The (Descended) Testicles

 

Male Reproductive System

Female Reproductive System


        

The word sex comes from the Latin word secare which means to separate or divide. Each of the 23 pairs of human chromosomes are separated from each other and placed within gametes called male sperm and female eggs. Human reproduction requires that the 23 chromosomes in the sperm be joined to the 23 chromosomes in the egg to form a new human being. The natural way this takes place is through sexual intercourse. This involves the male depositing sperm from his erect penis deep into the females lubricated vagina so they can travel through the cervix into the body of her uterus so one of them can swim to and join up with an egg.

 

To accomplish this task the male reproductive system (see above) is equipped with testicles (also called testes), which, under the direction of hormones (see below), produce sperm which travel through its genital duct system and external genitalia out of his body. The female reproductive system (see above) is equipped with external genitalia and a genital duct system to guide the sperm into her body toward an egg that has, under the direction of hormones, been released from one of her ovaries. The sperm and egg usually meet up in one of the fallopian tubes of the uterus where the newly formed one-celled zygote forms a new human life. It soon starts to divide becoming an embryo which then migrates into the body of the uterus and implants in its lining allowing it to grow and develop into a baby that exits the mother`s womb about nine months later. 

 

Although a given persons survival does not depend on having the right parts working properly for reproduction, we all know that without enough people having adequate sexual function, the existence of the human race would be impossible. Moreover, as difficult as it may be to explain the development of the different parts and control mechanisms needed for human males and females to reproduce, we must also realize that they must have come about simultaneously since neither a male nor a female is capable of continuing the human race without the other.

 

Despite this impressive array of the different structures of the male and female reproductive systems, with the right specifications being placed exactly where they need to be to allow them, under the control of a complicated hormonal system, to do what they`re supposed to do, some evolutionary biologists conclude that this set-up represents “bad design” and evidence for their theory; that life came about solely from the unguided and purposeless forces of natural selection acting on random variation (genetic mutation). In particular, they point to the descended human male testicles contained in a sack of skin called the scrotum that hangs outside his body. Since many other animals (including a few mammals) have their testes safely tucked up inside their body, neoDarwinists claim that for such a vital male organ to be placed in such a vulnerable position represents “bad design”. 

 

In this article I’ve chosen to cite just one critic, Dr. Abby Hafer, who received her doctorate in zoology from Oxford University and teaches human anatomy and physiology. The three composite quotes in the next section come from her book The Not-So-Intelligent Designer: Why Evolution Explains the Human Body and Intelligent Design Does Not. This is a very important topic for her and would seem to be the main reason for her book as in her introductory chapter she states “The male testicle is a great first argument against ID (intelligent design) in the human body, and this brings me to the alternative title for this book: Evolution, Intelligent Design and Men’s Testicles: Why Evolution Explains the Human Body and Intelligent Design Does Not”.

 

The Critic Speaks

The testicles hang outside the body in a sack of skin called the scrotum. Why? Because human body temperature is too hot for sperm production. Having normal body temperature be too hot for sperm production is bad design. So the testicles have to hang outside the body in the scrotum, thereby putting a vulnerable organ in a vulnerable place. Putting a valuable and vulnerable organ in such a vulnerable location is bad design. Men are put to all sorts of inconvenience and risk severe pain and worse because of this unfortunate positioning. One would think that God could do better. But if the testicles were designed, then one wonders why God didn’t protect them better. Couldn’t the Designer have put them inside the body, or encased them in bone, or at least put some bubble wrap around them? Is this the best that the Designer can do? 

 

But what if warm body temperature and sperm production just can’t go together? Here’s one solution. You’d think that the Designer would try to give us humans, who were made in his image, the best deal that he could manage, wouldn’t you? But he didn’t. Some warm-blooded animals have testicles that hang outside the body when this is needed, but can be pulled up inside the body out of harm’s way when this is the safer option. Actually lots of mammals get this deal. For instance, rats, mice, rabbits, guinea pigs can all do this. So when they want to breed, the testicles can hang outside and stay cool. But when they’re not breeding, they can be pulled up inside for safekeeping. Think of the convenience!  Many men would kill for this option. First off, men could control their fertility easily, in a convenient and nonpermanent way. They could pull their testicles in most of the time but when they wanted to breed, they could pull their testicles out for a few days to make fresh sperm. So who does the Designer like better—mice or men?

 

Does the Creator like frogs better than men, our cold-blooded relatives don’t have this problem, and their sperm-making equipment is safely inside them, where a vulnerable organ ought to be. It also turns out that warm body temperature and sperm production really can go together—just not in human. For instance, elephants, seals, whales, dolphins, manatees and rhinoceroses have internal testes. Birds are warm blooded too. In fact, they have higher body temperature than we do. But like frogs and elephants, their testicles are safely tucked up inside them where a vulnerable organ should be. So—does the Designer like birds better than us? Or did God make birds in his image? In other words, is the Designer a turkey?

