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Almost one third of U.S. adults have elevated low-density lipoprotein cholesterol, increasing their risk of atherosclerotic cardiovascular disease. The 2018 American College of Cardiology/American Heart Association Multisociety Cholesterol Management Guideline recommends maximally tolerated statin for those at increased atherosclerotic cardiovascular disease risk and add-on therapies (ezetimibe and PCSK9 inhibitors) in those at very high risk and low-density lipoprotein cholesterol ≥70 mg/dL. Prescription fill trends are unknown.Using national outpatient retail prescription data from the first quarter of 2017 to the first quarter of 2022, authors determined counts of patients who filled low-, moderate-, or high-intensity statins alone and with add-on therapies. The overall percentage change and joinpoint regression were used to assess trends. Analyses were conducted in March 2022-May 2022.During the first quarter of 2017 to the first quarter of 2022, patients filling a statin increased by 25.0%, with the greatest increase in high-intensity statins (64.1%, range=6.6-10.9 million). Low-intensity statins decreased by 29.2% (range=3.3-2.4 million). Concurrent fills of high-intensity statin and ezetimibe rose by 210% to 579,012 patients by the first quarter of 2022, with an increase in slope by the first quarter of 2019 for all statin intensities (p0.01). Concurrent fills of a statin and PCSK9 inhibitor increased to 2,629, 16,169, and 28,651 by the first quarter of 2022 for low-, moderate-, and high-intensity statins, respectively. For patients on all statin intensities and PCSK9 inhibitor, there were statistically significant increases in slope in the second quarter of 2019 and decreases in the first quarter of 2020.Patients filling moderate- and high-intensity statins and add-on ezetimibe and PCSK9 inhibitors have increased, indicating uptake of guideline-concordant lipid-lowering therapies. Improvements in the initiation and continuity of these therapies are important for atherosclerotic cardiovascular disease prevention.

Objective Describe the vaccination status, treatment, and outcomes of hospitalized, symptomatic pregnant women with Coronavirus Disease 2019 (COVID-19) and estimate whether treatment differs by pregnancy status among treatment-eligible (i.e., requiring supplemental oxygen per National Institutes of Health guidelines) women. Methods During January–November 2021, the COVID-19-Associated Hospitalization Surveillance Network completed medical chart abstraction for a probability sample of 2,715 hospitalized women aged 15–49 years with laboratory-confirmed SARS-CoV-2 infection. Of these, 1,950 women had symptoms of COVID-19 upon admission; 336 were pregnant. We calculated weighted prevalence estimates of demographic and clinical characteristics, vaccination status, and outcomes among pregnant women with symptoms of COVID-19 upon admission. We used propensity score matching to estimate prevalence ratios (PR), and 95% confidence intervals (CI) of treatment-eligible patients who received remdesivir or systemic steroids by pregnancy status. Results Among 336 hospitalized pregnant women with symptomatic COVID-19, 39.6% were non-Hispanic Black, 24.8% were Hispanic or Latino, and 61.9% were aged 25–34 years. Among those with known COVID-19 vaccination status, 92.9% were unvaccinated. One-third (32.7%) were treatment-eligible. Among treatment-eligible pregnant women, 74.1% received systemic steroids and 61.4% received remdesivir. Among those that were no longer pregnant at discharge (n = 180), 5.4% had spontaneous abortions and 3.5% had stillbirths. Of the 159 live births, 29.0% were pre-term. Among a propensity score-matched cohort of treatment-eligible hospitalized women of reproductive age, pregnant women were less likely than non-pregnant women to receive remdesivir (PR 0.82, 95% CI 0.69–0.97) and systemic steroids (PR 0.80, 95% CI 0.73–0.87). Conclusion Most hospitalized pregnant patients with symptomatic COVID-19 were unvaccinated. Hospitalized pregnant patients were less likely to receive recommended remdesivir and systemic steroids compared to similar hospitalized non-pregnant women. Our results underscore the need to identify opportunities for improving COVID-19 vaccination, implementation of treatment of pregnant women, and the inclusion of pregnant women in clinical trials.

