Common Pesticide Implicated Bee Colony Collapse Disorder

[MindMover]

Honeybee colonies have been mysteriously dying off all over the globe, leaving scientists scratching their heads—and important crops languishing in the fields unpollinated. Viruses, mites, pesticides and poor food choices have been fingered as potential culprits. And three new studies in the past week are taking aim at one of the most common types of agricultural insecticides.

Farmers worldwide have been using one popular neonicotinoid, imidacloprid, for about a decade to keep harmful insects off their cotton, corn, grains, potatoes, rice, vegetables and other crops. Like other neonicotinoids it targets the nervous system of insects, resulting in paralysis and death. Because honeybees (Apis mellifera) are insects, too, biologists have long suspected neonicotinoids as a possible force in colony collapse disorder.

Although most residue levels have not been found to kill bees on contact, the chemicals could conceivably do harm later on in these important pollinators—or their offspring–that ingest it either through nectar from sprayed crops or through the corn syrup that beekeepers feed to their bees; that syrup is made from insecticide-treated corn.

http://blogs.scientificamerican.com/observations/2012/04/06/common-pesticide-implicated-bee-colony-collapse-disorder/

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Sygenta is the Monsanto of Western Europe.....another major polluter and poisoner of our environment....

http://www.agprofessional.com/news/Syngenta-to-defend-atrazine-contamination-lawsuit-134636718.html

[Duer 157099]

1. I wonder what imidacloprid does to humans?

Alzheimer's anyone?

[mike_c]

3. millions of pet owners would likely disagree....

Advantage is imidicloprid, so millions of pet owners have it all over their homes. There is no data that suggests any link to human disease. None.

[MindMover]

4. Maybe it just hurts bees....?!!!!!

[mike_c]

8. well, it REALLY hurts fleas....

At least at the doses used on pets.

[Duer 157099]

5. It takes decades to develop Alzheimer's disease

I'm not sure we can say yet with confidence whether something is having an effect or not.

[Duer 157099]

6. Here is just the first thing a search turned up

Next step: do a PubMed search using the terms: ?4?2 nicotinic acetylcholine receptor AND Alzheimer's disease. I bet you get a hit or two.

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J Neurosci Res. 2011 Aug;89(8):1295-301. doi: 10.1002/jnr.22644. Epub 2011 Apr 28.
Activation and modulation of human ?4?2 nicotinic acetylcholine receptors by the neonicotinoids clothianidin and imidacloprid.
Li P, Ann J, Akk G.
Source

Department of Anesthesiology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
Abstract

Neonicotinoids are synthetic, nicotine-derived insecticides used for agricultural and household pest control. Though highly effective at activating insect nicotinic receptors, many neonicotinoids are also capable of directly activating and/or modulating the activation of vertebrate nicotinic receptors. In this study, we have investigated the actions of the neonicotinoids clothianidin (CTD) and imidacloprid (IMI) on human neuronal ?4?2 nicotinic acetylcholine receptors. The data demonstrate that the compounds are weak agonists of the human receptors with relative peak currents of 1-4% of the response to 1 mM acetylcholine (ACh). Coapplication of IMI strongly inhibited currents elicited by ACh. From Schild plot analysis, we estimate that the affinity of IMI for the human ?4?2 receptor is 18 ?M. The application of low concentrations of CTD potentiated responses to low concentrations of ACh, suggesting that receptors occupied by one ACh and one CTD molecule have a higher gating efficacy than receptors with one ACh bound. Interestingly, subunit stoichiometry affected inhibition by CTD, with (?4)(2) (?2)(3) receptors significantly more strongly inhibited than the (?4)(3) (?2)(2) receptors.

[mike_c]

9. just to be clear, those are post-synaptic gated ion channels in neurons...

...and nicotine binds to them as well. Alzheimer's disease is a gross structural abnormality caused by macrocellular plaque formation. It's hard to even hypothesize any reasonable connection.

[Duer 157099]

10. Yes, nicotine does bind, of course

But do you know that cells expressing such receptors are severely impacted in AD? I can imagine all sorts of hypotheses.

[mike_c]

11. well yes, but they're not impacted by anything having to do with nicotinic receptors....

If that were the case, there would be a massive smoking gun connection between AD and, um, smoking.

[Duer 157099]

12. It isn't as clear as you might think

and yes, there is no doubt whatsoever that there is a connection between AD and nicotinic receptors. It just isn't as simple as one might think.

Edit: wait, did you really write: "...they're not impacted by anything having to do with nicotinic receptors..."???

You sound like you know how to do a PubMed search. Please do one now just to prove to yourself that your statement is, um, inaccurate.

