We now have the full text of the Harvard Study by Alex Lu which can be downloaded from this Google Docs link:



The magnitude and the pattern of honey bee hive loss
during the winter months in this study resemble the reported
symptoms of CCD. The loss of 15 of 16 imidacloprid-
treated hives (94%) across 4 apiaries occurred
over a period of 10 weeks following the first hive death.
Dead hives were remarkably empty except for stores of
food and some pollen left on the frames (figure 3). The
dead hives, particularly for those treated with higher dosages
of imidacloprid, was preceded by the observation
of dead bees scattered on snow in front of the hives,
with diminished small clusters remaining the week before
death. Snow usually fell between weekly hive examinations
making the observation of scattered dead
honey bees in front of individual hives noticeable. Although
this observation is not quite reminiscent of the
reported CCD symptoms, it is important to consider that
if these hives were located in a warmer climate region,
such as in Florida USA where migratory hives overwinter,
bees exiting the hives would have dispersed some
distance from the hives and therefore would not be observed
in front of the hives.

The replicated controlled design of this in situ study in
the apiarian setting, and the survival of honey bees in 3
of 4 control hives (figure 4), eliminate the possibility
that hive deaths were caused by common suggested risk
factors, such as long-distance transportation of hives,
malnutrition, or the reported toxic effect of hydroxymethylfurfural,
a heat-formed contaminant during the
distillation process of making HFCS, to honey bees (Le-
Blanc et al., 2009). We used the same HFCS in both the
imidacloprid-treated and control hives. The loss of imidacloprid-
treated hives in this study is also highly unlikely
due to pathogen infection since the presence of neither
Nosema nor a large number of Varroa mites was
observed in hives during the summer and fall seasons.
In addition, all hives were treated with Apistan strips
and Fumagillin B, two effective treatments for parasite
prevention, prior to the winter season. Since all hives
were considered healthy as they went into fall season,
those pathogens posed very little threat to the health of
honey bee hives. The only dead control hive exhibited
symptoms of dysentery in which dead honey bees were
found both inside and outside of the hive, which is not
seen in the other 19 hives.

Data from this in situ study provide convincing evidence
that exposure to sub-lethal levels of imidacloprid
causes honey bees to exhibit symptoms consistent to
CCD months after imidacloprid exposure.
Should stressor
factors other than feeding honey bees with HFCS
containing imidacloprid cause CCD, the loss of honey
bees would not occur disproportionally on those imidacloprid-
treated hives. The survival of the control hives
unequivocally augments this conclusion. The study hypothesis
is further supported by the mortality data presented
in figure 2, which clearly demonstrates a dose-
response relationship, in which the highest imidacloprid
dose exterminates hives more quickly than the subsequent
doses in all 4 apiaries. Although imidacloprid, and
other neonicotinoid insecticides have been suggested as
a possible contributing factor to CCD because of its toxicity
in impairing foraging ability or triggering other
neuro-behavioral problems (e.g. failure to return to the
hive) in honey bees at sub-lethal doses (Suchail et al.,
2001; Rortais et al., 2005; Thompson and Maus, 2007;
Yang et al., 2008; Mullin et al., 2010), its attribution to
CCD in the apiary setting has never been documented.
The results from this study underscore the paucity of
research concerning the sub-lethal effects of pesticides
on CCD, particularly of neonicotinoids throughout the
yearly life cycle of entire honey bee colonies under
natural conditions (Maini et al., 2010; Spivak et al.,