A Contamination Theory of the Obesity Epidemic
This is a summary of a paper that I found open in a browser tab; I don’t recall where I came across it. I think it’s a nice paper, but it’s also 63 pages long and seemed worth a synopsis for those who wouldn’t otherwise tackle it.
Scott concluded in For, then Against, High-saturated-fat diets that the obesity crisis seemed to imply one of three answers:
That weight less is really hard and people in previous centuries had really hard lives and that’s why there was so little obesity back then.
That it’s “being caused by plastics or antibiotics affecting the microbiome or something like that”.
That there is hysteresis—once you become overweight it’s semi-permanent.
This paper argues for the second answer, and against the other two.
At the outset, there are reasons to be wary of this paper: neither author (who share a family name) appear to have expertise in applicable fields, and it appears to be set in Computer Modern Roman, hardly the style of a journal submission. So it’s coming from outside of traditional expertise. (I don’t have any expertise here either.)
With that in mind, the paper starts by posing a series of challenging facts about obesity. (References in the original:)
It’s new. One hundred years ago obesity was very rare (~1% of the population) but there were plenty of people who had enough to eat and, from our point of view, ate a lot of fattening foods.
It’s not just new, it seemed to suddenly kick off around 1980. “Today the rate of obesity in Italy, France, and Sweden is around 20%. In 1975, there was no country in the world that had an obesity rate higher than 15%”.
It’s still getting worse. It’s less in the news but if anything it’s accelerating in the US. This is despite Americans significantly cutting back on sugars and carbs since 2000.
It’s not just humans: lab animals and wild animals appear to be getting fatter over time too. (A surprise to me, but casual inspection seems to confirm that this is really a thing that reviewed papers are noting.)
Junk food from a supermarket fattens rats far more than giving them more of any macro-nutrient does. Somehow junk food is more than the sum of its sugars, proteins, and fats.
Across several countries, living at sea-level seems to increase obesity.
Diets produce modest reductions in weight over the span of weeks or months, but the weight comes back over time. There’s been a lot of searching for effective diets, but they’re all about the same in large populations.
The next section answers some of the competing explanations for obesity:
“It’s from overeating!”, they cry. But controlled overfeeding studies (from the 1970′s—pre-explosion) struggle to make people gain weight and they loose it quickly once the overfeeding stops. (Which is evidence against a hysteresis theory.)
“It’s lack of exercise”, they yell. But making people exercise doesn’t seem to produce significant weight loss, and obesity is still spreading despite lots of money and effort being put into exercise.
“It’s from eating too much fat”, rings out. But Americans reduced their fat intake in response to messaging about the evils of fat some decades ago and it didn’t help. Nor are low-fat diets very effective.
“It’s too much sugar / carbs”, you hear. But Americans reduced their sugar and (more generally) carb intakes over recent years and that didn’t help either. Gary Taubes’s study was a bit of a damp squib.
In this section there’s a hunter-gatherer tribe for everything. I’m a little suspicious of this line of evidence because these small human populations could plausibly have evolved to tolerate their specific environment but, if you want a group of humans with zero-percent obesity who eat 60%+ carbs, or 60%+ fat, this paper has one for you. They have plenty of food, they just live happily and remain thin.
Next the paper establishes that there is clearly some degree of homeostatic regulation of weight by the brain. You can damage a specific part of the brain and cause obesity. Or you can have a genetic flaw that results in fat cells not producing leptin, which results in an insatiable appetite. (But adding leptin to overweight people doesn’t work.)
Now the paper presents its thesis: it’s all caused by a subtle poison! Manufacture of which really took off slightly before 1980, and is increasing or is bio-accumulative. Diets don’t work because it’s not a diet problem. Supermarket food fattens rats much more than any macro-nutrient chow because supermarket food contains more of the contamination. Wild animals are getting fatter because they’re consuming it too. Living at sea-level means that your water supply has traveled much further and picked up more of it, which is why altitude is anti-correlated with obesity.
There are many drugs that cause weight gain and that appear to do so by acting on the brain, so these things can exist. This is hardly the first paper to suggest that certain chemicals contribute to the problem, but this paper is distinguishing itself by saying that it’s the dominant factor.
Three specific families of chemicals are detailed for consideration: antibiotics; per-, and poly-fluoroalkyls (PFAS); and lithium. All have ambiguous evidence.
Antibiotics certainly make animals fatter, but do they do the same to humans in the amounts consumed? If so, why aren’t places that use a lot in livestock fatter than those which use less? Why aren’t vegan diets magic for weight loss?
PFAS is a family of thousands of under-studied chemicals, but they doesn’t clearly cause weight gain in humans at plausible levels. But they are certainly getting everywhere.
Lithium clearly does cause weight gain in humans, but are the amounts that people are exposed to increasing, and they are large enough to cause weight gain?
