Behe Meets the Peaceful Science Forum

No, not at all. When Behe speaks of degradation, he is not referring to protein degradation but to degradation/loss of function. I invite you to read the review he wrote in 2010 on the subject.

Then, since he is trained as a biochemist, he is being deliberately deceptive, because that’s what the word means in a biochemical context.

Gil, we’ve just shown you evidence that indicates that your claims are false, and all you can do is point to Behe’s rhetoric? Rhetoric doesn’t trump evidence.

You’re doing the Nigel Tufnel “but my amp goes to 11” thing yet again…


Hi Gil,

You seem to have overlooked the following statement on p. 440 of Behe’s paper:

Although the rates of appearance of loss-of-FCT and modification-of-function mutations that degrade protein activity are always expected to be much greater than the rate of appearance of gain-of-FCT mutations, a separate question concerns what fractions of the mutations in those categories are adaptive.

It sure seems that Behe is classifying loss-of-FCT and modification mutations as inherently degrading to protein activity.

This is not the only problem I see here.

As has been explained multiple times in discussions about Lenski and Behe, biologists expect that functions useful in the wild (protection against predators that are absent in the lab, ability to metabolize food sources absent in the lab, etc.) will be lost/broken in the lab environment.

So I see several problems in Behe’s QRB paper:

  1. He does not acknowledge that the lab environment would skew the selection pressure on mutation types.
  2. He ignores the presence of gain-of-function mutations outside of the knockout protocols.
  3. The presence of orthologous sequences that can be turned on after knockouts shows that copy-and-diversification had previously occurred. But Behe has already admitted that copy-and-diversification is a “gain-of-FCT” change.

And that’s just a critique of the paper with respect to the literature in 2008. Since then, dozens of discoveries of novel genes (which are by definition gain-of-FCT) have been published.

May I suggest that you pay closer attention to the biologists’ critiques of Behe? That you would point to such a thoroughly debunked paper is surprising.



Always thought the “needle-in-a-haystack” argument was weak when Dembski was making it back in 2005. Nice to see experimental confirmation.


In the context of our discussion, protein activity and protein function are synonyms.

Adaptive loss of function mutations are not at all confined to the lab environment. in DD, Behe offers many examples of these in the wild.
And it happens that a 2021 paper in Nature Heredity give credence to Behe’s contention that “loss-of-function” mutations are prevalent in the evolutionary process, the sad thing being that the authors don’t bother to cite him.

That’s false. Perhaps familiarize yourself with Behe’s work before defending it?


OK…discuss the stability and activity/function of those TPM1 variants above while conflating activity and function.

No one ever said they were confined to the lab. Offering examples doesn’t support his quantitative claim that they dominate the evolutionary process.


There would be many reasons not to:

  1. Reviews review the primary literature, not other reviews.
  2. Behe’s review is about experimental evolution. This Heredity (not Nature Heredity) review is not.
  3. Both of those apply even if the authors of the Heredity review agreed with Behe, which I am confident they do not.
  4. Behe and Sanford falsely portray evolution as requiring new mutations. The Heredity review extensively covered existing polymorphisms, an elephant in the room that Behe and Sanford want to ignore.
  5. Behe and Sanford are claiming that LoF mutations dominate the evolutionary process. There is no suggestion in the Heredity review to that effect.

Another important case that falsifies Behe’s hypothesis is collagen. It is the most common protein in your body and is structural. Excess glucose caused by diabetes increases collagen glycation, making it too stable, which contributes to renal, cardiac, vision, and many other forms of deterioration. Here’s a lay summary:
Whoever figures out how to reverse this glycation will become very famous and rich, because it causes so much suffering and death.


I am very very familiar with Behe’s work. I did the French translation of DBB and I read his two other books as well as most of his articles and written exchanges with his critics. I have also followed many of his debates when they were available on YouTube, including the one you recently had with him.
This being said, I maintain my claim that in the context of our discussion of DD, protein activity and protein function are expressions that have similar meaning.

Quick correction: there is no Nature review. The paper is published in Heredity, a journal within the NPG publishing group. There is no such journal as Nature Heredity. There are a lot of Nature journals (Nature Genetics, Nature Neuroscience, Nature Ecology and Evolution, seemingly a new one monthly) but this is not one.

