Correcting professor Dave on "Darwin devolves"

 Answering Farina on Behe’s Work: Darwin Devolves

Jonathan McLatchie

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.

An interlude

 

Correcting professor Dave on the "edge of evolution"

 Answering Farina on Behe’s Work: The Edge of Evolution

Jonathan McLatchie

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

David Coppedge

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.

Which came first minds or maths

 

John Money:a brief history.

 John Money

Wikipedia

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]

The Reagan revolution: a brief history.

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

Wikipedia

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

Cornelius G Hunter

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.”

We are free to acknowledge free moral agency

 Free Will: What Are the Reasons to Believe in It?

Denyse O'Leary

University of Missouri psychology professor Kennon Sheldon’s message is neatly summed up in an opening statement: “Regardless of whether humans do or don’t have free will, psychological research shows it’s beneficial to act as if you do.”

The author of Freely Determined: What the New Psychology of the Self Teaches Us About How to Live (Basic Books, 2022) responds to philosophers who say that we do not have free will:

All my life, I’ve struggled with the question of whether humans have ‘free will’. It catalysed my decision to become a psychologist and continues to inspire my research to this day, especially as it relates to the kinds of goals people set for themselves, and the effects of goal-striving on people’s happiness and wellbeing.

I’ve come to the conclusion that people really do have free will, at least when it is defined as the ability to make reasoned choices among action possibilities that we ourselves think up…

Regardless of who is correct in this debate, my work has led me to a second conclusion that I consider even more important than whether we have free will or not. It’s that a belief in our own capacity to make choices is critical for our mental health. At the very least, this belief lets us function ‘as if’ we have free will, which greatly benefits us.

KENNON SHELDON, “THE THREE REASONS WHY IT’S GOOD FOR YOU TO BELIEVE IN FREE WILL,” PSYCHE, JUNE 15, 2023 

An Obvious Problem

Now, the obvious problem with his approach is that if we believe in free will simply because that belief is supposed to be good for our mental health, then we really don’t believe in it.

A simple example suffices: We sometimes hear that being optimistic is also better for mental health. In one sense, that’s true. If we focus on the positive things, our lives feel more pleasant and that is bound to be better for mental health. But what if we have no good reason for optimism? What if we live under an active volcano that shows signs of erupting? Optimism (“it probably won’t really happen this year”) could delay evacuation past the point of no return.

So let’s look back at free will in this light: If we believe that we have it — and that belief is true — we are empowered to deal with temptations and addictions, firm in the knowledge that we really can cast the deciding vote for our best possible outcome. But if free will is not true, we are setting ourselves up for delusion if we succeed and needless disappointment and misery if we fail. Not only that but we are participating in an unfair system where people are judged and punished for unwise or bad behavior that they cannot really help. So functioning “as if” we have free will turns out not to be very good at all.

“A Better Person”?

Sheldon goes on to say,

The second reason why I consider belief in free will to be beneficial is that it makes you a better person. Studies in social psychology show clearly that, if people become convinced that they have no free will, there can be negative effects on their ethical behaviour.

SHELDON, PSYCHE, 2023

Perhaps that’s true but it amounts to saying that perhaps we should be deluded for our own good. Even though delusions are said to be bad for us… Is there any light at the end of this tunnel? 

Sheldon offers a reason why some thinkers deny free will:

You might wonder why anyone would choose to believe in determinism, given the clear negative effects of this belief? There are several possible reasons. Some people might think that determinism is the most scientific and intellectually sophisticated position to take, and they like feeling smarter than others.

SHELDON, PSYCHE, 2023

Well, if science matters, the good news is that neuroscience provides sound reasons to believe in free will. As Stony Brook neurosurgeon Michael Egnor has pointed out, the work of neuroscience pioneer Benjamin Libet established that we certainly have “free won’t” — the ability to choose not to do something:

[W]hat he found was, when you made a decision to push the button [in a psychological experiment], you still had the brain wave that preceded the decision by half a second. But when you decided to veto pushing the button, there was no new brain wave at all. It was silent in terms of brain waves. But you did make the decision to veto. So he said that it wasn’t so much that you have free will but you have free won’t. That is, you have the ability to decide whether or not you are going to comply with what your brain is urging you to do. And that compliance is not material. It’s not a brain wave. It’s immaterial.

