Highlights
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Not surprisingly, one’s general level of anxiety is a fairly stable personality trait,3 a significant component of temperament
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But simply stating that we are each different only begs the question: What is it that makes us each psychologically distinct? The answer, of course, is that we each have a one-of-a-kind brain. As I explained in Synaptic Self,5 while all human brains are similar in overall structure and function, they are wired differently in subtle, microscopic ways that make us individuals
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These differences come about both because of the unique combination of genes we get from our two parents and because of the experiences we have as we go through life. Nature and nurture are partners in shaping who we are, and that partnership is played out in each of our brains
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Literary and religious writings and works of art over the ages reveal that people have always recognized the mental state we commonly refer to as anxiety today, even though they did not typically label it using angh or its linguistic descendants
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Anxiety was, for Freud, first and foremost “something felt,” a special “character of unpleasure.”20 Like the Greeks, he made a point of distinguishing Angst (anxiety) from Furcht (fear). Anxiety, Freud said, relates to the state itself, and disregards the object that elicits it, whereas fear draws attention precisely to the object.21 Specifically, Freud noted that anxiety describes a state of expecting danger or preparing for it, and of dreading it, even though the actual source of harm may be unknown; fear, however, requires a definite object of which to be afraid.22 He also distinguished between primary anxiety, which has an immediate object (essentially fear), and signal anxiety, which is objectless and involves a more diffuse or uncertain feeling that harm may come in the future (essentially anxiety).
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In Freud’s view anxiety is born out of a need to keep impulses based on stressful thoughts and memories, mostly about childhood, out of consciousness. Through the defense mechanism of repression, these impulses are hidden in the unconscious mind. When repression fails, the troubling impulses reach consciousness, and neurotic anxiety results. The impulses then need to be repressed again or “satiated” through neurotic “enactments” to relieve anxiety. The goal of Freud’s psychoanalytic method was to bring the cause of the neurotic anxiety, or what came to be called anxiety neurosis, into consciousness and eliminate its clandestine, subversive power
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In The Concept of Anxiety, published in 1844, before Freud was born, Kierkegaard made a distinction between fear, which has a specific object (similar to Freud’s Furcht, or primary anxiety), and anxiety, a kind of unfocused, objectless, future-oriented fear (comparable to Freud’s Angst and signal anxiety but with much less emphasis on pathology and a greater
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focus on consciousness).26 Because of its lack of an objective focus, Kierkegaard argued that anxiety (dread) was caused by “nothingness”: the despair that comes from the realization that we are not grounded in the world and are defined only by the practices in which we engage.
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Mainstream psychiatry today is biologically oriented and in this sense more aligned with Freud’s view that anxiety can become a pathological condition for which treatment is required to heal the troubled brain. Yet, while contemporary biological psychiatry recognizes the importance of Freud’s seminal contributions,33 it is divorced from his psychoanalytic theory.34
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Scientists and mental health professionals today are greatly influenced in their views of fear and anxiety by both Freud and Kierkegaard, who each regarded fear and anxiety as perfectly normal, yet unpleasant, feelings. In fear, as we have seen, the focus is on a specific external threat, one that is present or imminent, whereas in anxiety the threat is typically less identifiable and its occurrence less predictable—it is more internal, and in the mind more of an expectation than a fact, and can also be an imagined possibility with a low likelihood of ever occurring
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Can we really make a distinction between fear and anxiety given that both are anticipatory responses to danger and thus closely entwined? I think we can, and must
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As I will describe in later chapters, somewhat different brain mechanisms are engaged when the state is triggered by an objective and present threat as opposed to an uncertain event that may or may not occur in the future. An immediately present stimulus that is itself dangerous, or that is a reliable indicator that danger is likely to soon follow, results in fear. Anxiety may well also be present, but if the initial state is triggered by a specific stimulus, it is a state of fear. However, when the state in question involves worry about something that is not present and may never occur, then the state is anxiety. Fear can, like anxiety, involve anticipation, but the nature of the anticipation in each is different: In fear the anticipation concerns if and when a present threat will cause harm, whereas in anxiety the anticipation involves uncertainty about the consequences of a threat that is not present and may not occur.
