The association between dietary patterns before pregnancy and gestational diabetes mellitus: a matched case-control study in China.

BACKGROUND AND OBJECTIVES: We aimed to explore the relationship between dietary patterns and gestational diabetes mellitus (GDM) during pre-pregnancy six months using principal component analysis (PCA) and the geometric framework for nutrition (GFN). METHODS AND STUDY DESIGN: We conducted a case-control study that included 210 GDM pregnant women and 210 controls. The dietary intake of all participants was assessed by a validated semi-quantitative food frequency questionnaire (FFQ). Major dietary patterns were extracted by PCA. A conditional logistic regression model was used to determine whether specific dietary patterns are associated with the risk of GDM. Meanwhile, the relationship between dietary patterns and GDM was visualized using GFN. RESULTS: Four major dietary patterns were identified: "protein-rich pattern," "plant-based pattern," "oil-pickles-desserts pattern," and "cereals-nuts pattern." After adjustment for confounders, the "plant-based pattern" was associated with decreased risk of GDM (Q4 vs. Q1: OR = 0.01, 95% CI: 0.00-0.08), whereas no significant association was found in other dietary patterns. Moreover, there was no dietary intake of ice cream cones and deep-fried dough sticks for the population, which would produce fewer patients with GDM. Deep-fried dough sticks had statistically significant differences in the case and control groups (p < 0.001), while ice cream cones had the opposite result. CONCLUSIONS: The "plant-based pattern" may reduce the risk of GDM. Besides, although the "cereals-nuts pattern" had no association with GDM risk, avoiding the intake of deep-fried dough sticks could decrease GDM risk.

Associations of accelerometer-measured physical activity and sedentary time with renal function and chronic kidney disease: a national population-based study.

Introduction: There is limited information about the relationship between physical activity (PA) and sedentary behaviors in chronic kidney disease (CKD). Therefore, this study aims to explore the associations of accelerometer-measured PA and sedentary behaviors with CKD. Methods: A cross-sectional study was conducted using data from the National Health and Nutrition Examination Survey in the 2003-2004 and 2005-2006 survey cycles. A uniaxial accelerometer measured physical activity (PA) and sedentary time (ST). The associations of PA and ST with estimated glomerular filtration rate (eGFR) and odds of CKD adopted the generalized linear regression, multivariable logistic regression, and isotemporal substitution models. Results: A total of 5,990 adults with 605 CKD patients were included in this study. Compared with the individuals in the first quartile group, participants in the fourth quartile of low-intensity physical activity (LIPA), moderate to vigorous physical activity (MVPA), and ST were associated with 52% (35%, 65%) and 42% (14%, 62%) lower odds of CKD and 64% (17%, 131%) higher odds of CKD, respectively. Substituting 30 min/day of ST with equivalent LIPA/MVPA contributed to risk reduction in CKD. Discussion: The findings suggest that increased LIPA and MVPA and reduced ST were associated with a lower risk of CKD and that replacing ST with LIPA may decrease the risk of CKD.

Association between organophosphate esters exposure and all-cause and cause-specific mortality: a national population-based cohort study.

Exposure to organophosphate esters (OPEs) is associated with several chronic diseases, but the relationship with mortality risk is unclear. Therefore, we used the National Health and Nutrition Examination Survey 2011-2018 data to evaluate these relationships. 6,869 participants aged 18 years or older were included. Survival status information was obtained through the National Death Index through 31 December 2019. Multivariable COX regression model was adopted to calculate the hazard ratios (HRs) and 95% confidence intervals (CIs) for the relationships of urinary OPEs metabolites with mortality risk. During an average of 5.0 years of follow-up, 406 deaths were documented. After adjusting for confounders, bis(2-chloroethyl) phosphate was associated with an increased risk of all-cause mortality [HR (95%CI) = 1.12(1.05-1.20)] and cardiovascular mortality [HR (95%CI) = 1.15(1.04-1.26)]. Our study found that exposure to OPEs was significantly associated with increased risks of all-cause and cardiovascular mortality. Consequently, controlling OPEs exposure is needed to alleviate the health-related burden.

Combined effects of genetic predisposition and sleep quality on acceleration of biological ageing: Findings from the UK biobank cohort.

