Another bad year for religionists

Arkycharlie

Super Member
Another year has passed in which not a single valid scientific paper was published in which actual evidence FOR creation or for deities of any sort was even worked on, much less published.
Thus, the emptiness and uselessness of creationism in all its forms continues unabated.
Point us to a "valid scientific paper" in which ACTUAL EVIDENCE FOR abiogenesis has been published in the past year. Without abiogenesis, evolution is empty and useless, is it not?
 

evoguy313

Active member
Point us to a "valid scientific paper" in which ACTUAL EVIDENCE FOR abiogenesis has been published in the past year. Without abiogenesis, evolution is empty and useless, is it not?
Not in the least.
It is a common bit of creationist disinformation/desperation to demand that abiogenesis is linked to evolution, or that evolution needs abiogenesis. The ToE deals with the origin of species after life had begun. Pretty standard stuff.
Of course, I can present this from just the last few years, just from one researcher and his collaborators - and please note, not a single one of them is merely attacking some aspect of creation, while nearly every creation/ID paper I have ever seen has attacked evolution and NOT presented evidence in favor of YECism:


2021

Bristow, T.F., et al. (2021) Brine Driven Diagenesis of Clay Minerals in Gale Crater, Mars. Science, in press.

Tu, V.M., et al. (2021) A review of the phyllosilicates in Gale Crater as detected by the CheMin instrument on the Mars Science Laboratory, Curiosity rover. Minerals, in press.

Hazen, R.M., and Morrison, S.M. (2021) Mineralogical environments of the Hadean Eon: Templates for the Origins of Life? In: A. Neubeck and S. McMahon, Eds., Prebiotic Chemistry and the Origin of Life. Springer. In press.

2020

Hao, J., Knoll, A.H., Huang, F., Hazen, R.M., and Daniel, I. (2020) Cycling phosphorus on the Archean Earth: Part I. Continental weathering and riverine transport of phosphorus, Geochimica et Cosmochimica Acta, 273, 70-84.

Hao, J., Knoll, A.H., Huang, F., Schieber, J., Hazen, R.M., and Daniel, I. (2020) Cycling phosphorus on the Archean Earth: Part II. Phosphorus limitation on primary production in Archean ecosystems, Geochimica et Cosmochimica Acta, 280, 360-377.

Rampe, E.B., et al. (2020) Mineralogy of Vera Rubin Ridge from the Mars Science Laboratory CheMin instrument. Journal of Geophysical Research – Planets, 125, e2019JE006306.

Johnson, S., Graham, H., Des Marais, D.J., and Hazen, R.M. (2020) Detecting life on Earth and the limits of analogy. In Planetary Astrobiology (V. Meadows et al., eds.), pp. 121–150. Univ. of Arizona, Tucson, DOI: 10.2458/azu_uapress_9780816540068-ch005.

Castle, N., et al. (2020) Detection and Quantification of Minor Phases in CheMin X-Ray Diffraction Results from Mars. ACS Earth and Space Chemistry, in press.

Morris, R.V., et al.. (2020) Hydrothermal precipitation of sanidine (adularia) having full Al,Si structural disorder and specular hematite at Maunakea Volcano (Hawai’i) and Gale Crater (Mars). Journal of Geophysical Research – Planets, 125, e2019JE006324. http://dx.doi.org/10.1029/2019JE006324

Achilles, C.N, et al. (2020) Evidence for Multiple Diagenetic Episodes in Ancient Fluvial-Lacustrine Sedimentary Rocks in Gale Crater, Mars. Journal of Geophysical Research – Planets, 125, e2019JE006295. http://dx.doi.org/10.1029/2019JE006295

Fornaro, T., et al. (2020) UV Irradiation and near infrared characterization of laboratory Mars soil analog samples. Frontiers in Astronomy and Space Sciences. https://doi.org/10.3389/fspas.2020.539289

2019

Estrada, C,, Sverjensky, D.A., and Hazen, R.M. (2019) Selective adsorption of aspartate facilitated by calcium on [Mg(OH)2]-brucite. ACS Earth and Space Chemistry, 3, 1-7. DOI: 10.1021/acsearthspacechem.8b00081

Chan, M.A., et al. (2019) Deciphering biosignatures in planetary contexts. Astrobiology, 19, 28 p. doi: 10.1089/ast.2018.1903

Hao, J., Sverjensky, D.A., and Hazen, R.M. (2019) Redox states of Archean surficial environments: the importance of H2,g instead of O2,g for weathering reactions, Chemical Geology, 521, 49-58.

