Rosa Rubicondior: Refuting Creationism - How A Couple of Chance Mutations Led to Big Brains in Humans

Saturday, 29 March 2025

Refuting Creationism

How A Couple Of Chance Mutations Led To Big Brains In Humans

Microscopic image of a section of an electroporated, genetically modified chimpanzee brain organoid. Cell nuclei in blue, precursor cells in magenta, electroporated, genetically modified cells in green and dividing cells in orange.

Homo habilis is an extinct hominid species that lived between 2.8 and 1.5 million years ago. It is considered to be one of the earliest members of the genus Homo, and its name means "handy man" in Latin, reflecting its ability to make and use tools.

How did the large brain evolve? | DPZ

Creationists often struggle to explain why closely related species share identical genes located at the same locus on the same chromosome, typically resorting to the argument of common design rather than common descent. Even more challenging for creationists is when these shared genes exhibit slight modifications that result in significant differences between species, strongly supporting descent with modification.

A compelling recent example involves two genes, NBPF14 and NOTCH2NLB, identified by researchers from the German Primate Center - Leibniz Institute for Primate Research (DPZ) and the Max Planck Institute of Molecular Cell Biology and Genetics. These genes, modified specifically in humans, appear to explain the larger and more complex human brain compared to chimpanzees and bonobos. The research shows that NBPF14 and NOTCH2NLB act synergistically: one gene increases the production of neural progenitor cells, while the other facilitates their transformation into neurons capable of forming more extensive neural connections.

Together, these genetic modifications account for the remarkable increase in the size and complexity of the human brain relative to our closest primate relatives.

For an explanation of how two mutations with a low probability can quickly spread through the gene pool when they act synergistically, see my book Twenty Reasons To Reject Creationism: Understanding Evolution, pages 17-20, in which, using the example of a bacterium and two beneficial mutations acting synergistically, I show that the time take for 50% of the population to have both mutations is actually shorter than the time for 50% of the population to have just one mutation because, the accelerating effect of synergy increases the probability of both being inherited together.

This can explain why a large-brained archaic hominin appeared relatively suddenly in the fossil record. As we shall see, the fact that at least one of our ancestral species went through a narrow genetic bottleneck was ultimately highly beneficial because this reduces the time taken for the whole gene pool to acquire a neutral mutation by genetic drift alone.

What information do you have on the genes, NBPF14 and NOTCH2NLB, their role and evolution and how they differ from the counterparts found in chimpanzees, bonobos and gorillas?

The genes NBPF14 and NOTCH2NLB are notable primarily because of their roles in human brain evolution and their marked divergence from the genomes of chimpanzees, bonobos, and gorillas. Both are associated with human-specific evolutionary traits, particularly cognitive development and brain morphology.

NBPF14 (Neuroblastoma Breakpoint Family Member 14)

General Information:

Family: Part of the NBPF gene family, consisting of multiple copies primarily located on chromosome 1 (1q21.1-q21.2 region), known for copy-number variations (CNVs).
Function: Involved in neurogenesis, brain development, cognitive function, and possibly neuronal proliferation.
Protein domain: Contains DUF1220 protein domains (also known as Olduvai domains), which are highly duplicated in humans.

Role in Human Evolution:

Expansion of DUF1220 domains, including NBPF14, strongly correlates with increased brain size, cognitive abilities, and susceptibility to neurological conditions.
NBPF14 has undergone significant copy-number increases in humans compared to other great apes, making it a prime candidate in studies of human brain evolution.

Differences from Chimpanzees, Bonobos, and Gorillas:

Humans possess significantly more DUF1220 domains in NBPF14 than chimpanzees, bonobos, or gorillas.
The expansion in the NBPF gene family, especially in NBPF14, appears uniquely human, associated with increased cognitive complexity, brain volume, and potential vulnerability to certain neurodevelopmental disorders like autism and schizophrenia.

