Why I Mostly Eat Vegetarian Food

To begin, that title is very precisely worded. I am not a vegetarian. I am not a vegan. I have been teased because I’ve incautiously used the phrase “I’m mostly vegetarian” in the past. No, I choose to eat vegetarian (or even vegan) food, most of the time. This may be a confusing (and possibly indefensible) position but it is accurate. I have that choice, though, because I am no where near poverty or starvation (and, even at my poorest, starvation was pretty remote). But given that I have a choice, why do I?

Why Post This?

A couple weeks ago, a friend asked me (on twitter) if I was mostly vegetarian. This led to a brief discussion as to why but more specifically issues of labeling and honesty. I realized that perhaps I should post something because my eating choices aren’t just an arbitrary preference: they are triggered from real ethical concerns and writing about them might just draw a bit more attention to an issue I consider important.

To state that another way: I think humans (especially in the wealthy “developed world”) should be producing and eating fewer animal products. If that angers you, then this post will anger you. For some, it’s uncouth to talk about your moral positions as regards food, but less so for other things1. If it seems like I’m preaching, then perhaps I am. Does this mean I’m judging you personally, whoever you are? Honestly? Probably not. I’ve got better things to do. But I do wish the question received a bit more consideration.

Environmental Impact and Efficient Use of Resources

When I first modified my diet from “whatever I felt like”, I stopped eating seafood. Many fish and other sea life are endangered or threatened. Even animals with robust populations are often captured in extremely damaging ways. These days I will eat some seafood, but it’s because I have more information and understand the issues better.

But if I was giving up fish because of environmental damage, what about meat? Meat production is expensive (in resources) because we’re eating an animal that itself has to be fed. Since there’s not enough grass for the numbers we raise, we grow food for animals. In many cases, we could grow more food to directly eat rather than feeding it to animals.2 Somewhere around 80% of corn grown in the United States feeds animals. A great deal of the soy is also fed to animals. Most of this corn and soy is grown in huge monoculture fields, very intensively, using many inputs in the forms of pesticides, fertilizers, machinery, etc. The inputs could be used to support more direct food for humans — corn and soy are actually tasty and nutritious foods themselves. How many people could be fed using that land?

But the fertilizer and pesticide run-off and soil erosion are a huge problem. The Gulf of Mexico Dead Zone is a region of the ocean that intermittently becomes low in oxygen due to algae blooms feeding on nitrogen and phosphorus run-off. Low oxygen kills much of the life. Given how much agriculture in the Mississippi watershed supports raising animals for meat, the Gulf of Mexico Dead Zone may largely be due to our society’s consumption of meat. If we weren’t trying to feed so many animals, would runoffs be as disastrous?

Related to all of this is of course the problem of climate change and greenhouse gas emissions. There’s a lot of information on the internet only a google away, so I’ll leave you with a NY Times summary of a relatively recent consumer-oriented report on the emissions related to different types of foods. Short version: animal-based foods result in more greenhouse gas emissions than vegetable-based foods. One critical point that I personally needed reminding of is that cheese is actually worse than many meats and fish (e.g. tuna and chicken).

Animal Rights and Humane Treatment

This section was originally named “animal abuse” because that is what modern industrial animal “husbandry” looks like to me. Few would support treating a family dog the way cows or chickens are treated in a factory farm. I’m not going to describe these conditions. It’s frankly not something I want to summarize. Suffice to say that standard industrial animal conditions are cramped and diseased. There’s a reason antibiotics have to be used.

Even if the animals aren’t abused, what does it mean to eat meat? Eating meat (or fish) means: I’m ending the life of another living creature not much different from me. I don’t have an answer for myself, but I find myself increasingly uncomfortable with the idea of ending the life of an animal, especially vertebrates and octopi. Some of my favorite reading (and video) is about the diversity and complexity of life. How amazing it is that there’s all this life! And each little bit is doing its own little thing, whatever that is, in its own little place. Ending one of those lives seems pretty similar to ending my own and maybe I should consider that. It’s not that I learned anything new recently. I just seem to be interpreting differently. I don’t know that this perspective will entirely change my behavior, but it’s there.

