A Chemical Hunger – Part V: Livestock Antibiotics

[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]

Obesity in the United States – Dysbiosis from Exposure to Low-Dose Antibiotics? suggests that the obesity epidemic is driven by population-wide exposure to residual antibiotics from livestock cultivation, and the resulting impact on gut microbiota.

This is one of the most similar proposals to the theory presented in A Chemical Hunger, though they don’t go quite as far as we do, still attributing some of the influence to diet and exercise: “Most reports attribute the obesity epidemic to factors such as excess food energy intake, changes in diet and eating behavior, and increasing sedentary life style. Undoubtedly, these factors contribute, but can they all account for the rapid increase in this problem that occurred over the last two decades?”

They make a pretty compelling case. A large percentage of antibiotics are excreted in animal waste and end up in the water supply, where they affect natural microorganisms. Relevant to our interests, antibiotics are more and more prevalent in rivers as they make their way towards the ocean: “The only site at which no antibiotics were detected,” they write, “was the pristine site in the mountains before the river had encountered urban or agricultural landscapes. By the time the river had exited the urban area, 6 of the 11 antibiotic compounds that were monitored were found in the samples. At Site 5, which had both urban and agricultural influences all five of the TCs monitored were detected.”

Exposure has increased in the US over time, closely matched with the increasing prevalence of obesity — “practically overlapping with the counties with the highest obesity prevalence in the US.” Similar trends can be observed in other countries. For example, in Great Britain, by 1958, around 50% of British pigs were fed antibiotics, and nearly all piglets were given food containing tetracyclines. In West Germany in the 1960s, an estimated 80% of feeds for pigs, calves, and poultry contained antibiotics.

The Effects on Human Health of Subtherapeutic Use of Antimicrobials in Animal Feeds opens by saying, “The food-producing animal and poultry industries have undergone a dramatic change that began around 1950.” That’s a little earlier than we would expect, but depending on how you measure things, it took until the 70’s or 80’s before things really got rolling.

In meat animals, antibiotics often lead to weight gain, sometimes as high as 40% weight gain compared to control, and there’s reason to suspect that this might be linked to the microbiome. Gut microbiota influence energy intake and body weight in mammals, and even short courses of antibiotics can reduce gut microbiota and increase BMI in humans (though the BMI effect was only seen in some antibiotics).

There’s even a study where they put fecal matter from human twins into germfree mice. (This is one of the more creative study designs we’ve seen.) They started by finding pairs of twins where one twin was fat and the other twin was lean. This is pretty uncommon — normally, twins weigh the same amount. They transplanted fecal matter from the twins into mice and found that mice that got fecal matter from the obese twin gained weight — unless it was housed with one of the mice who got fecal matter from the lean twin.

However, there is also evidence against this picture. For one thing, Germany, Spain, Italy, and Japan all use a lot of antibiotics in their meat, and none of these countries is particularly obese. Australia and South Africa are both pretty obese, but both of these countries use less antibiotics than usual. This could maybe be reconciled if these countries use different kinds of antibiotics, but we would need to see that case made to evaluate it.

There’s also some evidence in favor of this theory that this paper didn’t review.

For one thing, people who eat fewer animal products have lower BMIs, and the effect seems to be dose-dependent. In a sample from 2002-2006, average BMI was lowest in vegans (23.6) and incrementally higher in ovo-lacto vegetarians (25.7), pescitarians (26.3), semi-vegetarians (27.3), and nonvegetarians (28.8). We can note that the BMI for vegans is about the same as that found in hunter-gatherers and in Civil War veterans in the 1890s. That said, everyone in this sample was a Seventh-Day Adventist, so they may not be all that representative.

India and Japan are the least obese of the developed countries. Both have obesity rates below 5%. India is the most vegetarian country on the planet and Japan, while not especially vegetarian, mostly consumes seafood in place of meat products.

