Stress: Causes

Pathogenesis (development of disease)

Acute stress in the sense of eustress is a healthy alarm signal of the organism. After a parasympathetic preliminary phase, which serves to provide energy, the sympathetic nervous system is activated and cortisol is released as the so-called “stress hormone.” This results in a variety of physiological reactions, such as an increase in heart rate, mobilization of fat and glucose reserves – which leads to an increase in muscle response – or an increase in blood clotting. Other autonomic systems, such as sexual function, are blocked. After the stressors are removed, the sympathetic excitation subsides in a final recovery phase, and the normal state is re-established. This eustress corresponds to innate behavioral patterns as a physiological principle for survival in the face of danger. One speaks of potentially damaging distress when a person, due to permanent stress, no longer has the possibility to react in the sense of the described stress phases. Mental conflicts or stress-triggering stimuli such as chronic pain thus lead to a constant sympathetic over-excitation and an increased cortisol level. According to Selye (1981), the body develops an adaptation syndrome as a result of constant stress stimuli. After an alarm phase and a phase of resistance, the phase of exhaustion develops. This adaptation syndrome occurs until the exhaustion phase when the mobilized energies cannot be dissipated by flight or attack or transformed by other behaviors, such as laughter and crying, emotional conversation, or sexual activity. Stress responses are seen under different ordering principles: for example, one type classification contrasts vagotonics and sympatheticotonics. Cardiovascular diseases are seen as an expression of an excessive sympathetic excitation, gastrointestinal diseases as a sign of an irritated parasympathetic nervous system. Unfortunately, the knowledge about the causal biological connections between stress and somatoform disorders is still very incomplete, precisely because of a multifactorial genesis. Stress interferes with a very fine regulatory system of neurotransmitters, hormones and the immune system. In addition, innate – genetic – and learned factors play a still largely unknown role. Chronic stress thus leads to long-term dysfunctions of the hypothalamic-pituitary-adrenal axis (HHNA) and the sympathetic nervous system, as well as glucocorticoid-associated neurotoxic effects. An example will be used to illustrate the biological relationship between stress and a disease, in this case depression:

It has been observed that patients with acute depression often have elevated cortisol levels. This cortisol level is still elevated weeks and months after the depression has subsided. Stress hormone regulation is thus significantly disturbed in depressed patients. After corticotropin-releasing hormone (CRH), which ultimately causes hypercortisolism, was isolated in the early 1980s, it was examined what other effects CRH has. CRH was identified as a neurotransmitter. In many series of studies, CRH itself has been shown to cause anxiety, sleep disturbances, lack of appetite, and psychomotor changes, all typical symptoms of depression. For CRH, two different receptors, the CRH 1 and the CRH 2 receptor, have been identified so far. It became evident that the overactivity at the CRH 1-receptor is decisive and that blocking drugs against its activity can be developed (Holsboer & Barden, 1996), which is currently still being researched. Thus, via stress hormone physiology, a link between increased cortisol secretion and depression was clearly found. In parallel with these studies, a chronic stress model of depression in animals was developed (Katz, 1981). Rats were exposed to severe stressors, such as swimming in cold water. In addition to typical “depressive” behavioral changes, the animals showed an increase in cortisol levels. These stress-induced changes could be treated with antidepressants. Chronic mild stress also results in anhedonia (inability to feel pleasure and joy), decreased activity, weight loss, and decreased sexual activity in analogy to the typical symptoms of depression. Chronic mild stress leads to hyperactivity of the pituitary-adrenal axis with hypertrophy of the adrenal gland and increased cortisol secretion.Furthermore, in these animals there is an increase – typical for depression – in adrenergic ß-receptors and serotonergic 5HT1A and 5HT2-receptors in the frontal cortex, hippocampus and hypothalamus, which in turn are reversible by administration of antidepressants. With these research findings, the relationship between enduring stress and depression can now be better understood. But long-term stress not only leads to depression (see Figure 1) but is a significant causative factor in cardiovascular disease (coronary heart disease (CHD) (Wulsin & Signal 2003; Joynt et al., 2003). Stress-and independently, depression-alter two major neurobiological axes, leading to hypercortisolism (see above) and sympatho-vagal imbalance. The consequences are the well-known autonomic dysfunctions (Nahshoni et al., 2004) and the metabolic syndrome. Another consequence is impaired hemostasis. All three syndromes increase the CHD risk. The CHD risk is supported by smoking, physical inactivity and an unhealthy diet, which in turn are themselves often a consequence of stress and depression (Deuschle, 2002). There is a comorbidity between depression and cardiovascular disease (Heßlinger et al., 2002). It should no longer be overlooked that stress and depression must be added to the known risk factors of coronary heart disease (CHD), such as smoking, type 2 diabetes mellitus, hypertension, or hyperlipidemia (Takeshita et al., 2002). Fig 1: Disturbed neurobiological axes in stress, depression, and CHD risk.

Etiology (causes)

Biographical causes

  • Occupations – occupations with exposure to noise
  • Socioeconomic factors – poverty

Behavioral causes

  • Consumption of stimulants
    • Alcohol
    • Nicotine (tobacco use)
  • Physical activity
    • High workload
    • Shift work
    • Underchallenge
  • Psycho-social situation
    • Bullying
    • Serious life cuts
    • Mental conflicts
    • Social isolation
  • High responsibility
  • Boredom
  • Perfectionism
  • Sleep deprivation
  • Lack of time

Causes due to illness

  • Anxiety
  • Chronic pain
  • Insomnia (sleep disorders)
  • Misophonia (“hatred of sounds”; form of reduced sound tolerance).
  • Diseases and their consequences

Medications The following is a list of medications that can lead to restlessness (nervousness) (A claim to completeness does not exist! ):

Environmental pollution – intoxications (poisonings).

  • Noise

Further

  • Poverty