Darwinism Vs.The real world.XXXVII

Puberty, Maturation, and Fertility: The Role of Information in Human Sexuality
Howard Glicksman 

Editor's note: Physicians have a special place among the thinkers who have elaborated the argument for intelligent design. Perhaps that's because, more than evolutionary biologists, they are familiar with the challenges of maintaining a functioning complex system, the human body. With that in mind, Evolution News is delighted to offer this series, "The Designed Body." For the complete series,  see here. Dr. Glicksman practices palliative medicine for a hospice organization.

The word sex comes from the Latin secare which means to separate or divide. Most one-celled organisms form offspring through asexual reproduction. It is asexual because there is no separation of genetic material. Therefore divided chromosomes do not need to be brought together and the new life produced is genetically identical to the original.

In contrast, most multi-cellular organisms form offspring in a much more complicated way called sexual reproduction. In humans, each of the chromosomes making up the 23 pairs containing the genetic material for life is separated from its partner and placed into gametes called male sperm and female eggs. Human reproduction involves sexual intercourse in which the male deposits sperm in the vagina of the female so they can move into the uterus and one of them can join its separated 23 chromosomes to the ones within the female egg in a process called fertilization. The fertilization of the female egg by the male sperm results in a one-celled zygote which then contains the full complement of genetic material and is distinct from its parents.

As difficult as it may be for evolutionary biologists to explain the blind and unguided development of the different organ systems and the body's ability to control them, because of the mechanism humans must use for reproduction they must also explain the simultaneous development of both males and females since neither is of any use to propagate the species without the other.

The three things needed for a human to reproduce are: (1) either be male or female and have all of the right sexual parts, (2) be able to produce enough sperm or release an egg into a fallopian tube, and (3) be able to participate in sexual intercourse so sperm is released into the vagina or have a clear path for sperm to swim toward the fallopian tubes.

In my last article, I showed that for the first few weeks of life the human embryo is asexual. That is because the primordial gonads have not declared themselves to be testes or ovaries yet. Notwithstanding where the embryonic structures that develop into mature sexual organs came from, the human embryo is destined to become female by default unless acted upon by specific chemicals. These include the Testis Determining Factor (TDF) (usually found on the Y chromosome), the enzymes needed to convert cholesterol into testosterone and testosterone into dihydrotestosterone, the androgen receptor on the Wolffian ducts and the tissue that will become male external genitalia, Anti-Mullerian Hormone (AMH) and the AMH receptor on the Mullerian ducts.

If all of these chemicals are present and working properly the human embryo will usually develop into a normal male. But if the TDF is absent it will usually develop into a normal female. However, if the TDF is present, directing the primordial gonads to become testosterone-producing testes, but the androgen receptor is absent or defective (Complete Androgen Insensitivity Syndrome (CAIS)), the result in an XY female. XY females occur in about one in twenty thousand "male" births and have testes instead of ovaries, no genital duct system and female external genitalia. So for the first decade of life they look like normal little girls. However, experience teaches that although humans are sexually differentiated as male or female at birth, they are not able to reproduce. Most children begin to show signs of their sexual development to come by the end of the first decade. Over the following years they will undergo sexual and bodily development in a process called puberty. Puberty is a constellation of physiological changes that, except in, for example, XY females, not only enables human beings to reproduce but also prepares them for their natural role in the family. Let's consider how this happens.

The hypothalamus and pituitary work to control many different vital hormones in the body. For example, the hypothalamus secretes Growth Hormone-Releasing Hormone, which stimulates the pituitary to release Growth Hormone (GH). As its name implies, GH is very important in the overall growth and development of the body. The hypothalamus also sends out Thyrotropin-Releasing Hormone (TRH), which tells the pituitary to send out Thyroid Stimulating Hormone (TSH). It is TSH that controls the production of thyroid hormone from the thyroid gland, which mainly affects the body's metabolic rate. Furthermore, the hypothalamus sends out Corticotropin-Releasing Hormone, which tells the pituitary to send out Adrenocorticotropin Hormone (ACTH). ACTH stimulates the adrenal glands to produce cortisol, another hormone that is important in the body's metabolism, in addition to androgenic hormones.

The hypothalamus and pituitary together control the production of a hormone such as thyroid hormone, or others, through a process called feedback inhibition. For example, the hypothalamus and the pituitary have specific receptors that allow them to sense the blood level of thyroid hormone. If it rises above what is needed the hypothalamus reduces its output of TRH and the pituitary lowers its output of TSH. The feedback of the thyroid hormone level in the blood serves to inhibit the release of TRH and TSH to maintain control of the blood level of thyroid hormone.