OBJECTIVE: Genetic risks can accelerate ageing, yet better quality sleep may slow down it. We thus examined the interaction and combined effects of genetic predisposition and sleep quality on the risk of accelerate aging. METHODS: This study included 407,027 participants from the UK Biobank. Sleep index of each participant was retrieved from the following seven sleep behaviors: snoring, chronotype, daytime sleepiness, sleep duration, insomnia, nap and difficulties in getting up. The biological age (PhenoAge) were estimated by corresponding algorithms based on clinical traits, and their residual discrepancies with chronological age were defined as the age accelerations (PhenoAgeaccel). We explored the interaction and combined effects of genetic risk and sleep quality on accelerated ageing by constructing a linear model. RESULTS: Compared with participants in low sleep quality group, those in medium and high sleep quality group decreased 0.727 (95%CI, 0.653 to 0.801) and 1.056 (95%CI, 0.982 to 1.130) years of PhenoAgeaccel, respectively. Compared with participants in low genetic risk group, those in medium and high genetic risk group increased 0.833 (95%CI, 0.792 to 0.874) and 1.543 (95%CI, 1.494 to 1.592) years of PhenoAgeaccel, respectively. There was interaction between the genetic risk and sleep quality (P-interaction<0.001). For combined effect, compared to the group with high sleep quality and lower genetic risk, people with low sleep quality and high genetic risk had 2.747 (95%CI, 2.602 to 2.892) years higher PhenoAgeaccel. CONCLUSION: Our findings elucidate that better sleep quality could lessen accelerated biological ageing especially among population with high genetic risk.

Environmental pollution to kidney disease: an updated review of current knowledge and future directions.

Environmental pollution significantly impacts global disease burden. However, the contribution of environmental pollution to kidney disease is often overlooked in nephrology. This review examines the growing body of research demonstrating the significant impacts of environmental pollutants, with a focus on air pollution as a primary factor, and acknowledges the roles of other pollutants, such as heavy metals, in the development and progression of kidney diseases. Short-term exposure to air pollution is linked with an increased risk of kidney disease-related events, including hospital admissions, and death, predominantly occurring in vulnerable populations. In contrast, long-term exposure, even at low to moderate levels, may lead to progressive pathophysiological changes, such as chronic systemic inflammation and oxidative stress, that contribute to the development of kidney disease. In addition, air pollution may exacerbate traditional kidney disease risk factors such as hypertension and diabetes, thereby accelerating disease progression. The review also explores how climate change may interact with various pollutants, including air pollution, influencing kidney disease indirectly. The examined evidence underscores the urgent need for an interdisciplinary approach to research further into environmental kidney disease. Environmental health policies could play a crucial role in the prevention, intervention, and improvement of kidney health worldwide.

Fatty acids metabolism in ozone-induced pulmonary inflammatory injury: Evidence, mechanism and prevention.

Ozone (O3) is a major air pollutant that directly threatens the respiratory system, lung fatty acid metabolism disorder is an important molecular event in pulmonary inflammatory diseases. Liver kinase B1 (LKB1) and nucleotide-binding domain leucine-rich repeat-containing protein 3 (NLRP3) inflammasome not only regulate inflammation, but also have close relationship with fatty acid metabolism. However, the role and mechanism of LKB1 and NLRP3 inflammasome in lung fatty acid metabolism, which may contribute to ozone-induced lung inflammation, remain unclear, and effective strategy for preventing O3-induced pulmonary inflammatory injury is lacking. To explore these, mice were exposed to 1.00 ppm O3 (3 h/d, 5 days), and pulmonary inflammation was determined by airway hyperresponsiveness, histopathological examination, total cells and cytokines in bronchoalveolar lavage fluid (BALF). Targeted fatty acids metabolomics was used to detect medium and long fatty acid in lung tissue. Then, using LKB1-overexpressing adenovirus and NLRP3 knockout (NLRP3-/-) mice to explore the mechanism of O3-induced lung fatty acid metabolism disorder. Results demonstrated that O3 exposure caused pulmonary inflammatory injury and lung medium and long chain fatty acids metabolism disorder, especially decreased dihomo-γ-linolenic acid (DGLA). Meanwhile, LKB1 expression was decreased, and NLRP3 inflammasome was activated in lung of mice after O3 exposure. Additionally, LKB1 overexpression alleviated O3-induced lung inflammation and inhibited the activation of NLRP3 inflammasome. And we found that pulmonary fatty acid metabolism disorder was ameliorated of NLRP3 -/- mice compared with those in wide type mice after O3 exposure. Furthermore, administrating DGLA intratracheally prior to O3 exposure significantly attenuated O3-induced pulmonary inflammatory injury. Taken together, these findings suggest that fatty acids metabolism disorder is involved in O3-induced pulmonary inflammation, which is regulated by LKB1-mediated NLRP3 pathway, DGLA supplement could be a useful preventive strategy to ameliorate ozone-associated lung inflammatory injury.

