Can God be a useful "scientific" hypothesis? Yes

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A logical consequence is an abstract thing. How do we test for that?

Yes, people can have opinions about that. But how do we come to a clear unambiguous decision?

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None of those are logical conclusions.

Much too vague to test. What do you even mean by “harm and degeneration”?

And that’s more word salad. This is hopeless.

And for the fifth time (though I may have lost count): how do you explain the end-Permian mass extinction? Is everything really for the best in this best of all possible worlds?

What isn’t necessary?

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No @Meerkat_SK5, and more importantly I was not asking you to.

I do expect you to substantiate your own claims, such as this one:

Your claim that we can “constrain the hypothesis within the context of human behavior” (i) is unsubstantiated, and (ii) (as I pointed out) appears to be contradicted by the doctrine of Divine Ineffability (according to which doctrine God is beyond description and comprehension).

And this one:

This claim is also unsubstantiated. And, given that I’ve seen Theodicy (part of “that” theology) discussed in connection to the animal kingdom, I also find it highly dubious.

As should be obvious to any reasonable reader, I was only bringing up those theological issues in order to impeach your claims.

Given the shear volume of your blather on this thread, that is a thoroughly unhelpful claim!

Link to the post please and, given how lengthy your posts generally are, indication of which part of that post you are refering to.

I have three problems with this ‘reply’ (and I use the word so loosely, to the point that it has fallen apart in a heap on the floor):

  1. This appears to be irrelevant to the issue I was raising.

  2. It appears to be utter balderdash, as I believe has been pointed out to you by numerous others.

  3. “How can you say this is still unfalsifiable …?” The answer is simple: I never stated this. I’d probably agree with the claim of unfalsifiability (see 2 above), but have not myself actually articulated it. Which makes it strange that you ask this question.

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By “random mutations”, evolutionary biologists mean that mutations occur regardless of their consequences. It is one of the most supported claims in evolutionary biology.

You don’t know what “new genetic information” means, but you claimed it wasn’t gotten in Lenski’s LTEE. You then go on to cite a paper, which doesn’t define what it meant by “new genetic information”. Aren’t you confused?

The paper authors seem confused as well. Their E. coli lines evolved the cit+ trait, just like in Lenski’s LTEE, but they deny its new. They made a conclusion contrary to their data.

The definition of life is completely irrelevant to our conversation, so is the issue of whether life originated in other places. This response further confirms you don’t really understand the things you say.

Remember you claimed the LTEE and PACE experiments (PACEE from now on) can be used to simulate the origin of the first cells and I pointed out that this wasn’t possible because both experiments depend on the existence of already existing lifeforms like the E. coli (which both use). Biological evolutionary experiments in general are only concerned with how life changed or changes following the origin of the earliest forms from organic matter. The origin of prebiotic life is completely out of the scope of modern evolutionary biology and its experimental methods like LTEE and PACEE.

If you feel you could scientifically test for God-driven evolution, go ahead and develop your methodology, validate and publish a peer-reviewed report of its performance, accuracy and other important details. Stop trying to use unsuitable experiments like LTEEs and PACEEs.

You are free to postulate God is responsible for body plans, but that hypothesis is unscientific until you put into a format that is testable.

We have been through this already. If this is one way to falsify your hypothesis of God-driven evolution, then your hypothesis is falsified because of the inactivity of GULOP in our genome.

In the absence of dietary vitamin C, we and other organisms who need it to survive die. If God drove our evolution to that point, then there is nothing good or loving about him. In contrast, if our evolution was unguided, the formation of GULO makes complete sense.

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So you literally don’t know what you’re talking about.

A few side points:

  • You should be able to access it fully, since it’s free access (here).
  • The only definition they provide for “new genetic information” (novel gene function) is on the page you linked to.
  • That definition is completely at odds with the Yockey quote you’re so fond of using.
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This may be the most perfect pair of sentences ever written by a creationist. The existence of this entire thread has now been justified.

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Benevolent Design Hypothesis

This explanation entails that sinister designs that seem to bring harm and degeneration have an underlying positive benefit to the species or population or other species. The positive benefit would involve maintaining or enhancing either survival or reproductive capabilities, or the ability to fit different environments.

