Dietary nutrients during gestation cause obesity and related metabolic changes by altering DNA methylation in the offspring.

Growing evidence shows that maternal nutrition from preconception until lactation has an important effect on the development of non-communicable diseases in the offspring. Biological responses to environmental stress during pregnancy, including undernutrition or overnutrition of various nutrients, are transmitted in part by DNA methylation. The aim of the present narrative review is to summarize literature data on altered DNA methylation patterns caused by maternal macronutrient or vitamin intake and its association with offspring's phenotype (obesity and related metabolic changes). With our literature search, we found evidence for the association between alterations in DNA methylation pattern of different genes caused by maternal under- or overnutrition of several nutrients (protein, fructose, fat, vitamin D, methyl-group donor nutrients) during 3 critical periods of programming (preconception, pregnancy, lactation) and the development of obesity or related metabolic changes (glucose, insulin, lipid, leptin, adiponectin levels, blood pressure, non-alcoholic fatty liver disease) in offspring. The review highlights that maternal consumption of several nutrients could individually affect the development of offspring's obesity and related metabolic changes via alterations in DNA methylation.

The Effect of Holder Pasteurization and Different Variants on Breast Milk Antioxidants.

BACKGROUND: After birth, breast milk (BM) is a known essential source of antioxidants for infants. We analyzed the non-enzymatic total antioxidant capacity (TAC), oxygen radical absorbance capacity (ORAC), and glutathione, calcium, transferrin, and total protein levels of human breast milk before and after Holder pasteurization (HoP). METHODS: The collected donor BM samples were pasteurized with HoP. RESULTS: HoP decreased TAC (-12.6%), ORAC (-12.1%), transferrin (-98.3%), and total protein (-21.4%) levels; HoP did not influence the glutathione concentration, and it increased the total calcium (+25.5%) concentration. Mothers who gave birth via Cesarean section had significantly lower TAC in their BM. TAC and glutathione levels were elevated in the BM of mothers over the age of 30. BM produced in the summer had higher glutathione and calcium levels compared to BM produced in the winter. The glutathione concentration in term milk samples was significantly higher in the first two months of lactation compared to the period between the third and sixth months. The transferrin level of BM for female infants was significantly higher than the BM for boys, and mothers with a BMI above 30 had increased transferrin in their samples. CONCLUSIONS: Antioxidant levels in human milk are influenced by numerous factors. Environmental and maternal factors, the postpartum age at breast milk collection, and Holder pasteurization of the milk influence the antioxidant intake of the infant.

Insulin, Testosterone, and Albumin in Term and Preterm Breast Milk, Donor Milk, and Infant Formula.

BACKGROUND: Infants have three options for feeding: their own mother's breast milk, donor milk, or infant formula. Insulin, testosterone, total protein, and albumin levels were measured in breast milk samples from the first 6 months of lactation, in donor milk samples, and in different infant formulas. METHODS: Mothers who gave birth to term (n = 19) or preterm (n = 19) infants were recruited to collect breast milk samples during the first 6 months of lactation. The Breast Milk Collection Center (Unified Health Institution, Pécs, Hungary) provided 96 donor milk (DM) samples for analysis in our study. Insulin, testosterone, total protein, and albumin levels were measured in breast milk, donor milk, and infant formulas. RESULTS: During the first 2 months of lactation, the concentration of insulin was lower (-27.4%) while the testosterone concentration was higher (+20.8%) compared to the period between the 3rd and 6th months only in the preterm breast milk samples. The infant formulas examined did not contain insulin or testosterone. Holder pasteurization (HoP) did not influence the level of testosterone in human milk, although HoP decreased the insulin (-53.6%) and albumin (-38.6%) concentrations. CONCLUSIONS: Diet impacts the hormone intake of infants, underlining the importance of breastfeeding and the possible supplementation of formula-fed infants.

