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The Scientific Impossibility of Evolution

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posted on Oct, 18 2018 @ 09:07 PM
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originally posted by: Phantom423
a reply to: dothedew

I'm afraid you're quite wrong on how organisms develop. Nature is quite remarkable in its efficiency. We don't develop useless blobs of cells unless they're cancerous or otherwise diseased. You might consider acquiring a freshman level biology book where this is all explained.


But that's his point. An evolving organ would have to go through a stage of uselessness, because there are so many component parts that are involved to become a functioning organ. Like your stomach - without the production of acid it cannot digest, but without an acid-resistant lining the acid would destroy the tissue. Not to mention the developmental necessity of organizing parietal cells in the correct location. Biology is absolutely fascinating and to attribute its complexity to randomness is stubborn atheism.
edit on 18-10-2018 by cooperton because: (no reason given)




posted on Oct, 18 2018 @ 09:43 PM
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a reply to: cooperton

Yes, I agree. And that's exactly what evolution is. A sequence of events that results in an outcome. Thank you for accepting the mechanism!

I don't necessarily agree with the randomness of outcomes. There are mathematicians who would argue this. I think your description of digestive functionality is very much to the point. This is how the engine of evolution works. I don't believe an organism has to go through a stage of uselessness. If that were true we would see groups of cells today that we would consider useless. But just like "junk genes", eventually science figures out their usefulness and why they are there in the first place. The human appendix is another good example. No one understood why we had an appendix until researchers discovered that it plays an important role by cleaning out bad bacteria. But your digestion analogy is a good one. It points exactly to the path of evolution and how nature engineers its products.




edit on 18-10-2018 by Phantom423 because: (no reason given)



posted on Oct, 19 2018 @ 06:56 AM
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originally posted by: Phantom423
a reply to: cooperton

Yes, I agree. And that's exactly what evolution is. A sequence of events that results in an outcome. Thank you for accepting the mechanism!

I don't necessarily agree with the randomness of outcomes. There are mathematicians who would argue this. I think your description of digestive functionality is very much to the point. This is how the engine of evolution works. I don't believe an organism has to go through a stage of uselessness. If that were true we would see groups of cells today that we would consider useless. But just like "junk genes", eventually science figures out their usefulness and why they are there in the first place. The human appendix is another good example. No one understood why we had an appendix until researchers discovered that it plays an important role by cleaning out bad bacteria. But your digestion analogy is a good one. It points exactly to the path of evolution and how nature engineers its products.



The point was we don't see useless sacs of intermediate tissue that remain in organisms. Like you said these are considered tumors by the body and often attacked by the immune system.

One mutation would have to create a plethora of histological, microbiological, and developmental advancements. To refer back to the stomach example, if a mutation were to occur that somehow created a protein that orchestrated the development and orientation of parietal cells into a hitherto useless pouch organ (stomach) which was in desperate need of an acid-producing cell, then I guess that would work. But that is just so implausible, because the organism needs the acid to digest food, and mutations are too random to quickly be able to gain the functionality needed to develop and emit HCl from parietal cells in a regulated manner.

This dilemma is present on every level of an organism - microbiology, organelles, cells, histology, organs and organ systems all need to be fine-tuned together. The reason we see adaptive mechanisms that can be interpreted as evolution is because all these pieces are already in play and taken for granted.

What good is a larger retina if the optic nerve can't handle all that information? If the ocular bones won't permit a larger eye ball? If the visual cortex couldn't process more information? If developmental cues cannot organize the cells in the enlarged retina? If homeostatic mechanisms aren't present in the expansion of retinal cells?

These are all the issues that need to be addressed when improving function to an organism. Genetic fragments being spewed together at random will not create these functional improvements, just like you wouldn't expect a monkey to be able to make coding improvements for facebook.


originally posted by: Phantom423
a reply to: cooperton

I don't necessarily agree with the randomness of outcomes.


So you believe it's intelligibly orchestrated?
edit on 19-10-2018 by cooperton because: (no reason given)



posted on Oct, 19 2018 @ 09:11 AM
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a reply to: cooperton




One mutation would have to create a plethora of histological, microbiological, and developmental advancements. To refer back to the stomach example, if a mutation were to occur that somehow created a protein that orchestrated the development and orientation of parietal cells into a hitherto useless pouch organ (stomach) which was in desperate need of an acid-producing cell, then I guess that would work. But that is just so implausible, because the organism needs the acid to digest food, and mutations are too random to quickly be able to gain the functionality needed to develop and emit HCl from parietal cells in a regulated manner.


