Ancient Genomes reveal origin and spread of malaria | Max-Planck-Gesellschaft
Sometimes, I can almost feel sorry for creationists, if only most of them weren't such arrogant, obnoxious liars, more interested in winning more simpletons for their cult than in truth.
It must be difficult when none of the available real-world evidence can be shoehorned successfully into the absurd mythology they want to teach to school children at tax-payers' expense as a prelude to establishing a self-appointing theocracy unaccountable to no-one but themselves.
I have written many of articles in this blog, and will no doubt write a great many more, detailing events in the history of the universe and of life on Earth in the long period of time before creationist superstition says the Universe was created in 6 days of a mythical 'Creation Week'.
I also write regular articles showing how, if life is intelligently designed, the only conclusion must be that the designer is an incompetent idiot and a sadistic, pestilential malevolence with so many parasites seemingly designed to cause suffering in the world. Creationists have been taught to blame the latter, indeed all the nasty stuff in the Universe, on 'The Fall' and 'sin', and have even been given some scientifically nonsensical but sciencey-sounding parrot squawks, 'Genetic entropy' and 'devolution' to throw in at the appropriate time.
The problem there, apart from giving away the fact that creationism is a religious cult, not a science, is the fact that if that had even a slight degree of merit, parasitism should have begun at this mythical 'Fall'.
Admittedly, the Bible is vague about the timing but the clear impression of the Adam & Eve legend it that it happen within weeks, or months, maybe a year or so after 'Creation Week', and before they had any children to inherit it, but certainly not 4,500 years later, unless Adam & Eve were ancient beyond belief when they decided to 'sin'.
And yet, here we have clear scientific evidence that two of the nasty little family of parasites of the Plasmodium genus that cause so much human death and suffering in the form of malaria, weren't around until about 5,500 years ago - some 4,500 years after the alleged 'Fall'.
And creationists shouldn't forget how their guru, Michael J Behe, denied them the opportunity to blame 'Sin' and his other scientifically nonsensical 'explanations', by using what he falsely claimed could not have evolved, being 'irreducibly complex' - anti-malarial drug resistance in P. falciparum - as evidence that their god created it.
What can you tell me about the malaria-causing Falciparum genus of parasites? The Plasmodium genus of parasites is responsible for causing malaria in humans and other animals. Here is a detailed overview:As I said, I can almost feel sorry for creationists, but they should have little difficulty lying about, misrepresenting or ignoring this inconvenient truth, just as they routinely do with the myriads of other scientific papers that daily casually refute creationism.
Overview of Plasmodium GenusGlobal Impact:
- Classification:
- Domain: Eukaryota
- Phylum: Apicomplexa
- Class: Aconoidasida
- Order: Haemosporida
- Family: Plasmodiidae
- Genus: Plasmodium
- Species Affecting Humans:
There are five main Plasmodium species that cause malaria in humans:
- Plasmodium falciparum: Causes the most severe form of malaria and is the most deadly.
- Plasmodium vivax: Causes milder malaria but can remain dormant in the liver and cause relapses.
- Plasmodium ovale: Similar to P. vivax, it can also cause relapses due to dormant liver stages.
- Plasmodium malariae: Causes a chronic infection that can last for many years if untreated.
- Plasmodium knowlesi: Primarily infects macaques but can also infect humans, leading to zoonotic malaria.
- Life Cycle: The Plasmodium life cycle involves two hosts: humans and Anopheles mosquitoes.
- In Mosquitoes:
- A mosquito bites an infected human and ingests gametocytes (sexual forms of the parasite).
- In the mosquito's gut, gametocytes mature into gametes, fuse to form zygotes, and develop into ookinetes.
- Ookinetes penetrate the gut wall and form oocysts.
- Oocysts burst, releasing sporozoites that migrate to the mosquito's salivary glands.
- In Humans:
- The infected mosquito injects sporozoites into the human bloodstream during a bite.
- Sporozoites travel to the liver, infect hepatocytes, and develop into schizonts, which release merozoites.
- Merozoites enter red blood cells, multiply asexually, and cause the cells to burst, releasing more merozoites and causing symptoms.
- Some merozoites develop into gametocytes, which can be taken up by another mosquito, continuing the cycle.
- Pathogenesis:
- Plasmodium falciparum: Known for causing severe and complicated malaria due to the high levels of parasitemia and sequestration of infected erythrocytes in the capillaries.
