Monday, 30 September 2019

Review: Nathan H. Lents “Human Errors – A Panorama of Our Glitches From Pointless Bones to Broken Genes”

Review: Nathan H. Lents Human Errors – A Panorama of Our Glitches From Pointless Bones to Broken Genes (2018: Houghton Mifflin Harcourt)

Cell biologist Nathan H Lents, professor of biology at John Jay College, The City University of New York has written an engaging, highly accessible book showing the interested layperson how the errors in our body from the gross anatomical down to the genomic levels attest to our evolutionary origins. Highly recommended.

One of the reasons why medical schools teach embryology is that many otherwise bewildering aspects of human anatomy are readily understood when the medical student sees how limbs, organs, and systems develop from a fertilised egg. Similarly, many of those quirks of human anatomy [1] become readily understandable when our evolutionary origins are studied. [2] The tortuous path taken by the recurrent laryngeal nerve past the larynx, down into the chest where it loops under the aorta before returning up the neck to its destination and the presence of so many decayed remnants of retroviral genes located at exactly the same location as the great apes are two examples which defy explanation if the human body was designed from scratch, but cease to be puzzling when evolutionary origins are factored in. As Lents puts it:
“Our flaws illuminate not only our evolutionary past but also our present and future. Everyone knows that it is impossible to understand current events in a specific country without understanding the history of that country and how the modern state came to be. The same is true for our bodies, our genes, and our minds. In order to fully grasp any aspect of the human experience, we must understand how it took shape.” [3]
One of the more common apologetics strategies creationists use is to appeal to intricate design in the human body as evidence against evolution. There is no denying that there are many elegant features in the human body; my favourite is counter-current multiplication in the loop of Henle which concentrates urine in the kidney. [4] However, as the field of evolutionary computation shows, mutation and selection are more than capable of effecting elegant design which can far exceed what a human designer can achieve. Design does not need a conscious designer.

The fact the watchmaker is blind means that it cannot look ahead to the future; evolution is ultimately a tinkerer which selects what works for the moment without considering whether what works now will become a liability in the future. For example, the bizarre QWERTY keyboard layout makes no sense for an electronic keyboard, but when we realise that we inherited the layout from mechanical typewriters, one that was chosen to stop the bars holding the letters of commonly-appearing letter pairs from hitting each other. Obviously, that is not a problem for electronic keyboards, but given that millions of people were proficient in typing on a QWERTY keyboard, it made sense to continue using a familiar layout rather than create a new one – even if it was more efficient – which would require many people costly weeks to relearn how to type again. Many otherwise baffling flaws in the human body are inherited from a remote ancestor in which the future flaws of that ancestral structure were not apparent.

Lents classifies these flaws into three groups:

1. Design structures that made sense in a previous environment
2. Incomplete adaptation
3. Limits of evolutionary change

An example of the first one he provides is the difficulty with which we lose weight compared with the ease with which we out it on, one which is a factor behind the obesity epidemic which has considerable medical implications ranging from osteoarthritis to diabetes mellitus to ischaemic heart disease. Human evolved in an environment where food security did not exist; being able to take advantage of a feast/famine environment to store fat for the lean times is a positive liability in a world in which cheap, readily accessible, high-energy food is everywhere. What once made sense in a past environment has become a liability in a new one.

Recognising changed environments allows one to understand the second class of flaws. Lents provides the example of the knee joint. It’s at best a middling design which as sportspeople know is prone to failure when stressed. One should not be too harsh on the knee given that it originally evolved in the quadruped ancestors of humans. Once our ancestors adopted a bipedal gait, the knee had to cope with a new set of forces which it had never encountered before. The knee is very much a work in progress, evolving from a quadruped design to one that is able to function in a biped. Since evolution works incrementally with what it inherits, it’s hardly surprising that problems will arise and that change will be slow. An excellent example can be seen in the panda which despite having an exclusively vegetarian design has the short gut and teeth of a carnivore. Even the gut bacteria of the panda bear the hallmarks of its omnivorous past rather than being custom-designed for a vegetarian diet. [6]

The radical changes required to give the panda an herbivorous gut and dentition simply don’t happen in an evolutionary instant, which is the point Lents makes in his third category of human defects, those contingent on what evolution has inherited and the limits of incremental change. Human examples Lents cites are the extra pointless bones in the human foot and the potential choking point caused by food and air passing through the throat. If given a clean sheet, a designer could readily provide a far more efficient and safer design, but evolution cannot do this as it is a tinkerer.

