The regulation of neurogenesis, the complex process of producing and differentiating new brain tissue cells, is influenced by a complex interaction of internal and external factors. Over the past decade, extensive research has been conducted on neurotrophins and their key role in adult neurogenesis, as well as their impact on diseases such as depression. Among neurotrophins, the brain-derived neurotrophic factor (BDNF) has been the subject of comprehensive studies on adult neurogenesis, and scientific evidence supports its necessity for neurogenesis in the subventricular zone of the hippocampus. A novel area of research is the emerging role of gut microbiota as a significant contributor to neurogenesis and neurotrophin production. Studies have shown that reduced BDNF levels can lead to mood disorders, which are observed in intestinal dysbiosis, characterized by an imbalance in the composition and quantity of the intestinal microbiota. There is evidence in the literature that there is a link between brain function and gut microbiota. Physical activity, and especially the regularity and intensity of exercise, is important in relation to the level of BDNF and the intestinal microbiota. Probiotics, prebiotics and physical activity may have a positive effect on the intestinal microbiota, and therefore also on the level of the brain-derived neurotrophic factor.

The role of inappropriate lifestyle in the etiology of polycystic ovary syndrome (PCOS) and its metabolic and reproductive complications has attracted much attention in recent years; however, most studies involve adult patients. Thus, the study aimed to compare dietary patterns, physical activity, metabolic, anthropometric and inflammatory markers of 14–18-year-old girls with and without PCOS (n = 61 and n = 35, respectively) as well as to assess correlations between concentrations of metabolic and inflammatory markers and macronutrient intake and to identify the independent predictors of PCOS, related to diet and physical activity (PA). Compared to the control group, PCOS girls consumed significantly more total fat (p = 0.0005), including both saturated (SFA) (p = 0.03), monounsaturated (MUFA) (p = 0.0003) and polyunsaturated fatty acids (PUFA) (p = 0.01). A significantly higher percentage of PCOS patients consumed high and medium glycemic index (GI) foods (p = 0.03) and represented a low level of PA, both during school and in leisure time (41.67 vs. 6.06%; p = 0.0001 and 32.79 vs. 5.71%; p = 0.003, respectively). The PCOS group had also significantly higher waist circumference (WC), C-reactive protein (CRP) (p = 0.01), LDL cholesterol (p = 0.01), fasting insulin (p = 0.002) and HOMA-IR (p = 0.006) levels. There was an inverse correlation between fiber intake and fasting insulin, (p = 0.0002, r = −0.37), HOMA-IR (p = 0.0004, r = −0.35), WC (p = 0.029; r = −0.222) and a positive relationship between high and medium GI diet and insulin concentration (p = 0.003; r = 0.3). An increase of 10 g/day in total fat intake per day increases the probability of PCOS by 1.4 times. If the SFA or MUFA intakes increase by 10 g, the probability of PCOS increase 1.7-fold and 2.5-fold, respectively. The consumption of foods with a medium GI raises the probability of PCOS by more than 3 times, after adjusting for age. The odds ratio decreased for the moderate and high PA at school/work and in leisure time. Further research in girls with PCOS is needed to test whether low GI and dietary fatty acid reduction combined with increased PA is effective in the nonpharmacological treatment and prevention of PCOS complications. ClinicalTrial.gov Identifier: NCT04738409.

Background/Objectives: Vitamin D deficiency is prevalent in higher-latitude regions and among older adults, and has been linked to depressive symptoms and cognitive decline, although the neurobiological link remains unclear. Brain-derived neurotrophic factor (BDNF) may be a key modulator and mediator of vitamin D-related neuroprotection. Methods: Selected databases (2009–2025) were searched for specific studies reporting vitamin D exposure, BDNF, and mood or cognitive outcomes. Risk of bias was appraised with RoB 2, Newcastle–Ottawa Scale or SYRCLE. Results: Thirteen studies were included. High-dose vitamin D improves mood primarily when levels are low. Supplementation of at least 2000 IU/day for 12 weeks reduced BDI scores by 1.7–7.6 points and increased BDNF levels by ~7%. Each 1 ng/mL increase in 25(OH)D levels decreased the likelihood of depressive symptoms, especially when BDNF levels were high. In animal studies vitamin D increases hippocampal BDNF and reverses stress-induced depressive behavioral deficits. Adequate vitamin D intake is associated with improved cognitive performance and a dose-dependent increase in BDNF. Each 10 ng/mL increase in 25(OH)D was associated with a 0.6-point increase in MMSE scores and a 15% increase in serum BDNF. Low vitamin D status in children may predict cognitive decline. Animal studies have shown that supplementation with 500–10,000 IU/kg for at least 3 weeks increased hippocampal BDNF and improved biochemical markers of aging. Conclusions: Vitamin D supplementation may support mood and cognition via BDNF modulation, especially in people with insufficient vitamin D levels (<30 ng/mL), but long-term, adequately powered studies with objective tools are required.

