Friday 30 June 2023
Still no simple beginning
On the Irreducible Complexity of Sperm Cells
Human reproduction is perhaps the quintessential example of teleology in biology. The process by which a fertilized egg develops into an infant over the space of nine months reveals exquisite engineering and ingenious design. Before this intricate process can even begin, there is a need for a sperm cell to fuse with an ovum — each carrying, in the case of humans, 23 chromosomes. This incredible feat bears the unmistakable hallmarks of conscious intent and foresight
Here , I will focus on the design characteristics of sperm cells. In a subsequent post, I will discuss the design features of the seminal fluid, and sperm capacitation. Sperm cells are comprised of three components — the head, the middle piece, and the flagellum — and hundreds of millions of them are carried in the seminal fluid that is released into the cervix through ejaculation during sexual intercourse. With each ejaculation, the male releases between two hundred and five hundred million sperm cells (approximately 100 million per milliliter of semen). Each of these three components, and the seminal fluid, is crucial to the sperm cell’s mission of fusing with an ovum to form a zygote (a fertilized egg). Let us consider each one in turn.
The Head
The head carries densely coiled chromatin fibers, containing the haploid genome — totaling half of the genetic material that will be inherited by the next generation (the other half will come from the mother’s egg cell). The tight packaging of the DNA serves to minimize its volume for transport.
On the tip of the sperm head is a membranous organelle, called the acrosome, that contains various hydrolytic enzymes. When these are secreted, they digest the egg cell membrane, thereby facilitating penetration of the ovum. Without the acrosome, the sperm cell will be unable to penetrate the egg cell membrane to fertilize the ovum. According to a review paper published in Frontiers in Cell and Developmental Biology:
Any structural or functional acrosomal abnormality could impair sperm fusion, and ultimately result in infertility. Moreover, studies have shown that intra-cytoplasmic insemination with sperm containing acrosomal abnormalities did not lead to successful fertilization, even in the absence of fertilization barriers, because the oocyte was unable to be efficiently activated…Thus, the acrosome is indispensable for fertilization.1
When a sperm reaches the vicinity of the egg, it undergoes a series of molecular interactions with the zona pellucida, which is a specialized extracellular matrix surrounding the egg. Specific receptors on the sperm’s plasma membrane, such as spermadhesins or integrins, recognize and bind to corresponding ligands on the zona pellucida. This binding triggers the activation of signaling pathways in the sperm. Binding of the sperm receptors to the zona pellucida ligands leads to an influx of calcium ions (Ca2+) into the sperm cell. This calcium influx is typically mediated by ion channels or receptors on the sperm’s plasma membrane, which are activated upon ligand-receptor binding. The increase in intracellular calcium levels initiates a signaling cascade within the sperm cell. Calcium ions act as second messengers and trigger the activation of various downstream signaling molecules and enzymes, including protein kinases. As a result of the calcium-mediated signaling cascade, the acrosome undergoes exocytosis. The membrane surrounding the acrosome fuses with the sperm’s plasma membrane, causing the release of the acrosomal contents, including enzymes such as hyaluronidase and acrosin. The enzymes released from the acrosome help degrade the glycoprotein matrix of the zona pellucida, allowing the sperm to penetrate and reach the egg’s plasma membrane. The acrosomal contents aid in the breakdown of the protective layers surrounding the egg, facilitating the fusion of the sperm and egg membranes.
The formation of the acrosome itself is divided into four stages. The first stage, the “Golgi phase,” is dependent upon the Golgi apparatus, which produces and packages the proteins and enzymes needed for acrosome formation. These proteins are then transported into the developing acrosome vesicle. In the second phase, the “cap phase,” the Golgi-derived vesicle (known as the proacrosomal vesicle) fuses with the anterior portion of the nucleus, forming a cap-like structure over the nucleus. The fusion of the vesicle with the nucleus is mediated by membrane trafficking processes. The proacrosomal vesicle contains enzymes, glycoproteins, and other components that are essential for acrosome maturation. In the third phase, the “acrosome phase,” the cap-like structure undergoes a series of structural changes, leading to the formation of the acrosome. The proacrosomal vesicle flattens and elongates, spreading over the anterior region of the nucleus. The Golgi-derived enzymes modify the proteins present in the proacrosomal vesicle, converting them into their active forms. The acrosomal membrane also undergoes changes, becoming specialized for the acrosome’s functions. In the final phase, the “maturation phase,” the acrosome undergoes further modifications and maturation. Enzymes within the acrosome become fully activated and the acrosomal matrix undergoes changes, becoming more condensed. The acrosomal granule, which is the central region of the acrosome, becomes highly electron-dense due to the accumulation of enzymes and proteins. The mature acrosome is now ready for its role in fertilization. For a more detailed description of this incredible process, I refer readers to a review paper on the “Mechanism of Acrosome Biogenesis in Mammals.”2
The Middle Piece
The middle piece consists of a central filamentous core, around which are many strategically placed mitochondria that synthesize the energy molecule adenosine triphosphate (ATP). The complexity and design of energy generation within the mitochondria — including the processes of glycolysis, the citric acid (or, Krebs) cycle, the electron transport chain, and oxidative phosphorylation — could be its own series of articles, but this is a topic for another day. For a good introduction to the phenomenal processes within the mitochondria, here are three animations from Harvard University that bring this fascinating organelle to life:
“Mitochondria: The Cell’s Powerhouse”
“Electron Transport Chain”
“ATP Synthase in action”
The ATP generated by the mitochondria energizes the power strokes of the flagellum, driving its journey through the female cervix, uterus, and uterine tubes. As such, the middle piece of the sperm cell is absolutely essential to its function of swimming through the female uterus and fallopian tube to fertilize her egg. Without the middle piece and its mitochondria, the sperm cells are completely immobile.
The Flagellum
Unlike a bacterial flagellum (which rotates like a motor), a sperm flagellum beats with a whip-like motion to produce motility. How does the flagellum work? In 2018, Jianfeng Lin and Daniela Nicastro elucidated the mechanism of flagellar motility.3 Their data indicated that “bending was generated by the asymmetric distribution of dynein activity on opposite sides of the flagellum”4 (dyneins are ATP-powered molecular motors that “walk” along microtubules towards their minus end). Their results also revealed that alternating flagellar bending occurs due to “a ‘switch-inhibition’ mechanism in which force imbalance is generated by inhibiting…dyneins on alternating sides of the flagellum.”5 In other words, regulatory signals lead to the inhibition of dynein motors on one side of the flagellum. Meanwhile, on the other side, the dyneins walk along the microtubules. The flagellum bends in one direction due to molecular linkers that resist this sliding. The flagellar bending alternates by repeatedly switching the side of dynein inhibition. Look here for an animation showing how this is thought to work.
