I am reviewing your article. You need to supply actual evidence for your explanation. “Well, I can’t believe evolution did it” is not evidence.
You have never supported this argument with evidence.
Still not seeing any evidence. All you can seem to say is that the nested hierarchy is part of his theory. It isn’t enough to say that he proposed it. There needs to be some evidence and reasoning behind it.
That’s word salad. It doesn’t mean anything.
We already have non-design explanations for these patterns.
A search for Hox pseudogenes finds many papers.
Sorry, those are not testable predictions. You can’t even explain what the heck quantum coherence is.
None of which rules out numerous and obvious violations of a nested hierarchy.
Lacks evidence.
No evidence of consciousness given.
Currently evolutionary theories also ascribe function to lncRNAs.
Hypotheses don’t demonstrate. Evidence demonstrates. You seem to think that you can just pronounce that X has function, and that is valid evidence of function. That’s not how it works. If you want to talk about pseudogenes, then you need to show evidence for function and the percentage of pseudogenes that have evidence of function.
It does no such thing since you don’t define nor give a way to measure organized complexity.
The causal role for function is nonsense. This is why your paper is rejected.
Any results would be nonsense if you use the causal role definition.
But those nested hierarchies would group organisms which live in the same environment and occupy similar niches together. Sharks with dolphins, for instance. Oilbirds with bats. Wolves with thylacines. Phalangers with flying squirrels. Hedgehogs with tenrecs. Seasnakes with eels.
Like what? What evidence are you looking for to support our explanation?
Correct, this is because it is just a hypothesis at this stage. Future research should reveal this. I told you this before.
Yes, but it only accommodates it rather than predict it.
They are because our theory posits consciousness as the self-collapse of the universal wave function, which aligns with established findings and predictions from Orch-OR theory:
Quantum Coherence in Microtubules: Orch-OR predicts quantum coherence (the preservation of quantum properties) in brain microtubules, which has been directly supported by experiments showing quantum vibrations in microtubule molecules, suggesting coherence under biological conditions.
Microtubules and Quantum States: Research demonstrates that microtubules contribute to critical cognitive functions, supporting Orch-OR’s claim that microtubules process quantum states relevant to consciousness.
Quantum Vibrations in Microtubules: Orch-OR proposes that microtubules exhibit vibrational modes to support quantum processing. Observed resonant vibrations at brain-relevant frequencies (EEG frequencies) align with Orch-OR predictions of quantum processing in microtubules.
Orchestrated State Reduction Timing: Orch-OR posits consciousness arises from the periodic “collapse” of quantum states within microtubules at frequencies matching EEG (10-40 Hz). Empirical evidence supports a connection between these frequencies and consciousness.
Anesthetics and Quantum Processes: Orch-OR predicts that anesthetics disrupt quantum coherence in microtubules, leading to loss of consciousness. Studies show that anesthetics affect microtubule dynamics, likely impacting coherence.
Tubulin Dipole Oscillations: Orch-OR suggests tubulin proteins in microtubules act as quantum bits (qubits) through dipole oscillations. Studies indicate that tubulin dimers exhibit dynamic dipole behavior needed for quantum processing, potentially serving as biological qubits.
Correct, but this is a good thing because it fully explains those observations compared to descent, which does not apparently.
What is your point here?
I have already provided evidence for your preferred definition of function and why this definition is more relevant to the common design theory than the common designer theory. Do you want me to refresh your memory and show you it again?
Empirical and objective evidence, the kind of evidence that all other theories in science are supported by. “The hypothesis says so, so it must be true” is not evidence.
Then it needs to be pulled from the paper until there is evidence.
We are back to parsimony. We already have natural processes that explain these observations. Inventing a supernatural cause that just happens to exactly mimic the natural process is dead on arrival.
You need evidence that microtubules are involved in consciousness.
I would strongly suggest you describe this evidence.
You have yet to show evidence of quantum processing.
What evidence?
Again, show this evidence.
Again, need evidence of quantum processing.
Common descent predicts a nested hierarchy. Common design does not.
