Journal of Nutrition Health & Aging最新文献

Background: Alzheimer's disease (AD) is characterized by the accumulation of abnormal proteins, such as β-amyloid and tau, in the brain, which precedes cognitive impairment. Although diabetes mellitus (DM) is a well-established risk factor for AD, few studies have investigated how the presence of DM affects the sequential pathogenesis of AD, specifically within the amyloid-tau-neurodegeneration (ATN) and cognition framework.

Objectives: This study aims to investigate the trajectories of ATN biomarkers in relation to the presence of DM in the preclinical and prodromal stages of AD.

Design: Participants with normal cognition (CN) or mild cognitive impairment (MCI) at baseline were included. Subjects were followed for 12-192 months, with neuroimaging and cognitive assessments conducted at every 12 or 24 months.

Setting: This study utilized data from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database.

Participants: A total of 603 participants aged 55-90 years were included, comprising 284 CN (25 with DM, 259 without DM) and 319 MCI (39 with DM, 280 without DM) individuals.

Measurements: ATN biomarkers were identified using florbetapir positron emission tomography (PET), flortaucipir PET, and magnetic resonance imaging (MRI), respectively. Cognition was assessed using the Clinical Dementia Rating-Sum of Boxes (CDR-SB) and Mini-Mental State Examination (MMSE). Moderation analysis was conducted to investigate the effect of DM on the association between ATN biomarkers of AD.

Results: Elevated amyloid standardized uptake value ratios (SUVRs) were associated with increased tau levels in the hippocampus, and this association was significantly enhanced by the presence of DM in MCI participants (p = 0.021). DM also strengthened the association between increased tau SUVR levels and neurodegeneration (indicated by decreased entorhinal cortical volumes; p = 0.005) in those with MCI. Furthermore, DM enhanced the association of decreased entorhinal (p = 0.012) and middle temporal cortex (p = 0.031) volumes with increased (worsened) CDR-SB scores in MCI participants. However, DM did not predict significant longitudinal changes in ATN pathology or cognitive decline in CN participants.

Conclusions: Our study suggests that DM may increase the risk of AD by accelerating each step of the A-T-N cascade in the prodromal stage of AD, underscoring the importance of DM management in preventing the MCI conversion to AD.

Background: The decline in daily living abilities (ADL) among older adults is a notable predictor of depressive symptoms and the occurrence of disease. However, the effects of changes in ADL disability on the progression of depression have not been extensively studied.

Objective: This research aims to examine the relationship between current ADL disability and depression in individuals aged 45 and older, as well as to explore how ADL disability influences the progression of depression in later life within China.

Methods: This study analyzed 7-year data from the China Health and Retirement Longitudinal Study (CHARLS), involving 2,205 middle-aged and older adults. The ADL disability (BADL: such as eating, dressing; IADL: such as shopping, cooking) were obtained using ADL scale (scores 0-12, lower is better), and depression was measured by the Center for Epidemiologic Studies Depression Scale (scores 0-30, lower is better). The latent growth curve and cross-lagged models were analyzed after adjusting relevant control variables to study the effect of ADL disability on the progression of depression.

Results: The mean values for depression, basic activities of daily living (BADL), and instrumental activities of daily living (IADL) varied from 9.44 to 11.08, 6.45 to 6.81, and 6.86 to 7.29, respectively. The analysis indicated a potential association between depression and ADL. Specifically, the trajectory of BADL was a significant predictor of both initial depression (β = 0.138, 95%CI = 0.039-0.237) and its trajectory (β = 0.579, 95%CI = 0.403-0.754). Although IADL did not significantly predict the trajectory of depression, it was a significant predictor of initial depression (β = 0.471, 95%CI = 0.404-0.538). Additionally, cross-lag regression analysis provided further support for the relationship between depression and BADL disability.

Conclusions: This research highlights how ADL disability can forecast future depression in Chinese middle-aged and older adults. The findings indicate a significant connection between ADL disability and both changes in and future instances of depression in this group. Therefore, it is crucial for the Chinese government to prioritize interventions that enhance physical functioning in the elderly, as such measures can effectively mitigate the worsening of depression and promote positive aging.

Background: Aging is associated with multiple neurodegenerative conditions that severely limit quality of life and can shorten lifespan. Studies in rodents indicate that in addition to extending lifespan, the ketogenic diet (KD) improves cognitive function in aged animals, yet long term adherence to KD in Humans is poor.

Objectives: To broadly investigate what mechanisms might be activated in the brain in response to ketogenic diet.

Methods: We conducted transcriptome wide analysis on whole brain samples from 13-month-old mice, 13-month-old mice fed a ketogenic diet for 1 month, 26-month-old mice, and 26-month-old mice fed a ketogenic diet for 14 months.

Results: As expected, analysis of differently expressed genes between the old (26 month) vs younger mice (13 month) showed clear activation of inflammation and complement system pathways with aging. Analysis between the 26-month-old animals fed ketogenic diet for 14 months with 26-month-old animals fed control diet indicate that long-term KD resulted in activation of LRP, TCF7L2 (WNT pathway), and IGF1 signaling. There was also a significant increase in the expression of SOX2-dependent oligodendrocyte/myelination markers, though TCF7L2 and SOX2 dependent gene sets were largely overlapping. Remarkably, the effect of 1 month of ketogenic diet was minimal and there was no congruence between gene expression effects of short-term KD vs long-term KD.

