Trends in Food Habits and Their Relation to Socioeconomic Status among Nordic Adolescents 2001/2002-2009/2010

Background

In the Nordic countries, substantial policy and intervention efforts have been made to increase adolescents'' consumption of fruit and vegetables and to reduce their intake of sweets and soft drinks. Some initiatives have been formulated in a Nordic collaboration and implemented at national level. In recent years, social inequalities in food habits have been attracted particular governmental interest and several initiatives addressing the socioeconomic gradient in food habits have been highlighted. However, few internationally published studies have evaluated how trends in adolescents'' food habits develop in the context of Nordic nutrition policy, or have compared differences between the Nordic countries.

Methods

The study was based on Danish, Finnish, Norwegian and Swedish cross-sectional data from the international Health Behaviour in School-Aged Children (HBSC) study, collected via three nationally representative and comparable questionnaire surveys in 2001/2002, 2005/2006 and 2009/2010. Food habits were identified by students'' consumption of fruit, vegetables, sweets and sugar sweetened soft drink. Socioeconomic status (SES) was measured with the Family Affluence Scale (FAS). Multilevel logistic regression was used to analyze the data.

Results

Trends in fruit consumption developed differently across countries, characterized by an increase in Denmark and Norway and more stable trends in Sweden and Finland. Vegetable consumption increased particularly in Denmark and to a lesser extent in Norway, whereas Sweden and Finland displayed stable trends. Decreased trends were observed for sweet and soft drink consumption and were similar in Norway, Sweden and Finland. Sweet consumption decreased across all survey years, whereas soft drink consumption decreased between 2001/2002–2005/2006 and was stable thereafter. Denmark displayed an increase between 2001/2002–2005/2006 followed by a similar decrease between 2005/2006–2009/2010 for both sweet and soft drink consumption. Socioeconomic inequalities in fruit and vegetable consumption were observed in all countries, with no cross-country differences, and no changes over time. Small but not significant cross-country variation was identified for SES inequalities in sweet consumption. Reduced SES inequalities were observed in Sweden between 2005/2006 and 2009/2010. SES was not associated with soft drink consumption in this study population, with the exception of Denmark for the survey year 2009/2010.

Conclusion

Different trends resulted in increased country differences in food habits during the time of observations. In survey year 2009/2010, Danish students reported a higher intake of fruit and vegetable consumption than their counterparts in the other Nordic countries. Finnish students reported the lowest frequency of sweets and soft drink consumption. Despite the positive dietary trends documented in the present study, the majority of Nordic adolescents are far from meeting national dietary recommendations. Our findings underline the need for more comprehensive initiatives targeting young people''s food habits as well as a more deliberate and focused action to close gaps in social inequalities that affect food choices.     

Effects of High Intensity Interval Training and Strength Training on Metabolic,Cardiovascular and Hormonal Outcomes in Women with Polycystic Ovary Syndrome: A Pilot Study

Background

Polycystic ovary syndrome is a common endocrinopathy in reproductive-age women, and associates with insulin resistance. Exercise is advocated in this disorder, but little knowledge exists on the optimal exercise regimes. We assessed the effects of high intensity interval training and strength training on metabolic, cardiovascular, and hormonal outcomes in women with polycystic ovary syndrome.

Materials and Methods

Three-arm parallel randomized controlled trial. Thirty-one women with polycystic ovary syndrome (age 27.2 ± 5.5 years; body mass index 26.7 ± 6.0 kg/m²) were randomly assigned to high intensity interval training, strength training, or a control group. The exercise groups exercised three times weekly for 10 weeks.

Results

The main outcome measure was change in homeostatic assessment of insulin resistance (HOMA-IR). HOMA-IR improved significantly only after high intensity interval training, by -0.83 (95% confidence interval [CI], -1.45, -0.20), equal to 17%, with between-group difference (p = 0.014). After high intensity interval training, high-density lipoprotein cholesterol increased by 0.2 (95% CI, 0.02, 0.5) mmol/L, with between group difference (p = 0.04). Endothelial function, measured as flow-mediated dilatation of the brachial artery, increased significantly after high intensity interval training, by 2.0 (95% CI, 0.1, 4.0) %, between-group difference (p = 0.08). Fat percentage decreased significantly after both exercise regimes, without changes in body weight. After strength training, anti-Müllarian hormone was significantly reduced, by -14.8 (95% CI, -21.2, -8.4) pmol/L, between-group difference (p = 0.04). There were no significant changes in high-sensitivity C-reactive protein, adiponectin or leptin in any group.

Conclusions

High intensity interval training for ten weeks improved insulin resistance, without weight loss, in women with polycystic ovary syndrome. Body composition improved significantly after both strength training and high intensity interval training. This pilot study indicates that exercise training can improve the cardiometabolic profile in polycystic ovary syndrome in the absence of weight loss.

Trial Registration

ClinicalTrial.gov NCT01919281     

Stimulation of serglycin and CD44 mRNA expression in endothelial cells exposed to TNF-alpha and IL-1alpha.

Serglycin is a widely distributed proteoglycan, previously assumed to be hematopoietic cell specific. However, the results presented show that serglycin mRNA is expressed outside the hematopoietic cell system. High levels of serglycin mRNA were detected in endothelial cells and smooth muscle cells, whereas low levels were detected in skin fibroblasts. To further analyze the importance of serglycin in endothelial cells, the expression of serglycin mRNA was measured following activation of an endothelial cell line derived from human umbilical cord vein (HUV-EC-C), by the proinflammatory cytokines TNF-alpha and IL-1alpha. The level of serglycin mRNA increased in a time- and dose-dependent way. TNF-alpha (7 ng/ml) was the most potent inducer, increasing the level of serglycin mRNA 2.5 times after 24 h of stimulation. Serglycin has been shown to be a ligand for CD44, a membrane protein expressed in endothelial cells. Following stimulation of the endothelial cells, the level of CD44 mRNA also increased. Again, TNF-alpha (7 ng/ml) turned out to be the most potent inducer, increasing the level of CD44 mRNA 5.5 times after 24 h of stimulation. Both TNF-alpha and IL-1alpha stimulation of the endothelial cells resulted in an increase in the total incorporation of [(35)S]sulfate into macromolecules, which probably indicates an increase in the total production of proteoglycans. A stimulation of endothelial cells by proinflammatory agents resulted in an increase in both serglycin and CD44 mRNA expression, indicating that serglycin, as well as CD44, may participate in the inflammatory process of leukocyte migration.     

Characterization of mutants within the gene for the adenovirus E3 14.7-kilodalton protein which prevents cytolysis by tumor necrosis factor.

The 14,700-Da protein (14.7K protein) encoded by the E3 region of adenovirus has previously been shown to protect mouse cells from cytolysis by tumor necrosis factor (TNF). Delineating the sequences in the 14.7K protein that are required for this activity may provide insight into the mechanism of protection from TNF by 14.7K as well as the mechanism of TNF cytolysis. In the present study, we examined the ability of 14.7K mutants to protect cells from lysis by TNF. In-frame deletions as well as Cys-to-Ser mutations in the 14.7K gene were generated by site-directed mutagenesis and then built into the genome of a modified adenovirus type 5 (dl7001) that lacks all E3 genes. dl7001, which replicates to the same titers as does adenovirus type 5 in cultured cells, has the largest E3 deletion analyzed to date. 51Cr release was used to assay TNF cytolysis. Our results indicate that most mutations in the 14.7K gene result in a loss of function, suggesting that nearly the entire protein rather than a specific domain functions to prevent TNF cytolysis.     

You Wouldn’t Spawn in a Septic Tank, Would You?

Environmental effects of salmon farming are controversial issues. In Northern Norway, cod fishers argue that the location of salmon pens in fjords results in the cessation of local cod spawning. Research supporting or rejecting such statements is scant. There is an absence of both short-term and long-term studies on the effects that salmon farming may have on wild fish stocks. There are few studies of local ecosystem relationships in general. This article explores fishers’ arguments about the effects of salmon farming. It discusses methods of assessing the reliability and validity of fisher knowledge, and contributes to the discussion on assets and limitations of narrative data and experiential knowledge.     