2018

Moore, E.K., Hao, J., Sverjensky, D.A., Jelen, B.I., Meyer, M., Hazen, R.M., and Falkowski, P.G. (2018) Geological and chemical factors that impacted the biological utilization of cobalt in the Archean Eon. Journal of Geophysical Research Biogeosciences,123, 743-759. DOI: 10.1002/2017G004067

Fornaro, T., Brucato, J.R., Feuillie, C., Sverjenski, D.A., Hazen, R.M., Brunetto, R., D’Amore, M., Barone, V. (2018) Binding of nucleic acid components to the serpentinite-hosted hydrothermal mineral brucite. Astrobiology, 18, 19 p. DOI: 10.1089/ast.2017.1784

Vaniman, D.T., et al. (2018) Gypsum, bassanite, and anhydrite at Gale crater, Mars. American Mineralogist, 103, 1011-1020.

Muscente, A.D., Prabhu, A., Zhong, H., Eleish, A., Meyer, M.B., Fox, P., Hazen, R.M., and Knoll, A.H. (2018) Quantifying ecological impacts of mass extinctions with network analysis of fossil communities. Proceedings of the National Academy of Sciences, doi = 10.1073/pnas.1719976115.

Rampe, E.B., et al. (2018) Sand mineralogy of the Bagnold Dunes, Gale crater, as observed in situ and from orbit. Geophysical Research Letters, 45, 9488-9497.

Fornaro, T., Boosman, A., Brucato, J.R., Loes ten Kate, I., Siljestrom, S., Poggiali, G., Steele, A., and Hazen, R.M. (2018) UV irradiation of biomarkers adsorbed on minerals under Martian-like conditions: hints for life detection on Mars. Icarus, 313, 38-60.

Bristow, T. F., et al.. (2018) Clay mineral diversity and abundance in sedimentary rocks of Gale crater, Mars, Science Advances, 4, eaar3330.

2017

Jiang, W., Pacella, M.S., Athanasiadou, D., Nelea, V., Vali, H., Hazen, R.M., Gray, J.J., and McKee, M.D. (2017) Chrial acidic amino acids induce chiral hierarchical structure in calcium carbonate. Nature Communications, 8, 15066.

Estrada, C.E., I. Mamajanov, J. Hao, D.A. Sverjensky, G.D. Cody, and R.M. Hazen (2017) Aspartate transformation at 200°C with brucite [Mg(OH)2], NH3, and H2: Implications for prebiotic molecules in hydrothermal systems. Chemical Geology, 457, 162-172.

Rampe, E.B., et al. (2017) Mineralogy of an ancient lacustrine mudstone succession from the Murray formation, Gale crater, Mars. Earth and Planetary Science Letters, 471, 172-185.

Hao, J., D. A. Sverjensky, and R. M. Hazen (2017) A model for late Archean chemical weathering and world average river water, Earth and Planetary Science Letters, 457,191-203.

Hao, J., D. A. Sverjensky, and R. M. Hazen (2017) Mobility of nutrients and trace metals during weathering in the late Archean, Earth and Planetary Science Letters, 471, 148-159.

Hazen, R.M. (2017) Chance, necessity, and the origins of life: A physical sciences perspective. Philosophical Transactions of the Royal Society A375, 20160353. DOI: 10.1098/rsta.2016.0353

Estrada, C., Sverjensky, D.A., and Hazen, R.M. (2017) Cooperative and inhibited adsorption of D-ribose with Ca2+ and Mg2+ onto brucite [Mg(OH)2] with divalent cations. ACS Earth Space Chemistry 1, 591-600.

