Low-carbohydrate diets for gestational diabetes

Nutrition therapy provides the foundation for treatment of gestational diabetes (GDM), and has historically been based on restricting carbohydrate (CHO) intake. In this paper, randomized controlled trials (RCTs) are reviewed to assess the effects of both low- and higher CHO nutrition approaches in GDM. The prevailing pattern across the evidence underscores that although CHO restriction improves glycemia at least in the short-term, similar outcomes could be achievable using less restrictive approaches that may not exacerbate IR. The quality of existing studies is limited, in part due to dietary non-adherence and confounding effects of treatment with insulin or oral medication. Recent evidence suggests that modified nutritional manipulation in GDM from usual intake, including but not limited to CHO restriction, improves maternal glucose and lowers infant birthweight. This creates a platform for future studies to further clarify the impact of multiple nutritional patterns in GDM on both maternal and infant outcomes

Barriers to and solutions for representative inclusion across the lifespan and in life course research: The need for structural competency highlighted by the COVID-19 pandemic

Exclusion of special populations (older adults; pregnant women, children, and adolescents; individuals of lower socioeconomic status and/or who live in rural communities; people from racial and ethnic minority groups; individuals from sexual or gender minority groups; and individuals with disabilities) in research is a pervasive problem, despite efforts and policy changes by the National Institutes of Health and other organizations. These populations are adversely impacted by social determinants of health (SDOH) that reduce access and ability to participate in biomedical research. In March 2020, the Northwestern University Clinical and Translational Sciences Institute hosted the Lifespan and Life Course Research: integrating strategies Un-Meeting to discuss barriers and solutions to underrepresentation of special populations in biomedical research. The COVID-19 pandemic highlighted how exclusion of representative populations in research can increase health inequities. We applied findings of this meeting to perform a literature review of barriers and solutions to recruitment and retention of representative populations in research and to discuss how findings are important to research conducted during the ongoing COVID-19 pandemic. We highlight the role of SDOH, review barriers and solutions to underrepresentation, and discuss the importance of a structural competency framework to improve research participation and retention among special populations

Circulating Soluble RAGE Isoforms are Attenuated in Obese, Impaired Glucose Tolerant Individuals and are Associated with the Development of Type 2 Diabetes

The soluble receptor for advanced glycation end products (sRAGE) may be protective against inflammation associated with obesity and type 2 diabetes (T2DM). The aim of this study was to determine the distribution of sRAGE isoforms and whether sRAGE isoforms are associated with risk of T2DM development in subjects spanning the glucose tolerance continuum. In this retrospective analysis, circulating total sRAGE and endogenous secretory RAGE (esRAGE) were quantified via ELISA, and cleaved RAGE (cRAGE) was calculated in 274 individuals stratified by glucose tolerance status (GTS) and obesity. Group differences were probed by ANOVA, and multivariate ordinal logistic regression was used to test the association between sRAGE isoform concentrations and the proportional odds of developing diabetes, vs. normal glucose tolerance (NGT) or impaired glucose tolerance (IGT). When stratified by GTS, total sRAGE, cRAGE, and esRAGE were all lower with IGT and T2DM, while the ratio of cRAGE to esRAGE (cRAGE:esRAGE) was only lower ( P &lt; 0.01) with T2DM compared with NGT. When stratified by GTS and obesity, cRAGE:esRAGE was higher with obesity and lower with IGT ( P &lt; 0.0001) compared with lean, NGT. In ordinal logistic regression models, greater total sRAGE (odds ratio, 0.91; P &lt; 0.01) and cRAGE (odds ratio, 0.84; P &lt; 0.01) were associated with lower proportional odds of developing T2DM. Reduced values of sRAGE isoforms observed with both obesity and IGT are independently associated with greater proportional odds of developing T2DM. The mechanisms by which each respective isoform contributes to obesity and insulin resistance may reveal novel treatment strategies for diabetes. </jats:p

