Krinn Post 2: A Year and Change

Last time you heard from her, Krinn had just put out a tumblr post titled An Ad-Hoc, Informally-Specified, Bug-Ridden, Single-Subject Study Of Weight Loss Via Potassium Supplementation And Exercise Without Dieting. After losing 6 lbs in our Low-Dose Potassium Community Trial, she decided not to stop as planned but instead to keep going, and in fact go even harder. Eventually she ramped up to around 10,000 mg potassium a day, and lost even more weight. 

Krinn also added an exercise habit that she described as a “naïve just-hit-the-treadmill exercise regimen”. Even with this in mind, her results still seem remarkable, because most people do not lose 50 lbs from starting a moderate treadmill habit: 

We published a short review of that original post on this here blog of ours. That was in July 2023. Now, Krinn is back, and more powerful than ever, with an untitled post we’ll call A Year And Change After The Long Post About The Potassium Experiment (AYACATLPATPE). 

The long and short of it is that Krinn kept taking high doses of potassium and kept losing weight, eventually reaching her goal of 200 lbs. There was a long plateau in the middle after she first brushed up against her goal, but she maintained the original weight loss and eventually lost the remaining weight:

In personal communication (see very bottom of this post), Krinn noted that:

One of the few things the graphs say really, really, really loudly is “Krinn lost 30+ pounds _and stayed that way for at least a year._” … one of the overwhelmingly common failure modes of existing interventions: people lose some weight and then gain some weight and end up fairly close to where they started. Whatever else happened in my experiment, it sure wasn’t that: I lost a significant amount of weight and then _stabilized._ That seems important.

This time we don’t have much to add, but as before we wanted to reproduce her post for posterity. And we do have a few thoughts, mainly: 

This seems like more evidence that high doses of potassium cause weight loss. It suggests that potassium is probably one of the active ingredients, maybe the only active ingredient, in the weight loss caused by the potato diet. Krinn was taking about as much potassium as you would get if you were eating 2000 calories of potatoes per day, and experienced similar weight loss. 

It’s good to be skeptical of single case studies, however rigorous and careful they may be, but here are a few things to keep in mind: 

Remember that participants in the Low-Dose Potassium Community Trial lost a small but statistically significant amount of weight (p = .014) on a dose much lower than what Krinn was taking — only about 2,000 mg of potassium a day on average, compared to Krinn’s ~10,000 mg per day. This can’t confirm the effects of the higher dose, but it is consistent with Krinn’s results, and the final sample size was 104 people.

There’s also at least one successful replication. Inspired by Krinn’s first report, Alex Chernavsky did a shorter potassium self-experiment and lost about 4 pounds over a two-month period, otherwise keeping his diet and exercise constant. He also provided this handy table: 

Finally, we know of two other people who are losing weight on high-potassium brines, at least one of them without any additional exercise. They’re both interested in publishing their results, probably in early 2025. So watch this space. :​) 

As before, we want to conclude by saying that Krinn is a hero and a pioneer. She is worth a hundred of the book-swallowers who can only comment and couldn’t collect a data point to save their life. If you want to do anything remotely like what Krinn did, please feel free to reach out, we’d be happy to help.


Here’s a reproduction of Krinn’s full report as it appears in her tumblr post:

A Year And Change After The Long Post About The Potassium Experiment 

A year and change after the long post about the potassium experiment, I reached my weight-loss goal. This is a quick, minimally-structured thought-dump about it. As before, this is part of a wider conversation that starts with A Chemical Hunger.

Methodology: I mostly kept doing what I’d been doing. Turned up the exercise dial a bit, turned down the potassium dial a bit. Both still, AIUI, quite high compared to American baseline. Some bad news — in addition to whatever confounding factors were present last time, there’s a few extra ones now from my life in general going very poorly. As before, here’s the data, Creative Commons Zero, good luck with whatever you try on it. After making it to one year of being fairly diligent, I decided to let things vary and see what happened — on the one hand, I’d gotten far enough towards my personal goal that I wasn’t too fussed about the last 10%, and on the other hand, if this works in general and even work when you’re kinda half-assing it, that too is great news.

Interpretations: There’s multiple ways this could go. Here are a few that were easy to think of.

  1. Potassium or potassium-plus-exercise caused me to lose weight
  2. Exercise caused me to lose weight and potassium was irrelevant
  3. Something else caused me to lose weight

I would prefer to believe that potassium-plus-exercise caused me to lose weight. The data I have and my experience of gathering/being that data, to some extent support that conclusion. Flipping that around, if I ask “does that data rule out this conclusion?” no it absolutely does not. But it’s important to note that the exercise-only conclusion is only slightly less-well-supported and the none-of-the-above explanation is much-less-well-supported but certainly not ruled out. I have a preferred explanation, but all three of these explanations are live.

My subjective experience of the thing was that there was an easy part and a hard part. In the easy part I lost weight at a pretty rapid and consistent pace. In the hard part, my weight changed less and went back and forth more than it went down. If you buy into SMTM’s “something is screwing up people’s lipostats” theory, this is very consistent with that theory: potassium reduced or removed the something, my weight briskly dropped back to a healthy range (the first 9 months of the graphs) and then stabilized. However, the competing theory of “Krinn was super out of shape and then she started exercising” is also supported by the graphs (not shown on the graphs: my fairly poor 2022 exercise habits — my long-term exercise habits have had some good stretches, but the plague years did not do good things for me there!). I’m not sure whether it matters that I shifted from mostly treadmill time to having a couple of walks around the neighborhood that I can do pretty much on autopilot (shout-out to Mike Duncan’s Revolutions, this show is the first time podcast as a medium has clicked for me and it’s a great show). I do think, though, that exercise is a bit more complicated than I was really grasping. That, in turn, makes me glad that I’m tracking three exercise metrics rather than just one — if I was going to track only one, it’d be exertion, but exertion, exercise minutes, and step count, together make it possible to at least take a guess at what qualities a day’s exercise had.

Regarding my own questions from the first post: 

How safe is this? When I made the first post I was antsy about “adding this much potassium to your diet is probably safe for people in generally good health” but now I’m pretty sure it’s true. Some health problems can take a long time to present themselves, but adding this much of something to your diet for two years and having it be fine, is pretty persuasive evidence that the thing is probably fine. It could still easily turn out to have negative health impacts that are important, but a huge swath of the things you’d be worried about, are vanishingly unlikely once you’ve hit the point of “I’ve been taking this for two years and I’m fine.”

Does this replicate? Well, it’s self-consistent for me, and I don’t want to gain 50 pounds and try again. I did not like the shape of my body at +50 pounds from where I am now! So this is a question for others.

How much do other nutrients matter? I don’t know. Mostly not equipped to rigorously check.

Does HRT matter? I’ll let you know if I can get back on HRT. I would definitely like to investigate this.

Does dieting matter? Probably: my diet changed involuntarily over the course of two years and that certainly matters to some extent, but one of my ground rules is that I’m focusing on controlling exercise and potassium, the things I can control. Diet is far more complex and also in my life particularly, more susceptible to unplanned, involuntary change, so I’m writing it off as a factor.

Does this help with cannabis-induced hunger? I think I was off-base/over-optimistic with this one and it either doesn’t matter or matters a small amount.

Is there a point where I get really hungry/tired or start accidentally starving? I did not reach such a point. I felt basically fine the whole time.

I was cooking with this though:

If you tell someone you want to lose weight and would like their advice, it is overwhelmingly likely that the advice will involve exercising more. Everyone has heard this advice. And yet, as Michael Hobbes observes  in a searing piece for Highline, “many ‘failed’ obesity interventions are successful eat-healthier-and-exercise-more interventions” that simply didn’t result in weight loss. Even if we as a society choose to believe “more exercise always leads to weight loss, most people just fuck up at it,” that immediately confronts us with the important question, why do they fuck up at it? and its equally urgent sibling, what can we learn from those who succeed at it to give a hand up to those who have not yet succeeded?