We can test this by studying nociceptive sensitizations in animals. For example, injury in animals can lead to long-lasting distress, whereby frequent exposure to pain-producing stimuli causes a progressively amplified response well after the injury has healed. This phenomenon has been referred to as “nociceptive sensitization.” Biomedical researchers have long viewed nociceptive sensitization as maladaptive because, in humans, it is associated with anxiety.

However, researchers have studied nociceptive sensitizations in squids and concluded that heightened sensitivity to pain helps these creatures evade predation. Since nociceptive sensitization is pervasive, it likely serves a similar benefit among other animals, as well.

Nociceptive Sensitization Reduces Predation Risk: Current Biology (cell.com)

We can also test this by studying carnivores or predators. They often are responsible for producing mass extinctions within herbivore populations. However, studies show how animal death and carnivorous activity play a necessary role in preventing the fixation of harmful viruses within populations that would potentially cause a herbivore population to become extinct.

Predators indirectly control vector-borne disease: linking predator-prey and host-pathogen models - PubMed (nih.gov)

Design Tradeoff hypothesis

This explanation involves the situational decision to deliberately diminish or lose one quality, quantity, or property of a design in return for gains in other aspects. In other words, one thing increases, and another must decrease.

We can test this by examining those bad designs from an engineer’s perspective and look for other qualities that may have increased. This would show the designer had a different goal in mind for that design then originally thought. As one professional engineer has suggested:

“…there are practical limitations to the width and length of vehicles, and heavier bumpers can reduce gas mileage and the maneuverability of the vehicle. The reality is that virtually every feature in a designed structure such as a car is a compromise between competing objectives: safety, comfort, aesthetics, cost, ease of manufacturing, ease of repair (an objective often overlooked), stability, speed and acceleration, and so forth. Generally, not every desirable objective can be met”.

Intelligent Design and Design Flaws: Jury-Rigged Design in Nature? (jefflindsay.com)

There are examples of this found in nature already:
Glycolytic strategy as a tradeoff between energy yield and protein cost | PNAS

An optimal bronchial tree may be dangerous - PubMed (nih.gov)

Simple, mass extinctions allows for a surge in biodiversity:

“Analysis of the fossil record of microbes, algae, fungi, protists, plants, and animals shows that the diversity of both marine and continental life increased exponentially since the end of the Precambrian.”

More importantly, Biodiversity benefits all life:

Biodiversity enhances the multitrophic control of arthropod herbivory | Science Advances (sciencemag.org)

Science Journals — AAAS (sciencemag.org)

Arguing that previous observations suggest that if there is a Divine intelligence that guided evolution, it probably operates and mimicks human behavior rather than natural law. In other words, it’s offering justification for a rational God for the operation of nature.

The evidence suggests that if there is a Divine intelligence that guided evolution, it mimics the behavior of humans NOT natural law:

“ There is nothing in the physico-chemical world [apart from life] that remotely resembles reactions being determined by a sequence [the genome] and codes between sequences [the genetic code]. The existence of a genome and the genetic code divides living organisms from non-living matter. ” (Computers and Chemistry, 24 (2000) 105-123)

“ Only the measurement of information in the genome and the transcription of information from DNA to RNA to protein are mathematically identical to the measurement of information and the transcription of written language. ”

Microsoft Word - 2005-11-16_Hubert_Yockey_reply_to_FTE_amicus.doc (ncse.ngo)

“ For experiments aimed at demonstrating chemically more complex processes, such as multistep syntheses mimicking biochemical pathways or genetic replication, repeated interventions by the experimentalist have been necessary .”

Prebiotic chemistry and human intervention | Nature Communications

No, this is your claim that you have not substantiated. You need to provide the article you are suggesting that makes this connection so I can properly address it. BTW, I was not trying to argue for the Christian God under this topic. The God of classical theism is the subject of this discussion.

Yes, my mistake. It was the wrong example. If God is infinite or non-contingent, then we would not get flawed designs in nature. That’s all I was suggesting.