Global, regional, and national burden of stroke attributable to extreme low temperatures, 1990-2019: A global analysis.

BACKGROUND: Extreme ambient temperatures have been linked to increased risks of stroke morbidity and mortality. However, global estimates of the burden of stroke due to extreme low temperatures are not well-defined. AIMS: This study aimed to determine the global burden of stroke due to extreme low temperatures and its spatiotemporal trend from 1990 to 2019. METHODS: Based on the Global Burden of Disease Study 2019, we obtained global, regional, and national data on deaths, disability-adjusted life years (DALYs), age-standardized mortality rate (ASMR), and age-standardized rate of DALYs (ASDR) of stroke attributed to extreme low temperatures, further stratified by age, sex, and sociodemographic index (SDI). RESULTS: Globally, in 2019, an estimated 474,000 stroke deaths with the corresponding ASMR (6.2 (95% uncertainty interval (UI): 4.6-7.9)) and ASDR (103.9 (95% UI: 77.0-134.5)) per 100,000 population, were attributable to extreme low temperatures. The most significant burden was observed in Central Asia, followed by Eastern Europe and East Asia. From 1990 to 2019, the global burden of stroke and its subtypes (ischemic stroke, intracerebral hemorrhage, and subarachnoid hemorrhage) attributable to extreme low temperatures exhibited a decrease in both ASMR and ASDR. Significant decreases in stroke burden occurred in the high-SDI regions, high-income Asia Pacific, and subarachnoid hemorrhage cases. Moreover, the ASMR and ASDR increased with age and were higher in males than females. CONCLUSION: The global stroke burden due to extreme low temperatures remains high despite a decreasing trend over the past three decades. The stroke burden due to extreme low temperatures was more notable for Central Asia, older people, and the male sex.

Chronic exposure to ambient air pollution and the risk of non-alcoholic fatty liver disease: A cross-sectional study in Taiwan and Hong Kong.

BACKGROUND: Information on the relation of air pollution with non-alcoholic fatty liver disease (NAFLD) is scarce. We thus conducted a large cross-sectional study in Asia to investigate the role of air pollution in NAFLD. METHODS: We recruited 329,048 adults (mean age: 41.0 years) without other liver disease (hepatitis and cirrhosis) or excessive alcohol consumption in Taiwan and Hong Kong from 2001 to 2018. The concentrations of nitrogen dioxide (NO2) and ozone (O3) were estimated using a space-time regression model, and the concentrations of fine particulate matter (PM2.5) was evaluated using a satellite-based spatio-temporal model. NAFLD was determined using either the fatty liver index (FLI) or the hepatic steatosis index (HSI). The NAFLD-related advanced fibrosis was defined according to BARD score or the fibrosis-4 (FIB-4). A logistic regression model was adopted to explore the relationships of ambient air pollution with the odds of NAFLD and NAFLD-related advanced fibrosis. RESULTS: We found positive relationships between PM2.5 and the odds of NAFLD and advanced fibrosis, with every standard deviation (SD, 7.5 µg/m3) increases in PM2.5 exposure being associated with a 10% (95% confidence interval [CI]: 9%-11%) increment in the prevalence of NAFLD and an 8% (95% CI: 7%-9%) increment in the prevalence of advanced fibrosis. Similarly, the prevalence of NAFLD and advanced fibrosis increased by 8% (95% CI: 7%-9%) and 7% (95% CI: 6%-8%) with per SD (18.9 µg/m3) increasement in NO2 concentration, respectively. Additionally, for every SD (9.9 µg/m3) increasement in O3 concentration, the prevalence of NAFLD and advanced fibrosis decreased by 12% (95% CI: 11%-13%) and 11% (95% CI: 9%-12%), respectively. CONCLUSION: Higher ambient PM2.5 and NO2 are linked with higher odds of NAFLD and advanced fibrosis. Our findings indicate that reducing PM2.5 and NO2 concentrations may be an effective way for preventing NAFLD. Further studies on O3 are warranted.

Low-carbohydrate diet and risk of cardiovascular disease, cardiovascular and all-cause mortality: a systematic review and meta-analysis of cohort studies.