This would mean that vegan diets would work really well for weight loss, right? Well, maybe. As we previously reviewed, all diets seem to work a little, and no diet seems to work all that well. We see something similar in vegetarian and vegan diets. A 2015 meta-analysis found that people assigned to vegetarian diets lost more weight than those assigned to nonvegetarian diets. People on vegan diets lost a little more weight than people on vegetarian diets, about 5.5 pounds (2.5 kg) to 3.3 pounds (1.5 kg). The studies differed quite a bit in the size of the effect, but all of them had similar conclusions. The other meta-analysis from 2015 found the same general pattern, and individual studies comparing different types of vegetarian and vegan diets seem to confirm this dose-dependent trend.

This looks a lot like other studies, where the differences between diets are technically reliable but so small as to be basically meaningless, but the possible dose-dependent effect is interesting.

The most interesting study might be this one, that compared a vegan diet to a conventional low-fat diet. So far so standard, but unlike most diet studies, which end after 12 or 18 months, this one followed up two years later. The vegan group not only lost more weight (4.9 kg versus 1.8 kg), they kept it off better at the two-year followup (3.1 kg versus 0.8 kg). On most diets people lose a little weight but then gain it right back, so the fact that people kept most of the weight off for two years is interesting. Even so, the amount of weight lost in an absolute sense is still quite small. It could take more than two years on a vegan diet for you to see all the effects — but if this were the case, you’d think people would have lost even more weight by year two, but that’s not what we see.

None of these are smoking guns. At best, they are consistent with the idea that some of these contaminants are more prevalent in animal-based foods. And we know that this can’t be about the animal products themselves, because hunter-gatherers and our ancestors in 1890 ate lots of meat and didn’t experience modern levels of obesity.

Consider:

Source: Wikipedia. Radioactive barrels not to scale.

Environmental contaminants tend to build up in animals through the plants they eat, so any contaminants in the environment will bioaccumulate, and concentrations will be higher in animals than in groundwater or in plants. Compounds in a farmer’s fields will end up in the corn or alfalfa fed to their cows, and the cows will end up getting an even larger dose, which will be passed on to the person who eats the resulting cheeseburger. So the fact that meat consumption is linked to obesity doesn’t necessarily implicate antibiotics. It could be something else in the meat.


[Next Time: SUSPECT NUMBER TWO]


18 thoughts on “A Chemical Hunger – Part V: Livestock Antibiotics

  1. r_c says:

    Do we know if the problem could be the absence of a natural product rather than the presence of a contaminant?

    e.g., antibiotics wipe out populations of bacteria in the environment but these populations produce natural products required to prevent obesity. How would we measure the presence of absence? Should we expect bacterial populations to consistently produce anti-obesity natural products on a global scale across all geographies? Unlikely but worth ruling out systematically.

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  2. rcastillo0516 says:

    Do we know if the problem could be the absence of a natural product rather than the presence of a contaminant?

    e.g., antibiotics wipe out populations of bacteria in the environment but these populations produce natural products required to prevent obesity. How would we measure the presence of absence? Should we expect bacterial populations to consistently produce anti-obesity natural products on a global scale across all geographies? Unlikely but worth ruling out systematically.

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  3. filipp8 says:

    Great work! Looking forward to read what’s next. I am wondering how environmental contaminants could explain Italy’s north south divide in obesity rates. So far most would explain the problem with dietary and sport differences net of educational level (+ higher prevalence of low educated individuals compared to the north).

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      1. filippotto89 says:

        There is free access microdata at the regional level (Multiscopo, see here: https://www.istat.it/it/archivio/129956) and several surveys conducted by the Istituto Superiore della Sanità (ISS) on different ages that would in principle allow to look at provinces (e.g. https://www.epicentro.iss.it/okkioallasalute/indagini). I can help navigating the websites if interested. I tried to ask for the primary school children data because the ISS survey is incredibly rich (cross section repeated with around 50.000 8-9 yo) but I eventually gave up – well, they actually gave up on me and stopped replying (not an easy country when it comes to data sharing).
        Italy is a pretty interesting case study because many Italians moved (and move) from southern regions to the north, and because differences across regions are incredibly high (Children: https://www.epicentro.iss.it/okkioallasalute/indagine-2019-dati and Adults: https://www.epicentro.iss.it/passi/dati/sovrappeso?tab-container-1=tab1).