It needs to be relevant to biology, not a hypothesis. The causal role of function is not relevant to biology. It’s a nonsense definition.
For example, researchers can redesign or refactor the genome of bacteriophage T7 to create an engineered surrogate optimized for human purposes, such as resistance to virus infection—a process observed in nature [97]. This showcases how genomes encoding natural biological systems can be systematically redesigned and rebuilt to serve scientific understanding or human intentions [97].
In one instance, scientists synthesized RNA molecules of a virus and reconstructed a poliovirus particle from scratch, without a natural template [97]. This was achieved by utilizing components from another virus, such as specialized proteins (enzymes), to construct an RNA virus capable of addressing the problem of unstable RNA [97]. Upon introducing this synthetic RNA virus into cells, it successfully generated infectious poliovirus particles [97]. The instability of RNA is a well-known challenge in the RNA world hypothesis, and similar solutions have been proposed, such as the Protein-first hypothesis [7].
Now, show me evidence of pure unguided processes producing viruses.
So are you saying that we need to provide evidence for every aspect of our theory before we can publish it in a scientific journal? If so, how come this standard is not applied to the Darwin’s theory of evolution?
How does Darwin’s theory explain viruses through HGT when they cannot be integrated into the Tree of Life framework because they lack cellular characteristics [50], and no single gene is universally shared among all viruses or viral lineages [50]. Remember, viruses are polyphyletic, having multiple evolutionary origins [50]. Moreover, the presence of horizontally transferred genes in organism genomes can complicate phylogenetic relationships, deviating from the clear vertical inheritance depicted by the Tree of Life [15,25].
This phenomenon blurs the lines of evolutionary descent, as genes from diverse sources may coexist within the genome of a single organism [15,25]. As a result, establishing a singular common ancestry for an organism based solely on its genes becomes challenging [15,25]. It is much easier from a common design perspective to explain these conflicts, but it also potentially explains the phylogenetic signal as well through future research and testable predictions.
Where are your testable predictions showing how descent models explain these discrepancies as well?
Based on this study, design definitely would predict it:
Software in the natural world: a computational approach to hierarchical emergence
Just read their article for all the evidence for those predictions:
Hameroff S., Penrose R. (2014a). Consciousness in the universe: a review of the ‘Orch OR’ theory. Phys. Life Rev. 11 39–78. [DOI] [PubMed] [Google Scholar]
These predictions can undergo validation through a comparative genomics approach, as demonstrated in the discovery of convergence between pandas [23]. Upon conducting tests, at least one adaptive gene and one positively selected gene will be identified within each order and family taxa in vertebrate groups that are considered basic types [96].
In the case of pandas, predictions regarding the 3D structures of HOXA3 and HOXC10, as well as the assessment of mutation effects, were made and subsequently confirmed [23].
W. Fang, K. Li, S. Ma, F. Wei, Y. Hu, Natural selection and convergent evolution of the HOX gene family in Carnivora. Front. Ecol. Evol. 11, 1107034 (2023).
Brownyn A. Lucas et al., “Evidence for Convergent Evolution of SINE-Directed Staufen-Mediated mRNA Decay,” Proceedings of the National Academy of Sciences, USA Early Edition (January 2018): doi:10.1073/pnas.1715531115.
That’s not evidence viruses were designed 4+ billion years ago.
Yes, you need evidence in support of your conclusions. It is applied to the theory of evolution in the very same way.
That’s not what I was responding to.
“The fossil record supports the design model through patterns of stasis and sudden appearances:”
That’s what I was responding to.
You also continue with the attacks on evolution. Design has to stand on its own, not simply attack other explanations.
That’s completely false. Nowhere in the paper does it describe the types of nested hierarchies found in biology. The paper is talking about nested functions with in a single piece of software. You need to ditch that reference and find one that actually addresses nested hierarchies like they are seen in biology.
At this point, @RTBsupporter either takes the advice or keeps arguing against the reviewer. If a paper is rejected without review then it needs major changes, but all @RTBsupporter wants to do is keep beating the same drum. Reminds me of the definition of insanity (advice I should probably take myself).