Background: Evidence for the long-term health effect of low-carbohydrate diets (LCDs) is inconsistent. Herein, we aimed to examine the associations of LCDs with cardiovascular disease (CVD) and all-cause and cause-specific mortality. Methods: We searched PubMed, EMBASE, and the Web of Science up to 26 July 2023 for eligible publications. Random-effect models were used to pool the summary relative risks (RRs) and 95% confidence intervals (CIs). Results: A total of 44 studies (17 articles) were included in the systematic review and 38 in the meta-analysis, including 223 657 all-cause deaths (771 609 participants), 14 046 cardiovascular deaths (274 807 participants), 18 264 CVD cases (405 631 participants), and 3634 coronary heart disease (CHD) cases (151 023 participants). Subsequently, the highest LCD score was compared with the lowest one and the pooled RRs (95% CIs) were 1.05 (0.96, 1.14; I2 = 65.1%; n = 13) for CVD, 1.43 (1.18, 1.72; I2 = 25.4%; n = 3) for CHD, 0.93 (0.81, 1.06; I2 = 0.0%; n = 2) for stroke, 1.03 (0.96, 1.10; I2 = 86.6%; n = 13) for all-cause mortality and 1.09 (0.99, 1.19; I2 = 65.1%; n = 10) for cardiovascular mortality. Conclusion: Our analysis showed positive associations of LCDs with CHD. Thus, vigilance is recommended for long-term adherence to this dietary pattern.

Spatiotemporal Trends of Stroke Burden Attributable to Ambient PM2.5 in 204 Countries and Territories, 1990-2019: A Global Analysis.

BACKGROUND AND OBJECTIVES: Previous studies suggested that long-term exposure to ambient fine particulate matter (PM2.5) is associated with increased risk of stroke. However, limited studies evaluated the stroke burden attributable to ambient PM2.5 globally, especially comprising across different regions, countries, and social-economic levels. We thus conducted this study to estimate the spatial and temporal trends of ambient PM2.5-related stroke burden by sex, age, and subtypes from 1990 to 2019 at global, regional, and national levels. METHODS: Information on the ambient PM2.5-related stroke burden from 1990 to 2019 was obtained from the Global Burden of Disease study 2019. The burdens of stroke attributable to ambient PM2.5 (i.e., age-standardized mortality rate [ASMR] and age-standardized disability-adjusted life-year rate [ASDR]) were estimated by sex, age, and subtypes from 1990 to 2019 at global, regional, and national levels. The estimated annual percentage change (EAPC) was used to evaluate the changing trends of ASDR and ASMR attributable to ambient PM2.5 from 1990 to 2019. The Spearman correlation coefficient was used to examine the correlation between sociodemographic index (SDI) and EAPC of ASMR and ASDR at the national level. RESULTS: In 2019, the global ambient PM2.5-related stroke mortality and disability-adjusted life years were 1.14 million and 28.74 million, respectively, with the corresponding ASDR and ASMR of 348.1 and 14.3 per 100,000 population, respectively. The ASDR and ASMR increased with age and were highest among male patients, in the middle SDI regions, and for intracerebral hemorrhage (ICH). From 1990 to 2019, the absolute death number of stroke attributable to ambient PM2.5 and the corresponding ASMR and ASDR were both in an increasing trend. The corresponding EAPCs in ASMR and ASDR were 0.09 (95% CI -0.05 to 0.24) and 0.31 (95% CI 0.18-0.44), respectively. The significant increases of ASMR and ASDR were observed in the low, low-middle, and middle SDI regions, and for ICH. However, a decreasing trend was observed in high and middle-high SDI regions, and for subarachnoid hemorrhage. DISCUSSION: The global burden of stroke attributable to ambient PM2.5 showed an increasing trend over the past 30 years, especially in male patients, low-income countries, and for ICH. Continued efforts on reducing the level of ambient PM2.5 are necessary to reduce the burden of stroke.

Burden of stroke attributable to high ambient temperature from 1990 to 2019: A global analysis.

