Biological Evolutionary Puzzles


Evolutionary biology tells us that many beneficial mutations happened in the past thousands of years ago like Blue Eyes or Lactose Tolerance in humans. But does the evidence support this claim? Not exactly.

Many mutations assumed from the distant past are perhaps only traits from normal reproduction or heredity. We have coined these as “ancient assumptions” because the claim is these mutations must have happened long ago as we find them today. This conclusion is not based on genetic information from the past because DNA in fossils is very rare and, at best, fragments. The claim is question-begging in that it looks at known genetic regions in the present and assumes these must-have transformed in the deep past– hundreds or thousands of years ago. These include (1) The Edison or less sleep mutation; (2) The Loss of ivory tusks in African elephants mutation; (3) The loss of wisdom teeth in humans mutation; (4) The Blue eyes mutation in humans; (5) The Lactose tolerance mutation in humans; (6) The loss of bitterness in almond tree mutation; and (7) The Murray beef mutation.

Sources are cited below each segment.

“The less sleep or Edison mutation”


DEC2 & hDEC2 mutation.

The Good: The gene thought to regulate sleep duration has the proclaimed benefit of requiring fewer hours of sleep for those with this genetic mutation. Popularizers of this beneficial mutation claim that sleeping 7 to 8 hours per night (such as the average) is a disadvantage compared to requiring fewer hours of sleep. The mutation allows (or more accurately causes) its carriers to function “normally” on only 4-5 hours of sleep per night. Some say perhaps Thomas Edison had this same mutation.-1

The reality: It is subjective to conclude that less sleep is better or regular. This mutation is known to directly cause the deletion of orexin neurons (receptor genes), resulting in narcolepsy. Also, it causes orexin signaling that negatively affects maintaining arousal (wakefulness) and sleep consolidation (quality sleep). Furthermore, administering orexin neurons experimentally increased arousal and decreased sleep duration. “Therefore, our findings provide insight into how orexin expression, which is involved in many biological functions, is regulated at a molecular level. We previously reported that the human DEC2 mutation contributes to short sleep duration in humans. Research also found decreased sleep durations in other animals, including flies and mice.-1. Regardless, “…the detailed mechanism of this sleep phenotype has remained elusive.” Clock genes, such as this mutation, are involved with tumor progression, playing an “important role in circadian rhythm, cell proliferation, apoptosis, hypoxia response, various stresses, and epithelial-to-mesenchymal transition (EMT) of tumor cells” -2. Therefore a mutation likely will manifest negatively within these areas as well. This negative feedback system is essential in 24-hour rhythmic regulation for circadian rhythm. The disturbance of circadian rhythm may induce metabolic syndrome, diabetes, Alzheimer’s disease, depression, sleep disorder, or cancer. Less sleep or nighttime work may increase cancer risk due to melatonin suppression. Mutations in the DEC2 gene are involved in the human short sleep phenotype and the regularization of sleep duration in mammals. Fewer hours of sleep are directly associated with excessive daytime sleeplessness, especially in children. Excessive sleepiness is associated with a 60% higher incidence of cancer and an 80% increased risk to children with neoplasm in the central nervous system. Sleep disorders account for 40% of the entire children with cancer! Also, the mutation is associated with the expression of DEC1, which is associated with human oral, breast, and pancreatic cancer cells.-2

All living beings from bacteria to human have circadian rhythm, which is dominantly regulated by clock genes (DEC2). The molecular mechanism of circadian rhythm depends on negative feed-back system by clock genes.”-2

(Mutated) Clock genes, major regulators of circadian rhythm, are involved in tumor progression…cell proliferation, apoptosis, hypoxia response, various stresses, and…tumor cells.“-2

Effects derived by heredity

Summary: The premise that less sleep is a benefit is very subjective. The quality of sleep and resulting wakefulness are more objectively positive attributes of sleep. First, any associated advantage from this mutation is not clear to researchers, concluding that any good benefits behind this proclaimed good mutation “remain elusive.” Perhaps the most critical role of quality sleep is found by maintaining good circadian rhythms. Good circadian rhythms are directly associated with good health and reduced disease. Also, the mutation is associated with many vastly harmful side effects, including narcolepsy, poor sleep quality, diabetes, Alzheimer’s Disease, depression, sleep disorders, and even increased risk of developing cancers, including breast and pancreatic. Children with this mutation have an 80% increased risk of developing central nervous system cancer, while any sleeping disorder in children increases cancer risks by 40%.