Achilles, C.N, et al.. (2017) Mineralogy of an active Eolian sediment from the Namib Dune, Gale Crater, Mars. Journal of Geophysical Research, Planets, 122, 2344-2361.

Moore EK, Hao J, Sverjensky DA, Jelen BI, Meyer M, Hazen RM and Falkowski PG Geological and chemical factors that impacted the biological utilization of cobalt in the Archean Eon. (in review)

Hao J, Sverjensky DA and Hazen RM Limits on the partial pressure of H2 in the Archean atmosphere during weathering of basaltic minerals. Geochemica et Cosmochimica Acta (in review)

Estrada C, Sverjensky DA and Hazen RM Selective adsorption of calcium-aspartate ligands onto [Mg(OH)2]-brucite: Implications for calcium in prebiotic chemistry. Astrobiology (in review)

Estrada C, Sverjensky DA and Hazen RM Enhanced and inhibited adsorption of D-ribose with Ca2+ and Mg2+ onto brucite [Mg(OH)2]. Geochimica et Cosmochimica Acta (in review)

Hazen RM Chance, necessity, and the origins of life. Philosophical Transactions of the Royal Society A (in review)

Estrada CE, Mamajanov I, Hao J, Sverjensky DA, Cody GD and Hazen RM (2017) Aspartate transformation at 200 °C with brucite [Mg(OH)2], NH3, and H2: Implications for prebiotic molecules in hydrothermal systems. Chemical Geology 457:162-172

Gherase D, Hazen RM, Krishnamurthy R and Blackmond DG (2017) Mineral-Induced Enantioenrichment of Tartaric Acid. Synlett 28(1):89-92

Wenge J, Pacella MS, Athanasiadou D, Nelea V, Vali H, Hazen RM, Gray JJ, McKee MD (2017) Chiral acidic amino acids induce chiral hierarchical structure in calcium carbonate. Nature Communications 8:15066​


I eagerly await your similar list of scientific research being done by creation scientists on Creation.
 
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rossum

Well-known member
No TBS. It has never been presented higher than the coloring book level.
Ah... So you were telling fibs before, you naughty boy. Your question was answered, but you didn't like the answer, it was a "coloring book" answer.

You are admitting that we did answer your question, but that you did not like the answers you were given.

All you have to do now is to be specific about what you don't like in our answers so we can fill in the details you want to see. Yes, that does mean you will have to do some work deciding where you want us to be more specific.
 

CrowCross

Super Member
Ah... So you were telling fibs before, you naughty boy. Your question was answered, but you didn't like the answer, it was a "coloring book" answer.

You are admitting that we did answer your question, but that you did not like the answers you were given.

All you have to do now is to be specific about what you don't like in our answers so we can fill in the details you want to see. Yes, that does mean you will have to do some work deciding where you want us to be more specific.
Oh boy, if that's your answer...I really fell sorry for your belief in the religion of evo-ism.
 

rossum

Well-known member
Oh boy, if that's your answer...I really fell sorry for your belief in the religion of evo-ism.
So, you have no specific problems with what you call a "coloring book" answer. That indicates that you do not want to put in the work on your side to tell us where you want additional detail. In effect, you are not sufficiently interested in seeing what a more detailed answer would be.

That attitude does not reflect well on yourself.
 

CrowCross

Super Member
So, you have no specific problems with what you call a "coloring book" answer. That indicates that you do not want to put in the work on your side to tell us where you want additional detail. In effect, you are not sufficiently interested in seeing what a more detailed answer would be.

That attitude does not reflect well on yourself.
I've been asking for additional details for years...but you evos can't get away from the coloring book answer.
 

TeabagSalad

Well-known member
I've been asking for additional details for years...but you evos can't get away from the coloring book answer.

If you understand how mutations can spread through a population then the way they add up is obvious. It doesn't need a complex explanation because it isn't a complex idea.

If you were to put some effort in and learn what DNA is and what mutations are, then try to understand how a beneficial mutation spreads through a population then you will understand how mutations add up.

So, can you learn what DNA is?
And, can you learn what mutations are?
 

CrowCross

Super Member
If you understand how mutations can spread through a population then the way they add up is obvious. It doesn't need a complex explanation because it isn't a complex idea.

