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Few studies have examined dietary protein intake and sources, in combination with longitudinal changes in brain structure markers. Our study aimed to examine the association between dietary protein intake and different sources of dietary protein, with the longitudinal rate of change in brain structural markers. A total of 2723 and 2679 participants from the UK Biobank were separately included in the analysis. The relative and absolute amounts of dietary protein intake were calculated using a 24 h dietary recall questionnaire. The longitudinal change rates of brain structural biomarkers were computed using two waves of brain imaging data. The average interval between the assessments was three years. We utilized multiple linear regression to examine the association between dietary protein and different sources and the longitudinal changes in brain structural biomarkers. Restrictive cubic splines were used to explore nonlinear relationships, and stratified and sensitivity analyses were conducted. Increasing the proportion of animal protein in dietary protein intake was associated with a slower reduction in the total hippocampus volume (THV, β: 0.02524, p < 0.05), left hippocampus volume (LHV, β: 0.02435, p < 0.01) and right hippocampus volume (RHV, β: 0.02544, p < 0.05). A higher intake of animal protein relative to plant protein was linked to a lower atrophy rate in the THV (β: 0.01249, p < 0.05) and LHV (β: 0.01173, p < 0.05) and RHV (β: 0.01193, p < 0.05). Individuals with a higher intake of seafood exhibited a higher longitudinal rate of change in the HV compared to those that did not consume seafood (THV, β: 0.004514; p < 0.05; RHV, β: 0.005527, p < 0.05). In the subgroup and sensitivity analyses, there were no significant alterations. A moderate increase in an individual’s intake and the proportion of animal protein in their diet, especially from seafood, is associated with a lower atrophy rate in the hippocampus volume.

A relationship may exist between selenium and kidney calculi, but there is a lack of research in this field at present. Our study explored the relationship between the serum selenium level and a medical history of adult kidney calculi. We utilized data from the National Health and Nutrition Examination Survey conducted between 2011 and 2016. Participants self-reported their history of kidney stones, while serum selenium levels were measured using inductively coupled plasma dynamic reaction cell mass spectrometry. Our findings indicate a negative correlation between serum selenium levels and the risk of kidney stone history. In the multiple-adjusted model, the lowest serum selenium level group had a higher risk than the other groups. The odds ratio (95% confidence interval) of ever having kidney stones for the highest serum selenium level group was 0.54 (0.33–0.88). In the results of stratified analysis, this relationship was still significant in the groups of women and those 40–59 years. We also found that as a nonlinear dose–response relationship between serum selenium levels and the history of kidney stones disease. In our research, we found that people with higher serum selenium levels had a lower risk of having a history of kidney stones. We concluded that selenium may have a protective effect on kidney stones. In the future, more population studies are needed to explore the relationship between selenium and kidney stones.

The association between iodine status and depressive symptoms has not been investigated in the general population. Therefore, we drew 8935 participants from the National Health and Nutrition Examination Survey (NHANES) 2007–2018 to explore their association. In NHANES, Inductively Coupled Plasma Dynamic Reaction Cell Mass Spectroscopy was utilized to measure urinary iodine concentration (UIC), and Patient Health Questionnaire-9 was used to assess depressive symptoms. Meanwhile, we fitted logistic regression and restricted cubic spline models. We found that high UIC was associated with a higher prevalence of depressive symptoms than the normal UIC group (OR: 1.50, 95% CI: 1.04–2.16). This association was particularly pronounced and further strengthened among females (OR: 1.90, 95% CI: 1.19–3.01) and participants aged 40–59 (OR: 1.90, 95% CI: 1.11–3.25). Moreover, we found that low UIC was associated with a high prevalence of depressive symptoms among females (OR: 1.50, 95% CI: 1.02–2.18). Moreover, the dose-response relationship between UIC and depressive symptoms presented a general trend of decreased, steady transiently, and then increased. We found that participants with high UIC had a higher prevalence of depressive symptoms than those with normal UIC. Meanwhile, we also found that females with low UIC had higher odds of reporting depressive symptoms.

