A Chemical Hunger – Interlude E: Bad Seeds

[PART I – MYSTERIES]
[PART II – CURRENT THEORIES OF OBESITY ARE INADEQUATE]
[PART III – ENVIRONMENTAL CONTAMINANTS]
[INTERLUDE A – CICO KILLER, QU’EST-CE QUE C’EST?]
[PART IV – CRITERIA]
[PART V – LIVESTOCK ANTIBIOTICS]
[INTERLUDE B – THE NUTRIENT SLUDGE DIET]
[PART VI – PFAS]
[PART VII – LITHIUM]
[INTERLUDE C – HIGHLIGHTS FROM THE REDDIT COMMENTS]
[INTERLUDE D – GLYPHOSATE (AKA THE ACTIVE INGREDIENT IN ROUNDUP)]

People have been asking us if we’re going to review the literature on seed oils. 

We weren’t aware this was such a popular theory when we wrote the series, so we didn’t think to address it. Briefly, this theory says that some of our food oils — usually soybean, corn, canola, cottonseed, and safflower oils, but sometimes others — are behind the modern meteoric rise in obesity rates. Clearly this is relevant to our interests. 

People are split over exactly what to call the culprit — seed oils, industrial seed oils, vegetable oil, etc. These terms may mean slightly different things to different people, but ultimately these are all a closely related set of theories. In this post, we will go with the term “seed oils” because it is the shortest. 

Here is just a small subset of the sources people sent us:

We haven’t read everything ever written on seed oils because there are a truly enormous number of pieces on this idea. But we do think it’s worthwhile to do our own review of the theory, so here goes. 

Plausibility

There are a number of things that make this hypothesis attractive. For one, these oils truly are in everything

One of the authors of this blog went on a couple dates with a girl who had a serious corn allergy. Unfortunately for her, corn oils and other corn byproducts are all over the damn place. She couldn’t eat out at restaurants or buy most prepared foods. She couldn’t have chocolate. She couldn’t even eat citrus, because corn proteins are a component in the pesticides/preservatives sprayed on citrus trees and fruit. She could eat apples if she peeled them, but even that was a risk. She mostly lived on rice, rice noodles, a small number of safe vegetables, and potatoes (which, to be fair, are the prince of food). 

And this is just corn! We’re looking for a factor that is omnipresent in the environment and difficult to escape regardless of one’s diet, and seed oils do seem to fit the bill.

We should also note that the contaminants theory more or less predicts something like seed oils. Any contaminant that causes obesity probably bioaccumulates in plants and animals. If it bioaccumulates in plants, then highly concentrated byproducts of those plants might contain higher concentrations of the contaminant. This would vary based on the species of plant (some will bioaccumulate more than others) but we would expect to see especially high levels of contaminants in some extremely concentrated food products. 

Seed oils are also highly processed (check out the cool/disturbing video at that link) so they have many opportunities to come into contact with industrial contaminants. “I thought it was going well,” says YouTube commenter Sam De Francesco, “up to the bit about using a chemical solvent to remove the remaining oil from the canola cake. It went downhill from there quickly.”

The two theories are complementary, and it’s possible that both could be true. We can even look at specific contaminants to see if there might be a connection.

There is some work on measuring the levels of PFAS in cooking oils, and they do record some PFAS being detected in “Edible Oil Samples from Markets in Beijing, China, in 2013”, including corn oil, soybean oil, etc. But these levels of contamination are in about the same range as PFAS found in other foods, like milk, not thousands of times higher.

We can’t find any actual measurements of lithium levels in different food oils. This paper finds no relationship between vegetable oil consumption and lithium in the blood plasma of 922 Germans, but the food consumption measure was all self-reported, and people are probably not fully aware of how much vegetable oil is in many foods. Some secondary sources (here, here) say that lithium is most concentrated in vegetables, cereals, and grains, which would sort of line up with the seed oil hypothesis, but we can’t find the primary sources for these claims, so take this one with a grain of salt for sure. 

Glyphosate’s Hail Mary

In a previous post, we took a look at glyphosate and concluded that it doesn’t seem like glyphosate could be a primary driver of obesity, and probably doesn’t contribute to obesity at all. There is one longshot hypothesis, however, of how glyphosate might play a role in the obesity epidemic, or at least the increase we’ve seen since the 1990s. 

