Creation Moment 12/5/2025 - Designed Diversity Model

And Adam called his wife's name Eve; 

because she was the mother of all living. 

Genesis 3:20

"The attack on the historicity of Adam and Eve began long ago (VanDoodewaard 2015; Carter 2015) and has increasingly been coming from within the church (Venema and McKnight 2017; Carter 2017). 

Many theistic evolutionists are aggressively advancing the argument

that Adam and Eve never existed, and so they must be either mythical or allegorical (Faulk 2004). 

They typically assert that there was no miraculous creation, no Edenic state, and no literal Fall. 

Perhaps the most popular science-based argument against a literal Adam and Eve is the claim that it would be impossible for just two people to give rise to all the genetic diversity we see in the human population today. Some theistic evolutionists have been aggressively promoting this claim (e.g., Venema 2010; Venema and McKnight 2017). 

On various forums and blogs, some are even claiming they can prove the human population has never been less than several thousand individuals, or that that human allele frequency distributions are proof against a literal Adam and Eve (e.g., Shaffner 2017a, 2017b).

Interestingly, other evolutionists caution that allele frequency analysis does not justify making dogmatic historical inferences (Myers, Fefferman, and Patterson 2008; Terhorst and Song 2015; Harpak, Bhasker, and Pritchard 2016; Baharian and Gravel 2018). This does not mean that allele frequency data are useless, however, only that one must be cautious when trying to derive historical models from them. 

We have been exploring the concept that Adam and Eve might have been created in a heterozygous state for more than a decade. We call this the Designed Diversity Model. 

Our 2005 version of the numerical simulation program Mendel’s Accountant (hereafter “Mendel”) included an “initial contrasting alleles” (ICA) option that was intended to enable the study of created diversity in a human population. At that time, we understood that the first human couple could have been designed with millions of variable genetic sites.

The Designed Diversity Model requires an expanded vocabulary. Traditionally it has been assumed that genetic variation only comes from mutations, giving rise to mutational variants (“mutational alleles”). However, given a miraculous creation, there could be a very different class of created variants (“designed alleles”). Mutational alleles and designed alleles would be different in several important respects. 

Mutational alleles need time to accumulate, 

while designed alleles can exist from the beginning. 

Mutational alleles are essentially random typographical errors in the genome and so are typically harmful, while designed alleles would logically be created to be beneficial. 

While mutational alleles always arise in a population as a single isolated copy, designed alleles would logically be created at higher frequencies.

It is widely understood that a mutational allele arises as a single copy – which is, therefore, on the verge of its own extinction. 

When a new mutation enters a population, its frequency is just one copy in a population of 2n (with n being the population’s size). Therefore, most mutational alleles are rapidly lost due to genetic drift within just a few generations (Rupe and Sanford 2013). 

While mutational alleles are typically very rare, designed alleles would typically be expected to be abundant, in accord with the nature of their function, and in accord with their initially designed frequencies. 

The smallest possible unit of genetic variation involves a single letter difference in the genome. Population geneticists call these single nucleotide variants (SNVs). 

If the minor allele is found at a frequency greater than 1%, such a variant allele is also called a single nucleotide polymorphism (SNP). For simplicity, and in keeping with the final report from the 1000 Genomes Project (1000 Genomes 2015), we will use the term “SNP” for all single nucleotide variations, regardless of their allelic frequency. 

The 1000 Genomes Project detected 84 million SNPs within the human population (1000 Genomes 2015). The vast majority of these are very rare alleles (about 64 million of the observed SNPs had allele frequencies of less than 0.5%). However, this is still a serious underestimate of how many rare human alleles exist. 

Given our current population size and mutation rate, every nucleotide site in the human genome should mutate many times every generation somewhere on this planet. Therefore, the number of

existing SNPs should be roughly the size of the genome (3 billion). But most of these variants are so rare that they are not detectable, due to limited sampling size. Most rare human alleles are unique to a single people group or sub-population. This indicates that most of these rare variants have arisen via mutation in the relatively recent past. We have previously proposed that, excluding rare alleles, a large fraction of currently observed human genetic diversity might have arisen from designed genetic variants that were built into Adam and Eve when they were first created (Sanford and Carter 2015a, 2015b). The latest analysis of the human genome (1000 Genomes 2015), indicates that there are only 8 million SNPs with allele frequencies of 5% or more. 

Hypothetically, most of these common alleles could be designed alleles. The average person living today carries 4–5 million SNP alleles (Levy et al. 2007). Therefore, a single human today accounts for a large fraction (approximately 30%) of all common genetic variation (Carter 2018). 

The African people groups tend to have slightly higher rates of polymorphism (Gurdasani et al. 2014; 1000 Genomes 2015). Since there are only about 8 million common SNPs in the human population, and since most of the SNPs in a single person are common SNPs, this means that any given person carries a very significant percentage of all the common genetic variants found across the world (Carter 2018). 

A single modern couple should carry most of the 8 million common SNPs that are ubiquitous in the human population. Obviously, the genomes of Adam and Eve could have contained this amount of diversity and much more (Sanford and Carter 2015a, 2015b).

Some fraction of the pre-Flood genetic diversity would be lost due to the genetic bottleneck of the Biblical Flood. However, population geneticists have known for decades that even the most extreme bottleneck (i.e., two people) can capture a significant amount of a population’s pre-bottleneck diversity, assuming the bottleneck only lasts for one or just a few generations and is followed by rapid population re-growth (Nei et al. 1975). 

In addition to the 8 million common alleles (most of which may be designed alleles), the 1000 Genomes Project identified another 64 million rare SNPs (most of which can be assumed to be mutational alleles). 

Q: How many generations would it take for 64 million mutations to accumulate? 

