Sooooo many of you sent me an instagram video by dr_idz, MBBS, MRes, DipIBLM in which he responds to a video by Sam Previte RD, CPT, CIEC - find.food.freedom on IG. For those who haven’t heard of him, dr_idz is an Instagram influencer and Lifestyle Medicine physical who is currently marketing a new book. Many of his posts use a common structure in which he introduces the topic, says “School’s in” discusses research around the topic, and ends with “Class Dismissed.” This video followed that format.

Regular readers know that my policy is not to link to weight stigma so I’ve transcribed the IG video and we’re going to take a look at the research he used to try to support his claims. These won’t all be deep dives because deep dives aren’t needed to draw the issues with his arguments into sharp relief. That said, if you’d like a deeper dive of any of these studies, please feel free to let me know in the comments.

Throughout I’ve indented quotes from dr_idz. You can skip them, avoid weight stigma, and still get the gist of the piece. That said, some of the studies discuss calories and caloric restriction so please take care as you read this.

At the beginning the video goes back and forth between a video created by Sam Previte and dr_idz’s commentary:

Sam Previte

“Being fat or having excess fat does not cause disease.”

dr_idz

Okay, so this dietitian, Find Food Freedom, blocked me years ago because she seemed unable to take on board constructive criticism, and this video is no different. Time for school.

Sam Previte

It’s true that many diseases are found more commonly in people that reside in larger bodies.
This does not mean that the weight itself causes the disease. Much of the evidence on this topic is based on epidemiologic research. Epidemiologic research goes association, not causation.

dr_idz

Okay, yes, some evidence is observational, but that does not mean that ob*sity is not causal in disease.

It is at this point that dr_idz begins to make claims while flashing various studies in the background. What I’ll be doing is bringing those studies to the foreground to see if they actually support the claims that he is making.

School’s in…

Dr_idz

Mechanistically, excess adipose tissue is literally an active endocrine organ. It secretes inflammatory cytokines, altars insulin signaling, secretes and impacts several hormones like higher leptin and lower adiponectin. It raises ectopic fat deposition in various organs and drives insulin resistance, dyslipidemia, and hypertension.

To support this he cites a paper called “Adipose tissue as an endocrine organ” by Erin E Kershaw and Jeffrey S Flier, 2024

Per OpenPayments, Erin E. Kershaw has taken $3,988.98 in general payments, $17,974.50 in research payments, and $704,154.78 associated research funding from the pharma and medical device industry. The majority of the general payments were from Eli Lilly and the majority of the associated research funding from Regeneron (who are in trials with a new weight loss drug) and Eli Lilly, marketer of Zepbound for weight loss.

Jeffrey S. Flier’s Harvard bio says he is “one of the country’s leading investigators in the areas of ob*sity and diabetes.” He also wrote an article for STAT called “How Pfizer ended up passing on my GLP-1 work back in the early ’90s” bragging that he was “part of what I believe was the earliest commercial effort to develop GLP-1 as a metabolic therapy”

So both of these authors have fully committed to profiting from weight loss which doesn’t automatically invalidate their findings but does cause concern about paradigm entrenchment and all the issues that come with it, including a tendency (consciously or subconsciously) to look for support for the paradigm they’ve aligned with/profit from.

For example, they begin their abstract “Adipose tissue is a complex, essential, and highly active metabolic and endocrine organ.”

This may be true, but what follows makes clear that their entire conceptualization of adipose tissue for this study involves the idea of “adverse metabolic consequences” of “excess” or “deficiency” of adipose tissue. This is a good example of researcher bias. Their idea wasn’t to study adipose tissue as an endocrine organ with a goal of understanding, it wasn’t even to confirm or reject a hypothesis that there are adverse consequences of “excess” or “deficient” amounts of adipose tissue. They don’t even bother to define “excess” or “deficiency”. Instead they seek to find possible pathways that adipose tissue in some unspecified amounts might create harm.

Here is their full claim, which I’ll break down bit by bit:

“The important endocrine function of adipose tissue is emphasized by the adverse metabolic consequences of both adipose tissue excess and deficiency. Adipose tissue excess or ob*sity, particularly in the visceral compartment, is associated with insulin resistance, hyperglycemia, dyslipidemia, hypertension, and prothrombotic and proinflammatory states (4). The prevalence of ob*sity and these associated morbidities, known as the metabolic syndrome, has reached epidemic proportions (4). Interestingly, adipose tissue deficiency or lipodystrophy is also associated with features of the metabolic syndrome in both humans and rodents (5). Furthermore, the prevalence of lipodystrophy in humans is increasing with the use of highly active antiretroviral therapy for HIV (5). Thus, both excess and deficiency of adipose tissue have harmful metabolic consequences and represent significant medical and socioeconomic burdens in the world today.”

I recently received peer review on an article that said that I should start by agreeing with the paper I was critiquing so I’ll start there. The authors are honest when they use the word “associated” here because they have not proven causality.

Also, they haven’t proven that “excess adipose tissue” actually causes diseases, they show that “excess adipose tissue” is associated with risk factors for disease, with the possible exception of hypertension.

Let’s take this piece by piece:

“Adipose tissue excess or ob*sity, particularly in the visceral compartment…”

These are three separate things.

“Adipose tissue excess” is an idea for which they offer no definition or diagnostic criteria.

Ob*sity is a construct based on a ratio of weight and height that gives no information as to amount of adipose tissue.

Adipose tissue in the visceral compartment (“excess” or otherwise) is fat that is gathered around internal organs which can be present in various amounts in people of very different body sizes and amounts of overall adipose tissue.

It does not get better from there:

“is associated with insulin resistance, hyperglycemia, dyslipidemia, hypertension, and prothrombotic and proinflammatory states”

“Associated” is doing a lot of work here, it can be helpful to remember it means “happens at the same time but causality is not known.” Also, with the possible exception of hypertension, these aren’t actually diseases, just risk factors or possible symptoms.

“The prevalence of ob*sity and these associated morbidities, known as the metabolic syndrome, has reached epidemic proportions”

The idea that higher-weight people existing is an “epidemic” is a clear example of weight stigma. But it’s more than that - remember just a few pieces ago when I was talking about Natasha Wiebe’s research and I said “One of the things I appreciate about Natasha’s work is that she points out where studies often stop in ways that allow for an assumption to be made that weight causes health issues. Then she actually does the research to see if the assumption holds”? Well, this is exactly what I was talking about. And exactly what Natasha and the author group were studying.

What did Natasha’s study ( “Associations of ob*sity, systemic inflammation, and hyperinsulinemia with the incidence of non-communicable chronic disease and mortality: A prospective cohort study” by Natasha Wiebe MMath et al.) find?

They found that while people with higher BMIs were at a higher risk for death, it appeared that risk was actually driven by inflammation, hyperinsulinemia or “something proximal and not directly due to BMI.”

They found that hyperinsulinemia typically precedes being/becoming higher-weight. While the sequence for weight and inflammation was less clear they found ““no evidence” that high adiposity “initiates the inflammatory cascade.”

They concluded that “As there are more people with metabolic syndrome without ob*sity than with ob*sity, future research should prioritise the study of how to best diagnose, monitor and treat inflammation and hyperinsulinemia rather than ob*sity.”

All of which to say that this study is far from proving that adipose tissue (in some undefined amount,) or “ob*sity” (which is not the same as adipose tissue) causes disease. Remember that dr_idz is trying to show that being fat or having “excess fat” causes diseases. Here we don’t have causality and, again, with the possible exception of hypertension, we don’t even have disease.

Dr_idz:
Now, we can look at other types of research like human randomized control trials. This study lasting two years split participants to a nutritionally-adequate a libertum diet or a 12% calorie-restricted diet. The calorie-restricted group lost seven and a half kilograms of body weight, and that directly led to improvements in all cardiometabolic markers, including LDL, Cholesterol Ratio, Systolic and Diastolic blood pressure, as well as improvements in C-reactive protein, insulin sensitivity index, and metabolic syndrome score.

He is simply wrong. The claim that caloric restriction/weight loss “directly led to improvements” is not possible to determine from the study design. If dr_idz doesn’t know that, it’s very concerning. If he does know that but he said it anyway, it’s perhaps even more concerning.

The study he is talking about is tKraus WE, Bhapkar M, Huffman KM, et al. 2 years of calorie restriction and cardiometabolic risk (CALERIE): exploratory outcomes of a multicentre, phase 2, randomised controlled trial. Lancet Diabetes Endocrinol. 2019;7(9):673-683. doi:10.1016/S2213-8587(19)30151-2

Let’s start again where we agree: It was, in fact, a two year trial.

Moving on.

First, note in the title the use of the term “exploratory outcomes.” The 218 total people in this trial were specifically characterized as “healthy normal weight and slightly overw*ight (BMI, 22 to 27.9 kg/m2) young men (21 to 50 y) and premenopausal women (21 to 47 y)” Said another way, these were people who did not have any diseases and who weren’t particularly fat so how is this to prove that fat causes disease as dr_idz is trying to do? In general the study design causes an issue if anyone is trying to claim that being higher-weight causes health issues, that weight loss solves health issues, and/or if they are trying to extrapolate these findings to other populations, including people whose BMIs are higher than this.

He’s also ignoring the fact that the study didn’t set out to test a 12% calorie-restricted diet. It set out to test a 25% calorie restricted diet, but the calorie restriction group could only manage an average caloric reduction of 11.9%. In fact, the first six months they averaged 19.5%, but that “decreased over time as might be expected to 9.1% (±0.7%) after 6 months, but averaged 11.7% (±0.7%) over the entire, two-year intervention”

“As might be expected…”So the researchers are basically admitting that this is not likely to be maintained long-term and of course a century of research strongly suggests that even if it was the caloric restriction and/or weight loss that caused the health improvements (and that’s a big if, since confounding variables can include improved food quality, increased movement, support, engagement with the healthcare system etc.) it’s not likely sustainable. This is further shown by the fact that the caloric restriction group was already regaining weight in year two since “weight loss from baseline averaged 8.4±0.3 kg (11.5%) at one year and 7.5±0.3 kg (10.4%) at two years.” Many health improvements were also receding by the end of the study.

But I digress. dr_idz is trying to prove that Sam Previt’s claim that “Being fat or having excess fat does not cause disease” is false. This study doesn’t show that and it made no effort to show that. It only included people who were either “normal weight or “slightly overw*ight” who, by the author’s own admission had “clinically normal risk factor at baseline.” Which is to say, these were people who either weren’t higher-weight or who were barely higher-weight who didn’t have health issues. Further, the study failed to control for or mitigate possible confounding variables.

dr_idz may have been confused because the authors vastly overstate their conclusions, grandiosely claiming that “there are no pharmacologic agents with such profound effect on such a broad range of cardiometabolic risk factors” despite a small effect that was receding over the two-year study. As a side note - do you know what does have that kind of profound effect? Engagement in movement/exercise/fitness, as I discussed when I reviewed huge analyses by Gaesser and Angadi, and Weeldryer et al. Other weight-inclusive interventions can also create impact on these factors.

Now might also be a good time to remember that when researchers actually tested the idea that small amounts of weight loss create health benefits, they found that it was more likely behavior change and other factors than the weight loss driving the health change. Despite this research being in the world, the researchers on this caloric deprivation study failed to even mention, let alone control for or mitigate, these known possible confounding variables. It could be that they are simply ignorant of the research that exists in their field, or that they are hoping nobody notices.

The same goes for dr_idz, but regardless, this study does not support his claims.

Let’s move on.

Dr_idz: We also have meta-analyses on 15 long-term control trials showing that intentional weight loss leads to a 15% reduced risk of all-cause mortality.

This is not even an accurate summary of the authors’ summary of the study he is citing (Kritchevsky, S. B., Beavers, K. M., Miller, M. E., Shea, M. K., Houston, D. K., Kitzman, D. W., & Nicklas, B. J. (2015). Intentional weight loss and all-cause mortality: a meta-analysis of randomized clinical trials. PloS one, 10(3), e0121993. https://doi.org/10.1371/journal.pone.0121993)

The study concludes “In ob*se adults, intentional weight loss may be associated with approximately a 15% reduction in all-cause mortality.”

Note the use of the word “may” in the authors’ conclusion statement. That’s because this analysis was not created to show causation and they have no idea if being higher-weight created any health issues (and they made no effort to do so.) Even in the actual topic of the analysis, the authors have not idea if it was the weight loss or, again, as other research has suggested, behavior changes and other factors actually created any reduction in all cause mortality.

I don’t know if dr_idz is shaky on the concept of correlation vs causation or if he is hoping his audience will be, but saying that this study “shows” that “intentional weight loss leads to” a reduced risk of all-cause mortality” makes it seem to me like either he missed the first day of research methods class (and every day after that) or he is purposely misrepresenting the study findings. Remember, this is the second time he has done this in three studies that he has reviewed.

In part 2 we’ll review the rest of the video including his (patently ridiculous) claim about “one of the best pieces of evidence we have to directly show the weight loss causing the improvement.”

We’ll continue this next class.

Want to learn more about the tools of the trade that the weight loss industry uses to trick us and what we can do about it? June’s online workshop is Exposing the Weight Loss Industry’s Secrets and Tricks with guest Louise Adams. We’ll talk about what they are doing, why they are doing it, and how we can pushback. All registrants get access to a video and there is a pay-what-you-can-afford option so that money isn’t a barrier. Details and Registration here!

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*Note on language: I use “fat” as a neutral descriptor as used by the fat activist community, I use “ob*se” and “overw*ight” to acknowledge that these are terms that were created to medicalize and pathologize fat bodies, with roots in racism and specifically anti-Blackness. Please read Sabrina Strings’ Fearing the Black Body – the Racial Origins of Fat Phobia and Da’Shaun Harrison’s Belly of the Beast: The Politics of Anti-Fatness as Anti-Blackness for more on this.

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Today I’m going to offer a sample letter that I have used with success when pushed to use “person-first language” for higher-weight people. First I’ll give a brief introduction into the issue, if you want to skip that, you can scroll down to where it says “Sample Letter.”

Person first language originated in disability community, where there has been and currently is a lot of conversation, transformation, and nuance happening (more on that later.) It has also begun to be more commonly used in other healthcare scenarios. It is the opposite of identity-first language. One example would be a person with Type 2 Diabetes (person-first language) versus a diabetic person (identify-first language.) In people with the same disability or health condition, some will prefer person-first language and others will prefer identity-first language.

This is much more convoluted when it comes to the use of person-first language for higher-weight people.

The weight loss industry (driven by Novo Nordisk and their astroturf “patient advocacy” organizations) seized upon person-first language as a way to forward their profit goal of declaring simply existing in a fat* body to be a disease (“treatable,” of course, with their interventions.)

That is how we got to a place where instead of simply describing higher-weight/fat bodies like we do tall, short, and thin bodies, we instead get the ridiculous “person with ob*sity,” the even more ridiculous “person affected by ob*sity,” and the ridiculous and grammatically criminal “person with overw*ight.”

In order to more effectively market this change, the weight loss industry is marketing the use of person first language as a stigma reduction method. It is not (in fact it creates greater stigma) which I’ve written about in detail previously. That said, they have almost endless money and, I would describe their behavior as displaying low-to-no ethics and so this naked attempt to take advantage of well-intentioned people’s desire to be less stigmatizing - by co-opting and decades of actual weight stigma work and redirect it toward weight loss industry profit - has been very successful as they put massive effort into pushing this into healthcare as quickly and broadly as possible.

