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What Happens in the Brain When We Feel Fear. And why some of us just can’t get enough of it

What Happens in the Brain When We Feel Fear?

Fear may be as old as life on Earth. It is a fundamental, deeply wired reaction, evolved over the history of biology, to protect organisms against perceived threat to their integrity or existence. Fear may be as simple as a cringe of an antenna in a snail that is touched, or as complex as existential anxiety in a human.

Whether we love or hate to experience fear, it’s hard to deny that we certainly revere it – devoting an entire holiday to the celebration of fear. Thinking about the circuitry of the brain and human psychology, some of the main chemicals that contribute to the “fight or flight” response are also involved in other positive emotional states, such as happiness and excitement. So, it makes sense that the high arousal state we experience during a scare may also be experienced in a more positive light. But what makes the difference between getting a “rush” and feeling completely terrorized?

We are psychiatrists who treat fear and study its neurobiology. Our studies and clinical interactions, as well as those of others, suggest that a major factor in how we experience fear has to do with the context. When our “thinking” brain gives feedback to our “emotional” brain and we perceive ourselves as being in a safe space, we can then quickly shift the way we experience that high arousal state, going from one of fear to one of enjoyment or excitement.

When you enter a haunted house during Halloween season, for example, anticipating a ghoul jumping out at you and knowing it isn’t really a threat, you are able to quickly relabel the experience. In contrast, if you were walking in a dark alley at night and a stranger began chasing you, both your emotional and thinking areas of the brain would be in agreement that the situation is dangerous, and it’s time to flee!

But how does your brain do this?

Fear reaction starts in the brain and spreads through the body to make adjustments for the best defense, or flight reaction. The fear response starts in a region of the brain called the amygdala. This almond-shaped set of nuclei in the temporal lobe of the brain is dedicated to detecting the emotional salience of the stimuli – how much something stands out to us.

For example, the amygdala activates whenever we see a human face with an emotion. This reaction is more pronounced with anger and fear. A threat stimulus, such as the sight of a predator, triggers a fear response in the amygdala, which activates areas involved in preparation for motor functions involved in fight or flight. It also triggers release of stress hormones and sympathetic nervous system.

This leads to bodily changes that prepare us to be more efficient in a danger: The brain becomes hyperalert, pupils dilate, the bronchi dilate and breathing accelerates. Heart rate and blood pressure rise. Blood flow and stream of glucose to the skeletal muscles increase. Organs not vital in survival such as the gastrointestinal system slow down.

A part of the brain called the hippocampus is closely connected with the amygdala. The hippocampus and prefrontal cortex help the brain interpret the perceived threat. They are involved in a higher-level processing of context, which helps a person know whether a perceived threat is real.

For instance, seeing a lion in the wild can trigger a strong fear reaction, but the response to a view of the same lion at a zoo is more of curiosity and thinking that the lion is cute. This is because the hippocampus and the frontal cortex process contextual information, and inhibitory pathways dampen the amygdala fear response and its downstream results. Basically, our “thinking” circuitry of brain reassures our “emotional” areas that we are, in fact, OK.

Being attacked by a dog or seeing someone else attacked by a dog triggers fear

Similar to other animals, we very often learn fear through personal experiences, such as being attacked by an aggressive dog, or observing other humans being attacked by an aggressive dog.

However, an evolutionarily unique and fascinating way of learning in humans is through instruction – we learn from the spoken words or written notes! If a sign says the dog is dangerous, proximity to the dog will trigger a fear response. We learn safety in a similar fashion: experiencing a domesticated dog, observing other people safely interact with that dog or reading a sign that the dog is friendly.

Fear creates distraction, which can be a positive experience. When something scary happens, in that moment, we are on high alert and not preoccupied with other things that might be on our mind (getting in trouble at work, worrying about a big test the next day), which brings us to the here and now.

Furthermore, when we experience these frightening things with the people in our lives, we often find that emotions can be contagious in a positive way. We are social creatures, able to learn from one another. So, when you look over to your friend at the haunted house and she’s quickly gone from screaming to laughing, socially you’re able to pick up on her emotional state, which can positively influence your own.

While each of these factors - context, distraction, social learning - have potential to influence the way we experience fear, a common theme that connects all of them is our sense of control. When we are able to recognize what is and isn’t a real threat, relabel an experience and enjoy the thrill of that moment, we are ultimately at a place where we feel in control. That perception of control is vital to how we experience and respond to fear. When we overcome the initial “fight or flight” rush, we are often left feeling satisfied, reassured of our safety and more confident in our ability to confront the things that initially scared us.