1- DEC2 modulates orexin expression and regulates sleep


“The Ivory Tusk loss Mutation in elephants”


AMELX or MEP1a Mutation.

The Good: It is estimated that 35,000 elephants are killed yearly for their ivory, so a reduction helps protect these threatened populations.-1 The female elephant, as measured since the 1940s, has a higher likelihood of being born “tusk-less” from about 18.5% to about 33% today. Tusks are associated with the teeth genes and are essentially overgrown molars used for various tasks. Since poaching has increased, it is believed that this mutation has caused this result to benefit the elephant population at large as a form of natural selection.

The reality is tusks are genetically passed by heredity. Any male born without tusks clearly has a degradative disability that leads to death. Due to changing environments, tusks are not needed by females. Also, poaching impacts the genetic pool of reproduction. Those carriers of the tusk gene are more likely to be killed than the tuskless. “They have this very compelling genomic data…(but) Scientists are still not sure which changes are causing a loss of tusks in either of the genes… “It appears that natural selection (as driven by gametes at reproduction) is the best and only answer as to why there has been a measurable reduction in the number of female elephants born tusk-less. The mutation has been isolated as a degradative disability in male elephants. There leaves little reason to believe that it is also a handicap for females—just not (usually) deadly. The findings here are largely anecdotal, as the prevalence of tuskless females has always been measurable. The rapid reduction of elephant populations combined with an ever-changing environment has led to a “bottleneck that strongly favors (the) tusk-less phenotype.”-1. Think about it this way: the elephants (primarily male but also females) with tusks are poached and killed. Those females that carry the tusk-less phenotype live and reproduce. Thus expanding this recessive trait with each passing year by genetic bottlenecking. This is natural selection (by environmental pressure) as a direct result caused by reckless human beings. The results are not due to mutations but are heredity favoring the recessive trait of tusk-less females. Finally, while there are anecdotal reports of tusk-less males in the populations of elephants worldwide, these are plausibly explained by either rare exceptions such as injuries or observer error–not beneficial mutations.

Researchers at Gorongosa National Park “noticed that the elephants with no incisors were usually female. The park has never seen a tuskless male, suggesting the trait related to tusklessness is sex-linked.-2

If a female elephant had one copy of the tuskless mutation, they would have no tusks. So, when the elephant reproduces, half of their daughters will have tusks, and the others will not have tusks at all. Half of the males will have tusks if their offspring is male, and the other half will die, possibly even before birth…”-2

Effects derived by normal heredity

Summary: Tusks are detrimental to male elephants used for various purposes but certainly as the primary form self-defense that includes the ability to gain a mate and reproduce. Tuskless male elephants face certain death. This supposed beneficial mutation has helped female elephants escape ivory hunters, and natural selection, not conversions, has likely played a role in this reality. Elephant parents carry hereditary traits (alleles) to pass tusks and tusklessness to offspring. Over recent decades, studies have found that due to various factors, including changing environments and ivory hunting, allele frequencies of female tusklessness have increased from 18.5% to 30%. This is evidence reflects natural selection pressures that are likely impacted by ivory hunting. Therefore, the benefit claims seem validated, but it is not. Why? Because identifying the genetic sequence of the gene responsible for female trustlessness is not due to any copy error mutation but are gene variants provided by the parents that are passed at reproduction. Because many tusked females have been hunted and removed from the gene pool, tusklessness has increased. It is that simple. Like brown or blue eyes in human beings, these are gene variants–presuming them to be due to an ancient mutation is not verifiable and is ultimately speculation. Any assumption of this occurring by a supposed beneficial mutation is based on ancient premise because we have always observed both tusk and tuskless female evidence.



