ADAM AND EVE, DESIGNED DIVERSITY, AND ALLELE FREQUENCIES
Jon Potter, FMS Foundation, 877 Marshall Rd, Waterloo, NY 13165, USA. jpotterm@gmail.com Bruce Potter, FMS Foundation, 877 Marshall Rd, Waterloo, NY 13165, USA. brucemp7@gmail.com John Baumgardner, Logos Research Associates, 24515 Novato Place, Ramona, CA 92065 USA. Johnrbaumgardner@gmail.com Wes Brewer, Computational Solutions LLC, P.O. Box 4752, Jackson, MS 39296, USA. wes@computational.io Rob Carter, FMS Foundation, 877 Marshall Rd, Waterloo, NY 13165, USA. rcarter@FMSFound.org John Sanford, FMS Foundation, 877 Marshall Rd, Waterloo, NY 13165, USA. jsanford@FMSFound.org
Pennsylvania: Creation Science Fellowship. International Conference on Creationism, ed. J.H. Whitmore, pp. 200–216. Pittsburgh, and Eve, designed diversity, and allele frequencies. In Proceedings of the Eighth Sanford, J., R. Carter, W. Brewer, J. Baumgardner, B. Potter, and J. Potter. 2018. Adam 201
ABSTRACT
just a few generations (Rupe and Sanford 2013). While mutational generation Flood-type bottleneck involving just three founding most mutational alleles are rapidly lost due to genetic drift within also been demonstrated using computer simulations of a single- a population of 2n (with n being the population’s size). Therefore, followed by rapid population re-growth (Nei et al. 1975). This has a new mutation enters a population, its frequency is just one copy in the bottleneck only lasts for one or just a few generations and is copy – which is, therefore, on the verge of its own extinction. When amount of a population’s pre-bottleneck diversity, assuming It is widely understood that a mutational allele arises as a single extreme bottleneck (i.e., two people) can capture a signicant population geneticists have known for decades that even the most logically be created at higher frequencies. due to the genetic bottleneck of the biblical Flood. However, in a population as a single isolated copy, designed alleles would Some fraction of the pre-Flood genetic diversity would be lost be created to be benecial. While mutational alleles always arise and so are typically harmful, while designed alleles would logically much more (Sanford and Carter 2015a, 2015b). alleles are essentially random typographical errors in the genome Adam and Eve could have contained this amount of diversity and while designed alleles can exist from the beginning. Mutational ubiquitous in the human population. Obviously, the genomes of important respects. Mutational alleles need time to accumulate, couple should carry most of the 8 million common SNPs that are Mutational alleles and designed alleles would be dierent in several variants found across the world (Carter 2018). A single modern a very dierent class of created variants (“designed alleles”). carries a very signicant percentage of all the common genetic alleles”). However, given a miraculous creation, there could be single person are common SNPs, this means that any given person from mutations, giving rise to mutational variants (“mutational SNPs in the human population, and since most of the SNPs in a Traditionally it has been assumed that genetic variation only comes Genomes 2015). Since there are only about 8 million common The Designed Diversity Model requires an expanded vocabulary. slightly higher rates of polymorphism (Gurdasani et al. 2014; 1000 variation (Carter 2018). The African people groups tend to have and should happen. for a large fraction (approximately 30%) of all common genetic accounting can and must happen, and valid genetic accounting can (Levy et al. 2007). Therefore, a single human today accounts genetic accounting in general. On the contrary, valid nancial The average person living today carries 4–5 million SNP alleles invalidate nancial accounting in general, nor does it invalidate even as there are bad or dishonest accountants. But this does not alleles could be designed alleles. It is true that there are bad or dishonest numerical simulations, frequencies of 5% or more. Hypothetically, most of these common 2015), indicates that there are only 8 million SNPs with allele 2013; Sanford et al. 2015). 2015b). The latest analysis of the human genome (1000 Genomes Nelson and Sanford 2013; Rupe and Sanford 2013; Sanford et al. and Eve when they were rst created (Sanford and Carter 2015a, Brewer et al. 2013b; Brewer et al. 2013c; Gibson et al. 2013; arisen from designed genetic variants that were built into Adam and Nelson 2012; Baumgardner et al. 2013; Brewer et al. 2013a; fraction of currently observed human genetic diversity might have al. 2007b; Baumgardner et al. 2008; Sanford et al. 2008; Sanford We have previously proposed that, excluding rare alleles, a large creationist and secular literature (Sanford et al. 2007a; Sanford et of real-world phenomena, and it has been widely validated in both rare variants have arisen via mutation in the relatively recent past. level scientists with proven expertise in the numerical simulation people group or sub-population. This indicates that most of these applied science. Furthermore, Mendel was developed by high- sampling size. Most rare human alleles are unique to a single widely tested and has become a powerful tool in many elds of these variants are so rare that they are not detectable, due to limited box”. This is unfortunate because numerical simulation has been should be roughly the size of the genome (3 billion). But most of Some may dismiss numerical simulation as an arbitrary “black somewhere on this planet. Therefore, the number of existing SNPs in the human genome should mutate many times every generation tallies nal outcomes on many dierent levels. our current population size and mutation rate, every nucleotide site transactions that take place over many generations, and nally serious underestimate of how many rare human alleles exist. Given exist in a population, accounts for enormous numbers of genetic had allele frequencies of less than 0.5%). However, this is still a dierent levels, Mendel tracks all of the old and new alleles that these are very rare alleles (about 64 million of the observed SNPs of nancial transactions and then calculate gain or loss at many human population (1000 Genomes 2015). The vast majority of corporation or government must faithfully track a vast number The 1000 Genomes Project detected 84 million SNPs within the Mendel is best understood as an accounting program. Just as a large nucleotide variations, regardless of their allelic frequency. with millions of variable genetic sites. (1000 Genomes 2015), we will use the term “SNP” for all single understood that the rst human couple could have been designed keeping with the nal report from the 1000 Genomes Project study of created diversity in a human population. At that time, we a single nucleotide polymorphism (SNP). For simplicity, and in contrasting alleles” (ICA) option that was intended to enable the a frequency greater than 1%, such a variant allele is also called Mendel’s Accountant (hereafter “Mendel”) included an “initial single nucleotide variants (SNVs). If the minor allele is found at (2018). Our 2005 version of the numerical simulation program letter dierence in the genome. Population geneticists call these diversity, for example, Hössjer et al. (2016a, 2016b), and Gauger The smallest possible unit of genetic variation involves a single ID proponents are now examining the concept of designed genetic and Francis (2016), and Jeanson and Tomkins (2017). Likewise, and in accord with their initially designed frequencies. recently in Lightner (2016), Jeanson and Tomkins (2016), Wood expected to be abundant, in accord with the nature of their function, appears at least as far back as Woodmorappe (1996), but also more alleles are typically very rare, designed alleles would typically be Sanford et al. ◀ Designed genetic diversity in Adam and Eve ▶ 2018 ICC 202 data. series of numerical simulations. We used Mendel simulations to We tested the Heterozygous Adam and Eve Model using a biblical Adam and Eve with the observed human allele distribution 3. Examining the Heterozygous Adam and Eve Model There are multiple genetic mechanisms that can reconcile the that the claim that “there is no possible way…” is overreaching. the population. c In this paper we will use logic and numerical simulation to show before and after the bottleneck, and P is the carrying capacity of A B the bottleneck occurs, R and R are the average reproductive rates distributions seen in today’s human population. b where i is the generation number, i is the generation number when could be plotted and could be compared to actual allele frequency the end of each experiment, the nal allele frequency distribution the dynamic population could still be tracked across generations.At Modications were made so that the changing allele frequencies in following formula: population bottlenecks, and subsequent population re-growth. The model population grows each generation according to the and examining the eects of small founder populations, mid-run initially created alleles, studying normal mutation accumulation, population. We improved older features that enabled such things as tracking to actual allele frequency distributions seen in today’s human where population size was continuously dynamic (changing). nal allele frequency distribution could be plotted and compared size function, so that special experiments could be conducted be tracked across generations. At the end of the experiment, the computer language “Go”. We included a new dynamic population changing allele frequencies in the dynamic population could still version of Mendel (“Mendel-Go”) written in the state-of-the-art and population re-growth. Modications were made so that the Mendel program (version 2.7.2), and also a completely redesigned founder population, population growth, a population bottleneck, To address these challenges, we developed a modied version of the initially created alleles, normal mutation accumulation, a small Mendel simulator. These improvements enabled such things as dismissed and calls for careful consideration. was developed. This was used to validate the output of the original human population.” This more technical objection is not easily At the same time, an entirely restructured program (Mendel-Go) specic patterns of allele frequencies that we see in the modern be conducted where population size was dynamically changing. claim becomes, “Adam and Eve could not possibly account for the dynamic population size function, so that special experiments could the variant alleles observed in the human population. The narrower The modied Mendel program (version 2.7.2) required a new objection can still be raised. It deals with the specic distribution of allele frequency distributions. observed amount of human genetic diversity, a more technical many generations, and tallies and plots nal outcomes, including While Adam and Eve could clearly have given rise to the currently enormous numbers of genetic transactions that take place over not reasonable. of virtual alleles that exist in a virtual population, accounts for way Adam and Eve could have given rise to so much diversity,” is As stated in the introduction, Mendel tracks the coming and going growing rapidly. In light of all this, the blanket claim, “There is no frequency patterns using Mendel version 2.7.2 and Mendel-Go. alleles would be greatly reduced in a population that is continuously We tested various historical