Yes, that’s one of the definitions of “random” mutations I am going off on but what is your point by telling me this.

Alright, here is my definition. New genetic information would be a new transporter, a new promoter, or a new metabolic pathway.

Sure, that’s fine. The experimental procedure I laid out before was mainly there to show that my hypothesis is testable at least in principle, which was my overall objective under this topic.

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  1. Even if your statement were true, it does not “constrain the hypothesis within the context of human behavior” – even if the purported Divine Intelligence does mimic human behavior does not mean that they must on all occasions mimic it.

  2. Your spammed quote-mines do not provide evidence for your claim. They do not in fact make any mention of anything resembling a “Divine intelligence” at all. I’m fairly certain that the authors whose work you are abusing would be thoroughly confused as to how you think their statements support your claim.

  3. [Addendum] Your second Yockey quote is pulled out of context from a section whose stated purpose is to directly contradict your claim that the material supports a (Divine) Intelligence:

Point Two: Information theory is not concerned with “patterns of intelligence”

So @Meerkat_SK5, you have merely succeeded in turning one unsubstatiated claim into two unsubstantiated claims. The original one being:

I merely mentioned that to explain why I found your claim to be “dubious”. It is therefore peripheral to the discussion. I read it a week or two back in connection to the question of whether animals go to heaven, and did not bookmark it. The fact that I cannot immediately produce it does not change the fact that the following statement (which I was referring to above) is unsubstantiated:

[Addendum: I could not find the original article I read, but this article seems to cover similar territory.]

So @Meerkat_SK5, you now have three unsubstantiated claims at issue with me (and I’m sure more with other members).

Do I need to point out to you that any further attempts to ‘substantiate’ these claims about a “Divine intelligence” and theology, with quote-mines from scientific sources that make no mention of such issues, will not only not be acceptable, but will be treated with outright derision? They are simply a non sequitor.

In any case this all seems to be approaching the stage of flogging a dead horse. If ‘God can be a useful scientific hypothesis’ (which I strongly doubt, and would suspect most theist scientists would doubt as well), it would appear (from the failure of this lengthy discussion) that @Meerkat_SK5 is not the right person to advance the claim.

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Notice that you didn’t even answer my question. And this covers too much ground to be useful, especially when the benefit may accrue to “other species”. Further, what you mention here would seem to be similar to what’s expected from natural selection. How would you tell the difference?

Apparently you don’t know what mass extinction is. Or even what extinction is. No, what you’re talking about here is death. Death is not extinction, and extinction is not mass extinction. Beyond that, your model is confused. If predation were merely good for the predator, wouldn’t that also fit your model? If it’s bad for the harmful virus, you’re free to ignore that. As long as you can find something good for somebody, somewhere, you declare victory.

Why do you say “deliberately”? Again, wouldn’t natural selection produce a similar result?

Only in recovery from a major loss in biodiversity. Now of course that may benefit some of the survivors, but you ignore most species, the ones that die, to concentrate on the few survivors. Once again, your model is vague enough to accommodate anything, and so is useless.

Please stop with the naked quotes from unattributed sources and inappropriate citations of papers you have not read.

More word salad. Please stop.

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Excellent. Let’s recap the line of thought leading to this point. It started with this:

You then clarified what you meant by that goal being achieved:

Thus, its clear that you think new genetic information cannot be produced in extant organisms. I further pressed you to clarify what you meant by new genetic information and you replied as follows:

To summarize, you believe new genetic information cannot be produced because God has achieved his creative goals and you even went ahead to specify what you meant by new genetic information. Thus, if I find examples of genes getting new promoters or new metabolic pathways evolving, then it falsifies your claim that evolution was or is guided by God, because if it was guided the production of new genetic information should have ceased (according to you).

In the first case, the emergence of a new promoter, Lenski’s LTEE provides a classic example. The diagram below beautifully refutes your claims, because it shows how the citT (citrate/succinate antiporter) gene was given a new promoter.

