Can God be a useful "scientific" hypothesis? Yes

Are you saying that that quote I highlighted on their article ended up not actually being there conclusion at the end of their paper? Because, although I paraphrased their quote, I don’t see where I paraphrased it so much that I ended up misrepresenting their conclusions. This is what they said in their “discussions” that made me think it was their conclusion:

"As stated above, our recursive GV-based model protocell demonstrated a primitive model cell cycle comprising four discrete phases. "

Can you show me where in their paper they might have suggested something different in which I did not pick up?

Yes, for starters because the quote said that it was a model. Your misrepresentation of their conclusion did not include that.

The authors never, ever claim that their model demonstrating a primitive cell cycle is sufficient to demonstrate “how lifelike cells emerged from nonliving matter,” the words you put in their mouths.

Do you think that your genome includes any genes that are involved in making arms, but not legs? Vice versa?

I split out the recent discussions centered around information (as they are off-topic for this long thread):

Please use those threads for those conversations and leave this thread for @Meerkat_SK5’s hypothesis.

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Alright, this will be my last round of large scale changes to my hypothesis before I start creating another topic that deals with a common design model for my hypothesis.

To @Jordan, make sure you read my last response to you. No need to respond back though.

Observations

A) Life is immaterial

B) Information in DNA is mathematically identical to human language

C) Positive results in pre-biotic experiments require human intervention

D) Mutations appear to be goal-directed

Does Evolution proceed by Divine intelligence?

Consciousness interacts with DNA to increase or decrease the rates of spontaneous mutations to significantly alter the ability of an organism to evolve or alter its susceptibility to disease under environmental stresses.

How? Proton-tunneling and quantum entanglement

Why? Make sure species survive, reproduce, and fill the biosphere.

Where? Every mutation is directly caused for a specific purpose

When? From RNA viruses leading up to humans

Who? A Monotheistic God

What? A Self-collapsing Universal wave-function

Methods

The rationale behind my approach will be based upon a principle regarding causation from past events, which was popularized by Charles Lyell who also influenced Charles Darwin and Stephen Meyer, of course. “Lyell argued that when scientists seek to explain events in the past, they should cite causes that are known from our uniform experience to have the power to produce the effect in question. Historical scientists should cite ‘causes now in operation’ or presently acting causes, which would be humans in this case.

This is because experiments in quantum physics has shown that only the conscious observer has the ability to choose which aspect of nature his knowledge will probe. We have seen the same effect happen in biochemistry and biology.

For example, A hydrothermal vent simulation experiment by researchers reported that they created protocells with the capacity to self-replicate continuously for multiple generations, mirroring the behavior of biological cells. They concluded that their work demonstrated how “lifelike” cells emerged from nonliving matter under conditions similar to the hydrothermal vents found on the early earth. However, they artificially and carefully designed or selected certain molecules such as phospholipids that play a key role in forming stable vesicles.

A recursive vesicle-based model protocell with a primitive model cell cycle | Nature Communications

Another experiment suggested the same thing but within the context of actual living cells. For instance, researchers assumed that mutations were only additive and the effect of each mutation is done singly. With this assumption, the striking result of this design is that the simple additivity assumption was validated.

The success of the method implied that additive mutations is big enough for engineering potent changes in activity. Researchers said, “The natural prevalence of nonadditivity in mutations may still be a point of debate, but it might be irrelevant to the protein engineer if the case of γ-humulene synthase is representative of nature as a whole.”

The intelligent design of evolution | Molecular Systems Biology (embopress.org)

However, inserting a human observer into the experiment is not enough to establish that a Divine intelligence was the cause because we are contingent beings. This is why another experiment showing an unguided process , in accordance with the second experiment that shows a guided process, is required.

If the unguided experiment produces negative results, it would show that there could not be any conscious life before simple life emerged and support the “necessary” attribute of this intelligent designer or conscious agent. This is because “necessity” is an intrinsic attribute of God’s nature, which means showing that God is not necessary in explaining and showing how a particular feature in nature is the same thing as falsifying the God hypothesis. Atheist Physicist ,Sean Carroll, would agree with me and I encourage everybody to watch this video from 3:00 to 20:00 for more:

God is not a Good Theory (Sean Carroll) - YouTube

However, it is important to note that we cannot apply the same reasoning to present day events because humans exist and ,thus, could have been responsible for the results equally as well. This is why I will propose other ways to test whether God is still guiding evolution in the present.

Predictions

If my hypothesis is true, then the second (unguided) experiments on hypothermal vents will produce negative results because it is not guided by the experimenter.

If my hypothesis is true, then the assumption of only additive mutations will produce the positive results in one of Lenski’s failed E.coli populations.

We should find enhanced survival capabilities from other animals that are undergoing “nociceptive sensitizations”.

We should find a different goal in mind from bad designs.

If my hypothesis is false, then the one successful E.coli population will eventually produce one large mutational change causing a single-step speciation and produce an entire genome chock full of metainformation.

If my hypothesis is false, then Lenski’s 11 other failed populations will eventually produce the same positive result.

If my hypothesis is false, then the second (unguided) experiment will produce a self-replicating molecule.

I think you are confusing “lifelike” with an actual living cell, which I agree they did not demonstrate. When I said “lifelike”, I meant it literally. What they produced imitated the first cell but was not actually living according to them. So there was no misrepresentation from me and if you insist that I did, then I honestly don’t know where you are getting that idea. Again, you need to actually provide a snippet of what they said to support your claim because I really don’t see where there is foul play here.

