This is about  bees in Arnot Forest, New York State, USA.
There has developed an isolated and resistant wild bee community :
https://www.apidologie.org/articles/apido/abs/2007/01/m6063/m6063.html

The authoritative researcher is Tom Seeley, who has been studying these survivor hives for many years.

Now, Tom Seeley always evasively responded to the repeated questions by Dee Lusby, which cell sizes these wild bees really build.
Again and again he responded very negative to Dee Lusby’s comments on the artificially enlarged cell size of our bees.

Now a very interesting study appeared, in which Tom Seeley was significantly involved. Sasha Mikheyev, Assistant Professor of Ecology and Evolution at the Okinawa Institute of Science and Technology (OIST) in Japan, is the primary author.

This scientific research from 2015 is about:

Some honeybee colonies adapt in wake of deadly mites

A new genetics study of wild honeybees offers clues to how a population has adapted to a mite that has devastated bee colonies worldwide. The findings may aid beekeepers and bee breeders to prevent future honeybee declines.

To read here:
http://news.cornell.edu/stories/2015/08/some-honeybee-colonies-adapt-wake-deadly-mites

and then Tom Seeley suddenly says that the bees are smaller in Arnot forest:

Tom Seeley said: 
The surviving bees evolved to be smaller, suggesting these bees might require less time to develop. Since the mites infest nursery cells in hives, the shorter development time may allow young bees to develop into adulthood before the mites can finish their development. Mite-resistant honeybees in Africa are also small and have short development times, Seeley said.

,

the full article:

A new genetics study of wild honeybees offers clues to how a population has adapted to a mite that has devastated bee colonies worldwide. The findings may aid beekeepers and bee breeders to prevent future honeybee declines.

The researchers genetically analyzed museum samples collected from wild honeybee colonies in 1977 and 2010; the bees came from Cornell University’s Arnot Forest. In comparing genomes from the two time periods, the results – published Aug. 6 in Nature Communications – show clear evidence that the wild honeybee colonies experienced a genetic bottleneck – a loss of genetic diversity – when the Varroa destructor mites killed most of the honeybee colonies. But some colonies survived, allowing the population to rebound.

“The study is a unique and powerful contribution to understanding how honeybees have been impacted by the introduction of Varroa destructor, and how, if left alone, they can evolve resistance to this deadly parasite,” said Thomas Seeley, the Horace White Professor in Biology at Cornell and the paper’s senior author. Sasha Mikheyev ’00, an assistant professor of ecology and evolution at Okinawa Institute of Science and Technology (OIST) in Japan, is the paper’s first author.

“The paper is also a clear demonstration of the importance of museum collections, in this case the Cornell University Insect Collection, and the importance of wild places, such as Cornell’s Arnot Forest,” Seeley added.

In the 1970s, Seeley surveyed the population of wild colonies of honeybees (Apis mellifera) in Arnot Forest, and found 2.5 colonies per square mile. By the early 1990s, V. destructor mites had spread across the U.S. to New York state and were devastating bee colonies. The mites infest nursery cells in honeybee nests and feed on developing bees while also transferring virulent viruses.

A 2002 survey of Arnot Forest by Seeley revealed the same abundance of bee colonies as in the late 1970s, suggesting that either new colonies from beekeepers’ hives had repopulated the area, or that the existing population had undergone strong natural selection and came out with good resistance.

By 2010, advances in DNA technology, used previously to stitch together fragmented DNA from Neanderthal samples, gave Mikheyev, Seeley and colleagues the tools for whole-genome sequencing and comparing museum and modern specimens.

The results revealed a huge loss in diversity of mitochondrial genes, which are passed from one generation to the next only through the female lineage. This shows that the wild population of honeybees experienced a genetic bottleneck. Such bottlenecks arise when few individuals reproduce, reducing the gene pool. “Maybe only four or five queens survived and repopulated the forest,” Seeley said.