I know that we are all tired as the weight loss industry continues its incessant, insatiable campaign for profits, and this might seem like something we can let slide but I think this is, in fact, something that we should go to the mat for or, more appropriately, we should to go to the mat against any time we can.

Again, individuals can choose the language they prefer for themselves (though those choices don’t happen in a vacuum and they can have a negative effect on others,) but when we’re considering general/published language, the use of person-first language for higher-weight people does many harmful things including:

• Advancing the weight loss industry goal of diseasifying a body size (regardless of actual health) to increase their market and profits, legitimizing the extremely questionable construct of “ob*sity” and leading to an increased number of people being harmed by their interventions

• Separating fat people from our bodies and turning fatness into an undesirable label that we are told everyone should want to get away from/avoid.

• Telling higher-weight people that we should be grateful to be less stigmatized because person-first language constructs our existence that is claimed (with plenty of direction from the weight loss industry) to be an epidemic/pandemic/global crisis… at least isn’t our fault because our existence is a “disease” that requires “treatment” and “prevention” so that higher-weight people cease to exist and are prevented from existing in the future. (It’s the old “we don’t want fat people treated badly, but we do want to eradicate them from the earth in a non-stigmatizing way” nonsense.) Of course there is no shame in having a disease of any kind, the issue is that body size simply doesn’t qualify scientifically or logically and the weight loss industry’s attempt to strong-arm this into existence is creating significant harm.

• Ignoring/erasing the true method of ending weight stigma which, instead of telling us that our bodies are wrong but it’s not our fault, is affirming and celebrating bodies of all sizes.

I believe it is critical that we not allow the weight loss industry and those (knowingly or unknowingly) working to advance their priorities to speak over and for actual fat positive anti-weight stigma advocates/experts.

All of that to say, I’ve heard from a number of people in healthcare and research who, even though they know better, are being pressured to acquiesce and use this language. It’s not just other people either, in several of my recent academic projects, including research, I’ve received pushback telling me that my use of “higher-weight” is stigmatizing and I must use person-first language to reduce stigma. (While fat is my preferred personal descriptor, it is also a reclaiming term with all of the complexities of a reclaiming term and so in academic work I often use higher-weight and/or use fat with an explanation of the choice of identify-first language generally and the terms I use specifically.)

This is a massive problem because if they can get us to acquiesce in order to be published, then we are giving our tacit approval and who is left to hold the line and demand not just the dignity but the safety of higher-weight people?

Below is the email (with in-text references) that I have created and sent back. I’ve used it three times now and it’s been successful each time though, of course, your mileage (and mine in future uses) may vary.

Finally, I’ll just say that this situation is infuriating because someone (at least in all of the cases it’s happened to me,) who is neither higher-weight nor an expert on weight stigma is telling me what terminology I have to use to avoid creating stigma against myself and people like me. Dude. Still, as I’ve said before, while impact is greater than intent, I think that intent matters (someone accidentally stepping on my foot who immediately moves and apologizes when I point it out is very different than someone who stomps on my foot on purpose who tells me they won’t stop because if they stopped stomping on my foot it would be stigmatizing me.)

Thus, while I think pushing back is completely essential (to the point that I would absolutely withdraw a publication before I would agree to use person-first language with “o-words” for higher-weight people,) I try to keep in mind that this person is likely well-meaning and has simply been reached by the deep pockets of the weight loss industry and address them accordingly.

Sample Letter

(As always, please feel free to modify this to work for you.)

Thank you so much for your communication and for your interest in ensuring that de-stigmatizing language is used. It is definitely an interest that I share and an area that I’ve studied, so I would like to provide some context.

Person first language emerged in disability community where there has been, and is, significant and nuanced conversation around the use of person-first versus identify-first language.

Janeszewski et al, 2025 discussed this in more detail (https://doi.org/10.1037/rep0000631)

As an example of transformation, The Association on Higher-Education and Disability has shifted to identify-first language and offers an explanation as to why in their statement on language

https://web.archive.org/web/20260109215326/https://www.ahead.org/professional-resources/accommodations/statement-on-language

This issue is even more complex for higher-weight people as the co-option of person-first language for use on higher-weight people was constructed primarily by the weight loss industry and pushed into healthcare and research primarily though weight loss industry funded organizations like the Obesity Action Coalition, The Obesity Society, EASO etc. This is part of the weight loss industry’s primary goal of pathologizing existence in a higher-weight body (regardless of health status) in order to increase their market. This is made plain in the 10-year plan by Novo Nordisk (manufacturers of the Wegovy weight loss medication) ilaid out in their 2015 annual report under the section “Obesity Care: Creating the Market from Scratch” (https://www.annualreports.com/HostedData/AnnualReportArchive/n/NYSE_NVO_2015.PDF)

Fat studies scholars, weight-inclusive health community, and fat liberation community reject the idea that higher-weight bodies are a condition and/or label that person-first language should be used to avoid, instead conceptualizing accurate descriptions of higher-weight bodies as simply neutral/positive attributes like tall, short, and thin.

Rather than reducing stigma, the use of person first language for higher-weight people can be more stigmatizing as it treats higher-weight bodies differently than other bodies (for example, we do not typically insist upon the use of “person with thinness,” or “person with tallness.”) The claim that accurately describing higher-weight bodies in a non-stigmatizing way requires a semantic work around that is not utilized in other size-based body descriptions is, in and of itself, a form of weight stigma and adds to the pathologization of higher-weight bodies which further adds to weight stigma.

Robins et al., 2025 (https://doi.org/10.1016/j.bodyim.2025.101860) sought to fill a gap in the literature around terminology. This gap has been created by the common research practice of asking people who aren’t higher-weight, and who often have a financial interest in pathologizing higher-weight bodies, what terms should be used to describe higher-weight bodies. This study asked higher-weight people their preferences and then made recommendations for clinicians and researchers:

“Prior research excludes those most affected by the terms used to describe them.
Weight-related term preferences are linked to beliefs about health and weight.
Preferring “fat” and nonmedicalized terms is associated with favorable outcomes.
Person first language, such as “person with overweight/obesity,” is not preferred.
Clinicians and researchers should utilize terms that don’t pathologize larger bodies.”

The APA’s Inclusive Language Guides recommends (https://www.apa.org/about/apa/equity-diversity-inclusion/language-guidelines)

“To avoid perpetuating weight stigma, use neutral terms that affirm and respect the dignity of all individuals regardless of their body size, such as “weight,” “lower weight,” and “higher weight” but does not take a position on general use of person or identify first language. That said, weight is not included in their specific discussion of person- vs identity-first language.

I believe there is a strong lived-experience and evidence basis to support the use of identity-first language (in this case higher-weight) as de-stigmatizing language in [this work] and I am asking to use that language as originally submitted.

Again, I truly appreciate your commitment to inclusive language and your willingness to engage in dialog on this subject.

Best,

~Ragen

So, are you dealing with this? If you have other ideas/options/references I would love to hear about them in the comments and if you use this I’d love to know how it goes!

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*Note on language: I use “fat” as a neutral descriptor as used by the fat activist community, I use “ob*se” and “overw*ight” to acknowledge that these are terms that were created to medicalize and pathologize fat bodies, with roots in racism and specifically anti-Blackness. Please read Sabrina Strings’ Fearing the Black Body – the Racial Origins of Fat Phobia and Da’Shaun Harrison’s Belly of the Beast: The Politics of Anti-Fatness as Anti-Blackness for more on this.

In Part 1 we looked at a study that questions common assumptions about weight and health. Today the lead author, Natasha Wiebe will share her reflections on her attendance and presentation of the paper at the Ob*sity Summit in Montreal, Quebec. (This summit is sponsored by Ob*sity Canada which is a weight loss industry funded astro-turf group, essentially the Canadian version of the Ob*sity Action Coalition, Novo Nordisk and Eli Lilly are reproducing this model all over the world, using these groups as Purdue Pharma did to claim they are “patient advocacy” organizations and lobby for their drug company funder’s priorities at the provider, patient, and policy level. Fun fact: they used to be called the Canadian Ob*sity Network, giving them my favorite acronym for one of these organizations.)

Here is Natasha’s letter sharing her experiences, thoughts, feelings, and opinions:

I am a mid-sized fat statistician working in medical research since 1999. Back in 2010, I was asked to work on a health technology assessment of bariatric surgery. As part of that work I came across the Swedish Ob*sity Study and grew interested in the control arm - the study group that received no bariatric surgery, other than advice to diet and exercise. People in that arm gained a small amount of weight over time. It confirmed to me what I thought was likely true, given my own lived experience, that diet and exercise has minimal, longterm, sustainable impact on weight.

Then, a number of years later, I learned about the Ob*sity Paradox. The “paradox” is that while more fat patients were being diagnosed with chronic diseases, these very same fat patients, on average, were living longer than their thin counterparts with these very same diseases.

Researchers continue to try very hard to explain away this “paradox”. Even today I saw a comprehensively written post on heart failure with preserved ejection fraction coming up with multiple reasons as to why this “paradox” need not be true, that fat patients are not living longer. Most of these arguments are based on the premise that the health system is screening, monitoring and treating fat patients more aggressively than thin patients, and that these interventions are why fat patients are outliving thin patients.

I cannot think of another example where marginalized groups were outliving non-marginalized groups because the health system worked better for them. In any case, for me, as someone who may have less intrinsic weight bias than the average fat or thin person, I thought why couldn’t it be? Why wouldn’t the body try to save itself … with fatness! After all, adiposity is an active immunological organ. (If that identifies me as someone who glorifies ob*sity, so be it!)

Since then, I have begun studying the ob*sity paradox myself, culminating in what may be my final paper supporting the ob*sity paradox (which would suggest that it need not be a paradox at all). In two population-representative datasets (the Canadian Health Measures Survey for Canada and the National Health and Nutrition Examination Survey for the US) and one very large cohort from the UK (the UK Biobank), we show that a higher body mass index associates with a lower risk of death after adjustment for a few key confounders – age, sex, smoking status, fasting insulin and C-reactive protein (a marker of inflammation). The results (dom-pubs.onlinelibrary.wiley.com/doi/10.1111/dom.70568) suggest that the majority of adults have metabolic syndrome (a condition antecedent to many chronic diseases) and that within metabolic syndrome, fatness appears to be protective against death.

I recognize that far too much money is being made off of weight loss (fueled by patriarchy, racism, capitalism, etc), so I decided to take my research to the Ob*sity Summit this past March 2026 to see if I could get even a few researchers or clinicians open to a different paradigm of fatness. The experience was varied: some good, some bad, and some truly ugly.

The good:

The short presentations were all earnest and integral scientific research, largely work with murine models and other preclinical studies that were very early in the research cycle.

Arya Sharma, the founder of the Ob*sity Canada, was asked to talk about the required 5% weight loss (WL) for good health outcomes. Over time, we have gone from targeting the “ideal” weight to 25% WL, 15%, 10%, and now 5% WL. Arya suggested that it was not the WL that matters but the health outcomes. He separated weight from health, but I am not sure many of the conference attenders truly absorbed that distinction.

I managed to talk to a few of the patient representatives. My sense was that they were open to a different paradigm around weight science but at this point in their lives, they were simply grateful that they were being treated with some kindness by the healthcare industry. (Note, they are coached to tell media at every opportunity that ob?sity is a disease.)

The bad:

A question from the floor was asked about the controversiality of the term ob*sity. The panelist, Arya Sharma, chose not to explain why it was controversial. Unfortunately, my experience with healthcare providers is that they truly do not know. Arya dismissed the question and suggested that the terminology was unimportant. (I sadly think this reaction may have reflected concerns about his legacy as the organization’s founder.)

Too many of the plenary sessions felt like grift to me. David Macklin’s talk was one of the hardest ones to listen too – basically you eat too much but it’s not your fault. (Nevermind that bariatric patients consume about 1000 calories per day and that the majority remain with a BMI >30 kg/m².)

There are too many people and industries making profit off of WL either through honorariums paid by industry, consulting practices coaching clinicians how to counsel with fat patients, social media influencing, or private clinics.

One speaker showed us their commercial conflicts of interests and then actively dismissed them as if commercial interests could not possibly affect what they had to say or think. (Note, this conference had 11 private sponsorships.)

The conference attenders were largely thin and not representative of the Canadian population. Naively, I expected to see more folks that looked like me. Outside of the patient representatives, there were few visibly fat attenders.

The ugly:

Yoni Freedhoff is a physician from Ottawa and I had seen him featured in at least one documentary on ob*sity and on other media platforms. I had low expectations, and he exceeded those. At the beginning of his talk, he shared the question that he had asked of a number of Large Language Models (like ChatGPT and Claude): how much weight a person could lose today given these latest WL drugs and bariatric surgery? They all gave some answer around 95% of excess weight. He then proceeded to talk about this as if this were science.

I heard no talk or discussion of adverse events related to these latest WL drugs, nor anything about the large research participant attrition in these clinical trials, or why doses deemed toxic to people with diabetes were considered acceptable targets for WL.

The hardest and most surprising part for me was the emphatic nodding in response to the speakers at many of the plenaries by what was largely a clinical audience. I think it was a response to ob*sity now being called a disease with a cure. Amen! What are we (us fat people) to do with this understanding? Where is the discernment and scientific reasoning?

My presentation had about 30 attendees. While I spoke, half the room looked angry and the other half looked pleasantly surprised at the results I was sharing. I suspect those that were excited by my findings will be discouraged by other collaborators. Hopefully a few will be encouraged to take a deeper look at the weight science (and the unproven assumptions) and at the possibility that our dominant paradigm of fatness is not just incomplete, but actively misleading.

I’m so grateful to Natasha for all of her work including this study, for braving this summit to spread the word about that work, and for sharing her experiences here!

Want to learn more about the inner workings of the weight loss industry? This month’s online workshop is Exposing the Weight Loss Industry’s Secrets and Tricks with guest Louise Adams. We’ll talk about what they are doing, why they are doing it, and how we can pushback. All registrants get access to a video and there is a pay-what-you-can-afford option so that money isn’t a barrier. Details and Registration here!

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*Note on language: I use “fat” as a neutral descriptor as used by the fat activist community, I use “ob*se” and “overw*ight” to acknowledge that these are terms that were created to medicalize and pathologize fat bodies, with roots in racism and specifically anti-Blackness. Please read Sabrina Strings’ Fearing the Black Body – the Racial Origins of Fat Phobia and Da’Shaun Harrison’s Belly of the Beast: The Politics of Anti-Fatness as Anti-Blackness for more on this.

Today’s discussion question comes from Kate who asks:

How do people handle food restrictions in terms of medical conditions? For example, there are certain foods patients with acid reflux are told to avoid. I have a friend/acquaintance who gets really "diet-y" when talking about her food re…

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I’ve previously written about research from Natasha Wiebe et al. that questions assumptions around weight and health. Today I’m back to discuss a new study “Associations of ob*sity, systemic inflammation, and hyperinsulinemia with the incidence of non-communicable chronic disease and mortality: A prospective cohort study” by Natasha Wiebe MMath, Stephanie Thompson MD, Peter Stenvinkel MD, Aminu Bello MD, Matthew T. James MD, and Marcello Tonelli MD.

