Dietary patterns and the risk of pregnancy-associated hypertension in the Danish National Birth Cohort: a prospective longitudinal study.

OBJECTIVE: To examine the association between mid-pregnancy dietary patterns and pregnancy-associated hypertension (PAH). DESIGN: A prospective longitudinal cohort study. SETTING: Denmark. POPULATION: About 55 139 Danish women with single enrolments and recorded food frequency questionnaire dates with complete information on dietary intake. METHODS: Women were eligible if they could speak Danish and were planning to carry to term. Diet was assessed using a validated semi-quantitative 360-item food frequency questionnaire and dietary patterns were derived using factor analysis. MAIN OUTCOME MEASURES: Gestational hypertension (GH) and pre-eclampsia (PE). RESULTS: Disease prevalence was 14% for GH (5491/39 362); 2% for PE (1168/54 778), and 0.4% for severe PE (234/55 086). Seven dietary patterns were characterised in the population, of which two were associated with PAH. The Seafood diet characterised by high consumption of fish and vegetables was inversely associated with the odds of developing GH [odds ratio (OR) 0.86; 95% CI 0.77-0.95)] and PE (OR 0.79; 95% CI 0.65-0.97). The Western diet characterised by high consumption of potatoes (including French fries), mixed meat, margarine and white bread increased the odds of developing GH (OR 1.18; 95% CI 1.05-1.33) and PE (OR 1.40; 95% CI 1.11-1.76). No association was seen with severe PE. CONCLUSIONS: We found protective associations of Seafood diet and harmful associations of Western diet with PAH. Dietary interventions encouraging the reduction of Western diet may contribute to a decrease of PAH. TWEETABLE ABSTRACT: Western diet increases (Seafood diet decreases) the likelihood of developing pre-eclampsia among Danish pregnant women.

Faster increase in body mass index between ages 8 and 13 is associated with risk factors for cardiovascular morbidity and mortality.

BACKGROUND AND AIMS: Excess childhood weight is associated with cardiovascular disease (CVD) in adulthood. Whether this is mediated through adult body mass index (BMI) and associated risk factors such as metabolic derangements remains unclear. The aim was to examine whether childhood BMI velocity (Δkg m(-2) per year) was associated with adult CVD mortality and to examine how adult BMI and cardiometabolic risk factors contribute to the association. METHODS AND RESULTS: Subjects were 1924 Icelanders born between 1921 and 1935 and living in Reykjavik when recruited into a longitudinal study from 1967 to 1991. From ages 8-13 years, BMI velocity was calculated to quantify the association between childhood growth and adult CVD mortality. Deaths from recruitment to 31 December 2009 were extracted from the national register. There were 202 CVD deaths among men and 90 CVD deaths among women (mean follow-up: 25.9 years). Faster BMI velocity from ages 8-13 years was associated with CVD mortality when comparing those in the highest versus lowest tertile with corresponding hazard ratio (HR) (95% confidence interval (CI)): 1.49 (1.03, 2.15) among men and 2.32 (1.32, 4.08) among women after adjustment for mid-life BMI and CVD risk factors. Faster childhood BMI velocity was associated with elevated CVD risk factors among men at mid-life but these associations were less pronounced among women. CONCLUSION: Faster increase in BMI from ages 8-13 years was associated with an increased CVD mortality risk. Children with early growth spurts coupled with excess weight gain during this transition period from childhood into adolescence should be closely monitored to ensure better health in adulthood.

Consumption of lead-shot cervid meat and blood lead concentrations in a group of adult Norwegians.

Several recent investigations have reported high concentrations of lead in samples of minced cervid meat. This paper describes findings from a Norwegian study performed in 2012 among 147 adults with a wide range of cervid game consumption. The main aim was to assess whether high consumption of lead-shot cervid meat is associated with increased concentration of lead in blood. A second aim was to investigate to what extent factors apart from game consumption explain observed variability in blood lead levels. Median (5 and 95 percentile) blood concentration of lead was 16.6 µg/L (7.5 and 39 µg/L). An optimal multivariate linear regression model for log-transformed blood lead indicated that cervid game meat consumption once a month or more was associated with approximately 31% increase in blood lead concentrations. The increase seemed to be mostly associated with consumption of minced cervid meat, particularly purchased minced meat. However, many participants with high and long-lasting game meat intake had low blood lead concentrations. Cervid meat together with number of bullet shots per year, years with game consumption, self-assembly of bullets, wine consumption and smoking jointly accounted for approximately 25% of the variation in blood lead concentrations, while age and sex accounted for 27% of the variance. Blood lead concentrations increased approximately 18% per decade of age, and men had on average 30% higher blood lead concentrations than women. Hunters who assembled their own ammunition had 52% higher blood lead concentrations than persons not making ammunition. In conjunction with minced cervid meat, wine intake was significantly associated with increased blood lead. Our results indicate that hunting practices such as use of lead-based ammunition, self-assembling of lead containing bullets and inclusion of lead-contaminated meat for mincing to a large extent determine the exposure to lead from cervid game consumption.