Conclusions: This work informs target identification efforts for aging and neurodegenerative disorder therapeutics discovery while also establishing differential effects of short-term vs long-term KD on gene expression in the brain.

Background and aims: Parkinson's disease (PD) is a chronic neurodegenerative disorder, and past research suggests that adherence to the Mediterranean diet (MD) may influence the risk of PD. However, there are varying conclusions among different studies regarding the correlation between long-term adherence to the MD and the occurrence of PD. This meta-analysis aimed to investigate the association between MD adherence and PD incidence.

Methods: This meta-analysis was registered on PROSPERO (CRD42024520410). We searched PubMed, Embase, Web of Science, and Cochrane databases to identify observational studies, including prospective cohorts, case-control, and cross-sectional studies, up to February 2024. Studies reported on MD adherence were included, with MD adherence categorized through a quantifying score or index. The pool odds ratios (ORs) and 95% confidence intervals (CIs) were calculated for the highest versus the lowest categories of MD score in relation to PD risk, using random-effects models. Additionally, bias assessment, heterogeneity assessment, sensitivity analysis, and subgroup analysis were performed. A total of 12 studies were included in the meta-analysis.

Results: The overall effect size of PD risk was as follows: compared to the lowest adherence to the MD, the highest adherence to MD showed a significant negative correlation with the incidence of PD, with an overall OR of 0.75 (95% CI: 0.66, 0.84). Specifically, in studies diagnosing PD, the overall OR was 0.83 (95% CI: 0.74, 0.94), while in studies diagnosing prodromal Parkinson's disease (pPD), the overall OR was 0.67 (95%CI: 0.59, 0.76). For individuals aged <60 years, the overall OR was 0.70 (95%CI: 0.62, 0.78), whereas, for those aged ≥60 years, the overall OR was 0.86 (95%CI: 0.74, 0.99).

Conclusions: The evidence from this meta-analysis demonstrates a significant negative correlation between adherence to MD patterns and the risk of PD, suggesting that the MD may serve as a protective factor for PD. This dietary pattern may be particularly beneficial in reducing the risk of pPD.

Background: Modifiable lifestyle behaviors significantly influence the risk of cognitive impairment. However, the cumulative effects of multidimensional lifestyle profiles on cognitive function remain poorly understood, as most studies examine individual lifestyle behaviors in isolation. This study aimed to identify distinct profiles of individuals based on healthy lifestyle behaviors and to examine associations between these profiles and cognitive function in older Chinese adults.

Methods: We used a prospective cohort, including 5381 participants of the Chinese Longitudinal Healthy Longevity Survey (CLHLS) between 2008 and 2018, aged 65 years and older with normal cognition at baseline. Questionnaires were used to collect self-reported data on healthy diet, sleep quality, physical activities, cognitive activities, and social activities. Repeated measures of the Mini-Mental State Examination (MMSE) were utilized to assess cognitive function. Latent Profile Analysis (LPA) was conducted to identify profiles characterized by similar characteristics of lifestyle behaviors. The resultant profiles, were then used to further explore associations with cognitive function using cox proportional hazard regression and linear mixed models.

Results: During a 10-year follow-up period, 2017 (37.5%) out of 5381 participants developed cognitive impairment. Three latent profiles were identified: (1) "active engagement" (n = 347, 6.4%); (2) "moderate engagement" (n = 627, 11.7%); and (3) "negative engagement" (n = 4407, 81.9%). Compared to negative engagement, the active profile had the lower risk of cognitive impairment (HR = 0.693, 95% CI: 0.553-0.868), longer years to develop cognitive impairment (mean = 7.818, range: 6.701, 8.935) and slower rate of annual cognitive decline (0.407 points per year). Similarly, the moderate engagement profile had the lower risk of cognitive impairment (HR = 0.781, 95% CI: 0.664-0.919), longer years to develop cognitive impairment (mean = 7.541, 95%CI: 6.464, 8.619) and slower rate of annual cognitive decline (0.297 points per year) compared to negative profile. Subgroup analysis revealed that there were no significant differences observed across any of the subgroups, including age, gender, year of schooling, marital status, residence, live alone, family economic status.

Conclusions: These findings imply the likelihood of an inverse correlation between the levels of engagement in healthy lifestyle behavior and the risk of cognitive impairment. Even adopting a few healthy lifestyle habits is superior to none at all, underscoring the value of lifestyle modifications for cognitive health.

Objectives: Findings regarding the effects of vitamin D supplementation on diabetes risk are inconclusive. Because inflammation and vitamin D levels are interconnected, we hypothesized that higher inflammation levels moderate the effects of vitamin D deficiency on diabetes risk.