If you were to put some effort in and learn what DNA is and what mutations are, then try to understand how a beneficial mutation spreads through a population then you will understand how mutations add up.

So, can you learn what DNA is?
And, can you learn what mutations are?
Your problem is explaining how a 2nd so-called beneficial mutation can happen and effect the original..then a 3rd, 4th, 5th..etc.....each increasing the firness of the trend that is evolving.
 

rossum

Well-known member
I've been asking for additional details for years...but you evos can't get away from the coloring book answer.
Which additional details? I posted a spreadsheet showing the effect of natural selection, but you dismissed that. If you don't tell us what you want then we can't show it to you.

Tell us exactly what you want to see, in specific terms, not general terms. Yes, you will need to do that work.
 

Arkycharlie

Super Member
It is a common bit of creationist disinformation/desperation to demand that abiogenesis is linked to evolution, or that evolution needs abiogenesis. The ToE deals with the origin of species after life had begun. Pretty standard stuff.

I eagerly await your similar list of scientific research being done by creation scientists on Creation.
It is evo disinformation/desperation to demand that evolution is not linked to and doesn't need abiogenesis. If abiogenesis had not occurred, what would there have been to evolve on planet earth? NOTHING! Assuming that abiogenesis had occurred, would not evolution have had to kick in with the first proto life form in order for it to eventually become a living organism? Where does abiogenesis end and evolution begin? Oh, I forgot, there's no link between the two, is there.
 

rossum

Well-known member
Your problem is explaining how a 2nd so-called beneficial mutation can happen and effect the original..then a 3rd, 4th, 5th..etc.....each increasing the firness of the trend that is evolving.
Ah. That is something specific that we can answer.

We start with a single beneficial mutations. Natural selection will spread that beneficial mutation through the population. For example, about one third of the human population have a beneficial mutation for lactase persistence. That is the target to aim at: the one third who have inherited that first beneficial mutation through natural selection. Note that I am not picking a beneficial mutation that 100% of the human population has inherited, like the genes to form our large brains.

So, some numbers. The average human has about 75 mutations. Our population is 7 billion (7e9) so in the whole population there are 75 x 7e9 = 5.25e11 mutation in total. There are 3e9 base pairs in the human genome, and for each base pair there are 3 possible point mutations, from the current value to any one of the other three values. This gives a total of 3 x 3e9 = 9e9 possible point mutations in the genome. Doing the division gives 5.25e11 / 9e9 = 58. Every possible point mutation happens 58 times in the human population on average.

Now two thirds of the population do not have the lactase persistence mutation, so we only need to deal with the one third that do have it: 58 / 3 = 19 copies of every point mutation. How many of these are going to impact the action of the same gene? A gene coding for 100 amino acids has 300 base pairs. So, over the whole human population 300 x 19 = 5700 mutation will affect that same gene.

The majority of mutations are neutral, so not affecting the operation of the gene in any way. The majority of the rest are deleterious. We can allow, say, 1% of mutations to the gene to be beneficial. 1% of 5700 = 57. At 0.5% beneficial that would be 28 individuals with two beneficial mutations.

So, in the human population as a whole, 57 (or perhaps 28) people have both the first beneficial lactase persistence mutation, and also a second beneficial mutation to the same gene. Being beneficial, that combination of two mutations will spread through the population by natural selection.

In every generation there will be mutations in all of the genome, somewhere in the population. The proportion of beneficial mutations will vary; the faster the environment is changing the more opportunities there are for beneficial mutations, and all possible point mutations are being tried somewhere. Fundamentally this is a result of population size, which is why species with small populations find it difficult to adapt to changing environments. They lack the necessary genetic variation to acquire enough beneficial mutations to adjust to fit the changing environment.

That was not a "coloring book" answer. I will be interested to see how you respond to it.
 

rossum

Well-known member
If abiogenesis had not occurred, what would there have been to evolve on planet earth? NOTHING!
Unless you accept what Darwin wrote:

There is grandeur in this view of life, with its several powers, having been originally breathed by the Creator into a few forms or into one; and that, whilst this planet has gone cycling on according to the fixed law of gravity, from so simple a beginning endless forms most beautiful and most wonderful have been, and are being evolved. (emphasis added)​

There is no problem with evolution if it could be shown that some deity created the first life on earth, and then let it evolve. Darwin called his book "On the Origin of Species", not "On the Origin of Life".
 

