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Five Questions about Human Errors for Proponents of Intelligent Design

When Charles Darwin first proposed natural selection as the mechanism of evolutionary change, he provided many different lines of reasoning. One of them was that he and other biologists had observed striking examples of suboptimal design in nature. If a creator-God was perfect and designed the world and everything in it according to His perfect plan, how could poor structure/function be explained? If we view the natural world as the product of evolutionary forces, however, imperfection is not so surprising. Rather, examples of poor design reveal interesting things about an organism’s evolutionary past, and that’s the thrust of my new book Human Errors.1

Because courts in the United States rightly determined that creationism is a religious doctrine, not a scientific one, its proponents changed their approach, practically overnight, restyling their position as the theory of “intelligent design,” or ID. By focusing on the seemingly scientific principle of “irreducible complexity” and only implying a vague, unnamed “designer,” supporters of ID claim it as a valid scientific theory, not a religious doctrine necessarily. Notwithstanding the fact that vanishingly few scientists support this theory and that neither were the courts fooled by the semantic shift, ID has become the dominant expression of creationism in the United States and is supported by around 40 percent of the population.2 Support for ID is strongly stratified by age, with only around 25 percent of those under age 30 in support, and is finally beginning to decline after years of holding steady.3

Glitches in nature, particularly in the human body, call out for an explanation.

Even if ID offered intellectual gains over creationism through the principle of irreducible complexity, and a focus on observations rather than biblical scripture, it did little to explain how poor design could be so rampant in creatures that were specifically designed by an intelligent force. Therefore, glitches in nature, particularly in the human body, call out for an explanation. Evolution usually provides elegant and deeply informative explanations. What are the explanations provided by ID? My book documents scores of these “human errors,” but I would love to know what intelligent design supporters say about these five in particular.

1. Why are we designed with nonfunctional pseudogenes?

In the human genome, there exist broken-down versions of once-functional genes. Formally called pseudogenes, these genetic elements have no function and are usually not expressed at all, but they bear striking resemblance to important and functional genes in other species. These genes were rendered inoperative by mutations and, in most cases, whatever function the genes once had we either no longer need or has been taken over by some other genes. In a few cases, however, the breakdown of the gene in question actually hobbles us in some specific way.

The most famous of the pseudogenes is called GULO. This gene normally functions in the synthesis of ascorbic acid, more commonly called vitamin C.4 The majority of animals on earth synthesize vitamin C for themselves, but primates cannot and therefore they (we!) must get it in our diet. The reason is because, long ago, in an ancestor of all primates, the GULO gene was disabled by a random mutation in either a sperm or egg cell. Through sheer chance, it became fixed in the population and has since accumulated many other mutations. But it is still easily recognizable. We have the GULO gene, but it’s broken.

For this reason, primates have been restricted to the climates where citrus fruits and other sources of vitamin C abound. It was once a mystery why humans had to consume vitamin C while none of our domesticated animals seem to need it. Evolutionary study has provided the fascinating answer, which also illuminates why primates live where they do around the globe. For example, it’s no coincidence that no primates besides humans are native to the content of Europe. Dietary vitamin C is scarce there and explains why scurvy was a major public health concern in Europe through pre-history and antiquity. We’ve since learned to incorporate foods that provide us with vitamin C.

Since creationists don’t believe in evolution, what is their explanation? It’s not that we don’t have the GULO gene. We do. It just doesn’t work. Why would an intelligent force intentionally design us with a broken gene? Give us a gene or don’t, but a broken version? What is that about?

Also, GULO is not the only pseudogene. We have thousands of formerly functional genes scattered throughout our genomes like rusting cars in a junkyard.5 We may even carry more broken genes than working ones. If this is design, it sure isn’t intelligent!

The human maxillary sinus cavity.

The human maxillary sinus cavity. Because the mucus collection duct is located at the top of the chamber, gravity cannot help with drainage. Illustration by Donald Ganley from Human Errors by Nathan H. Lents. Used by permission. All rights reserved, © Houghton Mifflin Harcourt.

2. Why do our nasal sinuses drain upward?

Have you noticed that, while we adults get 3 or 4 colds each year and our children can get 10 or more, our pets don’t seem to have this problem at all? One big reason for this is that our nasal cavities have a huge design flaw that those of dogs and cats don’t.

Nasal cavities are hollow, air-filled chambers through which air flows before heading down to the lungs. Lined with sticky surfaces called mucus membranes, these caverns warm and humidify the air and also trap particulates and microorganisms in the mucus. Normally, mucus is thin, clear, and watery, and is continually secreted, creating a constant flow of the sticky goo as it eventually drains into the throat where it can be swallowed and sent to the stomach for acid neutralization.

