In a recent article for Answers in Genesis, Harry F. Sanders III attempts to explain how defense/attack structures (DAS) such as venoms, armor, parasitism, carnivorous plant traps, and other offensive and defensive adaptations, could have originated in a world that was, according to young-earth creationist (YEC) theology, originally created free of death, predation, and suffering. Sanders proposes four categories of explanation: structures had a different pre-Fall use, structures were genetically hidden and later revealed, changes occurred in the target organism rather than the attacker, and parasites degenerated from originally benign relationships.

Here I examine each proposed mechanism and find them scientifically inadequate. The explanations lack specificity, offer no testable hypotheses, ignore vast bodies of relevant molecular, genetic, and phylogenetic evidence, and in several cases require more rapid and dramatic evolutionary change than mainstream science proposes creating what could be called a “hyperevolution paradox.” I present additional challenges to the YEC framework for DAS origins are presented, including evidence from convergent evolution of venom systems, the deep phylogenetic distribution of defense structures in the fossil record, molecular clock data, and the irreducible complexity of integrated predator-prey systems that defy simple repurposing narratives.

---

The existence of defense/attack structures (DAS) in the biological world has long presented one of the most difficult theological and scientific challenges for young-earth creationism (YEC). If the original creation was “very good” (Genesis 1:31), with no death, predation, or suffering, how did the staggering diversity of venoms, toxins, armor, parasitic life cycles, and predatory anatomies come to exist? This is not merely a peripheral question; it strikes at the coherence of the entire YEC model of biological history.

Sanders’ article, How Did Animals Develop Defense and Attack Structure?, published on February 25, 2026, by Answers in Genesis, represents the latest attempt to address this challenge. While the article is competently written and does cite relevant scientific literature on the organisms it describes, its proposed solutions to the DAS problem are, upon close examination, remarkably thin. Each proposed mechanism including “different use,” “revealed” genetic information, “different reaction,” and “different interaction”, amounts to little more than a speculative narrative unsupported by empirical evidence, devoid of testable predictions, and in many cases contradicted by the very biological data that Sanders himself cites.

This critique will examine each of Sanders’ four proposed explanations in turn, evaluating them against the available scientific evidence. It will then raise additional challenges to the YEC framework for DAS origins that Sanders does not address, drawing on molecular phylogenetics, convergent evolution, fossil evidence, and the integrated complexity of predator-prey systems.

The “Different Use” Hypothesis: Repurposed Structures

Sanders’ first proposed explanation is that many DAS had a different, benign function before the Fall. He suggests that the Venus flytrap “could have been used to trap pollen and detritus as meals,” that the thresher shark’s elongated tail could have been “used solely for swimming or potentially for breaking loose seagrass from its holdfasts,” that skunk spray may have functioned in “communication or territorial marking,” and that lamprey teeth “could have been used to scrape algae off rocks.”

The Venus Flytrap

The suggestion that the Venus flytrap’s snap-trap mechanism could have originally functioned to capture pollen and detritus is perhaps the most transparent example of the article’s speculative approach. The Venus flytrap (Dionaea muscipula) possesses an extraordinarily sophisticated prey-capture system involving trigger hairs, electrical signaling, rapid turgor-pressure changes, and the secretion of digestive enzymes. As Sanders himself notes, citing Volkov et al. (2008, 2011), the trap requires two touches of trigger hairs to close, uses electrical impulses, and then slowly digests captured prey. Every component of this system—from the trigger hairs to the digestive glands—is integrated toward the capture and digestion of animal prey. There is no known analog for a “pollen trap” of anything like this sort in the plant kingdom, and pollen grains do not trigger the mechanical responses that insect movement does. Furthermore, the digestive enzymes secreted by the trap are proteases designed to break down animal proteins, not the carbohydrate-rich walls of pollen grains. The suggestion that this entire integrated system was “originally” designed for pollen capture and was then seamlessly repurposed for animal prey capture is biologically implausible and constitutes pure ad hoc speculation.

