Anxiety

by Daniel Freeman

  • amygdala, the storehouse of unconscious fear memories;

  • anterior cingulate cortex (ACC), which helps control our fear reactions;

  • hippocampus, which stores contextual memories (for example, where we were and what we were doing when a frightening event occurred), and can therefore help us judge whether a situation is truly dangerous or merely resembles aspects of a previously threatening event.

  In people suffering from PTSD, the amygdala may be overactive and the ACC and hippocampus underactive. Indeed, there’s evidence to suggest that the ACC and hippocampus are actually smaller in people with PTSD, though whether that’s a result of the illness or a cause is unclear. (In fact, it may not be the whole hippocampus that is affected; recent research has highlighted atrophy in a specific region of the hippocampus in people with PTSD.)

  Without the moderating influence of the ACC and hippocampus, the amygdala may perceive threat where there is none – a hallmark of PTSD, and indeed of anxiety disorders in general.

  It’s been suggested that the hippocampus may shrink through the effects of the hormone cortisol. Cortisol, and related neurochemicals, are released via the hypothalamic-pituitary-adrenal (HPA) axis in order to key up the body to respond to potential threat. Scientists are investigating the idea that dysfunction in the HPA axis may play an important role in PTSD. So far, however, no consistent pattern has emerged.

  Research into the genetics of PTSD is scarce. What there is suggests only moderate heritability (around the 30–35% mark). Interestingly, there seems to be some overlap between genetic susceptibility to PTSD and to some types of the trauma that trigger the illness. This may be a result of the individual’s personality. Murray Stein and colleagues have speculated:

  an individual’s genetically influenced propensity toward neuroticism would lead the individual to experience more anger and irritability, making that person 1) more likely to get into fights (thereby increasing the risk of experiencing assaultive trauma) and 2) more likely to become highly emotionally aroused as a result of experiencing such traumata (thereby increasing the risk for PTSD symptoms).

  In some cases, then, personality may partly influence the likelihood of a person experiencing a trauma and of then developing PTSD. But we shouldn’t get carried away: most traumatic events occur out of the blue and regardless of the individual’s personality.

  Chapter 11

  Treatment

  Around one-third of the adult population reports difficulties with anxiety, with close to one in five having problems severe enough to meet criteria for a clinical disorder. And anxiety can feel horrible, as Holly Golightly pointed out back in Chapter 1. Anxiety, then, can be a big problem. How are we faring for solutions?

  In fact, simply establishing which treatments are effective is an immensely complex, labour-intensive business. The undoubted ‘gold standard’ for clinical research is what’s known as randomized controlled trials. These involve participants being randomly assigned to one of at least two groups. Group one will receive a specific treatment, and group two either a ‘control’ non-treatment (a placebo, for example) or an alternative treatment. (Sometimes trials will assess two or more treatments against a control.) Allocating participants randomly means that the composition of each group should be similar, and by following their outcomes, you can see whether the treatment has helped, over and above natural recovery.

  But even randomized controlled trials are not as straightforward as they can appear. This is why medical researchers are encouraged to follow the CONSORT (Consolidated Standards of Reporting Trials) guidelines. The latest CONSORT statement was issued in 2010, after seven years of consultations, and it has the backing of the leading medical journals (which is where most scientists hope to publish their results).

  Among the numerous factors CONSORT urges researchers to consider when designing and reporting a trial are: the nature of the patients selected (for example, how severe their problem; how long-lasting it is; whether they have other problems); the techniques used to randomly allocate participants to treatment groups (there are several alternatives); the nature of the control treatment; the composition and quality of the treatment being tested; what types of outcome are measured; whether the research assessors and patients were blind to treatment allocation; what to do about people who drop out of the trial; length of follow-up after the treatment has concluded; appropriate statistical analysis – and so on. And on.

  Unfortunately, not all clinical trials adhere to the CONSORT guidelines – and they didn’t exist at all until 1996. And even the best trials can only tell us about particular durations or dosages of treatment for a particular group over a particular time period. This means that there are uncertainties and gaps in knowledge. Hence clinicians often debate the question: what works for whom?

  What works?

  Establishing the efficacy of specific treatments, then, is an inordinately tricky business. And yet in the case of anxiety disorders, we do have a consensus.

  The number one treatment of choice is psychological therapy – principally cognitive behaviour therapy (CBT) and its variants. (We’ve highlighted the theoretical foundations of CBT in the chapters on specific disorders.) Anxiety occurs when we believe a situation is threatening. CBT’s core objective is to test the accuracy of those beliefs. This is achieved by carefully exposing individuals to the situations and feelings that they fear in a way that allows them to learn from the experience. When the tests are carried out in a controlled, graduated, and individually tailored fashion, the person discovers that they are actually much safer than they had thought and their anxiety decreases.

  But anxiety is also tackled with medication. For long-term treatment, SSRI antidepressants (such as paroxetine) are preferred. But in the short term, specific anxiolytic (anti-anxiety) drugs may be prescribed to help a patient cope with a crisis. The most commonly used anxiolytics are the benzodiazepines: these tend to work very rapidly and effectively, but can lead to tolerance (your body becomes used to the effects of the drug and therefore increasing doses are required) and to addiction – hence the recommendation that they only be used in the short term.

  The gains brought about by CBT are sometimes greater, and typically last longer, than those produced by medication. Moreover, medication can sometimes produce side effects – and giving them up can be tricky. This is why the UK’s National Institute for Clinical Excellence recommends CBT as the first line of treatment for each of the anxiety disorders, with SSRIs as a second choice. (We’ll look at the various treatment alternatives in greater detail below.)

  Interestingly, combining psychological therapy and medication doesn’t seem to bring any additional benefits. In fact, in some cases (panic disorder, for instance), medication may actually interfere with the therapy. This is because, in order to learn that you can cope with your anxiety in a controlled exposure, it’s necessary to really feel your fear – which is something anti-anxiety medication is intended, of course, to prevent.

  One interesting development, however, is the use of drugs to boost the effects of psychological therapy. It is early days, but promising results have been obtained with ‘cognitive enhancers’ such as D-cycloserine (drugs that quicken learning). D-cycloserine appears to speed up the progress made when individuals test out the accuracy of their fearful thoughts.

  What treatments are people receiving?

  As we’ve seen, official guidelines in the UK advocate the use of CBT to treat anxiety disorders. But how many people with anxiety disorders are actually receiving CBT – or indeed any other form of treatment?

  Not nearly enough, would seem to be the inevitable conclusion when you look at the data from a survey carried out for the NHS in 2007. Here are the percentages of people receiving no treatment at all:

  • Generalized anxiety disorder: 66%

  • Phobias: 43%

  • Obsessive-compulsive disorder: 69%

  • Panic disorder: 75%

  • Mixed anxiety and depressive
episode: 85%

  Here are the figures for people with anxiety disorders receiving medication only:

  • Generalized anxiety disorder: 18%

  • Phobias: 23%

  • Obsessive-compulsive disorder: 12%

  • Panic disorder: 8%

  • Mixed anxiety and depressive episode: 11%

  And now the figures for people with anxiety disorders receiving some form of counselling or therapy, either with medication or on its own, with the figure in bold denoting CBT:

  • Generalized anxiety disorder: 15%; 3%

  • Phobias: 34%; 11%

  • Obsessive-compulsive disorder: 18%; 4%

  • Panic disorder: 17%; 4%

  • Mixed anxiety and depressive episode: 5%; 1%

  One of the reasons CBT is so rarely used is a shortage of trained therapists. This is a situation the UK government has attempted to rectify by means of the Improving Access to Psychological Therapies scheme, which was launched in 2007 with the aim of training 3,600 new therapists.

  Medication

  Three main types of drugs are used to treat anxiety: SSRIs, benzodiazepines, and beta-blockers.

  SSRIs

  You might be surprised to discover that anxiety is treated with SSRIs (selective serotonin reuptake inhibitors). SSRIs, after all, are popularly regarded as anti-depressants. They were certainly marketed as anti-depressants when they appeared on the scene in the late 1980s. But their ability to dampen down feelings of anxiety has made them the primary pharmaceutical option for these disorders. Indeed, some experts have argued that they are more effective at treating anxiety than depression.

  Among the SSRIs commonly prescribed for anxiety problems are paroxetine, venlafaxine, and sertraline. Unlike the other drug options, they often take a few weeks to show benefits. Once SSRIs kick in, however, they can reduce our sense of threat and instead stimulate a feeling of calm contentment. How they do this is unknown. SSRIs increase the amount of serotonin in the brain, but what this means for anxiety isn’t well understood. As the psychiatrist David Healy has written: ‘We know a lot about where drugs go in the brain but very little about how they work.’

  Benzodiazepines

  Like many other drugs, the success of benzodiazepines owed much to luck. A scientist named Leo Sternbach synthesized chlordiazepoxide in 1955 while working for the pharmaceutical giant Hoffmann-La Roche, but could see no reason to continue working on it.

  Chlordiazepoxide sat in a corner of Sternbach’s lab for two years until a colleague, Earl Reeder, took another look. Reeder was astonished by the results, and the company was quick to see the potential. Chlordiazepoxide, renamed Librium, was introduced to the market in 1960, followed a few years later by diazepam (Valium).

  Benzodiazepines appeared to offer a safe, quick-acting cure for the effects of anxiety, and they were astonishingly popular. It’s perhaps not surprising that the public were so keen: benzodiazepines produce a sense of relaxation that resembles the feeling produced by alcohol. They do this by enhancing the effect of a neurochemical called gamma aminobutyric acid (GABA), which relaxes us when we’re anxious.

  Gradually, however, it was recognized that all was not quite as rosy in the benzodiazepine garden as it seemed. Unpleasant side effects were common, and stopping the drug could result in nasty withdrawal symptoms. In fact, the tide of scientific and popular opinion turned so conclusively that the brand name Valium was dropped.