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Prior to its duplication (fig a), the citT gene (blue segment, fig a) could only be expressed in the absence of oxygen. See those arrows which go down and take a turn to the right, they indicate promoter regions which are currently directing DNA transcription into RNA and for this context in the presence of oxygen. The promoter sequence of citT, if it were shown wouldn’t have had any arrow attached to it, because it would be bound by a repressor protein, preventing the transcription of genes downstream to it. This repressor protein is active in the presence of oxygen.

Lenski’s LTEE rolls on and one day, boom!, that citT gene is duplicated (alongside bits and pieces of its neighbours, fig b). This duplication event places citT downstream of the rnk promoter which is before the rnk gene (pink segment in fig a). The rnk promoter can be bound by RNA polymerase in the presence of oxygen to initiate transcription. The new location of citT allows it to be co-transcribed with bits of the rnk gene under oxygen-rich conditions.

If what I wrote is unclear, just know that what happened here is akin to transferring an employee (citT) to work with a “new” boss (rnk promoter) who has a different work schedule. See the source paper below for more details

For the second case, the emergence of new metabolic pathways, I present to you the PCP degradation pathway which newly emerged in the bacterium called Sphingobium chlorophenolicum. PCP is a man-made chemical which is quite toxic to living organisms including microbes. Serendipitously, the aforementioned bacterium was found to facilitate its degradation by some researchers many decades ago. Molecular investigations revealed the presence of a new, but still inefficient, metabolic or biotransformative pathway the bacterium evolved to degrade PCP. This is the pathway:

Screenshot_20210522-140904
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Some of the enzymes in the pathways were derived from HGT events (transfer of genetic material between bacteria without their asexual mode of reproduction), while others were derived from its common ancestor with a sister Sphingobium species.

An aside. In both examples I provided, we see a similar pattern in the evolution of new traits, which is inefficiency of those new traits post-actualization. When a trait is newly evolved. In Lenski’s LTEE, the earliest mutants with the Cit+ trait, utilized citrate quite poorly. The trait had to undergo further refinement, and it did through further mutations, enabling better utility of citrate as a carbon source. The PCP degradation pathway is currently in the “actualization” stage (just like the earliest CitT+ strains) because it is highly inefficient at degrading PCP, but will need to undergo refinement either in nature or in Copley’s (or maybe my) lab :wink:

With these examples, your version of the hypothesis of God-driven evolution is falsified, because new genetic information to use citrate under oxic conditions and degrade PCP via a new metabolic pathway were produced, even though it should have stopped according to you.

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I already explained why it does in previous posts because God is supposed to be bound by his own nature. For instance, the attributes of God have to work in accordance with each other in a logically consistent manner because he is who he is (i.e. the law of identity) and cannot not be who he is at the same time (i.e. law of non-contradiction).

This means that God cannot make himself cease to exist because this would conflict with him being a necessary being. God cannot make a square circle because this would conflict with his omniscience. God cannot lie because it would conflict with his omnibenevolence. God cannot make a rock so heavy that he cannot lift because it would conflict with his omni-potency.

God cannot create and develop a world that does not have God intimately involved in the process every step of the way because it would conflict with his “Personal’ nature. Thus, God must be true to “all” his attributes, because to do otherwise would be to deny his own self.

I agree, I was not trying to provide evidence that a Divine intelligence guided evolution. Instead, I was arguing that IF there is a God guiding evolution, we have good reasons to believe that this causal agent is probably Personal or relatable like us rather than mysterious. Thus, we can test it in accordance to human behavior by allowing human intervention to take place in experiments and have it count as potential evidence for or against the hypothesis. In other words, it was just an educated guess.

I encourage you to read this article. It’s basically a response to your article:

Where is God When Bad Things Happen? Why Natural Evil Must Exist (godandscience.org)

What I mean by “harm and degeneration” is a feature of an organism that is designed to impede on that organism or other organisms’ ability to survive, reproduce, and fit an environmental niche.

I am not sure what you mean by this.

Correct, I made it very clear that this hypothesis is an improvement of the Modern synthesis or add-on to what we already know, which means this is not about natural selection but it is about random mutations being undirected. I am merely arguing that mutations was never really random. That’s pretty much it.