Epigenetic Effect of Maternal Methyl-Group Donor Intake on Offspring's Health and Disease.

Maternal exposure to some dietary and environmental factors during embryonic development can affect offspring's phenotype and, furthermore, the risk of developing diseases later in life. One potential mechanism responsible for this early programming may be the modification of the epigenome, such as DNA methylation. Methyl-group donors are essential for DNA methylation and are shown to have an important role in fetal development and later health. The main goal of the present review is to summarize the available literature data on the epigenetic effect (DNA methylation) of maternal methyl-group donor availability on reproductivity, perinatal outcome, and later health of the offspring. In our literature search, we found evidence for the association between alterations in DNA methylation patterns caused by different maternal methyl-group donor (folate, choline, methionine, betaine) intake and reproductivity, birth weight, neural tube defect, congenital heart defect, cleft lip and palate, brain development, and the development of obesity and associated non-communicable diseases in later life. We can conclude that maternal methyl-group donor availability could affect offspring's health via alterations in DNA methylation and may be a major link between early environmental exposure and the development of diseases in the offspring. However, still, further studies are necessary to confirm the associations and causal relationships.

Thyroxine and Thyroid-Stimulating Hormone in Own Mother's Milk, Donor Milk, and Infant Formula.

Breastfeeding is widely supported in clinical and home practices, and it is known that different forms of infant feeding differ in hormone content. Thyroid hormones have essential physiological roles. In our study, we examined thyroid-stimulating hormone (TSH), thyroxine, and albumin levels in breast milk produced for term (n = 16) or preterm (n = 15) infants throughout the first 6 months of lactation. Moreover, we analyzed these components in donor human milk and in three different infant formulas. Term and preterm breast milk samples were collected monthly. The two groups had similar levels of TSH (18.4 ± 1.4 vs. 24.7 ± 2.9 nU/L), but term milk contained higher amounts of thyroxine (11,245.5 ± 73.8 vs. 671.6 ± 61.2 nmol/L) during the examination period. The albumin level was significantly higher in preterm breast milk than in term breast milk (328.6 ± 17.1 vs. 264.2 ± 6.8 mg/L). In preterm breast milk we detected downward trends in the levels of TSH (-30.2%) and thyroxine (-29.2%) in the 3rd through 6th month compared to the first 2 months of lactation. Microbiological safety of donor milk was ensured by Holder pasteurization (HoP). From the Breast Milk Collection Center of Pécs, Hungary, we enrolled 44 donor mothers into the study. HoP decreased TSH (-73.8%), thyroxine (-22.4%), and albumin (-20.9%) concentrations. Infant formulas used by the Neonatal Intensive Care Unit of the University of Pécs were found to not contain the investigated hormones, but their albumin levels were similar to the breast milk samples. The present study shows the lack of thyroid hormones in infant formulas compared to human milk and raises the question of whether formula-fed infants should be supplemented with thyroid hormones.

Association of Gln223 Arg polymorphism of the leptin receptor gene with indicators of energy expenditure in obese children.

OBJECTIVE: Gln223 Arg polymorphism of the leptin receptor (LEPR) gene is one of the most frequently examined polymorphisms of this gene and has been suggested to be associated with energy expenditure (EE). The aim of the present study was to investigate the association of this variant on indicators of EE-resting metabolic rate (RMR), postabsorptive and postprandial respiratory quotient (RQ), and food-induced thermogenesis (FIT)-in obese children. METHODS: The study included 486 genotyped children (obese, n = 355). RMR was measured by indirect calorimetry for 45 min. Subsequent to test-food consumption, FIT was measured in a subsample of obese children (n = 121, body mass index 31.9 kg/m(2) (mean ± SD 5.1). RESULTS: Obese children with the Gln223 Gln genotype showed a significantly lower post-absorptive and postprandial RQ (P = 0.0055 versus P = 0.0002, adjusted for age, sex, and lean body mass) than did groups of children with Gln223 Arg and Arg223 Arg genotypes. No significant differences were observed in FIT and RMR among the carriers and non-carriers of the 223 Arg allele. CONCLUSION: The significantly lower post-absorptive and postprandial RQ in the group of Gln223 Gln genotype children indicates that the fat oxidation of these children maybe increased before and subsequent to food consumption, which can be important in the planning of diet of these children.

