I dont think you are really addressing the problem. …

Comment on Southern Adventist University opens Origins Exhibit by Sean Pitman.

I dont think you are really addressing the problem. You hopefully suggest, “Many features, of dogs for example, are polygenetic – such as height or color, etc. For example, the determination of coat color and pattern is a polygenic in that these features are controlled by more than one gene or gene complex.”

Indeed that is true but at each of these polygenic sites there are only at maximum 4 possibilities in a [breeding] pair of 2.

That’s right, but a polygenic trait is not governed by a single site. It might help to get a few concepts straight here. “Quantitative traits refer to phenotypes (characteristics) that vary in degree and can be attributed to polygenic effects, i.e., product of two or more genes… Polygenic inheritance refers to inheritance of a phenotypic characteristic (trait) that is attributable to two or more genes and can be measured Quantitatively… Unlike monogenic traits, polygenic traits do not follow patterns of Mendelian inheritance (separated traits). Instead, their phenotypes typically vary along a continuous gradient depicted by a bell curve… Most phenotypic characteristics are the result of the interaction of multiple genes.” (Link)

Sometimes hundreds of genetic loci are involved in governing the expression of a given trait or feature. For example, height in humans is governed by the interaction of some 200 genetic regions. Genome-wide association studies in humans, laboratory animals, and outcrossed domesticated plants such as maize show that the genetic architecture of most phenotypes tested to date—including body size, body mass index, lipid level, and flowering time—appear to be under the control of hundreds of genes, each contributing a very modest amount to the overall heritability of a given trait. This makes a great deal of variety of expression of a given trait possible – even starting with a very small population (such a just two individuals). This is why my brother and I look so different despite having the very same parents. He has dark skin. I have light skin. He is hairy. I’m not. He has dark green eyes. I have light greenish blue eyes. etc. The is also why two dogs can produce a mix of very different looking puppies within the same litter – to include significant differences in color, hair texture, size, etc…

Of course, it not always the case that a wide variety of a phenotypic trait expressions is the result of a large number of genes. When it comes to modern dog breeds in particular, it seems like relatively few genetic regions of large phenotypic effect underlie most traits.

For example, dog size (the variation of which is greater across dog breeds than in any other terrestrial species) seems to be controlled mainly by six genetic regions (CFA15.44226659, CFAX.106866624, CFA10.11440860, CFAX.86813164, CFA4.42351982, and CFA7.46842856) – with a few dozen other more minor genetic influences. “The signal on CFA15 corresponds to the location of IGF1 which encodes a growth factor previously described to control a significant proportion of size variation across dog breeds. The CFA10 signal corresponds to the location of HMGA2, a gene known to affect body size variation in humans and mice. Both HMGA2 and a locus corresponding to the CFA7 signal, SMAD2, have been previously associated with dog body size. In contrast, the signals on CFA4 and CFAX hits have not previously been associated with body size variation in dogs. Interestingly, the CFA4 signal contains (among other genes) the STC2 locus, a known growth inhibitor in mice. The two signals on the X chromosome lie in separate LD blocks that each contains dozens of genes.”

http://www.plosbiology.org/article/info%3Adoi%2F10.1371%2Fjournal.pbio.1000451

So, although such traits in dogs are controlled by fewer genetic regions, it seems quite clear that far more than just “4 possibilities” could be produced by a single breeding pair when it comes to most phenotypic traits – depending upon the combination of these genetic loci and how they control the expression of a given trait.

Of course, “in all six regions, wolves are not highly polymorphic” – as would be expected since wolf morphology is fairly uniform (not having been bred to highlight unique morphologic features that could be isolated in relatively short order). Of course, there are additional allelic options, based on unique mutations, within modern dogs, as compared to the wolf…

For example, the short stubby legs of Dachshunds, Basset Hounds, Corgis, and the like have an extra copy of a gene that codes for Fibroblast Growth Factor 4 (FGF4). This extra gene is a mutated retrogene. Neither the introns nor the upstream promoter sequences of the gene are present in the inserted retrogene. However all exons are present, with no alterations in the coding sequence, as well as the 3′ UTR and poly-A tail – characteristic of retrotransposition of processed mRNA. The lack of introns normally found in FGF4 genes causes the retrogene version to malfunction. In short, this malfunctioning retrogene results in the overproduction of FGF4 transcript. The “atypical expression” of the FGF4 transcript in the chondrocytes apparently causes the inappropriate activation of one or more of the fibroblast growth factor receptors – such as FGFR3. An activating mutation in FGFR3 is responsible for > 95% of achondroplasia cases, the most common form of dwarfism in humans, and 60–65% of hypochondroplasia cases, a human syndrome that is more similar in appearance to breed defining chondrodysplasia (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2748762/). In other words, this overproduction of FGF4 is thought to disturb the normal process of limb growth during fetal development, such as turning on key growth receptors at the wrong time, leading to short legs in dogs. What happens is that the development of long bones is curtailed due to calcification of growth plates, resulting in short legs with a curved appearance.

This example illustrates the fact that dramatic phenotypic differences can be produced by gene dosage alterations – i.e., an increase or decrease in gene products. Mutations that cause an over or under production of gene products are not uncommon and can be realized in relatively short order – especially in larger populations.

Remember, it is far far easier for mutations to cause a loss or disruption or even a gain of the same basic type of pre-established functionality vs. the evolution of entirely novel, qualitatively novel, functionality – which does not happen at all beyond very low levels of functional complexity.

This is why such novel features in various breeds, such a dog breeds, or even “species” that were derived from the same ancestral gene pool, can be realized in such short order. They really have nothing truly new, qualitatively new, beyond very low levels of functional complexity – compared to what their original parents had. Almost all examples of the evolution of “new” functional traits or alleles are based on the disruption or loss of a pre-existing trait or functional system. And, those occasional examples of evolution where qualitatively novel functional systems are produced in observable time are all at very very low levels of functional complexity (requiring a minimum of no more than a few hundred specifically arranged amino acid residues).

That is why I argue that the current phenotypic variety of breeds, such as dogs, is based on front-loaded genetic information with very little if any qualitatively novel traits evolving which were not based on the quantitative increase or decrease of expression of pre-existing genetic elements – something that can be achieved in very short order.

I am again confused. Are you arguing for dogs derived from 2 wolves or not? If you take the genesis account literally which I understand you do, dogs are unclean and you must consider that they are therefore derived from the most severe genetic bottleneck possible.

What I’m saying here is that it would be possible to produce all or nearly all the phenotypic diversity of modern dog breeds within a very short time starting with only two individuals. I’m not quite sure why you think longer periods of time would be required for selective breeding to produce essentially the same degree of phenotypic variety that we see today? Where is the limiting factor here?

It would help your argument if you could point to an example of a reintroduction program where there was success with 2 genetically isolated animals. I certainly cannot find any.

If you care to read the paper on reintroduction of wolfs into yellowstone

http://www.ncbi.nlm.nih.gov/pubmed/17877715

You will see they followed the standard practice built up based on long experience and reintroducing around 40 animals. [It is argued whether sustainable populations are around 30 or if 50 are needed)

Which brings us back to our previous discussion about declining genomic quality over time. As already explained in some detail, this decline is due to the continual build-up of detrimental mutations in the gene pools of all slowly reproducing creatures far far faster than natural selection can get rid of them. The death rate required for natural selection to deal with this problem is simply far too high. That is why inbreeding within small groups of animals or people is such a big problem today. It enhances odds of the fixation of detrimental mutations within a population – resulting in a greater chance of genetic meltdown and extinction within a shorter time span. This is also why many modern dog pure-breeds suffer from far more genetic diseases than do hybrid dogs.

There is also, of course, the problem of the dangers of living in the wild – of dealing with random accidents, injuries, sickness, disease, infertility, ext. Increasing the population size helps to alleviate these problems when trying to start a new colony.

The experience with 4 avian species again shows that populations with low genome equivalents are subject to significant and life threatening inbreeding and loss of genetic diversity

http://www.ncbi.nlm.nih.gov/pubmed/20825445

2 genome equivalents is clearly in the unsustainable range according to all the current practical and theoretical models of population genetics.