[mike_c]

13. I think we're speaking at cross purposes here...

I didn't say that nicotinic receptors are unaffected. I said that the impacts of AD on neurons-- bearing nicotinic receptors-- are not caused by anything having to do with those receptors. They are damaged by amyloid plaque, at a much more macro scale than what's going on in those synapses. Consider too the dose response-- if binding non-target ligands to nicotinic receptors (so called BECAUSE they bind non-target nicotine) plays any role at all in causing AD, then smokers should have a much higher incidence than non-smokers who are exposed to low dose imidicloprid. There is no evidence at all to support this being the case, at least none that I'm aware of.

[Duer 157099]

14. And what I'm saying is

that the picture is not at all clear, certainly not clear enough to draw the conclusion that you have.

There is extreme controversy about the role that amyloid plays in AD, mainly because the picture remains so complex. But it is fact that at least some of the nicotinic receptors bind to amyloid-related peptides:

J Alzheimers Dis. 2011;23(2):335-47.
Functional interactions of fibrillar and oligomeric amyloid-? with alpha7 nicotinic receptors in Alzheimer's disease.
Lilja AM, Porras O, Storelli E, Nordberg A, Marutle A.
Source

Karolinska Institutet, Division of Alzheimer Neurobiology, Department of Neurobiology, Care Sciences and Society, Karolinska University Hospital Huddinge, Stockholm, Sweden.
Abstract

Amyloid-? (A? ) peptides in the brain of patients with Alzheimer's disease (AD) assemble into various aggregation forms that differ in size, structure, and functional properties. Previous studies have shown that A? binds to nicotinic acetylcholine receptors (nAChRs) and activates signaling cascades that result in the disruption of synaptic functions. These findings suggest a possible link between impaired cholinergic neurotransmitter function in AD and A? pathogenesis. However, it is not yet known how the different A? assemblies interact with specific nAChR subtypes. In the present study, we demonstrate that neurotoxicity in neuronal cells in culture induced by fibrillar A? (1-40) is prevented through an ?7 nAChR-dependent mechanism. The ?7 nAChR agonists varenicline and JN403 increased binding of the amyloid ligand [³H]PIB to fibrillar A? in AD frontal cortex autopsy tissue. This suggests that the presence of nAChR agonists may inhibit interaction of A? with ?7 nAChRs and prevent the formation of A?/?7 nAChR complexes. This interaction was confirmed in binding assays with [¹²⁵I]A? (1-40) and ?7 nAChRs in autopsy brain tissue homogenates from the frontal cortex. The functional effects of A? fibrils and oligomers on nAChRs were examined by measuring intracellular calcium ([Ca(2+)](i) levels. Oligomeric, but not fibrillar A? (1-40), increased [Ca(2+)](i) in neuronal cells, and this effect was attenuated by varenicline. Our findings demonstrate that fibrillar A? exerts neurotoxic effects mediated partly through a blockade of ?7 nAChRs, whilst oligomeric A? may act as a ligand activating ?7 nAChRs, thereby stimulating downstream signaling pathways.

As I'm sure you know, ligand binding isn't digital. Ligand A binds to receptor B and that is good; ligand C binds to receptor B and that is bad. There's a whole spectrum of how ligands and receptors interact

[mike_c]

7. this suggestion has been around for several years....

We've discussed it here before, so I'll stick with the short version. The data are quite equivocal about connections between neonicotinoids and CCD, just as the data are somewhat equivocal about whether CCD is a single, discrete phenomenon or whether it's a combination of colony "dwindling disorders" and "disappearing disorders" that have been documented for a century.

But regarding neonicotinoids-- some research has suggested a link between low dose (sub-lethal) neonicotinoid exposure and neurological damage in bees, but that has NEVER been shown to be a factor in CCD. And entomologists have looked hard for that evidence, so the connection is purely circumstantial, at best, and imaginary at worst. There have been a number of other putative causitive agents, including viruses, fungal infections, parasites, and husbandry issues that seem to have better support. In the report you cited, low exposure imidicloprid did kill colonies, but there hasn't been much evidence YET linking it to CCD. I mean, flamethrowers kill honeybee colonies too, but the simple fact that they do doesn't implicate them in CCD.

Personally, I suspect neonicotinoids might indeed be part of the problem, but it's important to remember that no data yet supports any single cause for CCD, and many entomologists are less than convinced that CCD even exists as it has been described in the popular press. Even if neonicotinoids are involved, simply removing them from use might not solve the problem because CCD might be a syndrome with multiple interacting causes rather than a single discrete pathology with a simple, identifiable cause. THAT is currently what most data suggest.