It goes without saying that, without the flagellum, the sperm cell is completely immotile and has no chance of fertilizing the egg.
Thus far, we have considered the irreducible complexity of the components of a sperm cell. In a subsequent article, we shall consider the design features of the seminal fluid and the process of sperm capacitation that takes place within the female reproductive tract.
Notes
Khawar MB, Gao H, Li W. Mechanism of Acrosome Biogenesis in Mammals. Front Cell Dev Biol. 2019 Sep 18;7:195.
Ibid.
Lin J, Nicastro D. Asymmetric distribution and spatial switching of dynein activity generates ciliary motility. Science. 2018 Apr 27;360(6387):eaar1968.
Ibid.
Ibid.
Continuing to massage the record?
Fossil Friday: Homo rudolfensis, Another Contentious Homo
Last week for Fossil Friday I posted some musings about Homo habilis and its controversial attribution to our genus. This week we will have a look at another disputed relative, Homo rudolfensis. Alexeev (1986) described the new species Homo (Pithecanthropus) rudolfensis from a single skull (KNM-ER 1470) discovered in 1972 by Richard Leakey at the 1.9 million year old Koobi Fora locality of the Turkana Lake (formerly known as Lake Rudolf) basin in East Africa (also see Wood 1999). The material was previously considered to be conspecific with Homo habilis, which is a hypothesis still entertained by some modern experts. However, the skull differs from Homo habilis in its flat face and larger brain volume as well as the more robust-australopithecine-like cheek teeth. Unfortunately, no associated postcranial remains are known yet (Berger et al. 2015), so that the most distinctive characters of the genus Homo and those for bipedal gait are unknown (Tuttle 2006: 253).
A New Digital Reconstruction
As for Homo habilis, Wood & Collard (1999a, 1999b, 2001) and Collard & Wood (2007, 2015) indeed advocated for transferring H. rudolfensis to the genus Australopithecus, which had already been suggested by other researchers (i.e., Walker 1976 and Lieberman et al. 1996). Walker & Shipman (1996) pointed out that “1470 might have a big braincase, but morphologically it was just an australopithecine.” A new digital reconstruction of the skull by Bromage et al. (2008) showed that it was somewhat less flat and the brain volume somewhat smaller, which made it even more similar to australopithecine skulls. Nevertheless, the latter study retained this species in the genus Homo. A co-author of this study was German paleoanthropologist Friedemann Schrenk, who at my university, Tübingen, was known by the sneering nickname the “Möllemann of German paleontology.” That was because he shared a notorious proclivity for PR stunts and media hype with the late German politician Jürgen Möllemann. He discovered a hominin mandible (UR 501) in Malawi, which he attributed to Homo rudolfensis and with an estimated age of 2.4 million years this would be much older than the holotype. Of course, publications on an early Homo make for much more sensational press releases than just another ape-man.
Anyway, Leakey et al. (2001) and Lieberman (2001) noted several striking similarities in the facial architecture of the newly described hominin Kenyanthropus platyops and the 1.6 million year younger H. rudolfensis, who could be a late survivor of the australopithecine-like Kenyanthropus lineage rather than an early Homo. The phylogenetic analysis by Cameron & Groves (2004) strongly confirmed the reclassification as Kenyanthropus rudolfensis by Cameron (2003). Cela-Conde & Ayala (2003) agreed that Homo rudolfensis (and H. habilis) should be grouped with Kenyanthropus platyops, but instead proposed to include all three within the genus Homo. That would place the origin of our genus 3.5 million years ago, in stark contradiction to all other experts and the unequivocal empirical evidence from the fossil record.
Four Hypotheses
Prat (2007) compared the four suggested alternative hypotheses: H. rudolfensis is conspecific with Homo habilis; H. rudolfensis and H. habilis are both distinct species of Homo; both species belong to the genus Australopithecus; or H. rudolfensis belongs to the genus Kenyanthropus. Prat came to the conclusion that Homo rudolfensis is distinct but her cladistic analysis suffers from several flaws. This is evident from the fact that the inclusion of the holotype of Kenyanthropus platyops did not just influence the polarity of some characters but produced a totally different tree topology with hardly any similarity to the tree recovered by excluding this taxon. The confidence level in any such highly unstable analyses should be very low for reasonable and unbiased scientists. However, having two early species of Homo is of course a highly desirable result for evolutionist paleoanthropologists, and so it is hardly surprising that almost all subsequent publications maintained the attribution of these two species to the genus Homo.
Awaiting Better Evidence
More recently, a more ancient origin of our genus has indeed been claimed by the discovery of a 2.8 million year old human mandible at Ledi-Geraru in the Afar region of Ethiopia, which was attributed to an early Homo (Villmoare et al. 2015). But this fossil combines primitive australopithecine traits with more derived features of later Homo, and it also suffers from the absence of any other cranial and postcranial characters that could support this claim. Considering the checkered history of grandiose claims and controversies in paleoanthropology, some caution may be wise until more and better evidence is found.
References
Alexeev VP 1986. The Origin of the Human Race. Progress Publishers, Moscow, 360 pp. https://archive.org/details/originhumanrace/page/1/mode/2up
Berger LR, Hawks J, de Ruiter DJ et al. 2015. Homo naledi, a new species of the genus Homo from the Dinaledi Chamber, South Africa. eLife 4:e09560, 1–35. DOI: https://doi.org/10.7554/eLife.09560
Bromage TG, McMahon JM, Thackeray JF, Kullmer O, Hogg R, Rosenberger AL, Schrenk F & Enlow DH 2008. Craniofacial architectural constraints and their importance for reconstructing the early Homo skull KNM-ER 1470. Journal of Clinical Pediatric Dentistry 33, 43–54. DOI: https://doi.org/10.17796/jcpd.33.1.8168115j12103nut
Cameron DW 2003. Early hominin speciation at the Plio/Pleistocene transition. HOMO 54(1), 1–28. DOI: https://doi.org/10.1078/0018-442X-00057
Cameron DW & Groves CP 2004. Bones, Stones, and Molecules: “Out of Africa” and Human Origins. Academic Press, Burlington (MA), xi+402 pp.
Cela-Conde CJ & Ayala FJ 2003. Genera of the human lineage. PNAS 100(13), 7684–7689.
DOI: https://doi.org/10.1073/pnas.0832372100
Collard M & Wood B 2007. Defining the Genus Homo. pp. 1575–1610 in: Henke W & Tattersall I (eds). Handbook of Paleoanthropology. 3 vols. Springer, Berlin, 2069 pp.