AIMS: To determine the global and regional burden of stroke due to high temperature and the spatiotemporal trends in 204 countries and territories from 1990 to 2019. METHODS: Based on Global Burden of Disease Study 2019, deaths, disability-adjusted life years (DALYs), and age-standardized mortality rate (ASMR) and age-standardized DALY rate (ASDR) for stroke attributable to high temperature (i.e. a daily mean temperature warmer than the theoretical minimum-risk exposure level (TMREL)) were calculated in global, geographical location, and country and analyzed by age, sex, subtypes, and socio-demographic index (SDI) from 1990 to 2019. The trends in ASMR and ASDR from 1990 to 2019 were estimated by linear regression model. The regression coefficients (ß) referred to a mean change of per year for ASMR or ASDR attributable to high temperature. RESULTS: The global burden of stroke attributable to high temperature had an increase trend from 1990 to 2019 (ß = 0.005, 95% uncertainty interval (UI) = 0.003-0.007 for ASMR and ß = 0.104, 95% UI = 0.066-0.142 for ASDR, respectively). Globally, in 2019, an estimated 0.048 million deaths and 1.01 million DALYs of stroke were attributable to high temperature, and the global ASMR and ASDR of stroke attributable to high temperature were 0.60 (95% UI = 0.07-1.30) and 13.31 (1.40-28.97) per 100,000 population, respectively. The largest burden occurred in Western Sub-Saharan Africa, followed by South Asia, Southeast Asia, and North Africa and the Middle East. ASMR and ASDR increased with age and were higher in males and for intracerebral hemorrhage, and were the highest in the low SDI regions. In 2019, the region with the largest percentage increase in ASMR and ASDR attributable to high temperature was Eastern Sub-Saharan Africa from 1990 to 2019. CONCLUSIONS: Stroke burden due to high temperature has been increasing, and a higher burden was observed in people aged 65-75 years, males, and countries with a low SDI. Stroke burden attributable to high temperature constitutes a major global public health concern in the context of global warming.

Spatiotemporal trends of cardiovascular disease burden attributable to ambient PM2.5 from 1990 to 2019: A global burden of disease study.

There is little known about the global burden of CVD attributable to ambient PM2.5 (referred to as CVD burden hereinafter) and its secular trend across different regions and countries. We aimed to evaluate the spatiotemporal trends in CVD burden at the global, regional and national levels from 1990 to 2019. Data on CVD burden including mortality and disability adjusted of life years (DALYs) from 1990 to 2019 were extracted from the Global Burden of Disease Study 2019. Cases, the age-standardized rate of mortality (ASMR) and DALYs (ASDR) were estimated by age, sex and sociodemographic index (SDI). Estimated annual percentage change (EAPC) was calculated to evaluate the temporal changing in ASDR and ASMR from 1990 to 2019. In 2019, 2.48 million deaths and 60.91 million DALYs of CVD were attributed to ambient PM2.5 globally. Most CVD burden occurred in males, elderly and the middle SDI region. At national level, Uzbekistan, Egypt, and Iraq had the highest ASMR and ASDR. Despite remarkable increase in number of DALYs and deaths of CVD worldwide from 1990 to 2019, we observed nonsignificant change in ASMR (EAPC: 0.06, 95 % CI: -0.01, 0.13) and slight increment in ASDR (EAPC: 0.30, 95 % CI: 0.23, 0.37). The EAPCs of ASMR and ASDR were negatively associated with SDI in 2019, while the low-middle SDI region exhibited the fastest growth of ASMR and ASDR with EAPCs of 3.25 (95 % CI: 3.14, 3.37) and 3.36 (95 % CI: 3.22, 3.49), respectively. In conclusion, the global CVD burden attributable to ambient PM2.5 has largely increased over the past three decades. The population growth, aging and SDI contributed to the heterogeneity of spatial and temporal distribution. Enforcing policy to improving air quality is required to halt the growing burden of PM2.5 on health.

Dietary intake and serum concentrations of vitamin A and vitamin E and pre-eclampsia risk in Chinese pregnant women: A matched case-control study.

Background: Many studies have suggested that the serum concentrations of vitamin A (VA) and vitamin E (VE) influence preeclampsia (PE) risk in pregnant women. However, few studies have assessed whether dietary intake and serum concentrations of VA and VE are correlated with PE risk. Methods: A 1:1 matched case-control study was conducted to explore the association between the dietary intake and serum concentrations of VA and VE and the risk of PE in pregnant Chinese women. A total of 440 pregnant women with PE and 440 control pregnant women were included in the study. Dietary information was obtained using a 78-item semi-quantitative food frequency questionnaire. Serum concentrations of VA and VE were measured by liquid chromatography-tandem mass spectrometry. Results: Compared with the lowest quartile, the multivariate-adjusted odds ratios [95% confidence interval (CI)] of the highest quartiles were 0.62 (95% CI: 0.40-0.96, P trend = 0.02) for VA, 0.51 (95% CI: 0.33-0.80, P trend =0.002) for ß-carotene, and 0.70 (95% CI: 0.45-1.08, P trend = 0.029) for retinol. Additionally, for serum VA and VE concentrations, the multivariate-adjusted odds ratios (95% CI) were 2.75 (95% CI: 1.24-6.13, P trend = 0.002) and 11.97 (95% CI: 4.01-35.77, P trend < 0.001), respectively. No significant association was seen between VE intake and PE risk. Conclusions: Dietary VA intake was negatively correlated with PE risk, and serum VA and VE concentrations were positively correlated with PE risk among pregnant Chinese women.