Filling in the Gaps

 

Male or Female?

Everyone knows that a human being is biologically either male or female. And most people know that the nucleus in each human cell normally contains 23 pairs of chromosomes which house the genetic material needed to produce the essential molecules for life.  There are even some who know that, in addition to providing 22 somatic chromosomes, the female egg always provides an X chromosome and the male sperm provides either an X or Y chromosome to make a female (XX) or a male (XY) human person. But what most people don’t know is how the body decides whether to make male or female parts and that without at least 12 properly working factors it either automatically becomes female by default or an infertile male. In other words, without at least these 12 properly working factors human life would be impossible.    

 

For the first 7 or 8 weeks of life the human embryo is asexual because the gonads haven’t yet declared themselves to be either testes or ovaries. Human embryology tells us that the undifferentiated gonads are destined to become ovaries by default unless acted upon by a molecule called the Testis Determining Factor (TDF). The genetic information needed to produce TDF is usually located on the Sex Determining Region of the Y chromosome (SRY).  This explains why a male must have a Y chromosome. By telling the primordial gonads to become testes, the TDF on the SRY is the 1st properly working factor, the master switch that makes the body go down the male track rather than female. But becoming a male with all the properly working parts for reproduction involves much more.

 

The testes produce testosterone, a steroid hormone derived from cholesterol. Five different chemical reactions using five different enzymes encoded on four different somatic chromosomes are used to convert cholesterol into testosterone (fig.1). If any one of these five enzymes were to be missing or not working properly, there would be no testosterone, no males and no humanity. If you’re keeping count, these represent the 2nd to 6th properly working factors needed for male fertility resulting in continuation of the human race.

 

  

Figure 1: Chemical Reactions/Enzymes to get Testosterone from Cholesterol

         

 

Each human embryo begins life with two different undeveloped genital duct systems, the (male) Wolffian ducts and the (female) Mullerian ducts. The Wolffian ducts have androgen receptors which if adequately stimulated by testosterone will direct them to develop into the male genital duct system consisting of the epididymis, vas deferens and seminal vesicle. If the primordial gonads become ovaries instead and there’s no testosterone around, or the androgen receptors are missing or not working properly, the Wolffian ducts automatically degenerate and disappear. In contrast, unless directed otherwise, the Mullerian ducts automatically develop into the female genital duct system consisting of the uterus, fallopian tubes, and upper vagina. The androgen receptor is the 7th properly working factor that’s needed for a fertile male human to reproduce the species.

 

In addition to testosterone, the testes also produce Anti-Mullerian Hormone (AMH). AMH attaches to the specific AMH receptors on the Mullerian ducts and directs them to degenerate and disappear. This is very important for male fertility because if both duct systems develop they physically interfere with each other which results in male sterility. Without these 8th and 9th properly working factors, male fertility would be impossible and so would human existence.

 

The external genitalia develop from the urogenital sinus, swellings, folds and tubercle. If the gonads do not become testes and produce testosterone these automatically develop into the female external genitalia which consists of the lower vagina, labia, and clitoris. For this tissue to become normal male external genitalia requires much more stimulation of the androgen receptors than what testosterone can provide. The cells in these tissues use an enzyme, called 5-alpha reductase to convert testosterone into dihydrotestosterone (DHT) which is a stronger stimulator of the androgen receptor (see fig. 1 above). When DHT attaches to the androgen receptors in these embryonic tissues it makes them develop into the penis, the scrotum and the prostate gland.

 

 

An XY male with a rare genetic disorder called 5-alpha reductase deficiency will have normally functioning testes and a normal male genital duct system but his external genitalia will be deformed and ambiguous making him incapable of participating in sexual intercourse and rendering him infertile. So, 5-alpha reductase is the 10th properly working factor needed for the male human to be able to perform sexual intercourse.

 

Figure 2: Testicular Descent
T = Testicle

G = Gubernaculum

 

 

 

In the later embryo and early fetal stages the testes are located in the back of the abdominal cavity just below the kidneys. As figure 2 shows, from the 8th to 15th week of gestation, during the transabdominal phase, the gubernaculum, a cord of gelatinous connective tissue mainly consisting of collagen and elastin fibers, pulls the testes forward and downward into the inguinal region (groin). Then from the 25th to 35th week of gestation, during the inguino-scrotal (passage) phase, the gubernaculum pulls the testis through the inguinal canal into the scrotum and usually by the 40th week this passageway closes up.