The evidence on the relationship of pyridoxal 5′-phosphate (PLP) with sleep-related problems is limited and controversial. Notably, there is a lack of studies on the general population and studies of the dose–response relationship. Therefore, we conducted a cross-sectional study to examine the associations between serum PLP concentration and sleep-related problems (sleep quality and sleep duration) in adults, using the data of the National Health and Nutrition Examination Survey 2005–2010. High-performance liquid chromatography (HPLC) was used to test PLP in blood samples. Sleep quality and sleep duration were based on self-reported data, with sleep quality categorized as sleep disorder, trouble falling asleep, waking up during the night, and daytime sleepiness. The primary analyses utilized logistic regression models and restricted cubic spline. Compared with the first quartile (Q1), the odds ratios (ORs) and 95% confidence intervals (CIs) of daytime sleepiness for the Q2 and Q3 of serum PLP concentrations were 0.76 (0.59–0.99) and 0.78 (0.62–0.98), respectively. The relationship was only significant for males. Furthermore, a non-linear dose–response relationship was observed between serum PLP concentration and the risk of daytime sleepiness. Compared with the normal sleep duration group, serum PLP concentrations were negatively associated with the risks of very short, short, and long sleep duration, with relative risk ratios (RRRs) of 0.58 (0.43–0.81) (Q4), 0.71 (0.61–0.83) (Q4) and 0.62 (0.34–0.94) (Q3), respectively. The average serum PLP concentrations were higher in people with normal sleep duration, suggesting a non-linear dose–response relationship. Our study indicated that serum PLP concentrations were negatively associated with daytime sleepiness, and this association may only exist in males. Moreover, it was also inversely related to abnormal sleep duration (very short, short, long) compared to normal sleep duration.

This study aimed to investigate the association between the alternative healthy eating index-2010 (AHEI-2010) with cognitive function and the mediating role of depressive symptoms in older adults using the data from the 2011–2014 National Health and Nutrition Examination Survey (NHANES). The AHEI-2010 was calculated from NHANES individual food data and Food Patterns Equivalents Database (FPED) diet data. Cognitive function was assessed by the Consortium to Establish a Registry for Alzheimer’s disease (CERAD, memory function indicator), Word Learning sub-test, digital symbol substitution test (DSST, processing speed indicator), animal fluency test (AFT, executive function indicator), and the comprehensive z-score (global cognition indicator). A weighted multiple linear regression model was used to explore the relationship between AHEI-2010 and cognitive function, and Karlson–Holm–Breen (KHB) method was used to explore the mediating effect of depressive symptoms. A total of 2644 participants were included in this study. Participants with higher AHEI-2010 scores were more likely to have higher scores in DSST, AFT, and comprehensive z-score compared with the lowest quartile. Depressive symptoms play a significant mediating role between AHEI-2010 and cognitive function. The proportion of mediating in CERAD, DSST, AFT, and comprehensive z-score was 14.14%, 9.10%, 9.15%, and 10.47%, respectively. This study found that higher dietary quality was associated with better cognitive function. In addition, depressive symptoms may be an important pathway linking diet and cognitive function.

Objective: This cross-sectional study aimed to explore the association between smoking cessation and depressive symptoms and investigate the mediating role of dietary quality. Methods: We used data from the 2007–2014 National Health and Nutrition Examination Survey. Logistic regression models were applied to evaluate the associations between smoking cessation and depressive symptoms. Stratified analysis was performed according to different HEI levels. We examined the mediating role of HEI in the relationship between depressive symptoms and cessation duration using the Karlson–Holm–Breen (KHB) method. Results: A total of 20,004 participants aged 20 years or older were included in the analyses. There were significant correlations between years for smoking cessation and depressive symptoms (OR: 0.985, 95% CI: 0.971~0.999) after adjusting for correlation covariables. A likelihood ratio test showed that there was an interaction between smoking cessation and diet quality (p = 0.047). In the mediation analysis, we estimated that the increase in HEI scores after quitting smoking could explain the 6.91% decline in depressive symptoms. Conclusion: In this cross-sectional study, smoking cessation showed a protective effect on depressive symptoms and that diet quality can influence and mediate this association.