Collard M & Wood B 2015. Defining the Genus Homo. pp. 2107–2144 in: Henke W & Tattersall I (eds). Handbook of Paleoanthropology. 3 vols. Springer, Berlin, xliii+2624 pp. DOI: https://doi.org/10.1007/978-3-642-39979-4_51
Tuttle RH 2006. Are Human Beings Apes, or are Apes People too? pp. 249–258 in: Ishida H, Tuttle R, Pickford M, Ogihara N & Nakatsukasa M (eds). Human Origins and Environmental Backgrounds. Springer Science, Boston (MA), x+282 pp. DOI: https://doi.org/10.1007/0-387-29798-7_19
Leakey MG, Spoor F, Brown FH, Gathogo PN, Kiarie C, Leakey LN & McDougall I 2001. New hominin genus from eastern Africa shows diverse middle Pliocene lineages. Nature 410(6827), 433–440. DOI: https://doi.org/10.1038/35068500
Lieberman DE 2001. Another face in our family tree. Nature 410(6827), 419–420. DOI: https://doi.org/10.1038/35068648
Lieberman DE, Wood BA & Pilbeam DR 1996. Homoplasy and early Homo: An analysis of the evolutionary relationships of H. habilis sensu stricto and H. rudolfensis. Journal of Human Evolution 30, 97–120. DOI: https://doi.org/10.1006/jhev.1996.0008
Prat S 2007. The Quaternary boundary: 1.8 or 2.6 millions years old? Contributions of early Homo. Quaternaire 18(1), 99–107.
DOI: https://doi.org/10.4000/quaternaire.1313
Villmoare B, Kimbel WH, Seyoum C et al. 2015. Early Homo at 2.8 Ma from Ledi-Geraru, Afar, Ethiopia. Science 347(6228), 1352–1355. DOI: https://doi.org/10.1126/science.aaa1343
Walker A 1976. Remains attributable to Australopithecus in the East Rudolf succession. pp 484–489 in: Coppens Y, Howell FC, Isaac GL & Leakey REF (eds). Earliest Man and Environments in the Lake Rudolf Basin. University of Chicago Press, Chicago (IL), 640 pp.
Walker A & Shipman P 1996. The Wisdom of the Bones: In Search of Human Origins. Knopf, New York (NY), 368 pp.
Wood B 1999. Homo rudolfensis Alexeev, 1986: Fact or phantom?. Journal of Human Evolution 36(1), 115–118. DOI: https://doi.org/10.1006/jhev.1998.0246
Wood B & Collard M 1999a. The Human Genus. Science 284(5411), 65–71. DOI: https://doi.org/10.1126/science.284.5411.65
Wood B & Collard M 1999b. The changing face of genus Homo. Evolutionary Anthropology 8(6), 195–207. DOI: https://doi.org/10.1002/(SICI)1520-6505(1999)8:6<195::AID-EVAN1>3.0.CO;2-2
Wood B & Collard M 2001. The meaning of Homo. Ludus Vitalis 9(15), 63–74. http://profmarkcollard.com/wp-content/uploads/2014/09/Wood-and-Collard-2001.pdf
On the anti-Darwinian bias of the natural law.
Intelligence Is Unnatural, and Why That Matters
One of the advantages we have in our study of nature is our ability to observe an entire “unpolluted” universe. By “unpolluted” I mean that as we look out from Earth, we observe an almost unlimited theater of the natural. And what do we observe? Mostly empty space, visibly interspersed with galaxies composed of stars and nebulae. The regularities of the laws of nature also reveal unseen actors such as dark matter and energy, planets, and even black holes.
Speaking of the laws of nature, the heavenly stage extends so far away that light’s finite speed shows us scenes that happened in the past — from about one and one fourth seconds in the past, when we look at the moon, to more than 13 billion years ago in recent images of distant galaxies revealed by the James Webb Space Telescope. The physical universe provides astronomers with a time machine for viewing nature throughout the history of the cosmos. And what we see confirms the unchanging nature of the laws of physics.
What Spectroscopy Reveals
Using spectroscopy, astronomers not only observe the large-scale features of the universe, but through analysis of the specific wavelengths of electromagnetic radiation received, details of the atomic components of stars and gas clouds also are revealed. In the past as well as in the present, both near to home in our solar system and out to the most distant reaches of the visible universe, the same atomic characters fill the arena of the universe. Throughout the entire long history of the universe and in every direction we look, nature has only managed to produce a very limited playlist of elements — 92 different elements, from hydrogen with one proton as its nucleus to uranium with 92 protons.1
The reason I emphasize the limited number of types of elements in the entire universe is to suggest that one of the characteristics of nature is its “sameness” or redundancy. Now, there’s a reason for this: natural outcomes are governed by natural law. Only four fundamental forces of nature exist. Gravity pulls masses together; the electromagnetic force has twice the fun and can both push and pull masses that possess electric charge. The strong nuclear force also pulls,2 but with restrictions. It only acts on nucleons (protons and neutrons, but not electrons), and it has an extremely short range of about one fermi (10-15 m). The weak force neither pushes nor pulls, but is responsible for certain decay processes of elementary particles.
An example of the sameness of the cosmos is seen in the limited range of star masses. From at least a billion trillion stars in the universe, we find that their masses vary only over a range of about 1800, from 8 percent of the sun’s mass up to about 150 times the sun’s mass. These mass limits are not accidental; they are fixed by the laws of physics.
Seemingly Endless Variations
But what about the seemingly endless variations in the palette of sunset colors and patterns in the western sky? Doesn’t that run counter to the concept of limited diversity of natural phenomena? Certainly, we all appreciate the beauty of the rosy colorations of clouds illuminated by the rays of the setting sun. However, if we spent a thousand evenings watching the sun set, the sky would simply depict variations on a theme, with amorphous shapes of clouds shaded with gradations of color. Air, clouds, and light all respond according to the laws of nature, limiting their arrangements to forms devoid of specific complexity. Sameness prevails.
Turning our gaze away from sky and stars to the biosphere of Earth, we are struck by diversity unlimited. First, consider the unbelievable range of sizes and forms and behaviors of the millions of species of creatures that have lived on Earth. From tiny diatoms to enormous dinosaurs, from worms to eagles, and ants to people, the variety of living forms on Earth is astonishing compared to the overall sameness of the entire non-living universe.
The stark contrast between our life-filled planet and the rest of the cosmos sharpens further when we take into account all of the things produced by humans throughout our relatively short history on the stage of existence. Clocks, cars, computers, castles, clothing, and can openers. Besides physical creations, humans have produced a fantastic variety of musical and literary forms and coding for computer programs. Our prolific creativity seems limitless, and the scope of what we make spans an enormously broad spectrum with a variety that’s anything but “more of the same.”