The paper also notes that things are even worse to think about because chemicals do complex things in the environment, and in animals. You don’t just have to think about the chemicals that are made, you have to worry about everything they can become. The paper includes the example of a factory in Colorado that made “war materials” and released some chemicals into the ground around the factory. It took several years for the chemicals to travel through the ground water to farms several miles away. During that time they had reacted to form 2,4-D, a herbicide, which killed crops on those farms. (The unreacted chemicals were also pretty nasty.)
Switching to speculation that should be blamed entirely on me, not the paper: it seems that there might be a tendency for any chemical that affects the regulation of adiposity to do so in the direction of obesity. There are several drugs that target the brain and cause weight gain, but fewer safe drugs that cause significant down regulation of weight. (If there were several such drugs, lots of people would be taking them.) Rather, drugs that cause weight loss often cause energy to be wasted from the body rather than changing the regulation of weight: DNP causing heat-loss, or SGLT2 inhibitors causing glucose excretion. Thus we might be facing a situation where multiple minor factors affect adipose regulation, but the overall effect is towards obesity because any effect tends to be in that direction.
The obvious example of something that causes down-regulation of weight is smoking. (We wouldn’t call it “safe” though.) I wonder whether the paper is overly focused on something that had a step change in prevalence shortly before 1980. It might have been building steadily in the prior decades but the 40%ish of American adults who smoked in the 60s/70s hid it for a while.
If we were to hypothesise that some environmental factor is causing a significant fraction of the obesity problem then how would we test it? It could well be the sum of multiple factors, some of which may be carried in water given the correlation with elevation. It seems that one would need groups of overweight people willing to consume exclusively provided water (from distillation) and a source of food that is somehow pristine. The half-life of PFAS, at least, is measured in years in humans, so the subjects would have to remain compliant with this proscribed diet for extended periods of time. In order to have control groups we would have to (double-blind) contaminate the pristine food with environmentally-plausible levels of candidate chemicals, I guess? Would that get past any IRB? The paper contains easier experiments, like having Kuwait change its desalination process or, more reasonably, have a car-mechanic company change grease, but these would only produce partial answers unless we got lucky and one factor dominates.
The environmental hypothesis is primarily one of exclusion, and this paper makes a good case. (Although one should have significant epistemological humility about any complex technical argument outside of one’s expertise.) And I haven’t even covered it all! The paper continues with arguments about paradoxical reactions and the occurrence of anorexia! There is much more within if this summary piqued an interest.
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The statistical silver bullet you’re looking for, assuming you can’t run multi-decade RCTs or convince entire countries to dramatically change their water policies (sounds a bit tricky?), is variance components analysis.
You want a variance component analysis equivalent to heritability, but for water/obesity. This is a perfect match: you have a very high-dimensional measurement (GC-MS of drinking water & foodstuffs), whose components you can’t observe because you don’t even know how many there are much less which ones (like the unknown chemicals that the original contaminants may react into along the way**), where direct prediction/regression would fail because it requires absurd amounts of data (especially given the statistical issues they outline), and where your original research question is not “where is the needle in the haystack” but “does this haystack have any needles at all”.
In behavioral genetics, if you plot pairs of people by their genetic similarity and their phenotypic similarity, you will find that people similar on both tend to cluster; and the more heritable the trait is, the more they cluster. You can do this for kinds of similarity which aren’t ‘genetic’. The idea of variance components is to switch from directly correlating/regressing the specific chemical levels in water, trying to measure the exact direct effect of each chemical on obesity, to instead asking, “how similar, in terms of overall water chemical composition, are similarly far or thin people? Do the chemical spectrums of fat people tend to look similar, and the spectrums of thin people look similar? Do they co-vary, and cluster?”
Think of the water GC-MS as a sort of fingerprint or high-dimensional summary. It doesn’t need to contain the actual critical datapoint, just a lot of correlates/proxies thereof (eg you can just shine some light on leaves and it’ll work!). The point is not to directly measure the culprit, but to indirectly measure how distant the datapoints are; perhaps chemical A shows up and chemical B does not show up clearly, and B is the real cause, but as long as chemical A correlates with chemical B (maybe it’s a different reaction product, or just gets manufactured or used in close correlation with B), then you will see that fatties tend to have close-together water spectra (because of A) and you will have strong evidence that “there is something in the water” because where the bad water clusters the fatties cluster.
So, you’d do something like record the BMI of 10,000 people, take a sample of their drinking water, GC-MS it (ideally, but many other analytical techniques could be used and maybe some would be better here, I’ll defer to any actual analytical chemists on that topic), and then plug into a mixed linear-model. You can plug in covariates as necessary (families/pedigrees to jointly model genetic heritability, ZIP codes, age, sex, local mining/factories, already known harmful contaminants the GC-MS detected, that sort of thing). This can be done at multiple levels: individuals nested in households, within regions, within countries, etc. The amount of covariance between the water spectrum and BMI measures the amount of variance the contents of the water en masse can explain, and depending on measurement error and whatnot, given the genetic heritability bounding how much water-heritability can explain, you should get somewhere <30%. Under most theories of obesity, it’s difficult to see why one would predict a water-heritability different from 0%*, especially if one has already included altitude/SES/household/region as covariates (which should cover all the obvious confounders like “maybe contaminated water is just a proxy for living in a poor region / having mining nearby / being poor”), so anything >0% is highly suspicious.