Notional Vegetarianism

Even before my friend asked that question, I’ve usually eaten vegetarian food. But since I was raised on meat (and especially beef), it is tasty to me. I don’t have a visceral disgust to the idea of eating meat. So I’m regularly (once a month perhaps) tempted by some beef (always “hippie beef” as I call it3). Very occasionally at a party or the like, the lure of bacon will catch me. I loved sushi before I mostly gave up fish, so I more frequently eat certain types of fish and seafood (e.g. local shellfish or domestic catfish or supposedly sustainable sushi). Though these exceptions are pretty rare because it’s often socially and practically infeasible to “be sure”.

But I do make exceptions. Sometimes it’s just easier. Or someone brought something very interesting looking to a party. Or our order was misunderstood at a restaurant and the item would go to waste. Or I’m at a very fancy restaurant and the interesting options involve meat or seafood (I sometimes call this “cultural eating”). Or I’m at a bar with a lot of friends and my only “safe” options are french fries and I know that only eating fries will make me a grumpy person all evening.

I’m not a saint and sometimes I rate my own hedonistic pleasure or social norms above consideration for the environment or animals. Waste bothers me a lot, so it’s easy to make an exception for non-vegetarian food that would otherwise be wasted. I rationalize and compromise with the world. But that sits less comfortably this week as I consider when and why I make exceptions.

The Fuzzy Shifting Line

So … what? I’m not eating vertebrate meat at all right now4. Most dairy or eggs that might be available to me while eating out is going to be factory-farmed, so that should be out (though until recently I too often ordered the eggs or cheese because it’s tasty). At home it’s pretty easy to eat vegan when I want. Aside from cheese and eggs (these at least I can be mostly sure don’t involve animal abuse), our groceries rarely include anything non-vegan. Almost all fish are right out, of course. Shellfish aren’t out for any (firm) reason, but it’s probably simpler to just not eat any seafood at all (and easier to explain too). I will likely sometime eat meat again, but I imagine it will be much less often than previously.

So, I’m still not a vegan or even strictly vegetarian. All I can say is that I mostly eat vegetarian or vegan food. And maybe this post will make a few more people think about eating less meat.

  1. I would include specific examples of less fraught moral discussions — whether spanking is child abuse or whether anonymous political donations are okay, for instance — but I suspect that would derail the argument when someone reading doesn’t agree that my particular choices are acceptable for polite discussion. So I put it here in a footnote.
  2. But, you might say, is that we could raise ungulates on grass in marginal lands that couldn’t be used for other agriculture. Raising meat animals on marginal land is a good use of resources if that’s your only option. But we have other options and a lot of marginal land use is increasingly destructive.
  3. Though perhaps “yuppie meat” would be a better phrase these days. It’s curious to me that everyone I talk to about this knows what I mean by “hippie meat” though.
  4. We’ll see how long it lasts — meat, especially beef, is tasty to me.

A Little Idea from Science Online Seattle

Monday, I went to the first event for Science Online Seattle. I had seen a tweet last week about it and signed up on a lark. I wasn’t even sure I would go — it doesn’t seem necessarily like something for a non-scientist. I was encouraged to go when I realized that someone I already knew was going. Still, it’s a little strange to show up in a law school classroom (very nice classroom with outlets at every seat!) to a room full of strangers that you are under the impression are all Awesome Scientists. Fortunately, most of the discussion was about how to make science more accessible and useful to researchers, journalists and “laymen” alike. The livestream is available online so I won’t try to summarize all the points. The twitter #sosea hashtag has a lot of side discussion and comments.

Engaging the Public

One topic1 brought up was that researchers in government agencies often can’t be open about what they are working on — strict public relations policies and risk aversion means that there’s little incentive to, for example, keep a blog of a research trip. One person even joked that no one wants pictures of a researchers having fun because a Congress person will see it and complain about wasting taxpayer money! Another issue brought up was how certain scientific questions (e.g. climate change) are extremely politicized. Another common theme was funding — crowd funding was brought up as an alternative to traditional methods (government funding is getting tighter) and specifically the new site Microryza which, in short, is Kickstarter for researchers2. The game Foldit is harnessing human minds to solve problems and lets non-scientists participate in science. Half the talk of the night was how to engage the public.