I guess I don’t know what your objection entails. Maybe you can pinpoint what exactly conflicts with my hypothesis or at least tell me why you think your objection is not based on a definition of species that I have not agreed upon yet?

The trait and the genetic arrangement may be novel, but *the mechanisms, genes, promoters, and metabolic pathways are NOT novel.*I am going to have to refer you to Hugh Ross to explain further:

"Well, it isn’t utterly new for E. coli to utilize citrate as a primary food source. E. coli utilizes citrate via a citrate fermentation cycle under anaerobic conditions just fine. Under anaerobic conditions, the bacteria produce a citrate/succinate antiporter that allows transport of citrate from the environment into the bacteria. Also, as mentioned before, citrate utilization by E. coli , although rare under aerobic conditions, has been observed before. In those instances, the acquisition of this novel function, like many acquisitions of new traits in microbes, is through the horizontal (from bug to bug) transfer of small circular pieces of DNA (known as plasmids) encoding new functional genes. They can grow aerobically on citrate because they produce a citrate transporter encoded by the plasmid DNA and regulated by plasmid promoters. The citrate transporter allows citrate uptake, and citrate is metabolized via the citric acid cycle.

But that’s not what’s going on in the Cit+ E. coli in the LTEE. It’s not horizontal gene transfer. It’s not due to contamination of the cultures. The citrate transporter is not being co-opted from another system. It’s not exaptation. All Cit+ bacteria in the Ara-3 lineage harbor a ~3 kb tandem repeat of a portion of the endogenous citT operon, resulting in the introduction of additional citT genes in the E. coli genome. (See figure below.) The critical (but not sole) changes hinge on the duplication of an endogenous promoter ( rnk ) that is active under aerobic conditions, the duplication of the citT gene, encoding a citrate transporter, and the juxtaposition of these elements in tandem repeats. The tandem copies of the citT gene are no longer under the regulatory control of the endogenous citG/citT promoter but are under the regulation of copies of an endogenous, downstream rnk promoter. The rnk-citT element allows the production of a citrate transporter under aerobic conditions, and this allows Cit+ E. coli to utilize the citrate in the growth media via mechanisms and metabolic pathways already present.

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The Ara-3 Cit+ bacteria utilize citrate through the preexisting metabolic pathway (citric acid cycle). The ability to do so is facilitated by production of citrate/succinate antiporters from a preexisting gene sequence that is now expressed under aerobic conditions by simply switching the promoter that controls its expression. It is a novel trait, but the mechanisms underlying it are not innovations of new genes or new promoters. The Cit+ bacteria did not evolve a new transporter, a new promoter, or a new metabolic pathway."

And I told you already that this does not falsify the hypothesis.

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Of course it does.

You said God behaves like humans.

A human wouldn’t design humans with a broken vitamin C gene so that we get scurvy, or a broken uricase gene so that we get gout.

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Scientific hypotheses are not mere explanations. A scientific “Benevolent Design Hypothesis” would involve a mechanism underlying design, not any explanation or justification for it.

You appear to have multiple misunderstandings about the scientific method.

No, we really can’t, because your hypothesis is in no way mechanistic.

It’s the only biologically relevant definition.

Why aren’t the new antibody sequences generated by mutation + selection during the immune response new information?

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I am glad you figured out how evolution could operate (Addendum: on further reading of your comment, its obvious you blindly echoed Ross’ erroneous claim about no new promoter emerging in Lenski’s LTEE). Don’t forget evolution works like a tinkerer: it takes preexisting parts (ranging from biomolecules to organs) and modifies or rearranges them to get novel features and it uses a collection of well-known mechanisms like gene duplications, fusions, HGT, etcetera to achieve these novel changes. Furthermore, I showed you a new metabolic pathway which evolved in S. chlorophenolicum that allowed it to degrade PCP (a pesticide that did not exist until humans created it).

Merely bringing this up shows you don’t understand how evolution operates, but I hope you do now.