Association between healthy maternal dietary pattern and risk for gestational diabetes mellitus.

BACKGROUND/OBJECTIVES: Gestational diabetes mellitus (GDM) is associated with negative health effects for mother and child. The aim was to investigate the association between maternal dietary patterns and GDM. SUBJECTS/METHODS: Prospective observational study including 168 pregnant women aged 18-40 years, recruited at routine 20-week ultrasound. All participants kept a 4-day weighed food record following recruitment (commencement: gestational weeks 19-24). Principal component analysis was used to extract dietary patterns from 29 food groups. A Healthy Eating Index (HEI) was constructed. All women underwent an oral glucose tolerance test in weeks 23-28. RESULTS: One clear dietary pattern (Eigenvalue 2.4) was extracted with positive factor loadings for seafood; eggs; vegetables; fruits and berries; vegetable oils; nuts and seeds; pasta; breakfast cereals; and coffee, tea and cocoa powder, and negative factor loadings for soft drinks and French fries. This pattern was labeled a prudent dietary pattern. Explained variance was 8.2%. The prevalence of GDM was 2.3% among women of normal weight before pregnancy (n=86) and 18.3% among overweight/obese women (n=82). The prudent dietary pattern was associated with lower risk of GDM (OR: 0.54; 95% CI: 0.30, 0.98). When adjusting for age, parity, prepregnancy weight, energy intake, weekly weight gain and total metabolic equivalent of task the association remained (OR: 0.36; 95% CI: 0.14, 0.94). Similar results were found when only including overweight or obese women (OR: 0.31; 95% CI: 0.13, 0.75). CONCLUSIONS: Adhering to a prudent dietary pattern in pregnancy was clearly associated with lower risk of GDM, especially among women already at higher risk because of overweight/obesity before pregnancy.

Different weight gain in women of normal weight before pregnancy: postpartum weight and birth weight.

OBJECTIVE: To identify the effect of different gestational weight gains among women of normal weight before pregnancy on babies' birth weights, and women's weights 18-24 months postpartum. METHODS: Two groups of women of normal weight before pregnancy (body mass index [BMI] 19.6-25.4 kg/m2) took part in the study (n = 200). They gained either moderate weight (9-15 kg) or high weight (18-24 kg) during pregnancy. From maternity records and telephone interviews, information on age, height, prepregnancy and postpartum weight, gestational weight gain, babies' birth weights, lactation, parity, and smoking habits was collected. RESULTS: High maternal weight gain during pregnancy resulted in mean birth weight 286 g higher than that of babies of mothers who gained moderate weight. The correlation coefficient between birth weight and gestational weight gain was 0.3 (P < .001). The postpartum weight of women with high weight gain during pregnancy was 2.6+/-0.38 kg (mean +/- standard error of the mean [SEM]) more than before pregnancy but the group of moderate weight gain weighed 0.1+/-0.47 kg less than before pregnancy (P < .001). However, most women in both groups (88.6%) regained normal weight, and prepregnant weight correlated strongly with the weight 18-24 months postpartum (r = 0.79, P < .001). There was not a significant correlation between the duration of lactation and postpartum weight loss (r = 0.04, P > .05). CONCLUSION: High gestational weight gain among women of normal weight before pregnancy increases birth weight and women's weight postpartum, compared with moderate weight gain. Prepregnant weight is more indicative of postpartum weight, and women reach normal weight again irrespective of gestational weight gain.

Association between size at birth, truncal fat and obesity in adult life and its contribution to blood pressure and coronary heart disease; study in a high birth weight population.

OBJECTIVE: The aim of the study was to assess the relationship between size at birth and obesity as well as truncal fat, and its contribution to cardiovascular risk in a high birth weight population. DESIGN: Cohort-study with retrospectively collected data on size at birth. SETTING: Reykjavik, Iceland. SUBJECTS: A total of 1874 men and 1833 women born in Reykjavik during 1914-1935. MAIN OUTCOME MEASURES: Size at birth. Adult weight, height and skinfold thickness measurements, systolic and diastolic blood pressure, fatal and nonfatal coronary heart disease (CHD). RESULTS: Birth weight was positively related to adult body mass index (BMI) in both genders (B=0.35+/-0.14 kg/m(2), adj. R(2)=0.015, P=0.012 and B=0.34+/-0.17 kg/m(2), adj. R(2)=0.055, P=0.043 in men and women, respectively). However, high birth weight was not a risk factor for adult obesity (BMI>/=30 kg/m(2)). In the highest birth weight quartile, the odds ratio (95% CI) for being above the 90th percentile of truncal fat was 0.7 (0.6-1.0, P=0.021) for men and 0.4 (0.3-0.8, P=0.002) for women, compared with the lowest birth weight quartile. Truncal fat and BMI were positively related to blood pressure in both genders (P<0.05), but not to CHD. The regression coefficient for the inverse association between birth weight and blood pressure hardly changed when adding truncal fat to the model. CONCLUSION: In this high birth weight population, high birth weight was related to higher BMI in adulthood without being a risk factor for adult obesity. The inverse association between birth weight and truncal fat in adulthood suggests a role for foetal development in determining adult fat distribution. The inverse relationship of birth weight to blood pressure seems not to be mediated through the same pathway as to truncal fat.