 

This last phase takes place by the gubernaculum undergoing changes in its structure at the direction of a hormone called insulin-like peptide 3 (INSL3) attaching to a relaxin/insulin-like family peptide receptor 2 (RXFP2). Failure of the testis to descend into the scrotum results in cryptorchidism which results in male infertility. So, INSL3 and RXFP2 are the 11th and 12th properly working factors needed for human male fertility.

 

In summary, the human embryo is destined to become female by default, or an infertile male, unless acted upon by at least 12 properly working factors. If any one were to be absent or defective then human reproduction would be impossible and so would human existence.

 

Male Maturation (Puberty)

Although humans are sexually differentiated as male or female at birth, they are not able to reproduce. Most children begin to show the beginning signs of sexual development by the end of the first decade. Over the next few years they undergo sexual and bodily maturation in a process called puberty. Puberty is a constellation of physiological changes that not only enables male and female humans to reproduce but also prepares them for their natural role in the family.

 

The production of the sex hormones is regulated by the hypothalamus and the pituitary. The hypothalamus secretes Gonadotropin-Releasing Hormone (GnRH) which attaches to specific receptors on certain cells in the pituitary and tells them to send out the gonadotropins, Follicle-Stimulating Hormone (FSH) and Luteinizing Hormone (LH). It is FSH and LH that attach to specific receptors on the testes or the ovaries to produce the sex hormones, testosterone in males and estrogen (and later progesterone) in females.

 

The hypothalamus and pituitary can detect the blood level of the sex hormones sent out by the gonads and in response they modulate the release of their hormones (see fig.3). If the blood level of the sex hormone goes up, the release of GnRH from the hypothalamus, and FSH and LH from the pituitary goes down. If the blood level of the sex hormone goes down, the release of GnRH from the hypothalamus, and FSH and LH from the pituitary goes up. This inverse relationship is called feedback inhibition. The blood level of the sex hormone feeds back on the hypothalamus and the pituitary and inhibits them so that together they keep the sex hormones at the proper level called a set point. Feedback inhibition is common to many hormone systems in the body.   

 

Figure 3: Hypothalamus-Pituitary-Gonad Axis (feedback inhibition)

                          

 

In the first decade of life it appears that the hypothalamus and the pituitary are very sensitive to the feedback inhibition of the sex hormones. This means that prior to puberty, very low levels of testosterone and estrogen are able to prevent the hypothalamus from releasing its GnRH and the pituitary its FSH and LH. This results in very low blood levels of testosterone and estrogen prior to puberty and so no sexual development.  

 

A few years before puberty the adrenals increase their output of androgens (male hormones) which causes a small growth spurt and the development of pubic and axillary hair in both sexes. What actually triggers the beginning of puberty is, as yet, poorly understood. However, what is known to happen is that the hypothalamus and the pituitary start to become progressively less sensitive to the sex hormones. This diminished feedback inhibition of the sex hormones on the hypothalamus and the pituitary results in them slowly increasing their output of GnRH and the gonadotropins, FSH & LH. By the time puberty is in full swing the levels of gonadotropins and the sex hormones have been raised significantly.

 

During male puberty, more FSH and LH attach to specific receptors in the testes and cause an increase in testosterone production while at the same time giving them the ability to produce sperm. Puberty in the male also results in the progressive increase and coarsening of facial, chest, axillary, abdominal, extremity, and pubic hair, with enlargement of the vocal cords and deepening of the voice. Moreover, with the associated increase in the pituitary output of Growth Hormone (GH), the male experiences a significant linear growth spurt and the development of his musculoskeletal system as well. Furthermore, along with the capacity for sperm production, puberty brings on enlargement of the penis, scrotum, and testes. Finally, testosterone not only plays a major role in sexual differentiation, development, and maturation, but also in the desire for sexual relations. In addition, testosterone is important in giving the male the ability to maintain an erection for adequate penetration into the vagina and ejaculation during sexual intercourse. All of these developments prepare the boy to become a man and later a father.

 

In summary, without at least GnRH, FSH, LH, estrogen and testosterone and their specific receptors, the right sensitivities of their target tissues and the negative feedback control mechanism that maintains the right levels and effectiveness of each hormone, the maturation of the male (and female) reproductive tissue would be impossible and so would human existence.

 

Male Fertility

For a man to be able to reproduce he has to send out enough sperm having a normal appearance and motility. Sperm production begins in the seminiferous tubules of the testes and ends in the epididymis where the sperm mature and are stored for ejaculation (see figure above).

 

The process of sperm production begins with germ stem cells dividing by mitosis to form two identical cells with the full complement of 23 pairs of chromosomes (diploid). Half of these cells remain as germ stem cells for lifelong sperm production. The other half go through two further divisions by meiosis to form four sperm cells. Instead of 23 pairs of chromosomes, each sperm contains only one set of 23 chromosomes (haploid), 22 somatic and 1 sex chromosome (X or Y).