It is important to keep in mind that everyone is different, with a unique sense of what we find scary or enjoyable. This raises yet another question: While many can enjoy a good fright, why might others downright hate it? Any imbalance between excitement caused by fear in the animal brain and the sense of control in the contextual human brain may cause too much, or not enough, excitement. If the individual perceives the experience as “too real,” an extreme fear response can overcome the sense of control over the situation.

This may happen even in those who do love scary experiences: They may enjoy Freddy Krueger movies but be too terrified by “The Exorcist,” as it feels too real, and fear response is not modulated by the cortical brain.

On the other hand, if the experience is not triggering enough to the emotional brain, or if is too unreal to the thinking cognitive brain, the experience can end up feeling boring. A biologist who cannot tune down her cognitive brain from analyzing all the bodily things that are realistically impossible in a zombie movie may not be able to enjoy “The Walking Dead” as much as another person.

So if the emotional brain is too terrified and the cognitive brain helpless, or if the emotional brain is bored and the cognitive brain is too suppressing, scary movies and experiences may not be as fun.

All fun aside, abnormal levels of fear and anxiety can lead to significant distress and dysfunction and limit a person’s ability for success and joy of life. Nearly one in four people experiences a form of anxiety disorder during their lives, and nearly 8 percent experience post-traumatic stress disorder (PTSD).

Disorders of anxiety and fear include phobias, social phobia, generalized anxiety disorder, separation anxiety, PTSD and obsessive compulsive disorder. These conditions usually begin at a young age, and without appropriate treatment can become chronic and debilitating and affect a person’s life trajectory. The good news is that we have effective treatments that work in a relatively short time period, in the form of psychotherapy and medications.

5 Things You Never Knew About Fear

Fear Is Physical

Fear is experienced in your mind, but it triggers a strong physical reaction in your body. As soon as you recognize fear, your amygdala (small organ in the middle of your brain) goes to work. It alerts your nervous system, which sets your body’s fear response into motion. Stress hormones like cortisol and adrenaline are released. Your blood pressure and heart rate increase. You start breathing faster. Even your blood flow changes — blood actually flows away from your heart and into your limbs, making it easier for you to start throwing punches, or run for your life. Your body is preparing for fight-or-flight.

Fear Can Make You Foggy

As some parts of your brain are revving up, others are shutting down. When the amygdala senses fear, the cerebral cortex (area of the brain that harnesses reasoning and judgment) becomes impaired — so now it’s difficult to make good decisions or think clearly. As a result, you might scream and throw your hands up when approached by an actor in a haunted house, unable to rationalize that the threat is not real.

Fear Can Become Pleasure

But why do people who love roller-coasters, haunted houses and horror movies enjoy getting caught up in those fearful, stressful moments? Because the thrill doesn’t necessarily end when the ride or movie ends. Through the excitation transfer process, your body and brain remain aroused even after your scary experience is over.

“During a staged fear experience, your brain will produce more of a chemical called dopamine, which elicits pleasure,” says Dr. Sikora.

Fear Is Not Phobia

If you’re slightly uneasy about swimming in the ocean after watching “Jaws,” the movie did what it set out to do. But if you find yourself terrorized, traumatized and unable to function at the mere thought of basking on the beach, you might be experiencing more than just fear.

The difference between fear and phobia is simple. Fears are common reactions to events or objects. But a fear becomes a phobia when it interferes with your ability to function and maintain a consistent quality of life. If you start taking extreme measures to avoid water, spiders or people, you may have a phobia.

Fear Keeps You Safe

“Fear is a natural and biological condition that we all experience,” says Dr. Sikora. “It’s important that we experience fear because it keeps us safe.” Fear is a complex human emotion that can be positive and healthy, but it can also have negative consequences. If a fear or phobia affects your life in negative and inconvenient ways, speak to your primary care provider, who can help determine the kind of treatment you might need.

Ralph Adolphs (RA): Fear can only be defined based on observation of behavior in a natural environment, not neuroscience. In my view, fear is a psychological state with specific functional properties, conceptually distinct from conscious experience; it is a latent variable that provides a causal explanation of observed fear-related behaviors. Fear refers to a rough category of states with similar functions; science will likely revise this picture and show us that there are different kinds of fear (perhaps a dozen or so) that depend on different neural systems.

