HIN7/440: Evidence-based Consumer Health Information - The need for unbiased risk communication

Online consumer health information is rapidly growing. At the same time an active part of patients and consumers in decision making about preventive or therapeutic interventions is increasingly demanded. The basis for informed consumer choice is the communication of evidence-based scientific data in a format that is clearly understood by most lay persons. The way study results are presented influence decisions by health care providers and patients or consumers alike. The impact of framing of outcome data as either relative or absolute differences is well recognized. Outcome data should be reported as absolute numbers, absolute risk reductions or numbers needed to treat or to screen rather than as relative risk reductions. Beyond the question of whether relative or absolute differences are used, outcome data can be framed by either emphasising achievable benefits or the lack of such benefits. Presentation of data as the proportion of patients who remain free of a target outcome rather than the proportion of patients who benefit from a certain intervention could substantially influence decision making. So far, studies evaluating the communication of treatment results to patients were focussed on the benefits of the respective interventions. Such an approach is incompatible with unbiased informed decision making by the patient, client or consumer. In order to communicate outcome data in an objective manner the whole possible spectrum of data presentation should be considered. Both, the proportion of persons who are likely to benefit as well as the proportion of persons who are unlikely to benefit or likely to be harmed should be presented with equal emphasis. Instruments to judge the quality of printed or online consumer health information do not include rating the framing of outcome data (e.g. http:/www.discern.org.uk).In order to establish an online system of evidence-based consumer health information that provides unbiased evidence-based communication of outcome data mammography screening was used as a model. After screening the literature according to evidence-based medicine criteria the information on benefits and risks of mammography screening has been compiled. Results are communicated as simple self explaining illustrations as well as original numbers equally emphasising the various aspects of the outcome. In addition, unbiased information is provided on the test efficacy of mammography screening (false positive, false negative results), on other potential side effects or other beneficial effects of mammography screening such as the number of diagnostic surgical interventions following mammography or the psychological sequaele thereof, data on total mortality and precision or lack of precision of results. The described mammography screening consumer information system is being evaluated with experts and the target consumer population with the final goal of an online evidence-based consumer health informatio

Barriers to Health Information and Building Solutions

Most stakeholders in the health care system-doctors, patients, and policy makers-have not been taught to apply evidence-based information to the many decisions that must be made daily. Little awareness of this problem exists, yet a better use of evidence could improve outcomes for patients, increase patient satisfaction, and lower costs. This chapter considers how the use of information that emerges from evidence-based medicine could be improved. "Health literacy" constitutes the first step. After a discussion of the barriers that exist to health literacy (e. g., lack of incentive to search for health information, non-standardized reporting of health results, and poor comprehension), possible remedies are presented. Raising health literacy by targeting individual stakeholder groups, such as patients and health care professionals, is debated as is the option of focusing on change in the overall health system. What is required to achieve a change both at the individual and system levels? Solutions are unlikely to generate systemic changes in center-based treatment variations. However, a change at one level may set off change in another. Finally, increasing awareness beyond the immediate professional community is necessary if systemic changes are to be made. The promotion of health literacy requires careful consideration to reach the various stakeholders throughout the health care system

Amyloid-β Protein Oligomer at Low Nanomolar Concentrations Activates Microglia and Induces Microglial Neurotoxicity*

Neuroinflammation and associated neuronal dysfunction mediated by activated microglia play an important role in the pathogenesis of Alzheimer disease (AD). Microglia are activated by aggregated forms of amyloid-β protein (Aβ), usually demonstrated in vitro by stimulating microglia with micromolar concentrations of fibrillar Aβ, a major component of amyloid plaques in AD brains. Here we report that amyloid-β oligomer (AβO), at 5–50 nm, induces a unique pattern of microglia activation that requires the activity of the scavenger receptor A and the Ca2+-activated potassium channel KCa3.1. AβO treatment induced an activated morphological and biochemical profile of microglia, including activation of p38 MAPK and nuclear factor κB. Interestingly, although increasing nitric oxide (NO) production, AβO did not increase several proinflammatory mediators commonly induced by lipopolyliposacharides or fibrillar Aβ, suggesting that AβO stimulates both common and divergent pathways of microglia activation. AβO at low nanomolar concentrations, although not neurotoxic, induced indirect, microglia-mediated damage to neurons in dissociated cultures and in organotypic hippocampal slices. The indirect neurotoxicity was prevented by (i) doxycycline, an inhibitor of microglia activation; (ii) TRAM-34, a selective KCa3.1 blocker; and (iii) two inhibitors of inducible NO synthase, indicating that KCa3.1 activity and excessive NO release are required for AβO-induced microglial neurotoxicity. Our results suggest that AβO, generally considered a neurotoxin, may more potently cause neuronal damage indirectly by activating microglia in AD