In part 1 we’ll discuss the study. In part 2 I’ll publish a piece written by Natasha about her experience attending a weight loss industry event to present her findings.

I want to thank Natasha not just for her work, and her write-up for part 2, but also her work on this piece including reading through an early draft and providing additional clarity and context!

One of the things I appreciate about Natasha’s work is that she points out where studies often stop in ways that allow for an assumption to be made that weight causes health issues. Then she actually does the research to see if the assumption holds.

A note that this study uses terms that are stigmatizing (ob*se, overw*ight, etc.). I also want to point out that while there will be a discussion of the possibility of factors that might contribute to people becoming higher-weight, and there is no harm in understanding that, it doesn’t mean that this information can (or should!) be used to attempt to decrease the existence of higher-weight people which does cause harm.

Summary

The only author with conflicts of interest had conflicts with pharmaceutical companies who sell weight loss drugs and are pushing the narrative that “ob*sity” is (somehow) both a disease and causes non-communicable diseases.

The researchers used he Canada Health Measures Survey which uses a population-representative design that collects data from Canadian residents in a two year cycle with data linkages that allow for longitudinal follow up. to test assumptions that being higher weight causes inflammation and/or hyperinsulinemia as well as testing assumptions about higher-weight and overall mortality and non-communicable diseases.

They found that while people with higher BMIs were at a higher risk for death, it appeared that risk was actually driven by inflammation, hyperinsulinemia or “something proximal and not directly due to BMI.”

They found that hyperinsulinemia typically precedes being/becoming higher-weight. While the sequence for weight and inflammation was less clear they found ““no evidence” that high adiposity “initiates the inflammatory cascade.”

They found that higher BMI was positively associated with hypertension (meaning this was more likely to occur in people with higher BMI,) and non-significantly with CVD and Type 2 Diabetes (meaning it’s as likely that any association they found was due to chance as it was that it was due to higher BMI) and inversely associated with cancer (meaning cancer was less likely for those with a higher BMI.)

They conclude that “As there are more people with metabolic syndrome without ob*sity than with ob*sity, future research should prioritise the study of how to best diagnose, monitor and treat inflammation and hyperinsulinemia rather than ob*sity.”

Deeper Dive

We’ll start, as always, with the authors.

Natasha Wiebe MMath - Department of Medicine, University of Alberta, Edmonton, Alberta, Canada

Stephanie Thompson MD - Department of Medicine, University of Alberta, Edmonton, Alberta, Canada

Peter Stenvinkel MD - Department of Clinical Science, Karolinska Institutet, Stockholm, Sweden

Disclosures: Peter Stenvinkel reports the following: advisory boards for Baxter,Astra Zeneca, GSK, Vifor, Alexion, CSL, Vera; research funding fromBayer, Astra Zeneca; honoraria from Astra Zeneca, Baxter, Astellas,Novo Nordisk, Pfizer/BSM, FMC, CSL, Danone; and advisory or lead-ership role for Astra Zeneca, GSK, Alexion, CSL, Boerhinger (later 2024), Vafeso (later 2024).

Aminu Bello MD - Department of Clinical Science, Karolinska Institutet, Stockholm, Sweden

Matthew T. James MD - Department of Medicine, University of Calgary, Calgary, Alberta, Canada

Marcello Tonelli MD - Department of Medicine, University of Calgary, Calgary, Alberta, Canada

Funding for the study was provided by the Cumming School of Medicine, University of Calgary

This is refreshing. The only author with any conflicts actually has conflicts of interest with multiple pharmaceutical companies who sell weight loss drugs and are pushing the narrative that “ob*sity” is (somehow) both a disease and causes non-communicable diseases.

The authors begin by noting that while being higher-weight is associated with non-communicable chronic diseases (NCDs), existing research fails to properly investigate whether hyperinsulinemia (high blood insulin) and/or C-reactive protein (a measure of inflammation) might actually be the driver of NCDs and mortality, including in higher-weight people..

The researchers also note that previous research has been limited by the lack of a population-representative design. This study utilized the Canada Health Measures Survey which uses a population-representative design that collects data from Canadian residents in a two year cycle with data linkages that allow for longitudinal follow up.

Data Sources and Cohort

The researchers used “five cycles of the Canadian Health Measures Survey (CHMS; 2007 to 2015) linked to vital statistics, hospitalisations and the Canadian Cancer Registry (CCR) to create a cohort representative of the general Canadian population. Through interviews and physical examinations, the CHMS collects information on demographics, physiological measurements, medical history, medication use and laboratory tests.”

The researchers used this data to create a study group of people 18 and older that included measures of BMI, CRP, and fasting insulin. They followed the participants until they were lost to follow up, the study ended (12/31/2019) or the participant died.

While the primary focus was on BMI, CRP, and fasting insulin the researchers considered alternatives by replacing BMI with waist-to-hip ratio (WHpR) and waist to height ratio (WHtR) in sensitivity analysis. For purposes of reporting (and content warning because this is language rooted in weight stigma) they considered “ob*sity” to be a BMI of 30 or more and “s*v*re ob*sity” to be a BMI of 40 or more.

Beyond just considering all-cause mortality they also planned to study NCDs that are considered to be related to being higher weight as identified by Guh et al, 2009 which correlated being higher weight with 18 NCDs “five cardiovascular diseases (specifically heart failure, hypertension, myocardial infarction, pulmonary embolism, stroke), eight cancers (specifically breast, colorectal, endometrial, oesophageal, kidney, ovarian, pancreatic, prostate), type II diabetes, asthma, osteoarthritis, gallbladder disease, and chronic back pain.” They “also studied cardiovascular disease (CVD: heart failure, myocardial infarction, pulmonary embolism, stroke), type II diabetes, hypertension, and cancers separately, where power allowed.”

They included 8,280 adults in the sample.

Discussion

Life expectancy/mortality

In their analysis the researchers found that both inflammation and hyperinsulinemia were strongly associated with a higher risk of mortality. They found that while people with higher BMIs were at a higher risk for death, it appeared that risk was actually driven by inflammation, hyperinsulinemia or “something proximal and not directly due to BMI.”

I’ll jump in here to remind us that inflammation has been shown to be a consequence of both weight stigma and weight cycling (which is the most common outcome of weight loss attempts, including with GLP-1 drugs for weight loss). When they adjusted for inflammation and blood insulin, people with higher BMI had lower mortality.

The study authors point out that since “at least 2005, research has suggested that the longest life expectancy was found for those who had a BMI of 25–29.9 and “perhaps higher still” in those with a BMI of 30–34.9. Critics, they note, have claimed that this is explained by collider bias (which, the authors explain, means that “selection into the study is influenced by the exposure of interest.” )However, in this study collider bias cannot explain the findings since they used a general population cohort which precluded selection bias, and the outcome of death is not subjective.

NCDs

They found that each of the tested exposures (high BMI, inflammation, and hyperinsulinemia) was “associated with a higher risk of one NCD or another.” Inflammation and high BMI (but not hyperinsulinemia) were associated with a higher risk of developing any NCD (as a pooled group) but when separated out into categories (CVD, hypertension, type 2 diabetes, cancer), the associations varied substantially.

Higher BMI was positively associated with hypertension (meaning these were more likely to occur in people with higher BMI,) and non-significantly with CVD and Type 2 Diabetes (meaning it’s as likely that any association they found was due to chance as it was that it was due to higher BMI) and inversely associated with cancer (meaning cancer was less likely for those with a higher BMI.)

The study authors are clear in their limitations section that they weren’t able to study weight stigma and weight cycling since they weren’t captured in the survey data they used so, here again, it is possible that weight stigma and/or weight cycling could be the cause of the associations with hypertension and CVD. Natasha explained “inflammation is likely to cover some of the effects of weight stigma and weight cycling - but not weight discrimination.”

Inflammation was positively associated with cancer, non-significantly associated with CVD and non-significantly with T2D, high fasting insulin was positively associated with T2D and non-significantly associated with CVD and hypertension.

Here the authors note that critics claim that high BMI (aka “ob*sity”) causes systemic chronic inflammation and hyperinsulinemia. However, randomized trials find that people who take insulin or sulfonylureas (medications that increase insulin within the body) tend to gain weight, while those who have weight loss surgery show that “fasting insulin and some inflammatory markers decrease before any weight is lost.” (That said, I disagree with the idea that weight loss surgery is an appropriate treatment for health issues which I discussed here.) When this information is combined with the authors previous meta-analysis, the authors note that the findings “clearly suggest that changes in fasting insulin precede changes in weight and not the other way around.”

Thus, they note that contrary to the common assumption that being higher-weight causes hyperinsulinemia (and so being higher-weight is to blame for negative outcomes) “it appears more plausible” that being higher-weight happens after hyperinsulinemia and may actually “mitigate some of the adverse consequences of the latter or of a proximal exposure like hyperglycaemia.”

You may have heard the idea that adipose tissue is metabolically active as if that’s the reason being higher-weight should be blamed for health issues, but these researchers point out that “adipose tissue is metabolically active and contributes to immune function” and so higher-weight may “act as a protective mediator (within metabolic syndrome) and temper acute exacerbations of NCDs.” Natasha clarified this for me, explaining “this is really the key idea. As Deb Burgard put it at the AWSIM conference during my poster presentation, increased adiposity may be compensatory, that’s really what I’m proposing - even if increasing adiposity contributes to hypertension, its ability to bridge acute illnesses of NCDs and delay death is far more beneficial to the host body.”

The authors then explain that evidence for the sequence around adiposity and inflammation (ie - which comes first) is less clear. They note that in observational studies of people who don’t have diabetes, the markers for inflammation come before increases in fasting insulin “and thus presumably precede” becoming higher-weight, but there is not good experimental data. They explain that there is “some preclinical work” that higher rates of adiposity may amplify inflammation, but “no evidence” that high adiposity “initiates the inflammatory cascade”. (Note: for a deeper dive into weight and inflammation, see this series with Dr. Zed Zha.)

Further complicating this is the fact that mechanistic studies find that certain cytokines “interfere with insulin signaling and thus may contribute to insulin resistance”. Rodent studies support a causal role of chronic inflammation and maybe insulin resistance preceding being higher-weight.

They make the important point that it isn’t enough to say that being higher-weight is associated with inflammation and hyperinsulinemia but, rather, we must distinguish being higher-weight from inflammation and hyperinsulinemia because people with a BMI of less than 30 also experience inflammation and/or hyperinsulinemia and need treatment for those specific conditions that is not just “lose weight” (as, I would argue, do higher-weight people.)

There are also, the authors point out, higher-weight people who do not have systemic inflammation or hyperinsulinemia who may be subjected to weight loss interventions (including drugs and surgeries) under the guise of treating these healthcare issues (which they don’t have). Thus, even if those interventions do have a benefit for these actual health conditions (and research suggests that if they do, the benefit comes from behavior change and/or the intervention itself rather than weight change) higher-weight people without these conditions who are subjected to these interventions would get no benefit but still be subject to the adverse events which can cause significant harm including death.

Finally the study authors conclude:

“As there are more people with metabolic syndrome without ob*sity than with ob*sity, future research should prioritise the study of how to best diagnose, monitor and treat inflammation and hyperinsulinemia rather than ob*sity.”

While this information isn’t necessary for weight-inclusive health to be an evidence-based paradigm, it is important research that supports the weight-inclusive paradigm and I am grateful to the researchers.

In Part 2, lead author Natasha Wiebe will share her experience of talking about this research at a weight loss industry event.

This month’s online workshop is Exposing the Weight Loss Industry’s Secrets and Tricks with guest Louise Adams. We’ll talk about what they are doing, why they are doing it, and how we can pushback. All registrants get access to a video and there is a pay-what-you-can-afford option so that money isn’t a barrier. Details and Registration here!

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*Note on language: I use “fat” as a neutral descriptor as used by the fat activist community, I use “ob*se” and “overw*ight” to acknowledge that these are terms that were created to medicalize and pathologize fat bodies, with roots in racism and specifically anti-Blackness. Please read Sabrina Strings’ Fearing the Black Body – the Racial Origins of Fat Phobia and Da’Shaun Harrison’s Belly of the Beast: The Politics of Anti-Fatness as Anti-Blackness for more on this.

In Part 1 we started talking about emails that I’ve been receiving from readers about the weight centric backslide including some initial ways that we can identify the issue and push back. Today we’re going to dig deeper.

Before we do that, I’m going to repeat from part 1 what I think is one of the most important things that we can do:

Hold the line on weight stigma

Perhaps one of the most massive and insidious campaigns that the weight loss industry is currently involved in is co-opting decades of actual anti weight stigma work by true anti weight stigma activists in order to sell weight loss. Their goal is to claim that anti weight stigma work should be about insisting that “ob*sity” is a treatable disease.

Now, if you tell people that their body is bad and it’s their fault, and then you tell them that their body is bad but it’s not their fault, you may reduce some weight stigma. But if you make it clear that their body was never bad, you can eliminate weight stigma and you’ll avoid creating additional stigma and exposing a group of people to weight loss “treatments” that have limited to no long-term “success” and high risks.

The weight loss industry is trying to claim that you can de-stigmatize higher-weight people while seeking to create a world where they don’t exist and that is beyond just being ridiculous (though it is,) because it is deeply harmful.

The idea that you can treat higher-weight people as a problem to be solved (an epidemic/pandemic/global crisis etc.) who should be treated/eradicated/prevented is incompatible with the idea of ending weight stigma.

A legitimate anti-weight stigma stance must include an unyielding stance against:

Implicit and explicit weight bias

Poor treatment of higher-weight people

Lack of inclusion/accommodation of higher-weight people

Any attempt to eliminate/reduce/prevent fatness/higher-weight bodies

Let me be clear, even if someone thinks that weight loss will make people healthier, there is still no way to say that being higher-weight is a bad thing/disease/epidemic/crisis et al without stigmatizing higher-weight people, because we are talking about a body size and not an actual health issue. I wrote about this in more detail here and I highly recommend Dr. Rachel Fox’s dissertation on the Anti-Ob*sity Assemblage for a deeper understanding.

Fight back against attempts to turn us into lobbyists/marketers for the weight loss industry

This is where lot of sneaky stuff is happening, including leveraging claims about marginalized populations to try to get us to become marketers and lobbyists for the weight loss industry. I’ve written about this in detail before, but as a quick review, if someone is trying to convince you to lobby for weight loss industry priorities (like insurance/Medicare coverage for weight loss drugs), if they are claiming that lack of access to weight loss interventions is a form of weight stigma or stigma of any kind, if they are trying to get you to legitimize the need for “ob*sity medicine” doctors, that’s an opportunity to push back, to call out the fact that they are asking you to lobby/market for the weight loss industry (which already has enough money to make any/all of their interventions affordable to anyone they want to) and to point out that weight-neutral interventions may offer offer the same/greater benefits with less risk, and sometimes far less risk.