models and their expected allele usually drift out of a population, the rate of loss of mutational Numerical Simulations only take about 80 generations. While most new mutational alleles 2. Analysis of Theoretical Allelic Distributions Based Upon population. Even for a human population of just 10,000, it would for comparisons with our numerical simulation results. one generation to accumulate 64 million mutations in the human very informative in themselves and provide controls (templates) population of over 7 billion people, it would require less than distributions for the current human population. These plots are mutations per person per generation, and assuming our current (MAF) plots. These plots reect the actual allele frequency mutations to accumulate? Given a mutation rate of roughly 100 The data were plotted using standard Minor Allele Frequency alleles). How many generations would it take for 64 million tabulated from the VCF-formatted data using custom Perl scripts. million rare SNPs (most of which can be assumed to be mutational Project page (accessed 17 Apr 2015). Allele frequency data were designed alleles), the 1000 Genomes Project identied another 64 2014), and chromosome 22 sequence data from the 1000 Genomes In addition to the 8 million common alleles (most of which may be Y chromosome, the mitochondrial chromosome (see Diroma et al. human population, we employed the latest sequence data for the millions of polymorphic alleles. In order to observe the actual allele frequencies of the current would be lost at the Flood, Noah’s family could have easily carried 1. Plotting Actual Allele Frequency Distributions been retained (Carter 2018). Thus, while some created diversity sisters), nearly 60% of the pre-Flood diversity would still have population. worst-case scenario (where Shem, Ham and Japheth married their allele frequency distribution similar to that now seen in the human 80% of the pre-Flood diversity (Carter and Powell 2016). Even in a whereby a miraculously created rst couple might give rise to an distantly related, the Ark-borne population could have carried up to logic and numerical simulations to examine genetic mechanisms of diversity. For example, if Noah’s three daughters-in-law were there were millions of designed SNPs in Eden. We have used simple originally designed variants, even though there would be some loss and Eve with a vast amount of internal genetic diversity, such that with the Flood scenario in terms of preserving most of the Our working hypothesis is that God miraculously created Adam couples (Carter and Powell 2016). Therefore, there is no problem METHODS Sanford et al. ◀ Designed genetic diversity in Adam and Eve ▶ 2018 ICC 203 200-generation biblical framework (including population growth, many generations, or the population will go extinct due to slightly designed alleles, plus accumulating mutational alleles, though a as is commonly assumed. This is essential for longer runs over gametes (50 sperm and 50 eggs). Mendel then tracked the initial where noted, we have made all mutations eectively neutral, would have been transmitted through 100 genetically independent new mutations being added per individual per generation. Except ospring that carried designed alleles from a rst couple, which designed alleles. We generally specify 1000 individuals, with 100 this using numerical simulations. We initially simulated 50 We simulated evolutionary human populations where there were no to the gene pool of a large human population. We then illustrate 6. Details of simulations of evolutionary populations gametogonia could represent a gene pool essentially equivalent alleles can “ip” over time). of individually designed gametogonia, and that these diverse as the minor allele (as genetic drift continues, the major and minor We rst explain that two designed people could have millions at which point we can empirically classify the less abundant allele The logic of this analysis is described in the Results section. “minor” allele. However, genetic drift will quickly “break the tie”, this could possibly generate the allele frequencies observed today. frequency of 50%, so we cannot initially dene the “major” or the potentially having its own unique genotype. We tested to see if allele pairs, both of the contrasting alleles will often start with a gametogonia) within Eden, with each gamete (or gametogonium) “ancestral” or “derived”. Likewise, when we specify designed individually designed each of the gametes (more accurately the simulate designed alleles, we cannot realistically adopt the terms We examined the logical outcome that would arise if God distributions we again need to clarify our terminology. When we 4. Examining the Designed Gametes Model When discussing designed alleles and their allele frequency neutral” (no eective selection). Only in a few special cases do we plot all alleles (1–99%). experiments, the magnitude of the tness eects was always “near- tally all alleles, but usually only plot the minor alleles (1–50%). the designed alleles would be either 0.25 or 0.50 or 0.75). For most making it redundant. For designed allele experiments, we always a ratio of either 50/50 or 25/75 (so all initial allele frequencies for it would appear as a mirror image of the minor allele distribution, chromosome in Eden, and so every designed allele pair would have a frequency 1 – f, if the major allele distribution was also plotted, Adam and Eve model, there would be just four copies of each for every minor allele at frequency f there exists a major allele at given equal but opposite tness eects). Under the heterozygous normal convention is that only the minor alleles are plotted. Since (1:1 or 1:3); and c) the tness eect per pair (pairs are normally was the “original” since allele frequencies change over time). The allele pairs and their locations; b) the ratio of the paired alleles allele frequency distribution data, they cannot know which allele function allows the specication of: a) the number of designed which are derived by mutation (when scientists look at real human function which establishes and tracks designed alleles. This new our simulations, we actually know which alleles are original and this model, we had to create within Mendel a new computational and 50% are plotted), while the major allele is simply assumed. In would be present at the beginning of a Mendel run. To simulate show the minor allele (i.e., only allele frequencies between 1% allele in a pair had its own designed function. Designed allele pairs rare (the minor allele). Thus, allele frequency plots normally only variants that were created as designed allelic pairs, wherein each frequently observed (the major allele), and that the mutant allele is In addition to mutational alleles, we simulated initial genetic It is usually also assumed that the original allele is the one most no selection happening, all mutational alleles would be drifting). is an “original” (ancestral) allele and a “mutant” (derived) allele. default mutational eect was “near-zero” (i.e., there was essentially all alleles arise via random mutations, so it is assumed that there mutation rate was 100 mutations per person per generation. Our allele frequencies from 1% to 99%. It is normally assumed that mutation rate and the eect of each mutation on tness. Our default whether we should plot allele frequencies from 1% to 50%, or arising mutational alleles, we only had to specify the population’s Another major data plotting issue involves the question of new mutation and each mutational allele. To simulate newly importance of this “invisible bin” in the Discussion section. in number. From its inception, Mendel has always tracked each distorts the scaling of any allele frequency plot. We will revisit the occurring, and mutation count per individual consistently increases sequencing errors; c) this rst bin is usually so large that it severely allele would always arise as a rare variant. Mutations are always and so can uctuate wildly; b) this rst bin incorporates all DNA word-processing errors in the genome. This type of mutational very rare alleles in this rst bin is very sensitive to sampling size the designed allele. Mutational alleles would arise essentially as etc. There are numerous practical reasons for this: a) detection of classically understood mutational allele, and the second type was of 1–2%, the next bin tallies alleles with a frequency of 2–3%, very dierent types of genetic variation. The rst type was the rst (left-most) bin tallies the number of alleles with a frequency Our simulations required the creation and tracking of two plot the very rare alleles. Instead, in our allele frequency plots the mutations and further recombination. alleles account for most of the allelic diversity, we tally, but do not generation allelic diversity would increase due to newly arising plot alleles with a frequency less than 1.0%. Although these rare number of genotypes in the second generation. In each succeeding However, following the standard convention, we do not normally recombination and segregation could have generated a large As stated above, all new mutations begin as very rare alleles. its own unique set of designed variants, normal chromosomal that include designed alleles each one of the 88 original autosomes in Eden could have carried 5. Complexities of plotting allele frequencies from simulations the currently observed human allele frequency distributions. Since heterozygous rst couple to generate allele distributions similar to maximum population size). discover which parameters settings, if any, might allow a highly a 6-person bottleneck in generation 9, and re-growth up to a pre-set Sanford et al. ◀ Designed genetic diversity in Adam and Eve ▶ 2018 ICC 204 frequencies (1–50%). Figure 2b is our benchmark for a stable Figure 2b follows the convention of only plotting the minor allele MT 1,074 2,618 424 seen, a large number of alleles have drifted to xation (100%). Y 1,233 60,446 7,491 2a shows the full range of allele frequencies (1–100%). As can be individual per generation, and it ran for 10,000 generations. Figure 22 2,504 918,038 215,313 population size was 1000, the mutation rate was 100 mutations per mutation/drift equilibrium is shown in Figure 2a. In this run the SNPs Chromosome n All SNPs of an allele frequency distribution of an evolutionary population in Common of polymorphisms in the population stops increasing. An example SNPs for each chromosome, based on 1000 Genomes Project data. frequency distribution stabilizes.At the same time, the total number the total number SNPs for each chromosome, and number of common population. When mutation/drift equilibrium is reached, the allele Table 1. Three chromosomes, the number of sequenced individuals (n), are drifting to xation as fast as new alleles are drifting into the population reach mutation/drift equilibrium, where older alleles chromosome is young. individuals is exceedingly slow. Only after deep time can a large The extreme scarcity of high-frequency alleles suggests the mitochondrial zero). The rate of drift in any population with 1,000 or more Project. The vast majority of SNPs in the rst bin (2,194) are not shown. to drift will very slowly drift toward the right (i.e., away from chromosome, based upon 1,074 individuals from the 1000 Genomes Figure 1c. The allele frequency distribution for the human mitochondrial population at very low initial frequencies and those that are