Background/Objectives: Cognitive impairment in alcohol use disorder (AUD) may reflect alcohol exposure, withdrawal, nutritional disruption, systemic illness, and social vulnerability. We evaluated prioritized human-adult evidence linking nutritional exposures with objective cognition and examined separately whether AUD severity modifies nutrition–cognition associations and whether nutritional disruption mediates the relationship between alcohol exposure and cognitive outcomes. Methods: This structured narrative review used documented multi-database retrieval, pre-access prioritization, full-text adjudication, evidence appraisal, and qualitative sensitivity scenarios. A targeted vitamin B12 update supplemented the baseline corpus. Results: Thiamine had the broadest and most clinically actionable evidence, but biomarker thresholds, optimal cognitive dosing, and independent treatment effects remained uncertain. Evidence for folate, vitamin B12, niacin outside pellagra, other micronutrients, diet, body mass index, and albumin was sparse, mixed, or nonspecific. The targeted B12 evidence was null or contradictory rather than supportive. Cognitive improvement during detoxification could not be separated from abstinence and bundled care. No included study verified causal mediation by nutrition or a formal nutrition-by-severity interaction. Conclusions: Nutritional assessment and prompt treatment of recognized deficiency remain clinically important, but the prioritized retrieved corpus does not justify nutrient-specific causal claims for typical AUD-related cognitive impairment. Longitudinal studies should align repeated nutrition, alcohol exposure, cognition, and function and prespecify interaction and mediation tests.
Background/Objectives: Coffee consumption and snacking are common dietary behaviours linked to cardiometabolic risk, and variants in BDNF and TCF7L2 have been associated with obesity and type 2 diabetes (T2DM). We examined whether glycaemic, adiposity, and lipid traits reflect these behaviours, these genotypes, or both, and whether BDNF (rs10501087) and TCF7L2 (rs4506565, rs7901695, rs7903146) genotypes modify the behavioural associations. Methods: In a cross-sectional study of Polish adults (NCT03792685; analytic cohort n = 1227), coffee consumption (never, weekly, daily) and snacking frequency (rare, frequent) were assessed by questionnaire (n = 905); outcomes were glucose and insulin area under the curve (AUC) from a 2-h 75 g oral glucose tolerance test (OGTT), glycated haemoglobin (HbA1c), fasting lipids, and bioimpedance body composition. Multivariable models were adjusted for age, sex, daily energy intake, and physical inactivity; all analyses, including gene × behaviour interaction tests, were exploratory, with false discovery rate (FDR) correction for multiple testing. Results: Daily coffee consumption was associated with a higher glucose AUC than never consumption (β = +0.045, 95% confidence interval [CI] 0.018–0.073; p = 0.001; FDR q = 0.094), with higher post-load glucose and insulin but similar fasting glucose and HbA1c; the association was robust in sensitivity analyses. Weekly coffee consumption was associated with higher high-density lipoprotein cholesterol (β = +4.75 mg/dL, 95% CI 1.49–8.02; p = 0.004; FDR q = 0.10). Frequent snacking was associated with higher body mass index, fat mass, and body fat percentage (nominal p = 0.034–0.049; FDR q = 0.26) and was not associated with coffee consumption. BDNF rs10501087 CT was nominally associated with lower T2DM odds than TT (odds ratio [OR] = 0.42, 95% CI 0.21–0.78; p = 0.009). The behavioural associations showed no detectable modification by genotype (184 interaction tests; none with FDR q < 0.05). Conclusions: Everyday dietary behaviour, particularly daily coffee consumption, was more consistently related to cardiometabolic traits than BDNF or TCF7L2 genotypes. The post-load glycaemic profile of daily coffee consumers, missed by fasting glucose and HbA1c, highlights the value of OGTT-based phenotyping in nutritional research. These exploratory findings do not support genotype-tailored advice on coffee or snacking.
Background/Objectives: Adherence to a Mediterranean diet (MedDiet) has been shown to improve women’s reproductive health. However, there is a lack of evidence on the potential efficacy in attenuating the intensity of global symptoms related to endometriosis. This was a cross-sectional analysis investigating the association between MedDiet (and associated lifestyle) adherence and intensity of global endometriosis symptoms in Australian women. Methods: Adherence to a MedDiet (and associated lifestyle) was assessed using the Mediterranean Diet Adherence Screener (MEDAS) and MEDiterranean LIFEstyle Index (MEDLIFE), and the impact of endometriosis symptoms was assessed using the Endometriosis Impact Questionnaire (EIQ-63). Results: A total of n = 103 participants (29.7 ± 8.6 years; BMI: 27.1 ± 6.8 kg/m2) were included in the final analyses. Participants reported moderate MEDLIFE adherence scores (12.1 ± 3.2) and low-to-moderate adherence to a MedDiet (5.6 ± 2.0). Few participants achieved normative serve size criteria for core dietary constituents of a MedDiet, including legumes (n = 14, 16.7%), fruit (n = 11, 13.1%), fish and seafood (n = 9, 10.7%), nuts (n = 15, 17.9%) and olive oil (n = 2, 2.4%). MEDLIFE index or MEDAS adherence were not associated with global impact symptoms of endometriosis. Conclusions: Despite the null findings, these results provide an important contribution to the existing literature, highlighting the importance of diet quality on women’s health more broadly. Exploration of these findings using well-controlled longitudinal analyses and robust clinical trials is needed to discover causal relationships.
Intellectual disability (ID) is frequently accompanied by a range of neuropsychiatric and neurological comorbidities, including anxiety, depression, autism spectrum disorder (ASD), attention-deficit/hyperactivity disorder (ADHD), sleep disturbances, and epilepsy. Conventional pharmacological treatments often provide partial relief and may be associated with adverse effects, prompting interest in adjunctive strategies such as phytotherapy. This review examines the current evidence on selected plant-derived compounds—particularly Crocus sativus (saffron), Bacopa monnieri, Curcuma longa (curcumin), and other botanicals—in the management of disorders associated with ID. Mechanistic pathways, clinical evidence, and safety considerations are critically discussed. Although some phytotherapeutic interventions have shown preliminary evidence of potential benefit and may modulate pathways involving neuroinflammation, oxidative stress, and neurotransmitter function, direct clinical evidence in individuals with ID remains limited. Further well-designed randomized controlled trials, particularly in ID-specific populations, are needed to establish efficacy, safety, optimal dosing, and clinical applicability.
Nutrition during early life may be an important determinant of long-term health. Preterm birth, affecting approximately 10% of deliveries worldwide, and intrauterine growth restriction (IUGR) are major perinatal conditions. The Developmental Origins of Health and Disease (DOHaD) hypothesis proposes that early nutritional and environmental exposures shape adult disease risk. This narrative review synthesizes epidemiological, cohort, animal, and interventional evidence on early nutrition and long-term outcomes in these infants. Rapid weight gain has been associated with later obesity and cardio-metabolic risk; however, this does not show that the tempo of gain, rather than attained size, carries the risk, and catch-up growth after preterm birth or growth restriction supports neurodevelopment. Preterm birth has been associated with a 53% higher risk of ischemic heart disease, whereas IUGR confers overlapping but distinct risks. Hypothesized mechanisms include epigenetic modification, structural organ deficits, hormonal reprogramming, gut-microbiome dysbiosis, and oxidative stress. Because the human evidence is almost entirely observational and vulnerable to confounding and to over-adjustment for attained body size, these associations should be read as hypotheses rather than established causal effects. Individualized, guideline-based and responsive feeding strategies, with support for mothers to provide their own milk, are needed to optimize immediate outcomes while limiting lifelong disease susceptibility.
