a comment.

Most of the side-effect stories are overblown. Apart from nausea and other stomach trouble most people already expect, the side effects in the news are rare, and some stories are anecdotes with no supporting studies. The side effects that have been measured become more common as the dose goes up, and that matters because many people are taking more of the drug than they need. That means the dose should be set with a doctor who monitors how the patient responds, rather than stepping up to the maximum on a fixed schedule.

· Dietary advice. Where it is on solid ground, where it is not, and how to tell the two apart.

· Predicted lifespan after a serious diagnosis. When a patient with cancer or another serious condition is given a number of months or years, where does that number come from? And what does it mean for one person?

· Living longer versus living well. Much of medicine aims at more years. Not all of it aims at better ones. When the two pull apart, the claims get hard to read.

A large proportion of the small but growing subscriber list supported the list and suggested additional topics. I will respond in the next subscriber newsletter.

Here is the first of the series. It asks what dietary research has settled, what it has not, and what survives of the common advice. There will be more of these.

We have all been told to cut fat, cut salt, take fish oil, eat five a day and eat plants instead of meat. I went through the studies behind seventeen of the most common recommendations and read each one with the six faults in mind.

The first thing to say is that dietary research is hard. People cannot remember what they ate, the people who eat well also live well in other ways, and a trial that could settle the question would take decades. Some of the research was sound, and it helped people who already had something wrong. But most of the recent claims rest on faulty research and are overblown. That does not make them false. It makes them unproven.

The paper ends with what anthropology adds. The populations that stayed free of heart disease ate a variety of plants and some meat, and stayed active. That is where the evidence leaves us.

The paper is on the site: A Healthy Skeptic Looks at Diet Research

The subject is the physician advice videos on YouTube. I read the transcripts of fifty of them, covering twenty-one topics from statins to menopause hormone therapy, and they all follow the same twelve-step script: the hook, the credential, the story, the mechanism, the prescription, and, at the end, the request to subscribe. The mechanism does the persuading. Almost every video explains one, and almost none provides a baseline for its numbers. The script is built for watch time, and the advice comes second.

The paper is on the site: The Script Behind Physician Advice Videos.

I’ve written the whole story up as a case study on the site: Dietary Cholesterol and Heart Disease. It starts with why the cholesterol you eat is not the cholesterol in your blood test. Then it takes four claims apart. The 17% headline leaves out how many people it affects. The studies behind it compare egg eaters with other people and can’t separate the egg from the eater. The 300 mg limit has no known source. And a 2025 trial said to clear eggs was too small to settle anything.

The takeaway

Eating eggs may raise LDL a little, but not at a level shown to affect your health. No one has tested whether cutting eggs prevents heart disease. The limits you’ve heard, 300 mg or one egg a day, don’t come from any line in the data.

The numbers and every source are in the case study: Dietary Cholesterol and Heart Disease at healthy-skepticism.com.

Thanks to the subscriber who suggested this topic.

The weaning story

Apple News is carrying a Women’s Health piece under the headline “Experts Say It’s Possible to Maintain Weight Loss After Quitting a GLP-1. Here Are the Exact Steps to Take.” Forbes ran a physician’s list of five strategies for the same purpose. Both take it as given that getting off the drug is the goal, and that a patient who follows the steps will get there.

I checked the steps against their evidence, and the result is on the site: Can You Really Wean Off a GLP-1? The short answer is no, not by any method that has been tested. No trial has compared weaning against stopping outright. The one built to do so has no results yet. In the trials that did stop the drug, most of the lost weight came back within a year. And the steps themselves, protein, fiber, exercise, weigh-ins, are the advice people were given before the drugs existed. That advice failed most of the people who followed it. That is why the drugs exist.

Why the goal is the shaming

The harm in these articles is not the advice. Protein and exercise are fine. The harm is the goal they set without any basis: that a reasonable patient should be working toward the day they stop.

Nobody writes that article about blood pressure pills. Nobody tells a person with type 1 diabetes that the exact steps will get them off insulin. Those are understood as maintenance treatments. A signal the body does not supply has to keep being supplied, and stopping means the condition comes back. GLP-1 drugs work the same way. Appetite is regulated by hormones, one of those hormones runs weak in people carrying extra weight, and the drug supplies it.

So when a magazine sets total weaning as the goal, it hands patients a test that most of them will fail, and then a verdict. The weight came back. You did not follow the steps well enough. That is the old willpower story wearing a lab coat, and it is the same story that made people feel they were cheating by taking the drug in the first place. I wrote about that one in the first issue: Is Taking a GLP-1 Drug Cheating?

The governor

The other story is JB Pritzker, in the Chicago Sun-Times on September 21. He has lost 80 pounds over two and a half years on a GLP-1 drug. He was diagnosed with type 2 diabetes at 58, went on insulin, switched to the GLP-1, and has been off insulin for nine months with normal blood sugar. He walks along the lake most mornings and plays tennis with his daughter.

Asked whether the drug is cheating, he said: “I don’t think it’s cheating. I think it’s what I need to succeed.” He described the food noise going quiet the way patients describe it. He used to want the whole cake. Now one slice is enough, and he does not walk around thinking about the next meal.