not lost linearly with time. Mutational alleles continuously enter the population, the number of accumulated mutations increases size, mutation rate, and time. For any biologically realistic drift, which is dependent on the parameter settings for population allele frequency distributions are determined by the rate of genetic In our evolutionary simulations, we have observed that mutational designed alleles 2. Illustrating the Evolutionary Model – simulations without proxy for the rest of the genome. essentially identical to chr22. Thus, in this case, chr22 is a suitable the 1000 Genomes database and have observed a distribution distribution for all human autosomal chromosomes included in scarcity of high-frequency alleles suggests that chromosome Y is young. majority of SNPs in the rst bin (52,955) are not shown. The extreme chr22 data. However, we have since calculated the allele frequency Y, based upon 1,209 individuals from the 1000 Genomes Project. The vast for this paper.At the time of submission, our analysis only included Figure 1b. The allele frequency distribution for the human chromosome in Table 1. Figure 1a is the allele frequency distribution benchmark Summary allele data for each of the three chromosomes are reported Project data for chr22, chrY, and chrM are shown in Figures 1a–c. The allele frequency distributions within the 1000 Genomes 1. Actual Allele Frequency Distributions RESULTS designed alleles start at a frequency of either 25% or 75%. all alleles, while the other would be homozygous. In this case, all is set to 0.5, then either Adam or Eve would be heterozygous for frequency of 50%.Alternatively, if the initial heterozygous fraction Eve are equally heterozygous and all designed alleles begin with vast majority of SNPs in the rst bin (702,725) are not shown. initially heterozygous. If the fraction is 1.0, then both Adam and 22, based upon 2,504 individuals from the 1000 Genomes Project. The we specify the fraction of individuals in the population who are Figure 1a. The minor allele frequency distribution for human chromosome tness increase if every “benecial” allele went to xation). Lastly, specify the upper limit of total tness benet (i.e., the hypothetical assign tness eects according to a Weibull distribution, and normally make all designed alleles co-dominant. We typically both alleles will always remain in the same linkage block. We locus. The sum of their allele frequencies must add up to 1.0, and pair represents two alternative nucleotides at the same genetic For our designed allele simulations, each initial contrasting allele designed alleles 7. Details of simulations of short-term populations with deleterious mutations, long before the simulation is complete. Sanford et al. ◀ Designed genetic diversity in Adam and Eve ▶ 2018 ICC 205 the curve is distinctly sharper in the Evolutionary Adam and Eve carry designed heterozygosity, while chrYand chrM would initially simulation (Figure 2b). See Figure 8 and Table 2. The bend in chrM. Therefore, it might be expected that the autosomes might distribution (Figure 1a) but is distinct from the evolutionary there would be only one progenitor chrY and only one progenitor an allele distribution that is clearly similar to the actually observed initially exist in four copies (enabling initial heterozygosity), while As can be seen, the Evolutionary Adam and Eve scenario yields perspective, because in Eden the autosomal chromosomes would larger human population and then give rise to modern humanity. 1b), and chrM (Figure 1c). This is not surprising from a creation and Eve scenario, wherein Adam and Eve derive naturally from a consistent with the observed allele distributions of chrY (Figure rebounds to its original size. This represents an Evolutionary Adam chromosome 22 (Figure 1a). However, this simulation is quite down to just two people for a single generation and then rapidly not look like the actually observed distribution of the autosomal 200 generations before the run is over. The population shrinks after just 200 generations. Yet the distribution in Figure 2d does Figure 2c shows an identical simulation, except a bottleneck occurs drift leading to a meaningful allele distribution spread, even generations. In this biblical framework, we see substantial genetic the frequency range of 3–15%. by rapid population rebound up to 1000. The run only lasts 200 bend in its distribution, compared to the evolutionary scenario, in generations, then there is a bottleneck down to 6 people, followed The actually observed allele distribution has a distinctly tighter starts with two individuals, there is rapid population growth for 10 distributions from the 1000 Genomes Project (Figure 8, Table 2). biblical timeframe and population dynamics. In this case the run distribution that is quite dierent from the actually observed allele Figure 2d shows a mutation accumulation simulation, but with a evolutionary population in deep time generates an allele frequency evolutionary allele distribution. Our simulation of this type of simulation. chrM (Figure 1c) allele distributions. Simulated and plotted using new Mendel-Go version. 1–50%. This plot is nothing like the actually observed autosomal allele distribution but is more similar to the actually observed chrY (Figure 1b) and bottleneck at generation 10; and a population growth and re-growth rate of 2.0 (doubling every generation). The plotted allele frequencies are from settings were an initial population size of two, a stable population size of 1000; 200 generations; 100 mutations per individual per generation; a Figure 2d. This distribution reects mutation accumulation in a biblical timeframe (case pc1fe3). There were no designed alleles. Key parameters 1.5 after the bottleneck. The plotted allele frequencies are from 1–50%. Simulated and plotted using new Mendel-Go version. were 1000 population size; 10,000 generations; 100 mutations per individual per generation; a bottleneck at generation 9,800; and a re-growth rate of single-generation bottleneck just 200 generations before the experiment ended (case i2e1e0). There were no designed alleles. Key parameters settings Figure 2c. This is what can be considered an evolutionary Adam and Eve scenario. This Figure has the same setting as Figure 2b but adds a severe and plotted using new Mendel-Go version. Figure 2b. This gure shows the same evolutionary simulation as Figure 2a, but with only minor alleles are plotted (0–50%). Case p0a098. Simulated and plotted using new Mendel-Go version. equilibrium. The same case is show in Figure 2b, but this plot shows the conventional plotting of only the minor alleles (1–50% frequencies). Simulated plots allele frequencies from 1–100% to show that xations (far right) are arising at a high rate, indicating that this population was in mutation/drift no designed alleles. Key parameters settings were 10,000 generations; 1000 population size; 100 mutations per individual per generation. This gure Figure 2a. Allele distribution of a simulated evolutionary population that is mature and is in mutation/drift equilibrium (case p0a098). There were Sanford et al. ◀ Designed genetic diversity in Adam and Eve ▶ 2018 ICC 206 growth, a severe population bottleneck to just 6 people in the tenth version 2.7.2. plotted allele frequencies from 1–100%. Simulated and plotted using Mendel but started with a population of two, followed by rapid population cal population dynamics greatly increase the rate of genetic drift. Mendel has same initial allele frequency and a time span of 200 generations, (6 individuals), followed by rapid growth up to 1000. As can be seen, bibli- 3b). A second, more biblically-realistic experiment involved the by rapid growth and an extreme single-generation bottleneck in generation 10 that in this time there had been very limited genetic drift (Figure severe population constrictions. The starting population size was 2, followed narrow bell-shaped curve that was still centered at 50%, indicating to Figure 3b, after 200 generations of drift, with no mutations, but with two population size of 1000, after 200 generations the distribution was a Figure 3c. This is a simple illustration of a designed allele distribution, similar single spike at 50%. Given this starting point, and given a constant frequencies from 1–100%. Simulated and plotted using Mendel version 2.7.2. happened, but in this timeframe the drift is modest. Mendel has plotted allele such runs is shown in Figure 3a. The allele “distribution” is a population with a constant population size of 1000. It is obvious that drift has The initial allele frequency distribution (rst generation) for all to Figure 3a, but after 200 generations of drift. It assumes no mutations and a linkage blocks, and nearly-neutral tness eects (i.e., no selection). Figure 3b. This is a simple illustration of a designed allele distribution, similar a short timeframe (200 generations), 989 designed allele pairs, 989 frequencies from 1–100%. Simulated and plotted using Mendel version 2.7.2. 50%. For these simulations we generally specied zero mutations, (unresponsive to selection). Note that in these cases Mendel has plotted allele bitrarily designated “deleterious” (red). These alleles are made nearly neutral We initially specied that all alleles start with an allele frequency of arbitrarily designated one allele “benecial” (green) and the other allele is ar- the minor allele but still show a full frequency range of 0–100%. desireable function and one has another alternative desireable function, we mutations arising). Note that most of these experiments show only frequency of 50%. Because for each contrasting allele pair, one allele has one We rst performed simulations with only designed alleles (no new with a 50/50 ratio, so all designed alleles in this experiment start with an initial initial frequency of 50%. generation of a simulation. In this example, all designed allele pairs begin A. Simulations involving only designed alleles, all having an Figure 3a. A simple illustration of a designed allele “distribution.”In the rst simulations to examine this question. from a massively heterozygous Adam and Eve? We used numerical Could the observed human allele frequency distributions be derived 3. Illustrating the Heterozygous Adam and Eve Model appear very young. designed variants, it seems possible that they might similarly invariant. If all the autosomal chromosomes initially lacked sense if these chromosomes were very young and were initially toward lower allele frequencies. These distributions only make SNP alleles, and their allele distributions are very strongly skewed This makes sense, because in all three cases there are very few non-variant Edenic chromosomes that lacked designed variants. be invariant. Figure 2d, like Figures 1b and 1c, may all reect Designed Gametes 7 0.84 A & E, Designed Alleles 6b 1.16 A & E, Adam and Eve 2c 0.70 Evolutionary Evolutionary 2b 5.75 Figure Model MSE (x10 ) -3 Corresponding the Designed Alleles and Designed Gametes models. 