These effects are logical sequelae of the prolonged activation of the SNS. Stress and inflammatory mediators, such as cytokines, also have important effects on mood, behaviour and emotion.⁷ Activation of the immune system via these immune mediators, such as takes place during an acute infection, induces sickness behaviour (apathy, lethargy, lack of motivation and appetite). This behaviour is the body’s way of ensuring that one takes the rest required to assist the body in recovering from an infection. Many of these symptoms are also seen in depression and a significant part of the reason may be because of the high levels of cytokines associated with high allostatic load. Some cytokines activate cerebral noradrenergic and serotonergic systems and so anxiety and depression are often seen as a mixed picture. It may also be part of the reason that depression occurs more frequently in people with medical disorders associated with immune dysfunction. From a therapeutic perspective it is important to remember that every investment in reducing anxiety, improving coping and enhancing wellbeing is a step towards reducing suicide risk.

MENTAL HEALTH INDICATORS

Measures of mental health in developed countries have not been heading in a positive direction in recent decades:

In spite of recent clinical and research advances, an increased burden of mortality and morbidity related to stress and mental ill health can be noted, especially in European societies and populations undergoing stressful transitions and dramatic changes. A societal syndrome, consisting of depression, suicide, abuse, risk-taking and violent behaviour as well as vascular morbidity and mortality, can be observed.⁸

Evidence suggests that the stress associated with modern life has been increasing at a surprisingly rapid rate: 45% over the past 30 years in some surveys.⁹ Depression currently ‘causes the largest amount of non-fatal burden, accounting for almost 12% of all total years lived with disability worldwide’¹⁰ and it is estimated that in Australia mental health issues, principally depression, will be the major cause of morbidity within the next two decades.¹¹ Among affluent countries around the world it is estimated that, by the year 2030, unipolar depression will account for over 1.5 times the burden of disease that will be accounted for by cardiovascular disease.¹² This is independent of the secondary effects of depression, such as it being an independent risk factor for heart disease and associated co-morbidities such as substance abuse.

The higher prevalence of poor mental health could be explained in part by an increased awareness of mental health issues. Aside from this it is apparent that many people have more pressured and stressful lives. The rapid increase in the amount of social change, job insecurity, the speed of life, escalating competitiveness, higher expectations and many other factors all contribute.

Today, higher rates of depression are occurring at younger ages. Suicidal ideation is surprisingly common in adolescents. Data suggest that 1 in 2 young people report experiencing high levels of psychological stress and as many as 25% of 15–24 year-olds presenting to a GP for any reason reported experiencing recent suicidal thoughts ¹³ despite the fact that most did not present for psychological reasons.

Evidence suggests that antidepressant medications in children and adolescents, although widely used, are not effective and that such approaches have to be questioned.^14,¹⁵ Part of their overuse may be driven by marketing forces and parental anxiety. Particularly in this group of patients it is important for attention to be paid to the social and domestic causes of stress and to the fostering of protective factors and resilience through education and community programs.

The causes of declining adolescent mental health are contributed to by a wide range of factors, including physical inactivity, poor nutrition, substance abuse and social influences. Some elements of youth culture and excessive pleasure-seeking behaviour may also be contributing factors. Although adolescents will ‘self-medicate’ for depression by using substances and promiscuous sexual behaviour, recent studies also suggest that substance abuse and promiscuous sexual behaviour precede and predict the later development of depression: ‘Engaging in sex and drug behaviors places adolescents, and especially girls, at risk for future depression.’^16a

Some groups on the fringe of society, such as the Goth subculture, seem to be at very high risk for self-harm and attempted suicide.¹⁷ Music is also a powerful modulator of emotion and behaviour and can significantly increase risk-taking behaviour.¹⁸ The assessment and management of mental health issues among adolescents therefore requires attention to such issues.

DOPAMINE AND REWARD SYSTEMS

Different brain pathways accord with differing approaches to pursuing fulfillment. Dopamine is a neurotransmitter with multiple actions at each level of the mesocorticolimbic reward pathway—it is intimately associated with the ability to experience pleasure and motivation.¹⁹ The pursuit of pleasure is a vital activity associated with survival. For example, we would not eat or reproduce unless it was pleasurable. Some people are, however, more genetically at risk of developing addictive behaviours, and the over-activation of the mesolimbic system can trigger addictions of various kinds. In such situations it requires increasingly intense and frequent stimuli to produce the same pleasure response; over time, this ‘tires’ the reward system, predisposing to anhedonia and depression. Dysfunction of dopamine transmission in the reward circuit is associated with symptoms such as anhedonia (inability to experience pleasure), apathy and dysphoria (disturbed mood). It is found in various neuropsychiatric disorders, including Parkinson’s disease, depression and drug addiction. Prolonged and significant stress early in life can also affect one’s dopamine pathways for life.²⁰ What begins as a pursuit of pleasure eventually becomes an uneasy retreat from the pain and anxiety associated with withdrawal. This has implications for the development of impulsivity and reactivity.

Increased dopamine release is also seen in the brain during the relaxation response. This is associated with reduced impulsivity or reactivity,²¹ which may have something to do with the development of emotional and impulse regulation associated with long-term meditation practice. This may also help to facilitate healthy lifestyle change.

Mood, neurochemistry and behaviour are intimately entwined. Mood affects behaviour and is a common reason for relapse into unhealthy behaviours.²² Major depression, for example, triples the risk of progression to daily smoking²³ but, conversely, a history of daily smoking nearly doubles the risk of major depression. In adolescents, experimental smoking very significantly increases the risk of taking up smoking as a habit. Depression, anxiety and peer smoking strongly predict the risk of experimental smoking, and depression and anxiety increase susceptibility to peer influence to establish risk-taking behaviours. Building resilience and emotional intelligence in adolescents, particularly boys, may therefore produce a number of benefits including the ability to avoid unhealthy behaviours. It also goes part of the way towards explaining why CBT and antidepressant medications both reduce relapse rates for smokers.^24,²⁵

Brain scans show that mental anticipation can have as significant an effect upon brain activity as physical stimulation. The thought of eating activates areas of the brain associated with rewards and pleasure.²⁶ As these centres are important in addictions it is likely that potential forms of therapy for treating addictions will be developed that target these biochemical reactions pharmacologically²⁷ and behaviourally.

STRESS AND PERCEPTION

Man is not disturbed by events but by the view he takes of them.²⁸

Epictetus

That stress is intimately related to perception is not a new concept. The mind has a key role in eliciting the stress response through its functions of perception, cognition, interpretation and conditioning. When perceptions are distorted or cognitions are irrational, this leads to a consequent inappropriate activation of the stress response.

