The Unintelligent Designer - Another Error-Prone Bungle to Compensate for a Bungled Design

Physiology

William Heath Robinson

Peacekeeper cells protect the body from autoimmunity during infection | Biological Sciences Division | The University of Chicago

A significant issue with our immune system is that it is poorly "designed." If it were truly the product of an intelligent designer, as creationists claim, that designer would hardly be competent enough to design a simple household item, let alone a complex biological system.

Because our immune system is so disorganized and inefficient, multiple layers of complexity have evolved to mitigate its worst shortcomings. However, these added layers themselves remain prone to errors, as they reflect the same flawed foundation. The central problem arises because the immune system must balance two contradictory requirements: it needs to be sensitive enough to identify and eliminate genuine threats, yet not so sensitive that it mistakenly attacks the body's own tissues.

While an omnipotent, supremely intelligent designer should have easily resolved such a contradiction, the reality is that our immune system frequently fails on both counts. It often permits pathogens and parasites to invade, and it also frequently turns against the body itself, leading to autoimmune diseases such as lupus, diabetes, multiple sclerosis, arthritis, and kidney or liver failure, among numerous other debilitating conditions that cause immense suffering.

Like the whimsical contraptions created by cartoonist William Heath Robinson — complex machines built from objects originally intended for entirely different purposes - the mammalian immune system is not designed top-down from a clear blueprint. Rather, it's built up gradually from one makeshift adaptation piled onto another, each new solution attempting to compensate for the shortcomings of earlier ones. Eventually, this process results in a ramshackle system so intricate that its complexity itself creates new opportunities for failure. Such complexity is not indicative of intelligent, purposeful design, which would typically favour simplicity and efficiency. Instead, it reflects an ad hoc, utilitarian approach driven by evolutionary constraints and an inability to anticipate future challenges.

And of course, this embarrassment for creationism is made worse by the fact that, according to Michael J. Behe, pathogenic parasites such as E. coli and Plasmodium falciparum are examples of irreducible complexity, so are, in creationist circles, unarguable 'proof' of intelligent design, so the immune system is allegedly designed by the designer of these pathogens to protect us from them.

It seems creationists have no difficulty in believing the same designer would design parasites to make sick, then design a system to protect us from its pathogenic designs, and even though that system doesn't work very well, it is nevertheless evidence of supreme intelligence.

New Book - Twenty Reasons To Reject Creationism: Understanding Evolution

This book looks at the ID/Creationism vs evolution debate from multiple angles and analyses why the science of evolutionary biology refutes the childish notion of intelligent design.

I wrote it because, creationism is dangerous. It replaces evidence-based knowledge with superstition and creates the impression that cultural prejudice and ignorant incredulity are better measures of reality than observation, analysis and reason.

Now more than ever we need our politicians, law-makers and captains of industry to be able to make sense of complex data and use it to make wise decisions, not dismiss it as based on ‘flawed’ concepts and the result of conspiracies designed to turn people away from the ‘truth’ as revealed in ancient texts declared to be holy. As is clearly shown in the Discovery Institute’s Wedge Document and in the wilful misrepresentations of science its fellows dutifully feed to the largely scientifically-illiterate public, there is a hidden political agenda that depends on people believing falsehoods and thinking anti-science is some sort of moral crusade to restore Western civilisation to a notional ideal golden age in pre-renaissance Europe when the slave trade was booming and witch-burning was a regular spectacle in the local town square.

This was a time when people like Copernicus and Galileo would be persecuted and deprived of their livelihood and even their life, for revealing the empirical evidence that Earth orbits the sun – not because they had falsified the data but because the data falsified the Bible. The sacred superstitions, even though empirically proved wrong, had to be defended against the truth as revealed by the physical data.

Refuting Creationism - Teenage Puberty, 15,000 Years Before 'Creation Week'

Human life in the European Pleistocene

AI generated (ChatGPT4.0)

Reconstruction of Romito 2, a 16-year-old teenager with a form of dwarfism who lived 11,000 years ago in southern Italy.

Drawing by: Olivier Graveleau.

Realities of Ice Age puberty - University of Victoria

The thing about this study from a creationist perspective is its two-fold refutation of basic creationist dogma.

Firstly, it is not so much that teenagers in the last Ice Age went through puberty at pretty much the same age as modern teenagers, despite an assumed improvement in the diet of modern people compared to that of a Pleistocene hunter-gatherer, but that there were actually human teenagers 15,000 years before creationist dogma says that there was an Earth.

Secondly, there is the fact that the remains of these teenagers are available for analysis, when the mythical global genocidal flood, so beloved of creationists, should have swept it all away.

But counter-factual creationism is never perturbed by scientific evidence because, as all creationists know, scientific evidence is either lies made up by evil scientists, or just plain wrong as 'proven' by the fact that creationist cult leaders say so and it doesn't conform with what a bunch of scientifically-illiterate Bronze Age pastoralists who thought the universe consisted of a small flat planet with a dome over it, made up in their origin myths.

Malevolent Designer - How Zebra Fish Can 'Heal' Blindness - And Humans Can't

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[right caption]

Zebrafish photoreceptor cells stimulated with blue light show correct electrical activity. The picture was taken using the microscope that was custom-built for this study.

Seeing the Future: Zebrafish Regenerates Fully Functional Photoreceptor Cells and Restores Its Vision — Center for Regenerative Therapies Dresden (CRTD) — TU Dresden

Readers may remember my recent post about how researchers have discovered that zebra fish can heal a transected spinal cord, and why creationists need to explain why their putative omnibenevolent designer apparently chose not to give this ability to all vertebrates, including its supposedly favourite special vertebrate, humans
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Was it because it prefers to watch paraplegics suffer or because it forgot how to?