This doesn’t require any RCTs (or interventions of any kind), longitudinal datasets, n in the millions, or any of the barriers to most of the proposed tests. You only need a cross-section of obesity/water-samples. Individual level is ideal, but doing it with geographic units can be useful too if that is what is available across enough units (individual n are much nosier than k, but also much easier to get high statistical power with). This may even already exist! Drinking water is often tested for many reasons, and obesity health data is standard medical data collected in almost any relevant research; so there ought to be a lot of possible cross-references.
* you could do this with food as well but I focus on water because water is a lot more consistent day to day, and food results would be ambiguous. A single day’s food is still not very representative of individual consumption (maybe your wife cooks healthy at home but then you eat processed garbage at the office, and the sample comes from the weekend), so it provides a very poor measurement of the overall diet’s chemical signature. And if you demonstrated a large food-heritability of obesity, this would just be taken as proving that “see? sugar / fat / calories / highly-palatable processing causes everything, just like we said all along!”, and be weak evidence for contamination at best.
** They also raise the problem of interactions & nonlinear responses. These are issues in behavioral genetics too, of course, with dominance/epistasis particularly, and can be dealt with similarly in the water context: “narrowsense” vs “broadsense” heritability covers simple additive vs interactions, and you can do things like DeFries-Fulker, I think, for nonlinear responses. My guess is that contamination would be ‘additive’ mostly, for similar underlying reasons as genetics tends to be ‘additive’: many interactions are just constants because they are done on a fixed background of chemistry, and promiscuous interactions average out to additive effects. But this is the sort of thing to worry about only after having done the straightforward work.
I wonder if the GC-MS exists for municipal water supplies already, and can just be aggregated and compared against population obesity rates? Less precise than doing it house-by-house, but much cheaper if someone has already done it for you and also it might not vary much house-by-house.
Yes, that is what I meant by geographic units. It has both advantages and disadvantages: data may already be available, and may be much more statistically-powerful; on the other hand, variance-components like BLUP usually are done with individuals available, and I’m not sure about the interpretation/correctness of doing it otherwise.
Have you ever seen or even heard of a person who is obese who doesn’t eat hyperpalatable foods? (That is, they only eat naturally tasting, unprocessed, “healthy” foods).
This seems like the occam’s razor expanation to me. Some of our new flavour/texture combinations are so rewarding that they easily overcome the natural stop signals, leading to excess caloric consumption in most (to a variable degree), which leads to weight gain in some.
A study which gave its participants a 1000cal/day dietary surplus found while some participants gained 14kg of fat over the course of the study (I think it was for 3 months), others gained as little as 4kg. As one would expect, there is genetic variance in one’s vulnerability to the effects of a harmful caloric surplus, and there is probably also genetic variance in one’s susceptability to hyperpalatable foods.
Tried this for many years. Paleo diet; eating mainly broccoli and turkey; trying to get most of my calories from giant salads. Nothing.
Might not be the right place to ask this question but: Have you tried bariatric surgery? I’m sure you’ve done a bunch of research and was wondering if you hadn’t because of something you’d read, or you had and it didn’t work, or some third thing.
The study I would like to see is giving obese people unlimited access to only natural foods for 3 months. They could add salt and spices, but no oil and definitely no sugar. The diet would be lean(ish) meats, fruits, vegetables and legumes (unsure if allowing nuts is a good idea as they’re extremely calorie dense, but technically they should be allowed under this definition).
I would be surprised if this didn’t work. Under this model I view hyperpalatble foods as equivalent to an addictive drug for obese people. Just as if you have a poor phenotype for alcoholism, you should avoid alcohol altogether, if you have a poor phenotype for the overconsumption of hyperpalatable foods, and a poor phenotype for the conversion of those extra calories into fat, you should avoid hyperpalatble foods.
People get fat eating fruits, which are obviously ‘natural’, and are basically candy. A lot of natural foods fail on the actual criteria (Cashews also fail, for instance.). Does it fill you up? Does it make you not want to keep eating (physical signals)? Are you satisfied enough (psychologically) to be done? Did it give you the nutrients you need (both for your health and to prevent cravings)? Is all of this finished before you ate too many calories?
Are you implying that there are examples of people like BDay mentioned, who are obese despite only eating fruits/nuts/meat/veggies? Or just that people can get fat while including fruit in the diet? I’d be surprised and intrigued if it were the former.