Medicare and most insurance plans already cover GLP-1 drugs for Type 2 Diabetes and other uses. So far the insurance companies have bene the only ones with enough power to slow down the endless lobbying from the weight loss drug companies (and the so-called “patient advocacy” groups they fund) for coverage of these drugs for weight loss. Even if someone believed that it was important that more people have access to these drugs for weight loss, lobbying for Medicare/Medicaid/Insurance coverage is lobbying for weight loss industry profits, they should lobby the companies themselves (remembering that both Novo Nordisk and Eli Lilly have their own private pharmacies!) to make the drugs more accessible.

Ask for the evidence

A common (dangerous) issue is people who are either part of the weight loss industry or have been trained by them (directly or simply through their massive media push) responding to legitimate concerns and critiques about weight loss interventions, particularly GLP-1 drugs, by blowing off the concern stating a “solution” for which there is little to no evidence.

Two of the most common common examples:

In the first example, someone points out the research that finds that the vast majority of people don’t remain on the GLP-1 drugs (the longest semaglutide study was 4 years and they lost 89.5% of the sample,) and that going off the drugs initiates rapid weight regain and loss of cardiometabolic benefits and possible unknown issues.

The response comes back to “just take the med forever, relapsing and remitting is part of the disease process” (which is why the weight loss industry is trying so hard in their attempts to redefine existing in a higher-weight body as a “chronic, lifelong, relapsing remitting disease” as a way to rebrand the weight cycling caused by their drugs.)

There is absolutely no evidence that this will create significant long-term weight loss or health benefits (which are two different things.) In fact, the tirzepatide withdrawal trial saw 10.5% of people who stayed on the drug for 88 weeks gain back 20% or more of the weight they lost in the first 36 weeks over the following 52 weeks (the rest may have been regaining but researchers obfuscated this by defining “maintained weight loss” has having regained less than 20%.)

In the second example, someone points out the significant loss of muscle mass on GLP-1 drugs…

The flip response is to “just eat protein and lift weights.”

Here again, there is not nearly enough evidence to state this as fact (even if, for example, the seniors on Medicare who are being pushed to take this drug could safely choke down however much protein they are told they need to, without compromising kidney function.)

And as a bonus, we have the n=1 refutation. This happens when someone believes that a single person who is (at least currently) happy with some weight loss intervention refutes any amount of evidence about the possible harms or lack of efficacy. You’ll see this on social media where someone is offering critiques about the evidence, or research that finds concerns about the intervention. Enter someone in the comment section: “This isn’t true because I’m doing it and [insert their person experience.]” Even if this isn’t a bot or a plant, it’s still not the same thing as a consideration of evidence.

When you see this happening, you can push back. One option that can be helpful, especially if you happen to be less confrontational (and that is a completely valid way of being!) is to ask for the evidence that supports these claims - you could say something like “That’s really interesting, I hadn’t seen that research, could you point me to it?” When someone tries to use a personal testimonial as a refutation you can ask “sorry, just to clarify, are you talking about your individual experience or the results of a trial or larger study?”

Refuse to accept the claim that information is shame

One of the ways that legitimate critique is shut down is by people claiming that anyone reporting on the issues with a weight loss intervention, offering critique or concern is “shaming” people who have chosen to attempt the intervention. This regularly happens to me despite the fact that I constantly say that I take a firm view of bodily autonomy and people are allowed to try to lose weight for whatever their beliefs or reasons, and that the reality is that someone people are bullied into weight loss by a healthcare system that holds their healthcare hostage for a weight loss ransom.

I also take a firm view of what constitutes the ethical, evidence-based practice of medicine which is where I have a problem with weight loss interventions, and is the point of my critique and analysis.

Here we can point out that while people aren’t obligated to read critiques about these weight loss interventions, discussing possible issues and analyzing/critiquing the research is not, in any way, shaming people who choose to attempt these weight loss interventions.

Finally, as I said in Part 1, pushing back is important, but at the end of the day I want to remind us that the biggest thing we can do to stop the weight centric backslide is to not become part of it. We have to remain vigilant and critical because the weight loss industry is using its massive resources to try to pull us in.

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*Note on language: I use “fat” as a neutral descriptor as used by the fat activist community, I use “ob*se” and “overw*ight” to acknowledge that these are terms that were created to medicalize and pathologize fat bodies, with roots in racism and specifically anti-Blackness. Please read Sabrina Strings’ Fearing the Black Body – the Racial Origins of Fat Phobia and Da’Shaun Harrison’s Belly of the Beast: The Politics of Anti-Fatness as Anti-Blackness for more on this.

Please feel free to add your thoughts below and if you asked a question and my answer missed the mark and/or you have follow-up questions, please feel free to …

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“Another question I have is about my young adult children, who are hearing from friends and media that thin = healthy. How do I share my views without getting preachy?”

This i…

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I’ve received a lot of reader emails like the one below from reader Jeannie.

I feel like I’m seeing so many people, including dietitians and doctors, who used to be staunchly non diet getting back on the weight loss bandwagon. Suddenly they’re all “you can fight weight stigma and promote weight loss” and “o-word is a metabolic disease” - and “use people first language” and it’s like they were claiming to be non diet but it was only because they didn’t think they could shrink us but now they think these drugs can and they are showing their true (anti fat) colors and people (including doctors) I thought respected me and believed in non diet care are showing me that they’ve always thought I would be better thin, or that my fatness is a disease, they just didn’t think they could make me thin (or not “diseased”) and now they do. Is there anything we can do to fight against this?

First of all thanks to reader Jeannie and to everyone who has emailed to ask me similar questions. I absolutely understand what you are saying and I’m noticing this as well. It can be any combination of frustrating, hurtful, painful, enraging, and harmful.

In Part 1 we’ll look at the basics and in Part 2 we’ll take a deeper dive into some options to help stop this weight-centric backslide.

A few things to note before we get started. Much of this backlash seems to be happening because of the massive marketing efforts of the companies selling GLP-1s for weight loss. GLP-1s are a solid Type 2 Diabetes drug and may have other actual health benefits (though the research must be very closely analyzed because there are currently serious issues.) The research around weight loss is even more troubling. In their 2015 annual report, Novo Nordisk announced a 10 year plan called “Ob*sity Care - Creating the Market from Scratch” in which they noted they their primary goal was to “convince” healthcare providers that “ob*sity” is a disease and that 5-10% weight loss created health benefits (a very questionable claim that I’ve written about before) so that their then weight loss GLP-1, Saxenda could reach its “full potential.” They’ve been systematically working on this for over ten years with an almost unlimited budget training patients and providers, influence peddling at the policy and institution level, so it’s not a surprise that some people have been swept into the backslide. That said, real harm is being done and so we have to stay vigilant. What can we do?

Set the goal

A lot of what is happening is beyond our (immediate) control. That doesn’t mean that we can’t push back and it doesn’t mean that pushing back can’t be successful, but it can take time and victories can be small, few, and/or far between. I’ve been thinking a lot about Dr. Art VanZee who was an early-and-often whistle blower on Purdue Pharma’s strategy and bad behavior around opioids - strategy and behavior that Novo Nordisk and Eli Lilly are using as a roadmap to market their GLP-1s for weight loss and other uses besides T2D. Dr. VanZee was harried, harassed, called an alarmist and a quack by everyone from other doctors to industry lobbyists, to powerful members of congress. But he was right, and he just kept telling the truth and pushing back until it all came out.

I try to consider activism to be a self-care practice. There is injustice and pushing back against it is one of the ways that I care for myself. Framing it like this helps me avoid burning out. Part of that is making the work itself the goal - I can’t control the outcome of my work, all I can do is do the work. When we make our work itself the goal, we can celebrate those more frequent victories which can help us keep going psychologically. So if we make the goal to pushback - against the weight loss industry talking points, against the diseasification of fatness and the backslide of people/providers who identify as weight-inclusive into diet culture, then we can celebrate the success of doing the work which can help support against the frustration, pain, and harm of what’s happening.

Let’s talk about the issue and what we can do about it.

Float above the flood

The weight loss industry, and in particular the pharma companies that are selling these GLP-1 weight loss drugs, are using a version of the political tactic known as “flooding the zone.” They have pockets that are almost unfathomably deep and they are using that money to push out a torrent of trials, studies, and media articles and to pay a gaggle of doctors to do the same and, in other cases, to pay food and beverage costs for “trainings” that amount to indoctrination. Here again they are following the playbook that worked incredibly well for Purdue Pharma and their sales of Oxycontin.

In 2024 alone OpenPayments shows that Novo Nordisk (including Novo Nordisk AS Denmark, Novo Nordisk Health Care AG Switzerland, Novo Nordisk Inc New Jersey, and Novo Nordisk US Research and Development Massachusetts) made $28,352,315.12 in general payments and $51,074,166.16 in research payments. Novo Nordisk Inc in New Jersey didn’t just make $25,453,923.72 in general payments, they made 494,195 separate payments - that’s a lot of influence being thrown around and, again, that’s just in a single year.

So they make up a definition for existing in a higher-weight body (aka “ob*sity”) as a chronic, lifelong, relapsing, remitting disease, they foist inappropriate “person first” language on higher-weight people and call it “anti stigma,” and then they use their massive budgets, media machine, and astroturf “patient advocacy” organizations (all of which create significant influence) and it seems like overnight we are seeing this language everywhere, leading a lot of people to believe that it’s settled science when, in fact, it’s neither settled nor science. Even for those who are not convinced, it creates a situation where providers fear judgment/harm to reputation/looking like quacks if they don’t get in line or if they speak out or push back.

And it’s not just research. The combination of widespread anti-fatness and industry marketing made GLP-1s a hot topic from media outlets to influencers, almost guaranteed to get the views and clicks they need. I subscribe to a massive number of medical and healthcare trade publications and and almost every one includes at least one article about GLP-1s. Many of these stories are “supported” with quotes from “experts” who are on the weight loss industry’s payroll, but aren’t disclosing that. (Remember when the NYT ran a piece basically lobbying for insurance coverage of these drugs and every expert quoted had taken money from the drug manufacturers but none of that was disclosed? I do.)

All of this can lead to people thinking that there is “so much evidence” that the weight loss industry’s claims must be true, or they simply hear weight loss industry talking points so often that they internalize and regurgitate them. ‘

There is also a confirmation bias issue - if people want these drugs to create weight loss (and not create adverse events/deaths) then they may, consciously or subconsciously, glom on to the first talking point they hear that relieves their stress about the critiques of and concerns about these drugs (and, of course, these talking points are developed and disseminated by the weight loss industry for exactly this purpose!)

To push back against this (and help keep ourselves from becoming sucked into it!) it is imperative that we stay skeptical and curious. We can make a point to know who is creating the information and what they stand to gain, to follow the money, to point out weight loss industry influence, and ask questions that help others do the same. Leave comments on media articles and in social media comment sections:

Who funded that study?

What were the conflicts of interest among the researchers?

What is the evidence for that claim?

Is that doctor who is quoted in that article taking money from the weight loss industry or are they part of the weight loss industry such that their quote/interview is in their profit interest? Was that fully disclosed? (Anytime I see a doctor making claims that align with the weight loss industry, I look them up on the OpenPayments database!)

Who funds that “patient advocacy” organization?

Is the person claiming to be giving a “patient perspective” actually trained by the weight loss industry and/or deeply financially involved with the weight loss industry (as we saw in the Lancet Commission’s “study” on ob*sity)?

Peel the spaghetti off the wall and inspect it

We are watching the weight loss industry try a lot of different claims, arguments, and even names to try to get healthcare providers and others onboard.

We hear that “ob*sity” is a “lifelong, chronic, relapsing remitting disease” (a definition made up by the weight loss industry to make up for the shortcomings of their interventions.) But we’re also told that “ob*sity” is a “brain disease” or maybe it’s a metabolic condition? Maybe it’s Adipose Based Chronic Disease (going pretty far for the acronym ABCD because if you say it fast if sounds like “ob*sity”?) or maybe it’s weight-related health conditions or they are ob*sity-related health conditions?

And diet drugs are now weight loss medications, or weight management medications, except when they are “anti-ob*sity medications.” (Often the same people claiming that they are “anti weight stigma’ are peddling anti-ob*sity medications which strikes me as what you would call a medication if you wanted to engage in the most possible weight stigma.) So “now anti-ob*sity medications” are part of “ob*sity care”?

This is well and truly ridiculous, but it’s also effective. They meet people where they are and then lead them to where they want them to be. Maybe they aren’t comfortable saying “anti-ob*sity” medications, but they are willing to buy into Adipose Based Chronic Disease. Claiming (based on some seriously questionable evidence) that fatness causes disease isn’t as good for the weight loss industry as claiming that fatness is a disease, but it still sells their interventions and it’s a step in the right direction for their current and future profits.

We’ve seen this same effect happen with diets themselves - they try different names to see what resonates and to try to distance themselves from legitimate critiques and/or to try to conflate the ideas of weight loss and health improvements, even though they are two different things.

One thing we can do is to call things what they are - I continue to use terms like weight loss interventions to keep the intention plain and to fight this conflation. I’ve already written about the issues with so-called “weight-related” (or “adipose based”) health issues and there would need to be significantly better evidence before I would buy into this.

Insist that people be clear - if the goal of the intervention is body size change then it’s a weight loss intervention. If the goal is some health benefit then that’s what the intervention (including medication) should be about (and what it should be dosed and titrated for) with no mention of weight loss.

Hold the line on weight stigma

Perhaps one of the most massive and insidious campaigns that the weight loss industry is currently involved in is co-opting decades of actual anti weight stigma work by true anti weight stigma activists in order to sell weight loss. Their goal is to claim that anti weight stigma work should be about insisting that “ob*sity” is a treatable disease.

Now, if you tell people that their body is bad and it’s their fault, and then you tell them that their body is bad but it’s not their fault, you may reduce some weight stigma. But if you make it clear that their body was never bad, you’ll can eliminate weight stigma and you’ll avoid creating additional stigma and exposing a group of people to weight loss “treatments” that have limited to no long-term “success” and high risks.

The weight loss industry is trying to claim that you can de-stigmatize higher-weight people while seeking to create a world where they don’t exist and that is beyond just being ridiculous (though it is,) because it is deeply harmful.

The idea that you can treat higher-weight people as a problem to be solved (an epidemic/pandemic/global crisis etc.) who should be treated/eradicated/prevented is incompatible with the idea of ending weight stigma.

A legitimate anti-weight stigma stance must include an unyielding stance against:

Implicit and explicit weight bias

Poor treatment of higher-weight people

Lack of inclusion/accommodation of higher-weight people

Any attempt to eliminate/reduce/prevent fatness/higher-weight bodies

Let me be clear, even if someone thinks that weight loss will make people healthier, there is still no way to say that being higher-weight is a bad thing/disease/epidemic/crisis et al without stigmatizing higher-weight people, because we are talking about a body size and not an actual health issues\. I wrote about this in more detail here and I highly recommend Dr. Rachel Fox’s dissertation on the Anti-Ob*sity Assemblage for a deeper understanding.

Pushing back is important, but at the end of the day I also want to remind us that one of the biggest things we can do to stop the weight centric backslide is to not become part of it ourselves. We have to remain vigilant and critical because the weight loss industry is using its massive resources to try to sweep us back in.

In part 2 we’ll look at more options to stop the backslide.

This month’s online workshop is Exposing the Weight Loss Industry’s Secrets and Tricks with guest Louise Adams. We’ll talk about what they are doing, why they are doing it, and how we can pushback. All registrants get access to a video and there is a pay-what-you-can-afford option so that money isn’t a barrier. Details and Registration here!

