I’ve been studying the amygdala for more than 30 years. When I started this work, research on this brain region was a lonely field of inquiry. The hippocampus was all therage, and I sometimes felt jealous of the attention lavished on this brain region because of its contribution to memory. These days, though, it is the amygdala that is in the spotlight. This little neural nugget has gone from an obscure area of the brain to practically a household word, one that has come to be synonymous with “fear.” And for many people, my name, too, is practically synonymous with “fear.” I am often said to have identified the amygdala as the brain’s “fear” center. But the fact is, I have not done this, nor has anyone else.
The idea that the amygdala is the home of fear in the brain is just that—an idea. It is not a scientific finding but instead a conclusion based on an interpretation of a finding. So what is the finding, what is the interpretation, and how did the interpretation come about?
The Finding: When the amygdala is damaged, previously threatening stimuli come to be treated as benign. The classic discovery was that monkeys with amygdala damage were “tamed;” snakes, for example, no longer elicited so-called fight-flight responses after amygdala damage. Later studies in rats by me, and others, mapped out the amygdala’s role in a neural system that detects and responds to threats, and similar circuits were found to be operative when the human brain processes threats.
The Interpretation: Since damage to the amygdala eliminates behavioral responses to threats, feelings of “fear” are products of the amygdala. People are indeed less responsive to threats when the amygdala is damaged (in humans amygdala damage can occur as a result of epilepsy or other medical conditions or their surgical treatment). Yet, these people can still experience (feel) “fear.” In other words, the amygdala is an important part of the circuit that allows the brain to detect and respond to threats but is not necessary to feel “fear.”
Brain imaging studies of healthy humans (people without brain damage) suggest something similar. When they are exposed to threats, neural activity in the amygdala increases and body responses (like sweating or increased heart rate) result. This is true even if the threatening stimuli are presented subliminally, such that the person is not consciously aware that the threat is present and does not consciously experience (feel) “fear.” Amygdala activity does not mean that fear is experienced.
The conclusion that the amygdala is the brain’s fear center wrongly assumes that the feelings of “fear” and the responses elicited by threats are products of the same brain system. While amygdala circuits are directly responsible for behavioral/physiological responses elicited by threats, they are not directly responsible for feelings of “fear.”
How did the interpretation come to be? We humans frequently feel afraid when we find ourselves freezing or fleeing when in harm’s way. In other words, these two things (the feeling and the body responses) tend to be tightly correlated in our conscious introspections. These introspections are talked about and become shared experiences that are ingrained as natural truths. Most people thus believe that the feeling of fear is the reason an animal or person runs from danger; or that the classic facial expression we know as “fear” is driven by feeling afraid. But when it comes to the brain, what is obvious is not always what is the case. The purpose of science is to go beyond the obvious to reveal the deeper truths that cannot be gleaned simply from observing nature.
One of the first things a scientist learns is that a correlation does not necessarily reveal causation. The interpretation that the amygdala is the brain’s fear center confuses correlation and causation. Actually, there are two confusions involved: (1) because we often feel afraid when we are responding to danger, fear is the reason we respond the way we do; and (2) because the amygdala is responsible for the response to danger, it must also be responsible for the feeling of fear.
From the beginning, my research suggested that the amygdala contributes to non-conscious aspects of fear, by which I meant the detection of threats and the control of body responses that help cope with the threat. Conscious fear, I argued in my books The Emotional Brain (Simon and Schuster, 1996) and Synaptic Self (Viking, 2002), and most recently in Anxious (Viking, 2015), is a product of cognitive systems in the neocortex that operate in parallel with the amygdala circuit. But that subtlety (the distinction between conscious and non-conscious aspects of fear) was lost on most people.
When one hears the word “fear,” the pull of the vernacular meaning is so strong that the mind is compelled to think of the feeling of being afraid. For this reason, I eventually concluded that it is not helpful to talk about conscious and non-conscious aspects of fear. A feeling like “fear” is a conscious experience. To use the word “fear” in any other way only leads to confusion.
The amygdala has a role in fear, but it is not the one that is popularly described. It’s role in fear is more fundamental and also more mundane. It is responsible for detecting and responding to threats, and only contributes to feelings of fear indirectly. For example, the amygdala outputs driven by threat detection alter information processing in diverse regions of the brain. One important set of outputs result in the secretion of chemicals throughout the brain (norepinephrine, acetylcholine, dopamine, serotonin) and body (hormones such as adrenalin and cortisol). In situations of danger, these chemicals alert the organism that something important is happening. As a result, attention systems in the neocortex guide the perceptual search the environment for an explanation for the highly aroused state. The meaning of the environmental stimuli present is added by the retrieval of memories. If the stimuli are known sources of danger, “fear” schema are retrieved from memory. My hypothesis, then, is that the feeling of “fear” results when the outcome of these various processes (attention, perception, memory, arousal) coalesce in consciousness and compel one to feel “fear.” This can only happen in a brain that has the cognitive wherewithal have the concept of “me,” or what Endel Tulving has called “autonoetic consciousness.” In a later post, I will elaborate on the autonoetic nature of our conscious feelings.
There’s nothing wrong with speculation in science (I just speculated about how feelings come about). But when a speculative interpretation becomes ingrained in the culture of science, and the culture at large, as an unquestioned fact, we have a problem. This is problem is especially acute in neuroscience, where we start from mental state words (like fear) that have historical meanings, and treat the words as if they are entities that live in brain areas (like the amygdala).
In sum, there is no fear center out of which effuses the feeling of being afraid. “Fear” is, in my view, better thought of as a cognitively assembled conscious experience that is related to threat processing, but that should not be confused with the non-conscious processes that detect and control responses to threats.
Postscript: Be suspicious of any statement that says a brain area is a center responsible for some function. The notion of functions being products of brain areas or centers is left over from the days when most evidence about brain function was based on the effects of brain lesions localized to specific areas. Today, we think of functions as products of systems rather than of areas. Neurons in areas contribute because they are part of a system. The amygdala, for example, contributes to threat detection because it is part of a threat detection system. And just because the amygdala contributes to threat detection does not mean that threat detection is the only function to which it contributes. Amygdala neurons, for example, are also components of systems that process the significance of stimuli related to eating, drinking, sex, and addictive drugs