Comment

Stressed brain, stressed heart?

Psychological birth trauma and childbirth-related posttraumatic stress disorder represent a substantial burden of disease with 6.6 million mothers and 1.7 million fathers or co-parents affected by childbirth-related posttraumatic stress disorder worldwide each year. There is mounting evidence to indicate that parents who develop childbirth-related posttraumatic stress disorder do so as a direct consequence of a traumatic childbirth experience. High-risk groups, such as those who experience preterm birth, stillbirth, or preeclampsia, have higher prevalence rates. The main risks include antenatal factors (eg, depression in pregnancy, fear of childbirth, poor health or complications in pregnancy, history of trauma or sexual abuse, or mental health problems), perinatal factors (eg, negative subjective birth experience, operative birth, obstetrical complications, and severe maternal morbidity, as well as maternal near misses, lack of support, dissociation), and postpartum factors (eg, depression, postpartum physical complications, and poor coping and stress).

The link between birth events and childbirth-related posttraumatic stress disorder provides a valuable opportunity to prevent traumatic childbirths and childbirth-related posttraumatic stress disorder from occurring in the first place. Childbirth-related posttraumatic stress disorder is an extremely distressing mental disorder and has a substantial negative impact on those who give birth, fathers or co-parents, and, potentially, the whole family. Still, a traumatic childbirth experience and childbirth-related posttraumatic stress disorder remain largely unrecognized in maternity services and are not routinely screened for during pregnancy and the postpartum period. In fact, there are gaps in the evidence on how, when, and who to screen.

Similarly, there is a lack of evidence on how best to treat those affected. Primary prevention efforts (eg, screening for antenatal risk factors, use of trauma-informed care) are aimed at preventing a traumatic childbirth experience and childbirth-related posttraumatic stress disorder in the first place by eliminating or reducing risk factors for childbirth-related posttraumatic stress disorder. Secondary prevention approaches (eg, trauma-focused psychological therapies, early psychological interventions) aim to identify those who have had a traumatic childbirth experience and to intervene to prevent the development of childbirth-related posttraumatic stress disorder. Tertiary prevention (eg, trauma-focused cognitive behavioural therapy and eye movement desensitization and reprocessing) seeks to ensure that people with childbirth-related posttraumatic stress disorder are identified and treated to recovery so that childbirth-related posttraumatic stress disorder does not become chronic.

Adequate prevention, screening, and intervention could alleviate a considerable amount of suffering in affected families. In light of the available research on the impact of childbirth-related posttraumatic stress disorder on families, it is important to develop and evaluate assessment, prevention, and treatment interventions that target the birthing person, the couple dyad, the parent-infant dyad, and the family as a whole. Further research should focus on the inclusion of couples in different constellations and, more generally, on the inclusion of more diverse populations in diverse settings. The paucity of national and international policy guidance on the prevention, care, and treatment of psychological birth trauma and the lack of formal psychological birth trauma services and training, highlight the need to engage with service managers and policy makers.

For at least a few centuries, if not millennia, psychological stress has been popularly believed to contribute to heart disease. Does psychological stress really contribute to heart disease? Are anecdotal, patient, and lay press reports that angina, heart attack, and even cardiac death are caused by stress based on fact, or are they just folklore? In this review, the study data supporting associations between stress and cardiovascular risk, as well as potential mechanisms by which psychological stress might contribute to heart disease and precipitate myocardial ischemia and infarction, are critically reviewed and summarized.

The aim of this study was to explore the role of art psychotherapy as a biopsychosocial approach to bodymind medicine in ameliorating the effects of psychophysical stress among people with non-metastatic cutaneous malignant melanoma (CMM), post-surgical resection.

Mixed methods.

This study followed a mixed-methods research design, utilising qualitative data gained from a 6-month weekly group art therapy intervention, including both the images made and explored during the 3-h sessions and the accompanying narratives. The narratives were the subject of thematic analysis. The quantitative data arose from ELISA assays for secretory immunoglobulin A (S-IgA) and secretory interferon-γ (S-IFN- γ), DTH (PPD) tests were delivered at timepoints t0, t1, t5, t13, t24 and t52, and questionnaires were delivered at t0, t24 and t52: MAC, HAD, COPE & EORTC-QLQ-C-30.

The findings of this study included themes of ‘otherness’ and ‘isolation’, which also preceded diagnosis, and an upward trend in S-IgA, which continued over time.

This study found that art psychotherapy promotes enhanced immunological function, coping skills and interpersonal relations. Positive psychoneuroimmunological change can result from group art psychotherapy, facilitating integration of psychological content in a supportive and interactive environment, which improves quality of life, thereby reducing the public health burden.