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*Note on language: I use “fat” as a neutral descriptor as used by the fat activist community, I use “ob*se” and “overw*ight” to acknowledge that these are terms that were created to medicalize and pathologize fat bodies, with roots in racism and specifically anti-Blackness. Please read Sabrina Strings’ Fearing the Black Body – the Racial Origins of Fat Phobia and Da’Shaun Harrison’s Belly of the Beast: The Politics of Anti-Fatness as Anti-Blackness for more on this.

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In part 1 we began discussing the study “Potential mechanisms for change in diabetes prevention programs: A systematic review” including the authors and the premise. Today we’ll look at the methodology and the findings.

Summary

The researchers sought to determine which of the multiple mechanisms, moderators, or mediators (MMMs) included in Diabetes Prevention Programs (DPPs) are actually responsible for any benefits of the programs. They found that the while there is a great deal of research on these programs, nearly half of the included research drew from only three data sets and most research failed to even consider how or why any program benefits were created. The researchers found no compelling evidence that supported any MMM in general and, specifically, they found “no evidence to suggest that weight loss is a significant mediator of improvement in the programmes or even that weight loss is not harmful.” In DPP research (and I will add any research that includes weigh loss) it is crucial to include a mechanism to determine whether some part of the intervention (behaviors, pharmacotherapy, support etc.) and/or weight loss created any benefits that are found, otherwise we will just continue on our current path of assumption without evidence that props up weight loss (and the weight loss industry) perhaps (and I would suggest very likely) to the detriment of higher-weight people.

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Deeper Dive

Research Methodology

The authors note that since Diabetes Prevention Programs (DPP) research typically uses efficacy research designs (that is, designs like randomized controlled trials that seek to find out if an intervention produces the result that is expected under circumstances that are ideal,) research that seeks to determine the actual mechanisms by which the results are produced would predominantly involve assessing mediators and moderators to “identify or provide support for mechanisms of change.”

The primary goal of this systematic review, then, was to look at the literature on DPPs to “investigate which mechanisms, moderators, or mediators (MMs) are responsible for improvement in physical health outcomes among participants in DPPs.” The secondary goal was to “assess the relative strength of the association of each MMM with physical health outcomes.” Their hypothesis was that “weight loss would be less strongly associated with improved (non-weight loss) physical health outcomes than other MMMs.”

They included studies conducted through 9/2019 that investigated interventions to prevent “diabetes onset, morbidity or mortality, or improving related risk factors.” They included studies of adults that considered MMMs of “the relationship between the intervention and the non-body weight physical health outcome(s) related to diabetes risk, onset, morbidity, or mortality” they started with 13,236 studies and, after screening they ultimately included 108 total studies including 502,257 participants in the review.

Findings

While testing suggested that the included studies had “generally good methodological quality,” 46% drew from just three datasets (the DPP, Action for Health in Diabetes Trial, and the Finnish Diabetes Prevention Study.)

The researchers note that in what they call a “voluminous body of literature on the efficacy of DPPs” very few consider how/why the programs create any benefit. In fact, out of their initial group of 7,487 studies, only around 1% tested to see how/for whom the intervention actually worked.

They did not find much unequivocal evidence to support any of the tested moderators or mediators. They note that several studies found that higher-weight people experienced significantly less benefit, no benefit, and even harm from the interventions. They weren’t able to robustly test their initial hypothesis because there was not much evidence to support any MMM. Further, they note that despite a “strong emphasis on weight loss in most DPPs and in clinical guidelines, relatively few studies tested whether a weight-related MMM” explained the effect.

This is something I want to take a moment on. There are so many guidelines that recommend weight loss to prevent or improve a health condition and there are few to no studies that actually test the MMMs in interventions to see if weight loss is actually the reason for the outcome. When this actually is tested, research generally does not support the idea that weight loss actually creates the outcome.

In fact, 79% of the time when weight-related MMMs were tested in the research, they “either were not supported or showed that DPPs were less effective or harmful” for higher-weight people. Only 8 of the included studies provided evidence that “explained how or for whom DPPs work to improve physical health,” 4 provided evidence of weight as a potentially harmful moderator or mediator, and 26 showed no effect for weight.

Conclusions

The researchers found “no compelling evidence” that supported any MMM in general and, specifically, they found “no evidence to suggest that weight loss is a significant mediator of improvement in the programmes or even that weight loss is not harmful.” (emphasis mine)

Again, this is a critical point given the research we do have about the harm of weight stigma, which the study authors note can be created by these programs, and weight cycling, which is the outcome of the vast majority of intentional weight loss attempts.

The article notes that there are clinical, research, and policy implications to their findings in that future researchers need to focus on understanding the actual mechanisms that drive DPP efficacy, “rather than developing and testing new programmes to target difficult-to-change and only putatively important mechanisms, such as body weight.” Further, they note that developing new weight-loss interventions is an “inappropriate target” given the fact that they did not find evidence that weight loss is “the most important, an important, or even not harmful mechanism.” They recommend that researchers shift from a focus on interventions with a number of potential mechanisms to completing the necessary testing to determine which mechanisms are the most successful.

Finally, they conclude that “because prescribing weight loss has both ethical and potentially iatrogenic risks, clinicians should be cautious about prescribing weight-loss-focused diabetes prevention interventions until evidence is established that weight loss is significant and non-harmful for diabetes prevention.” Iatrogenic harm, meaning harm that is created by the medical care/intervention, is something that research shows can happen through higher-weight people’s healthcare including through both medical weight stigma and weight cycling that is induced by medical weight loss recommendations but is rarely, if ever, considered.

This type of research is absolutely critical. Our culture, including healthcare education, has conditioned us to assume that any correlation between (small, typically temporary) weight loss and health impacts means that weight loss creates the health impact. Sometimes there isn’t even a “need” for correlational research - there is just an assumption that weight loss will make any and everything better. Plenty of weight loss interventions, including behavioral, pharmacotherapies, and surgeries, have risen to prominence (and profit!) based on these faulty assumptions. That is why research like this is so crucially important and I’m grateful to these researchers for this work.

If I’ve said it once (and I have) I’ve said it roughly 15 million times (and I have,) research, including and especially research involving weight loss, MUST include a mechanism to determine if body size change is the reason for any health improvement or if, in fact, it is about another aspect of the intervention like behavior change, support, or the impact of the drug itself (and no,GLP-1 weight loss researchers, just giving the control group a placebo and the exact same diet/exercise intervention does not count.) We must stop propping up weight loss (and, by extension, the weight loss industry,) by foisting weight loss interventions on higher-weight people without evidence.

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*Note on language: I use “fat” as a neutral descriptor as used by the fat activist community, I use “ob*se” and “overw*ight” to acknowledge that these are terms that were created to medicalize and pathologize fat bodies, with roots in racism and specifically anti-Blackness. Please read Sabrina Strings’ Fearing the Black Body – the Racial Origins of Fat Phobia and Da’Shaun Harrison’s Belly of the Beast: The Politics of Anti-Fatness as Anti-Blackness for more on this.

Diabetes Prevention Programs are a group of programs that are created to prevent the onset of Type 2 Diabetes, often in people who have been identified as at-risk. Most include behavior changes, social support, and include weight loss as a metric and/or the primary outcome.

The assumption is typically that any health changes and/or reductions in the development of T2D are because of any weight loss. In discussing these programs previously I’ve expressed the concern that any differences in health/T2D development were more likely due to behavior changes/support than any weight loss and that, because of their insistence on a weight-loss focus, the programs likely included much more restriction than is necessary to create any health changes, which could create harms including weight cycling (which can actually drive T2D,) weight stigma (which can actually drive T2D,) and disengagement from behaviors that might actually support health and make T2D less likely (with the clear and critical understanding that whether or not someone develops T2D involves myriad factors, many of which are completely outside of their control, including genetics.)

Enter the new systematic review “Potential mechanisms for change in diabetes prevention programs” which sought “to investigate potential mechanisms for change in diabetes prevention programs (DPPs), and assess the strength of associations.” Their hypothesis was that “ Weight loss would be less strongly associated with improved health than other mechanisms.”

Summary

A group of researchers, several of whom work in weight inclusive Type 2 Diabetes preventions and management, sought to fill a gap in research around Diabetes Prevention Programs (DPPs). These program seek to delay/prevent onset of Type 2 Diabetes and typically include multiple interventions but often target an end goal of weight loss. There is a significant lack of research that even attempts to determine which aspects of DPPs might actually be responsible for any benefits and which might be unhelpful or cause harm. These researchers undertook a systematic review to attempt to determine just that.

The Authors

We’ll begin, as we always do, with the authors. Spoiler alert, this is going to be much shorter than these typically are. The study received no funding and the authors disclosed no conflicts of interest. I’ll do my usual deeper dive into their work and, as a reminder, working in the space in which you are researching is not considered a conflict of interest that requires disclosure but is something that always makes me give extra scrutiny to methodology. As usual, if you want to skip this part you can scroll down to where it says “The Study.”

Margit I. Berman is an Associate Professor at the Graduate School of Professional Psychology at the University of St. Thomas. Dr. Berman is the author of a “A Clinician’s Guide to Acceptance-Based Approaches for Weight Concerns: The Accept Yourself! Framework” This is not a DPP program but does have a section on Health at Every Size™ approaches to Diabetes and Cardiovascular Health. [Note: that Health at Every Size is the trademarked brand of the Association for Size Diversity and Health)

Martha Burla - per LinkedIn currently works at the Feinberg School of Medicine in the Department of Medical Social Sciences where she supports research on patient reported outcomes and shared decision making. She is also pursuing a PhD in Health Sciences from Rush University with the hope of continuing to research patient decision making and autonomy.

Hannah Martin - per her Linkedin she is a PhD candidate at the University of Otago, Dunedin New Zealand. Her research focuses on Intuitive Eating

Megrette Fletcher - is the owner of Inclusive Diabetes Care, LLC which offers free and paid resources for weight-inclusive diabetes care. Full disclosure, Megrette and I have worked together including speaking on the same panel and on a writing project.

Elizabeth A. Michaels - per LinkedIn, works at Christopher Rural Health Planning Corporation Primary Care including Coordination of Diabetes Program in accordance with AADE Standards , Individualized Nutrition Consultation and Diet Instruction, Nutrition Therapy for Emotional Eating, Personalized Meal Plans and Recipe Development, Provision and Marketing of Community Health Classes, Development of Educational Resources and Materials, Diabetes Medication and Insulin Management, Continuous Quality Improvement Tracking, Patient Goal Setting and Ongoing Support, Auditor AADE Programs, and Development and initiation of CDCs Diabetes Prevention Program

Lauren Brittany Beach- Per LinkedIn they are an Assistant Professor at Northwestern University’s Department of Medicine Social Sciences and Department of Preventive Medicine in the Feinberg School of Medicine and “a leader with a strong track record of scientific research and business development across a wide variety of therapeutic areas, including infectious disease, oncology, cardiology, endocrinology, nephrology, rare disease, and more. In my roles as Assistant Professor, ADVOCATE Center Director, and Robert H. Lurie Comprehensive Cancer Center Executive Team member at the Northwestern University Feinberg School of Medicine, I am recognized for innovative and high impact contributions in research, mentorship, education, and service. I have 20 years of experience translating results from cutting-edge science into narratives that resonate with funding agencies, regulators, clinicians, and the public. I have experience directing interdisciplinary teams in the United States and globally of up to 60 people to solve complex research and operational challenges on time and on budget. Trained in genetics, law, and epidemiology, I am a skilled data scientist and technical writer with experience in research and regulatory communication in both the discovery and clinical research domains.”

Michelle L. May - per LinkedIn May is an Associate Professor in the Psychology Department at Arizona State University and the creator of the Am I Hungry? Mindful eating program offering “experiential mindful eating workshops, retreats, and corporate wellness programs. We have trained over 800 health and wellness professionals in over 40+ countries to offer mindful eating programs, coaching, and therapy in their communities, practices, and workplaces.“

Pamela J. Bagley - per LinkedIn Bagley is Coordinator of Biomedical Research Support at Dartmouth Biomedical Libraries.

Heather B. Blunt - is a Research and Education Librarian, Public Health Lead in Medical and Health Sciences at the Dartmouth Biomedical Libraries with subspecialties in Medical and Health Sciences

The Study

The authors begin by explaining diabetes prevention programs (DPPs), including that they can vary but often have multiple components including medical and/or psychosocial interventions. They point to the DPP-ILI (Intensive Lifestyle Intervention) as a typical intervention that focuses on creating 7% weight loss using multiple components. They also point out that in one study the DPP-ILI reduced diabetes incidence by 58% compared to a placebo, but that participants don’t necessarily find the program either “helpful or tolerable” and the programs often having drop out rates from 40-80%. They also note that the DPP-ILI contains multiple elements - change in weight, physical activity, food, social support, psychological change, education, and self-monitoring and self-awareness that may impact onset of diabetes. Finally, the authors point out that “despite their efficacy, it is possible that DPPs may include harmful elements such as exposure to weight stigma or healthism.” I’ll also add, based on about 100 years of research, exposure to the harms of weight cycling since the vast majority of people who lose weight will gain it back.

Here the researchers hit on an issue I would suggest is not just with DPPs but with all health interventions that are based on weight loss. As these authors put it, “it is striking how little is known about which components of these interventions cause a delay in diabetes onset, and which components may cause harm.” As is, again, the case with almost all, if not all , research that tries to claim that weight loss create health benefits, more than twenty years in, the research into the DPP-ILI “was not designed to test the relative contributions of dietary changes, increased physical activity, and weight loss to the reduction in the risk of diabetes.” Given our culture’s obsession with weight loss (driven by, and with tremendous profit to, the weight loss industry,) the assumption with the DPP (and in general) is always that weight loss (and, typically, very small amounts of weight loss) causes health benefits, literally ignoring all of the behavior changes and other components that precede both the (small, typically temporary) weight loss and the health changes/benefits. The researchers note that “clinicians have focused on the importance of weight loss…recommending weight loss, however, may be a particularly likely candidate to cause harmful or null effects in DPPs.”

Considering weight loss, the researchers note that long-term weight loss is “not achievable for most people” and, further, that weight loss programs can induce or exacerbate weight stigma and expose participants to discrimination. They point out that despite the “transient” nature of weight loss in DPPS, “the delayed onset of diabetes can be largely retained, suggesting that mechanisms other than weight loss may contribute to the benefits.”

In part 2 we’ll look at the study methodology and what they found.

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*Note on language: I use “fat” as a neutral descriptor as used by the fat activist community, I use “ob*se” and “overw*ight” to acknowledge that these are terms that were created to medicalize and pathologize fat bodies, with roots in racism and specifically anti-Blackness. Please read Sabrina Strings’ Fearing the Black Body – the Racial Origins of Fat Phobia and Da’Shaun Harrison’s Belly of the Beast: The Politics of Anti-Fatness as Anti-Blackness for more on this.

