Background: Coinfection with active tuberculosis (TB) is one of the leading causes of death in people living with HIV (PLWH) in Africa. This investigation explores the role of micronutrient supplementation in preventing active TB in PLWH.
Methods: A randomized trial of nutritional supplementation was conducted among antiretroviral- naïve (without previous antiretroviral treatment [ART]) HIV-infected people in Botswana between 2004 and 2009. The study had a factorial design with four arms: the selenium (Se) alone arm, the multivitamins (MVT) alone arm that contained vitamin B complex and vitamins C and E, the combined Se+MVT group and the placebo group. Those participants with prior or current active TB were excluded, as were participants with advanced HIV disease (CD4 <250 cells/μL) or who had already qualified for ART. HIV-positive adults (N=878) were followed monthly for study pill dispensation, every 3 months for CD4 cell count and every 6 months for viral load during 24 months or until they were started on ART.
Results: The participants' characteristics were not significantly different among the four groups at baseline. Supplementation with Se alone (hazard ratio =0.20, 95% confidence interval: 0.04, 0.95, P=0.043) and the two combined SE groups (Se and Se+MVT) had significantly lower risk of developing incident TB disease compared with placebo in multivariate adjusted models (hazard ratio=0.32, 95% confidence interval: 0.11, 0.93, P=0.036). Multivitamins alone did not affect the incidence of TB. Isoniazid preventive therapy was received by 12.2% of participants, a rate that was not significantly different among the four study arms (P=0.122) and the newly diagnosed cases.
Conclusion: Se supplementation, alone and with MVT, decreased the incidence of TB disease in PLWH who were ART-naïve. Supplementation with these micronutrients should be considered in HIV infection, prior to ART, in areas where TB and malnutrition are endemic.
The gut microbiome performs many crucial functions for the human host, but the molecular mechanisms by which host, microbe and diet interact to mediate health and disease are only starting to be revealed. Here we review the literature on how changes in the diet affect the microbiome. A number of studies have shown that within a geographic region, different diets (such as vegan vs. omnivore) are associated with differences in a modest number of taxa but do not reliably produce radical differences within the gut microbial community. In contrast, studies that look across continents consistently find profoundly different microbial communities between Westernized and traditional populations, although it remains unclear to what extent diet or other differences in lifestyle drive these distinct microbial community structures. Furthermore, studies that place subjects on controlled short term experimental diets have found the resulting alterations to the gut microbial community to generally be small in scope, with changes that do not overcome initial individual differences in microbial community structure. These results emphasize that the human gut microbial community is relatively stable over time. In contrast, short term changes in diet can cause large changes in metabolite profiles, including metabolites processed by the gut microbial community. These results suggest that commensal gut microbes have a great deal of genetic plasticity and can activate different metabolic pathways independent of changes to microbial community composition. Thus, future studies of the how diet impacts host health via the microbiome may wish to focus on functional assays such as transcriptomics and metabolomics, in addition to 16S rRNA and whole-genome metagenome shotgun analyses of DNA. Taken together, the literature is most consistent with a model in which the composition of the adult gut microbial community undergoes modest compositional changes in response to altered diet but can nonetheless respond very rapidly to dietary changes via up- or down-regulation of metabolic pathways that can have profound and immediate consequences for host health.
Background: The gluten free, casein free (GFCF) diet is heralded by strong anecdotal parental reports to greatly improve and even "cure" symptoms of Autism Spectrum Disorders (ASD). Yet to date, little conclusive empirical evidence exists supporting its use.
Objective: The purpose of this paper is to provide an overview of the state of the recent evidence regarding use of GFCF diet for treatment of individuals with ASD.
Methods: Five database providers (PubMed, Web of Knowledge, EBSCO, ProQuest, and WorldCat) were used to search 19 databases yielding a total of 491 articles that were published through February 2015. Peer reviewed articles published between 2005 and February 2015 were included for review if study participants were identified as having ASD and investigated the effects of the GFCF diet on ASD behaviors or the relationship between the diet and these behaviors.
Results: Evaluation of search results yielded 11 reviews, 7 group experimental studies including 5 randomized controlled trials, 5 case reports, and 4 group observational studies published during the last 10 years. These studies represent a marked increase in number of reported studies as well as increased scientific rigor in investigation of GFCF diets in ASD.
Conclusions: While strong empirical support for the GFCF diet in ASD is currently lacking, studies point to the need for identifying subsets of individuals (e.g., those with documented gastrointestinal abnormalities) who may be the best responders to the GFCF diet. Identifying these subsets is critically needed to enhance rigor in this research area. Until rigorous research supporting use of GFCF diet is reported, clinicians should continue use caution and consider several factors when advising regarding implementation of the GFCF diet for individuals with ASD.
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