Oh well, let’s see:

This is completely irrelevant, because no one denies this. What’s relevant is that several E. coli lines in the LTEE evolved the ability to use citrate as a carbon source under oxic conditions, by expressing the formerly suppressed citrate/succinate antiporter.

The citrate/succinate antiporter wasn’t co-opted, but the rnk promoter was.

This is false in two ways.

First, this is temporally false because the earliest Cit+ mutants had no duplicate rnk promoters, but were still able to uptake citrate. Later mutants, however, had duplicate rnk promoters.

Second, in a non-temporal sense this is false because whether we have two or more rnk - citT modules/duplicates, the CitT+ trait only depends on the duplication of the citT gene and its relocation downstream of the rnk promoter (or any other promoter that works under oxic conditions). In one of the CitT mutants, the duplicate citT was placed downstream of the rna promoter, not the rnk promoter.

No surprise here. Its how evolution works. Using what you have at present to make or do something new. The citric acid cycle itself was once new as well, built from other parts by the hands of that tinkerer called evolution.

In addition, it goes beyond just using catabolizing citrate in the citric acid cycle, but now doing so under oxygen-rich conditions. That’s novel.

Again no surprise here at how evolution could operate. The frequency at which Ross emphasizes this point about using preexisting parts and/or mechanisms to generate evolutionary novelties as if it were a counterpoint suggests the man, like Meerkat, does not understand how evolution works.

Which is just horrendously false with regards to a getting a new promoter. The Cit+ mutants evolved a new promoter for their citT gene to be transcribed under oxic conditions.

In addition, its quite easy to evolve new promoters from scratch. Happy reading:

https://www.nature.com/articles/s41467-018-04026-w

Word of advice. Stop getting your biology knowledge from an astronomer. If a blind man leads a blind man, both will fall into a pit.

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Then you are mixing up two quite different things. Any feature that’s “designed” to impede that organism’s abilities would be evidence of God, though a malevolent one. Natural selection works to improve those abilities, not degrade them. A feature that impedes other organisms abilities (such as the teeth and claws of predators) would be an improvement for the predator, and would likewise be evidence of natural selection. Now, Darwin famously said that any feature of an organism that existed solely for the benefit of a different species would argue against his theory. Maybe you should concentrate on finding those. But as it is, your ideas are confused and useless.

I mean that you have constructed a mishmash of many different sorts of phenomena, real examples of which either do not exist or are consistent with unguided evolution.

You made none of this clear at all. And it has nothing to do with whether mutations are directed. You have so far said nothing at all about mutations. Also, I don’t know if you were following the argument about what “random” means, but it isn’t clear that you know what you mean by it.

I don’t think you know what anything I’m saying means. No, this has nothing whatsoever to do with the definition of “species”. I’m pointing out that your hypothesis is so all-encompassing that anything at all would count as evidence for it in your mind. As long as some event or feature benefits some individual, or species, or segment of the biosphere, you count it as evidence for design. This is hopeless.

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There is no significant benefit to losing GULO activity. If you don’t get vitamin C in your diet or via supplements, you will die. That’s a massive design flaw.

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You have not in fact demonstrated that it is in God’s nature to mimic humanity, merely claimed (not particularly convincingly) that he does (at times) mimic humanity.

Given that neither of your quote-mined passages were talking about God “mimic[ing] the behavior of humans”, and in fact one of them was quote-mined from a section explicitly stating that “Information theory is not concerned with ‘patterns of intelligence’”, they do not constitute “good reason” for this claim. They do not in fact constitute any reason at all for accepting it.

  1. I offered the article as a refutation of your claim that theodicy was unrelated to the animal kingdom, not because I accepted its claims.

  2. In any case, why would I be interested in an article on the subject by Rich Deem, who (i) has no qualifications in theology, and (ii) is a professional creationism apologist (a group for which I have zero confidence in the honesty of)?

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Alright, I am going to bring some more clarity to what I am trying to argue. According to Ayala,

“Mutations are random or chance events because (i) they are rare exceptions to the fidelity of the process of DNA replication and because (ii) there is no way of knowing which gene will mutate in a particular cell or in a particular individual. However, the meaning of ‘random’ that is most significant for understanding the evolutionary process is (iii) that mutations are unoriented with respect to adaptation; they occur independently of whether or not they are beneficial or harmful to the organisms. Some are beneficial, most are not, and only the beneficial ones become incorporated in the organisms through natural selection.”