 

Sperm production in most mammals is exquisitely sensitive to temperature. To remain fertile the testes must be 2oC – 8oC below the core temperature. For the human male it’s 33oC, about 4oC below the normal core temperature of 37oC. The reasons for this are poorly understood. They seem to be related to there being an optimal temperature range for certain important enzymes used in the formation and maturation of human sperm to work properly as well as higher temperatures causing certain toxic chemicals to build up.

 

In this regard, it is interesting to note that in the last few decades scientists have discovered the presence of heat shock proteins (stress proteins) in all species, from bacteria to humans. Under stresses like heat, cold, UV light, wound healing and tissue remodeling, these chaperone proteins help to stabilize certain cellular proteins, allowing the cell to continue to function properly and prevent programmed death (apoptosis). Among other reasons, the presence and functionality of different stress proteins may explain why certain mammals, like elephants, and other animals like birds, that have a core temperature of 40oC, can produce adequate sperm despite having intra-abdominal (undescended) testes (see below).

 

The human male is able to produce sperm year-round. This means that his testes must always remain at the right temperature. Just because the testes are housed outside the body in the scrotum doesn’t automatically mean that this can be accomplished as physical and environmental factors may conspire against it. That’s why the male scrotum has several mechanisms in place to try to protect it and keep the temperature of the testis, as Goldilocks would say, “just right”. 

 

The testicle is surrounded and protected by a fibrous membrane called the tunica albuginea. Also, to prevent injury and facilitate mobility one testicle usually rides higher than the other and they are able to slide by each other without difficulty. In addition, the skin of the scrotum is very thin and baggy which allows for more loss of heat by radiation. It also has a high density of sweat glands which automatically kick into gear to give off heat by evaporation with elevations in temperature.

 

Moreover, within the scrotum, just below its surface is the dartos muscle and within the spermatic cord is the cremaster muscle. When the temperature drops, both the dartos and cremaster muscles automatically contract which reduces the scrotal surface area and loss of heat, and lifts the testis up closer to the warmer abdominal cavity respectively. When the temperature rises, both muscles relax which increases the scrotal surface area and loss of heat (dartos) and drops the testes further away from the warmer abdominal cavity (cremaster).

 

Furthermore, the arteries and veins which take blood to and from the testes in the scrotum (pampiniform plexus) are set up to pass close by each other to act as a counter-current heat exchange which helps to keep the testes cooler. 

 

In summary, without the protective tissue and temperature control mechanisms present within the male reproductive system, adequate sperm production would be impossible and so would human existence.

 

Three Questions

So, besides human testicles needing to be located in the scrotum to keep them cooler than the core body temperature to allow for proper sperm production, there’s a lot more to male fertility and human reproduction than what’s mentioned above by this critic. In other words, just because descended testicles are potentially at risk for injury and could possibly be considered “badly designed” doesn’t automatically mean that the human male (and female) reproductive systems came about by the unguided and purposeless forces of natural selection acting on random variation (genetic mutation).

 

To jump to this conclusion using this false dichotomy without pointing out what else is involved  and needs to be explained is frankly not only disingenuous but unscientific. In fact, it’s a non sequitur which in and of itself in no way “explains the human body” as the critic claims. Here are three questions to which this critic doesn’t even allude, never mind try to answer, which should give the reader pause.

           

In what order and from where did the new genetic and other information come that specifies the size, shape, assembly, material specifications and placement of all of the parts of the male and female reproductive systems and what is the real probability that these two systems could have come about simultaneously by undirected forces while remaining functional in intermediate organisms each step along the way? 

 

In what order and from where did the new genetic and other information come that specifies and controls the maturation process (puberty) of the reproductive organs and the secondary sexual characteristics for both male and female humans and what is the real probability that these two systems could have come about simultaneously by undirected forces while remaining functional in intermediate organisms each step along the way? 

 

In what order and from where did the new genetic and other information come that specifies the different parts needed for male testicular protection and temperature control and what is the real probability that such a system could have come about by undirected forces while remaining functional in intermediate organisms each step along the way? 

 

So, are you willing to accept the undirected forces of natural selection acting on random variation as the definitive answer to the above questions?  The “smoke and mirrors” of neo-Darwinism which doesn’t even try to account for the simultaneous development of the male and female reproductive systems, their later maturation and the mechanisms in place to protect and control the temperature of the testes to allow for adequate sperm production?

 

It’s important to realize that natural selection acting on random variation (genetic mutation) means exactly what it says. Over time, life required a gazillion bits of new genetic information (not natural selection) to bring about new structures with new functions. All natural selection did was preserve the life that was up and running properly and able to survive due to these gazillion undirected genetic mutations. But keep in mind, natural selection cuts both ways.