Associations between common genetic polymorphisms in the liver X receptor alpha and its target genes with the serum HDL-cholesterol concentration in adolescents of the HELENA Study.

OBJECTIVE: Genetic variability in the NR1H3 gene (encoding LXRα) and in several of its target genes is associated with serum HDL-cholesterol (HDL-C) concentrations. We sought to assess if these associations could be detected in adolescents. METHODS: Thirty-nine polymorphisms in NR1H3, ABCA1, APOE, CETP, PLTP and LPL were analysed in the HELENA study (n = 1144 European adolescents). RESULTS: The minor alleles of rs11039155 in NR1H3, rs2575879 in ABCA1, rs708272, rs17231506 and rs5882 in CETP and rs328 in LPL were associated with higher serum HDL-C concentrations (p ≤ 0.0012). The minor alleles of rs12221497 in NR1H3, rs1800978 in ABCA1 and the APOE ɛ4 allele were associated with lower HDL-C concentrations (p ≤ 0.01). The combined set of associated polymorphisms accounted for ∼6.6% of the variance in HDL-C. CONCLUSION: We report for the first time that polymorphisms in NR1H3 and its target genes ABCA1, APOE, CETP and LPL contribute to the genetic variance for HDL-C concentrations in adolescence.

Haplotype analysis of the apolipoprotein A5 gene in obese pediatric patients.

OBJECTIVE: Apolipoprotein A5 (APOA5) gene variants have been shown to be associated with elevated TG levels; the T-1131C (rs662799) variant has been reported to confer risk for the metabolic syndrome in adult populations. Little is known about the APOA5 variants in pediatric population, no such information is available for pediatric obesity at all. Here we examined four haplotype-tagging polymorphisms (T-1131C, IVS3 + G476A [rs2072560], T1259C [rs2266788] and C56G [rs3135506]) and studied also the frequency of major naturally occurring haplotypes of APOA5 in obese children. METHODS: The polymorphisms were analyzed in 232 obese children, and in 137 healthy, normal weight controls, using PCR-RFLP methods. RESULTS: In the pediatric patients we could confirm the already known adult subjects based association of -1131C, IVS3 + 476A and 1259C variants with elevated triglyceride concentrations, both in obese patients and in the controls. The prevalence of the APOA5*2 haplotype (containing the minor allele of T-1131C, IVS3 + G476A and T1259C SNPs together) was 15.5% in obese children, and 5.80% in the controls (p<0.001); multiple logistic regression analysis revealed that this haplotype confers susceptibility for development of obesity (OR=2.87; 95% CI: 1.29-6.37; p≤0.01). By contrast, the APOA5*4 haplotype (with -1131C alone) did not show similar associations. Our findings also suggest that the APOA5*5 haplotype (1259C alone) can be protective against obesity (OR=0.25; 95% CI: 0.07-0.80; p<0.05). CONCLUSIONS: While previous studies in adults demonstrated, that the APOA5 -1131C minor allele confers risk for adult metabolic syndrome, here we show, that the susceptibility nature of this SNP restricted to the APOA5*2 haplotype in pediatric obese subjects.

Common polymorphisms in six genes of the methyl group metabolism pathway and obesity in European adolescents.