In modern times, yes. Thank you for highlighting my point. This was not the situation, however, when gene pools were much closer to their original creation and had not yet built up so many detrimental mutations…

I really don’t know why you seem to be continually arguing for naturalistic mechanisms for scenarios around the miraculous global flood account. Can’t you accept that derivation of all populations from the ark is genetically untenable and accept it as miraculous. Creation science is intrinsically miraculous; turtles all the way down. Just accept it and don’t pretend it is some scientific hypothesis that can be tested by experiment. As prof Kent argues it is even worse because you not only try to argue a particular interpretation is scientifically valid but then pin your faith on your ability to argue the scientific validity. It’s a miracle. Move on to the consequences and you might not find it is so foundational.

There is no need to invoke God to explain the phenotypic diversity of living things beyond His original programming of the parental population – His “front-loading” of the gene pools if you will. God did not need to step in and create novel alleles within wolves or dogs in order for the diversity of dog breeds to be realized in very short order via natural processes that have been in place since the beginning of life on this planet. It is simply your lack of understanding that makes you think that a subsequent Divine miracle, or an ongoing series of miracles of deliberate design, would have to have been required. What? would you really have me believe that God was the one who stepped in and deliberately created the retrovirus FGF4 gene for the “inappropriate activation” of FGFR3? so that modern dogs could have stumpy legs? I suppose God also causes achondroplasia in humans? Come on now…

The same is true for the nature of the geologic / fossil records. No Divine miracle is required to explain most of their features from a Biblical perspective. Sure, there are still unanswered questions. However, the weight of evidence, science itself (true science that is), strongly supports the claims of the Bible. Faith in the reliability of the Bible as the true Word of God need not be blind or indistinguishable from wishful thinking…

Sean Pitman
www.DetectingDesign.com

Sean Pitman Also Commented

Southern Adventist University opens Origins Exhibit
@Pauluc:

I agree with Prof Kent. I think you have a few problems

1] You have used an arbitrary statistical limit to define a universal limits of evolutionary development and speciation

The limitation is not arbitrary. It is both observed in real time and can be calculated to show that it (a minimum requirement of 1000 specifically arranged residue positions) is the most likely limitation this side of trillions of years of time – from the perspective of RM/NS.

2] You have conceded that 80-90% of the genetic variation between species has been acquired over 4000 years. (I am surprised that you feel able to extend this to 5000 years given EG White’s writings.

It depends upon what type of variation you’re talking about. Certainly all variation at lower levels of functional complexity could easily be realized in this period of time.

3] You allow for rapid development of phenotype and novel repurposing of proteins in the development of evenomation

DNA can and does rapidly mutate – true.

4] You claim some value for a limit of 1000fsaar but do not seem able to identify concrete examples of this during speciation.

Speciation is not based on producing novel functional complexity beyond very low levels of functional complexity. In fact, speciation can be based on functionally neutral genetic changes. Also, there are no examples of evolving beyond the level of 1000 specifically arranged amino acid residues because it is statistically impossible to do so. Only variations at low levels of functional complexity can be or ever have been demonstrated.

5] Indeed comparative genomics between man and apes suggests that the differences between these species is mostly at the single nucleotide level and in gene duplications
http://www.ncbi.nlm.nih.gov/pubmed/19212409
http://www.ncbi.nlm.nih.gov/pubmed/19718026
http://www.ncbi.nlm.nih.gov/pubmed/21270892
http://www.ncbi.nlm.nih.gov/pubmed/20448178

and that there seems to be none of the barriers of 1000fsaar complexity that Sean suggests to limit evolution of homo sapiens from an hominid ancestor common with great apes.

Humans and apes are quite different in various respects, to include brain structure and function – which is thought to be based on numerous differences in genetic regions that code for miRNAs (around 8% of which are human specific).

“miRNAs recently have been implicated in synaptic development and in memory formation. As the species specific miRNAs described here are expressed in the brain, which is the most complex tissue in the human body, with an estimated 10,000 different cell types, these miRNAs could have a role in establishing or maintaining cellular diversity and could thereby contribute to the differences in human and chimpanzee brain … function.”