If you’ve read previous posts, you know that I care a lot about the public not being (mis-)led by fearful information about science. That hypothetical Congress person can only criticize researchers having fun on a trip if her constituents believe that narrative. But they won’t find it a meaningful narrative if it’s a common pastime for “normal people” to follow researchers groping with hard questions or posting neat pictures of the fruits of research. Climate change science “scandals” wouldn’t be so scandalous if people engaged more with scientific questions and the inherent ambiguity of results.

A Modest Suggestion

But how do you engage the public? Most people aren’t scientists or really have much training in it. Many think of scientists as a special priesthood. Some think that priesthood isn’t up to much good. But, in general, I think many people just feel disconnected from it: it’s not something “normal” people can be involved in. It’s too hard to understand. Non-experts can’t really judge.

The main products of research are journal articles. Many of them are essentially paid for by the public already. In any case, many are pretty freely available (though not enough!) “Gatekeepers” — journalists and scientists explaining new results — are useful to provide context and background. But that’s not enough.

Let us, the “layman”, actually read science articles! They are usually pretty short. Good ones are readable, even if you have to skip the statistics or spend a few minutes finding out what a word means. Bad ones often are confusing even ignoring the math. Exposure to the reasoning necessary to “prove” something exposes you to the complexity and ambiguity of science. Would people be so worried about the current scary health news story if they more often read the reviewed article and not just the overblown press releases? When the news claims the sky is falling but the journal article mentions only a small unexplained change with myriad possible explanations, would people worry so much? When an opinion piece doesn’t even link to good sources, would we pass it around credulously?

I realize it’s pretty optimistic to believe people (possibly with poor science and math basic education) would want to (or even be able) to read journal articles. I wouldn’t expect everyone to always go read the article that’s a source for the news. While I think even occasional article reading would improve how people view science, I don’t know how to get there. I just know that I get a lot out of them, even as a non-scientist3.

So, my non-scientist friends reading this, I hope you try reading a journal article sometime soon. It won’t be as mystifying as you think. Pick a topic you care about or a news story that worries you. Google the article title and you’ll probably find it. Feel free to skim it. Ask questions. Google the unknown words. Science is understanding the universe around you and that article is describing only a very, very tiny piece.

  1. I’m not really going to try to attribute specific thoughts to individuals. In one case I remember who said it, but for the rest I don’t recall exactly. I might be able to figure it out from the livestream but I’ll inevitably get a bunch wrong.
  2. Though thankfully they don’t require projects to have concrete results. Research just doesn’t always go where you expect!
  3. An undergraduate “computer science” degree doesn’t make me a scientist or even terribly more educated about science than most. I only took one semester each of chemistry and biology which is no more than humanities and non-technical degree programs at my school.

Is industrial farming causing antibiotic resistant infections?

In my last post, I summarized a few of the, to put it politely, bad outcomes of industrial animal agriculture (“factory farms”). This style of very intense animal husbandry is mainly feasible because of antibiotics1. But the current attempts to regulate antibiotic use have little to do with abuse of animals and everything to do with fears of disease in humans. In the previous post, I mentioned that there were “surprisingly few documented cases” of antibiotic-resistant bacteria being bred in livestock and then transferring to humans. I based this on my fairly limited memory of cases mentioned in Superbug by Maryn McKenna. I’d remembered being surprised when I read that book how few cases she gave.

I should have dug into this more. The reality is that there is much more evidence for it that I’d imagined, but that the evidence is complicated.

Why is it hard to answer?

The cases I’d remembered from Superbug were the (seemingly) straightforward cases where a human infection was found to be from a antibiotic-resistant bacteria and there was a simple causal link back to a farm where antibiotics were used and the animals carried the same strain. It’s not actually simple or easy to prove these. The steps seem simple enough:

  • Human is sick with an antibiotic-resistant bacterial infection.
  • Human recently interacted with a source for the infection, such as eating contaminated meat or working on a farm.
  • Animals on the farm are carrying the same strain as the human.
  • The animals were treated with a related antibiotic.