Conclusion: I’m gonna keep writing things down in my spreadsheet for the same reasons as last time. I’m not sure what exactly I’m going to do as far as twiddling the factors, because now my main goal is somewhere between “don’t gain weight again” and “see what happens,” but I do know that writing down what happens is Good Actually, so I’m going to keep doing that.


Slightly after publication, Krinn sent us these comments, which she agreed we could publish: 

Personal Communication

Dangit now I’m having the first draft effect: writing the first draft and sleeping on it tells me things I should have written. In this case, I think there’s a plausible reading that my experience supports the “potassium does something good at a high enough effect size to care about” line of argument because while the peaks of how much effort I put in were fairly high — the periods of combined high exercise and high potassium intake — the most noticeable effect was when I was ramping up on both of those in the first 9 months, and when I was in just-bumbling-through-like-an-average-human mode, the effect didn’t reverse itself. There were plateau periods and there were slow-reversion periods, but there was definitely no “you slacked off and now there’s rapid weight gain mirroring the rapid weight loss” effect. I think that’s positive? I think it’s plausible to read it as “once I got the majority of the weight loss effect, locking in that benefit was easy.”

In any case one of the questions I was interested in was “if this works, does it work well enough that an average person can successfully implement it?” and I am now convinced that that’s a clear “Yes”.

I wouldn’t say there’s any part of this experiment that I’m actively unhappy about, but I do find it a little frustrating that this is basically just another piece of evidence on the pile of “here’s something that is consistent with the lithium/potassium hypothesis, but that is also consistent with some other stuff, and my main observation is that Something Happened” — intellectually I feel sure that much solid science is built by assembling big enough piles of such evidence and then distilling it into “now we know Why Something Happened,” but putting one single bit of evidence on the pile is still something where I need to make my own satisfaction about it rather than having a well-established cultural narrative rushing to bring me “yes! you did the thing! Woohoo!”

Also thinking more about the potassium experiment I’m having one of those “hold on a minute, this should have been obvious to me” moments — one of the few things the graphs say really, really, really loudly is “Krinn lost 30+ pounds and stayed that way for at least a year.” That’s one of the crucial parts of the whole obesity thing, that second half, right? That’s one of the overwhelmingly common failure modes of existing intervention: people lose some weight and then gain some weight and end up fairly close to where they started. Whatever else happened in my experiment, it sure wasn’t that: I lost a significant amount of weight and then stabilized. That seems important.

Yessssss I get the smug clever-kitty feeling, this is exactly why I have that “ratchet” column in the spreadsheet: the last ratchet-tick day from more than a year ago (i.e. it’s locked in) was July 10th 2023, on which day my week-average weight was 212.4lbs, down 33.6lbs from the start of the year.

So that early period of dramatic weight loss is noteworthy because we can be confident that whatever the cause was — potassium, exercise, or something else — it caused durable weight loss, which is exactly the thing we are looking for.

This is a conclusion we couldn’t have reached in July 2023, with the major writeup I did, because at that point “something else happens and Krinn gains the weight back” was very possible, was one of the likely answers to “what comes next?”

Review of Krinn’s Self-Experiment Where She Lost Weight Taking High Doses of Potassium

Krinn is a reader who participated in our Low-Dose Potassium Community Trial. She lost 6 lbs taking low doses of potassium, and liked it enough that she decided to keep going, along with a new exercise habit to help support the weight loss. And she started trying higher doses of potassium, eventually ramping up to around 10,000 mg of potassium a day. 

This is a lot — way more than the average person gets from their diet, and a lot more than people added in the original potassium trial.

Krinn writes, “I decided to stabilize at about 10,000mg per day … because that’s about how much potassium people were getting during the SMTM potato diet community trial. … Aiming for that amount also meant that it would be easier to compare my results to something that worked decently well and to ask questions like ‘is there something special about whole potatoes, or is it mostly the potassium?’ If it’s mostly the potassium, you’d expect my results to be closer to the full-potato-diet results than to the low-dose-potassium results — which is what happened.” 

Indeed, she lost quite a bit of weight. Here’s the chart of her weight change so far: 

Having just passed six months on potassium, Krinn has published the current state of her results, along with her protocol, data, thoughts, and comments, in a tumblr post titled An Ad-Hoc, Informally-Specified, Bug-Ridden, Single-Subject Study Of Weight Loss Via Potassium Supplementation And Exercise Without Dieting (henceforth, AAHISBRSSSOWLVPSAEWD). Here’s an archive link if tumblr doesn’t work for you.

Krinn’s report is excellent — nuanced, detailed, and clearly written. She covers almost every aspect of her self-experiment better than we could, so we won’t try to restate her points. We recommend that you read the report for yourself. Instead we will focus on the few small areas where we can add some speculation or additional context.

(Krinn’s full report is also reproduced in an appendix below, because tumblr posts do not always have the best longevity and we figured it might be good for the report to exist in two places.)

Again, you may want to read what Krinn wrote before you take a look at our comments. But we will restate this part: while this seems to be working for Krinn, it’s not clear that high doses of potassium are safe for everyone, and they almost certainly are not safe if you have kidney disease or related diseases like diabetes. Do not try supplementing doses this high without consulting your physician, and absolutely do not try it if you have kidney problems or any conditions that might compromise your kidney function.

Ok, here are our thoughts: 

Optimal Weight Loss Brine

Originally, we argued that high doses of potassium alone might be responsible for weight loss on the potato diet. After all, eating nothing but potatoes does give you heroic doses of potassium.

In retrospect, that seems a little naïve. Sure, it could be just the potassium. But biology tends to be a bit more complicated than that. 

This insight was sparked in large part by Salt, Sugar, Water, Zinc: How Scientists Learned to Treat the 20th Century’s Biggest Killer of Children, an excellent piece by Matt Reynolds on the history of oral rehydration solution (ORS) for the treatment of cholera. ORS is very simple to make, but discovering the right formula was strangely difficult. 

At risk of oversimplifying (read the original piece), people knew that cholera patients needed electrolytes, but feeding them an electrolyte solution didn’t seem to help.

Through a series of coincidences, people eventually discovered that adding glucose to the electrolyte solution sometimes made the treatment work. But this didn’t immediately lead to a cure, because if you put too much glucose and salt in the solution, it made patients worse instead.

After more confusion, they discovered that sugar and sodium ions are absorbed together in the gut through a sodium-glucose cotransport protein, but you need the right concentration or it will dehydrate the patient instead, which often kills them. The solution was simple, but getting there was hard.

Getting sodium into someone’s body isn’t simple — you need to include glucose in your rehydration formula, and even then, you need to get the right ratios. This makes us suspicious that something similar might be the case for potassium.

Even if high doses of potassium are required for curing obesity, it seems pretty likely that potassium by itself isn’t the whole engine. So now we are looking for some other set of factors, probably other switches that are triggered when you eat ~100% potatoes, that might also be needed to make the gears of weight loss mesh. 

Magnesium

The most likely candidate at this point seems to be magnesium.

Potassium and magnesium serve many complementary roles in our biology, and the two minerals are often prescribed together. We spoke to a physician about this, and he pointed out that for patients with low potassium (hypoK), if you don’t have enough magnesium (hypoMg), you’ll be hypoK forever unless you fix the hypoMg first, because of “some renal excretion thing I think” (his words). See also this paper, which says: “magnesium replacement is often necessary before hypokalemia and potassium depletion can be satisfactorily corrected with potassium supplements.”

Electrolyte mixes, like LMNT and Snake Juice, are sometimes used for weight loss, and these mixes usually contain some amount of magnesium. Assuming that, by a process of natural selection (it’s a electrolyte-powder-eat-electrolyte-powder world out there), they have run across something like the right electrolyte ratios to cause weight loss, this also suggests that magnesium might be involved.