The central thesis I am trying to argue is that the “random” in mutations is an appearance.
For instance, ever since the ENCODE results, numerous studies have revealed that most, if not all, of these non-coding regions play an important role in the accurate functioning of the DNA in regards to neutral mutations (http://www.lncrnablog.com/).

The vast majority of mutations in regions that do encode proteins but are deleterious appears to be fine-tuned to lower the risk of harmful genetic changes. For instance, mutations have been shown to be guided by both the physical properties of the genetic code and the need to preserve critical protein function.

Evolution: are the monkeys’ typewriters rigged? | Royal Society Open Science (royalsocietypublishing.org)

Moreover, I argue that harmful mutations that do arise are regulated in a way that ensures the timely death of individuals so that resources are available for the young and preserve a balance between predator and prey populations because too many predators or prey can cause a collapse of the ecosystem.

Species with a Large Impact on Community Structure | Learn Science at Scitable (nature.com)

Lastly, I argue that beneficial mutations have not always been rare but directed. For instance, researchers performed a statistical study of the fossil record, using the origin and radiation of dicynodonts and sauropod dinosaurs as case studies to understand what caused the rapid increase in biodiversity for these dinosaur groups at specific points in history. They discovered that these animals did not show large biodiversity when they initially appeared on the scene. Instead, it took several million years before these two groups underwent radiation events. In both cases, bursts in biodiversity occurred after an extinction event. Thus, biological improvement was not connected with the first appearance of dicynodonts and sauropods that initiated an increase in biodiversity. Instead, the trigger appeared to be the extinction of other groups of organisms. [Just ask for reference]

Thus, I am saying that God has directed mutations over the course of history to either choose beneficial, neutral, or harmful mutations in order to guide evolution to improvement of either survival, reproductive abilities or to fit ecological niches.

I already I explained how we can theoretically test this additional mechanism to the evolutionary mechanism. So I will just move on and address everyone’s latest objections

The reason why falsifying my hypothesis this way is problematic is because it could be an example of Design Tradeoffs. This involves the situational decision to deliberately diminish or lose one quality, quantity, or property of a design in return for gains in other aspects. In other words, one thing increases, and another must decrease.

For example, Rubisco (ribulose 1,5-bisphosphate carboxylase/oxygenase) is the most abundant protein in nature that plays a crucial role in photosynthesis. However, the carbon fixation reaction happens gradually and inadequately. Moreover, rubisco can catalyze the reaction of oxygen with ribulose 1,5-bisphosphate to form unwanted compounds.

This seemingly inefficient enzyme has compelled researchers to focus their efforts on developing genetically engineered plants with better forms of rubisco that function with greater efficacy than those found in nature (Liu et al., 2010). As a result, genetically modified plants would boost food production around the world. Ellis wrote a commentary on this work, referring to it as “a superb example of unintelligent design” (Ellis, 2010).

However, previous research revealed that the difficulty of rubisco to discriminate between oxygen and carbon dioxide is not because of defective design, but instead stems from the inherent chemical nature of these two gases. To overcome this “confusion,” the enzyme slows down the carbon fixation reaction. Rubisco faces a trade-off between rate of reaction and discrimination between carbon dioxide and molecular oxygen (Tcherkez, et al. 2006). Moreover, in a response to Ellis’ commentary, Porter & Wollenweber (2010) argued that the efficiency of rubisco has no bearing on crop yields. [Just ask for references]

Thus, there could be different goals the designer had in mind or maybe there is an underlying function that may be found in the future like other psuedogenes.

The mechanisms would be “directed” mutations and natural selection

According to a following study, “We hypothesized that the isolation of such mutants should be relatively easy, would follow the same genetic trajectory as that identified in the LTEE, and would utilize information present on the chromosome and not involve evolution of new information (novel gene function). As such, we predicted that the extremely long time required for E. coli to evolve to Cit+ status was due to the LTEE conditions and not to potentiating genetic events requiring 33,000 generations.”