Well, now we have more evidence, if you accept the childish creationist 'intelligent [sic] design, nonsense, of how the same fish, have apparently been given another ability that would have hugely benefitted humans and other animals - they can repair damage to their visual receptors in their eyes, in other words, they can heal blindness.

A believer in intelligent [sic] design, must accept that, since their designer god apparently knew how to give this ability to zebra fish, it knew how to give it to all vertebrates and made the conscious decision not to.

Malevolent Designer News - How Creationism's Divine Malevolence Gave A Fish The Ability To Mend a Damaged Spine, But Not Humans

Top: fluorescently labeled cells in the spinal cord of a zebrafish recovering one week after injury.
Bottom: recovery four weeks after injury.

Zebra fish in the lab of Robin Tanguay at Oregan Stae University.

Photo: Lynn Ketchum

Zebrafish use surprising strategy to regrow spinal cord – Washington University School of Medicine in St. Louis

Just as amputees can't regrow a lost limb, so spine-injured patients can't repair a damaged spine, and yet, several species of amphibian can grow new limbs and Zebra fish can grow a new spinal cord.

Which leaves intelligent [sic] design creationists to explain why, if their putative designer can give some species the ability to regrow a lost limb or repair a transected spinal cord, he chose not to give that ability to his supposedly favourite, 'special' creation, humans.

But of course, those are not the only abilities and systems that could have been better in humans if the same designer designed other animals with superior abilities and systems:

Birds of prey have a vastly superior visual acuity to humans; birds in general have a much more efficient respiratory system which enables then to fly at heights at which we would be unconscious for lack of oxygen. Many animals have a vastly superior sense of hearing to what we have, and bats have a better immune system. Elephants and sharks both rarely get cancer, and so the list goes on.

Unintelligent Designer News - Is Creationism's Incompetent Designer Also A Racist?

National Aboriginal Community Controlled Health Organization (NACCHO) logo

Torres Strait family on Thursday Island.

Image source: Let’s Learn about the Torres Strait Islands, Oz Publishing.

Lupus is more common and severe in Aboriginal and Torres Strait Islander peoples. Learning why is crucial

The realisation that Australian Aboriginal people and Torres Strait Islanders are not only more prone to the autoimmune condition lupus but suffer a more severe form of it than Europeans, would be an embarrassment for creationists if they were aware of it and understood the implications for some of their most cherished superstitions.

It has long been known that Africans and Asians are more prone to lupus, but this study shows that Australian Aboriginal people and Torres Strait Islanders may have been singled out for special attention, if you believe these things are designed by creationism's putative designer.

In general terms. lupus is a failure if the immune system in that something triggers it to turn against the person instead of protecting them. As an example of design, it is an example of incompetence in the extreme. It's like creating an army to protect a country, only to have it turn on the people of that country and start massacring them, because it's mistaken them for invaders. This might be a feature of mal-formed banana republics, but it's hardly a sign of a well-designed civilised society.

But, of course, creationists have been primed to blame these design failures, like parasites, on the scientifically nonsensical 'genetic entropy' and 'devolution', but if that were to blame for the greater suffering of these Austronesians that would mean that they have 'devolved' further than other humans and so must have been subject to more 'genetic entropy'. But all humans have been around for the same length of time, whether you accept the science or believe the childish magic creation just a few thousand years ago, so what would cause this accelerated rate of 'genetic entropy' in a regional population?

Refuting Creationisn - Understanding Consciousness - No God(s) Required

Study reveals how an anesthesia drug induces unconsciousness | MIT News | Massachusetts Institute of Technology

One of creationism beloved gaps in which they try to shoehorn their ever-shrinking little god, is a scientific explanation for consciousness.

It is true that we don't yet have an explanation for consciousness but no gap in the scientific understanding of anything has ever been filled by a god, or to be more scientific, by an unproven, undetectable supernatural entity, so it's a strangely unrealistic view of science that any (or all) of creationism's gaps, real or imaginary are going to be the exception to the rule and somehow, one day, science is going to reveal the locally popular god in all its glory, having managed to hide itself for millennia.

Being inherently unfalsifiable, of course, there is no possible scientific methodology that could reveal any specified god as the indisputable cause of any phenomenon, so creationist belief that this is about to happen is delusional.

But back to the problem of consciousness.

Unintelligent Design - Why Do Males Have Useless Nipples? - It's Evolution, Naturally!

New mathematical model sheds light on the absence of breastfeeding in male mammals - News and events, University of York

Ask an intelligent [sic] design creationists why males have nipples, and you'll get lots of evasion and avoidance but no answer beyond mutterings about an 'ineffable god', and 'not knowing the minds of the creator', betraying the religious underpinning of creationism.

So, why exactly do males have nipples?

The answer is, of course, evolution.

Creationism in Crisis - How The Human Heart Evolved As Humans Adapted To An Active Life-Style

Study on architecture of heart offers new understanding of human evolution - Swansea University

According to research by an international team from Swansea University, Swansea, Glamorgan, Wales and the University of British Columbia, Okanagan, Canada, there is evidence that the human heart has evolved to facilitate the more active life-style of humans compared to their closest relatives, as they diversified.

Humans typically have a much more active life-style with a higher resting metabolic rate compared to chimpanzees. We also have larger brains. As hunter-gatherers, we typically walked and ran far more often and for much longer than do the other apes and we needed to lose the excess body heat this activity generated, so we needed a more hemodynamic heart able to meet those needs, which meant adaptations to changes in the twisting of the left ventricle (LV) - the chamber which pumps oxygenated blood around the body - during systole, and this meant a change in the degree of trabeculation inside the LV.