22. Further experimentation with parameter settings will improve the t of The threeAdam and Eve models all show a much tighter t to chromosome distribution. The most divergent model was the evolutionary simulation. tweaking parameters within a model to make the model t an expected The MSE is not a signicance test, but the results are a useful guide when frequency. Smaller values indicate a tighter t to the reference sequence. of the reference distribution (in this case, chromosome 22) at that same i i i – Ŷ ) , where Y is the value of the test distribution and Ŷ is the value 2 i Mean Squared Error (MSE) is simply the average of the error terms (Y (chromosome 22) and the normalized distributions of several models. The Table 2. Dierences between the normalized observed allele distribution Sanford et al. ◀ Designed genetic diversity in Adam and Eve ▶ 2018 ICC 207 spread along the x-axis. The resulting distribution was very similar for God to bless later generations with abundant “good” diversity on the far left, smoothly transitioning into the designed alleles premise of a miraculously created Adam and Eve, a logical way resulting distribution reects the relatively rare mutational alleles genotype for each gametogonium of Adam and Eve. Given the at 25%) were combined with mutational alleles (Figure 6b). The Lastly, we examined the feasibility that God designed a unique We then did an experiment where designed alleles (initially all Numerical Simulation 4. Illustration of the Designed Gametes Model Using Logic and from the observed allele distribution. selective sweeps, lineage extinctions, etc., as will be discussed. with the mode at 50%. This outcome is obviously very dierent growth rates, as well as various population dynamics such as the far left, and the designed alleles are spreading along the x-axis, exact shape of this curve would depend on the early population The resulting distribution reveals that the rare mutational alleles on to the actually observed allele distribution (Figure 8, Table 2). The alleles (initially all at 50%) with mutational alleles (Figure 6a). We did a preliminary simulation where we combined designed version 2.7.2. alleles allele frequencies from 1–100%. Simulated and plotted using Mendel D. Simulations combining both mutational alleles and designed spreading, resulting in a distribution that is nearly at. Mendel has plotted that can eclipse the eects of drift. When biblical population constrictions are added there is much more allele of numerous strong demographic forces (such as selective sweeps), approximates the lower section of the actual allele frequency distribution. When mutations are added and the scale is normalized, this type of curve them. In the Discussion section we will describe the implications this distribution is resembles a straight line sloping downward to the right. be expected to carry many low-impact linked alleles along with seen when designed alleles start out with a frequency of 50% (Figure 3c), frequency mutational alleles). Such strong selective sweeps would Instead of the “hump” that is observed in the middle frequency range as is “gap zone” separating the high-frequency created alleles and low- designed alleles have a distribution strongly skewed toward the left. impact alleles to the left and right extremes (this eectively lls mutations and a population with a constant population size of 1000. The emptying the central part of the distribution and driving the high similar to Figure 4a, but after 200 generations of drift. It assumes no These allele pairs responded rapidly to natural selection, eectively Figure 4b. This is a simple illustration of a designed allele distribution, favored) and major (green = more favored) alleles in this plot. 2.7.2. frequencies from 1–100%. Simulated and plotted using Mendel version within a biblical framework. We show both the minor (red = less a distribution strongly skewed toward the left. Mendel has plotted allele all at 50%) were assigned large tness eects and were simulated frequency of 25%, and after just 20 generations. The designed alleles have experiments a limited number of designed allele pairs (initially similar to Figure 3b, but with all initial minor alleles starting at a Figure 5 shows the eect of a series of selective sweeps. In these Figure 4a. This is a simple illustration of a designed allele distribution, selective sweeps C. Simulation involving high-impact designed alleles resulting in frequency plots to be rescaled). accumulate to high numbers (because this requires the y-axis of the diminishes greatly when mutational alleles are added and begin to fraction of allele pairs that start at 50%. The steepness of the slope the slope can be modulated by including in the simulation some allele frequency distribution. We have found that the steepness of this is the basic shape of the lower-most portion of the actual straight line that slopes downward to the right. When re-scaled, zero and the distribution’s bell-shaped curve has become a nearly what happens after 200 generations. The mode is now approaching left, with the mode shifting downward from 25%. Figure 4b shows after just 20 generations. Most of the distribution is shifting to the frequency distribution (Figure 1a). Figure 4a shows what happens allele frequency, it is much easier to approach the observed human Figure 3a, but with the spike located at 25%. With this lower initial frequency distribution (in the rst generation) would look just like show the minor alleles in such plots). In this case, the starting allele contrasting allele with allele a frequency of 75% (we generally only every allele pair where the minor allele frequency is 25%, there is a alleles that all began with a minor allele frequency of 25%. For Still more promising were simulations that involved designed initial frequency of 25% B. Simulations involving only designed alleles, all having an result in much more rapid allele frequency spreading. this biblical scenario, we see that two population constrictions can generation, followed by a rapid population rebound (Figure 3c). In Sanford et al. ◀ Designed genetic diversity in Adam and Eve ▶ 2018 ICC 208 Mendel’s parameter settings can obviously be ne-tuned to further while the evolutionary simulation had a distribution that was by far allele frequency distribution very similar to what is seen today. simulations were very similar to the actually observed distribution, to the chr22 distribution. As can be seen, all three Adam and Eve generate, in just 200 generations, and without any ancestors, an Table 2 shows the degree of dierence of each curve, compared the Designed Gametes Model enables a literal Adam and Eve to most clearly divergent from the actually observed distribution. our designed gametes simulation indicates. Figure 7 shows that observed distribution. However, the evolutionary simulation was is distinctly dierent from what is actually observed and what are similar to each other and largely overlap with the actually the evolutionary simulation (Figure2b) shows a distribution which of the curves that involve any type of Adam and Eve simulation similar types of allele distributions (Figure 8, Table 2). However, for the purpose of comparison. As can be visually discerned, all (Figure 7). As can be seen, both Figures 1a and Figure 7 yield very Figure 8 displays these ve normalized distributions side-by-side, generations, and the allele frequencies were tallied and plotted then grew rapidly again. The simulation was stopped after 200 Adam and Eve simulation involving designed gametogonia. rapidly, experienced a severe bottleneck at generation 10, and Eve simulation. Figure 7 represents the allele distribution of an allele pairs. We then simulated a biblical population that grew 6b represents the allele distribution of a heterozygous Adam and each linkage block was assigned a specied number of designed distribution of an evolutionary Adam and Eve simulation. Figure (100 chromosome sets). Each child had 989 linkage blocks, with a classical evolutionary simulation. Figure 2c represents the allele sampling of Adam and Eve’s gametes. We assumed 50 children 22 (shown in black). Figure 2b represents the allele distribution of but with their children, because their children would represent a allele distribution that is actually observed in human chromosome gametes, we did not start our simulation with Adam and Eve, simulations (Figures 1a, 2b, 2c, 6b, and 7). Figure 1a represents the to those observed today. To model designed diversity within Figure 8 helps us to compare the allele distributions of our ve key gametes might give rise to patterns of allele diversity similar 5. Comparing the Dierent Distributions We employed numerical simulations to illustrate how designed this will be addressed in depth in the Discussion section. God’s design. of our simulated populations is usually just 1000. This reason for diversity of linkage patterns, as might have been in accord with caveat regarding Figure 7 and all our other results, is that the size initial population of gametes could have also started with a great actually observed allele frequency data. However, a very important in accord with God’s design for mankind. In the same way, the improve the match between our Designed Gametes Model and the have started with almost any initial allele frequency distribution, This means that the variants in that rst human population could 2.7.2. frequencies from 1–100%. Simulated and plotted using Mendel version primordial gene pool that existed within Adam and Eve’s gametes. alleles into the “gap zone”. Note that in this case Mendel has plotted allele chromosomes, representing a very substantial sampling of the were linked to them. These “selective sweeps” drag many nearly-neutral large family, there could have been 100 or more dierent sets of them a great number of nearly-neutral designed and mutational alleles that the early patriarchs (Carter and Hardy 2015). In such an extremely distributions. Such high-impact designed alleles would sweep along with a very large family size, given the extreme longevity and vigor of transition between mutational allele distributions and designed allele Indeed, it is entirely feasible that Adam and Eve would have had region (in the range of 3-15%), that can arise where there is not a smooth generations would require that the rst family was very large. alleles have been strongly pushed to the left, lling the problematic “gap” transmit a large fraction of the original genetic diversity to later has driven all alleles out of the center of the distribution. The un-favored designed alleles (red) from the favored designed alleles (green). Selection comparable to the gene pool of a large human population. To In just 200 generations, selection has completely separated the un-favored Eden, this would potentially constitute an enormous gene poo1, positive and negative tness values which enabled strong natural selection. If there were individually designed gametes/gametogonia in with Figure 3a). However, the designed allele pairs were assigned strong linkage block patterns. designed allele pairs which are started with an initial frequency of 50% (as and Eve with observed allele frequencies, but also with observed Natural selection is one such force. This plot shows a limited number of that actively drive allele frequencies to change, and to change rapidly. Gametes Model appears to not only help reconcile a literal Adam diusive nature of genetic drift, there are many other variables in nature blocks that were designed, specic, and functional. Our Designed systematic selective sweeps. While Figures 3b and 5c reect the slow and gametic variants would logically have been created within linkage Figure 5. An illustration of high-impact designed alleles resulting in gametogonia (giving rise to sperm). In addition, all those designed designed SNPs in each egg. Similar