It is worth noting that all carnivorous plant lineages including sundews (Drosera), pitcher plants (Sarracenia, Nepenthes), butterworts (Pinguicula), and bladderworts (Utricularia), have independently evolved carnivory from non-carnivorous ancestors. Molecular phylogenetic studies indicate that carnivory has evolved independently at least six times in angiosperms (Ellison and Gotelli, 2009). Each lineage employs a distinct trapping mechanism, yet Sanders provides a “different use” explanation for only one. What were the pre-Fall functions of pitfall traps, flypaper traps, snap traps, bladder traps, and lobster-pot traps? The silence on these matters is telling.

The Thresher Shark

The proposal that the thresher shark’s elongated caudal fin was originally used “solely for swimming or potentially for breaking loose seagrass from its holdfasts” fares no better. Thresher sharks (genus Alopias) possess a caudal fin that constitutes roughly half their total body length—an extreme morphological specialization. Sanders himself cites Oliver et al. (2013), who documented that thresher sharks rely almost exclusively on tail-slaps to stun prey, with no evidence that lunging ever produced a successful feeding event. The biomechanics of the tail-slap are highly specialized: the tail generates forces sufficient to create cavitation bubbles in the water, stunning or killing small fish. This is not a general-purpose swimming fin that was incidentally repurposed; it is a specialized hunting weapon whose biomechanics are optimized for prey stunning. Sanders offers no mechanism by which a swimming fin would develop the specific kinematic properties needed for prey stunning, nor does he explain why a vegetarian shark would possess a body plan dominated by a hunting appendage.

Skunk Spray and Lamprey Teeth

The suggestion that skunk spray may have originally functioned in “communication or territorial marking” is offered without any supporting evidence or biological reasoning. While many mammals use scent marking for communication, the chemical composition of skunk spray (primarily thiols and thioacetates) is specifically optimized for noxiousness and deterrence, not information transfer. The spray glands of skunks are anatomically specialized for directed, pressurized delivery at distances up to several meters, a design feature that makes no sense for territorial marking.

Similarly, the claim that lamprey teeth “could have been used to scrape algae off rocks” ignores the oral disc morphology of parasitic lampreys. The sucker-like oral disc, lined with concentric rows of keratinous teeth and a rasping tongue (the piston), constitutes an integrated blood-feeding apparatus. The teeth are configured to grip flesh and create a seal, while the piston rasps through skin and scales. Larval lampreys (ammocoetes) are indeed filter feeders that consume algae and detritus—but they achieve this through an entirely different morphology involving a hood-like oral structure with no teeth. The adult parasitic lamprey’s oral apparatus is not a modified version of the larval feeding structure; it develops during metamorphosis as a fundamentally new anatomy. Sanders’ comparison to fruit bat teeth is also misleading: fruit bat dentition is adapted for crushing fruit, not for penetrating flesh and maintaining suction. The analogy obscures rather than illuminates.

The Core Problem with “Different Use”

The overarching problem with the “different use” hypothesis is that it treats complex, integrated biological systems as if they were generic tools that can be casually reassigned to new tasks. But biological structures are not like Swiss Army knives. The Venus flytrap’s snap-trap, the thresher shark’s hunting tail, the skunk’s spray apparatus, and the lamprey’s oral disc are each composed of multiple co-adapted components that function together specifically for their current purpose. Proposing that all of these were “originally” designed for some other benign function, but were then seamlessly repurposed after the Fall, requires a level of pre-programmed biological flexibility that is both unfalsifiable and explanatorily vacuous. No mechanism is proposed, no predictions are made, and no tests are suggested. The “different use” hypothesis is not a scientific explanation; it is a narrative convenience.

The “Revealed” Hypothesis: Hidden Genetic Information

Sanders’ second category of explanation posits that some DAS were not present before the Fall but existed as hidden or silenced genetic information that was later “revealed” through gene regulation changes or mutations. He writes that “the chemical structure of venom could have changed after the fall to become noxious, either due to mutations or due to preexisting genes that were disabled prior to the fall,” and that “genes involved in producing defense/attack structures could have been turned off or turned down to a point where their effects were unrecognizable.” He also suggests that gene duplication events could have transformed harmless digestive enzymes into venomous toxins.

