Harassment, stalking, threats and attacks targeting New Zealand politicians: a mental health issue

The harassment of politicians has significant psychosocial costs for both the victim and the perpetrator and represents an opportunity for mental health intervention. Abstract Objective: Due to the nature of their work, politicians are at greater risk of stalking, harassment and attack than the general population. The small, but significantly elevated risk of violence to politicians is predominantly due not to organised terrorism or politically motivated extremists but to fixated individuals with untreated serious mental disorders, usually psychosis. Our objective was to ascertain the frequency, nature and effects of unwanted harassment of politicians in New Zealand and the possible role of mental illness in this harassment. Methods: New Zealand Members of Parliament were surveyed, with an 84% response rate (n = 102). Quantitative and qualitative data were collected on Parliamentarians’ experiences of harassment and stalking. Results: Eighty-seven percent of politicians reported unwanted harassment ranging from disturbing communications to physical violence, with most experiencing harassment in multiple modalities and on multiple occasions. Cyberstalking and other forms of online harassment were common, and politicians felt they (and their families) had become more exposed as a result of the Internet. Half of MPs had been personally approached by their harassers, 48% had been directly threatened and 15% had been attacked. Some of these incidents were serious, involving weapons such as guns, Molotov cocktails and blunt instruments. One in three politicians had been targeted at their homes. Respondents believed the majority of those responsible for the harassment exhibited signs of mental illness. Conclusion: The harassment of politicians in New Zealand is common and concerning. Many of those responsible were thought to be mentally ill by their victims. This harassment has significant psychosocial costs for both the victim and the perpetrator and represents an opportunity for mental health intervention

How evidence‐based medicine is failing due to biased trials and selective publication

Evidence-based medicine (EBM) was announced in the early 1990s as a 'new paradigm' for improving patient care. Yet there is currently little evidence that EBM has achieved its aim. Since its introduction, health care costs have increased while there remains a lack of high-quality evidence suggesting EBM has resulted in substantial population-level health gains. In this paper we suggest that EBM's potential for improving patients' health care has been thwarted by bias in the choice of hypotheses tested, manipulation of study design and selective publication. Evidence for these flaws is clearest in industry-funded studies. We argue EBM's indiscriminate acceptance of industry-generated 'evidence' is akin to letting politicians count their own votes. Given that most intervention studies are industry funded, this is a serious problem for the overall evidence base. Clinical decisions based on such evidence are likely to be misinformed, with patients given less effective, harmful or more expensive treatments. More investment in independent research is urgently required. Independent bodies, informed democratically, need to set research priorities. We also propose that evidence rating schemes are formally modified so research with conflict of interest bias is explicitly downgraded in value

How evidence‐based medicine is failing due to biased trials and selective publication

Evidence-based medicine (EBM) was announced in the early 1990s as a 'new paradigm' for improving patient care. Yet there is currently little evidence that EBM has achieved its aim. Since its introduction, health care costs have increased while there remains a lack of high-quality evidence suggesting EBM has resulted in substantial population-level health gains. In this paper we suggest that EBM's potential for improving patients' health care has been thwarted by bias in the choice of hypotheses tested, manipulation of study design and selective publication. Evidence for these flaws is clearest in industry-funded studies. We argue EBM's indiscriminate acceptance of industry-generated 'evidence' is akin to letting politicians count their own votes. Given that most intervention studies are industry funded, this is a serious problem for the overall evidence base. Clinical decisions based on such evidence are likely to be misinformed, with patients given less effective, harmful or more expensive treatments. More investment in independent research is urgently required. Independent bodies, informed democratically, need to set research priorities. We also propose that evidence rating schemes are formally modified so research with conflict of interest bias is explicitly downgraded in value

Colonic transit studies to measure gastrointestinal motility in antipsychotic treated patients

This is the research protocol for an observational (cross-sectional) study investigating gastrointestinal motility in antipsychotic treated patients. Recruitment for this study will begin in 2014

Clozapine and the gastrointestinal tract

Clozapine is one of psychiatry’s most valuable medicines, improving outcomes for many people with schizophrenia whose illness has not responded adequately to other treatments. However, clozapine’s well-established advantages come at a price: a troublesome adverse-effect profile. Clozapine-induced gastrointestinal hypomotility (CIGH) is one of the most common—and serious—of these adverse effects, ranging in severity from mild constipation to fatal bowel obstruction and/or ischaemia. Mortality from these serious gastrointestinal complications is increasingly being reported in the literature. Most patients remain on clozapine for many years, sometimes compulsorily under mental health legislation. As compulsory treatment abrogates the usual patient right to self-determine the balance of risks and benefits, the prescriber has an even greater responsibility than usual to monitor and manage adverse effects. This thesis comprises a broad-ranging investigation into the epidemiology, aetiology, prevention, and treatment of CIGH. The objective is to improve the understanding, and consequently the management, of this important, but poorly understood and under-researched adverse effect