NOTCH2NLB (Notch 2 N-terminal Like B)

General Information:

Gene Family: Member of the NOTCH2-related gene family located on chromosome 1q21.1, close to the NBPF cluster, originating from duplications of the ancestral NOTCH2 gene.
Function: Regulates neural progenitor cell proliferation, expansion of cortical progenitor cells, and thus is involved in cortical development and enlargement of the cerebral cortex.
NOTCH2NL genes (NOTCH2NLA, NOTCH2NLB, NOTCH2NLC) are expressed highly in neural progenitor cells during cortical neurogenesis.

Role in Human Evolution:

Emerged specifically during recent human evolution (~3-4 million years ago) due to partial duplication and gene conversion events.
Thought to have driven expansion and increased complexity of the human cerebral cortex.
Strongly implicated in the evolutionary development of distinctively human brain traits, including increased cortical thickness, gyrification, and cognitive abilities.
Differences from Chimpanzees, Bonobos, and Gorillas:

Chimpanzees, bonobos, and gorillas completely lack functional NOTCH2NL genes. Humans uniquely possess functional NOTCH2NL genes, including NOTCH2NLB.
The chimpanzee genome contains truncated pseudogene versions, whereas gorillas and bonobos similarly lack fully functional orthologues.
Human-specific duplications and gene conversion events led to functional NOTCH2NL genes, representing a unique evolutionary innovation in Homo sapiens.

Evolutionary Implications of Both Genes:

Genomic Context:

Both genes reside within a complex genomic region on chromosome 1 (1q21), characterized by frequent structural rearrangements and duplications.
This genomic instability contributed to rapid evolution and divergence in these genes in humans, reflecting recent selective pressures on cognitive traits.

Adaptive Significance:

Expansion and functional emergence of these genes in humans correlate temporally and functionally with the rapid evolutionary expansion of the neocortex, increasing cognitive capabilities unique to our lineage.
However, this evolutionary advantage is counterbalanced by increased susceptibility to neuropsychiatric and developmental disorders (e.g., autism, schizophrenia, intellectual disabilities).

Summary of Key Differences:

NBPF14 (DUF1220):

Humans: Highly expanded copy-number and DUF1220 domain repetitions
Chimpanzees, Bonobos, Gorillas: Fewer DUF1220 domains, less complexity

NOTCH2NLB (NOTCH2NL):

Humans: Functional and intact, critical for cortical expansion
Chimpanzees, Bonobos, Gorillas: Non-functional pseudogenes or absent entirely

Cortical Development:

Humans: Significant impact on increased cortical complexity and size
Chimpanzees, Bonobos, Gorillas: Limited cortical complexity compared to humans

Neurological Disease Risk:

Humans: Increased susceptibility to neurological disorders
Chimpanzees, Bonobos, Gorillas: Comparatively lower susceptibility

Conclusion:

NBPF14 and NOTCH2NLB represent key examples of human-specific genomic innovations contributing significantly to brain evolution and cognitive complexity.
These genes underscore the evolutionary trade-off between enhanced cognitive capacities and susceptibility to neurological disorders.
Comparative genomic analyses highlight stark functional divergence between humans and other great apes, positioning these genes as crucial markers of recent human evolution.

ChatGPT4.5 [Response to user request]
Retrieved from https://chatgpt.com/

Information Continually updated

The research team have recently published their findings, open access, in Science Advances and explained it in a DPZ news release:

How did the large brain evolve?
New insights into the development of the human brain

Two specific genes that evolve exclusively in humans jointly influence the development of the cerebrum. Researchers from the German Primate Center - Leibniz Institute for Primate Research and the Max Planck Institute of Molecular Cell Biology and Genetics have discovered this in a recently published study. They have thus provided evidence that these genes contribute together to the evolutionary enlargement of the brain.
The results of the study show that the two genes act in a finely tuned interplay: one ensures that the progenitor cells of the brain multiply more, while the other causes these cells to transform into a different type of progenitor cell - the cells that later form the nerve cells of the brain. In the course of evolution, this interplay has led to the human brain being unique in its size and complexity.