Like potassium, most people are not getting enough magnesium, at least per the official recommendations. According to the NIH, you’re supposed to get 300-400 mg of magnesium per day. And potatoes are not only high in potassium, they are also pretty high in magnesium. Each potato contains about 40-50 mg of magnesium. Someone on the potato diet would be getting about 800-1,000 mg of magnesium per day.

If potassium and magnesium together are the cause of this weight-loss effect we’ve discovered, this would explain why potatoes are such a reliable way to cause weight loss, and why they’re often more effective than supplementing straight potassium.

All the above are just reasons for the hunch, but we also want to note that this hunch is supported by Krinn’s case study.

In her report, Krinn writes: 

My go-to snacks are cashews, pistachios, cherries, and granola bars.

Cashews and pistachios are particularly high in magnesium, providing 260 mg per 100 g and 110 mg per 100 g, respectively. We don’t know exactly how much cashew Krinn is consuming, but it’s likely that it’s giving her a respectable amount of extra magnesium.

We discussed this with Krinn over twitter DMs, where she said, “cashews are one of my go-to snack foods, so whatever amount I’m getting, I would be extremely surprised if I was getting something less than a healthy amount of magnesium in my diet.”

She also notes that she tends to consume the magnesium and the potassium relatively close to one another.

…another way to look at it is that “eating cashews” and “drinking gatorade+potassium” are never _that_ far apart

since the potassium stuff is spaced out 4–6 hours apart across the day, and I eat cashews at least once a day, that puts a ceiling on how far apart those two things could possibly be

We have no idea if it’s helpful or necessary to take potassium and magnesium at the same time, but it’s worth noting that Krinn tends to leave little daylight between them.

In short, we’ve suspected for a while that potassium might only cause weight loss, or might cause it more effectively, when combined with reasonable doses of magnesium. The potato diet would get this “for free”, since potatoes contain high amounts of both. This hunch predicts that people who lose weight by supplementing straight potassium will also likely be getting high doses of magnesium from some source, either from supplements or their diet. Krinn’s case matches that prediction.

We’ve also recently been corresponding with a participant from the half-tato diet, who told us that straight potassium seems to have some kind of effect for her, and who mentioned that she has been supplementing 266 mg magnesium a day as magnesium glycinate capsules. Not conclusive, but another hit for the prediction. 

Stearic Acid

Another possible connection is with stearic acid, a fatty acid found in “meat, poultry, fish, eggs, dairy products, and foods prepared with fats; beef tallow, lard, butterfat, cocoa butter, and shea butter are rich fat sources of stearic acid.”

If you’ve heard of this before, it’s likely from Fire in a Bottle (FIAB), a website/program/theory which argues that a diet high in stearic acid can cause weight loss. This is sometimes called The Croissant Diet (TCD), presumably in the hopes of confusing readers — you do not actually eat nothing but croissants. In fact, you don’t have to eat any croissants at all. But you do ideally eat lots of foods high in stearic acid, sometimes supplementing with additional stearic acid, and some people seem to lose weight when they do this.

We find the evidence for stearic acid to be pretty thin (though see FIAB for the other side). And there’s no theoretical reason to suspect that stearic acid influences potassium uptake or anything. But there are just a few hints, so we figured we might mention them here. 

One is from our half-tato diet. Most people lost only a small amount of weight on the half-tato diet, but one person (participant ​​25348806) lost 17 lbs in four weeks. This person gave us detailed notes about the rest of her diet, and this part jumped out in particular: 

…I also have dairy – at least one glass of milk a day (either raw whole milk or 2% or whole conventional) – and a small amount of juice or lemonade.  Some mornings I may have full fat yogurt with collagen and stearic acid (see fireinabottle.net) but not all mornings.  I have some extra potassium as well as other supplements.

For comparison, here’s what Krinn has to say about her fat intake: 

I use a generous hand when measuring out olive oil. I believe that if you need either milk taste or milk fat, you shouldn’t half-ass it, so when I need milk taste or milk fat, I rely on whole milk and heavy cream. Fats, generally, taste good. … Once in a while, dark chocolate, usually with the nuts and fruit.

Milk fat and chocolate (via cocoa butter) are both high in stearic acid. You’ll also notice that Krinn usually takes the chocolate with her cashews.

And remember that participant from the half-tato diet we mentioned at the end of last section? Based on these hints, we asked her if she also consumes a lot of stearic acid, and she told us she eats a whole lot of dairy fat, and chocolate “EVERY DAY” (her emphasis). 

This is certainly suggestive, but what doesn’t fit is the potato diet. Potatoes are high in both potassium and magnesium, so it would make sense if high doses of potassium and magnesium conspire to create the potato weight loss effect. But potatoes contain very little fat and approximately 0% stearic acid. The idea that you might need stearic acid to cause the potato effect is rather inconsistent with the potato diet, since you do not get appreciable amounts of stearic acid from potatoes.

That said, there are hints that people who are on half-tato, or who are supplementing potassium directly, do benefit from stearic acid. At the very least, we’ve noticed that some of the biggest success stories are people who have been getting decent amounts of stearic acid in their diet. Maybe stearic acid helps when you are getting less enormous doses of these minerals?

It’s always possible there’s some unknown connection — maybe the potato diet only works for people who already have sufficient reserves of stearic acid in their body. Or maybe some people need stearic acid for the effect to kick in and others don’t, for genetic reasons. Or maybe other fatty acids can substitute in a pinch, but stearic acid happens to be slightly better than average. But at this point, it definitely fits less well than magnesium. 

This Age Needs Heroes

We love everything that Krinn did here. She participated in a community trial, decided to keep going, and spun it into a self-experiment. She came up with her own design and attacked her questions in her own unique way. She did something interesting and she wrote it down so that all ingenious people could be informed thereof and consider the results for themselves.

More people should do what Krinn did, and get involved in the business of conducting science. Anyone else who wants to do anything else remotely like this should feel free to reach out, we’d be happy to help. We’re in the process of writing a whole series about how to conduct self-experiments, which may be a good starting point. Consider this your invitation.


Here’s a reproduction of Krinn’s full report as it appears in her tumblr post:

An Ad-Hoc, Informally-Specified, Bug-Ridden, Single-Subject Study Of Weight Loss Via Potassium Supplementation And Exercise Without Dieting

Here’s the short version: I lost 30 pounds in 6 months by chugging a bunch of potassium salt and exercising a lot. My subjective experience is that cranking my potassium intake way up made it possible to do a lot more exercise than I had been doing without also eating a lot more. Exercising more without also eating more led to weight loss (as one would hope!). I did not diet: I ate as I had been doing and as it pleased me to do. Do with the raw data as you please.

Losing weight this way is unusual and worth paying attention to because many things about increases and decreases in weight and obesity are very poorly understood. Many people would like their personal weight and obesity levels to be different, so anything that improves our collective understanding of how to make that happen is valuable. However, losing weight this way is an experiment: it’s not necessarily safe to do what I did! Part of why I did it was to find out what would happen, and if you have any kind of existing kidney problems then you definitely should not do what I did. Note to other transfemmes: if you’re taking spiro, that counts as a kidney problem.

I also don’t want to overstate the significance of this experiment: what I’ve been up to in the last 6 months amounts to a single data point that happens to also be 1,100 spreadsheet cells. It’s a data point that is highly suggestive, sure, but it would be extremely ambitious to say that it proves anything beyond “this worked for me” and perhaps “it’s not impossible for this to work”. I am writing about it because as far as I know, this particular experiment is something that nobody else has tried, and, again, anything that improves our collective understanding here is valuable.

The long version comes next: how I came to be doing this experiment, what I did in the experiment, what I plan to do next, and finally what I think about it all. The really long version is the ongoing conversation that this post is part of, starting with A Chemical Hunger, which is a book-length literature review about the 1980s–present global increase in obesity prevalence, also the posts about single-subject research where the same authors discuss the limits of what can be learned from experiences like mine, also the Experimental Fat Loss guy and his wide variety of diet-only experiments, also some critics who disagree.

