Randy Oliver's Critique of the 'Harvard Study'.

[Stromnessbees]

That's ok, Jon, you obviously like Randy Oliver's site. Now let's have a closer look:

This is the so called Harvard study:
http://www.hsph.harvard.edu/faculty/...e-disorder.pdf


My next post shows what Randy Oliver has to say about it.

Let's have a decent discussion about his comments, without derailing, moving bits about or ridicule.

Due to its length I had to split the article in two, and for ease of referencing I have divided it up into numbered sections.


1
Re this study, at first glance it appears to support the hypothesis that chronic exposure to field realistic doses of imidacloprid during summer and fall can lead to late winter collapse of the treated colonies. Unfortunately, there are a great deal of factual misrepresentations and
fuzzy thinking in the paper, which obviously was not peer reviewed by any bee biologist nor toxicologist. For example, the author stated in an interview:

"When other conditions cause hive collapse--such as disease or pests--many dead bees are typically found inside and outside the affected hives."

Could someone please refresh my memory? Other than in the case of tracheal mite, which diseases or pests leave many dead bees in a hive? (Note that starvation or acute pesticide toxicity would not fall into the category of "disease or pest").


2
My reading of the paper suggests that the author knows little about bees, little about pesticides, nothing about HFCS, had no understanding of the distribution of systemic pesticides in plants.


3
Let's look at a few more sentences from the paper:

"We hypothesized that the first occurrence of CCD in 2006/2007 resulted from the presence of imidacloprid ... 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."

As Bob and others have pointed out, CCD actually started occurring in 2004-2005.


4
"Second, while commercial beekeepers appear to be affected by CCD at a disproportional rate"

This is not true according to any of the surveys that I've seen.

", 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.... 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)."

It appears that the first cases of CCD preceded this time period, since any
HFCS produced from such treated corn would have necessarily have been produced
following the season of harvest.


5
The authors then cite a few studies that show that systemic insecticides
are translocated, as they are intended, throughout the plants. But then they stretch by
stating:

" 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."

My gosh, this is one helluva assumption! Without taking the time to simply confirm that Imd winds up in the kernels, the author *assumes* that it is concentrated there at high levels! An then further goes out on a limb by "assuming" that any such imidacloprid is then concentrated when the corn is used to produce HFCS (ignoring the fact that most corn is treated with clothianidin, rather than imidacloprid):


6
The paper turns into farce when the author states:

"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. The range of dosages used in this study from 20 to 400 ?g/kg were not only environmentally relevant"

Since when has 400 ppb ever been been considered to be "environmentally relevant"? Levels of 1-4 ppb are environmentally relevant; levels above 40 ppb are usually considered to be overtly toxic. So the 400 ppb figure is 100 - 400 times as strong as the normal measured levels in the field due to seed treatment.


7
But then the author goes into la-la land with some even wilder creative assumptions:

"Since there is no tolerance level for imidacloprid in HFCS, we applied a 10-fold concentrating factor, or 0.5 ppm (500?g/kg) of imidacloprid in HFCS, by taking into account
the uptake by corn plants from seeds that are treated with imidacloprid."

He simply created this "concentrating factor" out of thin air! He gave absolutely no justification for it. In the actual process of making HFCS, pesticides are largely removed. As I stated before, all that the author had to do would have been to ask Roger Simonds at the USDA Gastonia pesticide testing lab as to the actual measured levels of Imd in HFCS, and thus would not have brought embarrassment to Harvard Medical School by such a
ludicrous assumption.

"Therefore, we
are confident that the imidacloprid dosages applied in this study would be comparable, if not lower to those encountered by honey bees inside and outside of their hives."

Unfortunately, the authors' confidence is not supported by any actual field measurements whatsoever!


8
The authors state:

"There are several questions that remain unanswered as a result of this study. First, the systematic loss of sealed brood in the imidacloprid-treated and control hives may
indicate a common stress factor that was present across all 4 apiaries."

Like, maybe the field investigators should have taken a few nosema or varroa counts, rather than simply assuming that these common parasites weren't killing the colonies! For all we know, all the hives could have bee crawling with varroa or badly infected with nosema. One statement suggests that varroa was evident: "nor a large number of Varroa mites was
observed in hives during the summer and fall seasons," suggesting some something less than a "large" number of mites was indeed observed! And then they waited until October 5 to treat with Apistan strips, which are ineffective against mites in many areas of the U.S.


9
The authors, on a roll, simply do not know when to stop:

"If imidacloprid exposure is truly the sole cause of CCD, it might also explain the scenario in which CCD occurred in honey bee hives not fed with HFCS. Considering the sensitivity
of honey bees to imidacloprid as demonstrated in this study and the widespread uses of
imidacloprid and other neonicotinoid insecticides, pollen, nectar, and guttation drops produced from those plants would have contained sufficient amounts of neonicotinoid insecticide residues to induce CCD"

What are they talking about when they say "considering the sensitivity"? Even the lowest fed dosage (20 ppb) is about 5-20 times higher than that commonly found in nectar, and the other three doses were far higher--it is amazing to me that the colonies were not killed outright!


10
Oddly, I don't see any explanation as to why the investigators changed treatment dosages mid trial. To their credit, they initially treated the colonies with "field realistic" doses of the insecticide: 0.1 - 10 ppb (that would have actually have been a decent study). I suspect that after feeding the colonies for four straight weeks in July, and not noticing any adverse effects, that they then decided that they had better really hit the colonies hard if they wanted to support their hypothesis--so they arbitrarily ramped up the lowest dose to 200 times stronger, and the highest dose to 40x stronger (that oughtta do it!).

I can only imagine their surprise and disappointment when after then feeding colonies a full half gallon of obviously toxic treated syrup weekly for another 9 straight weeks, they still noted virtually no adverse effects! Note that the amount of broodrearing was unaffected at the 20, 40, and 200 ppb dosages, and only slightly depressed at the clearly toxic 400 ppb dose! Note that the colonies were all still alive at midwinter, 3 months after the dosing ended.