Learned patterns of coping and personality styles are generally more influential than the situation in activating the stress response. By understanding the basic mechanisms that underlie this process, it is possible to use strategies to deactivate it. Such strategies can include:

• meditation

• relaxation therapy

• cognitive-behaviour therapy (CBT)

• mindfulness-based cognitive therapy (MBCT)

• acceptance commitment therapy (ACT)

• dialectic behaviour therapy (DBT)

• rational-emotive therapy (RET).

These help to reverse the effects of inappropriate stress by attacking it at its cause—thought. Reviews of the literature suggest that cognitive and relaxation-based forms of stress management are the most effective strategies in general practice settings, and that working in groups potentiates outcomes.²⁹ A certain amount of stress can be useful in enhancing motivation. Furthermore, the fight-or-flight response can be entirely necessary in extreme situations. Aside from this, however, most of the stress experienced in daily life is neither necessary nor helpful in improving our ability to deal with a challenge. Most of the unhelpful stress experienced is associated with an agitated and unfocused mind that also has a limited capacity at the time to distinguish between present-time reality and imagination. Mental projections and anticipation are given a reality they do not deserve. Examples might include projecting fears into the future about upcoming exams or interviews or habitually recreating past anxieties and conflicts. Here the stressors are in the mind, not in reality, but the body will nevertheless faithfully translate this mentally generated stressor into the stress response. It will not stop until it is told to, regardless of whether the stressor is real or imagined. If one imagines a rope to be a snake, the body will react to the perception, not the reality. Even events that are actually happening at the time will only cause stress depending on the mental interpretation of them. To attribute our stress solely to the events around us and to ignore our own role in generating stress is disempowering and will lead to less than favourable therapeutic outcomes.

GENDER AND THE STRESS RESPONSE

Much of the early stress research focused on men, and hence the fight-or-flight response, which is largely a male response, has become the predominant paradigm in stress medicine. But there is good evidence to suggest that women do not respond to stressful situations in entirely the same way as men, emotionally, socially, behaviourally or physiologically. Reviews of the literature ‘suggest that the female stress response of tending to offspring and affiliating with a social group is facilitated by the process of “befriending”, which is the creation of networks of associations that provide resources and protection for the female and her offspring under conditions of stress’.³⁰

Both males and females have the capacity to activate the fight-or-flight response if required, but men are especially built for this response. Testosterone contributes significantly to this ³¹ and also has a role in the development of ‘rough- and-tumble play’ and sporting interests among boys. Excessive testosterone levels are implicated in excessive physical aggression and crime among men. Female aggression, on the other hand, is more ‘cerebral’—that is, it seems more likely to be expressed ‘in the form of gossip, rumour-spreading and enlisting the cooperation of a third party in undermining an acquaintance’.³²

The females of most species are more involved in tending the young because they have the biological or behavioural disposition to ‘tend-and-befriend’. In humans this effect is largely mediated through female hormones such as oxytocin and oestrogen.³³ Levels of these hormones are highest during activities like breastfeeding as well as in social interaction, massage and caring physical contact. These hormones have a calming or settling effect on stress and down-regulate the fight-or-flight response.³⁴ Women therefore have less of a tendency to become overly aggressive. None of this suggests that men cannot tend and befriend, or that women cannot elicit the fight-or-flight response when required, but it does suggest that each gender is more or less adapted for one or other response. This is an example of the complementarity of nature but equally it is part of the reason that men and women will respond in different ways to life events and therapies. Women, for example, will tend to feel more comfortable with talking-based therapies, especially dealing with emotional content, whereas men will more often wish to approach problems in an action-based way.

STRESS AND PERFORMANCE

One of the reasons that many people value stress is that they use it as a motivator to enhance performance. It is an assumption for many that if there were no stress there would be no performance. Inertia is, initially at least, a low-stress state but as stress increases, perhaps before an exam or a deadline, stress will often stimulate an increase in performance (Fig 8.1). If the stress remains manageable and is not too prolonged, then there tends not to be a significant problem. If, however, the stress escalates due to rising demands on performance, and stress is the only motivator being used to drive performance, then the person goes over the top of the stress-performance curve (red line) and finds that, despite high stress and energy consumption, performance drops. If this situation goes on for long, burnout soon eventuates.

FIGURE 8.1 Stress–performance curve

There is another option (green line). We will have had experiences when we functioned at our peak. In athletic circles this is called ‘the zone’; it is also called a ‘flow state’. In such a state there is an increased focus of attention and this has two significant effects. First, because attention is less monopolised by anxieties and fears there is a reduction in stress, leading to a sense of being inwardly calm. Secondly, because of the high level of focus or ‘restful alertness’, the resulting perceptiveness is associated with a high level of performance and efficiency. A hallmark of this state is a sense of effortlessness.

Unfortunately, burnout is common, particularly among doctors. A study of medical interns found a steady increase in the point prevalence of burnout, which peaked at a prevalence of 75%, 8 months into the intern year. Seventy-three per cent of interns met the criteria for psychiatric morbidity—that is, an anxiety or depressive disorder—on at least one occasion throughout the year.³⁵ For this reason, an increasing number of medical schools are introducing self-care skills into medical education to foster resilience for later careers. Burnout is measured by levels of things such as depersonalisation, lack of motivation and low sense of achievement.

Even in the absence of burnout, living and working in a ‘hyperkinetic environment’ encourages a lower level of focus, which some call ‘attention deficit trait’ (ADT).³⁶ In dealing with so much input coming at such a speed, a person tends to become increasingly reactive, adopts ‘black-and-white thinking’, has difficulty staying organised and setting priorities, and manages time poorly. It is often associated with a constant low level of panic and guilt. The management of ADT is through learning to focus or regulate attention, lifestyle maintenance, changing the environment to be less frenetic and learning how to stop at the end of the day.

Studies of learning styles indicate that certain motivation and learning styles need stress to drive performance, and others don’t. Biggs’ model describes three learning approaches: surface learning, achievement learning and deep learning.³⁷ Deep learners are driven by interest, not stress, and do not need stress to perform well. They integrate what they learn and tend to enjoy it far more. Surface learners tend to learn by rote and the main motivation is to avoid failure. Achievement learners often study hard but are motivated by ego-enhancement, that is, wishing to achieve well in order to earn respect or look good. Surface and achievement learners tend to need stress to perform. The highest achievers all use deep approaches, while third-class honours students tend to use surface approaches.³⁸

MIND AND BRAIN

In the field of MBM, there is much debate about the distinction, if any, between mind and brain. Are they the same, or does the mind communicate through the brain? In this view, mind is non-physical and is constituted by thought and emotion. The brain, on the other hand, is the physical organ that translates thought and emotion into biological and electrical activity and thereby regulates the body. The statement that an illness, pain or stress is ‘in the mind’ is correct, but it is also in the body.