How I came to be doing this

At the tail end of 2022, I noticed both that my BMI had hit 30 and that I had become very unhappy about my weight. There’s a specific photo where I didn’t realize until I saw the photo that my belly was hanging out over my waistband and it’s vividly unpleasant in my memory. Around the same time, I happened to find the potassium-supplementation community trial that the Slime Mold Time Mold folks were running. The value proposition was “this will be easy, cheap, and safe, but also it might not actually work,” and that sounded good to me, so I signed up for it and took a modest amount of potassium all through December and January. It kinda-sorta worked: I lost 6 pounds. Not nothing, but “it kinda-sorta worked” is the most one can really say about losing 6 pounds in 60 days.

The low-dose potassium delivered on all of what the SMTM folks promised, though. It was easy, cheap, and safe. So I kept doing it and, since I was already doing the potassium, decided that I should get an exercise habit going. I am a big believer in the idea that it’s a tremendous amount easier to go from doing Something to doing More Something than to go from doing Nothing to doing Something. The low-dose potassium got me through the first step: once I was doing Something about my weight, it was relatively easy to do More Something. When the community trial ended in early February, I didn’t have to worry about messing up its results by departing from the trial’s instructions, so I started taking more potassium and building my own experiment. I also kept in touch with the SMTM authors, who were very encouraging. 🐯💕

By late March I had brought myself up to daily amounts of potassium and exertion that seemed good to me, and I stuck with those. This is the first time in my life I’ve focused on trying to lose weight, and I was not fully prepared for how demoralizing it is that the weight change from day N to day N+1 sometimes seems perversely unrelated to what you were doing on day N. Fortunately I have experience with spreadsheets, so I put together a tracker for myself that focused on the trailing-week average of my daily weight and exercise measurements as well as long-term graphs. Three months of data were enough to put together a chart whose trendline said very, very clearly, “what you are doing is working — keep it up!” With any kind of long-term project it’s very important to create and sustain sources of feedback. All else being equal, the longer it takes before you can get a read on “is this going well or poorly?”, the worse it will go.

I decided that my goal would be to get my BMI from 30 (the lower limit of “obese”) to under 25 (the upper limit of “normal”). Happily, the math is very easy there: for my height, a BMI of 25 rounds off to 200lbs. I further decided that I was willing to spend all of 2023 working on this. That decision is why I’m writing this post now: halfway through a project is a natural time to pause and take stock.

What I did

By the end of March, my regimen was firmly settled and I kept at it through the end of June without further tinkering. The daily goals I settled on were 10,000mg of potassium and 1,200kcal of exertion. That amount of exercise worked out to be 90 to 100 minutes per day. For contrast, in 2022 my average amount of exercise per day was 15 minutes and my average exertion was 500kcal.

I used my smartwatch’s exertion number (“how many calories are you using above the amount you need to burn to be alive at all?”) and gradually walked up my daily goal, settling at 1,200kcal/day partially because it was working and partially because one hour of watch face equaling 100kcal was helpful for being able to read “how close to my goal am I?” without thinking hard about it. Most of the exercise was treadmill time, usually a brisk walk or light jog. Over the months I also did some running, some bicycling, and some hiking, but treadmill time was the reliable, unremarkable, do-this-every-day core of my exercise regimen. It took a while to ramp up to that amount of exertion and there were definitely days when I stumbled, for good reasons and bad. However, in general I hit the exertion goal and in particular had it absolutely dialed from early March to mid-April.

It was easier to be totally rigorous about the potassium-intake goal — it helped that that part only took a few minutes per day, instead of 90+ minutes! I used potassium chloride powder (whatever came up first on an Amazon search since all KCl should be alike) mixed with regular Gatorade (i.e. not the sugar-free kind) to make it taste okay (I recommend blue Gatorade, it’s the closest to appealing when kaliated — the yellow lemon-lime was meh and the fruit punch red was awful). I added two heaping teaspoons of KCl powder to a 20oz. bottle of Gatorade and drank that. KCl is about 52% potassium and a heaping teaspoon of it is about 6500mg, so I rounded up a smidge and called that 6600-and-a-bit milligrams of potassium per bottle. On Thursdays and Sundays I drank 2 full bottles and on other days 1.5 bottles. I recorded this as 10,000mg of potassium on regular days and 13,500mg on Thursdays and Sundays.

Is 10,000mg of potassium a lot? It’s a lot more than average! The SMTM potassium trial post contextualizes it helpfully:

For a long time, the recommended daily value for adults (technically, the “Adequate Intake”) was 4,700 mg of potassium per day. But most people don’t get anywhere near this amount. 

In every CDC NHANES dataset from 1999 to 2018, median potassium intake hovers around 2,400 mg/day, and mean intake around 2,600 mg/day. In this report from 2004, the National Academy of Medicine found that “most American women … consume no more than half of the recommended amount of potassium, and men’s intake is only moderately higher.” Per this paper, only 0.3% of American women were getting the recommended amount. Similarly low levels of intake are also observed in Europe, Mexico, China, etc. 

But in 2019, the National Academies of Sciences, Engineering, and Medicine changed the recommended / adequate intake to 2,600 mg/day for women and 3,400 mg/day for men. They say that the change is “due, in part, to the expansion of the DRI model in which consideration of chronic disease risk reduction was separate from consideration of adequacy,” but we can’t help but wonder if they changed it because it was embarrassing to have less than 5% of the population getting the recommended amount.

In any case, recommended potassium intake is something like 2,500 to 5,000 mg per day for adults, and many people don’t get enough.

Potatoes are exceptionally high in potassium. A single potato contains somewhere between 600 and 1000 mg of potassium, depending on which source you look at. They are the 6th highest in potassium on this list of high-potassium foods from the NIH, and 9th on this old list from the USDA. If you do the math, this means that someone on the potato diet, eating 2,000 kcal of potatoes a day, gets at least 11,000 mg of potassium per day, more than twice the old recommended intake.

This explanation is most of why I decided to stabilize at about 10,000mg per day: because that’s about how much potassium people were getting during the SMTM potato diet community trial. Because that community trial involved around 200 people, it was unlikely that there would be any truly heinous health effects from knocking back that much potassium, especially together with the anecdotal evidence that inspired the trial. Aiming for that amount also meant that it would be easier to compare my results to something that worked decently well and to ask questions like “is there something special about whole potatoes, or is it mostly the potassium?” If it’s mostly the potassium, you’d expect my results to be closer to the full-potato-diet results than to the low-dose-potassium results — which is what happened.

I measured those results in a very basic way: ordinary bathroom scale, first thing in the morning, every day. Considering how much noise there is in weight measurement, there’s just no advantage to measuring it more often. I kept the circumstances of the weigh-in simple and stable, trusting that that was good enough. I also measured exertion in two other forms — step count and exercise minutes — but that was mostly for my personal curiosity because both are basically downstream of exertion as such. Similarly, I tracked my sleep but didn’t expect that to matter a whole lot.

While I was affirmatively not dieting, I want to make sure to talk about my food habits because I could be missing something that’s easy for others to see as unusual but seems totally ordinary to me. My meals are heavy on pasta, rice, bread, and granola. I work diligently to get enough dietary fiber. I eat some meat but not a lot (eating a pound of meat in a week would be above average for me), and I enjoy coffee but not a tremendous amount of it since usually I make Chemex-style coffee and having a bunch of that in a day would be too time-intensive. My go-to snacks are cashews, pistachios, cherries, and granola bars. Like most people, I should eat more dark leafy greens than I do. I use a generous hand when measuring out olive oil. I believe that if you need either milk taste or milk fat, you shouldn’t half-ass it, so when I need milk taste or milk fat, I rely on whole milk and heavy cream. Fats, generally, taste good. I eat more whole food and food I personally cook than I eat packaged and processed food, and I only infrequently eat restaurant food (weekly pizza night, maybe twice a month other than that). I really like sour candies but basically stopped eating them last autumn after some very patient coaxing from my dentist. Once in a while, dark chocolate, usually with the nuts and fruit.