OBJECTIVE: The goal of the present study was to assess the relationship between the genetic variability in six genes of methyl group (CH(3)) metabolism and the risk of obesity. METHODS: Single nucleotide polymorphisms (SNP) were selected among the methylene-tetrahydrofolate reductase (MTHFR), methionine synthase (MTR), methionine synthase reductase (MTRR), cystationine betha-syntase (CBS), transcobalamin-II (TCN2) and paraoxonase-1 (PON1) genes. The associations between SNPs and the risk of obesity were assessed in a case-control study of obese and normal-weight adolescents (age: 14.9±1.2 years), and the relationship between SNPs and body fat markers (i.e., body mass index [BMI], percentage body fat [BF%] and waist circumference [WC]) in a cross-sectional study of 1 155 European adolescents (age: 14.8±1.4 years). Genotyping was performed on an Illumina system and plasma folate level was determined by immunoassay. RESULTS: In the case-control study, there was no evidence for any association between SNPs of MTHFR, MTR, CBS, TCN2 and PON1 and obesity (all p values ≥0.08). In contrast, two SNPs of MTRR were associated with a higher (rs10520873, Odds Ratio: 1.68 [1.18-2.39]; p=0.004) or lower (rs1801394, 0.61 [0.42-0.87]; p=0.007) risk of obesity. In the cross-sectional sample, rs1801394 was associated with lower BMI (p=0.03) and lower waist circumference (p=0.02). However, after Bonferroni correction these associations were no longer significant. No other significant association or interaction between folate levels and SNPs were detected for anthropometric variables. CONCLUSION: Our findings do not support an association between MTHFR, MTR, CBS, TCN2 and PON1 SNPs and obesity in adolescence. Further investigations are necessary to confirm the possible association between the rs1801394 variant of MTRR and obesity.

Attenuation of the effect of the FTO rs9939609 polymorphism on total and central body fat by physical activity in adolescents: the HELENA study.

OBJECTIVE: To examine whether physical activity attenuates the effect of the FTO rs9939609 polymorphism on body fat estimates in adolescents. DESIGN: Cross-sectional study. SETTING: Athens, Greece; Dortmund, Germany; Ghent, Belgium; Heraklion, Greece; Lille, France; Pécs, Hungary; Rome, Italy; Stockholm, Sweden; Vienna, Austria; and Zaragoza, Spain, from October 2006 to December 2007. PARTICIPANTS: Adolescents from the Healthy Lifestyle in Europe by Nutrition in Adolescence Cross-Sectional Study (n = 752). MAIN EXPOSURE: Physical activity. MAIN OUTCOME MEASURES: The FTO rs9939609 polymorphism was genotyped. Physical activity was assessed by accelerometry. We measured weight, height, waist circumference, and triceps and subscapular skinfolds; body mass index (BMI [calculated as weight in kilograms divided by height in meters squared]) and body fat percentage were calculated. RESULTS: The A allele of the FTO polymorphism was significantly associated with higher BMI (+0.42 per risk allele), higher body fat percentage (+1.03% per risk allele), and higher waist circumference (+0.85 cm per risk allele). We detected significant or borderline gene x physical activity interactions for the studied body fat estimates (for interaction, P = .02, .06, and .10 for BMI, body fat percentage, and waist circumference, respectively). Indeed, the effect of the FTO rs9939609 polymorphism on these body fat parameters was much lower in adolescents who met the daily physical activity recommendations (ie, >/=60 min/d of moderate to vigorous physical activity) compared with those who did not: +0.17 vs +0.65 per risk allele in BMI, respectively; +0.40% vs +1.70% per risk allele in body fat percentage, respectively; and +0.60 vs +1.15 cm per risk allele in waist circumference, respectively. CONCLUSION: Adolescents meeting the daily physical activity recommendations may overcome the effect of the FTO rs9939609 polymorphism on obesity-related traits.

Single nucleotide polymorphisms in the FADS gene cluster are associated with delta-5 and delta-6 desaturase activities estimated by serum fatty acid ratios.