The largest such cavities in humans are the maxillary sinuses just behind our cheek bones. In a perplexing example of poor design, the drainage spout for this sinus cavity is near the top of the chamber. Since fluids don’t tend to flow uphill, tiny hair-like structures called cilia have to work extra hard to direct the mucus up to the drain pipe, which happens also to be extremely skinny. Most of the time, they can handle this challenge, but if there is any uptick in the load of allergens, infectious agents, or even just dust, mucus gets thicker and more viscous and this is when the situation gets sticky, literally. As the thick and cloudy mucus pools in the bottom of the sinus cavity, infections brew. What kind of plumber would put the drain at the top?

3. Why are humans so bad at absorbing vitamins and minerals?

A quick scan of the USDA’s recommended daily intake of various micronutrients confirms what anyone who has tried to eat a healthy and well-balanced diet knows all too well: the human diet is incredibly demanding. A little bit of this, a little bit of that, not too much of that…. While the supplement industry has no doubt exaggerated this for profit, there is truth to the claim that humans have to worry much more about their diet than other animals seem to. In fact, many animals can do just fine on a very repetitive diet of just a few, or even just one, source of food. Why can’t we?

Human evolutionary history is marked by one thing above all else: variety and experimentation.6 Humans have explored and exploited every imaginable habitat and mode of living and the ability to thrive in diverse scenarios and survive on myriad sources of nourishment unfortunately became the necessity of a varied diet as our bodies became lazy about manufacturing micronutrients for ourselves. (See vitamin C, above).

One thing that humans are terrible at absorbing is calcium, which is unfortunate because it is vital for the functioning of every single cell in the body. So essential is calcium, that we strip it from our bones whenever we don’t ingest enough of it. The bizarre part is that even when we consume sufficient amounts of calcium, we still end up deficient because we are so bad at extracting it from our food. 200 million women around the world suffer from osteoporosis. In the US, the typical diet provides plenty of calcium and yet, one in three women and one in five men will suffer a bone fracture due to osteoporosis,7 usually after age 50. What gives?

We start our lives absorbing a respectable 60 percent of the calcium we consume as infants. This percentage drops steadily throughout life, reaching about 20 percent in early adulthood, and plummeting to around 5 percent in old age.8 And this is the sad state of affairs when we have adequate vitamin D in our diets. Without vitamin D, we basically don’t absorb any calcium at all. Adding insult to injury, even though many women need also to boost their iron intake to prevent or treat anemia, iron in a meal can interfere with the absorption of calcium! So can sodium. And potassium. Is it any wonder that most of us are deficient in calcium?

We also have trouble absorbing some vitamins, such as B12. Like all the herbivore animals, we have bacteria in our large intestine that synthesize plenty of B12. But we only absorb B12 in our small intestine.9 This means that someone can suffer macrocytic anemia due to vitamin B12 deficiency while simultaneously sending copious amounts of B12 to the toilet. Bad plumbing strikes again!

4. Why do humans have muscles and bones that have no function?

The human body has way too many bones. Most humans are born with around 300 bones. This number drops to around 206 by adulthood as bones begin to fuse together. These numbers are just averages, some people have some extras and some are missing some. That alone tells you that something funny is going on.

Our ankles and wrists have seven or eight separate bones in them and for no good reason. They are all pretty much fixed together, though not fused, so there is no value in them being separate at all. While redundancy is often a good thing in a physical structure, the additional bones do not make our ankles or wrists stronger. In fact, having so many attachment sites for tendons and ligaments makes strains and sprains more likely. After all, a chain is only as strong as its weakest link. Think of how common sprained ankles are in humans. Now think of how rare they are in our companion animals.

Formally called the coccyx, the entire tailbone is pointless as well. While most of us have four coccygeal vertebrae, some have one extra and some have one fewer. While we’ve long known that it was the remnant of the tail that almost all mammals except apes have, it was assumed that the stump that we’re left with was important because many tendons and ligaments attach to it. However, tens of thousands of coccygectomies have been performed for various reasons, including cancer of the coccyx, and patients have absolutely no long-term discomfort or loss of function after their tailbones are removed.10 The various attachments could be entirely redundant or purely vestigial, probably both.

Not connected to the tailbone, but near it, lies another pointless organ called the pyramidalis muscle. This muscle can tense the flesh between the anus and the testes or vulva but this has no importance to posture, continence, or anything. In fact, around 20 percent of the population is missing this muscle altogether and it is badly misshapen in many that do have it.11 Some believe that the pyramidalis muscle previously functioned to flex the tail that our ancestors had but lost its attachment to the tailbone as the tail regressed.