The newly gained insights not only provide a deeper understanding of the evolutionary development of our brain but could also help to better comprehend how certain developmental disorders or diseases of the brain arise.

Brain organoid of a chimpanzee in culture for 14 days.

Our findings deepen the fundamental understanding of brain development and provide new insights into the evolutionary origins of our large brain. In the long term, they could contribute to the development of therapeutic approaches for malformations of the brain.

Nesil Eşiyok, first author.
German Primate Center, Leibniz Institute for Primate Research
Göttingen, Germany.

Various methods were combined for the study: In addition to animal experiments with mice, alternative methods such as chimpanzee brain organoids were also used. ‘The remarkable feature of our study is that the results from animal experiments and alternative methods complement each other well and mutually confirm their findings. This not only emphasizes the high significance of our results, but could also help to reduce the need for animal experiments in the future by further developing, refining and confirming alternative methods,’ explains Michael Heide, the study’s lead researcher.

Publication
Nesil Eşiyok, Neringa Liutikaite, Christiane Haffner, Jula Peters, Sabrina Heide, Christina Eugster Oegema, Wieland B. Huttner, Michael Heide (2025)
A dyad of human-specific NBPF14 and NOTCH2NLB orchestrates cortical progenitor abundance crucial for human neocortex expansion.
Science Advances 11, DOI: 10.1126/sciadv.ads7543.

Abstract
We determined the roles of two coevolved and coexpressed human-specific genes, NBPF14 and NOTCH2NLB, on the abundance of the cortical progenitors that underlie the evolutionary expansion of the neocortex, the seat of higher cognitive abilities in humans. Using automated microinjection into apical progenitors (APs) of embryonic mouse neocortex and electroporation of APs in chimpanzee cerebral organoids, we show that NBPF14 promotes the delamination of AP progeny, by promoting oblique cleavage plane orientation during AP division, leading to increased abundance of the key basal progenitor type, basal radial glia. In contrast, NOTCH2NLB promotes AP proliferation, leading to expansion of the AP pool. When expressed together, NBPF14 and NOTCH2NLB exert coordinated effects, resulting in expansion of basal progenitors while maintaining self-renewal of APs. Hence, these two human-specific genes orchestrate the behavior of APs, and the lineages of their progeny, in a manner essential for the evolutionary expansion of the human neocortex.

INTRODUCTION
The remarkable expansion of the cerebral cortex over the past ≈2 millions of years of human evolution culminated in the strongly folded human neocortex, which is three times larger than that of our closest living relative, the chimpanzee (1–5). This tremendous increase in the size of the human neocortex is thought to be a basis for our higher cognitive abilities (1, 6–10). A key process underlying the evolutionary expansion of the neocortex is cortical neurogenesis, which typically occurs during fetal development and involves cortical neural stem and progenitor cells (cNPCs) (5–8, 11).

Two main classes of cNPCs can be distinguished within the two principal germinal zones of fetal neocortex: apical progenitors (APs) and basal progenitors (BPs) (6–8, 12, 13). APs reside in the primary germinal zone, the ventricular zone (VZ) lining the ventricle, and comprise the primary cNPCs, the neuroepithelial cells (NECs) (11, 14). With the onset of cortical neurogenesis, NECs transform into apical radial glia (aRG; also called ventricular radial glia) (6–8, 13, 15–17). BPs reside in the secondary germinal zone, the subventricular zone (SVZ), which lies basally adjacent to the VZ (18, 19). Two types of BPs can be distinguished: basal radial glia (bRG; also called outer radial glia) and basal intermediate progenitors (bIPs) (7, 20–22). In species with an expanded neocortex, notably primates and in particular human, the SVZ becomes subdivided into an inner (iSVZ) and an outer SVZ (oSVZ) (21, 23–25). The iSVZ largely corresponds to the SVZ of small brain-containing rodents, and the oSVZ with its abundance of bRG has been implicated in neocortex expansion (6, 8, 21, 22, 24, 26–29).

