Background: Polyamines, including spermidine (SPD), spermine (SPM) and putrescine (PUT), are essential for cellular physiology and various cellular processes. This study aimed to examine the associations of dietary polyamines intake and all-cause mortality and incident cardiovascular disease (CVD). Methods: This prospective cohort study included 184,732 participants without CVD at baseline from the UK Biobank who had completed at least one dietary questionnaire. Diet was assessed using Oxford WebQ, a web-based 24 h recall questionnaire, with polyamines intakes estimated from previous studies. Cox proportional models with restricted cubic splines were employed to investigate nonlinear associations. The primary endpoint was all-cause mortality or incident CVD (including CVD death, coronary heart disease and stroke). Results: During a median follow-up period of 11.5 years, 7348 (3.9%) participants died and 12,316 (6.5%) developed incident CVD. Polyamines intake showed nonlinear associations with all-cause mortality and incident CVD (P for nonlinear < 0.01). Compared to the lowest quintile group of dietary polyamines intake (≤17.4 mg/day), the quintile 2 to 5 groups demonstrated a reduced risk of all-cause mortality, with the lowest risk in quintile 2 group (>17.4–22.3 mg/day) (HR:0.82, 95% CI: 0.76–0.88). Similar results were observed for incident CVD, with the lowest risk in the quintile 4 group (>27.1–33.5 mg/day) (HR: 0.86, 95% CI: 0.82–0.92). Conclusions: We found that dietary polyamines intake was associated with a lower risk of all-cause mortality or incident CVD. Furthermore, our study identified an optimal range of dietary polyamines intake.

Natural polyamines, including spermidine (SPD), spermine (SPM) and putrescine (PUT), are evolutionarily conserved endogenous molecules crucially involved in central cellular processes. Their physiological importance may extend to the maintenance of cognitive function during aging. However, limited population-based epidemiological studies have explored the link between dietary polyamines and dementia risk. This study was a prospective analysis of 77,092 UK Biobank participants aged ≥ 60 years without dementia at baseline. We used Cox proportional hazard regression models to explore the associations between dietary polyamines and the risk of dementia, and restricted cubic splines to test the non-linear relationships. During a median follow-up of 12 years, 1087 incidents of all-cause dementia cases occurred, including 450 Alzheimer’s disease (AD) cases and 206 vascular dementia (VD) cases. The fully adjusted hazard ratios (HRs) for the upper fourth quintile of dietary SPD, in comparison with the lowest quintile of intake, were 0.68 (95% confidence interval [95% CI]: 0.66–0.83) for the risk of all-cause dementia, 0.62 (95% CI: 0.45–0.85) for AD and 0.56 (95% CI: 0.36–0.88) for VD, respectively. A 26% reduction in dementia risk [HR: 0.74, (95% CI: 0.61–0.89)] and a 47% reduction in AD [HR: 0.53, (95%CI: 0.39–0.72)] were observed comparing the third with the lowest quintiles of dietary SPM. Dietary PUT was only associated with a reduced risk of all-cause dementia in the fourth quintile [HR (95% CI): 0.82 (0.68–0.99)]. Reduced risk was not found to be significant across all quintiles. There were ‘U’-shaped relationships found between dietary polyamines and all-cause dementia, AD and VD. Stratification by genetic predisposition showed no significant effect modification. Optimal intake of polyamines was linked to a decreased risk of dementia, with no modification by genetic risk. This potentially suggests cognitive benefits of dietary natural polyamines in humans.

To evaluate the role of brain-derived neurotrophic factor (BDNF)-a crucial modulator of neural development and plasticity-in the association between prenatal maternal anxiety, depression, and perceived stress and child neurodevelopment in a prospective cohort study. We included 526 eligible mother-child pairs from the Shanghai Birth Cohort in the study. Maternal mental health was assessed at mid-pregnancy using Zung's Self-Rating Anxiety Scale, Center for Epidemiologic Studies Depression Scale, and Perceived Stress Scale. The concentration of BDNF in cord blood was measured by ELISA. The offspring neurodevelopment at 24 months of age was assessed using the Bayley Scales. Linear and non-linear regression models were used. The average cord blood BDNF levels were higher in female newborns and those born via vaginal delivery, full term, and normal birth weight. Prenatal maternal anxiety (β = -0.32; 95 % CI: -0.55, -0.09), depression (β = -0.30; 95 % CI: -0.52, -0.08), and perceived stress (β = -0.41; 95 % CI: -0.71, -0.12) scores were negatively associated with social-emotional performance at 24 months of age. However, no significant associations were found between prenatal maternal anxiety, depression, or perceived stress at mid-pregnancy and cord blood BDNF levels, as well as between cord blood BDNF levels and child neurodevelopment. Maternal mental health at different timepoints during pregnancy and generalizability of the results warrant further assessment. Prenatal mental health was not associated with cord blood BDNF level and that BDNF may not be a mediator in the association between prenatal mental health and child neurodevelopment.