OBJECTIVES: The global prevalence of non-alcoholic fatty liver disease (NAFLD) has risen to 25%, with Hispanic populations among those at greatest risk. We describe the prevalence of NAFLD in a cohort of Guatemalan adults and examine whether exposure to a protein-energy supplement from conception to age two years is associated with lower prevalence of NAFLD. METHODS: From 1969 to 1977, four villages in Guatemala were cluster-randomized to receive a protein-energy supplement (Atole) or a no-protein, low-energy beverage (Fresco). We conducted a follow-up of participants in the original study from 2015 to 2017. We assessed blood samples (n = 1093; 61.1% women; aged 37 to 53 years) for alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and estimated NAFLD prevalence using the liver fat score (calculated using fasting insulin, fasting AST, the AST/ALT ratio, and presence of metabolic syndrome and type 2 diabetes). We used generalized linear and logistic models, pooled and stratified by sex, to estimate the difference-in-difference effect of Atole from conception to age two years on NAFLD. RESULTS: Median ALT and AST were 19.7 U/L (interquartile range, IQR: 14.1, 27.4) and 26.0 U/L (IQR: 21.4, 32.8), respectively. The median NAFLD liver fat score was 0.2 (IQR: −1.2, 1.6) in women and −1.2 (IQR: −2.2, 0.5) in men (P

Pregnant women less frequently receive COVID-19 vaccination and are at increased risk for adverse pregnancy outcomes from COVID-19.This study aimed to first, describe the vaccination status, treatment, and outcomes of hospitalized, symptomatic pregnant women with COVID-19, and second, estimate whether treatment differs by pregnancy status among treatment-eligible (ie, requiring supplemental oxygen per National Institutes of Health guidelines at the time of the study) women.From January to November 2021, the COVID-19-Associated Hospitalization Surveillance Network completed medical chart abstraction for a probability sample of 2715 hospitalized women aged 15 to 49 years with laboratory-confirmed SARS-CoV-2 infection. Of these, 1950 women had symptoms of COVID-19 on admission, and 336 were pregnant. We calculated weighted prevalence estimates of demographic and clinical characteristics, vaccination status, and outcomes among pregnant women with symptoms of COVID-19 on admission. We used propensity score matching to estimate prevalence ratios and 95% confidence intervals of treatment-eligible patients who received remdesivir or systemic steroids by pregnancy status.Among 336 hospitalized pregnant women with symptomatic COVID-19, 39.6% were non-Hispanic Black, 24.8% were Hispanic or Latino, and 61.9% were aged 25 to 34 years. Among those with known COVID-19 vaccination status, 92.9% were unvaccinated. One-third (32.7%) were treatment-eligible. Among treatment-eligible pregnant women, 74.1% received systemic steroids and 61.4% received remdesivir. Among those that were no longer pregnant at discharge (n=180), 5.4% had spontaneous abortions and 3.5% had stillbirths. Of the 159 live births, 29.0% were preterm. Among a propensity score-matched cohort of treatment-eligible hospitalized women of reproductive age, pregnant women were less likely than nonpregnant women to receive remdesivir (prevalence ratio, 0.82; 95% confidence interval, 0.69-0.97) and systemic steroids (prevalence ratio, 0.80; 95% confidence interval, 0.73-0.87).Most hospitalized pregnant patients with symptomatic COVID-19 were unvaccinated. Hospitalized pregnant patients were less likely to receive recommended remdesivir and systemic steroids compared with similar hospitalized nonpregnant women. Our results underscore the need to identify opportunities for improving COVID-19 vaccination, implementation of treatment of pregnant women, and the inclusion of pregnant women in clinical trials.

Background Priming for cardiometabolic diseases, including non-alcoholic fatty liver disease (NAFLD), is hypothesized to begin in utero. The primary objective of this study is to determine whether there is an association between maternal nutritional status and offspring NAFLD. Methods Data come from the Avon Longitudinal Study of Parents and Children (ALSPAC) in the UK. The analytic sample included 3353 participants who had maternal information on pre-pregnancy BMI, gestational weight gain, diabetes, and free sugar intake as percent of total energy and were assessed for mild-severe hepatic steatosis at 24 years by transient elastography (controlled attenuation parameter score ≥ 248 dB/m). Multiple logistic regression was used to evaluate the association between maternal factors and offspring hepatic steatosis at 24 years. Results In confounder-adjusted models the independent associations for each maternal factor with mild to severe vs low hepatic steatosis at 24 years were: pre-pregnancy overweight (OR: 1.84, 95%CL: 1.43–2.38) or obesity (OR: 2.73, 95%CL: 1.84–4.03), more than recommended gestational weight gain (OR: 1.30, 95%CL: 1.04–1.64), diabetes (OR: 1.39, 95%CI: 0.87, 2.21), and high free sugar intake during pregnancy (OR: 1.04, 95% CI: 0.82, 1.33). These associations were largely mediated by BMI at 24 years, but not by birthweight or breastfeeding. Conclusions Our results suggest that maternal nutritional status is associated with the development of NAFLD in their adult offspring, although the relationship is largely mediated by offspring BMI in adulthood.

