Associations between vitamin D status in infants and blood lipids, body mass index and waist circumference.

AIM: To study the relationships between 25-hydroxyvitamin D status and blood lipids, insulin, glucose, body mass index and waist circumference in infants. METHODS: In a cross-sectional study, 255 infants aged 9 months with a blood sample for 25-hydroxyvitamin D were examined. Plasma 25-hydroxyvitamin D concentrations were analysed by chemiluminescent immunoassay. Associations between plasma 25-hydroxyvitamin D and high-density lipoprotein (HDL), low-density lipoprotein, total cholesterol, triglycerides, insulin, glucose, body mass index and waist circumference were analysed. RESULTS: Mean plasma 25-hydroxyvitamin D was 77.2 ± 22.7 nM. At the time of examination, 97% received vitamin D supplementation. 25-Hydroxyvitamin D was negatively associated with HDL (p = 0.003), cholesterol (p = 0.002) and triglycerides (p = 0.010) in multivariate analysis controlled for gender, season, body mass index, length, birth weight and breastfeeding. There were no associations between 25-hydroxyvitamin D and glucose or insulin (all p > 0.05). 25-hydroxyvitamin D was negatively associated with body mass index (p = 0.005) and waist circumference (p = 0.002) controlled for gender, season, breastfeeding, birth weight and length. CONCLUSION: Vitamin D status is negatively associated with blood lipids, body mass index and waist circumference in infants where nearly all received vitamin D supplements. Whether this has long-term health effects remains to be elucidated.

Vitamin D status in infants: relation to nutrition and season.

In a cross-sectional study, the primary objective was to assess the plasma concentration of 25-hydroxyvitamin D (25(OH)D) in healthy 9-month-old infants (n=255). The secondary objective was to evaluate nutritional variables and season in relation to 25(OH)D. The concentration of 25(OH)D was 77.2 ± 22.7 nmol/l (mean ± s.d.), ranging from 12 to 151 nmol/l. During the first 9 months, 97% received vitamin D supplementation (10 µg/day) and 89% had sufficient levels of 25(OH)D (50-250 nmol/l). In multiple regression analysis, controlled for body mass index (BMI) and intake of infant formula, a longer period of exclusive breastfeeding (P=0.026) and breastfeeding at 9 months (P=0.001) were both associated with lower levels. Dietary vitamin D intake was 4.4 ± 3.1 µg/day and in multiple regression analysis, controlled for BMI, intake of infant formula and mean energy intake, it was positively associated with 25(OH)D (P=0.001). There was a significant seasonal difference in 25(OH)D, with higher levels during summer-autumn compared with winter-spring (P=0.021) after control for BMI.

Cortical brain dysfunction in early schizophrenia: secondary pathogenetic hierarchy of neuroplasticity, psychopathology and social impairment.

Schizophrenia has the quality of a 'top-down' disorder with perturbation of self, and malattuned appraisal of basic experience of the outside world, and of intentionality. There is dissonance between the faculties of consciousness. The neuronal cortical network displays distributed activation of the sensory cortices during perception, and retroactivation during recall. This multimodal organization is sensitive to aberrations of structure and informational content during the metabolically dynamic phases of expansion and pruning in childhood and adolescence. There is substantial evidence of deviant function of the cortical network in schizophrenia. This includes increased neuronal density, reduced prefrontal capacity for activation, impaired fronto-temporal interaction during language production, defect monitoring of inner speech, activation of secondary sensory cortices during hallucinations, reduced cortical and thalamic volume, reduced thalamic activation (filtering) and sensitization of dopaminergic modulation. As a hypothesis the cortical defects lead to secondary causation of abnormalities at the levels of neuroplasticity, symptomatology and social competence. Suggestions for empirical testing are presented for the hypothesis that neocortical defects are primary, thalamic defects secondary and dopaminergic aberrations tertiary in the schizophrenic process. This testing of hypotheses involves prospective studies of patient groups at various ages of onset, as well as comparison of neurobiological measures in remitting vs. treatment-resistant cases.