Eugene Berezikov, Fritz Thuemmler, Linda W van Laake, Ivanela Kondova, Ronald Bontrop4, Edwin Cuppen & Ronald H A Plasterk, “Diversity of microRNAs in human and chimpanzee brain”, Nature Genetics, Vol 38 | Number 12 | December 2006 pp. 1375-1377.

The Y-chromosome is even more unique. A study published by Nature in early 2010 showed many striking differences between human and chimp chromosome structure, gene content, and even qualitatively unique genes between the two species. As far as looking at specific genes, the chimp and human Y-chromosomes seem to have a dramatic difference in gene content of up to 53 percent. In other words, the chimp is lacking approximately half of the genes found on a human Y-chromosome. Because genes occur in families or similarity categories, the researchers also sought to determine if there was any difference in actual gene categories. They found a shocking 33 percent difference. The human Y-chromosome contains a third more gene categories, entirely different classes of genes, compared to chimps.

Hughes, J.F. et al. 2010. Chimpanzee and human Y chromosomes are remarkably divergent in structure gene content. Nature. 463 (7280): 536-539.

For further discussion see:

http://www.detectingdesign.com/pseudogenes.html#Key

6] You define species classification as being arbritary but have some nebulous concept of a barrier of complexity for potential changes induced by the acquired changes which you concedes occurs rapidly and frequently.
This limit to complexity you relate to some theoretic 1000fsaar limit.

Again, this limit is both observable and calculable based on known distributions and densities of viable sequences in sequence spaces at various levels of functional complexity.

You seem to support models of rapid evolution by Darwinian mechanism inside a 1000fsaar limit; if you think them scientific they must be tested by reference to reality and real data. I suggest you look at the genomic data and point out the genetic differences that correspond to your 1000 FSAAR limit.

I’ve given you numerous examples already of systems that require a minimum of far more than 1000 specifically arranged residues. How many more examples do you need?

You might like to also comment on you model of evolution of all Y chromosome variation that exists today from a single Y chromosome 4000 years ago at the time of flood.

In case anyone suggests there were 4 males on the boat and therefore there were 4 Y chromosomes, Noah and his 3 sons would all have the one identical Y chromosome because of transmission from Noah to his sons. Humans in terms of Y chromosomes are equivalent to a breeding pair.

The variation in the Y chromosome in humans today, like all other unclean animals must therefore date to mutations in the last 4000 years.

http://www.ncbi.nlm.nih.gov/pubmed/20981092

All this genomic sequence is now freely available so there is no excuse for not testing it except the paucity of value you see in your arguments.

What testing would you want? Low level genetic changes can and do take place very fast – especially in larger populations. There are no examples of higher level changes because, statistically, they are impossible this side of a practical eternity of time.

Both Jeff Kent and I have both offered advice in publication of these experiments in the peer reviewed literature.

Until you give me some real evidence based on experimental data you seem to be simply doing what Bob Ryan abhors; telling just so stories.

Sit down. Do the math for yourself. Then, come back and talk to me about who is telling the just-so stories regarding the creative potential of random mutations and natural selection (RM/NS).

Sean Pitman
www.DetectingDesign.com


Southern Adventist University opens Origins Exhibit
@pauluc:

Thanks for that. Wise choice, that I knew given your intelligence you would make despite you vigorous defence of your near perfect pair model of origins. We will pass over the assumption that there are no deleterious mutations and that you discriminate against animals with variant expression of FGF4 and consider it deleterious. Why the prejudice against short legs?

When you disrupt a pre-existing system and this disruption has a beneficial effect, that doesn’t mean that this benefit wasn’t the result of a loss of pre-existing genetic information. It’s like a population of cave fish who have lost the ability to grow eyes. Such a mutation, in certain environments, is beneficial. It takes a lot of energy to maintain eyes that aren’t beneficial in the dark. Yet, mutations that result in the loss of ability to grow eyes are degenerative in nature in that they remove or disrupt pre-existing genetic information.

The same thing is true of mutations that disrupt the normal expression of FGF4 – which results in the abnormal structure of the stumpy legs of certain breeds of dog. Such mutations are degenerative in nature in that they aren’t based on anything new; they are based on the disruption or loss of pre-existing systems of function.

