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1.
BMJ ; 384: e077310, 2024 02 28.
Article in English | MEDLINE | ID: mdl-38418082

ABSTRACT

OBJECTIVE: To evaluate the existing meta-analytic evidence of associations between exposure to ultra-processed foods, as defined by the Nova food classification system, and adverse health outcomes. DESIGN: Systematic umbrella review of existing meta-analyses. DATA SOURCES: MEDLINE, PsycINFO, Embase, and the Cochrane Database of Systematic Reviews, as well as manual searches of reference lists from 2009 to June 2023. ELIGIBILITY CRITERIA FOR SELECTING STUDIES: Systematic reviews and meta-analyses of cohort, case-control, and/or cross sectional study designs. To evaluate the credibility of evidence, pre-specified evidence classification criteria were applied, graded as convincing ("class I"), highly suggestive ("class II"), suggestive ("class III"), weak ("class IV"), or no evidence ("class V"). The quality of evidence was assessed using the GRADE (Grading of Recommendations, Assessment, Development, and Evaluations) framework, categorised as "high," "moderate," "low," or "very low" quality. RESULTS: The search identified 45 unique pooled analyses, including 13 dose-response associations and 32 non-dose-response associations (n=9 888 373). Overall, direct associations were found between exposure to ultra-processed foods and 32 (71%) health parameters spanning mortality, cancer, and mental, respiratory, cardiovascular, gastrointestinal, and metabolic health outcomes. Based on the pre-specified evidence classification criteria, convincing evidence (class I) supported direct associations between greater ultra-processed food exposure and higher risks of incident cardiovascular disease related mortality (risk ratio 1.50, 95% confidence interval 1.37 to 1.63; GRADE=very low) and type 2 diabetes (dose-response risk ratio 1.12, 1.11 to 1.13; moderate), as well as higher risks of prevalent anxiety outcomes (odds ratio 1.48, 1.37 to 1.59; low) and combined common mental disorder outcomes (odds ratio 1.53, 1.43 to 1.63; low). Highly suggestive (class II) evidence indicated that greater exposure to ultra-processed foods was directly associated with higher risks of incident all cause mortality (risk ratio 1.21, 1.15 to 1.27; low), heart disease related mortality (hazard ratio 1.66, 1.51 to 1.84; low), type 2 diabetes (odds ratio 1.40, 1.23 to 1.59; very low), and depressive outcomes (hazard ratio 1.22, 1.16 to 1.28; low), together with higher risks of prevalent adverse sleep related outcomes (odds ratio 1.41, 1.24 to 1.61; low), wheezing (risk ratio 1.40, 1.27 to 1.55; low), and obesity (odds ratio 1.55, 1.36 to 1.77; low). Of the remaining 34 pooled analyses, 21 were graded as suggestive or weak strength (class III-IV) and 13 were graded as no evidence (class V). Overall, using the GRADE framework, 22 pooled analyses were rated as low quality, with 19 rated as very low quality and four rated as moderate quality. CONCLUSIONS: Greater exposure to ultra-processed food was associated with a higher risk of adverse health outcomes, especially cardiometabolic, common mental disorder, and mortality outcomes. These findings provide a rationale to develop and evaluate the effectiveness of using population based and public health measures to target and reduce dietary exposure to ultra-processed foods for improved human health. They also inform and provide support for urgent mechanistic research. SYSTEMATIC REVIEW REGISTRATION: PROSPERO CRD42023412732.


Subject(s)
Cardiovascular Diseases , Diabetes Mellitus, Type 2 , Humans , Food, Processed , Cross-Sectional Studies , Systematic Reviews as Topic , Cardiovascular Diseases/epidemiology , Cardiovascular Diseases/etiology
2.
Neurobiol Learn Mem ; 193: 107656, 2022 09.
Article in English | MEDLINE | ID: mdl-35792324

ABSTRACT

An increase in the age of surgical patients as well as the volume of surgeries is associated with a rise in perioperative neurocognitive disorders. These disorders encompass acute delirium and longer-term cognitive dysfunctions. Brain derived neurotrophic factor (BDNF) is a neurotrophin that plays a dynamic role in a series of neurological functions including neuroplasticity, neurogenesis and synaptic regulation. Given the possible alterations to brain physiology in response to surgery, this review aims to explore the relationship between changes in central and peripheral BDNF concentrations and perioperative neurocognitive disorders. Higher levels of Brain tissue and blood BDNF have been associated with better cognitive function; however, the nature of the association between BDNF and delirium is uncertain. Preclinical models point to a significant depletion in BDNF expression and signalling within the brain post-operatively, while preliminary human studies demonstrate depletions in serum BDNF concentration after surgery. These findings suggest that the reduced BDNF concentrations may be associated with post-operative cognitive dysfunction. Thus, understanding the BDNF expression/signalling pathways may present a promising avenue for managing perioperative neurocognitive disorders symptoms. Nonetheless, given that results were primarily derived from preclinical models, it is critical for these findings to be validated in humans to confirm the relevance of this promising target.