Design, setting, participants, and measurements: UK Biobank participants without pre-existing diabetes at baseline were included (N = 336,500). We first linked vitamin D and C-reactive protein (CRP; inflammation measure) levels with incident diabetes during a mean follow-up of 13.5 years (SD = 1.9). Then, we investigated the moderation effect of CRP on the associations between vitamin D deficiency (<10 ng/mL) and incident diabetes and performed subgroup analyses according to age (<60 vs. ≥60 years) and frailty status (frail; pre-frail; non-frail). Multivariate analyses were conducted using restricted cubic spline Cox proportional hazards regression models.

Results: Lower vitamin D and higher CRP levels were significantly associated with an increased risk of diabetes during follow-up. There was a significant interaction between vitamin D deficiency and CRP on incident diabetes (p < 0.001). In participants with higher levels of CRP, the hazard ratio of developing diabetes comparing participants who had vitamin D deficiency to those who did not was lower than that in participants with lower levels of CRP. The moderation effect of CRP was similar between younger and older adults but was stronger in frail or pre-frail older adults than in non-frail older adults.

Conclusion: Our findings indicate that the effect of vitamin D deficiency on incident diabetes may be affected by inflammation. This finding may explain the inconsistent results from vitamin D supplementation trials. Vitamin D supplementation without considering the potential impact of inflammation might prove unsatisfactory.

Objectives: Early-famine exposure was reported to be associated with metabolic associated fatty liver disease (MAFLD); however, it has not been fully elucidated whether the gene-famine interaction exist in this association. We aimed to investigate the association between early-life famine exposure in different genetic risk stratifications and the risk of MAFLD in adulthood.

Design, setting, participants, and measurements: The study included 8213 participants from the SPECT-China study. Famine exposure subgroups was defined according to the birth year. A genetic risk score (GRS) was constructed with single nucleotide polymorphisms associated with MAFLD in East Asians. Logistic models were used to examine the association of famine exposure and GRS with MAFLD.

Results: Early-life famine exposure was positively associated with MAFLD after adjusting for multiple confounders (OR (95% CI): fetal-exposure 1.3(1.11-1.53), childhood exposure 1.12(1-1.25)). Meanwhile, with per SD increment of GRS (2.49 points), the OR(95%CI) of MAFLD was 1.1(1.04-1.16). In high GRS group, fetal-exposure was positively associated with 45% higher risk of MAFLD (1.45(1.15-1.83)). In men, neither in low or high GRS subgroups observed an association between early-life famine exposure and MAFLD. But in women with high GRS of MAFLD, fetal-exposure was positively associated with even higher risk of MAFLD (1.64(1.22-2.22)).

Conclusion: The positive association between early-life famine exposure and MAFLD is intensified by high genetic susceptibility of MAFLD in women and in general population in China; while this association does not exist in men or in those with low genetic risk scores.

Objectives: The aim of the study was to investigate associations between risk of malnutrition and risk of rehospitalisation and death in older hospital patients, and whether the possible associations were modified by age, gender, comorbidity or Ambulatory Care Sensitive Conditions (ACSCs).

Design: Prospective cohort study.

Setting: Somatic hospital in Western Norway.

Participants: 9,768 hospital admissions for patients aged ≥65 years.

Measurements: Information on the risk of malnutrition was based on nutritional risk screening data from 34 point prevalence surveys conducted between 2008 and 2018. Risk of malnutrition was assessed using Nutritional Risk Screening 2002 (NRS 2002) during the initial hospital admission. Outcomes and possible effect modifiers were obtained from the hospital's patient administration systems. The short-term outcome was the length of initial hospital stay. Long-term outcomes included total number of days in hospital, number of hospital stays and risk of death within one year following nutritional risk screening. Statistical analysis involved negative binomial and Cox regression models with adjustment for age, sex and number of diagnoses at time of nutritional risk screening.

Results: Overall, 34% of the patients were classified as being at risk of malnutrition. A higher proportion of the initial admissions were related to ACSCs for patients at risk of malnutrition than for those not at risk. Risk of malnutrition was associated with longer initial hospital stay (adjusted hazard ratio (95% confidence intervals) 1.31 (1.25, 1.37)), more days in hospital (adjusted risk ratio 1.25 (1.18, 1.32)) and a higher risk of having more than two hospital admissions the year following nutritional risk screening (adjusted risk ratio 1.16 (1.07, 1.26)). Patients at risk of malnutrition also had an increased risk of death within one year (adjusted hazard ratio 2.45 (2.25, 2.67)). All associations were more pronounced in the '65-69' and '70-79' age groups compared to the 80+ years age group, and in patients with fewer than four diagnoses compared to patients with four or more diagnoses. No significant interaction was detected between sex and risk of malnutrition with regard to patient outcomes.

Conclusion: Older patients at risk of malnutrition have a higher risk of rehospitalisation and death during the first year after nutritional risk screening compared with those not at risk. Among patients at risk of malnutrition, the initial hospital admissions were more often due to ACSCs. The impact of the risk of malnutrition on outcomes appears stronger in patients aged 65-79 years and in patients with less comorbidity. These findings underline the importance of nutritional risk screening and subsequent nutritional support in all groups of older patients.