In the context of heart ventricles, what are trabeculae and what is their function? Trabeculae (also known as trabeculae carneae) are irregular ridges of muscle found on the inner walls of the ventricles of the heart. They play several important roles in the function of the heart:

1. Structural Support: Trabeculae carneae help reinforce the ventricular walls. Their irregular structure provides additional strength and prevents the walls from sticking together during contraction, thereby maintaining the heart's shape and integrity.
2. Facilitation of Blood Flow: The trabeculae carneae create a more turbulent flow of blood within the ventricles, which can help with the efficient mixing of blood and ensure a more thorough contraction and expulsion of blood from the ventricles during systole.
3. Conduction System: Some trabeculae carneae are involved in the conduction system of the heart. For example, the moderator band (a type of trabecula) in the right ventricle contains part of the right bundle branch of the bundle of His. This helps coordinate the contraction of the right ventricle by ensuring that the electrical impulses are transmitted efficiently.
4. Reduction of Blood Stagnation: By creating a complex surface within the ventricles, trabeculae carneae reduce the likelihood of blood stagnation, which can prevent clot formation and improve overall blood flow dynamics.

In summary, trabeculae carneae serve to strengthen the ventricular walls, enhance blood flow, support the heart's electrical conduction system, and reduce the risk of blood clots by preventing blood from pooling in the ventricles.

What is meant by 'ventricular twist'?

'Ventricular twist' refers to the complex motion of the heart's ventricles during the cardiac cycle, particularly during the contraction (systole) and relaxation (diastole) phases. This twisting motion is also known as 'ventricular torsion' or 'ventricular rotation.' Here’s a more detailed explanation:

Mechanics of Ventricular Twist

1. Twisting Motion During Systole: During systole, the ventricles contract to pump blood out of the heart. The base (the top part of the ventricles, near the atria) of the heart rotates in a counterclockwise direction (when viewed from the apex), while the apex (the bottom tip of the heart) rotates in a clockwise direction. This results in a wringing motion, similar to wringing out a wet towel.
2. Untwisting Motion During Diastole: During diastole, the ventricles relax and fill with blood. The previously twisted ventricles now untwist, helping to create a suction effect that aids in the efficient filling of the ventricles with blood.

Significance of Ventricular Twist

1. Efficient Blood Ejection: The twisting motion enhances the efficiency of the heart’s pumping action. By adding a rotational component to the contraction, the heart can expel blood more forcefully and completely.
2. Diastolic Suction: The untwisting or recoil of the ventricles during diastole contributes to the rapid filling phase. This elastic recoil generates a negative pressure that helps draw blood into the ventricles more efficiently.
3. Mechanical Synchrony: The coordinated twisting and untwisting ensure that the contraction and relaxation phases are well-synchronized, promoting optimal cardiac function and maintaining a steady and efficient blood flow throughout the body.
4. Clinical Relevance: Abnormalities in ventricular twist mechanics can be indicative of various cardiac pathologies, such as heart failure, myocardial infarction, or cardiomyopathies. Therefore, measuring and analyzing ventricular twist can provide valuable diagnostic and prognostic information.

Measurement of Ventricular Twist
Ventricular twist can be assessed using advanced imaging techniques such as speckle-tracking echocardiography (STE) or cardiac magnetic resonance imaging (MRI). These techniques allow for detailed visualization and quantification of the rotational mechanics of the heart.

In summary, ventricular twist is a crucial aspect of the heart’s mechanics, contributing to the efficient ejection and filling of blood in the ventricles. It is essential for maintaining optimal cardiac function and can be an important parameter in the assessment of heart health.

The team has shown there is a negative correlation between the degree of trabeculation and LV systolic twist. The inner wall of the LV of a healthy human heart is comparatively smooth. Their results are published in the journal Communications Biology and explained in a Swansea University News release:

An international research team from Swansea University and UBC Okanagan (UBCO) has uncovered a new insight into human evolution by comparing humans’ hearts with those of other great apes.

Despite humans and non-human great apes having a common ancestor, the former has evolved larger brains and the ability to walk or run upright on two feet to travel long distances, likely to hunt.

Now, through a new comparative study of the form and function of the heart, published in Communications Biology, researchers believe they have discovered another piece of the evolutionary puzzle.

The team compared the human heart with those of our closest evolutionary relatives, including chimpanzees, orangutans, gorillas, and bonobos cared for at wildlife sanctuaries in Africa and zoos throughout Europe.

During these great apes' routine veterinary procedures, the team used echocardiography—a cardiac ultrasound—to produce images of the left ventricle, the chamber of the heart that pumps blood around the body. Within the non-human great ape's left ventricle, bundles of muscle extend into the chamber, called trabeculations.

The left ventricle of a healthy human is relatively smooth, with predominantly compact muscle compared to the more trabeculated, mesh-like network in the non-human great apes. The difference is most pronounced at the apex, the bottom of the heart, where we found approximately four times the trabeculation in non-human great apes compared to humans.

Bryony Curry, first author
Centre for Heart, Lung and Vascular Health
School of Health and Exercise Sciences
University of British Columbia, Kelowna, BC, Canada.

The team also measured the heart's movement and velocities using speckle-tracking echocardiography, an imaging technique that traces the pattern of the cardiac muscle as it contracts and relaxes.