Subject(s)
Cognitive Dysfunction , Delirium , Brain-Derived Neurotrophic Factor/metabolism , Cognition/physiology , Cognitive Dysfunction/etiology , Humans , Neuronal Plasticity
3.
Cognition ; 222: 105012, 2022 05.
Article in English | MEDLINE | ID: mdl-34998243

ABSTRACT

The brain-time account posits that the physical timing of sensory-evoked neural activity determines the perceived timing of corresponding sensory events. A canonical model formalises this account for tasks such as simultaneity and order judgements: Signals arrive at a decision centre in an order, and at a temporal offset, shaped by neural propagation times. This model assumes that the noise affecting people's temporal judgements is primarily neural-latency noise, i.e. variation in propagation times across trials, but this assumption has received little scrutiny. Here, we recorded EEG alongside simultaneity judgements from 50 participants in response to combinations of visual, auditory and tactile stimuli. Bootstrapping of ERP components was used to estimate neural-latency noise, and simultaneity judgements were modelled to estimate the precision of timing judgements. We obtained the predicted correlation between neural and behavioural measures of latency noise, supporting a fundamental feature of the canonical model of perceived timing.


Subject(s)
Auditory Perception , Visual Perception , Acoustic Stimulation , Auditory Perception/physiology , Humans , Judgment/physiology , Touch , Visual Perception/physiology
4.
Adv Nutr ; 12(5): 1681-1690, 2021 10 01.
Article in English | MEDLINE | ID: mdl-33873204

ABSTRACT

Numerous observational studies have investigated the role of the Dietary Inflammatory Index (DII®) in chronic disease risk. The aims of this umbrella review and integrated meta-analyses were to systematically synthesize the observational evidence reporting on the associations between the DII and health outcomes based on meta-analyses, and to assess the quality and strength of the evidence for each associated outcome. This umbrella review with integrated meta-analyses investigated the association between the DII and a range of health outcomes based on meta-analyses of observational data. A credibility assessment was conducted for each outcome using the following criteria: statistical heterogeneity, 95% prediction intervals, evidence for small-study effect and/or excess significance bias, as well as effect sizes and P values using calculated random effects meta-analyses. In total, 15 meta-analyses reporting on 38 chronic disease-related outcomes were included, incorporating a total population of 4,360,111 subjects. Outcomes (n = 38) were examined through various study designs including case-control (n = 8), cross-sectional (n = 5), prospective (n = 5), and combination (n = 20) study designs. Adherence to a pro-inflammatory dietary pattern had a significant positive association with 27 (71%) of the included health outcomes (P value < 0.05). Using the credibility assessment, Class I (Convincing) evidence was identified for myocardial infarction only, Class II (Highly suggestive) evidence was identified for increased risk of all-cause mortality, overall risk of incident cancer, and risk of incident site-specific cancers (colorectal, pancreatic, respiratory, and oral cancers) with increasing (more pro-inflammatory) DII score. Most outcomes (n = 31) presented Class III (Suggestive) or lower evidence (Weak or No association). Pro-inflammatory dietary patterns were nominally associated with an increased risk of many chronic disease outcomes. However, the strength of evidence for most outcomes was limited. Further prospective studies are required to improve the precision of the effect size.


Subject(s)
Diet , Neoplasms , Humans , Meta-Analysis as Topic , Observational Studies as Topic
5.
Mol Psychiatry ; 26(1): 134-150, 2021 01.
Article in English | MEDLINE | ID: mdl-33144709

ABSTRACT

The field of nutritional psychiatry has generated observational and efficacy data supporting a role for healthy dietary patterns in depression onset and symptom management. To guide future clinical trials and targeted dietary therapies, this review provides an overview of what is currently known regarding underlying mechanisms of action by which diet may influence mental and brain health. The mechanisms of action associating diet with health outcomes are complex, multifaceted, interacting, and not restricted to any one biological pathway. Numerous pathways were identified through which diet could plausibly affect mental health. These include modulation of pathways involved in inflammation, oxidative stress, epigenetics, mitochondrial dysfunction, the gut microbiota, tryptophan-kynurenine metabolism, the HPA axis, neurogenesis and BDNF, epigenetics, and obesity. However, the nascent nature of the nutritional psychiatry field to date means that the existing literature identified in this review is largely comprised of preclinical animal studies. To fully identify and elucidate complex mechanisms of action, intervention studies that assess markers related to these pathways within clinically diagnosed human populations are needed.


Subject(s)
Depression/metabolism , Depression/physiopathology , Diet/psychology , Animals , Depression/genetics , Epigenesis, Genetic , Gastrointestinal Microbiome , Humans , Inflammation , Oxidative Stress
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