Depression is an emotional state that is also associated with a range of other symptoms and somatic effects. These are mediated via the neurotransmitter and hormonal changes associated with depression and the rich interconnections between emotional and cognitive centres in the brain. Although there are undoubtedly changes in neurotransmitter profiles in the brain associated with depression, serotonin being the most important, sophisticated brain-imaging techniques are making it clear that thought and belief have a major role in driving brain activity. Functional MRI (fMRI), for example, can show that changes in brain activity associated with the placebo response when a person receives a mock antidepressant is biologically similar to that in people who receive the active drug. Such observations are impossible to explain with the view that the cause of recovery from depression is purely a chemical one. The same is also seen in people who receive placebo analgesics by mapping regional metabolic changes in parts of the brain that modulate the pain response.^39,⁴⁰ Interestingly, brain scans mapping the recovery from depression associated with cognitive approaches demonstrate that it is via different pathways than those associated with pharmacological therapies.^41,⁴²

In various chronic pain syndromes, the changes in the brain associated with stress and sympathetic nervous system reactivity sensitise the pain pathways in the brain to register pain messages even with relatively low-level stimuli and in the absence of tissue damage. To the person experiencing the chronic pain syndrome, the experience of pain feels real. This is part of the reason that chronic pain and other manifestations of somatisation are such common accompaniments to emotional states such as depression, anxiety and burnout. It also explains, at least in part, why it is often difficult to demonstrate tissue damage associated with pain in various conditions such as chronic musculoskeletal pain, chronic low back pain, chronic fatigue syndrome and fibromyalgia.⁴³ Sustained attention and arousal are crucial in creating and sustaining the neural loops associated with chronic pain.⁴⁴ In other words, when a person becomes highly vigilant and reactive to pain messages, the brain will fire off pain messages with fewer and fewer stimuli. From a therapeutic perspective, this may be part of the reason that attention regulation exercises, such as mindfulness meditation, help in chronic pain syndromes. It is likely that the reduced reactivity to sensations may actually help to ‘rewire’ the brain in a way that minimises these effects.

Depression, stress and other psychological and emotional states are undoubtedly associated with physical sequelae. For instance, it has been shown that chronic severe depression is associated with a fivefold-increased risk of coronary heart disease independent of other risk factors.⁴⁵ These effects are not just the result of changes to one neurotransmitter—serotonin. There is a huge variety of biochemical, physiological and hormonal changes relevant to the cardiovascular system that are associated with depression. It therefore follows that treating depression with antidepressants does not significantly reduce the risk of cardiovascular disease. If, however, thought changes biology, then changing thought for the better among depressed patients should have a more significant effect in reducing the risk of cardiovascular disease, which it does. A meta-analysis of 23 studies clearly showed major reductions in ongoing morbidity and mortality for cardiac patients who received, as part of their rehabilitation, psychosocial interventions aimed at improving coping and emotional health.⁴⁶ The increased risk for those with no psychosocial treatment as a part of their ongoing management was 1.70 for mortality and 1.84 for recurrence. The conclusions drawn from this study were unambiguous: ‘The addition of psychosocial treatments to standard cardiac rehabilitation regimens reduces mortality and morbidity, psychological distress, and some biological risk factors … It is recommended to include routinely psychosocial treatment components in cardiac rehabilitation.’

The above discussion has given some indication of the scope and potential of MBM.

MAPPING MIND AND BRAIN

The vast and rapidly expanding field of neuroscience is providing plausible ways of understanding the mind–body connection. Mapping of the brain began in the early twentieth century. Specific functions could be attributed to specific regions of the brain, although this early work led to some naive and simplistic approaches to managing mental illness and behavioural problems. Psychosurgical techniques such as the frontal lobotomy have understandably been relegated to history, although other techniques such as electroconvulsive therapy (ECT) remain in use, and newer techniques such as transcranial magnetic stimulation (TMS) are being developed. The mainstay of the management of mental illness since the 1960s has been pharmaceutical. In more recent times, psychotherapies have accumulated more evidence supporting their use.

Many long-held myths about the brain have recently been challenged, particularly since the rise of neuron-imaging techniques. It was once thought that, after initial development, the CNS changes very little for the rest of the lifespan, but it is now becoming increasingly obvious that major modification of the brain takes place in response to experience, memory, attention and emotion. This is called ‘neuroplasticity’. It suggests that although maladaptive reactions and ways of coping can become ‘wired’ into the circuitry of the brain, from a therapeutic perspective these reactions can also be wired out again, given the right strategies and persistence. The adaptability of the brain is exemplified by experiments on the effects of stress on the animal brain.⁴⁷ It was demonstrated that remodelling, particularly of the amygdala, which is associated with emotions and anxiety states, took place over a few weeks. This ‘rewiring’ is reversed if the animal is allowed to return to a stress-free environment. Such modelling and remodelling is more rapid in younger animals than in older animals. From a developmental perspective, it has significant implications for the long-term development of anxiety and depression. Memory of emotionally traumatic events with a high level of emotional reactivity reinforces the pairing of the thought with the emotion and accompanying physiological response. In its most extreme form it leads to post-traumatic stress disorder.

There are a number of changes to the brain associated with persistently high allostatic load. The brain is biochemically and structurally very responsive to stress hormones. The hippocampus, important for learning and memory, tends to atrophy and is vulnerable to the effects of stress and trauma. This has implications for the later development of dementia. The prefrontal cortex is important for working memory, and executive functions such as reasoning, emotional regulation, immune modulation and extinction of learning. The prefrontal cortex also plays a key role in modulating the stress response ⁴⁸ but it too tends to atrophy through stress. The amygdala, on the other hand, which mediates the physiological and behavioural fear response, shows growth in response to persistent stress. Other parts of the brain have also been shown to be involved in the stress and fear responses.

States of mind such as those induced by mindfulness meditation are associated with changes in brain activity, specifically activation of the left frontal lobe, which is associated with better mood and improved immunity.⁴⁹ A predominance of left-sided anterior prefrontal activation is associated with positive affect and optimism. Other studies also link meditation to specific changes in brain activity associated with attention regulation and control of the autonomic nervous system.⁵⁰ Long-term meditation is now thought to have effects on brain structure and to slow age-related neuronal loss,⁵¹ particularly in brain regions associated with attention, interoception and sensory processing. These were significantly thicker in meditators than in matched controls. Meditation ‘might offset age-related cortical thinning’ and provide ‘evidence for … cortical plasticity’, probably a result of down-regulation of the stress hormones associated with allostatic load and implicated in acceleration of brain ageing.

THE PLACEBO RESPONSE

The placebo response is probably the most widely known example of the mind–body interaction. It refers to when a clinically significant effect is derived from the use of a chemically inert substance that the subject believes to be an active compound. In drug trials it is the most consistent confounding factor. Apart from the difficulty of identifying the mechanisms by which it is mediated, the placebo effect also makes it difficult to determine the effectiveness of medications, and can produce unwanted ‘side effects’—this is called the ‘nocebo effect’.