In short, your argument there is no such thing as a degenerative mutation, informationally speaking, is clearly mistaken. A correct understanding of this concept is vital to understanding the creative potential and very clear limits of the Darwinian mechanism of RM/NS.

Lets recap what we do agree on

1] A genetically bottle-necked population such as 2 Daschunds lacks the genetic diversity to allow rapid selection of phenotypic novelty by selection among allelic variants. imposing a bottleneck on a non-bottle-necked population of wolves is also suspect so you choose 100 pairs.

This is not the reason why I would choose 100 pairs vs. a single pair of wolves with non-degenerative gene pools. The reason, as already explained, is only a timing issue. The 100 pairs would be more rapidly adaptive in the near term. However, in the long term the offspring and larger population from single pair of genetically perfect wolves would be just as adaptive . . . due to the evolution of novel alleles over the course of time.

2] In this you seem to be accepting the conventional scientific view that a bottle-necked population is undesirable as it has dramatically decreased repertoire in their gene pool and high levels of homozygosity. Lack of variation rather than deleterious mutation is the issue.

Not true. Deleterious mutations are far more problematic for modern gene pools than is the lack of allelic diversification. It is the enhanced expression of recessive detrimental mutations that is the primary threat.

Sure, modern environments have far more virulent pathogens than did the original environment when all gene pools were still perfect or near perfect. Various alleles have evolved over time to more effectively deal with these pathogens. The loss of these allelic variations would make modern bottlenecked populations more susceptible to disease. However, as already explained, this was not the problem it is today right after the Flood since pathogens had not yet evolved to their current levels of virulence.

3] You accept that wolves and their subfamily dogs, foxes, jackal and coyotes are all derived from 2 animals living 4000 years ago. This by definition is a genetic bottleneck

Yes. And their allelic diversification since that time is not miraculous since it can be explained by rapid low-level allelic evolution.

4] These animals had 2 genomes and maximum of 4 haplotypes and alleles for every gene. Any additional alleles has arisen subsequently as random or non-random mutations.

Yes . . . although I don’t exactly know what you mean by “non-random mutations”?

5] The vast majority of the SNP (>2.5million) arose in the progeny of this pair by mutations over a period of 4000 years.

Give or take a thousand years or so, yes.

5] The multiple DLA alleles at the class II arose denovo since these 2 animals provided the 4 original alleles.

You mean HLA alleles? – yes.

6] Similarly in man [assuming 8 people on the ark and that Noahs sons were the progeny of he and his wife, and that his daughter in laws were unrelated to each other and to Noah and his wife and were heterzygous] there were a total of 10 alleles at HLA B. this means that 1590 of the HLA-B alleles currently recognized by genotype in man have arisen denovo over the last 4000 years.

Yes.

7] In this case if we accept Seans value of 1600 HLA-B allels then 99.3% of the variation seen today has arisen by chance mutations and selection.

Yep.

8] If we conservatively estimate the HLA-B serological specificities associated with amino acid changes and differences in peptide binding are 60 and all of the 10 HLA-B alleles in the 8 people on the boat were associated with serological specificity then we can assume that at least 83% of the variation in the highly functional amino acid changes in HLA-B seen the current population were derived by chance mutations.

That’s right.

9] There seems little reason to argue that the same process that must occur in highly polymorphic systems such as the MHC do not occur in other gene systems.

Other genes also experience random mutations and allelic variations – more rapidly in larger populations.

9] If between 83% and 99% of the variation in the progeny of 2 animals and 8 humans arose rapidly over 4000 years and in the case of canines this acquired variation was able to generate at least the species wolves, coyote, foxes and Jackals, it is hard to then mount a consistent criticism that species can never arise by acquired mutations.

That’s right. It’s not that different “species” can’t evolve because the species concept isn’t based on measures of novel functional complexity within different gene pools. All genetic definitions of species are based on non-functional aspects of genetic mutations, or at least don’t take into consideration the level of functional complexity involved. Given these species definitions which are not based on functionality, on levels of functional complexity, it is very easy to rapidly evolve novel species via the mechanism of RM/NS.

