Daily skin-to-skin contact in full-term infants and breastfeeding: Secondary outcomes from a randomized controlled trial

This randomized controlled trial evaluated the effect of a 5-week daily skin-to-skin contact (SSC) intervention between mothers and their full-term infants, compared with care-as-usual, on exclusive and continued breastfeeding duration during the first post-natal year. Healthy pregnant women (n = 116) from a community sample were enrolled and randomly allocated to the SSC or care-as-usual condition. SSC mothers were requested to provide one daily hour of SSC for the first five post-natal weeks. Twelve months post-partum, mothers indicated the number of exclusive and continued breastfeeding months. Multiple regression analyses were conducted using intention-to-treat, per-protocol and exploratory dose–response frameworks. In intention-to-treat analyses, exclusive and continued breastfeeding duration was not different between groups (exclusive: 3.61 ± 1.99 vs. 3.16 ± 1.77 months; adjusted mean difference 0.28, 95% confidence interval [CI] ?0.33 to 0.89; p = 0.36; continued: 7.98 ± 4.20 vs. 6.75 ± 4.06 months; adjusted mean difference 0.81, 95% CI ?0.46 to 2.08; p = 0.21). In per-protocol analyses, exclusive and continued breastfeeding duration was longer for SSC than care-as-usual dyads (exclusive: 4.89 ± 1.26 vs. 3.25 ± 1.80 months; adjusted mean difference 1.28, 95% CI 0.31–2.24; p = 0.01; continued: 10.81 ± 1.97 vs. 6.98 ± 4.08 months; adjusted mean difference 2.33, 95% CI 0.13–4.54; p = 0.04). Exploratory dose–response effects indicated that more SSC hours predicted longer exclusive and continued breastfeeding duration. This study demonstrates that for the total group, the 5-week daily SSC intervention did not extend exclusive and continued breastfeeding duration. However, for mothers performing a regular daily hour of SSC, this simple and accessible intervention may extend exclusive and continued breastfeeding duration by months. Future studies are required to confirm these promising findings. Trial registration: Netherlands Trial Register (NTR5697).     

Chemotherapy-induced neurotoxicity: the value of neuroprotective strategies

Chemotherapy-induced peripheral neuropathy (CIPN) is a common major dose-limiting side effect of many chemotherapeutic agents, including platinum compounds, taxanes, vinca alkaloids, thalidomide and newer agents such as bortezomib. The incidence and degree of neuropathy depends on the type of cytotoxic drug, the duration of administration, cumulative dose and pre-existing peripheral neuropathy. Because of increasing survival rates of patients treated with neurotoxic agents, CIPN is accompanied by a significant decrease in the patient's quality of life among cancer survivors. Therefore, several neuroprotective strategies, including calcium/magnesium infusion, amifostine, gluthatione, glutamine, acetyl-L-carnitine and erythropoietin as most promising, have been investigated to decrease the neurotoxicity without compromising anti-tumour efficacy. However, clinical evidence for the efficacy of these drugs is sparse. In this review we will give an outline of the neurotoxic effects of chemotherapeutic agents, their clinical manifestations and potential neuroprotective strategies.     

Mechanisms underlying the effects of prenatal psychosocial stress on child outcomes: beyond the HPA axis

Accumulating evidence from preclinical and clinical studies indicates that maternal psychosocial stress and anxiety during pregnancy adversely affect child outcomes. However, knowledge on the possible mechanisms underlying these relations is limited. In the present paper, we review the most often proposed mechanism, namely that involving the HPA axis and cortisol, as well as other less well-studied but possibly relevant and complementary mechanisms. We present evidence for a role of the following mechanisms: compromised placental functioning, including the 11β-HSD2 enzyme, increased catecholamines, compromised maternal immune system and intestinal microbiota, and altered health behaviors including eating, sleep, and exercise. The roles of (epi)genetics, the postnatal environment and the fetus are also discussed. We conclude that maternal prenatal psychosocial stress is a complex phenomenon that affects maternal emotions, behavior and physiology in many ways, and may influence the physiology and functioning of the fetus through a network of different pathways. The review concludes with recommendations for future research that helps our understanding of the mechanisms by which maternal prenatal stress exerts its effect on the fetus.     