Harnessing the clinical potential of the placebo response raises ethical issues, as it is held to be unethical to mislead a patient. On the other hand, demystifying the placebo response has the potential to negate a significant part of the clinical response for many treatments.

Conditions that seem to be most subject to the placebo effect are those most influenced by emotion, perception and interpretation. Hence, the placebo effect for antidepressants, anxiolytic agents and analgesics is extremely high. To illustrate, reviews of the published research data suggest that the level of placebo effect of antidepressants is 60–80%; that is, only 20–40% of the clinical effect can be attributed to the chemical. More recent reviews, which include unpublished as well as published data, suggest that antidepressants are no better than placebo for mild–moderate depression and only marginally better than placebo even for severe depression.^52,⁵³ This is not surprising if one considers that fMRIs on patients receiving antidepressants show that brain activation in those receiving the drug is almost identical to that of those who receive a placebo.³⁹ Recovery from depression through cognitive therapies is via different neurological pathways than those activated by drugs. In the future it may be possible to use patients’ brain scans to identify those who are more likely to respond to drug or cognitive therapies.^42,⁵⁴ fMRI also shows that giving a placebo to a person in pain leads to a different cascade of neuron-chemical changes than those associated with mood regulation—rather, one associated with pain pathways.⁵⁵ Explanations for such phenomena are difficult unless one takes a more metaphysical view of the relationship between mind, brain and biology.

Surgical techniques are rarely subjected to placebo-controlled trials but when they are, the results are interesting. For example, a trial on arthroscopic knee surgery for osteoarthritis found that ‘the outcomes after arthroscopic lavage or arthroscopic debridement were no better than those after a placebo procedure’.⁵⁶

THE EXPERIENCE OF PAIN

The experience of pain is ‘holistic’ in the sense that the mental, emotional and physical are all involved. Pain is not localisable to any one centre of the brain, but is dependent on the interaction of many centres that register, modify or amplify pain signals. Such pain pathways can be affected by attention, mood, emotion, fear and cognition.

Empathy, or experiencing another’s pain, has biological correlates. Again, under fMRI, empathy has been shown to be associated with similar changes in brain activity to those in the loved one actually experiencing the pain. Although the body is not registering physical pain, in empathy a person ‘suffers’ emotionally as they would if they were experiencing physical pain.⁵⁷ ‘Stress’ also affects acute and chronic pain perception. Chronic pain syndromes are very common in individuals with anxiety, depression, poor coping and high levels of helplessness and hopelessness. Equally, it is often difficult to identify somatic disease in such conditions as burnout, multiple chemical sensitivity, chronic musculoskeletal pain, chronic low back pain, chronic fatigue syndrome and fibromyalgia. In chronic pain syndromes, evidence suggests that neural loops become sensitised to register the experience of pain with minimal stimuli. They are maintained by ‘sustained attention and arousal’ in that the person is constantly vigilant for, and reactive to, pain messages.^58,⁵⁹ It may be through the reversal of such effects that practices such as mindfulness, which reduce arousal and reactivity and refocus attention, have excellent long-term effects in the management of chronic pain.⁶⁰

The comorbidity of chronic pain and depression may be partly explained by the fact that pain alters the hippocampus and gene expression, and reduces neurogenesis. In total, this adds up to the sensitisation of the nervous and limbic systems, in depressed patients.⁶¹

Chronic pain conditions are responsive to a range of mind–body interventions. For example, a study ⁶² of irritable bowel patients found that 71% initially responded to hypnosis and, of these, 81% maintained their improvement in the longer term. This correlated with improvements in quality of life, anxiety or depression scores, and led to a reduction in consultation rates and medication use. These benefits were still demonstrable after 5 years.

No management of a chronic pain syndrome should be considered complete without attention to the mind–body interaction. Taking a mind–body approach, however, will require a patient to have both insight and motivation.

THE EFFECTS OF STRESS REDUCTION

Psychological stress affects every system of the body. For example, there are effects on cardiac risk factors such as:

• increased blood pressure

• increased cholesterol

• increased platelet adhesiveness

• poor diet and sedentary behaviour

• addictive behaviours, including smoking.

Stress affects immune function (see section on psychoneuroimmunology, later in this chapter), slows wound healing ^63,⁶⁴ and alters genetic function, damage and repair (see section on genetic expression, later in this chapter). The implications are enormous.

The relaxation response, on the other hand, reverses the harmful effects of the inappropriate activation of the stress response. The ‘relaxation response’ was first coined by Professor Herbert Benson of Harvard University.⁶⁵ Although it can be fostered in a variety of ways, the effects are similar: a relaxed physical condition and a focused and alert mental state. This state of body and mind is sometimes called ‘restful alertness’.

Some of the physical and psychological effects of stress that can be reversed through stress reduction techniques are listed in Boxes 8.1 and 8.2.⁶⁶ Overall there is a restoration of physiological balance or homeostasis. This movement towards balance, efficiency and health is natural and will take place automatically if it is not interfered with. Similarly, the mind will return to happiness and contentment if it is allowed.

BOX 8.1 Physiological benefits of relaxation and stress reduction

• Marked decrease in oxygen consumption, respiratory and metabolic rate and economy, and lower catechol receptor sensitivity ⁶⁷^–⁶⁹

• Reduction in blood pressure and heart rate ⁷⁰

• Reduction in serum cholesterol ⁷¹

• Better control and lower rate of complications for diabetics ⁷²

• Increase in skin resistance and decrease in blood lactate ⁷³

• Changes in EEG patterns, including an increase in alpha and theta waves and EEG coherence ⁷⁴

• Reduction in epileptic seizure frequency ⁷⁵

• Changes in neurotransmitter profile, including high serotonin ⁷⁶

• Selective increase in cerebral blood flow ⁷⁷

• Reduction in cortisol levels ⁷⁸

• Reduced TSH and T₃ levels ⁷⁹

• Improved response time and reflexes ⁸⁰

• Improvement in proprioception, perceptiveness of hearing and other senses ^51,⁸¹

• Immune regulation—improved immune function, reduced inflammation and better response to immunisation ⁸²

• Neuroplasticity—increased left prefrontal lobe activity, thicker grey matter (prefrontal lobes)⁵¹

• Reduced calcium loss associated with high cortisol ⁸³

• Adjunct to therapy for a variety of illnesses such as heart disease, cancer, chronic pain,⁸⁴ asthma,⁸⁵ diabetes⁸⁶

• Reduced mortality (cardiac, cancer and all-cause mortality)⁸⁷

BOX 8.2 Psychological benefits of stress reduction

• Decreased anxiety ^88,⁸⁹

• More optimism, decreased depression ^90,⁹¹

• Improved coping capabilities ⁹²

• Improved wellbeing ⁹³

• As an adjunct to psychotherapy ⁹⁴

• Reduced reliance upon drugs (prescribed and non-prescribed) or alcohol ⁹⁵

• Improved sleep—more restful, less insomnia and, in time, less sleep needed ⁹⁶

• Reduced aggression and criminal tendency ⁹⁷

• Improved IQ and learning capabilities, including the aged and intellectually impaired ^98,⁹⁹

• Greater efficiency and output and reduced stress at work ¹⁰⁰

• Reduced ‘attentional blink’ and greater ability to absorb information ¹⁰¹

• Better time management and improved concentration, academic performance and memory ¹⁰²^–¹⁰⁴

• Reduction in personality disorders and ability to change undesired personality traits ^105,¹⁰⁶

• Greater emotional intelligence and emotional regulation ¹⁰⁷

Meditation is possibly the most powerful way of eliciting the relaxation response. Physiological and psychological benefits are cumulative when such exercises are practised over time. They work largely by reversing the unwanted effects of high allostatic load as well as helping to facilitate healthy behaviour change.