BACKGROUND The importance of body fat distribution in the development of nonalcoholic fatty liver disease (NAFLD) is unclear. OBJECTIVE To examine whether total and truncal fat deposition patterns in childhood/adolescence are associated with NAFLD risk at 24 years. METHODS Data were from 1657 participants in the Avon Longitudinal Study of Parents and Children. Transient elastography was used to assess hepatic steatosis (low/moderate/severe) at 24 years and dual-energy X-ray absorptiometry was used to assess total body fat percent (TBF%) and trunk fat percent (TrF%) at 9, 13, 15, 17, and/or 24 years. Linear mixed models were constructed with quadratic age to examine trajectories of TBF% and TrF% by steatosis at 24 years, adjusting for confounders. RESULTS In both sexes, TBF% trajectories from 9 to 24 years followed a similar pattern based on steatosis group (P = .83 for boys and P = .14 for girls for age2 *steatosis fixed effect). However, at all ages TBF% was higher for moderate/severe vs low steatosis at 24 years (P

OBJECTIVES: Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of metabolic syndrome and is characterized by elevated levels of fat in the liver. NAFLD can begin in childhood, although the origins of the disease are not well characterized. Elevated alanine aminotransferase (ALT) is often used to screen for NAFLD. Our objectives are to 1) examine whether elevated ALT at 24 y is associated with hepatic steatosis and 2) describe whether ALT trends from 9 to 24 y differ by hepatic steatosis grade at 24 y. METHODS: We used data from a UK population-based birth cohort study (ALSPAC). Patients with 2 to 4 ALT measurements (at 9, 15, 17, 24 y) were included; pregnant women and high alcohol consumers were excluded. To assess hepatic steatosis, controlled attenuation parameter (CAP) scores from Fibroscan were measured at 24 y. We categorized CAP scores into steatosis grades [none (S0: 279 dB/m)]. We used a Pearson's chi-square test to determine whether elevated ALT at 24 y (>19 U/L in women, >30 U/L in men) was associated with steatosis grade. We used sex-stratified linear mixed models to assess trend differences of log-transformed ALT levels from 9 to 24 y between the different steatosis grades at 24 y. RESULTS: The final sample size was 1156 (41.4% male). At 24 y, among those with elevated ALT, 17.5% had severe steatosis (S3), while among those with normal ALT only 4.8% had S3 (P

Pediatric guidelines for the management of nonalcoholic fatty liver disease (NAFLD) recommend a healthy diet as treatment. Reduction of sugary foods and beverages is a plausible but unproven treatment.To determine the effects of a diet low in free sugars (those sugars added to foods and beverages and occurring naturally in fruit juices) in adolescent boys with NAFLD.An open-label, 8-week randomized clinical trial of adolescent boys aged 11 to 16 years with histologically diagnosed NAFLD and evidence of active disease (hepatic steatosis10% and alanine aminotransferase level ≥45 U/L) randomized 1:1 to an intervention diet group or usual diet group at 2 US academic clinical research centers from August 2015 to July 2017; final date of follow-up was September 2017.The intervention diet consisted of individualized menu planning and provision of study meals for the entire household to restrict free sugar intake to less than 3% of daily calories for 8 weeks. Twice-weekly telephone calls assessed diet adherence. Usual diet participants consumed their regular diet.The primary outcome was change in hepatic steatosis estimated by magnetic resonance imaging proton density fat fraction measurement between baseline and 8 weeks. The minimal clinically important difference was assumed to be 4%. There were 12 secondary outcomes, including change in alanine aminotransferase level and diet adherence.Forty adolescent boys were randomly assigned to either the intervention diet group or the usual diet group (20 per group; mean [SD] age, 13.0 [1.9] years; most were Hispanic [95%]) and all completed the trial. The mean decrease in hepatic steatosis from baseline to week 8 was significantly greater for the intervention diet group (25% to 17%) vs the usual diet group (21% to 20%) and the adjusted week 8 mean difference was -6.23% (95% CI, -9.45% to -3.02%; P .001). Of the 12 prespecified secondary outcomes, 7 were null and 5 were statistically significant including alanine aminotransferase level and diet adherence. The geometric mean decrease in alanine aminotransferase level from baseline to 8 weeks was significantly greater for the intervention diet group (103 U/L to 61 U/L) vs the usual diet group (82 U/L to 75 U/L) and the adjusted ratio of the geometric means at week 8 was 0.65 U/L (95% CI, 0.53 to 0.81 U/L; P .001). Adherence to the diet was high in the intervention diet group (18 of 20 reported intake of3% of calories from free sugar during the intervention). There were no adverse events related to participation in the study.In this study of adolescent boys with NAFLD, 8 weeks of provision of a diet low in free sugar content compared with usual diet resulted in significant improvement in hepatic steatosis. However, these findings should be considered preliminary and further research is required to assess long-term and clinical outcomes.ClinicalTrials.gov Identifier: NCT02513121.