“What are some pieces of advice for dealing with medical situations where fat people's bodies are not always considered? (Examples: I was told to do the Heimlich on a larger person by getting them to stand with their back…

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A couple of months ago, Anna Whelan, MD, FACOG and I did a workshop on weight-neutral reproductive care. During that workshop there were a number of questions about working with fertility specialists and Dr. Whelan mentioned the she has a resource that she sends to providers to help higher-weight patients receive weight-inclusive care and she very kindly agreed to agreed to share it. I’ve copied it below. This can be used as a template for your doctor to communicate with your fertility specialists, it can also be modified for you to communicate with fertility specialists.

Some other incredible resources for higher-weight patients navigating reproductive care:

Nicola Salmon’s Fat Fertility resources.

Jen McLellan’s Plus Mommy resources.

I have a piece about emergency contraception for higher-weight people here

You can get the video of Dr. Whelan and my workshop. There is a pay-what-you-can-afford option so that money isn’t a barrier.

Here is Dr. Whelan’s letter, republished with her permission and my gratitude!

Patient name was referred to us for discussion of how to optimize pregnancy outcomes due to their higher weight/BMI. We discussed that BMI is a poor measurement of health and most of the data regarding BMI and adverse pregnancy outcomes contains multiple confounders. Additionally, the effect of weight stigma experienced by individuals in larger bodies contributes significantly to adverse outcomes both in obstetrics and in general medicine [1,2 ].

The current data regarding BMI over 30 and pregnancy shows a small increase in rates of miscarriage and recurrent miscarriage. However, in studies where patients then lost weight, the rates of miscarriage did not decrease (indicating that it is likely not the body weight that caused the increased rate of miscarriage) and there is likely an unmeasured confounder [3 ].

Data from a systematic review of small cohort studies from the 1960s-early 2000s demonstrated an increased risk (OR 1.26-2.2) for congenital malformations among individuals with BMI ≥ 30 [4]. However, more contemporary studies have not consistently corroborated this finding [5,6]. Additionally, among patients who lost weight through bariatric surgery, rates of congenital malformations were similar to individuals with elevated BMI who had not lost weight, again indicating this finding may be due to an unmeasured confounder [7].

Individuals with BMI ≥ 30 are at an increased risk for gestational diabetes and preeclampsia. Research has demonstrated that some of this increased risk for gestational diabetes may be due to the experience of weight stigma [2]. In order to decrease the risk of gestational diabetes we recommend regular physical activity (150 minutes a week of moderate exercise such as brisk walking) and varied diet with adequate protein, fiber, and complex carbohydrates. In order to decrease the risk of preeclampsia, a low dose aspirin (81 mg) is recommended daily from 12 weeks until delivery.

Prior research has demonstrated that the rate of stillbirth may be increased among individuals with BMI ≥ 30 based on two studies. However, these studies excluded significant portions of the population and are unable to evaluate provider bias, sufficiency of stillbirth evaluation and mitigating factors. However, in order to decrease risk and identify fetuses at risk of compromise we recommend serial assessment of fetal growth starting at 24 weeks and antenatal testing starting at 37 weeks with weekly NSTs.

It is reasonable to consider induction of labor between 39 and 40 weeks, but if testing is reassuring it is also reasonable to wait until 41 weeks.

[NOTE: This section deals specifically with a patient with a history of anorexia and may be customized based on individual patient history/experiences.] We discussed that weight loss is NOT recommended to decrease obstetric risk specifically in their case due to a history of anorexia. Eating disorders have the highest mortality of any mental health condition and are associated with significant adverse pregnancy outcomes.

Additionally, weight loss is not sustainable as over 95% of individuals will regain the weight they lose within 1 year. Weight cycling, the process of losing weight via dieting/restriction (especially crash dieting) and then regaining weight afterwards, is directly associated with adverse health outcomes including cardiovascular disease, osteoporosis and mortality. We discussed that achieving weight loss has not been consistently proven to increase likelihood of pregnancy, decrease rate of miscarriage, or decrease risks of other adverse outcomes such as rates of congenital malformations, preeclampsia, gestational diabetes and stillbirth.

References:

1. Phelan SM, Burgess DJ, Yeazel MW, Hellerstedt WL, Griffin JM, van Ryn M. Impact of weight bias and stigma on quality of care and outcomes for patients with obesity. Obes Rev. Apr 2015;16(4):319-26.

2. Tomiyama AJ, Carr D, Granberg EM, et al. How and why weight stigma drives the obesity 'epidemic' and harms health. BMC Med. Aug 15 2018;16(1):123.

3. Ribeiro LM, Sasaki LMP, Silva AA, et al. Overweight, obesity and assisted reproduction: A systematic review and meta-analysis. Eur J Obstet Gynecol Reprod Biol. Apr 2022;271:117-127.

4. Stothard KJ, Tennant PW, Bell R, Rankin J. Maternal overweight and obesity and the risk of congenital anomalies: a systematic review and meta-analysis. JAMA. Feb 11 2009;301(6):636-50.

5. Pulliam L, Trammel S, Dean JH, Sianko N. Neural Tube Defects in South Carolina 1992-2019: A Review of Risk Factors. South Med J. Apr 2025;118(4):201-205.

6. Akhter Z, Rankin J, Ceulemans D, et al. Pregnancy after bariatric surgery and adverse perinatal outcomes: A systematic review and meta-analysis. PLoS Med. Aug 2019;16(8):e1002866. doi:10.1371/journal.pmed.1002866

Thanks to Dr. Whelan for sharing her work. If there are specific resources that you would find helpful for me to publish here, please let me know in the comments!

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*Note on language: I use “fat” as a neutral descriptor as used by the fat activist community, I use “ob*se” and “overw*ight” to acknowledge that these are terms that were created to medicalize and pathologize fat bodies, with roots in racism and specifically anti-Blackness. Please read Sabrina Strings’ Fearing the Black Body – the Racial Origins of Fat Phobia and Da’Shaun Harrison’s Belly of the Beast: The Politics of Anti-Fatness as Anti-Blackness for more on this.

In part 1 we looked at the authors and introduction of “Once-weekly semaglutide 7·2 mg in adults with ob*sity (STEP UP): a randomised, controlled, phase 3b trial.”

Summary

The trial over-represented cis women (who have been found to have greater weight loss on GLP-1s) and underrepresented People of Color with no trans or non-binary representation. Taking the 7.2mg dose vs the 2.4mg dose resulted in an average of 3.1% more weight loss (about 8 pounds) over 72 weeks. Based on Novo Nordisk’s pricing of the drug, the 7.2mg group would have paid $900 ($50/month) more than the 2.4mg group during the study period. Many of the actual health benefits touted by the authors (blood pressure, hsCRP) were small and/or failed to reach statistical significance. The biggest difference in terms of adverse events was a disruption to sense of touch including unusual, unpleasant or painful sensations that occurred in 22.9% of the 7.2mg group and 6% of the 2.4mg group.

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Deeper Dive

Before we get into the nuts and bolts I want to discuss a section they called “evidence before this study” (as always, I’ll indent the study content so that you can skip it if you’d like and still get the point of the piece.)

“Although we did not conduct a systematic literature search before doing this study, evidence shows that semaglutide 2-4 mg is effective for weight management.

I was always taught that giving an answer without showing your work was frowned upon. Note, again, there is no definition for “effective” weight management. They are benefiting from years of attrition as the weight loss industry systematically lowered what was considered “effective” weight loss to almost nothing. They may not have done their homework, but I did, or I should say we did. In our recent article about GLP-1s, Angela Meadows, Louise Adams and I created tables for tirzepatide and semaglutide that show the topline results, adverse events, and weight loss for each of the phase 3 placebo controlled weight loss trials, you can find them in the supplemental materials here.

However, some people did not reach their individual treatment goals with this dose in the STEP 1 trial in people with overw*ight or ob*sity. Modelling and simulation of semaglutide at different doses has suggested that a dose higher than the currently approved 2·4 mg might provide further bodyweight reduction and health benefits without jeopardising safety.”

What an odd thing to say. The STEP 1 trial did not have individual treatment goals, that’s not how trials work. They gave a group of people the drug and a group of people the placebo and then wrote up the results. The idea of “individual treatment goals” concept gives them a lot of leeway though to claim “success’ based on a number that isn’t specified.

Participants

The study included three groups. The semaglutide 7.2mg group had 1,005 participants. The semaglutide 2.4mg and the placebo group each had 201 participants.

When there is this kind of imbalance I always wonder if they are trying to stack the deck around adverse events. Adverse events are reported as a percentage, but these are also participants who are recording anything that they feel. You need 20 people out of 200 to nausea at some point during 72 weeks to get to 10%, but you need 100 people out of 1,000. I always wonder if a comparison to much smaller groups means that incidental side effects that aren’t related to the drug in the smaller group (in this case in both the placebo and 2.4mg group) might be making the side effects, especially things that are more common generally, from the drug seem more even than they are?

The 7.2mg group was 74.9% female and 50.1% male (with no trans or nonbinary representation in the trial.) The 2.4mg group was 68.2% female and 31.8% male and the placebo group was 73.1% female and 26.9% male.

There are also things to think about here. A meta-analysis of studies with almost 20,000 patients found that cis women lost 4.1% more weight than cis men. So if the 7.2mg group has a higher percentage of cis women than the 2.4mg group does, then it may give the 7.2mg group a little boost in weight loss. The authors themselves admit this vaguely, saying “The majority of participants were female, which might have introduced sex-specific biases in the reported data.”

Overall the study was 85.5% white, 8.6 Black, 4.5 Asian, 1.2% other, 0.2% missing, and 4.5% Hispanic.

This is significant because Novo Nordisk continues to target Communities of Color for intervention/insurance lobbying of their drug while underrepresenting these same communities in their trials.

Findings

So even with the possible advantage of having more cis-women, the semaglutide 7.2mg group took 3 times the dose to lose 3.1% more weight (which worked out to an average of about 8 pounds). Remember when I said I thought they were softening us up for lackluster results? Here they are.

Also, on NovoCare (Novo Nordisk owns its own pharmacy, yikes) the 7.2mg dose, at $399, costs $50 per month more than the 2.4mg dose at $349) (The 0.5mg dose it $199 which may be why Novo doesn’t seem too excited to figure out if any health benefits of the drug can be achieved on lower doses, but that that’s a subject for another day.)

So, in this 18 month study, people would have paid an extra $900 to lose an average of 8 additional pounds.

In terms of other health indicators, they claim:

Significant improvements in blood pressure and hsCRP were seen from baseline to week 72 with semaglutide 7 • 2 mg versus placebo

Note that they are comparing semaglutide 7.2mg to PLACEBO and finding statistically significant differences, but what is the difference between the existing 2.4mg dose and the 7.2mg dose?

The difference in systolic bp between 7.2mg and 2.4mg was -1.2 and did not reach statistical significance.

The difference in diastolic bp was -1.5 and did reach statistical significance.

The difference in hsCRP was 0.94 and did not reach statistical significance.

So again, not much of a difference given the 3x higher dose (and the extra cost). Also, they note that most participants who were receiving lipid-lowering or anti-hypertensive medications at baseline had no changes to their medications over the 72 weeks across all groups.

Moreover, like all of their trials, there is no mechanism to tell if any health benefits were due to the mechanism of the drug itself, behavior changes, or body size changes.

Adverse Events

7.2mg vs 2.4mg

Overall adverse events: 87.5% vs 84.1%

Mild: 80.2% vs 76.6%

Moderate: 50.4% vs 48.3%

Severe: 8.1% vs 10.4%

Serious: 6.8% vs 10.9%

First of all, I’ve heard some folks have confusion about the difference between severe and serious adverse events so I wanted to take a moment on this. “Severe” is part of a grading system that refers to the intensity of the event. So if stomach pain is an adverse event, it could be graded as mild, moderate, severe (life-threatening and fatal are also grades on this scale). “Serious” refers to the outcome of the event, and is typically reserved for events that can post a threat to the ability to function or the patient’s life. An event can be severe but not serious, for example, a severe headache.

Even if these numbers are accurate (and not the result of the group size differences as I mentioned before) these strike me as pretty big numbers - about half of people have moderate events and somewhere between 8 and 10% are severe. Almost 7% to almost 11% have serious adverse events? Especially considering how widely these drugs are being prescribed (and how widely the weight loss industry lobby is trying to get them prescribed,) that is a lot of people.

Adverse events leading to dose reduction: 18.5% vs 12.4%

Adverse events leading to permanent discontinuation: 5.4% vs 4.0%

As a reminder, these are people who signed up to be in a trial of weight loss medications, they went through an informed consent process and they are, in theory, quite motivated and 4-5% permanently discontinued the medication because of adverse events and 12-18.5% reduced their dose and that’s just in 72 weeks. Remember that weight is rapidly regained when the drugs are ceases and, while there is no evidence to support this, the weight loss industry is claiming that people have to stay on the drugs for life to even have a chance of maintaining weight loss. Again, not only is there not a reason to believe it will work, there’s not a reason to believe that people can stay on the drugs that long.

There is one adverse event I want to discuss more, Dysaesthesia. This is listed in the adverse events table. If you follow the symbol to the fine print you learn that they define this as [items in brackets are added by me and not part of the original research text] “allodynia [extreme sensitivity to touch], burning sensation, dysaesthesia [disruption to sense of touch unusual, unpleasant or painful sensations], hyperaesthesia [sensations felt very intensely], pain of skin, paraesthesia [tingling, numbness or pins and needles], sensitive skin, skin burning sensation, skin discomfort, and skin sensitisation”.

At any rate, this cluster of adverse events was experienced by 22.9% of the 7.2mg group versus 6% of the 2.4mg group (it was not an adverse event at all in the original STEP 1 trial at all.)

The researchers claim that “Dysaesthesia adverse events were mild for most participants who experienced them: and that “Most participants recovered from the event by the end of the trial.” Of course we don’t know if they will come back and for those who hadn’t recovered, we don’t know how this impacts their life/quality of life.

This strikes me as a big deal and perhaps a high price to pay for losing an average of 8 extra pounds (at least short term.)

These adverse events are also important when we consider these drugs for secondary uses. For example, it may have a benefit for hypertension, but we also need to look at how not just the benefit of actual hypertension meds compares but also the adverse event profile.

The dose comparisons themselves are on shaky ground. In the limitations section the authors point out that

It was also valuable to compare both doses of semaglutide for all endpoints; however, due to the prespecified statistical hierarchy, exploratory post-hoc comparisons were underpowered and therefore not fully representative of the differences between semaglutide 7 • 2 mg and 2-4 mg.

They designed this study so this is really on them. Now, statistically underpowered studies happen, especially where research resources are limited and that doesn’t mean that the results aren’t worth considering. That said, it seems like a company with pretty much endless funds that is putting together a trial comparing dose differences, could create a trial with sufficient statistical power to accurately compare the dose differences.

Their overall claim:

Results from the STEP UP trial therefore support a favourable benefit-risk profile of semaglutide 7 • 2 mg for weight management in people with ob*sity, and suggest that a higher dose of semaglutide up to 7 • 2 mg per week could be used to achieve greater clinical benefits in people not reaching therapeutic goals with once-weekly semaglutide 2 • 4 mg.

The claim of a “favourable benefit-risk profile” seems to be a bit of a judgment call, there’s not much more weight loss and not many more other health benefits than with semaglutide 2.4mg and the adverse events, particularly the Dysaesthesia cluster experienced by more than 22% of the 7.2mg group, seem concerning to me.