Background: Previous studies showed lutein and zeaxanthin (L and Z) may influence cognitive function by different mechanisms. Our study aimed to be the first to examine whether the risk of non-alcoholic fatty liver disease (NAFLD) mediated the possible association between the dietary intake of L and Z and cognitive function. Methods: We conducted a cross-sectional analysis of participants aged 60 years or over in the National Health and Nutrition Examination Survey (NHANES) 2011–2014. Multivariable linear regression was used to investigate the association between the dietary intake of L and Z and cognitive function, and structural equation modeling tested the mediation effect. Results: The fatty liver index for the United States population (US FLI) acted as a mediator in the association between the higher intake of L and Z and the Animal Fluency Test, the Digit Symbol Substitution Test (DSST), and composite score and mediated 13.89%, 17.87%, and 13.79% of the total association in dietary L and Z intake (14.29%, 13.68%, and 10.34% of the total association in total L and Z intake), respectively. Conclusion: Our study indicated the potential role of the risk of NAFLD as a mediator of associations between the dietary intake of L and Z and cognitive function in the geriatric American population.

Background: As life expectancy increases, cognitive performance decline in the elderly has become one of the major global challenges. We aimed to evaluate the association of dietary vitamin D (VD), serum 25-hydroxyvitamin D3 (25(OH)D3), 25-hydroxyvitamin D2 (25(OH)D2), and total 25-hydroxyvitamin (25(OH)D) concentration with cognitive performance in older Americans. Methods: The data from the National Health and Nutrition Examination Survey (NHANES), 2011–2014 was used. The cognitive performance was assessed by the Consortium to Establish a Registry for Alzheimer’s Disease (CERAD) Word Learning sub-test, Animal Fluency test, and Digit Symbol Substitution Test (DSST). A binary logistic regression model was applied to evaluate the association between VD and cognitive performance, and restricted cubic spline model was adopted to evaluate the dose–response relationship. Results: While comparing to the lowest dietary VD intake group, the multivariate adjusted odds ratios (ORs) and 95% confidence intervals (CIs) of the highest dietary VD intake group were 0.51 (0.36–0.72) for the Animal Fluency test score and 0.45 (0.31–0.66) for DSST score, respectively; and those of serum total 25(OH)D and 25(OH)D3 concentration were 0.68 (0.47–0.97) and 0.62 (0.44–0.86) for DSST score. L-shaped relationships were identified for dietary VD intake, serum total 25(OH)D and 25(OH)D3 concentration with cognition performance. The associations between dietary VD intake, serum total 25(OH)D and cognitive performance were non-significant when stratified by gender. Conclusions: The study indicates that dietary VD intake, serum total 25(OH)D and 25(OH)D3 concentration were positively associated with cognitive performance. Further studies are needed to clarify the possible effects of dietary VD intake and serum 25(OH)D2, 25(OH)D3 on cognitive performance.

The relationship between ω-3 and ω-6 fatty acids consumption and sleep disorders or duration are controversial. Therefore, we used the data of the National Health and Nutrition Examination Survey 2007–2016 in this cross-sectional study to explore their relationships. ω-3 and ω-6 fatty acids consumption was assessed using two 24 h dietary recall interviews. Sleep disorders and sleep duration were based on self-reported data. Logistic regression models and restricted cubic spline analyses were used. Compared with tertile one, the odds ratios (ORs) and 95% confidence intervals (CIs) of sleep disorders for the second tertile of ω-6 fatty acid intake and the highest tertile of ω-6:ω-3 ratio were 1.30 (1.04–1.62) and 1.36 (1.08–1.70), respectively. Inverse U-shaped and linear dose–response relationships were observed between dietary ω-6 fatty acid intake and ω-6:ω-3 ratio and sleep disorders, respectively. In addition, ω-3 fatty acid consumption was adversely related to sleep disorders in men and the OR (95% CI) was 0.68 (0.49–0.95). Compared with normal sleep duration, ω-3 fatty acid consumption was negatively related to very short, short, and long sleep duration risk. The relative risk ratios (RRRs) were 0.53 (0.35–0.81), 0.79 (0.67–0.93), and 0.81 (068–0.98), respectively. The RRR of very short sleep for ω-6 fatty acid consumption was 0.57 (0.45–0.73). Our study indicates that ω-6 fatty acid consumption and the ω-6:ω-3 ratio are positively associated with the risk of sleep disorders, while the negative association between ω-3 fatty acids and sleep disorders may exist only in men. Furthermore, ω-3 and ω-6 fatty acid consumption are negatively related to the risk of non-normal sleep duration.

