Open-label placebos (OLPs) are placebos without deception in the sense that patients know that they are receiving a placebo. The objective of our study is to systematically review and analyze the effect of OLPs in comparison to no treatment in clinical trials. A systematic literature search was carried out in February 2020. Randomized controlled trials of any medical condition or mental disorder comparing OLPs to no treatment were included. Data extraction and risk of bias rating were independently assessed. 1246 records were screened and thirteen studies were included into the systematic review. Eleven trials were eligible for meta-analysis. These trials assessed effects of OLPs on back pain, cancer-related fatigue, attention deficit hyperactivity disorder, allergic rhinitis, major depression, irritable bowel syndrome and menopausal hot flushes. Risk of bias was moderate among all studies. We found a significant overall effect (standardized mean difference = 0.72, 95% Cl 0.39–1.05, p < 0.0001, I2 = 76%) of OLP. Thus, OLPs appear to be a promising treatment in different conditions but the respective research is in its infancy. More research is needed, especially with respect to different medical and mental disorders and instructions accompanying the OLP administration as well as the role of expectations and mindsets.
Increased intake of vegetables is associated with a lower risk of dementia and slower rates of cognitive decline in older age. Yet, evidence that this association is also valid for high fruit consumption is lacking.
Preventing Alzheimer's disease (AD) would require knowledge about its etiology to a degree of detail not yet available. The major hurdle in understanding the disease lies in teasing out the various causes and their complex interactions. Since considerable data have accrued showing that the essential trace element selenium (Se) might play different roles in the progression of AD, we conducted a systematic review of the literature regarding Se and AD. We identified 9 placebo-controlled studies (6 were multiple supplement trials including Se, 1 was ongoing), 4 prospective, 4 cross-sectional, 15 case control, 24 autopsy studies, as well studies in animals and cells. There is an absence of consistent clinical evidence as to whether supplementation of Se is beneficial in the treatment of AD and how Se levels are altered in brain, cerebrospinal fluid, and blood of patients with AD. Some longitudinal and cross-sectional studies, however, show an association of Se status and cognitive function. Findings from molecular biology reveal a decisive role of Se in the pathogenesis of AD. In summary, the current state of knowledge provides no evidence for a role of Se in the treatment of AD, but allows speculation on a potential preventive relevance. Large trials of long-term duration could provide definitive answers.
Objective: Obesity is a risk factor of dementia. Current forecasts of dementia prevalence fail to take the rising obesity prevalence into account. Design and Methods: Embase and Medline were searched for observational studies on the association between overweight (BMI 25-30 kg/m 2 ) or obesity (BMI > 30 kg/m 2 ) and dementia and pooled the effect sizes by meta-analysis. The population attributable risk (PAR) was calculated for different time points and adjusted them for confounders. Based on current prevalence rates of dementia and demographic forecasts, patient numbers were calculated and adjusted by the growth rates of PAR. . If obesity is included into forecast models, the prevalence of dementia is estimated to be 7.1 million (6.9, 7.3) and 11.3 million (10.9, 11.7) for the United States in 2030 and 2050, respectively. In China, the estimate is 13.1 million (12.8, 13.3) in 2030 and 26.2 million (25.1, 27.4) in 2050. These figures are 9% and 19% higher for the United States and China, respectively, than forecasts that rely solely on the demographic change. Conclusion: The past and ongoing increase in midlife obesity prevalence will contribute significantly to the future prevalence of dementia and public health measures to reduce midlife obesity are simultaneously primary prevention measures to reduce the risk of dementia.Obesity (2013) 21, E51-E55.
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