In a 5-year multifactorial risk reduction intervention for healthy men with at least one cardiovascular disease (CVD) risk factor, mortality was unexpectedly higher in the intervention than the control group during the first 15-year follow-up. In order to find explanations for the adverse outcome, we have extended mortality follow-up and examined in greater detail baseline characteristics that contributed to total mortality.

Long-term follow-up of a controlled intervention trial.

The Helsinki Businessmen Study Intervention Trial.

The prevention trial between 1974–1980 included 1,222 initially healthy men (born 1919–1934) at high CVD risk, who were randomly allocated into intervention (n=612) and control groups (n=610). The 5-year multifactorial intervention consisted of personal health education and contemporary drug treatments for dyslipidemia and hypertension. In the present analysis we used previously unpublished data on baseline risk factors and lifestyle characteristics.

40-year total and cause-specific mortality through linkage to nation-wide death registers.

The study groups were practically identical at baseline in 1974, and the 5-year intervention significantly improved risk factors (body mass index, blood pressure, serum lipids and glucose), and total CVD risk by 46% in the intervention group. Despite this, total mortality has been consistently higher up to 25 years post-trial in the intervention group than the control group, and converging thereafter. Increased mortality risk was driven by CVD and accidental deaths. Of the newly-analysed baseline factors, there was a significant interaction for mortality between intervention group and yearly vacation time (P=0.027): shorter vacation was associated with excess 30-year mortality in the intervention (hazard ratio 1.37, 95% CI 1.03–1.83, P=0.03), but not in the control group (P=0.5). This finding was robust to multivariable adjustments.

After a multifactorial intervention for healthy men with at least one CVD risk factor, there has been an unexpectedly increased mortality in the intervention group. This increase was especially observed in a subgroup characterised by shorter vacation time at baseline. Although this adverse response to personal preventive measures in vulnerable individuals may be characteristic to men of high social status with subclinical CVD, it clearly deserves further investigation.

Despite the increased risk for cardiovascular morbidity associated with vital exhaustion (VE), the underlying pathophysiological mechanisms remain unclear. Allostatic load may constitute the missing link between VE and cardiovascular diseases. The aim of the present study was to investigate whether men with different degrees of VE would differ in terms of allostatic load, chronic stress, and social support.

The Men Stress 40 + study sample consisted of N = 121 apparently healthy men aged 40 to 75 years. The following allostatic load markers were aggregated to create a cumulative index of biological stress: salivary cortisol, salivary dehydroepiandrosterone sulfate (DHEA-S), waist-to-hip-ratio, systolic and diastolic blood pressure. Long-term cortisol and DHEA were additionally measured in hair. Chronic stress and social support were assessed via validated questionnaires. Groups of mildly, substantially, and severely exhausted men were compared using one-way ANOVAs with appropriate post-hoc tests.

Men who reported mild or severe levels of vital exhaustion had the highest scores on the cumulative index of biological stress. Hair cortisol was unrelated to vital exhaustion; hair DHEA was highest in men with substantial levels of exhaustion. Men with mild exhaustion reported the lowest levels of chronic stress, while men with severe exhaustion reported the lowest levels of social support.

Signs of allostatic load are detectable in vitally exhausted men at a stage where no major cardiovascular consequences have yet ensued.

Manual therapy initiates a cascade of neurophysiological changes in various systems including the peripheral nervous system, autonomic nervous system and the endocrine system. Of particular focus of this review was the hypothalamic-pituitary-adrenal (HPA) axis. When faced with a stressor, the HPA axis provides the frontline of defence resulting in the production of cortisol, measurement of which has been shown to be a reliable indicator of HPA axis activity. Manual therapy has been shown to influence the HPA axis. However, a functional cross-talk has been clearly demonstrated between the HPA axis and the hypothalamic-pituitary-gonadal (HPG) axis, with cortisol and testosterone inhibiting each other at all levels. This mutual inhibition may mean that multiple measures across these two systems (HPA-HPG axis) should be considered to provide an accurate representation of stress physiology. The balance between testosterone and cortisol represented as a ratio termed T/C ratio has been used for this purpose. Given the implicit role of the HPA-HPG axis in pain and inflammation and an apparent gender difference in pain perception and treatment response, T/C ratio may be of interest to osteopaths as it may enable us to capture the holistic effects of osteopathy.

This review revisits the function of the HPA axis in pain and inflammation, presents a dual hormone approach in measuring the HPA axis and evaluates the implications for osteopathic practice and research.