But all of these steps are remarkably hard to prove in practical terms. All kinds of problems can crop up:

  • How do you prove that the resistant bacteria X causing an infection didn’t gain the resistance factors from normally harmless bacteria Y that the patient already had?
  • You can’t identify the source of the human infection clearly. This is especially difficult if you don’t have full data. What if the infection is Salmonella but the patient hasn’t eaten any obvious source (chicken)? The possible sources include every food item that might have been cross-contaminated. The FDA has become really good at this for food products not expected to have contamination (candy, vegetables, etc) but generally no one bothers to trace infectious agent origins unless a lot of people are affected.
  • The source (such as meat) has to be traced back to the originated farm. This can be really hard. If you buy conventional ground beef in a grocery store, it could contain meat (and bacteria) from any of hundreds or thousands of animals from multiple farms, slaughtered at different times, etc.
  • By the time you find the farm, maybe none of the animals living there were part of the population from which your source was taken, so the expected strain may not exist in the population any more.

There are of course more complications possible. My main sources for the following are several review articles234. If you read only one of them, I recommend Swartz2.


Straightforward Evidence

These are cases where someone has traced a specific infection back to a zoonotic source.

  • A major outbreak of Salmonella in 1985 was traced from human consumption of hamburgers, thru the meat-processing plants and eventually all the way back to dairy farms where the cattle were raised25 (dairy cows are often made into hamburger at end of productive life).
  • A specific case of ceftriaxone-resistant Salmonella occurred in a child in Nebraska that was eventually traced back to cattle treated with antibiotics on his father’s farm. Notably the strain was actually found to be resistant to a large number of antibiotics (not all used to treat Salmonella infections in humans, of course): “ampicillin, chloramphenicol, tetracycline, sulfisoxazole, kanamycin, and streptomycin as well as to broad-spectrum cephalosporins (e.g., cephalothin) and expanded-spectrum cephalosporins (e.g., ceftriaxone, which is used in humans, and ceftiofur, which is used in animals), aztreonam, cefoxitin, gentamicin, and tobramycin.”6
  • A comparison study7 was done with poultry workers at both battery and free-range style farms. The battery farms were fed antibiotics (as is typical). The workers were tested before and after for Escherichia coli, specifically looking for resistant varieties. The results showed that workers caring for birds being fed antibiotics quickly began to harbor resistant varities of E. coli in their stool, similar to the poultry.

These are some of the major direct cases that I’ve found (no doubt I’ve missed some!) The indirect evidence for particular organisms is much more substantial, indicating that zoonotic-origin antibiotic-resistant infections are probably relatively common, but proving it for particular cases is much harder.

Indirect Evidence


Several Campylobacter spp. cause a significant proportion of gastroenteritis cases in the United States (otherwise known as “food poisoning”). It is not usually treated with antibiotics because for most individuals it doesn’t greatly improve recovery speed. Chickens are treated with quinolone antibiotics to prevent infections and quinolone-resistant strains of Campylobacter have been found in chickens, chicken products, and human beings289. Significantly, a Danish study10 demonstrated that domestically acquired infections were significantly less likely to be quinolone-resistant strains: quinolones are rarely used on chickens in Denmark.


Salmonella of the food-poisoning variety is usually acquired from food: undercooked meat or eggs or food that has been cross-contaminated (though you can also catch it from wild and pet reptiles such as turtles!) There are numerous strains of it and they are frequently the subject of recalls due to major outbreaks. There have been several cases where a particular strain is more prevalent in animals and human infections are linked to animal reservoirs11. Antibiotic-resistant Salmonella has been found in ground meat12.

A US federal government program (NARMS) monitors Salmonella cases and tests for resistance on a proportion, allowing us to know over time which strains exist and which are resistant. Swartz2 summarizes this confusing data. The results are mixed: some strains look to be gaining resistance and affecting humans, other perhaps not. Resistant strains of Salmonella may even be associated with more frequent bloodstream infections and hospitalizations13.


Vancomycin-Resistant Enterococcus (VRE) are often acquired in the hospital and are nearly untreatable. There is some evidence that a similar antibiotic (avoparcin) used in animals creates a reservoir for continued VRE infections in humans, at least in Europe which decreased when avoparcin use decreased (summarized in Swartz2 and Smith14). The evidence here is fairly confusing to me, but certainly worrisome.

Convincing? Should we worry?

Considering I’m a dilettante just poking around PubMed and other sources, this is not exactly a complete review of the literature. Previous to looking into this a bit more, I had a vague notion that treating animals with antibiotics (subtherapeutically in most cases) definitely led to resistant infections in humans. After looking the literature, I’m well convinced that it does indeed happen. But like all things in science, it’s more complicated. For example, for Salmonella it may only be happening for some strains and not others. Why is that? Is it a risk for humans? Moreover, transfer of resistance genes between bacteria is really hard to demonstrate in practice, which is one of the major fears I’ve read about.