“Less Wisdom Teeth Mutation”


PAX9 & MSX1 difference Mutation-1. {d, b, c}

The Good: The presumption is that the jawline has become smaller (due to another mutation, MYH16), which is said to have restricted the human jaw size, also related to the supposed growing brain size. Some have evolved to get fewer wisdom teeth as an act of natural selection. The belief reasons that as we continue to grow, humankind will not have any wisdom teeth one day. Today the presumption is this random gene mutation occurred nearly 400,000 years ago or longer. Those born with this mutation in the gene for teeth have gained the beneficial attribute of requiring fewer wisdom teeth extractions.

The reality: This genetic trait is hereditary and far from unusual. This gene affects about 20%-40% of the human population with less than four wisdom teeth. Some humans get double wisdom teeth—up to eight teeth.-2 The most obvious answer is natural selection and the operation of heredity. Perhaps over the centuries, isolated gene sequences that include teeth have been turned off. It mi ht be as simple as we do not need wisdom teeth as we did hundreds of years ago. However, at best, misinformation is associated with a spontaneous mutation of the distant past. Geneticists can identify where the genetic sequence resides that accounts for wisdom teeth, but there is no ancient DNA sample to compare against to confirm this speculation. The mutation that is supposed to reduce the number of molars (wisdom teeth) is our deduction as to what might have happened in the distant past. This claim is not empirically based but speculations on genetic evidence and not from genetic evidence. “Are wisdom teeth genetic? The answer is complicated. Ances ryDNA looks at…genetic markers related to wisdom teeth to estimate whether or not you developed all four wisdom teeth. (Howe er), there are still a lot of unknowns about the role genetics plays in tooth development — particularly wisdom teeth because they aren’t present at birth like the rest of your teeth are. As genetics are complicated, and there may be other factors besides your genes, this trait is hard to pred, So even if your genetic markers predict an absence of wisdom teeth, you may still have them.”-3. In other words, claiming a beneficial mutation as the cause behind reduced wisdom teeth production is highly dubious, not explained by evidence but, as it turns out, a math formula.

Perhaps the greatest significance of the study is that it demonstrates how the evolutionary development of our bodies can be described mathematicallyHaving a formula to describe these features could help us understand some of the greatest mysteries of our evolutionary history.”-2

Derived by heredity– ancient assumption inferences

Summary: The gene sequences that control wisdom teeth are genetically passed as variants derived from the parents. As we have pointed out repeatedly, identifying the genetic sequence does not provide evidence for an ancient mutation for elements of heredity. Heredity emerges from the sex cells of the parents that provide variants the ultimately form gametes that create the offspring at conception. This process has nothing to do with copy error mutations. Any presumption of an ancient mutation cannot be verified because no such DNA sample can verify a pre-mutated sample, rendering this as speculation. Due to changing needs for molars, slight changes may have been made due to natural selection. Any assumption of this occurring due to a beneficial mutation is based on speculation because, as far as we know, humans have always had various genes that affect wisdom teeth production.




“Blue Eyes Mutation”


OCA2 Mutation. {b, d

The Good: The presumption is that the emergence of blue eyes in humans happened by a mutation in a single human ancestor about 6,000-10,000 years ago. Therefore, those born with this mutation in the eye gene have gained the attribute of having blue eyes, which is considered neither a positive nor negative trait.-1

The reality: Hereditary function finds that the sex cells of the parents produce gametes that emerge as various traits in the offspring called allele frequencies. Some of these expressions (traits) are dominant because they happen more often, while others are recessive because they emerge less often. Some aspects of eye color function by a pigment called melanin that produces the brown color. Lower melanin has less pigment and, therefore, green, hazel, or blue eyes.-2 These traits are merely speculated as emerging from a mutation long ago but persist in the present as trait options called gene variants or alleles.-3. Claiming such hereditary traits as being derived by a distant mutation assumes that Universal Common Descent is factual, and therefore these changes “must” have happened by mutations. These are merely speculations on the evidence and not what is empirically known regarding the evidence.