When reviewing the list of Roundup Ready crops, varieties designed to be sprayed with huge doses of glyphosate, we couldn’t help but notice that soybeans, corn, canola, and cotton are all on the list (though not safflower). As a result, these crops are sprayed with much more glyphosate than normal. This seems like kind of a weird coincidence. You’ll also recall that in 2016, the EPA found glyphosate in 63.1% of corn samples and 67.0% of soybean samples they tested

The level of contamination was quite low in all of these samples, but seed oils are highly concentrated, so the levels of contamination in corn oil could potentially be hundreds of times higher. That said, we haven’t been able to find any data on glyphosate levels in any of these oils, so it’s hard to tell. There’s some evidence that glyphosate is in more foods than officially recognized (thanks to commenter Louis for finding this one!), but that’s not a direct connection to seed oils per se. We also found one claim that glyphosate “does not mix with oil, so there are negligible glyphosate residues in vegetable oil from treated crops such as soybeans, canola and corn”, but this is from gmoanswers.com.

Challenges

The seed oil account of obesity also has several weaknesses, which make the hypothesis seem less likely.

First of all, it seems unlikely that there is a problem with the sources of the oils themselves. Soybeans and corn have been eaten for centuries without a wave of obesity. Rapeseed (you know this as the source of canola oil) is yet another Brassica, which people have been eating forever. 

(Ok rapeseed is a Brassica but not a Brassica Oleracea, just let us have this one.)

It could all be in the dose, though. These seed oils are highly concentrated — hundreds or thousands of servings of the relevant vegetable are needed to make one serving of the oil — so if there is some corn enzyme that is harmless at a small dose but dangerous when the dose is 100x higher, that could lead to corn being harmless but corn oil being an issue. A common saying among seed oil proponents is “the dose makes the poison,” and that certainly might be the case.

We notice that the seed oils under suspicion were developed around 1900-1930, which seems a little too early to match the timeline for obesity. People have been eating more and more of them over time, but this trend took off around 1940 and doesn’t show a clear inflection point around 1980. This isn’t damning evidence, but it doesn’t quite fit the pattern. 

Image courtesy of Jeff Nobbs, reproduced with permission of the author

In addition, seed oils face the same problems faced by every food-based explanation for the obesity epidemic.

Seed oils have a hard time accounting for patterns like obesity being related to altitude, and wild animals also becoming obese. Maybe wild animals are eating scraps of human food out of dumpsters behind the 7-11, but it’s not clear why people at low altitudes would be eating more seed oils than people at high altitudes.

Seed oils also seem unable to account for the big differences between obesity rates in different professions. It doesn’t seem like people in different professions are likely to eat different amounts of seed oils, but they do seem likely to be exposed to different contaminants at work.

Similarly, there is a large amount of variance in obesity rates between countries, and there has been for a long time. Why is the Middle East so obese? Why has Kuwait always been one of the most obese countries in the world? Why was Kuwait 20% obese in 1979, back when the obesity rate for the US was only 13%? It doesn’t seem like seed oils could be behind the high rates of obesity in the Middle East, which limits the possible role they could play in driving the obesity epidemic.

Health Claims

Of course, what we’re really interested in is whether or not seed oils are related to weight gain and obesity.

It’s unfair to look through a literature and start with some random papers. You want to let the theory’s supporters point you to the evidence they feel is strongest, the evidence they think is most important. We wanted to look at the strongest possible argument, the sort of case that only a supporter could put together. So we decided to start by looking at one person’s case against seed oils.

For this purpose, we decided to focus on work by Jeff Nobbs, because his series was the best of the many arguments we saw, and we want to engage with the strongest version of the theory. Nobbs cites lots of primary sources, links directly to them, and tells you which parts of the findings he thinks are relevant. He doesn’t hit you in the face with a bunch of biochem claims right out of the gate. He doesn’t engage in name-calling and doesn’t try to scare the reader by going on about how dirty or unnatural seed oils are, something we can’t say about some of the other sources we saw. He just shares the evidence that convinced him and explains why he thinks it’s important.