In Chapter 1, “Pointless Bones and Other Anatomical Errors”, Lents looks at design flaws in the skeletal and nervous systems including the inverted retina, the poor drainage of the nasal sinus, and the already-mentioned knee and ankle joints. Take the inverted retina. Unlike cephalopods (octopuses, squids, and cuttlefish), the vertebrate retina is backwards, with the light-sensing cells pointing away from the light. The reason the vertebrate eye is inverted is that in the common ancestor of all vertebrates, the direction of the light-sensing cells made little difference to how well that organism could sense light. However, as the vertebrate eye evolved from a light-sensitive patch to a globe, the backwards-pointing retina was kept, simply because the changes in the developmental pathway of the retina required to get the lights cells pointing the right way around were not trivial and amenable to incremental change. They were ‘locked in’, with the result that the retina points away from the light, leaving us with a blind spot with no light-sensing cells in the part of the retina where the nerves and blood vessels exit and enter the eye. From a medical point of view, this backwards-pointing retina predisposes us to problems such as vision loss from retinal detachment, macular degeneration, diabetic retinopathy and retinal haemorrhage. [7] These would simply not be an issue if the retina was like that of the cephalopod, with light cells pointing towards the light.

One design flaw which when pointed out positively shouts the quadruped ancestry of humans is the location of the drainage holes in the nasal sinuses. Sufferers of sinusitis are all too aware of the misery that comes when the sinuses fail to clear and become infected. Lents points out that wild animals rarely suffer from sinus infections, with the main reason behind our susceptibility being that the drainage point in the maxillary sinuses are in the wrong place:
“Specifically, one of the important drainage-collection pipes is installed near the top of the largest pair of cavities, the maxillary sinuses, located underneath the upper cheeks. Putting the drainage-collection point high within these sinuses is not a good idea because of this pesky thing called gravity. While the sinuses behind the forehead and around the eyes can drain downward, the largest and lowest two cavities must drain upward. Sure, there are cilia to help propel the mucus up, but wouldn’t it be easier to have the drainage below the sinuses rather than above them? What kind of plumber would put a drainpipe anywhere but at the bottom of a chamber?” [8]
Lents notes that the evolutionary transition from mammals with a long snout to facilitate the important sense of smell to vision-oriented primates with a smaller snout, and then to humans with an even flatter face with smaller sinuses and thinner drainage ducts, likely secondary to the changes required to hold our large brains is the likely cause of our poor sinus drainage. Again, when evolutionary contingency and the tinkering nature of evolution is factored in, the sinus anatomy makes sense. However, it is not the design one would employ if creating a human from scratch.

In Chapter 2, “Our Needy Diet”, Lents, notes that humans fail to make many vitamins that other animals can synthesise from scratch while are predisposed to trace mineral deficiencies, requiring a demanding diet. Unlike most animals, humans (and most of the primates), most bats, guinea pigs and many fish cannot synthesise vitamin C, meaning they require a reliable dietary source. Without vitamin C, we cannot synthesise the connective tissue protein collagen; prolonged vitamin C deficiency results in scurvy which is fatal if not treated. The precise reason behind our inability to synthesise vitamin C is that the last gene in the biosynthetic pathway, L-gulonolactone oxidase (GULO) has been crippled by a mutation, turning it into a pseudogene. As primates have a diet high in fruit, it is likely that the mutation in the GULO gene of the common ancestor of the haplorhines (the suborder of primates including tarsiers, Old World monkeys, apes, and New World monkeys) would not have caused problems given that the loss of biosynthesised vitamin C would have been made up by the dietary source. As reversing the loss of function of a gene lost through mutation is difficult at best, [9] primates have evolved to be very efficient at making the most of all the vitamin C in the diet:
“humans, however, absorb dietary vitamin C at a much higher rate. But even though we have learned to eat food with ample vitamin C and even though our bodies are better at extracting these micronutrients from food, we have not managed to fully compensate for this malfunction. It’s still a very poor design. In the days before fresh food from faraway places was readily available to people, scurvy was a common and often deadly disease.” [10]
In chapter 3,”Junk in the Genome” Lents continues his zoom down in scale from the gross anatomical to the biochemical to the genomic level. A large part of the human genome – possibly up to 90% [12] serves no function. Lents provides examples of such ‘junk’ DNA such as pseudogenes, endogenous retroviral elements, and retrotransposons. One of the best-known examples of a pseudogene in the human genome is the GULO pseudogene which Lents raised in the previous chapter.