A Problem of Scale

This hypothesis drastically underestimates the molecular complexity of venom systems. Snake venom, for example, is not a single toxic compound that can be produced by flipping a genetic switch. A comprehensive phylogenetic analysis by Fry (2005) demonstrated that the snake venom proteome arose through at least 24 independent gene recruitment events, drawing from diverse protein families including phospholipase A₂, metalloproteinases, serine proteases, three-finger toxins, cystatin, kunitz-type proteinase inhibitors, and many others. Each of these toxin families has undergone extensive gene duplication, neofunctionalization, and accelerated evolution under positive selection (Vonk et al., 2013; Shibata et al., 2018). The king cobra genome alone reveals that venom toxin genes have been co-opted from genes expressed in a wide variety of tissues, with at least two distinct mechanisms: gene hijacking/modification and duplication of non-toxin genes followed by selective venom gland expression (Vonk et al., 2013).

This is not a matter of “silencing” a few genes. It involves the coordinated evolution of specialized venom glands, novel regulatory elements, venom delivery systems (fangs, grooved teeth, or modified salivary ducts), and dozens of toxin gene families—each with multiple paralogs that have undergone independent evolutionary trajectories. Castoe et al. (2024), whom Sanders himself cites, demonstrated that rattlesnake venom gene expression is regulated by diverse and complex mechanisms operating at fine evolutionary scales, including changes in chromatin accessibility, transcription factor binding, and post-transcriptional regulation. The notion that all of this complexity was “pre-loaded” into a prelapsarian genome as silenced information waiting to be activated is not consistent with what we observe in these genomes.

The Hyperevolution Paradox

Here we encounter what may be the most fundamental problem for the YEC model: the hyperevolution paradox. Sanders suggests that gene duplications, mutations, and regulatory changes produced the full diversity of venom systems, parasitic adaptations, and predatory morphologies we observe today. But within the YEC timeline, all of this had to occur within roughly 4,500 years (post-Flood) or at most 6,000–10,000 years (post-Fall). The irony is striking: YEC advocates routinely argue that evolution cannot produce complex new features, yet their own model requires evolutionary changes of a scope and speed that far exceeds anything proposed by mainstream evolutionary biology. Mainstream science places the origin of snake venom glands at approximately 60–80 million years ago, at the base of the colubroid radiation (Fry, 2005; Vidal and Hedges, 2002). The YEC model compresses this into a few thousand years—a rate of molecular evolution orders of magnitude faster than anything observed or proposed in the peer-reviewed literature.

This paradox is not limited to snake venom. Venom systems have evolved independently more than 100 times across the animal kingdom (Schendel et al., 2019), in lineages as diverse as cnidarians, cephalopods, arthropods (spiders, scorpions, insects), fish, reptiles, and mammals. A recent comparative transcriptomic study by Zancolli et al. (2022) demonstrated convergent gene expression profiles across venom glands from 20 species representing eight independent origins of venom. Under the YEC model, all 100+ independent origins of venom must have occurred in parallel, within a few thousand years, by a combination of gene duplication, mutation, and regulatory rewiring—the very processes that YEC proponents typically dismiss as incapable of producing novel complexity.

The Problem of Integrated Systems

Sanders’ “revealed” hypothesis also fails to account for the fact that venom is useless without a delivery system. Snake venom requires not only the toxin proteins but also specialized venom glands, ducts, and fangs—the latter having evolved independently at least three times in snakes (in vipers, elapids, and atractaspidids). Stonefish venom requires 18+ specialized spines connected to venom glands via ducts. Jellyfish venom requires cnidocytes—arguably the most morphologically complex organelle known—which discharge at extraordinary speed and force to puncture prey and inject venom. Were all of these delivery systems also “silenced” in the prelapsarian genome? If so, this amounts to claiming that God created organisms with complete, functional predatory and defensive weapon systems that were simply hidden, awaiting activation—a claim that raises profound theological questions about the nature of a “very good” creation.

The “Different Reaction” Hypothesis: Changed Targets

Sanders’ third explanation, applied specifically to poison ivy, is that the target organism changed rather than the plant. He notes that most herbivorous animals are unaffected by urushiol and suggests that “a mutation, either shortly after the fall or shortly after the flood,” broke “the normal tolerance humans displayed toward urushiol.”