One last thing before I wrap this up. Despite the existence of the 2.4mg dose which some of this study’s authors told (and are still telling) the media is “game-changing,” Novo Nordisk got expedited FDA approval of this drug through Commissioner’s National Priority Voucher pilot program which “seeks to expedite approval of applications that address critical national health priorities, such as bringing innovative therapies to the American people, addressing large unmet medical needs, promoting domestic manufacturing, and increasing affordability.” As a voucher recipient Novo was “entitled…to benefits including enhanced communications and rolling review to allow for a shortened review time.” I am disappointed that this is the kind of drug that the FDA is expediting and I’ll point out that the FDA has made a habit of giving Novo Nordisk priority reviews for its weight loss drugs, though that is a subject for another day.

For today I have to wonder what will happen to people on this new megadose of the drug long-term? What happens when they go off the drug? And how will we possibly know, when Novo Nordisk is shirking its duties to report post market adverse drug events to the FDA? In an ideal world researchers who were not either taking money from a drug company or directly employed by, and shareholders, of them would evaluate drugs in trials with rigorous methodology, drawing unbiased conclusions. Unfortunately, this is far from an ideal world and so we always need to look beyond the abstracts and press releases for these drugs.

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*Note on language: I use “fat” as a neutral descriptor as used by the fat activist community, I use “ob*se” and “overw*ight” to acknowledge that these are terms that were created to medicalize and pathologize fat bodies, with roots in racism and specifically anti-Blackness. Please read Sabrina Strings’ Fearing the Black Body – the Racial Origins of Fat Phobia and Da’Shaun Harrison’s Belly of the Beast: The Politics of Anti-Fatness as Anti-Blackness for more on this.

Hello Subscribers and happy Friday. Thank you so much for supporting my work here. This week’s topic comes from Dev:

What are some manageable, actionable steps we could choose to take towards decreasing institutional weight stigma and barriers? For example, if I'm in a waiting room without armless chairs, I'll often mention to the receptionist that there…

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You may have heard that Semaglutide was approved by the FDA at a new dose of 7.2mg for weight loss (a lot of you did because the requests to write about this have been pouring in!) The FDA approved the new dose based on a 72 week trial called “Once-weekly semaglutide 7·2 mg in adults with ob*sity (STEP UP): a randomised, controlled, phase 3b trial” In part 1 we’ll discuss the authors and the introduction, in Part 2 we’ll look at the findings.

Summary

Semaglutide was originally a Type 2 Diabetes medication that showed a small side effect of weight loss. The minimum therapeutic dose of semaglutide for T2D is 0.5mg. Originally the maximum dose was 1mg and it still is in many European countries. In the US, the maximum dose was eventually increased to 2mg. The manufacturer of the drug (Novo Nordisk) noted the weight loss side effect and decided to create a “weight loss” drug by giving people a larger dose of 2.4mg to maximize the side effect of weight loss. So people who were taking the weight loss dose could be taking up to about five times the amount of those taking the drug for type 2 diabetes.

Novo decided why stop at 5 times the minimum T2D dose when you could give almost 14.5 times the minimum T2D dose and 3 times the existing weight loss megadose! Enter the drug trial “Once-weekly semaglutide 7·2 mg in adults with ob*sity (STEP UP): a randomised, controlled, phase 3b trial”

Every author is either financially conflicted or an employee and stockholder at Novo Nordisk. Nordisk didn’t just fund the study, they designed it, oversaw it, collected and analyzed the data, and drafted the manuscript, paying for the medical writing and editorial support.

The introduction is a dance wherein they continually assure us that the current weight loss dose (2.4mg) is “effective” and that the 7.2mg dose is needed, while also softening the ground for the findings to be, I would guess, pretty minimal.

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Deeper Dive

Let’s start as we always do, with the authors. I think this is important to document these vast conflicts of interest, but I also understand that reading it can have a somnolent effect (trust me, I understand - so can the research that goes into writing this section!) So I’ve done three things to try to help:

1. I’ve highlighted the conflicts with the study funder, Novo Nordisk so you can just skim that.

2. I’ve provided links to openpayments as well as amounts for the authors who are listed there so you can juts get a sense of the money involved.

3. You can skip this section entirely by scrolling down to where it says “Let’s look at the introduction” in large bold type.

The listed authors are below. I’ve included the information from the study disclosures, highlighting the specific conflicts with the study funder, I’ve included financial information from OpenPayments.com where it was available for US-based healthcare providers.

Sean Wharton, MD

Disclosures: SW has received payment or honoraria from AstraZeneca, Bausch Health Canada, Boehringer Ingelheim, Eli Lilly, Metsera, Neurogastrix, Novo Nordisk, and Regeneron for academic talks to colleagues; has been provided with medical writing support from AstraZeneca, Boehringer Ingelheim, Bausch Health Canada, Eli Lilly, and Novo Nordisk; and has an unpaid leadership role in The Ob*sity Society, and Ob*sity Canada [both of which take significant funding from Novo Nordisk].

Paula Freitas, PhD

Disclosures: PF has received payment or honoraria from Amryt, Bia!; Boehringer Ingelheim, FaesFarma, Janssen, Lilly, Merck, Novartis, NovoNordisk, Pronokal, and Sanofi, along with support to attend meetings from Bia!, Medinfar, NovoNordisk, and Sanofi.

Jøran Hjelmesæth, MD

Disclosures: JH has received payment or honoraria from Novo Nordisk, Eli Wly, VIVUS, and AstraZeneca; and has received fees to participate on a data safety monitoring board or advisory board for Novo Nordisk, Eli Lilly, and VIVUS.

Maria Kabisch, PhD

Disclosures: MK is a full-time employee of, and holds shares in, Novo Nordisk; and is named on a US patent for semaglutide (”Semaglutide in Medical Therapy”, Patent Number: US 12,029,779 B2)

Kristian Kandler, MD

Disclosures: KK is a full-time employee of, and holds shares in, Novo Nordisk.

Ildiko Lingvay, MD

Disclosures: IL has received grants from Boehringer Ingelheim, Dexcom, Eli Lilly, Novo Nordisk, Roche, and Pfizer, with all payments made to her institution; has received payment or honoraria from AbbVie, Altimmune, Alveus Therapeutics, Amgen, Antag Therapeutics, AstraZeneca, Bayer, Betagenon, Bioio, Biomea, Boehringer Ingelheim, Cannot, Cytoki Pharma, Eli Lilly, Intercept, Janssen/J&J, Juvena, Keros Therapeutic, Mediflix, Merck, Metsera, Neurocrine, Novo Nordisk, Pharmaventures, Pfizer, Regeneron, Roche, Sanofi, Shionogi, Source Bio, Structure Therapeutics, TARGET RWE, Terns Pharma, The Comm Group, Verdiva Bio, WebMD, and Zealand Pharma; and has received support to attend meetings from AstraZeneca, Boehringer Ingelheim, Novo Nordisk, and Eli Lilly

Per OpenPayments

$129,391.04 in general payments
$783,570.26 in associated research funding
Novo Nordisk is her top patron for both forms of funding

Maria Quiroga, MD

Disclosures: MDLAQ-P is a fulltime employee of Novo Nordisk and holds shares in Novo Nordisk, Eli Lilly, and Genmab

Per LinkedIn she is an Associate Medical Director at Novo Nordisk

Julio Rosenstock, MD

Disclosures: JR has received research grants from Amgen, Applied Therapeutics, AstraZeneca, Biomea Fusion, Boehringer Ingelheim, Carmot, Corcept, Eli Wly, Hanntl, Merck, Novartis, Novo Nordisk, Oramed, Regeneron, Pfizer, Sanofi, Structure Therapeutics and Terns; and has served on scientific advisory boards and received honorarium or consulting fees from Amgen, Applied Therapeutics, Biomea Fusion, Eli Wly, Hanntl, Novo Nordisk, Oramed, Regeneron, Regor, Roche, Sanofi, Structure Therapeutics, and Terns; and received honoraria for lectures from Eli Lilly, Novo Nordisk, and Sanofi

Per OpenPayments between 2018 and 2024
General Payments - $1,486,867.18
Research Payments - $431,236.85
Associated research funding - $20,949,578.63

Novo nordisk is her second highest general payment patron

Eli Lilly is her top research payment patron

Eli Lilly is her top associated research funding patron with over 11.2M with Novo Nordisk coming in a strong second placed with over $4.4M

Prof W Timothy Garvey, MD

Disclosures: WTG has received grants as a principal investigator from Novo Nordisk, Eli Lilly & Co, Pfizer, Epitomee, Neurovalens, Zealand, Cannot/Roche, Terns Pharmaceuticals, Viking Therapeutics, and Pfizer, and for research from the UAB Diabetes Research Center (DK079626) funded by the US National Institutes of Health and National Institute of Diabetes and Digestive and Kidney Diseases, with all payments made to his institution; has received consulting fees as an advisory board member from Boehringer Ingelheim, Eli Lilly, Novo Nordisk, Pfizer, Fractyl Health, Alnylam Pharmaceuticals, Inogen, Zealand, Allurion, Carmot/ Roche, Terns Pharmaceuticals, Neurocrine, KEROS Therapeutics, Gan & Lee, NodThera, and Regereron; has received fees to participate on a data safety monitoring board or advisory board for Boehringer Ingelheim and Eli Lilly; and is an unpaid member of the The Lancet Diabetes Endocrinology Commission on definition and diagnostic criteria of clinical ob*sity, American Association of Clinical Endocrinology (AACE) update of ob*sity treatment algorithm, American Diabetes Association (ADA) nutrition recommendations update, and ADA Standards of Care for Ob*sity.

He also has his own page on the Novo Nordisk website: https://sciencehub.novonordisk.com/speakers/timothy-garvey.html

OpenPayments (Interestingly, he is listed as W. Timothy Garvey on the research but William T. Garvey on OpenPayments)

General Payments - $338,059.61
Research Payment Records - $3,456.86
Associated research funding - $2,817,062.68

Novo Nordisk is his top patron, by far

Study Funding

Novo Nordisk isn’t just the study funder, they were also very heavily involved “The funder provided the trial product, designed the study, oversaw its conduct, monitored study sites, and collected and analysed the data; investigators were responsible for study-related medical decisions and data collection. This manuscript was drafted under the guidance of the authors, with medical writing and editorial support paid for by the funder.”

So those are the authors, as usual massive conflicts of interest all around and deep involvement by Novo Nordisk in the research.

Let’s look at the introduction

As always, I’ve indented their words, you can skip them and still get the gist of the piece.

As the global prevalence of ob*sity approaches one billion people,’ there is a need for treatment options that will allow people with ob*sity to reach their individual treatment goals to improve their health. Effective management of ob*sity requires options to reduce the risk of ob*sity-related complications and improve quality of life and wellbeing.

Some things to note here. First, the citation for the “global prevalence of ob*sity” is from an 2024 study creating estimates using data from 1990-2022. It does not control for the impact of weight loss interventions over that time, which is important since about a century of research has shown that the vast majority of weight loss attempts end in complete weight regain with up to 66% resulting in weight gain over baseline. I’m not saying there is anything wrong with being/becoming higher-weight, rather that the weight loss industry has spent the last century peddling an intervention which commonly results in the opposite of the intended effect, and then using their own failure to insist that we need more/more dangerous/more expensive interventions delivered earlier and more often.

Weight-neutral interventions have been shown to provide similar health benefits with far less risk. I would suggest that the responsible thing to do would be to use weight-neutral comparator groups, rather than testing against a placebo and an old-fashioned weight loss diet.

Further remember that “ob*sity-related complications” are health issues that happen to people of all sizes but get called “ob*sity-related” when higher-weight people have them (including and especially when the weight loss industry is trying to sell weight loss interventions.)

There is a continuously emerging landscape of effective ob*sity treatments, with many currently in development.

Note that they don’t offer any definition for “effective” and they are talking about treatments for which every author has conflicts of interest. This is the start of an amusing part of this study - specifically that they don’t want to damage the marketing for the existing drug dose, so they have to find a way to prop up their current drug/dose (semaglutide 2.4mg) while also hyping up the tested drug/dose (semaglutide 7.2).

Once-weekly subcutaneous semaglutide 2 • 4 mg, a G LP-1 receptor agonist, has been extensively investigated in the global phase 3 STEP clinical trial programme. In the

STEP 1 trial, semaglutide 2-4 mg provided superior bodyweight reduction versus placebo, with a mean change of -14-9% versus -2-4%, respectively, after 68 weeks (estimated treatment difference [ETD] -12 -4% [95% CI -13-4 to -11 -5]; p<0 -0001), and was well tolerated.

Semaglutide 2 • 4 mg is approved for weight management and for the reduction of major adverse cardiovascular events for people with established cardiovascular disease and a BMI of 27 kg/m2 or greater.

We’re going to get into this in more depth later, but remember that the cardiovascular trial rode to FDA approval on the back of an extremely ethically questionable publicity stunt and the “benefit” was a 1.5% absolute risk reduction that was not statistically significant for women, Black people, Hispanic people, those under 55 or over 75, and those with a BMI above 35. Also, most of the cardiovascular impact happened before weight was lost. I wrote about this in detail here.

The benefits of semaglutide 2 -4 mg also include decreased pain for those with knee osteoarthritis

Here the authors were honest that they had no idea if decreased pain was due to weight loss, behavior change, or the impact of the drug which may have “antiinflammatory and antidegradative effects.” It’s also not at all clear that semaglutide is superior to other drugs (including metformin) or other treatments for knee OA. I wrote about this here.

and improved glycaemic status for those with prediabetes.

They gave people who didn’t have type 2 diabetes a megadose of a type 2 diabetes drug and their blood sugar was lowered? The phrase Big Whoop comes to mind. The idea of prediabetes is controversial but even if that wasn’t the case, one wonders if the drug could have had that effect at a significantly lower dose.

Tirzepatide is a peptide engineered from the glucose-dependent insulinotropic polypeptide (GIP), investigated at once-weekly doses of 5 mg, 10 mg, and 15 mg.19 In the SURMOUNT-1 trial, all doses of tirzepatide provided superior bodyweight reduction versus placebo, with a mean change of -15 -0% (ETD -11 -9% [95% CI -13·4 to -10·4]; p<0-001) with the 5 mg dose, -19-5% (-16 -4% [-17 -9 to -14-8]; p<0 -001) with the 10 mg dose, and -20-9% (-17-8% [-19-3 to -16-3]; p<0 -001) with the 15 mg dose versus -3 -1% with placebo after 72 weeks, and all doses were well tolerated.19 In the SURMOUNT-5 trial, conducted in adults with overw*ight or ob*sity and at least one ob*sity-related complication, without type 2 diabetes, the mean percentage change in bodyweight was -13 -7% (95% CI -14-9 to -12 -6) with semaglutide 1-7 mg or 2-4 mg, and -20-2% (-21·4 to -19-1) with tirzepatide 10 mg or 15 mg after 72 weeks.