That is why the Biblical concept of unique “kinds” of gene pools is more accurate as far as the limits of evolutionary divergence is concerned. Unique kinds of gene pools that are based on qualitatively unique functional elements beyond very low levels of functional complexity are isolated from each other. These lines of complexity cannot be transgressed by any mindless evolutionary mechanism.

10] You can of course invoke miracles. Indeed I think it is the only logically consistent conclusion given your premises.

Why would I need to do that? I ask you again, where is the need to invoke miracles here? beyond the original creation of the various “kinds” of gene pools and their potential for rapid genetic and phenotypic diversity over time?

1] All species variation arose over 4000 years from an extremely bottle-necked population

Within the same “kind” of gene pool, yes.

2] Mutations account for any variation not present in the original near perfect pair.

Yes . . . without the need to invoke additional miracles of intelligent design.

3] These mutations cannot generate anything useful or novel that can contribute to the phenotypic development of breeds or species.

Not true. Mutations can and do contribute useful as well as novel elements to the phenotypic development of breeds and “species”. I’ve specifically explained this concept several times to you.

I have great faith in your ability to reconcile these but I do not have the intellectual horsepower to do so except by invoking miracles.

That is because you draw no distinction between levels of functional complexity within gene pools.

Sean Pitman
www.DetectingDesign.com


Southern Adventist University opens Origins Exhibit
@pauluc:

A pubmed search for “sequence space” AND “functional complexity” yielded 30 publications none of which convey your perspective but do follow the scientific tradition of testing models against biological data in order to understand the operation of the natural world.

That’s right. There are no papers, of which I am aware, that detail the limitations of the Darwinian mechanism of RM/NS when it comes to levels of functional complexity.

Of course, the basic concept of different levels of functional complexity is fairly well defined in literature. However, no one has gone to the next step and detailed the limitations that this concept presents to Darwinian mechanism of RM/NS. No one has published anything at all about the average time necessary for random mutations to find anything qualitatively novel at various levels of functional complexity.

Yet, this concept is not beyond reach for scientific investigation. In fact, there is enough information for anyone interested in this question to sit down and work out the math for him/herself. The results are quite surprising – from an Darwinian perspective anyway. There is a very clear exponential decline in evolutionary potential with each linear increase in the level of functional complexity under consideration.

Now, don’t take my word for it. Do the math yourself. Don’t simply rely on what you read in literature. Why not actually do some of your own investigation into this question?

For example for speciation

1] We say that with time there is accumulation of genetic change or mutations by a variety of mechanisms including point mutations, indels, duplication events and within a population there is thus variation and selection for a phenotype that reflects a favourable genotype. With time pheotypic selection leads to genetically isolated populations which you can call a species.

Great! I have no problem with this except for the fact that it details no limitations to the potential for producing qualitatively novel systems of function beyond very low levels of functional complexity.

2] You start with a model of all possible protein sequences. Calculate the possibility that anything big and complex is statistically impossible within your sequence space matrix and then decide this is the basis of limitations of “RM/NS” and the limit of speciation. You may well be right but you do not seem to appreciate that at least to me without anchoring your model to real data and observations it appears just theory and conjecture over reality, an instance of argument from incredulity that does nothing to advance science.

My model is anchored to real data and observations. The data is available. You can determine the density of potentially viable protein sequences in sequence spaces at various levels of functional complexity. From this density, you can determine the most likely minimum Hamming distance between any one viable island cluster of protein sequences and the next closest viable/potentially beneficial sequence. Then, you can determine the average number of mutations necessary to get across this minimum likely gap distance…

As it turns out, the minimum likely gap distance increases in a linear manner with each linear increase in the level of functional complexity under consideration. With each linear increase in the gap distance, the average number of mutations needed to cross the gap increases exponentially…

I’ve explained this all in detail on my website.

http://www.detectingdesign.com/flagellum.html#Calculation

Sean Pitman
www.DetectingDesign.com


Recent Comments by Sean Pitman

Science and Methodological Naturalism
Very interesting passage. After all, if scientists are honest with themselves, scientific methodologies are well-able to detect the existence of intelligent design behind various artifacts found in nature. It’s just the personal philosophy of scientists that makes them put living things and the origin of the fine-tuned universe “out of bounds” when it comes to the detection of intelligent design. This conclusion simply isn’t dictated by science itself, but by a philosophical position, a type of religion actually, that strives to block the Divine Foot from getting into the door…


Revisiting God, Sky & Land by Fritz Guy and Brian Bull
@Ron:

Why is it that creationists are afraid to acknowledge the validity of Darwinism in these settings? I don’t see that these threaten a belief in God in any way whatsoever.