Low-Carbohydrate Diets for Gestational Diabetes

Nutrition therapy provides the foundation for treatment of gestational diabetes (GDM), and has historically been based on restricting carbohydrate (CHO) intake. In this paper, randomized controlled trials (RCTs) are reviewed to assess the effects of both low- and higher CHO nutrition approaches in GDM. The prevailing pattern across the evidence underscores that although CHO restriction improves glycemia at least in the short-term, similar outcomes could be achievable using less restrictive approaches that may not exacerbate IR. The quality of existing studies is limited, in part due to dietary non-adherence and confounding effects of treatment with insulin or oral medication. Recent evidence suggests that modified nutritional manipulation in GDM from usual intake, including but not limited to CHO restriction, improves maternal glucose and lowers infant birthweight. This creates a platform for future studies to further clarify the impact of multiple nutritional patterns in GDM on both maternal and infant outcomes

Sleep, Glucose Variability, CVD Risk & CV Stress in Young Adults with T1DM

Poor glucose control is believed to contribute importantly to cardiovascular disease (CVD) – a leading complication and cause of death in people with Type I Diabetes Mellitus (T1DM). Good sleep also has been shown to play an important role in maintaining cardiovascular and metabolic health, and sleep quality is reduced in people with T1DM. To test the hypotheses that glucose variations are causally related to sleep disruption and that sleep disruption mediates inflammation and CVD risk in individuals with T1DM, two aims were proposed: 1) to quantify sleep disturbances and to determine their relationship to glucose variability and 2) to define the relationship between sleep disruption and markers of CVD risk in young adults with T1DM. 30 young adults, age 18-30, were enrolled. Subjects wore a continuous glucose monitoring system and a sleep/activity monitor in home for three days and two nights and underwent polysomnography (PSG) in the laboratory on the third night. The amount of power in five electroencephalogram (EEG) Bands – Delta and Theta (characteristic of sleep); Alpha, Beta and Gamma (characteristic of wakefulness) – was tracked throughout the PSG study night. Wavelet coherence analysis revealed a strong but time-varying and frequency specific coupling between glucose and sleep measured by both actigraphy and PSG. Evidence for a causal relationship between glucose and brain activity was provided by Granger causality analysis. Increasing glucose caused increasing Alpha and decreasing Theta and Delta power, suggesting that glucose changes disturb sleep by causing arousal or awakening. Increases in Beta and Delta power consistently caused increasing glucose levels while increasing Theta power caused decreasing glucose. These findings support a bi-directional relationship between glucose and brain activity during sleep. Further, findings supported that both sleep disruption and poor glycemic control mediate increased inflammatory processes in T1DM. Tumor Necrosis Factor-α increased during the sleep period. Only subjects with good glycemic control exhibited a normal pattern of decreased IL-6 upon awakening. Findings from this study demonstrate a bi-directional relationship between sleep and glucose changes, and that both sleep disruption and glycemic control may play important roles in mediating levels of inflammation, which are associated with CVD development in T1DM

Sleep-disordered breathing in pregnancy: A developmental origin of offspring obesity?

Sleep-disordered breathing (SDB) worsens over pregnancy, and obstructive sleep apnea is associated with serious maternal complications. Intrauterine exposures that provoke insulin resistance (IR), inflammation, or oxidative stress may have long-term offspring health consequences. In obesity, worsening maternal SDB appears to be an exposure that increases the risk for both small- or large-for-gestational-age (SGA, LGA, respectively), suggesting distinct outcomes linked to a common maternal phenotype. The aim of this paper is to systematically review and link data from both mechanistic rodent models and descriptive human studies to characterize the impact of maternal SDB on fetal development. A systematic review of the literature was conducted using PubMed, Embase, and CINAHL (01/2000-09/2019). Data from rodent (9 studies) and human models (48 studies, 5 meta-analyses) were included and reviewed using PRISMA guidelines. Evidence from rodent models suggests that intermittent maternal hypoxia results in mixed changes in birth weight (BW) followed by accelerated postnatal growth, while maternal sleep fragmentation results in normal BW followed by later metabolic derangement. Human studies support that maternal SDB is associated with both SGA and LGA, both of which may predispose offspring to later obesity. Evidence also suggests a link between SDB, inflammation, and oxidative stress that may impact maternal metabolism and/or placental function. SDB is common in pregnancy and affects fetal growth and development. Given that SDB has significant potential to adversely influence the intrauterine metabolic environment, larger, prospective studies in humans are urgently needed to fully elucidate the effects of this exposure on offspring metabolic risk