While this is perhaps the most scientifically defensible of Sanders’ proposals in its broad outlines—indeed, the human immune response to urushiol is a T-cell-mediated hypersensitivity reaction that varies in intensity among individuals—it applies to only an extremely narrow subset of DAS. It does nothing to explain venom, predatory anatomy, parasitism, or the vast majority of defense structures. Furthermore, the argument actually undermines the YEC position: if urushiol sensitivity in humans is the result of a post-Fall mutation, this implies that mutation and natural selection can modify complex immune system responses in a few thousand years—precisely the kind of evolutionary change that YEC proponents typically argue is impossible.

The argument also fails to grapple with the ecological purpose of urushiol in Toxicodendron species. Research suggests that urushiol functions as an antifungal and antimicrobial compound, protecting the plant from pathogen attack (Senchina, 2008). If the purpose of urushiol is plant defense against microbial pathogens, then it was designed as a defensive compound from the start—which brings us right back to the original DAS problem.

The “Different Interaction” Hypothesis: Degenerated Relationships

Sanders’ final category of explanation is applied to parasites. He suggests that Sacculina barnacles “were a form of symbiont with their current crab hosts before the fall and degenerated into their present form,” that Cymothoa tongue-replacing isopods “most likely were free-living or perhaps symbionts,” and that some roundworms transitioned from free-living to parasitic lifestyles.

The Implausibility of Degeneration from Symbiosis

The claim that Sacculina barnacles were once symbionts is perhaps the most strained of all the proposals in the article. Sacculina is a rhizocephalan barnacle that has undergone such extreme morphological modification for parasitism that adult females are essentially unrecognizable as arthropods. They lack a gut, appendages, and segmentation. Their body consists primarily of a network of root-like tendrils (the interna) that penetrate throughout the host crab’s body, absorbing nutrients directly from the hemolymph. The reproductive body (the externa) protrudes from the crab’s abdomen. Sacculina castrates its host, modifies the host’s behavior and morphology (including feminizing male crabs), and hijacks the host’s brood-care behavior to disperse its own larvae.

To claim that this organism was once a “symbiont” that “degenerated” into its present form is to claim that it lost its entire body plan—its digestive system, its appendages, its segmentation—and simultaneously evolved a root-like nutrient absorption system, host castration mechanisms, behavioral manipulation capabilities, and a complex parasitic life cycle involving a free-swimming nauplius larva, a cypris larva that settles on a crab, and an injected kentrogon stage that develops into the internal network. This is not “degeneration.” It is an astonishing example of evolutionary specialization that required the acquisition of multiple novel features. In mainstream biology, the evolution of rhizocephalan parasitism from free-living barnacle ancestors is well-supported by phylogenetic evidence and is understood to have occurred over tens of millions of years (Glenner and Hebsgaard, 2006). Sanders’ model requires it to have happened in a few thousand years—again, hyperevolution on a scale that dwarfs any mainstream proposal.

The Scope of Parasitism

The article’s treatment of parasitism is also hopelessly incomplete. Sanders discusses three examples—Cymothoa, Sacculina, and lampreys—but parasitism is not an anomaly requiring a few case-by-case explanations. It is a dominant ecological strategy. Estimates suggest that parasites may constitute more than 40% of all described species (Dobson et al., 2008), and parasitic lineages have arisen independently in virtually every major animal phylum. The diversity of parasitic strategies is staggering: endoparasites, ectoparasites, parasitoids, kleptoparasites, brood parasites, social parasites, and hyperparasites, each requiring specialized anatomical, physiological, and behavioral adaptations. Many parasites have multi-host life cycles requiring sequential infection of two or more unrelated host species—a level of ecological integration that defies any simple “degeneration” narrative.

Consider the trematode Dicrocoelium dendriticum (the lancet liver fluke), which requires three hosts: a snail, an ant, and a grazing mammal. The parasite manipulates the behavior of infected ants, causing them to climb to the tips of grass blades at night, where they are more likely to be consumed by grazing mammals. This three-host life cycle with behavioral manipulation cannot have “degenerated” from a symbiotic relationship. It is a complex, multi-step adaptation that must function as an integrated system or not at all. How does Sanders’ “different interaction” hypothesis account for the origin of multi-host parasitic life cycles within a few thousand years?