I’ve tried the whole foods diet, and I’ve personally found it surprisingly hard to overeat, even when I let myself eat as many fruits and nuts as I want. You can only eat so many cashews before they start to feel significantly less appetizing. And after I’ve eaten 500 cal of cashews in one sitting, the next time I’m feeling snacky, those cashews still sound kinda meh. Fruit is certainly easier to eat, but still after the fourth or fifth clementine I feel like “ok that’s enough” (and that’s probably only ~300 calories). Whereas I could easily eat 500 cal of candy without breaking a sweat.
I think one major roadblock to overeating with fruit is that it takes effort to eat. You have to peel an orange, or cut up a kiwi or melon, or bite off the green part of a strawberry. There’s a lot more work involved in eating 500 cal of fruit than there is in unwrapping a candy bar or opening a party size bag of chips.
So all of this rambling is just to say that I’m somewhat skeptical of the claims that “fruit (nuts) are mostly sugar (fat) and are calorie dense, and you can overeat them just like you can with junk food”. I think it’s surprisingly hard in practice to do so (and it’s much less enjoyable than overeating junk food).
Fruits have lots of fibers. Fibers both reduce sugar absorption in the guts and slow it down, evening the amount of sugar that gets in the blood stream over time (avoiding peaks that cause mass insulin production followed by a sugar dip when insulin keeps being produced while sugar intake drops, causing sudden fatigue). Fibers also fill the stomach, stretching it which signals satiety. You only get those benefits if you eat the whole fruit. In juices, slushies and the like, the fibers have been cut in small pieces and they effect is significantly reduced.
I disagree only in that I don’t think the amount of fiber is sufficient to make up for it.
I was not stating that I believe a whole foods diet won’t be helpful for many people, just pointing out that not all whole foods are good if you need to lose weight. Most diets work a little, and whole foods is one people find easy to understand (and, I suspect, to live with.) It isn’t just better than nothing, it could genuinely be useful.
I am implying that adding fruit to a diet is not helpful whatsoever to weight (unless you want to gain weight and just need more calories.) Fruit makes many people much hungrier due to very high sugar and general carb counts, and causes both physical and psychological cravings, while not providing the fats and proteins people need to stop craving food. I do not know of someone trying a fruit only diet (which would be very stupid), so I can’t say I have evidence that they would be fat if eating only fruit.
I do agree with you that the minimal extra effort to prepare the fruits for eating does often help reduce the amount eaten, but I would say this works much better for people that don’t have significant physiological cravings to eat. If you are normal weight and healthy, it isn’t that bad to eat fruit once in a while, just like a cookie or two won’t hurt you. For people that actually have trouble due overeating, fruit is still very binge-able. (Fruit cravings are definitely something I’ve seen a lot of in the obese people I know.)
Minimally processed meats and most vegetables are not prone to fattening people, while I believe certain nuts (like cashews) are. Cashews are not particularly satiating (notably, the body only finds saturated fats satiating, not unsaturated), and do not fill the stomach either. For the same (high) number of calories it would be vastly harder to eat it in meat than cashews, even if you like meat more. I have nothing against fat being part of the diet, but cashews just don’t work that well.
edit: moved a paragraph, changed the spelling of a word
Given the massive changes in fruits from selective breeding, I disagree. I would classify most fruits in the hyperpalatable category.
How many of the bananas in the article below are you going to eat?
https://www.sciencealert.com/fruits-vegetables-before-domestication-photos-genetically-modified-food-natural
And then there is the issue of availability in nature. Most fruits are only available seasonally in nature but we have fixed that. This temporary availability in quantity may be IMHO what drives binge eating of sweet foods. Because in nature it is a case of use it or lose it.
Oh, huh—looks like this paper is the summary of the blog series that “Slime Mold Time Mold” has been written about it? Guess I can read this paper to skip to the end, since not all of it is posted yet. :P
The altitude correlation would seem to suggest drinking water in particular as a culprit, and suggests a simple and straightforward study that would settle the question once and for all: randomize a group of households to either receive reverse osmosis filters on their taps, or not, then track whether the people in those households become obese.
I checked whether this study has been performed, and as far as I can tell, it hasn’t. There have been studies that randomly installed reverse osmosis filters, but they were checking for something else and didn’t track peoples’ weight.
Another effect of altitude is the atmosphere, and there is evidence that the active ingredient in altitude decreasing weight is the thin atmosphere. For example, “One study on rats found that they ate 58% less one day after being transported to Pike’s Peak, and were still eating 16% less per day two weeks afterwards.” The immediate effect strongly suggests that it’s not caused by anything in the water source.
See page six of the paper for the authors dealing with this point. It’s certainly a potential explanation, but the map of obesity in the US does seem to suggest that being, say, at the mouth of the Mississippi basin is much worse than being on the west coast, despite them both being at sea level.
The mouth of the Mississippi basin is much poorer than the West Coast, and has a lot fewer Asians (who are exceptionally thin). I’d guess those things probably play a role.
Educational attainment is strongly correlated with obesity rate across US states:
I used this obesity dataset from the CDC and this educational attainment dataset from the USDA.