Current evidence on the relationship of phytoestrogens with sleep is limited and contradictory. In particular, studies on individual phytoestrogens and sleep have not been reported. Thus, this study aimed to appraise the associations of individual phytoestrogens with sleep disorders and sleep duration. This cross-sectional study comprising 4830 adults utilized data from the National Health and Nutrition Examination Survey 2005–2010. Phytoestrogens were tested in urine specimens. Sleep disorders and sleep duration were based on a self-reported doctor’s diagnosis and usual sleep duration. The main analyses utilized logistic and multinomial logistic regression models and a restricted cubic spline. In the fully adjusted model, compared with tertile 1 (lowest), the odds ratios (95% confidence intervals (CIs)) of sleep disorders for the highest tertile of urinary concentrations of enterolactone, enterodiol, and O-desmethylangolensin were 0.64 (0.41–1.00), 1.54 (1.07–2.21), and 1.89 (1.26–2.85), respectively. Linear inverse, approximatively linear positive, and inverted L-shaped concentration–response relationships were found between enterolactone, enterodiol, and O-desmethylangolensin and sleep disorders, respectively. Compared with normal sleep (7–8 h/night), the relative risk ratio (RRR) (95% CI) of very short sleep for enterolactone was 0.56 (0.36–0.86), and the RRR (95% CI) of long sleep risk for genistein was 0.62 (0.39–0.99). Furthermore, negative associations of genistein with sleep disorders and enterolactone with long sleep risk, as well as positive associations of enterodiol with both long and very short sleep, were observed in the stratified analysis by age or gender. Finally, a notable finding was that urinary O-desmethylangolensin concentration was positively related to sleep disorders in both females aged 40–59 years and non-Hispanic Whites but inversely associated with sleep disorders in both females aged 60 years or over and other Hispanics. Our findings suggested that enterolactone and genistein might be beneficial for preventing sleep disorders or non-normal sleep duration among adults, and enterodiol might be adverse toward this goal. However, the association of O-desmethylangolensin with sleep disorders might be discrepant in different races and females of different ages.

The aim of this study was to examine the association of coffee, caffeinated coffee, decaffeinated coffee and caffeine intake from coffee with cognitive performance in older adults. we used data from the National Health and Nutrition Examination Survey (NHANES) 2011−2014. Coffee and caffeine intake were obtained through two 24-hour dietary recalls. Cognitive performance was evaluated by the Consortium to Establish a Registry for Alzheimer’s Disease (CERAD) test, Animal Fluency test and Digit Symbol Substitution Test (DSST). Binary logistic regression and restricted cubic spline models were applied to evaluate the association of coffee and caffeine intake with cognitive performance. A total of 2513 participants aged 60 years or older were included. In the fully adjusted model, compared to those reporting no coffee consumption, those who reported 266.4−495 (g/day) had a multivariate adjusted odd ratio (OR) with 95% confidence interval (CI) of 0.56(0.35−0.89) for DSST test score, compared to those reporting no caffeinated coffee consumption, those who reported ≥384.8 (g/day) had a multivariate-adjusted OR (95% CI) of 0.68(0.48−0.97) for DSST test score, compared to the lowest quartile of caffeine intake from coffee, the multivariate adjusted OR (95% CI) of the quartile (Q) three was 0.62(0.38−0.98) for the CERAD test score. L-shaped associations were apparent for coffee, caffeinated coffee and caffeine from coffee with the DSST test score and CERAD test score. No significant association was observed between decaffeinated coffee and different dimensions of cognitive performance. Our study suggests that coffee, caffeinated coffee and caffeine from coffee were associated with cognitive performance, while decaffeinated coffee was not associated with cognitive performance.