I ate as I had been doing: I ate the food I felt like eating and ate as much of it as I felt like eating. If I felt like eating more or less, I did that. Since I wanted to keep the exercise habit going regardless of whether or not I lost weight, it was very important to me to not make the exercise any more difficult than it had to be. Going hungry would definitely make it more difficult, so I avoided doing that. One way in which I’m very sure my experience generalizes is, it’s much easier to persuade people to try “add this supplement to what you’re already eating” than to get them to try “replace all of your current food with potatoes,” especially when talking about long-term or indefinite-duration changes.

What I plan to do next

I’ll be thrilled if I can recapture something like the 7-week March/April streak I had going. Most days in this period (44 out of 49) were PB days (i.e. a day where my trailing-week-average weight was the lowest it had been since the start of the year) and no two consecutive days in this period were non-PB days (i.e. if a day wasn’t a PB day, both the day before and the day after were PB days). I was losing almost 2lbs per week and exercising a lot and I felt great. However, my intuition is that that was the honeymoon period of going from mostly-sedentary to exercising regularly, and that I should expect further progress to be more difficult, to be like the less impressive results I got in May and June.

Still, the thing as a whole has definitely been successful enough that I’m going to keep at it until the end of the year, re-evaluating again in December (and maybe when I hit my weight-loss goal, which should happen around halfway between now and then). Since I’m using January 1st as my anchor date for the start of the experiment, it lines up nicely with the calendar if I just keep going all year and see what happens. Besides, I only need 6 months more to generate a year of data, while someone going from a cold start would need a whole year.

Given that I have a setup that is working pretty well, I’m reluctant to tinker with it. I might add one more high-potassium day in addition to Thursdays and Sundays, and I might start tracking some extra data — even though I’m not trying to change them, recording my food habits seems like the most helpful additional thing I could record.

If I develop health problems I’m gonna pull the ripcord (and post about it). There are already too many shitty fake weight loss regimens in the world that fuck up the health of people who try them, we do not need more.

What I think about it

Since I’m the one doing this experiment, I get to be excited about how it’s working out for me personally, which is to say, very well indeed. Right now it seems pretty certain that I’ll be able to reach my goal of losing ~50lbs in a long-term-sustainable way and just as importantly, getting myself to a much better baseline state of physical fitness. I feel pretty great about that part!

The experiment is not just for me, though: the reason it’s an experiment rather than just “I’m trying to lose weight” is that I am keeping track of things carefully such that other people could carry out the same steps I did and get results similar to or different from mine and ideally everyone eventually comes to pretty firm conclusions about whether this — losing weight via potassium and exercise without dieting — works or not. My chugging potassium and Gatorade for six months to a year is the very beginning of that process, and I expect that the difficult parts of the process will be carried out by people with more expertise and resources than me.

I also expect that I have not tumbled to the One Weird Trick for weight loss that everyone else just overlooked. As someone with plenty of programming experience, I have a hearty suspicion towards “well, it worked on MY setup” stories. One obvious alternate explanation for my successful weight loss is “well yeah, you doubled your exertion and kept your food intake the same, of course you lost weight” — but I don’t find that explanation satisfying. To start with, if it were that easy, people would do it more often. There are a tremendous number of people who would like to lose weight and a tremendous marketplace of devices, services, and professionals to help them use exercise for that purpose, and yet in a 20-year NCHS study, average exercise rose without obesity falling. It’s also very, very easy to find fat people who exercise plenty — you will find them more or less anywhere you find lots of people exercising, as well as in places like sumo stables. A member of my family has taken up powerlifting in the last year, making him both fitter and heavier by quite a bit.

Additionally, there’s studies like Keating 2017 concluding that short-term exercise intervention doesn’t do enough to matter, or like the Wu 2009 work concluding that exerise-and-dieting isn’t meaningfully better than just dieting over periods of 6+ months, and then there’s the STRRIDE study, Slentz 2004, concluding that jogging 20 miles a week can get people to lose about 7 pounds over 8 months. The STRRIDE study caught my eye because it’s pretty similar to what I did: they took obese mostly-sedentary folks, had them exercise more, and forbade them from eating less. However, once you do the math the results are much less similar: the average STRRIDE participant did around half the exercise I’ve done for at most a fifth of the weight loss (i.e. around 1lb/month vs. around 5lbs/month and around 3mi/day vs. 7mi/day). If someone else told me “Krinn, your naïve just-hit-the-treadmill exercise regimen is 2.5x as effective as an exercise regimen supervised & measured by professionals,” I would want them to provide some compelling evidence for that.

If you tell someone you want to lose weight and would like their advice, it is overwhelmingly likely that the advice will involve exercising more. Everyone has heard this advice. And yet, as Michael Hobbes observes in a searing piece for Highline, “many ‘failed’ obesity interventions are successful eat-healthier-and-exercise-more interventions” that simply didn’t result in weight loss. Even if we as a society choose to believe “more exercise always leads to weight loss, most people just fuck up at it,” that immediately confronts us with the important question, why do they fuck up at it? and its equally urgent sibling, what can we learn from those who succeed at it to give a hand up to those who have not yet succeeded?

I find the SMTM authors’ metaphor for this helpful:

[exercising more and eating less] is not an explanation any more than “the bullet” is a good explanation for “who killed the mayor?” Something about the potato diet lowered people’s lipostat set point, which reduced their appetite, which yes made them eat fewer calories, which was part of what led them to lose weight. Yes, “fewer kcal/day” is somewhere in the causal chain. No, it is not an explanation.

Since I’ve been doing this for six months, I feel pretty certain that the potassium is doing something positive for me and I’m entirely willing to put in another six months to find out what happens for me. Finding out whether that generalizes is beyond my power: all I can do is explain what worked for me, one middle-aged Seattle housewife, and hope that it’s useful to people who are in a position to do serious work about it.

One kind of serious work that’s available is the very cool analytic techniques that other people in this conversation have used while looking at their data. If you are the kind of person to get elbows-deep in R or Matlab, feel free to grab my day-by-day measurements for that (I release this data under Creative Commons’ CC0 if that’s relevant to you). I’m not going to do that, though, partially because it’s been a long time since I last used R but mostly because of the thing I said earlier about my whole experiment basically being one data point. If you have a data series, then yeah, get in there with some numeric interrogation, but if you only have one data point, that data point is what it is and statistical analysis can’t really add to it. All I can claim here is that this is a new data point: people going about their everyday lives do not spontaneously increase their potassium intake severalfold and the background work from the SMTM potato diet and potassium community trials tell me that no-one’s run a study looking directly at what happens if you do increase your potassium intake that much.

Do you want to increase your potassium intake that much? If you do, I have to re-emphasize the potassium community trial‘s safety warning: if you have existing kidney problems, do not try this. Also I’m gonna deploy the boldface again to make sure I get this across to other trans women: on this topic, taking spiro counts as a kidney problem! I am not a doctor and I’m extremely not your doctor, you should talk to your actual doctor if you have any kind of potential kidney issues and even if you’re in good health and want to try chugging a bunch of potassium, you should titrate up gradually the way the SMTM writeup suggests (which is also the way I did).

In addition to a general spirit of responsibility, those warnings are important because otherwise just telling you that this is easy would sound like a recommendation. Did I mention that the experiment was easy? Easy easy. Piss easy. Lemon squeezy, etc. Of course building an exercise habit wasn’t easy, but the potassium part didn’t make it easier or harder, and the potassium part itself was pretty trivial. Mix this powder into Gatorade a couple times per day, drink it, done.

That said, if you do want to try this, godspeed and please write down how it goes for you. I recommend building positive reinforcement into whatever you use to track it; my personal spreadsheet for this is adorned with color-coding and happy emoji. I also recommend at least thinking about the following questions, whether you’re going to do this, evaluate the results of this, or both.