 

Based on what we know about how life actually works neo-Darwinism may explain the survival of the fittest but not the arrival of the fittest. That’s because when it comes to survival, logic tells us that the same power that natural selection had to preserve human life when the male and female reproductive systems simultaneously came into existence, later matured and testicular protection and thermoregulation worked properly, would have also prevented it from surviving if any one of the parts of these systems were missing, misplaced or defective.

 

The known engineering principles needed to bring about the functional capacities of all of these parts that resulted in human existence means that, in principle, not only does Darwin’s theory of gradualism fail, but so do all the other neo-Darwinian attempts to replace it. What do you think?

 

Comments

On reviewing Dr. Hafer’s concerns about descended testicles, it becomes clear that for her (and many of her colleagues) critiquing ID must be very easy. First, find one part of an organ system from which humans may suffer, but which does not impact personal or race survival, or in her case, just make one up. Then, without detailing the underlying material, cellular and molecular bases to support your criticism and proposed alternatives, claim that the organ system is “badly designed”. Finally, tell a “just so” story without any specifics about where the information came from for the formation and assembly of the organ system’s parts and the control mechanisms involved in development and achieving adequate function, claiming Evolution—the undirected forces of natural selection acting on random variation—as the only explanation for causation.

 

Dr. Hafer’s critique, which is mainly based on observation without much detail is set against an ideologically and (in her own words) politically conceived straw man—a caricature of what ID truly represents. She tells us that “The standard for systems that evolve is “good enough to not cause death before reproduction, (whereas) the standard for ID is designed by an infallible Creator. Human bodies are just too badly put together to stand up to even reasonable design specifications, much less infallible ones.”

 

She doesn’t seem to understand that, at a bare minimum, she would need to answer all three of the above questions to meet “the standard for systems that evolve” because that is what is really needed for them to be “good enough to not cause death before reproduction.”

 

In contrast, to paraphrase what one of my engineering acquaintances has said “For goodness sake, if it works it must have some sort of reasonable design specifications. After all there are an infinite number of ways that it can fail whereas there are usually only a few ways that it can work.”

 

ID holds that certain features of the universe and of living things are best explained by an intelligent (not necessarily an infallible) cause and not an undirected process such as natural selection acting on random variation (genetic mutation) alone. By taking into account the information needed to form and assemble the parts for a given organ system along with what it takes for development and to maintain control to allow adequate function, ID actually asks the right questions and in looking for the answers must follow the evidence wherever it leads. And when you come to understand what it really takes for life to survive you realize that Evolution doesn’t even come close to doing this—case in point—Dr. Hafer’s criticism.  

 

At the end of Dr. Hafer’s introductory chapter she tells the reader that “There is real science here.” Then, on the next page, in her opening paragraph, as noted in her first critique above, she says that the testicles are outside the body in “a sack of skin called the scrotum because the body’s temperature is too hot for sperm production”, that “having normal body temperature be too hot for sperm production is “bad design” and that’s why “the testicles have to hang outside the body in the scrotum”.

 

Yes, technically, there is real science in this statement, but unfortunately, not very much. It consists of simple gross anatomy with a light touch of (patho)physiology. Without explaining the cellular and molecular basis for why when the temperature of the testes is as high as the body’s core temperature it negatively impacts human sperm production, Dr. Hafer’s statement of this representing “bad design” is but mere opinion. And a poorly informed opinion at that.

 

At present there are many different theories as to the exact cellular and molecular mechanism(s) by which elevated testicular temperature diminishes human sperm production. Moreover, it’s not just humans that are affected by this phenomenon but almost all mammals. Furthermore, despite apparently all of these mammals having been “badly designed” they are all currently thriving. So one has to look askance at the critic and wonder “What’s your point?” 

 

But, more importantly, if we take the not unreasonable position that maybe in humans, and almost all other mammals, adequate sperm production requires a temperature lower than the body’s core temperature (as noted above by 2oC-8oC) then having placed the testicles in the scrotal sacks outside the body to accommodate this physiological requirement should be seen, by those with an open mind, to represent, not “bad design” but evidence of foresight and intelligent and purposeful design. 

 

In his book “Foresight: How the Chemistry of Life Reveals Planning and Purpose” Dr. Marcos Eberlin, a Senior Fellow with the Center for Science and Culture at the Discovery Institute states “No foresight, no life: The need to anticipate—to look into the future, predict potentially fatal problems with the plan, and solve them ahead of time—is observable all around us. It is clear that life is full of solutions whose need had to be predicted to avoid various dead-ends. Put another way, many biological functions and systems required planning to work. These features speak strongly against modern evolutionary theory in all its forms, which remains wedded to blind process.”