Essential and toxic element concentrations in blood and urine and their associations with diet: results from a Norwegian population study including high-consumers of seafood and game.

The first aim of the study was to evaluate calculated dietary intake and concentrations measured in blood or urine of essential and toxic elements in relation to nutritional and toxicological reference values. The second aim was to identify patterns of the element concentrations in blood and urine and to identify possible dietary determinants of the concentrations of these elements. Adults with a known high consumption of environmental contaminants (n=111), and a random sample of controls (n=76) answered a validated food frequency questionnaire (FFQ). Complete data on biological measures were available for 179 individuals. Blood and urine samples were analyzed for selenium, iodine, arsenic, mercury, cadmium and lead. Principal component analysis was used to identify underlying patterns of correlated blood and urine concentrations. The calculated intakes of selenium, iodine, inorganic arsenic and mercury were within guideline levels. For cadmium 24% of the high consumer group and 8% of the control group had intakes above the tolerable weekly intake. Concentrations of lead in blood exceeded the bench-mark dose lower confidence limits for some participants. However, overall, the examined exposures did not give rise to nutritional or toxicological concerns. Game consumption was associated with lead in blood (B(ln) 0.021; 95%CI:0.010, 0.031) and wine consumption. Seafood consumption was associated with urinary cadmium in non-smokers (B(ln) 0.009; 95%CI:0.003, 0.015). A novel finding was a distinct pattern of positively associated biological markers, comprising iodine, selenium, arsenic and mercury (eigenvalue 3.8), reflecting seafood intake (B 0.007; 95%CI:0.004, 0.010). The study clearly demonstrates the significance of seafood as a source of both essential nutrients and toxic elements simultaneously and shows that exposure to various essential and toxic elements can be intertwined.

Dietary mercury exposure in a population with a wide range of fish consumption--self-capture of fish and regional differences are important determinants of mercury in blood.

Human, low level, chronic exposure to mercury (Hg) from fish is of concern because of potential neurodevelopmental and cardiovascular toxicity. The purpose of the study was to 1) measure total mercury (THg) in blood and estimate dietary exposure in a population group with a wide range of seafood consumption, 2) assess the intake and blood concentration in relation to tolerable intake values, 3) characterise dietary sources, and 4) to investigate the relationship between dietary THg with THg in blood (BTHg), including factors that can explain the variance in BTHg concentrations. The participants (n=184) filled in an extensive food frequency questionnaire which was combined with a database on THg concentrations in Norwegian food, and donated blood and urine. Median consumption of seafood was 65 g/day (range 4 to 341 g/day). The calculated mean dietary THg exposure was 0.35 (median 0.30) µg/kg body weight/week. Seafood contributed on average 95% to the exposure. The JECFA Provisional Tolerable Weekly Intake (PTWI) of 1.6 µg MeHg/kg bw/week was not exceeded by any of the participants. BTHg ranged from 0.6 to 30 µg/L, with a mean of 5.3 (median 4.0 µg/L). There was a strong relationship between total seafood consumption and BTHg concentrations (r=0.58 95%CI: 0.48, 0.67) and between estimated THg dietary exposure and BTHg (r=0.46 95%CI: 0.35, 0.57). Fish consumption, sex, catching >50% of their seafood themselves, and living in coastal municipalities were significant factors in linear regression models with lnBTHg. Including urinary Hg in the regression model increased the explained variance from 54% to 65%. In a toxicokinetic model, the calculated dietary intake appeared to moderately underestimate the measured BTHg among the participants with the highest BTHg. Only two of the participants had BTHg slightly above a value equivalent to the JECFA PTWI, but none of them were women in fertile age.

Lower consumption of cow milk protein A1 beta-casein at 2 years of age, rather than consumption among 11- to 14-year-old adolescents, may explain the lower incidence of type 1 diabetes in Iceland than in Scandinavia.