MICHAEL EGNOR, “HOW A NEUROSCIENTIST IMAGED FREE WILL (AND “FREE WON’T”),” MIND MATTERS NEWS, MARCH 19, 2020 

What Quantum Mechanics Shows

Physicist Marcelo Gleiser also notes that science does not really support the view that free will is an illusion: “[T]he mind is not a solar system with strict deterministic laws. We have no clue what kinds of laws it follows, apart from very simplistic empirical laws about nerve impulses and their propagation, which already reveal complex nonlinear dynamics.” In any event, quantum mechanics shows that nature is indeterminate at the fundamental level and that the observer’s decision of what to measure plays a role in what happens. One outcome is that a number of younger thinkers accept free will as consistent with the evidence.

In other words, we can accept free will based on the evidence. There is no particular need to think that it might be a possibly pleasant delusion.

A theory of devolution?

 Is Adaptation Actually a Fight to Stay the Same?

Andrew McDiarmid

On a new episode of ID the Future, host Casey Luskin talks with Eric Anderson on location at this year’s Conference on Engineering and Living Systems (CELS). The two discuss an intriguing new engineering-based model of bounded adaptation that could dramatically change how we view small-scale evolutionary changes within populations of organisms. In presenting his argument for natural selection, Charles Darwin pointed to small changes like finch beak size and peppered moth color as visible evidence of an unguided evolutionary process at work. Many have adopted this perspective, quick to grant the Darwinian mechanism credit for micro-, if not macro-, evolution. But Anderson and other attendees at the CELS conference are starting to promote a different view. “We need to stop saying organisms are partly designed,” says Anderson. “We need to view them as deeply designed and purposeful, active and engaged in their environments, and capable of adapting within their operating parameters.” To get a fascinating glimpse of this novel approach to biology, download the podcast or listen to it here .

On professor Dave and the bacterial flagellum

 Answering Farina on Behe’s Work: Bacterial Flagella

Jonathan McLatchie

In a previous article, I began a series of four responses to YouTuber Dave Farina (aka “Professor Dave”) about his video reviewing Dr. Michael Behe’s three books. Here I will turn my attention to Mr. Farina’s comments regarding bacterial flagella.

In relation to the flagellum, the video complains about Behe’s “dishonest usage of terminology pertaining to machinery,” including phrases such as “outboard motor,” “drive shaft,” “universal joint,” “bushings,” and “clutch and braking system.” In reality, this terminology is used widely in the scientific literature. It’s not unique to Behe. On the contrary, in reference to flagella, the literature is full of such terms including “motor”,1 “drive shaft,”2 “universal joint,”3“bushing,”4 and “clutch.”5 The word “machine” itself has a wide circulation.6 Is Farina going to charge the entire flagella research community with dishonesty as well?

Co-option Scenarios for the Origins of Bacterial Flagella

According to the video, “A flagellum that merely twitches instead of rotating smoothly would also produce motion and thus could be selected for.” But a type IV pilis, which enables twitching motility (a form of bacterial translocation over moist surfaces), is very different from a flagellum. Twitching motility occurs by extension, tethering, and retraction of the type IV pilus, which functions in a manner akin to a grappling hook. A flagellum, on the other hand, rotates as it is driven by a proton motive force across the cell membrane. The assembly mechanisms of pili and flagella are also quite different.

The video complains that Behe fails to acknowledge the existence of alternative flagellar systems that are simpler than the model system found in Salmonella species and Escherichia coli. However, the fact that an alternative system lacks a specific component that is essential in another system does not mean that the former lacks an alternative mechanism for achieving the same outcome. The most robust concept of irreducible complexity understands it as a property of a system that is contributed to by multiple subfunctions, the removal of one of which causes the overall system to effectively cease performing its job. Note that each individual subfunction could, in principle, be performed by multiple protein components. Likewise, a single protein component could perform more than one of those subfunctions. Furthermore, the identity of the specific components performing each respective subfunction could differ from one organism to the next. It is therefore not the identity of the structural parts that is important in an irreducibly complex system, but rather the essential functions that need to be performed in order for a higher-level objective to be realized.