We found that the degree of trabeculation in the heart was related to the amount of deformation, rotation and twist. In other words, in humans, who have the least trabeculation, we observed comparatively greater cardiac function. This finding supports our hypothesis that the human heart may have evolved away from the structure of other non-human great apes to meet the higher demands of humans’ unique ecological niche.

Bryony Curry.

A human’s larger brain and greater physical activity compared to other great apes can also be linked to higher metabolic demand, which requires a heart that can pump a greater volume of blood to the body.

Similarly, Higher blood flow contributes to humans’ ability to cool down, as blood vessels close to the skin dilate—observed as flushing of the skin—and lose heat to the air.

In evolutionary terms, our findings may suggest selective pressure was placed on the human heart to adapt to meet the demands of walking upright and managing thermal stress.

What remains unclear is how the more trabeculated hearts of non-human great apes may be adaptive to their own ecological niches. Perhaps it’s a remaining structure of the ancestral heart, though, in nature, form most often serves a function.

Dr Aimee Drane, co-corresponding author
International Primate Heart Project
Cardiff Metropolitan University, Cardiff, UK
And Faculty of Medicine
Health and Life Sciences
Swansea University, Swansea, UK

The research team is grateful to the staff and volunteers who care for the animals in the study, including the teams at Tchimpounga Wildlife Sanctuary (Congo), Chimfunshi Wildlife Sanctuary (Zambia), Tacugama Chimpanzee Sanctuary (Sierra Leone), Nyaru Menteng Orangutan Rescue and Rehabilitation Center (Borneo), the Zoological Society of London (UK), Paignton Zoo (UK), Bristol Zoo Gardens (UK), Burgers’ Zoo (Netherlands) and Wilhelma Zoo (Germany).

Abstract
Although the gross morphology of the heart is conserved across mammals, subtle interspecific variations exist in the cardiac phenotype, which may reflect evolutionary divergence among closely-related species. Here, we compare the left ventricle (LV) across all extant members of the Hominidae taxon, using 2D echocardiography, to gain insight into the evolution of the human heart. We present compelling evidence that the human LV has diverged away from a more trabeculated phenotype present in all other great apes, towards a ventricular wall with proportionally greater compact myocardium, which was corroborated by post-mortem chimpanzee (Pan troglodytes) hearts. Speckle-tracking echocardiographic analyses identified a negative curvilinear relationship between the degree of trabeculation and LV systolic twist, revealing lower rotational mechanics in the trabeculated non-human great ape LV. This divergent evolution of the human heart may have facilitated the augmentation of cardiac output to support the metabolic and thermoregulatory demands of the human ecological niche.

Introduction
Mammals are a remarkably diverse class of vertebrates, capable of inhabiting every major biome on the planet. This diversity is associated with a vast range of environmental stressors and interspecific differences in posture and locomotion, creating very different hemodynamic challenges. Despite this remarkable diversity, the gross structure of the mammalian heart is highly conserved across species; retaining four chambers and a complete interatrial and interventricular septum¹.

Although the gross structure of the mammalian heart is conserved, interspecific features exist. For example, heart shape varies considerably across species, from broad and flat in whales to long and narrow in terrestrial ungulates2. Variation in the cardiac phenotype is also present among closely-related mammals², indicative of evolutionary divergence. While comprehensive data examining cardiac structure and function across the entire Hominidae taxon do not exist, preliminary work suggests that the left ventricle (LV) of adult male chimpanzees (Pan troglodytes) may be morphologically distinct from that of humans³. Prominent myocardial trabeculations, characterized by protrusions of the endocardium into the LV cavity with intertrabecular recesses, were previously observed in adult male chimpanzees³. This trabeculated phenotype differs from the relatively smoother ventricular wall typically observed in healthy humans⁴, suggesting that there may have been species-specific selective pressures on the heart during the evolution of Hominidae³.

Cardiac morphology and function are closely linked⁵; therefore, the discrete structural attributes of the chimpanzee and human LV likely coincide with differences in systolic and diastolic ventricular function. Such interspecific cardiac phenotypes may be the result of selection for the hemodynamic demands associated with each species’ ecological niche (i.e., the habitat and the role a species plays within an ecosystem). Indeed, previous data has shown that resting metabolic rate⁶, physical activity and daily locomotion⁷ are far greater in humans in comparison with other great apes, and so it is not surprising that cardiac output is also comparatively higher in humans³. The larger cardiac output in humans is likely supported by comparatively greater LV systolic and diastolic function (e.g., myocardial rotation and deformation), including LV twist³. LV twist, which is dependent upon the helical angulation of the aggregated cardiomyocytes^8,9,10, is characterized by counter-directional rotation of the LV base and apex during systole. Together with the velocity of LV untwisting during diastole, LV twist helps facilitate efficient filling and ejection of the ventricle, especially during periods of heightened metabolic and thermoregulatory demand^11,12.

The functional advantages associated with a LV capable of greater twist and untwisting velocity, combined with the preliminary data in adult male chimpanzees³, prompt the hypothesis that the human heart has diverged from a trabeculated ancestral phenotype to support the specific metabolic and thermoregulatory demands of the human niche. To test this hypothesis, we compared LV structure across all extant great apes using 2D echocardiography and further explored trabeculation in a subset of post-mortem chimpanzee (Pan troglodytes) hearts. We then compared LV rotation and deformation between human and non-human great apes to explore whether the trabeculated phenotype is associated with differences in LV systolic and diastolic functional mechanics. Our findings point to evolutionary divergence of the human LV away from the phenotype of all other non-human great apes, which may have had important implications for cardiac function in early humans.