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With the arrival of DSM-III in 1980, anxiety neurosis was divided into two separate states, a partition based on research findings by the psychiatrist Donald Klein.52 Klein had been studying a new experimental drug, imipramine, to treat hospitalized schizophrenic patients in the hope of reducing their high levels of anxiety. The patients claimed that their anxiety levels were unchanged, but the staff noted a dramatic decrease in the frequency with which these patients would show up at the nurses’ station complaining of physiological symptoms (inability to breathe, racing heart, dizziness) and psychological distress (feeling terrified that they were about to die). These brief bouts of intense fear (or, as they came to be called, panic attacks) were lessened after several weeks of treatment. Benzodiazepines, drugs like Valium, by contrast, reduced chronic anxiety but did not help with panic attacks. Findings such as these led Klein to distinguish between two broad kinds of anxiety disorders: generalized anxiety disorder (GAD) and panic disorder. While Freud anticipated this distinction, because he discussed anxiety as a general condition that sometimes had physiological symptoms similar to those in a panic attack, he did not distinguish these as different subcategories of anxiety neurosis
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The term “anxiety disorders” thus originally arose to subsume two states of anxiety (GAD and panic) and was retained when additional conditions were added. But the label “anxiety disorders” gives short shrift to the fact that most of the conditions included also involve fear (e.g., fear of specific objects or situations in specific and social phobic disorders; fear elicited by somatic sensations, such as heart palpitations or shortness of breath, in panic disorder). Therefore, I prefer to describe these states as fear and anxiety disorders, conditions in which maladaptive fear and/or anxiety plays a central role. With this in mind, I break with the DSM-5 categorization and include PTSD in my discussion of fear and anxiety because it involves maladaptive fear (fear of trauma-related cues)
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Together, fear and anxiety disorders are the most prevalent of all psychiatric problems in the United States, affecting about 20 percent of the population
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What determines who will be likely to suffer from a fear or anxiety disorder? For example, why does only a relatively small proportion of people exposed to a trauma develop PTSD?60 David Barlow has proposed that three factors make people vulnerable to these disorders61
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One is genetics or other biological factors in the brain
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Another source of vulnerability involves general psychological processes, such as an individual’s tendency to perceive situations as unpredictable and uncontrollable. The third factor listed by Barlow is specific learning experiences. If a child is given excessive attention when ill, he may continue to use “sick behaviors” as a way to attract attention and sympathy
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It should be noted that psychological processes and learning experiences are, in the end, also biological in nature, because they are products of the brain and as such are also subject to genetic influences and the influence of gene-environment interactions, or what is called epigenetics.
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the close connection between fear and anxiety demands that these two emotions be understood together. A key factor that links them is that they both depend on mechanisms in the brain that detect and respond to threats to well-being
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Threats, whether present or anticipated, real or imagined, demand action. As many others have noted, threat detection provides preparation for fight or flight.65 We are all familiar with the fight-flight response, the defensive emergency reaction that is triggered when we encounter present or anticipated threats, and that moves into overdrive when we are under stress (see Chapter 3). This whole-body reaction is mobilized to help us survive an encounter with danger. When it is in play, our conscious mind is consumed with fear or anxiety, and often with both. Threat processing is at the heart of fear and anxiety.
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In this book I will be less concerned with the disorders themselves than with the question of how threat processing contributes to maladaptive feelings of fear and anxiety in these disorders.67 People who suffer from them are hypersensitive to threats, which seize and hold their attention, a condition sometimes called hypervigilance
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Feelings of fear, in my view, result when we become consciously aware that our brain has nonconsciously detected danger.80 How does this happen? It all starts when an external stimulus, processed by sensory systems in the brain, is nonconsciously determined to be a threat. Outputs of threat detection circuits then trigger a general increase in brain arousal and the expression of behavioral responses and supporting physiological changes in the body. Signals from the behavioral and physiological responses of the body are sent back to the brain, where they become part of the nonconscious response to danger (sensory components of these responses can be “sensed” just like sights or sounds). Brain activity then comes to be monopolized by the threat and by efforts to cope with the harm it portends. Threat vigilance increases—the environment is scanned to figure out why we are aroused in this particular way. Brain activity related to all other goals (eating, drinking, sex, money, self-fulfillment, etc.) are suppressed. If, via memory, environmental monitoring reveals that “known” threats are present, attention becomes focused on these stimuli, which are consciously “blamed” for the aroused state. Memory also allows us to know that “fear” is the name we give to experiences of this type (starting in childhood, we build up templates of what it is like to be in states we label with emotion words). When the various factors or ingredients are integrated in consciousness, an emotion, specifically the conscious feeling of fear, is thus compelled. But this can only happen if the brain in question has the cognitive wherewithal to create conscious experiences and interpret the contents of these experiences in terms of implications for one’s well-being. Otherwise, the brain and body responses are a motivational force that guide behavior in the quest to stay alive, but the feeling of fear is not a part of the process. This does not mean that the feeling of fear is a mere by-product. For once it exists, it opens up the resources of the conscious brain to the quest to survive and thrive
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One important implication of the ideas to be developed in this book is that they reveal a disconnect between the troubling feelings of fear and anxiety that motivate people to seek help and the way research on those feelings—including research on how to find new treatments to allay them—is conducted and interpreted. Consciousness is no longer a taboo subject in science, and much progress has been made in this area in recent years. Yet research on fear and anxiety disorders in animals, and also in humans, that I and others have conducted is often focused on how the brain detects and responds to threats, processes that operate nonconsciously. Although this work is very relevant to understanding conscious fear and anxiety, it has to be understood in the proper context. Responses to threats, in spite of common practice, are not foolproof markers of conscious feelings, even in humans, and likewise should not be assumed to be so in animals
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Contrary to the popular opinion of laypeople and many scientists, I argue that we have not inherited feelings like fear or anxiety from animals; we have instead inherited mechanisms that detect and respond to threats. When these threat-processing mechanisms are present in a brain that can be conscious of its own activities, conscious feelings of fear or anxiety are possible; otherwise threat processing mechanisms motivate behavior but do not necessarily result in or involve feelings of fear or anxiety
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I believe we should restrict the use of emotion words like “fear” to conscious feelings, such as the feeling of being afraid. Brain systems that detect threatening stimuli and control behavioral and physiological responses elicited by these stimuli should not be described in terms of fear. The latter systems operate nonconsciously in humans, and although they contribute to feelings of fear, they are not fear mechanisms per se. This chapter explains why I think the distinction between mechanisms that detect and respond to threats outside the realm of consciousness, as opposed to mechanisms that create conscious feelings of fear, is so important for our conception of fear and its partner, anxiety.