In Part 1 of his series, Nobbs does a really great job describing how levels of chronic disease and obesity are increasing, and reviewing the evidence for just how weird this is. He hits a number of the same points we made in our review of the mysteries surrounding obesity, and often he makes a more compelling case for their weirdness than we did. In particular, he does a better job describing how exercise rates are increasing. We especially like this figure: 

Image courtesy of Jeff Nobbs, reproduced with permission of the author

Part 2, called Death by Vegetable Oil: What the Studies Say, reviews a number of studies that suggest that seed oils (Nobbs prefers the term vegetable oil, but it’s essentially the same thing) contribute to health conditions like cancer, dementia, and weight gain. In this series we are primarily interested in obesity, so we will stick to the weight gain results.

In this post, Nobbs references four studies showing an obesity-seed oil connection:

In one study, rats were divided into different groups receiving diets identical in fat, protein, and carbohydrate calories but differing in the source of the fats. The rats in the group receiving fat from safflower oil had a 12.3% increase in total body weight compared to the rats eating traditional fats [6].

In a randomized trial on rabbits, three groups of rabbits were given access to identical foods, with only one difference: the first group of rabbits was fed unheated vegetable oil, the second group was fed vegetable oil that had been heated once, and the third group was fed vegetable oil that had been repeatedly heated multiple times. Everything else about their diets was kept the same [7].

The outcome? Compared to the group of rabbits eating unheated oil, the group eating single heated oil gained 6% more weight, and the group eating repeatedly heated oil gained 45% more weight!

A 2020 study in mice showed that consumption of soybean oil leads not only to weight gain, but also to gene dysregulation that could cause higher rates of neurological conditions like autism, Alzheimer’s disease, anxiety, and depression [8].

In another mouse study, feeding mice the equivalent of 2 tablespoons of canola oil per day is associated with worsened memory, learning ability and weight gain, along with “considerable neuronal damage” and increased formation of beta-amyloid plaques, the signature of Alzheimer’s disease [10].

Links 8 and 10 are to news sites, not to the original research papers, but as far as we can tell, 8 is probably this paper and 10 appears to be this paper.

We do want to mention at this point that all of these studies were conducted on animals, not humans. (Nobbs also knows this, of course.) We recognize the value of animal studies and we often cite them ourselves, but it’s curious that there seem to be no studies showing that seed oils cause weight gain in humans — more on this in a bit.

These sources describe what Nobbs says they do, showing connections between seed oil consumption and weight gain. And in fact there are many other studies that also show this connection — this study shows soybean oil led to more weight gain than other oils (in mice), this study shows soybean oil led to more weight gain than fish oil and palm oil (in rats), and this study shows safflower oil led to higher levels of leptin (but not body weight) compared to animal-based fats (also in rats).

However, there are also studies that show essentially no difference between seed oils and other oils in terms of weight gain. For example, in this study soybean oil led to an equal amount of weight gain as lard and palm oil, and canola oil led to less weight gain than the other three (still in rats), and in this study lard, sunflower oil, and palm olein oil led to nearly identical weights (mercifully, in vervets this time). 

Many other studies find the exact opposite, that seed oils cause less weight gain than other fats, including animal fats. For example, this paper found that a butter-rich diet led to more weight gain than a canola-rich diet (in rats), this paper found that a lard diet led to greater weight gain than safflower oil (in mice), and mice that were started on a lard diet and then switched to safflower oil actually started losing weight, this paper reviewed the literature and found that pretty much any high fat diet leads to some weight gain (in rats and mice), and the paper Body Fat Accumulation Is Greater in Rats Fed a Beef Tallow Diet than in Rats Fed a Safflower or Soybean Oil Diet found what it says on the tin. 

Even this is only a small selection of the large number of papers on this topic. Some of these papers are probably better than others — some we should take seriously, and others we should discount. Probably a bunch of these studies are crap. If someone wants to do a deep dive into these papers, and all the other ones out there, to try to figure out the state of the literature, we would be interested in reading that piece. But even if someone did a deep dive, we doubt there would be a clear result. It’s hard to look at this literature and say anything more than “wow that looks complicated”.

This is just one of those very large literatures where you have to be careful about drawing a conclusion from only a few studies. “Some studies where seed oils lead to more weight gain than other fats, some studies where they lead to less, and a couple studies where there’s no difference” is what we should expect to see if there is a small effect in either direction, or no effect at all.

There certainly doesn’t seem to be a strong effect here. If the effect were strong, it would be detected more reliably. So if seed oils have an effect on weight gain (in mice, rats, and vervets), it’s a weak effect at most, and it’s not clear from the evidence whether seed oil causes more or less weight than other fats.