There is also the Palmaris Longus muscle in our forearms. While a more substantial version of this muscle likely helped our ancestors by providing strong grip while swinging from trees, it is useless to us today. Between 10–20 percent of the population is missing this muscle entirely and they do not measure weaker grip strength for its absence.12 In fact, so useless is this muscle that surgeons routinely use its connecting tendon as the source of tissue grafts when they need a new tendon to repair a badly broken wrist.13

5. Why are humans so inefficient with reproduction?

The one thing that a species absolutely must be able to do is reproduce, so this is an area that humans must have mastered, right? Not even close. In fact, humans may be the least fertile of the apes. More than 10 percent of couples have trouble conceiving14 and when you consider what all can go wrong, it’s understandable.

To begin with, the ovaries are not even physically attached to the fallopian tubes and so eggs are sometimes squirted pointless into the abdominal cavity. Although it’s very rare, a roving sperm can actually fertilize one of these misplaced eggs and start a life-threatening abdominal pregnancy. On the male side, sperm have no sense of direction and swim in right-handed corkscrews, unable to turn left. This is part of the reason why hundreds of millions of them are needed for one to reach the egg. Many men have low sperm count or motility and many women have unpredictable ovulation cycles, meaning that the simple act of helping the meandering sperm and rudderless egg find each other is often not so simple.

But even when conception occurs, pregnancy is far from certain. More often than not, embryos fail to implant in the uterine wall before menstruation begins. In nearly half of those, chromosomal errors are to blame for an embryo’s failure to thrive,15 but in the larger portion, there is no apparent defect. The embryo simply bounces off the uterine wall and is lost with the endometrium at the end of the month. That so many perfectly healthy embryos are lost for failure to implant is especially painful for families trying to grow.

To demonstrate how out of step with other animals this is, female mice that copulate with a vasectomized male undergo the physiological steps of gestation, a phenomenon called pseudopregnancy.16 So confident is her body in its own fertility, and that of her mate, that a female mouse just assumes she’s pregnant any time she’s had sex. Her corpus luteum will persist, her uterine wall will thicken, and she will begin to lactate. Pseudopregnant mice even build nests in preparation for the nonexistent pups. Pseudopregnancy lasts 10–14 days in mice, nearly half the normal gestational period. It can last over a month in cats and two months in pigs.

Even when humans have managed to get and stay pregnant, the biggest danger of all still awaits. While modern technologies, from soap to Cesarean sections, have all but turned this page, giving birth was previously among the most dangerous moments of a woman’s life. As recently as 2000, almost 3% of childbirths in Sierra Leone resulted in maternal death and this is much reduced from just a half-century past.17 How much riskier was childbirth during the classical and pre-historical periods?

Being born is risky also. We do okay in developed countries, but there are four countries even today that suffer from greater than 10 percent infant mortality rate. The highest is Afghanistan where 12.1 percent of babies born do not survive the first year of life. In 1950, most countries were close to 20 percent on this measure.18 We are a spectacularly fragile species, but our evolution holds the explanation. Our pelvic girdle narrowed as we evolved to walk in an upright manner, with our upper legs jutting straight down and remaining within the same plane with each stride. Then, our craniums experienced an explosion of growth not long after. In a risky compromise of these two adaptations, we are born long before we are really ready, helpless and sickly.

The relative sizes of female pelvises and infant heads in (from left to right) chimpanzees, Australopithecus afarensis, and modern humans.

The relative sizes of female pelvises and infant heads in (from left to right) chimpanzees, Australopithecus afarensis (“Lucy”), and modern humans. Illustration by Donald Ganley from Human Errors by Nathan H. Lents. Used by permission. All rights reserved, © Houghton Mifflin Harcourt.

Once again, this is far out of step with other animals. For most of our fellow mammals, childbirth is not a dramatic affair. Cows and horses seem to barely notice when they give birth and the offspring are ambling about within minutes. Gorillas often continue to eat and care for other children as they give birth. It is just we humans, the supposed pinnacles of creation, who bear the awful burden of a treacherous childbirth.

Errors Abound

While the great majority of the quirks and glitches that I discuss in my book are the results of compromises, tradeoffs, and the inherent limits of evolution, some of them cannot possibly be seen as anything other than “bad design.” While evolution usually has an answer to the questions raised by these design flaws, if an unsatisfying one, what answer is offered by the theory of intelligent design? When creationists try to duck this question in creative ways (as they already have in responses to my book), this too is telling. What makes a theory scientific is its explanatory power and it’s ability to make testable predictions about future discoveries.