  • How safe is it, in general rather than for me particularly, to chug this much potassium? This is the big one: “just mix potassium salt into Gatorade and drink it a few times a day” is so incredibly easy that even if the effect size is small, it could benefit a huge number of people, but of course it doesn’t benefit them if it’s not actually safe to do that.
  • Does this replicate? If it’s not safe it matters a lot less whether it replicates, so the safety question comes first, but if it is safe, then one would immediately want to find out whether it works for 1% of people, 10% of people, or 50% of people.
  • How much do other mineral nutrients, particularly sodium and magnesium, matter for this? Maybe they need to be combined in some specific way, as this Twitter thread suggests.
  • Do sex hormone levels matter? I’m a trans woman and I’ve been having problems with access to HRT in this timeframe. Given how many things in one’s body testosterone and estrogen affect, and given that previous obesity research has shown differences based on hormone profiles, that’s definitely something to keep an eye on. Also because spironolactone in particular messes with renal function and potassium metabolism, I expect that it affects this. Digression: spironolactone is total bullshit as an anti-androgen of first resort. It sucks and I hate it and I should have switched to other anti-androgens even sooner than I did. If you’re using spironolactone as an anti-androgen because it was the first thing your doctor tried for that, you really should try something else and see if that works.
  • I steadfastly avoided dieting. I like my existing diet just fine, and that’s why I preferred the “what if I just chug a bunch of potassium” plan. All else being equal, I’d rather try things that let me eat what I like than things that require throwing my relationship with food into upheaval. But of course you wonder, what would happen if you did combine dieting and exercise and potassium? The ExFatLoss guy has been busy trying a lot of diet-only interventions and he’s got a lot of interesting results. I am not the person to try it, but it’s one of the obvious things to try, so I hope someone does try it.
  • How does this interact with the munchies? If you decide to try what I tried and you, like me, enjoy living somewhere where marijuana is legal, I think you should look at whether the potassium changes how you experience marijuana-induced hunger/overeating. One of the things I found very striking about the matter is that it was possible for me to chug enough potassium that the marijuana-induced hunger was drastically reduced. I expected the opposite since the potassium was causing me to eat less (relative to exertion) at other times. However, I have very strong habits about marijuana (exactly twice a week, edibles only, same amount every time) and I’m not willing to change them for this, so who knows how this aspect will work out for others. Definitely something to keep an eye on, though. Even if I wasn’t losing weight, the potassium reduces marijuana-induced overeating enough that I’d probably keep going with it just for that effect.

Conclusion

I spent 6 months trying to lose weight with lots of potassium and exercise but without dieting. So far I have succeeded. Unless something disastrous comes up, I’m going to keep trying it for at least another 6 months and going to keep recording what I’m doing. I’m particularly curious to see where I’ll plateau, since I assume at some point I’ll start getting really hungry and/or tired instead of accidentally starving. I hope that my experience and the data I’ve recorded from it, are useful to people who are looking into questions about obesity and weight. Please feel free to use my data and my writeup (this post) for that. If you want to try doing as I’ve done, good luck and stay safe: this has worked for me but it is still experimental, it might be unsafe and/or fail to work for you.

Peer Review: Obesity II – Establishing Causal Links Between Chemical Exposures and Obesity

A new paper, called Obesity II: Establishing Causal Links Between Chemical Exposures and Obesity, was just published in the journal Biochemical Pharmacology (available online as of 5 April 2022). Authors include some obesity bigwigs like Robert H. Lustig, and it’s really long, so we figured it might be important. 

The title isn’t some weird Walden II reference — there’s a Part I and Part III as well. Part I reviews the obesity epidemic (in case you’re not already familiar?) and argues that obesity “likely has origins in utero.”

“The obesity epidemic is Kurt Cobain’s fault” is an unexpected but refreshing hypothesis

Part III basically argues that we should move away from doing obesity research with cells isolated in test tubes (probably a good idea TBH) and move towards “model organisms such as Drosophila, C. elegans, zebrafish, and medaka.” Sounds fishy to us but whatever, you’re the doctor.

This paper, Part II, makes the case that environmental contaminants “play a vital role in” the obesity epidemic, and presents the evidence in favor of a long list of candidate contaminants. We’re going to stick with Part II today because that’s what we’re really interested in.

For some reason the editors of this journal have hidden away the peer reviews instead of publishing them alongside the paper, like any reasonable person would. After all, who could possibly evaluate a piece of research without knowing what three anonymous faculty members said about it? The editors must have just forgotten to add them. But that’s ok — WE are these people’s peers as well, so we would be happy to fill the gap. Consider this our peer review:

This is an ok paper. They cite some good references. And they do cite a lot of references (740 to be exact), which definitely took some poor grad students a long time and should probably count for something. But the only way to express how we really feel is:

Seriously, 43 authors from 33 different institutions coming together to tell you that “ubiquitous environmental chemicals called obesogens play a vital role in the obesity pandemic”? We could have told you that a year ago, on a budget of $0. 

This wasted months, maybe years of their lives, and millions of taxpayer dollars making this paper that is just like, really boring and not very good. Meanwhile we wrote the first draft of A Chemical Hunger in a month (pretty much straight through in October 2020) and the only reason you didn’t see it sooner was because we were sending drafts around to specialists to make sure there wasn’t anything major that we overlooked (there wasn’t).

We don’t want to pick on the actual authors because, frankly, we’re sure this paper must have been a nightmare to work on. Most of the authors are passengers of this trainwreck — involved, but not responsible. We blame the system they work under.

We hope this doesn’t seem like a priority dispute. We don’t claim priority for the contamination hypothesis — here are four papers from 2008, 2009, 2010, and 2014, way before our work on the subject, all arguing in favor of the idea that contaminants cause obesity. If the contamination hypothesis turns out to be right, give David B. Allison the credit, or maybe someone even earlier. We just think we did an exceptionally good job making the case for the hypothesis. Our only original contributions (so far) are arguing that the obesity epidemic is 100% (ok, >90%) caused by contaminants, and suggesting lithium as a likely candidate. 

So we’re not trying to say that these authors are a bunch of johnny-come-latelies (though they kind of are, you see the papers up there from e.g. 2008?). The authors are victims here of a vicious system that has put them in such a bad spot that, for all their gifts, they can now only produce rubbish papers, and we think they know this in their hearts. It’s no wonder grad students are so depressed! 

So to us, this paper looks like a serious condemnation of the current academic system, and of the medical research system in particular. And while we don’t want to criticize the researchers, we do want to criticize the paper for being an indecisive snoozefest.

Long Paper is Long

The best part of this paper is that comes out so strongly against “traditional wisdom” about the obesity epidemic:  

The prevailing view is that obesity results from an imbalance between energy intake and expenditure caused by overeating and insufficient exercise. We describe another environmental element that can alter the balance between energy intake and energy expenditure: obesogens. … Obesogens can determine how much food is needed to maintain homeostasis and thereby increase the susceptibility to obesity. 

In particular we like how they point out how, from the contaminant perspective, measures of how much people eat are just not that interesting. If chemicals in your carpet raise your set point, you may need to eat more just to maintain homeostasis, and you might get fat. This means that more consumption, of calories or anything else you want to measure, is consistent with contaminants causing obesity. We made the same point in Interlude A. Anyways, don’t come at us about CICO unless you’ve done your homework. 

We also think the paper’s heart is in the right place in terms of treatment: 

The focus in the obesity field has been to reduce obesity via medicines, surgery, or diets. These interventions have not been efficacious as most people fail to lose weight, and even those who successfully lose substantial amounts of weight regain it. A better approach would be to prevent obesity from occurring in the first place. … A significant advantage of the obesogen hypothesis is that obesity results from an endocrine disorder and is thus amenable to a focus on prevention. 

So for this we say: preach, brothers and sisters.