There are a few reasons the authors might not have cited Behe. In the “historical context” section of their paper they could have cited Behe, reasonably IMO, but a glance at the section and the few papers cited there suggests to me that it would have been a bit odd. The Heredity paper is about genomics and population genetics, and not really about LOF alleles in adaptation. So the “historical context” paragraph focuses on early hints that LOF, especially on genomic scales, was an important aspect of evolutionary change. Those early hints began in the late 90s and the authors cite one influential review article from 1999. Here is what the Heredity authors write:

Only relatively recently, through discoveries enabled by the availability of molecular sequence data, were alternative views of adaptive loss-of-function alleles formalized, most notably with the “less is more” ideas proposed by Olson.

That paper (by Maynard Olson) is linked below, and is open access, and at a glance you should be able to see that it advances the specific proposal of LOF and adaptation, more than a decade before Behe’s QRB review. Behe does not cite Olson, and that IMO is more notable than the Heredity authors not citing Behe.

Anyone who thinks that Behe’s QRB review broke new conceptual ground should read this paragraph by Olson, published almost 12 years before Behe’s review.

Because mutations that lead to loss of function are numerous, this class of change (if adaptive) is the most likely outcome when a novel selection acts on a population. Loss-of-function mutations will occur far more often than will a shift in the target specificity of a protein or in the patterns of spatial or temporal regulation of a gene—and certainly will occur more often than a gene will acquire a new regulatory system. Once its function is lost—unless the lesion involves a complete deletion of the gene—the mutated gene will persist in the genome and may be available for reversion if the selective environment shifts once more. Evidence supporting the plausibility of the “less-is-more” hypothesis comes from both mammalian and microbial genetics. Here, on the basis of diverse examples drawn from these organisms, I propose the testable view that gene loss is a major motif of molecular evolution.


Nobody here is disputing that adaptive loss of function mutations occur, nor is anyone here disputing that they can predominate under many circumstances, including in the wild. What is being disputed is Behe’s overall thesis, which is not only that this process occurs, but that it is the net, long-term outcome of the evolutionary process basically under any circumstance, such that the complexity we see in life couldn’t be produced by evolution as we currently understand it. There’s just no good evidence for such a grandiose claim. There is lots of evidence against it. He first derived this “net” effect view of evolution largely from a review of a handful of studies of evolution in a few simple, synthetic lab environments where organisms were taken from their enormously complex wild-type environments and evolved in simple, constant, flask environments.

Evolution is a combination of multiple processes with their own varying biases that can fluctuate in magnitude over time, as conditions change. Some times conditions change and become simpler, with fewer or no ecological opportunities that reward new functions, and then you just get a sort of optimization by any unnecessary genetic material and gene expression being shut off and eventually suffers deactivating if not deletion mutations. This can of course not go on indefinitely, as eventually no more functions or genes can be lost without incurring strong fitness penalties, as you’ve essentially removed everything non-essential and which doesn’t positively contribute to fitness in that environment.
Once this floor is reached, there is no other way to go but either to stay there, or to increase in complexity again when conditions allow (and you might ask entirely legitimately, what conditions do allow this?).

Of course, the “cost” of excess genetic material depends largely on population size. Generally speaking, selection for single-celled organisms such as bacteria is much more efficient at removing excess DNA, because of their huge population sizes. This situation is often times much more relaxed for large multicellular eukaryotes. Hence for multicellular eukaryotes, more complexity is allowed.

The “streamlining” effect of selection can also be counterbalanced by other processes that can have inherent tendencies for complexification. There are now multiple well-known examples of constructive neutral evolution driving up complexity. Microsatellite DNA amplifications, actively transposing retrotransposons, and other types of selfish genetic elements can drive up genome size and add to the constructive neutral evolution process.