When considering the role of the various types of cNPCs in the evolutionary expansion of the neocortex and the associated increase in cortical neurogenesis, both the lineage of cNPCs and their modes of division are key (12, 30–32). The canonical lineage of cortical neurogenesis is: APs make BPs make neurons. Initially, both NECs and a portion of aRG undergo symmetric proliferative divisions, which eventually increases the number of radial units (33, 34). With the progression of cortical neurogenesis, an increasing proportion of aRG switch to asymmetric self-renewing divisions, which yield one aRG daughter and one newborn BP daughter, with the latter migrating to the SVZ.

Both types of BPs can self-amplify by symmetric proliferative divisions, and can undergo neuron-generating divisions. bRG typically do the latter by asymmetric self-renewing divisions, which yield one bRG daughter and one newborn neuron that then migrates to the cortical plate. bIPs typically generate neurons by symmetric consumptive division (11, 12, 15, 35–37). In these cNPC lineage and division mode scenarios, it is essential to realize that a mere expansion of the AP pool size, without a concomitant increase in BP generation, is insufficient for neocortex expansion (6, 8, 38).

In light of the fact that neocortex expansion is particularly relevant in the case of human evolution, a research focus has been to study genomic alterations that have occurred specifically during human evolution and that differentially affect the abundance, behavior, and activity of human cNPCs in comparison to cNPCs of other primates (19, 39, 40). Such human-specific genomic alterations include both small changes such as nucleotide substitutions, as well as large changes that led to the emergence of novel genes that evolved specifically in the human lineage (41–44). With regard to the evolutionary expansion of the human neocortex, the latter genes, referred to as human-specific genes, are of particular interest if they are preferentially expressed in human cNPCs as opposed to neurons. While a number of such human-specific genes have been identified over the past decade (45) [summarized in Heide and Huttner (46)], functional studies dissecting how these genes affect cNPCs have addressed only two of them, ARHGAP11B and the NOTCH2NL genes (NOTCH2NLA-C) (45, 47, 48). Thus, ARHGAP11B has been shown to increase both, the generation of BPs from aRG and the self-renewal of BPs. Hence, the human-specific gene ARHGAP11B fulfills the abovementioned criterion that an increase in BPs is essential for neocortex expansion. In support of this concept, ARHGAP11B expression in fetuses of the common marmoset increases the size of the neocortex and induces its folding, phenotypes that were found to be associated with a specific increase in the abundance of BPs, notably bRG and in particular in the oSVZ (44).

In contrast, in the case of the human-specific NOTCH2NL genes, it has been shown that expression of the NOTCH2NLA variant in the embryonic mouse neocortex increases the proportion of cycling BPs in the SVZ, but not of APs in the VZ (45). Conversely, two comprehensive studies (47, 48) have reported that the expression of the NOTCH2NLB variant in embryonic mouse neocortex increases aRG abundance in the VZ without increasing BP abundance in the SVZ. Mechanistically, NOTCH2NLB has been shown to activate Notch signaling by inhibiting the interaction between Notch and Dll1 in a cell-autonomous manner, thereby promoting the self-renewal of aRG (47, 48). In light of the notion that a mere expansion of the AP pool size, without a concomitant increase in BP generation, is insufficient for neocortex expansion, this finding by Suzuki et al., if confirmed, would imply that NOTCH2NLB alone is unlikely to be able to cause an expansion of the neocortex during human evolution.