- Plasmodium vivax and Plasmodium ovale: Can cause relapses due to hypnozoites (dormant liver stages).
- Plasmodium malariae: Known for causing long-term infections with periods of low-level parasitemia.
- Plasmodium knowlesi: Can lead to severe and rapidly progressing malaria, often misdiagnosed as P. malariae due to morphological similarities.
- Symptoms:
- Initial symptoms include fever, chills, headache, muscle pain, and malaise.
- Severe malaria can lead to anemia, respiratory distress, cerebral malaria (particularly with P. falciparum), and multi-organ failure.
- Diagnosis:
- Microscopy of blood smears (thick and thin) is the gold standard.
- Rapid diagnostic tests (RDTs) detect specific antigens produced by Plasmodium species.
- Molecular methods like polymerase chain reaction (PCR) offer high sensitivity and specificity.
- Treatment:
- Uncomplicated Malaria: Artemisinin-based combination therapies (ACTs) are the first-line treatment.
- Severe Malaria: Intravenous artesunate is recommended.
- P. vivax and P. ovale: Requires treatment with primaquine or tafenoquine to eliminate hypnozoites and prevent relapses.
- Prevention:
- Vector Control: Use of insecticide-treated bed nets (ITNs) and indoor residual spraying (IRS).
- Chemoprophylaxis: Antimalarial drugs for travelers to endemic areas.
- Vaccination: RTS,S/AS01 (Mosquirix) is the first malaria vaccine approved for children in some African countries.
- Research: Ongoing efforts to develop more effective vaccines and new antimalarial drugs.
- Malaria caused by Plasmodium species is a major public health issue, particularly in tropical and subtropical regions.
- Efforts to control and eradicate malaria involve a combination of medical treatment, vector control, and public health initiatives.
- Drug resistance, particularly in *P. falciparum*, poses significant challenges to treatment and control efforts.
How scientists from the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany worked out when the Plasmodium genus is the subject of a research paper in Nature and a news release from the Max Planck Institute:
Origin and spread of malariaFor more technical details, we have the abstract and introduction to the team's open access paper in Nature:
Scientists reconstruct ancient genomes of the two most deadly malaria parasites, Plasmodium vivax and Plasmodium falciparum
In a new study, an international team of researchers led by the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, reconstructed the evolutionary history and global spread of malaria over the past 5,500 years, identifying trade, warfare, and colonialism as major catalysts for its dispersal.
Malaria, one of the world’s deadliest infectious diseases, is caused by several species of single-celled parasites that are transmitted via the bite of infected Anopheles mosquitoes. Despite major control and eradication efforts, nearly half of the world’s population still lives in regions where they are at risk of contracting malaria, and the World Health Organization estimates that malaria causes nearly 250 million infections and more than 600,000 deaths each year.
Beyond this massive modern impact, malaria has strongly shaped our human evolutionary history.
Although largely a tropical disease today, only a century ago the pathogen’s range covered half the world’s land surface, including parts of the northern USA, southern Canada, Scandinavia, and Siberia. Malaria’s legacy is written in our very genomes: genetic variants responsible for devastating blood disorders such as sickle cell disease are thought to persist in human populations because they confer partial resistance to malaria infection.
Megan Michel, lead author
Department of Archaeogenetics
Max Planck Institute for Evolutionary Anthropology, Leipzig, Germany.
And Max Planck-Harvard Research Center Archaeoscience of the Ancient Mediterranean.
[The Max Planck-Harvard Research Center Archaeoscience of the Ancient Mediterranean is a research collaboration between the Max Planck Institute for Evolutionary Anthropology and the Initiative for the Science of the Human Past at Harvard University.]
Despite this evolutionary impact, the origins and spread of the two deadliest species of malaria parasites, Plasmodium falciparum and Plasmodium vivax, remain shrouded in mystery. Malaria infections leave no clear visible traces in human skeletal remains, and scant references in historical texts can be difficult to decipher. However, recent advances in the ancient DNA field have revealed that human teeth can preserve traces of pathogens present in a person’s blood at the time of death, providing an opportunity to study illnesses that are normally invisible in the archaeological record.