Derived by heredity– ancient assumption inferences

Summary: The gene sequences that eye coloration is known to be genetically passed as variants derived from the parents at conception (forming the various traits by gametes). As we have pointed out repeatedly, identifying any specific genetic sequence does not provide evidence for an ancient mutation–it just identifies the variants as they exist in the present. Heredity emerges from the sex cells of the parents that provide variants of the ultimate form of gametes that create the offspring at conception. This process has nothing to do with copy error mutations in the present. The assumption that eye pigmentation is due to mutation is based on a supposed ancient mutation (that was never observed by assumed). This claim is not empirical because no complete DNA sample exists from 6,000-10,000 years ago (of course). Any assumption of this occurring due to a beneficial mutation is based on speculation because, as far as we know, humans have always had various genes that affect eye coloration. Brown eye traits are dominant and blue eyes (or colorations that are not brown) are recessive. These gene variants have nothing to do with a copy error mutation in the present–only based on speculation.




“Lactose Tolerance Mutation”

Hereditary, Ancient Assumptions, Due to a Feedback Loop (not a mutation)

LCT (lactose) 2q21 Mutation. {b, d}

The Good: It is not hard to understand how digesting dairy (lactose) is a benefit. Evolution presumes that humans developed the ability to digest dairy products by a mutation between 2,000 – 20,000 years ago from a region near modern-day Turkey. The idea concludes that humans domesticated cows, goats, and sheep.-1. Repeated exposure to the lactase enzyme ultimately caused a genetic mutation that enabled humans to digest dairy.

The reality: First, the biological mechanism that enables lactose digestion is by a (very complex) feedback loop—not by any single mutation (see diagram). Second, lactose is a sugar broken down by an enzyme called lactase provided by heredity (lactose intolerance is a recessive trait-2). Third, all humans become more susceptible to lactose intolerance after being weaned.-3 Forth, while fragments of DNA have been discovered, any genetic claims from thousands of years ago rely only on assumptions because isolating any fully mappable samples of DNA, both before and after the mutation, simply does not exist empirically. In other words, fifth, this proclaimed beneficial mutation is only speculation and not supported by any verifiable evidence. Finally, the reality seems correct that lactose intolerance is a mutational disability.

Ancient assumptions

Summary: The biological mechanisms behind lactose digestion are complex, using a feedback loop that breaks the molecular bond by a highly specialized enzyme called lactase. This enzyme separates the sugar from the lactose molecule so it can be digested. Humans are born to digest lactose because their mothers feed them breast milk. As we age, the genetic expressions behind lactose digestion fade. The rate of this recession varies between individuals, but most all humans are less capable of lactose digestion than at birth. The idea that lactose tolerance emerged by a mutation fails superficial scrutiny. If human beings could not digest lactose from the beginning (from breast milk), then the species would have perished. The biological system has nothing to do with any mutation but a feedback loop. This supposed beneficial mutation of lactose tolerance developed in antiquity is falsified. The assumption that lactose tolerance developed from a prior intolerance is nonsensical. Like eye coloration in humans, this claim is not empirically established due to a mutation because no complete DNA sample existed from 6,000-10,000 years ago (of course). Any assumption of this occurring due to a beneficial mutation is based on speculation because, as far as we know, humans can always digest lactose. If not, we would not be here!




“Almond Tree non-bitter taste mutation”


Wild Gene mutation resulted in a loss of amygdalin (bitter flavor).