It is evidence when assessed using the principle of causation. Effects observed in past events should be explained by causes known from uniform experience to produce similar effects—a methodology championed by Charles Lyell and embraced by Darwin [94]. Lyell argued that explanations for past events must rely on observed causes in our uniform experience [94]. Darwin applied this principle to demonstrate that natural selection was causally sufficient to explain observed effects in past events [94].
Similarly, our argument for a direct design framework follows the same principle. Human-engineered viruses exhibit modularity, adaptability, and functionality, which align with the observed properties of natural viruses. This parallel suggests that intentional design is a causally sufficient explanation for the origin of viruses, consistent with the principle of causation.
We agree that evidence is essential for any framework, including ours. That said, when presenting our conclusions, we explicitly acknowledged their tentative nature, noting that cognitive science and evolutionary biology also offer explanations for the observed design principles without invoking intelligent design. This acknowledgment aligns with scientific rigor and openness to alternative interpretations.
Additionally, while evidence is critical, it is worth noting that Richard Owen’s framework, which predates Darwin’s theory, provided explanations for much of the same biological evidence. Owen’s approach offered insights into nested hierarchies and structural patterns without reliance on natural selection, highlighting that multiple frameworks can interpret the same data. This historical context suggests that requiring definitive conclusions in support of design, while Darwin’s theory was allowed to build iteratively, may apply a double standard.
Our intention was not to attack evolutionary theory but to emphasize that our design model offers a distinct explanatory framework that complements or differs from existing theories. We explicitly stated that our conclusions were tentative to avoid overstating the design model’s scope.
Moreover, design frameworks can and do stand on their own, as demonstrated by their ability to generate testable predictions (e.g., quantum coherence in Hox clusters or functional modularity in viral genomes). These predictions are independent of critiques of evolutionary mechanisms and provide a basis for empirical testing. We are not relying on weaknesses in evolution to validate design; instead, we propose that design principles provide a causally sufficient alternative for specific phenomena.
I am not sure what you are getting at here. Can you elaborate?
That is not the point of why I mentioned the study. Let me break it down to you…
The study demonstrates how nested hierarchies are used in engineered systems, like software, to manage complexity through principles such as ease of maintenance, scalability, and adaptability. Hierarchical organization in software serves practical design goals, making systems efficient and manageable. The authors then extend these ideas by drawing parallels between software architectures and biological hierarchies. They argue that the same organizational principles that underpin nested hierarchies in software can also be observed in biological systems, suggesting that macroscopic processes in biology exhibit computational properties similar to those found in software systems.
While the study primarily focuses on software, the structural principles it describes (e.g., modular reuse and adaptability) are relevant to biological systems. We extend this analogy to propose that similar principles could explain nested patterns in viruses, particularly their role in increasing host adaptability or functionality. For example, viruses have been shown to increase an organism’s ability to survive, reproduce, or utilize hostile environments.
Gaelen R. Burke and Michael R. Strand, “Polydnaviruses of Parasitic Wasps: Domestication of Viruses to Act as Gene Delivery Vectors,” Insects 3, no. 1 (2012): 91–119, doi:10.3390/insects3010091.
I understand, but the intention of my response was to clarify and provide the evidence unique to our theory. Using the selection-effect definition, our theory predicts specific patterns that align with observed biological phenomena. This evidence distinguishes our framework from other explanations.
If additional evidence is required, we are open to further refinement. However, as you noted, interpretations of other forms of evidence often align with Darwinian explanations, which underscores the need for unique predictions within any framework, including ours.
You’re absolutely right, and I appreciate your patience during our discussion. My intent has been to explore every angle and extract as much constructive insight as possible before making the necessary major revisions to the paper on the preprint server. I value the feedback provided here and will use it to strengthen the manuscript moving forward, regardless of the final decision.
Humans weren’t around 4+ billion years ago, so you have no causation.
Owen’s framework does not offer an explanation because it does not predict a nested hierarchy from first principles. Common ancestry and vertical inheritance does predict a nested hierarchy from first principles. That’s the difference. There is absolutely no reason why different archetypes should fit into a nested hierarchy.
