I’ve gotten some requests to revisit a blog post from a couple of years ago, as the authors of the paper I eviscerated in that essay have published again on the same subject. If you don’t have time to re-read that post, the upshot was that some researchers did a poorly-controlled experiment with beehives and insecticide-laced artificial nectar, then made lots of wild headline-grabbing claims about how they’d found the cause of colony collapse disorder (CCD).
Having been stung by my withering criticism – or perhaps having simply completed a high school-level course in experimental design – the same team is back again with the same argument. Their new paper appears in the same highly sketchy journal, but it’s a bit better than the previous one. That’s not to say the data come anywhere near proving what they’re trying to claim. However, they did at least do a couple of additional controls.
For example, they used two different artificial nectars, high fructose corn syrup (HFCS) and a sucrose solution, and analyzed both beforehand to see if they were already contaminated with neonicitinoid insecticides. They weren’t. That was one of the things I had called for in my previous criticism. The lack of detectable insecticide residues in the HFCS actually undercuts the theory they put forth in their previous study, but let’s let that slide for now.
The investigators also tracked the outdoor temperature throughout the study, accounting for the extreme weather variability we get here in Massachusetts. The 2012-2013 winter was considerably milder than the 2010-2011 season in which the previous study occurred. Otherwise the protocol was pretty similar, with experimental hives getting artificial nectar laced with various quantities of insecticide and controls getting unadulterated nectar. The experimental hives fared worse.
So that’s the smoking gun, right? Well, that’s certainly what Lu et al. seem to think:
The results from this study not only replicate findings from the previous study on imidacloprid and extend to clothianidin, but also reinforce the conclusion that sub-lethal exposure to neonicotinoids is likely the main culprit for the occurrence of CCD.
But the experimental hives didn’t develop CCD. They had fewer bees in them at the end of the winter and produced less brood, and six of the twelve treated colonies died compared to only one of the six controls, so the treated colonies do seem sicker. However, the dead hives contained many dead bees, and the surviving insecticide-treated hives had little or no brood and/or no queens. In CCD, the bees abandon the hive, leaving behind brood and a queen but no dead bees. What Lu et al. are doing here is equivalent to looking at a heart attack and calling it cancer. Insecticide-laced nectar may indeed make beehives sick, but there’s no evidence in this paper that insecticides cause CCD.
The new work also suffers from one of the other major flaws of the previous study; the entire project took place in New England. Yes, this is a lovely part of the country, but the commercial hives that seem to be most susceptible to CCD don’t stay in one place. They get loaded onto trucks and driven thousands of miles north and south to provide pollination services to crops along the way. They experience a sort of eternal summer, and all of the hives in the Lu et al. study did just fine in the summer – it was winter that killed them. The experiment just isn’t a very good model of reality.
There are other groups publishing papers on this subject, though. Many of them are even doing good science. Most are much more circumspect about their claims than Lu et al., which is appropriate: the whole CCD story is clear as mud right now. Does sub-lethal insecticide exposure cause CCD? Nobody knows. But we can be certain that making bold claims from shoddy data won’t get us any closer to an answer.