Socioeconomic inequality in overweight/obesity among US children: NHANES 2001 to 2018.

Background: Previous research has found that the prevalence of childhood overweight/obesity varies depending on household income, ethnicity, and sex. The goal of our research is to examine changes over time in socioeconomic inequality and the prevalence of overweight/obesity among American children under five by sex and ethnicity. Methods: This cross-sectional analysis used data from the National Health and Nutrition Examination Surveys (NHANES) collected from 2001-02 to 2017-18. Overweight/obesity in children under five [Body Mass Index (BMI)-for-age z-score >2 standard deviations] was defined according to the World Health Organization (WHO) growth reference standard. The slope inequality index (SII) and the concentration index (CIX) were used to measure the socioeconomic inequality in overweight/obesity. Results: Between 2001-02 and 2011-12, childhood overweight/obesity in the United States decreased from 7.3% to 6.3%, and had increased to 8.1% by 2017-18. However, this pattern varied widely by ethnicity and sex. For both the 2015-16 and 2017-18 surveys, overweight/obesity was more concentrated in the poorest household quintile for overall Caucasian children ((SII = -11.83, IC 95% = -23.17, -0.49 and CIX = -7.368, IC 95% = -13.92, -0.82) and (SII = -11.52, IC 95% = -22.13, -0.91 and CIX = -7.24, IC 95% = -13.27, -1.21), respectively) and for males of other ethnicities [(SII = -13.93, IC 95% = -26.95, -0.92) and CIX = -8.55, IC 95% = -0.86, -16.25] and (SII = -21.19, IC 95% = -40.65, -1.74) and CIX = -13.11, IC 95% = -1.42, -24.80), respectively). In the last three surveys, overweight/obesity was also more concentrated in the poorest household quintile for the overall children of other ethnicities. With the exception of African American females in the 2013-14 survey, for whom overweight/obesity was significantly concentrated in a quintile of the richest households (SII = 12.60, 95% CI = 0.24, 24.97 and CIX = 7.86, 95% CI = 15.59, 0.12); overweight/obesity was found to be concentrated in the richest household quintile for overall African American children, but not significantly so. Conclusions: Our findings give an update and reinforce the notion that overweight/obesity in children under the age of five has increased and that related wealth inequalities are a public health problem in the United States.

Folate, vitamin B6, and vitamin B12 intakes are negatively associated with the prevalence of hypertension: A national population-based study.

We hypothesized that the prevalence of hypertension is related to B-vitamin intake in the general population, but it has not been sufficiently studied. This study aimed to investigate the intakes of dietary folate, vitamin B6, and vitamin B12 concerning hypertension in US adults. A total of 55 569 adults from National Health and Nutrition Examination Survey III and 1999-2014 were included in this study. Nutrient intake was collected from subjects through one or two 24-hour dietary reviews. Multiple logistic regression models were used to examine the relationship between these nutrient intakes and hypertension. Among male participants, dietary folate, vitamin B6, and vitamin B12 intakes were significantly and negatively associated with the prevalence of hypertension, with multivariate-adjusted odds ratios (ORs) of 0.61 (95% confidence interval [CI], 0.55-0.68), 0.65 (95% CI, 0.59-0.72), and 0.84 (95% CI, 0.75-0.95) for the highest quartile group compared with the lowest group. Results were similar for female participants, with multivariate-adjusted ORs of 0.63 (95% CI, 0.57-0.71), 0.60 (95% CI, 0.53-0.66), and 0.87 (95% CI, 0.77-0.98) for the highest quartile group. Moreover, there was a linear trend (Ptrend < .001) in both men and women that the prevalence of hypertension tended to decrease with increased intake of folate, vitamin B6, and vitamin B12; however, the decreases above the third quartile were negligible. Dietary folate, vitamin B6, and vitamin B12 were significantly associated negatively with hypertension, indicating that these nutrients might have a protective effect against hypertension in United States adults.

Iron supplementation and deworming during pregnancy reduces the risk of anemia and stunting in infants less than 2 years of age: a study from Sub-Saharan Africa.

