Fight, flight, freeze… or just hack someone else’s brain?

As we know, there are three basic survival strategies in the wild. Encountered danger? In that case, fight, flee (“run”), or play dead (“freeze”/”hide”). But here’s the thing: while we thought this was an exhaustive menu, evolution decided not to stop there. As it turns out, there is a fourth, far more sophisticated path in the wild. Let’s call it “hack your neighbor’s neurobiology.”

Imagine: you are a huge, strong tropical cockroach. An emerald cockroach wasp (which is about three times smaller than you) flies up to you and gives you a quick sting. You are alive, you are conscious, your legs are working. But you… don’t want anything anymore. The wasp delivers a second, surgically precise sting directly into the cockroach’s subesophageal ganglion (the brain). Its venom acts as a perfect blocker of octopamine—the neurotransmitter responsible for initiative and the motivation to move. The cockroach is not paralyzed! It simply completely loses its free will. It is in a state of severe apathy. The wasp takes the giant by its antenna and, like a compliant dog on a leash, leads it to its burrow, where it will lay an egg on it. The larva will eat the cockroach alive, and the cockroach won’t even attempt to escape.

There is also the famous Toxoplasma (Toxoplasma gondii). This single-celled parasite desperately needs to get into a cat’s intestine—that is the only place where it can reproduce. But how do you get there if you are currently inside a mouse? Toxoplasma doesn’t just wait for the mouse to be eaten by chance. It takes control! The parasite forms microscopic cysts in the amygdala of the mouse’s brain, as a result of which the mouse completely loses its innate terror of the smell of cat urine, or even begins to experience slight sexual arousal from it. The mouse goes out into the open on its own, searches for a cat, and predictably becomes its lunch.

Another very cool example: the lancet fluke—a flatworm that needs to get from an ant into the stomach of a sheep or a cow. It penetrates directly into the ant’s subesophageal ganglion and takes the helm like a seasoned truck driver. In the evening, when it gets cold, the parasite forces the ant to separate from the colony, climb to the very tip of a tall blade of grass, and cling to it firmly with its jaws. The ant hangs there and waits to be swallowed by a cow. But do you know what is most amazing? If the cow doesn’t come during the night, and in the morning the sun begins to blaze (which could cause the ant to dry up and die along with the parasite), the worm releases control! It allows the ant to unclench its jaws, descend to the ground, and hide in the shade. The ant spends the whole day living its usual ant life, and in the evening, the parasite presses the button again: “Time to climb the blade of grass!”. And so it goes until they are eaten.

Why is this so cool? When we hear the word “parasite,” we imagine someone who just drinks blood or steals nutrients. But evolution has shown: information and control over behavior are the most valuable resources. These creatures do not control the victim through fear. They use perfect knowledge of neuropharmacology. They synthesize analogues of dopamine, serotonin, various alkaloids and proteins that “hack” the neural circuits of other species. This is not a random system glitch, but the result of millions of years of harsh evolutionary selection. Those who learned to change the host’s behavior in their favor survived and reproduced much more effectively than those who just sat and waited for a miracle. And nature didn’t give a damn about philosophical concepts like “free will”!

What does this mean for us, humans? Acting upon the neurobiology of an opponent who threatens us with harm—for the sake of bio-enhancing morality or as a violence inhibitor—is also not some “madman’s rambling,” but a fully successful strategy supported by millions of years of evolution, which is becoming technologically more accessible to us every day. If you don’t like such an approach at all, then look at yourself and propose full recognition of the Non-Aggression Principle (NAP) and the impermissibility of violence in exchange for the limitation of biotech weapons that affect behavior.

Voluntarist, Bitarch

What exactly in our brain makes us non-violent

Voluntarist, Bitarch

Extremely interesting and important results were demonstrated by experiments on the use of anti-aggressive agents in mice and rats. It turned out that some of them are capable of reducing the manifestation of attacking aggression on their part, while not affecting defensive aggression and other non-aggressive forms of behavior and social communication. To be more specific, we are talking about agonists that activate serotonin 5-HT1A/1B receptors.

These results align with the theory that many species possess innate inhibitors of aggressive behavior, which prevent causing harm and killing members of their own species. In the case of humans, a model of the violence inhibition mechanism (VIM) was even developed, which also explains the development of empathy. Based on this theory, violence in intraspecific relationships should be viewed as a pathological rather than a natural form of behavior. Especially since even in many territorial, social, and armed species, the level of lethal violence still does not exceed 1%, and according to various evidence, only no more than 2% of people do not experience strong resistance to committing murder.

We also see that defensive aggression, unlike attacking aggression, is indeed a natural form of behavior, and the work of the violence inhibitor does not stop it in the presence of an immediate threat to life in the environment. This was well demonstrated by the administration of the 5-HT1A agonist alnespirone to rats. It had an extremely selective effect; the strong reduction in aggressiveness did not prevent the rats from resorting to defensive behavior when encountering an aggressive peer.

Various genetic evidence demonstrates that certain variants of the 5-HT1A/1B receptor genes, as well as three other genes associated with the 5-HT system—TPH2, MAO A (also known as the “warrior gene”), and SERT—lead to increased aggressiveness in animals and humans. For example, in one study, impulsive and aggressive alcoholics were found to have differences in the 5-HT1B gene compared to healthy people and non-aggressive alcoholics. This study covered two different groups of people: Finns and a Native American tribe. Mutations in the MAO A gene have long been known as a cause of abnormal manifestations of aggression in men.

According to the violence inhibition mechanism model, the direct result of its dysfunction is calloused-unemotional (CU) traits in children and psychopathy in adults. Changes in the function of 5-HT1B receptors in certain parts of the brain were found in people with aggressive traits and psychopathic traits. A difference in the 5-HT1B gene genotype was present in children with calloused-unemotional traits.

It should be noted that dozens of genes and a large number of systems influence aggressiveness. However, the violence inhibitor remains a specific mechanism expressed by a limited number of receptors and genes. Firstly, this is simply important for inhibiting aggression most effectively. Secondly, other forms of pharmacological intervention, such as the use of antipsychotics (like haloperidol), beta-blockers, drugs affecting GABA neurotransmitters, and 5-HT2 receptor agonists and antagonists (many psychedelics belong to the former), result only in a non-selective reduction of aggressiveness, suppressing defensive aggression and other forms of behavior, and causing side effects.

Understanding the nature of the violence inhibitor and its limitation to a small number of receptors and genes can not only tell us a lot about violence itself, but also help in creating a solution aimed against it as a pathological form of behavior inherent in a minority of people. And the essence of such a solution is simple: returning to them the inhibiting control over aggression that is natural for the majority, through the use of appropriate pharmacological or even gene-therapeutic drugs.

This material briefly describes the content of the article titled “Neurophysiology and Genetics of the Violence Inhibition Mechanism“, which you may refer to for greater detail.