Maria Weyermann

Acquisition of Helicobacter Pylori Infection in Early Childhood: Independent Contributions of Infected Mothers, Fathers, and Siblings

OBJECTIVES:Infected siblings, mothers, and fathers have all been suggested to be major sources for Helicobacter pylori acquisition among children, but few studies have addressed the potential role of various family members simultaneously.METHODS:A systematic review was performed on studies investigating intrafamilial transmission of childhood H. pylori infection. Within the Ulm Birth Cohort Study, which consists of 1,066 healthy newborns, born between November 2000 and November 2001 and followed up to age 4, and their siblings and parents, the independent role of the infection status of parents and siblings in transmission of H. pylori among children at age 4 was assessed.RESULTS:Among four studies reporting infected mothers and siblings as independent risk factors for childhood H. pylori infection, odds ratios (ORs) for childhood infection given an infected sibling decreased meaningfully after adjustment for maternal infection status. Within the Ulm Birth Cohort Study, the prevalence of infection was 3.0% among index children at age 4. In bivariate analyses, maternal, paternal, and sibling infection were all strongly and significantly related to infection of the child. However, after multivariate adjustment, only maternal infection persisted as the single strong and significant risk factor (OR 13.0, 95% confidence interval 3.0–55.2).CONCLUSIONS:These patterns suggest that mutual control for H. pylori status of other family members is crucial for estimating the role of mothers, fathers, and siblings in the transmission of childhood H. pylori infection. In populations with low H. pylori prevalence the infected mother is likely to be the main source for childhood H. pylori infection.

Duration of breastfeeding and risk of overweight in childhood: a prospective birth cohort study from Germany

Background:Whereas a recently published meta-analysis showed that ever breastfeeding reduces the risk of obesity in childhood significantly, the recent literature describing the relationship between duration of breastfeeding and risk of overweight or obesity in childhood remains inconclusive.Methods:Between November 2000 and November 2001, all mothers and their newborns were recruited after delivery at the Department of Gynecology and Obstetrics at the University of Ulm, Germany. Active follow-up was performed at the age of 12 months and 24 months.Results:Of the 1066 children included in the baseline examination, information on body mass index was available for 855 (80%) at the 2-year follow-up. At this age 72 children (8.4%) were overweight and 24 (2.8%) were severely overweight. Whereas 76 children (8.9%) were never breastfed, 533 children (62.3%) were breastfed for at least 6 months, and 322 children (37.7%) were exclusively breastfed for at least 6 months. Compared to children who were breastfed for less than 3 months, the adjusted odds ratio (OR) for overweight was 0.4 (95% confidence interval (CI) 0.2–0.8) in children who were breastfed for at least 6 months. When considering the time of exclusive breastfeeding, the adjusted OR for overweight was 0.8 (95% CI 0.4; 1.5) in children who were exclusively breastfed for at least 3 but less than 6 months and 0.4 (95% CI 0.2; 0.9) in children who were exclusively breastfed for at least 6 months compared to children who were exclusively breastfed less than 3 months.Conclusion:These results highlight the importance of prolonged breastfeeding for the prevention of overweight in children.

The mother as source of Helicobacter pylori infection

Background: To further elucidate the intrafamilial transmission of Helicobacter pylori infection, we investigated the occurrence of infection by parental infection status in a large community-based birth cohort of children from Germany. Methods: Parental infection (at birth) and childrens infection (at age 3 years) were determined by 13C-urea breath test and by monoclonal antigen stool test. Results: Twenty of 834 children (2.4%) were found to be infected. The odds ratio for H. pylori infection of the child was 12.9 (95% confidence interval = 3.2–52.5) if the mother was infected and 1.4 (0.4–4.6) if the father was infected, after adjustment for infection status of the other parent and for nationality. The number of older siblings was not a risk factor for H. pylori infection of the child. Conclusions: This longitudinal study suggests that infected mothers are the main source of H. pylori infection of their children.

Adipokines in human milk and risk of overweight in early childhood: A prospective cohort study

Background: Multiple studies have suggested that breast-feeding can prevent obesity, but the evidence remains inconclusive. The concentrations of specific constituents of human milk, such as adipokines, may play a role in this relationship, and these have rarely been considered. We assessed the role of adiponectin and leptin in human milk in childhood overweight. Methods: Between November 2000 and November 2001 all women delivering at the Department of Gynecology and Obstetrics at the University of Ulm, Germany were invited to participate in the study together with their healthy newborns. Milk samples were collected 6 weeks postpartum. Adiponectin and leptin levels were determined by commercially available ELISA. Active follow-up was performed at age 12 and 24 months. Results: Of the 674 breast-fed children, 56 (8%) were overweight at the age of 2 years. Median adiponectin and leptin levels in milk were 10.9 ng/mL and 174.5 pg/mL, respectively. Adjusted odds ratio for overweight at the age of 2 was 1.6 (95% confidence interval = 1.0–2.6) per unit increase of log adiponectin and 1.1 (0.8–1.5) per unit increase of log leptin. Among children who were breast-fed for at least 6 months, adjusted odds ratios were 2.1 (1.1–4.2) per unit increase of log adiponectin, and 1.1 (0.7–1.6) per unit increase of log leptin. Conclusion: High levels of adiponectin in maternal milk may be a risk factor for childhood overweight.

Genetic variants in the FADS gene cluster are associated with arachidonic acid concentrations of human breast milk at 1.5 and 6 mo postpartum and influence the course of milk dodecanoic, tetracosenoic, and trans-9-octadecenoic acid concentrations over the duration of lactation.