The rest of the paper is boring to read and inconclusive. If you think we’re being unfair about how boring it is, we encourage you to go try to read it yourself.

Specific Contaminants

The paper doesn’t even do a good job assessing the evidence for the contaminants it lists. For example, glyphosate. Here is their entire review:

Glyphosate is the most used herbicide globally, focusing on corn, soy and canola [649]. Glyphosate was negative in 3T3-L1 adipogenic assays [650], [651]. Interestingly, three different formulations of commercial glyphosate, in addition to glyphosate itself, inhibited adipocyte proliferation and differentiation from 3T3-L1 cells [651]. There are also no animal studies focusing on developmental exposure and weight gain in the offspring. An intriguing study exposed pregnant rats to 25mg/kg/day during days 8-14 of gestation [652]. The offspring were then bred within the lineage to generate F2 offspring and bread to generate the F3 progeny. About 40% of the males and females of the F2 and F3 had abdominal obesity and increased adipocyte size revealing transgenerational inheritance. Interestingly, the F1 offspring did not show these effects. These results need verification before glyphosate can be designated as an obesogen.

For comparison, here’s our review of glyphosate. We try to, you know, come to a conclusion. We spend more than a paragraph on it. We cite more than four sources.

We cite their [652] as well, but we like, ya know, evaluate it critically and in the context of other exposure to the same compound. We take a close look at our sources, and we tell the reader we don’t think glyphosate is a major contributor to the obesity epidemic because the evidence doesn’t look very strong to us. This is bare-bones due diligence stuff. Take a look: 

The best evidence for glyphosate causing weight gain that we could find was from a 2019 study in rats. In this study, they exposed female rats (the original generation, F0) to 25 mg/kg body weight glyphosate daily, during days 8 to 14 of gestation. There was essentially no effect of glyphosate exposure on these rats, or in their children (F1), but there was a significant increase in the rates of obesity in their grandchildren (F2) and great-grandchildren (F3). There are some multiple comparison issues, but the differences are relatively robust, and are present in both male and female descendants, so we’re inclined to think that there’s something here. 

There are a few problems with extending these results to humans, however, and we don’t just mean that the study subjects are all rats. The dose they give is pretty high, 25 mg/kg/day, in comparison to (again) farmers working directly with the stuff getting a dose closer to 0.004 mg/kg.

The timeline also doesn’t seem to line up. If we take this finding and apply it to humans at face value, glyphosate would only make you obese if your grandmother or great-grandmother was exposed during gestation. But glyphosate wasn’t brought to market until 1974 and didn’t see much use until the 1990s. There are some grandparents today who could have been exposed when they were pregnant, but obesity began rising in the 1980s. If glyphosate had been invented in the 1920s, this would be much more concerning, but it wasn’t.

Frankly, if they aren’t going to put in the work to engage with studies at this level, they shouldn’t have put them in this review. 

If this were a team of three people or something, that would be one thing. But this is 43 specialists working on this problem for what we assume was several months. We wrote our glyphosate post in maybe a week?

Some of the reviews are better than this — their review of BPA goes into more detail and cites a lot more studies. But the average review is pretty cruddy. For example, here’s the whole review for MSG:

Monosodium glutamate (MSG) is a flavor enhancer used worldwide. Multiple animal studies provided causal and mechanistic evidence that parenteral MSG intake caused increased abdominal fat, dyslipidemia, total body weight gain, hyperphagia and T2D by affecting the hypothalamic feeding center [622], [623], [624]. MSG increased glucagon-like peptide-1 (GLP-1) secretion from the pGIP/neo: STC-1 cell line indicating a possible action on the gastrointestinal (GI) tract in addition to its effects on the brain [625]. It is challenging to show similar results in humans because there is no control population due to the ubiquitous presence of MSG in foods. MSG is an obesogen.

Seems kind of extreme to unequivocally declare “MSG is an obesogen” on the basis of just four papers. On the basis of results that seem to be in mice, rats, mice, and cells in a test tube, as far as we can tell (two of the citations are review articles, which makes it hard for us to know what studies they specifically had in mind). Somehow this is enough to declare MSG a “Class I Obesogen” — Animal evidence: Strong. In vitro evidence: Strong. Regulatory action: to be banned. Really? 

Instead, we support the idea of — thinking about it for five minutes. For example, MSG occurs naturally in many foods. If MSG were a serious obesogen, tomatoes and dashi broth would both make you obese. Why are Italy and Japan not more obese? The Japanese first purified MSG and they love it so much, they have a factory tour for the stuff that is practically a theme park — “there is a 360-degree immersive movie experience, a diorama and museum of factory history, a peek inside the fermentation tanks (yum!), and finally, an opportunity to make and taste your own MSG seasoning.” Yet Japan is one of the leanest countries in the world.

As far as we can tell, Asia in general consumes way more MSG than any other part of the world. “Mainland China, Indonesia, Vietnam, Thailand, and Taiwan are the major producing countries in Asia.” Why are these countries not more obese? MSG first went on the market in 1909. Why didn’t the obesity epidemic start then? We just don’t think it adds up. 

(Also kind of weird to put this seasoning invented in Asia, and most popular in Asia, under your section on “Western diet.”)

Adapted from Fig. 3

Let’s also look at their section on DDT. This one, at least, is several paragraphs long, so we won’t quote it in full. But here’s the summary: 

A 2017 systematic review of in vitro, animal and epidemiological data on DDT exposures and obesity concluded the evidence indicated that DDT was “presumed” to be obesogenic for humans [461]. The in vitro and animal data strongly support DDT as an obesogen. Based on the number of positive prospective human studies, DDT is highly likely to be a human obesogen. Animal and human studies showed obesogenic transmission across generations. Thus, a POP banned almost 50 years ago is still playing a role in the current obesity pandemic, which indicates the need for caution with other chemical exposures that can cause multigenerational effects.

We’re open to being convinced otherwise, but again, this doesn’t really seem to add up. DDT was gradually banned across different countries and was eventually banned worldwide. Why do we not see reversals or lags in the growth of obesity in those countries those years? They mention that DDT is still used in India and Africa, sometimes in defiance of the ban. So why are obesity rates in India and Africa so low? We’d love to know what they think of this and see it contextualized more in terms of things like occupation and human exposure timeline.

Review Paper

With a long list of chemicals given only the briefest examination, it’s hard not to see this paper as overly inclusive to the point of being useless. It makes the paper feel like a cheap land grab to stake a claim to being correct in the future if any of the chemicals on the list pan out.

Maybe their goal is just to list and categorize every study that has ever been conducted that might be relevant. We can sort of understand this but — why no critical approach to the material? Which of these studies are ruined by obvious confounders? How many of them have been p-hacked to hell? Seems like the kind of thing you would want to know! 

You can’t just list papers and assume that it will get you closer to understanding. In medicine, the reference for this problem is Ioannidis’s Why Most Published Research Findings Are False. WMPRFAF was published in 2005, you don’t have an excuse for not thinking critically about your sources.

Despite this, they don’t even mention lithium, which seems like an oversight. 

Oh right, Kurt Cobain IS responsible for the obesity epidemic

We wish the paper tried to provide a useful conclusion. It would have been great to read them making their best case for pretty much anything. Contaminants are responsible for 50% of the epidemic. Contaminants are responsible for no more than 10% of the epidemic. Contaminants are responsible for more than 90% of the epidemic. We think phthalates are the biggest cause. We think DDT is the biggest cause. We think it’s air pollution and atrazine. Make a case for something. That would be cool.

What is not cool is showing up being like: Hey we have a big paper! The obesity epidemic is caused by chemicals, perhaps, in what might possibly be your food and water, or at work, though if it’s not, they aren’t. This is a huge deal if this is what caused the epidemic, possibly, unless it didn’t. The epidemic is caused by any of these several dozen compounds, unless it’s just one, or maybe none of them. What percentage of the epidemic is caused by these compounds? It’s impossible to say. But if we had to guess, somewhere between zero and one hundred percent. Unless it isn’t. 