Then there are circumstances where the environment starts selecting for novel functions. When you’re down near that floor of complexity where nothing else can be lost without incurring a fitness cost, new ecological opportunities can open up and reward innovations(gain of function mutations). A novel carbon compound enters the environment, and then suddenly this enzyme that has this weird inherent side-activity that never did anything is suddenly useful, so now amplifications of this enzyme gene are beneficial, and now there’s selection for enhancing this side-activity in some of these duplicates and so you get complexification by gain-of-function mutations through the innovation-amplification-divergence process. You now have two enzymes each specialized towards one function each, where before you just had one. Add more novel environmental challenges and rewards, and you get the opportunity for selection to reward more innovation.


The Heredity paper had a good point at the beginning that provides some interesting contrast.

One would think that Behe would have made a big deal of that point, the CCR5 deletion that confers resistance to HIV, in a book aimed at laypeople, but then the deletion occurred a few thousand years ago. Behe clearly doesn’t want any of his minions thinking about existing genetic variation, because then his hypothesis crumbles.


That’s not a good foundation for understanding.

Have you read any of the scientific literature that Behe cites? What about any of the literature that Behe doesn’t cite?


I’m sorry; did I claim anywhere that loss-of-function mutations never, ever happen in the wild? Kindly show me where I did so and I will immediately amend my error!

Here’s what I did say:

  1. The ratio of loss-to-gain mutations is expected to be different in the lab than in the wild, and therefore
  2. Behe’s sweeping generalization about evolution in the wild, based on the ratio in lab experiments, is bad science.

I would love to hear your thoughts on what I actually said, @Giltil.


EDIT: As I read back through the thread, I realize that I made several other points that you have not addressed, @Giltil

Behe ignores the presence of gain-of-function mutations outside of the knockout protocols.

The presence of orthologous sequences that can be turned on after knockouts shows that copy-and-diversification had previously occurred. But Behe has already admitted that copy-and-diversification is a “gain-of-FCT” change.

And that’s just a critique of the paper with respect to the literature in 2008. Since then, dozens of discoveries of novel genes (which are by definition gain-of-FCT) have been published.

I would love to hear your thoughts on these critiques, as well.


After rereading what you initially wrote, and thanks to your last clarifications, I can now see that you didn’t say that LOF mutations don’t happen in the wild at all.

No. Behe acknowledge that adaptive GOF mutations can happen both in the lab and in the wild. But his contention is simply that adaptive LOF mutations largely overwhelm in number adaptive GOF mutations, whether in nature or in the lab. He has captured this idea with what he called the first rule of adaptive evolution, which says: Break or blunt any functional coded element whose loss would yield a net fitness gain.

I think that the data accumulated since 2008 strengthen, not weaken, Behe’s thesis in DD.
Now, I would be happy if you could offer some examples demonstrating the emergence of novel gene by RV + NS.

BSC4. Antifreeze glycoproteins in northern gadids. T-urf13? To pick a few.


Supporting that contention would require a wide breadth of knowledge and quantitation, neither of which Behe bothers with. Recall his pratfall with immunology in the Dover trial.

He has not supported that rule with data.

I’m pretty certain that you are not familiar with the data. If you disagree, what is the most recent paper from the primary literature that you have read–and understand well enough to discuss without any copy/pasting from the paper or from what others say about it, only copy/pasting the data (figures and tables)?


My point was that his quantitative analysis of the ratio of mutation types relies almost exclusively on experiments conducted in labs.

Allow me to refresh your memory:

In Behe QRB Table 1, only 8 “wild” mutations were examined, of which half are not loss-of-function. This dataset is vastly too small to support any broader conclusions.

Behe QRB Tables 2, 3, and 4 all examine the ratio of mutations in laboratory experiments.

And that’s it! That is the entirety of the data on which Behe relies to speculate that the ratio observed in the wild would (supposedly) overwhelmingly favor loss-of-function mutations rather than gain-of-function.

Anyone who has taken an entry level probability and statistics course can recognize that Behe’s conclusions are invalid.

Extensive examples have been discussed in this very forum. I notice that you have not participated in any of those threads, so I post links to them below so you can read the research papers that are linked in the threads. You will find that your diligence in reading the threads and the papers cited will be rewarded by the revelation of a fascinating body of research that you have never seen before. Enjoy!



32 posts were split to a new topic: Introducing Geremey (and Behe)