The threat is when you see no limitations to natural mindless mechanisms – where you attribute everything to the creative power of nature instead of to the God of nature.

God has created natural laws that can do some pretty amazing things. However, these natural laws are not infinite in creative potential. Their abilities are finite while only God is truly infinite.

The detection of these limitations allows us to recognize the need for the input of higher-level intelligence and creative power that goes well beyond what nature alone can achieve. It is here that the Signature of God is detectable.

For those who only hold a naturalistic view of the universe, everything is attributed to the mindless laws of nature… so that the Signature of God is obscured. Nothing is left that tells them, “Only God or some God-like intelligent mind could have done this.”

That’s the problem when you do not recognize any specific limitations to the tools that God has created – when you do not recognize the limits of nature and what natural laws can achieve all by themselves.

Sean Pitman
www.DetectingDesign.com


Revisiting God, Sky & Land by Fritz Guy and Brian Bull
@Bill Sorensen:

Since the fall of Adam, Sean, all babies are born in sin and they are sinners. God created them. Even if it was by way of cooperation of natural law as human beings also participated in the creation process.

God did not create the broken condition of any human baby – neither the physical or moral brokenness of any human being. God is responsible for every good thing, to include the spark or breath of life within each one of us. However, He did not and does not create those things within us that are broken or bad.

“The owner’s servants came to him and said, ‘Sir, didn’t you sow good seed in your field? Where then did the weeds come from?’ ‘An enemy did this,’ he replied. “The servants asked him, ‘Do you want us to go and pull them up?'” Matthew 13:27-28

Of course, all humans are indeed born broken and are in a natural state of rebellion against God. However, God is not the one who created this condition nor is God responsible for any baby being born with any kind of defect in character, personality, moral tendency, or physical or genetic abnormality. God did not create anyone with such brokenness. Such were the natural result of rebellion against God and heading the temptations of the “enemy”… the natural result of a separation from God with the inevitable decay in physical, mental, and moral strength.

Of course, the ones who are born broken are not responsible for their broken condition either. However, all of us are morally responsible for choosing to reject the gift of Divine Grace once it is appreciated… and for choosing to go against what we all have been given to know, internally, of moral truth. In other words, we are responsible for rebelling against the Royal Law written on the hearts of all mankind.

This is because God has maintained in us the power to be truly free moral agents in that we maintain the Power to choose, as a gift of God (Genesis 3:15). We can choose to accept or reject the call of the Royal Law, as the Holy Spirit speaks to all of our hearts…

Remember the statement by Mrs. White that God is in no wise responsible for sin in anyone at any time. God is working to fix our broken condition. He did not and does not create our broken condition. Just as He does not cause Babies to be born with painful and lethal genetic defects, such as those that result in childhood leukemia, He does not cause Babies to be born with defects of moral character either. God is only directly responsible for the good, never the evil, of this life.

Sean Pitman
www.DetectingDesign.com


Revisiting God, Sky & Land by Fritz Guy and Brian Bull
@Ron:

Again, your all-or-nothing approach to the claims of scientists isn’t very scientific. Even the best and most famous of scientists has had numerous hair-brained ideas that were completely off base. This fact does not undermine the good discoveries and inventions that were produced.

Scientific credibility isn’t based on the person making the argument, but upon the merits of the argument itself – the ability of the hypothesis to gain predictive value when tested. That’s it.

Sean Pitman
www.DetectingDesign.com


Gary Gilbert, Spectrum, and Pseudogenes
Don’t be so obtuse here. We’re not talking about publishing just anything in mainstream journals. I’ve published several articles myself. We’re talking about publishing the conclusion that intelligent design was clearly involved with the origin of various artifactual features of living things on this planet. Try getting a paper that mentions such a conclusion published…

Sean Pitman
www.DetectingDesign.com