logic would apply to Adam’s existed in Eve’s ovaries. Eve might have had a vast number of the number of variant alleles and linkage blocks that could have been genetically unique. Therefore, there is almost no limit to would have been miraculously formed and could potentially have not have formed in the normal way – so each gametogonium However, assuming that Eve was created, not born, her eggs could born with a vast number of eggs already formed in their ovaries. in her mother’s womb. In other words, women are normally woman’s egg cells form from her gametogonia while she is still gametogonia (the cells that give rise to gametes). Normally, a would be to create within Adam and Eve genetically diverse Sanford et al. ◀ Designed genetic diversity in Adam and Eve ▶ 2018 ICC 209 God’s design, both for humans and for all living things. populations in deep time (Figure 2b). We have simulated the Flood. It is reasonable to expect that diversity would be part of human allele distribution. We have simulated evolutionary and rapid fragmentation of populations into sub-populations after low-frequency alleles, and hence line up with the actually observed with natural selection, it optimally enables rapid local adaptation result in allele distribution patterns that are strongly skewed toward mutation/selection. In addition, when designed diversity is coupled dicult to understand how such designed allelic variation could variations of this type cannot rationally be attributed to Darwinian loaded into the genomes of Adam and Eve. However, it is more talents such as mathematical or artistic genius. Desirable human It is easy to envision a great deal of genetic diversity being front- forms of human beauty, and the various types of human gifts and This should be especially obvious when we consider the various and plotted using new Mendel-Go version. (i.e., variations that are desirable, and have no pathological eects). Figure 8). Mendel has plotted allele frequencies from 1–50%. Simulated variants can credibly account for all the “good diversity” we see this distribution is compared to the actual allele distribution (Figure 1a, that nearly all non-neutral mutations are deleterious, only designed The accumulated mutational alleles are shown in red. Note how similar see within the human race today. Since all parties acknowledge pairs (purple alleles are less favored and gold alleles are more favored). the most coherent explanation for the benecial variations that we mutational alleles (case 824f). There were 296,700 initial designed allele the idea of “designed diversity” is a logical deduction. It provides parameters and a mixture of initial designed alleles and accumulating If we start with the premise of a miraculously createdAdam and Eve, alleles starting at 25%). We performed this simulation using biblical combining both mutational and initially designed alleles (with all designed Sanford 2017). Figure 6b. This is a heterozygous Adam and Eve simulation. A simulation highly contested within the eld of paleoanthropology (Rupe and from 1–100%. Simulated and plotted using Mendel version 2.7.2. that are popularly claimed to be “transitional fossils” are actually distribution, in the range of 3–20%. Mendel has plotted allele frequencies with the human evolutionary model involves the fact that the bones which started at a frequency of 50%. Note the problematic “gap” in the longer than two letters long. A fourth serious problem associated The broad bulge centered on 0.50 represents the designed alleles – all of requires a vast number of specic nucleotide strings that are much of which remain rare throughout the 200 generations of the experiment. ancestral population (Sanford et al. 2015). Yet human evolution far left is due to the continuous accumulation of mutational alleles, most is from the actual allele distribution (Figure 1a). The spike of alleles on the x a nucleotide string consisting of only two letters in a human-like combination of Figure 2d and Figure 3c. Note how dierent this distribution turns out that it would take at least 84 million years to create and and a mixture of designed and created alleles. This run is essentially a has a third glaring problem called “the waiting time problem”. It generations later severe single generation bottleneck with 6 individuals), falsied (Cordova and Sanford 2017). The human evolution model simulation using biblical parameters (an initial population of two, and ten However, the spontaneous nylonase claim has recently been designed alleles (all designed alleles starting at 50%). We performed this that it is easy to create new functional biological information. Figure 6a. A preliminary simulation combining both mutational and The counter-claim has been that the famous nylonase gene is proof human, has been demonstrated on many levels (Marks et al. 2013). creating the biological information that makes life, and makes us population into a human population. The enormous diculty of of new information that would be required to change an ape no credible way that mutation/selection can create the vast amount with the human evolutionary model is the fact that there is simply degeneration and eventual extinction. A second profound problem very slightly deleterious. This should result in continuous genetic for the millions of rare alleles in the human population should be mutations (Sanford 2014). Many of the mutations that account time due the relentless accumulation of slightly deleterious strong evidence that human populations cannot survive in deep many fundamental problems of its own. For example, there is we must rst point out that the human evolutionary model has Eve might be reconciled with the observed allele distributions, Before we address the various ways in which a literal Adam and consistent with the Word of God. by providing reasonable evidences and credible models that are revealed them to us. The best we can do is to encourage the faithful to understand the thoughts or actions of God, except as He has signicant topic. Even as Bible believers, we should not pretend be a great deal of humility on all sides as we explore this very inherent limits of historical science. Thus, we suggest there should Any origin-of-man model will have signicant problems due to the DISCUSSION the most divergent. Sanford et al. ◀ Designed genetic diversity in Adam and Eve ▶ 2018 ICC 210 like. It is an ever-present, entropic dissipation. Not only is the are shrinking. At the same time the people of India, many parts of This is a diusion model – very slow, very steady, very clock- to collapse.At present European, Japanese, and Korean populations uctuations in the gametic gene pool, generation after generation. went global. Multiple factors caused Native American populations Drift is thought to happen almost exclusively due to tiny sampling the recent past, the European population exploded as colonialism in composition due to war, conquest, disease, technology, etc. In the actually observed allele distribution. human population has continuously experienced dramatic changes gametic sampling) will greatly reduce the time needed to generate has been due to many other demographic factors. For example, the realistic understanding of how alleles change (apart from mere of changing allele patterns has not been due to random drift but drift and allele frequency change. We are convinced that a more consider recent human history, it is clear that the primary cause suggest there is a real need for a more realistic model of genetic much faster than classic random genetic drift can accomplish. We patterns to change much faster than has ever been simulated. If we demographic forces that can cause allele frequencies to shift much more powerful than genetic drift, causing allele frequency to generate the observed number of SNPs. Likewise, there are is always being subjected to strong demographic forces that are alleles but as created alleles. This greatly reduces the time needed We suggest that for higher organisms any real global population from a creation perspective, we see many SNPs not as mutational profoundly wrong. to modern humanity in just a few hundred generations. However, (no sub-populations). Both of these assumptions are known to be perspective, it would seem impossible for two people to give rise natural selection happening; and 2) there is perfect random mating genetic drift, both of which require deep time. Given that extremely unrealistic biologically. It assumes that; 1) there is no primarily by random accumulation of mutations and random standard model of genetic drift extremely slow and weak, it is Most geneticists assume allele frequency distributions arise bottlenecking is inherent and integral. align surprisingly well with the actually observed allele frequency data. a bottleneck is entirely post hoc, while for the creation model purposes of comparison. Clearly, a number of dierent biblical models require genetic bottlenecking, for the evolutionary model to invoke (Designed Alleles Model), and 7 (Designed Gametes Model), plotted for 2b (Evolutionary Model), 2c (Evolutionary Adam and Eve Model), 6b size constriction. While both the evolutionary and biblical models Figure 8. The normalized distributions of Figures 1a (chromosome 22), biblical simulations clearly require at least one severe population in order to match the actually observed allele distribution, our the distant past (all bottlenecks seem to tighten the bend). Similarly, evolutionists need to invoke a long-term population bottleneck in order to reconcile evolutionary simulations with the real data, distribution, compared to the actually observed distribution. In simulation (Figure2b) indicates a distinctly softer “bend” in the curves into closer alignment with the actual data. The evolutionary can invoke hypothetical mechanisms to bring their simulated allele frequency distribution. Both evolutionists and creationists to yield allele distributions that better match the actually observed All of the types of simulations listed above can be further ne-tuned actually observed allele distribution. version. our evolutionary simulation that was most discordant with the frequencies are from 1–50%. Simulated and plotted using new Mendel-Go similar to the actually observed allele distribution. Again, it was gold (favored alleles). All alleles were near-neutral. The plotted allele Adam and Eve simulations could yield allele distributions very shown in red, while designed alleles are purple (un-favored alleles) or simulation was halted in the 200 generation. Mutational alleles are were closest to the actually observed distribution. All three of our th (3 reproducing couples), and then regrowth up to 1000 individuals. The shown quantitatively in Table 2, which shows which distributions population grows for 9 generations, followed by a biblical bottleneck while the evolutionary simulation was most discordant. This is also and Eve’s designed gametes (gametegonia) (case w35b49). This initial types of Adam and Eve simulations closely aligned with chr22, with 50 ospring of Adam and Eve who were derived from 100 of Adam 2b, 2c, 6b, and 7, side-by-side. It is visually obvious that the three Figure 7. This is a designed gametes simulation. The population begins pool (Figure 7). Figure 8 shows the distributions of Figures 1a, that their sperm and egg cells would represent a very large gene their millions of gametogonia created genetically distinct – such and