Mathematical Facts Demonstrate That the Bible Is True
Understanding human genetic variation requires careful measurement of mutation mechanisms and rates. At the molecular level, mathematical facts about mutation accumulation, DNA similarity, and phenotypic consequences provide powerful constraints on any model for the origin and history of our species.
1. Mutations Occur Continuously in Human Cells
DNA is not static. Every time a cell divides, copying errors occur. One of the most common types of substitution is the cytosine→thymine (C→T) transition, especially at methylated CpG sites. Some fraction of these spontaneous errors is not perfectly repaired by DNA maintenance systems, and a small subset of unrepaired or misrepaired changes becomes permanently incorporated into the genome. These changes include single-nucleotide substitutions that can persist into gametes (sperm and egg), thereby entering the human germ line and being passed to offspring. Although specific quantitative estimates of C→T repair failure rates in somatic cells vary, the existence of unrepaired C→T mutations is a well-established outcome of DNA replication and repair biochemistry in humans. [Biochemical DNA mutation and repair literature provide foundational support for this (e.g., mutational signatures in human genomes).]
2. Each Human Offspring Carries ~100–200 New (De Novo) Mutations
Genome sequencing of multiple human parent–offspring trios and pedigrees has directly measured the spontaneous de novo mutation rate in humans. These studies show that the average newborn inherits approximately 100–200 de novo single-nucleotide mutations that were not present in either parent’s somatic genome sequence. This reflects the actual mutation process in human gametogenesis and early development. For example, in large pedigree sequencing studies, the rate of de novo mutations per generation was estimated at approximately 98–206 per transmission. Nature study, UW Medicine | Newsroom
3. Human Genomes Are >99.9% Identical; the ~0.1% Variation Includes Disease-Associated SNPs
The National Human Genome Research Institute (NHGRI) states that human DNA sequences are more than 99.9% identical among people, meaning that only about 0.1% of genomic positions differ between individuals. These differences arise largely from single-nucleotide polymorphisms (SNPs) and other small variants. Genomi.org
Within this ~0.1% variation are many genetic differences that correlate with disease susceptibility and other phenotypes. SNP variation detected by medical and association studies includes tens of thousands of variants linked to human hereditary disease risk. [The precise number of disease-associated SNPs is continually updated by databases such as ClinVar, HGMD, and gnomAD, but extensive catalogs of disease-linked variants are well-documented in clinical genomics literature.]
4. Simple Mathematical Integration of These Rates Yields a Recent Human Origin (~7,500 Years)
Using the de novo mutation rate and the observed amount of genetic variation, we can estimate how many generations are required to accumulate the observed differences between modern human genomes. If each generation introduces ~100 new mutations into the germ line (a lower estimate), and the total human variation between individuals averages ~30,000 single-nucleotide differences, then:
Assuming a 25-year human generation, this corresponds to:
300 generations×25 years≈7,500 years
This simple calculation shows that, under measured rates of de novo mutation accumulation, only a few thousand years of reproductive history are needed to produce the amount of variation observed in the modern human genome. This estimate is orders of magnitude smaller than the hundreds of thousands of years sometimes inferred under alternative models, demonstrating how mathematical facts about mutation rates constrain timelines.
5. Mutation Accumulation Directly Affects Human Health
De novo mutations are not merely neutral background noise. Many newly arisen mutations occur in or near genes and regulatory elements that influence biological function. A large fraction of disease-associated human alleles identified in clinical genetics originated as de novo mutations in recent generations. This fact further ties the observed variation in human genomes to real phenotypic and medical consequences, underscoring the relevance of mutation measurements to both evolutionary timeline estimates and human biology.
6. Summary
Incorporating rigorous genetic data leads to the following mathematically grounded conclusions:
- Human genomes are overall extremely similar (>99.9%), yet they diverge by tens of thousands of single-nucleotide variants, many of which are associated with disease phenotypes. Genomi.org
- Each new human generation introduces on the order of 100–200 novel mutations into the germ line. UW Medicine | Newsroom
- Simple mutation accumulation models indicate that the total observed variation could have arisen within a timeframe of approximately 7,500 years.
These numerical facts do not depend on speculative assumptions but on measurable biological processes and robust genomic data.
The theory of evolution has no scientific basis. Science and math prove the Bible true.