Moreover, pointing to homologues of flagellar proteins does not undermine the argument from irreducible complexity, since co-opting those proteins to produce a flagellar system requires multiple co-incident changes in order for the new system to be realized. For example, flagellar-specific proteins would not confer a selective advantage until incorporated into the flagellar system. But the necessary proteins that serve roles in other systems will not become incorporated into the flagellar system before these flagellar-specific proteins arise. This is quite aside from the need to have complementary protein-protein binding interfaces, as well as a choreographed assembly system to ensure that the proteins are assembled in the appropriate order.

Resurrecting a Flagellum

In a 2016 article at Evolution News, Behe asks, 

W]hy doesn’t [Kenneth Miller] just take an appropriate bacterial species, knock out the genes for its flagellum, place the bacterium under selective pressure (for mobility, say), and experimentally produce a flagellum — or any equally complex system — in the laboratory? (A flagellum, after all, has only 30-40 genes, not the hundreds Miller claims would be easy for natural selection to rapidly redesign.) If he did that, my claims would be utterly falsified. But he won’t even try it because he is grossly exaggerating the prospects of success.

The video by Farina comments, 

hilariously, [Behe] is oblivious to the fact that this precise experiment was carried out the year before. Here’s the paper. Gene deletion produced two strains of bacteria with no flagellum. They then introduced selective pressure for motility by depleting the nutrients in the colony. Within 96 hours, both strains had regenerated flagellar motility by a pathway involving two successive point mutations in genes that served other purposes.

However, the paper that Farina cites7 does not do this at all. Not for the first time with this video, I wonder if he has in fact read the paper. All that the researchers deleted was the flagellar master switch protein, FleQ, in Pseudomonas fluorescens. After a few days of incubating the bacterial cells on Petri dishes, they reacquired their ability to grow flagella. The genetic basis for this reactivation of the flagella is that another master switch protein, NtrC, that is a structurally similar homolog of FleQ — responsible for turning on genes involved in nitrogen metabolism — already had the ability, to some extent, to cross-bind to the promoter usually bound by FleQ. When produced in excess, as a result of a broken regulator, NtrC was thus able to drive flagellar synthesis. As a consequence of this mutation, the bacterial cell lost its ability to regulate its nitrogen metabolism genes. An article in The Scientist describes this research:

But while the re-evolved flagella enabled the bacteria to access food supplies at the farthest reaches of the Petri dish, the ability came at a price. ‘The bacteria that became much better at swimming were much worse at nitrogen regulation,’ said Johnson. However, she added, ‘sometimes the advantage can be so great that it’s worth paying that cost because otherwise you die.’

Thus, contrary to the Farina video’s claims, this paper does not document the de novo evolutionary origins of a bacterial flagellum at all — far from it. In fact, Behe has already addressed the paper here.

The Waiting Times Problem

In 2004, Michael Behe and David Snoke published a paper in the journal, Protein Science.8 About this paper, Farina has three complaints. The first complaint is that, “Behe and Snoke found that the target sequence did actually evolve, in population sizes and timeframes that are entirely realistic, and if anything, quite small compared to real-world populations. The paper literally proves them wrong and they somehow count it as a win anyway.” Farina mentions Behe’s expert testimony at the 2005 Kitzmiller v. Dover trial:

When questioned about his 2004 paper, Behe tacitly acknowledged that the population size in their model was orders of magnitude smaller than real-world bacterial populations, which had the effect of vastly underestimating the rate at which such “irreducible” traits could evolve… In one striking exchange, Behe acknowledged a paper which indicated that there are more prokaryotes in a single ton of soil than in his model population, and that there is a lot more than one ton of soil on Earth.