AIM: To compare the consumption of the cow milk proteins A1 and B beta-casein among children and adolescents in Iceland and Scandinavia (Norway, Denmark, Sweden and Finland) as this might explain the lower incidence of type 1 diabetes (per 100,000/year, 0-14 years) in Iceland. METHODS: The consumption of A1 beta-casein in each country among 2- and 11- to 14-year-old children was calculated from results on food intake and on cow milk protein concentration. The consumption values were then compared and evaluated against the incidence of type 1 diabetes. RESULTS: There was a significant difference between the consumption of A1 (p = 0.034) as well as the sum of A1 and B (p = 0.021) beta-casein in Iceland and Scandinavia for 2-year-old children. In the same age group, consumption of A1 beta-casein correlated with the incidence of type 1 diabetes in the countries (r = 0.9; p = 0.037). No significant difference in consumption of A1 or the sum of A1 and B beta-casein was found for 11- to 14-year-old adolescents. CONCLUSION: This study supports that lower consumption of A1 beta-casein might be related to the lower incidence of type 1 diabetes in Iceland than in Scandinavia. Additionally it indicates that consumption in young childhood might be of more importance for the development of the disease incidence than consumption in adolescence.

Variation in consumption of cow milk proteins and lower incidence of Type 1 diabetes in Iceland vs the other 4 Nordic countries.

BACKGROUND: The incidence of Type 1 diabetes is lower in Iceland than in the other 4 Nordic Countries. Earlier studies have showed that the cow milk proteins A1 and B beta-casein, suggested to be diabetogenic, are in lower amount in Icelandic cow milk than in milk from the other 4 Nordic Countries, and the per capita consumption of these proteins correlates with the incidence of Type 1 diabetes. OBJECTIVE: To investigate whether lower consumption of the cow milk protein bovine serum albumin (BSA) (suggested to be diabetogenic) or higher consumption of immunoglobulin (Ig) or lactoferrin (LF) (suggested to be protective) is related to the lower incidence of Type 1 diabetes in Iceland. METHODS: The per capita consumption of milk proteins was calculated from an international database on consumption of milk and milk products and from the analysis of cow's milk samples. The samples were randomly collected from the largest consumption areas in Iceland and in the other 4 Nordic Countries. RESULTS: The per capita consumption of BSA was higher in Iceland (0.79 +/- 0.02 g/person per day) (mean +/- SEM) than in the other 4 Nordic Countries (0.43 +/- 0.05 g/person per day) (p = 0.025). The per capita consumption of Ig was also higher in Iceland than in the other 4 Nordic Countries (p = 0.025), while the consumption of LF was similar. Consumption of these 3 individual milk proteins did not correlate with the incidence of Type 1 diabetes in the 5 countries studied. CONCLUSION: Consumption of BSA, Ig or LF does not seem to explain the lower incidence of Type 1 diabetes in Iceland, compared with the other 4 Nordic Countries, while A1 and B beta-casein may contribute to varying diabetogenicity of cow's milk and explain the difference in incidence of Type 1 diabetes.

Different beta-casein fractions in Icelandic versus Scandinavian cow's milk may influence diabetogenicity of cow's milk in infancy and explain low incidence of insulin-dependent diabetes mellitus in Iceland.

OBJECTIVES: To compare children with insulin-dependent diabetes mellitus (IDDM) with controls in Iceland regarding their consumption of cow's milk in infancy, and to investigate the beta-casein fractions in Scandinavian and Icelandic cow's milk. The A1 variant of beta-casein has been shown to be diabetogenic in animal studies, and suggestions have been made that the B variant of beta-casein acts similarly. Differences in the relative proportions of beta-casein fractions might explain the lower incidence of IDDM in Iceland than in Scandinavia. METHODS: A retrospective case-control study on IDDM patients and matching controls was performed in Iceland to compare their diets in infancy. Fifty-five children with IDDM born in Iceland over a 16-year period and randomly collected controls (n = 165) were recruited to the study. Mothers of the children answered questions on breastfeeding habits and on when cow's milk products were introduced. Samples of cow's milk from randomly selected milk batches from the largest consumption areas in Iceland and Scandinavia were collected. The milk samples were freeze-dried and their beta-casein fractions were analyzed using capillary electrophoresis. RESULTS: No significant difference was found between IDDM patients and controls in the frequency and duration of breastfeeding or the first introduction of cow's milk products. The analyses of milk samples showed that the percentage of the A1 and B variants of beta-casein in Icelandic milk was significantly lower than in the milk from the Scandinavian countries. CONCLUSIONS: Cow's milk consumption in infancy is not related to IDDM in Iceland. The lower fraction of A1 and B beta-caseins in Icelandic cow's milk may explain why there is a lower incidence of IDDM in Iceland than in Scandinavia.