The production of the sex hormones is regulated in the same way 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 and estrogen, respectively.

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 the blood levels of testosterone and estrogen being very low prior to puberty.

A few years before puberty the adrenals increase their output of androgenic hormones which causes a small growth spurt and the development of pubic and axillary hair. What actually triggers the beginning of puberty is, as yet, poorly understood. However, what is known to happen is that the hypothalamus and pituitary start to become progressively less sensitive to the sex hormones. The gradually diminishing feedback inhibition of the sex hormones on the hypothalamus and pituitary results in their slowly increasing their output of GnRH and the gonadotropins, FSH and LH, respectively. By the time puberty is in full swing, the levels of gonadotropins and the sex hormones have risen 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 these developments prepare the boy to become a man and later a father.

During puberty in the female, more FSH and LH attach to specific receptors in the ovaries and cause an increase in estrogen production while at the same time giving them the ability to develop an egg. Puberty in the female results in an increase in mainly pubic and axillary hair that is not as coarse as in the male. Moreover, breast development takes place so that the potential mother will be able to provide breast milk for her infant. In addition, an increase in Growth Hormone (GH) results in a significant linear growth spurt and development of her musculoskeletal system as well. Puberty also brings on enlargement of the external genitalia and increased mucous production within the vagina and uterus. Finally, along with the capacity for egg development, the increase in FSH, LH, and estrogen allows for ovulation, where the egg is released and can enter the fallopian tube.

Inside the fallopian tube the egg can meet and join with the sperm, which has been deposited into the vagina by the male during sexual intercourse, to form new human life. After ovulation, the ovaries mainly secrete the pregnancy hormone called progesterone. The estrogen before ovulation, and the progesterone after ovulation, attach to specific receptors in the lining of the uterus to make it thicken up and produce more mucous helping it to prepare for pregnancy. If a pregnancy does not take place, the gonadotropins (FSH, LH) and the female sex hormone levels (estrogen, progesterone) drop precipitously to cause the lining of the uterus to shed in the process called menstruation. The first menstrual period generally marks the beginning of female fertility and usually takes place on a monthly basis for the next thirty or forty years.

All these developments prepare the girl to become a woman and later a mother. However, during puberty an XY female will develop normal breasts and in every way look like a normally maturing woman, except when she fails to menstruate. Investigation will then uncover her as yet unknown (even to her) secret.

Remember that an XY female has Complete Androgen Insensitivity Syndrome (CAIS). In this case, the testes form testosterone, but since the androgen receptors are absent or not working, the Wolffian ducts degenerate and the external genitalia become female. However, in addition to testosterone the testes also produce Anti-Mullerian Hormone (AMH), which attaches to specific AMH receptors on the Mullerian ducts and makes them degenerate as well. So the XY female has neither a male nor female genital duct system and her vagina ends in a blind pouch. If an XY female has testes instead of ovaries how can she develop breasts during puberty?

The answer lies in the fact that breast development does not, per se, depend only on estrogen but rather the ratio between estrogen and testosterone. Since during puberty the normal XY male produces lots of testosterone and relatively small amounts of estrogen, his breast tissue does not develop. During puberty the normal XX female produces lots of estrogen and only relatively small amounts of testosterone, so her breast tissue does develop. Although an XY female has testes that produce lots of testosterone, because there are no androgen receptors for it to take effect, this allows the small amount of estrogen she produces to dominate and cause breast development. In fact, without any androgenic effects in their bodies, XY females are some of the most femininely attractive women in the world.

As noted above, the human embryo is destined to become female by default unless several other chemicals swing into action to make it become a normal male. But that's only part of the story because for the first several years of life, humans, whether male or female, cannot reproduce. Puberty first involves an as yet unexplained reduction in feedback inhibition so there can be a significant increase in the release of GnRH from the hypothalamus and FSH and LH from the pituitary. This also requires the presence of specific receptors on their target tissues. It leads to the testes being able to produce sperm and more testosterone and the ovaries being able to release an egg and more estrogen (and progesterone) so males and females can reproduce.

It is information, wrapped in chemical signals, that makes the embryo become male or female and initiates puberty, thus making human reproduction possible. As Stephen Meyer observes in the Discovery Institute film The Information Enigma, the major discovery of the last half of the 20th century was that it is information that drives biology. In generating information, all human experience points to a mind rather than a random and unguided material process.


But clinical experience teaches that just having all of the parts present for reproduction doesn't automatically guarantee fertility and the natural ability to bring about new human life. That's what we'll begin to explore next time.

On the collapse Darwinism's prima facie case.

Alleged Instances of Observed Speciation -- Evolution's Smoking Gun Is Still Missing
Editor's note: William Dembski and Jonathan Wells, leading figures in the intelligent design movement, are co-authors of The Design of Life: Discovering Signs of Intelligence in Biological Systems. Originally published by the Foundation for Thought and Ethics, this path-breaking work explores some of the most important arguments for intelligent design in biology. To celebrate the launch of Foundation for Thought & Ethics Books as an imprint of Discovery Institute Press, we will be publishing excerpts from the book here at Evolution News. Through July 8, we will also be making the book available for only $10 -- that's more than a 70 percent discount, and it includes both the full-color hardcover and an accompanying CD with additional materials. If you haven't read this classic book, now is your chance! Order now, because this special discount won't last long.

Despite the absence of evidence for the ability of reproductive isolation to harness the mechanisms of genetic change and thereby to produce new species, some Darwinists still claim that there are many instances of observed speciation.1 But most of these alleged instances are in fact analyses of existing species that are used to defend one or another theory of how they might have originated -- such as the theories of allopatric and sympatric speciation, or the bottleneck and founder effects. Analyzing existing species to support one or another theory of speciation, however, is not the same as observing speciation in action.

There actually are some confirmed cases of observed speciation, but these are due to an increase in the number of chromosomes, or "polyploidy." Such cases, however, are limited to flowering plants and result from hybridizing two species to form a new one.2 Furthermore, according to evolutionary biologist Douglas Futuyma, speciation that results from polyploidy (also called "secondary speciation") "does not confer major new morphological characteristics . . . [and] does not cause the evolution of new genera" or higher taxonomic levels.3 Darwinian evolution, by contrast, depends on taking a single existing species and splitting off new species from it (called "primary speciation"), which then in turn diverge and split, diverge and split, over and over again. Only primary speciation, and not secondary speciation, could produce the branching-tree pattern required by Darwinian evolution.

Of the many instances of observed speciation alleged by Darwinists, only five come close to claiming observed primary speciation. First, in 1962, from a single lab population of Drosophila (fruit flies), J.M. Thoday and J.B. Gibson bred only those flies with the highest and lowest number of bristles (the insect equivalent of hair). After 12 generations, the experiment produced two populations that not only differed in bristle number but also showed "strong though partial isolation." Yet Thoday and Gibson not did claim to have produced a new species. Furthermore, other laboratories were unable to reproduce their results.4

Second, in 1958 Theodosius Dobzhansky and Olga Pavlovsky started a laboratory population of fruit flies using a single female of a strain from Colombia. Crosses between that fly and several other strains produced fertile hybrids in the laboratory. In 1963, however, similar crosses yielded sterile hybrids. In 1966, Dobzhansky and Pavlovsky concluded that the strain they had introduced in 1958 had become "a new race or incipient species . . . in the laboratory at some time between 1958 and 1963."5 But Coyne and Orr, writing in 2004, suspect their results were "due to contamination of cultures by other subspecies."6 In any case, Dobzhansky and Pavlovsky reported only a "new race or incipient species," not a new species.

Third, in 1964 biologists collected some marine worms in Los Angeles Harbor and used them to start a lab colony. When they went back to the same location 12 years later, the original population had disappeared, so they collected worms from two other locations several miles away, and these were used to start two new lab colonies. In 1989, researchers found that the two new colonies could interbreed with each other but not with the Los Angeles Harbor colony that had been started 25 years earlier. In 1992, James Weinberg and his colleagues called this an observed instance of "rapid speciation," based on the assumption that the original colony had "speciated in the laboratory, rather than before 1964."7 A few years later, however, tests performed by Weinberg and two others showed that the original population was "already a species different from" the two new colonies "at the time when it was originally sampled in 1964."8 No speciation had occurred.

Fourth, in 1969 E. Paterniani reported an experiment on maize in which breeding was permitted only between individuals possessing two extremes of a particular trait. Paterniani noted the development of "an almost complete reproductive isolation between two maize populations" but did not claim that a new species had been produced.9

Fifth and last, in the 1980s William R. Rice and George W. Salt subjected a population of fruit flies to eight different environments. They then took the flies that preferred the two most extreme environments and allowed only them to breed. Within thirty generations the flies had sorted themselves into two populations that did not interbreed. Even so, Rice and Salt did not claim to have produced two new species. More modestly, they believed only that "incipient speciation" had occurred.10

So, of the five alleged instances of observed primary speciation, only one (Weinberg's) claimed to have observed actual speciation -- and it was later retracted. The other four (one of which could not be reproduced by other scientists and one of which was not controlled for contamination) claimed only some degree of reproductive isolation or "incipient speciation."

What is "incipient speciation"? Darwin wrote: "According to my view, varieties are species in the process of formation, or are, as I have called them, incipient species."11 But how can we possibly know whether two varieties (or races) are in the process of becoming separate species? St. Bernards and Chihuahuas are two varieties of dog that cannot interbreed naturally, but they are members of the same species. Maybe they are on their way to becoming separate species, or maybe not. The two varieties of Rhagoletis pomonella described in the previous section do not interbreed in the wild, but they look exactly alike and are still capable of mating in the laboratory. Like different breeds of dogs, they are still members of the same species. Calling them "incipient species" amounts to no more than a prediction that they will eventually become separate species. But maybe they won't. Short of waiting to see whether the prediction comes true, we can't really know. And given our limited lifespans, we don't have time to wait (at least not by conventional evolutionary timescales).

Darwinists therefore discount the lack of observed instances of primary speciation by saying that it takes too long to observe them. But if it takes too long for scientific investigators to observe primary speciation, then there will never be anything more than indirect evidence for the first and most important step in Darwinian evolution. Darwinists claim that all species have descended from a common ancestor through variation and selection. But until they can point to a single observed instance of primary speciation, their claim must remain an unverified assumption, not an observed scientific fact. University of Bristol bacteriologist Alan H. Linton made precisely this point when in 2001 he assessed the direct evidence of speciation: 

None exists in the literature claiming that one species has been shown to evolve into another. Bacteria, the simplest form of independent life, are ideal for this kind of study, with generation times of twenty to thirty minutes, and populations achieved after eighteen hours. But throughout 150 years of the science of bacteriology, there is no evidence that one species of bacteria has changed into another. . . . Since there is no evidence for species changes between the simplest forms of unicellular life, it is not surprising that there is no evidence for evolution from prokaryotic [e.g., bacterial] to eukaryotic [e.g., plant and animal] cells, let alone throughout the whole array of higher multicellular organisms.12

So except for secondary speciation, which is not what Darwin's theory needs, there are no observed instances of the origin of species. As evolutionary biologists Lynn Margulis and Dorion Sagan wrote in 2002: "Speciation, whether in the remote Galápagos, in the laboratory cages of the drosophilosophers, or in the crowded sediments of the paleontologists, still has never been directly traced."13 Evolution's smoking gun is still missing.

References:

(1) See Catherine A. Callaghan, "Instances of Observed Speciation," The American Biology Teacher 49 (1987): 34–36; Joseph Boxhorn, "Observed Instances of Speciation," The Talk.Origins Archive, September 1, 1995, available online (last accessed January 9, 2007); Chris Stassen, James Meritt, Annelise Lilje, and L. Drew Davis, "Some More Observed Speciation Events," The Talk.Origins Archive, 1997, available online (last accessed January 9, 2007).

(2) See Justin Ramsey and Douglas W. Schemske, "Neopolyploidy in Flowering Plants," Annual Review of Ecology and Systematics 33 (2002): 589–639; D. M. Rosenthal, L. H. Rieseberg, and L. A. Donovan, "Re-creating Ancient Hybrid Species' Complex Phenotypes from Early-Generation Synthetic Hybrids: Three Examples Using Wild Sunflowers," The American Naturalist 166(1) (2005): 26–41.

(3) Douglas J. Futuyma, Evolution (Sunderland, Mass.: Sinauer Associates, 2005), 398.

(4) J.M. Thoday and J. B. Gibson, "Isolation by Disruptive Selection," Nature 193 (1962): 1164–1166. J. M. Thoday and J. B. Gibson, "The Probability of Isolation by Disruptive Selection," The American Naturalist 104 (1970): 219–230. Coyne and Orr, Speciation, 138.

(5) Theodosius Dobzhansky and Olga Pavlovsky, "Spontaneous Origin of an Incipient Species in the Drosophila Paulistorum Complex," Proceedings of the National Academy of Sciences 55 (1966): 727–733.

(6) Coyne and Orr, Speciation, 138.

(7) James R. Weinberg, Victoria R. Starczak, and Daniele Jörg, "Evidence for Rapid Speciation Following a Founder Event in the Laboratory," Evolution 46 (1992): 1214–1220.

(8) Francisco Rodriquez-Trelles, James R. Weinberg, and Francisco J. Ayala, "Presumptive Rapid Speciation After a Founder Event in a Laboratory Population of Nereis: Allozyme Electrophoretic Evidence Does Not Support the Hypothesis," Evolution 50 (1996): 457–461.