This has already been worked out in the lab. I'll look up a few papers later on today. But again, we're talking about de novo genes. Whatever protein it will code for, if any, may require more than one mutation. There are hundreds of thousands of proteins. If you wanted to understand the sequence of events for a single protein, you'd have to start with the mutation(s), then transcription and nucleic acid production to generate the peptides required, etc. I don't know where you get "this useless pouch organ". Can you give me an anatomical example of what you're referring to?




What good is a larger retina if the optic nerve can't handle all that information? If the ocular bones won't permit a larger eye ball? If the visual cortex couldn't process more information? If developmental cues cannot organize the cells in the enlarged retina? If homeostatic mechanisms aren't present in the expansion of retinal cells?


If that's the case, why do we have functional eyes? We have functional eyes because the process of natural selection kicks out mutations which don't work. So if you have a person with a very large retina that doesn't work with the optic nerve, you certainly have an anomaly. But most people have functional eyes which means that developmentally mutations, transcription, translation, protein generation - all the parts of the process - work.




These are all the issues that need to be addressed when improving function to an organism. Genetic fragments being spewed together at random will not create these functional improvements, just like you wouldn't expect a monkey to be able to make coding improvements for facebook.


And that's exactly what evolution does - most of the time it improves the functionality of an organism. The process is not random. The code is embedded in the DNA. If it were random, the output would be random and it isn't. Most of us have two eyes, two ears a nose and so forth. So there is a process - a step-by-step process that accomplishes the goal and satisfies the organism's requirement.

I don't see a problem here. The problems that you outline have been worked out. If the problems as you describe them had not been worked out by nature, we wouldn't have eyes.
edit on 19-10-2018 by Phantom423 because: (no reason given)

edit on 19-10-2018 by Phantom423 because: (no reason given)



posted on Oct, 19 2018 @ 11:47 AM
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originally posted by: cooperton
One mutation would have to create a plethora of histological, microbiological, and developmental advancements. To refer back to the stomach example, if a mutation were to occur that somehow created a protein that orchestrated the development and orientation of parietal cells into a hitherto useless pouch organ (stomach) which was in desperate need of an acid-producing cell, then I guess that would work. But that is just so implausible, because the organism needs the acid to digest food, and mutations are too random to quickly be able to gain the functionality needed to develop and emit HCl from parietal cells in a regulated manner.


Define what you mean by "food".

I agree a lot of this can seem implausible when looking at the development of organisms in their current state. But think about what the earliest multicellular organisms must've been like. My guess is they weren't eating steak and potatoes and didn't have stomachs. Chances are the earliest lifeforms lived in water and energy intake came by way of ingesting simple organic compounds. Planktons and things of that nature. Small things.


originally posted by: cooperton
What good is a larger retina if the optic nerve can't handle all that information? If the ocular bones won't permit a larger eye ball? If the visual cortex couldn't process more information? If developmental cues cannot organize the cells in the enlarged retina? If homeostatic mechanisms aren't present in the expansion of retinal cells?

Think about what the earliest most primitive forms of eyeballs were. Likely light-sensing cells of some sort. Since plants can sense light then there's some plausibility. Some.

Research the origin of hox genes. Not sure you'll get answers, but your questions seem more suited to development than evolution, I think. I'm still fascinated by how it all happened and where the origin of morphological body plans comes from. That it all happened by itself to me is just as amazing as if it happened by some external influence. Self assembly, self organization, self regulation and so on... Why do chemicals do what they do? What governs the laws of interaction and attraction? Deconstruct it as far down as you can go, then work your way back up.

edit on 19-10-2018 by PhotonEffect because: (no reason given)



posted on Oct, 19 2018 @ 11:54 AM
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a reply to: PhotonEffect

I agree that mutations alone aren't the only factor and that genetics gets a lot more attention these days since the Human Genome Project released their data and Svante Paabo at Max Planck released all of his data on ancient genetics extractin in Neanderthal.

I also think that I heritability of epigenetics could play a larger roll in secondary processes like Punctuated Equilibrium. Epigenetics would explain a lot regarding PE and why we see such static morphology and then in short periods (geologically speaking of course) we see a wide array of diversity.Likewise, Epigenetics could have played a larger role in the Cambrian Explosion which as you know well, is the single largest and fairly quick, geologically, adaptive diversification event in the fossil record. But that also could change because if everyone is being honest, the fossil record for that time frame is incredibly sparse so the appearance of rapid adaptation, morphological on phenotypic diversification could be just that. How it appears because of the limited amount of strata that remains from that time frame.