Another problem with the weight gain results in rodents and monkeys is, why do none of the human studies find the same thing? Nobbs cites a number of studies on people, but none of the ones we looked into show any evidence that seed oils cause weight gain in humans. 

Let’s take a look. The Los Angeles Veterans Administration Study specifically mentions, “the unrestricted consumption of the two diets had no significant effect on average body-weight.” The Minnesota Coronary Experiment reports BMI in both conditions and finds them to be nearly identical, 24.6 versus 24.5. 

The MARGARIN Study reports BMI for all conditions and finds no difference in people who ate diets with margarine made with more fat from vegetable oil versus margarine made with less fat from vegetable oil. 

The Sydney Diet-Heart Study had two groups start out with similar BMIs (25.4 vs. 25.1) and BMI in both groups went down by a similar, small amount (ending up at 24.5 vs 24.3) after 12 months, regardless of whether they were eating mostly safflower oil and margarine, or mostly olive oil and butter.

These studies generally run for several years and have much higher sample sizes than the studies run on animals, and of course they’re looking at humans. If there’s no evidence in these studies that people gain weight when eating seed oils, then any effect of seed oils on weight would have to be very small or very subtle. Or, there might be no effect at all.

In fact, this is pretty strong evidence against seed oils causing obesity. If seed oils cause weight gain when people eat them, why didn’t seed oils cause weight gain when people ate them? Sure we didn’t review every study out there, but these are four rather large studies (a couple hundred to a couple thousand people each) and all of them show an effect of seed oil on weight that is absolutely zilch, bupkis, nothing. This is more than “no smoking gun”, this is “suspect was in another country giving a speech in front of 10,000 people on live TV.”

Rigor

And also… ok, we do want to pick on the rigor here, just a little.

Nobbs says, “In the Los Angeles Veterans Administration Study, the group of participants who increased fat from vegetable oil–while keeping total fat the same–were 82% more likely to die from cancer compared to the control group that didn’t increase fat from vegetable oil.” 

This sounds very impressive — but as far as we can tell, it is referring to this result: “31 of 174 deaths in the experimental group were due to cancer, as opposed to 17 of 178 deaths in the control group.” This is about 82% more in the experimental group, but as you can see, the absolute numbers are quite small. 

This difference is not even statistically significant, which the authors note, giving p = .06. In addition, they begin the discussion by noting, “The experience of other investigators using similar diets has not been the same.” They mention a couple other studies, including one from London which tested a diet high in “soya-bean oil”, where there were 6 cancer deaths in the control group and only one cancer death in the group eating a diet high in “soya-bean oil”.

We see something similar in the other studies. Nobbs mentions that “the group consuming more vegetable oil had a 62% higher rate of death during the seven-year study compared to the group eating less vegetable oil” in the Sydney Diet-Heart Study. Again, this sounds like a lot. We’re not entirely certain which result he’s referring to, but as far as we can tell this is also not significant, p = .051. In fact, every p-value reported in this paper seems to be between .02 and .13, which does not inspire confidence and is probably an indicator of p-hacking. Either way, the majority of these results are not statistically significant, and if we were to apply a simple correction for multiple comparisons, none of them would be.

In the MARGARIN Study, the “seven times higher” figure refers to one death in the less-vegetable-oil group and seven deaths in the more-vegetable-oil group. The authors note that this is “not significant because of the small numbers.” They don’t report a p-value here, so we double-checked their analysis just to be sure and found the same thing, p = .096.

The evidence in the Minnesota Coronary Experiment is a little more mixed, but the authors themselves do not seem to have access to the raw data, and in reference to the apparent increased mortality in adults over 65, say, “in the absence of the raw data, however, we cannot determine the statistical significance of this finding.”

Nobbs did a good job reviewing the literature and providing direct references to the studies he draws his conclusions from. But the literature on weight gain in animals is far larger and more mixed than many people realize, and doesn’t clearly point to seed oils causing obesity. The literature on seed oil consumption in humans consistently shows that seed oils cause no more weight gain than other fats. When we took a closer look at some of these studies, we found serious problems with several of the analyses. The evidence here is weak at best. 

This doesn’t mean that seed oils, or vegetable oils, or whatever you want to call them, are good for you. They may still be very bad for you, and the case for other health effects (including a connection with cancer) seems stronger. But it doesn’t look like they could be a major cause of the obesity epidemic, and probably, they play no role at all.