Sleep, Stress, and Cardiometabolic Health in Women of Childbearing Age with Overweight and Obesity

Background: Sleep is important for health, but its relationship to cardiometabolic health in women of childbearing age remains unclear. Furthermore, stress, unmet basic needs, and lack of physical activity may be related to disrupted sleep and poor cardiometabolic health in women of childbearing age and these relationships may differ by ethnicity. The purposes of this study were to investigate the relationship between sleep, markers of cardiometabolic health, stress, unmet basic needs, and physical activity in women of childbearing age with overweight or obesity and identify if these relationships differed between women that identified as Latino/Hispanic and non-Latino/Hispanic ethnicity. Methods: A secondary cross-sectional analysis was conducted using baseline data from a trial that embeds healthy eating and activity into a national home visiting program, Parents as Teachers. The sample was stratified based on self-reported ethnicity (Hispanic/Latino or non-Hispanic/Latino). Pearson's and Spearman's correlations were used to determine bivariate relationships among sleep, cardiometabolic variables, stress, unmet basic needs, and physical activity. Results: Two hundred seventy-six women, 46% of whom identified as Hispanic/Latino, were included in the analysis. Body mass index (BMI) was significantly correlated with sleep disturbance (??=?0.23, p?=?0.01) in women who identify as Hispanic/Latino. Stress was positively related to sleep disturbance, sleep duration, and unmet needs for both groups of women. BMI was correlated with unmet basic needs in women who identified as non-Hispanic/Latino (??=?0.25, p?=?0.01). Conclusions: Our results suggest that sleep, stress, and basic needs are important in understanding cardiometabolic health in women of childbearing age and these relationships differ depending on ethnicity. Clinical Trial Registration Number: NCT03758638

Effects of acute aerobic exercise on circulating sTLR and sRAGE profiles in normal‐ and abnormal‐glucose‐tolerant individuals

Abstract BMI‐matched normal‐ (NGT, n = 10, 41 ± 4y, 35.6 ± 3.0 kg/m2) and abnormal‐glucose‐tolerant (AGT, n = 16, 51 ± 3y, 34.3 ± 1.5 kg/m2) participants were evaluated for body composition, metabolic health (oral glucose tolerance test [OGTT]), and VO2max. Participants also completed a treadmill walking test at 65% VO2max for 30 min. Total sRAGE, esRAGE, sTLR2, and sTLR4 were assessed via ELISA, and cRAGE was calculated. AGT exhibited greater (p  0.05) following AE. sTLR4 tended to be 36% lower in AGT than NGT (main effect, p = 0.096) and did not change following AE (p > 0.05). Total sRAGE and isoforms were similar (p > 0.05) between groups and did not change following AE (p > 0.05). sTLR2 was correlated with (p < 0.05) basal BG (r = −0.505) and OGTT AUC (r = −0.687). sTLR4 was correlated with basal BG (p < 0.10, r = −0.374) and OGTT AUC (p < 0.05, r = −0.402). Linear regressions were predictive of sTLRs in the basal state (sTLR2: R2 = 0.641, p = 0.01; sTLR4: R2 = 0.566, p = 0.037) and after acute exercise state (sTLR2: R2 = 0.681, p = 0.004, sTLR4: R2 = 0.568, p = 0.036).These findings show circulating sTLR profiles are disrupted in AGT and acute AE minimally modulates their levels