The GULO pseudogene in humans and the other primates is inactivated in exactly the same way [11] which is of course consistent with common descent. It beggars imagination that humans and primates would have been specially created not only without the ability to synthesise vitamin C but with exactly the same inactivating mutation. If humans were intentionally designed not to synthesise vitamin C, it is hard to see why they would have a broken GULO gene created in the first place.

Endogenous retroviral elements are the remnants of ancient retroviral infections which inserted themselves in the DNA of ancient sperm / egg cells and subsequently became passed down to the next generation of cells along with the rest of the human DNA. Over time, this retroviral-sourced DNA has picked up mutations and gradually degenerated to the point where they are largely harmless genetic fossils, incapable of reactivating as fully-operational retroviruses. [13] What is truly fascinating is that around 8 percent of the genome, approximately the same amount as exists in coding DNA is of viral origin:
“Around 8 percent of the DNA inside every single cell of your body consists of remnants of past viral infections, nearly a hundred thousand viral carcasses in all. Humans share some of these carcasses with cousins as distant as birds and reptiles, meaning that the viral infections that originally created them took place many hundreds of millions of years ago and these viral genomes have been passed along, silently and pointlessly, ever since.” [14]
Apart from the question of why a specially-created human genome would be made to look as if around 8% of it was of viral origin, the fact humans and primates share many identical ERV elements at the same place – exactly as one would expect if humans and apes shared common ancestry. [15]

In chapter 4 “Homo sterilis”, Lents observes that for a species whose population numbers in the billions, our reproductive capacity is quite inefficient when compared with other animals. Reasons for this include relatively late age of onset of sexual maturity (which when combined with high human mortality rates pre-modern medicine meant many people died before reproducing), low sperm count and motility, concealed ovulation (human females do not provide unmistakable physiological signs indicating peak fertility), the high number of pregnancies that that result in spontaneous abortion. As Lents observes
“These glitches in the reproductive system are especially maddening—and painful—for couples trying to conceive. And they are all bug, no feature; there is no justification for the spontaneous abortion of a perfectly healthy embryo or for the apparent failure of seemingly healthy reproductive organs to establish a pregnancy in the first place.” [16]
It’s not just conception and early pregnancy in which human reproduction shows many flaws. Childbirth is particularly dangerous, a point which modern medicine has helped reduce as any comparison of infant and maternal mortality rates both in the developing world and the pre-modern medicine era of now-developed countries with modern rates shows. Again, we are anomalous when comparing pre-modern medicine infant mortality rates with wild animals:
“While chromosomal errors and failures to implant are probably just as high among our ape relatives, miscarriages, stillbirths, and infant deaths during delivery are quite rare in other animals, especially primates. One-year infant mortality for wild animals is difficult to measure with certainty, but the best estimates for the other apes is 1 to 2 percent, making their birthing process several times more dangerous than that of humans in the modern United States but several times less dangerous than that of people in Mali or Afghanistan or the pre-1950 United States.” [17]
Lents also comments on how childbirth is more of a problem for humans when compared with other animals, and argues that the disparity between the evolution of the brain and the rest of the body are major factors here:
“If you’ve witnessed the birth of another mammal species, you’ll know that it is usually not a dramatic affair. Cows seem to barely notice when they give birth. Gorilla mothers often continue eating or caring for other children during delivery. The difficulties we associate with childbirth are uniquely human, the product of the rapid evolution of a large cranium together with the failure of evolution to keep up with those changes.” [18]
On this point, it is fair to note that there have been some recent challenges to the obstetrical dilemma that argues human infants are born ‘early’ to ensure that their heads are still able to fit through a narrow pelvis before further head growth makes this impossible. Biological anthropologist Holly Dunsworth has argued against the obstetric dilemma, noting that human pregnancy is only marginally longer than that of apes, standing in contrast with the obstetric dilemma which asserts that it is shorter when compared with an ideal pregnancy length if we did not have a narrow pelvis. [19] Irrespective of whether this is true or not, the central point that human fertility is remarkably inefficient and pregnancy / childbirth dangerous remains true.