 

Most reasonable people would see that since higher temperature negatively impacts sperm production, then having placed the testes in a cooler environment, which being in the scrotal sacks outside the body affords, could be included in what Dr. Eberlin calls “solutions to potentially fatal problems.” As noted above, undescended testes (cryptorchidism) results in infertility. So, universal cryptorchidism would result in human extinction. Not having descended testicles is clearly an example of Dr. Eberlin’s thesis, “No foresight, no life.”

 

Dr. Hafer then moves onto make believe and hyperbole by first stating (correctly) that the descended testicle within the scrotum is potentially vulnerable to injury.  But without accounting for this necessity and the protective mechanisms involved, concludes that “Putting a valuable and vulnerable organ in such a vulnerable location is bad design.” Then without any supportive evidence (she could have at least surveyed the several male endorsers of her book), she makes the outrageous statement that “Men are put to all sorts of inconvenience and risk severe pain and worse because of this unfortunate positioning.”

 

One can only assume that this has been accepted by her male supporters because of her obvious lack of personal experience in this regard and the desire to promote her book. If any man were to have written these words he would be laughed out of academia and excoriated by his own sex.   

 

Although the testicles have several abovementioned protective mechanisms in place to prevent injury this does not preclude the possibility that their owners may participate in activities like contact sports and violence that puts them in harm’s way. The incidence of injury in these situations is considered to be less than one-percent and rarely if ever, leads to permanent infertility—certainly not enough to put the survival of the human race at risk. As for the “all sorts of inconvenience and risk of severe pain and worse”, based on my personal and medical experience I have no idea what she’s talking about. And so I conclude, neither does she.

 

In the second critique Dr. Hafer says “But what if warm body temperature and sperm production just can’t go together?  Some warm-blooded animals have testicles that hang outside the body when this is needed, but can be pulled up inside the body out of harm’s way when this is the safer option. Actually lots of mammals get this deal. For instance, rats, mice, rabbits, guinea pigs can all do this. So when they want to breed, the testicles can hang outside and stay cool. But when they’re not breeding, they can be pulled up inside for safekeeping.”

 

What are we to make of this statement? Is she stepping back from her earlier assertion that “having normal body temperature be too hot for sperm production is bad design” by realizing (without giving any cellular or molecular details of why) that, like a machine gives off heat with work, so too, this situation for the testicles may just be due to the laws of nature?  

 

And since this situation would impact all warm-blooded animals, not just humans, what are we to make of there being a tiny subset of small ones that can pull their testicles “up inside their body out of harm’s way when this is the safer option” or “when they want to breed”? This circumstance doesn’t seem to point to an undirected random process but to another case of foresight and purposeful intelligent design.

 

And of course, all of this should therefore engender more questions. Like what exactly is the mechanism involved here and where did it come from? It appears that it’s the same reflexive contraction of the cremaster muscle in the spermatic cord that allows human males to retract their testicles up towards the groin but not inside the abdomen like these small animals can when stimulated to do so under stress or cold conditions. This happens not voluntarily but as an automatic reflex in response to appropriate stimuli. It’s not based on a decision made by these small animals to breed and to even intimate this (even in jest) is sheer nonsense.

 

Based on this assumption and then by merely extrapolating, without taking into account human experience and the differences in body size and anatomy, Dr. Hafer then presents this contraction ability as a possible solution to her imaginary “bad designed (human) male testicles” problem. She opines “Think of the convenience!  Many men would kill for this option. First off, men could control their fertility easily, in a convenient and nonpermanent way. They could pull their testicles in most of the time but when they wanted to breed, they could pull their testicles out for a few days to make fresh sperm.”

 

Notwithstanding her apparent limited knowledge of what it really means to be a man with dignity, integrity, self-control and a proper regard for chastity and sexual relations, she says this without mentioning what anatomical and neuromuscular changes and new control mechanisms would be needed to accomplish this. I for one would not relish having my testicles taking up space in my groin, lower abdomen or pelvis. I think most men would agree. Once, again, rather than just making assumptions she could have at least asked the men who endorsed her book to state their agreement to her thesis on the testicle but they know how the rest of us would react.

 

Then she tells us that “You’d think that the Designer would try to give us humans, who were made in his image, the best deal that he could manage, wouldn’t you? But he didn’t. So who does the Designer like better—mice or men?”

 

It seems to never occur to Dr. Hafer that it`s precisely because we were “created in His image” that we men weren’t given what she calls “the best deal that he could manage”. That’s because, as opposed to her point of view most men would rather be controlled by and think with their brains, not their testicles. History has shown that the latter situation ends up destroying the family and ultimately civilization. So, maybe it’s a good thing that, as she implies, the Designer likes mice more than men. We’re just blessed to know for certain that because we’ve been created in His image the Designer loves men more than mice. 