Still, what would happen if we greatly decreased (or even banned) subtherapeutic — prophylactic and growth-enhancing — uses of antibiotics on animals? The main outcome seems that we would be able to raise fewer animals, but in better conditions generally, and meat and dairy would become a bit more expensive. Lipsitch3 and Smith15 argue that perhaps there would be little medical impact from restricting antibiotics in animals in cases where there are already resistant-bacteria in humans — the horse has left the barn. In any case, the research supports reducing many uses of antibiotics in animals to mitigate demonstrable effects in human beings.

A follow-on post to this one may cover some links to some random studies I found interesting or curious when looking into this issue. Spelunking through science articles is fun though sometimes disturbing.

  1. Tellingly, though, it’s possible to create inhumane conditions for animals even without antibiotics. Some “organic”, “free range” chicken eggs are from hens raised in batteries just like “conventional” operations. But due to the conditions and the fact that antibiotics can’t be given, the facility must be kept nearly sterile.
  2. Swartz, M. 2002. Human diseases caused by foodborne pathogens of animal origin. Clin. Infect. Dis. 34:S111-S122. 2
  3. Lipsitch M, Singer RS, and Levin BR. 2002. Antibiotics in agriculture: when is it time to close the barn door? Proc Natl Acad Sci U S A. 2002 Apr 30;99(9):5752-4. 2
  4. ML Cohen and RV Tauxe. 1986. Drug-resistant Salmonella in the United States: an epidemiologic perspective. Science 21 November 1986: Vol. 234 no. 4779 pp. 964-969.
  5. Spika JS, et. al. 1987. Chloramphenicol-resistant Salmonella newport traced through hamburger to dairy farms. N Engl J Med 1987; 316:565-570. I sadly wasn’t able to actually go read this article as it’s not accessible to me, so I’m going off the references to it in other literature and the abstract.
  6. Fey PD, Safranek TJ, et. al. 2000. Ceftriaxone-resistant salmonella infection acquired by a child from cattle. N Engl J Med. 2000 Apr 27;342(17):1242-9.
  7. Ojeniyi AA. 1989. Direct transmission of Escherichia coli from poultry to humans. Epidemiol Infect. 1989 Dec;103(3):513-22.
  8. Smith KE, et. al. 1999. Quinolone-resistant Campylobacter jejuni infections in Minnesota, 1992-1998. N Engl J Med. 1999 May 20;340(20):1581-2.
  9. Zhao S, et. al. 2010. Antimicrobial resistance of Campylobacter isolates from retail meat in the United States between 2002 and 2007. Appl Environ Microbiol. 2010 Dec;76(24):7949-56.
  10. Engberg J, et. al. 2004. Quinolone-resistant Campylobacter Infections in Denmark: Risk Factors and Clinical Consequences. Emerg Infect Dis. 2004 Jun;10(6):1056-63.
  11. Akkina JE, et al. 1999. Epidemiologic aspects, control, and importance of multiple-drug resistant Salmonella Typhimurium DT104 in the United States. J Am Vet Med Assoc 1999; 214:790–8.
  12. White DG, et. al. 2001. The isolation of antibiotic-resistant salmonella from retail ground meats. N Engl J Med. 2001 Oct 18;345(16):1147-54.
  13. Varma JK, et. al. 2005. Antimicrobial-resistant nontyphoidal Salmonella is associated with excess bloodstream infections and hospitalizations. J Infect Dis. 2005 Feb 15;191(4):554-61.
  14. Smith DL, Dushoff J, and Morris JG. 2005. Agricultural antibiotics and human health. PLoS Med. 2005 Aug;2(8):e232.
  15. Smith DL, et. al. 2002. Animal antibiotic use has an early but important impact on the emergence of antibiotic resistance in human commensal bacteria. Proc Natl Acad Sci U S A. 2002 Apr 30;99(9):6434-9.

Antibiotics and Industrial Livestock Production: Not Just Superbugs

The FDA is finally issuing regulations and recommendations on use of antibiotics in livestock! They are unfortunately voluntary regulations but considering the FDA proposed doing this in 1977 but got shutdown by Congress, this is good news. It’s taken more than thirty years for the FDA to officially say that many uses of antibiotics in meat and dairy production are dangerous.