The threshold for population-level optimal red blood cell (RBC) folate concentration among women of reproductive age for the prevention of neural tube defects has been estimated at 906 nmol/L; however, the dose-response relationship between folic acid intake and blood folate concentrations is uncharacterized. To estimate the magnitude of blood folate concentration increase in response to specific dosages of folic acid under steady-state conditions (as could be achieved with food fortification), a systematic review of the literature and meta-analysis was conducted. Of the 14,002 records we identified, 533 were selected for full-text review, and data were extracted from 108 articles. The steady-state concentrations (homeostasis) of both serum/plasma and RBC folate concentrations were estimated using a Bayesian meta-analytic approach and one-compartment physiologically-based pharmacokinetic models. RBC folate concentrations increased 1.78 fold (95% credible interval (CI): 1.66, 1.93) from baseline to steady-state at 375–570 µg folic acid/day, and it took a median of 36 weeks of folic acid intake (95% CI: 27, 52) to achieve steady-state RBC folate concentrations. Based on regression analysis, we estimate that serum/plasma folate concentrations increased 11.6% (95% CI: 8.4, 14.9) for every 100 µg/day folic acid intake. These results will help programs plan and monitor folic acid fortification programs.

The primary treatment for nonalcoholic fatty liver disease (NAFLD) in children is lifestyle change, including a healthier diet. However, there are no agreed upon expert recommendations for a specific diet in the prevention or treatment of NAFLD. In this study, we review studies published between 2015 and 2017 contributing to further understanding of the role of diet in the development and progression of NAFLD, particularly those addressing sugars and dietary patterns.Multiple recent studies have expanded on earlier evidence that suggests that high intake of sugars plays a causal role in the development of NAFLD, including several recent experimental studies in adults and children that support a unique effect of fructose consumption on liver fat accumulation. Evidence also points to protective effects of dietary patterns that include but are not limited to minimizing sugar intake, Dietary Approaches to Stop Hypertension (DASH), high protein and the Mediterranean diet. The effect of diet may act through its impact on the microbiome, and may be modified by presence or absence of genetic polymorphisms (nutrigenomics) and several new studies demonstrate this.Diet appears to be a powerful tool in the prevention and treatment of NAFLD. It is imperative that researchers and clinicians continue to hone in on the mechanistic pathways and specific diets to reverse the growing morbidity and mortality of NAFLD.

Background: Dietary guidelines recommend consumption of 1% or skim (i.e. non-fat) milk for children >2 years due to concerns about the role of saturated fat in raising low-density lipoprotein cholesterol (LDL) levels and cardiovascular disease risk. Low- or non-fat milk is also recommended to promote energy balance and reduce obesity risk. While more recent evidence in adults suggests no association between milkfat and cardiovascular disease risk, this association has not been well studied among children who tend to be the highest consumers of milk. No known studies have demonstrated an association between milkfat consumption and lipid levels in children. Our objective was to determine if there is an association between milk fat consumption and risk of dyslipidemia and obesity among U.S. children. Methods: We used cross-sectional data from children 2-19 years from the National Health and Nutrition Examination Survey (NHANES) 2011-2014 (n=7261). Usual milkfat intake (i.e. never/rare milk consumption, non-fat, 1%, 2%, or whole) was self-reported by parent or child. Lipid levels (12-19 years only) and adiposity (BMI z-score and weight category [underweight, normal, overweight, or obese] in all ages) were assessed by trained staff using standardized methods. Covariates included child age, sex, household income, race/ethnicity, physical activity, dieting, and total energy intake. We used multivariate linear and logistic regression models to examine the association between milkfat consumption and our outcomes and conducted pairwise comparisons to assess differences between different milkfat consumers. Results: Most children consumed 2% milk (42.3%), followed by whole (26.1%), 1% milk (11.7%), never/rare consumption (10.2%), and nonfat (9.7%). We found no significant trends in mean cholesterol (total, HDL, LDL) with consumption of milk with greater fat content. There was a significant trend towards higher triglycerides as milkfat intake increased (p=0.01) though this association was stronger among 2% milk compared to whole fat consumers. We found no significant trend in prevalence of each BMI category across milk fat intake. Pairwise comparisons demonstrated that usual consumption of 1% and 2% milkfat was associated with both higher BMI Z-score and odds of obesity compared to whole milk. Conclusion: We found no significant linear trend between usual %milk fat consumed and indicators of cardiovascular disease (BMI-Z and lipid levels) in children, except for triglycerides which rose as milkfat intake increased. However, triglycerides were higher among the 2% compared to whole milkfat consumers. Overall, whole milk was not associated with increased indicators of cardiovascular disease risk in children.