BACKGROUND: In sub-Saharan Africa, infant anemia, stunting and low birth weight remains major public health problems. It is unclear whether prenatal iron supplementation and/or deworming can reduce the risk of infant stunting, anemia and low birth weight. The aim of this study was to investigate the relationship between iron supplementation and/or deworming and stunting, anemia, and low birth weight in infants under two years of age in sub-Saharan Africa. METHODS: Our studies examined pooled data from Demographic and Health Surveys (DHS) in twenty-three African countries collected between 2014 and 2020. childhood anemia and stunting in infants under the age of two were the primary outcomes. Iron supplementation and deworming during prenatal visits were the main exposure variables. A multivariate logistic regression model was used to investigate these relationships. RESULTS: The prevalence of stunting was 29.9%, severe stunting was 10.6%, childhood anemia was 74.3%, childhood severe anemia was 3.2%, and low birth weight was 16.4%, respectively. The use of prenatal iron supplementation alone was associated with a significant reduction of childhood anemia [aOR (95% CI) = 0.9 (0.8-1.0)]. Prenatal deworming alone was associated with a significantly reduced risk of stunting [aOR (95% CI) = 0.7 (0.8-1.0)], childhood anemia [aOR (95% CI) = 0.7 (0.8-0.9)], and low birth weight [aOR (95% CI) = 0.7 (0.8-1.0)]. Prenatal iron supplementation plus deworming or iron supplementation (with or without deworming) were not associated with childhood anemia, infant stunting and low birth weight. CONCLUSIONS: In Sub-Saharan Africa, prenatal deworming alone has the potential to improve infants' outcomes. Childhood anemia was improved with prenatal iron supplementation alone. Our recent findings indicate the necessity for prospective studies on the association between prenatal iron supplementation plus deworming and childhood anemia, stunting and low birth weight.

Isolated systolic or diastolic hypertension and mortality risk in young adults using the 2017 American College of Cardiology/American Heart Association blood pressure guideline: a longitudinal cohort study.

BACKGROUND: Little is known regarding the health effects of different hypertension phenotypes including isolated systolic hypertension (ISH), isolated diastolic hypertension (IDH), and systolic and diastolic hypertension (SDH) defined by the 2017 American College of Cardiology (ACC)/American Heart Association (AHA) guideline among young adults. We conducted this longitudinal study using time-varying analyses to evaluate the relationship between cardiovascular/all-natural mortality risk and different hypertension phenotypes in young adults. METHODS: A total of 284 597 young adults (aged 18-39 years) were recruited between 1996 and 2016. Participants were classified into eight mutually exclusive BP groups: normal blood pressure (BP), elevated BP, stage 1 IDH, stage 1 ISH, stage 1 SDH, stage 2 IDH, stage 2 ISH, and stage 2 SDH. The outcomes were cardiovascular and all-natural mortality. RESULTS: After a median follow-up of 15.8 years, 2341 all-natural deaths with 442 cardiovascular deaths were observed. When compared with individuals with normal BP, the multivariable adjusted hazard ratios (95% confidence interval) of cardiovascular mortality was 1.39 (1.01-1.93) for elevated BP, 2.00 (1.45-2.77) for stage 1 IDH, 1.66 (1.08-2.56) for stage 1 ISH, 3.08 (2.13-4.45) for stage 1 SDH, 2.85 (1.76-4.62) for stage 2 IDH, 4.30 (2.96-6.25) for stage 2 ISH, and 6.93 (4.99-9.61) for stage 2 SDH, respectively. In consideration to all-natural mortality, similar results were observed for stage 1 SDH, stage 2 ISH, and stage 2 SDH; but not for elevated BP, stage 1 IDH, stage 1 ISH, and stage 2 IDH. CONCLUSION: Young adults with stage 1 or stage 2 ISH, IDH, and SDH are at increased risk of cardiovascular death than those with normal BP. Regardless of BP stage, SDH was associated with a higher cardiovascular mortality risk than IDH and ISH.

Dietary carbohydrate quantity and quality and risk of cardiovascular disease, all-cause, cardiovascular and cancer mortality: A systematic review and meta-analysis.