The contrast between variety in living forms on just one planet, compared to the vast sameness of the non-living universe suggests a clear-cut distinction between even the simplest living organisms and non-living arrangements of matter. An objective consideration of the flourishing creativity of human endeavors compared to the routine instinctual behaviors of other creatures further suggests a categorical difference between human beings and other creatures.
A Physics Point of View
The exceptionalism manifested by humans, when compared to the predictably limited outcomes of non-living matter, is evidence that the choices and actions of intelligent beings are not governed by the laws of physics. My body is affected by gravity, but the force of gravity doesn’t determine what I eat for lunch. My cellular biochemistry is affected by the electromagnetic force, but my decision about what topic to address in my next article is not. The strong force holds the nuclei of my carbon atoms together, but it in no way determines what color my wife will choose to paint the living room.
How did we become so unnaturally creative? The Judeo-Christian tradition offers one possible answer. The belief that human beings are made in the image of God resonates with the unique creativity expressed by humanity throughout history. The more closely related the created is to the Creator, the more attributes of the one are to be expected in the other.
With our intelligent and creative minds, we can bring together the raw materials of the natural universe into an unlimited variety of forms that are both functional and purposive. Human expression manifests the unnatural attributes of creating art, literature, and technology — outcomes that would never arise by the influence of natural processes alone. Freedom and creativity complement one another; neither will flourish under controlling forces. If the forces of nature governed our thoughts and actions, would we see the vast panoply of creative human expression displayed throughout the history of civilization? It seems not.
Notes
A few more (or fewer) natural elements could be considered, depending on whether one includes those that are extremely rare or have a very short half-life.
The strong force becomes repulsive for inter-nucleon distances less than about 0.5 fermi.
Thursday 29 June 2023
Missing links aplenty?
Long Necks in Sauropod Dinosaurs — By Neo-Darwinism or Intelligent Design?
Editor’s note: We are delighted to direct readers to a new paper by geneticist Wolf-Ekkehard Lönnig, “A Brief Note on the Multiple Independent Origins of the Long Necks in Sauropod Dinosaurs: Neo-Darwinism or Intelligent Design?” What follows is the paper’s abstract:
Convergence is a deeply intriguing mystery, given how complex some of the structures are. Some scientists are skeptical that an undirected process like natural selection and mutation would have stumbled upon the same complex structure many different times.
MEYER, MINNICH, MONEYMAKER, NELSON, SEELKE1
Now it is precisely the phenomenon of convergence that poses further major problems for neo-Darwinism. For if the one-time emergence of completely “adapted” organs or characteristics through selection of random mutations can hardly be explained, the multiple formation of similar organs elutes the neo-Darwinian interpretation even further.
HENNING KAHLE2
Abstract
The phenomenon of complex convergences by selection of random mutations is “a deeply intriguing mystery” and “poses further major problems for neo-Darwinism,” because “if it is highly improbable for a complex solution to evolve once, ‘convergent evolution’ only exacerbates the improbability.” In contrast, “what we do know […] is that intelligence can take a solution to a problem and apply it in different circumstances over and over again” (see references in the text). I have chosen 20 examples (of at least 36 according to D’Emic 2023) of such long-necked sauropod dinosaurs and shown and discussed them in the article below.
Chronological occurrence of the 20 genera distributed in 9 families of the sauropod dinosaurs mentioned and shown in the present article. Note please that 5 and 4 of the genera arose almost simultaneously. And “nearly all did arise independently” (D’Emic, mail 26 June 2023 to W.-E. L.). Figure by Roland Slowik (Dietzenbach, Germany) for the present article (20 June 2023).
Now, the origin of the ingeniously intricate long necks (and their correspondingly fine-tuned body anatomy) in sauropod dinosaurs has been postulated to have arisen more than 35 times independently of each other by selection of random mutations. The improbability that such transformations having happened by natural selection of random or accidental or haphazard DNA mutations is again being multiplied almost unimaginably. The improbability of neo-Darwinian evolution thus becomes virtually immeasurable. How do our Darwinian friends react to such objections?
Well, they presuppose their evolutionary worldview as sacrosanct, unassailable, and irrefutable. They then argue that the origin of such sophisticated features must be so very easy, so utterly simple, that they can evolve even many dozens of times independently of each other almost everywhere in the realm of living beings.3 I met that “explanation” first in an article by Mayr and Salvini-Plawen. My comment: Hats off for such naïvety.
Comparing ID with Neo-Darwinism
Applying Dembski’s Explanatory Filter to this question, we get the following answers:
Law: There is no law that produces long necks inevitably under any defined ecological conditions.
Vast improbability: Fulfilled — chance to be excluded.
Specification: Fulfilled.
In comparing neo-Darwinism with the theory of intelligent design, we find the latter to be definitely the superior explanation.
Read the rest at, “A Brief Note on the Multiple Independent Origins of the Long Necks in Sauropod Dinosaurs: Neo-Darwinism or Intelligent Design?”
Wednesday 28 June 2023
Correcting professor Dave on "Darwin devolves"
Answering Farina on Behe’s Work: Darwin Devolves
In three previous articles (here, here, andhere ), I began a series of four responses to You-Tuber “Professor Dave” Farina’s video review of Michael Behe’s three books. In this final post, I will turn my attention to Farina’s comments regarding Darwin Devolves.
Hemoglobin and C-Harlem
In Darwin Devolves, Behe contends that the majority of helpful mutations are deleterious rather than constructive, since there are far more ways to gain an advantage by breaking than by building something. Says the Farina video:
If Behe had bothered to look at some of the most well-documented examples of evolutionary change, he’d know that this isn’t the case. In fact, he should know this is nonsense based on examples he himself described in his other works. For example, in Edge of Evolution, Behe describes a hemoglobin allele called HbC-Harlem, which, similar to the allele that causes sickle-cell disease, confers resistance to malaria, with, as Behe describes, “the advantages but not the drawbacks of sickle.”