Plasma appearance of unesterified astaxanthin geometrical E/Z and optical R/S isomers in men given single doses of a mixture of optical 3 and 3'R/S isomers of astaxanthin fatty acyl diesters

Appearance, pharmacokinetics and distribution of astaxanthin all-E-, 9Z- and 13Z-geometrical and (3R,3'R)-, (3R,3'S)- and (3S,3'S)-optical isomers in plasma fractions were studied in three middle-aged male volunteers (41-50 years) after ingestion of a single meal containing first a 10-mg dose equivalent of astaxanthin from astaxanthin diesters, followed by a dose of 100 mg astaxanthin equivalents after 4 weeks. Direct resolution of geometrical isomers and optical isomers of astaxanthin dicamphanates by HPLC after saponification showed that the astaxanthin consisted of 95.2% all-E-, 1.2% 9Z- and 3.6% 13Z-astaxanthin, of (3R,3'R)-, (3R,3'S; meso)- and (3S,3'S)-astaxanthin in a 31:49:20 ratio. The plasma astaxanthin concentration-time curves were measured during 76 h. Astaxanthin esters were not detected in plasma. Maximum levels of astaxanthin (C(max)=0.28+/-0.1 mg/l) were reached 11.5 h after administration and the plasma astaxanthin elimination half-life was 52+/-40 h. The C(max) at the low dose was 0.08 mg/l and showed that, the dose response was non-linear. The (3R,3'R)-astaxanthin optical isomer accumulated selectively in plasma compared to the (3R,3'S)- and (3S,3'S)-isomers, and comprised 54% of total astaxanthin in the blood and only 31% of total astaxanthin in the administered dose. The astaxanthin Z-isomers were absorbed selectively into plasma and comprised approximately 32% of total astaxanthin 6-7.5 h postprandially. The proportion of all-E-astaxanthin was significantly higher in the very low density lipoproteins and chylomicrons (VLDL/CM) plasma lipoprotein fraction than in the high density lipoproteins (HDL) and low denisty lipoproteins (LDL) fractions (P<0.05). The results indicate that a selective process increase the relative proportion of astaxanthin Z-isomers compared to the all-E-astaxanthin before uptake in blood and that the astaxanthin esters are hydrolyzed selectively during absorption.     

Notch1 Gene Mutations Target KRAS G12D-expressing CD8+ Cells and Contribute to Their Leukemogenic Transformation

Acute T-cell lymphoblastic leukemia/lymphoma (T-ALL) is an aggressive hematopoietic malignancy affecting both children and adults. Previous studies of T-ALL mouse models induced by different genetic mutations have provided highly diverse results on the issues of T-cell leukemia/lymphoma-initiating cells (T-LICs) and potential mechanisms contributing to T-LIC transformation. Here, we show that oncogenic Kras (Kras G12D) expressed from its endogenous locus is a potent inducer of T-ALL even in a less sensitized BALB/c background. Notch1 mutations, including exon 34 mutations and recently characterized type 1 and 2 deletions, are detected in 100% of Kras G12D-induced T-ALL tumors. Although these mutations are not detected at the pre-leukemia stage, incremental up-regulation of NOTCH1 surface expression is observed at the pre-leukemia and leukemia stages. As secondary genetic hits in the Kras G12D model, Notch1 mutations target CD8⁺ T-cells but not hematopoietic stem cells to further promote T-ALL progression. Pre-leukemia T-cells without detectable Notch1 mutations do not induce T-ALL in secondary recipient mice compared with T-ALL tumor cells with Notch1 mutations. We found huge variations in T-LIC frequency and immunophenotypes of cells enriched for T-LICs. Unlike Pten deficiency-induced T-ALL, oncogenic Kras-initiated T-ALL is not associated with up-regulation of the Wnt/β-catenin pathway. Our results suggest that up-regulation of NOTCH1 signaling, through either overexpression of surface NOTCH1 or acquired gain-of-function mutations, is involved in both T-ALL initiation and progression. Notch1 mutations and Kras G12D contribute cooperatively to leukemogenic transformation of normal T-cells.