The predictions are word salad. I would work towards making those predictions plainer and related to specific experiments and specific outcomes.
They don’t demonstrate why separate programs would fall into a nested hierarchy, and those of us who actually code software have been telling you this over and over. The nested hierarchy exists BETWEEN SPECIES, not within a single genome which is the analogy you are drawing with this reference.
Again, this reference doesn’t work. You need another one.
Arguing the same thing over and over (with more cowbell) isn’t going to work. You need to change the argument. Owen’s framework doesn’t work because it doesn’t predict a nested hierarchy from first principles. OR theory is highly contested within science, so you should look for something that has a much stronger consensus if you are going to challenge evolutionary mechanisms based on an additional theory. You have also completely failed to address the observations of random mutations, be it by viral insertion, indel/substitutions, or HGT. For that matter, if you are going to claim that viruses are being controlled by a consciousness for the better of the organism and species then you need to address the harm that retroviruses cause, such as AIDS caused by HIV and higher cancer rates caused by HTLV-1.
In its current form, I would be absolutely stunned if it is even sent out for review at any reputable journal.
All those unused reference numbers suggest @RTBsupporter isn’t actually writing these replies, he’s just copying fragments that he thinks might be relevant from some other document.
You might as well be responding to a trained parrot.
The methodology we employ draws from Richard Owen’s framework, which integrates theological and scientific perspectives. Owen interpreted science through the lens of scripture, particularly the Genesis narrative, and viewed natural laws as expressions of a rational Creator [21,55]. This alignment allowed Owen to bridge scientific observations with a broader theological framework, including the Christian understanding of God as both divine and human, embodied in Jesus [71].
From this perspective, Jesus as the universal designer implies a form of human agency extending to the origins of life, aligning with the causation necessary for the design of viruses. This theological integration posits that humans, through the divine aspect of Jesus, have always existed, providing the foundational causation for viruses and their role in creation.
You know what. I think you guys may have a valid point but for different reasons. Let me approach this differently:
Consider endogenous viral elements (EVEs), which reflect ancient viral invasions integrated into genomes. For example, nudivirus-derived EVEs in certain wasps function as gene delivery systems to suppress host immune defenses. This intricate system exhibits principles of modularity, adaptability, and reuse—hallmarks of design.
Nested hierarchies could naturally emerge as a design byproduct aimed at optimizing survival, reproduction, and integration into ecosystems. For instance:
EVEs align with nested patterns, as their presence correlates with shared ancestry but also reflects functional modularity.
The modular design of viruses, integrating into host genomes and enhancing survival, mirrors human-engineered systems like software.
Therefore, if a designer’s goal is to maximize efficiency and adaptability, nested patterns would be expected, providing a rationale for their presence in biological systems. Owen’s framework aligns with this principle by attributing structural order to a universal archetype, allowing for both nested hierarchies and functional modularity.
Can you tell me which predictions you are referring to here?
Design Features and Efficiency: Research will verify that alleged design flaws (e.g., those identified by Lents) contribute to quantifiable increases in efficiency for survival, reproduction, and adaptation [41].
Adaptive Genes in Vertebrates: At least one adaptive and one positively selected gene will be identified in each order and family within vertebrate taxa [96].
ERV Functionality: Over 50% of ERVs will exhibit context-dependent or regulatory functions, consistent with findings from ENCODE.
Endorestiform Nucleus: Correlations between this brain structure’s size and fine motor control will distinguish humans from animals displaying burial or religious behaviors [60].
There are conflicts between anatomically-based family trees and those inferred from molecular similarities within reptile and mammal phylogenetic groupings
These predictions are grounded in specific observations and can be empirically tested.
While Penrose’s Orch-OR theory and Owen’s archetype share some conceptual similarities, they are fundamentally different in their scope and mechanisms. These differences allow Owen’s framework to avoid most of the criticisms directed at Orch-OR.
We acknowledge in the paper that some criticisms of Orch-OR, such as concerns about testability and empirical validation, may overlap with those of Owen’s theory. However, Owen’s framework is less vulnerable to these critiques because it draws on established biological and structural principles, rather than speculative quantum phenomena.