13 thoughts on “A Chemical Hunger – Interlude E: Bad Seeds

  1. Max says:

    Much easier to test effects of seed oil consumption with rats than with humans. As you pointed out seed oils are almost everywhere. So if a study is done with some people eating bread with butter and others bread with margarine the difference in seed oil consumption between the two groups might not be all that large.

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  2. Folkie says:

    I will play devils advocate here.
    “Seed oils have a hard time accounting for patterns like obesity being related to altitude, and wild animals also becoming obese. ”
    I have more trouble with the wild animal part.
    If vegetable oils pathway is the pro-inflamatory action of omega-6 fatty acids, altitude is sorta known to improve imflamation markers. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0070081
    It could also help compounding with pollutants by increasing inflamation levels in the liver similar to how PNALD in the US was caused by soy bean oil formulations while the epa/dha heavy formulations avoided the problem entirely. More adult livers will process pro-inflamatory compounds better, but maybe they add yet more stress to the liver and reduce how much of certain substances like pesticides it can detoxify.
    This argument probably might also work for products with high free fructose content.
    In any case, there’s likely not a single cause.

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    1. Brennan says:

      Oh, it also explains another mystery with obesity that you DIDN’T mention – that despite obesity being heavily correlated with the per capita gdp of a COUNTRY, it’s also negatively correlated with income WITHIN countries – poor folks in the US are much more obese than the rich, despite poorer countries having lower overall obesity rates.

      This sounds like a paradox until you realize that processed foods are extremely cheap, but only widely available in highly industrialized societies, people in non-industrialized countries still mostly grow their own food and/or buy raw ingredients directly. While richer people in America can afford more expensive whole foods and have time to cook for themselves or money to hire someone.

      The same mystery is also IMHO a big argument against the contaminant theory, there’s no obvious reason why socioeconomic status or being Hispanic would universally expose you to more hypothetical contaminants, but those groups have historically tended towards highly processed foods due to reasons of cost and convenience (and in many cases access, so-called “food deserts” often simply don’t have whole foods available!)

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      1. tweid says:

        I’d argue that actually, contaminant theory and processed food go hand in hand – after all, processed food is theoretically bad _because_ it is full of some particular contaminant, right?

        And all the way back in the first post, the author mentions the ‘cafeteria diet’ as one of the main mysteries. The potential (modest but real?) benefits of a whole foods diet comes up in Part III.

        That being said, I question the idea that status or race wouldn’t affect your exposure to contaminants. After all, incomes and ethnicity aren’t spread evenly across the country. Lower income people, in particular, might be forced to live closer to industry, or in crowded urban areas, which might have more contaminants (note the increase in lithium concentration in urban areas in Part VII).

        The link between income and obesity is definitely worth exploring, though, and I feel like there should be at least a post on processed foods and what kind of contaminants might be in them.

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      2. Brennan says:

        Somehow i messed up the threading on my original post, oops… Anyway, contaminant theory could certainly go with processed foods, but Occam’s razor would dictate that the simpler case would be that highly processed food in and of itself is sufficient to throw off our body’s ability to regulate fat storage and caloric intake.

        It certainly doesn’t seem implausible either, you hear a lot about the “hunger” hormone but hunger and satiety are both potentially relevant and have something like 12 different hormones involved in how we feel them – see here https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2777281/.

        It’s entirely reasonable that some of these hormonal responses dictating when and how much we eat simply don’t adequately adjust for the extremely high density and easily digested macro-nutrients in modern processed food. Or some of them could signal based on micronutrient density; or even the presence of compounds that aren’t nutritionally relevant but still common, or stuff like fiber in our intestines.

        Anyway, as far as environmental exposure to contaminants goes, again it’s not impossible or anything for it to be correlated with income! It would just seem to be a highly unusual pattern that affects specifically lower-income people in developed countries. Like you mention industry, but manufacturing, mining, industrial agriculture, etc are just as common in countries like China or India or Latin America and yet we often don’t see the same issues with obesity. On the other side of things, we see that countries like Palau and Tuvalu have huge recent issues with obesity, and they have basically no industry at all and rely on things like tourism and subsistence agriculture.