TibiasDad

Well-known member
Ah. That is something specific that we can answer.

We start with a single beneficial mutations. Natural selection will spread that beneficial mutation through the population. For example, about one third of the human population have a beneficial mutation for lactase persistence. That is the target to aim at: the one third who have inherited that first beneficial mutation through natural selection. Note that I am not picking a beneficial mutation that 100% of the human population has inherited, like the genes to form our large brains.

So, some numbers. The average human has about 75 mutations. Our population is 7 billion (7e9) so in the whole population there are 75 x 7e9 = 5.25e11 mutation in total. There are 3e9 base pairs in the human genome, and for each base pair there are 3 possible point mutations, from the current value to any one of the other three values. This gives a total of 3 x 3e9 = 9e9 possible point mutations in the genome. Doing the division gives 5.25e11 / 9e9 = 58. Every possible point mutation happens 58 times in the human population on average.

Now two thirds of the population do not have the lactase persistence mutation, so we only need to deal with the one third that do have it: 58 / 3 = 19 copies of every point mutation. How many of these are going to impact the action of the same gene? A gene coding for 100 amino acids has 300 base pairs. So, over the whole human population 300 x 19 = 5700 mutation will affect that same gene.

The majority of mutations are neutral, so not affecting the operation of the gene in any way. The majority of the rest are deleterious. We can allow, say, 1% of mutations to the gene to be beneficial. 1% of 5700 = 57. At 0.5% beneficial that would be 28 individuals with two beneficial mutations.

So, in the human population as a whole, 57 (or perhaps 28) people have both the first beneficial lactase persistence mutation, and also a second beneficial mutation to the same gene. Being beneficial, that combination of two mutations will spread through the population by natural selection.

In every generation there will be mutations in all of the genome, somewhere in the population. The proportion of beneficial mutations will vary; the faster the environment is changing the more opportunities there are for beneficial mutations, and all possible point mutations are being tried somewhere. Fundamentally this is a result of population size, which is why species with small populations find it difficult to adapt to changing environments. They lack the necessary genetic variation to acquire enough beneficial mutations to adjust to fit the changing environment.

That was not a "coloring book" answer. I will be interested to see how you respond to it.
A question from a lurker…if 99% of non-neutral mutations are harmful, then don’t we have a 99% greater opportunity for harm than beneficial and would not these negative mutations have a negative impact on the 1% positive, greatly hampering if not destroying any the advancements that the positive mutations may have caused? In other words, there is a 99% greater chance that mutations would destroy the human race before the 1% could gain enough to traction to advance the race.

Doug
 

Arkycharlie

Super Member
Unless you accept what Darwin wrote:

There is grandeur in this view of life, with its several powers, having been originally breathed by the Creator into a few forms or into one; and that, whilst this planet has gone cycling on according to the fixed law of gravity, from so simple a beginning endless forms most beautiful and most wonderful have been, and are being evolved. (emphasis added)​

There is no problem with evolution if it could be shown that some deity created the first life on earth, and then let it evolve. Darwin called his book "On the Origin of Species", not "On the Origin of Life".
My comments were not addressed to you.
 

CrowCross

Super Member
Which additional details? I posted a spreadsheet showing the effect of natural selection, but you dismissed that. If you don't tell us what you want then we can't show it to you.

Tell us exactly what you want to see, in specific terms, not general terms. Yes, you will need to do that work.
The spread sheet didn't answer the question. If I remember correctly the numbers were alo made up.
 

CrowCross

Super Member
Ah. That is something specific that we can answer.

We start with a single beneficial mutations. Natural selection will spread that beneficial mutation through the population.
May spread. Not will spread.

For example, about one third of the human population have a beneficial mutation for lactase persistence. That is the target to aim at: the one third who have inherited that first beneficial mutation through natural selection. Note that I am not picking a beneficial mutation that 100% of the human population has inherited, like the genes to form our large brains.