The NOTCH2NLB gene, located on the long arm of chromosome 1 at position 1q21.1, lies adjacent to another human-specific gene preferentially expressed in cNPCs, NBPF14 (41, 49), which shows strongest expression in aRG (45). NBPF14 belongs to the neuroblastoma breakpoint family (NBPF) of genes. NBPF genes are defined by the presence of a protein domain called Olduvai domain (previously known as DUF1220) (50), whose molecular function is currently unknown. While the molecular mechanism underlying the function of NBPF14 has not yet been elucidated, one member of the NBPF gene family, NBPF1, has been suggested to play a role in metabolic regulation by fine-tuning mitochondrial function, indicating a potential role of Olduvai domain(s) in this context (51). Genomic and phylogenetic analyses revealed that a large number of NBPF gene family members are found in the primate lineage, with the greatest number of members present in human (50, 52). It has been suggested that NBPF14 and NOTCH2NLB evolved jointly as a two-gene module in the human lineage (49). In light of the coexpression of these two genes in human cNPCs, notably in aRG (45, 46, 49), the question arises whether these human-specific genes can affect cNPCs in a coordinated, potentially synergistic, manner.

Here, we analyzed the role of NBPF14 during prenatal neocortical development, focusing on the effects of this human-specific gene on cNPCs and its possible functional interaction with NOTCH2NLB. To this end, we have used automated microinjection into aRG of embryonic mouse neocortex and electroporation of chimpanzee cerebral organoids. We confirm that NOTCH2NLB amplifies aRG, without increasing the generation of BPs, implying that this human-specific gene alone is unlikely to be able to cause an expansion of the neocortex during human evolution. Our functional analyses reveal that NBPF14 induces delamination of cNPCs from the VZ by modifying the cleavage plane orientation of mitotic aRG, thereby increasing the abundance of bRG in the developing neocortex. We further provide evidence that the combined expression of NBPF14 and NOTCH2NLB expands the BP pool while maintaining the self-renewal capacity of APs. Our data therefore provide a paradigmatic example of how two coevolved human-specific genes, NBPF14 and NOTCH2NLB, located adjacent to each other on chromosome 1, act in a coordinated and synergistic manner in aRG during cortical development. This concerted action of these genes likely has contributed to the increase in neocortex size during human evolution.

So, what does this mean for theories of human evolution? We have two mutations, neither of which conveys much advantage on their own. In other words, the mutation is neutral.

To Understand this, I had the following conversation with ChatGPT4.5. It's worth following it through to the end:

Assuming that neither mutation gave any survival advantage on their own, how could we calculate how long it would take for both mutations to be present in the same individual so the full effects of synergy could be realised?

To estimate the time it would take for two neutral mutations, neither providing a selective advantage individually, to appear together in the same individual through random genetic drift, we use the principles of population genetics and probability theory.

Here's a simplified but rigorous approach to the calculation:
Step 1: Understanding the Problem

Neutral mutations: Neither mutation confers an advantage or disadvantage alone.
Initial assumption: Each mutation occurs independently at a low frequency (initially just one individual).
Goal: Calculate the expected waiting time until both mutations co-occur in the same individual.

Step 2: Defining Variables

Let’s define clearly:

$N$ : Effective population size (number of breeding individuals).
$μ$ : Mutation rate per gene per generation (probability of the mutation occurring).
Each mutation event is independent.

We assume each mutation arises once spontaneously in a single individual, after which it can drift randomly through the population.
Step 3: Calculating the Probability of Fixation for a Neutral Mutation

A neutral mutation has the following probability of eventually becoming fixed in a diploid population: $\begin{matrix} (1) & P_{fixation} = \frac{1}{2 N} \end{matrix}$ This is because every allele, in neutral theory, has an equal probability of becoming fixed that depends only on its initial frequency (1 individual out of $2 N$ total alleles).

Thus, the probability of fixation of a neutral mutation is very small in large populations.
Step 4: Average Time to Fixation for Neutral Mutations

The average time for a neutral allele to either become fixed or lost through random drift in a diploid population is approximately: $\begin{matrix} (2) & T_{fixation or loss} \approx 4 N \end{matrix}$

This means, on average, it takes about $4 N$ generations for a neutral allele to either become fixed or disappear from the population entirely.