 

In her third critique Dr. Hafer tells us frogs, and other cold-blooded animals, some mammals like elephants, and other warm-blood animals like birds, actually have internal testes which provide adequate sperm production. In other words, she’s been holding out on us all this time. There really are warm-blooded animals that can have adequate sperm production while their testes are at body temperature. And at least for them Dr. Hafer can stop fretting and put her mind at ease because “their sperm-making equipment is safely inside them, where a vulnerable organ ought to be.” She says this with full knowledge that her narrow perspective and concern has not impacted mammalian survival one bit and so stands in direct opposition to her criticism of “bad design”.

 

But, given the information above, the inquisitive reader is more likely to wonder not only how this can be but also how it came about? What is the mechanism within birds, which has a core temperature of 40oC-41oC, far above humans, that allows them to be able to produce adequate sperm and where did if come from? What about elephants? Whatever it is that helps them to have adequate sperm production at their core temperature (36oC) would have to have come about before, or at least at the same time, as they lost the ability for their testicles to descend. And how did that happen?  

 

The testes of birds have a lot of heat shock protein A2 (HSPA2). This allows their spermatic cells and important proteins within them to continue to function at higher temperatures. But what about mammals like the elephants? The same may apply to them as well. And it turns out that in the elephant fetus there is no evidence for the gubernaculum as the INSL3 and RXFP2 genes needed for its formation and proper function are either absent or defective (see above).

 

Interesting!  None of this is mentioned in Dr. Hafer’s book. But this speaks to mechanism, to the how and why, which is what ID is all about. Follow the evidence wherever it leads. Don’t just ignore it and hope nobody notices so you can tell a “just so” story while leaving out almost all of the most important details.

 

As Dr. Hafer’s critique demonstrates, this is the essence of neo-Darwinism. Base your theory just on how life looks, not on how it actually works. Engineers (and physicians) don’t have the luxury of practicing their professions based mostly on theory. At the end of the day, if they can’t make it work (or cure someone), then it doesn’t matter what their proposal says—it’s wrong!

 

Laufmann’s Triple Filter

Not understanding the objectives of the designer

 

Based on what she’s written, it would seem that without realizing it and understanding what it really means, Dr. Hafer frequently stumbles on the true objective of the designer, i.e. to create humanity in His image. This, by physical and chemical necessity requires human beings to be warm-blooded. And it’s being warm-blooded with a core temperature of 37oC that puts human sperm production at risk because it does best at 33oC.

 

Warm-blooded means; using enough energy to maintain control of the body’s core temperature (usually above the ambient) so the different enzymes used in thousands of vital chemical reactions within the body’s trillions of cells remain functional and the membrane surrounding them remains intact. As noted above, this means that for most warm-blooded male mammals, the temperature inside the body is usually too high for adequate sperm production. All of this necessitates their testicles having to be located just outside the body in the cooler scrotal sacks.  

 

There are advantages and disadvantages to being either cold-blooded or warm-blooded. In particular, since the efficiency of chemical reactions in the cell is dependent on the core temperature, being warm-blooded allows for more activity within colder environments. Warm-blooded animals are therefore, in general, able to forage for food faster and defend themselves better within a wider temperature range than cold-blooded ones. In addition, warm-blooded animals are able to support highly-complex energy-dependent organs like the mammalian brain.  

 

Being created in the image of the Designer affords us many intellectual capacities that require us to have the most complex brains in the world. This consists of a large cerebral cortex and many more connecting fibers between the different regions of the brain. All of this requires us to be warm-blooded in order to maintain this highly complex organ.

 

But there’s even more to consider. Given Dr. Hafer’s position about the Designer (or lack of one) her apparent view of male sexuality not surprisingly seems to lack a moral sense of self-control and responsibility. But having been created in the image of the Designer also affords us the ability, if we are inclined to do so, to image the Designer, by fulfilling our vocation to love as He loves. This is accomplished in the sacrament of marriage where the husband and wife image the love of God through their intimate exclusive and life-long relationship and bodily communion that is open to life.

 

Maybe that’s why the Designer didn’t give us retractable testicles so we could take control of our fertility as we please—what Dr. Hafer called “the best deal”.  Maybe, rather than listening to Dr. Hafer, the Designer had something else in mind—something Dr. Hafer never considered—living life totally for God and neighbor. That’s definitely not a “bad design”.  

 

Not accounting for the functional requirements, constraints and trade-offs

It is evident from the above that the functional requirement of the testicles to produce enough healthy sperm is constrained by the ambient temperature which must be about 4oC below the body’s core temperature (37oC). This is why one of the trade-offs for male reproductive health is, as Dr. Hafer puts it, “to place such a valuable organ (like the testicle) in a vulnerable position” outside the body in the cooler scrotum. However, this critique seems overblown as the human race has flourished for about 300,000 years despite her narrow and overwrought concern.