In Chapter 5, “Why God Invented Doctors”, Lents comments on the morbidity and mortality caused by autoimmune diseases and allergies, in which the immune system misfires, and mistakes the human body for invading pathogens (autoimmunity) or mounts a disproportionate response to non-threatening foreign body (allergy). Autoimmune diseases definitely cause considerable morbidity and mortality, but here I must admit that the force of the argument here was less compelling than the previous chapters. Lents is definitely correct when he notes
“But to call our immune system perfectly designed would be equally inaccurate. There are millions of people who once happily walked this planet only to meet their demise because their bodies simply self-sabotaged. When bodies fight themselves, there can be no winner.” [20]
but any argument about how evolutionary flaws precipitate disease in humans would be made even more compelling by looking at the genomic flaws that are partly responsible. John Avise’s 2010 PNAS paper “Footprints of nonsentient design inside the human genome” [21] Avise comments on the large number of human diseases attributable to genetic mutation, and pre-empts a possible rebuttal from an evolution denialist:
“An apologist for the intelligent designer might be tempted to claim that such deleterious mutations are merely unavoidable glitches or secondary departures from a prototypical human genome that otherwise was designed and engineered to near perfection. As I will briefly describe in the next two sections, however, this excuse would be untenable, because all human genomes are also littered with inherent (endogenous) design flaws.” [22]
These genomic flaws include the presence of introns – large non-coding sections splitting up the coding section of genes into sections. The process of making a protein requires the introns to be excised out of the RNA copy of the gene, and mutations at intron-exon borders can result in genetic disorders. Avise notes that around 33% of genetic disorders can be attributed in some cases to errors in how this intron processing occurs:
For example, it has long been known that mutations at intron-exon borders often disrupt premRNA splicing in ways that alter gene products and lead to countless genetic disabilities, including various cancers and other metabolic defects. There is also good evidence that the number of introns in human genes is positively correlated with a gene’s probability of being a disease-causing agent. [23]
Avise continues by noting how overly-complex gene regulation, the existence of mitochondrial DNA with a higher mutation rate than nuclear DNA, genetic mutations arising from abnormal chromosome pairing during meiosis due to duplicate genes, and mobile genetic elements. A designer creating the human genome from scratch would arguably not write such flaws into its very structure.

Chaper 6, “A Species of Suckers” leaves behind the body and looks at the human mind, specifically human cognitive biases. It’s an accessible, informative overview of cognitive biases, particularly if you don’t have the time to read Daniel Kahneman’s “Thinking Fast and Slow” [24]. There is no doubt that many problems the human species faces come from the fact that our brains have evolved in an environment utterly unlike the one in which we now live. As Lents notes:
“In other words, human bodies and brains have not changed much in the past twelve thousand years. This is a kind way of saying that we are not adapted to this life. We are adapted to Pleistocene life. And perhaps nowhere is this clearer than in the way we perceive the world around us” [25]
In the Pleistocene world, the human who stopped to think about whether the strange rustling sound was a big cat with a hunger for human flesh or simply a gust of wind quite likely would not have survived long, meaning there were good evolutionary reasons to evolve the ability to make quick judgements, However, a brain tuned to make quick life-or-death decisions can make errors, which can be a problem in a world where critical thinking and deliberate decision-making is important. What makes the problem even more frustrating is that even when we know we are not creatures of logic and rationality, we still make those mistakes:
“What does make cognitive biases qualify as defects is that they are not the result of an overtaxed system; they are patterns of mistakes that are made over and over again. Even worse, they are deeply ingrained and resistant to correction. Even when people know that their brains tend to get something wrong, and even when they’re given all the information needed to get things right, there are some mistakes that they’ll just keep on making.”[26]

There are a number of books already in print on the evolutionary origin of human design flaws [27], but Lent’s is anything but redundant given that he manages to combine accessibility with an irenic tone (the lack of which was a significant drawback in the otherwise excellent “The Not-So-Intelligent Designer” by Abby Hafer. It’s definitely one to add to the library.