  Benzodiazepines (also known as ‘minor tranquillizers’) are still widely prescribed for some anxiety problems, though are only recommended for short-term use: usually two to four weeks. Commonly used varieties include chlordiazepoxide (Librium) and diazepam (the former Valium), lorazepam (Ativan), bromazepam (Lexotan), alprazolam (Xanax), and clorazepate (Tranxene).

  Beta-blockers

  At the 2008 Beijing Olympics, North Korean competitor Kim Jong-su became the first ever pistol shooter to be expelled from the Games after testing positive for a banned substance. The substance in question was the drug propanolol, a beta-blocker, and it cost Kim Jong-su his silver and bronze medals.

  Why a pistol shooter might be tempted to take a beta-blocker is no mystery. These drugs – of which propanolol was the first to be developed, in the late 1950s – quickly prevent many of the physiological symptoms of anxiety, such as elevated heart rate, perspiration, and trembling.

  Beta-blockers are principally prescribed to treat cardiovascular problems such as high blood pressure or angina. But they are thought to be widely used by orchestral musicians and other performers to control the effects of nerves. While beta-blockers may help with specific, short-term situations, they aren’t recommended for long-term treatment of anxiety disorders.

  Cognitive behaviour therapy

  CBT was developed by the American psychiatrist Aaron Beck (born 1921), initially as a treatment for depression. As the psychologist Gillian Butler has written, CBT is ‘based on the recognition that thoughts and feelings are closely related. If you think something is going to go wrong, you will feel anxious; if you think everything will go fine, you will feel more confident.’ So CBT therapists work with their clients to identify and evaluate negative thoughts and the unhelpful behaviours that often result.

  CBT isn’t a narrowly prescriptive programme. Exactly how it is applied to anxiety (or indeed any other problem) depends on the nature of the disorder and the person being treated. Treatment is based on the construction of detailed models showing how a disorder is caused, maintained, and overcome. As more is discovered, the model is updated and the therapy evolves accordingly.

  (Incidentally, one of the problems commonly treated with CBT is hypochondriasis, which is the fear that one is suffering from a serious illness. Hypochondriasis is often referred to as ‘health anxiety’. The psychiatric classification systems, however, don’t categorize it as an anxiety disorder, though many experts believe it would be more logical to do so.)

  At the core of CBT for anxiety is the idea that fear is a product of interpretation. We are frightened not because something awful is happening, but because we believe it will happen in the future. To overcome your anxiety, you must test out your interpretation by experiencing the situation you fear. And you must do so without adopting any of the safety behaviours you would ordinarily use in order to cope. If you can do that, you will discover that your fears are misplaced.

  For example, a person suffering from OCD who fears contamination would be encouraged to seek out dirty environments, and to resist the compulsion to wash repeatedly afterwards as they would ordinarily do. An individual with panic disorder might be asked to visit a place they would usually avoid and to stay there even when they feel the sensations of panic. If they can ride out the panic, rather than fighting it, they’ll find out that what they dreaded – a heart attack, perhaps, or fainting – didn’t occur. And a person with social phobia might be shown videos of themselves in a social situation, once when using their safety behaviours (avoiding eye contact, for example, or carefully rehearsing everything they say) and once without those safety behaviours. They can then see that their safety behaviours aren’t in fact helping. They’ll probably also discover that they come across much better than they had imagined. Below we describe CBT for two problems in a little more depth.

  CBT for phobias

  CBT has been used very successfully to tackle a wide range of phobias. One notable example is the programme developed by Lars-Göran Öst, Professor of Psychology at the University of Stockholm, to treat people with a spider phobia. The programme is extremely brief, comprising just a one-hour assessment followed by a three-hour exposure session.

  During those three hours, Öst guides the individual through a series of increasingly demanding tasks. As is normal in CBT exposure, Öst models the required behaviour for the client. Letting the person see exactly what’s involved before they attempt a task helps encourage and relax them.

  First, the person is taught to catch a small spider in a glass bowl; then to touch the
spider; and finally to let the spider walk on their hand. Before the second task, the person is asked what they expect will happen. Öst notes: ‘Almost 100 per cent of our patients say that the spider will crawl up on their hands, up the arm and underneath the clothes.’ But the individual soon discovers that their interpretation is mistaken: in fact, the spider runs away.

  Once the client has completed the three tasks, they repeat them with a series of increasingly large spiders. By the end of the session, the person will have the two biggest spiders walking around on their hands – a pretty remarkable achievement considering how they felt about spiders just a few hours previously.

  Öst has developed a similar treatment for people suffering from blood-injection-injury phobias. In this case, clients are shown a series of increasingly gory images of wounds, operations, and the like. But these phobias are unlike any others: rather than the individual’s blood pressure rising when confronted by the feared object or situation, it drops. And so, to prevent the person fainting when they see blood, Öst teaches them to detect the earliest signs of a fall in blood pressure and to respond by repeatedly tensing their muscles. This ‘applied tension’ increases the individual’s blood pressure, thus enabling them to proceed with the exposure task.