Also, the mouth of the Mississippi basin does seem to be at a lower elevation than the West Coast:
That’s a map of highest elevation by county. I don’t think most people in LA County (third from bottom on the California coast) live above 6800 feet, because most people don’t live on mountains even if one exists in their county.
Oops, sorry.
The map of average elevation by county looks similar, but you are right that this matters very little because people are disproportionally likely to live in low elevations.
Reverse osmosis filters will already be more common in some places that have harder water (and decided that softening it at the municipal level wouldn’t be cost-effective). If there was fine grained data available about water hardness and obesity levels, that might provide at least a little signal.
Heads up: the given link to the paper seems to be broken, because it links to a 4 page paper called “The Beginning of Time” which is entirely unrelated to nutrition and your post.
Based on this Wayback snapshot it seems to be a paper called “A Contamination Theory of the Obesity Epidemic” by Ethan Ludwin-Peery and Sarah Ludwin-Peery. I was able to download the PDF of the paper at this link (the main body of the PDF is 63 pages as claimed in this LW post, and the PDF is dated July 3, 2021, which is just before this LW post was published, so it is likely the version of the paper being discussed here).
Yes, I can’t get it either.
The possibility of a broken link (now or in the future) is one of several reasons why it would have been a good idea to mention the title of the paper and the authors’ names.
Note that Korea and Japan have very low obesity rates (around 2-3%), despite being highly developed and having widespread availability of hyper-palatable food. Definitely worth to check whether some chemicals are more present literally everywhere else than in those two countries.
Contra the obvious genetic hypothesis, genetically similar China and Taiwan have very high rates of obesity. I don’t know whether Koreans and Japanese might be genetically closer to each other than to Han Chinese.
Given the Confucian influence on the culture of Korea and Japan, maybe it is peer pressure that keeps people from becoming overweight? Plausible, so it might be worth to look into the case of hikkikomoris, which is the Japanese phenomenon of refusing to leave your room/apartment for months or years while being supported (usually) by your parents. As such, they are likely not actively managing their weight. They are obviously a hard group to survey, but these studies looked into characteristics of hikkikomori and neither mentioned overweight, so that is a point for cultural or genetic reasons.
However, your linked paper says that Japanese that move to America do tend to gain weight, so it cannot all just be genetics.
I wonder whether Asian kids adopted by non-Asian parents are more often overweight than kids raised by Asian parents.
This is very interesting. You certainly can’t argue with the availability of hyperpalatable food in these countries. To the extent they are less available in stores, that would be the result of people wanting them less.
Perhaps the consumption is lower because of their culture (mimesis effects). People eat what those around them eat, and the traditional diet is culturally sticky enough in Japan and South Korea that, in spite of the availability of hyperpalatable foods, people still follow it for the majority of meals. However, this explanation requires a reason why this is not the case in other places, especially genetically and (I’m guessing somewhat) culturally similar places like China and Taiwan.
It’s not like South Korea and Japan have failed to pick up on the addictive aspects of other areas of modern culture, like the internet. So I don’t understand why diet would be different for them.
How do hikikomori plan their meals? If their parents are handling a lot for them, are the parents also implicitly regulating food they provide? Alternatively, is a habitual clockwork pattern of delivery food an implicit form of regulation?
EDIT: My complete thoughts are here: https://goodtosell.substack.com/p/a-response-to-a-contamination-theory
https://www.jeffnobbs.com/posts/what-causes-chronic-disease
I’ll add more and fix this up tomorrow at my pc. Sorry bout the sloppiness and the formatting, you’ll see why I was so excited. I really can’t stress just how much this adds up. It’s really quite uncanny. I encourage anyone to just read that instead of me, but I gave this a shot for when you’re done with that.
Just found this, it reminded me of your post, as I’d been thinking about it a ton.
Looks to me like it’s vegetable oils. Practically fits everything perfectly. The new addition to our diet. They were only invented about a hundred years ago. They’re in nearly everything packaged in the supermarket—hence why it looks environmental, why the rats got fat, why the processed food looks bad, even why the Cubans got skinnier, since these oils are highly implicated in global trade.
If you look at what soybean oil does in mice studies it’s kind of ridiculous. Not a medical professional, so who knows. Especially how it solves most of the points addressed in that paper.
Changed over the last hundred years
Yep
With a major shift around 1980
For the 1980 thing, I think the author focuses on that date a little too much anyways, it’s a monotonic increase in both oils and obesity all the way up.
-It could be a threshold that got passed around that time—it looks like that’s about when the average man went from just under to just about overweight BMI
-Perhaps a large cohort was hitting a certain age around that time
-Global trade really starts kicking off
And whatever it is, there is more of it every year
Yep. See source.
It doesn’t affect people living nonindustrialized lives, regardless of diet
Global trade, new invention from USA, ticks this box for me.
But it does affect lab animals, wild animals, and animals living in zoos
Lab animals fed store bought food, yep. Wild animals, no source from what I can tell, surely raccoons are eating plenty of cheetos nowadays.