Clozapine and the gastrointestinal tract

Clozapine is one of psychiatry’s most valuable medicines, improving outcomes for many people with schizophrenia whose illness has not responded adequately to other treatments. However, clozapine’s well-established advantages come at a price: a troublesome adverse-effect profile. Clozapine-induced gastrointestinal hypomotility (CIGH) is one of the most common—and serious—of these adverse effects, ranging in severity from mild constipation to fatal bowel obstruction and/or ischaemia. Mortality from these serious gastrointestinal complications is increasingly being reported in the literature. Most patients remain on clozapine for many years, sometimes compulsorily under mental health legislation. As compulsory treatment abrogates the usual patient right to self-determine the balance of risks and benefits, the prescriber has an even greater responsibility than usual to monitor and manage adverse effects. This thesis comprises a broad-ranging investigation into the epidemiology, aetiology, prevention, and treatment of CIGH. The objective is to improve the understanding, and consequently the management, of this important, but poorly understood and under-researched adverse effect

Research Protocol: Comparing gastrointestinal motility in clozapine-treated patients before and after laxative treatment

This is the research protocol for a study considering the effectiveness of commonly used laxatives in clozapine-treated patients. We will compare gastrointestinal motility times (as measured by radiopaque marker transit tests) before and after laxative treatment in psychiatric inpatients treated receiving clozapine. Laxative treatment will be informed by the Porirua Protocol, which involves monitoring gastrointestinal function, with doses of docusate & senna adjusted in response to constipation symptoms, to a maximum of 4 tablets daily, with macrogol 3350 added when docusate & senna is inadequate

Spatiotemporal Mapping Techniques Show Clozapine Impairs Neurogenic and Myogenic Patterns of Activity in the Colon of the Rabbit in a Dose-Dependent Manner

Background: Clozapine, an antipsychotic used in treatment-resistant schizophrenia, has adverse gastrointestinal effects with significant associated morbidity and mortality. However, its effects on defined patterns of colonic contractile activity have not been assessed.Method: We used novel radial and longitudinal spatiotemporal mapping techniques, combined with and monitoring of ambient lumen pressure, in ex vivo preparations of triply and of singly haustrated portions of rabbit colon. We identified the contractile patterns of mass peristalses, fast phasic, and ripple contractions and directly qualified the effects of clozapine, at concentrations of 10 μmol/L, 20 μmol/L, and 30 μmol/L, and of norclozapine, the main metabolite of clozapine, on contractile patterns. The effects of carbachol, serotonin and naloxone on clozapine-exposed preparations were also determined. Tetradotoxin was used to distinguish neurogenic from myogenic contractions.Results: At 10 μmol/L, clozapine temporarily abolished the longitudinal contractile components of mass peristalsis, which on return were significantly reduced in number and amplitude, as was maximal mass peristaltic pressure. These effects were reversed by carbachol (1 μmol/L) and to some extent by serotonin (15 μmol/L). At 10 μmol/L, myogenic ripple contractions were not affected. At 20 μmol/L, clozapine had a similar but more marked effect on mass peristalses with both longitudinal and radial components and corresponding maximal pressure greatly reduced. At 30 μmol/L, clozapine suppressed the radial and longitudinal components of mass peristalses for over 30 min, as well as ripple contractions. Similar dose-related effects were observed on addition of clozapine to the mid colon. At 20 μmol/L, norclozapine had opposite effects to those of clozapine, causing an increase in the frequency of mass peristalsis with slight increases in basal tone. These slightly augmented contractions were abolished on addition of clozapine. Concentrations of norclozapine below 20 μmol/L had no discernible effects.Conclusion: Clozapine, but not norclozapine, has potent effects on the motility of the rabbit colon, inhibiting neurogenic contractions at lower concentrations and myogenic contractions at higher concentrations. This is the likely mechanism for the serious and life-threatening gastrointestinal complications seen in human clozapine-users. These effects appear to be mediated by cholinergic and serotonergic mechanisms. Spatiotemporal mapping is useful in directly assessing the effects of pharmaceuticals on particular patterns of gastrointestinal motility