Low-grade systemic inflammation and the workplace.

BACKGROUND: Psychosocial and physical stressors can elicit the stress response, co-ordinated by interactions between neuroendocrine and inflammatory processes. The central role of the immune system, specifically low-grade systemic inflammation, is sometimes overlooked in work-related stress research. OBJECTIVE: To review evidence that work-related psychosocial and physical stressors can stimulate a low-grade systemic inflammation which, through interactions with the neurohormonal systems, may impact on the well-being and productivity of workers. METHODS: Literature searches were performed by databases and by hand. Databases used included Interface - EBSCOhost Research Databases; PsycINFO; Academic Search Complete; Africa-Wide Information; CINAHL; E-Journals; MEDLINE and PsycARTICLES. RESULTS: Psychosocial stressors, infections, poor indoor air quality, musculoskeletal injuries and chemicals can stimulate a low-grade systemic inflammation that may adversely affect workers' mental and physical health, as well as productivity. The psychological and physical effects caused by infection-induced inflammation are generally referred to as sickness behaviour and those caused by poor indoor air quality as sick building syndrome. CONCLUSIONS: Stressor-induced low-grade systemic inflammation can be a causal factor in the physical and behavioural symptoms of work-related stress. It is therefore important that those involved with the health of workers be cognisant of inappropriate or chronic low-grade inflammation as a potential health hazard.

Stimulants and growth in children with attention-deficit/hyperactivity disorder.

Initial suggestions that suppression of growth may be an intrinsic characteristic of attention-deficit/hyperactivity disorder (ADHD) have now largely been disproven. Although controversy persists regarding the possible negative effect of adrenergic stimulants on growth in children with ADHD, the consensus that appears to be reached in the scientific literature is that stimulant usage may cause a manageable attenuation of growth in these children. Since it is known that stimulants increase the amount of dopamine and noradrenaline in the synapse, this writing suggests that these increases in dopamine and noradrenaline are responsible for the growth attenuation in these children. It appears that increased amounts of dopamine and noradrenaline have the ability to inhibit the secretion of growth hormone and growth-related hormones such as prolactin, thyroid hormones, sex hormones and insulin. Therefore, it would be reasonable to suggest that the increases in dopamine and noradrenaline caused by stimulant usage can disrupt the homeostasis of both growth hormone and growth-related hormones, generating the potential for the suppression of growth.

Autonomic correlates at rest and during evoked attention in children with attention-deficit/hyperactivity disorder and effects of methylphenidate.

OBJECTIVE: The aim of this study was to assess autonomic nervous system functioning in children with attention-deficit/hyperactivity disorder (ADHD) and to examine the effects of methylphenidate and focussed attention. METHOD: Children with ADHD (n = 19) were tested while they were stimulant free and during a period in which they were on stimulants. On both occasions, autonomic nervous system functioning was tested at baseline and during focussed attention. Autonomic nervous system functioning of control subjects was also tested at baseline and during focussed attention. Autonomic nervous system activity was determined by means of heart rate variability (HRV) and skin conductivity analyses. Attention was evoked by means of the BioGraph Infiniti biofeedback apparatus. HRV was determined by time domain, frequency domain and Poincaré analysis of RR interval data. Skin conductivity was determined by the BioGraph Infiniti biofeedback apparatus. RESULTS: The main findings of this study were (a) that stimulant-free children with ADHD showed a sympathetic underarousal and parasympathetic overarousal of the sympathovagal balance relative to control subjects; (b) methylphenidate shifted the autonomic balance of children with ADHD towards normal levels; however, a normal autonomic balance was not reached, and (c) stimulant-free children with ADHD exhibited a shift in the sympathovagal balance towards the sympathetic nervous system from baseline to focussed attention; however, methylphenidate appeared to abolish this shift. CONCLUSIONS: Stimulant-free children with ADHD have a parasympathetic dominance of the autonomic balance, relative to control subjects. Methylphenidate attempts to restore the normal autonomic balance in children with ADHD, but inhibits the normal autonomic nervous system response to a cognitive challenge. CLINICAL APPLICATIONS: These results indicate that methylphenidate may have a suppressive effect on the normal stress response. Although this may be of benefit to those who interact with children who suffer from ADHD, the implications for the physiological and psychological well-being of the children themselves are debatable. Further research is needed. LIMITATIONS OF THE STUDY: Only 19 children with ADHD and 18 control subjects were tested. Further studies should include prior testing in order to exclude children with possible co-existing learning disabilities. Cognitive function and emotional responses of children with ADHD were not tested.

The effect of sympathomimetic medication on cardiovascular functioning of children with attention-deficit/hyperactivity disorder.

OBJECTIVE: The aim of this study was to investigate the effects of sympathomimetic medication on the cardiovascular system of children with attention-deficit/hyperactivity disorder (ADHD). METHODS: Cardiovascular functioning of children with ADHD (n = 19) was tested while the children were stimulant free and during a period in which they were on stimulant medication. Electrocardiograms (ECGs) were obtained by means of a Schiller CardioLaptop AT-110 ECG recorder using the standard 12-lead cable positioning for a resting ECG. Blood pressure was measured by means of a stethoscope and mercury sphygmomanometer. RESULTS: The main findings of this study were that methylphenidate usage is associated with increases in heart rate (HR) and blood pressure (BP), and that it does not adversely affect HR-corrected QT and JT intervals or cardiac dispersion values. CONCLUSION: Methylphenidate causes an increase in HR as well as increases in both systolic and diastolic BP, but no change in cardiac depolarisation and repolarisation duration or homogeneity.