No, it’s you who does not understand what I am arguing. This is not about refuting evolution but showing how my hypothesis could be refuted. As you suggested, we would not expect this from an unguided process but we would expect this from a guided one. So if we saw innovations of new genes and new transporter and new metabolic pathway, then it would show a possible condition in which advanced life could have arose without human intervention and thus falsifying the hypothesis. So thank you for proving how God is a testable hypothesis.

But this is not how we test for my hypothesis because it readily allows that natural selection can effect some changes in populations. The right question is not ‘Can natural selection do anything?’ but rather ‘Can natural selection do everything on its own without human intervention?’

Or it could be a design tradeoff. For instance, the bronchial system in the human lung is not optimally designed to produce maximum efficiency in distributing air with minimal dissipation and it is relatively oversized. However, it has been suggested that the design actually is optimal when one considers physiological variability: a more optimal design of the bronchial tree would result in many more humans suffering from asthma and other lung disorders . [just ask for reference]

Again, the attributes of God have to work in accordance with each other in a logically consistent manner because he is who he is (i.e. the law of identity) and cannot not be who he is at the same time (i.e. law of non-contradiction). God must be true to “all” his attributes, because to do otherwise would be to deny his own self.

So NO. If it was truly a Sinister design, it would be evidence against my hypothesis.

As I told Michael, thank you for showing how my hypothesis is testable because it involves God “directed” mutations and natural selection.

I addressed this at the top

No, it just means that it is not the best way to falsify it, as I explained to another user.

I explained logically how and why God must be consistent with his nature based on the laws of logic. Do you want me to copy and paste this again?

I already explained how all three observations COMBINED gives us reason to infer that it is probably personal like us. You have yet to explain why those observations do not show it. Instead, all you did was cherry picked one of them and isolated it from the other observations to make your conclusion. I never argued that that one observation suggests patterns of intelligence.

No, this was not my argument. I merely responded to your assertion that our inability to comprehend, understand, and predict God’s actions applies to both nature and humanity. It has nothing to with Theodicy and even if it does, I already addressed it by explaining the Benevolent design hypothesis.

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Where does anyone on that blog reveal any such thing?

My question was about antibody genes, not the LTEE. Why would you quote my question and follow it with a non-answer?

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You may think so, but you never really do.

Case in point: That paragraph conflates two quite separate ideas. The randomness of mutations (or not) has nothing to do with the existence (or not) of junk DNA. And the ENCODE results are a joke. And showing that one or a few lncRNAs are functional does nothing to imply that the entire genome is functional. Finding a black swan doesn’t tell you that all swans are black.

You have confused mutation with fixation, though the authors of the study did not.

You can argue that, but do you have any evidence? Your reference certainly has nothing to do with your claim.

Vast confusion on your part here. Dicynodonts are not dinosaurs. You present no evidence of directed mutation. That mass extinctions decrease diversity, which subsequently recovers, is no surprise and needs no divine intervention.

Still word salad. There has been no improvement in your argument. Perhaps you could use some divine intervention. Certainly extinction of most of your words would improve it.

You haven’t. If both beneficial and deleterious mutations are directed, and if both extinction and radiation are directed, there’s nothing that could falsify divine intervention.

You have once again demonstrated that no evidence can falsify your claims, since anything could have a function we haven’t discovered. This is just another version of the “mysterious ways” defense.

Instead you have shown that your hypothesis can’t be refuted by any conceivable data.

Only because your hypothesis is specifically about a benevolent god. But benevolent toward whom? Not, apparently, toward trilobites or pantodonts, or upwards of 99% of all species that have ever lived. He does seem to really like filaria worms, but that interferes with his liking for humans. Very confusing.

Not so fast. First you will have to find a feature that exists solely for the benefit of a different species. Have you?

Sadly, no.

True, but you never managed to explain why his nature has to be what you claim. Very little in any of your conclusions actually follows from your premises, so invoking the laws of logic is ironic at best.

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