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Unfortunately, the limbic system theory continues to be prominent in both lay and scientific discussions of the emotional brain in spite of its evolutionary basis having been discredited.
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I thought that a different approach was needed, one that made minimal starting assumptions about how emotions are organized in the brain. The approach I took was to follow the flow of information in the brain from the sensory system that processes a stimulus to the muscles that control the responses to it. Somewhere along that pathway would be mechanisms that detect the significance of the stimulus and trigger the appropriate responses. Limbic areas might well be implicated, but the point was to have an objective approach to the circuitry rather than one that presumed to know the answer before the research was done.
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When studying split-brain patients, you can’t help but picture signals flowing from point to point in the brain to construct what we are seeing, remembering, thinking, and feeling, and in controlling behavior.
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Conceiving of brain functions in terms of information flow had become inevitable with changes in the psychological zeitgeist. For decades behaviorists had dominated psychology, shunning all talk of mind, consciousness, and other unobservable inner factors (whether in the mind or brain) in explaining behavior.7 A science of psychology, they said, must be based on observable events—stimuli and responses. But by the 1970s behaviorism had been supplanted by the cognitive approach, which treated the mind not as a place where conscious experiences occur so much as an information-processing system that connects stimuli with responses, and that does not necessarily involve consciousness.8 Split-brain studies fit perfectly within this intellectual framework
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When we showed the patient’s right hemisphere an emotional stimulus, the left hemisphere could not name it but could rate its emotional valence. This suggested that the cognitive processes involved in perceiving what a stimulus is are separable in the brain from the processes that evaluate its emotional significance. I wanted to figure out how emotional significance was added to a stimulus as it flowed, in the form of information, through the brain. Because there was no way to pursue detailed brain mechanisms in humans, I turned to studies of rats.
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Neuroscience was formed in 196911
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The field of neuroscience was officially born as a discipline when the Society for
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These researchers showed that when an innocuous stimulus, such as a tone, was paired with mild electric shocks, it elicited freezing behavior, whether tested after a few minutes, or days or weeks later (Figure 2.2). Freezing is an innate defensive response that is just as important to animals as its more familiar partners, fight and flight.21 (Indeed, as discussed in the next chapter, the fight-flight reaction is now often described as freeze-fight-flight.) The tone also produces increases in blood pressure, heart rate, and respiration and releases hormones like adrenalin and cortisol,22 providing physiological support for energy-demanding defensive behaviors.
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I thought that with all the tools available in the Reis laboratory, I could use the Kandel strategy, in conjunction with Pavlovian conditioning procedures, to trace the flow of information that enabled a meaningless stimulus to elicit fear responses in mammals (rats) following fear conditioning. This should be possible, I reasoned, because the responses, which are expressed the same in all rats, are driven by a specific stimulus that was completely under my control as an experimenter. As a result, I might be able to trace the flow of the stimulus processing from the CS sensory system to the CR motor system
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Through this research, the amygdala came to be viewed as a key component of the brain’s fear system
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the question of what exactly a fear system does has turned out to be a tricky issue.