But this “example of evolutionary change” shows precisely the opposite of what Farina wants. As Behe explains in The Edge of Evolution, “Hereditary persistence of fetal hemoglobin (HPFH) is already widespread in Africa, ameliorating the problems of the sickle gene.”1 Surprisingly, however, “the C-Harlem gene, which builds directly on the foundation of the sickle gene and would entirely eliminate the drawbacks of the sickle mutation, has not yet turned up in Africa, where it would do the most good.”2 The reason for this is that the move from regular hemoglobin to C-Harlem would require two co-dependent mutations, whereas the sickle-cell trait requires only one. The probability of getting the sickle-celled trait in any individual is about one in a hundred million. Assuming a population size of a million people, it should thus be expected to arise spontaneously approximately every hundred generations, which is within the reach of evolutionary processes. For the two necessary mutations needed for hemoglobin C-Harlem to occur at the same time, the probability is a hundred million multiplied by a hundred million, which is 1016. As Behe summarizes, “With a generation time of ten years and an average population size of a million people, on average it should take about a hundred billion years for that particular mutation to arise — more than the age of the universe.”3Nonetheless, hemoglobin C-Harlem has arisen, and was first documented relatively recently in New York City.4 But this is because the initial sickle-cell trait was already adaptive, since it conferred resistance to the malarial parasite. Thus, natural selection can preserve the sickle-celled trait (requiring only a single mutation) first and then acquire the second mutation (building on the first), thereby giving rise to the C-Harlem trait, which confers an even greater advantage. It looks like Mr. Farina did not review this example very carefully.
Cit+ in E. coli
As Farina’s second example, he notes,
[Dr. Behe] also describes the aforementioned Cit+ trait in the E. coli of the LTEE [Richard Lenski’s long-term evolution experiment], which has a new metabolic option, without compromising any existing pathways, literally debunking himself yet refusing to acknowledge it.
I have already addressed this example (see here), so I will not belabor the point further. Suffice it to say that Behe discusses Lenski’s work at length in Chapter 7 of Darwin Devolves, and Farina fails to engage with anything Behe writes concerning the long-term evolution experiment.
De Novo Gene Birth
Another complaint in the Farina video is that,
As you are likely beginning to see, creationists [sic] have a sadistic obsession with painting evolution as some kind of destructive force, but to do so they have to ignore a long and expanding list of completely new genes rapidly evolving everywhere we look. There are many papers like this one examining the concept of de novo genes. These are new genes that originate when previously non-expressed DNA becomes protein-coding and preserved via natural selection due to promoters arising near previously non-coding sections of DNA. So, we have a section of DNA that was not a gene, which is now a gene. New genes. We used to think this was rare, but once we figured out how to look for them, by identifying protein-coding sequences that aren’t protein coding in all the most closely related species, we started finding them all over the place.
The review paper Farina cites, by Stephen Branden Van Oss and Anne-Ruxandra Carvunis, notes (as is common in review papers dealing with this subject) that, for a long time, “the consensus view was that virtually all genes were derived from ancestral genes, with Francois Jacob famously remarking in a 1977 essay that ‘the probability that a functional protein would appear de novo by random association of amino acids is practically zero’.”5 But “though de novo gene birth was once viewed as a highly unlikely occurrence, there are now several unequivocal examples of the phenomenon that have been described.”6 In other words, though it was once thought that the origins of fundamentally new genes from non-coding sequences was essentially impossible, the fact that we observe a plethora of taxonomically-restricted genes, rather than being taken as a disconfirmed prediction of evolution, is taken to show that de novo genes can be birthed by evolution quite readily after all. Evolutionary theory, remarkably, is taken to be completely insensitive to disconfirming evidence.
Moreover, though some examples of taxonomically restricted genes bear some resemblance to non-coding stretches of DNA in related species, this is not so with the majority of cases. Furthermore, there is no convincing mechanistic scenario by which non-coding DNA may be transformed into genes coding for proteins that are ready to fulfil a functional role.
Polar Bears
According to Farina,
Perhaps the best evidence that Darwin Devolves is nonsense is that Behe had to flat out lie to defend it. In a discussion of Behe’s treatment of documented adaptations in polar bears, Dr. Nathan Lents pointed out that Behe did not accurately represent the findings of a paper he cited, when he claimed that virtually all adaptations that polar bears have to their arctic climate are actually damaging in some way. In response, Behe provided a table from that paper, showing that all the documented mutations are either “possibly damaging” or “probably damaging.” But he must have thought nobody would check up on him, since Dr. Lents showed that Behe sneakily omitted two columns and many rows, and the omitted data, unsurprisingly, tell a very different story… Apart from the two restored columns, look at all those rows that say “benign,” meaning not harmful in effect. You know, the exact opposite of what Behe is claiming?
This claim has been rebutted thoroughly elsewhere (such as here). In brief, Behe nowhere denies that non-adaptive neutral mutations are common in evolution. Rather, his thesis is that the vast majority of positively selectedmutations are damaging, since there are far more ways for an organism to acquire an advantage by breaking something than there are ways to gain an advantage by building something new. In Darwin Devolves, Behe contended that “65 to 83 percent of helpful, positively selected genes are estimated to have suffered at least one damaging mutation.”7 Given that the entire chart from the Liu et al. paper, cited by Behe, is some 47 rows long and 8 columns wide, it made more sense to reproduce only the portion of the chart that was relevant to supporting his point. There is nothing duplicitous here. Behe omitted from the chart the data from the HVar algorithm (instead showing only the results of the HDiv algorithm) and also left out instances where the HDiv algorithm predicted that a mutation was benign. This served Behe’s purpose of confirming for his readers that up to 14 of the 17 genes examined (i.e., 83 percent) were probably or possibly damaging. The instances where a mutation was not predicted to be damaging (i.e., those listed as benign) do not contradict Behe’s thesis, since Behe never denied that many mutations are benign. Indeed, a significant majority of mutations are benign (e.g., the third codon position may be substituted without altering the amino acid sequence). But Behe’s thesis is that the vast majority of adaptive mutations (which make up a minority of mutations overall) are destructive rather than constructive. There is nothing in the chart that invalidates or undermines this thesis.
Conclusion
Farina’s video rebuttal directed at Behe’s work misrepresents Behe at multiple points. Moreover, Farina misreads several papers that he cites in his video, failing to understand how they intersect with Behe’s critiques of evolutionary theory. There is also little that is new to see in his video. Many of his criticisms of Behe have been made before by others and addressed in detail elsewhere. In short, despite Mr. Farina’s smug condescension and patronizing demeanor, he fails to mount a credible critique of Dr. Behe’s thesis.
Notes
Behe MJ, The Edge of Evolution: The Search for the Limits of Darwinism (Free Press, 2007), 29.
Ibid.
Ibid., 110.
Bookchin RM, Nagel RL, and Ranney HM. Structure and properties of hemoglobin C-Harlem, a human hemoglobin variant with amino acid substitutions in 2 residues of the beta-polypeptide chain. Journal of Biological Chemistry 1967; 242:248-255.
Van Oss SB, Carvunis AR. De novo gene birth. PLoS Genet. 2019 May 23;15(5):e1008160.
Ibid.
Behe MJ, Darwin Devolves: The New Science About DNA That Challenges Evolution (HarperOne, 2020), 17.
Correcting professor Dave on the "edge of evolution"
Answering Farina on Behe’s Work: The Edge of Evolution
In two previous articles (here and here), I began a series of responses to YouTuber “Professor Dave” Farina’s video about Michael Behe’s three books. In this essay, I turn my attention to Mr. Farina’s comments regarding The Edge of Evolution.
Malaria
In the video, Farina claims that “[Dr. Behe] seems to think that for any given biochemical trait, like drug resistance or disease immunity, there is one way, and only one way, to accomplish that job, despite he himself describing the biochemical details of more than one form of malaria resistance found in humans.” Actually, in The Edge of Evolution, Behe discusses the biochemical details of malarial resistance to two different drugs, namely, atovaquone and chloroquine. In regard to chloroquine resistance, Behe described the Plasmodium falciparum chloroquine resistance transporter, coded by the pfcrt gene, which is recognized to be of primary importance in conferring chloroquine resistance.1 This pump naturally functions as a peptide transporter. Mutations that enable the transporter to pump chloroquine impair its ability to pump peptides and actually entail a significant fitness cost to the parasite.2 As Behe explains in The Edge of Evolution, at least two co-dependent amino acid substitutions are necessary for this chloroquine resistance phenotype3 — and public health data suggests that it occurs approximately once in every 1020 cells.4 From this, it may be predicted that an adaptation requiring four co-dependent substitutions would arise in every 1040 malarial cells. Given that less than 1040 organisms have likely ever existed on earth5, this number is quite prohibitive. The challenge is even more acute when we are dealing with complex animals such as mammals, which have far, far fewer individuals. Until relatively recently, the effective population size of hominids, for instance, was only in the range of 10,000-20,000 individuals. If it is challenging for complex traits to evolve in single-celled organisms, it is much, much more difficult for them to evolve in more complex organisms. For a more detailed treatment of this subject, I refer readers to this article by Casey Luskin.
Farina contends that,
Behe butchers the concept of fitness landscapes in a way that is both extremely basic and completely undermines his argument…In one time or place, a particular genotype might be extremely fit, but in a different time or place, it might have low fitness. Behe completely misses this trivial detail. He argues that crossing “valleys” is impossible via evolutionary processes, since any intermediate between two peaks or two high-fitness genotypes will be low fitness, and selected against. In making this argument, he assumes that fitness landscapes are constant, and genotypes have fixed fitness values, regardless of environmental or ecological conditions.
But for many complex adaptations, such as those described in Behe’s books, a fitness benefit is not realized until multiple co-dependent mutations have arisen. A protein that stably folds, in order to mutate into a fundamentally different fold, will have to pass through a fitness valley where it does not stably fold and no longer performs its role. Such a protein will not be selected for under an alternative set of environmental conditions. It seems that, again, Farina fails to understand Behe’s argument.
Bizarrely, Farina asserts that “it’s quite amusing to note that if Behe considers [antimalarial] drug resistance to be impossible to evolve, it means that he believes in a god who deliberately bestowed plasmodia with resistance to our drugs in order to ensure that we continue to contract malaria. Gee, what a swell guy.” But this, too, betrays a misunderstanding of what Behe argues in The Edge of Evolution. He does not deny that malarial parasites have acquired resistance to chloroquine and other antimalarial drugs. Quite the contrary. Rather, as discussed above, he notes that malarial resistance to chloroquine has arisen and that it occurs approximately once in every 1020 cells. He then uses this data to extrapolate to a case requiring twice as many co-dependent changes to bring about, and he points out that this problem is far more acute in the case of more complex organisms like large mammals, with much smaller population sizes, longer generation turn-over times, and lower mutation rates.
Interestingly, this same misrepresentation of The Edge of Evolution was made by Nathen Lents in his review of Darwin Devolves (discussed by Casey Luskin here). This makes me wonder whether Farina has in fact read Behe’s book for himself, or whether he is relying upon others, such as Lents, for his information about what is in the book.
HIV
In his video, Farina takes issue with Behe’s claims concerning HIV that “there have been no significant basic biological changes in the virus at all” and “There have been no reports of new viral protein-protein interactions developing in an infected cell due to mutations in HIV proteins.”6 He cites the Vpu example discussed in part one. However, as Behe acknowledged years ago, this was one example he had overlooked in The Edge of Evolution. Nonetheless, it does not significantly impact the thesis of the book, since the statement may be modified to assert that “There have been hardly any reports of new viral protein-protein interactions developing in an infected cell due to mutations in HIV proteins,” despite the fact that “HIV has almost certainly altered its proteins at one point or another in the past few decades enough to cover all of shape space.”7 Behe does not deny that new protein-protein binding sites have arisen by mutations in HIV. In fact, he explicitly states that its mutated proteins must have bound many molecules, though “none seem to have helped it” such that they were preserved by selection.8 The reason for this is what Behe dubs the problem of restricted choice — “That is, not only do new protein interactions have to develop, there has to be some protein available that would actually do some good.”9 Vpu is one exception where it did apparently help. But given how much better an evolver HIV is relative to essentially any other organism (with its 109-1010 individual viruses per infected person and its mutation rate of 10-4, meaning that all possible double point mutations will arise in each virus in one individual every single day), the problem is certainly much more acute for other life forms.
Notes
Sidhu AB, Verdier-Pinard D, Fidock DA. Chloroquine resistance in Plasmodium falciparum malaria parasites conferred by pfcrt mutations. Science. 2002;298(5591):210-3.
Felger I, Beck HP. Fitness costs of resistance to antimalarial drugs. Trends Parasitol. 2008;24(8):331-3.
Summers RL, Dave A, Dolstra TJ, Bellanca S, Marchetti RV, Nash MN, Richards SN, Goh V, Schenk RL, Stein WD, Kirk K, Sanchez CP, Lanzer M, Martin RE. Diverse mutational pathways converge on saturable chloroquine transport via the malaria parasite’s chloroquine resistance transporter. Proc Natl Acad Sci USA.2014;111(17):E1759-67.
White NJ. Antimalarial drug resistance. J Clin Invest. 2004; 113(8):1084-92.
Whitman WB, Coleman DC, Wiebe WJ. Prokaryotes: the unseen majority. Proc Natl Acad Sci U S A. 1998; 95(12):6578-83.
Behe MJ, The Edge of Evolution: The Search for the Limits of Darwinism (Free Press, 2007), 139.
Ibid., 157-158.
Ibid.
Ibid., 157.
Nothing simple about these beginnings.