It has something to do with palatable human snackfoods, unrelated to nutritional value
Yep. Unrelated to carb or fat content.
It differs in its intensity by altitude for some reason
Also think they’re a bit too focused on this one, maybe there’s a mechanism, maybe Colorado is an outlier. There’s a lot of talk of lipids, and oxidization in papers about veggie oils, perhaps that’s something—less oxygen, less oxidization, less CVD? I don’t have the expertise. Maybe it’s something else for that.
And it appears to have nothing to do with our diets Not so sure about that one
Some quotes and my rebuttals:
Well, not the macronutrient contents. I think we have plenty of studies that show low fat vs low carb etc is kinda a wash. But surely there’s plenty of vegetable oil in all those processed foods.
For an abrupt shift, 1980 is when the USA started guidance going against saturated fats….and we replaced lard and butter with veggie (soybean) oil.
Same location, new lifestyle? If they didn’t also move, I don’t see why you should say it’s in the water, vs a complete diet makeover. Note that these oils do all these things to rats. The oils also seem to act on their brains, messing with the hypothalamus which from what I could tell seems somewhat implicated in set point type stuff.
Diet won’t work—only potatoes did. Whole foods does. Those get rid of veggie oils for sure. Switching from fats to carbs won’t get rid of the veggy oils that are in near all processed foods though.
Oils are in doritos (ingredient 2), in froot loops even, presumably in ‘fried pork skins’. As for wedding cake, couldn’t find a good label on the internet, if it’s store bought it’s probably there though.
I actually doubt it’s chemical contaminants—you’d think China with the factories and air pollution, or the Congo with mines and terrible water would be worse than us. The USA really cleaned up its air in the past 60 years or so, no dice on that in my book.
Finally, I don’t have a horse in this race, i posted some thoughts a few weeks ago here too with an entirely different explanation. I don’t usually get emotional about science, and try to kill my bias. But something smells here. This works way too well, it’s new, it’s simple, why is this not one of the first things anyone thinks of? The people who wrote the paper in the OP didn’t address this at all, when veggie oils are in nearly everything and absolutely exploded from nothing about a hundred years ago. I’ve done a fair bit more digging, there are allegations of corruption—especially of Proctor and Gamble (crisco) buying out the American Heart Association essentially. I’m skeptical, but it does seem like they were throwing some money around in support of Crisco.
Per the source:
Tldr, vegetable oils were invented about 100 years ago, highly promoted around when they started to turn on saturated fats, and line up with close to every mystery the authors assert. It’s also a way simpler explanation.
I think this problem is extremely real but the academic studies overstate them, because people who succeed with their first diet and keep succeeding don’t sign up for diet RCTs. They’re selecting diet-resistant people.
Adderall (and other similar stimulants) are known to suppress appetites. They’re not a great choice to prescribe as an appetite suppressant, due to their major other effects and since it doesn’t seem to affect everyone, but they do work.
Other examples of drugs that also seem to work for weight loss are GLP-1 agonists, which are relatively new and potentially promising.
No doubt environmental factors should be considered. Assuming for a moment it’s plastics in the water, say, I’m curious what mechanisms would explain why we don’t see really obvious trends by geographic area (independent of other factors). For example, it’s of course not all environmental because people in the same neighborhood/family have different outcomes.
To throw my hat in the ring: all things metabolic seem highly intertwined. I faced an interesting trillemma once upon a time—I had high blood sugar, high cholesterol, and low testosterone(alcoholism). I initially cut calories: that was tough because my testosterone declined even more, and burning fat also “releases” (not a technical term) cholesterol from the fat back to the bloodstream. But I improved blood sugar. After that miserable time, I messed around with a lot of different things, but ultimately settled on a general healthy whole-foods based diet, lifting weights, and hiit. Worked like a charm. What was interesting to me was how everything failed at once, and in roughly the same proportion: my cholesterol and blood sugar were just hitting the danger zone, and my testosterone was just about hypogonadal. Interesting, because you would think one acute stressor would affect, say, only blood sugar. But that’s not the case, it seemed as if the system was highly interconnected, and “slack” could be taken from one parameter to improve another. Along the same line, it seemed as if the whole system could be tightened up all at once as well, by a holistic approach. But focusing on blood sugar came to the detriment of cholesterol and testosterone. So one bad input could turn all the outputs, even the non-direct relationships, bad all at once. But the opposite was not true.
Another thing, anecdotally I’ve observed that generally people either stay at a good weight, or pretty much always decline monotonically, once they hit some sort of inflection, i.e. insulin resistance, past a threshold. Rarely do you see that their tendency goes from effortlessly maintaining 150lbs>effortlessly maintaining 155lbs. It seems more that they effortlessly maintain 150lbs, then something breaks, and they add weight until they are old enough to have even bigger problems. This may be why the acceleration at once, perhaps the average level of some cumulative damage /other measure went from just under to just over said threshold around 1980.
