{'fraction_non_alphanumeric': 0.044072948328267476, 'fraction_numerical': 0.03252279635258359, 'mean_word_length': 5.377906976744186, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Does dehydroepiandrosterone decrease the risk or progression of Alzheimer's dementia?

A2009 systematic review included five trials (n5560) that assessed the effects of dehydroepiandrosterone (DHEA) supplementation on cognitive function in adults older than age 50 yearswithout dementia. The studymost relevant to the question included in the review was a 2008 randomized controlled trial (RCT) trial of 225 healthy individuals (51% women, age range 55–85 years), who were nonsmokers, had not previously taken hormone therapy, and were not selected based on DHEA levels. Treatment consisted of 50 mg daily oral DHEA supplementation, with a placebo control group. Function and quality of life were assessed at baseline, 3, 6, and 12 months using standardized scales including the Beck’s Depression Index, Medical Outcomes Study 36-item Short Form Survey, Life Satisfaction Index-Z, Satisfaction With Life Scale, Female Sexual Function Index (women), and International Index of Erectile Function (men). Circulating levels of DHEA were alsomeasured.During the study, circulatingDHEA levels of the treatment group significantly increased, with levels two to four times higher as compared to those of the baseline. However, no statistically significant changes in cognitive function measures were detected between groups. A 2003 pilot RCT (n558) examinedDHEA supplementation (50 mg twice daily) versus placebo in individuals meeting the clinical criteria of the National Institutes of Neurological and Communicative Disorders and Stroke (NIH) for Alzheimer’s dementia. Nineteen treated and 14 control patients completed the trial; dropouts from the trial were due to adverse events (n56), poor compliance (n52), withdrawal of consent (n59), development of exclusion criteria (n53), loss to follow-up (n52), and “other” reasons (n53). There was no significant effect of supplementation on the primary reported endpoint of changes in scores measured by the Alzheimer’s disease Assessment Scale-Cognitive and Clinicians Interview-Based Impression of Change with Caregiver Input instruments at 6 months. By contrast, a 2010 nonrandomized clinical trial in Japan enrolled 27 women (age 65–90 years with mild-tomoderate cognitive impairment (Mini-Mental Status Examination [MMSE] score range 10–28) to study the effects of DHEA supplement on cognitive function and activities of daily living. Twelve received DHEA 25 mg daily for 6 months; 15 in the control group not receiving DHEA were matched with the treatment group based on age and cognitive function. Change in cognitive functionwasmeasured by the MMSE, the Hasegawa Dementia Scale-Revised (HDS-R), and the Barthel Index (BI) administered at baseline, 3, and 6 months. After 6 months, in the treatment group, DHEA and DHEA-S levels were increased 2-fold to 3-fold as compared to those at baseline. At 6 months, the treatment group showed improved cognitive scores versus the control group by comparing the differences between the scores at baseline and those at 6months (MMSE [total possible score 30], +0.6 vs –2.1,P,.05; HDS-R [total possible score 30], +2.8 vs –0.3, P,.05; BI [total possible score 100], +3.7 vs –2.7,P5.05).Weaknesses of the study included small sample size, nonrandomization, andunclear clinical relevance of the findings.