And Adam ....
and begat a son in his own likeness, ....
Genesis 5:3
"By comparing DNA from different humans around the world, it has been found that all humans 
This means that there is very little polymorphism, or variation. Much evidence of this genetic continuity has been found. For example, Dorit et al. examined a 729-base pair intron (the DNA in the genome that is not read to make proteins) from a worldwide sample of 38 human males and reported no sequence variation. This sort of invariance
‘ … likely results from either a recent selective sweep, a recent origin for modern Homo sapiens, recurrent male population bottlenecks, or historically small effective male population sizes … any value of Q [lowest actual human sequence diversity] > 0.0011 predicts polymorphism in our sample [and yet none was found] … . The critical value for this study thus falls below most, but not all, available estimates, thus suggesting that the lack of polymorphism at ZFY [a locus, or location] is not due to chance.’
After citing additional evidence of low variation on the Y chromosome, they note in their last paragraph that their results ‘are not compatible with most multiregional models for the origin of modern humans.’ Knight et al. have had similar research results:
‘We obtained over 55 kilobases of sequence from three autosomal loci encompassing Alu repeats for representatives of diverse human populations as well as orthologous sequences for other hominoid species at one of these loci. Nucleotide diversity was exceedingly low. Most individuals and populations were identical. Only a single nucleotide difference distinguished presumed ancestral alleles from descendants. These results differ from those expected if alleles from divergent archaic populations were maintained through multiregional continuity. The observed virtual lack of sequence polymorphism is the signature of a recent single origin for modern humans, with general replacement of archaic populations.’These results are quite consistent with a recent human origin and a global flood. Evolutionary models of origins did not predict such low human genetic diversity. Mutations should have produced much more diversity than 0.1% over millions of years. And yet this is exactly what we would expect to find if all humans were closely related and experienced a relatively recent event in which only a few survived. Research is needed to determine what variation should actually be present in the human genome—what would we expect within an evolutionary framework, and how does that compare with what we find? These results could have a great impact on biological evolution, population genetics, and could provide telling results about the age of the humankind. It could also affect the so-called molecular clock.
Another piece of evidence involves single nucleotide polymorphisms (hereafter SNPs), which are mutations common to the human genome (meaning that many humans share them), being present in the human population at a frequency of roughly 1%. These provide great insight into both medical
Linkage disequilibrium (or LD) supports the same conclusion. Genes are located on chromosomes in cells, and these genes may either be far away or close to each other. All of the genes that are located on one chromosome are said to be linked. When cells divide through meiosis, crossing over (or genetic recombination) often occurs. This involves two chromosomes aligning and swapping segments of DNA, resulting in genes getting shuffled around.
The closer two genes are together, the more likely that they will be inherited together—because they are close, it is unlikely that they will be separated during crossing over. When this holds true, genes are said to be in linkage disequilibrium—a state where they are not thoroughly mixed, but tend to be inherited together.
Likewise, if genes are thoroughly mixed, they are in equilibrium. LD has provided much evidence for a population bottleneck, because humans contain long-range LD, or LD that extends quite far in the genome, meaning that many genes tend to be inherited together. This type of evidence has been found in Northern Europe, for example. In fact, data gathered by Reich et al., suggests that in general, blocks of LD are large in humans, because many genes are closely associated. The explanation of this can have significant implications:
‘Why does LD extend so far? LD around an allele [or variant form of a gene] arises because of selection or population history—a small population size, genetic drift or population mixture—and decays owing to recombination [crossing over], which breaks down ancestral haplotypes [blocks of SNPs]. The extent of LD decreases in proportion to the number of generations since the LD-generating event. The simplest explanation for the observed long-range LD [such as what we find in humans] is that the population under study experienced an extreme founder effect or bottleneck: a period when the population was so small that a few ancestral haplotypes gave rise to most of the haplotypes that exist today.’This study concluded with the possibility that 50 individuals may have founded the entire population of Europe. This evidence is also quite consistent with a historical global flood." CMI