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took a different approach from the ones described above. I thought that the Darwinian commonsense idea was flawed because it attributed too much to conscious fear, and the central state view was flawed because it ignored conscious fear. I believed conscious and nonconscious states both played roles, but the roles needed to be kept separate
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was compelled toward my view by the split-brain studies I had done earlier. Gazzaniga and I noticed that the left hemisphere of a split-brain patient often commented on behaviors that were produced by the right hemisphere. One might expect that in people with this condition the left hemisphere would be surprised when it saw its body doing something for a reason that it (the left hemisphere) was not aware of. Instead, the left hemisphere took these unexpected behaviors in stride and wove them into its stream of thought. This was a fascinating phenomenon, so we designed some studies to explore it
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Basically, we coaxed the right hemisphere to respond behaviorally and then simply asked the left hemisphere, “Why did you do that?” Without hesitation, time and time again, the left hemisphere came up with an explanation. For example, when the patient was urged to stand up via stimuli presented to his right hemisphere, in response to our query as to why he did that, his left hemisphere said he needed to stretch; when he waved, it was because he thought he saw a friend out the window; he scratched his hand because it itched. These were fabrications on the part of the conscious brain, explanations for why the body responses were being generated. Gazzaniga and I proposed that the human brain does this all the time
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While we are not always privy to the motivations underlying the responses controlled by our brains, consciousness ties the loose ends together by coming up with an interpretation that unifies the mind and behavior by filling in the blanks of an otherwise incomplete mental pattern
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Gazzaniga called this the interpreter theory of consciousness
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And I used this idea to explain how
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nonconscious processes that underlie emotional responses contribute to the conscious feelings that we experience
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In the late 1890s Walter Cannon, who would later introduce the fight-flight concept, was researching the digestive system of animals.18 He noticed that when an animal was stressed, its digestion was disrupted—specifically, the peristaltic contractions of stomach muscles ceased. This led him to pursue the role of the nervous system in emotionally arousing situations. He went on to explore how the autonomic nervous system (ANS) controls the physiology of the body in challenging circumstances, such as those involving threats or other stressors. Cannon called this the emergency response, a term he used interchangeably with fight-flight response.
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Hans Selye, working around the same time as Cannon, extended the emergency reaction system to include the adrenal cortex and its hormone, cortisol.23 Cortisol, a steroid hormone, also contributes to energy regulation. It is released from the adrenal cortex by adrenocorticotrophic hormone (ACTH), which itself is released by the pituitary gland.
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As a result of Cannon and Selye’s work, the emergency reaction (or alarm response, as Selye called it) came to be viewed as being controlled by two complementary physiological axes: the sympathoadrenal axis, involving the sympathetic nervous system and adrenaline released from the adrenal medulla, and the pituitary-adrenal axis, involving the release of cortisol from the adrenal cortex (Figure 3.3). The response of the sympathoadrenal axis is rapid, occurring within seconds of encountering a threat. The pituitary-adrenal axis, by contrast, is slower and not fully expressed for minutes or even hours
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The psychiatrist Donald Klein has proposed another physiological response, the suffocation alarm response,26 which is triggered by internal physiological threat signals, such as an excess of carbon dioxide (hypercapnia), leading to “air hunger” (shortness of breath). Whereas the sympathoadrenal and pituitary-adrenal responses are relevant to all forms of fear and anxiety, the suffocation alarm system is particularly relevant to a subgroup of patients with panic disorder. These people, Klein suggests, have a hypersensitive suffocation alarm system, which falsely detects a dangerous level of CO2 and leads to hyperventilation, which in turn produces an actual rise in CO2 (due to short, fast inspiration). The resulting dizziness and light-headedness lead the person to misinterpret the physiological changes and worry and dread follow in the panic-stricken person. Klein’s hypothesis is supported by data27 but is viewed as controversial by some researchers.28
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Breathing on autopilot is controlled by respiratory circuits in the medulla and pons of the hindbrain that connect to the muscles of the lungs.176 Neurons in these are sensitive to CO2 and acidity (see earlier discussion), and this plays a key role in their control over the contraction of the diaphragm muscles, which in turn control the amount of air we take in to balance CO2 and oxygen in our body. In addition to this automatic breathing control, we also have voluntary control of air intake and how fast or slow we breathe. Singing involves voluntary breath control, as does playing a flute, saxophone, or harmonica. Conscious control of this process is achieved by interactions between the executive control functions of the neocortex and the neurons in the medulla–spinal cord that control breathing
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When someone is stressed, it is common to advise, “Just take a deep breath.” This folk wisdom has a grain of truth to it. During stress the sympathetic nervous system dominates, overshadowing the parasympathetic system. The result is fast heart rate, but low heart rate variability, and shallow breathing.178 When one breathes in the slow, measured way that is commonly taught in meditation, yoga, and relaxation training, the vagus nerve, which controls the parasympathetic nervous system, becomes more active, and the balance between the sympathetic and parasympathetic system improves. As a result, heart rate variability increases, and the times when it is somewhat slower provide
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windows of opportunity exists for automatic processes to drive heart rate down and thus reduce elevated blood pressure and other sympathetic responses