Eve begin as the rst couple just 200 generations ago, having time of Noah. We have simulated biblical populations where Adam design (Figures 5b), with a subsequent population bottleneck at the couple just 200 generations ago, being massively heterozygous by where Adam and Eve are created miraculously as the rst human rise to modern humanity. We have simulated biblical populations single-generation bottleneck, and then in just 200 generations give derive from an evolutionary population, constituting an extreme evolutionary Adam and Eve scenarios, where Adam and Eve Sanford et al. ◀ Designed genetic diversity in Adam and Eve ▶ 2018 ICC 211 thinking. Historical rapid lineage expansions that have happened have simulated a single but more prolonged population bottleneck to ignore such alleles in our plots, we cannot ignore them in our of Babel (which may well have been chaotic/violent). We might our histograms and linear graphs. While it is a practical necessity growth among the emerging tribes, following the dispersion out the un-plotted alleles in the “invisible bin” (frequencies 0–1%) of just six reproducing adults; and c) a possible stall in population in our very large population. These nearly countless rare alleles are consisting of just two people; b) the tiny post-ood population of model the billions of very rare alleles that are now accumulating perhaps three such episodes: a) the tiny initial population in Eden, to model extremely large populations. In particular, we cannot of generations. Fortunately, the biblical model provides two and Amajor limitation of numerical simulation is that it lacks the ability one episode where the population size is very small for a number spreading required that early in the simulation there must be at least demographic stirring. to a near standstill (Carter and Powell 2016). Substantial allele change allele frequencies are natural selection and other types of population size reaches 1,000 or more, classical genetic drift grinds is essentially irrelevant, and the only meaningful factors that only happens when a population is relatively small. As soon as the Therefore, in larger global populations, classical genetic drift of 3–20%. It is generally assumed that accelerated genetic drift size, demographic stirring is not directly tied to population size. is essential for lling the allele distribution “gap” in the range of classical genetic drift is almost entirely a function of population Most importantly, we required accelerated genetic drift, which we show in Figure 8. It is important to realize that while the rate eectively accelerates allele spreading, yielding the distributions population size, and more than one initial allele frequency. in our simulations. We observe that this “correction factor” very formula. This included several instances of reduced or constrained for the complete absence of any natural “demographic stirring” allele distributions when we added other key elements to our 10,000 individuals. Our smaller populations help compensate We found that our results began to approximate the modern conventionally assumed historical human population size of observed allele frequency distribution. a maximal population size of 1000 individuals, instead of the problematic for us to reconcile the designed diversity model to the All the simulation experiments recorded in this paper employed (Figure 6a). Based upon our preliminary simulations, it seemed need some type of correction factor. being squeezed into the rst bin on the far left of the histogram account demographic stirring, population models and simulations a nearly vertical distribution, with almost all mutational alleles complicated and challenging to realistically simulate. To take into distribution along the x-axis, while the mutational alleles had forces in their models for the simple reason that these factors are with newly arising mutations, the designed alleles had a humped paper), have failed to include these important demographic distribution (Figure 1a). When designed alleles were combined People doing genetic simulations (including the authors of this distributions dierent from the actually observed allele frequency simulation should take into consideration demographic stirring. were over-simplied (Figures 3a, 3b, 3c, 4a, 4b, 6a) and yielded sampling error. We suggest all future population modeling and Our preliminary simulations of a heterozygous Adam and Eve should eclipse that special type of drift that is simply diusion/ population constrictions that accelerated genetic drift. stirring should greatly accelerate the rate of genetic drift and 1. Adam and Eve were created heterozygous, followed by we suggest that it is ubiquitous in nature. Any type of demographic allele distribution. the term demographic stirring to describe this phenomenon, and help us reconcile a literal Adam and Eve with the observed human act to “stir” the gene pool of any global population. We propose what we have learned about the three primary mechanisms that should be obvious that there are numerous demographic forces that encouraged by what our simulations show. We summarize below on diusion alone, without taking into account ocean currents. It reduced population size for demographic stirring, we are very would be trying to study ocean chemistry or marine biology based realism. Despite the complication associated with substituting and the exact rate becomes unpredictable. Another illustration of demographic correction factor to achieve greater biological But if there is any type stirring, the rate of mixing is much faster degree of demographic stirring and should include some type the added solution will diuse very slowly and at a constant rate. and simulations should eventually take into consideration some liquid carefully added to water. If there is very little initial mixing, selection and lineage expansions. Ideally, all population models at a much higher rate, can be seen when we consider a colored the numerous major demographic factors such as natural A simple illustration of how genetic drift might really be operating correction factor – but it seems to us better than entirely ignoring shifts should eective accelerate allele spreading. We acknowledge that reducing population size is not a perfect of massive global demographic shifts. All such major demographic population that Mendel is neither currently simulating or plotting. study, involving 92 scientists, clearly shows the historical reality there is an enormous reservoir of SNPs in the actual human in the early human population (Narasimhan et al. 2018). This number of actually observed human polymorphisms. Therefore, released that demonstrates rapid and massive demographic shifts SNPs into the 1–99% frequency range, helping to explain the large only change extremely slowly. A major new paper has just been any type of demographic stirring would draw large numbers of populations are older than they really are, and that populations can rapidly from thousands of people to billions of people. Realistically, are ignored, genetic simulations will consistently indicate that rare alleles that would accumulate as the human population grew drift” (i.e., accelerated allele frequency change). If these forces frequency bins. Our simulations fail to model the vast number of man has existed. Logically, these forces should cause “accelerated these types of genetic change have been going on for as long as should pull many alleles out of the invisible bin and into higher Africa, and many Muslim populations are exploding. Arguable all at the expense of other sub-populations (Narasimhan et al. 2018), Sanford et al. ◀ Designed genetic diversity in Adam and Eve ▶ 2018 ICC 212 the earth), seems to imply rapid adaptive population fragmentation. nature, yet both of their distributions are very similar. They both mandate to “ll the earth” (i.e., ll all the environmental niches in are striking in that these two chromosomes are very dierent in their it enables very rapid adaptation to local conditions. The biblical the actual allele distributions of chrY and chrM. These distributions One reason why designed diversity makes so much sense is that allele distributions of the autosomal chr22. But we also generated series of powerful selective sweeps can clearly help ll “the gap”. We have primarily compared our simulated results with the actual alternatives that can change allele frequencies rapidly (Figure 5). A histogram bin into the 1–15% histogram bins. We used selective sweeps as just one example to illustrate non-drift rare mutational alleles, moving them from the invisible 0–1% events. dynamics could rapidly amplify many of the countless un-plotted expansions, lineage extinctions, and other fast-acting population historical populations surged forward. These types of population such as selective sweeps, migration/invasion, explosive lineage alleles must have diminished over time, even as the alleles of other less time. These other factors consist of numerous active processes Rohde et al. 2004). Therefore, the frequencies of many human are much more eective in shifting allele frequencies, and in much the vast majority of all lineages go extinct (Helgason et al. 2003; perfectly random mating. Yet there are various other forces that today are the descendants of the lucky lineages that survived, as is essentially no selection, and that the global population has genocides and shrinkages. It is obvious that all people living models (including ours) assume all alleles are neutral, that there we see a long series of explosive human expansions, along with over very deep time. It is a passive and slow process. Most drift change allele frequencies. Looking backwards in human history, in changing allele frequencies except in very small populations or other important demographic factors that could very rapidly Genetic drift is really just a type of diusion and is quite impotent numerical simulation. However, we are not yet able to simulate rapid demographic shifts that can be easily demonstrated using make our simulations more biologically realistic. We used selective sweeps as our example because they are selective sweeps and dierential sub-population expansions to We believe that we must eventually factor in forces such as and constituting desirable poly-genic (quantitative) traits. genetic drift. in coordination each other, constituting functional linkage blocks, combined with various demographic forces other than classical designed alleles of this type would naturally be designed to work 2. Adam and Eve were created with internal designed diversity, purpose, one favored over the other, depending on habitat. Lastly, for every designed allele pair both variants would have a designed generations after the ood. time), they would be created at relatively high frequencies, and an episode of accelerated mutation accumulation in the rst 25–50 alleles would be very abundant from the rst generation (no waiting simulating a growth pause after the Babel event; and c) simulating should respond to selection very rapidly. This is because designed adjusting the ratio of mutational alleles versus designed alleles; b) other types of adaptive selection) should be very common, and We may be able to enhance the current distribution further by: a) rare. However, given designed alleles, selective sweeps (and all the actually observed biological allele frequency distributions. and because mutations that are strongly-benecial are vanishingly distributions that plot as smooth curves and closely approximate to be very rare. This is because benecial mutations are very rare, able to discover parameter settings that produce allele frequency Given only mutational alleles, selective sweeps would be expected versus mutational alleles. By modulating these variables, we were in dierent frequency classes; and c) the ratio of designed alleles allele distributions when we simulated this scenario (Figure 5). and duration of bottlenecks; b) the ratio of the designed alleles mutational alleles. In less than 200 generations we observe smooth that shape the allele frequency distribution included: a) the number that will be carried along will include both designed alleles and the observed allele frequencies. In this model, the primary factors linked. This is what is called a “selective sweep”. Those variants a very long way toward reconciling a literal Adam and Eve with carry with them countless nearly-neutral variants that happen to be In summary, modeling a heterozygous Adam and Eve brings us are driven toward the far left or far right of our plots, they will be moving toward a frequency of zero. As these high-impact pairs the actually observed allele distribution (Figure 7). the same time, in that habitat the corresponding minor allele would 50%), we found our distributions could be ne-tuned to align with that allele would increase rapidly toward xation in that habitat. At of 25%, another type starting with an initial allele frequency of more adaptive in one habitat than the other, so the frequency of pairs (for example, one type starting with an initial allele frequency Given a pair of high-impact alleles, one allele will typically be When we added a blend of two or more types of designed allele of selective progress and so allows for extremely rapid adaptation. 6b). functional linkage sets at high frequency. This amplies the rate toward higher allele frequencies, eectively lling the gap (Figure Furthermore, such designed variants would already exist as fully frequencies, while the mutational alleles drifted substantially then slowly move from allelic near-extinction to allelic xation. the designed alleles substantially drifted toward lower allele to wait for just the right set of mutations to arise serendipitously and (starting at 25%), with the two primary bottlenecks, we saw that frequency, enabling very rapid selective progress. There is no need When we combined mutational alleles with designed alleles present from the rst generation, and are already present at high rebound after the ood (Carter and Hardy 2015). “waiting time” is required. All the required genetic variants are bottleneck at the time of the Flood, and moderately rapid population to cause selection-driven adaptation. This is because no extended rapid population growth after Adam and Eve, a single-generation Designed alleles represent the most eective and the most rapid way with the biblical account, which seems to require moderately alleles on hand that could rapidly respond to natural selection. to accomplish the same thing, however we sought to be consistent Therefore, it would be reasonable to have a limited class of designed Sanford et al. ◀ Designed genetic diversity in Adam and Eve ▶ 2018 ICC 213 only seem logical for the Creator to pre-program designed diversity histories from nite allele frequency spectra. Theoretical Population Baharian, S., and S. Gravel. 2018. On the decidability of population size to what we see today. Indeed, given a miraculous creation, it would genetic diversity, could have given rise to allele distributions similar genetic variation. Nature 52:68–74. miraculously created people, if endowed with appropriate designed 1000 Genomes Project Consortium. 2015. A global reference for human REFERENCES In summary, our research indicates that it is reasonable that two analysis. like if there had never been a Fall. We gratefully thank Stephen Lee for advice regarding statistical reect, with wonder, upon what the human race might have been ACKNOWLEDGEMENTS biblical model is not only reasonable, it has inspired the authors to of His design, and the nature of His providential planning. This appears to have enabled rapid human adaptation after the ood. to appropriately reect the glory of God, the beauty and elegance to Darwinian mutation/selection. In addition, designed diversity to falsify. More than a strong counter-argument, this model seems talents. Human traits of this type cannot rationally be attributed consistent with what is observed, it would appear to be very hard forms of human beauty and the various forms of human gifts and audacious claim that “There is no way…”. This model is not only diversity”. This is especially true when we consider the various within the genome. This model seems to most eectively refute the the genetic diversity found within the human race is “designed a vast number of fully functional and fully integrated linkage blocks most coherent, powerful, and compelling explanation for most of would not just create a vast amount of diversity, it would also create Given the premise of a miraculously created Adam and Eve, the have logically been organized into functional linkage blocks. This “demographic stirring” and how it may accelerate genetic drift. Under the Designed Gametes Model, functional variants would linkage patterns. Future research will examine the concept of actually observed distribution. given rise to our current human allele patterns and our current The designed gametes allele distribution was very similar to the explanation for how Adam and Eve might have simultaneously in tness eect. The plotted allele frequencies were from 1–50%. robust, and in our opinion is even elegant. It seems to be the best allele, and a gold (favored) allele. All alleles were nearly-neutral we see today. The designed gametes model appears to be especially in Figure 7. Each designed allele pair had a purple (un-favored) that two people could give rise to the human allele distribution that generation. The subsequent allele frequency spectrum is shown genetic mechanisms seem to falsify the claim that there is “no way” up to 1000 individuals. The simulation was halted in the 200 and Eve’s originally created gametogonia. Together, these various th by a biblical bottleneck (3 reproducing couples), and then regrow population expansions; and 3) designed diversity within Adam The population was allowed to grow for 9 generations, followed as selective sweeps, lineage extinctions, and dierential sub- the designed alleles initially having a spectrum of frequencies. above, combined with more powerful demographic forces such population was designed with 989,000 or more allele pairs, with drift associated with multiple population constrictions; 2) as of Adam and Eve’s designed gametes (gametegonia). This initial Eve’s four sets of chromosomes followed by accelerated genetic with 50 ospring of Adam and Eve, who were derived from 100 mechanisms include: 1) designed diversity within Adam and designed gametes simulations model a population that begins distribution now seen in the human population. These genetic gametes might give rise to modern allele frequencies. Our can reconcile a literal Adam and Eve with the allele frequency We have used numerical simulation to illustrate how designed show that there are several Designed Diversity mechanisms that In this paper we have used logic and numerical simulation to “gene pool” comparable to a large human population. CONCLUSIONS original population of reproductive cells could have represented a own unique set of alleles and its own unique linkage patterns. That they are undermining the faith of millions of souls. unique. Every gamete in Eden could have been designed with its may be mistaken, and to prayerfully consider the possibility that Adam and Eve. Each gametogonium could have been genetically Adam and Eve to very carefully consider the possibility that they There could have been a vast number of created gametogonia within brethren who have been so vigorously arguing against a literal diversity. appears to be reckless and destructive. We exhort our Christian 3. Adam and Eve’s created gametogonia contained designed the historical Adam and Eve that is coming from within the church Scripture and the faith of millions of people–this militant attack on many mutational alleles and have them drift to higher frequencies. appears to be incorrect. Given what is at stake–the authority of been too little time for these chromosomes to accumulate very seriously over-reaching. In light of the current study, that claim seem to reect very young chromosomes. It appears that there has and Eve could ever give rise to our current allele distribution) was very similar to chrY and chrM. These chrY and chrM distributions evolutionist’s claim that “there is no way…” (that a literal Adam genome, all human chromosomes would have allele distributions Although the issues are complex, it is now very clear that the theistic that if we could strip all the designed alleles out of the rest of the We began to investigate these issues more than a decade ago. would be the result of newly accumulating mutations. We suggest had zero designed alleles, and all the observed polymorphisms help give rise to the specic allele distributions observed today. four copies, but as single ancestral copies. Thus, they would have genetic drift, selective sweeps, and sub-population surges), could two very special chromosomes would have existed in Eden, not in could be several ways that natural processes (such as accelerated consistent with the Heterozygous Adam and Eve Model. These research indicates that after the miraculous creation event, there the polymorphic alleles have very low frequencies. This is remarkable if He did not include benecial types of variation. Our have very few high-frequency polymorphisms. Overwhelmingly, into the genomes of the rst couple. In retrospect, it would seem Sanford et al. ◀ Designed genetic diversity in Adam and Eve ▶ 2018 ICC 214 Pennsylvania: Creation Science Fellowship. Skinner, I. Bergmann,A. Le Cabec, S. Benazzi, K. Harvati, and P. Gunz. Conference on Creationism, ed. J.H. Whitmore, pp. 133-151. Pittsburgh, Hublin, J., A. Ben-Ncer, S.E. Bailey, S.E. Freidline, S. Neubauer, M.M. mitochondrial chromosome. In Proceedings of the Eighth International doi:10.5048/BIO-C.2016.4. independent histories of the human Y chromosome and the human history part 2: A unique origin algorithm. BIO-Complexity 4:1–36. Carter, R.W., S.S. Lee, and J.C. Sanford. 2018. An overview of the Hössjer O., A. Gauger, and C. Reeves. 2016b. Genetic modeling of human the Flood bottleneck. Journal of Creation 32, no. 2:124–127.. approaches. 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Sanford. 2017. Contested Bones. Waterloo, New York: 122. common ancestry of all living humans. Nature 431:562–566. genotypic and phenotypic diversity. Answers Research Journal 9:81– Rohde, D.L.T, S. Olsen, and J.T. Chang. 2004. Modelling the recent Jeanson, N.T., and J. Lisle. 2016. On the origin of eukaryotic species’ origin of Homo sapiens. Nature 546:289–292. 337, no. 6099:1159–1161. 