Gifted Microbes Elevate the Case for Intelligent Design to the Entire Biosphere
Far from being humble, primitive steppingstones to higher life, microbes display superpowers that so-called “higher” forms of life depend on. Here are some recent examples.
Never Say Forever
So-called “forever chemicals” known as PFAS (poly-fluoroalkyl substances) have been in the news as a pollution concern because they resist breakdown for decades in the soil and water. UC Riverside says that our lust for industrial applications comes at a price:
Chlorinated PFAS are a large group in the forever chemical family of thousands of compounds. They include a variety of non-flammable hydraulic fluids used in industry and compounds used to make chemically stable films that serve as moisture barriers in various industrial, packaging, and electronic applications.
The “unusually strong carbon-to-fluorine bonds” in these compounds make them resistant to natural decomposition. Yujie Men’s team at UCR recently found two species of bacteria, Desulfovibrio aminophilus and Sporomusa sphaeroides, that know how to break those bonds.
“What we discovered is that bacteria can do carbon-chlorine bond cleavage first, generating unstable intermediates,” Men said.
“And then those unstable intermediates undergo spontaneous defluorination, which is the cleavage of the carbon-fluorine bond.”
The team believes that providing these naturally occurring bacteria with nutrients like methanol in groundwater could increase their numbers. If they are not present, contaminated water could be inoculated with the bacteria. Why try to imitate their chemistry prowess when they are already at work doing what is needed? Just pamper them and PFAS can disappear.
The UCR team published their award-winning findings in Nature Water, but the bacteria are the deserving ones for a prize. This discovery adds to other abilities of bacteria to degrade pollution:
Microbes have long been used for biological cleanup of oil spills and other industrial pollutants, including the industrial solvent trichloroethylene or TCE, which Men has studied.
But what’s known about using microorganisms to clean up PFAS is still in its infancy, Men said. Her discovery shows great promise because biological treatments, if effective pollutant-eating microbes are available, are generally less costly and more environmentally friendly than chemical treatments. Pollutant-eating microbes can also be injected into difficult-to-reach locations underground.
While not an excuse to pollute, the findings give hope for cleaning our messes with gifted microbes.
Proficient Sorters
Some of the rare earth elements (REE) that are high in demand these days are difficult to separate. Again, a gifted bacterium is able to sort them better than humans can, announced researchers at Penn State. A protein in a bacterium may help pave the way for “green tech” with less cost.
Rare earth elements, like neodymium and dysprosium, are a critical component to almost all modern technologies, from smartphones to hard drives, but they are notoriously hard to separate from the Earth’s crust and from one another.
Penn State scientists have discovered a new mechanism by which bacteria can select between different rare earth elements, using the ability of a bacterial protein to bind to another unit of itself, or “dimerize,” when it is bound to certain rare earths, but prefer to remain a single unit, or “monomer,” when bound to others.
Instead of requiring toxic chemicals to do the separation, bacteria equipped with the LanM protein may be able to do it cleanly and quickly. The news item says that this bacterium lives on buds of English oak trees. Its ability to discriminate similar elements is very precise:
“This was surprising because these metals are very similar in size,” Cotruvo said. “This protein has the ability to differentiate at a scale that is unimaginable to most of us — a few trillionths of a meter, a difference that is less than a tenth of the diameter of an atom.”
Nature has reported on Penn State’s welcome discovery.
Mercury Impacts Earth
Concerned about mercury in your tuna and other seafood? Bacteria are coming to the rescue here, too. Scientists at Oak Ridge National Laboratory warn of the dangers of methylated mercury:
Methylmercury is a neurotoxin that forms in nature when mercury interacts with certain microbes living in soil and waterways. It accumulates at varying levels in all fish — particularly large predatory fish such as tuna and swordfish — and, when consumed in large quantities, can potentially cause neurological damage and developmental disorders, especially in children.
While microbes are involved in the formation of the toxin, scientists at Oak Ridge have discovered two species of methanotrophic bacteria that can degrade it.
Bacteria called methanotrophs feed off methane gas and can either take up or break down methylmercury, or both. Methanotrophs are widespread in nature and exist near methane and air interfaces, and both methane and methylmercury are usually formed in similar anoxic, or oxygen-deficient, environments.
To single out how and which methanotrophs perform demethylation, the ORNL-led team — along with methanotroph experts from the University of Michigan and Iowa State University — investigated the behavior of many different methanotrophs and used sophisticated mass spectrometry to analyze methylmercury uptake and decomposition by these bacteria. They discovered that methanotrophs such as Methlyosinus trichosporium OB3b can take up and break down methylmercury, while others such as Methylococcus capsulatus Bath only take up methylmercury.
In either case, the bacteria’s interactions can lower mercury toxicity levels in water.
The work is published in the open-access journal Science Advances by the AAAS. Perhaps safe tuna sandwiches are in our future, thanks to microbes.
Gut Helpers
A health partner inside our GI tract that many of us never heard of is named Akkermansia muciniphila. After enjoying a tuna sandwich, we depend on this little bacterium that lives inside us to avoid metabolid disorders. Here’s what it does for us, according to Phys.org’s report on findings at Duke University:
A. muciniphila can make up as much as 3 to 5% of the biota found in stool. It is present in wild animals, and its abundance in humans seems critical for healthy physiological functions, as abnormal levels are associated with immune disorders, pregnancy complications, cancer, neurological disorders and every kind of metabolic disease.
This gut germ helps regulate lipid biosynthesis and cholesterol levels. Would evolution generate as many redundant machines as this bacterium possesses?
A. muciniphila is known to use mucins as its preferred nutrient source. Mucins are large, highly glycosylated proteins that comprise the bulk of the intestinal mucus lining. The study found that, despite having the capability to produce a wide range of glycoside hydrolase enzymes, estimated to be around 60, only a few are needed to degrade intestinal mucins. This redundancy means that even if there were a mutation in one or most of these genes, the organism would still have the ability to survive.
Learn more about this essential microbe in Nature Microbiology.
Ocean Fertilizer
Another microbe — this one a cyanobacterium — performs a vital function for life in the seas. New Scientist describes how it changes its behavior depending on light levels.
These bacteria don’t just provide food for other organisms, they also turn nitrogen from the atmosphere into chemicals that other photosynthetic organisms can use. They fertilise vast areas of the ocean that would otherwise be too poor in nutrients for anything to grow, says [Ulrike] Pfreundt.
“It’s the living fertiliser for the oceans, essentially,” she says. “They provide a very large part of the nitrogen that is fixed in the ocean, and a whole lot of other organisms that sequester CO2 depend on this nitrogen.”