At the same time, the surviving bees show high genetic diversity in their nuclear genes, passed on by dying colonies that still managed to produce male bees. The nuclear DNA showed widespread genetic changes, a signature of adaptation. “Even when a colony is not doing well, it can still produce a batch of males, so nuclear genes were not lost,” Seeley said.

The data also show a lack of genes coming from outside populations, such as beekeepers’ bees.

The surviving bees evolved to be smaller, suggesting these bees might require less time to develop. Since the mites infest nursery cells in hives, the shorter development time may allow young bees to develop into adulthood before the mites can finish their development. Mite-resistant honeybees in Africa are also small and have short development times, Seeley said.

Next, the researchers will study which genes and traits confer resistance to Varroa mites. The findings may help beekeepers to avoid pesticides for controlling mites and to trust the process of natural selection, and bee breeders to develop bees with the traits that have enabled bees to survive in the wild.

The study was funded by the OIST and the North American Pollinator Protection Campaign.

Here is the full study:
https://www.nature.com/articles/ncomms8991

also as a pdf for download.

The vast majority of mitochondrial genetic diversity in the old population (blue) has been lost in the modern population (red). The most common haplotype present in many modern bees and one of the old bees is identical to the mitochondrial haplotype 53 of A. mellifera ligustica (Italian). The modern population seems to have descended from a relatively small number of queens.

wild bee hive in Arnot Forest:

A comment:

a beekeeper colleague has sent me a very interesting comment about Tom Seeley:

Hello,

Two weeks ago I was in Weimar, germany,  at a bee Symposium, where also Seeley has given some lectures on the resistant bees in Arnot Forest.

I asked him if he knew the bees of Dee Lusby and if the resistance of the bees in Arnot forest was also achieved through small cells.

He replied that he knew the method of Dee but did not have contact with her, but he tested small cells and could not determine resistance in these hives.

He also said that the resistance of Lusbys bees was only due to here africanized bees and had totally different genetics.

In that respect your article surprised  me, since some days ago you
just stated the opposite. It was also incomprehensible to me that the researchers did not team up with beekeepers to further promote bee health and its conservation.

Greeting W.

This is very interesting what Tom Seeley has said in Weimar.
He allegedly tested small cells and then found no resistance among his hives.
BUT he clearly states that the bees are smaller in the Arnot forest:

Tom Seeley said: 
The surviving bees grew smaller, suggesting that these bees need less time to develop. As the mites infest bee brood cells, the young bee can develop through the shorter breeding season before the mites can complete their own development. Mite-resistant honey bees in Africa are also small and have short development times, Seeley said.

.

And this is also highlighted in the research report:

Changes in body size and shape
Having found evidence of selection on developmental genes, we predicted that we would find morphological changes over time. Indeed, there has been an overall reduction in body size (head width: n = 64, t43.3 = -8.0, P = 4.0 × 10-10; intertegular span: n = 64, t62.8 = -8.6, P = 3.35 × 10-12; ………. African honey bees, which show resistance to V. destructor, are smaller than European honey bees honey bees of african descent.

.

And smaller bees require the construction of smaller cells in the brood nest, much like the african bees, which build cell sizes around 4.7mm.

So why Tom Seeley is not able to imitate the situation of the small bees in the Arnot Forest? They are smaller and resistant, but he can not do it!

Now Erik Österlund recently gave a lecture in Graz, Austria,  and Tom Seeley was also among the speakers.
Erik is a vehement advocate of small cells. He told me that he repeatedly asked T. Seeley about cell size of the bees in the Arnot Forest. He squirmed and did not want to make a definite statement, Erik said.
This researcher Tom Seeley is a bit suspicious to me, because I red how he reported that he deliberately killed a resistant hive in Arnot forest in order to examine it. He handled a cyan compound and by his clumsiness he almost poisoned himself, he reports.
Why on earth do you have to kill a survivor bee hive to be able to examine it ???

And now comes the supreme impudence of Tom Seeley. He answered in Weimar to the question of our colleague:

He also said that the resistance of Lusbys bees was only due to here africanized bees and had totally different genetics.