Discussion (part of)

[…]

Collectively, the findings of this study support evolutionary divergence of the human LV away from a trabeculated ancestral phenotype, towards a ventricular wall with a proportionately greater compact myocardium. We propose that this adaptive evolution occurred to support the requirements of the human ecological niche, including an augmented cardiac output to facilitate sustained bipedal physical activity, a larger brain, and the associated metabolic and thermoregulatory demands.

Fig. 1: Comparison of left ventricular trabeculation in great apes.

The bullseye plots represent the trabecular:compact (T:C) ratio for each segment of the left ventricle. The outer layer of the bullseye plots represents the basal segments, the middle and innermost layers represent the midpapillary and apical segments of the left ventricle, respectively. Red segments correspond to an average T:C ratio of >2; orange segments correspond to an average T:C ratio >1.5–2; yellow segments correspond to an average T:C ratio of >1–1.5; green segments correspond to an average T:C ratio of >0.5–1; blue segments correspond to an average T:C ratio of <0.05. Echocardiographic images of the parasternal short-axis at the apex are shown at end-diastole. *No data were available for the basal or midpapillary segments in the orangutans due to artifact from laryngeal air sacs. †These T:C ratios compare favorably with other reports in healthy human cohorts, ranging from 0.2 to 0.9^65,66. ‡Anatomical labels have been provided in accordance with the conventional guidelines for cardiac chamber quantification by the American Society of Echocardiography and European Association of Cardiovascular Imaging⁵². However, we note that this clinical convention does not align with the recognized anatomical approach and may result in confusion across disciplines—see ref. ⁶⁷ for further clarification.

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Fig. 2: Graphical representation of the trabecular:compact (T:C) ratio for each segment of the left ventricle in chimpanzees.

The outer layer of the bullseye plots represents the basal segments, the middle and innermost layers represent the midpapillary and apical segments of the left ventricle, respectively. Red segments correspond to an average T:C ratio of >2; orange segments correspond to an average T:C ratio >1.5–2; yellow segments correspond to an average T:C ratio of >1–1.5; green segments correspond to an average T:C ratio of >0.5–1; blue segments correspond to an average T:C ratio of <0.05. Infant age class includes individuals of ≤4 years of age, juveniles between 5–7 years of age, sub-adults between 8-11 years of age and adults ≥12 years of age.

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Fig. 3: Comparison of left ventricular morphology and mechanical indices of ventricular function between chimpanzees and humans.

Shortening along the long axis of the left ventricle (i.e., longitudinal strain) and deformation at the apex (i.e., apical circumferential and apical radial strain) were averaged across a mixed-sex, adult cohort of chimpanzees (n = 136) and represented in maroon. Blue reflects the deformation patterns of a mixed-sex, adult human cohort (n = 34). Dashed line represents aortic valve closure. Gray shading to the left of dashed line represents systole and white represents diastole.

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Fig. 4: Relationship between markers of left ventricular (LV) function and apical trabeculation in the extant Hominidae taxon.

a Peak LV systolic apical rotation, shown in red, in a mixed-sex, adult cohort of humans (male n = 18, female n = 16), chimpanzees (male n = 59, female n = 51), bonobos (male n = 2, female n = 4), gorillas (male n = 4, female n = 6) and orangutans (male n = 10, female n = 6). b Peak LV systolic twist, shown in green, and (c) peak diastolic untwisting velocity, shown in blue, in a cohort of humans (male n = 18, female n = 16), chimpanzees (male n = 47, female n = 43), bonobos (male n = 1, female n = 3) and gorillas (male n = 4, female n = 5). Analyses of LV twist and untwisting velocity were not possible in all individuals, nor any of the orangutans due to artifacts from laryngeal air sacs, hence the reduced sample size. The exponential plateau curve is shown, with the 95% confidence bands represented by the dotted line. The mean and standard error are shown in black for each species.

Curry, B.A., Drane, A.L., Atencia, R. et al.
Left ventricular trabeculation in Hominidae: divergence of the human cardiac phenotype. Commun Biol 7, 682 (2024). https://doi.org/10.1038/s42003-024-06280-9

Copyright: © 2024 The authors.
Published by Springer Nature Ltd. Open access.
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)

No crumbs of comfort there for creationists as the authors attribute everything to evolution by natural selection as humans diverged from the other great apes, nor is there any hint of a doubt that such an evolutionary divergence occurred.

The interesting thing from a biologists point of view is how the changes to the human heart reflect changes in our life-style as we adopted an upright gait and a hunter-gatherer life-style, necessitating running and walking long distances with additional demands on our heart to cope with the additional oxygen required and to dissipate the excess heat these activities generated, in addition to the increased demands our large brains were already imposing on our circulatory and thermoregulatory systems.

More work is now needed to understand whether the retention of this degree of trabeculation in the other apes has a benefit or whether it has simply been retained from a common ancestor. If the former, what evolutionary trade-off has there been for humans in losing these benefits?

Malevolent Designer News - How Creationism's 'Intelligent Designer' COULD Have Designed Us To Survive A Heart Attack - But Chose Not To

Zebra fish, Danio rerio

Source: Encyclopædia Britannica

Why can zebrafish regenerate damaged heart tissue, while other fish species cannot? – @theU

If you're foolish enough to believe the claims of creationist frauds that we were intelligently designed by an omniscient, omnibenevolent god, then the work of four researchers at Utah University, USA, should be a cause for concern.

They have shown how the zebra fish is 'designed' to survive a heart attack by repairing the damaged cardiac muscle unlike humans and other mammals who replace the damaged muscle with non-functional scar tissue, which can cause several life-limiting problems for those who survive the initial attack.