However, this objection stems from Farina’s misreading of the paper. As Behe himself explains in the very transcript that Farina cites, “forming a new disulfide bond might require as few as two point mutations. But forming other multi-residue features such as protein-protein binding sites might require more.” The graph below (figure 6 of the paper) shows Behe and Snoke’s estimate of the time to fixation (along the y-axis) versus the number of substitutions needed for a new feature to evolve (along the x-axis). On the top axis, values for the needed population sizes are given. The point is that, as the number of needed co-dependent mutations increases, so too does the needed population size and waiting time to fixation.

As Behe and Snoke explain in the paper, in a scenario where three substitutions are required for a novel feature to arise, a population size of roughly 1011 individuals is necessary for it to become fixed over the course of 108 generations (108 generations is marked as a horizontal bar on the figure). If the complex trait in question requires even more substitutions, it would require considerably more time. If six mutations were needed, the average population size required for it to become fixed in 108 generations would be on the order of 1022 individuals. Given that 1030 is a plausible estimate of the number of microorganisms on the entire planet9, these numbers become prohibitive very quickly.

The second complaint is that, “In their model, Behe and Snoke permitted only single-base mutations and natural selection — no recombination, no duplications beyond the initial presumed one, no other evolutionary changes.” But the authors explicitly say that “Because the model presented here does not include recombination, the results can be considered to be most applicable to a haploid, asexual population.” Nonetheless, they do note in the conclusion to their paper that “the results also impinge on the evolution of diploid sexual organisms,” since large multicellular organisms have much, much smaller population sizes than bacteria. If the evolution of complex features is difficult for microorganisms (with their massive population sizes and short generation turnover times), how much more so for large animals? Though one might counter, in the case of diploid sexual species, that recombination allows for neutral mutations to occur separately in a population and to later combine by sexual recombination, Christiansen et al. have shown, in a paper published in Theoretical Population Biology, that “Recombination lowers the waiting time until a new genotypic combination first appears, but the effect is small compared to that of the mutation rate and population size” (emphasis added).10

Finally, Farina complains that “They also specified a pre-determined target sequence and only considered the simulation to have been ‘successful’ if that specific target evolved.” But this is incorrect. Rather, the paper provides estimates for how many organisms would be required, and over how long a time frame, for multiple co-dependent mutations (none of which by themselves confers an advantage) to become fixed in a population.

Notes

Minamino T, Imada K, Namba K. Molecular motors of the bacterial flagella. Curr Opin Struct Biol. 2008; 18(6):693-701.

Johnson S, Furlong EJ, Deme JC, Nord AL, Caesar JJE, Chevance FFV, Berry RM, Hughes KT, Lea SM. Molecular structure of the intact bacterial flagellar basal body. Nat Microbiol. 2021; 6(6):712-721.

Kitao A, Hata H. Molecular dynamics simulation of bacterial flagella. Biophys Rev. 2018; 10(2):617-629.

Yamaguchi T, Makino F, Miyata T, Minamino T, Kato T, Namba K. Structure of the molecular bushing of the bacterial flagellar motor. Nat Commun. 2021 Jul 22;12(1):4469.

Blair KM, Turner L, Winkelman JT, Berg HC, Kearns DB. A molecular clutch disables flagella in the Bacillus subtilis biofilm. Science. 2008;320(5883):1636-8.

Sowa Y, Berry RM. Bacterial flagellar motor. Q Rev Biophys. 2008 May;41(2):103-32.

Taylor TB, Mulley G, Dills AH, Alsohim AS, McGuffin LJ, Studholme DJ, Silby MW, Brockhurst MA, Johnson LJ, Jackson RW. Evolution. Evolutionary resurrection of flagellar motility via rewiring of the nitrogen regulation system. Science. 2015; 347(6225):1014-7.

Behe MJ, Snoke DW. Simulating evolution by gene duplication of protein features that require multiple amino acid residues. Protein Sci. 2004; 13(10):2651-64.

Whitman WB, Coleman DC, Wiebe WJ. Prokaryotes: the unseen majority. Proc Natl Acad Sci U S A. 1998; 95(12):6578-83.

Christiansen FB, Otto SP, Bergman A, Feldman MW. Waiting with and without recombination: the time to production of a double mutant. Theor Popul Biol.1998;53(3):199-215.

How hubris sinks the unsinkable.

 Shades of Titanic — Probing the Wreck of the Unsinkable Enlightenment

David Klinghoffer

The week that the submersible Titan was revealed to have been instantaneously flattened on its way down to the wreck of the Titanic, David Berlinski spoke with Jame Lileks and Peter Robinson on Ricochet about the wreck of the Enlightenment. Much like the Titanic, and a bit like the Titan, so much was expected at the glorious launch of the experiment in human reasoning — yet down it went to disaster, not least in the 20th century with its horrors.

Writing yesterday in the Wall Street Journal, Peggy Noonan suggested that the story of the Titanic haunts us in part because its demise came two years before the start of the century’s great catastrophe, World War I: “the reason the Titanic endures is that there was an immediate connection in the public mind with the Great War. The 20th century was to be the century of progress.” Interesting connection. Science and reason were supposed to transform the world for the good instead of soaking it in gore. In his books — Human Nature and his latest, Science After Babel — Berlinski probes the causes behind that failure. “A cold wind is blowing,” the mathematician and philosopher observes, revealing how “fragile” the Enlightenment dream really was. The conversation with Dr. Berlinski begins at 31:45.

Gentleman thief?

Another conspiracy theory become just plain conspiracy?

A wonder of ancient engineering

Speaking of ID...

 How to Discuss Intelligent Design with Friends

Evolution News

On a classic episode of ID the Future, Tom Gilson — author, senior editor with The Stream, and occasional contributor to Evolution News — tackles the question of how best to discuss intelligent design (ID) with friends and associates skeptical of the theory. There is so much misinformation about the theory of ID that many well-intended people reject not the actual theory but a silly caricature, a straw man. They don’t realize that ID is not an argument from ignorance but an inference to the best explanation based on positive evidence for design and negative evidence against competing materialistic explanations. It involves abductive reasoning, a standard mode of reasoning in the historical sciences. When in conversation with someone who understands none of this, Gilson suggests using the Socratic method and, in particular, posing three questions designed to turn down the heat, promote dialogue, and draw the other person into a discovery of the actual theory of intelligent design. Try it with friends, colleagues, and family members! Download the podcast or listen to it here

No Jehovah,no Justice,no Peace here's why.

   The pseudo-religious bureaucracies of this age have given religion/worship a bad name.Likely many would agree with Indian statesman Jawarlal Nehru when he said that the spectacle of organised religion in India and elsewhere filled his mind with horror,and that it seems almost always to stand for superstition,ignorance,bigotry,exploitation,the vested interest of entrenched elites and the like.But long before Nehru now famous religious leader/teacher Jesus Christ had some choice words for the leaders of the dominant religion of his time and place: Matthew23:13KJV "But woe unto you scribes and pharisees,!For ye shut up the kingdom of heaven against men:For ye go in yourselves,neither suffer ye them that are entering to go in.Woe unto you,scribes and pharisees,hypocrites!For ye devour widows houses,and for a pretence make long prayer:Therefore ye shall receive the greater damnation.

   Two things to note in Jesus censure 1)The hypocrisy of these religious leaders separated them from God 2)Their hypocrisy turned others away from the God's truth.How?The bible suggest two ways 1)Matthew23:15ESV "Woe to you, scribes and pharisees,hypocrites!For you travel across sea and land to make a single proselyte,and when he becomes a proselyte,you make him twice as much a child of hell as yourselves."

  2)2Peter2:2 "Many will follow their sensuality,and because of them the way of truth will be blasphemed."

 On account of its bringing his name and kingdom into disrepute pseudo-religion in general and Christendom in particular is in the cross hairs of Jehovah's war machine.The bible tells us that soon pseudo-religion will pay a heavy price for its political meddling, greed and hypocrisy.Revelation19:2"because His judgments are trued and righteous,e

because He has judged the notorious prostitutef

who corrupted the earth with her sexual immorality;

and He has avenged the blood of His •slaves

that was on her hands.g"

There are of course those who urge an abandonment of the quest for the creator God.They claim that accepting a status of cosmic orphanhood and making new gods of chance,necessity,matter and self are the only way to free ourselves from the abuses of the past.To begin with militant atheist have been every bit as unsuccessful on liberating their flock from the racism,nationalism,militarism and greed that have always been the main triggers of conflict as theistic pseudo-religionists have.Additionally there are practical reasons that universal justice and peace are simply not possible apart from Jehovah's assertion of his rightful sovereignty over the globe

 1)Only Jehovah as creator can claim unimpeachable legitimacy as a global governor,there plain and simply is no man or group of men(or angels for that matter)that can be trusted with that kind of authority,apart from the fact that it is a universally accepted legal principle that the creator be recognised as legal owner of what he has produced.Jehovah is totally independent of his creation and is thus morally incorruptible,What could anyone possibly offer him as a bribe?A new luxury car?Tickets to the big game?A case of champagne perhaps?With him in charge mankind will finally have a ruler worthy of utter confidence and loyalty.

2)Jehovah is not learning on the job the very wisest among us human or superhuman is only just beginning to understand how to get the most out of Jehovah's creation Jehovah has been there and done that so to speak.No more guessing games with people's lives,health and prosperity.

3)Only Jehovah has the might/smarts to bring leviathan and his hordes to heal.There is a reason that the criminal and otherwise sociopathic elements of society always seem ahead of the agencies charged with countering them.Why instead they have consistently succeeding in corrupting the wider society.Some might be prepared to acknowledge behind the scenes influences on the human level.They might be less willing to acknowledge the Bible's warning that the corruption of the main institutions of our global civilisation extends to the realm of the superhuman see Ephesians6:12.Until our civilisation is rid of these malignant minds human and superhuman advances in technology will continue to be more of a curse than a blessing.

  4)Only Jehovah can guarantee infallible judgement.Not only is he first hand witness to all wrongdoing and right doing he can read hearts.This means that under his rule not only will we finally have a ruler worthy of our complete trust we will have fellow servants worthy of our complete trust.Picture a society with no need for

police,soldiers,spies,security personnel of any kind,courts,magistrates,judges,jails,locks,keys.Impossible you say?Certainly in the atheistic universe we could entertain no such hope.

 5)Justice delayed is Justice denied the saying goes.What about when justice never arrives?The number of unsolved crimes on the files of this world's law enforcement agencies is in the tens of thousands some of these are horrific indeed heartbreaking murders.What about those who have been erroneously convicted crimes they never committed What about past victims of state sponsored injustice.Jehovah is not only mankind's only hope of a just future he ALONE can counter the injustices of the past.

What is a hominid?

 Fossil Friday: To Be or Not to Be Homo

Gunter Bechly

The fossil hominin Homo habilis was described 1964 by famous paleoanthropologist Louis Leakey and his colleagues from the 1.9 million year old Olduvai Gorge locality in Tanzania (Leakey et al. 1964). Even though this taxon is only known from a small and highly incomplete collection of isolated bone fragments, it has become the crucial hominid species that supposedly bridges the gap between the ape-like australopithecines and our human genus Homo. Because of the association of the bones with stone tools it has been named Homo habilis, which means “handy man.” However, its alleged position as transitional form is quite controversial (also see Gibbons 2011, Luskin 2007, 2015), and even the validity of the species has been questioned because it seems to be “a wastebasket taxon, little more than a convenient recipient for a motley assortment of hominin fossils” (Tattersall 1992). Homo habilis certainly was not the ancestor of later Homo species, because he is too recent and coexisted with early Homo ergaster, thus leaving a distinct gap between australopithecines and the genus Homo (Hawks et al. 2000).

A Dubious Attribution?

Since its small brain volume falls within the range of australopithecines, several scientists very early doubted the attribution of H. habilis to the genus Homo. Also the hand and feet are more ape-like and exhibit clear adaptations for climbing. Walker & Shipman (1996: 132) said that H. habilis is even more ape-like than Lucy, and Spoor et al. (1994) even remarked in their comparative study of hominid labyrinthine morphology that “The specimen Stw 53 provisionally attributed to H. habilis, differs from all other hominids … [and] shows greatest similarities to the pattern observed for large cercopithecoids …[which] suggest that Stw53 relied less on bipedal behaviour than the australopithecines”. Holly Smith (1994) concluded from the comparative study hominid patterns of dental development that gracile australopithecines and H. habilis remain classified with African apes. Wood & Collard (1999a, 1999b, 2001), Collard & Wood (2007, 2015) could show that in none of the crucial character H. habilis is closer to Homo than to Australopithecus.

An Assignment Rejected

Therefore, they suggested that H. habilis should be transferred to the genus Australopithecus, which was also supported by Hartwig-Scherer (1999) and Schwartz & Tattersall (2015). This assignment was rejected by Harcourt-Smith (2007) based on postcranial characters, while Berger et al. (2015) agreed that “postcranial remains of H. habilis appear to reflect an australopith-like body plan”. Spoor et al. (2015) found that the mandible of H. habilis is remarkably primitive and more similar to Australopithecus afarensis. They also reconstructed a slightly larger brain volume for the holotype and clarified the definition of the taxon Homo habilis, but cautioned that the results raise questions about its phylogenetic relationships. It is also very much contradicting Darwinian expectations, that the oldest specimens of Homo habilis, such as the 2.3 million year old specimen no. AL 666-1, possess more advanced characters than the younger holotype specimen OH 7, which lived more than a half million years later. One of the most striking contradictions is the fact that the bones of Homo habilis and many other animals were found in the context of so-called “butchering sites” together with stone tools, and in the neighbourhood of rock circles that very much look like the stone huts still used by modern nomadic tribes of the region (Leakey 1972: 24).

These rock circles and huts demonstrably originated at the same time as Homo habilis, which obviously suggests that this ape-like creature was rather the animal prey of contemporary human hunters than a human ancestor and producer of stone tools. Otherwise, we would have to believe highly implausible hypothesis that an ape-like creature with an ape-sized brain and climbing adaptations built stone huts like modern humans. Anyway, the majority of evolutionists of course ignored all such doubts among the experts and blindly embraced Homo habilis as a cherished “missing link” without asking inconvenient and potentially career-threatening questions.

Reference

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

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

Gibbons A 2011. Who Was Homo habilis—And Was It Really Homo? Science 332(6036), 1370–1371. DOI: https://doi.org/10.1126/science.332.6036.1370

Harcourt-Smith WEH 2007. The Origins of Bipedal Locomotion. pp. 1483–1518 in: Henke W, Tattersall I (eds). Handbook of Paleoanthropology. 3 vols. Springer, Berlin, 2069 pp.

Hartwig-Scherer S 1999. “Homo” habilis ab jetzt kein Mensch mehr. Studium Integrale Journal 6(2), 85–87. http://www.si-journal.de/index2.php?artikel=jg6/heft2/sij62-5.html

Hawks J, Hunley K, Lee S-H & Wolpoff M 2000. Population Bottlenecks and Pleistocene Human Evolution. Molecular Biology and Evolution 17(1), 2–22. DOI: https://doi.org/10.1093/oxfordjournals.molbev.a026233

Holly Smith B 1994. Patterns of Dental Development in Homo, Australopithecus, Pan, and Gorilla. American Journal of Physical Anthropology 94(3), 307–325. DOI: https://doi.org/10.1002/ajpa.1330940303

Leakey MD 1972. Olduvai Gorge: Volume 3, Excavations in Beds I and II, 1960-1963. Cambridge University Press, Cambridge (UK), xix+306 pp.

Leakey LSB, Tobias PV & Napier JR 1964. A new species of the genus Homo from Olduvai Gorge. Nature 202(4927), 7–9. DOI: https://doi.org/10.1038/202007a0

Luskin C 2007. Paleoanthropologists Disown Homo habilis from Our Direct Family Tree. Evolution News August 9, 2007. https://evolutionnews.org/2007/08/paleoanthropologists_disown_ho/

Luskin C 2015. As a Taxonomic Group, “Homo habilis” Is Challenged in the Journal Science. Evolution News September 9, 2015. https://evolutionnews.org/2015/09/as_a_taxonomic_/

Schwartz JH & Tattersall I 2015. Defining the genus Homo. Science 349(6251), 931–932. DOI: https://doi.org/10.1126/science.aac6182

Spoor F, Wood B & Zonneveld F 1994. Implications of early hominid labyrinthine morphology for the evolution of human bipedal locomotion. Nature 369(6482), 645–648. DOI: https://doi.org/10.1038/369645a0

Spoor F, Gunz P, Neubauer S, Stelzer S, Scott N, Kwekason A & Dean MC 2015. Reconstructed Homo habilis type OH 7 suggests deep-rooted species diversity in early Homo. Nature 519(7541), 83–86. DOI: https://doi.org/10.1038/nature14224

Tattersall T 1992. The Many Faces of Homo habilis. Evolutionary Anthropology 1(1), 33–37.

Walker A & Shipman P 1996. The Wisdom of the Bones: In Search of Human Origins. Knopf, New York (NY), 368 pp.

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

Natural antifreeze vs. Darwin.

 Blood Viscosity and Freezing Temperatures — A Titanic Problem

Emily Reeves

Editor’s note: With the RMS Titanic tragically back in the news this week, we thought of this article from last year by biochemist Emily Reeves. She notes a question about the character Jack in the movie Titanic, and addresses a fascinating problem in marine biology.

Dr. Gregory Sloop is a Montana physician who knows a thing or two about the cardiovascular system. He has an article in the journal BIO-Complexity highlighting the sleek design of the Antarctic icefish that allows it to live in super-cold waters without freezing to death.

Icefish, aka the family Channichthydiae, survive at 0oC in the Southern Ocean by maintaining blood viscosity at the set point of 3.27 centipoise — a level nearly identical to human blood. They do this without hemoglobin, which is the primary determinant of human and other red-blooded animals’ blood viscosity.

Since icefish don’t have hemoglobin, how do they maintain blood viscosity? Also, how do they breathe? Turns out they maintain viscosity at freezing temperatures primarily by using a special type of glycoprotein: the antifreeze protein. And because oxygen has a higher solubility at lower temperatures, icefish don’t need an oxygen transport molecule like hemoglobin. 

Why Jack Froze

In case you were wondering, blood viscosity is the technical reason why Jack (Rose’s buddy aboard the Titanic) froze in less than 23 minutes, but icefish can survive for 15 years in water of a freezing temperature. Viscosity increases at lower temperatures, and at 0oC human blood reaches a viscosity that is not compatible with life. This is because hemoglobin as a protein is not able to keep viscosity low enough at freezing temperatures. But the antifreeze protein can (think: custom design).

While a viscosity too high is incompatible with life, a low viscosity is also unsuitable for sustaining life. This is because a properly functioning cardiovascular system must have optimized laminar flow and low vascular resistance, which can be achieved only through coordinated control of blood viscosity and specification of vascular geometry.

Stop Criticizing Icefish

Dr. Sloop says icefish have been criticized for expending nearly 22 percent of their basal metabolic rate pumping their hemoglobinless blood compared to at most 5 percent in temperate fish. But he reminds his readers that’s just the cost of doing business in the chilly — well technically, freezing — waters of the Southern Ocean.

Sloop also emphasizes that everything about the icefish is like a custom-fitted suit — appropriate for niche needs. Features included for dealing with the extreme cold are a high-output, low resistance vasculature where the diameter of muscle capillaries is 2-3 times larger than those of other fish.

These fish also have a heavy heart which delivers a larger stroke and therefore higher volume. Together these features enable a high-output, high-velocity, low-pressure, and low-resistance circulation.

Truly, every part of these incredible creatures is optimized for cold. Could all these custom changes be the result of random mutation? Dr. Sloop thinks that is very unlikely. What do you say?

Continuing to rethink the unthinkable

Yet another shot at explaining black holes