 

But, more importantly, Dr. Hafer (and most of her colleagues) misses out on the most obvious potential complication from the way the male reproductive system is set up. It’s something that definitely would have impacted the survival capacity of our ancient male ancestors and so could be seen as another trade-off due to the constraints that nature applies to sperm production. What I’m talking about are inguinal hernias, which are much more prevalent in men than in women.

 

Taber’s Medical Dictionary defines a hernia as “the protrusion of anatomical structure through the wall that normally contains it.” As noted above, during gestational development the testicle migrates from up near the kidney and moves down into the scrotal sack by passing through the abdominal wall and into the inguinal canal (groin). After this takes place, the opening from the abdomen into the inguinal canal closes up. But if this doesn’t happen correctly this can allow tissue to re-enter it in what is called a congenital inguinal hernia. And even if it does close properly it still remains as a potential space for tissue to re-enter it in later life in what is called an acquired inguinal hernia. Weakened tissues and heavy lifting often contribute to this in 25% of males throughout their lifetime (fig. 4).  

 

Figure 4: A piece of small bowel has migrated down to the testes in an inguinal hernia. The internal (deep) inguinal ring is the opening from the abdomen to the inguinal canal. The external (superficial) inguinal ring is the exit from the inguinal canal to the scrotum.

 

 

The necessity for the testicle and spermatic cord to move from inside the abdomen through a passageway that remains a potential weak spot, mainly for males at birth and later in life, clearly would have put our ancient ancestors at risk for inguinal hernias. Depending on its size and the amount and type of tissue within it (fatty tissue and/or a loop of small intestine) some men find it to be just a nuisance whereas others find it debilitating.

 

When the tissue within the inguinal hernia can’t be pushed back into the abdomen (reduced) then it is said to be incarcerated and this puts it at risk of strangulation. Strangulation of an inguinal hernia is a life-threatening condition where muscle tightening and swelling within the restricted space results in reduced blood flow which causes tissue death and brings on other complications, all of which can soon lead to total body death.

 

As noted above, the incidence for hernia surgery in men in their lifetime is 25%. Moreover 20 million surgical repairs of inguinal hernias are done annually throughout the world. Furthermore, about one-quarter of those are done emergently, usually due to incarceration and possible life-threatening strangulation, which in one study had a mortality of 6%. This goes to show you that the risk of inguinal hernia from the need for males to have descended testicles for adequate sperm production would have impacted the survivability of our ancient male ancestors much more than any of what Dr. Hafer describes as her “bad design” concerns. Nevertheless, from an engineering perspective, since humanity has continued to survive over the last 300,000 years, the trade-off has been worth it because the system continues to work.          

 

Failure to acknowledge user abuse and degradation over time

As already noted above, men are well aware of the vulnerability of their valuable reproductive organs but are quite capable of protecting them. Just because they engage in activities that put them at risk of injury does not necessarily mean that they’ve been “badly designed”. More importantly, because of the potential for developmental defects in the groin due to the need for the testicles to descend, males are particularly at risk for congenital and acquired inguinal hernias and their associated complications. Moreover, with aging the muscles of the lower abdomen and groin can weaken and with improper lifting of very heavy objects can bring on, or at least, aggravate, inguinal hernias which can result in other problems as noted above. 

 

Finally, male fertility is negatively impacted by various activities, conditions and toxins. This includes overheating of the testicles from frequent saunas or wearing tightly fitting underwear, anxiety, depression, smoking, alcohol, marijuana, viral and sexually transmitted infections, vitamin and mineral deficiencies, toxins, radiation, surgery, medications, diabetes, thyroid disease, aging and obesity. 

 

Yet, despite all of these circumstances having the potential to negatively impact adequate sperm production and with it human survival, it would appear that even user abuse and degradation has been taken into account by the Designer. 

 

Conclusion

The fact that human male testicles descend into the scrotum during gestation to keep their temperature 4oC below the body’s core temperature so that years later (after puberty) they can have adequate sperm production, even though this puts them at some risk for external injury, points to foresight. What Dr. Marcos Eberlin defines as “The need to anticipate—to look into the future, predict potentially fatal problems with the plan, and solve them ahead of time.” To claim, as Dr. Hafer and many of her colleagues do, that this represents “bad design” in the human body is not only misguided but, based on engineering principles, totally absurd. What do you think?

 

 


Also see Dr. Glicksman's Series on

"Beyond Irreducible Complexity"

"Exercise Your Wonder"

"On Being Alive"


Howard Glicksman M. D. graduated from the University of Toronto in 1978. He practiced primary care medicine for almost 25 yrs in Oakville, Ontario and Spring Hill, Florida. He now practices palliative medicine for a Hospice organization in his community. He has a special interest in how the ethos of our culture has been influenced by modern science’s understanding and promotion of what it means to be a human being.

Comments and questions are welcome.

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