Joy, Guilt, Anger, Love (13 page)

This entire set of fear responses occurs unconsciously and within milliseconds. As they unfold, we gradually become aware of them, but we don’t actually need to be conscious of them for them to take place. The American psychologist William James makes this clear in his seminal essay ‘What is an emotion?’, published in 1884. In this essay, James formulated his influential thoughts on how we ‘emote’. At that time, the prevailing theory on emotions described them as some sort of mental state of awareness of our reaction to a fact or a change in the environment. In turn, this mental perception would trigger a cascade of physical responses. So, applying this theory in the case of fear: seeing a bear in the woods would first make us be afraid and, consequently, the state of fear would in turn let us start to tremble and shake. James thought this sequence of events was wrong and that what happens is exactly the reverse. He said that we feel afraid because we tremble and shake, not the other way around. Emotions are first and foremost our bodily reactions. Then comes the feeling, or the awareness of them.

He was so convinced about this order of sequence in the way we emote that he went on to say that if we took away from emotions the bodily symptoms, there would be nothing left. Only a cold and neutral ‘state of intellectual perception’ would remain.

‘What kind of emotion of fear would be left, if the feeling neither of quickened heart-beats, the shallow breathing, trembling lips or weakened limbs, goose-flesh, visceral stirrings were not present, it is impossible to think.’
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But let’s go back to the distinction between fear and anxiety. Fear has a specific target. What about anxiety? Well, anxiety is not as simple. Anxiety is usually a fear of the indefinite, something that we cannot always explain or even locate in space and time. It is unpredictable, and often the anticipation of an unknown or not necessarily incumbent threat. Just as I did the night Robert called me, we feel edgy and jittery about the possibility of negative or catastrophic occurrences that may never actually materialize. In other words, anxiety is fear that is looking for a reason.
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Anxiety’s pedigree

Anxiety’s obscure and opaque reasons are good at hiding, but it is worth searching for them. Sigmund Freud devoted a lot of time to this hunt. Freud was convinced that ‘anxiety was a nodal point at which the most various and important [psychological] questions converge, a riddle whose solution would be bound to throw a flood of light on our whole mental existence’.
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Towards the end of the nineteenth and the beginning of the twentieth century, a disease began to seep through modern cities, especially among the upper class and working professionals. It mainly consisted of stomach unease, headaches, neuralgia and general fatigue and was rapidly spreading, much as flu might, in response to the rapid urbanization and the increasingly frenetic and hectic lifestyle spawned by the industrialized world. Across the pond, the American physician George Beard called this new condition ‘neurasthenia’ to indicate the over-excitation or ‘exhaustion’ of the nervous system and believed it was particularly common among Americans, saying that American society generated much more excitation of the nervous system than did European society.
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Indeed, ‘American nervousness’ or ‘Americanitis’ became popular synonyms for the disease.
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Freud concurred with the idea that the gruelling unease that he observed in patients was somehow related to the unremitting stress of urban life but thought there had to be more than external factors causing it. He named this condition ‘anxiety neurosis’ and suspected it was the result of an opposition between an individual’s constitution, desires and aspirations and what modern civilization demanded of him or her.

As you probably know, on his quest to find the inner causes of neurosis Freud received and listened to a large number of patients as they lay on a couch in his small practice in Vienna. Freud had been inspired to do this by his friend Josef Breuer, another Viennese physician, who hypnotized his patients and let them talk about themselves during their hypnotic states.

After examining a large number of cases, Freud theorized neurosis as the manifestation of unresolved conflicts that mostly had their origins in childhood and were often connected to traumatic experiences, frequently of a sexual nature. In general, a neurotic was someone who repressed the discharge of some kind of psychic energy that kept trying to emerge. So he continued to listen to his patients to help them unearth those memories, thus letting the reasons for their unresolved distress surface. One of the notable features of this kind of therapy was that a patient’s symptoms mostly disappeared when the moment of their first occurrence was evoked and when forgotten unpleasant or traumatic events connected to those symptoms were recalled to memory.

An emblematic example of this mechanism, one that impressed and inspired Freud, was that of Anna O., one of Breuer’s patients.
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Anna had presented with a nervous cough, visual disturbances, paralysis of the left side of her body, as well as some speech problems. Bizarrely, she at some point also manifested an acute form of hydrophobia. For several weeks she had not been able to drink any liquid. Something as innocuous as a glass of water revolted her and made her nervous, but she couldn’t explain why. During a hypnotic session, it emerged that once, in the house of an English woman to whom she was paying a visit, she had caught sight of a dog drinking from a glass. The scene disgusted her, but her manners forbade her to say anything to her host. After recalling this episode, however, she was able to drink again.

It might be worthwhile to summarize what subsequently became of the concept of neurosis.

During the course of the last century, as the number of mental ills afflicting the population increased, doctors thought it necessary to list them all in one book. To that end, in 1952 the American Psychiatric Association published a volume called
Diagnostic and Statistical Manual of Mental Disorders
(or DSM for short). Created to help psychiatrists agree on how to define and recognize mental pathology, the book was supposed to work as an instruction manual, listing the symptoms to observe and by which to identify each disorder among a variety of patients. The book, which is now considered the essential reference for everyone working in mental health and involved in the diagnosis and treatment of psychiatric disorders, had a basic aim of unifying the language of diagnosis. Thus by consulting the pages of the DSM, two psychiatrists living in two different cities, or even two different countries, could use the same parameters of diagnosis for patients showing similar symptoms.