Step 5: Probability of Both Mutations Occurring Simultaneously

Two neutral mutations arising independently will each drift through the population. The chance that both will occur in the same individual at random (assuming both remain at low frequency) is initially extremely low. Therefore, realistically, the full synergistic effect would occur most reliably if at least one mutation becomes widespread or fixed first.

Thus, we have two scenarios:

Scenario A: Both mutations drift neutrally and remain rare:

Probability that one individual acquires both mutations simultaneously purely by random mating (assuming each mutation frequency = $1 / (2 N)$ ) is roughly:
$\begin{matrix} (3) & P_{simultaneous} \approx \frac{1}{(2 N) \times (2 N)} = \frac{1}{4 N^{2}} \end{matrix}$ This scenario is improbable in large populations and generally negligible as a practical mechanism.

Scenario B (More realistic): One neutral mutation drifts to higher frequency (or fixation), then the second mutation arises later:

First mutation fixation takes about $4 N$ generations on average (neutral fixation).
Once fixed, every individual carries this mutation. Now we await the second mutation:

The second mutation appears at a mutation rate $μ$ per generation.
Expected waiting time for this second mutation to appear (once) is approximately:

$\begin{matrix} (4) & T_{second mutation} \approx \frac{1}{μ} \end{matrix}$ Then, the time required for this second mutation to spread neutrally again (if it needs to be widespread to realise a beneficial synergy widely) will again be approximately $4 N$ generations.

Thus, total expected time under realistic conditions is about: $\begin{matrix} (5) & T_{total} \approx 4 N + \frac{1}{μ} + 4 N = 8 N + \frac{1}{μ} \end{matrix}$
Step 6: Example Calculation (for illustrative purposes)

Suppose we assume:

Effective population size ( $N$ ) = 10,000 individuals.
Mutation rate ( $μ$ ) = $1 \times 10^{- 8}$ per generation per gene.

Then:

Time to fixation of the first mutation ≈ $4 N = 4 \times 10, 000 = 40, 000$ generations
Waiting time for the second mutation ≈ $1 / μ = 1 / 10^{- 8} = 10^{8}$ generations (very long!)
Another 40,000 generations to become widespread.

Total ≈ $40, 000 + 100, 000, 000 + 40, 000 \approx 100, 080, 000$ generations.

This illustrates that, under purely neutral conditions with realistic mutation rates, it's extremely improbable for two neutral mutations to independently appear and synergise quickly without any selection pressure.

Step 7: If Selection is Introduced

If, instead, the second mutation offers even a slight advantage once the first mutation is common, then selection greatly accelerates its spread and reduces total time drastically.

Conclusion and Interpretation:

Under purely neutral conditions (no selection), the co-occurrence of two neutral mutations would take an exceptionally long time.
Realistically, synergy is more likely to evolve if one mutation fixes first neutrally, and the second mutation, once it appears, immediately confers a selective advantage in the presence of the first.

In your scenario (human brain evolution with NBPF14 and NOTCH2NLB), it’s very likely at least one of these genes became widespread due to neutral drift first, and the subsequent occurrence of the second mutation quickly offered a survival or reproductive advantage, significantly accelerating fixation and allowing synergy to be realised far more rapidly.

This calculation underscores the critical importance of selective advantage—even slight—in driving evolutionary innovation more efficiently than neutral drift alone.

In a small population then, the time for one neutral mutation to reach fixation can be fairly short. The second mutation would then find a 'pre-primed' population. If the presence of both then gave a significant survival advantage, then the population could quite quickly have both mutations.

Yes, your reasoning is precisely correct. Here's a more explicit explanation:

Neutral Mutations in Small Populations

In small populations, neutral mutations can reach fixation relatively quickly. The average time to fixation for a neutral mutation is approximately: $\begin{matrix} (5) & T_{fixation (neutral)} \approx 4 N \end{matrix}$
For example, in a small population (e.g., $N = 100$ ), the expected time to fixation for a neutral mutation would be about 400 generations—comparatively short on evolutionary timescales.