Many studies have explored the association between n-3 fatty acids and depression, but research on the associations of n-6 fatty acids and n-6:n-3 ratio with depression is more scarce, and the results are controversial. Therefore, we conducted this cross-sectional study to explore the associations of n-3 and n-6 fatty acid intakes and n-6:n-3 ratio with the risk of depressive symptoms using data from National Health and Nutrition Examination Survey (NHANES) 2009−2016. Dietary data on n-3 and n-6 fatty acids were obtained through two 24-h dietary recall interviews, and were adjusted by energy. Depressive symptoms were measured by PHQ-9 (nine-item Patient Health Questionnaire). We applied logistic regression and restricted cubic spline models to assess the relationships of n-3 and n-6 fatty acids intake and n-6:n-3 ratio with the risk of depressive symptoms. A total of 17,431 individuals over 18 years old were enrolled in this study. In the multivariate-adjusted model 2, compared with the lowest category, the highest odd ratios (ORs) with 95% confidence intervals (CIs) for n-3 fatty acid intake and n-6:n-3 ratio were 0.71 (0.55−0.92) and 1.66 (1.10−2.50), and middle OR (95% CI) for n-6 fatty acid intake was 0.72 (0.56−0.92), respectively. Our study suggests that n-3 and n-6 fatty acids intake were inversely associated with the risk of depressive symptoms, while the n-6:n-3 ratio was positively associated with the risk of depressive symptoms.

The association between serum zinc level and preeclampsia (PE) remains controversial. A systematic literature search was performed in PubMed, Web of Science and Embase for relevant available articles. The articles were limited to those in English from January 1990 to April 2015. Observational studies evaluating the association between serum zinc level and PE were included. The I2 was used to assess heterogeneity and the random effect model (REM) was adopted as the pooling method. The pooled standard mean difference (SMD) with 95% confidence interval (CI) was used to estimate the association between serum zinc level and PE. Seventeen observational studies were included. Compared with healthy pregnancy controls, PE patients have lower serum zinc level in 14 studies about total PE (SMD (95% CI): −0.587 (−0.963, −0.212), Z = 3.06, p for Z = 0.002; I2 = 88.4%, p for I2 < 0.0001). In subgroup analysis, a lower serum zinc level in PE patients compared with healthy pregnancy controls was observed in studies conducted in Asia, studies with zinc level measured in serum, and studies involving fasting participants. The SMD did not differ significantly between studies with healthy pregnancy controls matched by individual age (yes or no), and by individual gestational age (yes or no), respectively. Results from this meta-analysis indicate that serum zinc level in PE patients is significantly lower than that in healthy pregnancy controls. A moderate amount of zinc supplementation during pregnancy is advocated to reduce the incidence of PE.

We conducted this cross-sectional study in the American general population to explore the association of dietary n3 and n6 fatty acids intake and the risk of hypertension. We used data from the National Health and Nutrition Examination Survey (NHANES) 2007−2014 in this study. We obtained dietary n3 and n6 fatty acids data through two 24 h dietary recall interviews and n3, n6 fatty acids intake were adjusted by weight. We defined hypertension as now taking prescribed medicine for hypertension or blood pressure above 130/80 mmHg. We applied binary logistic regression, multinomial logistic regression, and restricted cubic spline to evaluate the associations of dietary n3 and n6 fatty acids intake with hypertension. A total of 18,434 participants were included in this study. In the multivariate-adjusted model 2, the odds ratios (ORs) with 95% confidence interval (CI) of hypertension were 0.58 (0.49−0.68), 0.53 (0.45−0.63), and 0.92 (0.80−1.06) for the highest versus the lowest tertile of dietary n3, n6 fatty acids intake and n6:n3 ratio, respectively. Further excluded participants with hypertension history, the ORs with 95% CI of newly diagnosed hypertension were 0.60 (0.50−0.73), 0.52 (0.43−0.62), and 0.95 (0.79−1.14) for the highest versus lowest tertile of dietary n3, n6 fatty acids intake and n6:n3 ratio, respectively. Dose-response analyses showed that the risk of hypertension was associated with dietary n3 and n6 fatty acids intake. Our study suggested that dietary n3 and n6 fatty acids intake were inversely associated with the risk of hypertension in US adults.