Background/Objectives: Primary dysmenorrhea (PD) is a condition characterized by painful pelvic cramps onsetting shortly before menses and lasting for 3 days, negatively impacting the quality of life of young females. Further, menstrual cycle disorders are common in athletes. This study investigated differences in dietary habits, hormonal and immuno-metabolic parameters, and susceptibility to disordered eating attitudes (DEAs) between dysmenorrheic (D group) and non-dysmenorrheic (no-D group) young female basketball players. It also aimed to identify risk factors for PD, focusing on nutrition, anthropometric parameters, and biochemical markers. Materials and Methods: The study included 25 female basketball players (mean age: 16 years), categorized into D and no-D groups. Blood samples were analyzed for hormonal, metabolic, and inflammatory markers, including follicle-stimulating hormone, luteinizing hormone, total testosterone, androstenedione, dehydroepiandrosterone sulfate, estradiol, sex hormone-binding globulin, cortisol, prolactin, fasting glucose, fasting insulin, C-reactive protein, lipid profile, and 25-hydroxyvitamin D3. Dietary intake was assessed via a three-day food record, and DEA susceptibility was evaluated using the Eating Attitudes Test (EAT-26). Logistic regression identified independent PD risk factors. Results: The D group had significantly higher EAT-26 scores and prolactin and cortisol levels than the no-D group (p = 0.0284, p = 0.0108, p = 0.0035, respectively). Elevated prolactin, cortisol, and EAT-26 scores were associated with increased PD risk (OR = 1.75; OR = 1.02; OR = 1.14). Conclusions: Female basketball players with PD show higher prolactin and cortisol levels and greater DEA susceptibility. These factors may contribute to PD risk, warranting further research.

The study examined 110 samples of baby products based on rice, wheat, maize and multi-grains available on the western Polish market in order to detect the level of deoxynivalenol (DON) by means of HPLC (high-performance liquid chromatography) with a fluorescence detector (HPLC-FLD). DON was detected in 9.09% of the infant food samples, with an average and maximum level of 107.8 ± 30 and 148 μg/kg, respectively. The highest concentration of DON was detected in food for infants: wheat-based (mean 121 ± 7.07, 4.8%), multi-grain (mean 118 ± 5.65, 4.25%) and maize-based (mean 100 ± 37.96; 35.30%). No high DON content and high estimated daily intake were observed in the analyzed products. However, in order to minimize the harmfulness associated with the presence of DON in food for infants and young children, a risk assessment should be performed based on the monitoring results.

Background: Metabolic syndrome (MetS) and related disorders, such as insulin resistance, pose significant health risks in middle-aged women, including cognitive decline. Chronic inflammation, characterized by elevated levels of interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-α), has been identified as a key mechanism linking metabolic disturbances to neurodegenerative processes. Methods: This study aimed to examine the associations between metabolic disorders, inflammatory markers, and cognitive function among middle-aged women. A cross-sectional study was conducted on 179 non-smoking perimenopausal and postmenopausal women aged 43–73 years. Anthropometric, metabolic, and cognitive parameters were assessed, including body mass index (BMI), waist-to-height ratio (WHtR), fasting glucose (GLU), triglycerides (TG), IL-6, TNF-α, and Mini-Mental State Examination (MMSE) scores. Logistic regression models were applied to evaluate the relationships between inflammation, MetS components, and cognitive impairments. Results: Women with insulin resistance showed significantly worse metabolic profiles and lower MMSE scores (23.98 vs. 24.91, p = 0.032). IL-6 levels were strongly associated with hypertriglyceridemia (OR = 1.096, 95% CI: 1.044–1.151, p < 0.001) and insulin resistance (OR = 1.068, 95% CI: 1.030–1.107, p < 0.001), while TNF-α correlated with abdominal obesity (WHtR OR = 1.429, 95% CI: 1.005–2.031, p = 0.047). Moreover, TNF-α was a significant predictor of cognitive impairments (OR = 1.362, 95% CI: 1.153–1.610, p < 0.001), whereas IL-6 showed no significant association. Conclusions: These findings highlight that TNF-α may be a key inflammatory marker associated with metabolic disturbances and cognitive decline in middle-aged women. IL-6 appears to be more specifically linked to lipid abnormalities and insulin resistance. Targeted interventions to reduce inflammation may moderate metabolic and cognitive risks in this population.