Effect Size

The paper spends almost no time talking about effect size, which we think is 1) a weird choice and 2) the wrong approach for this question. 

We don’t just care about which contaminants make you gain weight. We care about which contaminants make you gain a concerning amount of weight. We want to know which contaminants have led to the ~40 lbs gain in average body weight since 1970, not which of them can cause 0.1 lbs of weight gain if you’re inhaling them every day at work. These differences are more than just important, they’re the question we’re actually interested in!

For comparison: coffee and airplane travel are both carcinogens, but they increase your risk of cancer by such a small degree that it’s not even worth thinking about, unless you’re a pilot with an espresso addiction. When the paper says “Chemical ABC is an obesogen”, it would be great to see some analysis of whether it’s an obesogen like how getting 10 minutes of sunshine is a carcinogen, or whether it’s an obesogen like how spending a day at the Chernobyl plant is a carcinogen. Otherwise we’re on to “bananas are radioactive” levels of science reporting — technically true, but useless and kind of misleading.

The huge number of contaminants they list does seem like a mark in favor of a “the obesity epidemic is massively multi-causal” hypothesis (which we discussed a bit in this interview), but again it’s hard to tell without seeing a better attempt to estimate effect sizes. The closest thing to an estimate that we saw was this line: “Population attributable risk of obesity from maternal smoking was estimated at 5.5% in the US and up to 10% in areas with higher smoking rates”.

Stress Testing

Their conclusion is especially lacking. It’s one thing to point out that what we’re studying is hard, but it’s another thing to deny the possibility of victory. Let’s look at a few quotes:

“A persistent key question is what percent of obesity is due to genetics, stress, overnutrition, lack of exercise, viruses, drugs or obesogens? It is virtually impossible to answer that question for any contributing factors… it is difficult to determine the exact effects of obesogens on obesity because each chemical is different, people are different, and exposures vary regionally and globally.”

Imagine going to an oncology conference and the keynote speaker gets up and says, “it is difficult to determine the exact effects of radiation on cancer because each radiation source is different, people are different, and exposures vary regionally and globally”. While much of this is true, oncologists don’t say this sort of thing (we hope?) because they understand that while the problem is indeed hard, it’s important, and hold out hope that solving that problem is not “virtually impossible”. Indeed, we’re pretty sure it’s not. 

They’re pretty pessimistic about future research options:

“We cannot run actual ‘clinical trials’ where exposure to obesogens and their effects are monitored over time. Thus, we focus on assessing the strength of the data for each obesogen.”

Assessing the strength of the data is a good idea, but this is leaving a lot on the table. Natural experiments are happening all the time, and you don’t need clinical trials to infer causality. We’d like to chastise this paper with the following words:

[Before] we set about instructing our colleagues in other fields, it will be proper to consider a problem fundamental to our own. How in the first place do we detect these relationships between sickness, injury and conditions of work? How do we determine what are physical, chemical and psychological hazards of occupation, and in particular those that are rare and not easily recognized?

There are, of course, instances in which we can reasonably answer these questions from the general body of medical knowledge. A particular, and perhaps extreme, physical environment cannot fail to be harmful; a particular chemical is known to be toxic to man and therefore suspect on the factory floor. Sometimes, alternatively, we may be able to consider what might a particular environment do to man, and then see whether such consequences are indeed to be found. But more often than not we have no such guidance, no such means of proceeding; more often than not we are dependent upon our observation and enumeration of defined events for which we then seek antecedents.

… However, before deducing ‘causation’ and taking action we shall not invariably have to sit around awaiting the results of the research. The whole chain may have to be unraveled or a few links may suffice. It will depend upon circumstances.

Sir Austin Bradford Hill said that, and we’d say he knows a little more about clinical trials than you do, pal, because HE INVENTED THEM. And then he perfected them so that no living physician could best him in the Ring of Honor– 

So we think the “no clinical trials” thing is a non-issue. Sir Austin Bradford Hill and colleagues were able to discover the connection between cigarette smoking and lung cancer without forcing people to smoke more than they were already smoking. You really can do medical research without clinical trials.

They did not do this

But even so, the paper is just wrong. We can run clinical trials. People do occasionally lose weight, sometimes huge amounts of weight. So we can try removing potential obesogens from the environment and seeing if that leads to weight loss. If we do it in a controlled manner, we can get some pretty strong evidence about whether or not specific contaminants are causing obesity.

Defeatism

Our final and biggest problem with this paper is that it is so tragically defeatist. It leaves you totally unsure as to what would be informative additional research. It doesn’t show a clear path forward. It’s pessimistic. And it’s tedious as hell. All of this is bad for morale. 

The paper’s suggestions seem like a list of good ways to spend forever on this problem and win as many grants as possible. This seems “good” for the scientists in the narrow sense that it will help them keep their tedious desk jobs, jobs which we think they all secretly hate. It’s “good” in that it lets you keep playing what Erik Hoel describes as “the Science Game” for as long as possible:

When you have a lab, you need grant money. Not just for yourself, but for the postdoctoral researchers and PhDs who depend on you for their livelihoods. … much of what goes on in academia is really the Science Game™. … varying some variable with infinite degrees of freedom and then throwing statistics at it until you get that reportable p-value and write up a narrative short story around it.

Think of it like grasping a dial, and each time you turn it slightly you produce a unique scientific publication. Such repeatable mechanisms for scientific papers are the dials everyone wants. Playing the Science Game™ means asking a question with a slightly different methodology each time, maybe throwing in a slightly different statistical analysis. When you’re done with all those variations, just go back and vary the original question a little bit. Publications galore.

If this is your MO, then “more research is needed” is the happiest sound in the world. Actually solving a problem, on the other hand, is kind of terrifying. You would need to find a new thing to investigate! It’s much safer to do inconclusive work on the same problem for decades.

This is part of why we find the suggestion to move towards research with “model organisms such as Drosophila, C. elegans, zebrafish, and medaka” so suspicious. Will this solve the obesity epidemic? Probably not, and certainly not any time this decade. Will it allow you to generate a lot of different papers on exposing Drosophila, C. elegans, zebrafish, and medaka to slightly different amounts of every chemical imaginable? Absolutely.

(As Paul Graham describes, “research must be substantial– and awkward systems yield meatier papers, because you can write about the obstacles you have to overcome in order to get things done. Nothing yields meaty problems like starting with the wrong assumptions.’”)

With all due respect to this approach, we do NOT want to work on obesity for the rest of our lives. We want to solve obesity in the next few years and move on to something else. We think that this is what you want to happen too! Wouldn’t it be nice to at least consider that we might make immediate progress on serious problems? What ever happened to that? 

Political Scientist Adolph Reed Jr. once wrote that modern liberalism has no particular place it wants to go. “Its métier,” he said, “is bearing witness, demonstrating solidarity, and the event or the gesture. Its reflex is to ‘send messages’ to those in power, to make statements, and to stand with or for the oppressed. This dilettantish politics is partly the heritage of a generation of defeat and marginalization, of decades without any possibility of challenging power or influencing policy.“

In this paper, we encounter a scientific tradition that no longer has any place it wants to go (“curing obesity? what’s that?”), that makes stands but has a hard time imagining taking action, that is the heir to a generation of defeat and marginalization. All that remains is a reflex of bearing witness to suffering. 

We think research can be better than this. That it can be active and optimistic. That it can dare to dream. That it can make an effort to be interesting. 

Why do we keep complaining about this paper being boring? Why does it matter? It matters because when the paper is boring, it suggests that the idea that obesity is caused by contaminants isn’t important enough to bother spending time on the writing. It suggests people won’t be interested to read the paper, that no one cares, that no care should be taken in the discussion. That nothing can be gained by thinking clearly about these ideas. It suggests that the prospect of curing obesity isn’t exciting. But we think that the prospect of curing obesity is very exciting, and we hope you do too!