In the animal kingdom, any hunt for a meal or encounter with a predator is a matter of life and death. To survive both, animals have evolved a multitude of weapons, of which venoms may be one of the most and effective.
But building a chemical weapon presents an evolutionary dilemma. Should venom be optimised to disarm prey, or to cause rapid pain to deter predators? Our suggests that in snakes, a meal comes before self-defence.
are complex chemical cocktails. Their composition is shaped fundamentally by their intended purpose. Predatory venoms disrupt multiple tissues and organs at once to immobilise prey. On the other hand, defensive venoms have only one job: to cause rapid, intense pain to deter predators. Think of a bee sting, for example.
These differences create a conundrum. What if an animal wants to use its venom for both predation and defence? This is not a trivial question, because the storage capacity of venom glands is limited, and producing venoms is thought to carry an energetic cost. That opens the door to an evolutionary trade-off: investing resources into one function might leave less for the other.
Venomous snakes are probably the best-studied venomous organisms, and for a good reason. Unfortunately, snakebite remains a , especially in tropical countries. More than 100,000 people die yearly and more than 400,000 people suffer lifelong injuries as a consequence of snakebite.
In theory, antivenoms could prevent many of those deaths, but there is another problem. Snake venoms are extremely variable, not just between species but also between different populations of the same species. This means that antivenoms developed for one region can in another. Understanding what drives this immense venom variation is the first step towards more effective treatments.
Snakes use their venoms both for hunting and self-defence. We have good evidence that diet is the central factor shaping venom composition in many snakes. In contrast, defence against predators has as an important evolutionary driver, and never in comparison with diet.
Based on the results of a , we suspected that species that hunt easy, low-risk prey such as insects might not need a highly lethal predatory venom, freeing up resources to invest in more defensive, pain-inducing compounds instead.
To test this idea, we looked at a group of venomous snakes called meadow vipers (Vipera ursinii and relatives). These curious little snakes live in the lowland steppes and alpine meadows of Eurasia. Their diet is unusual among vipers, as they eat mostly or almost entirely grasshoppers, crickets and locusts.
On the other hand, they also regularly fall prey to predators like birds of prey, badgers and foxes. It’s exactly the kind of pressure that might favour a defensive venom.
For our study, we travelled to where their populations can be found across Europe to obtain venom by “milking” them. It’s a process that causes no harm to the snakes, and they were released back to their habitats afterwards. We also collected venom from other European vipers like the adder (V. berus), asp viper (V. aspis) and nose-horned viper (V. ammodytes), which mostly feed on more dangerous prey, like rodents.
If our trade-off theory held, we would expect these venoms to be more predatory and less pain-inducing than those of meadow vipers.
Putting venom to the test
To measure pain, we tested the venoms on cultures of specialised sensory neuron cells. These are cells responsible for detecting harmful stimuli in the body. If such a cell is activated to produce pain, calcium ions flow into the cell. So, to track whether venom triggered these cells, we treated them with a fluorescent dye that reacts to calcium and measured the emitted fluorescence.
To our surprise, regardless of diet, none of the tested venoms activated these cells, not even that of the insect-feeding meadow vipers. So, it appears that European viper venoms, like in most snakes, probably evolved to overcome prey rather than to fend off predators.
All this does does not mean that viper bites don’t hurt. They do. But it seems that the pain is mostly caused as a side effect of other venom actions, such as inflammation, tissue degradation or muscle spasms.
There are however exceptions elsewhere in the snake world. Some toxins found in lanceheads and coral snakes do directly stimulate pain receptors. However, such toxins have been documented in only a handful of species and their ecological function remains enigmatic.
That means the story of snake venom is far from complete. Rather than revealing a universal rule, our findings suggest that, at least in European vipers, the evolutionary pressure to catch prey has outweighed the need to deter predators. Understanding where that pattern holds – and where it doesn’t – could help explain why snake venoms vary so dramatically, an essential step towards developing better treatments for snakebite around the world.