What am I saying? It’s probably fundamentally super complicated. I almost don’t even think we’re lacking in data or really in understanding of the basics—it seems we need a statistical revolution to really get to the bottom of this. My intuition tells me that the answer is there, it’s just not going to be a simple linear correlation. Same goes for most complex systems too, by the way. Or, equally likely, God just starts fucking with us when we try to figure out things that he simply wills, so he fudges the data
Perhaps it is carbon dioxide. Here is a paper on it:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3341709/
To summarize, the idea is that high partial pressure of CO2 causes blood pH to change, which influences the body’s regulatory mechanisms and eventually leads to obesity.
At higher altitudes the carbon dioxide fraction in the air is unchanged, but the partial pressure is lower. I’d expect that lower partial pressures of CO2 would mean less effect on blood pH.
This was my guess too, but they later did another study with rats and it did not show significant effects.
https://sciencenordic.com/climate-change-denmark-obesity/four-years-later-is-co2-making-us-fat/1440745
My layman’s understanding (and personal experience based on self-experimentation over the past decade trying to get to a healthy weight range) has been that this is a threshold problem. For generations we’ve been gradually making intentional and unintentional changes to diet, activity, and environment that make it a little harder for our bodies to regulate weight, until eventually we use up the slack and start actually gaining.
I think this is important, because if true, it means that there will never be a silver bullet, nor a single solution at either an individual or societal level. It also means the solutions don’t have to look like the proximal cause that “pushed us over the edge” if it’s easier to reverse changes that happened much earlier, or if we need to do other things to overcome sources of hysteresis in our bodies’ weight-regulation systems. We have a lot of possible levers: Reducing pollution, eliminating exposure to certain chemicals, curing some infections, altering diet composition and methods of food preparation, altering timing and number of meals, altering speed and social context of eating, reducing various forms of stress, varying all the different dimensions of type and duration of exercise, changing how we sleep, changing indoor lighting and air quality, changing time spent outdoors, improving hydration, reducing chronic inflammation, and that’s just what I thought of in two minutes. It is hard to do plan and stick to enough self-experimentation over a long enough time to find out what actually works for an individual, even for very smart and educated people.
I’ve called this the “phlogiston” theory of obesity—something systemic and undetected is at work.
It’s not necessarily wrong, there’s certainly some evidence that the same behavior 100 years ago would have had different results. On the other hand, the general alleviation of poverty and famines, as well as the presence of “hyper-processed” foods like Oreos are certainly part of the reason and are largely ignored.
If I had to guess what the “phlogiston” is, I would guess CO2 concentration. I don’t have any evidence whatsoever, but it’s a politically-convenient theory and the timing mostly works.
Ignored by this paper or this post? The blog posts the paper is supposedly based on explicitly considers it tho this post doesn’t mention it. Other commenters do mention this.
But more widely, I’ve seen those reasons mentioned very frequently.
Maybe you think these are largely ignored because they have been investigated and they didn’t (and don’t) seem promising?
For a while I had a theory that “sugar in a beverage not paired with bulky food” added calories without the human brain/whatever noticing and having the satiety mechanism(s?) kick in when the right calorie consumption level was hit. The archetypal study here would involve carefully measuring how many calories like this, C, that a person consumed per week, and then C/3500 is how many pounds per week they should gain over time.
I dunno if this is true, but it seemed close enough to likely to be true that I started rejiggering my habits and feelings about food to try to get my personal C “close to zero when left to my own habits and choices”. If I’m just going to “drink” now, I try to basically only drink water or milk. Not ALWAYS. Sometimes I find myself craving orange juice, but I try to eat other similar fruits first, before I fall back to a cup of delicious delicious citric acid flavored sugar water.
Is there a tribe that drinks a LOT of fruit juice?
The big obvious macrocausal elephant in the room is corn, and how corn is in everything, and how cows are fattened on it (so milk and burgers are actually corn), and then there’s HFCS, and corn oil, and so on. Cheap edible calories, as far as the eyes can see.
(You might link the “fruit” juice theory with the corn theory, because a lot of juice is just sugar water with fruit flavorants and a lot of sugar is corn based. If you’re not careful, an attempt to drink apple juice will lead you to actually drink “corn” juice.)
If we follow the corn calories, I could imagine them cascading out, through pets, and lab animals, and into the garbage, and into mice and possums (and anything that eats mice and possums)… but NOT into deer nor any other non-garbage-eating herbivores.
The wild animals seems surprising to me. I feel like I can probably suggest animals where it is NOT happening… like: I bet it is not happening in polar bears. How detailed was the analysis here? This seems like the place to find some “surprises” that constrain the causality more precisely.
I know people who only drink water and have issues with their weight, so this isn’t the only answer. I’d definitely believe that it plays a role though.