Genetic variability in the FADS1-FADS2 gene cluster [encoding delta-5 (D5D) and delta-6 (D6D) desaturases] has been associated with plasma long-chain PUFA (LCPUFA) and lipid levels in adults. To better understand these relationships, we further characterized the association between FADS1-FADS2 genetic variability and D5D and D6D activities in adolescents. Thirteen single nucleotide polymorphisms (SNPs) were genotyped in 1,144 European adolescents (mean +/- SD age: 14.7 +/- 1.4 y). Serum phospholipid fatty acid levels were analyzed using gas chromatography. D5D and D6D activities were estimated from the C20:4n-6/C20:3n-6 and C20:3n-6/C18:2n-6 ratios, respectively. Minor alleles of nine SNPs were associated with higher 18:2n-6 levels (1.9E-18

Breast-feeding modulates the influence of the peroxisome proliferator-activated receptor-gamma (PPARG2) Pro12Ala polymorphism on adiposity in adolescents: The Healthy Lifestyle in Europe by Nutrition in Adolescence (HELENA) cross-sectional study.

OBJECTIVE: The peroxisome proliferator-activated receptor-gamma2 (PPARG2) Pro12Ala polymorphism has been associated with a higher BMI and a lower risk of type 2 diabetes in adulthood. The association between adiposity and PPARG variants can be influenced by environmental factors such as early growth, dietary fat, and (as recently shown) breast-feeding. The objectives of this study were to assess 1) the influence of the PPARG2 Pro12Ala polymorphism on adiposity markers in adolescents and 2) a possible modulating effect of breast-feeding on these associations. RESEARCH DESIGN AND METHODS: Data on breast-feeding duration, BMI, and genotypes for the Pro12Ala polymorphism were available for 945 adolescents (mean age 14.7 years). The breast-feeding duration was obtained from parental records. We measured weight, height, waist circumference, and six skinfold thicknesses. RESULTS: No significant associations between the Pro12Ala polymorphism and any of the above-mentioned anthropometric parameters were found. There were significant interactions between the PPARG2 Pro12Ala polymorphism and breast-feeding with regard to adiposity measurements (all adjusted P < 0.05). Indeed, in children who had not been breast-fed, Ala12 allele carriers had higher adiposity parameters (e.g., Delta BMI +1.88 kg/m(2), adjusted for age, sex, and center, P = 0.007) than Pro12Pro adolescents. In contrast, in breast-fed subjects, there was no significant difference between Ala12 allele carriers and Pro12Pro children in terms of adiposity measurements, whatever the duration of breast-feeding. CONCLUSIONS: Breast-feeding appears to counter the deleterious effect of the PPARG2 Pro12Ala polymorphism on anthropometric parameters in adolescents.

Single-nucleotide polymorphism of CD36 locus and obesity in European adolescents.

CD36 is a membrane receptor with a wide variety of functions, including the regulation of energy metabolism, fat storage, and adipocyte differentiation. To assess the relationship between CD36 gene single-nucleotide polymorphisms (SNPs) and obesity in adolescents, we evaluated the relationship between CD36 SNPs and the risk of obesity in a case-control study composed of 307 obese (age = 15.0 +/- 1.1 years) and 339 normal-weight adolescents (age = 14.6 +/- 1.1 years). To validate the results, we assessed the relation between the same SNPs and percentage of body fat (BF%) and BMI in 1,151 European adolescents (age = 14.8 +/- 1.4 years). SNPs with a minor allele frequency >0.10 were selected to tag CD36. Genotyping was performed on an Illumina system. Four SNPs (rs3211867, rs3211883, rs3211908, and rs1527483) were associated with increased risk of obesity in the case-control study (odds ratio (OR) (95% confidence interval)): 1.96 (1.26-3.04], P = 0.003; 1.73 (1.16-2.59), P = 0.007; 2.42 (1.47-4.01), P = 0.0005 and 1.95 (1.25-3.05), P = 0.003, respectively). The same four SNPs were associated with higher BMI (P < 0.05) and BF% (P < 0.04) in the validation study. Further analyses identified a haplotype (frequency: 0.05) carrying the minor allele of these SNPs as being associated with obesity (OR: 2.28; P = 0.0008) in the case-control study and with excess adiposity (i.e., higher BF% (P = 0.03) and BMI (P = 0.04)) in the validation study. Our data suggest that genetic variability at the CD36 gene locus could be associated with body weight variability in European adolescents but these findings require replication.

Associations between common genetic polymorphisms in angiopoietin-like proteins 3 and 4 and lipid metabolism and adiposity in European adolescents and adults.

CONTEXT: Plasma-borne angiopoietin-like proteins (ANGPTL) act as endocrine factors on their target tissues. Because ANGPTL3 and ANGPTL4 play important roles in lipid metabolism and the regulation of adiposity in mice, we hypothesized that genetic variability at the ANGPTL3 and ANGPTL4 genes loci might influence lipid metabolism and fat deposition in humans. OBJECTIVE: The aim of the study was to examine the association between ANGPTL3 and ANGPTL4 genetic polymorphisms and metabolic phenotypes in adolescent and adult samples. DESIGN AND PARTICIPANTS: Two independent population-based studies, one composed of 1144 adolescents (mean age, 14.8 +/- 1.4 yr) from nine European countries (the HELENA study) and the other composed of 1155 adults (age range, 35-65 yr) from Northern France (the MONICA Lille study), were genotyped for one ANGPTL3 polymorphism and four ANGPTL4 polymorphisms. RESULTS: The ANGPTL3 rs11207997 polymorphism (minor allele frequency, 0.32) was associated with lower plasma HDL-cholesterol and apolipoprotein A-I levels in both adolescents (P = 0.0004, P = 0.00006, respectively) and adults (P = 0.03, P = 0.02, respectively). The ANGPTL4 rs4076317 polymorphism (minor allele frequency, 0.29) was associated with a higher percentage of body fat (P = 0.02) in adolescents and a higher waist-to-hip ratio (in interaction with the peroxisome proliferator-activated receptor gamma Pro12Ala polymorphism) in adults (P = 0.0004). CONCLUSION: The present study underlines the role of ANGPTL3 in HDL-cholesterol metabolism as early as in adolescence. Our data also suggest possible associations between ANGPTL4 polymorphisms and body fat, but these findings require replication.

Obesity related programming statements in infant feeding policies in five European countries.

The aim of this study was to know how the early nutrition programming concept and its relation with long-term diseases such as obesity is reflected in policy recommendations on infant nutrition in five European countries (Finland, Germany, Hungary, Spain and England). After collating and evaluating infant nutrition policy documents, statements about early nutrition programming, as the origin of diseases such as obesity, were analysed. The number of policy documents analysed were 38 (England: 10, Finland: 2, Germany: 11, Hungary: 8, Spain: 7) with a total of 455 statements identified and categorized into 53 different health outcomes. Obesity was mentioned in 5.5% (n = 25) of the statements, the third most frequent outcome after allergy (14.1%, n = 64) and health in general (5.7%, n = 26). Twenty six percent (n = 6) of the obesity related statements referred to short-term duration of the effects, 48% (n = 12) to medium-term, 24% (n = 6) to long-term effects and the rest were not identified. Only 22% of the obesity statements were evidence based. The link between infant feeding and obesity is integrated into policy documents, but most of the statements did not fully specify the short, medium and long term health implications. Action may be required to keep documents up to date as new evidence emerges and to ensure the evidence base is properly recorded.

Prevalence of metabolic syndrome in European obese children.

UNLABELLED: The rapid rising prevalence of childhood obesity is related to increased risk of obesity-related diseases during adulthood. The aim of the present study was to review the data concerning the prevalence of metabolic syndrome (MS) in European children and adolescents (Part 1) and to determine and compare the prevalence of MS among overweight and obese children, and adolescents in five European countries using four MS definitions (Part 2). In total, 1 241 European obese children from five different countries (France: n =283, Greece: n =145, Italy: n =274, Poland: n =90, and Hungary: n =449) were studied for MS according to the definition of Ferranti et al., the World Health Organisation, the National Cholesterol Education Program and the International Diabetes Federation. We used age- and sex-specific cut-off values for the diagnosis of high blood pressure and increased waist circumference. The prevalence of MS was 35.7%, 31.4%, 20.3%, and 16.4%, respectively, according to the above-mentioned definitions. Only 6.3-8.8% of obese adolescents were free from any risk factors and the clustering of three risk factors or more was very high: 20.3-35.7% (depending on the type of definition). A total of 12.2% of children had MS and 55.8% were free from MS according to all four definitions. CONCLUSIONS: The prevalence of MS is high among European obese children whatever criteria are used. There is an urgent need to achieve consensus concerning the definition of MS in adolescents and children.

Association of n-6 long-chain polyunsaturated fatty acids to -866 G/A genotypes of the human uncoupling protein 2 gene in obese children.

AIM: To investigate the association of plasma fatty acids with the -866 G/A polymorphism of uncoupling protein 2 (UCP2) in obese children. METHODS: Fatty acid composition of plasma phospholipids and sterol esters were investigated in 80 obese children. RESULTS: Values of dihomo-gamma-linolenic acid (C20:3n-6) were significantly lower in children with the -866 A/A (n = 12) than in those with the -866 G/A (n = 34) or -866 G/G (n = 34) genotype in plasma phospholipids (3.01 [0.42] vs. 3.56 [1.02] vs. 3.53 [0.84], % weight/weight, median [interquartile range], p < 0.05), and were significantly lower in children with the -866 A/A genotype than in the other two groups in plasma sterol esters (0.73 [0.22] vs. 0.92 [0.23] vs. 0.94 [0.25], p < 0.05). Phospholipid C20:3n-6 and arachidonic acid (C20:4n-6) values showed only in children with the -866 G/G and -866 G/A genotypes significant positive correlations with plasma insulin concentrations. CONCLUSIONS: Significantly lower values of C20:3n-6 can be detected in obese children with the homozygous (-866 A/A) mutation of UCP2 than in equally obese children with heterozygous mutation or the normal genotype. High glucose-stimulated insulin response is associated with high plasma C20:3n-6 and C20:4n-6 values only in obese children with the G allele of the -866 G/A polymorphism.

Association of n-3 and n-6 long-chain polyunsaturated fatty acids in plasma lipid classes with inflammatory bowel diseases.

In order to establish the biochemical basis for dietary interventions, we investigated the fatty acid composition of plasma lipid classes in patients with inactive inflammatory bowel disease. In this cross-sectional study thirty patients with ulcerative colitis (UC), twenty-one with Crohn disease (CD) and twenty-four controls were investigated (mean age: UC, 40.8 (sd 12.1); CD, 37.6 (sd 11.0); control, 31.5 (sd 8.4) years). Fatty acid composition of plasma lipids was determined by high-resolution capillary GLC. In plasma phospholipids, significantly higher values of eicosapentaenoic (20 : 5n-3), docosapentaenoic (22 : 5n-3) and gamma-linolenic (18 : 3n-6) acids were found in control patients and patients with UC as compared to patients with CD [median % (weight by weight), control v. UC v. CD : 20 : 5n-3, 0.09 (interquartile range (IQR) 0.05) v. 0.14 (IQR 0.10) v. 0.16 (IQR 0.10), P < 0.05; 22 : 5n-3, 0.14 (IQR 0.10) v. 0.27 (IQR 0.16) v. 0.31 (IQR 0.10), P < 0.001; 18 : 3n-6, 0.02 (IQR 0.02) v. 0.03 (IQR 0.02) v. 0.05 (IQR 0.03), P < 0.05]. When compared to the control, values of the principal n-3 and n-6 long-chain PUFA, arachidonic acid (20 : 4n-6) and DHA (22 : 6n-3) were significantly higher in patients with UC but not in patients with CD [median % (w/w), UC v. control: 20 : 4n-6, 8.43 (IQR 3.23) v. 6.92 (IQR 2.96), P < 0.05; 22 : 6n-3, 1.22 (IQR 0.56) v. 0.73 (IQR 0.39), P < 0.05]. As seen there are considerable differences between the long-chain PUFA status of patients suffering from UC or CD. The data obtained in the present study do not support the concept of eicosapentaenoic acid or DHA deficiency in patients with either UC or CD.

Systematic review of fatty acid composition of human milk from mothers of preterm compared to full-term infants.

BACKGROUND: Fatty acid composition of human milk serves as guidance for the composition of infant formulae. The aim of the study was to systematically review data on the fatty acid composition of human milk of mothers of preterm compared to full-term infants. METHODS: An electronic literature search was performed in English (Medline and Medscape) and German (SpringerLink) databases and via the Google utility. Fatty acid compositional data for preterm and full-term human milk were converted to differences between means and 95% confidence intervals. RESULTS: We identified five relevant studies publishing direct comparison of fatty acid composition of preterm versus full-term human milk. There were no significant differences between the values of the principal saturated and monounsaturated fatty acids. In three independent studies covering three different time points of lactation, however, docosahexaenoic acid (DHA) values were significantly higher in milk of mothers of preterm as compared to those of full-term infants, with an extent of difference considered nutritionally relevant. CONCLUSION: Higher DHA values in preterm than in full-term human milk underlines the importance of using own mother's milk for feeding preterm babies and raises the question whether DHA contents in preterm formulae should be higher than in formulae for full-term infants.

[Genetic markers and personality traits in eating disorders--preliminary results]. / Genetikai és személyiségfaktorok vizsgálata evészavarokban.

INTRODUCTION: The multidimensional approach of the ethiopathogenesis of eating disorders include the genetic, biologic, psychosocial effects, and premorbid personality markers. AIM/METHOD: To determine the potential relation between genetic and personality trate and state factors, and also to investigate the connection of clinical symptoms and diagnostic subgroups. The serotonin transporter gene (VNTR) polymorphism was investigated by polymerase chain reaction (PCR) technology, the personality factors were determined by the Temperament and Character Inventory (TCI) inventory. RESULTS: Among patients with bulimia nervosa (BN) the short allele of serotonin transporter gene was more frequent than in anorexia nervosa (78% vs. 67%), and in both groups it was more common than in the general population (43%). Patients with anorexia nervosa (AN) have higher scores in the scale of harm avoidance (61,2 vs. 51.4), but in bulimia nervosa the novelty seeking (54.5 vs. 44.2) and the reward dependence factors (53.2 vs. 46.5) were more significant. In the self-directedness (BN: 42.7; AN: 44.3) and the cooperativeness scales (BN: 51.2; AN: 44.6) both groups show lower scores, which could implicate personality disorder in the background of the eating disorders. Anorexic patients with the 10 allele show similar personality factors like patients with bulimia nervosa, while with the 12 allele (homozygotes), their factors were more likely the factors of patients with classic anorexic symptoms. CONCLUSION: Our data strength the role of specific personality factors in the background of the symptoms of eating disorders. Among patients with bulimia nervosa the 10 allele were more frequent, which could indicate the role of the serotonin system in developing eating disorders. Two subgroups were differentiated among patients with anorexia nervosa in relation with personality factors; the factors of patients with the 12 allele homozygotes were similar to the classical factors of anorexia nervosa, while patients with the 10 allele were like bulimic patients. Our results could improve our knowledge with newer aspects concerning the etiology of eating disorders, that might be used in broadening our preventive and therapeutic facilities in the future.