.

Ed & Dee Lusby got their bees analysed in 1986 by Prof. dr. N. Koeniger from  the institute of bee investigations in Frankfurt, Germany.
This has been published on Dee’s website for many years, but again and again the same hostility towards Dee Lusby appeares.
https://beesource.com/point-of-view/dee-lusby/lusbys-bee-biometrics/

Here Professor Koeniger wrote:

We did the biometrics now and it resulted in clear differences of your black bees compared to the usual U.S. mixture. Your bees are quantitatively significant more towards Apis mellifera carnica und Apis mellifera caucasica. The Italian influence is very limited.

.

the original letter:

Prof. Dr. N. Koeniger
INSTITUT FUR BIENENKUNDE
(Polytechnische Gesellschaft)
Fachbereich Biologie der J. W. Goethe-Universitat
Frankfurt am Main

6370 Oberursel 1
Im Rothkopf 5
W.-Germany

May 12, 1986

Dear Mr. and Mrs. Lusby,

Thanks for the letter of March 19th and the samples of bees. We did the biometrics now and it resulted in clear differences of your black bees compared to the usual U.S. mixture. Your bees are quantitatively significant more towards Apis mellifera carnica und Apis mellifera caucasica. The Italian influence is very limited.

We thank you again for your hospitality. Hope to meet you some day again. Attached you will find the values of your samples (cubital index).

Sincerely

N. Koeniger

As Professor Koeniger says, the bees of Ed & Dee Lusby are clearly related to Carnica and Caucasica bees and show a clear difference to usual american bees.

This has been public since 1986 and why does Tom Seeley dare to assert that Lusby’s bees are africanized and that their resistance results in this fact?

Does he do it purposely to discredit her?

Small Cell Beekeeping (4.9 mm) vs. Large Cell (5.4 mm) for Natural Varroa Control

1. The Central Thesis of resistantbees and Dee Lusby. The core idea is that the European honey bee evolved with a natural brood cell size of approximately 4.9 millimeters, which equates to 820 to 860 cells per square decimeter. There is solid historical evidence for this: measurements taken across Europe, North Africa, India, and the United States between 1865 and 1968, including from pioneers like Langstroth, Root, Grout, Betts, and Georgandas, consistently show values within this range. The thesis argues that a methodological measurement error introduced by Baudoux in the early 20th century led to an overestimation of the natural cell size. As a result, the actual 4.9 mm values were mistakenly reinterpreted as approximately 5.4 mm, thus establishing the current artificial standard. Therefore, Dee Lusby concludes that the widespread shift to the 5.4 mm cell represents a human-induced artificial mutation, a modification that stressed bees and made them vulnerable to the Varroa mite. Returning to the original 4.9 mm cell is seen as the way to restore the co-evolutionary balance and natural resistance.

2. Seeley’s Findings from the Arnot Forest Bees. In contrast, researcher Tom Seeley studied a wild population of bees in New York’s Arnot Forest that managed to survive the arrival of Varroa without any human intervention. Seeley identified two key adaptations in these surviving bees: a smaller body size than commercial bees and a shorter than normal brood period. According to his analysis, this shortened brood cycle is the primary mechanism that disrupts the Varroa mite’s reproductive cycle, preventing the mite from completing its reproduction inside the cell. However, a significant limitation of Seeley’s study is that he did not prove that the use of small cells is the cause of the resistance. He attributes the resistance to the short brood cycle, which is a consequence of natural selection, not to the cell size itself. In fact, Seeley has mentioned that his own experiments with artificial 4.9 mm cells did not consistently induce resistance, introducing a major point of discrepancy.