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  4. George Herold says:

    Yup certainly one candidate chemical. Just to make things more complicated, it could be that exposure during some part of our life cycle is what sets the lipostat (the fat ‘setpoint’.) Like in the womb, or breast feeding, or during puberty. It seems like there must be more than ‘just something in the diet’.

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  5. Mahmud says:

    Does this suggest an antidote is a special extra level of pro-biotics? I know a few like LG have been shown to reduce visceral fat.

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  6. Jack Peterson says:

    There’s a (somewhat related) natural experiment kicking off in Taiwan that you might find interesting. For a long time, Taiwan had banned US pork imports due to the presence of ractopamine, but just last year they reversed course and decided to allow US pork imports (https://www.reuters.com/article/us-taiwan-politics/taiwan-lawmakers-approve-imports-of-additive-fed-u-s-pork-idUSKBN28Y0ZF).

    Ractopamine is not an antibiotic. However, it seems particularly relevant as a potential obesity-promoting contaminant because it is added to feed in order to increase weight gain. (Specifically lean muscle, but any food additives that are put there with the goal of messing with animals’ natural weight seem highly suspicious to me.)

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  7. gerard says:

    I was very interested in your serial at first, then after thinking more I think it’s a fool errand to search for an unique reason, a smoking gun, and it’s part of the very american search for a quick fix (well, maybe you are not from the USA I just don’t know but if not you should be:-))
    Looking at the number for different countries you see so many variations that it’s difficult not to think that there is no single cause: for example, if a single chemical compound was the culprit, why in some countries should the men be more overweight, while in other countries it’s the women ? It does not make sense, we are a single species so it’s difficult to avoid the conclusion that social norms have an influence (young women need to be slim to find a partner in many countries tradition). In my country the poor people are markedly overweight, obesity is diminishing according to wealth. Also in the USA the Amish are a marked exception to the general tendency, but it does not seem to be related to what they eat (they eat a lot BTW): Amish people having sedentary occupation (a small proportion) seem to get overweight too.
    So in a word, weight regulation is managed by a lot of mechanisms, some social. When all are removed by progress, things go awry. I think that in my country rich are slimmer because they work more: they work more because they are rich, success is marked by having a second home, *owning* a second home: it means having to manage it, and it’s a lot of work. These houses have 2 level and there is a stair between levels (installing a lift in a family house would be insane at the current price levels). Week-ends are busy for the rich, while poors are in a rented social housing, with nothing special to do in the week-ends -they are not allowed to make changes in their flats, and most breakage are covered by the rent. Social housing have typically 5-6 levels but these days there is always a lift (it’s mandatory because of disabled people). Lifts were not common in 1970 in my country. As we are a bipedal special there is not much penalty to walk wearing some weight, but as soon as you begin to climb, it’s painful. If you have 5 levels of stairs to climb, you are reminded that you need to regulate your eating. Remove this problem thanks to the magical lifts, and eating too much is not so much of a problem. Very rich people can make other people do jobs in their many houses of course, but once the social pattern has set that poor=fat, they can’t afford to get overweight as it would be a social status loss, so they exercise/diet.
    Your altitude mystery could be explained also in this way: usually high level countries are mountains, where you have to actually climb hills to get to a lot of places…

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  8. MTSowbug says:

    The link at “In meat animals, antibiotics often lead to weight gain, sometimes as high as 40% weight gain compared to control” does not lead to an article. Could you revise the link, possibly with a DOI?

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    1. Thanks for catching this. The paper is from 1950 and as far as we can tell, doesn’t have a DOI. Unfortunately we can’t find a better link (if anyone reading this has one, we will happily replace the current link), but the citation is:

      Luecke, R. W., McMillen, W. N., & Thorp Jr, F. (1950). The effect of vitamin B12, animal protein factor and streptomycin on the growth of young pigs. Arch. Biochem., 28, 326-327.

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