        At the end of the day, it just seems to me that y’all are looking for a contaminant that:
        – Is seemingly affecting every country in the world at ever-increasing rates
        – Affects specifically poor folks in countries, but only when they get rich
        – Is HEAVILY affected by national borders (compare Yemen to Saudi Arabia or Sudan to Egypt)
        – Started exposure in some countries as early as the turn of the 20th century but didn’t have an effect before that
        – Seemingly isn’t easily visible in blood or urine tests
        – Hasn’t been discovered to be HEAVILY correlated with obesity before now.

        With such restrictive conditions, it seems to me that the chances of there being something that fulfils those conditions are pretty vanishingly small no? Like it’d certainly be possible, but there’d be a truly astonishing amount of money involved in finding an obesity cause as simple as “this specific contaminant or agent” and the inevitable profitable cures this could lead to, I just don’t buy that it’s likely that no one has found something up ’till now 🙂

        On the other hand, convincing people to meaningfully permanently change their diet is hard as hell and not particularly profitable, and as you noted being mentioned in part III what evidence there is around whole food diets is very promising – and that’s only based on a few studies that essentially just involved a bunch of doctors saying “hey eat this way”. If the effect is real, there is no doubt in my mind that a truly controlled trial on patients in a controlled setting where ALL food intake could accurately be monitored would show even better results – both compliance and reporting accuracy are notoriously poor for participants in nutrition studies haha

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  3. Mahmud says:

    So far this doesn’t seem to be any more compelling than the antibiotic hypothesis article.

    The two strong ones seem to be lithium and PFAS with (I think) lithium being the stronger of the two but PFAS giving it a run for the money. Good on the astralcodex team for intensifying the case for lithium.

    Perhaps plastics or microplastics is the next area of research? Also perhaps some contaminants popped up in the 70s and mysteriously didn’t show an effect until the 80s so there may be something there.

    Something, God knows what, happened in this era.

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  4. Brennan says:

    Boss, there’s a pretty simple explanation that I don’t think anyone has mentioned yet – that highly processed food, regardless of nutritional content, causes obesity.

    The most recent study on this is this one https://www.cell.com/cell-metabolism/fulltext/S1550-4131(19)30248-7, which mentions many related studies and found that when letting randomly assigned people eat as much as they wanted of nutritionally matched ultra processed and unprocessed diets, the ultra processed diet group gained roughly 1 lb a week and ate ~500 more calories daily, while the unprocessed group actually LOST about a lb a week.

    Of couse, this doesn’t rule out the presence of a contaminant or pollutant in ultra processed food that is responsible for the effect, but it explains ALMOST all the mysteries you mention.

    – TV dinners and the like originated in the 50s, when we start to see the trend towards higher BMI. Foods have continued to get more heavily engineered and processed since, and make up a higher than ever portion of american diets. Old folks who actually cook for themselves have basically died out, explaining why older folks are now fatter than younger. Looking only at obsesity instead of average BMI also obscures that BMIs were rising earlier, just to a less extreme level (consistent with a smaller percentage of the diet composed of processed foods)
    – No government that I’m aware of has taken steps to avoid consumption of processed foods, and it’s only until recently that they’ve been theorized as a culprit at all.
    – Traditional diets across the world vary ENORMOUSLY but almost never result in obesity. In comparison, I’m not aware of a single country that has not trended towards the convenience and low cost of highly processed food as they industrialized, and we’ve seen the exact same trend towards obesity in industrial nations across the world.
    – The effect likely exists independent of macro and micronutrient composition, so changes in fat, sugar, or vegetable oil consumption don’t affect it.
    – Animal food has ALSO grown more processed, including not just pet food but also lab animals and feral animals who eat human food (indeed, you linked a study to this effect when talking about rats growing fat on a cafeteria style diet! the SC rats maintained consistent weight on a diet that was functionally just ground up grains and pig meat/bones)
    – Diets don’t work because participants only lose weight due to strict calorie control, and when going back to eating normally after weight loss the processed foods ’cause them to gain weight back again. This is also why there’s no “magic bullet” diet – some diets like vegetarian diets (see here https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5466943/) seem to maintain lower weights, but it’s fundamentally because they tend to consist of less processed foods – after all, American meat consumption hasn’t risen THAT much since the 19th century, though it has risen somewhat.

    Of course, it’s likely there are other factors at play as well. The variations by altitude aren’t easily explained by this, and it’s almost certain that other metabolic or genetic factors can affect the weight gain caused by processed foods or make certain people and groups susceptible to obesity from them.