3. The Global Field Evidence from the resistantbees Network. In contrast to laboratory results or Seeley’s limited studies, the resistantbees network presents massive, long-term empirical evidence. For decades, thousands of colonies across multiple climates and countries have been managed without any chemical treatments, exclusively using small (4.9 mm) cells. This includes pioneers Dee and Ed Lusby with 700 colonies in Arizona, Erik Österlund with 650 in Sweden, Hans-Otto Johnsen with 650 in Norway, Kirk Webster with 400 to 700 in Vermont, Terje Reinertsen with 400 in Norway, Dean Stiglitz’s network with several hundred in the USA, and the ResistantBees group with 100 colonies on La Palma. The existence and continued success of these operations, many of them commercial, demonstrates that the method works on a real-world scale and in very diverse conditions.

4. Key Quantitative Results: Hans-Otto Johnsen’s Test. A particularly robust piece of evidence is the controlled test conducted by Johnsen between 2002 and 2004, directly comparing colonies on large 5.5 mm cells with colonies on small 4.9 mm cells. The results were striking. First, the average honey harvest was 24% higher in the small cell group, at 44.5 kilograms compared to 36 kilograms in the large cell group. Second, the Varroa load was drastically reduced: the natural mite drop at its peak was only 2 mites per day in the small hives, compared to 7 mites per day in the large ones. Likewise, an alcohol wash in the autumn showed 14% mites per 100 bees in the small group, compared to 29% in the large group. Furthermore, the small cell colonies were stronger (about one brood box more) and showed a more uniform and consistent honey production. Johnsen’s conclusion, as a commercial beekeeper wintering 650 colonies, was clear: he could not find any negative effect of small cell size on bee colony performance.

5. Points of Agreement Between Seeley and resistantbees. Despite their differences, both approaches share fundamental principles. They agree on the use of zero chemical treatments, the importance of natural selection (allowing weak colonies to die), natural feeding (no sugar syrup or pollen substitutes), the use of pure wax with no chemical residues, respect for natural swarming because it creates brood breaks that harm Varroa, and the need for an unrestricted brood nest. Seeley even agrees that the surviving Arnot bees are smaller, which is entirely consistent with small-cell biology.

6. Points of Disagreement or Different Emphasis. The fundamental disagreement lies in the cause and the tool. For Seeley, the primary resistance mechanism is the shorter brood period, and the smaller bee size is a consequence of that, not a cause. For the resistantbees network, the small cell size (4.9 mm) is the necessary cause and the practical tool to achieve this resistance. Seeley bases his conclusion on genomic and morphometric evidence from a single wild population, while resistantbees relies on historical data and decades of field success on a global scale. Moreover, for Seeley, the solution would be to wait for natural selection to act over decades, whereas for resistantbees, the solution is applicable today: any beekeeper can switch to 4.9 mm cells and get results.

7. Critical Clarifications Regarding Other Projects. Two important clarifications are necessary. First, Cuba is not a valid example of large-cell, treatment-free beekeeping. Although many wild colonies survive there, the managed colonies in Cuba use 5.3 mm cells and need to resort to drone comb trapping to survive. Second, the European Varroaresistenz 2033 project, despite its funding and ambition, has not achieved results comparable to those of the resistantbees network. Finally, it is crucial to understand that the small cell is not a magic solution on its own. Its success within the resistantbees network is always accompanied by an integrated management system including local breeding, zero chemicals, natural feeding, and harsh selection.

8. General Conclusion. There is a significant discrepancy between the academic research represented by Seeley, who correctly identifies the short brood cycle as a resistance mechanism but does not support the small cell as a tool, and the global empirical evidence from resistantbees, which demonstrates that thousands of small-cell colonies survive and produce more honey without treatments. A possible reconciliation is that using the small 4.9 mm cell may be a practical and reproducible way to induce the same shorter brood period that Seeley observed as a result of natural selection in the Arnot Forest. If this is true, the resistantbees network has achieved on a large scale what Seeley documented in a single wild population, but in a way that is applicable by any beekeeper today. The evidence presented, including historical data, long-term field studies, and quantified commercial results like Johnsen’s, suggests that the small-cell approach deserves serious reconsideration by the scientific and beekeeping community.