A: Given a mutation rate of roughly 100 mutations per person per generation, and assuming our current population of over 7 billion people, it would require less than one generation to accumulate 64 million mutations in the human population. 

Even for a human population of just 10,000, it would only take about 80 generations. While most new mutational alleles usually drift out of a population, the rate of loss of mutational alleles would be greatly reduced in a population that is continuously growing rapidly. In light of all this, the blanket claim, “There is no way Adam and Eve could have given rise to so much diversity,” is not reasonable. 

While Adam and Eve could clearly have given rise to the currently

observed amount of human genetic diversity, a more technical objection can still be raised. It deals with the specific distribution of the variant alleles observed in the human population. The narrower claim becomes, “Adam and Eve could not possibly account for the specific patterns of allele frequencies that we see in the modern human population.” This more technical objection is not easily dismissed and calls for careful consideration.

To address these challenges, we developed a modified version of the Mendel program (version 2.7.2), and also a completely redesigned version of Mendel (“Mendel-Go”) written in the state-of-the-art computer language “Go”. 

We included a new dynamic population size function, so that special experiments could be conducted where population size was continuously dynamic (changing). We improved older features that enabled such things as tracking initially created alleles, studying normal mutation accumulation, and examining the effects of small founder populations, mid-run population bottlenecks, and subsequent population re-growth. 

Modifications were made so that the changing allele frequencies in the dynamic population could still be tracked across generations. At the end of each experiment, the final allele frequency distribution could be plotted and could be compared to actual allele frequency distributions seen in today’s human population. In this paper we will use logic and numerical simulation to show that the claim that “there is no possible way…” is overreaching. There are multiple genetic mechanisms that can reconcile the Biblical Adam and Eve with the observed human allele distribution data.

Our simulations required the creation and tracking of two very different types of genetic variation. 

The first type was the classically understood mutational allele, and the second type was the designed allele. 

Mutational alleles would arise essentially as word-processing errors in the genome. This type of mutational allele would always arise as a rare variant. Mutations are always occurring, and mutation count per individual consistently increases in number. Our default mutation rate was 100 mutations per person per generation. Our default mutational effect was “near-zero” (i.e., there was essentially no selection happening, all mutational alleles would be drifting). 

In addition to mutational alleles, we simulated initial genetic variants that were created as designed allelic pairs, wherein each allele in a pair had its own designed function. Designed allele pairs would be present at the beginning of a Mendel run. 

Under the heterozygous Adam and Eve model, there would be just four copies of each chromosome in Eden, and so every designed allele pair would have a ratio of either 50/50 or 25/75 (so all initial allele frequencies for the designed alleles would be either 0.25 or 0.50 or 0.75). 

In our evolutionary simulations, we have observed that mutational allele frequency distributions are determined by the rate of genetic

drift, which is dependent on the parameter settings for population size, mutation rate, and time.

Mutational alleles continuously enter the population at very low initial frequencies and those that are not lost to drift will very slowly drift toward the right (i.e., away from zero). The rate of drift in any population with 1,000 or more individuals is exceedingly slow. Only after deep time can a large population reach mutation/drift equilibrium, where older alleles are drifting to fixation as fast as new alleles are drifting into the population. 

When mutation/drift equilibrium is reached, the allele frequency distribution stabilizes. At the same time, the total number of polymorphisms in the population stops increasing. 

We first performed simulations with only designed alleles (no new mutations arising). The allele “distribution” is a single spike at 50%. Given this starting point, and given a constant population size of 1000, after 200 generations the distribution was a narrow bell-shaped curve that was still centered at 50%, indicating that in this time there had been very limited genetic drift. 

----A second, more Biblically-realistic experiment involved the same initial allele frequency and a time span of 200 generations, 

*but started with a population of two, 

*followed by rapid population growth, 

*a severe population bottleneck to just 6 people in the tenth generation, 

*followed by a rapid population rebound. 

In this Biblical scenario, we see that two population constrictions can result in much more rapid allele frequency spreading.

Still more promising were simulations that involved designed alleles that all began with a minor allele frequency of 25%. For every allele pair where the minor allele frequency is 25%, there is a contrasting allele with allele a frequency of 75%. 

In this case, the starting allele frequency distribution (in the first generation)  the spike located at 25%. With this lower initial allele frequency, it is much easier to approach the observed human frequency distribution.... after just 20 generations. Most of the distribution is shifting to the left, with the mode shifting downward from 25%. .... what happens after 200 generations. The mode is now approaching zero and the distribution’s bell-shaped curve has become a nearly straight line that slopes downward to the right. When re-scaled, this is the basic shape of the lower-most portion of the actual allele frequency distribution. 

These allele pairs responded rapidly to natural selection, effectively emptying the central part of the distribution and driving the high impact alleles to the left and right extremes (this effectively fills “gap zone” separating the high-frequency created alleles and low frequency mutational alleles). Such strong selective sweeps would be expected to carry many low-impact linked alleles along with them. 

If there were individually designed gametes/gametogonia in Eden, this would potentially constitute an enormous gene poo1, comparable to the gene pool of a large human population. 

To transmit a large fraction of the original genetic diversity to later generations would require that the first family was very large. Indeed, it is entirely feasible that Adam and Eve would have had a very large family size, given the extreme longevity and vigor of the early patriarchs (Carter and Hardy 2015). In such an extremely large family, there could have been 100 or more different sets of chromosomes, representing a very substantial sampling of the primordial gene pool that existed within Adam and Eve’s gametes. This means that the variants in that first human population could have started with almost any initial allele frequency distribution, in accord with God’s design for mankind. In the same way, the initial population of gametes could have also started with a great diversity of linkage patterns, as might have been in accord with God’s design."

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