    But I’m not aware of any other theory that is both strongly supported by all the studies done so far in both humans and animals, and so easily and convincingly explains how obesity and metabolic syndrome have very consistently risen in frequency in every country and population in the world as they industrialized. When you feed people or animals processed food, especially junk food, they almost invariably eat more calories and gain weight without intentional aggressive caloric restriction, and if you feed people exclusively whole foods and unprocessed foods they don’t.

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  5. Oriol says:

    Although the oil theory isn’t a smoking gun for sure, the usage of different fats in Europe (France with higher usage of butter than the US, or Spain and Italy using mostly olive and sunflower oil) might help explain some of the variance on the data.

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  6. mkg says:

    Perhaps lipid oxidation rate explains the correlation with higher altitudes. Seed oils oxidize faster in humid and hot conditions and the effect is large. And of course, oxidize faster in the presence of more oxygen. This would predict that cold, dry, low oxygen environments (i.e. colorado) will see much less oxidation and that hot, humid environments (the Mediterranean / middle east) will see much more oxidation. Perhaps this also explains the middle east being an outlier in obesity rates (and also an outlier in import rates since nothing grows in the desert, allowing for more time to oxidize their oils).

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6657719/
    https://www.frontiersin.org/articles/10.3389/fpls.2020.573681/full

    http://www.kuwait.climatemps.com/humidity.php#:~:text=The%20average%20annual%20relative%20humidity,July%20to%2065%25%20in%20December.

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  7. Jonathan says:

    Seems to me that the professions highest in obesity are also the most stressful jobs. Since stress is related to weight gain, perhaps this is a confounding variable?

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  8. Audax says:

    I think this undersells the case that vegetable oils are contributing to obesity. The hypothesis is that an environmental contaminant causes obesity, right? But if you consider linoleic acid or some other major component of vegetable oil as a contaminant, it seems unfair to use human studies where they switch people to vegetable oil for only 12 months and say that proves that it can’t cause obesity:
    >”If seed oils cause weight gain when people eat them, why didn’t seed oils cause weight gain when people ate them?”
    Compare this to the PFAS section where none of the human PFAS examples have a one-year exposure in adulthood that causes obesity. If you did this, maybe it would cause obesity, but if it didn’t then it wouldn’t disprove the PFAS hypothesis. For PFAS it looks like exposure over the course of life, including pregnancy and early childhood. Or persistent decades-long occupational exposure. This is the exact type of “exposure” to seed oils in the form of fried foods and packaged foods that happens, particularly among poorer people. (Think of the type of fat in the food you can find in a gas station — “Motor Vehicle Operators” are the highest obesity profession)

    Animal obesity is one of the mysteries that seems to point away from soybean oil and other seed oils. But the animals https://royalsocietypublishing.org/doi/10.1098/rspb.2010.1890 were being fed by humans, not eating a wild-type diet. I don’t find the assertion that their diets were consistent over the course of decades because they were “lab-controlled” convincing. Can we really be sure that the fats that made their way to primates in a cage in California stayed exactly the same at the same time that the fatty acid distribution for the entire human food supply and the literal biomass of humanity was radically changed? That they fed the primates the exact same type of grains for 30 years? If they’re feeding them meat, the fatty acid distribution of the meat has changed because of the changes in animal feed.

    The other citation was for horses. Look up contemporary horse feed and you’ll frequently find dehulled soybean meal, soybean oil, ground soybean hulls and the like.

    Liked by 1 person

  9. Daniel says:

    Review of the actual raw data of the Minnesota Coronary Experiment:

    Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73) (https://www.bmj.com/content/353/bmj.i1246)

    Conclusions:

    Available evidence from randomized controlled trials shows that replacement of saturated fat in the diet with linoleic acid effectively lowers serum cholesterol but does not support the hypothesis that this translates to a lower risk of death from coronary heart disease or all causes. Findings from the Minnesota Coronary Experiment add to growing evidence that incomplete publication has contributed to the overestimation of the benefits of replacing saturated fat with vegetable oils rich in linoleic acid.

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  10. I was just rereading this and realized a flaw in the point about the Sydney Diet-Heart Study. The participants are already not fat (BMI of ~25). They have a good deal less weight to lose, and it would surprise me if that were not very relevant to the amount they could lose.

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