To explore malaria’s enigmatic history, an international team of researchers representing 80 institutions and 21 countries reconstructed ancient Plasmodium genome-wide data from 36 malaria-infected individuals spanning 5,500 years of human history on five continents. These ancient malaria cases provide an unprecedented opportunity to reconstruct the worldwide spread of malaria and its historical impact at global, regional, and even individual scales.
Following biomolecular breadcrumbs in the Americas
Malaria is endemic in tropical regions of the Americas today, and scientists have long debated whether P. vivax, a malaria species adapted to survive in temperate climates, may have arrived via the Bering Strait with the peopling of the continent or traveled in the wake of European colonization. To track the parasites’ journey into the Americas, the team analyzed ancient DNA from a malaria-infected individual from Laguna de los Cóndores, a high-altitude site situated in the remote cloud forests of the eastern Peruvian Andes.
Genomic analysis revealed remarkable similarity between the Laguna de los Cóndores P. vivax strain and ancient European P. vivax, strongly suggesting that European colonizers spread this species to the Americas within the first century or so after contact.
Amplified by the effects of warfare, enslavement, and population displacement, infectious diseases, including malaria, devastated Indigenous peoples of the Americas during the colonial period, with mortality rates as high as 90 percent in some places.
Dr. Evelyn K. Guevara, co-author
Department of Archaeogenetics
Max Planck Institute for Evolutionary Anthropology, Leipzig, Germany
And Department of Forensic Medicine
University of Helsinki, Helsinki, Finland.
Remarkably, the team also uncovered genetic links between the Laguna de los Cóndores strain and modern Peruvian P. vivax populations 400 to 500 years later.
In addition to showing that malaria spread rapidly into what is a relatively remote region today, our data suggest that the pathogen thrived there, establishing an endemic focus and giving rise to parasites that are still infecting people in Peru today.
Dr. Eirini Skourtanioti, co-author
Max Planck Institute for Evolutionary Anthropology, Leipzig, Germany
And Max Planck-Harvard Research Center Archaeoscience of the Ancient Mediterranean.
Malaria on the march in Europe
While the role of colonialism in the spread of malaria is evident in the Americas, the team uncovered military activities that shaped the regional spread of malaria on the other side of the Atlantic. The cemetery at the Gothic cathedral of St. Rombout’s in Mechelen, Belgium was located adjacent to the first permanent military hospital (1567-1715 CE) in early modern Europe. Ancient human and pathogen DNA identified local cases of P. vivax among the general population buried before the construction of the military hospital, while individuals buried after its construction included cases of the more virulent P. falciparum malaria.
Most interestingly, we observe more cases of malaria in non-local male individuals from the military hospital period. We also identified several individuals infected with P. falciparum, a species that thrived in Mediterranean climates before eradication but was not thought to be endemic north of the Alps during this period.
Dr. Federica Pierini, co-author
Department of Archaeogenetics
Max Planck Institute for Evolutionary Anthropology, Leipzig, Germany.
These virulent cases were found in non-local male individuals of diverse Mediterranean origins, who were likely soldiers recruited from northern Italy, Spain, and other Mediterranean regions to fight in the Hapsburg Army of Flanders during the 80 Years’ War.
Himalayan trade and a surprising high-altitude infectionWe find that the large-scale troop movements played an important role in the spread of malaria during this period, similar to cases of so-called airport malaria in temperate Europe today. In our globalized world, infected travelers carry Plasmodium parasites back to regions where malaria is now eradicated, and mosquitoes capable of transmitting these parasites can even lead to cases of ongoing local transmission. Although the landscape of malaria infection in Europe is radically different today than it was 500 years ago, we see parallels in the ways in which human mobility shapes malaria risk.
Alexander Herbig, co-corresponding author
Department of Archaeogenetics
Max Planck Institute for Evolutionary Anthropology, Leipzig, Germany.
On the other side of the world, the team unexpectedly identified the earliest known case of P. falciparum malaria at the high Himalayan site of Chokhopani (ca. 800 BCE), located along the Kali Gandaki River Valley in the Mustang District of Nepal. At 2800 meters above sea level, the site lies far outside the habitat range for both the malaria parasite and the Anopheles mosquito.
Human genetic analysis revealed that the infected individual was a local male with genetic adaptations for life at high altitude. However, archaeological evidence at Chokhopani and other nearby sites suggests that these Himalayan populations were actively engaged in long-distance trade.The region surrounding Chokhopani is cold and quite dry. Neither the parasite nor the mosquitoes capable of transmitting malaria can survive at this altitude. For us this raised a key question: how did the Chokhopani individual acquire the malaria infection that may have ultimately led to his death?
