Promotion of faster weight gain in infants born small for gestational age - Is there an adverse effect on later blood pressure?

Background - Being born small for gestational age is associated with later risk factors for cardiovascular disease, such as high blood pressure. Promotion of postnatal growth has been proposed to ameliorate these effects. There is evidence in animals and infants born prematurely, however, that promotion of growth by increased postnatal nutrition increases rather than decreases later cardiovascular risk. We report the long-term impact of growth promotion in term infants born small for gestational age ( birth weight < 10th percentile).Methods and Results - Blood pressure was measured at 6 to 8 years in 153 of 299 ( 51%) of a cohort of children born small for gestational age and randomly assigned at birth to receive either a standard or a nutrient-enriched formula. The enriched formula contained 28% more protein than standard formula and promoted weight gain. Diastolic and mean ( but not systolic) blood pressure was significantly lower in children assigned to standard compared with nutrient-enriched formula ( unadjusted mean difference for diastolic blood pressure, - 3.2 mm Hg; 95% CI, - 5.8 to - 0.5; P = 0.02) independent of potential confounding factors ( adjusted difference, - 3.5 mm Hg; P = 0.01). In observational analyses, faster weight gain in infancy was associated with higher later blood pressure.Conclusions - In the present randomized study targeted to investigate the effect of early nutrition on long-term cardiovascular health, we found that a nutrient-enriched diet increased later blood pressure. These findings support an adverse effect of relative "overnutrition" in infancy on long-term cardiovascular disease risk, have implications for the early origins of cardiovascular disease hypothesis, and do not support the promotion of faster weight gain in infants born small for gestational age

Association of Baseline Metabolomic Profiles With Incident Stroke and Dementia and With Imaging Markers of Cerebral Small Vessel Disease.

BACKGROUND AND OBJECTIVES: Cerebral small vessel disease is a major cause of stroke and dementia. Metabolomics can help identify novel risk factors to better understand pathogenesis and predict disease progression and severity. METHODS: We analysed baseline metabolomics profiles from 118,021 UK Biobank participants. We examined cross-sectional associations of 325 metabolites with MRI markers of small vessel disease, evaluated longitudinal associations with incident stroke and dementia, and ascertained causal relationships using Mendelian randomization. RESULTS: In cross-sectional analyses, lower levels of apolipoproteins, free cholesterol, cholesteryl esters, fatty acids, lipoprotein particle concentrations, phospholipids, and triglycerides were associated with increased white matter microstructural damage on diffusion tensor MRI. In longitudinal analyses, lipoprotein subclasses of very large HDL were associated with increased risk of stroke, and acetate and 3-hydroxybutyrate were associated with increased risk of dementia. Mendelian randomization analyses identified strong evidence supporting causal relationships for many findings. A few metabolites had consistent associations across multiple analysis types. Increased total lipids in very large HDL and increased HDL particle size were associated with increased white matter damage (Lower FA: OR: 1.44, 95% CI: 1.07-1.95, and OR: 1.19, 95% CI: 1.06-1.34, respectively; MD: OR: 1.49, 95% CI: 1.11-2.01, and OR: 1.24, 95% CI: 1.11-1.40, respectively) and increased risk of incident all stroke (HR: 4.04, 95% CI: 2.13-7.64, and HR: 1.54, 95% CI: 1.20-1.98, respectively) and ischaemic stroke (HR: 3.12, 95% CI: 1.53-6.38; HR: 1.37, 95% CI: 1.04-1.81). Valine was associated with decreased MD (OR: 0.51, 95% CI: 0.30-0.88) and had a protective association with all-cause dementia (HR: 0.008, 95% CI: 0.002-0.035). Cholesterol in small HDL had an inverse association with incident all stroke (HR: 0.17, 95% CI: 0.08-0.39) and ischaemic stroke (HR: 0.19, 95% CI: 0.08-0.46) that was supported by evidence of a causal association with MRI-confirmed lacunar stroke (OR: 0.96, 95% CI: 0.93-0.99). DISCUSSION: In this large-scale metabolomics study, we found multiple metabolites associated with stroke, dementia, and MRI markers of small vessel disease. Further studies may help inform development of personalised prediction models and provide insights into mechanistic pathways and future treatment approaches.This research was conducted using the UK Biobank under application number 36509. Funding was provided by the Cambridge British Heart Foundation Centre of Research Excellence (RE/18/1/34212) and a British Heart Foundation programme grant (RG/F/22/110052). Infrastructural support was provided by the Cambridge University Hospitals NIHR Biomedical Research Centre (BRC-1215-20014). ELH is funded by the Alzheimer’s Society (AS-RF-21-017). HSM is supported by a NIHR Senior Investigator Award. The views expressed in this publication are those of the authors and not necessarily those of the NIHR, NHS, or UK Department of Health and Social Care

A Case of Rapid Fading of Visual Function

Headache; Vomiting; Difficulty readingA 33-year old female with a 2-week history of episodic headache accompanied with vomiting. Previous history significant for malignant melanoma, excised from left thigh.VA: 20/20 OURapid blurring of stimuli in right hemi-fiel

A Spatial Working Memory Component to Visuospatial Neglect

In the hemispatial neglect syndrome, usually due to a right inferior parietal lesion, patients tend to only search the ipsilateral half of the visual scene. Several lines of research suggest that multiple components underlie the neglect syndrome but a common theme has been a bias of attention. In an experimental paradigm using a visual search task a single case study indicated impaired spatial working memory (SWM) across saccades contributing to abnormal search in neglect