The Good: Almond seeds from wild species contain amygdalin, a bitter chemical that converts into cyanide inside the human body. According to researchers, consuming wild almonds is fatal. A single gene mutation in wild almond trees resulted in a variety that no longer synthesizes amygdalin. When humans discovered this non-bitter almond species, they cultivated them, which is continued till today.-1

The reality: The emergence of this variant is due to genetic expressions at reproduction and not any mutation. The wild strain already carried the gene without amygdalin that was passed to the offspring forms used today for commercial almond cultivations. This is an example of a miscategorized “mutation” associated with gene variants provided by gametes are reproduction that is preexisting and not de novo (novel) variations due to mutations.

Heredity– ancient assumptions

Summary: The genes for the bitterness variety of almonds preexisted from the sex cells of the parents (alleles). This has nothing to do with mutation. Geneticists have identified the sequence associated with this variety, but this does not equate to an empirical mutation. As with so many supposed ancient mutations, it is presumed that this happened long ago. Again, there are not fully sequenced DNA molecules to confirm that this mutation occurred– this is speculated. What we know for sure is the variety of almonds comes from other preexisting gene variants of, you guessed it, other almond trees.


“Murray Gray Beef Cattle mutation”


The Good: Murray Gray is a cattle breed obtained accidentally from a traditional cow species. The c lives produced by the specific cow were more productive than those made by the others. Farmers soon noticed the difference and started breeding from the offspring. The Murray breed, with some of the most favorable characteristics, has become popular all over Australia and then spread to various other countries.-1

Heredity- ancient assumptions

The reality: This cow species emerged by natural selection due to genetic expressions at reproduction– not any specific mutation. The offspring with the most desired traits were isolated for commercial farming. This is an example of a miscategorized “mutation” associated with gene variants provided by gametes at reproduction. Gamet s were preexisting within the parents and were not created de novo (novel or new information) variations due to mutations.

Summary: The genes for the variety of cattle that ultimately formed that “Murray Gray” came from preexisted from the sex cells of the parents (alleles) formed at conception–not due to mutation. Like all the various breeds of dogs that emerged from the Grey Wolf, all the breeds of cattle come from other cows. Geneticists have identified the sequence associated with genetic variation, but this identification does not equate to an established mutation. As with so many supposed ancient mutations, it is presumed that this happened long ago. Again, there are not fully sequenced DNA molecules to confirm that this mutation occurred– this is speculated. Speculated based on the presumed starting point that universal common descent is correct. So, UCD proves an ancient UCD? This is a logical fallacy. We know for sure that the wide variety of almonds (like all other living organisms) comes directly from heredity. Gene variants are preexisting from the parents (the mommy and daddy cows). The Murray Gray Cattle is an isolated (bottlenecked) artificially selected breed derived by heredity, not mutation.


Mutations, such as The Edison, Loss of ivory tusks, loss of wisdom teeth, Blue eyes, Lactose tolerance, almond tree, or the Murray beef, are all known to be derived today by normal reproduction or heredity. They have nothing to do with any mutation– except one presumed to have happened in the ancient past. The presupposition is that these effects manifested long ago by beneficial mutations. This conclusion simply cannot be substantiated based on fossil evidence lacking fully mappable DNA sequences but rarely has random fragments. In other words, there are no “pre-mutational” sequences to verify the claim; they do not exist besides as assumptions.

Low quantity, degraded and fragmented DNA, and contamination are the four issues that we have with ancient DNA,” says Bastien Llamas, an ancient DNA expert at the Australian Centre for Ancient DNA at the University of Adelaide.

“Can we really extract ancient DNA from dinosaurs?” Deborah Devis, Oct, 2021 -1

Therefore, such conclusions are not empirically established but are merely assumptions made upon the existing genetic material today. Presuming that modern sequences “must” have evolved is a logical fallacy of question-begging. The conclusion and the effect are the same– the effect is proven by the cause and the cause by the effect (circular logic). These observable “good” traits are merely speculation of presumed mutations of the ancient past, and no evidence can directly substantiate the claim. The specific genetic region that affects these attributes is perhaps well known in the present, but the pre-mutational genetic sequences are only imaginary because fully mappable DNA molecules simply do not exist in fossils.