Some insurance companies are interested in the health benefits of stress reduction and meditation. This interest is based on the findings of some large audits. One compared 600,000 non-meditators to 2000 meditators.¹⁰⁸ The findings demonstrated reduced illness rates and medical care utilisation in every disease category. For example, there was an 87% reduction in heart disease and a 55% reduction in tumours among those who meditated compared with those who didn’t. Follow-up over an 11-year period showed further improvements, with an overall 63% reduction in healthcare costs (that is, 63 cents in the health dollar saved), with less than one-eleventh the number of hospital admissions for cardiovascular disease, one-third the number for cancer and one-sixth the number for mental disorders and substance abuse, in meditators compared with non-meditating controls.¹⁰⁹ These studies did not control for all lifestyle and personality factors, and so self-selection and healthy lifestyle change would have contributed to the results along with direct physiological benefits. On the strength of the evidence, some insurance companies in the United States and Europe offer substantial reductions in life insurance premiums of up to 30% for those who regularly practise an approved form of meditation, in this case transcendental meditation (TM).

PSYCHONEUROIMMUNOLOGY

The mind in addition to medicine has powers to turn the immune system around.¹¹⁰

Jonas Salk (discoverer of the polio vaccine)

In recent decades there has been an explosion of research into how psychological factors affect the immune system. Put simply, psychoneuroimmunology (PNI) means that the mind is connected to the immune system via the nervous and endocrine systems. These effects have major implications for susceptibility to infections and cancer, response to allergens, and the modulation of autoimmune and inflammatory conditions. As it would be hard to find a disease process that is not influenced by immune function, PNI should be considered an important factor in the development of any illness.

Although the notion that the mind affects our resistance to disease dates back thousands of years, PNI began to gain credence in the mid-1970s. Communication between the CNS and the immune system takes place via ‘hard wiring’ (nerves) and a ‘postal system’ (blood-borne hormones and neurotransmitters). By these two means the CNS communicates with every element of our immune defences in a bi-directional feedback system.^111,¹¹² Over 70 neurotransmitter receptors have been found on the surface of white blood cells. Especially important in the feedback loop are the limbic system in the brain, primarily concerned with emotion, and the prefrontal lobes. A predominance of left-prefrontal lobe activity is associated with better mood, optimism, intense positive emotion response to emotionally positive stimuli and an ability to minimise negative affect in daily life.¹¹³^–¹¹⁵ This correlates with greater natural killer (NK) cell activity. Predominantly right-brain active people experience lower mood, more pessimism and intense negative emotion in response to emotionally negative stimuli. The right prefrontal lobe is more important for antibody and immunoglobulin response.¹¹⁶

The ‘chemistry of thought’ is not localised to the brain, because the same neurotransmitter receptors are found in virtually every tissue in which they are sought. This goes a long way to explaining how emotional states such as stress, anxiety and depression cause distant physiological effects and affect susceptibility to disease. Also important is the fact that drugs that have psychoactive properties are also found to affect immune function and have clinically relevant side effects on immunity. Furthermore, the blood–brain barrier is made more porous by stress ¹¹⁷ and PNI mechanisms may play a role in the development of psychiatric disorders.³

There are many ways of measuring immune status. The commonly used measures of immunity are simply the number and types of immune cells—this indicates ‘how large the army is’ but tells us little about how well it is functioning. Tests of immune cell function are more specialised and expensive but are designed to give a more important indicator of how well the cells are performing their designated roles.¹¹⁸ Such tests include measuring white blood cell ‘proliferation’ in response to an antigenic challenge and measuring how well NK cells kill tumour cells through a cytotoxic activity assay. These tests are performed in vivo. Other tests are performed in vitro by measuring the body’s ability to stimulate antibodies or the delayed-type hypersensitivity response (allergic response). Negative emotional states have a negative effect on immunity largely by affecting how well immune cells carry out their core functions, such as lymphocyte proliferation in response to infection¹¹⁹ or by inhibiting NK cell activity,¹²⁰ rather than having major effects on cell numbers. In terms of day-to-day health, the size of the army, though important, may be of secondary importance to how well that army is performing. For these reasons compromised immune function due to stress is harder to pick up on standard blood tests, which give cell counts but tell us little about how well those cells are functioning.

Immune cells discriminate ‘self’ from ‘non-self’ and do not attack self unless that cell has become a threat, as in cancer, or it has become infected by a virus. Immune dysfunction occurs when immune cells lose their ability to discriminate between self and non-self, attacking healthy tissue inappropriately or not attacking things that should be attacked. The former, through inflammatory mechanisms, leads to autoimmune and inflammatory diseases, and the latter, through immunosuppression, predisposes to infections and cancer. During high-stress periods there is a shift towards the type-2 immune response and type-2-mediated conditions (infections, latent viral expression, allergic conditions and autoimmune conditions).¹²¹ This inappropriate response is called immune ‘dysregulation’ and partially explains the increased incidence or relapse of such illnesses during high-stress periods (Box 8.3).

Immune cells mirror emotional states ¹²² and emotional states are associated with a variety of disease states, whether as a result of an accumulation of many small stressors or the impact of large ones. An accumulation of small daily stressors can be as detrimental to health as major stressors, if not more so.¹²³ Changes in immune cell numbers and function start to occur within five minutes of an event that is perceived to be stressful.¹²⁴ Depending on the reaction to the stressor, that effect can remain for up to 72 hours afterwards.¹²⁵ If a person perceives that they have some control over the situation or control over their response to the situation, then they are partially protected from the stress and its consequent immunosuppressive effects. People who perceive that they have no control over the event or their response to it, especially if they are anxious to be in control, experience prolonged negative effects on immune function.