The functional properties that define the state of fear are those that, in the light of evolution, have made this state adaptive for coping with a particular class of threats to survival, such as predators. Fear has several functional properties—such as persistence, learning, scalability and generalizability—that distinguish emotion states from reflexes and fixed-action patterns, although the latter can of course also contribute to behavior.

The neural circuits that regulate an animal’s fear-related behavior exhibit many of these same functional properties, including in the mouse hypothalamus2, are initial evidence that this brain structure is not merely involved in translating emotion states into behaviors, but plays a role in the central emotion state itself. Neuropsychological dissociations of fear from other emotions show that fear is a distinct category.

Michael Fanselow (MF): Fear is a neural–behavior system that evolved to protect animals against environmental threats to what John Garcia called the external milieu (as opposed to the internal milieu), with predation being the principal driving force behind that evolution (for example, as opposed to a toxin). This is the organizing idea behind my definition of fear. The complete definition must also include the signals giving rise to fear (antecedents) and objectively observable behaviors (consequents). The neuroscientific support for this definition is that many signals of external threat, such as cues signaling possible pain, the presence of natural predators and odors of conspecifics that have recently experienced external threats, all activate overlapping circuits and induce a common set of behaviors (for example, freezing and analgesia in rodents). Equally important as neuroscientific support is support from fieldwork, which has repeatedly shown that behaviors such as freezing enhance survival in the face of predators.

Lisa Feldman Barrett (LFB): I hypothesize that every mental event, fear or otherwise, is constructed in an animal’s brain as a plan for assembling motor actions and the visceromotor actions that support them, as well as the expected sensory consequences of those actions. The latter constitute an animal’s experience of its surrounding niche (sights, sounds, smells, etc.), including the affective value of objects. Here ‘value’ is a way of describing a brain’s estimation of its body’s state (i.e., interoceptive and skeletomotor predictions) and how that state will change as the animal moves or encodes something new. The plan is an inference (or a set of inferences) that is constructed from learned or innate priors that are similar to the present conditions; they represent the brain’s best guess as to the causes of expected sensory inputs and what to do about them.

The function most frequently associated with fear is protection from threat. The corresponding definition of fear is an instance an animal’s brain constructs defensive actions for survival. A human brain might construct inferences that are similar to present conditions in terms of sensory or perceptual features, but the inferences can also be functional and therefore abstract, and thus they may or may not be initiated by events that are typically defined as fear stimuli and may or may not result in the behaviors that are typically defined as fear behaviors. For example, sometimes humans may laugh or fall asleep in the face of a threat. In this view, fear is not defined by the sensory specifics of an eliciting stimulus or by a specific physical action generated by the animal; rather, it is characterized in terms of a situated function or goal: a particular set of action and sensory consequences that are inferred, based on priors, to serve a particular function in a similar situation (for example, protection).

In cognitive science, a set of objects or events that are similar in some way to one another constitute a category, so constructing inferences can also be described as constructing categories. Another way to phrase my hypothesis, then, is that a brain is dynamically constructing categories as guesses about which motor actions to take, what their sensory consequences will be, and the causes of those actions and expected sensory inputs. A representation of a category is a concept, and so the hypothesis can also be phrased this way: a brain is dynamically constructing concepts as hypotheses about the causes of upcoming motor actions and their expected sensory consequences. The concepts or categories are constructed in a situation-by-situation manner, so they are called ad hoc concepts or categories. In this way, biological categories can be considered ad hoc conceptual categories.

Kay Tye (KT): Fear is an intensely negative internal state. It conducts orchestration of coordinated functions serving to arouse our peak performance for avoidance, escape or confrontation. Fear resembles a dictator that makes all other brain processes (from cognition to breathing) its slave. Fear can be innate or learned. Innate fear can be expressed in response to environmental stimuli without prior experience, such as that of snakes and spiders in humans and to predator odor in rodents. Fear associations—primarily studied in the context of Pavlovian fear conditioning—are the most rapidly learned (one trial), robustly encoded and retrieved, and prone to activate multiple memory systems. Given its critical importance in survival and its authoritarian command over the rest of the brain, fear should be one of the most extensively studied topics in neuroscience, though it trails behind investigation of sensory and motor processes due to its subjective nature. Watching others exhibit the behavioral expressions and responses of fear may invoke emotional contagion or support learning about the environment. The usage of the term ‘fear’ in the field of behavioral neuroscience has taken on a related—but distinct—meaning through the extensive use and study of a very stereotyped behavioral paradigm originally termed ‘fear conditioning’. Fear conditioning is arguably the most commonly used behavioral paradigm in neuroscience and has been most comprehensively mined in terms of neural circuit dissection with rodent models but has also been used in humans, primates and even invertebrates. Fear conditioning refers to the Pavlovian pairing of a conditioned stimulus (most often an auditory pure tone) with a foot shock that is most often presented upon the termination of the conditioned stimulus.