The recommendations apparently don’t exclude use for preventing disease so it’s unclear to me how this will significantly reduce use of antibiotics. Tom Philpott posted a good overview of why these regulations are probably inadequate. But I’m still glad to see the FDA say something official.

Most of the news emphasizes the risk that prophylactic use of antibiotics in livestock risks creation of antibiotic-resistant bacteria which might transfer to humans. There are surprisingly few documented cases1 considering the extent of use. If we gave humans antibiotics in the same manner as livestock, you would be taking regular low-dose antibiotics, almost like vitamins. We regulate antibiotic use in humans so that they are (hopefully) only used when medically necessary to cure disease. But we administer antibiotics to livestock for a different reason: to support concentrated, intensive animal production. That has downsides beyond human health.

Animal Welfare: Many who swear off “factory farm meat” do so because of a concern for animal welfare. Industrial livestock production requires the animals to be held in tight quarters. Hens, for example, often have their beaks trimmed to keep them from pecking their neighbors because they are packed so tightly. Dairy cattle often get infected udders due to the conditions. Cattle in intensive operations suffer from diseases of the feet from standing in manure. Antibiotics are given to the animals in a preventative fashion: the close quarters and filth would certainly cause infections without them, either killing them or reducing yield.

Waste is Wasted: The waste produced from industrial animal operations results in huge lagoons of waste that are regulated under the Clean Water Act. Most of this waste ferments, unused, breeding unknown micro-organisms, seeping into local water tables until it is finally used as fertilizer. Occasionally it floods out of containment. Nearby residents live with interesting aromas. That waste is literally going to waste. The waste is eventually used as fertilizer but in modern operations there is so much that it is applied too liberally, leading to runoff. We could be burning the methane for energy production and then processing the waste (including better fertilizer2).

Industrial Monocropping: The large number of animals raised in intensive operations require huge amounts of feed. Most industrial livestock aren’t fed grass or whatever it is the animal would eat on that idyllic farm we think of as children. Cattle, for example, are fed a lot of corn3. Pigs are fed soy and meat by-products. A major driver of monoculture fields of corn and soy is demand from livestock operations. The largest single use of the US corn crop is for animal feed45. Our current industrial corn and soy production methods require a lot of inputs (water, pesticides and fertilizer) and monoculture agriculture presents challenges for pest management. Reducing demand for industrial meat would reduce demand for corn and soy. This would mean less fertilizer and pesticide runoff6 and less water consumption7.

Reducing antibiotic use in industrial livestock farming could force major changes in how animals are raised. Americans are already eating less meat. I really hope the FDA can make these regulations work (or make them mandatory if voluntary fails). Less intensive animal farming could significantly improve land usage throughout the United States. I’m not certain that limiting antibiotics to medically necessary reasons would significantly reduce the number and size of intensive operations, but I certainly hope it does.

Update at 18:55 PDT: I didn’t describe very clearly exactly what the FDA is trying to regulate. Specifically, they are trying to stop the use of human-relevant antibiotics for non-medical purposes. A very common non-medical use is currently to encourage growth (for some reason low-dose antibiotics seem to encourage rapid growth). Unfortunately, antibiotics used to treat animals “at risk of getting a specific illness” is not being restricted (even voluntarily). Since this use can justify regular low doses of antibiotics (since many animals are at risk of illness due to the crowding), it doesn’t seem likely these regulations will actually significantly decrease use. My hope is the FDA will eventually expand the rules.

  1. The book Superbug summarizes the cases.
  2. And apparently bedding for dairy operations.
  3. Also, bizarrely, cattle are often fed meat and bone meal.
  4. See World Agricultural Supply and Demand Estimates Report from the USDA.
  5. The second is ethanol production which has its own problems.
  6. Runoff into the Gulf of Mexico results in a dead zone where sea life is reduced severely.
  7. A significant amount of corn is irrigated from the Ogallala Aquifer.

Is HFCS killing honeybees?

This morning, while browsing the social networks, I was linked to two different pages about a new study that is claimed to show that pesticide-laden high fructose corn syrup (HFCS) is the cause of Colony Collapse Disorder (CCD) in honeybees. One was a retweet from William Gibson linking to the Harvard press release. The other were some friends linking to a Mongobay story.