Lactose toleration is about a gene not turning off.
So, some numbers. The average human has about 75 mutations.

Of the 75 mutations how many will you consider as beneficial? 25?
Our population is 7 billion (7e9) so in the whole population there are 75 x 7e9 = 5.25e11 mutation in total. There are 3e9 base pairs in the human genome, and for each base pair there are 3 possible point mutations, from the current value to any one of the other three values. This gives a total of 3 x 3e9 = 9e9 possible point mutations in the genome. Doing the division gives 5.25e11 / 9e9 = 58. Every possible point mutation happens 58 times in the human population on average.

Example rejected...beneficial mutations are not mentioned. Many of those mutations... 99%... would be harmful or some what harmful where the person survives and reproduces introducing this harmful result into their offspring which over millions of years might spread through the population.
Now two thirds of the population do not have the lactase persistence mutation, so we only need to deal with the one third that do have it: 58 / 3 = 19 copies of every point mutation. How many of these are going to impact the action of the same gene? A gene coding for 100 amino acids has 300 base pairs. So, over the whole human population 300 x 19 = 5700 mutation will affect that same gene.

Sounds like you're prescribing death.

Of course you never did mention how many are beneficial.
The majority of mutations are neutral, so not affecting the operation of the gene in any way. The majority of the rest are deleterious. We can allow, say, 1% of mutations to the gene to be beneficial. 1% of 5700 = 57. At 0.5% beneficial that would be 28 individuals with two beneficial mutations.

So you finally presented a number...1%....as beneficial. Problem is you made up that number. Why not 0.000,000,001%
So, in the human population as a whole, 57 (or perhaps 28) people have both the first beneficial lactase persistence mutation, and also a second beneficial mutation to the same gene. Being beneficial, that combination of two mutations will spread through the population by natural selection.

Another problem....assuming there was a second beneficial mutation. How long before it spreads to the population?
Your numbers drop from 7 billion down to 1.
In every generation there will be mutations in all of the genome, somewhere in the population. The proportion of beneficial mutations will vary; the faster the environment is changing the more opportunities there are for beneficial mutations, and all possible point mutations are being tried somewhere. Fundamentally this is a result of population size, which is why species with small populations find it difficult to adapt to changing environments. They lack the necessary genetic variation to acquire enough beneficial mutations to adjust to fit the changing environment.

Once again population size creates another problem for you as the number of people with the 2nd beneficial is 1. Your population has now become local to the beneficial mutation and the 7 billion people number can't be used.
That was not a "coloring book" answer. I will be interested to see how you respond to it.
Your reply didn't use a real number but rather a made up number of 1%. Your post fails because you used made up numbers. As I said above...Why not use 0.000,000,001% as a beneficial mutation rate?
 

Temujin

Well-known member
A question from a lurker…if 99% of non-neutral mutations are harmful, then don’t we have a 99% greater opportunity for harm than beneficial and would not these negative mutations have a negative impact on the 1% positive, greatly hampering if not destroying any the advancements that the positive mutations may have caused? In other words, there is a 99% greater chance that mutations would destroy the human race before the 1% could gain enough to traction to advance the race.

Doug
A harmful mutation damages the individual who has it, weakening its chances of passing on its genes, including the harmful mutation, to the next generation. Those individuals who do inherit the harmful mutation are similarly handicapped. The harmful mutation will quickly disappear from the population simply because any individual who has it will be less successful in passing it on. On the other hand, beneficial mutations give more success in breeding, are more likely to pass on and increase in the population.

Think of a relay race with 100 competitors. One has a regular baton, representing the beneficial gene. All the others have, instead of a baton, a live hagfish. There may be more of them, but my money is on the regular baton being the only runner left after a few changes. Of course, hundreds of new competitors join the race at each change over, most of them carrying hagfish. Despite this, over time the proportion of runners with regular batons increases while the hagfish keep getting eliminated.

Does that help? Great to hear from a lurker by the way. You should post here more often. We can do with new runners, whatever kind of baton they are carrying.
 
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