When I said that epigenetics was "new" I guess I should have been a little more clear as I meant 'new' as a somewhat widely known by non professionals. Epigenetics was a small blip until my 3rd year of school. It had never been mentioned in any of my high school courses or even any of the first or second year courses. It wasn't until we started honing in on what our focus would be for the next several years and you were lucky enough to take a random class and even then, it wasn't a topic of focus until grad school. That was 20+ years ago now and today, most people have at least heard of epigenetics. Likewise, it didn't get a lot of love from students or professors unless someone was compiling data for their dissertation. Which leads to your point, lack of funding and grants because it takes extraordinary evidence to support it and lack of funding or grant money kills a lot of research early on. I know that all too well first hand trying to get funding for research that I was told by peers and mentors alike, was a waste of my time, energy and resources and that pursuing it would be career suicide. 12 years later with better techniques for extracting ancient genetics, I ended up being correct but not before having to deal with the internal politics and ass covering soured me on the whole process.

And please... Ramble away. I always like seeing differing perspectives on the topic. You can't learn anything without keeping your mind open and rambling, spitballing hypothesizing etc... Is how all good science (and bad for thst matter) begins.



posted on Oct, 19 2018 @ 12:11 PM
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a reply to: peter vlar

Not to interrupt your conversation, but this article appeared in Phys.org this week. It's relevant to the epigenetic conversation.




Study documents paternal transmission of epigenetic memory via sperm October 17, 2018, University of California - Santa Cruz





Studies of human populations and animal models suggest that a father's experiences such as diet or environmental stress can influence the health and development of his descendants. How these effects are transmitted across generations, however, remains mysterious.

Susan Strome's lab at UC Santa Cruz has been making steady progress in unraveling the mechanisms behind this phenomenon, using a tiny roundworm called Caenorhabditis elegans to show how marks on chromosomes that affect gene expression, called "epigenetic" marks, can be transmitted from parents to offspring. Her team's most recent paper, published October 17 in Nature Communications, focuses on transmission of epigenetic marks by C. elegans sperm.

In addition to documenting the transmission of epigenetic memory by sperm, the new study shows that the epigenetic information delivered by sperm to the embryo is both necessary and sufficient to guide proper development of germ cells in the offspring (germ cells give rise to eggs and sperm).

"We decided to look at C. elegans because it is such a good model for asking epigenetic questions using powerful genetic approaches," said Strome, a distinguished professor of molecular, cell, and developmental biology. Epigenetic changes do not alter the DNA sequences of genes, but instead involve chemical modifications to either the DNA itself or the histone proteins with which DNA is packaged in the chromosomes.

These modifications influence gene expression, turning genes on or off in different cells and at different stages of development. The idea that epigenetic modifications can cause changes in gene expression that are transmitted from one generation to the next, known as "transgenerational epigenetic inheritance," is now the focus of intense scientific investigation. Read more at: phys.org...


phys.org...



posted on Oct, 22 2018 @ 03:04 PM
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a reply to: PhotonEffect

Its called science, things are always missing. So your point is?



posted on Oct, 22 2018 @ 03:06 PM
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a reply to: peter vlar

It makes me wonder how much scientific advancement has been stifled due to the lack of funding or proper attention. I have to believe that evolutionary studies has been impacted in some ways. What might we know about the world if scientists had free reign and unlimited resources to pursue their hunches or passion projects.




Epigenetics would explain a lot regarding PE and why we see such static morphology and then in short periods (geologically speaking of course) we see a wide array of diversity.Likewise, Epigenetics could have played a larger role in the Cambrian Explosion which as you know well, is the single largest and fairly quick, geologically, adaptive diversification event in the fossil record.


It has to in my opinion, and not with just PE related events, but with all adaptive evolutionary events ( at differing degrees of course). Populations couldn't survive waiting around for "organism x genome" to mutate at just the right time in just the right gene, then hopefully be fit enough to propagate in environments that shift rapidly. This doesn't make sense to me. Out of this strict adherence to genetic determinism, we get things like Neutral Theory - which to me is a pendulum swing in the complete opposite direction of the MES. Point is these theories, whether it be MES or NT, rely centrally on variation being created by a change in the underlying sequence, and that these changes are random and will directly yield x phenotype. I think this could be why we get such opposing views on evolution of populations (i.e. selectionists vs neutralists), statistically speaking.



posted on Oct, 22 2018 @ 03:06 PM
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a reply to: Noinden

Why don't you answer the question.



posted on Oct, 22 2018 @ 03:10 PM
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a reply to: Phantom423

So what's your take away?



posted on Oct, 22 2018 @ 05:04 PM
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a reply to: PhotonEffect

I did. I said that something is missing. As we are talking science, I am NOT going to put my own personal biases in this.