Two things in that interview matter for this issue. He waited to go public until he was confident the weight loss would persist. And he did not announce a plan to get off the drug. He described a treatment that is working and a life that is better for it. That is what maintenance looks like when the patient is not being shamed about it.

The takeaway

Getting off the drug is not a goal the evidence supports. No taper has been tested against stopping, and the advice offered for holding the loss is the advice that failed before the drug. Staying on a treatment that works is not a failure. It is what maintenance means, and nobody owes anyone a demonstration that they tried to quit.

Whether to continue, taper, or stop is a decision for you and your doctor. The papers say what the evidence can and cannot promise. They do not say what you should do.

Sources: Pines JM, Forbes, 7 September 2026. Women’s Health headline via Apple News, September 2026. Sfondeles T, Chicago Sun-Times, 21 September 2026. Wilding JPH et al. Diabetes, Obesity and Metabolism 2022;24:1553–1564. Aronne LJ et al. JAMA 2024;331:38–48. Budini B et al. eClinicalMedicine 2026;93:103796. Yevusiak T et al. PLoS One 2026;21(7):e0354237 (the REST protocol). Mann T et al. American Psychologist 2007;62:220–233. Sumithran P et al. New England Journal of Medicine 2011;365:1597–1604.

What Is a Healthy Skeptic

This paper explains the foundations of healthy skepticism. You do not need it to read anything else on the site, but everything here rests on it, and it is where the name for readers of this newsletter comes from.

Two careful people read the same study and reach opposite conclusions. Neither has misread it. How is that possible? The paper answers that, with a vaccine argument, a drug advertisement, a tax audit, and a jury as the test cases.

What Is a Healthy Skeptic (PDF, 4 pages)

Is Nicotine Good for You?

The second paper is a case study, the kind this newsletter said it would take up: a claim in circulation, worked through. Nicotine pouches are being sold as a focus aid, a brain protector, and a safer habit, with a Stanford neuroscientist and a well-known investor among the promoters. “Nicotine is good for you” turns out to be four claims, and each of them has a true fact under it. The paper takes them one at a time and shows where the step from the fact to “good for you” goes wrong. Four of the six faults, in one product.

Is Nicotine Good for You? (PDF, 5 pages)

Subscribers get something extra. Between issues I’ll send subscriber-only posts about the newsletter itself: what’s coming up, what I’m looking at, and how the project is evolving.

Subscribers also get the course materials. The Healthy Skepticism course covers six faults in medical reasoning over five sessions. The slides, the take-home summaries, and a paper on each fault are on the website at healthy-skepticism.com/students.html, behind a password. Subscribers get the password.

More importantly, subscribers get to weigh in. Before I write the next issue, I want to hear what claims or headlines you’d like me to look at. Reply to any post or use the Substack app. I read every message.

It’s free. One email a week, plus the occasional subscriber post. You can unsubscribe any time.

People taking semaglutide or tirzepatide, sold as Ozempic, Wegovy, Mounjaro and Zepbound, often report a particular discomfort. Not about side effects or cost, but about legitimacy. They feel they are taking a shortcut around something they should have managed themselves. Friends and family sometimes say so out loud.

That feeling rests on an assumption worth examining: that body weight is under voluntary control, and that a medication which reduces appetite substitutes for effort the person should have supplied.

The assumption is wrong, and the reasons are not controversial.

Appetite is a regulated system, not a decision

Body weight is centrally regulated. Signals released from the gut, the pancreas, and fat tissue are integrated in the brain, mainly in the hypothalamus, and those signals govern food intake and energy expenditure.

Sumithran P et al., New England Journal of Medicine 2011;365:1597-1604.

This inverts the usual picture. Hunger is not generated by choice and then overridden by willpower. It is produced by a control system that receives hormonal inputs and sets the strength of the drive to eat. Conscious effort works on top of that system, not in place of it.

One of those inputs is glucagon-like peptide-1, usually written GLP-1. It is released by cells in the intestinal lining when food arrives. It slows the emptying of the stomach, increases the sensation of fullness, prompts the pancreas to release insulin, and suppresses the release of glucagon.

Madsbad S, Diabetes, Obesity and Metabolism 2014;16:9-21.

What happens when you lose weight by dieting

This is the finding that does the most damage to the willpower story, and it comes from a study with an unusually clean design.

Fifty people with overweight or obesity completed a ten-week very-low-energy diet and lost roughly 13.5 kg on average. Their appetite hormones were measured three times: before the diet, immediately after it, and again at 62 weeks.

A year after the weight loss, the hormonal picture had not returned to where it started. Leptin, peptide YY, cholecystokinin, insulin, ghrelin, gastric inhibitory polypeptide and pancreatic polypeptide all remained significantly different from their pre-diet values. Ghrelin, which drives hunger, remained elevated. So did the participants' own reported hunger.

Sumithran P et al., New England Journal of Medicine 2011;365:1597-1604 (n = 50).

A year after losing the weight, these people were hungrier than before they started. Nothing about their character had changed. Their physiology had.