1. Readers familiar with the literature on evolutionary medicine will immediately be aware of the allusion to Lewis Held Jr Quirks of Human Anatomy – An Evo-Devo Look at the Human Body (2009: Cambridge University Press). Held’s book is also recommended, but it is aimed at a more academic audience than Lents’ book.
2. Which is why Randolph Nesse has rightly argued for evolutionary biology to be taught as one of the basic clinical sciences in medical school to provide “an integrative framework that links otherwise disparate bits of knowledge”. See Nesse R.M., et al “Making evolutionary biology a basic science for medicine Proceedings of the National Academy of Sciences Jan 2010, 200906224; DOI: 10.1073/pnas.0906224106
3. Nathan H. Lents Human Errors – A Panorama of Our Glitches From Pointless Bones to Broken Genes (2018: Houghton Mifflin Harcourt)
5. Adam Marczyk “Genetic Algorithms and Evolutionary Computation” The TalkOrigins Archive. Accessed 30th September 2019
6. Guo W et al (2018) Metagenomic Study Suggests That the Gut Microbiota of the Giant Panda (Ailuropoda melanoleuca) May Not Be Specialized for Fiber Fermentation. Front. Microbiol. 9:229.doi: 10.3389/fmicb.2018.00229
7. Novella, S. “Suboptimal Optics: Vision Problems as Scars of Evolutionary History” Evo Edu Outreach (2008) 1: 493.
8. Lents, ibid.
9. Though not completely impossible. Ten years ago, Bekpen et al provided evidence to show that the IRGM gene in primates was deactivated after the insertion of an Alu retrotransposon, only to be ‘resurrected’ by the insertion of a retrotransposon. Expecting events like this to restore human vitamin C synthesis however is probably less likely than winning the powerball lottery. Bekpen C, Marques-Bonet T, Alkan C, Antonacci F, Leogrande MB, Ventura M, et al. (2009) Death and Resurrection of the Human IRGM Gene. PLoS Genet 5(3): e1000403.
10. Lents, op cit.
11. Yang, H. (2013) Conserved or lost: molecular evolution of the key gene GULO in vertebrate vitamin C biosynthesis. Biochemical genetics, 51:413-425. doi: 10.1007/s10528-013-9574
12. Larry Moran Theme: Genomes & Junk DNA Sandwalk Feb 8 2008
13. Sometimes, this retroviral genetic material can be co-opted by the host for another function. One of the best-known examples is Syncitin-1, a protein involved in placental development which is of viral origin, having entered the primate genome over 25 million years ago. See Mi S, et al “Syncytin is a captive retroviral envelope protein involved in human placental morphogenesis.” Nature. 2000 Feb 17;403(6771):785-9.
14. Lents, op cit
15. The classic paper on how ERV insertions can be used to construct robust primate phylogenies is Welkin E. Johnson and John M. Coffin “Constructing primate phylogenies from ancient retrovirus sequences” PNAS (1999) 96: 10254-10260
16. Lents, op cit
17. ibid
18. ibid
19. Dunsworth, H. M. There Is No "Obstetrical Dilemma": Towards a Braver Medicine with Fewer Childbirth Interventions. Perspectives in Biology and Medicine (2018) 61:249-263.
20. Lents, op cit.
21. John C. Avise “Footprints of nonsentient design inside the human genome” Proceedings of the National Academy of Sciences May 2010, 107 (Supplement 2) 8969-8976
22. ibid, p 8972
23. ibid, p 8973
24. Daniel Kahneman Thinking Fast and Slow (2011: Penguin UK)
25. Lents, op cit.
26. ibid
27. I’ve already mentioned Held Jr. Two others are Abby Hafer’s The Not-So-Intelligent Designer (2015: Cascade Books) and John Avise’s Inside the Human Genome: A Case for Non-Intelligent Design (2010: OUP)