Just to recap; a heart attack is caused when an artery supplying blood to the heart muscle becomes blocked, so depriving the muscle of oxygen. Unless cleared very quickly, the muscle will die and will be replaced with scar tissue which lacks the contractile ability of cardiac muscle. How much this affects the functioning of the heart will depend on how much muscle was damaged.
How the zebra fish heart is able to repair itself is the subject of an open access paper in the journal Biology Open and of a news release from Utah University:

Evolution News - An Atlas Of The Human Ovary Shows Common Ancestry of Mammals

Ovarian follicle

Human ovarian follicle

First atlas of the human ovary with cell-level resolution is a step toward artificial ovary | University of Michigan News

This piece of research caught my eye, not so much because it refutes creationism with its daft notion of the special creation of humans as separate from all the other animals but because it's reminiscent of the research I used to be involved with in my first profession - a research technician in Oxford University's Department of Human Anatomy.

The research our small group was doing involved the hormonal control of reproduction in guinea pigs, which involved preparing light microscope slides of sections of guinea pig ovaries, and later on, transmission electron micrographs of ovarian tissues.

Like humans, guinea pigs have oestrus cycles where they periodically shed eggs from their ovaries regardless of whether they have mated or not. This is unlike some other mammals which ovulate soon after mating, stimulated to do so by the act of mating. Unlike human females, guinea pigs are only receptive for two or three days before and just after they ovulate. Outside that receptive period, they have a closure membrane that makes penetration impossible.

Unintelligent Design - RuBisCO Is Slowly Evolving - And Becoming Even More Embarrassing For Any Creationist Who Understands It

Photo by Kumiko SHIMIZU on Unsplash

The world’s most prolific CO₂-fixing enzyme is slowly getting better | University of Oxford

The world’s worst enzyme, ribulose-1,5-bisphosphate carboxylase/oxygenase, or RuBisCo as it is known, has featured in these blog posts several times and it described in my book, The Unintelligent Designer: Refuting the Intelligent Design Hoax as an example of the lack of intelligence in biological systems, and, as such, why it would be a major embarrassment to creationists - if they understood it.

Briefly, RuBisCo is one of the most ancient enzymes known and became an essential component of photosynthesis early on in the history of life on Earth when the first cyanobacteria evolved the ability to use the energy from sunlight to fix the carbon in atmospheric carbon dioxide (CO₂) to build the sugar glucose. Eventually, these photosynthesising cyanobacteria became incorporated into plant cells as the chloroplasts to produce the green plants at the base of most food chains. Because it is so inefficient, it quickly became probably the most abundant enzyme on Earth, making up with quantity what it lacked in quality.

But, evolution, unlike good intelligent design, is a one-way, utilitarian process in which whatever works better than preceded it will be retained and will provide the next basis for further evolution, because evolution has no mechanism to scrap a bad design and start again as any backward step will inevitably be worse, so will be quickly eliminated.

Tell me all about RuBisCo and why it's so inefficient.

RuBisCo, or ribulose-1,5-bisphosphate carboxylase/oxygenase, is an enzyme crucial for the process of carbon fixation in plants, algae, and some bacteria. It catalyzes the first major step of the Calvin cycle, which is the primary pathway for carbon dioxide fixation in photosynthesis. Despite its importance, RuBisCo is often considered inefficient for several reasons:

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Information current at January 2022

Creationism in Crisis - A Mystery In Plant Evolution - 125 Million Years In The Making In That Long Pre-'Creation Week' History Of Life On Earth

A bushel of tomatoes at the CSHL Uplands Farm.

A 'Ginormous' tomato produced by an unregulated CLV3 gene.

From Ciren D, Zebell S, Lippman ZB (2024)

An evolutionary mystery 125 million years in the making | Cold Spring Harbor Laboratory

In an example of one of those lovely gaps in the record of the evolution of a species into which creationists try to shoehorn their ever-shrinking and increasingly homeless little god, there is something about the evolution of tomatoes and Arabidopsis thaliana that scientists can't yet explain.

But the problem for creationists is that this gap is somewhere in the evolutionary history of these plants that occurred almost 125 million years before creationism’s god decided to create a small flat planet with a dome over it to keep the water above the sky out, centred on the Middle East, in what creationists like to call 'Creation Week'.

The problem comes from the fact that what creationists think is a science and history text book was written by ignorant people who knew nothing of the world outside their small part of it and who had no idea about the history of the planet or of life on it, so they wrote an imaginative story to fill the gap in their knowledge and understanding, and, quite understandably, got almost every aspect of it complete wrong.

And of course, they would never have imagined that one day someone almost as ignorant as they were, would gather their tales into a book and declare it to be the inerrant word of a god - an idea that would be hilarious if it wasn't taken seriously by adults who can become dangerously violent when their superstition is questions.

The mystery that Cold Spring Harbor Laboratory (CSHL) biologists have uncovered is that sometime during the last 125 million years, tomatoes and Arabidopsis thaliana plants experienced an extreme genetic makeover. Just what happened remains unclear. But the mystery surrounds CLV3, a gene key to healthy plant growth and development.

CLV3 controls the growth of fruit in these plants and, if uncontrolled will result in large, even gigantic, fruits, so there is an evolutionary trade-off between a few large fruits and lots of smaller fruits. The mystery is just how and why this balance was achieved differently in two distantly-related plants.

As the CSHL press release explains:

Unintelligent Design - The Heath-Robinson Workaround For A Design Fault In The Immune System

A dendritic cell, one of the cells of the innate immune system where cGAS plays a major role.