Associate Professor Christina Warinner, co-author
Associate Professor of Anthropology
Harvard University, Cambridge, MA, USA
And Group Leader at the Max Planck Institute for Evolutionary Anthropology.[Professor Aldenderfer's excavations in the region have revealed its long-distance trade connections].We think of these regions today as remote and inaccessible, but in fact the Kali Gandaki River Valley served as a kind of trans-Himalayan highway connecting people on the Tibetan Plateau with the Indian subcontinent. Copper artifacts recovered from Chokhopani’s burial chambers prove that the ancient inhabitants of Mustang were part of larger exchange networks that included northern India, and you don’t have to travel very far to reach the low-lying, poorly drained regions of the Nepalese and Indian Terai where malaria is endemic today.
Professor Mark Aldenderfer, co-author
Distinguished Professor Emeritus
Department of Anthropology and Heritage Studies
University of California, Merced, Merced, CA, USA.
The team believes that the man likely traveled to a lower-altitude malaria-endemic region, possibly for trade or other purposes, before returning or being brought back to Chokhopani, where he was later buried. The intimate details revealed by ancient DNA give clues to the myriad ways that infectious diseases like malaria spread in the past, giving rise to our current disease landscape.
Past and future of a dynamic disease
Today, the human experience of malaria is at a crossroads. Thanks to advances in mosquito control and concerted public health campaigns, malaria deaths reached an all-time low in the 2010s. However, the emergence of antimalarial drug-resistant parasites and insecticide-resistant vectors threatens to reverse decades of progress, while climate change and environmental destruction are making new regions vulnerable to malaria vector species. The team hopes that ancient DNA may provide an additional tool for understanding and even combating this public health threat.
For the first time, we are able to explore the ancient diversity of parasites from regions like Europe, where malaria is now eradicated. We see how mobility and population displacement spread malaria in the past, just as modern globalization makes malaria-free countries and regions vulnerable to reintroduction today. We hope that studying ancient diseases like malaria will provide a new window into understanding these organisms that continue to shape the world we live in today.
Johannes Krause, senior author
Director of Archaeogenetics
Department of Archaeogenetics
Max Planck Institute for Evolutionary Anthropology, Leipzig, Germany
And Max Planck-Harvard Research Center for the Archaeoscience of the Ancient Mediterranean.
AbstractSo, a lot for creationists to unpack and dismiss here. First, we have the evidence that the scientists rely entirely on the Theory of Evolution to explain the observed facts, with no hint of adopting creationist superstitions, the way creationist cult leaders have been predicting any day now, real soon - for the last half a century.
Malaria-causing protozoa of the genus Plasmodium have exerted one of the strongest selective pressures on the human genome, and resistance alleles provide biomolecular footprints that outline the historical reach of these species1. Nevertheless, debate persists over when and how malaria parasites emerged as human pathogens and spread around the globe1,2. To address these questions, we generated high-coverage ancient mitochondrial and nuclear genome-wide data from P. falciparum, P. vivax and P. malariae from 16 countries spanning around 5,500 years of human history. We identified P. vivax and P. falciparum across geographically disparate regions of Eurasia from as early as the fourth and first millennia BCE, respectively; for P. vivax, this evidence pre-dates textual references by several millennia3. Genomic analysis supports distinct disease histories for P. falciparum and P. vivax in the Americas: similarities between now-eliminated European and peri-contact South American strains indicate that European colonizers were the source of American P. vivax, whereas the trans-Atlantic slave trade probably introduced P. falciparum into the Americas. Our data underscore the role of cross-cultural contacts in the dissemination of malaria, laying the biomolecular foundation for future palaeo-epidemiological research into the impact of Plasmodium parasites on human history. Finally, our unexpected discovery of P. falciparum in the high-altitude Himalayas provides a rare case study in which individual mobility can be inferred from infection status, adding to our knowledge of cross-cultural connectivity in the region nearly three millennia ago.