2017. New fossils from Jebel Iroud, Morocco and the pan-African Pennisi, E. 2012. ENCODE Project writes eulogy for junk DNA. Science Sanford et al. ◀ Designed genetic diversity in Adam and Eve ▶ 2018 ICC 216 Perspectives; and 5) coauthor of the book Contested Bones. and has contributed to multiple open source projects. published proceedings entitled Biological Information–New software engineer for six years. He specializes in web technologies Science from Rochester Institute ofTechnology and has worked as a organizer/editor of the Cornell symposium and subsequently Foundation. He has his BS and Masters degrees in Computer numerical simulation of the mutation/selection process); 4) lead Jonathan Potter is a research associate for Feed My Sheep of Mendel’s Accountant (a comprehensive and biologically realistic Gun”); 2) author of the book Genetic Entropy; 3) co-developer contributing to several open source projects. have been: 1) primary inventor of the Biolistic Process (the “Gene years of experience in developing open source code, including Sheep Foundation. John’s most signicant contributions to science recently in cloud and edge computing. He has 2 patents, and 15 president of Logos Research Associates, and president of Feed My engineer for 33 years, rst on IBM’s supercomputers, and more scientic publications, and several dozen patents. John is presently from Clarkson University. He has worked for IBM as a software research for 37 years. This research resulted in more than 100 He has degrees in computer science and mechanical engineering As a Cornell University professor, John Sanford conducted genetic Bruce Potter is a research associate for Feed My Sheep Foundation. THE AUTHORS at Southern California Seminary in the San Diego area. Santee, California: Institute for Creation Research. in Santa Ana, California, and teaches science apologetics courses Woodmorappe, J. 1996. Noah’s Ark: a Feasibility Study [pp. 176–195]. a senior research associate with Logos Research Associates based Kregel. genetics relating to the origin and history of life. John currently is in the Garden?, ed. A. Chou, pp. 75–100. Grand Rapids, Michigan: Accountant,acomputermodelforexploringkeytopicsinpopulation Wood, T.C., and J.W. Francis. 2016. Genetics of Adam. In What Happened he has been part of a small team that has developed Mendel’s that the earth is thousands, not billions, of years old. Since 2005 Scripture After Genetic Science. Brazos Press, Grand Rapids, MI. Venema, D.R., and S. McKnight. 2017. Adam and the Genome: Reading documented multiple independent lines of radioisotope evidence on the Radioisotopes and the Age of the Earth (RATE) team that Perspectives on Science and Christian Faith 62, no. 3:166–178. in connection with Noah’s Flood. Beginning in 1997 he served human-ape common ancestry and ancestral hominid population sizes. research undergirding the concept of catastrophic plate tectonics Venema, D.R. 2010. Genesis and the genome: genomics evidence for Since the early 1980’s he has undertaken most of the primary Reformation Heritage Books. computational physics research during most of his scientic career. Hermeneutics, and Human Origins. Grand Rapids, Michigan: from UCLA and worked at Los Alamos National Laboratory in VanDoodewaard, W. 2015. The Quest for the Historical Adam: Genesis, Associates. He has a Ph.D. in geophysics and space physics Answers Research Journal 10:45–54. Dr. John Baumgardner is vice-president of Logos Research obfuscation regarding refutation of the human chromosome 2 fusion, Tomkins, J. 2017. Debunking the debunkers: a response to criticism and ice age climate modeling. since 2005 and also has worked with Larry Vardiman/ICR on post Journal 8:379–390. Korea. Furthermore, he has worked on Mendel’s Accountant team wide DNA similarity using Nucmer and LASTZ. Answers Research almost a decade teaching computer science in both South and North algorithm and a complete reanalysis of chimpanzee and human genome- Tomkins, J. 2015. Documented anomaly in recent versions of the BLASTN companies and organizations around the world. He has spent own consulting company in which he has worked with numerous functional. Answers Research Journal 6:293–301. computational hydrodynamic codes for the US Navy, he started his Tomkins, J. 2013. The human beta-globin pseudogene is non-variable and Engineering. After spending a number of years developing 25:7677–7682. LLC. He is a graduate of MIT and has a PhD in Computational Proceedings of the National Academy of Science (USA) 112, no. Dr. Wes Brewer is a consultant for Computational Solutions of demographic inference based on the sample frequency spectrum. Terhorst, J., and Y.S. Song. 2015. Fundamental limits on the accuracy obtain his PhD in Marine Biology. physics and electronics before going to the University of Miami to evolution. BioEssays 30:470–479. He then spent four years teaching high school biology, chemistry, Templeton, A.R. 2008. The reality and importance of founder speciation in Applied Biology from the Georgia Institute of Technology in 1992. generate the graphic in the discussion thread (Shaner 2017a)]. and other issues related to biblical creation. He obtained a BS in https://github.com/glipsnort/bottleneck [This was the software used to in Atlanta, Georgia. He is currently researching human genetics around with demographic bottlenecks. Retrieved May 15, 2018, from Dr. Robert W. Carter is a senior scientist and speaker for CMI-USA Shaner, S., 2017b. Bottleneck: a forward genetic simulator for playing Sanford et al. ◀ Designed genetic diversity in Adam and Eve ▶ 2018 ICC
J.H. Whitmore, pp. 200–216. Pittsburgh, Pennsylvania: Creation Science Fellowship. diversity, and allele frequencies. In Proceedings of the Eighth International Conference on Creationism, ed. Sanford, J., R. Carter, W. Brewer, J. Baumgardner, B. Potter, and J. Potter. 2018. Adam and Eve, designed Recommended Citation Conference on Creationism. Browse the contents of this volume of The Proceedings of the International dc@cedarville.edu. The authors are solely responsible for the content of their work. Please address questions to DigitalCommons@Cedarville, the Centennial Library, or Cedarville University and its employees. published in our journals do not necessarily indicate the endorsement or reect the views of See next page for additional authors publication. However, the opinions and sentiments expressed by the authors of articles which means that all articles are available on the Internet to all users immediately upon FMS Foundation DigitalCommons@Cedarville provides a publication platform for fully open access journals, Bruce Potter Logos Research Associates Part of the Genetics Commons, and the Numerical Analysis and Scientic Computing Commons John Baumgardner Follow this and additional works at: https://digitalcommons.cedarville.edu/icc_proceedings Fluid Physics International Wes Brewer FMS Foundation Robert W. Carter FMS Foundation John C. Sanford Adam and Eve, Designed Diversity, and Allele Frequencies 2018 Print Reference: Pages 200-216 Article 8 Volume 8 on Creationism The Proceedings of the International Conference https://digitalcommons.cedarville.edu/icc_proceedings/vol8/iss1/8 This conference proceeding is available in The Proceedings of the International Conference on Creationism: John C. Sanford, Robert W. Carter, Wes Brewer, John Baumgardner, Bruce Potter, and Jon Potter Authors Adam and Eve, Designed Diversity, and Allele Frequencies Copyright 2018 Creation Science Fellowship, Inc., Pittsburgh, Pennsylvania, USA www.creationicc.org 200 and McKnight 2017). On various forums and blogs, some are even have also been thinking along these lines. For example, the idea aggressively promoting this claim (e.g., Venema 2010; Venema We call this the Designed Diversity Model. Other creation authors human population today. Some theistic evolutionists have been have been created in a heterozygous state for more than a decade. two people to give rise to all the genetic diversity we see in the We have been exploring the concept that Adam and Eve might Adam and Eve is the claim that it would be impossible for just when trying to derive historical models from them. Perhaps the most popular science-based argument against a literal frequency data are useless, however, only that one must be cautious state, and no literal Fall. 2016; Baharian and Gravel 2018). This does not mean that allele typically assert that there was no miraculous creation, no Edenic 2008; Terhorst and Song 2015; Harpak, Bhasker, and Pritchard so they must be either mythical or allegorical (Faulk 2004). They dogmatic historical inferences (Myers, Feerman, and Patterson advancing the argument that Adam and Eve never existed, and caution that allele frequency analysis does not justify making 2017; Carter 2017). Many theistic evolutionists are aggressively (e.g., Shaner 2017a, 2017b). Interestingly, other evolutionists been coming from within the church (Venema and McKnight frequency distributions are proof against a literal Adam and Eve (VanDoodewaard 2015; Carter 2015) and has increasingly less than several thousand individuals, or that that human allele The attack on the historicity of Adam and Eve began long ago claiming they can prove the human population has never been INTRODUCTION designed alleles, designed gametes, founder eects, allele frequency distribution, numerical simulation. human origins, demographic stirring, genetics, mutation, genetic drift, population bottleneck, designed diversity, KEY WORDS compelling reason to reject Adam and Eve based on modern allele frequencies. the observed human allele frequencies is clearly over-reaching and appears to be theologically reckless. There is no population. However, the genetic argument that there is no way that a literal Adam and Eve could have given rise to We cannot know how God created Adam and Eve, nor exactly how Adam and Eve gave rise to the current human of the very same type as are now seen in modern man. simulation to show that two people, if they contain designed alleles, can in fact give rise to allele frequency distributions can help reconcile a literal Adam and Eve with the human allele frequency distributions seen today. We use numerical In this paper we have critically examined these arguments. Our analyses highlight several genetic mechanisms that it is claimed that observed human diversity disproves a literal Adam and Eve. frequency of either 25%, 50%, or 75%. Today, most allelic variants have frequencies in the range of 0–10%. Therefore, The logic here is that, since there were only four sets of chromosomes in Eden, all variants would have had an initial It is also claimed that the currently observed human allele frequency patterns could not arise from a single couple. and talents; 2) the many forms of human beauty; and 3) the various ways people have rapidly adapted to new habitats. have been pre-programmed into their genomes. This could logically provide the genetic basis for: 1) our human gifts have been created with “designed diversity”. We have previously shown that a vast amount of genetic variation could Yet, Adam and Eve could have been created massively heterozygous. We have argued for over a decade that they could high mutation rates, logically leading to rapid extinction. were true, all observed variations would have to arise recently via random mutations. This would require incredibly population. This implicitly assumes Adam and Eve would have been created without internal genetic diversity. If this it would be impossible for a single human couple to give rise to the genetic diversity seen in the modern human Theistic evolutionists present multiple genetic arguments against a literal Adam and Eve. One key argument asserts