Additional Challenges to the YEC Framework

Beyond the specific inadequacies of Sanders’ four proposed mechanisms, several broader lines of evidence pose formidable challenges to any young-earth model for DAS origins.

Deep Fossil Record of DAS

Defense and attack structures appear very early in the fossil record—far earlier than the YEC model can accommodate even within its own framework. Sanders acknowledges fossils of animals eating each other, citing Wilby and Martill (1992) and Ahlberg et al. (2023) on trilobite gut contents. But within the YEC framework, these fossils are supposed to represent organisms deposited during the Flood (approximately 4,500 years ago). The problem is that DAS appear in the very earliest animal fossils. The Cambrian explosion (~540–520 million years ago in the conventional timeline) is characterized by the simultaneous appearance of both predators and heavily armored prey. Trilobites possess compound eyes, enrolled body plans for defense, and calcified exoskeletons from their first appearance. Anomalocaris, the apex predator of Cambrian seas, had grasping appendages specifically adapted for capturing prey. If all of these organisms were created during Creation Week, they were created with DAS already in place—which contradicts the premise of a “very good” creation lacking predation. If they developed DAS after the Fall but before the Flood, the YEC timeline gives them at most ~1,656 years (from the Fall to the Flood in the Ussher chronology) to evolve armored exoskeletons, compound eyes, grasping appendages, mineralized teeth, and venom systems from scratch.

Convergent Evolution of Venom

As noted above, venom systems have evolved independently more than 100 times across the animal kingdom (Fry et al., 2009; Casewell et al., 2013; Schendel et al., 2019). This includes cnidarians (jellyfish, anemones, corals), cephalopods (octopuses, cone snails), arachnids (spiders, scorpions, ticks), insects (bees, wasps, ants), myriapods (centipedes), fish (stonefish, lionfish, stingrays), reptiles (snakes, lizards, including the Komodo dragon), and mammals (platypus, solenodons, shrews). Each independent origin involves the recruitment of different protein families into venom, the evolution of distinct venom glands and delivery systems, and lineage-specific patterns of gene duplication and neofunctionalization.

Zancolli et al. (2022) performed a comparative transcriptomic analysis of venom glands from 20 species representing eight independent origins and found evidence of convergent gene expression profiles, suggesting that similar molecular toolkit components are repeatedly co-opted for venom production across distantly related lineages. Under the YEC model, all 100+ independent venom origins must have occurred within a few thousand years, in parallel, across unrelated “kinds.” No mechanism has been proposed to explain how organisms that supposedly lacked venom in the original creation could independently evolve functionally convergent venom systems at such an extraordinary rate. Sanders’ article does not even acknowledge the existence of this problem.

Coevolutionary Arms Races

Many DAS exist not in isolation but as components of coevolutionary arms races between predators and prey, parasites and hosts, or herbivores and plants. The classic example is the coevolution between rough-skinned newts (Taricha granulosa) and common garter snakes (Thamnophis sirtalis) in the Pacific Northwest. The newts produce tetrodotoxin (TTX), one of the most potent neurotoxins known, in their skin. Garter snakes in sympatric populations have evolved resistance to TTX through specific amino acid substitutions in their sodium channel proteins (Geffeney et al., 2005). The geographic mosaic of TTX levels in newts and resistance levels in snakes provides direct evidence of an ongoing coevolutionary escalation.

Under the YEC model, both the newt’s TTX production and the snake’s TTX resistance must have evolved after the Fall, yet they show a tight coevolutionary geographic pattern that implies a long history of reciprocal selection. How could this geographic mosaic—with graduated levels of toxin and resistance precisely matched across populations separated by mountain ranges—have developed in only a few thousand years? The YEC model offers no explanation.