BACKGROUND & AIMS: Evidence remains conflicted on the association between dietary carbohydrate quantity and quality and risk of cardiovascular disease, all-cause, cardiovascular and cancer mortality, and such meta-analyses are lacking. The study aimed to conduct a systematic review and meta-analysis to synthesize the knowledge about their associations and to explore the dose-response relations. METHODS: We comprehensively searched PubMed, EMBASE, and Web of Science up to March 2022 for observational studies investigating the associations in adults. Random effect model was used to estimate the summary relative risks (RRs) and 95% confidence intervals (CIs) and the dose-response association was explored by restricted cubic splines. RESULTS: We obtained the data from 41 eligible studies. Compared with participants with lowest dietary carbohydrate intake, those with highest intake had an RR of 1.10 (95% CI 1.03-1.17, I2 = 52.8%) for cardiovascular disease, 1.10 (0.98-1.24, I2 = 65.5%) for coronary heart disease (CHD), 1.20 (1.08-1.34, I2 = 0) for stroke, 1.07 (1.00-1.14, I2 = 61.9%) for all-cause mortality, 1.02 (0.92-1.14, I2 = 51.3%) for cardiovascular mortality, and 1.01 (0.89-1.13, I2 = 56.7%) for cancer mortality. For each 5 %E increase in dietary carbohydrate intake, the summary RR was 1.02 (1.00-1.04, I2 = 66.8%) for cardiovascular disease, 1.04 (1.01-1.06, I2 = 0) for stroke but not significant for other outcomes. Restricted cubic splines showed linear associations with risk of cardiovascular disease (Pnon-linearity = 0.143), CHD (Pnon-linearity = 0.508), stroke (Pnon-linearity = 0.654) and non-linear associations with all-cause mortality (Pnon-linearity = 0.008) and cardiovascular mortality (Pnon-linearity = 0.055). Limited studies were found on the association of cardiovascular disease and mortality with dietary carbohydrate quality using a multidimensional and integrated indicator. CONCLUSIONS: Increased consumption of dietary carbohydrate intake is associated with increased risk of cardiovascular disease, stroke, and all-cause mortality. Linear relation was found for cardiovascular disease and stroke but non-linear relation for all-cause mortality. More studies are warranted to investigate the association of dietary carbohydrate quality using a combined indicator and cardiovascular disease and mortality.

Cardiovascular Mortality, Habitual Exercise, and Particulate Matter 2.5 Exposure: A Longitudinal Cohort Study.

INTRODUCTION: Habitual exercise may amplify the respiratory uptake of air pollutants in the lung, exacerbating the adverse effects of air pollution. However, it is unclear whether this can reduce the health benefits of habitual exercise (referred to as leisure-time exercise). Thus, the combined effects of habitual exercise and chronic exposure to ambient fine particulate matter 2.5 on cardiovascular mortality were examined among adults in Taiwan. METHODS: A total of 384,128 adults were recruited between 2001 and 2016 and followed up to May 31, 2019. Participants' vital status was obtained by matching their unique identification numbers with records of cardiovascular death in the National Death Registry of Taiwan. A time-varying Cox regression model was used to analyze the data. Analyses were conducted in 2021. RESULTS: Cardiovascular death risks were inversely associated with habitual exercise and positively associated with chronic exposure to particulate matter 2.5. The beneficial effects of habitual exercise on cardiovascular mortality were not modified by chronic exposure to particulate matter 2.5. Inactive participants with high particulate matter 2.5 exposure exhibited a 123% higher risk of cardiovascular death than high-exercise-group participants exposed to low levels of particulate matter 2.5 (95% CI=89, 163). CONCLUSIONS: High level of habitual exercise combined with low exposure level of ambient particulate matter 2.5 is associated with the lowest risk of cardiovascular death. A higher level of habitual exercise is associated with a lower risk of cardiovascular death at all levels of particulate matter 2.5 exposure studied. The results indicate that habitual exercise is a safe health promotion strategy even for people residing in relatively polluted regions.

Life-course exposure to ambient fine particulate matter and hypertension in adulthood: a longitudinal cohort study.

PM2.5-hypertension association were well documented in adults, while the effects of life-course exposure to PM2.5 on adulthood hypertension remained unclear. This study aimed to investigate the associations between life-course exposure to ambient PM2.5 and incident hypertension in adulthood in Asia. We included 4272 participants with 17,814 medical visits from two open cohorts in Taiwan and Hong Kong between 2000 and 2018. We used a satellite-based model to assess 2-year average PM2.5 exposure at a resolution of 1 km2. A linear mixed model was used to examine the association with blood pressure. A Cox regression model with time-dependent covariates was used to examine the overall association with the development of hypertension in adulthood. Life-course mixed models were used to examine the effects of PM2.5 exposure at different life stages on blood pressure and hypertension. For every 10 µg/m3 increase in PM2.5, the overall risk of adulthood hypertension increased by 40% (95% confidence interval [CI] 8-80%). The health effects of PM2.5 exposure at different life-stages on incident hypertension were generally independent of each other. In critical model, the risk of developing hypertension increased 23%, 27%, and 55% for each 10 µg/m3 increase in PM2.5 exposure during school age, adolescence, and adulthood, respectively. Similar associations were found between life-course PM2.5 exposure and blood pressure. Association between PM2.5 and adulthood hypertension can be traced back to childhood. Our study suggests that life-course control of air pollution exposure should be implemented to alleviate the huge burden of adulthood hypertension.