Saska Tuomasjukka

Blackcurrant seed oil for prevention of atopic dermatitis in newborns: a randomized, double-blind, placebo-controlled trial.

Background The present increased incidence of atopic diseases has been associated with an altered intake of essential fatty acids (EFAs). The composition of blackcurrant seed oil (BCSO) corresponds to the recommended dietary intake of EFAs, and as a dietary supplement could, in small doses, modify the imbalance of EFAs in an efficient way.

Black currant seed oil supplementation of mothers enhances IFN-γ and suppresses IL-4 production in breast milk.

The first year of infancy is crucial for the development of atopic immune response. Inadequate early Th1 and Treg responses and increased production of Th2 cytokines are associated with atopy. Breast milk contains several immunomodulatory cytokines and other factors that might influence the maturation of the infants immune system. We assessed the cytokines in breast milk of mother of newborn infants and their associations with black currant seed oil (BCSO) supplementation during pregnancy, mothers atopic status and the development of infants atopic dermatitis.

Pro-inflammatory and Th2-type cytokine responses in PBMC in infants are associated with parental smoking

During infancy, a disturbed cytokine balance leads to an atopic immune response. Many risk factors have been associated with the development of atopy. These include parental smoking, elevated cord blood IgE, early exposure to pets and family history of atopy, but the knowledge of their impact on cytokine balance is limited.

The glycaemic response to rolled oat is not influenced by the fat content

Oat is promoted as a low-glycaemic index food. Our aim was to measure the effect of the fat content of oat in glycaemia and insulinaemia and compare it with the effect of wheat. The study design was a double-blind, randomised cross-over study with four treatment segments. Eight healthy males attended four study sessions in which porridge made from four different raw materials was consumed: rolled oat (O), defatted rolled oat (DO), rolled whole wheat (W) or rolled whole wheat with added oat fat (WF). Available carbohydrate content was analysed enzymatically, and was adjusted to 50 g in each test meal. Fat content per meal was either 6.1 g (O, WF) or approximately 1.9 g (W, DO). Venous plasma glucose, insulin and triacylglycerol concentrations were measured at 0, 30, 60, 90, 120 and 180 min. All products caused a rapid increase in glucose with a peak at 30 min, where W and WF were significantly higher than O (0 = 0.006). Also insulin peaked at 30 min (no differences). A 4.2 g difference in fat content between O and DO or W and WF did not result in any significant differences in their glycaemia or insulinaemia. W and O did not differ in their overall glycaemic or insulinaemic responses. The removal of two-thirds of oat fat did not affect the postprandial plasma triacylglycerol concentration. The present study shows that neither the glycaemic nor the insulinaemic response to rolled oat is affected by the fat content, and that rolled wheat differed from rolled oat in terms of peak glucose concentration only.

Regio-distribution of stearic acid is not conserved in chylomicrons after ingestion of randomised, stearic acid-rich fat in a single meal.

Stearic acid from conventional food is well absorbed, but the fate of synthetic randomized stearic acid in fat absorption and subsequent metabolism is unclear. In this study, we examined the postprandial triglyceridemia following an ingestion of randomized stearic acid-rich fat. Following a 12-h fast, nine healthy young males ate a hamburger meal with 16.7 g of stearic acid (30% in triacylglycerol (TAG) sn-2 position, fully randomized). Postprandial blood samples were collected for 450 min, and the stearic acid content in chylomicron (CM, Svedberg flotation rate >400) TAG and the proportion of stearic acid in the sn-2 position were measured by tandem mass spectrometry at peak (180 min) and late (360 min) triglyceridemia. Of all stearic acid in CM TAG, 23% and 22% were in the sn-2 position at peak and late triglyceridemia (P<.004 and P<.001, respectively). This suggests a 68% and 62% conservation of sn-2 stearic acid, respectively. Peak postprandial TAG concentration and incremental area under the TAG curve showed a higher correlation with the fasting CM TAG (r=0.88, P<.01 and r=0.72, P<.05, respectively) than with total fasting plasma TAG (r=0.73, P<.05 and r=0.24, nonsignificant, respectively). In an earlier study, we showed that the absorption efficiency of the stearic acid of the meal was normal, with only marginal amounts of mainly sn-1,3 stearic acid found in the feces. In conclusion, we showed that sn-2 stearic acid is underrepresented in the postprandial CM TAG following an ingestion of fully randomized fat.