Chemotherapy-induced peripheral neuropathy and its association with quality of life: a systematic review

Background

The objective of this study was to systematically review all available literature concerning chemotherapy-induced peripheral neuropathy (CIPN) and quality of life (QOL) among cancer patients.

Methods

A computerized search of the literature was performed in December 2013. Articles were included if they investigated CIPN and QOL among cancer patients. Twenty-five articles were selected and were subjected to a 13-item quality checklist independently by two investigators.

Results

The methodological quality of the majority of the selected studies was adequate to high. The included studies differed tremendously with respect to study design (19 prospective studies, 5 cross-sectional, 1 both cross-sectional and prospective), patient population (lung, colorectal, ovarian, endometrial, cervical or breast cancer, lymphoma, acute lymphoblastic leukemia, or a mixed population), number of included patients (ranging from 14 to 1643), and ways to assess CIPN (objectively, subjectively, or both). Of the 25 included studies, 11 assessed the association of CIPN on patients’ QOL. While three of these studies did not find an association between CIPN and QOL, the others concluded that more CIPN was associated with a lower QOL.

Implications for cancer survivors

Although the included studies in this systematic review were very diverse, which impedes drawing firm conclusions on this topic, CIPN is likely to have a negative association with QOL. The variety of the studied patient populations and chemotherapeutic agents in the existing studies calls for further studies on this topic. These studies are preferably prospective in nature, include a large number of patients, and assess QOL and CIPN with validated questionnaires.     

Parent–Infant Attachment Insecurity and Emotional Eating in Adolescence: Mediation through Emotion Suppression and Alexithymia

Emotional eating (EE), the propensity to eat in response to emotions, is thought to have its origins in the early parent–infant relationship. This study tested the hypothesis that infant attachment insecurity results in EE in adolescence through the increased use of the emotion regulation strategy suppression of emotions and subsequent alexithymia. At the age of 15 months, parent–infant attachment security (n = 129) was observed with two abbreviated attachment measures: the shortened strange situation procedure (SSSP), and the shortened attachment Q-set (S-AQS). At the age of 12 years, children completed self-report questionnaires to assess the suppression of emotions, alexithymia, and EE. At the age of 16 years, EE was measured again. The mediation models indicated that lower parent–infant attachment security predicted increased use of suppression of emotions, which was related to increased alexithymia, and in turn more EE at the age of 12 years. These results were similar and significant for both attachment measures, and also (marginal) significant with EE at the age of 16 years as an outcome. Lastly, when parental caregiving quality was included, the models with the SSSP as predictor remained significant, but the models with the S-AQS became insignificant. These results indicated that to a certain extent, infant attachment security could predict adolescent EE above and beyond parental caregiving quality.     

Normal Weight but Low Muscle Mass and Abdominally Obese: Implications for the Cardiometabolic Risk Profile in Chronic Obstructive Pulmonary Disease

Background

It is well established that low muscle mass affects physical performance in chronic obstructive pulmonary disease (COPD). We hypothesize that combined low muscle mass and abdominal obesity may also adversely influence the cardiometabolic risk profile in COPD, even in those with normal weight. The cardiometabolic risk profile and the responsiveness to 4 months high-intensity exercise training was assessed in normal-weight patients with COPD with low muscle mass stratified by abdominal obesity.

Hepatocyte nuclear factor (HNF)1A and HNF4A substitution occurring simultaneously in a family with maturity‐onset diabetes of the young

Introduction Maturity‐onset diabetes of the young (MODY) is a monogenic form of diabetes mellitus characterized by an early age at onset, autosomal dominant inheritance and a primary defect in the function of the B‐cells of the pancreas. We report a family with two members carrying a substitution in both the hepatocyte nuclear factor (HNF)1A and HNF4A gene simultaneously. Case report A 39‐year‐old man was referred because of mild diabetic retinopathy. Because of a dominant presentation of diabetes in his family, genetic testing was performed. Sequence analysis of the genes involved in MODY‐1–3 revealed the presence of an amino acid substitution in the HNF1A as well as the HNF4A gene. Both substitutions were also detected in his mother. The HNF1A substitution has been described previously as pathogenic, whereas the HNF4A substitution had not been found previously. The HNF4A substitution was located in a conserved region of the protein and, additionally, the proband and his mother had high birthweights and low triglyceride levels, both of which are associated with pathogenic HNF4A substitutions. Conclusions To our knowledge this is the first reported family carrying both a substitution of HNF1A and HNF4A gene simultaneously. The exact contribution of each substitution to the phenotype of our subjects remains to be further elucidated, however, given the high birthweights and the low triglyceride levels in those with both substitutions, it is reasonable that the HNF4A substitution is pathogenic.     

Microalbuminuria and Cardiovascular Autonomic Dysfunction Are Independently Associated With Cardiovascular Mortality: Evidence for Distinct Pathways: The Hoorn Study

OBJECTIVE

Microalbuminuria is associated with cardiovascular mortality, particularly among individuals with type 2 diabetes, but the mechanisms underlying this association are not completely understood. Microalbuminuria is known to be associated with cardiovascular autonomic dysfunction (C-AD), and C-AD in turn is associated with cardiovascular mortality. The purpose of this study, therefore, was to investigate whether C-AD can explain the relationship between microalbuminuria and cardiovascular mortality.

RESEARCH DESIGN AND METHODS

We studied 490 individuals from a population-based cohort of individuals aged 50–75 years who were followed for a median period of 13.6 years. Microalbuminuria was defined as an albumin-to-creatinine ratio ≥2.0 mg/mmol in an early-morning spot-urine sample. Ten parameters reflecting different aspects of cardiovascular autonomic function were measured and compiled into a total score of C-AD (mean of separate z scores). The association between C-AD and microalbuminuria was estimated by multiple linear regression, and relative risks (RRs) for cardiovascular mortality were estimated by Cox proportional hazards analyses.

RESULTS

After adjustments for age, sex, glucose tolerance status, and other risk factors, C-AD was associated with microalbuminuria (β = 0.16 [95% CI 0.01–0.33]), and both microalbuminuria (RR 2.09 [1.07–4.08]) and C-AD (1.74 [1.04–2.89]) were associated with cardiovascular mortality. These associations did not change after further mutual adjustment for C-AD (2.13 [1.09–4.17]) or microalbuminuria (1.76 [1.05–2.94]), respectively.

CONCLUSIONS

Both microalbuminuria and C-AD are independently associated with cardiovascular mortality, and the excess mortality attributable to microalbuminuria cannot be explained by C-AD.Microalbuminuria is associated with an increased risk of cardiovascular disease and mortality (1). This association is independent of other known cardiovascular risk factors such as hypertension, dyslipidemia, obesity, smoking, and impaired renal function (1,2). Several mechanisms, notably endothelial dysfunction and low-grade inflammation, have been proposed to explain, at least in part, the increased risk of cardiovascular mortality in individuals with microalbuminuria (3). Cardiovascular autonomic dysfunction (C-AD) could potentially constitute another such mechanism.Indeed, we as well as others have previously shown that C-AD is associated with microalbuminuria, especially in individuals with impaired glucose metabolism (IGM) and type 2 diabetes (4–6). Two proposed mechanisms explaining this association are, first, a disturbance in glomerular arteriolar autoregulation, which in turn may result in an inability to counteract glomerular hypertension (7), and, second, a reduced drop in nightly blood pressure due to C-AD, both of which may result in microalbuminuria (8). In addition, C-AD is associated with cardiovascular mortality (9,10) and can potentially link microalbuminuria to cardiovascular mortality by arrhythmogenic or atherogenic effects, for example, by promoting vascular calcification and arterial stiffness (11).In view of these considerations, we investigated, in a prospective cohort study, whether C-AD can explain the relationship between microalbuminuria and cardiovascular mortality or, alternatively, whether both microalbuminuria and C-AD are independently associated with cardiovascular mortality. These hypotheses have never been investigated in the general population and could have clinical relevance because the first hypothesis suggests that C-AD should be targeted to decrease mortality risk in individuals with microalbuminuria and, conversely, the second hypothesis suggests that both microalbuminuria and C-AD can be used for estimating the risk of cardiovascular mortality.