'Pre-primed' Population

Once the first neutral mutation becomes fixed, every individual in the population carries this mutation. Thus, the population becomes 'pre-primed' or genetically predisposed to immediately benefit if a complementary mutation appears.
The second mutation, if arising later in this genetically "prepared" context, can then immediately interact beneficially with the first mutation, creating synergy.

Second Mutation Providing Selective Advantage

If the second mutation significantly enhances survival, reproduction, or cognitive abilities (such as brain complexity), natural selection rapidly amplifies its frequency in the population.
Under selection, the fixation time is drastically reduced compared to neutral drift. Even a modest advantage significantly speeds up fixation, typically within tens or a few hundred generations, rather than thousands or millions.

Overall Time Frame: Realistic Scenario

A realistic scenario in a small population might look like this:

Step
Approximate Timeframe

Neutral fixation of first mutation
Several hundred generations (short)

Appearance of second mutation
Dependent on mutation rate; possibly hundreds or thousands of generations

Fixation of second mutation (under selection)
Tens to a few hundred generations (very fast)

Thus, a small population provides a powerful evolutionary context for rapid adaptive evolution, particularly when two mutations interact synergistically.

Implications for Human Evolution

In the context of human brain evolution (such as with NBPF14 and NOTCH2NLB):

Early human populations (likely small and fragmented) provided precisely the kind of scenario you describe, enabling rapid fixation of beneficial synergies once mutations arose.
This scenario neatly explains rapid evolutionary events, particularly those associated with significant cognitive leaps in early human populations.

Conclusion

Your hypothesis is entirely plausible and aligns well with known evolutionary principles: In small populations, neutral mutations can quickly become widespread, "pre-priming" the population for subsequent beneficial mutations. Once both mutations interact synergistically to confer selective advantages, rapid evolutionary change follows.

ChatGPT4.5 [Response to user request]
Retrieved from https://chatgpt.com/

Information Continually updated

Given the tendency of archaic human populations to form small, genetically isolated groups that subsequently merged, as recent research indicates, it is entirely plausible that one of these groups evolved both mutations, rapidly acquiring cognitive abilities that provided significant advantages over other groups.

A recent paper, which I discussed in detail here, provides evidence for precisely this scenario. It describes how an isolated population passed through a severe genetic bottleneck before expanding and eventually merging with a larger population. Remarkably, this smaller group appears to have contributed around 80% of the genetic heritage shared by modern humans, Neanderthals, and Denisovans.

It therefore seems highly likely that these two key mutations arose within this smaller population, granting them—and consequently us—the capacity for larger brains, enhanced cognition, and sophisticated communication skills characteristic of modern Homo sapiens.

This scenario is entirely consistent with evolutionary theory and illustrates how mutations can confer significant advantages. This directly counters the creationist claim that mutations are invariably harmful and thus incapable of driving evolution.

Advertisement

What Makes You So Special? From The Big Bang To You

How did you come to be here, now? This books takes you from the Big Bang to the evolution of modern humans and the history of human cultures, showing that science is an adventure of discovery and a source of limitless wonder, giving us richer and more rewarding appreciation of the phenomenal privilege of merely being alive and able to begin to understand it all.

Available in Hardcover, Paperback or ebook for Kindle

Ten Reasons To Lose Faith: And Why You Are Better Off Without It

This book explains why faith is a fallacy and serves no useful purpose other than providing an excuse for pretending to know things that are unknown. It also explains how losing faith liberates former sufferers from fear, delusion and the control of others, freeing them to see the world in a different light, to recognise the injustices that religions cause and to accept people for who they are, not which group they happened to be born in. A society based on atheist, Humanist principles would be a less divided, more inclusive, more peaceful society and one more appreciative of the one opportunity that life gives us to enjoy and wonder at the world we live in.

Available in Hardcover, Paperback or ebook for Kindle

Advertisement

Amazon