©EPFL/iStock photos (Design Cells)

The “switch” that keeps the immune system from attacking the body - EPFL

A Machine for Testing Golf Drivers - William Heath-Robinson

A characteristic of designs by creationism's putative intelligent designer, is the needless complexity which often arises because earlier solutions were suboptimal and either didn't work very well or tended to cause problems that needed to be mitigated with another layer of (often suboptimal) complexity.

This is also a characteristic of systems 'designed' by a mindless natural process with no power or mechanism for scrapping a suboptimal design and starting again and no ability to predict the future and design for problems which will arise later.

In fact, what creationists think is evidence of a supreme intelligence, more often seems to resemble the designs of the British cartoonist and eccentric designer, William Heath-Robinson, who was famous for his machines designed to solve every-day problem, which were invariably far more complex than they need have been, and which incorporated everyday objects such as umbrellas, full coal-scuttles for counter-weights, lengths of knotted string and stepladders balanced on upright pianos to give them enough height. Take away any of these unlikely components and the whole machine would fail, in an almost perfect metaphor for how evolution can exapt pre-exiting structures from other processes and structures for novel functions, to give the appearance of irreducible complexity.

And yet they work, or at least look as though they would if anyone ever made one.

An example of a Heath-Robinson machine in mammalian 'design' was revealed by a scientists working at the Swiss École polytechnique fédérale de Lausanne (EPFL), who have discovered how the body prevents the immune system from attacking itself.

But, as the very many auto-immune diseases show, this system is far from perfect and frequently fails, sometime with serious, even fatal, consequences.

But the whole immune system is only needed because something designed pathogens such as bacteria, viruses and other parasites, apparently to attack us and make us sick in the first place. Parasites are a source of conflict for creationists who have to believe both that the putative designer god is the only entity capable of designing living things, and that something else created parasites because their god wouldn't do such a thing, and both that their god is omnipotent, but powerless against that other designer.

So, what is this mechanism the EPFL researchers have discovered?

Their findings are the subject of an open access paper in Nature and is explained in an EPFL news release:

Unintelligent Design News - Why Women Are More Prone To Lupus Than Men - Evolution, Or Does Creationism's God Just Hate Women More?

The classic 'butterfly rash' of systemic lupus erythematosus (SLE)

Lupus and other autoimmune diseases strike far more women than men. Now there's a clue why

In my days as an operational paramedic, I once had to move a 26 your old women to hospital because lupus had made her so ill her blood pressure was below the safe level to maintain her renal function.

It was so low I couldn't even sit her up to carry her down stairs without her losing consciousness, so I had to run a couple of units of IV fluid into her to bring it up enough to make it safe to move her. She really was profoundly ill and at death's door. But such was the nature of the profession that, having delivered her safely to hospital and handed her over to the care of doctors and nurses, that was the end of my role in her care, so I never heard the outcome.

The autoimmune condition, lupus erythematosus, is caused by a malfunction of the immune system in which something triggers it to turn against the sufferer's own body instead of the invasive pathogens from which it has evolved to protect us. Although, of course, a creationist would hotly dispute the idea that a system like our immune system evolved at all, and would insist that it was intelligently [sic] designed by their favourite, evidence-free, supernatural deity without whom nothing can be created, presumably because they believe chemistry and physics don't know how to behave without a magic god telling them.

But an intelligently-designed immune system would only malfunction and turn against the person it is supposedly designed to protect if it were either incompetently designed or malevolently designed and is doing what it was designed to do - randomly increasing the suffering in the world. The evidence is that lupus is far more common in women than in men by a ratio of 9:1, which begs the question, does the designer just hate women more than men or was he more diligent when designing men's immune system then when designing women's?

The answer, as anyone who understands anatomy and physiology and particularly, evolution, will tell you, is that as an evolved system, we can expect compromises and a lack of perfection because evolution is a utilitarian process with no foresight and no reverse gear, so we are stuck with a sub-optimal immune system that evolved in an ancient ancestor, maybe even a pre-vertebrate ancestor. Certainly, all known vertebrates have one, and some, like that of bats, is far superior to ours.

Now a team of researchers at Stanford University School of Medicine, Stanford, CA, USA have worked out why lupus is far more common in women than men. Ther results are published, open access, in Cell and explained in a Stanford Medical news release. But first, a little AI background:

Closing In On Abiogenesis - How Amino Acids Become Peptides in Water Droplets - No Magic Required

Professor R. Graham Cooks has studied the chemistry of water droplets for decades, discovering insights into cancer detection, drug discovery and early Earth chemistry.

Purdue University file photo/Andrew Hancock

A tripeptide (example Val-Gly-Ala) with green marked amino end (L-valine) and blue marked carboxyl end (L-alanine)

Chemistry professor R. Graham Cooks expands research of water droplet interfaces that offer the secret ingredient for building life - Purdue University Department of Chemistry

One of the puzzles of how the earliest proteins were built from amino acids was that the reaction of joining two amino acids together is a condensation reaction in which a molecule of water is eliminated when the -C-OH of one amino acid binds to the H₂N-C- of the other amino acid in what is known as a peptide bond:

-C-OH + H₂N-C- → -C-NH-C + H₂O;
but how could this happen in an aqueous solution?

In 2022, Professor R. Graham Cooks' team at Purdue University found the answer: It is due to the peculiar properties at the surface of droplets of water. Because of the way electrostatic forces align the water molecules at the surface, it behaves as though it is extremely dry, and highly acidic. These conditions provide the perfect conditions for a condensation reaction to occur, resulting in a peptides.