(9) E. Paterniani, "Selection for Reproductive Isolation Between Two Populations of Maize, Zea mays L.," Evolution 23 (1969): 534–547.

(10) William R. Rice and George W. Salt, "Speciation via Disruptive Selection on Habitat Preference: Experimental Evidence," The American Naturalist 131 (1988): 911–917. See also Coyne and Orr, Speciation, 138–141.

(11) Darwin, Origin of Species, 111.

(12) Alan Linton, "Scant Search for the Maker," The Times Higher Education Supplement (April 20, 2001), Book Section, 29, available online with registration (last accessed January 9, 2007).


(13) Lynn Margulis and Dorion Sagan, Acquiring Genomes: A Theory of the Origins of Species (New York: Basic Books, 2002), 32.

Why the geekocracy will not save us.

Science, Knowledge, and the "Epistemic Horizon"
David Klinghoffer

National Review Online's Kevin Williamson has sometimes rubbed me the wrong way, but in the 24 hours or so since Neil deGrasse Tyson shot off his "#Rationalia" tweet, Williamson composed an essay in response that can only be called profound. Tyson, the "dumbest smart person on Twitter," proposed a "virtual country," with a "one-line Constitution: All policy shall be based on the weight of evidence." In reply, Williamson offers the image of a limit to knowledge, an "epistemtic horizon" like the "event horizon" of a black hole.

Read it all for yourself, but this is the conclusion and upshot:

The epistemic horizon is not very broad. We do not, in fact, know what the results of various kinds of economic policies or social policies will be, and there isn't any evidence that can tell us with any degree of certainty. The housing projects that mar our cities weren't supposed to turn out like that; neither was the federal push to encourage home-ownership or to encourage the substitution of carbohydrates for fats and proteins in our diets. A truly rational policy of the sort that Tyson imagines must take into account not only how little we know about the future but how little we can know about the future, even if we consult the smartest, saintliest, and most disinterested experts among us.
That is part of the case for limited government and free markets. Government can do some things, such as guard borders (though ours chooses not to) and fight off foreign invaders. There are things that it cannot do, even in principle, such as impose a "rational" order on the nation's energy markets, deciding that x share of our electricity supply shall come from solar, y share from wind, z share from natural gas, all calculated to economic and environmental ideals. That is simply beyond its ken, even if all the best people -- including Tyson, from time to time -- pretend that it is otherwise. Free markets go about solving social problems in the opposite way: Dozens, or thousands, or millions, or even billions of people, firms, organizations, investors, and business managers trying dozens or thousands of approaches to solving social problems....

There isn't a road to Rationalia. There are billions of them, negotiated by individuals and institutions dozens or hundreds of times a day, every time they make a significant choice. Government programs are, by their nature, centralized, unitary, and static attempts to impose a rational order on complexity beyond the understanding of the people who would claim to manage it....

It isn't ideology that imposes a relatively narrow circle on what government planners can do. And, with all due respect to the genius of F. A. Hayek ("The curious task of economics is to demonstrate to men how little they really know about what they imagine they can design"), it isn't only economics, either. The limitations on human knowledge are real, and they are consequential. As men like him have done for ages, Tyson dreams of a world of self-evident choices, overseen by men of reason such as himself who occupy a position that we cannot help but notice is godlike. It's nice to imagine ruling from an Olympus of Reason, with men and nations arrayed before one as on a chessboard.

Down here on Earth, the view is rather different, and the lines of sight inside the epistemic horizon are not nearly so long as our would-be rulers imagine.

I would add -- and this he doesn't say -- that the idea of a limit or horizon to knowledge goes far beyond politics, economics, urban planning, the issues that seem to animate Kevin Williamson. It includes faith, notwithstanding the certainty of the New Atheists and some religious spokesmen as well. In this context, I think of the Talmud's interesting gnomic statement warning of four boundaries of reality beyond which we are better off not seeking to gaze -- "what is above, what is below, what was before, and what will be after."
The idea of an epistemic horizon definitely includes science, especially historical scientific theories that seek to lay bare biological origins. Everyone who speaks about science in public should be reminded of this.

I don't mean we can never have an informed opinion on how life arose, became complex and diverse. That's exactly what we talk about when we talk about intelligent design. But the horizon should be kept in view when we hear Darwinian evolution asserted as "fact" -- "as much a fact as gravity or erosion," in a typical formulation. No, that is wrong.


ID advocates don't talk that way -- ID as "fact," rather than a tentative inference. And good for them. That modesty is a point in favor of the design argument.