The Chill of Fear

Dread requires only a tenth of a second to take root

A copse can beckon, with its dappled leaves and songbird trills. But linger past twilight, and tree, bush, and animal assume different dimensions. Trunks thicken and loom, bushes snatch at clothing, and the rustlings and skitters of feather and claw magnify. You become unsettled, unnerved. You run.

You do this because you’re afraid. Even without direct evidence of danger, you’re compelled to flee, to protect yourself. Why this compulsion? It’s the work of your amygdala, a tiny almond–shaped structure in your brain. Sensory signals alert it; in turn, it triggers a cascade of activity, deluging your body with messages that widen your eyes, prick your ears, accelerate your heart, quicken your breathing, wrench your stomach, moisten your palms, and launch a full–body, organ–clenching, corpuscle–filling chill. You run quite simply because fear grips you.

“You could call the amygdala a relevance detector,” says Nouchine Hadjikhani, an HMS associate professor of radiology who specializes in capturing the activity of the brain as it reacts to fear–provoking stimuli. “In less than 100 milliseconds, just one–tenth of a second, sensory information reaches the amygdala, which signals your brain to be aware. All your systems become more receptive. You’re now ready to fight, freeze, or flee.”

The good news is that, should the terror prove benign, you’ll not long be in fear’s thrall. For while your amygdala is providing survival insurance by spurring action, sensory clues are also traveling to your prefrontal cortex. The amygdala’s action buys you additional milliseconds, during which you might glimpse a light, stumble upon a traveled road, or receive other sensory stimuli that your prefrontal cortex will use to temper the initial response. You will calm, completing an arc of reaction that has been key to mammalian survival through eons.

Investigating what drives that arc of reaction spurs much of today’s research into the molecular mechanisms of the fear response. HMS scientists are providing tantalizing insights by explaining how we decipher danger in the gazes or body movements of others, by informing treatments for conditions such as post–traumatic stress disorder, and even by providing clues to the gender–based underpinnings of human response to fear.

Fear Factors

A 2005 poll of U.S. teenagers revealed the power that emotion can have in searing fear–filled memories deeply; despite the teens’ limited direct experience, terrorist attacks, war, and nuclear war held top–ten berths in a list of fears. This finding hints at a phenomenon that Hadjikhani and her colleagues study: the contagion of fear. In her research, Hadjikhani has found that humans, like other animals, can experience fear indirectly, the result of another’s glance or muscle tensing, or, on a larger scale, that electric connection that turns a milling crowd into a stampeding throng.

Nouchine Hadjikhani

“We’re born into this world with a system to read other people’s expressions,” says Hadjikhani. “Ten minutes after we’re born, we’re already oriented more to faces than to objects.” In 2008, Hadjikhani and colleagues reported on their investigation of one aspect of facial expression—the gaze—and its role in communicating danger. They found that while a direct gaze from a fear–filled face triggers activity in fear–response regions of the brain, the response is not as complex as that elicited by a fear–filled face in which the eyes are averted. A direct gaze signals an interaction between participants who know themselves to be non–threatening. But an averted gaze, “pointing with the eyes,” as the researchers call it, flags a possible environmental danger and sparks activity in brain regions skilled at reading faces, interpreting gazes, processing fear, and detecting motion.

In other research, Hadjikhani found that the brain can recognize happy and fearful expressions in body movements. A fearful posture—hands held open and in front of the body like shields, for example—activates brain regions that oversee emotion, vision, and action, while postures of happiness—arms loosely held from the body as if opened to embrace—spur activity only in vision–processing regions. These physical communications of actual or perceived danger offer one avenue to developing a conditioned fear, a learned response founded upon emotion and impressed so firmly within memory that it remains active for a lifetime.