Main
Malaria is a vector-borne disease caused by protozoa in the genus Plasmodium and is transmitted by female anopheline mosquitoes4. It is a major cause of human morbidity and mortality, with an estimated 240 million cases and more than 600,000 fatalities in 2020 (ref. 5). Beyond its current health impact, malaria has profoundly influenced human evolution, exerting one of the strongest identified selective pressures on the human genome. Congenital haematological conditions, including sickle-cell disease, G6PD deficiency and thalassaemia, have persisted because they confer partial resistance to malaria, indicating a long-term relationship between the pathogen and human populations6.
Of the five primary human-infecting Plasmodium species, P. falciparum and P. vivax account for the vast majority of malaria disease burden today, whereas P. malariae, P. ovale wallikeri and P. ovale curtisi are less common and cause milder symptoms4. Previous research indicates that P. falciparum emerged through zoonosis from gorillas in sub-Saharan Africa7. Date estimates for the most recent common ancestor of extant P. falciparum strains range from less than 10,000 to 450,000 years ago8,9,10.
The emergence of P. vivax is generally considered to pre-date that of P. falciparum, but its evolutionary origins are less well understood. Early mitochondrial analyses supported an origin in Southeast Asia, placing P. vivax in a clade of Plasmodium species infecting macaques and other Southeast-Asian primates11,12. Analyses based on nuclear data, including phylogenies and patterns of nucleotide diversity, have provided further support for an Asian origin13. However, parasites of the African great apes, notably P. carteri and P. vivax-like, are now thought to constitute the closest relatives of P. vivax10,14,15. Together with the near-fixation of the Duffy-negative allele in many human groups in sub-Saharan Africa, this provides strong support for an African origin for P. vivax1. The Duffy antigen, encoded by the FY locus, facilitates P. vivax erythrocyte invasion, and individuals homozygous for the Duffy-negative allele were once considered completely immune to P. vivax malaria1,6. Accumulating evidence demonstrates that populations with high rates of Duffy negativity can maintain low levels of P. vivax transmission, and the phenotype seems to reduce the efficiency of erythrocyte invasion and provide protection against blood-stage infection16. Thus, proponents of the African-origin hypothesis argue that a long history of selection pressure exerted by P. vivax drove increases in the Duffy-negative phenotype, making these populations less susceptible to P. vivax infection today. Interestingly, some human groups in Papua New Guinea have a Duffy null allele that seems to have arisen through an independent mutation. Indeed, the low frequency and long haplotype associated with the Papua New Guinea variant support more recent positive selection in people living in Oceania than in those in sub-Saharan Africa17.
As well as the evolutionary constraints, variation in pathogenesis between P. vivax and P. falciparum contributes to their distinct geographical distributions and ecologies. Because of its higher virulence, morbidity and mortality, P. falciparum requires a larger population of susceptible hosts to sustain transmission. Consequently, some researchers have theorized that hunter-gatherer population densities were probably too low to support the emergence of P. falciparum, which instead may have proliferated with the development of agriculture in sub-Saharan Africa1. Climate also poses distinct constraints on the ranges of these two species, with P. vivax able to survive and develop at lower temperatures than P. falciparum18,19. Finally, P. vivax forms hypnozoites in its dormant hepatic stage, and reactivation months or even years after an initial infection can re-initiate the Plasmodium life cycle, enabling further transmission4. Hypnozoites enable P. vivax to overwinter in the human host when low temperatures limit vector activity. Combined with its greater tolerance for cold temperatures, this capacity enables P. vivax to survive in temperate regions, whereas P. falciparum is generally restricted to tropical and subtropical zones1.
Because Plasmodium species are obligate intracellular pathogens, their contemporary distributions reflect patterns of human mobility, as well as the evolutionary, physiological and ecological constraints acting on the parasite, human host and mosquito vector. However, relatively little is known about the timing and routes by which Plasmodium spp. spread around the globe. In the palaeopathological literature, cribra orbitalia and porotic hyperostosis have been considered to be indicators of severe malarial anaemia20,21. However, their presence should be interpreted with caution because these skeletal lesions are not pathognomonic for the identification of malaria cases in the archaeological record22,23, and the two conditions probably have different underlying aetiologies24,25. Recurrent fevers are described in Vedic and Brahmanic texts from the first millennium BCE, and Hippocratic texts from the late fifth or early fourth century BCE provide the first unambiguous references to malaria in the Mediterranean world1,3. However, retrospective diagnosis of malaria poses considerable challenges, and many time periods and regions are missing from the historical record26. Although written sources and congenital haematological conditions provide indirect evidence of the historical range of malaria, uncertainty persists over which species contributed to selective processes in specific regions, as well as how the selective dynamics played out over time1,2.
Tracing the history of Plasmodium spp. in the Americas is of particular interest, given the limited number of transoceanic contacts that may have facilitated transmission. P. falciparum is likely to have reached the Americas with colonizers from Mediterranean Europe or as a result of the trans-Atlantic slave trade, but the potential pre-contact origin of American P. vivax is still debated27. Some scholars suggest that P. vivax reached the American continent with its first human inhabitants, and cite as evidence both its high nucleotide diversity and the presence of divergent mitochondrial lineages in American parasite populations28. Others argue that American P. vivax may derive from pre-colonial-era contacts with Oceanian seafarers27. Finally, P. vivax, as well as P. falciparum and many other Eurasian pathogens, may have reached the Americas during the European colonial era28,29,30. A contact-era introduction of Plasmodium spp. is consistent with the absence of malaria-resistance alleles in the Indigenous peoples of the Americas31. Further support for this hypothesis comes from analyses of the only historical European P. vivax genomic dataset available to date, which derives from a 1944 blood slide from Spain’s Ebro Delta. Analysis of nuclear single-nucleotide polymorphism (SNP) data places Ebro1944 close to contemporary South and Central American P. vivax strains30.
The ability to retrieve ancient bacterial and viral DNA preserved in human skeletal material is providing a fuller picture of the evolution, origins and global dissemination of historically important pathogens32. However, attempts to retrieve ancient DNA from Plasmodium spp. have until now had limited success33. Apart from Ebro1944 (refs. 30,34,35), the available ancient Plasmodium datasets have so far been restricted to two partial mitochondrial genomes from southern Italy dating to the first and second century CE36. Here we identify P. falciparum, P. vivax and P. malariae infections in 36 ancient individuals from 16 countries spanning 5,500 years of human history from the Neolithic to the modern era. Using two new in-solution hybridization capture bait sets, we generate high-coverage ancient Plasmodium mitochondrial genomes and genome-wide nuclear data, which demonstrate that the European expansion of P. vivax greatly pre-dates evidence from written sources. Genomic data from now-eliminated European P. falciparum and P. vivax strains provide an unprecedented opportunity to explore gaps in the genomic diversity of modern Plasmodium populations, enabling a fuller picture of the origins and transmission routes of human malaria parasites. Finally, contextualizing ancient genomic data from P. falciparum and P. vivax alongside archaeological information and human population genetics reveals the critical role of human mobility in the spread of malaria in past populations.
Ancient Plasmodium spp. data generation
To identify ancient malaria cases, we performed a metagenomic analysis of previously produced shotgun-sequenced libraries from more than 10,000 ancient individuals (Methods). Ancient DNA libraries found to possess traces of Plasmodium DNA were enriched using two new hybridization capture reagents targeting the mitochondrial and nuclear genomes of Plasmodium spp. In total, we identified 36 malaria cases, comprising 10 P. falciparum infections, 2 cases of P. malariae and 21 P. vivax infections, along with 2 individuals co-infected with P. falciparum and P. malariae as well as 1 P. vivax–P. falciparum co-infection (Fig. 1, Supplementary Table 1 and Supplementary Note 1). We analysed these ancient mitochondrial and nuclear datasets alongside modern Plasmodium data and published shotgun reads from the Ebro1944 blood slide30,34,35,37,38.
Michel, M., Skourtanioti, E., Pierini, F. et al.
Ancient Plasmodium genomes shed light on the history of human malaria. Nature (2024). https://doi.org/10.1038/s41586-024-07546-2
Copyright: © 2024 The authors.
Published by Springer Nature. Open access.
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)
Second, we have the evidence that these species of parasite originated several thousand years after the mythical 'Fall' so we can rule of the traditional excuses for parasites - which, if the myth had any explanatory power, should have happened several thousand years earlier.
And we have the evidence of a parasite that appears to have no other purpose but to make humans sick and die, and of course, the prolific waste in their reproduction and the evidence of evolutionary arms races that belie any claim of intelligence behind their creation.
The Unintelligent Designer: Refuting The Intelligent Design Hoax
The Malevolent Designer: Why Nature's God is Not Good
Illustrated by Catherine Webber-Hounslow.
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