Molecular Clock Evidence

Molecular clock analyses consistently date the divergence of major venom toxin gene families to tens or hundreds of millions of years ago. For example, the Toxicofera hypothesis places the earliest acquisition of venom in squamate reptiles at approximately 170–185 million years ago, based on molecular phylogenetic analyses (Fry et al., 2006; Shibata et al., 2018). Even if one were to dispute specific divergence dates, the relative branching order of toxin gene families within snake genomes shows patterns of gene duplication and divergence that are consistent with deep evolutionary time and wholly inconsistent with a few thousand years of post-Fall modification. The synonymous substitution rates in venom toxin genes provide an independent molecular clock that cannot be reconciled with the YEC timeline without invoking mutation rates orders of magnitude higher than anything observed in any living organism.

The Theological Problem of Pre-Programmed Suffering

Sanders himself hints at a significant theological difficulty when he writes: “Because God knew, before he ever created Adam, that man would fall, he may have made the world in such a way as to be prepared for it.” This is a remarkable admission. If God “pre-programmed” organisms with hidden venom systems, parasitic capabilities, and predatory anatomies—knowing they would be activated by the Fall—then the distinction between a “very good” creation and a creation designed for predation and suffering becomes vanishingly thin. This is not a creation that was corrupted by sin; it is a creation that was engineered from the beginning to produce suffering upon activation of a divine trigger. Many theologians, including those within the Reformed tradition, have noted that this view effectively makes God the designer of biological evil, merely deferring its expression to a later date (see Murray, 2008, for a philosophical treatment of this issue).

Furthermore, as I have explored extensively in my work on the prelapsarian acacia and the “good creation” (Duff, 2012), the YEC assumption that any feature associated with competition, defense, or predation must be a post-Fall corruption reflects a misunderstanding of the Hebrew tov (“good”) in Genesis 1. The text describes creation as functionally fit for its intended purpose—not as a paradise free of all ecological interactions that modern humans might find aesthetically displeasing. The projection of a modern, sentimentalized view of nature onto the Genesis text is exegetically unwarranted.

The Absence of Testable Hypotheses

Perhaps the most damning feature of Sanders’ article is the complete absence of testable hypotheses. A scientific explanation, however preliminary, should generate predictions that can be evaluated against empirical data. Sanders’ four mechanisms generate no such predictions. Consider what testable predictions would be expected if the YEC model were correct:

If the “different use” hypothesis were correct, we should be able to identify vestigial features of original benign functions in current DAS. Where are the remnants of the Venus flytrap’s “pollen capture” anatomy? Where is evidence that lamprey oral discs retain any trace of a hypothetical algae-scraping function?

If the “revealed” hypothesis were correct, we should find evidence of recently silenced or recently activated gene networks in venom systems—regulatory elements that still bear the signatures of recent switching. Instead, comparative genomics reveals deep, conserved regulatory architectures with ancient phylogenetic signatures.

If the “different interaction” hypothesis were correct, parasites should show clear molecular signatures of very recent divergence from free-living relatives—on the order of thousands, not millions, of years. Instead, molecular phylogenetics consistently places the origins of major parasitic lineages deep in geological time.

None of these predictions are confirmed. The YEC model for DAS origins makes no predictions that distinguish it from the null hypothesis of “we don’t know, but God did something.” It is, in the words of Karl Popper, unfalsifiable—and therefore, by the standard criteria of scientific inquiry, not a scientific hypothesis at all.

Conclusion

Sanders’ article represents a sincere attempt to address one of young-earth creationism’s most difficult problems, and it is more forthcoming than many YEC treatments in acknowledging the genuine difficulty that DAS pose. However, its proposed solutions are scientifically inadequate by any reasonable standard. Each mechanism—different use, revealed genetic information, different reaction, and degenerated interactions—is offered as an untested, ad hoc narrative that ignores the molecular, genetic, phylogenetic, and paleontological evidence that bears directly on the question.

The article ultimately reveals the fundamental tension at the heart of the YEC approach to biology: the need to simultaneously deny that evolution can produce complex new features while requiring evolution to produce an extraordinary diversity of complex new features—venoms, parasitic life cycles, predatory anatomies, defensive armor—in a fraction of the time available under mainstream models. This hyperevolution paradox is not resolved by Sanders’ article; it is deepened.

As scientists and as Christians, we do better when we allow the evidence to speak clearly rather than forcing it into predetermined theological conclusions. The natural world’s defense and attack structures are remarkable testimonies to the power of evolutionary processes operating over deep time. Acknowledging this does not diminish the Creator; it deepens our appreciation for the intricate and ongoing processes through which the natural world has been providentially sustained.