That is your answer.



posted on Oct, 22 2018 @ 06:58 PM
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originally posted by: PhotonEffect

if scientists had free reign and unlimited resources to pursue their hunches or passion projects.



The Golden Age



posted on Oct, 23 2018 @ 06:02 AM
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a reply to: PhotonEffect

I think it's a very exciting area of research for molecular biologists. As Peter mentioned previously, although epigentics has been around for decades, it's only recently that instrumentation and methodology has allowed scientists to deduce how epigenetics interfaces with chromosomal mutations and the evolutionary process.

The implications for disease are huge. There are a number of articles that point to epigenetics as a significant new pathway to fight disease like cancer. Here's an article about gliomas - a nasty cancer of the brain:

Oncogenic Activities of IDH1/2 Mutations: From Epigenetics to Cellular Signaling



Trends Isocitrate dehydrogenase 1 and 2 (IDH1/2) mutations are frequent in brain cancer, acute myeloid leukemia, and other cancers, and are associated with a better prognosis in both astrocytomas and glioblastomas.

Mutations in IDH1/2 occur at specific amino acid residues and cause gain-of-function leading to the production and accumulation of the oncometabolite R-2HG.

R-2HG regulates the activity of numerous αKG-dependent enzymes involved in epigenetic regulation, chromatin modifications, RNA methylation, mTOR signaling, response to hypoxia, and collagen maturation.

Pharmacological inhibitors specific to the mutated forms of IDH1/2 efficiently diminish R-2HG levels and allow differentiation of cancer cells, and are currently under clinical investigation.


Gliomas and leukemias remain highly refractory to treatment, thus highlighting the need for new and improved therapeutic strategies. Mutations in genes encoding enzymes involved in the tricarboxylic acid (TCA) cycle, such as the isocitrate dehydrogenases 1 and 2 (IDH1/2), are frequently encountered in astrocytomas and secondary glioblastomas, as well as in acute myeloid leukemias; however, the precise molecular mechanisms by which these mutations promote tumorigenesis remain to be fully characterized. Gain-of-function mutations in IDH1/2 have been shown to stimulate production of the oncogenic metabolite R-2-hydroxyglutarate (R-2HG), which inhibits α-ketoglutarate (αKG)-dependent enzymes. We review recent advances on the elucidation of oncogenic functions of IDH1/2 mutations, and of the associated oncometabolite R-2HG, which link altered metabolism of cancer cells to epigenetics, RNA methylation, cellular signaling, hypoxic response, and DNA repair.

www.sciencedirect.com...

We've known about oncogenes for decades but the full blown mechanism as to how cancers develop hasn't been worked out. Epigenetics adds a very significant factor to uncovering that mechanism.

Epigenetics is more evidence that evolutionary theory is correct. We see a new area of research that ties right in to how chromosomal mutations affect an organism - for good or for bad.

And think of the role epigenetics will play going forward when humans leave this planet and populate the solar system and then further into our galaxy. We won't be in spacesuits forever. Eventually, humans will evolve into a new species compatible with the environments that we go to.

If I were a molecular biologist, that's the area of research I would be in - it's new, it's exciting and extremely relevant.


edit on 23-10-2018 by Phantom423 because: (no reason given)



posted on Oct, 23 2018 @ 06:14 AM
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a reply to: PhotonEffect




It makes me wonder how much scientific advancement has been stifled due to the lack of funding or proper attention. I have to believe that evolutionary studies has been impacted in some ways. What might we know about the world if scientists had free reign and unlimited resources to pursue their hunches or passion projects.


Money is important. But new ideas, new approaches, designing new experiments are more important. It's the guy/gal who thinks out of the box, who takes the risk in the lab to ask questions and forge ahead in research.