Acute stress alters quantitative and functional components of cellular immunity, and individuals vary markedly in the magnitude of their response. These differences can be predicted by individual variability in perception and consequent stress-induced hypothalamic-pituitary-adrenal-axis (HPA-axis) and SNS activation. Those who have higher SNS reactivity to stress (increased blood pressure, heart rate, catechol secretion) have the greatest disturbance to immunity and susceptibility to infection in response to stressful events. These variations are of clinical significance.¹²⁶ High cortisol reactors with high levels of life events have approximately double the incidence of verified upper respiratory infection than high reactors with low levels of life events and low reactors irrespective of their life event scores.¹²⁷ This has been further illustrated in studies measuring the stress levels of medical interns and their correlation with immunity.¹²⁸

Salivary immunoglobulin A (S-IgA) is the first line defence against infection in the respiratory gastrointestinal and urinary systems, and is one of the easiest markers of immune competence to measure. Low levels of S-IgA are associated with increased risk of infection ^129,¹³⁰ and have been found to be reduced by stressful life events such as exam pressure, social isolation,¹³¹ grief,¹³² anxiety¹³³ and the ‘need to have power and to influence others’.¹³⁴ Positive emotional states, however, are associated with immunoenhancement.^135,¹³⁶ S-IgA can be increased or decreased for 4–5 hours even by inducing positive (e.g. care and compassion) or negative (e.g. anger and frustration) emotions for only 5 minutes.¹³⁷ Mental and emotional states also influence the speed of wound healing due to the effects on interleukins and cytokines.¹³⁸

In response to ‘standardised stressors’ some people experience immunoenhancement and others immunosuppression, depending on the person’s perception of the event. Studies of life stress and its impact on cancer incidence have had similar findings. In determining the impact of stress upon health it is important to take into account the individual’s perception and coping style. Those with positive perceptions and coping styles consistently experience immunoenhancement, including improved NK cell activity and S-IgA, and those with negative perceptions and coping styles consistently experience immunosuppression.¹³⁹^–¹⁴¹ Furthermore, those who have higher SNS reactivity to stress as measured by increased blood pressure, heart rate and catechol secretion also seem to have the greatest disturbance to immunity when under stress.¹⁴² Immune change is also predicted by brain activity.¹⁴³

Lifestyle factors can also influence immune function significantly (see Table 8.1).¹⁴⁴ A healthy lifestyle helps our immune function to operate at an optimal level. No lifestyle factor is innately ‘good’ unless it is at the right level. For example, exercise prior to infection can enhance immunity and be protective against becoming ill, but high-intensity exercise after infection can worsen the infection and the symptoms. Very intense or prolonged exercise, because of the effects on allostatic load, can reduce immunity and predispose to infections. Elite athletes, for example, tend to have poor immunity.¹⁴⁵ So too much and too little exercise are both associated with poor immunity, as are too much and too little sleep. Being employed is good for health but too little or too much work is associated with poor health.¹⁴⁶

TABLE 8.1 Lifestyle and effect on natural killer cell activity ¹⁴⁴

Behaviour	Advantage in NK activity (%)
Exercise	47
Managing stress	45
Enough sleep	44
Balanced meals	37
Not smoking	27
Eating breakfast	21
Working moderate hours	17
Avoiding alcohol	0

An unhealthy lifestyle is promoted by stress ¹⁴⁷ and depression,¹⁴⁸ and therefore effective stress management is a prerequisite for sustained healthy lifestyle change.¹⁴⁹ Meditation,¹⁵⁰ psychological interventions such as CBT,^151,¹⁵² a positive attitude and humour¹⁵³ are all powerful immune system stimulants in that they help to reverse the immunosuppressive effect of stress.

The abovementioned fluctuations in immune function are significant factors in susceptibility to infection.¹⁵⁴ The likelihood of contracting a clinical infection when exposed to a virus is directly proportional to the level of stress that the host was experiencing not just at the time of exposure but during the preceding months. The severity of a viral illness, such as influenza, is greater with higher stress levels.¹⁵⁵ There is also a strong link between high stress and relapse for chronic infections such as herpes viruses,¹⁵⁶ HIV and shingles. Such viruses lie dormant and are more able to reactivate when the immune system is depleted. Data show that stress and social connectedness are important factors affecting the rate of progression of HIV to AIDS.¹⁵⁷ Those who were experiencing above-average levels of stress and had below average levels of social support were 2–3 times more likely to progress to AIDS over a 5-year follow-up. For every one severe stressor per 6-month study interval, the risk of early disease progression to AIDS was doubled.¹⁵⁸ Such observations indicate the importance of offering psychological interventions as a part of standard care. For example, giving CBT to HIV-positive men reduced depression and anxiety, and these changes were paralleled by reductions in stress hormones, improvements in white cell counts¹⁵⁹ and elevation of DHEA (dehydroepiandrosterone),¹⁶⁰ which is also an important hormone in patients with chronic fatigue syndrome.

Studies of medical students ¹⁵² during the exam period reveal profound immunosuppression, with lowered NK-cell activity, a 90% reduction in gamma interferon and lowered response of T-cells, which corresponds with the tendency to succumb to illness during or just after exams. Students who learn and practise relaxation techniques show significantly better immune function and less illness in exam periods. Even keeping a journal about significant life events is associated with improved immune function and fewer doctor visits for infectious disease.¹⁶¹ Carers have been found to exhibit immune suppression proportional to the level of distress they feel.¹⁶² The degree of immunosuppression observed in those going through a stressor such as marital separation is proportional to the amount of negative emotion and difficulty the person experiences in letting go.

AUTOIMMUNE AND INFLAMMATORY ILLNESSES

Mediators of inflammation play an important role in many illnesses. Cytokines can be typed as type 1 (e.g. γ-interferon) or type 2 (e.g. interleukin-10). A high ratio of type 1 to type 2 leads to what is called a ‘type-1 response’ and a low ratio leads to a ‘type-2 response’. It has been shown that during high-stress periods there is a shift towards the type-2 response, which partially explains the increased incidence of type-2-mediated conditions including infections, latent viral expression, allergic conditions and autoimmune conditions during high-stress periods.¹⁶³ Thus, psychological state not only regulates the level of immune response but also the type of response. This inappropriate immune response is called immune ‘dysregulation’. Autoimmune diseases are associated with immune dysregulation, whether the response is directed to the joints in rheumatoid arthritis or the myelin sheath in multiple sclerosis. Even coronary heart disease has a significant inflammatory component. PNI offers potential explanations of the mechanisms by which stressful life events and unsupportive social environments can trigger and exacerbate a variety of autoimmune diseases.¹⁶⁴^–¹⁶⁶