Importantly, both frameworks challenge the sufficiency of random mutations as the sole driver of evolutionary processes. Owen’s theory is not intended to replace evolutionary mechanisms but rather to complement them by emphasizing the role of overarching design principles and structural constraints in shaping biological diversity.
These distinctions, along with our acknowledgment and response to potential criticisms, ensure that Owen’s theory is presented on a strong foundation that aligns with broader scientific consensus.
Thank you for pointing this out. Our model does not dismiss random mutations but posits that viral systems and other genomic elements were initially designed with the machinery to facilitate adaptive changes.
Regarding harmful retroviruses, such as HIV or HTLV-1, we address this within the context of microbial evolution:
Pathogen Evolution: Viruses and microbes were created for beneficial purposes, but mutations and horizontal gene transfer (HGT) allowed some to become pathogenic. For instance:
E. coli O157 likely arose through toxin gene transfer from Shigella.
HIV originated from SIV through host-jumping events.
Design and Decay: These harmful adaptations reflect design decay rather than flawed design. Initially beneficial systems adapted to new environments in ways that became detrimental.
Thus, the harmful aspects of retroviruses do not negate their original purpose as part of a designed system, but rather illustrate how environmental and genetic changes repurpose designed elements.
“It is evidence when assessed using the principle of causation. Effects observed in past events should be explained by causes known from uniform experience to produce similar effects—a methodology championed by Charles Lyell and embraced by Darwin [94]. Lyell argued that explanations for past events must rely on observed causes in our uniform experience [94]. Darwin applied this principle to demonstrate that natural selection was causally sufficient to explain observed effects in past events [94].”
Those are made up hallmarks of design. Viruses naturally adapt through evolutionary mechanisms. They contain genes, so of course they are modular. The replicate, so of course there is reuse. All of these are non-design features.
No, they wouldn’t. This is something you have made up from whole cloth.
Describe the experiment and expected results based on this prediction.
We would expect to see adaptation through evolutionary mechanisms.
You use a nonsense definition of function, so this fails right away.
What does this have to do with anything?
As expected from evolutionary mechanisms.
There is no reason why Owen’s archetypes should fall into a nested hierarchy.
Frameworks don’t challenge anything. Only evidence can do that.
It seeks to replace common ancestry between lineages. That’s not complementary.
That’s a big fail. Is this supposed consciousness not in control?
You are essentially saying heads you win, tails I lose. That’s nonsense.
Let me clarify and simplify my earlier explanation:
Owen’s theory involves a universal common designer, which is conceived as an eternal, divine human. This designer provides the causal explanation necessary for the design of viruses. The existence of this designer is supported by theological and scientific reasoning followed by scientific evidence, making this an inference grounded in evidence rather than an assumption.
While these features might appear to result from evolutionary mechanisms, we argue they reflect front-loaded design. This view synthesizes Owen’s archetype theory with the virus-first hypothesis. For example, the prediction that over 50% of ERVs will exhibit context-dependent or regulatory functions aligns with findings from ENCODE, suggesting intentionality and modularity in viral design.
The modular and reusable nature of viral elements, analogous to human-engineered systems, supports the notion of purposeful design rather than random processes.
This inference is based on the vera causa principle advocated by Charles Lyell, which emphasizes causes observed in uniform experience. Observations of viruses demonstrate effects consistent with those seen in human-engineered systems, such as modularity and efficiency.
However, I am not claiming this applies universally. The model predicts nested patterns in many cases but also anticipates violations where design goals dictate deviations.
Testing Alleged Design Flaws:
Experimental Setup: Select organisms with alleged design flaws, such as human heart issues or the GULO gene deficiency.
Data Collection Methods: Measure survival rates, reproductive success, and adaptation to environmental changes in organisms with and without the alleged design flaws.
Statistical Tests: Use statistical analysis, such as t-tests or ANOVA, to compare the performance metrics between organisms with and without the alleged design flaws.