Our world could not function without microbes such as these, and uncountable numbers of additional species remain to be discovered. They are far from being mere primitive steppingstones to complex life. Without their engineering prowess to degrade harmful substances and provide nutrients for others, large organisms — animals and plants — could not exist. This elevates the evidence for intelligent design beyond cells and individuals to the entire biosphere.
Tuesday 27 June 2023
John Money:a brief history.
John Money
John William Money (8 July 1921 – 7 July 2006) was a New Zealand American psychologist, sexologist and professor at Johns Hopkins University known for his research on human sexual behavior and gender.
Working with endocrinologist Claude Migeon, Money established the Johns Hopkins Gender Identity Clinic, the first clinic in the United States to perform sexual reassignment surgeries.[1] Money advanced the use of more accurate terminology in sex research, coining the terms gender role and sexual orientation.[2][3] Despite widespread popular belief, Money did not coin 'gender identity'.[4] Money pioneered drug treatment for sex offenders in order to extinguish their sex drives.[5] He began testing anti-androgen medications on offenders as early as 1966, which yielded successful results.[6]
Starting in the 1990s, the work and research conducted by Money has been subjected to significant academic and public scrutiny. A 1997 academic study criticised Money's work in many respects, particularly in regard to the involuntary sex-reassignment of the child David Reimer, and Money's sexual abuse of Reimer and his brother when they were children.[7][8] Some of Money's sessions involved Money forcing the two children to perform sexual activities with each other, which Money then photographed.[9][10] David Reimer lived a troubled life, eventually committing suicide at 38; his brother died of an overdose at age 36.[11][12]
Money's writing has been translated into many languages and includes around 2,000 articles, books, chapters and reviews. He received around 65 honours, awards and degrees in his lifetime.[2]
File under "well said" XCIV
"We have just enough religion to make us hate, but not enough to make us love one another."
Jonathan Swift
The Hindu/Muslim rivalry:a brief history.
Hindu–Islamic relations
Interactions between the followers of Islam and Hinduism began in the 7th century, after the advent of the latter in the Arabian Peninsula. These interactions were mainly by trade throughout the Indian Ocean. Historically, these interactions formed contrasting patterns in northern and southern India. In the north, there is a long-standing historical influence from Muslim rulers and Christian rulers dating back to the Delhi Sultanate of the 13th century. The patterns of relationship between Hindus and Muslims have been different between north and south India. While there is a history of conquest and domination in the north, Hindu-Muslim relations in Kerala and Tamil Nadu have been peaceful.[1] However, historical evidence has shown that violence had existed by the year 1700 A.D.[2]
In the 16th century, the Mughal Empire was established. Under the Mughals, India experienced a period of relative stability and prosperity.[3] The Mughals were known for their religious tolerance, and they actively patronized the arts and literature. During the Mughal era, Indian art and culture thrived, with the construction of grand monuments such as the Taj Mahal and the Red Fort. While the Mughals fostered religious harmony and cultural advancements and nurtured Hindu scholars, poets, and artists, facilitating a dynamic cultural interchange that enriched both Islamic and Hindu traditions, there were instances of religious conflicts between the Mughals and the Rajput over control of territories. Aurangzeb was criticized for his policies of religious intolerance towards Hindus.[4][5]
During the 17th to 19th centuries, India was ruled by the British, who introduced a policy of divide and rule to maintain their control over the country.[6][7][8] The British also introduced a system of separate electorates, which further exacerbated the divide between the Hindu and Muslim communities.[9][10] The Indian Rebellion of 1857, also known as the First War of Independence, was a major uprising against British rule in India. The rebellion was fueled by a range of grievances, including economic exploitation, social and religious discrimination, and political oppression.[11][12][13] While the rebellion was not solely based on religious tensions between Hindus and Muslims, these tensions did play a role in fueling the conflict. During the rebellion, there were instances of both Muslim and Hindu soldiers and civilians fighting together against the British, as well as instances of conflict between the two communities.[14][15][16]
Islam and Hinduism share some ritual practices, such as fasting and pilgrimage, but their views differ on various aspects. There are also hundreds of shared ritual spaces, called dargahs (literally, “doorway” or “threshold”), for Hindus and Muslims. These mark shrines for revered Muslim (frequently Sufi) leaders and are visited by both Muslims and Hindus. Their interaction has witnessed periods of cooperation and syncretism, and periods of religious discrimination, intolerance, and violence. As a religious minority in India, Muslims are part of the Indian culture and have lived with Hindus for over 13 centuries. Despite the longtime assertion that the origins of Muslim-Hindu tensions were greatly attributed to 19th Century British colonial rule in India, it has been argued that Britain had little influence on constructing the religious identities of Islam and Hinduism in the region and that divisions existed beforehand as well.[17] For example, 18th-century Mughal–Maratha Wars. Ajay Verghese argues that the Hindu-Muslim conflict in India can be better understood by analyzing the historical relationship between the two communities. He contends that precolonial India was marked by a fluidity of religious identity and that religious boundaries were not always clear-cut. This led to a degree of intermingling between Muslims and Hindus, but also created conditions for tension and conflict.[2]
Ps. What I would add is that most of these "religious" rivalries are really political rivalries masquerading as religious rivalries.
Darwinists' problem is not with design but the designer.
New Study Reveals How the Shape of My Nose Arose
It is ironic that Charles Lyell, whose seminal, if flawed, work in geology—the barrister is sometimes known as the father of modern geology—positively influenced Charles Darwin’s development of evolutionary theory—the young Darwin read Lyell’s book as he sailed around the world in the H.M.S. Beagle—and who helped to arrange for Darwin’s first formal, if awkward, presentation of his theory—an event precipitated by Wallace’s Ternate letter—was one of the last of the intelligentsia to accept Darwin’s new formulation of Epicureanism, known as evolution.
At one point an exasperated Darwin asked Lyell—it always comes down to metaphysics—if he believed “the shape of my nose was designed?” If Lyell did think so then, Darwin added, “I have nothing more to say.” The infra-dignitatem, or infra-dig for the irreverent, argument, which insisted that it was beneath the dignity of the Creator to stoop so low as to dwell in the details of the world, had been promoted by no less than the father of natural theology John Ray and Platonist Ralph Cudworth, and in Darwin’s day was in full swing. Its influence on the young Darwin was clear in the naturalist’s early notebooks, and here in his appeal to Lyell. One look at one’s nose is all one needs to know about origins. Obviously we evolved. Now, a century and a half later, science finally has its say in the matter.
A new Study out of, appropriately enough, England, now reveals the underlying genetic details that influence the shape of our noses. It seems there are four genes that influence the width and length of our olfactory device and, as the press release informs us, “The new information adds to our understanding of how the human face evolved.”
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