Raising the Dread

According to the National Institute of Mental Health, roughly 19 million people in the United States have mental illnesses that involve persistent, outsized fear responses to seemingly ordinary stimuli. A door slam becomes a gun’s report to a shattered combat veteran, for example, while smoke from burning leaves might trigger smell–based memories of pyres for a genocide survivor. Among the anxiety disorders linked to conditioned fear responses is one that’s much in the news: post–traumatic stress disorder.

For more than a decade, Vadim Bolshakov, an HMS associate professor of psychiatry and director of McLean Hospital’s Cellular Neurobiology Laboratory, has explored fear–driven disorders by investigating their molecular bases in the brains of rats. One early finding from his laboratory showed that learned fear changes the way the animals’ brains operate, offering a mechanism for conditioned fear’s persistence.

Vadim Bolshakov

Bolshakov and colleagues taught rats to associate a harmless stimulus, a tone, with a painful event, a shock to their feet. The researchers found that neurons in the rodent amygdala exhibited remarkable sensitivity to the tone, so much so that the neurons continued to fire after the stimulus was removed. This sensitivity, known as long–term potentiation, is important to memory acquisition. It is normally modulated by glutamate, a chemical that is released into the synaptic spaces between neurons when a message is being passed, but then is deactivated to prevent message over–expression. Bolshakov’s team showed that the amygdala’s heightened sensitivity was the result of too much glutamate, either because the clean–up process failed or, as the researchers postulated, because production of the chemical went into overdrive.

Other studies by Bolshakov and colleagues identified two proteins essential to the innate and learned fear responses. When the researchers blocked production of one of the proteins, stathmin, fear–conditioned mice were less able to recall the learned fear—and lost the ability to recognize dangers that normally would have kicked their innate fear response into high gear. Blocking the gene that produced a protein known as transient receptor potential channel 5, normally found in high concentrations in the amygdala, decreased the rodents’ neurons’ sensitivity to cholecystokinin, a neuropeptide released when the innate fear response is triggered or a learned fear is recalled.

These insights are welcomed by Roger Pitman, an HMS professor of psychiatry, and Mohammed Milad, an HMS assistant professor of psychiatry. Based at Massachusetts General Hospital, these researchers seek to tease out treatments for people with anxiety disorders such as post–traumatic stress disorder.

Location, Location, Location

Roger Pitman

Or, as Pitman and colleagues discovered several years ago, people might be helped to stave off a fear–filled memory by preventing it from consolidating in the first place. In a controlled study of patients entering Mass General’s emergency department after traumatic experiences—assaults or car accidents, for example—Pitman provided some participants with a placebo and others with propranolol, a drug that blocks the effects of the hormone adrenaline. At follow–up interviews participants listened to audiotapes of their own accounts of their trauma the day it occurred. Propranolol recipients had weaker physical responses to the tapes than placebo users, who showed physical signs of the stirring of their fearful memory despite time’s passage.

Replicating these results has proven difficult, however, so Pitman and colleagues have shifted their focus to reactivating traumatic memories in people with post–traumatic stress disorder and then administering an anti–stress drug to try to weaken the memory’s reconsolidation.

Reliving a fear, even a trauma–induced one, is not necessarily pathologic, Milad points out. Recalling the source of high emotion or injury can serve as a safeguard, a warning that our brains can tap as needed. In addition, time often softens the intensity of response.

“Say you’re in a car accident,” Milad adds. “It occurs at a particular intersection at the same time a certain song is playing on the radio. For a period following that accident, whenever you go through that intersection or hear that song, you will re–experience at some level your initial fear. If over time nothing horrible happens to rekindle your memory, your conditioned response to either stimulus will lessen until the fear is extinguished. This extinction doesn’t erase the initial learned fear; instead, it leads to forming a new memory, a ‘safety memory.’ The learned fear—the neuronal connections that the experience formed within your amygdala and between your amygdala and certain cortical structures—remains.”

For some, the trauma never lessens. In people with post–traumatic stress disorder, Milad and Pitman have found that two brain regions involved in extinction, the hippocampus and a region of the prefrontal cortex, function at a lesser capacity, while activity in the amygdala and the dorsal anterior cingulate, a region involved in cognition and motor control, rachets up. These findings may explain the unending rawness that trauma–induced fears bring to people with the disorder.



Further reading


Documentaries, videos and podcasts


How Your Brain Processes Fear

October 31, 2019

Merel Kindt: The Neuroscience of Fear Memory Erasure

June 23, 2014

The Amygdala and Fear Conditioning

October 9, 2016


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