BACKGROUND Breastfeeding is considered an optimal nutritional source of n-6 (omega-6) and n-3 (omega-3) fatty acids (FAs) for the proper visual and cognitive development of newborn children. In addition to maternal nutrition as an important regulator of FA concentrations, first results exist on an association of breast-milk FAs with single nucleotide polymorphisms (SNPs) in the FADS gene cluster, which encodes the rate-limiting enzymes in the elongation-desaturation pathway of long-chain polyunsaturated fatty acids (LC-PUFAs). OBJECTIVE We analyzed the influence of FADS SNPs on breast-milk FA concentrations and their time course during lactation in the Ulm Birth Cohort study, which comprised 772 nursing mothers at 1.5 mo after giving birth, and in a subset of 463 mothers who were still breastfeeding at 6 mo postpartum. DESIGN We conducted linear regression analysis of 8 FADS SNPs with FA concentrations at both time points separately and assessed the genotype effect over time in a longitudinal analysis by using a generalized estimating equation regression model. RESULTS We observed significant associations of FADS genotypes with arachidonic acid (AA) concentrations and the 20:4n-6/20:3n-6 ratio at both time points but no association of FADS SNPs with the time course of AA concentrations. A longitudinal analysis of FAs other than LC-PUFAs by genotype over time showed associations for dodecanoic acid, cis-15-tetracosenoic acid, and trans-9-octadecenoic acid. CONCLUSIONS Maternal FADS genotypes are associated with breast-milk AA concentrations and might therefore influence the supply of this FA for children. Furthermore, our data indicate an interrelation between the LC-PUFA pathway and saturated and monounsaturated FAs.

Adipokines in cord blood and risk of wheezing disorders within the first two years of life

Background Adipokines are involved in the regulation of many inflammatory processes and are present at very high concentrations in cord blood of term infants.

Fatty Acid Profile Comparisons in Human Milk Sampled From the Same Mothers at the Sixth Week and the Sixth Month of Lactation

Objectives: To compare fatty acid composition of human milk at 2 different stages of lactation and investigate the relation between trans isomeric and long-chain polyunsaturated fatty acids (LCPUFAs) in human milk at the sixth month of lactation. Subjects and Methods: We investigated human milk samples obtained at the sixth week and sixth month of lactation from 462 mothers who participated in a large birth cohort study. Fatty acid composition of human milk lipids was determined by high-resolution capillary gas-liquid chromatography. Results: Fat contents of human milk increased significantly between the sixth week and sixth month of lactation (1.63 [2.06] and 3.19 [3.14], g/100 mL; median [interquartile range], P < 0.001). Percentage contributions to human milk fatty acid composition of nearly all polyunsaturated fatty acids also increased significantly (linoleic acid: 10.09 [4.41] and 11.01 [4.53], arachidonic acid: 0.46 [0.32] and 0.48 [0.23], α-linolenic acid: 0.69 [0.42] and 0.75 [0.41], and docosahexaenoic acid: 0.17 [0.23] and 0.23 [0.15], % wt/wt, P < 0.001). Values of the 18-carbon trans octadecenoic acid (C18:1n-7/9t) significantly inversely correlated to linoleic acid (r = −0.24, P < 0.001), α-linolenic acid (r = −0.19, P < 0.001), and arachidonic acid (r = −0.43, P < 0.001). In contrast, we found no correlation between the 16-carbon trans hexadecenoic acid (C16:1n-7t) and the same LCPUFAs. Conclusions: Data obtained in the present study indicate increasing fat contents with stable or increasing percentage contribution of LCPUFAs in human milk samples between the sixth week and at the sixth month of lactation, and the availability of 18-carbon trans isomeric fatty acids is inversely associated to the availability of several LCPUFAs in human milk at the sixth month of lactation.

Role of Lewis A and Lewis B blood group antigens in Helicobacter pylori infection.

Background and aims.  We investigated the prevalence of Helicobacter pylori infection in a large group of women to determine whether there was an association of current infection status with Lewis blood group antigen A and B phenotype.

Helicobacter pylori-specific immune response in maternal serum, cord blood, and human milk among mothers with and without current Helicobacter pylori infection

We assessed the patterns of Helicobacter pylori (H. pylori) specific maternal antibodies in maternal serum, cord blood, and milk, which might play a role in prevention of H. pylori infection because transferred to the infant. Between November 2000 and November 2001, mothers were recruited after delivery of their offspring. H. pylori infection status was determined by 13C-urea breath test (UBT). Specific H. pylori antibody profiles were analysed using commercial H. pylori–specific enzyme-linked immunosorbent assay and Western blots. Among 898 mothers, 23% had a current H. pylori infection. Median H. pylori IgG antibody titers in serum and cord blood of UBT-positive mothers were 23.8 U/mL and 24.0 U/mL, respectively. Whereas prevalences of H. pylori–specific antibodies in serum of UBT-negative mothers were clearly lower than those among UBT-positive mothers, patterns of H. pylori–specific IgA antibodies in milk were similar among UBT-positive and UBT-negative mothers. Neonates born from H. pylori–infected women are provided with large amounts of transplacentally transferred specific IgG H. pylori antibodies. Breast-fed neonates are additionally provided with specific IgA antibodies in human milk. Notably, the latter may also be activated if exposure of the mother to H. pylori might have been long time ago and been cleared in the meantime.

Plasma insulin levels in childhood are related to maternal factors – results of the Ulm Birth Cohort Study

The cardiovascular risk factor profile of a child as well as the development of body weight are influenced by genetic and childhood factors. Circulating insulin concentrations reflect the metabolic cardiovascular risk and may trigger weight gain. We aimed at identifying parental and childhood factors which may influence fasting plasma insulin concentrations in children.