Each year around the world, it is estimated that 300,000 neonates are born with a neural tube defect. Many countries, however, are still lacking comprehensive birth defects surveillance registries. Comprehensive birth defects surveillance systems can help countries understand the magnitude and distribution of the problem. These systems can also provide information about biological, contextual, social and environmental determinants of birth defects. This information in turn can be used to identify effective and implementable solutions, and to evaluate prevention and management strategies to improve quality performance. This paper summarizes the development and implementation of an online pre-course training and in-person surveillance workshop conducted between 2014 December and 2015 March for representatives from six African countries. Feedback given by participants provided valuable lessons learned that can be applied to subsequent trainings and workshops.

BACKGROUND:Folate-sensitive neural tube defects (NTDs) are an important, preventable cause of morbidity and mortality worldwide. There is a need to describe the current global burden of NTDs and identify gaps in available NTD data. METHODS AND FINDINGS:We conducted a systematic review and searched multiple databases for NTD prevalence estimates and abstracted data from peer-reviewed literature, birth defects surveillance registries, and reports published between January 1990 and July 2014 that had greater than 5,000 births and were not solely based on mortality data. We classified countries according to World Health Organization (WHO) regions and World Bank income classifications. The initial search yielded 11,614 results; after systematic review we identified 160 full text manuscripts and reports that met the inclusion criteria. Data came from 75 countries. Coverage by WHO region varied in completeness (i.e., % of countries reporting) as follows: African (17%), Eastern Mediterranean (57%), European (49%), Americas (43%), South-East Asian (36%), and Western Pacific (33%). The reported NTD prevalence ranges and medians for each region were: African (5.2-75.4; 11.7 per 10,000 births), Eastern Mediterranean (2.1-124.1; 21.9 per 10,000 births), European (1.3-35.9; 9.0 per 10,000 births), Americas (3.3-27.9; 11.5 per 10,000 births), South-East Asian (1.9-66.2; 15.8 per 10,000 births), and Western Pacific (0.3-199.4; 6.9 per 10,000 births). The presence of a registry or surveillance system for NTDs increased with country income level: low income (0%), lower-middle income (25%), upper-middle income (70%), and high income (91%). CONCLUSIONS:Many WHO member states (120/194) did not have any data on NTD prevalence. Where data are collected, prevalence estimates vary widely. These findings highlight the need for greater NTD surveillance efforts, especially in lower-income countries. NTDs are an important public health problem that can be prevented with folic acid supplementation and fortification of staple foods.

Patient data from Maison de Naissance (MN), a rural maternity clinic in Haiti, were analyzed to determine the prevalence of pregnancy-related hypertensive disorders and the extent to which maternal weight and age are associated with these disorders in the MN population.A case-control study design was used with cases defined as pregnant women who were presented at MN with pregnancy-related hypertensive disorders (pregnancy-induced hypertension, pre-eclampsia or eclampsia) and controls defined as those women who delivered babies at MN and were not diagnosed with a pregnancy-related hypertensive disorder. The final cohort size was 622 controls and 67 cases. Odds ratios were calculated using multivariate logistic regression.The incidence of pre-eclampsia and eclampsia was 7.0%. Older maternal age at delivery (OR = 3.18; 95%CI: 1.31, 7.76) and higher maternal weight (OR = 3.24; 95%CI: 1.76, 5.98) measured during prenatal care were significantly associated with pregnancy-related hypertensive disorders. Prenatal care was not significantly associated with reduced risk of pre-eclampsia/eclampsia.The prevalence of pregnancy-related hypertensive disorders was high relative to rates in other developing countries. More is required to reduce the rate of pre-eclampsia perhaps by targeting older and women with high weight for preconception and more intensive prenatal care.