Tirzepatide for weight loss (brand name Zepbound) is semaglutide for weight loss (Wegovy)’s main competitor. That said, nearly all of the authors (who aren’t Novo Nordisk employees) also have conflicts of interest with tirzepatide’s manufacturer Eli Lilly. The beef here likely comes from the fact that Lilly conducted the (completely unnecessary) SURMOUNT 5 trial to replicate both tirzepatide and semaglutide’s original weight loss trials just to demonstrate (again!) that tirzepatide caused more weight loss at least short term. (I lay awake at night and think about better ways to use however much money was spent on this.) I wrote about this here. It’s possible that Novo is trying to position semaglutide 7.2mg as being as good/better than tirzepatide at creating (at least short-term) weight loss.

Despite the effectiveness of current treatments for weight management, some individuals will not reach the therapeutic goals that are associated with greater bodyweight reduction.

Here we go. The “therapeutic goals that are associated with greater body weight reduction” is a lot of words to say, absolutely nothing, really. They aren’t going to commit to a “therapeutic goal” and they want to reiterate that their current drug dose is “effective.” Now, I’m not saying that there are drugs that are effective for which a larger dose might make sense, I’m saying that this drug isn’t it and I’m saying that the idea of “effectiveness” is in serious question.

It was deemed relevant to investigate a higher dose of semaglutide 7 • 2 mg to establish whether this dose provides further benefits and can help those for whom the current treatment landscape is inadequate.

Is it just me or is this starting to sound like a book report written by someone who didn’t read the book?

Incremental reductions in bodyweight after the maximum benefits have been reached with a lower dose can positively affect these people’s lives.

Something tells me that they are prepping us to learn that this new dose doesn’t do very much above what the current dose does but to believe that it’s still important.

Modelling and simulation of efficacy and exposure data from the phase 3a STEP (subcutaneous semaglutide 2 -4 mg) and OASIS (oral semaglutide) programmes suggested that increasing the dose of semaglutide might provide further bodyweight reduction and health benefits without jeopardising safety or significantly increasing the risk of adverse events. In the OASIS 1 study, exposure to oral semaglutide tripled during the escalation from 14 mg to 25 mg, without leading to an increased rate of adverse events,”

Modelling and simulation? To me this seems more like “we wanted to try a higher dose so that we could create as much (short term) weight loss as tirzepatide so here is our pretty weak justification.”

and the exposure response in the STEP programme revealed that gastrointestinal adverse events plateau at higher exposures.

Note that gastrointestinal adverse events are by far the most common but are definitely not the most serious adverse events associated with these drugs.

As a result of these findings, it was deemed appropriate to investigate an increased dose of subcutaneous semaglutide without further additional intermediate increases in the titration schedule.

The (I would argue wholly inadequate) answer to the question “Why are you jumping from 2.4mg to 7.2mg?” Even if the gastrointestinal side effects plateau, we don’t know what will happen with the serious, sometimes fatal side effects. This trial isn’t long enough to determine that and Novo Nordisk just got in trouble for failing to report serious adverse events and death to the FDA after other drugs, including semaglutide, had been approved. The FDA characterized Novo’s violations and subsequent responses as “suggest[ing] systemic failures with your surveillance, receipt, evaluation, and reporting of ADEs to FDA,” and noted that their failure to determine the root causes of the violations “raises concerns about your firm’s ability to monitor the safety of your products.” I wrote about this here.

The aim of the STEP UP trial was to assess the efficacy and safety of once-weekly semaglutide 7 • 2 mg versus placebo, and also versus semaglutide 2 • 4 mg, as an adjunct to lifestyle intervention, in adults with ob*sity without type 2 diabetes.

So they are calling the drug an adjunct to lifestyle intervention, even though they highlight the (at least short term) weight loss created by the drug over the placebo group, which also includes the exact same “lifestyle intervention” (lifestyle intervention here having the meaning of an old fashioned diet/exercise weight loss intervention that has, again, been failing for about 100 years).

“Eat less and exercise more, why can’t I quit you?” - These authors, probably.

So those are the authors and that’s the introduction. In Part 2 we’ll look at what they found (and what they didn’t.)

HAPPENING TONIGHT! This month’s online workshop is Movement in a Bigger Body with Leslie Jordan Garcia. This workshop is for anyone who wants to learn more about weight-inclusive movement/fitness with the understanding that nobody is obligated to participate, but every body should be welcome. There is a pay-what-you-can-afford option and all registrants get a video in case you can’t make it live. Details and Registration are here!

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*Note on language: I use “fat” as a neutral descriptor as used by the fat activist community, I use “ob*se” and “overw*ight” to acknowledge that these are terms that were created to medicalize and pathologize fat bodies, with roots in racism and specifically anti-Blackness. Please read Sabrina Strings’ Fearing the Black Body – the Racial Origins of Fat Phobia and Da’Shaun Harrison’s Belly of the Beast: The Politics of Anti-Fatness as Anti-Blackness for more on this.

Recently I wrote about research around GLP-1s and nutritional deficiencies. In summary, we looked at a study that showed that most of the clinical trials aren’t studying this at all, and that when studies do consider this there are concerning findings, and, finally, the implications of all this.

I was recently contacted by a Chicago-area private practice dietitian (MS, RDN, LDN) who had, in fact, written a letter to the editor of the journal that published one of the articles I looked at in Part 2, Malnutrition is Common in Patients Utilizing Glucagon-Like Peptide-1 Agonists Prior to Total Joint Arthroplasty, published in the journal Arthroplasty Today. The letter made important points about the study itself (including the lack of a Registered Dietitian among the authors) as well as issues with the measures chosen and more.

This is where I would link to the published letter, except that it’s not published. It was rejected, not on the merits of its arguments she told me, but with a single sentence:

“We appreciate your letter to the editor but I am not sure that we typically have registered dietician [sic] comment or collaborate on our research."

This seems to me to be part of a massive issue within the world of research. Journals, (which are often run by people with a profit interest in what they publish, though that’s a subject for another day,) choose not only whose work to publish and whose work not to publish, but also choose what critiques (if any) of that work are published.

This is how a letter to the editor from a nutrition expert about a study undertaken in her area of expertise is rejected because she is a a nutrition expert…by editors who either can’t spell dietitian, or didn’t think it was important enough to spell correctly (editor’s note: I apologize. In the editing process I shortened this paragraph including removing a larger section about the journal itself, which included an explanation that while the journal says that “Arthroplasty Today is also a forum for information relating to the advocacy mission of the American Association of Hip and Knee Surgeons” suggesting the misspelling, it’s also possible that the person who wrote the email came from somewhere in the world where dietician is used. Not including that caveat was my mistake and I apologize and thank those who caught it and let me know.)

This systematic silencing of viewpoints not based on merit but based on who “deserves” to publish and critique research (and, often, who profits from the research avoiding critique) is a big reason why this Substack exists. While Arthroplasty Today decided not to publish this letter, I will. As the letter’s author pointed out to me “These are critical conversations if we are going to have studies that accurately assess malnutrition in people on these drugs (and I’d hate for low-quality measures or methods to be the reason people throw out malnutrition studies and say they’re unreliable, people are fine, don’t worry about it, etc.)”

I’ll print the letter in it’s entirely (with permission, of course) and then offer some thoughts:

Letter to the Editor of Arthroplasty Today:

Evaluating Malnutrition in Patients Using GLP-1s

As a registered dietitian, I was delighted to see research on malnutrition in patients using GLP-1s in the Jodoin study (Malnutrition is Common in Patients Utilizing Glucagon-Like Peptide-1 Agonists Prior to Total Joint Arthroplasty) [1]. Thank you for addressing this critical topic and growing concern as more people are prescribed these medications. However, I was disappointed to see no registered dietitian among the authors, and I have concerns about the markers that were evaluated.

Any study on malnutrition should include a registered dietitian (RD). RDs are credentialed professionals who have a minimum of a graduate degree from an accredited dietetics program, have completed supervised practice, have passed a national exam, and continue professional development throughout their careers. These food and nutrition experts work in numerous settings, including research, community health, and inpatient and outpatient clinical care. RDs are a critical part of the healthcare team, especially as it relates to the use of GLP-1s and anything that impacts patients’ nutritional status.

Importantly, the joint advisory from the American College of Lifestyle Medicine, the American Society for Nutrition, the Ob*sity Medicine Association, and The Ob*sity Society on nutritional priorities to support GLP-1 therapy for ob*sity recommend that patients prescribed a GLP-1 receive counseling from an RD [2]. In practice, if the prescribing provider does not refer the patient to an RD, other members of the healthcare team, including orthopedic surgeons, must recognize this gap in care and refer the patient to an RD.

While retrospective chart reviews contain inherent limitations, the lab values chosen to indicate malnutrition in the Jodoin study are largely unreliable markers for malnutrition. For example, serum calcium does not indicate calcium intake nor calcium status [3]. Why was that marker chosen?

Additionally, albumin and total protein are not reliable markers of malnutrition, and prealbumin is questionable at best. These markers are susceptible to changes related to stress and inflammation and may also be in the normal range when the patient is indeed malnourished [4].

Although there are no standardized diagnostic criteria for malnutrition, the Academy of Nutrition and Dietetics and the American Society for Parenteral and Enteral Nutrition have recommended characteristics for the documentation and identification of adult malnutrition in a 2012 consensus statement. These characteristics include insufficient energy intake, weight loss, loss of muscle mass, loss of subcutaneous fat, fluid accumulation that may mask weight loss, and diminished functional status as measured by handgrip strength. The consensus statement notes, “indicators of inflammatory response traditionally used as indicators of malnutrition (ie, serum albumin, prealbumin) should be interpreted with caution.” [4] The Academy/ASPEN indicators for diagnosing malnutrition (AAIM) tool has been validated [5].

Thank you for your attention to the topic of malnutrition and GLP-1 use! I hope to see much more research in this area, as well as RDs as authors and the use of reliable markers of malnutrition.

References
[1] Jodoin Z, Young WH, Sheikh D, Pena B, Moore CC, Buttacavoli F. Malnutrition is Common in Patients Utilizing Glucagon-Like Peptide-1 Agonists Prior to Total Joint Arthroplasty. Arthroplasty Today. 2025;35:101865. DOI:10.1016/j.artd.2025.101865

[2] Mozaffarian D, Agarwal M, Aggarwal M, Alexander L, Apovian CM, Bindlish S, et al.; for the American College of Lifestyle Medicine, the American Society for Nutrition, the Obesity Medicine Association & The Obesity Society. Nutritional priorities to support GLP-1 therapy for obesity: a joint advisory from the American College of Lifestyle Medicine, the American Society for Nutrition, the Obesity Medicine Association, and The Obesity Society. Amer J Clin Nutr. 2025;122(1):344-367. DOI: 10.1016/j.ajcnut.2025.04.023

[3] Houillier P, Froissart M, Maruani G, Blanchard A. What serum calcium can tell us and what it can’t. Nephrol Dial Transplant. 2006;21(1):29-32. DOI: 10.1093/ndt/gfi268

[4] White JV, Guenter P, Jensen G, Malone A, Schofield M; Academy of Nutrition and Dietetics; American Society for Parenteral and Enteral Nutrition. Consensus statement of the Academy of Nutrition and Dietetics and American Society for Parenteral and Enteral Nutrition: characteristics recommended for the identification and documentation of adult malnutrition (undernutrition). J Acad Nutr Diet. 2012;112(5):730-738. doi: 10.1177/0148607112440285

[5] Compher C, Jensen GL, Malone A, Morgan S, Becker S, Cresta L,et al. Clinical Outcomes Associated With Malnutrition Diagnosed by the Academy of Nutrition and Dietetics and American Society for Parenteral and Enteral Nutrition Indicators of Malnutrition: A Systematic Review of Content Validity and Meta-Analysis of Predictive Validity. J Acad Nutr Diet. 2024;124(8):1058–1074.e4. DOI: 10.1016/j.jand.2024.02.002

I want to first point out that I’m so grateful for this letter because while I was able to discuss aspects of the research, I’m not a registered dietitian and the information in this letter is outside of my area of expertise. This is why we need to collaborate (for example, just as a random hypothetical, including RDs on author teams studying nutritional deficiencies.)

In reference to the “joint advisory from the American College of Lifestyle Medicine, the American Society for Nutrition, the Ob*sity Medicine Association, and The Ob*sity Society” I think their recommendation to refer GLP-1 patients to an RD is an important point in the Letter to the Editor. Outside of that context I want to point out that the Ob*sity Medicine Association and The Ob*sity Society exist as trade/lobbying groups for the weight loss industry and so, in general, any and all advice they offer should be heavily scrutinized.

I have no idea why these researchers chose the markers they did, but I do want to point out that many of the markers for malnutrition indicated by The Academy/ASPEN are things that these drugs are trying to create in higher-weight people such that, once again as the brilliant Deb Burgard has pointed out, what is diagnosed and treated in thinner people is being prescribed to fatter* people.

I also want to point out that the one study I looked at in my previous piece that took dietitian visits into account (Nutritional deficiencies and muscle loss in adults with type 2 diabetes using GLP-1 receptor agonists: A retrospective observational study, Butsch et al. 2025 DOI: 10.1016/j.obpill.2025.100186) found that nutritional deficiencies were actually more likely among patients who had a dietitian visit within the first 6 months compared with those who didn’t. Now, this is a complex finding and the study wasn’t created to understand this phenomenon. It could be that patients experiencing symptoms of malnutrition were more likely to be referred to a dietitian, creating a “chicken and egg” situation, it could be that they were sent to traditional, weight-centric dietitians who prioritized with loss over adequate nutrition (not all weight-centric dietitians make this mistake all the time, but many of them do and the idea that it’s reasonable to do “whatever it takes” to create weight loss and only when the person is thin consider their health is horrifyingly common.)

So I agree that it’s important for people taking drugs that manipulate their hunger mechanically and psychologically in ways that can cause nutritional deficiencies (which is what GLP-1s do and how they create weight loss, at least temporarily) should certainly receive expert support to ensure that they are at the very least, taking in adequate nutrition. That said, it seems at least possible that some dietitians could actually exacerbate the problem so if it were me, I would seek out a weight-inclusive, non-diet dietitian (More-Love.org has a list here and they are also included in the ASDAH.org list of their member/providers.)

Finally, those performing/publishing research about nutrition/nutritional deficiencies etc who find themselves saying something akin to “I am not sure that we typically have registered dietician comment or collaborate on our research” should, instead of pasting that into a email and sending it, consider how including actual experts with extensive training in nutrition could improve research about nutrition.

I’m going to be part of a free webinar, CDR-Approved for 1.5 CEUs and meets ethics/health equity requirement! As part of the Weight Inclusive Toolkit Initiative, this webinar explores weight-inclusive care and evidence-based interventions, centers student lived experiences, and offers actionable, trauma-informed strategies to build more inclusive, supportive learning environments. April 21, 2026 from 12:00-1:30pm EST. Click here for details and registration!

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*Note on language: I use “fat” as a neutral descriptor as used by the fat activist community, I use “ob*se” and “overw*ight” to acknowledge that these are terms that were created to medicalize and pathologize fat bodies, with roots in racism and specifically anti-Blackness. Please read Sabrina Strings’ Fearing the Black Body – the Racial Origins of Fat Phobia and Da’Shaun Harrison’s Belly of the Beast: The Politics of Anti-Fatness as Anti-Blackness for more on this.

This week’s post was suggested by Dev who asked for “Ideas and resources for handling situations with schools. For example, my kids often come home with instructions that they may bring a "healthy snack" to eat. For class parties, they ask some parents …

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