From what I know of deer behavior, they are quite happy to eat corn right off the field, so much so that deer from agriculturally-worked areas (the flat areas of northwestern Ohio, for example) taste less “gamey” than wood-dwelling deer of hilly areas (in southeast Ohio). Maybe there is a way to use hunting data and use one as a control group against the other.
After reading the whole thing I don’t think he disposed of the hyperpalatability hypothesis. That was the weakest part of the series.
One other thing that was missing related to sugars and seed oils. I have not been able to find any ‘native’ poulation with access to large quantities of both. You do have some with access to large amounts of fruit or honey, as mentioned. And also some (Kalahari desert dwellers eat large amounts of Omega 6 rich mongongo nuts “why farm when the world has mongongo nuts”) with access to large quantities of Omega 6 oils, one alleged culprit in seed oils. But I don’t see any that have both, Processed foods are rich in both and this is novel.
Still it is worth reading IMHO and I find myself somewhat convinced that Li has a role.
My larger-bodied theory is that the “work-week” & all of its over-regulated time tables, don’t properly co-relate to most people’s biological needs. “Rushed” anything is seen as negative, I’ve never felt good a single minute when the word “rush” was in my head. With a work-week regulation of everything is the expectation, fall off the horse & your troubles become worse. Your peer evaluation goes down, the work will not be offloaded or considered too much for one person, it is compounded, or you must act like an “ubermensch” for as long as it takes to get caught up. Remembering that you fell off the horse precisely because of the weight you carried without these extra burdens, you must now “rush”. I thinked the mental directive, “rush”, triggers over-feeding because of it’s base narrative of “need”, which has overlap with survival instincts. This is the pyschological feed that turns the modern worker into a slave. Constant retriggering of the “need” directive, makes of man a mule & a yoke.
I also posit that overall population feeling is transferrable, at least for high-contact groups. Which is most to all people. Telepathy or not, I can feel the anxiety of someone through all of their cues & I pay the cost of giving my “attention” to their “direction” by inheriting a distinct percentage of their feeling, depending on my attention input weight. When people feel aggressive, their peers feel aggressed by inheriting a bit of the aggression. This is a telephone game, where average response to high stimulation by those whose “need” directives are perpetually retriggering decides the overall feeling state of those with professions that require high-contact & high #’s of people met per day.
Persistence wears down resistance,
eventually the body’s natural weight regulation “capacitors” break, or at least conform to the new norm, hence the semi-permanence of weight gain after the initial deflowering of the non-obese individual.
This secondary theory could use a lot of work, & costs a decent amount of energy for me to add clarity to, but I believe in everything I’ve written
One possibility not mentioned is the removal of an environmental contaminant: 1980 corresponds to phase-out of leaded gasoline. Could it be that lead was making us (and all the animals) both dumber and skinnier?
I don’t think that explains why the US has a stronger obesity epidemic then France.
It’s a long shot, but how about oxygen deficiency? Our cells’ mitochondria use oxygen to produce ATP by ‘burning’ glucose. Could less oxygen mean less energy consumption and therefore more fat storage? All I could find about the evolution of oxygen concentration is on https://en.wikipedia.org/wiki/Oxygen#Later_history: Oxygen levels in the atmosphere are trending slightly downward globally, possibly because of fossil-fuel burning.
We’d expect altitude to be positively correlated with obesity, though.
There are studies, and studies of studies, showing that exposure to various PFAS chemicals are positively correlated with weight gain. I really think PFAS is the culprit. The extent that many municipal water systems are contaminated with PFAS has only recently been coming to light. People have been taking in a lot more PFAS contamination than they realize.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7723340/
I’m currently living the “clinical & pristine” diet outcome that you have theorized would be worth studying. I drink only distilled water w/ a small amount of added electrolytles, & eat only foods that came out of the Soylent meal replacement boom(that also scored the highest on my [enjoyment, body-feeling, satiety, satisfaction, company ethics] matrix compared to their competitors.) eaten only at room temperature or above(I have a strong belief, from approximation by body reactions & a few co-opters in the form of Gwern & a few studies, that cold foods are not digested properly & may slow metabolism, thus creating whatever behavioral/biological domino effect that would have. Sub-optimal.).
I collapsed into this diet outcome after a ferocious bout with a feeling-set [depression, low-motivation, erratic eating habits, inability to formulate coherent strategies] that I recognized as externally motivated. I changed a few other things, but this was one of the outcomes that my BNN’s gradient descent collapsed towards, I had never heard of microplastics or flouride being a nuerotoxin, which has led me to believe in the “mathematicians are often wrong about the details, right about the answer” form of epistemy. I think “something’s in the water”. It’s a shame I’m not closer to the problem, but a few years ago I thought it was the gutter-or-the-grave, so baby steps I suppose.
If use is ever found for someone with my diet composition, I’d be more than willing to pony-up my bio-metric data. I have a strong suspicion that diet composition is well related.
I’d wonder about the effect of atmospheric pollutants. Altitude would clearly also have an effect if obesity was being caused by pollutants in the air.