The authors put it plainly: the signals that encourage weight regain do not revert after diet-induced weight loss, and long-term strategies are needed to counteract that change.

Related work found that the drop in energy expenditure after large weight loss can persist for years. The body defends its former weight from both directions. It burns less and it wants more.

Fothergill E et al., Obesity 2016;24:1612-1619.

Where GLP-1 fits

GLP-1 signalling runs weaker in people with obesity than in people whose weight regulation is working. This has been measured in a large standardized study spanning normal weight through obesity, and it holds whether or not the person has any problem with blood sugar.

Faerch K et al., Diabetes 2015;64:2513-2525 (the ADDITION-PRO study, 1,462 participants).

So the signal that tells the brain a meal has arrived and fullness should follow is arriving faint.

What the medication does

Semaglutide and the related drugs activate the same receptor that natural GLP-1 activates. They are engineered to resist the enzyme that destroys natural GLP-1 within about two minutes, which is why they can be given weekly instead of by continuous infusion.

Functionally, the medication supplies a regulatory signal the body is not producing at sufficient strength. Appetite falls not because the person has acquired discipline but because the system that generates hunger is finally receiving the input it needs.

This is why the experience patients describe is so consistent, and so strange to them. The constant background negotiation about food goes quiet. That is not willpower arriving late. It is a control loop closing.

Why "cheating" does not apply

Set the biology aside for a moment. The concept itself does not fit.

Cheating means gaining an unfair advantage in a contest. Managing your own health is not a contest. There is no opponent, and no prize awarded for suffering more on the way to the same outcome.

Corrective lenses are not cheating at seeing. Insulin is not cheating at glucose regulation. A hip replacement is not cheating at walking. In each case a bodily function is not being performed adequately and a medical intervention performs it instead. Nobody asks the patient to first prove they tried hard enough without it.

Obesity attracts the accusation and short-sightedness does not. That distinction is not a scientific one. It is an inherited moral story about body weight that the physiology does not support.

What this means about stopping

The same explanation says something about how these drugs are likely to be used, and patients hear it as bad news when it is not.

If the medication supplies a signal the body is not producing at sufficient strength, then stopping returns you to the state in which it was not being produced. The weight comes back. This is not a failure of the drug, and it is not evidence that the loss was artificial.

It is what maintenance treatment looks like. Nobody expects blood pressure to stay down after the pills stop, or thyroid hormone to be a course you finish. Insulin is the closest parallel: a signal the body cannot supply in sufficient quantity, replaced for as long as that remains true.

Weight returning after you stop is the argument working, not failing. A signal that has to be supplied has to keep being supplied.

A natural question is whether a lower maintenance dose can hold the new weight. This is not yet established practice: no trial has tested a maintenance regimen, and guidelines are silent on it. Finding your maintenance dosage is something you need to do with your doctor's support.

If someone tells you it is cheating

Most of the time the remark is not an argument. It is a reflex, and it does not survive a question.

The useful question is what they think you are cheating at. There is no contest here, and once that is said out loud the accusation usually has nowhere to go.

If they want the substance, it fits in three sentences. Your body regulates weight with hormones, not with resolve. One of those hormones runs weak in people carrying extra weight. The medication supplies it, the way glasses supply focus a lens no longer provides.

And if they say the weight will come back if you stop: yes, that is how maintenance treatment works. It is true of blood pressure medication and of insulin, and nobody calls those cheating either.

You do not owe anyone a demonstration that you suffered enough first.

The paper with its full reference list: Is Taking a GLP-1 Drug Cheating?

This paper is educational and is not medical advice. Decisions about starting, continuing, or stopping any medication belong with you and your physician.

If a claim is puzzling you, send me an email. I will reply and consider it for the next newsletter. If this one was useful, forward it to one person who would want it.

Murray Cantor PhD

Medical information arrives every day. Headlines, drug advertisements, guidelines, test results, diagnoses. Most of it is harder to read than it looks. This newsletter exists to help you read it.

There will be three kinds of postings.

• The everyday recommendations, such as BMI ranges and blood pressure targets.

• The large public arguments, such as the one over vaccines.

• New claims as they surface online, taken up while people are still talking about them.

When I applied my mathematical training to the medical claims reaching the public, I found that the numbers are usually computed correctly. What breaks is the reasoning wrapped around the numbers, and it breaks in the same six ways. I call them faults, and each has a plain question that exposes it.

· Relative reporting. What does a 36% improvement from taking a drug really mean?

· Probability reversal. Does a positive COVID test mean I have it? Does a negative mean I’m not contagious?

· Arbitrary categories. How concerned should you be if your systolic blood pressure goes from 119 to 120?

· The Bernoulli fallacy. Why does the published medical advice keep changing?

· The causal leap. Does bird watching prevent dementia?

· The syndrome trap. If two people have the same diagnosis, what do they actually have in common?

There is a short paper on each at healthy-skepticism.com, free to read and share.

The goal is not to make you distrust medicine. The progress is real. The goal is a better conversation with the people who treat you.

Nothing here is medical advice. Decisions about your care belong to you and your doctor.

If a claim is puzzling you, send me an email. I read every

Murray Cantor PhD