Look at one of this year's Nobel Prize winners: Frances Arnold




Research: Arnold is credited with pioneering the use of directed evolution to create enzymes (biochemical molecules—often proteins—that catalyze, or speed up, chemical reactions) with improved and/or novel functions.[17] The directed evolution strategy involves iterative rounds of randomly mutating proteins' genes and screening for proteins with improved functions and it has been used to create useful biological systems, including enzymes, metabolic pathways, genetic regulatory circuits, and organisms. In nature, evolution by natural selection can lead to proteins (including enzymes) well-suited to carry out biological tasks, but natural selection can only act on existing sequence variations (mutations) and typically occurs over long time periods.[18] Arnold speeds up the process by introducing mutations in the underlying sequences of proteins; she then tests these mutations' effects. If a mutation improves the proteins' function she can keep iterating the process to optimize it further. This strategy has broad implications because it can be used to design proteins for a wide variety of applications.[19] For example, she has used directed evolution to design enzymes that can be used to produce renewable fuels and pharmaceutical compounds with less harm to the environment.[17]


New ideas, new research - that's what it's all about.

edit on 23-10-2018 by Phantom423 because: (no reason given)



posted on Oct, 23 2018 @ 12:07 PM
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a reply to: Noinden




As we are talking science, I am NOT going to put my own personal biases in this.

I don't have any issue with that. I asked a scientific question, not a personal one - but I would still accept your personal opinion. You're an expert in the field so you, more than most here, are in a position to provide an intellectual answer. Unless there isn't an answer? Or my question was a bad one... In which case, "I don't know" or "Your question is a bad one" is fair too.

But for what it's worth - we're subjective beings. As much as you'd like to think you're being 100% impartial and obejective in your scientific endeavors, at the end of the day the results require an analysis by a subjective mind. If scientists didn't harbor differing opinions or interpretations of scientific evidence (whatever it may be) then science wouldn't actually advance forward.

Good day to you sir



posted on Oct, 23 2018 @ 12:33 PM
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a reply to: PhotonEffect

To be fair, what I was attempting to do was a rather... Grandiose idea and 21/22 years ago, we simply didn't have the technology to do the work I was proposing. At least not in a way that could satisfy reasonable doubts. It took a team of people working under so,some much smarter than I am who already had access to the technology and had the know how to implement his idea and then have it independently reproduced. I was searching for a needle in a hayfield trying to locate genetic remains of potential African virology ingression into Neanderthal populations in Europe. There's still no clear answer to exactly why they disappeared as a distinct sub species but some of my ideas were proven correct, like definitive hominid admixture in the Levant. We do know that Neanderthal genes I grossing into H. Sapiens populations helped to confer immunity to some European diseases that we were susceptible to but whether or not H. Sapiens brought diseases into Europe that were potential deadly Neanderthal is still a big question mark.



posted on Oct, 23 2018 @ 02:21 PM
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a reply to: PhotonEffect

It was not scientific, as no evidence has been provided to make a hypthesis, let alone a theory. So I am not going to weigh in. You said in your opinion something is missing, and I said that was science, something is always missing. I'm not currently involved in any bioinformatic work, so I'd have to go tie up my PC for weeks crunching some datta, to get even a small bit of information.



posted on Oct, 23 2018 @ 02:36 PM
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originally posted by: PhotonEffect
a reply to: Noinden




As we are talking science, I am NOT going to put my own personal biases in this.

I don't have any issue with that. I asked a scientific question, not a personal one - but I would still accept your personal opinion. You're an expert in the field so you, more than most here, are in a position to provide an intellectual answer. Unless there isn't an answer? Or my question was a bad one... In which case, "I don't know" or "Your question is a bad one" is fair too.

But for what it's worth - we're subjective beings. As much as you'd like to think you're being 100% impartial and obejective in your scientific endeavors, at the end of the day the results require an analysis by a subjective mind. If scientists didn't harbor differing opinions or interpretations of scientific evidence (whatever it may be) then science wouldn't actually advance forward.

Good day to you sir


here is what happens when scientists disagree on the interpretation of a given set of data. they propose a hypothesis, design an experiment, execute the experiment, and collect the data. rinse and repeat. with every cycle, the picture acquires a little more resolution until a high definition collection of repeatable observations forms the foundation for what is called a "theory".



posted on Oct, 26 2018 @ 10:39 PM
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originally posted by: Noinden
a reply to: PhotonEffect

It was not scientific, as no evidence has been provided to make a hypthesis, let alone a theory. So I am not going to weigh in.


My question was regarding convergence of the LP phenotype, a real evolutionary phenomenon. Nothing non scientific about it. You didn't seem to have an issue weighing in w/ your opinions earlier in this thread, claiming no Epigenetics, so I figured I'd work off of what you started.



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