I’m not confused. You falsely attributed the conclusion to them that:

They made no such claim that this actually happened, so your misrepresentation is especially egregious.

And when you wrote “demonstrated how lifelike cells emerged,” you misrepresented the authors’ conclusions. They made no claims about what actually happened.

I explained it and predictably, you ignored my explanation:

So given that you haven’t addressed those at all, it’s hard to take that claim seriously.

Hence, the construction of a recursive model protocell may represent a first step towards an advanced model protocell, which in some respects could mimic evolution.

See the qualifications there? Big difference. If you honestly can’t see that enormous difference (bolded) while falsely portraying the authors as being immodest about their conclusions, it provides yet another data point indicating a fundamental misunderstanding of the scientific method.

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A, B and D are unequivocally false.

C is just an iteration of the Third Law.

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How does that quote show that they did not conclude that their model demonstrated “lifelike” molecules emerged from non-life?

All it does is refute that the claim that their model demonstrated how actual living cells emerged from non-life, which I never claim they did. I am really not following you here.

“We found that four discrete phases (ingestion, replication, maturity and division) emerged spontaneously during our pursuit of a constructive approach towards a recursive model protocell. Our model protocell completed this primitive model cell cycle, in which individual processes in each phase collaborated with the next, specifically responding to external stimuli from the environment…”

"As stated above, our recursive GV-based model protocell demonstrated a primitive model cell cycle comprising four discrete phases. However, the mechanism of division of our model protocell in the division phase seems too simple for a living cell. "

A) “ 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)

B) "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)

D) Numerous studies have revealed that many of these non-coding regions play an important role in the accurate functioning of the DNA in regards to neutral mutations.

Toddler: An Embryonic Signal That Promotes Cell Movement via Apelin Receptors (nih.gov)

(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.

" Our observations suggest that the mutation rate has been evolutionarily optimized to reduce the risk of deleterious mutations. Current knowledge of factors influencing the mutation rate—including transcription-coupled repair and context-dependent mutagenesis— do not explain these observations, indicating that additional mechanisms must be involved.

Evidence of non-random mutation rates suggests an evolutionary risk management strategy | Nature

The 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.

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

Lastly, It appears beneficial mutations need to be frequent to produce real changes:

“Some believe that recent work in developing protein mutant libraries supports the hypothesis that nonadditivity is the rule rather than the exception, and occurs much more often than believed previously (Zaccolo and Gherardi, 1999).
Others have put forth both theoretical and experimental evidence suggesting that, though frequent nonadditivity of mutations is still a possibility in these contexts, its existence is not yet supported well (Drummond et al , 2005). Since the method of Yoshikuni et al identifies only additive mutations, the success of the method implies that the space of well-behaved, additive mutations is big enough for engineering potent changes in activity

The intelligent design of evolution | Molecular Systems Biology (embopress.org)

I am seriously not following you here. What does this have anything to do with what I said and argued?

For starters, it doesn’t include anything about molecules.

Why did you misrepresent their conclusions as not including even a single qualification?

Do you even know what I mean by “qualification” or “conditional”?

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Then why do you guys reject applying how we measure information in written language to DNA?

::confused face::

You just said the measurement of information in a genome and its translation and transcription is mathematically identical to measurement of information in written language!!!

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@Meerkat_SK5

You still seem to be conflating quote-mines with actual evidence.

I would like to pay particular attention to one of your claims:

This is not substantiated by:

Please note that Yokey states that “only the measurement of information” is “mathematically identical”, not that the information itself is identical.

Analogously, to state that “the process of measurement of the weight of an elephant and a flea are identical” (i.e. in both cases you use a set of scales), does not mean that the weight of an elephant and a flea is identical.

In fact he precedes this statement with the statement that:

Information theory measures information completely without regard to meaning when it is applied to language and completely without regard to specificity when it is applied to proteins.

Yockey’s whole section was arguing that this commonality in mere measurement does not imply a deeper shared common meaning.

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As usual, the cited source (Computers and Chemistry, 24 (2000) 105-123) differs from the text ‘quoted’ by @Meerkat_SK5, which can be found elsewhere. @Meerkat_SK5 is still lying about his sources.

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Yes, it is actually a quote from his Kitzmiller response. It also contains nothing about “a Divine intelligence that guided evolution” or whether “it mimics the behavior of humans NOT natural law”. Further proof that quote-mines aren’t evidence.

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I’m shocked!!!

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This was pointed out to @Meerkat_SK5 nearly 300 posts ago.

He didn’t stop misusing Yockey’s words then, and he won’t now.

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Welcome to Apologetic Groundhog Day. :stuck_out_tongue:

groundhog

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Protocells are “lifelike” molecules. This is a semantic game you are playing now and I am no longer going to play it with you.

Sure, that’s fine. I will just fall back to the analogous inference since I just realized that a literal interpretation of the relation between DNA information and human information is not necessary for my hypothesis to be valid.

Grammar of protein domain architectures | PNAS

This is classic. You accuse me of Lying about my source but you failed to realize that this source originally came from you. I merely started to use it afterwards. :joy:

You took the text from Yockey’s Kitzmiller response, but cited his paper in Computers and Chemistry.

You have a habit of cutting-and-pasting text from one document, yet citing a different document. In short, you lie about your sources.

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