This study aimed to explore the association between dietary fiber intake and hypertension risk using 2017 American College of Cardiology/American Heart Association Blood Pressure Guidelines. Data from the National Health and Nutrition Examination Survey 2007–2014 were used in this study. Dietary fiber data were obtained through two 24-h dietary recall interviews. Hypertension was defined as systolic blood pressure (SBP) ≥ 130 mmHg or diastolic blood pressure (DBP) ≥ 80 mmHg or treatment with hypertensive medications. Logistic regression models and restricted cubic spline models were applied to evaluate the associations between dietary intakes of total, cereal, vegetable, and fruit fiber and hypertension. A total of 18,433 participants aged 18 years or older were included in the analyses. After adjustment for age, gender, body mass index (BMI), race, educational level, smoking status, family income, and total daily energy intake, compared with the lowest tertile, the odds ratios (95% confidence intervals) of hypertension for the highest tertile intakes of total, cereal, vegetable, and fruit fiber were 0.62 (0.52–0.75), 0.80 (0.67–0.96), 0.82 (0.69–0.98), and 0.86 (0.71–1.04), respectively. Dose-response analyses revealed that the risk of hypertension was associated with total fiber intake in a nonlinear trend, while the relationships were linear for cereal and vegetable fiber intakes. Our results suggested that the intakes of total, cereal, and vegetable fiber, but not fruit fiber, were associated with a decreased risk of hypertension in U.S. adults.

Several epidemiological studies have evaluated the association between calcium intake and the risk of ovarian cancer. However, the results of these studies remain controversial. Thus, we performed a meta-analysis to explore the association between calcium intake and the risk of ovarian cancer. Pubmed, Embase and Web of Science were searched for eligible publications up to April 2017. Pooled relative risks (RRs) with 95% confidence intervals (CIs) were calculated using the random-effects model. Small-study effect was estimated using Egger’s test and the funnel plot. Among 15 epidemiological studies involving 493,415 participants and 7453 cases eligible for this meta-analysis, 13 studies were about dietary calcium intake, 4 studies about dairy calcium intake and 7 studies about dietary plus supplemental calcium intake. When comparing the highest with the lowest intake, the pooled RRs of ovarian cancer were 0.80 (95% CI 0.72–0.89) for dietary calcium, 0.80 (95% CI 0.66–0.98) for dairy calcium and 0.90 (95% CI 0.65–1.24) for dietary plus supplemental calcium, respectively. Dietary calcium was significantly associated with a reduced risk of ovarian cancer among cohort studies (RR = 0.86, 95% CI 0.74–0.99) and among case-control studies (RR = 0.75, 95% CI 0.64–0.89). In subgroup analysis by ovarian cancer subtypes, we found a statistically significant association between the dietary calcium (RR = 0.78, 95% CI 0.69–0.88) and the risk of epithelial ovarian cancer (EOC). This meta-analysis indicated that increased calcium intake might be inversely associated with the risk of ovarian cancer; this still needs to be confirmed by larger prospective cohort studies.

Many epidemiologic studies have explored the association between dairy product consumption and the risk of non-Hodgkin lymphoma (NHL), but the results remain controversial. A literature search was performed in PubMed, Web of Science and Embase for relevant articles published up to October 2015. Pooled relative risks (RRs) with 95% confidence intervals (CIs) were calculated with a random-effects model. The dose-response relationship was assessed by restricted cubic spline. A total of 16 articles were eligible for this meta-analysis. The pooled RRs (95% CIs) of NHL for the highest vs. lowest category of the consumption of total dairy product, milk, butter, cheese, ice cream and yogurt were 1.20 (1.02, 1.42), 1.41 (1.08, 1.84), 1.31 (1.04, 1.65), 1.14 (0.96, 1.34), 1.57 (1.11, 2.20) and 0.78 (0.54, 1.12), respectively. In subgroup analyses, the positive association between total dairy product consumption and the risk of NHL was found among case-control studies (RR = 1.41, 95% CI: 1.17–1.70) but not among cohort studies (RR = 1.02, 95% CI: 0.88–1.17). The pooled RRs (95% CIs) of NHL were 1.21 (1.01, 1.46) for milk consumption in studies conducted in North America, and 1.24 (1.09, 1.40) for cheese consumption in studies that adopted validated food frequency questionnaires. In further analysis of NHL subtypes, we found statistically significant associations between the consumption of total dairy product (RR = 1.73, 95% CI: 1.22–2.45) and milk (RR = 1.49, 95% CI: 1.08–2.06) and the risk of diffuse large B-cell lymphoma. The dose-response analysis suggested that the risk of NHL increased by 5% (1.05 (1.00–1.10)) and 6% (1.06 (0.99–1.13)) for each 200 g/day increment of total dairy product and milk consumption, respectively. This meta-analysis suggested that dairy product consumption, but not yogurt, may increase the risk of NHL. More prospective cohort studies that investigate specific types of dairy product consumption are needed to confirm this conclusion.