Droplets of water are everywhere in nature, from the spray of breaking waves, the splash of raindrops, waterfalls, trickling streams to aerosols of water in clouds and fog.

And Professor Cooks's team at Purdue have now shown that these conditions also occur at the macro, centimeter scale as water evaporates on, for example rocks or the margins of hydrothermal pools. They have also shown that these reactions, in the presence of oxazolones (produced by the dehydration of amino acids) preserve the chirality of the peptides so the resulting peptides are 'L' enantiomers, as found in all living organisms.

As the Purdue University press release says:

The study adds to the body of evidence that the surface of water drops represents a uniquely active physical and chemical system. Present are very high electric fields and extreme acidity that drives dehydration of amino acids to form peptides. Studies of the chemistry at water droplet interfaces offer new insights into the early stages of life's chemical evolution.

Significance

This study provides experimental evidence identifying oxazolones as the key intermediates in prebiotic peptide synthesis. These compounds yield the dipeptides upon reaction with water and generate tripeptides in the presence of other amino acids. These key steps in protein formation occur in pure water droplets. Amino acid chirality is preserved in forming the oxazolone and the addition of amino acids during peptide chain extension shows a strong chiral preference, viz. the aqueous droplet chemistry represents a simple route to chirally pure polypeptides. A direct connection between this intermediate and the dipeptide isomer, oxazolidinone, is demonstrated by simple hydration/dehydration. The oxazolone/oxazolidinone-mediated mechanism also occurs in macroscopic wet–dry cycling, establishing a strong connection between macroscopic and microscopic peptide synthesis.

Abstract

Peptide formation from amino acids is thermodynamically unfavorable but a recent study provided evidence that the reaction occurs at the air/solution interfaces of aqueous microdroplets. Here, we show that i) the suggested amino acid complex in microdroplets undergoes dehydration to form oxazolone; ii) addition of water to oxazolone forms the dipeptide; and iii) reaction of oxazolone with other amino acids forms tripeptides. Furthermore, the chirality of the reacting amino acids is preserved in the oxazolone product, and strong chiral selectivity is observed when converting the oxazolone to tripeptide. This last fact ensures that optically impure amino acids will undergo chain extension to generate pure homochiral peptides. Peptide formation in bulk by wet-dry cycling shares a common pathway with the microdroplet reaction, both involving the oxazolone intermediate.

Qiu, Lingqi; Cooks, R. Graham
Oxazolone mediated peptide chain extension and homochirality in aqueous microdroplets
Proceedings of the National Academy of Sciences (PNAS) 121(2). DOI: 10.1073/pnas.2309360120

© 2024 PNAS.
Reprinted under the terms of s60 of the Copyright, Designs and Patents Act 1988.

And so that day that creationist frauds must be dreading, when science finally closes their favourite gap in which to force-fit their ever-shrinking little god finally slams as shut as all the other gaps it used to occupy in the minds of scientifically illiterate believers, gets a little closer. Only yesterday we learned how simple metabolic biochemical cycles can be produced from simple precursors, all of which were present on the pre-biotic Earth and without protein enzymes, and here we see how the proteins that could catalyse and improve those processes could also arise from simple precursors that were also present.

I wonder what disinformation the frauds who feed pseudo-science to the creation cult are preparing for that eventuality.

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Unintelligent Design - How Ovulation Goes Wrong Because It Wasn't Intelligently Designed

[left caption]

[Right caption/credit]

Gene expression atlas captures where ovulation can go awry | Cornell Chronicle

Back in the late 1960s and early 1970, in what seems like a different lifetime now, I was a senior research assistant in the Oxford University/MRC Neuroendocrinology Research Unit, researching the hormonal control of ovulation in guinea pigs. Two of our tools were radioimmunoassays I had adapted for measuring extremely low levels of a hormone in guinea pig anterior pituitary glands known as luteinizing hormone (LH), and another similar assay for measuring the level of the steroid progesterone in guinea pig blood.

Sadly, having worked for close on two years towards producing a research paper with hundreds of assay results, thousands of microscope slides, hundreds of electron micrographs and a freezer full of samples waiting to be assayed, the government pulled the rug from under our feet by withdrawing our research funding, and I was made redundant, so my work was never published. Disillusioned and with a young family to support, I left research and perused a career in the NHS Ambulance Service instead - but that's a different story, and not relevant to the subject of this blogpost, which illustrates how much science has progressed in the last 50-60 years.

Researchers are no longer researching the hormonal control of ovulation but the fine details of the genetic control of the process of ovulation at the cell level, and what they've found is that the process is far from intelligently designed by anything resembling a perfect, omniscient, omnipotent designer. It is a process that is so complex that it can, and does, go wrong. An intelligent designer who didn't want random women to be unable to shed viable eggs, could have designed a less complicated process, but you can depend on creationism's putative intelligent[sic] designer to never do something simple when there is a far more complicated and wasteful way to achieve the same result.

The research, published a few days ago in Proceedings of the National Academy of Sciences, was led by Iwijn De Vlaminck, associate professor of biomedical engineering in Cornell Engineering, and Yi Athena Ren, assistant professor of animal science in the College of Agriculture and Life Sciences. The paper’s lead author is Madhav Mantri, Ph.D., now a postdoctoral researcher at Stanford University.

The team used a form of RNA tagging to map the gene expressions that occur during ovarian follicle maturation and ovulation in mice.

This spatial transcriptomics map depicts the cell types of a mouse ovary undergoing hormone-induced ovulation

The research is explained in a Cornell University Press release: