Erasing Fears & Traumas Based on the Modern Neuroscience of Fear

The episode opens by presenting itself as a discussion of the neuroscience of fear, and of trauma and post-traumatic stress disorders. The host, who introduces himself as a professor of neurobiology and ophthalmology at Stanford School of Medicine, says fear has a long history in biology and psychology. His claim is that roughly the last 10 years of neuroscience have clarified two things: the neural circuits that control the fear response, and some ways to extinguish fears using behavioral therapies, drug therapies and brain-machine interfaces. He promises both an account of the biology and practical tools for confronting fear and trauma.

He previews a recently published study in which five minutes a day of deliberate exposure to stress was reported to relieve longstanding depressive and fear-related symptoms. He calls it a "somewhat counterintuitive" example of using stress to combat fear. The study's details and the protocol drawn from it are held back for later in the episode, so this section offers no evidence about its design or results.

The stated plan has three parts. First comes the biology of fear and trauma at the level of cells, circuits, connections and chemicals. Next is why fear sometimes, though not always, turns into trauma. Last is how fear is unlearned, or extinguished. Within that plan the host flags what he calls a key surprise:

we can't just eliminate fears; we actually have to replace fears with a new positive event.

The host also states that the podcast is separate from his teaching and research roles at Stanford, and he thanks the sponsors.

The host classes fear as an emotion but explicitly avoids the long-running debate over what an emotion is. He offers a working view instead: emotions combine bodily responses, such as a faster heart rate, changes in blood flow and sensations of the skin warming or cooling, with cognitive components such as thoughts and memories. He sets aside questions about how many emotions exist and how different people experience them, saying a future episode will cover them. He treats fear narrowly as a physiological and cognitive response because that framing leads to concrete mechanisms and practical tools for dealing with unwanted fear.

He then defines fear by what it is not. He describes stress as a physiological response: a faster heart rate, usually faster breathing, blood flow redirected to some areas of the brain and body and away from others, and a hypervigilance that is typically narrower in space, "like a soda-straw view of the world." Anxiety tends to be stress about some future event, though the word can mean other things. The relationship he proposes runs in one direction. Fear cannot occur without several, if not all, elements of the stress response and some elements of anxiety. Stress and anxiety, however, can occur without fear.

Trauma gets what he calls an operational definition, meaning a definition people agree on well enough to hold a conversation. As he defines it, trauma means some fear occurred and that fear became embedded or activated in the nervous system so that it reappears when it is maladaptive. His example is waking in the morning with no frightening stimulus present and suddenly experiencing something like a panic attack. He labels this post-traumatic stress, or post-traumatic fear. He also defines panic attacks as extreme fear without any fear-inducing stimulus, which he says is "kind of like trauma." Phobias are extreme fear of something specific, such as spiders, heights, flying or dying.

He says the purpose of this layering is to simplify, not to create a "word soup." With the related terms laid out, he narrows the focus to fear and trauma as biological and cognitive processes, so he can examine how fears form, how they are undone, and how new memories can replace earlier fearful experiences.

The host introduces autonomic arousal through the autonomic nervous system. He notes that "autonomic" means automatic but calls the term somewhat of a misnomer, because some aspects of the system can be controlled. The system governs digestion, urination, sexual behavior, stress, and the timing of wakefulness and sleep. It has two branches. The sympathetic branch, which he says has nothing to do with sympathy, increases alertness and vigilance, and he compares it to an accelerator. The parasympathetic branch is the calming system. He describes the two as a seesaw that sets overall alertness. As he speaks, he describes himself as alert but calm, with the seesaw roughly level or tilted slightly toward the sympathetic side. Sleepiness would tilt it the other way.

He singles out the HPA axis as a recurring theme of the episode. HPA stands for hypothalamic-pituitary-adrenal. The hypothalamus sits deep at the base of the brain and contains many areas that regulate temperature, sexual desire, hunger and thirst. It has "accelerators and brakes" for these drives, so it can also suppress them. The pituitary, near the roof of the mouth, releases hormones into the bloodstream. Through it, the hypothalamus can trigger or block the release of hormones such as cortisol and the hormones that stimulate the ovaries, testes and adrenals. The adrenal glands sit above the kidneys and receive both neural and hormonal signals. The two outputs he stresses are adrenaline, also called epinephrine, and cortisol. He adds that these "stress hormones" are not always tied to stress, because they are also involved in waking from sleep.

The key property he draws out is timing. The HPA axis can make the body alert and ready for action right away. It can also trigger chemicals that give that alertness "a very long tail" before it switches off. He links this to trauma. The triggering event can be very brief, such as a car that nearly hits you or a sudden gunshot lasting around 500 milliseconds to one second, yet the fear response can keep reverberating. He says the longer-lasting component can change connections between brain areas and the working of organs like the heart and lungs. It can also feed back to the brain to control gene expression, which can take many days and build new circuits and chemicals that embed fear in the brain and body.

He acknowledges this might sound depressing, and he says the fast and slow phases have an adaptive reason without spelling it out in this section. His hopeful point is that the same gene expression and long arc of the fear response, which he likens to a phantom living in the system, can also be used to undo the response: to extinguish it and replace it with nonfearful associations.

The circuit discussion starts with the amygdala, an almond-shaped structure found on both sides of the brain. The host's central reframing is that fear includes a reflex. He builds the analogy from the spinal reflex triggered by stepping on something sharp. One foot lifts, and a second reflex extends the other leg so you don't fall. Fear similarly involves a reflex. It speeds the heart, raises vigilance, switches on attention and makes energy available for movement and thought. Meanwhile the circuits for calm, for sleep and for taking in the whole visual and auditory environment shut down. He describes the amygdala as essentially the final common pathway of this threat reflex.

the way I'd like you to think about the amygdala is not as a fear center, but that it's a critical component of the threat reflex.

He calls this reflex "kind of a dumb response": generic rather than sophisticated. In his account, its generality is one of the system's strengths. It is not designed around any one object of fear. He notes there are debates, and "probably some good data," suggesting that human babies are innately afraid of things like heights, snakes or spiders. He also says the debate depends on the quality of the experiments. His broader claim is that people can become afraid of anything if the threat system is activated together with some external experience. That raises the question the rest of the section answers: how specific triggers such as a spider, a car accident or public speaking get attached to a reflex that "doesn't really know what to be afraid of."

The host explains that the amygdala belongs to a larger amygdaloid complex. Depending on which neuroanatomist does the dividing, the complex has 12 to 14 areas. He uses the field's joke about "lumpers" and "splitters" to explain why the count varies, places himself in between, and settles on 12. The point he draws is that the amygdala generates threat reflexes by integrating many kinds of information. Inputs from memory systems such as the hippocampus, and from the senses (vision, hearing, smell, taste and touch), flow into the lateral portion of the complex.

He describes two main output pathways. The first goes to threat-response structures: