Helicobacter pylori infection and colorectal cancer risk: evidence from a large population-based case-control study in Germany.

Evidence concerning the role of Helicobacter pylori infection in the development of colorectal cancer remains controversial. The authors assessed the association of H. pylori seroprevalence with risk of colorectal cancer in a large population-based case-control study from Germany in 2003-2007. Serum antibodies to H. pylori in general and the cytotoxin-associated gene A protein (CagA) were measured in 1,712 incident colorectal cancer cases and 1,669 controls. The association between H. pylori seroprevalence and colorectal cancer risk was estimated by logistic regression, with adjustment for potential confounders and stratification by age group, sex, anatomic subsites, and cancer stage. Overall, H. pylori seroprevalence was higher in cases (46.1%) than in controls (40.1%), resulting in an age- and sex-adjusted odds ratio of 1.30 (95% confidence interval (CI): 1.14, 1.50). Adjustment for established colorectal cancer risk factors decreased the odds ratio to 1.26 (95% CI: 1.09, 1.47), with a further reduction to 1.18 (95% CI: 1.01, 1.38) after additional adjustment for previous colorectal endoscopy. Stratified analyses showed risk elevation to be essentially confined to left-sided colorectal cancer, with an odds ratio of 1.22 (95% CI: 1.02, 1.45), suggesting that H. pylori infection may be associated with a small yet relevant risk increase in the left colorectum.

Helicobacter pylori infection is strongly associated with gastric and duodenal ulcers in a large prospective study.

BACKGROUND & AIMS: Infection with Helicobacter pylori (H pylori) is a risk factor for peptic ulcer disease (PUD), but there are limited longitudinal data on the associations between infection and incident gastric or duodenal ulcers. METHODS: Information on potential risk factors, lifetime history of PUD, and serologic measurements of H pylori infection were obtained from a German cohort of 9953 adults, 50 to 74 years old at baseline (2000-2002). The incidence of ulcers was determined by questionnaires sent to study participants and general practitioners 2 and 5 years later, and was validated by medical records. RESULTS: A lifetime history of PUD was reported by 1030 participants, and during the follow-up period 48 had a first gastric and 22 had a first duodenal ulcer. Infection with H pylori strains that express cytotoxin-associated gene A (cagA) was significantly associated with a lifetime history of PUD (odds ratio, 1.75; 95% confidence interval [CI], 1.50-2.04). Based on longitudinal analyses with physician-validated end points, the adjusted hazard ratios for incident gastric and duodenal ulcer disease were 2.9 (95% CI, 1.5-5.5) and 18.4 (95% CI, 4.2-79.9), respectively, among patients infected with cagA-positive strains of H pylori. CONCLUSIONS: In cross-sectional analysis, infection with cagA-positive strains of H pylori was associated with a 1.75-fold increased risk of peptic ulcer disease. Longitudinal analyses revealed an 18.4- and 2.9-fold increased risk for duodenal ulcer and gastric ulcer, respectively. The proportion of PUD that is attributable to H pylori infection might be larger than previously believed.

Genetic variation in the prostate stem cell antigen gene and upper gastrointestinal cancer in white individuals.

BACKGROUND & AIMS: An association between gastric cancer and the rs2294008 (C>T) polymorphism in the prostate stem cell antigen (PSCA) gene has been reported for several Asian populations. We set out to determine whether such an association exists in white individuals. METHODS: We genotyped 166 relatives of gastric cancer patients, including 43 Helicobacter pylori-infected subjects with hypochlorhydria and gastric atrophy, 65 infected subjects without these abnormalities, 58 H pylori-negative relatives, and 100 population controls. Additionally, a population-based study of chronic atrophic gastritis provided 533 cases and 1054 controls. We then genotyped 2 population-based, case-control studies of upper gastrointestinal cancer: the first included 312 gastric cancer cases and 383 controls; the second included 309 gastric cancer cases, 159 esophageal cancer cases, and 211 controls. Odds ratios were computed from logistic models and adjusted for confounding variables. RESULTS: Carriage of the risk allele (T) of rs2294008 in PSCA was associated with chronic atrophic gastritis (adjusted odds ratio [OR], 1.5; 95% confidence interval [CI]: 1.1-1.9) and noncardia gastric cancer (OR, 1.9; 95% CI: 1.3-2.8). The association was strongest for the diffuse histologic type (OR, 3.2; 95% CI: 1.2-10.7). An inverse association was observed between carriage of the risk allele and gastric cardia cancer (OR, 0.5; 95% CI: 0.3-0.9), esophageal adenocarcinoma (OR, 0.5; 95% CI: 0.3-0.9), and esophageal squamous cell carcinoma (OR, 0.4; 95% CI: 0.2-0.9). CONCLUSIONS: The rs2294008 polymorphism in PSCA increases the risk of noncardia gastric cancer and its precursors in white individuals but protects against proximal cancers.

Incidence and risk factors for the development of chronic atrophic gastritis: five year follow-up of a population-based cohort study.

Chronic atrophic gastritis (CAG) is a well-established precursor of intestinal gastric cancer. However, data on incidence of CAG are rare, especially from population-based studies. The aim of this analysis was to estimate the incidence of CAG in a large population-based study among older adults from Germany and to identify major risk factors associated with its development. In the baseline and 5-year follow-up examinations of the ESTHER study, serological measurements of pepsinogen (PG) I and II and Helicobacter pylori antibodies were performed in 5,229 women and men, aged 50-74 years at baseline. Information on additional potential risk factors was obtained by questionnaire. CAG was defined by PGI < 70 ng/mL and PGI/PGII < 3. In total, there were 58 (1.1%) incident CAG cases. CAG incidence increased with increasing age from 0.5% in age group 50-54 years to 2.1% in age group 70-74 years. Seropositivity with H. pylori was strongly associated with CAG incidence, with adjusted odds ratios of 5.0 [95% confidence interval (CI): 1.6-15.8] and 11.3 (95% CI: 4.2-30.0) for participants with cytotoxin associated gene A (cagA) negative and cagA positive H. pylori infection at both baseline and follow-up compared to those without H. pylori infection, respectively. Gender, education, smoking, alcohol consumption and family history of gastric cancer were not significantly associated with CAG incidence. Incidence of CAG is rather low in the German population. Older age and infection with H. pylori are key risk factors for the development of CAG.

DNA repair gene polymorphisms and risk of chronic atrophic gastritis: a case-control study.

BACKGROUND: Recent studies have reported associations of DNA repair pathway gene variants and risk of various cancers and precancerous lesions, such as chronic atrophic gastritis (CAG). METHODS: A nested case-control study within the German population-based ESTHER cohort was conducted, including 533 CAG cases and 1054 controls. Polymorphisms in eleven DNA repair genes (APEX1, ERCC1, ERCC2/XPD, PARP1 and XRCC1), in CD3EAP/ASE-1 and PPP1R13L were analysed. RESULTS: No association was disclosed for any of the analysed polymorphisms. Nor did stratified analyses according to ages < 65 and ≥ 65 years show any significant association with CAG risk. CONCLUSIONS: The results of this large German case-control study do not reveal associations of DNA repair pathway polymorphisms and risk of CAG. On the basis of a large number of CAG cases, they do not support associations of DNA repair pathway SNPs with CAG risk, but suggest the need of larger studies to disclose or exclude potential weak associations, or of studies with full coverage of candidate genes.

Apparent incidence of Helicobacter pylori in adulthood: to what extent do new infections reflect misclassification?

BACKGROUND: Helicobacter pylori infection is a key risk factor for a variety of gastrointestinal diseases. About half of the world population is infected. Most infections are acquired early in childhood, but the occurrence of new infections among adults has also been suggested. METHODS: We review epidemiological studies providing estimates of incidence of H. pylori infection among adults and evaluate to what extent incidence estimates might have been affected by measurement error of infection status. RESULTS: Thirty-two studies could be included in the review. Annual incidence was lower than 1.0 % in 17 studies; no correlation between length of follow-up and cumulative incidence was observed. Apparent cumulative incidences of the magnitudes observed in most studies would be expected, because of less than perfect sensitivity and specificity of the diagnostic tests, even in the absence of any true new infections. CONCLUSION/IMPACT: Apparent incidence rates of H. pylori infection among adults in Western populations should be interpreted with utmost caution.

Grb2-associated binder 1 (Gab1) genetic polymorphism, Helicobacter pylori infection, and chronic atrophic gastritis among older adults from Germany.

Grb2-associated binder 1 (Gab1) plays an important role in the regulation of cell growth and transformation. A single nucleotide polymorphism (SNP) (rs3805246) in the Gab1 gene has been suggested to be related to the risk of Helicobacter pylori infection and chronic atrophic gastritis (CAG) in a study from Japan. We aimed to assess the associations in a population-based study from Germany. In the baseline examination of ESTHER, a population-based study conducted in Saarland, serum pepsinogen I and II and H. pylori serostatus were measured by ELISA. The Gab1 SNP (rs3805246) was genotyped in 351 serologically defined CAG cases and 351 age- and sex-matched non-CAG controls. A nonsignificant association was observed between the Gab1 SNP and CAG, with an adjusted odds ratio of 1.15 (0.85-1.55) for AA/AG carriers compared to GG carriers. The magnitude of the association did not change when the analysis was restricted to H. pylori seropositive subjects. Furthermore, no significant relation was found between the SNP and H. pylori seropositivity among non-CAG controls. We could not confirm a major association between Gab1 SNP (rs3805246) and the predisposition to H. pylori infection and CAG in this study population from Germany. Further studies with larger sample size are needed to clarify a potential modest effect of Gab1 genetic polymorphisms.

Incidence of chronic atrophic gastritis: systematic review and meta-analysis of follow-up studies.

Chronic atrophic gastritis (CAG) is an important precursor lesion of intestinal gastric cancer. As it is typically asymptomatic, epidemiological data on the incidence of CAG are sparse. We aimed to provide an overview of published data on CAG incidence (overall and according to risk factors) from follow-up studies. Articles with information on incidence of CAG published in English until 26th of July 2009 were identified through a systematic MEDLINE and EMBASE search. Data extracted include study characteristics and key findings regarding the incidence of CAG. A meta-analysis was performed on the association between Helicobacter pylori infection and CAG incidence. Overall, data on CAG incidence were available from 14 studies, in 7 studies incidence could be estimated according to H. pylori infection. Most studies were conducted in symptomatic or high risk populations and the maximum number of incident cases was 284. Incidence estimates ranged from 0 to 11% per year and were consistently below 1% in patients not infected with H. pylori. The highest incidence was observed in a special study conducted on ulcer patients treated by proximal gastric vagotomy. Rate ratios for the association between H. pylori infection and CAG incidence ranged from 2.4 to 7.6 with a summary estimate of 5.0 (95% confidence interval: 3.1-8.3). Incidence of CAG is very low in the absence of H. pylori infection. There is a need for more population-based studies to provide comparable estimates of incidence and the impact of risk factors in the development of CAG.

Alcohol consumption and chronic atrophic gastritis: population-based study among 9,444 older adults from Germany.

Moderate alcohol consumption has been suggested to facilitate elimination of Helicobacter pylori infection which is a key risk factor for chronic atrophic gastritis (CAG) and gastric cancer. The aim of our study was to assess the association of alcohol consumption with CAG among older adults from Germany. In the baseline examination of ESTHER, a population-based study conducted in Saarland, serological measurements of pepsinogen I and II (for CAG definition) and H. pylori antibodies were taken in 9,444 subjects aged 50-74 years. Moderate current (<60 g/week) and lifetime (

Helicobacter pylori infection and chronic atrophic gastritis: associations according to severity of disease.

BACKGROUND: Helicobacter pylori infection is an established risk factor for chronic atrophic gastritis. However, estimates of the strength of this association have varied widely, possibly due to clearance of the infection in severe stages of chronic atrophic gastritis, which may lead to underestimation of the association. We assessed the association of H. pylori infection with chronic atrophic gastritis according to severity of disease. METHODS: We measured serum pepsinogen I and II (as surrogates for chronic atrophic gastritis) and antibodies against H. pylori by ELISA in 9444 men and women aged 50-74 years in a population-based study in Saarland, a state of Germany. The association between H. pylori and chronic atrophic gastritis (defined as pepsinogen I <70 ng/mL and pepsinogen I/II-ratio <3) was analyzed after stratification of chronic atrophic gastritis cases by quintiles of pepsinogen I as proxy marker for severity of chronic atrophic gastritis. RESULTS: When all cases were included, the odds ratio for the association with Chronic atrophic gastritis for H. pylori infection alone was 2.9 (95% confidence interval 2.3-3.6); it was 4.1 (3.2-5.2), for H. pylori infection that was positive for the presence of Ig G antibodies specific to the cytotoxin-associated gene A (CagA) protein-a well-established virulence factor of H. pylori. These ORs ranged from 11 (5.2-22) and 16 (7.7-34) for the quintile of cases with highest pepsinogen I (least severe cases) to 1.0 (0.7-1.6) and 0.9 (0.5-1.5) for the quintile of cases with lowest pepsinogen I (most severe cases). Five of 7 cases with CagA-seropositivity but negative H. pylori serostatus (a pattern indicative of past infection) were in the group of most severe cases. CONCLUSIONS: Our results support the hypothesis of major underestimation of the association of H. pylori and chronic atrophic gastritis, due to clearance of the infection in advanced stages of the disease. These results suggest that the association is much stronger than estimated by most epidemiologic studies to date.

Association of Helicobacter pylori infection with chronic atrophic gastritis: Meta-analyses according to type of disease definition.

Helicobacter pylori is a major risk factor for chronic atrophic gastritis (CAG). A large variety of definitions of CAG have been used in epidemiologic studies in the past. The aim of this work was to systematically review and summarize estimates of the association between H. pylori infection and CAG according to the various definitions of CAG. Articles on the association between H. pylori infection and CAG published until July 2007 were identified. Separate meta-analyses were carried out for studies defining CAG based on gastroscopy with biopsy, serum pepsinogen I (PG I) only, the pepsinogen I/pepsinogen II ratio (PG I/PG II ratio) only, or a combination of PG I and the PG I/PG II ratio. Numbers of identified studies and summary odds ratios (OR) (95% confidence intervals) were as follows: gastroscopy with biopsy: n = 34, OR = 6.4 (4.0-10.1); PG I only: n = 13, OR = 0.9 (0.7-1.2); PG I/PG II ratio: n = 8, OR = 7.2 (3.1-16.8); combination of PG I and the PG I/PG II ratio: n = 20, OR = 5.7 (4.4-7.5). Studies with CAG definitions based on gastroscopy with biopsy or the PG I/PG II ratio (alone or in combination with PG I) yield similarly strong associations of H. pylori with CAG. The association is missed entirely in studies where CAG is defined by PG I only.

Epidemiologic findings on serologically defined chronic atrophic gastritis strongly depend on the choice of the cutoff-value.

Chronic atrophic gastritis (CAG), a precursor of intestinal gastric cancer, is mostly ascertained noninvasively by serum pepsinogens in epidemiologic studies. However, serological definitions vary widely. We aimed to investigate the impact of this variation on estimated prevalence of CAG and its association with its main risk factors, age and Helicobacter pylori infection. Serum pepsinogen I and II and antibodies against H. pylori were measured by ELISA among 9,444 women and men aged 50-74 years in a population-based cohort study in Saarland/Germany. Application of the various definitions resulted in a wide range of prevalence estimates of CAG prevalence (2.1%-8.2%, with an outlier of 18.8% for one particular definition) and its associations with age and H. pylori infection (age adjusted odds ratios, OR, for CagA positive H. pylori infection: 0.98-4.48). Definitions of CAG based on both pepsinogen I and the pepsinogen I/II ratio or on the pepsinogen I/II ratio only revealed much clearer associations with both age and H. pylori infection than definitions of CAG based on pepsinogen I only (ORs for H. pylori infection: 1.45-4.48 and 0.86-1.30, respectively). Epidemiologic findings on CAG lack comparability due to the heterogeneity in serologic definitions of CAG. The association of age and H. pylori infection with CAG may be strongly underestimated in studies in which CAG is defined by pepsinogen I only.

Prevalence of chronic atrophic gastritis in different parts of the world.

Chronic atrophic gastritis (CAG) is a well-established precursor of intestinal gastric cancer, but epidemiologic data about its occurrence are sparse. We provide an overview on studies that examined the prevalence of CAG in different parts of the world. Articles containing data about the prevalence of chronic atrophic gastritis in unselected population samples and published until November 2005 were identified by searching the MEDLINE database. Furthermore, the references in the identified publications were screened for additional suitable studies. Studies comprising at least 50 subjects were included. Forty-one studies providing data on the prevalence of CAG in unselected population samples could be identified. CAG was determined by gastroscopy in 15 studies and by pepsinogen serum levels in 26 studies. Although results are difficult to compare due to the various definitions of CAG used, a strong increase with age, the lack of major gender differences, and strong variations between populations and population groups (in particular, relatively high rates in certain Asian populations) could be observed quite consistently. We conclude that CAG is relatively common among older adults in different parts of the world, but large variations exist. Large-scale international comparative studies with standardized methodology to determine CAG are needed to provide a coherent picture of the epidemiology of CAG in various populations. Noninvasive measurements of CAG by pepsinogen levels may be particularly suited for that purpose.

Restrained and external-emotional eating patterns in young overweight children-results of the Ulm Birth Cohort Study.

Childhood obesity is one of the greatest public health challenges in Western countries. Abnormal eating behavior is thought to be a developmental trajectory to obesity. The Eating Pattern Inventory for Children (EPI-C) has not been used for children as young as eight years, and possible associations with body weight have not yet been established. Five hundred and twenty-one children of the Ulm Birth Cohort Study (UBCS; age eight) filled out the EPI-C and BMI was assessed. Adequacy of the scales was tested with confirmatory factor analysis and a MANOVA and cluster analysis established associations between eating patterns and BMI. The factor structure of the EPI-C was confirmed (GFI = .968) and abnormal eating behavior was associated with overweight (χ(2)(8) =79.29, p<.001). The EPI-C is a valid assessment tool in this young age group. Overweight children consciously restrain their eating.

Gastric parietal cell antibodies, Helicobacter pylori infection, and chronic atrophic gastritis: evidence from a large population-based study in Germany.

BACKGROUND: Striking similarities between autoimmune gastritis and Helicobacter Pylori (H. pylori)-associated gastritis have suggested a potential link between these two pathologic conditions in the progression of chronic atrophic gastritis (CAG); however, evidence has remained conflicting. METHODS: Serum pepsinogen I and II, and antibodies against H. pylori in general, the cytotoxin-associated gene A protein (CagA) and parietal cells were measured by ELISA in 9,684 subjects aged 50 to 74 years. Antigastric parietal cell antibody (APCA) prevalence was examined in the overall population and according to sex, age, and H. pylori serostatus. The association between APCA prevalence and CAG was assessed by logistic regression, overall and according to H. pylori status, controlling for potential confounding factors. RESULTS: Overall APCA prevalence was 19.5%. APCA prevalence was strongly associated with CAG, and the association was increasing with increasing severity of CAG. Furthermore, the association between APCA and CAG was even stronger among H. pylori-negative subjects [odds ratio (OR) = 11.3; 95% confidence interval (CI): 7.5-17.1)] than among H. pylori-positive subjects (OR = 2.6; 95% CI: 2.1-3.3). CONCLUSIONS: APCA may play a role on the development of gastric atrophy, irrespective of H. pylori infection. IMPACT: Assessment of APCA might be a useful complement to established markers (such as pepsinogens and H. pylori antibodies) in screening for CAG.

Helicobacter pylori infection, chronic atrophic gastritis and major cardiovascular events: a population-based cohort study.

OBJECTIVE: There is debate whether infection with Helicobacter (H.) pylori, the main inducer of chronic atrophic gastritis (CAG), is a risk factor for cardiovascular disease and premature mortality. METHODS: Serological measurements of H. pylori infection and pepsinogen (PG) I and II were obtained in a population-based German cohort of 9953 older adults (50-74 years). Cox regression was employed to estimate hazard ratios (HR) and 95% confidence intervals (CI) for myocardial infarction, stroke, cardiovascular and all-cause mortality during five-year follow-up. RESULTS: According to serology, 4977 participants (51.9%) were infected with H. pylori (2604 with cytotoxin-associated gene A (cagA) strains) and 541 (5.7%) had CAG (PGI<70 ng/mL and PGI/PGII<3). During follow-up, 540 participants died (163 from cardiovascular causes), 170 experienced a primary myocardial infarction and 241 had a stroke. Neither cytotoxin-associated gene A (cagA) negative nor cagA positive H. pylori infections were associated with an increased risk for myocardial infarction, stroke or all-cause mortality. Intriguingly, infection with cagA positive H. pylori strains was inversely associated with cardiovascular mortality (HR, 0.62; CI: 0.41-0.94). No statistically significant associations were observed for the small group of participants with CAG, but point estimates of adjusted HRs for myocardial infarction, stroke and cardiovascular mortality were all below 1 (0.71, 0.59 and 0.65, respectively). CONCLUSIONS: Our results do not support the hypothesis that H. pylori infection or CAG are risk factors for cardiovascular disease or mortality and instead suggest an inverse relationship of cagA positive H. pylori infection with fatal cardiovascular events.

Polymorphisms in MUC1, MUC2, MUC5B and MUC6 genes are not associated with the risk of chronic atrophic gastritis.

Mucins represent major components of the mucous layer in the stomach, protecting the underlying epithelium from acid, mechanical trauma, proteases and pathogenic bacteria. Previous studies have shown an association of neoplastic transformation in the stomach with aberrant mucin levels, suggesting a potential role of genetic variation in mucin genes in the development of gastric cancer (GC). We assessed the association of genetic variation in candidate single nucleotide polymorphisms (SNPs) in mucin genes with the risk of chronic atrophic gastritis (CAG), a well-established precursor of GC in the German population-based ESTHER study. We genotyped MUC1 T31T, MUC2 L58P, MUC2 V116M, MUC5B E34G, MUC5B R51W, MUC5B rs2014486 (intronic) and MUC6 V619M for 533 serologically defined CAG cases and 1054 age- and sex-matched controls. None of the analysed SNPs was associated with CAG. However, large studies are needed to disclose or exclude potential weak associations of these SNPs with CAG risk.

Gestational weight gain and body mass index in children: results from three german cohort studies.

INTRODUCTION: Previous studies suggested potential priming effects of gestational weight gain (GWG) on offspring's body composition in later life. However, consistency of these effects in normal weight, overweight and obese mothers is less clear. METHODS: We combined the individual data of three German cohorts and assessed associations of total and excessive GWG (as defined by criteria of the Institute of Medicine) with offspring's mean body mass index (BMI) standard deviation scores (SDS) and overweight at the age of 5-6 years (total: n = 6,254). Quantile regression was used to examine potentially different effects on different parts of the BMI SDS distribution. All models were adjusted for birth weight, maternal age and maternal smoking during pregnancy and stratified by maternal pre-pregnancy weight status. RESULTS: In adjusted models, positive associations of total and excessive GWG with mean BMI SDS and overweight were observed only in children of non- overweight mothers. For example, excessive GWG was associated with a mean increase of 0.08 (95% CI: 0.01, 0.15) units of BMI SDS (0.13 (0.02, 0.24) kg/m(2) of 'real' BMI) in children of normal-weight mothers. The effects of total and excessive GWG on BMI SDS increased for higher- BMI children of normal-weight mothers. DISCUSSION: Increased GWG is likely to be associated with overweight in offspring of non-overweight mothers.

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.

Alcohol consumption, serum gamma-glutamyltransferase, and helicobacter pylori infection in a population-based study among 9733 older adults.

PURPOSE: Moderate alcohol consumption has been suggested to facilitate the elimination of Helicobacter pylori infection as the result of its antibacterial effect. We aimed to assess the associations of current and lifetime alcohol consumption as well as serum gamma-glutamyltransferase (GGT), an established biomarker of alcohol consumption, with H. pylori infection in a large population-based study. METHODS: In the baseline examination of the ESTHER study, serological measurements of antibodies against H. pylori and GGT measurements were taken in 9733 subjects ages 50 to 74 years. Information on lifestyle factors and medical history were obtained by self-administered standardized questionnaire. RESULTS: A significant inverse association, in dose-response manner, was observed between both current and lifetime alcohol consumption and H. pylori seropositivity. The estimates based on lifetime consumption were more pronounced than the results for current consumption, and such inverse associations were found both for men and women. Stronger relations were observed for those who only drank wine or mixed drinkers compare with those who only drank beer. Furthermore, there was a significant inverse dose-response relationship between serum GGT levels and H. pylori seropositivity, which was selectively observed among alcohol drinkers. CONCLUSIONS: In conclusion, our results support the hypothesis that moderate alcohol consumption may facilitate elimination of H. pylori.