‘Neurosis’ was listed in the first edition of the DSM. In that edition, neuroses were a broad category in which emotional distress manifested itself through various physiological and mental disturbances. In a way, being neurotic was a slight alteration of normal behaviour. The same broad class of ‘anxiety neurosis’ was maintained in the second edition of the manual published in 1968, but was dramatically dismantled in the third. The shift to the third edition of the DSM marked an important chapter in the history of psychiatry and laid the foundations for the current system for categorizing anxiety and all other classes of mental illness. In essence, the new edition got rid of the term neurosis – and of everything else that conserved a psychoanalytic meaning – and mainly separated panic attacks and panic disorders from other forms of anxiety, principally because they responded to different kinds of medication.
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The fourth edition kept this main separation and introduced new forms of anxiety, each with its own set of symptoms.
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The classification included: specific phobia, namely fear of a specific object or situation that is usually out of proportion to the actual danger, for instance an exaggerated fear of spiders; social phobia, or social anxiety disorder, the fear of social situations; agoraphobia, the fear of public spaces; post-traumatic stress disorder (PTSD), the manifestation of anxiety in the wake of past exposure to a traumatic event or terrifying threat; panic disorder, in which the sufferer experiences unexpected and frequent episodes of intense fear (like panic attacks); and obsessive–compulsive disorder, characterized by intrusive thoughts and the need to relentlessly pursue a thought or action to get rid of a fear – for instance, having to wash your hands obsessively because you are afraid of catching bacteria.

Another category is generalized anxiety disorder, or GAD for short. Were you to read through the diagnostic criteria for GAD you might conclude that they apply to everybody you know including yourself. Indeed, the DSM says that in order to qualify for a GAD diagnosis, you need to experience the following: excessive and difficult-to-tame anxiety and worry ‘occurring more days than not for at least 6 months about a number of events or activities (such as work or school performance)’. You should also manifest three or more of the following symptoms: ‘restlessness or feeling keyed-up or on edge; being easily fatigued; difficulty concentrating or mind going blank; irritability; muscle tension; sleep disturbance (difficulty falling or staying asleep, or restless unsatisfying sleep)’. The worry should also not be about something specific and should ‘cause clinically significant distress or impairment in social, occupational, or other important areas of functioning’ in life.

The DSM is supposed to facilitate the detection of disorders in people who seriously need medical support. But, given these criteria, who wouldn’t qualify for such a diagnosis? In a way, GAD is therefore closest to the condition formerly labelled neurosis and represents the ordinary type of anxiety that creeps up on us on a regular basis.

Of note is that, clearly, GAD and the other types of anxiety listed in the DSM are all arbitrary constructs of psychiatrists, illnesses generated by the medical establishment and based on clinical symptoms, not their biology. The disorders are monolithic entities for convenient diagnosis that by themselves tell us nothing about the individual’s experience of the disorder.

It is important to remark that at both the symptomatic and the biological level there is considerable overlap across the diagnoses. The various forms of anxiety share their primary neural substrates. Similarly, genes underlying the manifestation of one form of anxiety also play a role in the manifestation of another form (I will talk about this again in more detail in the next chapter).

Fear conditioning

Unfortunately, a bout of anxiety doesn’t always knock at our door. It ambushes us when we least expect it. However, it usually needs something to set it off and such a trigger can often seem innocuous.

Also, worry begets a cascade of other worries, and hearing about recession, or any other trigger, can revive deeper concerns, which are often connected to memories of traumatic events, or more broadly to other unresolved conflicts or problems in our lives. The mechanism of the association between a trigger and the subsequent arrival of a fearful response has long been at the centre of research on fear and anxiety and is related to general theories of behavioural conditioning, which explore how organisms learn to behave in a certain way as a response to changes in their environment.

You may be familiar with the famous experiment of the drooling dogs, conducted by the Russian scientist Ivan Petrovich Pavlov, who in 1904 was awarded the Nobel Prize. Pavlov was using dogs to study the function and mechanisms of the digestive system. Just as our mouths water when we are in front of a succulent meal, when a dog encounters food its saliva starts to dribble. One day, Pavlov noticed that when he or his colleagues visited the dogs in the laboratory, the dogs started to salivate even when there was no food for them. It turned out that the dogs were reacting to the lab coats. Whenever the dogs were given food, the scientist offering them a meal was wearing a white lab coat, so the dogs had learnt to associate the white coat with the arrival of food. Later Pavlov changed the stimulus and struck a bell each time the dogs were fed. After a while, each time the dogs heard a bell, even in the absence of food, their saliva drooled.

A typical laboratory fear-conditioning experiment goes like this: a rat or a mouse is placed in a cage and exposed to a trigger, often a buzzing tone, after which the animal receives a mild electric shock to the feet. The buzz works to
condition
the rodent to the arrival of the next shock. After a few of these pairings, the buzz acquires aversive properties and when presented to the animal it brings about typical behavioural and physiological fear responses. Most often, as soon as it hears the sound, the scared animal anticipates the shock by freezing.

A rodent’s fear responses are similar to those of humans. We, too, freeze in our tracks. Imagine your reaction, for instance, when you hear your boss or partner pronounce those four laconic words: ‘we need to talk’. If you are anything like me, the normal reaction is to freeze for a moment like those caged rats, because we can be quite sure we are in for some trouble. Then blood circulation races, the heart starts to pound and so on, as described above. Our attention and concentration focus, we are on alert. For many of us, this is because the last time we heard those words we probably had a memorable fight. Those four words function like the buzz in the fear-conditioning experiment. Particularly if reminiscent of traumatic events, external cues like those threatening words can function as conditioned stimuli that trigger a variety of anxious responses. All of this takes energy. Fear and anxiety are draining.

Anxiety in the brain

Although conceptually distinct, fear and anxiety share their anatomical position in the brain, and twenty years and more of research have mapped their underlying neural circuits, almost down to the single neuron.