You are correct that adaptation can occur through evolutionary mechanisms. However, this prediction is intended to challenge common descent rather than the mechanisms of evolution. By demonstrating the functional benefits of traits traditionally considered flaws, this approach highlights the plausibility of a common design framework.
This critique is specific to Owen’s theory and valid as an objection. However, the nested patterns observed in biological systems could naturally emerge as a byproduct of functional and modular design principles. For example:
Viruses and EVEs display functional modularity that aligns with nested patterns.
Nested hierarchies optimize adaptability, functionality, and scalability in biological systems, similar to engineered systems.
Agreed. This is why evidence supporting the virus-first hypothesis and its alignment with Owen’s framework provides a direct challenge to Darwinian explanations. If viral systems predate cellular life and exhibit design-like properties, they undermine the sufficiency of common descent and natural selection alone.
Common descent theory is a separate theory from natural selection and how it came about. So I don’t see how this is relevant to what I said.
While the common descent framework focuses on lineage relationships, Owen’s theory addresses the origin of structures and functions. These are separate but complementary aspects. For example:
Common descent explains the phylogenetic relationships between species.
The design model explains the emergence of complex systems and nested patterns.
This distinction allows both frameworks to coexist without contradiction.
It depends on what you mean by being in control.
Our model suggests that viruses represent front-loaded designs, indicating that the designer is not actively controlling every event but instead implemented a system capable of self-regulation and adaptation. This aligns with human design practices, where systems are created to achieve specific objectives and maintained with minimal intervention once those goals are met.
This approach explains key events in evolutionary history, such as the development of multicellular life, while acknowledging that not every detail is accounted for within this model.
This prediction is grounded in empirical testing to avoid such an interpretation:
Prediction: Alleged harmful design features, such as those outlined by Rubicondior [73], will demonstrate measurable benefits to survival, reproduction, or adaptation.
For example:
Features traditionally considered harmful, like the human appendix or certain genetic redundancies, may prove advantageous under specific conditions.
This contrasts with the Darwinian view that natural selection operates solely through fitness maximization at the individual level, without regard for collective benefits.
By testing these claims, we aim to demonstrate that design principles offer a viable alternative explanation.
And if I ask for evidence, I will get the usual run around that usually dead ends in “because Owen says so”.
That prediction is meaningless if you are using the causal role for determining function.
No, it doesn’t.
Humans make ice. Does this mean all ice in the universe is made by humans? No. This is a nonsense argument. Just because humans can do something does not mean nature is not capable of it.
People used to die of scurvy.
People die of heart disease.
As soon as you are shown negative effects you then claim “decay”. This seems entirely unfalsifiable.
It doesn’t challenge common descent. I can’t understand how finding positively selected genes challenges common descent. We can even see this happening at the species level.
They don’t exhibit design-like properties. This is just an empty assertion.
“You are correct that adaptation can occur through evolutionary mechanisms. However, this prediction is intended to challenge common descent rather than the mechanisms of evolution.”
You continually contradict yourself.
Anything could be the byproduct of design principles. Again, a quote from Romanes’ essay from 140 years ago:
Your entire premise was already refuted 140 years ago.
This has already been shown to be false. When shown the falsification of this prediction, you claim “decay”.
Christian theology, while it includes the idea that Jesus has always existed doesn’t necessarily have him being human for all that time.
But even if he was, which is the best case for your claim, there would still have only been one human 4bya, not humans.
It wasn’t. You were asked to quote the relevant passages from your paper. You weren’t asked to copy and paste bits of it instead of replying. You definitely weren’t asked to do so without making it clear which parts of your replies were your own words and which were from the article you asked us to review.
This leads to (at least) two problems.
The first is that one of the reasons you were asked to quote the relevant sections of your sources was to find out if you understood the well enough to identify the relevant sections. Since you’re now posting those sections without marking them as such, we’re left with the probability that you don’t understand your own posts.
Second, that paper was (supposedly) authored by Ross and Rana, not you. By posting sections of it as your own words, you are (if it was by them) plagiarizing them.
Since the first and last parts of your post were nonsense, I see no point in DynorodTMing the rest.