My Reply to Dr. Packer

Michael Egnor

I’m grateful to Dr. Alan Packer, Senior Editor of Nature Genetics, for his thoughtful comments on my recent post Spit-Brain Research, in which I addressed claims made by Perry et al. about their paper “Diet and the Evolution of Human Amylase Gene Copy Number Variation.” Dr. Packer makes some good points with which I agree, and some points with which I disagree.

Dr. Packer correctly points out that my reference to the authors’ paper linked not to the research paper itself but to the authors’ press release about their paper. Of course, the journal in which the paper was published (Nature Genetics) was clearly indicated in my post, and the authors’ press release to which I linked gave the issue (September 9th), so readers of my post had no difficulty locating the Nature Genetics article if they chose to do so. Regrettably, Nature Genetics limited public access to the paper by charging a non-trivial fee to access it. A brief abstract was available for free, but I see nothing wrong with my link to the press release. The press release is the authors’ own explanation and promotion of their research to the media and to the public. Evolution News and Views’ primary purpose is to “presen[t] analysis” of “news coverage [that] has been sloppy, inaccurate, and in some cases, overtly biased.” Critiquing scientists’ irresponsible public claims for Darwinism is entirely within ENV’s primary purpose.
Dr. Packer does raise some scientific issues that warrant discussion. He correctly points out that “[i]n fact, the paper by Perry et al. makes no claim whatsoever for a link between ‘spit’ and human brain evolution (the word ‘brain’ never appears in the paper).” Yet in their press release the authors credit their research with groundbreaking insight into brain evolution three times:

A new ability to supplement the diet with calorie-rich starches could have fed our large brains and…fueled our unrivaled colonization of the planet, Dominy said. [emphasis mine]

For Dominy and his coauthors, the finding goes beyond the mouth. In pondering human origins, Dominy said, anthropologists have long been stumped by the sudden, nearly simultaneous increases in our brain size….[emphasis mine]

“That’s the big mystery of paleoanthorpology,” Dominy said. “What changed? Why did our earliest human ancestors deviate from the pattern we see in living apes to evolve this incredibly large brain…”[emphasis mine]

Why did the authors repeatedly stress the importance of their research to brain evolution in their press release when, as Dr. Packer accurately points out, they never made any connection between their data and brain evolution in their peer-reviewed scientific article in Nature Genetics? They never even used the word brain in their scientific article, so why was there such inconsistency between the authors’ scientific assertions in Nature Genetics and their public claims in their press release? And especially, why would Dr. Packer imply that the authors’ inconsistent scientific and public assertions reflected on my forthrightness, rather than on the authors’?
I will be more careful in the future to distinguish between evolutionary biologists’ public claims about their research and the actual scientific evidence that they publish in journals. Evolutionary scientists often inflate the implications of their research to the public — highlighting specious materialistic interpretations of their work — while maintaining a softer and more professional tone in scientific journals.
Dr. Packer next takes exception to my satire of the authors’ work. Yet I merely quoted or paraphrased their press release, which begins, “To think that world domination could have begun in the cheeks…” The authors make wild assertions about their saliva research, repeatedly claiming relevance to brain evolution and referring to insight that it provides into “…the big mystery of paleoanthropology…” and “…our unrivaled colonization of the planet…”. My references to the authors’ statements were simply quotes or paraphrases from the authors themselves. That was the point of my post — evolutionary biology is difficult to satirize, because the outlandish quality of its claims leaves little room for exaggeration. In admonishing me for satirizing the authors’ claims, Dr. Packer inadvertently makes my point. Evolutionary biology is the only scientific discipline in which mere quotation or paraphrase can invoke credible allegations of satire.
Finally, Dr. Packer implies that I underestimated the importance of the science in the paper — that is, that I underestimated the importance of the authors’ study of the comparative genetics of salivary amylase in humans and several non-human primates. I’m not a geneticist, but I don’t doubt Dr. Packer’s opinion on the importance of inter-individual gene copy variation. He noted that it is “likely to explain a significant amount of human variation.” Interesting stuff, but Dr. Packer’s implicit characterization of the current state of knowledge of the phenotypic expression of gene amplification as cutting edge research raises a troubling question. Darwinists have claimed for quite a while that gene amplification is a clear and well understood process by which random genetic variation can give rise to new functional biological complexity. Of course, the only way that gene amplification could be preserved by natural selection is if it has phenotypic expression, and the only way that we could be sure that gene amplification was indeed a real source of novel biological complexity would be if we had a deep understanding of the phenotypic expression of gene amplification. Yet Dr. Packer characterizes the phenotypic expression of multiple gene copies as “one of the most exciting areas of human genetics.” Which of course means that the phenotypic expression of gene amplification isn’t the least bit clear and well-understood.
Either gene amplification is a well-understood way to increase functional biological complexity, or the research on the phenotypic expression of gene amplification is an “exciting area of human genetics.” Dr. Packer’s faux pas is an example of a common evolutionary motif: the emphatic claim that some evolutionary assertion is a ‘fact,’ and the subsequent announcement of groundbreaking research confirming it. Evolutionary biologists would do well to meet periodically to reconcile their stories. Either gene amplification is a well-understood source of new biological complexity, or it’s an exciting new area of research. It can’t be both.
As for Perry et al.’s paper in Nature Genetics, readers are invited to read it and judge for themselves. It’s rather technical, of course, and the discussion seems a bit desultory. The authors describe various facets of their comparative genetics of human and non-human primate salivary amylases, particularly variations in copy number and in inter-individual copy variation and variation in salivary amylase protein expression. While (as noted) the authors make no reference at all to the brain, they refer repeatedly to evolution and to natural selection:

Hominin evolution is characterized by significant dietary shifts…[emphasis mine]

Studies of evolution of amylase in humans and our close primate relatives may provide insight…[emphasis mine]

Natural selection may have influenced AMY1 copy number…[emphasis mine]

These CNV’s have experienced similar evolutionary pressures…[emphasis mine

natural selection has shaped AMY1 copy number…[emphasis mine]

We favor a model in which AMY1 copy number has been subject to positive or directional selection…[emphasis mine]

To understand better the evolutionary context of human AMY1 copy number variation…[emphasis mine]

…this expression pattern may have evolved to facilitate the digestion…[emphasis mine]

…demonstrating the importance of starchy foods in human evolution…[emphasis mine]

And the final sentence of the paper:

The characterization of copy number variation among humans and between humans and other primates promises considerable insight into our evolutionary history.

So are these evolutionary inferences, as distinct from the actual data on comparative genetics of salivary amylases, good science? To answer this question, I ask Dr. Packer to permit me a little speculation. Imagine that the data on human and ape amylase gene copy number and variation were different from the data compiled by the authors. Of course the data could take any of a number of permutations — humans could have had fewer copies of salivary enzymes than apes, or less copy number variation, etc. What inferences could be drawn?
What if humans had low salivary amylase gene copy number, and apes had high copy number? How could the authors invoke evolutionary theory to explain these observations? The authors could assert that human vulnerability (our relative inability to digest tubers) led to a need for interdependence and socialization to ensure survival, and gave rise to human cooperation, altruism, language, and civilization. This is of course explained by natural selection. The press release: ‘We Were Weak, So Now We’re Strong: Evolutionary scientists report groundbreaking research on how an evolutionary vulnerability led to the emergence of humans…’
What if humans had low intraspecies salivary amylase copy variation, and apes had high intraspecies variation? No problem. The evolutionary theory: low human intraspecies copy variation is evidence for strong evolutionary conservation — providing further evidence that human ability to digest tubers provided enhanced energy for evolutionary adaptation or that human vulnerability (inability to digest tubers) generated a need for interdependence, gave rise to cooperation, brain growth, altruism, language, and civilization. Natural selection is consistent with either of the evolutionary hypotheses! The press release: ‘Old Genes Are Good Genes!: Scientists make groundbreaking discovery linking surfeit (or lack) of critical enzymes in saliva to human evolution and world domination…’
What if humans and apes both had high salivary amylase gene copy numbers? The evolutionary explanation: abundant salivary amylase was essential for human and ape evolution, because it allowed digestion of energy-rich tubers, thereby facilitating human and ape brain growth and giving rise to intraspecies cooperation and altruism. More evidence for natural selection! The press release: ‘Scientists Discover What Makes All Primates’ Mouths Water…”
What if humans and apes both had low salivary amylase copy numbers? The evolutionary explanation: paucity of salivary amylase is essential for human and ape evolution — lack of ability to digest energy-rich tubers caused need for interdependence gave rise to ape cooperation, and to human brain evolution, altruism, language, civilization. Clear evidence for natural selection! Press release: Hard Times Make Good Species: Could world domination have begun in the cheeks…”
Perry et al.’s inference to natural selection is irrelevant to the specific data in their paper. ‘Natural selection’ could be invoked for any permutation of their data. Yet in science, inferences must depend on data, and must be subject to falsification by data. Inferences that are independent of data, such as the inference that amylase gene copy number and variation are explained by natural selection, aren’t scientific inferences at all, because the inference to selection could be drawn from any data on the comparative genetics of salivary enzymes. Of course, individual stories as to how the adaptation arose can be adjusted to fit data, but the fundamental inference to ‘natural selection’ is untested.
At the core of Darwin’s theory of evolution are two hypotheses: heritable variation arose randomly, without teleology, and individuals that were rendered more reproductively successful by heritable variation were more reproductively successful. When applied to several-million-year-old genes for salivary enzymes, the first hypothesis — that heritable variation arose without teleology — is untested, and the second inference — that reproductively successful individuals are reproductively successful — is a tautology. The inference to ‘evolution’ in the authors’ paper is an inference to the untested and to the tautological. The authors would have us believe that their inference to evolution is cutting-edge science. Yet the synthesis of ‘untested’ and ‘tautological’ isn’t science at all.
The authors would no doubt protest that some aspects of selection can be tested, and Dr. Packer points out that ‘robust’ statistical methods were applied to questions of positive selection, negative selection, and neutral drift. Yet what do these terms mean? Positive selection means the heritable variation helped, negative selection means it hurt, and neutral drift means it didn’t matter. Any heritable variation — non-teleological or teleological — would meet one of these three criteria, so how do the ‘robust’ statistical methods provide evidence for natural selection acting on random variation? One could apply the same ‘robust’ statistical methods to genetic engineering — some inserted genes improve a function, some hinder it, and some don’t matter. Yet one could not draw the inference that Darwin’s theory was at work — on the contrary, the variation was intelligently designed. Robust statistics don’t redeem unfounded inferences.
In the words of National Academy of Sciences member Phil Skell:

I found that Darwin’s theory had provided no discernible guidance, but was brought in, after the breakthroughs, as an interesting narrative gloss. … Darwinian explanations for such things are often too supple: Natural selection makes humans self-centered and aggressive — except when it makes them altruistic and peaceable. Or natural selection produces virile men who eagerly spread their seed — except when it prefers men who are faithful protectors and providers. When an explanation is so supple that it can explain any behavior, it is difficult to test it experimentally, much less use it as a catalyst for scientific discovery.
(Philip L. Skell, “Why do we invoke Darwin?,” The Scientist, Vol. 19(16):10 (August 29, 2005).)

So why the gratuitous inference to natural selection? It certainly makes salivary enzyme research more interesting. Without inferences to evolution (especially brain evolution), the press release would have garnered little attention (‘Ape Saliva Differs from Human Saliva, Scientists Announce…’). Perhaps the inference to natural selection is merely part of a desire to market Darwinism to the public. The authors’ study will no doubt be added to the ‘overwhelming evidence’ in support of Darwin’s theory of evolution, even though the specific data in the study are irrelevant to the inference to natural selection. Natural selection is invoked to explain anything, and there are as many evolutionary stories as there are permutations of data — all explained by natural selection. Inference from data to theory in evolutionary research hews to a pattern:
Inquiry- legitimate scientific inference based on data (‘humans have high salivary amylase gene copy number and variation compared to non-human primates’)
Story- High salivary amylase gene copy number and variation facilitated an energy-rich diet of tubers…
Tautology- (i.e. Natural Selection) Hominina whose reproductive success was enhanced by this adaptation were more reproductively successful…
Hyperbole- …”promises considerable insight into our evolutionary history.”
Publicity- Press release: “That’s the big mystery of paleoanthorpology…Why did our earliest human ancestors… evolve this incredibly large brain…To think that world domination could have begun in the cheeks…”
What is the scientific legitimacy of the evolutionary inferences in Perry et al.’s paper? Carefully considered, the paper merely invokes stories about the digestive benefits of salivary enzymes (better digestion means that we have more energy!), draws an inference to ‘natural selection’ that is unlinked in any meaningful way to data, and claims significant new insight into the origin of man.
Evolutionary theory — the unmoored inference to ‘selection’ that can be drawn from any permutation of data — is less science than a speculative pastime, all too often antecedent to a press release. The publication of such unscientific evolutionary speculation in Nature Genetics, and its defense by a senior editor of that journal, demeans science.

Michael Egnor

Senior Fellow, Center for Natural & Artificial Intelligence
Michael R. Egnor, MD, is a Professor of Neurosurgery and Pediatrics at State University of New York, Stony Brook, has served as the Director of Pediatric Neurosurgery, and award-winning brain surgeon. He was named one of New York’s best doctors by the New York Magazine in 2005. He received his medical education at Columbia University College of Physicians and Surgeons and completed his residency at Jackson Memorial Hospital. His research on hydrocephalus has been published in journals including Journal of Neurosurgery, Pediatrics, and Cerebrospinal Fluid Research. He is on the Scientific Advisory Board of the Hydrocephalus Association in the United States and has lectured extensively throughout the United States and Europe.