For example, stress is associated with increased inflammation, pain and disease activity in rheumatoid arthritis patients.¹⁶⁷ Those with supportive relationships and better coping skills are noted to have lower levels of inflammatory hormones such as interleukins.¹⁶⁸ ‘Irrational beliefs [that are stress-inducing] are associated with increased inflammation process, among apparently healthy individuals.’¹⁶⁹ There are also established links between major depression, early life stress and adverse health outcomes in inflammatory diseases.¹⁷⁰ Systemic lupus erythematosus (SLE) is also significantly affected by life stress,¹⁷¹ as is multiple sclerosis.¹⁷² From a clinical perspective, the important point is that the comprehensive treatment of any inflammatory or autoimmune illness requires the management of life stress, but unfortunately such interventions are too often ignored or seen as being of peripheral importance. Innovative studies, such as the following, have shown significant promise:

• clearing psoriasis twice as quickly when orthodox medical treatment is combined with meditation ¹⁷³

• improving outcomes for rheumatoid arthritis and asthma patients by enhancing positive emotional adjustment with journal writing as a form of stress release ¹⁷⁴

• including CBT in the management of rheumatoid arthritis.¹⁷⁵

ALLERGIES

As with immunosuppression, it is possible to classically condition allergies by pairing a stimulus with exposure to the allergen.¹⁷⁶ At present it is not known whether they can be un-conditioned. Unhealthy lifestyle and poor physical and mental health practices have been implicated in the aggravation of allergies.¹⁷⁷ The reverse hypothesis—that stress reduction reduces allergies—is still to be comprehensively tested, but some evidence suggests that it can play a role. For example, the treatment of atopic dermatitis was more successful and required fewer topical steroids when it was combined with relaxation therapy, CBT and an education program.¹⁷⁸ It has been further demonstrated that stress is an important prognostic factor for response to immunotherapy.¹⁷⁹

STRESS AND IMMUNISATION

The efficacy of vaccination such as with the hepatitis B or influenza vaccines is affected by stress. Those who are stressed prior to vaccination have significantly worse antibody and T-cell response,^180,¹⁸¹ and reducing stress has been demonstrated to improve response to flu vaccination.⁴⁹

PSYCHOGENETICS

The DNA or genetic code contains the blueprint for the whole body. Each human shares 99.9% of their genes with other humans, which means that the other 0.1% account for all the differences between humans. Until recently, genes and genetic expression were looked upon as largely fixed but now, as with the neurosciences, this thinking is being revised.

Genotype is the information coded into the genes, whereas phenotype is what the genes express. Many genes contained within a genotype may lie dormant or not be expressed at any given time. The activation and deactivation of various genes trigger the onset and progression of many diseases.

Studies on animals and humans ^182,¹⁸³ have revealed that psychological stress can induce DNA damage and chromosomal aberrations. Mental state can not only increase the number of genetic mutations, but can also impair the body’s ability to repair damage.¹⁸⁴ DNA damage is particularly important in the genesis of cancer,¹⁸⁵ which is also affected by genetically modulated cell replication, cell death (apoptosis) and cancer suppressor genes. Damage to these genes can lead to cancer.

DNA repair capacity (DRC) is a measure of the cell’s ability to repair damage. Stresses, such as coping with trauma, while increasing oxidative damage to DNA, also stimulate compensatory DNA repair mechanisms.¹⁸⁶ During periods of high stress, such as during exams, compared to periods of low stress, such as after vacations, there is an increase in DRC in most people,¹⁸⁷ implying an adaptive response to increased DNA damage. Those with higher and more consistent stress and mood disturbance have high DNA damage but no increase, or even a reduction, in DRC in high-stress periods, suggesting that the response has been impaired in some way. The implications may be significant. For example, studies comparing DRC in women with and without breast cancer showed that the DRC of those with cancer was lower than that in the control group.¹⁸⁸ A 1% decrease in DRC corresponded to a 22% increase in breast carcinoma risk, with younger breast cancer patients having a more significant reduction in DRC. Thus, DRC may be a useful marker in predicting susceptibility.

Psychological state affects genetic expression in other ways. A genetic predisposition to an illness—such as addictive behaviours,¹⁸⁹ cardiovascular reactivity,¹⁹⁰ depression,¹⁹¹ schizophrenia¹⁹² and asthma¹⁹³—is commonly activated by stress. Rather than saying that stress is the cause of the illness, it might be more accurate to say that it is a common trigger for many disease processes. In schizophrenia, for example, the ‘normal in-growth of dopamine fibres during late adolescence and their formation of aberrant connections with abnormal intrinsic cortico-limbic circuits could “trigger” the onset of symptoms in those who carry the constitutional vulnerability for schizophrenia’. In terms of genetic tendency to addictive behaviours, ‘stresses, such as drug use and social adversity, in adolescence or early adult life may propel the neuro-developmentally impaired individual over a threshold into frank psychosis’.¹⁹⁴ Drug-seeking behaviour can be triggered by various factors, including ‘priming injections’, drug-associated environmental stimuli and stress. Drug-associated stimuli and stress may activate this system via neural circuits from the prefrontal cortex, amygdala and HPA-axis.

Psychological and social factors also significantly affect the rate of genetic ageing. Telomeres can be used as a marker of genetic age. A study of healthy premenopausal women found that psychological stress, in terms of both perception and chronicity, is significantly associated with higher oxidative stress, lower telomerase activity (the enzyme that repairs telomeres) and shorter telomere length. Women with the highest levels of perceived stress compared with low-stress women had telomeres shorter on average by the equivalent of 9–17 years of additional ageing.¹⁹⁵ This has many implications for understanding how stress promotes earlier onset of age-related diseases. Mental illness is a major risk factor for CVD. Part of this may be associated with accelerated genetic ageing. Telomere shortness and low telomerase activity are associated with exaggerated autonomic reactivity (allostatic load) to acute mental stress and elevated nocturnal catechol secretion. Low telomerase activity is also associated with risk factors for CVD—smoking, lipids, high blood pressure, high fasting glucose and greater abdominal adiposity (metabolic syndrome).¹⁹⁶

The inherited disposition to depression can be activated by the interaction between heredity and upbringing. Developmentally, this is crucial for risk later in life. Childhood trauma (CT) and genetic factors contribute to the pathophysiology of depression, and experience of at least one type of CT is reported by 80% of adults with depression. The common traumas include physical neglect, emotional abuse and emotional neglect. There is an earlier age of onset of depression in those with CT and earliest onset in those with highest CT.¹⁹⁷ Children raised in deprived environments can consequently have severe cognitive and behavioural difficulties and poor response to stress lasting into adulthood. These changes are associated with ongoing alterations in gene expression, ‘environmental programming’ and downstream effects on the HPA axis.¹⁹⁸

From a research perspective, the new field of psychogenetics has the potential to explain the mechanisms of illness and recovery. From a therapeutic perspective, it is important to give attention to mental and emotional health in the prevention and management of any chronic health condition.

PERSONALITY AND ILLNESS

The notion that personality directly affects our physical health has a long history. For example, mythology and religion have long related moral and emotional character to health and healing. A relationship between personality and illness undoubtedly exists, but the depth of that relationship is unknown, imprecise and hard to determine because of the interrelation between psychology, upbringing, environment and health behaviours. This having been said, care needs to be taken in discussing this issue, for a number of reasons.

• Although objective self-examination and a sense of personal responsibility for behaviour is useful, one should avoid the tendency towards self-blaming or fatalism, which are common reactions.

• Giving information on the role of personality and emotional style in leading to illness can do more harm than good if it is not delivered with the skills and support to modify unhelpful traits.

• Personality is just one causal factor, albeit an important one, interplaying with others, such as environment, lifestyle and genetic predisposition.

• Much modern mythology concerning the relationship between personality and illness—for example, the idea that a lack of communicativeness will express itself through specific forms of cancer such as laryngeal cancer—cannot be supported by evidence.

• Personality is not fixed, although it takes persistent and conscious effort to change a long-held personality trait.

Any emotional ‘state’, even anger, has its place if it is appropriate to the situation, is not ‘over-expressed’ or ‘under-expressed’ and is left in the past once the situation is over. A person will generally know if the expression is appropriate or inappropriate by the after-effects. A personality ‘trait’, on the other hand, will tend to reflect a conditioned or ‘default’ response to situations. A tendency to experience and express anger, regardless of its appropriateness and usefulness, will rarely be helpful for oneself or others. It is such traits that are associated with poor mental and physical health.

Research in this field is inherently difficult due to the varying personality classifications and interpretations. Classifying personality types by clustering groups of traits together can be simplistic and risks ignoring the infinite variation and subtlety of human character and psychology. For example, studies of type A (hard-driving, ambitious, aggressive etc) personalities give inconsistent findings. Some suggest it is a risk factor for heart disease, but others do not.¹⁹⁹ More recent and decisive studies have concentrated more on individual traits, such as anger or hostility, rather than combining a number of traits. This may make more sense, as personality traits are blended differently in every individual and traits can be interpreted differently. One person might be ambitious or hard-driving, for example, but in a very compassionate and altruistic way, whereas another may be self-centred. Assertiveness can be useful or destructive, depending on which aspect of our nature is asserting itself. A person with emotional intelligence may experience anger but will be able to determine whether it is worth expressing or not.

Be that as it may, some research has demonstrated that particular personality types may be predisposed to particular types of illnesses. For example, the personality types listed below have been implicated, with differing incidences, in cancer, coronary heart disease (CHD) and overall mortality when individuals with these personality types were followed over 10 years.²⁰⁰

• Type 1: Cancer-prone individuals tended to hopelessness, helplessness and suppression of emotion.

• Type 2: CHD-prone individuals tended to anxiety, aggression and ambition, and express emotion inappropriately.

• Type 3: A mixture of the other types were intermediate in terms of amount and type of illness.

• Type 4: These people suffered far less illness. They tended to live more in harmony with themselves and others, communicated better, tended to optimism, were more self-aware and remained calmer under stress.

Establishing an unambiguous causal relationship between personality and illness is inherently difficult. Other lifestyle factors may not be controlled. Testing the hypothesis that altering personality traits alters future risk of disease is also difficult. Some research has suggested that minimising unhelpful personality traits and communication patterns and enhancing better ones has a positive long-term effect on physical and psychological health.^201,²⁰¹ Cancer-prone and heart-disease-prone individuals given ‘autonomy training’ over 6 months had far lower all-cause and cause-specific mortality than the control group. This suggests that as personality markers change, so too does the disease profile.

Other studies on patients with established and severe CHD ²⁰² show that those with a ‘type D’ personality are nearly five times more likely to have another acute myocardial infarction (AMI) in the next 6–10 years. Type D personality is made up of two main elements: a high level of negative affect (anxiety, anger, worry etc) and a tendency to withhold the expression of these emotions. Emotional stress and its suppression have also been found to increase the number of ischaemic episodes by a factor of 2.2, even when controlled for other factors.²⁰³ Among emotions, chronic anger and hostility seem to be most unhealthy, not just for CHD risk but also possibly for cancer risk^204,²⁰⁵ and survival.²⁰⁶ Other studies have given conflicting results.²⁰⁷ Part of the discrepancy is explained by the fact that many studies do not control as stringently for individual perception and coping style. People perceive the same events differently. For example, two people undergoing divorce will respond differently. For one it may be a relief of stress and for another a trauma, and in each case the physiological, endocrine and immune response will react to the perception of the event rather than the event itself. Therefore, the former is at minimal increased risk of illness, whereas the latter has a much higher risk.

Personality traits are far more malleable than they are often assumed to be, given the right support and motivation. Personality is in part genetic (nature) and in part ‘learned’ (nurture). It can be learned, and unlearned. Important elements in autonomy training, which is a behavioural approach, are self-awareness, relaxation, improved communication and behavioural strategies such as practising new ways of dealing with stressful situations. It is delivered within a support group setting and shows a lot of overlap with other approaches like mindfulness, positive psychology and emotional intelligence. Without awareness, insight and motivation it is all but impossible to change personality traits, except by the less conscious path of consistent conditioning and reinforcement.

In conclusion, advising a patient that the mind has an important role in the genesis, experience and progression of an illness is not to tell them that it is ‘all in the mind’. Rather, it is to emphasise that the state of the mind affects the body. The two are not separate. The body expresses what is happening on deeper emotional levels. As Plato would have said, prevention and therapy, therefore, must include help on the psychological as well as the physical level, if it is to achieve its potential.

MIND–BODY INTERVENTIONS

You ought not to attempt to cure the body without the soul.

Plato (Charmides)

Almost any therapy that affects a person’s mental and emotional states, because it will have consequent effects on their physical state, could be considered a mind–body therapy. For example, various meditative techniques have been found to be helpful for a range of conditions as diverse as epilepsy, premenstrual syndrome, menopausal symptoms, mood and anxiety disorders, and coping with serious illnesses, with few or no significant adverse events reported.²⁰⁸ Yoga therapy also has a range of benefits.²⁰⁹ Mind–body techniques will be helpful as adjuncts or alternatives in a far wider range of illnesses and symptoms but evidence on their efficacy sometimes lags behind community and practitioner experience. It is important that a GP who wishes to use mind–body strategies in the consulting room has adequate training. Although largely safe, their efficacy can be diminished and the potential for adverse events increased when used by inexperienced practitioners.

Techniques that can be included in the classification of mind–body therapies are described below.

A range of therapies use mindfulness principles, including mindfulness-based stress reduction (MBSR),²¹⁰ mindfulness-based cognitive therapy (MBCT),²¹¹ as well as acceptance commitment therapy (ACT) and dialectic behaviour therapy (DBT). There is a high level of clinical and research interest in mindfulness-based therapies because of promising outcomes in mental health²¹² and neurosciences. Mindfulness uses meditative practices in conjunction with a range of cognitive strategies.²¹³