References

Note: References to Sanders’ article are from H.F. Sanders III, “How Did Animals Develop Defense and Attack Structures?” Answers in Genesis, February 25, 2026. All references cited by Sanders are acknowledged; additional references are listed below.

Casewell, N.R., Wüster, W., Vonk, F.J., Harrison, R.A., and Fry, B.G. (2013). Complex cocktails: the evolutionary novelty of venoms. Trends in Ecology & Evolution 28: 219–229.

Castoe, T.A., et al. (2024). Diverse gene regulatory mechanisms alter rattlesnake venom gene expression at fine evolutionary scales. Genome Biology and Evolution 16(7): evae110.

Dobson, A., Lafferty, K.D., Kuris, A.M., Hechinger, R.F., and Jetz, W. (2008). Homage to Linnaeus: how many parasites? How many hosts? Proceedings of the National Academy of Sciences 105: 11482–11489.

Duff, J. (2012). The prelapsarian acacia and the good creation: on the origin of thorns. The Natural Historian. https://thenaturalhistorian.com/2017/01/23/on-the-origin-of-thorns-the-prelapsarian-acacia-and-the-good-creation/

Ellison, A.M. and Gotelli, N.J. (2009). Energetics and the evolution of carnivorous plants—Darwin’s “most wonderful plants in the world.” Journal of Experimental Botany 60(1): 19–42.

Fry, B.G. (2005). From genome to “venome”: molecular origin and evolution of the snake venom proteome inferred from phylogenetic analysis of toxin sequences and related body proteins. Genome Research 15: 403–420.

Fry, B.G., Roelants, K., Champagne, D.E., et al. (2009). The toxicogenomic multiverse: convergent recruitment of proteins into animal venoms. Annual Review of Genomics and Human Genetics 10: 483–511.

Fry, B.G., et al. (2006). Early evolution of the venom system in lizards and snakes. Nature 439: 584–588.

Geffeney, S.L., Fujimoto, E., Brodie, E.D. III, Brodie, E.D. Jr., and Ruben, P.C. (2005). Evolutionary diversification of TTX-resistant sodium channels in a predator-prey interaction. Nature 434: 759–763.

Glenner, H. and Hebsgaard, M.B. (2006). Phylogeny and evolution of life history strategies of the parasitic barnacles (Crustacea, Cirripedia, Rhizocephala). Molecular Phylogenetics and Evolution 41: 528–538.

Murray, M.J. (2008). Nature Red in Tooth and Claw: Theism and the Problem of Animal Suffering. Oxford University Press.

Oliver, S.P., Turner, J.R., Gann, K., Silvosa, M., and Jackson, T.D. (2013). Thresher sharks use tail-slaps as a hunting strategy. PLoS ONE 8(7): e67380.

Schendel, V., Rash, L.D., Jenner, R.A., and Undheim, E.A.B. (2019). The diversity of venom: the importance of behavior and venom system morphology in understanding its ecology and evolution. Toxins 11(11): 666.

Senchina, D.S. (2008). Fungal and animal associates of Toxicodendron spp. (Anacardiaceae) in North America. Perspectives in Plant Ecology, Evolution and Systematics 10(3): 197–216.

Shibata, H., et al. (2018). The habu genome reveals accelerated evolution of venom protein genes. Scientific Reports 8: 11300.

Vidal, N. and Hedges, S.B. (2002). Higher-level relationships of caenophidian snakes inferred from four nuclear and mitochondrial genes. Comptes Rendus Biologies 325: 987–995.

Volkov, A.G., Markin, V.S., and Jovanov, E. (2008). Active movements in plants. Plant Signaling and Behavior 3(10): 778–783.

Vonk, F.J., et al. (2013). The king cobra genome reveals dynamic gene evolution and adaptation in the snake venom system. Proceedings of the National Academy of Sciences 110(51): 20651–20656.

Zancolli, G., et al. (2022). Convergent evolution of venom gland transcriptomes across Metazoa. Proceedings of the National Academy of Sciences 119(1): e2111392119.