Speaking as part of a new series at Gresham College, Professor Robin May introduced the discussion on fear as perhaps the most fundamental and basal human emotion. This evolutionary conserved process is the easiest to understand because its primary purpose is to keep us alive. May began his lecture by noting how instinctively humans relate to mortal terror, such as the feeling invoked by Turner's painting of a shipwreck. The rapid, visceral nature of fear means that it bypasses higher cognitive thought, tapping into our most fundamental feelings.
The biological root of this powerful response lies deep within the brain, involving the hypothalamus, which regulates basic autonomic functions like breathing and blood pressure, and the adjacent, almond-shaped amygdalae. Because fear must activate swiftly, these structures are close to the core of the brain and often trigger a response, like jumping at a loud noise, before the higher parts of the brain have processed the event. This immediate biological activation drives the release of fear hormones, most notably adrenaline, from the adrenal glands. Adrenaline primes the body for fight-or-flight, causing an elevated heart rate, constricted blood vessels to raise blood pressure, and sweating. The dilation of the pupils is another key feature, maximizing light intake to prioritize vague, peripheral perception suitable for quickly locating a threat over fine focus. The effectiveness of this biological response is so pronounced that filmmakers use devices to measure pupil dilation in audience testing to confirm a movie's scary effect.
This intrinsic biology of fear is also subject to feedback loops. Professor May cited an experiment where volunteers watched a horror movie after being injected with either a placebo or adrenaline. Those given adrenaline rated the movie as scarier, exhibited stronger pupil dilation, and formed a more potent memory of the film. This suggests that intervening in the physiological response—such as taking a deep breath—can calm the mental response. However, this mechanism also means that highly fearful events create very strong, protective memories.
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When this system malfunctions, it can lead to debilitating conditions like panic disorder, defined by repeated, unexplained panic attacks. These disorders impact a significant number of people, affecting approximately 2.7% of the US population in a given year, and are roughly twice as common in women. Genetic factors play a role, with variation in the gene producing the enzyme Catechol-O-methyltransferase (COMT) being particularly relevant. A common variant makes this enzyme less efficient at breaking down fear-triggering neurotransmitters like adrenaline, leading to a more profound and prolonged fear response.
Furthermore, individuals with panic disorder may exhibit heightened sensitivity to rising CO2 levels, a basal panic inducer. Interestingly, the CO2 response is so basal that patient "SM," a woman whose amygdalae died due to Urbach-Wiethe syndrome, still experienced panic when exposed to CO2, despite being otherwise fearless.
Beyond pathology, natural variation in fear is also highly modulated, with an estimated 30-50% heritability component. May noted the wide gap between those who love roller coasters and those who avoid heights. This variation is strongly linked to genes that regulate GABA (gamma aminobutyric acid) signaling. GABA acts as a crucial neurotransmitter that "tunes" the core adrenaline response, suggesting individual fear levels may be highly modulated by these tuning factors. The GABA axis is especially interesting because its levels can be influenced by diet, opening a potential route for future non-interventionist ways to influence fear responses.
The presentation also explored the fascinating, external influences on fear and bravery. For instance, the parasite Toxoplasma gondii, which needs to infect cats to complete its life cycle, infects rodents and removes their fear of felines. When this parasite forms cysts in the human brain, infected individuals are twice as likely to engage in risky behaviors, such as car crashes or opening a business (and subsequently going bankrupt), suggesting the microbe modulates human risk perception. A less invasive microbial influence stems from the gut microbiome. The trillions of bacteria in the gut produce and break down neurotransmitters, including GABA. Experiments on mice confirm that germ-free mice are significantly more anxious, and researchers can induce bravery through microbiome transplantation, suggesting that gut bacteria may influence our fear response.
Finally, Professor May addressed the concept of sensing fear through scent. While humans are thought to have lost the functional vomeronasal organ used by dogs and rodents to detect fear pheromones, experiments demonstrate a subliminal response in humans. Sniffing sweat collected from skydivers (fear-induced sweat) causes the sniffer's amygdala to activate and makes them respond more potently to scary faces, indicating that the brain responds biologically to volatile, scent-based signals of fear. Professor May concluded on an optimistic note, stating that learning enough about the biology of fear offers the best ability to help people whose lives have been negatively impacted by this basal emotion get better faster.