As far as I can tell, the only creationist response to human design flaws is, “That’s just the way it is.” This is not a scientific answer and offers no exploratory way forward. END

About the new book

We like to think of ourselves as highly evolved creatures. But if we are evolution’s greatest creation, why are we so badly designed? We have retinas that face backward, the stump of a tail, and way too many bones in our wrists. We must find vitamins and nutrients in our diets that other animals simply make for themselves. Millions of us can’t reproduce successfully without help from modern science. We have nerves that take bizarre paths, muscles that attach to nothing, and lymph nodes that do more harm than good. And that’s just the beginning of the story. As biologist Nathan H. Lents explains, our evolutionary history is a litany of mistakes, each more entertaining and enlightening than the last. As we will discover, by exploring human shortcomings, we can peer into our past, because each of our flaws tells a story about our species’ evolutionary history. A rollicking, deeply informative tour of our four-billion-year-long evolutionary saga, Human Errors both celebrates our imperfections—for our mutations are, in their own way, a testament to our species’ greatness—and offers an unconventional accounting of the cost of our success.

About the Author

Dr. Nathan H. Lents is Professor of Biology at John Jay College of the City University of New York, where he is also the director of the honors programs. He also maintains The Human Evolution Blog and hosts the science podcast This World of Humans. He is the author of Not So Different: Finding Human Nature in Animals and Human Errors: A Panorama of Our Glitches, from Pointless Bones to Broken Genes.

References
  1. Lents, N. H. 2018. Human Errors: A Panorama of our Glitches, from Pointless Bones to Broken Genes. Houghton Mifflin Harcourt. https://thehumanevolutionblog.com/book-human-errors/
  2. Shermer, M. 2006. Why Darwin matters: The case against intelligent design. Macmillan.
  3. Green, E. Intelligent Design: Slowly Going Out of Style? The Atlantic. 9 June 2014
  4. https://bit.ly/2HNWxUc
  5. 5 Torrents, D., Suyama, M., Zdobnov, E., & Bork, P. 2003. A genome-wide survey of human pseudogenes. Genome research, 13(12), 2559–2567.
  6. Tattersall, I. 2001. How we came to be human. Scientific American, 285(6), 56–63.
  7. Johnell, O., & Kanis, J. A. 2006. An estimate of the worldwide prevalence and disability associated with osteoporotic fractures. Osteoporosis international, 17(12), 1726–1733.
  8. Gallagher, J. C., Riggs, B. L., Eisman, J., Hamstra, A., Arnaud, S. B., & Deluca, H. F. 1979. Intestinal calcium absorption and serum vitamin D metabolites in normal subjects and osteoporotic patients: effect of age and dietary calcium. The Journal of clinical investigation, 64(3), 729–736.
  9. Herbert, V. 1988. Vitamin B-12: plant sources, requirements, and assay. The American Journal of Clinical Nutrition, 48(3), 852–858.
  10. Balain, B., Eisenstein, S. M., Alo, G. O., Darby, A. J., Cassar-Pullicino, V. N., Roberts, S. E., & Jaffray, D. C. 2006. Coccygectomy for coccydynia: case series and review of literature. Spine, 31(13), E414–E420.
  11. Monkhouse, W. S., & Khalique, A. (1986). Variations in the composition of the human rectus sheath: a study of the anterior abdominal wall. Journal of anatomy, 145, 61.
  12. Thompson, N. W., Mockford, B. J., & Cran, G. W. 2001. Absence of the palmaris longus muscle: a population study. The Ulster medical journal, 70(1), 22.
  13. Wehbe, M. A. 1992. Tendon graft donor sites. Journal of Hand Surgery, 17(6), 1130–1132.
  14. 14 Mascarenhas, M. N., Flaxman, S. R., Boerma, T., Vanderpoel, S., & Stevens, G. A. 2012. National, regional, and global trends in infertility prevalence since 1990: a systematic analysis of 277 health surveys. PLoS medicine, 9(12), e1001356.
  15. Baart, E. B., Martini, E., van den Berg, I., Macklon, N. S., Galjaard, R. H., Fauser, B. C. J. M., & Van Opstal, D. 2005. Preimplantation genetic screening reveals a high incidence of aneuploidy and mosaicism in embryos from young women undergoing IVF. Human Reproduction, 21(1), 223–233.
  16. Dewar, A. D. 1959. Observations on pseudopregnancy in the mouse. Journal of Endocrinology, 18(2), 186–190.
  17. Trends in Maternal Mortality: 1990 to 2015. Geneva, World Health Organization, 2015.
  18. The World Factbook. 2012. The Central Intelligence Agency, Washington D.C.
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