Infant Sleep Predicts Attention Regulation and Behavior Problems at 3–4 Years of Age

This longitudinal study assessed the role of early sleep patterns in predicting attention regulation and behavior problems. Sleep of 43 infants was assessed using actigraphy at 12 months of age and then reassessed when the children were 3–4 years old. During this follow-up, their attention regulation and behavior problems were also assessed using a computerized test and parental reports. Lower quality of sleep in infancy significantly predicted compromised attention regulation and behavior problems. These findings underscore the need to identify and treat early sleep problems.     

Vitamin D, insulin secretion, sensitivity, and lipids: results from a case-control study and a randomized controlled trial using hyperglycemic clamp technique

OBJECTIVE

Vitamin D deficiency is associated with an unfavorable metabolic profile in observational studies. The intention was to compare insulin sensitivity (the primary end point) and secretion and lipids in subjects with low and high serum 25(OH)D (25-hydroxyvitamin D) levels and to assess the effect of vitamin D supplementation on the same outcomes among the participants with low serum 25(OH)D levels.

RESEARCH DESIGN AND METHODS

Participants were recruited from a population-based study (the Tromsø Study) based on their serum 25(OH)D measurements. A 3-h hyperglycemic clamp was performed, and the participants with low serum 25(OH)D levels were thereafter randomized to receive capsules of 20,000 IU vitamin D₃ or identical-looking placebo twice weekly for 6 months. A final hyperglycemic clamp was then performed.

RESULTS

The 52 participants with high serum 25(OH)D levels (85.6 ± 13.5 nmol/L [mean ± SD]) had significantly higher insulin sensitivity index (ISI) and lower HbA_1c and triglycerides (TGs) than the 108 participants with low serum 25(OH)D (40.3 ± 12.8 nmol/L), but the differences in ISI and TGs were not significant after adjustments. After supplementation, serum 25(OH)D was 142.7 ± 25.7 and 42.9 ± 17.3 nmol/L in 49 of 51 completing participants randomized to vitamin D and 45 of 53 randomized to placebo, respectively. At the end of the study, there were no statistically significant differences in the outcome variables between the two groups.

CONCLUSIONS

Vitamin D supplementation to apparently healthy subjects with insufficient serum 25(OH)D levels does not improve insulin sensitivity or secretion or serum lipid profile.Type 2 diabetes is a chronic condition associated with increased risk of micro- and macrovascular morbidity (1). The underlying pathophysiological mechanisms include insulin resistance combined with a relative deficit of insulin secretion from the pancreas, usually accompanied by systemic inflammation (2). The number of people suffering from the disease is increasing globally (2). Effective preventive means are therefore needed, and modifiable risk factors should be identified and explored.Vitamin D insufficiency, which is reported to be highly prevalent (3), might be such a factor. The vitamin D receptor (4) and the enzyme 1-α hydroxylase (5), which is necessary for the production of the active form of the hormone 1,25(OH)₂D (1,25-dihydroxyvitamin D), are present in pancreatic β-cells. Accordingly, vitamin D has been reported to increase glucose-mediated insulin secretion in animal studies (6). In vitro, 1,25(OH)₂D increases the expression of the insulin receptor and enhances insulin-mediated glucose transport (7). Although less explored, the anti-inflammatory effects of vitamin D might also affect diabetes development (8).Consistent with this, observational data from a number of epidemiological studies show an inverse association between serum 25(OH)D (25-hydroxyvitamin D) and glucose levels (9–12), insulin resistance (11–18), and prevalence of type 2 diabetes (18–20). However, to demonstrate a causal relation between vitamin D and glucose metabolism, evidence from randomized and adequately powered placebo-controlled intervention trials is needed. As recently reviewed, the studies published thus far are heterogeneous regarding dose and formulation of vitamin D treatment, duration, and inclusion criteria; most use indirect measures of insulin secretion and sensitivity; and the results are inconsistent (21).In the sixth Tromsø Study in 2008, serum 25(OH)D was measured in nearly 12,000 subjects. On the basis of these measurements, we invited subjects with low or high serum 25(OH)D levels to a follow-up study where insulin sensitivity and secretion were evaluated with the hyperglycemic clamp technique. Thereafter, the subjects with low serum 25(OH)D levels were invited to a 6-month intervention study to compare the effect of vitamin D₃ 20,000 IU twice per week with placebo on the same measures. As we previously have found cross-sectional and longitudinal associations between serum 25(OH)D levels and serum lipids (22), measurements of serum lipids were also included.     

Chemical genomic profiling for identifying intracellular targets of toxicants producing Parkinson's disease.

The yeast deletion collection includes approximately 4700 strains deleted for both copies of every nonessential gene. This collection is a powerful resource for identifying the cellular pathways that functionally interact with drugs. In the present study, the complete pool of approximately 4700 barcoded homozygous deletion strains of Saccharomyces cerevisiae were surveyed to identify genes/pathways interacting with 1-methyl-4-phenylpyridinium (MPP(+)) and N,N-dimethyl-4-4-bipiridinium (paraquat), neurotoxicants that can produce Parkinson's disease. Each yeast mutant is molecularly "barcoded" the collections can be grown competitively and ranked for sensitivity by microarray hybridization. Analysis data from these screens allowed us to determine that the multivesicular body pathway is an important element of toxicity induced by both MPP(+) and paraquat. When yeast genes that when deleted showed sensitivity to MPP(+) and paraquat toxicity were analyzed for their homology to human genes, 80% were found to have highly conserved human homologs (with e < 10(-8)). Future work will address if these human genes may also functionally interact with MPP(+) and paraquat toxicity.     

Consumption of fruits,vegetables and fruit juices and differentiated thyroid carcinoma risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) study

Fruit and vegetable (F&V) intake is considered as probably protective against overall cancer risk, but results in previous studies are not consistent for thyroid cancer (TC). The purpose of this study is to examine the association between the consumption of fruits, vegetables, fruit juices and differentiated thyroid cancer risk within the European Prospective Investigation into Cancer and Nutrition (EPIC) study. The EPIC study is a cohort including over half a million participants, recruited between 1991 and 2000. During a mean follow‐up of 14 years, 748 incident first primary differentiated TC cases were identified. F&V and fruit juice intakes were assessed through validated country‐specific dietary questionnaires. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox regression models adjusted for potential confounding factors. Comparing the highest versus lowest quartile of intake, differentiated TC risk was not associated with intakes of total F&V (HR: 0.89; 95% CI: 0.68–1.15; p‐trend = 0.44), vegetables (HR: 0.89; 95% CI: 0.69–1.14; p‐trend = 0.56), or fruit (HR: 1.00; 95% CI: 0.79–1.26; p‐trend = 0.64). No significant association was observed with any individual type of vegetable or fruit. However, there was a positive borderline trend with fruit juice intake (HR: 1.23; 95% CI: 0.98–1.53; p‐trend = 0.06). This study did not find any significant association between F&V intakes and differentiated TC risk; however a positive trend with fruit juice intake was observed, possibly related to its high sugar content.