So that’s kind of worrying, right?

The study itself makes a very strong claim:

From the ecological and apicultural perspectives, the results from this study show a profound and devastating effect of low levels of imidacloprid in HFCS on honey bee colonies… It is likely that CCD was caused by feeding honey bees with low levels of imidacloprid in HFCS throughout their lifecycle in which toxicity occurred during the larval/pupal stages and was later manifested in the adult honey bees.

That should require a convincing mechanism and very strong data. The study, as written, doesn’t. The basic hypothesis is fairly believable:

  • Bee keepers use HFCS as a cheap supplement food for their bees (since humans take most of their honey).
  • Neonicotinoid pesticides in large enough doses can directly kill bees.
  • Residues from these pesticides have been found in nectar and pollen.
  • Corn crops have been increasingly treated with these pesticides.
  • HFCS likely contains these pesticides.
  • Maybe bees eating small amounts of pesticide-laden HFCS can lead to CCD.

This is the part a layman is likely to read. Isn’t it pretty believable? To make it even more believable, neonicotinoid pesticides are banned in Europe. Plus, other studies investigating CCD have show a possible link to these pesticides (certainly, bees have been outright killed by misapplication of these pesticides). I’m convinced! Aren’t you?

But the study has some major flaws, as pointed out in a Wired article and a response from Bayer (who manufactures some of these pesticides). But please read the study itself because I think some of these should jump out to a critical reader. The following are some that bothered me the most.

Pesticide Feeding Levels Unjustified

The study feeds differing levels of imidacloprid (a neonicotinoid pesticide) in HFCS to various bee colonies (as well as HFCS containing no added pesticide as a control). But there is little justification for why those levels were chosen. There’s some hand-waving about levels of pesticide residues found in pollen and nectar, but that doesn’t really tell us much about how much would be in the HFCS that beekeepers would actually feed their bees. The explanation given is:

Lastly, several earlier reports have shown that corn and sunflower plants grown from genetically engineered seeds treated with imidacloprid, one of the neonicotinoid insecticides, produce pollen with average levels of 2.1 and 3 μg/kg of imidacloprid, respectively (Suchail et al., 2001, Rortais et al., 2005). Furthermore, a recent paper published during the course of this in situ study showed elevated imidacloprid residue levels of 47 mg/L in seedling corn guttation drops germinated from seeds treated with 3 different neonicotinoid insecticides-treated (including imidacloprid) corn plants that are high enough to kill honey bees instantaneously (Girolami et al., 2009). These study results lend credence to our hypothesis that the systemic property of imidacloprid is capable of being translocated from treated seeds to the whole plant, including corn kernels and therefore likely into HFCS.

However, the actual dosages chosen to be fed are not really explained. They varied wildly between hives — one hive was fed a range from 0.1 µg/kg (at four weeks) to 20 µg/kg (at nine weeks) while other hives were fed 10.5 µg/kg and 400 µg/kg. Why so much more after nine weeks? It’s not at all clear why this difference. I can guess — perhaps the literature indicates pesticide residues vary wildly over the season. But I shouldn’t have to guess. The only significant mention in the methods as to why the levels were chosen is:

The dosages used in this study were determined to reflect imidacloprid residue levels reported previously (Suchail et al., 2001; Bonmatin et al., 2005; Rortais et al., 2005; Girolami et al., 2009). Imidacloprid was initially fed to honey bees at 0.1, 1, 5, and 10 μg/kg in HFCS for 4 weeks starting on July 1st 2010, followed by 20, 40, 200, and 400 μg/kg for another 9 weeks, which ended on September 30th 2010.

But these are presumably just the residue levels discussed in the introduction which are residue levels in pollen, nectar and corn guttation drops1. How did the study authors calculate how much pesticide to add to mimic the amounts in commercially available HFCS?

Why does 2005/2006 HFCS matter?

The authors are very concerned about replicating HFCS used in 2005/2006 (when CCD supposedly began):

We hypothesized that the first occurrence of CCD in 2006/2007 resulted from the presence of imidacloprid (1-((6chloro-3-pyridinyl) methyl)-N-nitro-2-imidazolidinimine, CAS# 138261-41-3), in high-fructose corn syrup (HFCS), fed to honey bees as an alternative to sucrose-based food. There are three facts to support this hypothesis. First, since most of the suspected but creditable causes for CCD were not new to apiculture, there must have been an additional new stressor introduced to honey bee hives contemporaneous with the first occurrence of CCD during the winter months of 2006 and early 2007. Second, while commercial beekeepers appear to be affected by CCD at a disproportional rate, their beekeeping practices have been relatively unchanged during these years except for the replacement of honey or sucrose with HFCS as the supplemental sugar source for economic and convenient reasons. This is because many of the commercial beekeepers leave very little honey in their hives to sustain honey bees through the winter months, and therefore require the least expensive alternative for honey. Although the replacement of honey/sucrose-based feeds with HFCS among commercial beekeepers took place much earlier than 2006/2007, it was the timing of the introduction of neonicotinoid insecticides to the cornseed treatment program first occurring in 2004/2005 that coincides with CCD emergence (Bonmatin et al., 2005; Benbrook, 2008).

Later in the discussion:

One apparent deficiency, in addition to the small number of honey bee hives used in this study, is that we were not able to obtain HFCS manufactured in 2005/2006 for use in this experiment. Instead, we used food-grade HFCS fortified with different levels of imidacloprid, mimicking the levels that are assumed to have been present in the older HFCS.

Colony collapses are still occurring. If this is the cause of CCD, why should it matter that they replicate levels that may have existed (again, entirely unproven) in the past, when the problem supposedly began? If this is the cause of CCD (or even a major one) then surely levels of pesticide residues in HFCS should be an ongoing concern.

Why not just measure pesticide concentrations directly?

The biggest problem that bothers me about this study is that it claims that HFCS contains low-level pesticide residues, then attempts to demonstrate what levels of them will kill a colony, but never actually talks about measuring pesticide concentrations directly! This seems just completely obvious to me. If for some reason that’s hard to measure (the Wired article talks a bit about that), then don’t the authors need to provide a clear discussion as to why they chose the pesticide residue levels they used? As it is, I’m left to assume they chose these levels because it got them results.

A Minor Point

In the introduction, the authors mention genetically modified crops:

The wide-spread planting of genetically engineered corn seeds treated with elevated levels of neonicotinoid insecticides, such as imidacloprid since 2004 (Van Duyn, 2004), and their acute toxicity to honey bees led us to hypothesize a link between CCD and feeding of HFCS containing neonicotinoid insecticides.

This is mentioned again in the discussion:

We have validated the study hypothesis in which the initial emergence of CCD in 2006/2007 coincided with the introduction of genetically engineered corn seeds treated with imidacloprid and other neonicotinoid insecticides.

Corn grown in the US today is commonly a GE variety, so pretty much any new pesticide applied to corn crops will be applied specifically to GE corn crops. So why mention it except to invoke fear of genetic engineering? The problem, the authors claim, is the use of an insecticide, not genetically engineered crops. It strikes me as manipulative to mention “GE corn” in a context where any corn would likely be GE because to uncritical readers2 it implies that the “GE” part had something to do with it. It is likely an inadvertent inclusion. However, given the degree of fearful reporting related to agricultural sciences, it is unfortunate.

The aforementioned Wired article and a response from Bayer make some further critical points that I find credible:

  • The pesticide used in this study isn’t even one commonly applied in the United States.
  • The studied failed to gather enough data (enough bee hives) to achieve statistical significance.
  • Given other research showing many other possible triggers for CCD (fungi, mites, virii, bacteria, etc), a study claiming a very particular cause should at least give a nod to why these other causes aren’t as likely.

Given that the lead author, Chensheng Lu, is quoted in Wired saying:

“The hives were dead silent,” he said. “I kind of ask myself: Is this the repeat of Silent Spring? What else do we need to prove that it’s the pesticides causing colony collapse disorder?”

I think it pretty clear the author truly believes that pesticides are causing bee hive collapses. Unfortunately, this study isn’t very convincing to me, even if I think it likely pesticides are somehow involved with CCD.

  1. “Corn guttation drops” are drops of xylem from corn plants.
  2. Specifically, the mainstream media tends to take quotes from science reports and attribute more meaning to irrelevant parts than is warranted. Obviously we should expect more competence in science journalism, but scientists can help avoid some of the worst of it by not writing confusing papers.